MOYA – MOYA SYNDROME
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CLINICAL IMAGING OF THE BRACHIAL PLEXUS:
CLINICAL IMAGING OF THE BRACHIAL PLEXUS:
Himadri S. Das, N. Medhi, P. K. Sharma, P. Goswami, P. Hazarika, B. J. Sharma
Primus Imaging, Guwahati
The Brachial Plexus (BP) is comprised of the roots, trunks, divisions, cords, and branches.
ANATOMY
The brachial plexus originates from the anterior divisions of the spinal nerve roots of C5-T1. Variations in innervation are occasionally present. A “pre-fixed” BP occurs when C4 replaces T1 as a dominant contributor. A “post-fixed plexus is present when BP receives contributions from C6 – T2. These variations appear to have little clinical significance.
The BP is formed in the majority by the anterior divisions of the spinal nerves of C5 – T1 that forms its roots. The roots of the BP then combine to form the 3 trunks (upper, middle, lower). The roots of C5 and C6 combine to form the upper trunk, while the roots of C8 / T1 combine to form the lower trunk. The C7 root is the sole contributor of the middle trunk.
The trunks of the BP then split into anterior and posterior divisions. These divisions combine to form the cords of the BP. The cords of the BP are named (posterior, lateral, medial) according to their relationship with the adjacent subclavian artery. The posterior divisions of the upper, middle and lower trunk combine to form the posterior cord. The anterior divisions of the upper and middle trunks combine to form the lateral cord, and the anterior division of the lower trunk continues to form the medial cord.
The BP terminates in various branches, which supply motor sensory innervation to the upper extremity. The suprascapular nerve is the only terminal branch that originates from a trunk of the BP.
FIG1: ANATOMY OF THE BP
PERIPHERAL NERVES THAT ORIGINATE FROM CORDS OF THE BRACHIAL PLEXUS
Branches from the lateral cord
Lateral pectoral nerve
Musculocutaneous never
Lateral head of the median nerve
Branches from the median cord
Medial pectoral nerve
Medial cutaneous nerve of the upper arm
Medial cutaneous nerve of the forearm
Medial root of the median nerve
Branches from the posterior cord
Upper subscapular nerve
Thoracodorsal nerve
Lower subscapular nerve
Axillary nerve
Radial nerve
SURGICAL ANATOMY
The surgical classification is based on the relationship of the BP to the clavicle and divides it into supraclavicular, retroclavicular, and infraclavicular segments. The supraclavicular BP contains the roots and trunks and is situated in the posterior triangle between the anterior and middle scalene muscles.
The retroclavicular plexus contains the divisions and is located posterior to the clavicle adjacent to the subclavian artery. The infraclavicular plexus also courses adjacent to the subclavian artery and contains the cords and portions of the distal branches of the BP.
RADIOGRAPHIC ANATOMY
The radiologist can identify specific portions of the BP based on certain anatomic structures, which are easily seen on imaging studies. The fascial plane between the anterior and middle scalene muscles contains the roots and cords of the BP. The divisions and cords course adjacent to the subclavian artery. Thus, any mass that is adjacent to the subclavian artery is in close proximity to the divisions and cords of the BP. The branches of the BP are difficult to identify individually on imaging studies. However, it may be safely assumed that a mass in the axillary region is likely to involve the terminal branches of the cords.
FIG 2(a): CORONAL T1 WEIGHTED MR SEQUENCE
FIG 2(b): AXIAL T1 WEIGHTED MR SEQUENCE
Abbreviations: Clavicles (C), subclavius muscles (SUB), external jugular vein (XJ), internal jugular vein (J), subclavian veins (SV), axillosubclavian veins (AXV), coracoid processes (CP), brachiocephalic artery (BR), first ribs (FR), trachea (T), right lung (RL), and left lung (LL) are labelled for reference. The aorta (A) and pulmonary artery (P) are labeled to identify the heart.
CLINICAL SCENARIO:
Clinical features of a brachial plexopathies are often vague and non-specific. Symptoms include motor, sensory and sometimes, autonomic disturbances of the supraclavicular region, shoulder, and upper extremity. Motor weakness is primarily seen in those patients with obstetric-related palsies and avulsions of anterior roots. Sensory deficits are more often related to those patients with neoplastic and/or radiation induced plexopathies. Neoplastic plexopathies tend to be more painful and progress more rapidly than radiation-induced ones.
