Functional Magnetic Resonance Imaging (fMRI) in Neuroradiology:

Brain chrischan 600

Brain chrischan 600 (Photo credit: Wikipedia)

BOLD fMRI paradigms generally have several periods of rest alternating with several periods of activation. Images are then compared over the entire activation to the rest periods. Images obtained over the first 3 to 6 seconds of each period are generally discarded due to the delay in hemodynamic response. Alternating paradigms are used because the signal intensity generated by the MRI scanner drifts with time.

fMRI BOLD is best used for studying processes that can be rapidly turned on and off like language, vision, movement, hearing and memory. The study of emotion is hampered by its slow and variable onset and its inability to be quickly reversed. Some have, however, succeeded in using this technique to study emotional processes.

BOLD fMRI is very sensitive to movement so that tasks are limited to those without head movement, including speaking. BOLD fMRI is also limited in that artifacts are often present in brain regions that are close to air (ie. sinuses). Thus there are some problems in observing important emotional regions at the base of the brain like the orbitofrontal and medial temporal cortices. Another problem is that sometimes observed areas of activation may be located more in areas near large draining veins rather than directly at a capillary bed near the site of neuronal activation. Neurologists and neurosurgeons are beginning to use this technique clinically to noninvasively map language, motor and memory function in patients undergoing neurosurgery.

The secondary somatosensory cortex is colored ...

The secondary somatosensory cortex is colored green and the insular cortex brown in the top right portion of this image of the human brain. Primary somatosensory cortex is green in the top left. (Photo credit: Wikipedia)

Two fMRI methods have been developed for measuring cerebral blood flow. The first method, called intravenous bolus tracking, relies on the intravenous (iv) injection of a magnetic compound such as a gadolinium-containing contrast agent and measuring its T2 weighted signal as it perfuses through the brain over a short time period of time.

Areas perfused with the magnetic compound show less signal intensity as the compound creates a magnetic inhomogeneity that decreases the T2 signal. The magnetic compound may be injected once during the control and once during the activation task and relative differences in blood flow between the two states may be determined to develop a perfusion image. Alternatively one can measure changes in blood few over time over time after a single injection to generate a perfusion map.

Although gadolinium-based contrasts are not radioactive, the number of boluses that can be given to an individual is limited by the potential for kidney toxicity with repeated tracer administration. This technique also only generates a map of relative cerebral blood flow, not absolute flow as in the text technique. Arterial spin labeling is a T1 weighted noninvasive technique where intrinsic hydrogen atoms in arterial water outside of the slice of interest are magnetically tagged (“flipped”) as they course through the blood and are then imaged as they enter the slice of interest.

Brain scanning technology is quickly approachi...

Brain scanning technology is quickly approaching levels of detail that will have serious implications (Photo credit: Wikipedia)

Arterial spin labelling is noninvasive, does not involve an IV bolus injection, and can, thus, be repeatedly performed in individual subjects. Also, absolute regional blood flow can be measured which cannot be easily measured with SPECT or BOLD fMRI and requires an arterial line with PET. As absolute information is obtained, cerebral blood flow can be serially measured over separate imaging sessions such as measuring blood flow in bipolar subjects as they course through different disease states. Absolute blood flow information may be important in imaging such processes as anxiety which may be hard to turn on and off. For instance, in social phobics, a relaxation task may be imaged on one day and anticipating making a speech may be imaged on the next day. Comparing these separate tasks in different imaging sessions would not be possible with BOLD fMRI. Arterial spin labelling has some limitations in that it takes several minutes to acquire information on a single slice of interest. Therefore, one must have a specific brain region that one is interested in examining. Also, as it currently takes several minutes to acquire a single slice, it would be tedious obtaining enough images on this slice within a single session to make a statistical statement on a given subject.Brain scanning technology is quickly approaching levels of detail that will have serious implications (Photo credit: Wikipedia)

2. Diffusion-Weighted Imaging (DWI)

Diffusion-weighted imaging is very sensitive to the random movement of 1 H in water molecules (Brownian movement). The amount of water diffusion for a given pixel can be calculated and is called the apparent diffusion coefficient (ADC). Areas with low ADC value (ie. low diffusion) appear more intense. ADC values are direction sensitive. For instance, if images are taken perpendicular to myelin fiber tracts like the optic chiasm, arcuate fasciculus, or corpus callosum, ADC values will be lower than if the images are taken along the length of these fibers. This is thought to because there is little diffusion across myelin sheaths. Thus, ADC direction sensitivity permits detection of Myelination and may allow researchers to understand in greater detail myelin development in infants. On the other hand, this direction sensitivity hampers the study of diffusion in other processes as ADC values differ, depending on the imaging plane (axial, coronal or sagittal). There are now ways to calculate average ADC values incorporating all planes for each pixel, removing “artifacts” due to the direction of acquisition. Removing the directional diffusion sensitivity has been helpful in studying stroke.

While it is currently unclear now diffusion-weighted imaging will be useful in studying psychiatric disorders, it hold great promise for changing the clinical management of acute ischaemic stroke by potentially refining the criteria for patients most likely to benefit from thrombolytic therapy.

3. MRI Spectroscopy (MRS):

MRI spectroscopy (MRS) offers the capability of using MRI to noninvasively study tissue biochemistry. In the conventional and functional MRI techniques listed. The hydrogen atom in water is the main one that is flipped (resonated). In MRS, either 1H atoms in other molecules or other atoms such as 31P, 23Na, K, 19F or Li are flipped. Within a given brain region called a voxel, information on these molecules is usually presented as a spectrograph with precession frequency on the x-axis revealing the identity of a compound and intensity on the y-axis, which helps quantify the amount of a substance. The quantity of a substance is related is related to the area under its spectrographic peak; the larger the area, the more of a substance that is present.

The reason why several molecules can be identified and quantified within a single scan is that the resonant magnetic pulse has a bandwidth over a narrow precession frequency range os that it can flip several molecules at once. The signal intensity at each of these precession frequencies can then be identified using a complicated mathematical procedure called a Fourier transform. For a given precession frequency (or spectrographic peak of a given molecule), information can also be presented spatially as metabolic maps which are created with similar principles to the 1H atom in water spatial map in conventional MRI. The spatial resolution of these maps is generally less than that of conventional MRI as the substance concentration is much less than that of water. Consequently, the minimum area needed to obtain a visible signal is greater.

The two most widely used MRS techniques involve either viewing 1H atoms in molecules other than water or 31P-containing molecules. In 1H MRS, the water signal must first be suppressed as it is much greater than the signal from other 1H-containing compounds and has overlapping spectroscopic peaks with compounds.

Compounds that can be resolved with 1H-MRS include:

a) N-acetylaspartate (NAA) which is though to be a neuronal marker that decreases in processes where neurons die;

b) Lactate which is a product of anaerobic metabolism and may indicate hypoxia;

c) Excitatory neurotransmitters glutamate and aspartate;

d) The inhibitory neurotransmitter gamma-amino butyric acid (GABA);

e) Cytosolic choline which includes primarily mobile molecules involved in phospholipid membrane metabolism but also small amounts of the neurotransmitter acetylcholine and its precursor choline;

1. Myolinositol which is important in phospholipoid metabolism and intracellular second messenger systems; and

2. Creatine molecules such as creatine and phosphocreatine which usually have relatively constant concentrations throughout the brain and are often used as relative reference molecules (ie. one may see NAA concentration reported as the ratio NAA/creatine in the literature).

Phosphorus (31P) MRS allows the quantification of ATP metabolism, intracellular pH, and phospholipid metabolism. Mobile phospholipid, including phosphomonoesters (PME – putative cell membrane building blocks) and phosphodiesters (PDE – putative cell membrane breakdown products) can also be measured, supplying information on phospholipid membrane metabolism.

MRS is an useful tool to be used in the characterization of tumor, stroke and epileptogenic tissue and in presurgical planning.

Limitations

MRS is restricted to studying mobile magnetic compounds. As neurochemical receptors are noted usually mobile, they cannot be measured with MRS. Thus, receptor-ligand studies in psychiatry are still the domain of SPECT and PET. Another problem with MRS is that due to the low concentrations of many of the imaged substances, larger areas than with water are needed to obtain detectable signals. Larger volume units imaged over longer periods are thus used with this technique, limiting both temporal and spatial resolution compared with conventional MRI and BOLD-fMRI. However, stronger magnetic fields which can spread out precession frequencies over a wider range may improve this resolution.

Conclusions

While there are currently no clinical indications for ordering any of these fMRI techniques, they hold considerable promise for unraveling the neurocircuitry and metabolic pathways of numerous disorders in the immediate future and in further helping in diagnosis and treatment planning.

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Anatomy of the Cerebral Venous System & Dural sinuses

Revised diagram of cranial sinuses (in the hum...
Image via Wikipedia

Anatomy of the Cerebral Venous System & Dural sinuses

Authors: Himadri S. Das, P.Hatimota, P.Hazarika, C.D.Choudhury,

Institution: Matrix, 1st Byelane Tarun Nagar, G.S.Road, Guwahati-5

cerebral venous sinus anatomy.paper IRIA 2009.ghy

Address for Correspondence:

Dr Himadri Sikhor Das, MD, PDCC

Matrix, 1st Byelane Tarun Nagar

, G.S.Road, Near Rajiv Bhawan

Guwahati-781005

Tel:+0361-2464969

Email: drhsdas@gmail.com

Abstract:

Cerebral venous system can be divided into superficial and deep systems. The superficial system comprises of sagittal sinuses and cortical veins and these drain superficial surfaces of both cerebral hemispheres. The deep system comprises of lateral sinus, straight sinus and sigmoid sinus along with draining deeper cortical veins. Both these systems mostly drain themselves into internal jugular veins. The veins draining the brain do not follow the same course as the arteries that supply it. Generally, venous blood drains to the nearest venous sinus, except in the case of that draining from the deepest structures, which drain to deep veins. These drain, in turn, to the venous sinuses. The superficial cerebral veins can be subdivided into three groups. These are interlinked with anastomotic veins of Trolard and Labbe. However, the superficial cerebral veins are very variable. They drain to the nearest dural sinus.  The superolateral surface of the hemisphere drains to the superior sagittal sinus while the posteroinferior aspect drains to the transverse sinus. The veins of the   posterior fossa are variable in course and angiographic diagnosis of their occlusion is extremely difficult. Blood from the deep white matter of the cerebral hemisphere and from the

basal ganglia are drained by internal cerebral and basal veins, which join to form the great vein of Galen that drains into the straight sinus. With the exception of wide variations of basal vein, the deep system is rather constant compared to the superficial venous system. Hence their thrombosis is easy to recognize.

Key Words: Cerebral veins, MR, Venogram, thrombosis, TOF

Introduction

Cerebral venous system can be divided into two basic components.

A) Superficial System;

The superficial system comprises of sagittal sinuses and cortical veins and these drain superficial surfaces of both cerebral hemispheres.

B) Deep System;

The deep system comprises of lateral sinus, straight sinus and sigmoid sinus along with draining deeper cortical veins. Both these systems mostly drain themselves into internal Jugular veins.

A) Superficial cerebral venous system

The superficial cerebral veins (Figure1 and 2) can be divided into three collecting systems. First, a mediodorsal group draining into superior sagittal sinus (SSS) and the straight sinus (SS); Second, a lateroventral group draining into the lateral sinus; and third, an anterior group draining into the cavernous sinus. These veins are linked by the great anastomotic vein of Trolard, which connects the SSS to the middle cerebral veins. These are themselves connected to the lateral sinus (LS) by the vein of Labbe. The veins of the posterior fossa may again be divided into three groups:

1) Superior group draining into the Galenic system,

2) Anterior group draining into Petrosal sinus and

3) Posterior group draining into the torcular Herophili and neighboring transverse sinuses.

The veins of the posterior fossa are variable in course and angiographic diagnosis of their occlusion is extremely difficult. The Superior Sagittal Sinus (SSS) (Figure 3) starts at the foramen caecum and runs backwards towards the internal occipital protuberance, where it joins with the straight sinus and lateral sinus to form the torcular Herophili. Its anterior part is narrow or sometimes absent, replaced by two superior cerebral veins that join behind the coronal suture.

This fact should be borne in mind while evaluating for cerebral venous thrombosis (CVT). The SSS drain major part of the cerebral hemispheres. The cavernous sinuses drain blood from the orbits, the inferior parts of the frontal and parietal lobes and from the superior and inferior petrosal sinuses. Blood from them flow into the internal jugular veins.

The straight sinus is formed by the union of inferior sagittal sinus and the great vein of Galen. The inferior sagittal sinus runs in the free edge of falx cerebri and unites with the vein of Galen to form the straight sinus. It runs backwards in the center of the tentorium cerebelli at the attachment of the falx cerebri, emptying into the torcular Herophili at the internal occipital protuberance.

The lateral sinuses extend from torcular Herophili to jugular bulbs and consist of a transverse and sigmoid portion. They receive blood from the cerebellum, the brainstem and posterior parts of the hemisphere. They are also joined by some diploic veins and small veins from the middle ear. There are numerous LS anatomic variations that may be misinterpreted as sinus occlusion.

B) Deep cerebral venous system

The deep cerebral veins are more important than superficial veins from the angiographic point of view. Three veins unite just behind the interventricular foramen of Monro to form the internal cerebral vein (Figure 4). These include choroid vein, septal vein and thalamostriate vein. The Choroid vein runs from the choroid plexus of the lateral ventricle. The Septal vein runs from the region of the septum pellucidum in the anterior horn of the lateral ventricle and the thalamostriate vein runs anteriorly in the floor of the lateral ventricle in the thalamostriate groove between the thalamus and lentiform nucleus. The point of union of these veins is called the venous angle.

Revised diagram of cranial sinuses (in the hum...


The internal cerebral veins of each side run posteriorly in the roof of the third ventricle and unite beneath the splenium of the corpus callosum to form the great cerebral vein. The internal cerebral veins, which lie within 2 mm of the midline, are the most important deep veins since they can be used to diagnose midline shifts. The great cerebral vein of Galen is a short (1-2 cm long), thick vein that passes posterosuperiorly behind the splenium of corpus callosum in the quadrigeminal cistern. It receives the basal veins and the posterior fossa veins and drains to the anterior end of the straight sinus where this unites with the inferior sagittal sinus.

The basal vein of Rosenthal begins at the anterior perforated substance by the union of anterior cerebral vein, middle cerebral vein and the striate vein. The basal vein on each side passes around the midbrain to join the great cerebral vein. In summary, blood from the deep white matter of the cerebral hemisphere and from the basal ganglia, is drained by internal cerebral veins and basal veins of Rosenthal, which join to form the great vein of Galen that drains into the straight sinus (Figure 2). With the exception of wide variations of basal vein, the deep system is rather constant compared to the superficial venous system so their thrombosis is easy to recognize.

Specific features of Cerebral Venous System in Pathophysiology

of Cerebral Venous Thrombosis

The cerebral veins and sinuses neither have valves nor tunica muscularis. Because they lack valves, blood flow is possible in different directions. Moreover, the cortical veins are linked by numerous anastamoses, allowing the development of a collateral circulation and probably explaining the good prognosis of some cerebral venous thromboses. Lack of tunica muscularis permits veins to remain dilated. This is important in understanding the huge capacity to compensate even an extended occlusion. Venous sinuses are located between two rigid layers of duramater. This prevents their compression, when intracranial pressure rises. Superficial cortical veins drain into SSS against the blood flow in the sinus, thus causing turbulence in the blood stream that is further aggravated by the presence of fibrous septa at the inferior angle of the sinus.

Revised diagram of cranial sinuses (in the hum...
Image via Wikipedia

This fact explains greater prevalence of SSS thrombosis. In addition to draining most of the cerebral hemisphere, the superior sagittal sinus also receives blood from diploic, meningeal and emissary veins. Same is the case with other dural venous sinuses. This explains the frequent occurrence of CVT as a complication of infective pathologies in the catchments areas e.g. cavernous sinus thrombosis in facial infections, lateral sinus thrombosis in chronic otitis media and sagittal sinus thrombosis in scalp infections. The dural sinuses especially the SSS contain most of the arachnoid villi and granulations, in which absorption of CSF takes place. So dural sinus thrombosis blocks villi and leads to intracranial hypertension and papilloedema.

References

1. Sutton D., Stevens J.: Vascular Imaging in Neuroradiology in Textbook of radiology and Imaging, volume 2 by Churchill Livingstone New York 2003, pp1682-87.

2. Ryan S.P., Mc Nicholas M.M.J., Central Nervous system in Anatomy for diagnostic Imaging by W.B. Saunders Company Ltd. London. 1998, pp 77-80.

3. Kido DK, Baker RA, Rumbaugh Calvin L. Normal Cerebral Vascular Anatomy. In: Abrams Angiography, Vascular and Interventional Radiology by Abrams HL, Third Edition. Little, Brown and Company, Boston. USA. 1983 pp 257-68.

4. Meder JF, Chiras J. Roland J, Guinet P, Bracard S, Bargy F. Venous territories

of the brain. J Neuroradiol 1994; 21:118 – 33.

5. Einhaupl KM, Masuhr F.Cerebral Venous and Sinus thrombosis – an update Eur J Neurol 1994; 1: 109 – 26.

6. Huang, Y.P., and Wolf, B.S. Angiographic features of fourth ventricle tumors with special reference to the posterior inferior cerebellar artery. Am J Radiol. 1969; 107:543.

7. Hacker H: Normal Supratentorial veins and dural sinuses. In: Newton TH, Potts DG, eds: Radiology of Skull and Brain. Angiography. Book 3. St Louis: Mosby; 1974; 2:1851-77.

8. Weissleder R., Wittenberg J. Neurological Imaging in Primer of Diagnostic Imaging, Third Edition. Philadelphia: Mosby 2003: p 492.

9. Krayenbuhl HA, Yasargil MG. Cerebral Angiography (2nd ed.). London: Butterworth 1968.10. Dora F and Zileli T: Common Variations of the lateral and occipital sinuses at the confluence sinuum. Neuroradiology 1980; 20 : 23 – 7.

11. Taveras J.M..: Angiography in Neuroradiology Third Edition. Baltimore: Williams & Wilkins. 1996 pp 998.

12. Wolf, B.S., Newman, C.M. and Schlesinger, B. The diagnostic value of thedeep cerebral veins in cerebral angiography. Am J Radiol. 1962; 87:322.

13. Wolf B S, Huang Y P, Newman C.M. The superficial Sylvian venous drainage system. Am J Radiol. 1963; 89:398.

14. Wolf B S, Huang YP. The subependymal veins of the lateral ventricles. Am J Roentgenol Radium Ther Nucl Med. 1964; 91:406-26.

15. Parkash C, Bansal BC. Cerebral venous thrombosis. J Indian Acad Clin Med. 2000; 5: 55 – 61.

16. Kalbag RM, Woolf AL. Etiology of cerebral venous thrombosis in cerebral venous thrombosis publ. Ed Kalbagh RM, Wolf AL. Volume1. Oxford University Press London, 1967; pp 238.

