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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Functional Magnetic Resonance Imaging (fMRI) in Neuroradiology:

DTI Color Map
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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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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 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.

NEURO-RADIOLOGY PEARLS

Stroke

ATHEROSCLEROSIScauses 90% of thromboembolic disease & vascular stenosis

1. Etiology – focal endothelial change or subtle injury allows LDL & macrophage into intima Smooth muscle cells recruited & filled with fatty esters – foam cells. Fibrotic cap covers core of dead foam cells .Associated inflammation allows granulation tissue & neovascularity. Plaques ,hematoma & necroses acts as nidus for thrombi

2. Imaging – angio remains gold standard, US, CT & MRA alsoUS – peak systolic velocity best parameter for assesing stenosis . Angio done to – 1) determine degree of stenosis & ulceration 2) Identify tandem lesions in siphon or intracranialy 3) evaluate existing or potential collateral circulation. CT – identifies vessel ectasia & mural calcification .MRI – flow voids do not exclude significant stenosis

3. Carotid Origin Stenosis – endarterectamy helps if 70-99% delayed veiws show “string sign” of high grade stenosis.

4. Tandem Lesion – distal stenosis of carotid also seen in 2%hemodynamic effect additive, usually in siphon, PTA needed

5. Collateral Circulation – critical severe stenosis or occ circle of willis #1, complete in only 25%patent anterior communicating artery usually adequate to allow clamping external carotid to ophthalmic good, few others adequate

6. Subclavian Stealocculusion of proximal subclavian or arch, irregular flow reversed in vertebral artery to supply arm & shoulder. Atherosclerotic Diseases can effect any proximal great vessel or arch

7. Intracranial Atherosclerotic Disease – irregular lumen & stenosis can lead to tortuous vessels & fusiform aneurysms
Basal ganglia disease

Basal Ganglia Hemorrhage Horizontal

CEREBRAL ISCHEMIA AND INFARCTION

1. Physiology – central & peripheral portions differ. Central nidus quickly irretrievably damaged this is the zone of frank Cerebral Infarction. Penumbra – peripheral cells viable but at risk for hours. Zone of generalized neuronal necrosis, support cells left . Selective neuronal necrosis – only most vulnerable neurons. Ion homeostatsis lost: C++, Na+, & Cl- accumulate. Anerobic glucolysis causes metabolic acidosis. Free Radicals accumulate, cytoskeleton breaks down, cell dies

2. Selective Vulnerability – sensitivity to ischemia varies. Neurons most vulnerable are astrocytes, oligodendrocytes, microglia, Hippocampal pyramidal fibres most sensitive of the neurons. Neocortical layers III, V & VI, purkinje & neostriatum, Thalmus, Basal Ganglia, Centrum Semiovale susceptable ,long single arteriole vulnerable to anoxia & hypoperfusion. Vascular Watersheds – cortex & Cb in adults & term infants in deep perventricular region in premature babies. Adults – occurs in the WM near caudate or frontoparital Hyperacute Infarcts –

Acute Infarcts – 12-48hrsCT – sulcal effacement, low density basal ganglia, Gray-White interface lost – Insular ribbon sign. MRI – Hyperintensity on T2 develops in 8hrs associated with mass effect in 25%, usually mild, maximum at 5 days. Meningeal enhancement adjacent to infarct

5. Subacute Infarcts – 2 days – 2wks CT – 24-48hrs wedge shaped area of low attenuation visible. Edema & mass effect increases initially, subsides by 4-7 days. hemorrhagic transformation at 1-3 days, .Contrast enhancement from BBB breakdown, gyral or RING develops at 3-4 days & can last 8-10 wks, 20% seen only with a contrast scan, but NOT good for Pt . MRI – meningeal & intravascular enhancement decreases at 2-4 days. parenchymal enhancement begins & can last for weeks. T2 begins to fade as protiens from cell lysis spill out, 1-2 wks – T1 post-contrast striking, T2 NormalWallerian Degeneration – hypodense band in corticospinal tract

6. Chronic Infarcts – > 2 weeks. Gliosis & volume loss are hallmark of stroke residua. Both CT & MRI show well delineated encephalomalacia. Ipsilateral ventricle enlarges, dystrophic calcification rare. Hemmorhagic areas develop predictably

7. Lacunar Infarcts – 25% of all strokes, basal ganglia & thalami mostly affected. single long penetrating vessel to deep cerebral gray matter. CT – usually only seen with associated WM disease. MRI – dec T1, Inc T2 – DDx – subependymal myelin palloror ,Virchow-Robin – enlarged perivascular spaces

8. Hypoxic-Ischemic Enchephalopathy – global rather than focal. Etiology is prolonged hypotension, asphyxia, or CO poisoning.Basal Ganglia & border zones most sensitive.

Pseudolaminar Necrosis – Generalized cortical ischemia. layers III, V & VI effected along with caudate & putamen9.

Hemorrhagic Infarcts – easily detected by CT& MRI – standard images have poor sensitivty

10. Cerebellar Infarcts– rare due to extensive collarterals. Present with Vertigo, ataxia, nausea & vomiting. 90% occur in PICA distribution, congenital abscence. 25% enhance, most at subacute, gyral or ring type CT Finding Summary – Normal up to 24hrs. Peak mass effect at 2-5d, gone by 2nd week, Peak enhancement in 2nd week, predominately gray matter.