Long-term complications resulting from brachial plexopathies include muscle wasting, upper extremity edema, osteoporosis, joint contractures, complex regional pain syndromes and/or sympathetically mediated pain, and joint degeneration.
There are certain clinical findings that help to localize the inciting lesion and thus permit radiologists to focus their diagnostic evaluation. The phrenic nerve receives contributions from C3 – C5. Because of this overlap in innervation with the upper roots of the BP, a plexopathy associated with a paralyzed diaphragm indicates involvement of the upper plexus. The rhomboid and serratus anterior muscles are innervated by proximal branches of the BP (C5 – C7). Thus, rhomboid muscle paralysis or winging of the scapula is indicative of a proximal injury.
The Erb-Duchene palsy is most often a consequence of birth injury which results from shoulder dystocia during a vertex vaginal delivery. Obstetrical palsies tend to occur more often in larger babies, breech or forceps deliveries, and after prolonged labors. The right shoulder is more commonly affected because the head is usually in a left occiput anterior position. Excessive traction on the head and neck results in an injury limited to the C5 and C6 nerve roots. Patients with an Erb’s palsy have characteristic physical findings which consist of adduction and internal rotation of the arm with pronation of the forearm.
Several associated clinical findings implicate a lower BP lesion. The stellate ganglion receives contributions from C8-T1. Thus, a brachial plexopathy associated with an ipsilateral Horner’s syndrome is indicative of a lesion involving the lower BP. The classic Dejerine-Klumpke palsy is due to a failure to deliver the upper extremities before the head during a breech vaginal delivery. Forcible abduction of the arms causes excessive stretching and results in an injury to the nerve roots of C7-T1. This injury involves the lower intrinsic hand muscles, and the radial innervated extensors. Such an injury characteristically results in a paralysed (“claw”) hand. Because of the overlap in innervation with the stellate ganglion, Klumpke’s palsy may also be associated with ipsilateral Horner’s syndrome.
Several findings may be indicative of a more severe injury to the BP. A plexopathy associated findings similar to a Brown-Sequard syndrome may suggest a proximal nerve root avulsion and spinal cord injury. A nail limb with complete absence of deep tendon reflexes is indicative of a complete disruption of the BP.
INDICATIONS OF MR IMAGING:
1. Are symptoms unilateral or bilateral? The presence of bilateral brachial plexopathies is usually associated with a lesion in the epidural space or neural foramina, and these patients should be evaluated initially with a dedicated imaging study of the cervical spine.
2. Is there a history of trauma? These patients often require dedicated sectional imaging studies of the cervical spine to supplement the evaluation of the peripheral components of the plexus.
3. Is there an associated mass in the neck, supraclavicular fossa or axilla? Characterization of a palpable mass may require the use of double-echo-T2-weighted rather than SE-T2 weighted sequence and the administration of intravenous contrast.
4. Are the symptoms produced by a particular arm position? Hand pain with arm elevation of a common finding with thoracic outlet syndrome secondary to a cervical rib, and identification of a cervical rib on a frontal radiograph should prompt further evaluation of the subclavian and axillary arteries rather than the soft-tissue components of the brachial plexus.
5. Does the patient have a prior history of carcinoma? Studies of patients with a history of malignancy require a careful search for abnormal signal within the trabecular bone of the cervical spine, clavicle, scapula, and shoulder as well as the soft tissues adjacent to the nerves. This is especially important if pain is the only presenting symptom.
6. Is there a history os surgery or radiation therapy to the affected axilla, neck or supraclavicular fossa? Images of the affected side in these patient are often confusing and oblique coronal and sagittal imaging of the opposite brachial plexus is often useful for comparison and identification of subtle changes.
IMAGING IN VARIOUS PATHOLOGIES OF THE BRACHIAL PLEXUS:
TRAUMA
The initial imaging evaluation in patients with a post-traumatic brachial plexopathy should consist of plain films of the cervical spine, shoulder, clavicle and chest. These plain films should be assesses for fractures of subluxations which could account for the acute neurological deficit.
Posttraumatic nerve root avulsion of the BP results from forcible trauma which separates the arm from the shoulder. This may result in stretching and tearing of fibrous attachments which extends from the nerves to their respective transverse processes. Pseudomeningoceles arise from tears of the dura and arachnoid membranes caused by the root sleeves being pulled out into the intervertebral foramen. Nerve root avulsion results if the traction force exceeds the elastic tolerance of the root. Spinal cord injury may occur from direct contusion or by avulsion of the nerve root. Thus, it is possible to have post-traumatic Pseudomeningoceles without a coexistent nerve root avulsion. Conversely, approximately 20% of clinical nerve root avulsions are not associated with a pseudomeningocele.