17. Wasay M, Azeemuddin M. Neuroimaging of Cerebral Venous thrombosis. J Neuroimaging 2005; 15:118-28.

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Functional Magnetic Resonance Imaging (fMRI) in Neuroradiology:

DTI Color Map
Image via Wikipedia


Functional Magnetic Resonance Imaging (fMRI) in Neuroradiology:

Dr Himadri S.Das

First, the most commonly used fMRI technique called BOLD-fMRI (Blood-Oxygen-Level-dependent fMRI) potentially offers imaging with a temporal resolution on the order of 100 milliseconds and a spatial resolution of 1-2 millimeters, which is much greater than that of PET and SPECT scanning. This means that transient cognitive events can potentially be imaged and small structures like the amygdala can be more readily resolved. Most fMRI techniques are noninvasive and do not involve the injection of radioactive materials so that a person can be imaged repeatedly. This allows imaging of a patient repeatedly through different disease states or developmental changes Third, with fMRI, one can easily make statistical statements in comparing different functional states within an individual in a single session. Thus, fMRI may be of important use in understanding how a given individual’s brain functions and perhaps, in the future, making psychiatric diagnoses and treatment recommendations. It is in fact already starting to being used in presurgical planning to map vital areas like languages, motor function, and memory.

The four main applications of MRI for functional information can be categorized as :-

1. BOLD-fMRI which measures regional differences in oxygenated blood.

2. Perfusion fMRI which measures regional cerebral blood flow.

3. Diffusion-weighted fMRI which measures random movement of water molecules and

4. MRI spectroscopy, which can measure certain cerebral metabolites noninvasively.

1. BOLD-fMRI (Blood-Oxygen-Level-Dependent fMRI)

BOLD-fMRI is currently the most common fMRI technique

With this technique, it is assumed that an area is relatively more active when it has more oxygenated blood compared to another point in time. This is based on the principle that when a brain region is being used, arterial oxygenated blood will redistribute and increase to this area. This principle has one limitation: there is a time lag of 3-6 seconds between when brain region is activated and blood flow increases to it . During this time lag of 3-6 second, in fact, the activated areas experience relative decrease in oxygenated blood as oxygen is extracted by the active regional neurons. Afterward, the amount of blood flowing to the area far out weighs the amount of oxygen that is extracted so that oxygenated blood is now higher. Although images can be acquired every 100 msecs with echoplanar (a type of rapid acquisition) BOLD fMRI, this predictable but time varied delayed onset of the BOLD response limits the immediate temporal resolution to several seconds instead of the 100 msec potential. In the future, researchers may be able to improve the temporal resolution of fMRI by measuring the initial decrease in oxygenated blood with activation.

BOLD fMRI is a relative technique in that it must compare images taken during one mental state to another to create a meaningful picture. As images are acquired very rapidly (ie. a set of 15 coronal brain slices every 3 seconds is commonly) one can acquire enough images to measure the relative differences between two states to perform a statistical analysis within a single individual. Ideally, these states would differ in only one aspect so that everything is controlled for except the behavior in question.

BOLD fMRI paradigms generally have several periods of rest alternating with several periods of activation. Images are then compared over the entire activation to the rest periods. Images obtained over the first 3 to 6 seconds of each period are generally discarded due to the delay in hemodynamic response. Alternating paradigms are used because the signal intensity generated by the MRI scanner drifts with time.

fMRI BOLD is best used for studying processes that can be rapidly turned on and off like language, vision, movement, hearing and memory. The study of emotion is hampered by its slow and variable onset and its inability to be quickly reversed. Some have, however, succeeded in using this technique to study emotional processes.

BOLD fMRI is very sensitive to movement so that tasks are limited to those without head movement, including speaking. BOLD fMRI is also limited in that artifacts are often present in brain regions that are close to air (ie. sinuses). Thus there are some problems in observing important emotional regions at the base of the brain like the orbitofrontal and medial temporal cortices. Another problem is that sometimes observed areas of activation may be located more in areas near large draining veins rather than directly at a capillary bed near the site of neuronal activation. Neurologists and neurosurgeons are beginning to use this technique clinically to noninvasively map language, motor and memory function in patients undergoing neurosurgery.

Two fMRI methods have been developed for measuring cerebral blood flow. The first method, called intravenous bolus tracking, relies on the intravenous (iv) injection of a magnetic compound such as a gadolinium-containing contrast agent and measuring its T2 weighted signal as it perfuses through the brain over a short time period of time.

Areas perfused with the magnetic compound show less signal intensity as the compound creates a magnetic inhomogeneity that decreases the T2 signal. The magnetic compound may be injected once during the control and once during the activation task and relative differences in blood flow between the two states may be determined to develop a perfusion image. Alternatively one can measure changes in blood few over time over time after a single injection to generate a perfusion map.

Although gadolinium-based contrasts are not radioactive, the number of boluses that can be given to an individual is limited by the potential for kidney toxicity with repeated tracer administration. This technique also only generates a map of relative cerebral blood flow, not absolute flow as in the text technique. Arterial spin labeling is a T1 weighted noninvasive technique where intrinsic hydrogen atoms in arterial water outside of the slice of interest are magnetically tagged (“flipped”) as they course through the blood and are then imaged as they enter the slice of interest.

Arterial spin labelling is noninvasive, does not involve an IV bolus injection, and can, thus, be repeatedly performed in individual subjects. Also, absolute regional blood flow can be measured which cannot be easily measured with SPECT or BOLD fMRI and requires an arterial line with PET. As absolute information is obtained, cerebral blood flow can be serially measured over separate imaging sessions such as measuring blood flow in bipolar subjects as they course through different disease states. Absolute blood flow information may be important in imaging such processes as anxiety which may be hard to turn on and off. For instance, in social phobics, a relaxation task may be imaged on one day and anticipating making a speech may be imaged on the next day. Comparing these separate tasks in different imaging sessions would not be possible with BOLD fMRI. Arterial spin labelling has some limitations in that it takes several minutes to acquire information on a single slice of interest. Therefore, one must have a specific brain region that one is interested in examining. Also, as it currently takes several minutes to acquire a single slice, it would be tedious obtaining enough images on this slice within a single session to make a statistical statement on a given subject.

2. Diffusion-Weighted Imaging (DWI)

Diffusion-weighted imaging is very sensitive to the random movement of 1 H in water molecules (Brownian movement). The amount of water diffusion for a given pixel can be calculated and is called the apparent diffusion coefficient (ADC). Areas with low ADC value (ie. low diffusion) appear more intense. ADC values are direction sensitive. For instance, if images are taken perpendicular to myelin fiber tracts like the optic chiasm, arcuate fasciculus, or corpus callosum, ADC values will be lower than if the images are taken along the length of these fibers. This is thought to because there is little diffusion across myelin sheaths. Thus, ADC direction sensitivity permits detection of Myelination and may allow researchers to understand in greater detail myelin development in infants. On the other hand, this direction sensitivity hampers the study of diffusion in other processes as ADC values differ, depending on the imaging plane (axial, coronal or sagittal). There are now ways to calculate average ADC values incorporating all planes for each pixel, removing “artifacts” due to the direction of acquisition. Removing the directional diffusion sensitivity has been helpful in studying stroke.

While it is currently unclear now diffusion-weighted imaging will be useful in studying psychiatric disorders, it hold great promise for changing the clinical management of acute ischaemic stroke by potentially refining the criteria for patients most likely to benefit from thrombolytic therapy.

3. MRI Spectroscopy (MRS):

MRI spectroscopy (MRS) offers the capability of using MRI to noninvasively study tissue biochemistry. In the conventional and functional MRI techniques listed. The hydrogen atom in water is the main one that is flipped (resonated). In MRS, either 1H atoms in other molecules or other atoms such as 31P, 23Na, K, 19F or Li are flipped. Within a given brain region called a voxel, information on these molecules is usually presented as a spectrograph with precession frequency on the x-axis revealing the identity of a compound and intensity on the y-axis, which helps quantify the amount of a substance. The quantity of a substance is related is related to the area under its spectrographic peak; the larger the area, the more of a substance that is present.

The reason why several molecules can be identified and quantified within a single scan is that the resonant magnetic pulse has a bandwidth over a narrow precession frequency range os that it can flip several molecules at once. The signal intensity at each of these precession frequencies can then be identified using a complicated mathematical procedure called a Fourier transform. For a given precession frequency (or spectrographic peak of a given molecule), information can also be presented spatially as metabolic maps which are created with similar principles to the 1H atom in water spatial map in conventional MRI. The spatial resolution of these maps is generally less than that of conventional MRI as the substance concentration is much less than that of water. Consequently, the minimum area needed to obtain a visible signal is greater.

The two most widely used MRS techniques involve either viewing 1H atoms in molecules other than water or 31P-containing molecules. In 1H MRS, the water signal must first be suppressed as it is much greater than the signal from other 1H-containing compounds and has overlapping spectroscopic peaks with compounds.

Compounds that can be resolved with 1H-MRS include:

a) N-acetylaspartate (NAA) which is though to be a neuronal marker that decreases in processes where neurons die;

b) Lactate which is a product of anaerobic metabolism and may indicate hypoxia;

c) Excitatory neurotransmitters glutamate and aspartate;

d) The inhibitory neurotransmitter gamma-amino butyric acid (GABA);

e) Cytosolic choline which includes primarily mobile molecules involved in phospholipid membrane metabolism but also small amounts of the neurotransmitter acetylcholine and its precursor choline;

1. Myolinositol which is important in phospholipoid metabolism and intracellular second messenger systems; and

2. Creatine molecules such as creatine and phosphocreatine which usually have relatively constant concentrations throughout the brain and are often used as relative reference molecules (ie. one may see NAA concentration reported as the ratio NAA/creatine in the literature).

Phosphorus (31P) MRS allows the quantification of ATP metabolism, intracellular pH, and phospholipid metabolism. Mobile phospholipid, including phosphomonoesters (PME – putative cell membrane building blocks) and phosphodiesters (PDE – putative cell membrane breakdown products) can also be measured, supplying information on phospholipid membrane metabolism.

MRS is an useful tool to be used in the characterization of tumor, stroke and epileptogenic tissue and in presurgical planning.

Limitations

MRS is restricted to studying mobile magnetic compounds. As neurochemical receptors are noted usually mobile, they cannot be measured with MRS. Thus, receptor-ligand studies in psychiatry are still the domain of SPECT and PET. Another problem with MRS is that due to the low concentrations of many of the imaged substances, larger areas than with water are needed to obtain detectable signals. Larger volume units imaged over longer periods are thus used with this technique, limiting both temporal and spatial resolution compared with conventional MRI and BOLD-fMRI. However, stronger magnetic fields which can spread out precession frequencies over a wider range may improve this resolution.

Conclusions

While there are currently no clinical indications for ordering any of these fMRI techniques, they hold considerable promise for unraveling the neurocircuitry and metabolic pathways of numerous disorders in the immediate future and in further helping in diagnosis and treatment planning.

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LYMPHATIC SUPPLY OF HEAD & NECK WITH SPECIAL REFERENCE TO CT / MR IMAGING OF CERVICAL LYMPH NODES.








Preglandular, postglandular, prevascular, postvascular, and intravascular. The preglandular and prevascular groups are located anterior to the submandibular gland and facial artery, respectively. The postglandular and postvascular groups are posterior to these structures. Differing from the parotid gland in embryological development, there is no true intraglandular node; however, occasionally, a node has been identified inside the capsule of the gland. The submandibular nodes drain the ipsilateral upper and lower lip, cheek, nose, nasal mucosa, medial canthus, anterior gingiva, anterior tonsillar pillar, soft palate, anterior two thirds of the tongue, and submandibular gland. The efferent vessels drain into the internal jugular nodes. For the submental nodes, 2-8 nodes are located in the soft tissues of the submental triangle between the platysma and mylohyoid muscles. These nodes drain the mentum, the middle portion of the lower lip, the anterior gingiva, and the anterior third of the tongue. The efferent vessels drain into both the ipsilateral and contralateral submandibular nodes or into the internal jugular group.








The internal jugular chain consists of a large system covering the anterior and lateral aspects of the internal jugular vein, extending broadly from the digastric muscle superiorly to the subclavian vein inferiorly. As many as 30 of these nodes may exist, and they have been arbitrarily divided into upper, middle, and lower groups. The efferents of these nodes eventually pass into the venous system via the thoracic duct on the left and multiple lymphatic channels on the right. These nodes drain all the other groups mentioned. Direct efferents may be present from the nasal fossa, pharynx, tonsils, external and middle ear, Eustachian tube, tongue, palate, laryngopharynx, major salivary glands, thyroid, and parathyroid glands. Although fairly consistent, these drainage patterns are subject to alteration with malignant involvement or after radiotherapy. In such cases, rerouting is possible, with metastases arising in unusual sites. Metastases have also been shown to skip first-echelon nodes and manifest in the lower internal jugular group.


The nodes found in level II are located around the upper third of the internal jugular vein, extending from the level of the carotid bifurcation inferiorly to the skull base superiorly. The lateral boundary is formed by the posterior border of the SCM muscle; the medial boundary is formed by the stylohyoid muscle. Two subzones are also described; nodes located anterior to the spinal accessory nerve are part of level IIa, and those nodes posterior to the nerve are located in level IIb. The middle jugular lymph node group defines level III. Nodes are limited by the carotid bifurcation superiorly and the cricothyroid membrane inferiorly. The lateral border is formed by the posterior border of the SCM muscle; the medial margin is formed by the lateral border of the sternohyoid muscle. Level lV contains the lower jugular group and extends superiorly from the omohyoid muscle to the clavicle inferiorly. The lateral border is formed by the posterior border of the SCM muscle; the medial margin is formed by the lateral border of the sternohyoid muscle. The lymph nodes found in level V are contained in the posterior neck triangle, bordered anteriorly by the posterior border of the SCM muscle, posteriorly by the anterior border of the trapezius, and inferiorly by the clavicle. Level V includes the spinal accessory, transverse cervical, and supraclavicular nodal groups. Level VI lymph nodes are located in the anterior compartment. These nodes surround the middle visceral structures of the neck from the level of the hyoid superiorly to the suprasternal notch inferiorly.


Furthermore, the presence of cervical adenopathy has been correlated with an increase in the rate of distant metastasis. Unfortunately, clinical palpation of the neck demonstrates a large variation of findings among various examiners. Although both inexpensive to perform and repeat, palpation findings are generally accepted as inaccurate. Both the sensitivity and specificity are in the range of 60-70%, depending on the tumor studied. Because of the known low sensitivity and specificity of palpation, a neck side without palpable metastases is at risk of harboring occult metastasis, with the risk determined by the characteristics of the primary tumor. The incidence of false-negative (occult) nodes based on physical examination findings varies in the literature from 16-60%. Before the introduction of diagnostic imaging, particularly CT scan, clinical palpation was shown to be inadequate for detecting cervical metastasis. Soko et al reported that only 28% of occult cervical metastases were found by clinical palpation. Martis reported a 38% prevalence of occult metastasis based on clinical examination findings



Ultrasound : Ultrasound is reported superior to clinical palpation for detecting lymph nodes and metastases. The advantages of ultrasound over other imaging modalities are price, low patient burden, and possibilities for follow-up. Sonographs of metastatic lymph node disease characteristically find enlargement with a spherical shape. Commonly, nodes are hypoechoic, with a loss of hilar definition. In cases of extranodal spread with infiltrative growth, the borders are poorly defined. Common findings of metastases from squamous cell carcinoma are extranodal spread and central necrosis together with liquid areas in the lymph nodes. Lymph node metastases from malignant melanoma and papillary thyroid carcinoma have a nonechoic appearance that mimics a cystic lesion. Sonography also is useful for assessing invasion of the carotid artery and jugular vein. Because lymph nodes of borderline size cannot be reliably diagnosed using ultrasound alone, ultrasound-guided fine-needle aspiration and cytologic examination of the nodes in question can be easily performed. The result of the aspirate examination depends on the skill of the ultrasonographer and the quality of the specimen (ie, harboring an adequate number of representative cells). Using this technique, most studies report that a sensitivity of up to 70% can be obtained for the N0 neck.










Magnetic resonance imaging: The value of MRI is its excellent soft tissue resolution. MRI has surpassed CT scanning as the preferred study in the evaluation of cancer at primary sites such as the base of the tongue and the salivary glands. The sensitivity of MRI exceeds that of clinical palpation in detecting occult cervical lymphadenopathy. Size, the presence of multiple nodes, and necrosis are criteria shared by CT scanning and MRI imaging protocols. Most reports indicate that CT scanning still has an edge over MRI for detecting cervical nodal involvement. Advances in MRI technology (e.g., fast spin-echo imaging, fat suppression) have not yet surpassed the capacity of CT scanning to identify lymph nodes and to define nodal architecture. Central necrosis, as evaluated by unenhanced T1- and T2-weighted images, has been shown to provide an overall accuracy rate of 86-87% compared with CT scanning, which has an accuracy rate of 91-96%. The use of newer Contrast media, especially supramagnetic contrast media agents, hopefully will improve the sensitivity of MRI.




8.Van den Brekel MW: Lymph node metastases: CT and MRI. Eur J Radiol 2000 Mar; 33(3): 230-8[Medline].

Contrast Media Administration Guidelines by the ACR (American College of Radiology) Version 6 – 2008

Contrast Media Administration Guidelines by the ACR (American College of Radiology) Version 6 – 2008

NEURO – IMAGING IN PSYCHIATRY

NEURO – IMAGING IN PSYCHIATRY

Dr Himadri Sikhor Das

In psychiatry Neuroimaging is primarily used to aid in differential diagnosis. The clinical value of neuroimaging is used to demonstrate underlying organic brain pathology as a possible cause of disturbed mental status. Pathognomonic image profiles indicative of specific psychiatric disorders have not yet been fully identified; thus for the time being neuroimaging studies are finding only limited utility in identification of specific primary psychiatric diseases. In the future, however neuroimaging techniques may be used to make or confirm psychiatric diagnoses and neuroimaging profiles may be incorporated into the diagnostic criteria of certain psychiatric disorders. However in the future, imaging data may be valualable for predicting natural courses of illness as well as monitoring response to treatment.

MRI IMAGING IN PSYCHIATRIC ILLNESSES: -

Although specific clinical decisions must be mode on a case-to-case basis, tentative guidelines regarding the indications for structural neuroimaging in psychiatry have been suggested. These should be considered for patients who meet any of the four following criteria: -

1. Acute mental status change (including those of affect, behaviors or personality), plus any of:
- Age > 50 years
- Abnormal neurological examination.
- History of significant head trauma (i.e. Head trauma resulting in loss of consciousness or neurological sequelae)

2. New onset psychosis
3. New onset delirium or dementia of unknown etiology.
4. Prior to an initial course of ECT.

In addition to the above which focus on acute presentation; neuroimaging should also be considered when a patient’s distorted metal status proves refractory. Following these criteria a very low proportions of brain lesion associated with treatable general medical conditions could be missed. Move specifically, older age groups, psychiatric inpatients and patients with co-morbid medical illness likely will present the highest rate of positive findings. Finally an even higher percentage of patients may benefit from negative findings in a more subtle fashion i.e., as a consequence of the reassurance attained from having gross structural pathology ruled out and the primary psychiatric diagnoses solidified.

ROLE OF MRI IN CLINICAL NEUROSCIENCE: -

MRI is seen to play an important role in clinical neuroscience research in psychiatry. In general studies are done with two aims: -

- First images from large cohorts of patients and comparison subjects are reserved in order to identity pathological change that occurs in ill individuals.
- Second general research approach in to ask focused questions about the volume or shape of specific brain tissue types or structure to provide evidence regarding the involvement of these structures in the pathophysiology of specific conditions.

RECENT IMAGING MODALITIES: Recent advances in NMR and nuclear medicine techniques are finding more and more importance in pursuing active research work in Psychiatric diseases as well providing new insights into the human brain. With the advent of functional imaging, processes like memory, emotion, thought etc are being researched by scientists all over the world.

I. NUCLEAR MEDICINE (PET/SPECT):

Nuclear medicine procedures used for diagnosis and research of psychiatric conditions generally utilize PET and SPECT scans. These methods show blood flow by imaging trace amounts of radioisotopes. PET however can measure metabolism revealing how well the body is functioning. Use of radioactive tracers is well suited to studies of epilepsy, schizophrenia, Parkinson’s disease and stroke. Both PET and SPECT depict the distribution of blood into tissues, but PET does so with greater accuracy.

PET scanners watch the way the tissue cells (eg. brain cells) consume substances such as sugar (glucose). The substance is tagged with a radioisotope and brewed in a small, low energy cyclotron. The isotope has a small half-life meaning it loses half of its radioactivity only within minutes or hours of being created. Injected into the body the radioactive solution emits positrons wherever it flows. The positrons collide with electrons and the two annihilate each other releasing a burst of energy in the form of two gamma rays. These rays shoot in opposite directions and strike crystals in a ring of detectors around the patient’s head causing the crystals to light up. A computer records the location of each flash and plots the source of radiation, translating the data into an image. By tracing the radioactive substance a doctor can pinpoint areas of abnormal brain activity or determine the health of cells. Unlike PET, which specially requires a cyclotron on site, SPECT uses commercially available radioisotopes greatly reducing the cost of operation.

II. FUNCTIONAL MAGNETIC RESONANCE IMAGING (FMRI) IN PSYCHIATRY.

First, the most commonly used fMRI technique called BOLD-fMRI (Blood-Oxygen-Level-dependent fMRI) potentially offers imaging with a temporal resolution on the order of 100 milliseconds and a spatial resolution of 1-2 millimeters, which is much greater than that of PET and SPECT scanning. This means that transient cognitive events can potentially be imaged and small structures like the amygdala can be more readily resolved. Most fMRI techniques are noninvasive and do not involve the injection of radioactive materials so that a person can be imaged repeatedly. This allows imaging of a patient repeatedly through different disease states (i.e. imaging a bipolar patient through manic, depressive, and euthymic states) or developmental changes (ie. Learning cognitive stages of development, stages of grief recovery). Third, with fMRI, one can easily make statistical statements in comparing different mental states within an individual in a single session. Thus, fMRI may be of important use in understanding how a given individual’s brain functions and perhaps, in the future, making psychiatric diagnoses and treatment recommendations. It is in fact already starting to being used in presurgical planning to map vital areas like languages, motor function, and memory.

The four main applications of MRI yielding functional information in psychiatry can be categorized as: -
1. BOLD-fMRI that measures regional differences in oxygenated blood.
2. Perfusion fMRI, which measures regional cerebral blood flow.
3. Diffusion-weighted fMRI which measures random movement of water molecules and
4. MRI spectroscopy, which can measure certain cerebral metabolites noninvasively.

1. BOLD-fMRI (BLOOD-OXYGEN-LEVEL-DEPENDENT FMRI):

BOLD-fMRI is currently the most common fMRI technique. With this technique, it is assumed that an area is relatively more active when it has more oxygenated blood compared to another point in time. This is based on the principle that when a brain region is being used, arterial oxygenated blood will redistribute and increase to this area. BOLD fMRI is a relative technique in that it must compare images taken during one mental state to another to create a meaningful picture. As images are acquired very rapidly (ie. a set of 15 coronal brain slices every 3 seconds is commonly) one can acquire enough images to measure the relative differences between two states to perform a statistical analysis within a single individual. Ideally, these states would differ in only one aspect so that everything is controlled for except the behavior in question.

BOLD fMRI paradigms generally have several periods of rest alternating with several periods of activation. Images are then compared over the entire activation to the rest periods. BOLD fMRI is best used for studying processes that can be rapidly turned on and off like language, vision, movement, hearing and memory.
BOLD fMRI is very sensitive to movement so that tasks are limited to those without head movement, including speaking. BOLD fMRI is also limited in that artifacts are often present in brain regions that are close to air (ie. sinuses). Thus there are some problems in observing important emotional regions at the base of the brain like the orbitofrontal and medial temporal cortices. Another problem is that sometimes observed areas of activation may be located more in areas near large draining veins rather than directly at a capillary bed near the site of neuronal activation.

Currently, there are no indications for BOLD fMRI in clinical psychiatry, although this technique holds considerable promise for unraveling the neuroanatomic basis of psychiatric disease. It may be of potential help in sorting out diagnostic heterogeneity and treatment planning in the future. Neurologists and neurosurgeons are beginning to use this technique clinically to noninvasively map language, motor and memory function in patients undergoing neurosurgery.

2. PERFUSION fMRI:

Two fMRI methods have been developed for measuring cerebral blood flow. The first method, called intravenous bolus tracking, relies on the intravenous (iv) injection of a magnetic compound such as a gadolinium-containing contrast agent and measuring its T2 weighted signal as it perfuses through the brain over a short time period of time.

Areas perfused with the magnetic compound show less signal intensity as the compound creates a magnetic inhomogeneity that decreases the T2 signal. The magnetic compound may be injected once during the control and once during the activation task and relative differences in blood flow between the two states may be determined to develop a perfusion image. Alternatively one can measure changes in blood few over time over time after a single injection to generate a perfusion map.

This technique also only generates a map of relative cerebral blood flow, not absolute flow as in the text technique. Arterial spin labeling is a T1 weighted noninvasive technique where intrinsic hydrogen atoms in arterial water outside of the slice of interest are magnetically tagged (“flipped”) as they course through the blood and are then imaged as they enter the slice of interest.

Arterial spin labelling is noninvasive, does not involve an IV bolus injection, and can, thus, be repeatedly performed in individual subjects. Also, absolute regional blood flow can be measured which cannot be easily measured with SPECT or BOLD fMRI and requires an arterial line with PET. As absolute information is obtained, cerebral blood flow can be serially measured over separate imaging sessions such as measuring blood flow in bipolar subjects as they course through different disease states. Absolute blood flow information may be important in imaging such processes as anxiety, which may be hard to turn on and off. For instance, in social phobics, a relaxation task may be imaged on one day and anticipating making a speech may be imaged on the next day. Comparing these separate tasks in different imaging sessions would not be possible with BOLD fMRI. Arterial spin labelling has some limitations in that it takes several minutes to acquire information on a single slice of interest. Therefore, one must have a specific brain region that one is interested in examining. Also, as it currently takes several minutes to acquire a single slice, it would be tedious obtaining enough images on this slice within a single session to make a statistical statement on a given subject.

3. DIFFUSION-WEIGHTED IMAGING (DWI)

Diffusion-weighted imaging is very sensitive to the random movement of 1 H in water molecules (Brownian movement). The amount of water diffusion for a given pixel can be calculated and is called the apparent diffusion coefficient (ADC). Areas with low ADC value (ie. low diffusion) appear more intense. ADC values are direction sensitive. While it is currently unclear now diffusion-weighted imaging will be useful in studying psychiatric disorders, it hold great promise for changing the clinical management of acute ischaemic stroke by potentially refining the criteria for patients most likely to benefit from thrombolytic therapy.

4. MRI SPECTROSCOPY (MRS):

MRI spectroscopy (MRS) offers the capability of using MRI to noninvasively study tissue biochemistry. In the conventional and functional MRI techniques listed. The hydrogen atom in water is the main one that is flipped (resonated). In MRS, either 1H atoms in other molecules or other atoms such as 31P, 23Na, K, 19F or Li are flipped. Within a given brain region called a voxel, information on these molecules is usually presented as a spectrograph with precession frequency on the x-axis revealing the identity of a compound and intensity on the y-axis, which helps quantify the amount of a substance. The quantity of a substance is related is related to the area under its spectrographic peak; the larger the area, the more of a substance that is present.

The two most widely used MRS techniques involve either viewing 1H atoms in molecules other than water or 31P-containing molecules. In 1H MRS, the water signal must first be suppressed as it is much greater than the signal from other 1H-containing compounds and has overlapping spectroscopic peaks with compounds.

Compounds that can be resolved with 1H-MRS include:

a) N-acetylaspartate (NAA) which is though to be a neuronal marker that decreases in processes where neurons die;
b) Lactate which is a product of anaerobic metabolism and may indicate hypoxia;
c) Excitatory neurotransmitters glutamate and aspartate;
d) The inhibitory neurotransmitter gamma-amino butyric acid (GABA);
e) Cytosolic choline which includes primarily mobile molecules involved in phospholipid membrane metabolism but also small amounts of the neurotransmitter acetylcholine and its precursor choline;

1. Myolinositol which is important in phospholipoid metabolism and intracellular second messenger systems; and
2. Creatine molecules such as creatine and phosphocreatine, which usually have relatively constant concentrations throughout the brain and are often used as relative reference molecules (ie. one may see NAA concentration reported as the ratio NAA/creatine in the literature).

Phosphorus (31P) MRS allows the quantification of ATP metabolism, intracellular pH, and phospholipid metabolism. Mobile phospholipid, including phosphomonoesters (PME – putative cell membrane building blocks) and phosphodiesters (PDE – putative cell membrane breakdown products) can also be measured, supplying information on phospholipid membrane metabolism.

MRS can be used to identify regional biochemical abnormalities. For example, P-MRS studies of euthymic bipolar patients have revealed decreased frontal lobe PMEs (cell membrane building blocks) compared with healthy controls. However, when bipolar patients become either manic or depressed, their PMEs increase.

These findings appear to be unrelated to medication treatment. The finding of decreased frontal PMEs in euthymic bipolars has also been demonstrated in schizophrenia and speculatively accounts for the finding of decreased frontal lobe metabolism in both of these disorders. The schizophrenia finding also appears to be medication-independent.

MRS may also be of future help in the differential diagnosis of certain psychiatric diseases such as dementia. In normal aging, there is a decrease in PMEs and increase in PDEs. In early Alzheimer’s Dementia compared with healthy controls. Some believe that a decrease in NAA coupled with an increased myoinositol lever helps in differentiating probable Alzheimer’s Dementia from healthy age-matched controls as well as other dementias (usually decreased NAA but normal myoinositol levels).

With MRS, changes in metabolic activity can be measured over time within an individual scanning session. MRS can also be used to measure changes in metabolic activity between sessions, such as before and after medication treatment. For example, Satlin et al. (1997) used 1H MRS to measure midparietal lobe cytosolic choline levels in 12 Alzheimer’s subjects before and after treatment with Xanomeline, an M1 selective cholinergic agonist, or placebo. Additionally, MRS can be used to measure drug levels of certain psychotropic drugs. The magnetic elements Li and F do not naturally occur in the human body but they are fund in psychotropic drugs; lithum for Li and fluoxetine and stelazine for F. For example, studies have consistently found that the brain concentrations of lithium are about 0.5 that of serum Li levels and correlate with treatment response.

For psychiatry, MRS is a research to be used in the characterization of tumor, stroke and epileptogenic tissue and in presurgical planning.

LIMITATIONS:

MRS is restricted to studying mobile magnetic compounds. As neurochemical receptors are noted usually mobile, they cannot be measured with MRS. Thus, receptor-ligand studies are still the domain of SPECT and PET. Another problem with MRS is that due to the low concentrations of many of the imaged substances, larger areas than with water are needed to obtain detectable signals. Larger volume units imaged over longer periods are thus used with this technique, limiting both temporal and spatial resolution compared with conventional MRI and BOLD-fMRI. However, stronger magnetic fields which can spread out precession frequencies over a wider range may improve this resolution.

A brief view of recent findings are outlined.

PSYCHOTIC DISORDERS:

Research studies have identified a large number of pathologies in at last some subjects of schizophrenia for eg, the main regions sharing consistent abnormalities in schizophrenia have been frontal & temporal lobe structures. Volume decreases have been found in 62% of 37 studies of the whole temporal lobe, in 81% of 16 studies of the superior temporal gyrus and in 77% of 30 studies of the medial temporal lobe. Temporal lobe volume reduction may be uni or bilateral with deficits observed more commonly in left temporal lobe. Frontal lobe volume reductions have been reported in 55% of all published studies. Regional volume reductions have been reported in thalamus and corpus callosum. Interestingly, basal ganglia volumes may increase during treatment with typical, but not atypical neuroleptic agents. Recently studies in children have also shown findings consistent with the adult findings.

MOOD DISORDERS:

Major Depression

The spectrum of affective illness is very broad, ranging from single episodes of depressed mood, which are self-limited to life-long, treatment-refractory despondency with recurrent suicidality. Proposed that both primary and secondary mood disorders may involve abnormalities in specific frontosubcortical circuits that regulate mood. Depression is observed frequently in persons with degenerative diseases of the basal ganglia, such as Huntington’s disease, Parkinson’s disease, Wilson’s disease.

In older adults, frontal lobe atrophy and an increasing burden of T2 weighted, high signal intensity lesions have been correlated with late-life depression. Evidence suggests that depression may be seen following focal damage to critical brain regions as well as in response to diffuse brain injury. As the amygdala plays a key role in the brain’s integration of emotional meaning with perception and experience, volumetric studies of this brain structure currently are being reported. Sheline et al. have observed decreased amygdalar core nuclei volumes in depressed subjects increased amygdalar volumes in depressed patients. Mervaala et al. have noted significant amygdalar asymmetry (right smaller than left) in severely depressed subjects.

Strokes and tumors located in left sided frontal regions have been associated with new onset depression and less commonly; right-sided lesions may lead to manic symptoms. Subcortical lesions, especially of the caudate and thalamus, also can lead to mood dysregulation, with right sided lesions again being more commonly associated with mania. 30 MR studies with most consistent finding observed in 10 of 12 studies is a three-fold increase in the presence of WMH. The etiology of these WMH in bipolar patients is not clear, rates of alcohol and substance abuse, smoking cardiovascular risk factors contribute. As in schizophrenia some patients with bipolar disorder have increased lateral and third ventricular volume. Brain regions with volume deficits in bipolar include the cerebellum, especially in patients who are older or how have had multiple episodes of mania toxic effects of alcohol abuse lithium treatment.

Reduced volume and altered activity of subgenual prefrontal cortex in familial bipolar disorder has been reported. Subgenual cingulate cortex volume more recently increased amygdalar volumes have been seen in persons with bipolar disorder. Limited available data suggest that panic attacks may arise, in a minority of cases, as a consequence of ictal activity and that brain MR may identify a reasonably high yield of septo-hippocampal abnormalities in the subpopulation of panic patients who also have electroencephalogram abnormalities. Emission tomography studies generally have observed increased orbitofrontal and cingulate blood flow and glucose utilization, with decreased caudate perfusion. Hippocampal volume reductions on the order of 5% to 12% have been reported, which are of a lesser magnitude than those observed in AD or temporal-lobe epilepsy.

Neuroimaging studies of Dementing illness constitute a very active area of ongoing research. A great deal of attention has been paid to the hippocampus, as progressive atrophy has been reported to correlate with memory loss in a number of studies of both healthy adults and individuals with dementing illnesses. Recently have suggested that other regions of interest (e.g. entorhinal cortex, anterior cingulate and the banks of the superior temporal sulcus) may show larger rates of change in structural volume, over the for the hippocampal formation. Assessment of the medial occipitemporal, inferior and middle temporal gyri in demented elderly also has been suggested as a means to predict progression to AD. Alternatively, measurement of global cerebral volume also has been proposed as a means to assess disease progression. In healthy older adults, ventricular volume has been shown to increase by approximately 1.5 cm / year, suggesting that brain tissue loss is relatively slow in the absence of degenerative disorders. Frontotemporal dementia (FTD) may be distinguished from AD on the basis of anterior hippocampal atrophy (AD).

Decreases in the area of the body and posterior subregions of the corpus callosum have been reported in autistic individuals. Anorexia nervosa has been strongly associated with cerebral ventricular enlargement as well as gray and white matter deficits. Refeeding is associated with some improvement in ventricular and white matter volumes but gray matter volume deficits tend to persist, as do some neurocognitive impairments. Anorexia and bulimia may be associated with hyponatremia, which can lead to the development of central pontine myelinolysis.

Substance Use Disorders.

Alcohol-induced ventricular and sulcal enlargement have been observed by many. Regional atrophy of the corpus callosum and the hippocampus also have been reported. The cerebellum appears to be particularly sensitive to alcohol-induced damage. In addition to atrophic changes, diffuse white matter hyperintensities, suggestive of demyelination have been observed in T2 weighted examination of asymptomatic alcoholics. Signal intensity changes within the globus pallidus also have been observed in persons with cirrhosis, which may improve following liver transplantation.

Wernicke korsakoff syndrome results from nutritional deficiencies and may be precipitated by glucose administration to thiamine deficient alcoholics. The neuroanatomic change most closely associated with Wernicke Korsakoff syndrome in mamillary body atrophy although regional changes in the thalamus, orbitofrontal cortex and mesial temporal lobe also have been reported. Central pontine myelinolysis often is detected in alcoholics and presumably arises from rapid correction of electrolyte imbalance in severe hyponatremia. Extrapontine lesions also may be observed in CPM patient, affecting the cerebellar peduncles, basal ganglia and the thalamus. Marchiafava Bignami disease is a rare hemispheric disconnection syndrome typically associated with chronic alcoholism. MBD often is associated with hypointense T1 weighted or hyperintense T2 weighted lesions of the corpus callosum, suggestive of demyelination. Alcohol discontinuation and nutritional supplementation may contribute to recovery from MBD.

Stimulant Dependence.

Cocaine dependence recently has been associated with an increased incidence of WMH on T2 weighted imaging studies an incidence rate for asymptomatic stroke of approximately 3% in abstinent former cocaine users. Abuse of amphetamine and methampetamine also have been associated with cerebral ischaemia.

Other Drugs

Lipophilic adulterants present in preparations of vaporized heroin may produce signs of a toxic leukoencephalopathy. Chronic use of combined heroin and cocaine has been associated with increased pituitary volume as well as reduced prefrontal and temporal cortex volume. Solvent abuse has been linked to loss of gray white matter tissue differentiation, increased perivascular white-matter signal hyperintensities and cerebral atrophy.