Both CT Myelography and MR imaging may be used to evaluate patients with post-traumatic brachial plexopathies. The characteristic findings in a posttraumatic BP stretch injury are Pseudomeningoceles which may be detected by both CT Myelography and MR imaging. Thin section CT Myelography (1mm-3mm thick sections) allows for consistent visualization of the ventral and dorsal nerve roots within the spinal canal and is therefore the preferred imaging modality.
Absence of a nerve root shadow on CT Myelography is indicative of nerve root avulsion. Nerve root or dural thickening seen on MR imaging is suggestive of nerve root avulsion or edema. Recent technical advances in MR imaging permit improved visualization of the nerve roots within the spinal canal in normal patients, however, these advanced techniques are mostly limited to tertiary institutions and are not currently in general use. MR imaging does allow visualization of Pseudomeningoceles , which do not fit with contrast on CT Myelography. The role of MR Myelography for evaluating BP injuries is currently being evaluated.
Other post-traumatic lesions which may result in a brachial plexopathy include hematomas, vascular compression from pseudoaneurysm formation, and complete disruption of the brachial plexus. The presence of intramedullary or extramedullary haematoma may be detected with MR imaging. MR imaging is superior to CT for evaluating for the presence and extent of soft tissue injuries.
FIG 3: CORONAL T2 W IMAGE SHOWING POST TRAUMATIC PSEUDOMENINGOCELE
TRAUMATIC CAUSES OF BRACHIAL PLEXOPATHY
Fractures of the cervical spine or clavicle
Nerve root avulsion with or without an associated pseudomeningocele
Soft tissue edema
Hematoma
NONTRAUMATIC CAUSES OF BRACHIAL PLEXOPATHY
Primary neural tumors such as meningioma and schwannomas
Metastatic disease
Pan coast tumor
Post irradiation injury
Radiculopathy secondary to disk disease
Bony abnormalities such as cervical rib.
NEOPLASM’S
A variety of neoplasms may involve the BP. These lesions may be classified as tumours of neural (primary) and of non-neural origin (secondary). Primary BP tumors most commonly arise from the nerve sheaths. The most common benign neural tumors are neurofibromas and schwannomas. Neurofibromas are the most common neural tumor to involve the BP. Histologically; these lesions are unencapsulated tumors that are felt to arise from the nerve fascicles. One-third of these lesions occur in patients with Neurofibromatosis type 1 (NF-1) while two- thirds of cases are sporadic. Neurofibromas arising in patients with NF –1 occur with equal incidence in males and females. These tumors are characteristically multiple and plexiform in appearance with diffuse involvement of the BP. In contrast, sporadic neurofibromas are more commonly seen in females (2-3:1 female to male ratio). Sporadic neurofibromas are typically solitary and most likely originate in the supraclavicular BP. Schwannomas are the second most common neural tumor involving the BP.
The imaging features of solitary neurofibromas are essentially indistinguishable from those of the schwannomas. On CT, these lesions have similar attenuation to muscle and enhance variably with contrast. Both tumors may be associated with bony remodeling. On MR imaging, these two lesions are isointense to muscle on T1W sequences and hyperintense on T2W sequences. Both tumors typically enhance following intravenous Gadolinium administration. The diagnosis of neurofibromas may be made with a high degree of confidence if the lesions have a plexiform appearance or occur in a patient with NF-1.
Malignant neural tumors are very rare and consist mostly of fibro sarcomas and neurogenic sarcomas (malignant neurofibromas). Secondary neoplasms may extend to involve the adjacent BP. These lesions may also be either benign or malignant. Benign masses which involve the BP include: lipoma, lipoblastoma, desmoid, lymphangioma, myoblastoma, osteochondroma, and ganglioneuroma.
Malignant neoplasms which may involve the BP are commonly due to direct extension from a Pancoast tumor or metastatic disease. Involvement of the BP by direct extension of a Pancoast tumor may be suspected in patients who present with supraclavicular pain, weakness and paresthesias. Imaging findings suggestive of BP invasion by a superior sulcus tumor are obliteration of the apical fat and proximity of the mass to the BP. Tumors which have been reported to metastasize to the BP include breast, lymphoma, bladder, gastrointestinal, testicular, thyroid, lung, melanoma, head and neck, and sarcomas.