CONCLUSIONS:

While there are currently no clinical indications for ordering any of these fMRI techniques, they hold considerable promise for unraveling the neurocircuitry and metabolic pathways of psychiatric disorders in the immediate future and in further helping in psychiatric diagnosis and treatment planning.

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Acute and non acute Schmorl’s nodes,disc vascularization : MR findings & recent concepts

 

Disc degeneration itself is a normal process in the elderly, beginning

as early in the twenties. There are 3 complications of degenerative disease of

the spinal column, making the normal process to a pathologic condition for

the individual : disc hemiation, spinal stenosis, and erosive osteochondritis.

MRI of erosive osteochondritis is characterized by disc vascularization and

bone marrow edema, both imaging features also found in infectious

spondylitis. Schmorl’s nodes can become vascularized like disc tissue in

erosive osteochondritis. There exist two types of Schmorl’s nodes: intraosseous

hemiation of nucleus pulposus tissue through the cartilaginous

endplate and hyaline cartilage proliferation originating in the trabecular bone

in erosive osteochondritis.

In disc degeneration, erosions of the adjacent vertebral endplates can be

present. However, the peripheral cortical bone of the vertebra is intact in disc

degeneration and frequently sclerosis can be found. Disc infections, on the

other hand, are frequently associated with destruction of the cortical borders

of the vertebra, the distinct dark rim of the endplate is then often focally not

visible on T1-weighted images. A gas density on CT is helpful to

distinguish degenerative disc vascularization in erosive osteochondritis from

spinal infection.

There is a high prevalence of degeneratively affected lumbar discs in MRI

examinations of people without back pain, and all degrees of disc

degeneration can be generally found in asymptomatic populations. However,

band-like vascularity in the disc space at the disco-vertebral junction is

associated with severe painful back syndromes . As bony changes and spurs at the endplates

are absent or only moderately developed segmental instability may play a causative role in

 the development of disc vascularity. Secondary disc vascularization represents a clinical condition

which can be diagnosed easily only by means of contrast enhanced MRI.

Therefore, MRI protocols in the work-up of patients with painful back

syndromes should include the application of paramagnetic contrast medium

and sagittal imaging planes after contrast medium injection, when previous

CT studies do not show disc herniation or other significant findings to explain

the patients symptoms. Degenerative disc vascularization is an important

differential diagnosis to bacterial spondylitis. It can be causative for pain in

patients with post-discectomy syndrome.

Gadopentetate dimeglumine enhanced MR imaging examinations of the

lumbar and thoracic spine is indicated for Schmorl’s nodes,

vascularization of Schmorl’s nodes, and associated bone marrow edema.

Sagittal T2-weighted SE and T1-weighted enhanced and non-enhanced SE

images with and without fat suppression  may be employed.

 

 

 

As the prevalence of Schmorl’s nodes decreases with age from youth to

adulthood, healing may be possible. Therefore, proliferative processes must

take place in the area of intraosseous herniation. At postmortem microscopic

examination, abnormal cartilage proliferation was noted in a 16 years old boy

with juvenile kyphosis in abnormal vertebrae and growth plates. In the

peripheral regions of the Schmorl’s nodes, where the vertebral bodies are in

contact with the node, growth of cartilaginous cells can occur. After

intraosseous herniation, ingrowth of vessels takes place from the adjacent

bone marrow into the periphery of the node and will progress to the center of

the node. It can be hypothesized that vascularization is requisite for cartilage

formation. Subsequent ossification contributes to sclerosis. By this

mechanism, sclerotic healing may be possible after ossification of the

cartilage.

 Only very few Schmorl’s nodes become symptomatic. Vascularity may be a

normal attempt to heal intraosseous cartilaginous hernias and is not

necessarily accompanied by back pain. However, enhancing Schmorl’s nodes

were bigger and more often accompanied by bone marrow edema in patients

with back pain than in those without. Enhancing Schmorl’s nodes should not

be confused with tumor or infection.

 

 

 

Suggested reading:

 

1.

Modic MT, Steinberg PM, Ross JS, Masaryk TJ, Carter JR
Degenerative disc disease: asessment of changes in vertebral bony
marrow with MR imaging.Radiology 1988; 166:193-199

 

2.Ross JS, Modic MT, Massaryk TJTears of the annulus fibrosus: assessment
with Gd-DTPA-enhanced MR imaging.AJR 1990; 154:159-162

 

3.Hamanishi C, Kawabata T, Yosii T, Tanaka SSchmorl’s nodes on
magnetic resonance imaging. Their incidence andclinical relevance.
Spine 1994; 19:450-453

 

4.Resnick D, Niwayama GIntravertebral disk herniations:
Cartilaginous (Schmorl’s) nodes.Radiology 1978; 126:57-65

 

5.Martel W, Seeger JF, Wicks JD, Washbum RLTraumatic lesions
of the discovertebral junction in the lumbar spine.Am J Roentgenol
1976; 127:457-464
6. Dr Axel Staebler, M.D. MR in D/D of disc space pathology :
Disc vascularization in acute degeneration ,
spondylitis,enhancing schmorls nodes :

MR MORPHOLOGY IN INTRACRANIAL TUBERCULOMAS

MR Morphology of Intracranial Tuberculomas

Dr. H. S. Das, Dr. N. Medhi, Dr. B. Saharia, Dr. S. K. Handique

Introduction:

Tuberculomas represent a common neurological disorder in developing countries, forming 12-30% of all intracranial masses – (1,2). Furthermore the incidence of intracranial TB in patients with AIDS is also increasing, the highest incidence recorded being 2.3% – (3,4) in one study to 18% in another – (5). Prompt diagnosis is mandatory since any delay in increased morbidity and mortality. Unfortunately the diagnosis is not always possible on the basis of clinical and epidemiological data, since clinical manifestations are nonspecific – (7,8) and objective evidence of systemic tuberculosis or exposure to the disease may be absent in upto 70% of the cases – (9). The role of CT in diagnosis of CNS tuberculomas in well established, nevertheless CT findings should be interpreted with caution since neoplastic, fungal or parasitic diseases may cause similar changes on CT – (10). Recently Magnetic Resonance (MR) Imaging has shown advantage over CT in the detection of intracranial pathology – (11) and its value in the diagnosis of infections diseases of the central nervous system (CNS) has been reported – (12,13). Although tubercular meningitis can not be differentiated from other meningitides on the basis of MR findings; but intraparenchymal tuberculomas show characteristic T2 shortening not found in most other space occupying lesions – (14). Thus in the appropiate clinical setting tuberculomas should be considered. Here, we report our experience in using MR for the evaluation of patients with intracranial tuberculoma.

Patients and Methods:

10 Patients with intracranial tuberculomas were evaluated with MR in our institution between August ’95 to August’ 99. 8 males and 2 females between 5-45 years (Mean 22.9 years) were included in this study. MRI was performed on a 1-tesla super conductive magnet. Standard spin echo techniques were used to obtain multiplanar T1 and T2 weighted images. Contrast was used in 6 patients. The diagnosis of CNS tuberculosis was made after proper integration of data from the surgical and medical findings. Data included positive biopsy in 2 patients; analysis of blood and CSF (elevation in 2 cases); positive response to anti tubercular drugs in 6 patients and MR findings. Initial CT was done upon admission to the hospital in all ten cases. MR was done to visualize the full extent of the lesion, to differentiate these lesions from other diseases affecting the brain and to delineate the contents (necrotic centre, capsule and surrounding edema). None of the patients tested positive for HIV.

Results:

Tuberculomas were supratentorial in 9 patients and infratentorial in 1. All but one patient had single lesions, which were located at the cortico-subcortical junction of the cerebral hemispheres and in the brainstem in 2 patients. 1 patient had a cerebellar tuberculoma. On MR intracranial tuberculoma caused prolongation of the T1 relaxation time which was most marked at the centre of the lesion. 5 patients had lesions hypointense to normal brain; 4 patients had lesions isointense and 1 patient had a mixed signal with hypointensity predominating on T1 weighted images. On the T2 weighted sequences the MR appearance varied. In six patients the centre of the lesion gave hypointense (dark) signal while the periphery gave a hyperintense (bright) signal relative to the brain parenchyma due to surrounding oedema. In 2 patients the centre of the lesion was hyperintense with a hypointense rim surrounded again by diffuse hyperintensity due to edema.

Follow up CT in 6 patients during the course of antituberculous drugs showed reduction in the six of the lesion as well as the oedema as a result of therapy. 2 patients positive biopsy while 2 patients were lost to follow up. Following contrast infusion in 6 patients ring enhancing lesions were observed in 4 patients, disc enhancing lesion size of less than 1 cm, 3 patients had lesion size of more then 2 cms while the lesion size varied between 1-2 cms in the rest of the 6 patients. 2 out of the 10 patients presented with meningitis, which shows diffuse thick meningeal contrast enhancement presumably due to granulation tissue. These 2 patients also had different degrees of hydrocephalus.

Discussion:

Tuberculomas develop in the brain when the initial Rich’s focus does not rupture into the meninges but expands locally within the parenchyma due to greater resistance of host tissues to the infecting organism (5). Meningitis can cause borderline encephalitis resulting in direct infiltration of the brain parenchyma and multiple small tuberculomas which coalesce to form mature tuberculomas – (16).

Tuberculomas have different appearances on T2 weighted images depending on their stage of evolution. At an early stage of formation of tuberculomas, an inflammatory reaction occurs; the mass has an abundance of giant cells and a capsule poor in collagen. At this stage the mass is isointense on T1 and T2 weighted images. At a later stage, the capsule becomes rich in collagen. When small tuberculomas coalesce to become larger lesions they give low signal on T2 weighted images because of fibrosis, scar tissue and free radicals produced by macrophages during active phagocytosis – (17).

22 of the 27 cases (84%) of NCS tuberculoma in the literature clearly showed low signal on T2 weighted images – (8, 18, 19, 20). 5 (16%) had lesions with central high signal thought to represent caseating pathologic examination revealed tuberculoma with dense reactive fibrosis.

In another study out of 97 patients presumed to harbour cerebral tuberculomas (of which 11 were confirmed by biopsy and 73 showed a therapeutic response to AKT) the lesions were either homogenously hypointense or revealed a central hyperintense nidus within the hypointense lesion on T2 weighted images (21).

Based on a histopathological grading of 7 proven tuberculomas, Gupta et al (22) concluded that the signal intensity on T2 weighted images is variable and dependant on the relative proportion of macrophages, cellular infiltrates and fibrosis. Granulomas, which were frankly hyperintense on T2 weighted images, exhibited increased cellular infiltrates, scantly macrophages and little fibrosis; while the hypointense lesions showed grater numbers of macrophages; more fibrosis and gliosis – (22). Large amounts of lipids were reported to contribute to the T2 shortening in 2 of the granulomas analysed by localized proton spectroscopy – (22). MR is of value to visualize the full extent of the lesion, in differentiation of the lesion with other diseases of the CNS (e.g. fungal granuloma, haemorrhagic metastases and “granulo-nodular” stage of neurocysticercosis) and to delineate the different components of the lesion (necrotic center, capsule and surrounding oedema), which is not always possible with CT.

References:
1. Dastur HM, Desai AD (1965): A comparitive study of brain tuberculomas and gliomas based upon 107 case records of each. Brain 88: 375-396.
2. Laitha VS, Marker FE, Dastur DK, tuberculosis of the Central Nervous System. Neurology (India) 1980; 28: 197-201.
3. Anderson KM, MacMillan JI (1975) Intercranial Tuberculoma: an Increasing Problem in Britain. I. Neurolo Neurosurg Pshchiatry 38: 194-201.
4. Bishburg E, Sundaram G, Reichan LB; Kapila R (1986) CNS tuberculosis with AIDS its related complexes. Ann Intern Med 105: 210-213.
5. Intracranial tuberculosis is AIDS: CT and MRI findings. M.F. villomoria, J Dela Torre, F. Fortea, L. Munoz, T. Hernadez and J. J. Alarcon: (1992) Neuroradiology 34: 11-14.
6. Harder E, Al-Jawi MZ; Carney P (1983): Intracranial Tuberculoma; Conservative management. Am J. Med 74: 570-576.
7. Lehrer H. Venkatesh B, Girolamo R, Smith A (1973): Tuberculoma of the brain (revisited) AJR 118 : 594-600.
8. Talamas O, Del Brutto OH; Garcia Ramos G (1989): Brainstem Tuberculoma; an analysis of 11 patients, Arch Neurol.
9. De Angelis LM (1981) Intracranial tuberculoma: Case report and review of literature. Neurology 31: 1133-1136.
10. Wrishber L, Nice C, Karx M (1984) Cerebral computer tomography : a text atlas, Saunders. Philadelphia.
11. Brant-Zawadzki M, Davis PL, Crooks LE (1983) : NMR demonstration of cerebral abnormalities : Comparision with CT AJNR 4 : 120-126.
12. Davidson HD, Steiner RE (1965) MRI in infections on the CNS AJNR 6 : 120-126.
13. Schorth G; Kretzchmar K; Gawehn J, Voigt K (1987): Advantages of MRI in the diagnosis of cerebral infection. Neuroradiology 29: 120-126.
14. Kioumehr, MR Dadsetan, SA Rooholamini, A, AU (1994): Central Nervous System Tuberculosis: MRI. Neuroradiology 36: 93-96.
15. Dastur DK, Lalitha VS: The many facets of neurotuberculosis. An epitome of neuropathology. In Zimmerman RA (ed). Progress in neuropathology Vol. 2 New York. Grune and Stration 1973, 351, 108.
16. Dastur DK, (1983) Neurosurgically relevant aspects and pathognesis of intracranial and intraspinal tuberculomas. Neurosurg Rev. 6 : 103-110.
17. Chang KH, Han MH, Roh JK et al (1990): Gd-DTPA enhanced MR Imaging in intracranial tuberculosis. Neuroradiology 32: 19-25.
18. Gupta RK, Jena A, Sharma A, Guha DK (1988) MR imaging of intracranial tuberculoma, J. computer Assist Tomong. 121: 280-285.
19. Salgado P, Del Brutto OH, Talamas O, Zenteno MA, Rodriguez Carbajal J, Neuroradiology (1989) 31 : 299-302. Intracranial tuberculoma: MR imaging.
20. Dastur HM (1983) Diagnosis and neurosurgical treatment in tuberculous diseases of the CNS. Neurosurgery 6: 11-113.
21. Desai SB, Shah VC, Tavri OJ, Rao P, MRI more specific than CT in cranial tuverculomas. Neuroradiology (1991) : 33 (Suppl).
22. Gupta RK, Pandey B, Khan EM, Mittal P, Gujral RB, Chhabra DK. Intra cranial tuberculomas: MRI signal intensity correlation with histopathology and localized proton spectroscopy. Mag. Res. Imaging (1993), 11: 443-449.

MR Imaging in Multiple Sclerosis: Overview and role of MR imaging: Article by Dr H.S.Das:

Multiple sclerosis (MS) is an idiopathic inflammatory and most common demyelinating disease of the CNS. Most people with this disease are affected in their prime of their lives, usually between 20 and 40 years of age though exceptions have been documented. Cause of this disease remains unknown. Genetic, viral, autoimmune and environmental factors have been implicated in the disease.

 Pathologic hallmark of MS is multicentric and multiphasic CNS inflammation and remyelination scattered over space and time. In MS, cells of the immune system invade the CNS and destroys the myelin cover leading to demyelination of the axon and damage to the axon itself. In response, other cells of the CNS produce a hard sclerotic lesion (“ the MS plaque”) around the multiple demyelinated sites. Areas of axonal damage can be measured by magnetic resonance spectroscopy (MRS) and is found to correlate with clinical disability. Few lesions in non eloquent areas do not produce clinical symptoms or nerological dysfunction. Such lesions are referred to as “silent lesions”. Approximately 1 per 1000,000 people acquire MS internationally. Throughout adulthood , the female to male ratio is 2:1.

Clinical features:

Sensory problems occur in 20%-50% of patients and are often the earliest symptoms. These manifest as tingling, tight band feeling, crawling sensations etc are found in the extremities and in the trunk and are referred to as paresthesias. Few patients may experience an electric like sensation that goes down the back and legs with head or neck motion (Lhermitte’s sign).

Optic neuritis is the presenting symptom in 15%-20% of patients with MS and usually starts with blurring of vision followed by loss of vision. May appear on one side followed by a later appearance in the other. It rarely involves both eyes simultaneously.

Spasticity occurs due to cortico-spinal tract involvement . Occurs with the initial attack of MS in 30%-40% of patients. It is present in 60% of patients with progressive disease. Usually legs are involved more than the arms.

Other clinical features of MS includes gait and balance incoordination, bladder & bowel dysfunction, fatigue (the single most complaint of people with MS), heat sensitivity, cognitive and emotional dysfunctions etc.

Diagnosis of MS is based on a classic presentation (optic neuritis, transverse myelitis, paresthesias etc) and on the identification of other neurological abnormalities, which is indicated by the patients history and clinical examination. Typical findings in MRI greatly help to establish diagnosis of MS. Patients with atypical presentations and /or a normal or atypical MRI may require evoked potential studies to know about subclinical neurological abnormality. CSF analysis is done to exclude treatable conditions and to document immunological activity in the CNS. Oligoclonal bands are present in over 90% of definite MS, though these can be seen in other inflammatory diseases and in 7% of normal controls. An IgG index of >0.7 is seen in 86%-94% of MS patients and is usually the first CSF abnormality in early MS. 25% patients show elevated protein levels. Presence of myelin basic protein in CSF indicates demyelination though these also can be seen in other neurological conditions like infections, infarct etc. However this protein can be found in the first 2 weeks after a substantial exacerbation in 50%-90% of patients.

Course of disease: The natural course of MS is highly variable and it is impossible to predict the nature, severity or timing of progression in a given patient. Patients with sensory problems tends to have a better prognosis than those with spasticity or paralysis. Another factor that influences prognosis is age of onset. Disease progression tends to be more rapid in patients who experience their first symptoms after age 40. Other factors predictive of rapid progression include male gender, frequent attacks and burden of disease as detected by MRI scans.

Classifications of MS :

Clinically definite MS is further categorized according to disease course. Relapsing-remitting MS (RR-MS) is characterized by symptoms that develop over a period of a few hours to a few days, followed by recovery and a stable course between relapses. Approximately 80% of patients are initially dignosed with relapsing-remitting MS. Almost 50% of patients with relapsing- remitting MS eventually develop secondary-progressive MS (SP-MS) characterized by gradual neurological deterioration with or without superimposed acute relapses. If there is continual disease progression from onset with only minor fluctuation the classification becomes primary-progressive MS (PP-MS). PP-MS occurs in approximately 10 % of patients and mostly who are > 40 years of age. Progressive-relapsing MS (PR-MS), a rare from of the disease, is characterized by gradual neurological deterioration from the onset of symptoms to subsequent relapses.

MR IMAGING IN MS :

MR imaging is the modality of choice in patients with MS . Use of MRI in MS was first described by Young et al in 1981. Previously spin echo ( SE ) sequences like T1, T2 and PD weighted images are commonly used to screen patients with MS. Recently fast or turbo spin echo ( FSE & TSE ) techniques with similar PD and T2 weighted lesion contrast has become popular because this sequences utilize ¼ to 1/3rd of acquisition time. Very small lesions can be missed on FSE sequences because of edge blurring, but taking thinner slices compensates it.

Recent MR developments in imaging of white matter disease :

Nowadays FLAIR ( fluid attenuated inversion recovery ) sequences are widely used because heavily T2 weighted images can be obtained with CSF suppression and enables greater lesion conspicuity in the gray white interface areas. Another technique is EPI ( echo planar imaging ). Use of EPI FLAIR is very useful in detecting early lesions that do not enhance such as Demyelinating disease, acute infarcts and infection.

Diffusion weighted imaging (DWI) :

Normal white matter exhibit anisotropic diffusion with increased diffusion parallel to white matter fibers and restricted diffusion present perpendicular to these fibers. Demylination results in increase in extracellular space which in turn results in increase in water diffusion and diffusion coefficient as compared to normal white matter. Hence in MS, both in acute and chronic plaques there will be increase in diffusion coefficient. Acute plaques has higher diffusion coefficient than chronic plaques probably due to gliosis in chronic plaques. Currently modalities like DTI ( diffusion tensor imaging ) and FA ( fractional anisotropy ) are being utilized for more research in MS.

Quantative magnetisation transfer ( MT ) technique :

Useful in MS patients on drug therapies to know the disease activity. In active plaques there is little demyelination and their MT ratio is slightly reduced which indicates that lesions are most likely to respond to methylprednisolone and more likely to disappear. In contrast chronic plaques have more demyelination and very low MT ratio. These are unlikely to respond to any drug therapy. This technique is now applied to other white matter disease also.

Magnetic resonance spectroscopy (MRS) :

This technique does not produce images but graphs that display levels of metabolites as zones of different colors or shades of gray known as spectroscopic images. In MS tissue metabolite like NAA ( N – acetyl aspartate ) is decreased in chronic plaques and remains normal in active plaques.

MR appearance of MS lesions:

Lesions are typically nodular or ovoid in appearance. Size varies from few mm to more than 1cm. Lesions have propensity to involve the large white matter tracts particularly corpus callosum, medial longitudinal fasciculus and middle cerebellar peduncle. Lesions can also be found in juxtacortical location involving the “U” fibres, along the perimedullary veins at the calloso-septal interface and also in periventricular location giving rise to the classical “Dawson’s fingers appearance”. MS lesions however can involve any portion of the white matter. Recently presence of “ Subcallosal Striations”has been described using sagittal FLAIR sequence. These are thin white lines radiating from the calloso-septal interface and represents the earliest manifestation of MS in this location. Occasionally, MS lesions present as large lesions with mass effect and vasogenic edema indistinguishable from brain tumor by MR imaging ( tumefactive MS plaque). Other nonspecific findings include thinning of the corpus callosum, dirty white matter on T2 weighted images and deposition of non haem iron in the basal ganglia with progression of the disease

Spinal MS :

Spinal MS has a predilection for the cervical spinal cord ( 67 % of cases), with preferential eccentric involvement of the dorsal and lateral areas of the spinal cord abutting the subarachnoid space around the cord. About 55 to 75 % of patients with MS have spinal lesions at some point of time during the course of the disease. As many as 20% of spinal MS lesions are isolated. Spinal lesions enhance after contrast administration. Enhancement may last for 2 to 8 weeks. Steroids do not suppress enhancement of active plaques. Chronic plaques do not enhance and often demonstrate focal cord atrophy. Lesions of other etiologies ( eg, viral myelitis, ADEM ) may resemble MS plaques and must be considered along with the clinical history and the patients sign and symptoms.


 

 


Legends for photos:

Fig1: T2 sagittal image showing Cord change in MS

Fig2. FLAIR coronal image showing plaques (bright lesions) in the supra & infratentorial compartments of brain. Notice the upper cervical cord lesion.

Fig3:. T2 weighted axial image showing multiple Demyelinating plaques (bright lesions) in bilateral periventricular areas.

Typical MR morphology of MS lesion:

Initially MS lesions are isointense to mildly hypointense (black) on T1 weighted images. With time, the hypointensity progresses to develop the so called “T1 black hole”. Some lesions show slight peripheral hyperintensity surrounding the lesion due to presence of free radicles in the surrounding inflammatory tissues. On T2 and PD weighted images the lesions are usually hyperintense (bright).

Role of contrast administration in MS :

In MS contrast enhanced MRI plays an important role depending on the clinical context. Contrast enhancement in general indicates the presence of active inflammatory process. Non enhancing lesions are thought to be chronic lesions. Presence of enhancing and non enhancing lesions is strong evidence to indicate that these multiple lesions are separated in time supporting diagnosis of MS. Presence of ring enhancement suggest reactivation of an old lesion, the central nonenhancing portion representing the “burnt out” portion of the lesion. An incomplete or open ring enhancement is more indicative of an MS lesion.

MR imaging criteria for clinical progression to MS in patients with clinically isolated syndromes ( CIS). MS typically presents as an acute reversible episode of neurologic dysfunction.

Paty et al ( 1988 ) : 4 lesions ( Paty A)

  • : 3 or more lesions, including 1 periventricular lesion ( Paty B)

  • Sensitivity 86 %, Specificity 54 %

Fazekas et al (1988) : 3 lesions with 2 of the following properties.

  • : 5 or > 5 mm diameter of lesion.

  • : Infratentorial or periventricular location.

  • : Sensitivity 86 %, Specificity 54 %

Barkhof et al ( 19 97 ) : 4 lesions criteria

  • : 1 or > 1 Juxtacortical lesion.

  • : 1 or > 1 enhancing lesion or > 9 nonenhancing lesion.

  • : 1 or > 1 infratentorial lesion.

  • : 3 or > 3 periventricular lesions. ( Sensitivity and specificity 73% )

Proposed new diagnostic category : MR imaging supported definite multiple sclerosis ( MRISDMS)

At least one MS –like clinical episode with appropriate clinical findings, remission not necessary.

Abnormal MR image findings ( strongly suggestive of MS).

  • Four or more white matter lesions ( > 3 mm diameter ).

  • 3 lesions with at least one located in periventricular location.

  • One or more of the following specific features.

  • Involvement of corpus callosum.

  • Infratentorial location.

  • Oval shape.

  • > 6 mm in diameter.

  • Some but not all enhancing.

Variants of MS –

Balo’s concentric sclerosis :- Rare, affects young adults, last for few months, concentric bands of intact myelin and demyelinated zones, responds to steroid.

Devic’s disease :- ( neuromyelitis optica) Spinal cord and optic nerves affected. Brain spared . Brain MRI normal. MRI spine shows striking lesions.

Marburg’s disease :- Acute form of MS. Fulminant and progressive.

Schilder’s disease :- Rare, affect children, visual problems and cortical blindness, Seizures, headache, vomiting, large bilateral hemispheres demyelination.

Monophasic syndromes :- Optic neuritis, acute transverse myelitis, ADEM

 

 

 

 

IMAGING IN CEREBRAL VASCULAR PATHOLOGIES:

 

IMAGING IN CEREBRAL VASCULAR PATHOLOGIES:

 

EVOLUTION OF INTRACRANIAL HEMATOMA

 

1. Immediate


- liquid with 95% O2 saturated Hb, T2 hyper, T1 iso within seconds platelets thrombi form & cells aggregate

 2. Hyper acute stage -

4-6 hrs, fluid serum begins to disperse

Protein clot retracts, red cells become spherical, oxy

Early peripheral edema begins, T2 iso, T1 iso

OxyHb is diamagnetic with no unpaired electrons,

CT – isodense for 1-3hrs, then becomes dense, 60-100HU
3. Acute stage

- 7-72 hrs, red cells begin to compact, deoxyhb

Central portion T2 hypo, T1 iso

DeoxyHb is paramagnetic with 4 unpaired electrons, T2 shortening

Sheilded from H2O by globin, prevents T1 shortening

No proton-electron relaxation enhancement can occur

Edema pronounced in periphery

Dense on CT, window width of 150-250 best

 

4. Subacute stage -

1-4 wks, methemoglobin starts day 4

Begins at periphery & progresses towards anoxic center

Cells begin to lyse at 1 week releasing metHb, decrease in edema

Perivascular inflammatory reaction begins with macrophage at periphery

Ring Enhancement caused by this process

T1 BRIGHT due to 5 unpaired electrons exposed by globin change

Proton-electron relaxation enhancement does occur

Periphery affected 1st, middle remains iso initially

T2 HYPO early when methemoglobin still in RBC

BRIGHT once the cell breaks down & Hb diluted in water

CT attenuation decreases approx 1.5HU per day

CT is NOT an accurate indicator of age, due to variable Hb etc

 

5. Early Chronic stage

- >4wks, edema & inflammatory reaction subside

Vascular proliferation encroaches on haematoma decreasing its size

Dilute uniform pool of extracellular metHb with vascular walls

Macrophage contain ferritin & hemosiderin at periphery

T2 hypo due to strong magnetic susceptibility

T1 iso due to fact that hemosiderin is water insoluble

Hypodense on CT unless rebleeding has occurred

6. Late Chronic stage -

cystic or collapsed with dense capsule

Vascular proliferation gradually forms fibrotic matrix with macrophage

Infants may resolve completely

Ferritin laden scar persists for years in adults

10% calc with residual hypodense focus in 40%

Gradient echo is helpful in detecting Haem in low field MRI’s

OVERVIEW OF HEMORRHAGE CAUSES

Underlying cause often hidden by the bleed. Intraventricular extension associated with 10% mortality

 

1. Neonatal Hemorrhage – germinal matrix hemorrhage secondary to prematurity

thin walled, proliferating vessels in subependyma of lateral caudothalamic groove

involution occurs at 34 wks when all cells have migrated

No hemorrhage in utero or beyond first 28 days post birth

 

Grade I – Hemorrhage confined to germinal matrix, can be bilateral

Grade II – rupture into normal size ventricles

Grade III – intraventricular hemorrhage with Hydrocephalus

Grade IV – extension to adjacent hemispheric white matter

Can be seen by US in acute & subacute, lucent if chronic

 

Term Infants – Hemorrhage usually secondary to trauma, subdural mostly

Asphyxia & infarction most commonly in non-traumatic cases

Posterolateral lentiform nuclei & ventral thalamus most susceptible

 

2. Hypertension – Most common cause of nontraumatic bleed in adult

Lenticulostriate & Pontine vasculatures mostly involved, penetrating branches of MCA

Usually spontaneous in elderly patients, basal ganglia mostly

Vessels often abnormal, ruptured microanuerysms etc

50% have hemorrhage dissection into ventricles, poor prognosis

Lobar white matter hemorrhage in 20%, cerebellum 10%, midbrain & brainstem rare

Originates along perforating branches near dentate nuclei

Active bleeding usually lasts <1hr

Edema progresses for 24-48hrs, 25% die in this period

Hypertensive Encephalopathy – occurs secondary to elevated BP

Toxemia (Most common) – autoregulation overwhelmed especially in posterior aspect

Overdistention of arteriole leads to BBB breakdown

Reversible vasogenic edema results, frank hemorrhage rare

Cortical petechia & subcortical hemorrhage possible, especially in occipital regions

Increased T2 in external capsule & basal ganglia more common

Chronic renal Diseases, TTP, & Hemolytic-Uremic syndrome other causes

 

3. Hemorrhagic Infarction

Arterial Infarction – hemorrhage when endothelium reperfused

Occurs in 50%, but only seen in 10%, sensitivity: MRI>CT

Cortex & basal ganglia from MCA distribution most commonly, 24-48hrs later

Pseudolaminar Cortical Necrosis – generalized hypoxia

Middle layers usually effected, gyriform hemorrhage

Nonhemorrhagic ischemic changes can occur, gyri calcification possible

Venous Infarction – usually associated with dural sinus thrombosis

Dura around sinus will enhance, clot stays hypodense (empty delta sign)

More likely to effect white matter than cortex

4. Aneurysms – 90% of nontraumatic subarachnoid hemorrhage

Headache common presenting sign for aneurysm, CT best for acute SAH

Blood usually fills ambient cisterns & sylvian first

90% of blood cleared from CSF in 1wk

MRI better for subacute or chronic SAH, dirty CSF

Superficial siderosis – hemosiderin deposit on meninges

Cerebellum brainstem & cranial nerves also coated – neurological dysfunction

Giant aneurysms >2.5cm often have intramural hemorrhage

most from carotid, cavernous portion most common, all ages

75% have calc if thrombosed, none otherwise

Charcot-Bushard Aneurysm – secondary to HTN

5. Vascular Malformations -

AVM & Cavernous Angioma commonly

Most bleed into parenchyma rather than subarachnoid space

Arteriovenous Malformation – pial, dural or mixed, No cap bed

Pial AVM’s – hemorrhage @ 2% per year, often in previously normal young pts

70% bleed by 1st exam, repeated hemorrhage can simulate neoplasm

Central nidus with gliosis & encephalomalacia

Dural AVM’s – no central nidus, SAH or subdural

hemorrhage rare unless drainage through cortical veins

 

Cavernous Angioma – bleed @ .5% per year, freq repeated bleeds

Popcorn like with mixed signal foci & hemosiderin ring

Venous Angiomas – bleed rare, similar hematoma of other malformations

Medusa like collection of dilated medullary veins

Capillary Telangiectasias – usually small & clinically silent

may see multiple small foci of hemosiderin on T2

INTRACRANIAL ANEURYSMS & VASCULAR MALFORMATIONS

Charcot-Bushard Aneurysm – secondary to Hypertension

20% multiple, higher incidence in females.

Look for familial causes such as Polycystic Kid Disease

 

SACCULAR ANEURYSMS

Berrylike out pouching from arterial bifurcation

Include intima & adventitia, media ends with normal vessel

1. Etiology – hemodynamic induced injury, abnormal shear forces most commonly

Trauma, infection, tumor, drug abuse & AV malformations

Berry Aneurysms – associated with polycystic kidney Diseases & aortic coarctation

2. Incidence – 1% of angios & 5% of postmortems

Multiple in 20%, esp in females & polycystic kidney Diseases

Bilateral in 20%, esp at cavernous sinus, Pcom & MCA trifurcation

Occur age 40-60 unless traumatic or mycotic,

 

3. Associated Conditions – occur at anomalous vessels & AVM

Inc pressure ie HTN & aortic coarctation

Systemic Diseases – Marfan’s, fibromuscular dysplasia, polycystic kidney diaeases

 

4. Location – 30% at anterior communicating, 30% at posterior communicating, 20% MCA origin

10% in post circulation especially basilar artery bifurcation

traumatic or mycotic occur anywhere

5. Clinical Presentation – asymptomatic until rupture or giant >2.5cm

1-2% risk of rupture per year, 3.5% risk of surg

No different risk with HTN, age, sex or multiplicity

All should be repaired if >3yr life expectancy

Subarachnoid Hem – clinical grade by Hunt & Hess scale I-V

Vasospasm most common cause of morbidity, 30% die

highest bleed rate in 1st 24hrs, 50% rebleed in 2wk

CT – shows SAH in >80% of ruptured aneurysms

Cavernous sinus aneurysms can compress Nerves III-VI

TIA, Seizures & embolic ischaemia less common

 

Giant Aneurysms – most from supraclinoid carotid, all ages

Fibrous vascular walls, rarely rupture, Symptoms secondary to mass effect

Partially Thrombosed Aneurysms – 75% have curvilinear calcification

CT most specific for these with target seen

NO calc if not thrombosed

D/D – Meningioma, both erode sella & lat sphenoid

aneurysm has no associated hyperostosis or atherosclerosis

 

6. Appearance of Saccular Type – catheter angiography definitive

asses for relation to vessel, adjacent branches & vasospasm

essential in assessment of nontraumatic SAH

Thrombosed aneurysm will have no finding, 15%

may see mass effect if large

irregularity or local vasospasm can indicate rupture

D/D vascular loops & infundibuli (embryonic funnel <2mm)

CT may show bone erosion in long standing case

Patent aneurysms enhance intensely w contrast

Location of SAH can be prognostic indicator

Ambient cisterns anterior to brainstem probably just venous rupture

No repeat angio needed

Suprasellar cistern to lateral sylvian fissure

more aneurysmal pattern, must do F/U angio

MRI dependent on pattern of flow, turbulence & clot

may have wall enhancement with gadodiamide, laminated with thrombosis

 

7. Traumatic Aneurysm -

nonpenetrating usually occur at skull base, or shear

hyperextention stretches ICA over lat C1

 

8. Mycotic Aneurysms – Secondary to infection of arterial wall, rare <10%

adventitia & muscularis disrupted, thoracic aorta commonly

Angio – occur dist to usual location, 2nd branch MCA commonly

most common cause of multiple MCA aneurysms

usually small, staph & strep most common, inc in child

bleed into parenchyma or SAH equal incidence

Medical Treatment usually sufficient to control, surgery if enlarge on angio

Mucor & Aspergilla invade direct from nasopharynx cause thrombosis & infarct more often than aneurysm

 

9. Oncotic Aneurysms – usually extra cranial, exsanguinate freq

tumor may implant or cause emboli, primary or metastatic

 

10. Flow-Related Aneurysms – seen with AVM’s in 30%

distal ones most likely to hemorrhage

 

11. Vasculopathies – rare but seen with SLE, infarct & TIA commonly

Takayasu’s Arteritis – 9:1 female, inflammation & stenosis most commonly

prox arch vessels, L subclavian commonly, often occludes

Fibromuscular Dysplasia – up to 50%, dissection & A-V fistula, 65% bilateral

Cocaine – 50% with CNS symptoms have SAH, may be secondary to HTN treatment

several drugs cause vasculitis .