The imaging modality of choice in patients with possible neoplastic invasion of the BP is MR imaging due to its multiplanar capability and high soft tissue characterization. Previous studies have shown MRI to have a high sensitivity (100%) in detecting neoplastic involvement of the BP. The extent of disease is also better depicted with MRI than with CT. Coronal T1W images are especially helpful for assessing the status of the apical fat in patients with Pancoast tumors and evaluating the relationship of masses to the BP.
INFLAMMATORY
Inflammatory processes may involve the BP include radiation therapy, neuritis, and infections. Radiation therapy (RT) may injure the BP and cause a plexopathy. Three classical syndromes of RT induced brachial plexopathy have been described. The most common form is a delayed progressive radiation fibrosis. The remaining two forms of radiation damage are a reversible or transient plexopathy and an acute ischemic plexopathy.
Radiation- induced brachial plexopathy is the most common and severe peripheral nervous system complication of RT. Radiation damage to the BP appears to be dose related and most likely occurs in patients who have received doses in excess of 6000 cgys. It is most commonly seen in females who have been treated with RT for breast cancer. The plexopathy tends to be delayed and progressive with the majority of patients presenting atleast 6 months after the completion of RT. The initial symptoms include paresthesias, followd by pain and weakness. These symptoms typically occur in upper trunk distribution with weakness of the arm flexors and shoulder abduction. Pain can accompany these paresthesias but it usually occurs late in the course of this syndrome. However, other reports suggest that RT induced plexopathies are generalized and that the distribution of the deficits is not helpful in separating this variety of plexopathy from a neoplastic one. Histologically in RT –induced plexopathy, there is dense fibrous tissue encasing the BP with Wallerian degeneration. On physical examination, radiation- induced brachial plexopathy may result in reflex abnormalities, intrinsic muscle weakness, muscle atrophy and lymphedema.
MRI is the modality of choice for evaluating patients previously treated with RT to the supraclavicular region. The imaging findings of RT –induced brachial plexopathy are diffuse thickening and enhancement of the BP without a focal mass. The presence of a focal mass in a patient treated with RT is suspicious for recurrent tumor and requires further evaluation, especially in patients treated with doses less than 6000 cgys. Horner’s syndrome is rarely caused by RT alone and, when present, is also strongly suggestive of recurrent tumor.
Active inflammation of the BP is termed “brachial neuritis” (BN). Its etiology may be due to a primary viral infection (cytomegalovirus, coxsackie), or complication from prior infection. BN may also result as a complication of previous serum vaccine, antibiotic, or other drug administration. Idiopathic and heredofamilial forms of BN have also been described. Patients with BN typically present between the third to seventh decades of life. The condition is slightly more common in males than in females (2.4::1). Clinically, these patients present with an ache in the supraclavicular region and shoulder. The pain often worsens over a 3-10 day period and may be followed by weakness and sensory and reflex impairment. In most cases, the disease is self limited and subsides over a 6 to 12 week period. However, residual deficits occur in some patients. MRI is the modality of choice in patients suspected of having BN. The MRI findings are diffuse thickening, abnormal T2W signal intensity, and abnormal enhancement of the BP on the gadolinium enhanced images.
Infectious processes involving the BP most commonly involve its supraganglionic portion and are most likely due to discitis with associated epidural abscesses. Involvement of the more distal components of the BP is unusual and may be due to extension from and adjacent infection.
MISCELLANEOUS
The clinical symptoms of degenerative cervical disc disease may mimic those of a brachial plexopathy; therefore, evaluation of the cervical spine should be included in imaging studies of the BP. Eighty to ninety percent of cervical radiculopathies involve the C6 (C5/C6 disc) and C7 (C6/C7 disc) roots. Patients may present with numbness, pain, sensory loss, and diminished reflexes at the affected levels. These symptoms may be exacerbated by coughing, sneezing, or lateral head movements.