 

FUSIFORM ANUERYSMS

Etiology – atherosclerosis, exaggerated arterial ectasia

media damaged, stretches & elongates, frequent mural thrombus

Vertebrobasilar Dolichoectasia – Common site, older patient

often thrombus producing brainstem infarcts

can also compress local stem causing nerve palsies

Imaging – enhances if patent, hyperintense if thrombosed

curvilinear calcification pathognomonic, may cause skull base erosion

 

DISSECTING ANEURYSMS

Etiology – intramural blood from tear in intima

may narrow or occlude lumen, may distend subadventitia

do not confuse with Pseudoaneurysm, a encapsulated hematoma

Presentation – usually extracranial unless severe trauma

Commonly in midcervical ICA & vertebral from C2 to skull base

Catheter angio remains procedure of choice for assesment

 

INTRACRANIAL VASCULAR MALFORMATIONS

1. Parenchymal AVM – congenital, dilated arteries & veins without capillary bed

98% solitary, multiple in Osler-Weber-Rendu & Wyburn-Mason

Incidence – 85% supratentorial, peak 20-40y, 25% children

Hemorrhage in 85% with 3% per year risk, seizure 25%, deficit 25%

Size not predictive, deeper & smaller ones bleed more

Parenchymal commonly, also common cause of SAH if

Vascular Steal – atrophy due to vasculopathy of feeding vessel

atrophic low density regions & hematoma with high density

Overlying meninges thick & hemosiderin stained

Angio – shows feeding arteries & tortuous veins

often wedge shaped, possible to appear Normal if thrombosed

GBM may simulate but usually has tissue between vessels

10% have aneurysms in feeding arteries, can bleed

 

Cryptic AVM’s – not seen by angio, 10%

CT – often absent w/o contrast, 25% have mild curvilinear calcification

mixed increased & decreased density if seen, Mild mass effect possible

Enlarged post venous sinuses but not cavernous sinus

Calcification seen in

MRI – honeycomb of flow voids, increased signal if thrombosed

hemorrhage in different stages often present

No significant intervening brain tissue, D/D : GBM

TX – resection if unruptured, must be completely removed

Aneurysms must be treated separately, increased risk for bleed

 

2. Dural AVM’s & Fistulae – form within a venous sinus

no discrete nidus, multiple microfistulae, occluding sinus frequent

Follow recanulation of thrombosed sinus, 10% of all AVM’s

Transverse or Sigmoid sinus commonly, Bruits & headache most common

Cavernous sinus AVM – proptosis, retro orbital pain, proptosis

SAH common if reflux flow forced into cortical veins

Carotid-Cavernous fistula related, follow trauma

Occipital & Meningeal branch of ext carotid #1 feeders

CT often N, MRI may show dilated cortical veins

 

3. Mixed - 15%, if parenchymal AVM recruits arteries from dural supply

 

4. Capillary Telangiectasias – multiple nests of dilated capillaries

Common in pons & Cerebellum, usually incidental

Gliosis of adjacent brain & hemosiderin staining from hem possibly

Cavernous Angiomas assoc or simply the extreme form

Osler-Weber-Rendu – hereditary hemorrhagic Telangiectasias

25% have brain abnormalities, most are true AVM’s

Visceral angio dysplasia with scalp & mucous membrane telangiectasia

2nd most common lesion to venous angioma at autopsy

Not visualized by angio, may present with epistaxis

CT may faintly enhance, faint on MRI

5. Cavernous Angiomas – Hemangioma or cavernoma

Circumscribed nodule of honeycomb sinusoidal vascular spaces

separated by fibrous bands but no intervening neural tissue

frequently MULTIPLE HEMATOMAS at different stages, reticulated core of vessels

Supratentorial 80% but can occur anywhere, 50% multiple

Most Common vascular lesion identified, 20-40y/o

Seizure, deficits & bleed most common presenting features

Angio does NOT visualize, possible faint blush in early venous

CT shows freq Calc, variable enhancement, can simulate neoplasm

MRI – popcorn like appearance on T2 due to multiple hem

multiple areas of signal drop-out due to hemosiderin

VENOUS MALFORMATIONS

1. Venous Angioma – dilated anomalous veins converge on central vein

Etiology – remnant embryonic venous system, usually solitary

assoc with migrational abnormalities & cavernous Angiomas in 30%

Asymptomatic, Hemorrhage very rare unless from associated cavernous angioma

CT – may show linear tuft of vessels post contrast

located in deep White Matter of cortex or Cerebellum, commonly adjacent to frontal horn

MRI – shows stellate tributary veins into prominent collector vein

gliosis or hemorrhage seen in only 15%

Angio – the only vascular malformation with a single draining vein

Medusa head appearance on venous phase of angio

 

2. Vein of Galen Aneurysm – enlargement of Galenic system

Secondary to arteriovenous fistulae from choroidal arteries

AVM in thalmus or midbrain can also cause this

Present at birth with high-out put cardiac failure, cranial bruit +

Macrocephaly with obstructive hydrocephalus, deficits & ocular symptoms

US shows bi-directional flow in vein of Galen

Angio demonstrates either choroidal artery or thalmoperforating feeder

dilation to venous varix with or without distal stenosis

if stenosed distally will often thrombose

CT – large enhancing midline mass posterior to 3rd ventricle

Hydrocephalus frequent but hemorrhage rare

enhancing serpentine vessels in thalamic region

3. Venous varix – assoc with several intracranial vascular abnormalities

Enlarged & thin veins resulting in SAH, hydrocephalus & increased ICP

Sinus Pericranii – venous haemangioma adherent to outer skull, deep to galea

supplied from intracranial sinus & blood returns to sinus

present with enlarging fluctuant soft tissue mass, enlarge with crying

often secondary to trauma, often resolved with prolonged compression

Frontal commonly, parietal next, most near sagittal sinus, can be very lateral

Skull Film – usually sharp margins, vascular honeycombs possible

CT – shows strong uniform enhancement

MRI – well delineated ovoid or fusiform areas variable signal

Venous Cavernoma – subcutaneous lesions of scalp

blood supply from external carotid, drain to external jugular

 

4. Orbital Venous Varix – rare vascular malformation in orbit

Causes intermittent proptosis & diplopia with valsalva & bending over

Disappear completely with axial views, use tourniquet on jugular vein

 

NEONATAL HEMORRAGE

Caudothalamic groove – between head of caudate & thalamus

both make up lateral wall of lateral ventricle, terminates in Monroe

Foramen of Monroe – divides frontal & body portions of ventricles

thalmus entirely posterior, caudate head anterior, choroid enters it

 

1. Subependymal Hemorrhage – preterm infants <32wks

Correlates with size of germinal matrix at birth, largest 24-32wks

involutes & is absent by 40wks, last in inferior lateral wall of frontal

lies inferior to ependyma, superior to head of caudate & anterior to thalmus

Usually occurs in first 3 days, always by 7-8 days

 

Grade 0 – Normal

Grade I – Subependymal alone

Grade II – intraventricular with no ventriculomegaly

Grade III – Hydrocephalus,

Grade IV – intraparenchymal

grade does not predict ultimate outcome, may progress

Serial studies required, only applies to germinal matrix hemorrhage

 

2. Parenchymal Hemorrhage – extends farther lateral than germinal matrix

can be “grade IV”, but not all secondary to germinal matrix bleed

most extend from SHE (Subependymal haemorrhage) to frontal or parietal lobes

Hypoxia & Hypercapnia implicated as etiology

stress causes vessels to dilate & burst

Phase 1 – echogenic like SEH for 1-2wks

Phase 2 – central Hypoechoic, bright peripheral rim 2-4wks

Phase 3 – retracts & settles into dependent position

Phase 4 – necrosis & phagocytosis complete, encephalomalacia

Cerebellar hematoma best scaned in coronal behind ear

assoc with mortality of 50%.

 

3. Choroidal Hemorrhage – usually grade II or III

Second cause of intraventricular hemorrhage not caused by SEH

Difficult to discern from normal choroid on US

asym scanning can show marked asym in choroid size

isolated choroid hematoma simulates ventricular hematoma with no hydrocephalus

Myelomeningocele assoc with pedunculated choroid

CT more reliable than US for Dx

D/D – Choroid Papilloma, very rare, consider if CSF clear on tap

all assoc with hydrocephalus, enhance intensely on CT

HEMORRHAGIC NEOPLASMS & CYSTS

 

1. Malignancy Related Coagulopathy – esp with leukemia & chemotherapy

systemic neoplasms can be assoc with term coagulopathy

 

2. Intratumoral Hematomas – 10%, malignant , Astrocytoma’s are most common.

Neovascularity, central necrosis, plasminogen activators etc contribute

Heterogeneous, incomplete hemosiderin ring, edema persist

multiple lesions & min edema suggests nonneoplastic cause

Cysts & slow growing cystic neoplasm like cranio rarely bleed

Oligodendroglioma, neuroectodermal & teratoma hemorrhage frequently

Ependymoma & choroid tumors – frequent SAH & hemosiderosis

Pituitary Adenoma – may bleed more frequently than astrocytoma

Lymphoma rarely bleed unless with AIDS

Renal cell Ca, chorio Ca, melanoma, thyroid & lung mets, 15%

 

3. Nonneoplastic Hemorrhagic Cysts -rare, colloid cysts never bleed

Rathke cleft cysts & Arachnoid cysts more commonly bleed

Arachnoid cysts bleed secondary to trauma, bridging vessels rupture

sometimes assoc with subdural hematoma

MISCELLANEOUS CAUSES OF BENIGN INTRACRANIAL HEMORRHAGE

1. Amyloid Angiopathy – Most common cause of bleed in elderly patient with no HTN

nonbranching fibrillar protiens form beta-pleated sheets

Deposit is Cortical & leptomeningeal vessels

extend from small vessels to brain parenchyma

Contractile elements replaced by the crystals

Multiple hematomas frequent & occurs at cortico medullary junction

basal ganglia & brainstem not affected

2. Infection & vasculitis – rare, increased chance if immuncompromised

septic emboli – mycotic aneurysms & hemorrhagic infarct

10% of Infective endocarditis have SAH or parenchymal

Aspergillosis & other fungi directly invade vessel

Thrombosis, infarction & hem result

Herpes Simplex II – the only encephalitis assoc with hematoma

 

3. Recreational Drugs – 50% have preexisting AVM or aneurysm

Cocaine can induce an acute hypertensive episode, vasospasm

also enhances platelet aggregation, dural sinus thrombosis

amphetamine & PCP also associated with hemorrhage

endothelial damage & necrotizing vasculitis

 

4. Blood Dyscrasias & Coagulopathies – iatrogenic or acquired

Vit K deficiency, hepatocellular diseases, antibody against clot, DIC

Anticoagulants, thrombolytics, aspirin, Etoh abuse, chemo

15% of all intracranial hemorrhage on anticoagulants

Supratentorial, intraparenchymal bleeds most common

 

 

 

MR MORPHOLOGY IN INTRACRANIAL TUBERCULOMAS

MR Morphology of Intracranial Tuberculomas

Dr. H. S. Das, Dr. N. Medhi, Dr. B. Saharia, Dr. S. K. Handique

Introduction:

Tuberculomas represent a common neurological disorder in developing countries, forming 12-30% of all intracranial masses – (1,2). Furthermore the incidence of intracranial TB in patients with AIDS is also increasing, the highest incidence recorded being 2.3% – (3,4) in one study to 18% in another – (5). Prompt diagnosis is mandatory since any delay in increased morbidity and mortality. Unfortunately the diagnosis is not always possible on the basis of clinical and epidemiological data, since clinical manifestations are nonspecific – (7,8) and objective evidence of systemic tuberculosis or exposure to the disease may be absent in upto 70% of the cases – (9). The role of CT in diagnosis of CNS tuberculomas in well established, nevertheless CT findings should be interpreted with caution since neoplastic, fungal or parasitic diseases may cause similar changes on CT – (10). Recently Magnetic Resonance (MR) Imaging has shown advantage over CT in the detection of intracranial pathology – (11) and its value in the diagnosis of infections diseases of the central nervous system (CNS) has been reported – (12,13). Although tubercular meningitis can not be differentiated from other meningitides on the basis of MR findings; but intraparenchymal tuberculomas show characteristic T2 shortening not found in most other space occupying lesions – (14). Thus in the appropiate clinical setting tuberculomas should be considered. Here, we report our experience in using MR for the evaluation of patients with intracranial tuberculoma.

Patients and Methods:

10 Patients with intracranial tuberculomas were evaluated with MR in our institution between August ’95 to August’ 99. 8 males and 2 females between 5-45 years (Mean 22.9 years) were included in this study. MRI was performed on a 1-tesla super conductive magnet. Standard spin echo techniques were used to obtain multiplanar T1 and T2 weighted images. Contrast was used in 6 patients. The diagnosis of CNS tuberculosis was made after proper integration of data from the surgical and medical findings. Data included positive biopsy in 2 patients; analysis of blood and CSF (elevation in 2 cases); positive response to anti tubercular drugs in 6 patients and MR findings. Initial CT was done upon admission to the hospital in all ten cases. MR was done to visualize the full extent of the lesion, to differentiate these lesions from other diseases affecting the brain and to delineate the contents (necrotic centre, capsule and surrounding edema). None of the patients tested positive for HIV.

Results:

Tuberculomas were supratentorial in 9 patients and infratentorial in 1. All but one patient had single lesions, which were located at the cortico-subcortical junction of the cerebral hemispheres and in the brainstem in 2 patients. 1 patient had a cerebellar tuberculoma. On MR intracranial tuberculoma caused prolongation of the T1 relaxation time which was most marked at the centre of the lesion. 5 patients had lesions hypointense to normal brain; 4 patients had lesions isointense and 1 patient had a mixed signal with hypointensity predominating on T1 weighted images. On the T2 weighted sequences the MR appearance varied. In six patients the centre of the lesion gave hypointense (dark) signal while the periphery gave a hyperintense (bright) signal relative to the brain parenchyma due to surrounding oedema. In 2 patients the centre of the lesion was hyperintense with a hypointense rim surrounded again by diffuse hyperintensity due to edema.

Follow up CT in 6 patients during the course of antituberculous drugs showed reduction in the six of the lesion as well as the oedema as a result of therapy. 2 patients positive biopsy while 2 patients were lost to follow up. Following contrast infusion in 6 patients ring enhancing lesions were observed in 4 patients, disc enhancing lesion size of less than 1 cm, 3 patients had lesion size of more then 2 cms while the lesion size varied between 1-2 cms in the rest of the 6 patients. 2 out of the 10 patients presented with meningitis, which shows diffuse thick meningeal contrast enhancement presumably due to granulation tissue. These 2 patients also had different degrees of hydrocephalus.

Discussion:

Tuberculomas develop in the brain when the initial Rich’s focus does not rupture into the meninges but expands locally within the parenchyma due to greater resistance of host tissues to the infecting organism (5). Meningitis can cause borderline encephalitis resulting in direct infiltration of the brain parenchyma and multiple small tuberculomas which coalesce to form mature tuberculomas – (16).

Tuberculomas have different appearances on T2 weighted images depending on their stage of evolution. At an early stage of formation of tuberculomas, an inflammatory reaction occurs; the mass has an abundance of giant cells and a capsule poor in collagen. At this stage the mass is isointense on T1 and T2 weighted images. At a later stage, the capsule becomes rich in collagen. When small tuberculomas coalesce to become larger lesions they give low signal on T2 weighted images because of fibrosis, scar tissue and free radicals produced by macrophages during active phagocytosis – (17).

22 of the 27 cases (84%) of NCS tuberculoma in the literature clearly showed low signal on T2 weighted images – (8, 18, 19, 20). 5 (16%) had lesions with central high signal thought to represent caseating pathologic examination revealed tuberculoma with dense reactive fibrosis.

In another study out of 97 patients presumed to harbour cerebral tuberculomas (of which 11 were confirmed by biopsy and 73 showed a therapeutic response to AKT) the lesions were either homogenously hypointense or revealed a central hyperintense nidus within the hypointense lesion on T2 weighted images (21).

Based on a histopathological grading of 7 proven tuberculomas, Gupta et al (22) concluded that the signal intensity on T2 weighted images is variable and dependant on the relative proportion of macrophages, cellular infiltrates and fibrosis. Granulomas, which were frankly hyperintense on T2 weighted images, exhibited increased cellular infiltrates, scantly macrophages and little fibrosis; while the hypointense lesions showed grater numbers of macrophages; more fibrosis and gliosis – (22). Large amounts of lipids were reported to contribute to the T2 shortening in 2 of the granulomas analysed by localized proton spectroscopy – (22). MR is of value to visualize the full extent of the lesion, in differentiation of the lesion with other diseases of the CNS (e.g. fungal granuloma, haemorrhagic metastases and “granulo-nodular” stage of neurocysticercosis) and to delineate the different components of the lesion (necrotic center, capsule and surrounding oedema), which is not always possible with CT.

References:
1. Dastur HM, Desai AD (1965): A comparitive study of brain tuberculomas and gliomas based upon 107 case records of each. Brain 88: 375-396.
2. Laitha VS, Marker FE, Dastur DK, tuberculosis of the Central Nervous System. Neurology (India) 1980; 28: 197-201.
3. Anderson KM, MacMillan JI (1975) Intercranial Tuberculoma: an Increasing Problem in Britain. I. Neurolo Neurosurg Pshchiatry 38: 194-201.
4. Bishburg E, Sundaram G, Reichan LB; Kapila R (1986) CNS tuberculosis with AIDS its related complexes. Ann Intern Med 105: 210-213.
5. Intracranial tuberculosis is AIDS: CT and MRI findings. M.F. villomoria, J Dela Torre, F. Fortea, L. Munoz, T. Hernadez and J. J. Alarcon: (1992) Neuroradiology 34: 11-14.
6. Harder E, Al-Jawi MZ; Carney P (1983): Intracranial Tuberculoma; Conservative management. Am J. Med 74: 570-576.
7. Lehrer H. Venkatesh B, Girolamo R, Smith A (1973): Tuberculoma of the brain (revisited) AJR 118 : 594-600.
8. Talamas O, Del Brutto OH; Garcia Ramos G (1989): Brainstem Tuberculoma; an analysis of 11 patients, Arch Neurol.
9. De Angelis LM (1981) Intracranial tuberculoma: Case report and review of literature. Neurology 31: 1133-1136.
10. Wrishber L, Nice C, Karx M (1984) Cerebral computer tomography : a text atlas, Saunders. Philadelphia.
11. Brant-Zawadzki M, Davis PL, Crooks LE (1983) : NMR demonstration of cerebral abnormalities : Comparision with CT AJNR 4 : 120-126.
12. Davidson HD, Steiner RE (1965) MRI in infections on the CNS AJNR 6 : 120-126.
13. Schorth G; Kretzchmar K; Gawehn J, Voigt K (1987): Advantages of MRI in the diagnosis of cerebral infection. Neuroradiology 29: 120-126.
14. Kioumehr, MR Dadsetan, SA Rooholamini, A, AU (1994): Central Nervous System Tuberculosis: MRI. Neuroradiology 36: 93-96.
15. Dastur DK, Lalitha VS: The many facets of neurotuberculosis. An epitome of neuropathology. In Zimmerman RA (ed). Progress in neuropathology Vol. 2 New York. Grune and Stration 1973, 351, 108.
16. Dastur DK, (1983) Neurosurgically relevant aspects and pathognesis of intracranial and intraspinal tuberculomas. Neurosurg Rev. 6 : 103-110.
17. Chang KH, Han MH, Roh JK et al (1990): Gd-DTPA enhanced MR Imaging in intracranial tuberculosis. Neuroradiology 32: 19-25.
18. Gupta RK, Jena A, Sharma A, Guha DK (1988) MR imaging of intracranial tuberculoma, J. computer Assist Tomong. 121: 280-285.
19. Salgado P, Del Brutto OH, Talamas O, Zenteno MA, Rodriguez Carbajal J, Neuroradiology (1989) 31 : 299-302. Intracranial tuberculoma: MR imaging.
20. Dastur HM (1983) Diagnosis and neurosurgical treatment in tuberculous diseases of the CNS. Neurosurgery 6: 11-113.
21. Desai SB, Shah VC, Tavri OJ, Rao P, MRI more specific than CT in cranial tuverculomas. Neuroradiology (1991) : 33 (Suppl).
22. Gupta RK, Pandey B, Khan EM, Mittal P, Gujral RB, Chhabra DK. Intra cranial tuberculomas: MRI signal intensity correlation with histopathology and localized proton spectroscopy. Mag. Res. Imaging (1993), 11: 443-449.