Brachial plexopathy may also be caused by cervical ribs. Cervical ribs are present in approximately 1% of the population and are symptomatic in 10% of affected individuals. They are more common in females than in males (2:1) and are unilateral in 50% – 80% of individuals. Occasionally, a cervical rib may be attached to the first rib by a fibrous band. The BP may be affected by cervical ribs in one of two ways. The cervical rib may be positioned so that the BP must cross over it to enter the axilla, thereby stretching the lower trunk. Secondly, the cervical rib may narrow the space between the posterior aspect of the first rib and the anterior scalene muscle reducing the area through which the BP and subclavian artery course. The cervical rib syndrome is felt to result from compression of the lower trunk of the BP as it crosses over the cervical rib or by compression of the lower trunk by a fibrous band that attaches to the first rib. The symptoms consist of pain and /or paresthesias along the ulnar border of the forearm and hand and motor weakness in a similar distribution. Continued compression may result in muscle wasting which initially involves the thenar eminence but may also spread to involve the small muscles of the hand.
REFERENCES :
Som P.M, Curtin H. Head & Neck Imaging, 4th edition, 1998, Mosby Inc, Volume-II, Mosby Inc, page no 22217-2225
Mukherji SK, Castillo M, Wagle A. Brachial Plexus. Seminars in CT, US and MR imaging 1996; 17:519
Posniak HV, Olson MC, Dudiak CM, Wisniewski R, O’Malley C. MR imaging of the Brachial Plexus. AJR 1993; 161:373-379
Guha A, Graham B, Kline DG, Hudson AR. Brachial Plexus injuries. In: Wilkins RH, Rengachary SS, Eds. Neurosurgery 2nd ed. New York, NY: McGraw-Hill 1996:3121-3134
England JD, Summer AJ. Nontraumatic Brachial plexopathy. In: Wilkins RH, Rengachary SS, eds. Neurosurgery 2nd ed. New York, NY: McGraw-Hill 1996:3245-3250
Davies ER, Sutton D, Bligh AS. Myelography in brachial plexus injury. Br J Radiol 1966; 362-371
El-Gammel T, Brooks BS, Freedy RM, Crews CC. MR Myelography: imaging findings. AJR 1995; 164:173-177
Bowen BC, Verma A, Brandon AH, Fiedler JA. Radiation induced brachial plexopathy: MR imaging with clinical correlation AJNR 1996; 17:1932-1936
IMPROVING RADIOLOGICAL SERVICES IN INDIA ALONG THE LINES, OBSERVATIONS AND SUGGESTIONS PROPOSED BY EUROPEAN RADIOLOGICAL ASSOCIATION STANDARDS 2003:
IMPROVING RADIOLOGICAL SERVICES IN INDIA ALONG THE LINES, OBSERVATIONS AND SUGGESTIONS PROPOSED BY EUROPEAN RADIOLOGICAL ASSOCIATION STANDARDS 2003:
Dr Himadri S. Das
Guwahati, Assam
At the introductory meeting held at IAEA headquarters in Vienna in March 2003 on Thematic Planning for Diagnostic Radiology, representatives of the IAEA indicated that the Agency wished to take a more holistic approach to the improvement of global radiological services by helping to develop adequate standards for the 135 Member States, and by developing partnerships with other organizations with similar interests. Within IAEA there are already four programs in the health area covered by the Division of Human Health namely Nuclear Medicine, Radio Biology, Dosimetry/Physics & Nutrition. The focus is on identifying a role for nuclear sciences and technology in addressing human health problems particularly in developing countries, rather than duplication of activities already covered by other agencies, i.e. a complementary and co-coordinating role with a focus on patient radiological services, rather than strictly regulatory aspects. Specific concerns expressed during the meeting included the absence of access to Radiology services for two thirds of the world’s population, and the predicted growth in malignant disease in both developed and developing countries over the next decade requiring significant Investment in trained staff and equipment.
Access to health care should be a basic human right. Diagnostic Radiology is fundamental to the proper assessment and monitoring of many diseases processes, and is required in around 25% of medical Interventions. The challenge is to maximise the utilisation of diagnostic equipment in a timely fashion to expedite diagnosis and initiate appropriate treatment. Emergency Radiology services are now required on a 24 hour / 7 day week basis. Screening for early diagnosis of disease e.g. breast and lung cancer and vascular disease, provides an organizational, financial and ethical challenge. Research into the next developments in imaging is required. Many of these stem from the genomics project, and the requirement for molecular imaging and cellular imaging, in order to promptly identify disease processes and follow response to therapy.