HEAD & NECK NODAL IMAGING

Cervical Nodes

Variable size. Typically, as many as 75 nodes are located on each side of the neck. Nodes contain a sub capsular sinus below a prominent capsule, into which lymphatic fluid drains. This capsule is often the first site of metastatic growth. The fluid permeates into the substance of the node (composed of a cortex and a medulla) and exits through the hilum to enter more lymphatic vessels. These nodes are located between the superficial cervical and prevertebral fascia and, thus, are very amenable to surgical removal. The lymphatic fluid eventually enters the venous system at the junction of the internal jugular and subclavian veins. Many nodal descriptions exist today; Rouvière’s is the classic model.

The occipital nodes are in the superficial group, which includes 3-5 nodes. This group of nodes is localized between the sternocleidomastoid (SCM) and trapezius muscles, at the apex of the posterior triangle. These nodes are superficial to the splenius capitis. The deep group includes 1-3 nodes. This group of nodes is located deep to the splenius capitis and follows the course of the occipital artery. These nodes drain the scalp, the posterior portion of the neck, and the deep muscular layers of the neck.

The postauricular nodes vary in number from 2 to 4; they are located in the fibrous portion of the superior attachment of the SCM muscle to the mastoid process. Postauricular nodes drain the posterior parietal scalp and the skin of the mastoid region.

The parotid nodes can be divided into intraglandular and extraglandular groups. The extraglandular parotid nodes are located outside but adjacent to the parotid gland, where they drain the frontolateral scalp and face, the anterior aspects of the auricle, the external auditory canal, and the buccal mucosa. Embryologically, the lymphatic system develops before the parotid gland, which surrounds the intraglandular nodes as it develops. The intraglandular nodes drain the same regions as the extraglandularnodes, to which they interconnect and then drain into the upper jugular group of lymph nodes. As many as 20 parotid nodes may be found.

The submandibular nodes are divided into 5 groups:

Preglandular, postglandular, prevascular, postvascular, and intracapsular. The preglandular and prevascular groups are located anterior to the submandibular gland and facial artery, respectively. The postglandular and postvascular groups are posterior to these structures. Differing from the parotid gland in embryological development, there is no true intraglandular node; however, occasionally, a node has been identified inside the capsule of the gland. The submandibular nodes drain the ipsilateral upper and lower lip, cheek, nose, nasal mucosa, medial

canthus, anterior gingiva, anterior tonsillar pillar, soft palate, anterior two thirds of the tongue, and submandibular gland. The efferent vessels drain into the internal jugular nodes. For the submental nodes, 2-8 nodes are located in the soft tissues of the submental triangle between the platysma and mylohyoid muscles. These nodes drain the mentum, the middle portion of the lower lip, the anterior gingiva, and the anterior third of the tongue. The efferent vessels draininto both the ipsilateral and contralateral submandibular nodes or into the internal jugular group.

The sublingual nodes are located along the collecting trunk of the tongue and sublingual gland and drain the anterior floor of the mouth and ventral surface of the tongue. These nodes subsequently drain into the submandibular or jugular group of nodes.

The retropharyngeal nodes are divided into a medial and lateral group, located between the pharynx and the prevertebral fascia. The lateral group, located at the level of the atlas near the internal carotid artery, consists of 1-3 nodes, which may extend to the skull base. The medial group extends inferiorly to the postcricoid level. This group drains the posterior region of the nasal cavity, sphenoid and ethmoid sinuses, hard and soft palates, Nasopharynx, and posterior pharynx down to the postcricoid area. Management of these nodes must be considered if any Malignancy arises from the mentioned drainage areas.

The anterior cervical nodes are divided into the anterior jugular chain and the juxtavisceral chain of nodes. The anterior jugular chain nodes follow the anterior jugular vein, located superficial to the strap muscles. These nodes drain the skin and muscles of the anterior portion of the neck, and the efferent vessels empty into the lower internal jugular nodes. The juxtavisceral nodes are separated into the prelaryngeal, parathyroid, pretracheal, and paratracheal nodes. Prelaryngeal nodes are located from the thyrohyoid membrane to the cricothyroid membrane and drain the larynx and the thyroid lobes. A single Delphian node is often found overlying the thyroid cartilage.

The pretracheal group consists of nodes between the isthmus of the thyroid gland down to the level of the innominate vein. Varying from 2-12 in number, these nodes drain the region of the thyroid gland and the trachea and receive afferent flow from the prelaryngeal group. The pretracheal efferents empty in the internal jugular group and the anterior superior mediastinal nodes.

The paratracheal nodes lie near the recurrent laryngeal nerve and drain the thyroid lobes, parathyroid glands, subglottic larynx, trachea, and upper esophagus. The efferent vessels travel to the lower jugular group or directly toward the junction of the internal jugular vein and theSubclavian vein. The anterior nodes drain bilaterally because the midline of the neck has no division. Treatment must be planned accordingly when a tumor is located in subjacent draining areas.

The lateral cervical nodes are divided into superficial and deep groups. The superficial group follows the external jugular vein and drains into either the internal jugular or transverse cervical nodes of the deep group. The deep group forms a triangle bordered by the internal jugular nodes,the spinal accessory nodes, and the transverse cervical nodes. The transverse cervical nodes, forming the base of the triangle, follow the transverse cervical vessels and may contain as many as 12 nodes. These nodes receive drainage from the spinal accessory group and from collecting trunks of the skin of the neck and upper chest. The spinal accessory chain follows the nerve of the same name and may account for as many as 20 nodes. This chain receives lymph from the occipital, postauricular, and suprascapular nodes and from the posterior aspect of the scalp, nape of the neck, lateral aspect of the neck, and the shoulder.

The internal jugular chain consists of a large system covering the anterior and lateral aspects of the internal jugular vein, extending broadly from the digastric muscle superiorly to the subclavian vein inferiorly. As many as 30 of these nodes may exist, and they have beenarbitrarily divided into upper, middle, and lower groups. The efferents of these nodes eventually pass into the venous system via the thoracic duct on the left and multiple lymphatic channels on the right. These nodes drain all the other groups mentioned. Direct efferents may be present from the nasal fossa, pharynx, tonsils, external and middle ear, Eustachian tube, tongue, palate, laryngopharynx, major salivary glands, thyroid, and parathyroid glands. Although fairly consistent, these drainage patterns are subject to alteration with malignant involvement or after radiotherapy. In such cases, rerouting is possible, with metastases arising in unusual sites.Metastases have also been shown to skip first-echelon nodes and manifest in the lower internal jugular group.

The most widely accepted terminology was originally described by a group of head and necksurgeons at Memorial Sloan-Kettering Hospital. This classification uses neck levels or zones and divides each side of the neck into 6 separate regions. Level I is bordered by the body of the mandible, anterior belly of the contralateral digastric muscle, and anterior and posterior bellies of the ipsilateral digastric muscle. Two nodal subgroups are found. The submental group (Ia) is found in the submental triangle (anterior belly of the digastric muscles and the hyoid bone), and the submandibular group (Ib) is found within the submandibular triangle (anterior and posterior bellies of the digastric muscle and the body of the mandible).

The nodes found in level II are located around the upper third of the internal jugular vein, extending from the level of the carotid bifurcation inferiorly to the skull base superiorly. The lateral boundary is formed by the posterior border of the SCM muscle; the medialboundary is formed by the stylohyoid muscle. Two subzones are also described; nodes located anterior to the spinal accessory nerve are part of level IIa, and those nodes posterior to the nerve are located in level IIb. The middle jugular lymph node group defines level III. Nodes are limited by the carotid bifurcation superiorly and the cricothyroid membrane inferiorly. The lateral border is formed by the posterior border of the SCM muscle; the medial margin is formed by the lateral border of the sternohyoid muscle. Level lV contains the lower jugular group and extends superiorly from the omohyoid muscle to the clavicle inferiorly. The lateral border is formed by the posterior border of the SCM muscle; the medial margin is formed by the lateral border of the sternohyoid muscle. The lymph nodes found in level V are contained in the posterior neck triangle, bordered anteriorly by the posterior border of the SCM muscle, posteriorly by the anterior border of the trapezius, and inferiorly by the clavicle. Level V includes the spinal accessory, transverse cervical, and supraclavicular nodal groups. Level VI lymph nodes are located in the anterior compartment. These nodes surround the middle visceral structures of the neck from the level of the hyoid superiorly to the suprasternal notch inferiorly.

Evaluating neck metastases based on physical examination findings has been the classic method for patients with new tumors in the head and neck. The single most important factor in determining prognosis is whether nodal metastasis is present. Survival rates decrease by 50% when nodal metastases are present. Furthermore, the presence of cervical adenopathy has been correlated with an increase in the rate of distant metastasis. During the clinical evaluation, carefully palpate the neck, with specific attention to location, size, firmness, and mobility of each node. Direct attention to nodes that appear fixed to underlying neurovascular structures or visceral organs or that demonstrate skin infiltration. The description of each node becomes an important part of the medical record, which can be used to assess the response to treatment or the progression of the disease.

Unfortunately, clinical palpation of the neck demonstrates a large variation of findings among various examiners. Although both inexpensive to perform and repeat, palpation findings are generally accepted as inaccurate. Both the sensitivity and specificity are in the range of 60-70%, depending on the tumor studied. Because of the known low sensitivity and specificity of palpation, a neck side without palpable metastases is at risk of harboring occult metastasis, with the risk determined by the characteristics of the primary tumor. The incidence of false-negative (occult) nodes based on physical examination findings varies in the literature from 16-60%. Before the introduction of diagnostic imaging, particularly CT scan, clinical palpation was shown to be inadequate for detecting cervical metastasis. Soko et al reported that only 28% of occult cervical metastases were found by clinical palpation. Martis reported a 38% prevalence of occult metastasis based on clinical examination findings

Debate persists over the relative merits of imaging in the evaluation of the neck for metastatic disease. Studies that correlate radiologic and histopathologic findings show that early microscopic metastases can be present in nodes smaller than 10 mm that demonstrate no stigmata of neoplasia (i.e., central necrosis, extracapsular spread). Evidence of early metastatic disease in clinically occult nodes is minimal and may evade the efforts of the pathologist and radiologist.

Ultrasound :

Ultrasound is reported superior to clinical palpation for detecting lymph nodes and metastases. The advantages of ultrasound over other imaging modalities are price, low patient burden, and possibilities for follow-up.

Sonographs of metastatic lymph node disease characteristically find enlargement with a spherical shape. Commonly, nodes are hypo echoic, with a loss of hilar definition. In cases of extranodal spread with infiltrative growth, the borders are poorly defined. Common findings of metastases from squamous cell carcinoma are extranodal spread and central necrosis together with liquid areas in the lymph nodes. Lymph node metastases from malignant melanoma and papillary thyroid carcinoma have a nonechoic appearance that mimics a cystic lesion. Sonography also is useful for assessing invasion of the carotid artery and jugular vein. Because lymph nodes of borderline size cannot be reliably diagnosed using ultrasound alone, ultrasound-guided fine-needle aspiration and cytologic examination of the nodes in question can be easily performed. The result of the aspirate examination depends on the skill of the ultrasonographer and the quality of the specimen (ie, harboring an adequate number of representative cells). Using this technique, most studies report that a sensitivity of up to 70% can be obtained for the N0 neck.

CT scans

Since its debut in the 1970s, CT scans have been an invaluable tool in all fields of medicine, including the evaluation of head and neck cancer. Since the advent of high-resolution systems and specific contrast media, fine-cut CT scanning has allowed the detection of pathological cervical nodes of smaller size that may be missed by clinical examination. CT scanning is now used routinely for the preoperative evaluation of the neck because, presumably, it helps decrease the incidence of occult cervical Lymphadenopathy. Introduced in 1998, multiple-spiral CT scanning promises further improvement of temporal and spatial resolution (in the longitudinal axis). This technique permits rapid scanning of large volumes of tissue during quiet breathing. The volumetric helical data permit optical multiplanar and 3-dimensional reconstructions. Improvement of the assessment of tumor spread and lymph node metastases in arbitrary oblique planes is another advantage of the spiral technique.

Criteria for the identification of questionable nodes are also evolving as technology advances. Central necrosis remains the most specific finding suggestive of nodal involvement, but its absence does not exclude metastasis. Unfortunately, metastasis is usually quite rare or not visible in small lymph nodes, where detection would be crucial. Because of the higher imaging resolution, various studies have reduced the traditional values of 10-15 mm for a node to be suggestive. Many authors have proposed a minimal axial diameter of 11 mm for the submandibular triangle and 10 mm for the rest of the neck. Other criteria include the presence of groups of 3 or more borderline nodes and the loss of tissue planes.

Magnetic resonance imaging

The value of MRI is its excellent soft tissue resolution. MRI has surpassed CT scanning as the preferred study in the evaluation of cancer at primary sites such as the base of the tongue and the salivary glands. The sensitivity of MRI exceeds that of clinical palpation in detecting occult cervical lymphadenopathy. Size, the presence of multiple nodes, and necrosis are criteria shared by CT scanning and MRI imaging protocols. Most reports indicate that CT scanning still has an edge over MRI for detecting cervical nodal involvement. Advances in MRI technology (eg, fast spin-echo imaging, fat suppression) have not yet surpassed the capacity of CT scanning to identify lymph nodes and to define nodal architecture. Central necrosis, as evaluated by unenhanced T1- and T2-weighted images, has been shown to provide an overall accuracy rate of 86-87% compared with CT scanning, which has an accuracy rate of 91-96%. The use of newerContrast media, especially supramagnetic contrast media agents, hopefully will improve the sensitivity of MRI.

Positron emission tomography and single-photon emission computed tomography

Some studies have demonstrated that positron emission tomography may be able to detect nodal metastases in lymph nodes that are negative for disease based on CT scan or MRI findings. Single-photon emission computed tomography imaging with fluorodeoxyglucose or thallium also reportedly detects nodal metastases. The use of positron emission tomography in combination with immunoimaging using monoclonal antibodies might further enhance accuracy.

None of the currently available imaging techniques can help depict small tumor deposits inside lymph nodes. Characteristics of metastatic lymph nodes that can be depicted are the size and presence of noncontrast-enhancing parts inside metastatic lymph nodes caused by tumor necrosis, tumor keratinization, or cystic areas inside the tumor. Only rarely does tumoral tissue enhance more than reactive lymph node tissue; in these rare cases, the tumor can be visualized within a reactive lymph node.

Patients who need an evaluation for a possible nodal malignancy require a comprehensive multidisciplinary evaluation of all potential sites of drainage to that node to identify its primary source. This includes a thorough evaluation of potential primary sites using endoscopic techniques. When appropriate, include laryngoscopy, esophagoscopy, bronchoscopy, and examination of the nasopharynx. If no primary source is identified, taking blind mucosal biopsy samples of the most likely head and neck subsites is essential. Complete documentation of nodal characteristics by clinical examination and palpation guide the examiner in using adjunctive radiological tools to exclude occult nodal metastasis

References:

Chen Z, Malhotra PS, Thomas GR, et al: Expression of proinflammatory and proangiogenic cytokines in patients with head and neck cancer. Clin Cancer Res 1999 Jun; 5(6): 1369-79[Medline].

Curtin HD, Ishwaran H, Mancuso AA, et al: Comparison of CT and MR imaging in staging of neck metastases. Radiology 1998 Apr; 207(1): 123-30[Medline].

Haor SP, Ng SH: Magnetic resonance imaging versus clinical palpation in evaluating cervical metastasis from head and neck cancer. Otolaryngol Head Neck Surg 2000 Sep; 123(3): 324-7[Medline].

Merritt RM, Williams MF, James TH, Porubsky ES: Detection of cervical metastasis. A meta-analysis comparing computed tomography with physical examination. Arch Otolaryngol Head Neck Surg 1997 Feb; 123(2): 9-52[Medline].

Safa AA, Tran LM, Rege S, et al: The role of positron emission tomography in occult primary head and neck cancers. Cancer J Sci Am 1999 Jul-Aug; 5(4): 214-8[Medline].

Southwick, HW, Slaughter, DP, Trevino, ET: Elective neck dissection for intraoral cancer. Arch Surg 1960; 80: 905-9.

Stacker SA, Caesar C, Baldwin ME, et al: VEGF-D promotes the metastatic spread of tumor cells via the lymphatics. Nat Med 2001 Feb; 7(2): 186-91[Medline].

Van den Brekel MW: Lymph node metastases: CT and MRI. Eur J Radiol 2000 Mar; 33(3): 230-8[Medline].

MAGING IN CEREBRAL VASCULAR PATHOLOGIES: EVOLUTION OF INTRACRANIAL HEMATOMA

IMAGING IN CEREBRAL VASCULAR PATHOLOGIES:

EVOLUTION OF INTRACRANIAL HEMATOMA

1. Immediate
- liquid with 95% O2 saturated Hb, T2 hyper, T1 iso within seconds platelets thrombi form & cells aggregate

2. Hyper acute stage -

4-6 hrs, fluid serum begins to disperse

Protein clot retracts, red cells become spherical,

Early peripheral edema begins, T2 iso, T1 iso

OxyHb is diamagnetic with no unpaired electrons,

CT – isodense for 1-3hrs, then becomes dense, 60-100HU


3. Acute stage
- 7-72 hrs, red cells begin to compact, deoxyhb

Central portion T2 hypo, T1 iso

DeoxyHb is paramagnetic with 4 unpaired electrons, T2 shortening

Sheilded from H2O by globin, prevents T1 shortening

No proton-electron relaxation enhancement can occur

Edema pronounced in periphery

Dense on CT, window width of 150-250 best

4. Subacute stage -

1-4 wks, methemoglobin starts day 4

Begins at periphery & progresses towards anoxic center

Cells begin to lyse at 1 week releasing metHb, decrease in edema

Perivascular inflammatory reaction begins with macrophage at periphery

Ring Enhancement caused by this process

T1 BRIGHT due to 5 unpaired electrons exposed by globin change

Proton-electron relaxation enhancement does occur

Periphery affected 1st, middle remains iso initially

T2 HYPO early when methemoglobin still in RBC

BRIGHT once the cell breaks down & Hb diluted in water

CT attenuation decreases approx 1.5HU per day

CT is NOT an accurate indicator of age, due to variable Hb etc

5. Early Chronic stage


- >4wks, edema & inflammatory reaction subside

Vascular proliferation encroaches on haematoma decreasing its size

Dilute uniform pool of extracellular metHb with vascular walls

Macrophage contain ferritin & hemosiderin at periphery

T2 hypo due to strong magnetic susceptibility

T1 iso due to fact that hemosiderin is water insoluble

Hypodense on CT unless rebleeding has occurred

6. Late Chronic stage -
cystic or collapsed with dense capsule

Vascular proliferation gradually forms fibrotic matrix with macrophage

Infants may resolve completely

Ferritin laden scar persists for years in adults

10% calc with residual hypodense focus in 40%

Gradient echo is helpful in detecting Haem in low field MRI’s

OVERVIEW OF HEMORRHAGE CAUSES

Underlying cause often hidden by the bleed. Intraventricular extension associated with 10% mortality

1. Neonatal Hemorrhage – germinal matrix hemorrhage secondary to prematurity

thin walled, proliferating vessels in subependyma of lateral caudothalamic groove

involution occurs at 34 wks when all cells have migrated

No hemorrhage in utero or beyond first 28 days post birth

Grade I – Hemorrhage confined to germinal matrix, can be bilateral

Grade II – rupture into normal size ventricles

Grade III – intraventricular hemorrhage with Hydrocephalus

Grade IV – extension to adjacent hemispheric white matter

Can be seen by US in acute & subacute, lucent if chronic

Term Infants – Hemorrhage usually secondary to trauma, subdural mostly

Asphyxia & infarction most commonly in non-traumatic cases

Posterolateral lentiform nuclei & ventral thalamus most susceptible

2. Hypertension – Most common cause of nontraumatic bleed in adult

Lenticulostriate & Pontine vasculatures mostly involved, penetrating branches of MCA

Usually spontaneous in elderly patients, basal ganglia mostly

Vessels often abnormal, ruptured microanuerysms etc

50% have hemorrhage dissection into ventricles, poor prognosis

Lobar white matter hemorrhage in 20%, cerebellum 10%, midbrain & brainstem rare

Originates along perforating branches near dentate nuclei

Active bleeding usually lasts <1hr

Edema progresses for 24-48hrs, 25% die in this period

Hypertensive Encephalopathy – occurs secondary to elevated BP

Toxemia (Most common) – autoregulation overwhelmed especially in posterior aspect

Overdistention of arteriole leads to BBB breakdown

Reversible vasogenic edema results, frank hemorrhage rare

Cortical petechia & subcortical hemorrhage possible, especially in occipital regions

Increased T2 in external capsule & basal ganglia more common

Chronic renal Diseases, TTP, & Hemolytic-Uremic syndrome other causes

3. Hemorrhagic Infarction

Arterial Infarction – hemorrhage when endothelium reperfused

Occurs in 50%, but only seen in 10%, sensitivity: MRI>CT

Cortex & basal ganglia from MCA distribution most commonly, 24-48hrs later

Pseudolaminar Cortical Necrosis – generalized hypoxia

Middle layers usually effected, gyriform hemorrhage

Nonhemorrhagic ischemic changes can occur, gyri calcification possible

Venous Infarction – usually associated with dural sinus thrombosis

Dura around sinus will enhance, clot stays hypodense (empty delta sign)

More likely to effect white matter than cortex

4. Aneurysms - 90% of nontraumatic subarachnoid hemorrhage

Headache common presenting sign for aneurysm, CT best for acute SAH

Blood usually fills ambient cisterns & sylvian first

90% of blood cleared from CSF in 1wk

MRI better for subacute or chronic SAH, dirty CSF

Superficial siderosis – hemosiderin deposit on meninges

Cerebellum brainstem & cranial nerves also coated – neurological dysfunction

Giant aneurysms >2.5cm often have intramural hemorrhage

most from carotid, cavernous portion most common, all ages

75% have calc if thrombosed, none otherwise

Charcot-Bushard Aneurysm – secondary to HTN

5. Vascular Malformations

AVM & Cavernous Angioma commonly

Most bleed into parenchyma rather than subarachnoid space

Arteriovenous Malformation - pial, dural or mixed, No cap bed

Pial AVM’s – hemorrhage @ 2% per year, often in previously normal young pts

70% bleed by 1st exam, repeated hemorrhage can simulate neoplasm

Central nidus with gliosis & encephalomalacia

Dural AVM’s – no central nidus, SAH or subdural

hemorrhage rare unless drainage through cortical veins

Cavernous Angioma – bleed @ .5% per year, freq repeated bleeds

Popcorn like with mixed signal foci & hemosiderin ring

Venous Angiomas – bleed rare, similar hematoma of other malformations

Medusa like collection of dilated medullary veins

Capillary Telangiectasias – usually small & clinically silent

may see multiple small foci of hemosiderin on T2

INTRACRANIAL ANEURYSMS & VASCULAR MALFORMATIONS

Charcot-Bushard Aneurysm – secondary to Hypertension

20% multiple, higher incidence in females.

Look for familial causes such as Polycystic Kid Disease

SACCULAR ANEURYSMS

Berrylike out pouching from arterial bifurcation

Include intima & adventitia, media ends with normal vessel

1. Etiology - hemodynamic induced injury, abnormal shear forces most commonly

Trauma, infection, tumor, drug abuse & AV malformations

Berry Aneurysms – associated with polycystic kidney Diseases & aortic coarctation

2. Incidence – 1% of angios & 5% of postmortems

Multiple in 20%, esp in females & polycystic kidney Diseases

Bilateral in 20%, esp at cavernous sinus, Pcom & MCA trifurcation

Occur age 40-60 unless traumatic or mycotic,

3. Associated Conditions – occur at anomalous vessels & AVM

Inc pressure ie HTN & aortic coarctation

Systemic Diseases – Marfan’s, fibromuscular dysplasia, polycystic kidney diaeases

4. Location - 30% at anterior communicating, 30% at posterior communicating, 20% MCA origin

10% in post circulation especially basilar artery bifurcation

traumatic or mycotic occur anywhere

5. Clinical Presentation – asymptomatic until rupture or giant >2.5cm

1-2% risk of rupture per year, 3.5% risk of surg

No different risk with HTN, age, sex or multiplicity

All should be repaired if >3yr life expectancy

Subarachnoid Hem – clinical grade by Hunt & Hess scale I-V

Vasospasm most common cause of morbidity, 30% die

highest bleed rate in 1st 24hrs, 50% rebleed in 2wk

CT – shows SAH in >80% of ruptured aneurysms

Cavernous sinus aneurysms can compress Nerves III-VI

TIA, Seizures & embolic ischaemia less common

Giant Aneurysms - most from supraclinoid carotid, all ages

Fibrous vascular walls, rarely rupture, Symptoms secondary to mass effect

Partially Thrombosed Aneurysms – 75% have curvilinear calcification

CT most specific for these with target seen

NO calc if not thrombosed

D/D – Meningioma, both erode sella & lat sphenoid

aneurysm has no associated hyperostosis or atherosclerosis

6. Appearance of Saccular Type – catheter angiography definitive

asses for relation to vessel, adjacent branches & vasospasm

essential in assessment of nontraumatic SAH

Thrombosed aneurysm will have no finding, 15%

may see mass effect if large

irregularity or local vasospasm can indicate rupture

D/D vascular loops & infundibuli (embryonic funnel <2mm)

CT may show bone erosion in long standing case

Patent aneurysms enhance intensely w contrast

Location of SAH can be prognostic indicator

Ambient cisterns anterior to brainstem probably just venous rupture

No repeat angio needed

Suprasellar cistern to lateral sylvian fissure

more aneurysmal pattern, must do F/U angio

MRI dependent on pattern of flow, turbulence & clot

may have wall enhancement with gadodiamide, laminated with thrombosis

7. Traumatic Aneurysm

nonpenetrating usually occur at skull base, or shear

hyperextention stretches ICA over lat C1

8. Mycotic Aneurysms – Secondary to infection of arterial wall, rare <10%

adventitia & muscularis disrupted, thoracic aorta commonly

Angio – occur dist to usual location, 2nd branch MCA commonly

most common cause of multiple MCA aneurysms

usually small, staph & strep most common, inc in child

bleed into parenchyma or SAH equal incidence

Medical Treatment usually sufficient to control, surgery if enlarge on angio

Mucor & Aspergilla invade direct from nasopharynx cause thrombosis & infarct more often than aneurysm

9. Oncotic Aneurysms – usually extra cranial, exsanguinate freq

tumor may implant or cause emboli, primary or metastatic

10. Flow-Related Aneurysms – seen with AVM’s in 30%

distal ones most likely to hemorrhage

11. Vasculopathies – rare but seen with SLE, infarct & TIA commonly

Takayasu’s Arteritis – 9:1 female, inflammation & stenosis most commonly

prox arch vessels, L subclavian commonly, often occludes

Fibromuscular Dysplasia – up to 50%, dissection & A-V fistula, 65% bilateral

Cocaine – 50% with CNS symptoms have SAH, may be secondary to HTN treatment

several drugs cause vasculitis .

FUSIFORM ANUERYSMS

Etiology – atherosclerosis, exaggerated arterial ectasia

media damaged, stretches & elongates, frequent mural thrombus

Vertebrobasilar Dolichoectasia – Common site, older patient

often thrombus producing brainstem infarcts

can also compress local stem causing nerve palsies

Imaging – enhances if patent, hyperintense if thrombosed

curvilinear calcification pathognomonic, may cause skull base erosion

DISSECTING ANEURYSMS

Etiology – intramural blood from tear in intima

may narrow or occlude lumen, may distend subadventitia

do not confuse with Pseudoaneurysm, a encapsulated hematoma

Presentation – usually extracranial unless severe trauma

Commonly in midcervical ICA & vertebral from C2 to skull base

Catheter angio remains procedure of choice for assesment

INTRACRANIAL VASCULAR MALFORMATIONS

1. Parenchymal AVM – congenital, dilated arteries & veins without capillary bed

98% solitary, multiple in Osler-Weber-Rendu & Wyburn-Mason

Incidence – 85% supratentorial, peak 20-40y, 25% children

Hemorrhage in 85% with 3% per year risk, seizure 25%, deficit 25%

Size not predictive, deeper & smaller ones bleed more

Parenchymal commonly, also common cause of SAH if

Vascular Steal – atrophy due to vasculopathy of feeding vessel

atrophic low density regions & hematoma with high density

Overlying meninges thick & hemosiderin stained

Angio – shows feeding arteries & tortuous veins

often wedge shaped, possible to appear Normal if thrombosed

GBM may simulate but usually has tissue between vessels

10% have aneurysms in feeding arteries, can bleed

Cryptic AVM’s – not seen by angio, 10%

CT – often absent w/o contrast, 25% have mild curvilinear calcification

mixed increased & decreased density if seen, Mild mass effect possible

Enlarged post venous sinuses but not cavernous sinus

Calcification seen in

MRI – honeycomb of flow voids, increased signal if thrombosed

hemorrhage in different stages often present

No significant intervening brain tissue, D/D : GBM

TX – resection if unruptured, must be completely removed

Aneurysms must be treated separately, increased risk for bleed

2. Dural AVM’s & Fistulae – form within a venous sinus

no discrete nidus, multiple microfistulae, occluding sinus frequent

Follow recanulation of thrombosed sinus, 10% of all AVM’s

Transverse or Sigmoid sinus commonly, Bruits & headache most common

Cavernous sinus AVM – proptosis, retro orbital pain, proptosis

SAH common if reflux flow forced into cortical veins

Carotid-Cavernous fistula related, follow trauma

Occipital & Meningeal branch of ext carotid #1 feeders

CT often N, MRI may show dilated cortical veins

3. Mixed – 15%, if parenchymal AVM recruits arteries from dural supply

4. Capillary Telangiectasias – multiple nests of dilated capillaries

Common in pons & Cerebellum, usually incidental

Gliosis of adjacent brain & hemosiderin staining from hem possibly

Cavernous Angiomas assoc or simply the extreme form

Osler-Weber-Rendu – hereditary hemorrhagic Telangiectasias

25% have brain abnormalities, most are true AVM’s

Visceral angio dysplasia with scalp & mucous membrane telangiectasia

2nd most common lesion to venous angioma at autopsy

Not visualized by angio, may present with epistaxis

CT may faintly enhance, faint on MRI

5. Cavernous Angiomas – Hemangioma or cavernoma

Circumscribed nodule of honeycomb sinusoidal vascular spaces

separated by fibrous bands but no intervening neural tissue

frequently MULTIPLE HEMATOMAS at different stages, reticulated core of vessels

Supratentorial 80% but can occur anywhere, 50% multiple

Most Common vascular lesion identified, 20-40y/o

Seizure, deficits & bleed most common presenting features

Angio does NOT visualize, possible faint blush in early venous

CT shows freq Calc, variable enhancement, can simulate neoplasm

MRI – popcorn like appearance on T2 due to multiple hem

multiple areas of signal drop-out due to hemosiderin

VENOUS MALFORMATIONS

1. Venous Angioma – dilated anomalous veins converge on central vein

Etiology – remnant embryonic venous system, usually solitary

assoc with migrational abnormalities & cavernous Angiomas in 30%

Asymptomatic, Hemorrhage very rare unless from associated cavernous angioma

CT – may show linear tuft of vessels post contrast

located in deep White Matter of cortex or Cerebellum, commonly adjacent to frontal horn

MRI – shows stellate tributary veins into prominent collector vein

gliosis or hemorrhage seen in only 15%

Angio – the only vascular malformation with a single draining vein

Medusa head appearance on venous phase of angio

2. Vein of Galen Aneurysm – enlargement of Galenic system

Secondary to arteriovenous fistulae from choroidal arteries

AVM in thalmus or midbrain can also cause this

Present at birth with high-out put cardiac failure, cranial bruit +

Macrocephaly with obstructive hydrocephalus, deficits & ocular symptoms

US shows bi-directional flow in vein of Galen

Angio demonstrates either choroidal artery or thalmoperforating feeder

dilation to venous varix with or without distal stenosis

if stenosed distally will often thrombose

CT – large enhancing midline mass posterior to 3rd ventricle

Hydrocephalus frequent but hemorrhage rare

enhancing serpentine vessels in thalamic region

3. Venous varix – assoc with several intracranial vascular abnormalities

Enlarged & thin veins resulting in SAH, hydrocephalus & increased ICP

Sinus Pericranii – venous haemangioma adherent to outer skull, deep to galea

supplied from intracranial sinus & blood returns to sinus

present with enlarging fluctuant soft tissue mass, enlarge with crying

often secondary to trauma, often resolved with prolonged compression

Frontal commonly, parietal next, most near sagittal sinus, can be very lateral

Skull Film – usually sharp margins, vascular honeycombs possible

CT – shows strong uniform enhancement

MRI – well delineated ovoid or fusiform areas w variable signal

Venous Cavernoma – subcutaneous lesions of scalp

blood supply from external carotid, drain to external jugular

4. Orbital Venous Varix – rare vascular malformation in orbit

Causes intermittent proptosis & diplopia with valsalva & bending over

Disappear completely with axial views, use tourniquet on jugular vein

NEONATAL HEMORRAGE

Caudothalamic groove – between head of caudate & thalamus

both make up lateral wall of lateral ventricle, terminates in Monroe

Foramen of Monroe – divides frontal & body portions of ventricles

thalmus entirely posterior, caudate head anterior, choroid enters it

1. Subependymal Hemorrhage – preterm infants <32wks

Correlates with size of germinal matrix at birth, largest 24-32wks

involutes & is absent by 40wks, last in inferior lateral wall of frontal

lies inferior to ependyma, superior to head of caudate & anterior to thalmus

Usually occurs in first 3 days, always by 7-8 days

Grade 0 – Normal

Grade I – Subependymal alone

Grade II – intraventricular with no ventriculomegaly

Grade III – Hydrocephalus,

Grade IV – intraparenchymal

grade does not predict ultimate outcome, may progress

Serial studies required, only applies to germinal matrix hemorrhage

2. Parenchymal Hemorrhage – extends farther lateral than germinal matrix

can be “grade IV”, but not all secondary to germinal matrix bleed

most extend from SHE(Subependymal haemorrhage) to frontal or parietal lobes

Hypoxia & Hypercapnia implicated as etiology

stress causes vessels to dilate & burst

Phase 1 – echogenic like SEH for 1-2wks

Phase 2 – central Hypoechoic, bright peripheral rim 2-4wks

Phase 3 – retracts & settles into dependent position

Phase 4 – necrosis & phagocytosis complete, encephalomalacia

Cerebellar hematoma best scaned in coronal behind ear

assoc with mortality of 50%.

3. Choroidal Hemorrhage – usually grade II or III

Second cause of intraventricular hemorrhage not caused by SEH

Difficult to discern from normal choroid on US

asym scanning can show marked asym in choroid size

isolated choroid hematoma simulates ventricular hematoma with no hydrocephalus

Myelomeningocele assoc with pedunculated choroid

CT more reliable than US for Dx

D/D – Choroid Papilloma, very rare, consider if CSF clear on tap

all assoc with hydrocephalus, enhance intensely on CT

HEMORRHAGIC NEOPLASMS & CYSTS

1. Malignancy Related Coagulopathy – esp with leukemia & chemotherapy

systemic neoplasms can be assoc with term coagulopathy

2. Intratumoral Hematomas – 10%, malignant , Astrocytoma’s are most common.

Neovascularity, central necrosis, plasminogen activators etc contribute

Heterogeneous, incomplete hemosiderin ring, edema persist

multiple lesions & min edema suggests nonneoplastic cause

Cysts & slow growing cystic neoplasm like cranio rarely bleed

Oligodendroglioma, neuroectodermal & teratoma hemorrhage frequently

Ependymoma & choroid tumors – frequent SAH & hemosiderosis

Pituitary Adenoma – may bleed more frequently than astrocytoma

Lymphoma rarely bleed unless with AIDS

Renal cell Ca, chorio Ca, melanoma, thyroid & lung mets, 15%

3. Nonneoplastic Hemorrhagic Cysts -rare, colloid cysts never bleed

Rathke cleft cysts & Arachnoid cysts more commonly bleed

Arachnoid cysts bleed secondary to trauma, bridging vessels rupture

sometimes assoc with subdural hematoma


MISCELLANEOUS CAUSES OF BENIGN INTRACRANIAL HEMORRHAGE

1. Amyloid Angiopathy – Most common cause of bleed in elderly patient with no HTN

nonbranching fibrillar protiens form beta-pleated sheets

Deposit is Cortical & leptomeningeal vessels

extend from small vessels to brain parenchyma

Contractile elements replaced by the crystals

Multiple hematomas frequent & occurs at cortico medullary junction

basal ganglia & brainstem not affected

2. Infection & vasculitis - rare, increased chance if immuncompromised

septic emboli – mycotic aneurysms & hemorrhagic infarct

10% of Infective endocarditis have SAH or parenchymal

Aspergillosis & other fungi directly invade vessel

Thrombosis, infarction & hem result

Herpes Simplex II – the only encephalitis assoc with hematoma

3. Recreational Drugs – 50% have preexisting AVM or aneurysm

Cocaine can induce an acute hypertensive episode, vasospasm

also enhances platelet aggregation, dural sinus thrombosis

amphetamine & PCP also associated with hemorrhage

endothelial damage & necrotizing vasculitis

4. Blood Dyscrasias & Coagulopathies – iatrogenic or acquired

Vit K deficiency, hepatocellular diseases, antibody against clot, DIC

Anticoagulants, thrombolytics, aspirin, Etoh abuse, chemo

15% of all intracranial hemorrhage on anticoagulants

Supratentorial, intraparenchymal bleeds most common

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