It is appropriate that the worst cases are prioritized, i.e. third world and highly populated countries like India, or those affected by recent conflicts, are supported in the provision of, at least, basic radiology services. The development of pilot centres of excellence as already in effect in the WHO initiative would be a good starting point. These could be hospital and/or community based and should offer the possibility of providing a “critical mass” of trained Radiologists and Radiographers and support staff drawn from the indigenous population, with practical support and encouragement from outside gencies and national governments.
These could provide the framework for the development of training programmes and benchmarks for staff development, and are more likely to have basic infrastructure, e.g. a reliable electrical supply, required to underpin an ongoing radiological service, and the pump priming of sustained academic development.
Basic X-ray equipment, which is robust and easy to maintain, should be provided. Image processing using film based systems may require a lower initial investment, but Computed Radiography (CR) systems offer lower revenue expenditure in the long term and the possibility of image transmission (tele-radiology) or reporting/second opinion, if the local telecommunications system is capable of supporting this technology. Basic Ultrasound equipment has become cheaper and more sophisticated and small portable units have now got quite sophisticated capability including colour Doppler imaging. These are invaluable in obstetric assessment, as well as general abdominal and small parts: thyroid, testis, breast, etc. evaluation, and also for vascular evaluation and paediatric cerebral examination. With good tuition, those with basic anatomy and pathology training can master the operational skills without too much difficulty. Training programmes could be provided on a “fellowship” basis. The capital cost of CT scanners has relatively declined in recent years. Regular planned maintenance is essential. Modern X-Ray tubes are relatively resilient. A properly planned CT examination is a flexible and powerful diagnostic tool and should be available in any “core” hospital department. Targeted contrast agents and the development of new MRI sequences leading to functional imaging are of particular importance, especially in Neuro-Radiology. Collaborative multi centre studies are required and could be supported.
Radiology services require teamwork and the involvement of trained Radiographers, Clerical/Administrative staff and Medical Physicists. Nowadays IT Staff are essential to support Radiology Information Systems (RIS), Picture Archiving and Communications Systems (PACS) and integration with Hospital Information Systems (HIS). These arrangements support the provision of comprehensive Radiology services and are usually based in hospitals or clinics.
Lack of comprehensive training leads to emphasis on one modality, sometimes undertaken by physicians with no formal Radiological training. Similarly, absence of reliable up-to-date equipment also limits the quality and range of diagnostic & therapeutic options. In the worst scenario, as indicated above, there is a complete absence of Radiological services, often compounded by other fundamental problems: starvation, lack of clean water, electricity and telecommunications, and the presence of endemic diseases – AIDS, malaria, hepatitis, Tuberculosis etc.
In Europe, postgraduate training in Radiology lasts for five years, following medical qualification and experience. Modalities used are: X-ray Fluoroscopy, Ultrasound, Computed Tomography (CT) and Magnetic Resonance Imaging (MRI). Recently, Positron Emission Tomography (PET) has been added to the diagnostic armamentarium – often in conjunction with CT (e.g. CTPET).
The situation in India is after basic medical qualification (MBBS degree) and general medical experience, postgraduate training in Radiology (MD) lasts for three years. Diploma courses (DMRD) are offered in few places. Some Radiologists sub-specialise, usually on the basis of Interest in one or other organ systems, but most Radiologists conduct a Radiological practice utilizing Radiographic Images derived from X ray, USG & doppler with CT, MRI etc being available in few Governmental Hospitals, nursing homes, general purpose diagnostic centres and the likes. New entrants are corporate hospitals with ultramodern equipments but these lack the experience of properly trained Radiologists WITH the experience of using such machines.
The Government, Radiological Associations and regulatory bodies could help to:
1. Co-operate in the provision of training and educational standards
2. Inspect and advise on training centres
3. Encourage the development of national legislative requirements in Radiation protection. Provide quality and benchmarking guidelines for Radiology Department management.
4. Upgrading Guidelines on Pregraduate and Postgraduate training in Radiology and in Continuing Medical Education. Referral Guidelines for physicians setting out an appropriate radio diagnostic approaches.
5. Encourage Radiologists to provide leadership in the provision of high standards in radiological services.
Significant funding is required if we are to compete with our international colleagues who have been successful in attracting huge government funding to new national radiological research institutes. The world of Diagnostic Radiology is a referral specialty of medicine providing services in medical imaging and image guided Interventional techniques to the patients of Medicine and allied practitioners, surgeons, oncologists and other medical specialists.
NEURORADIOLOGY DIFFERENTIAL DIAGNOSES
Neuroradiology Differential Diagnoses
(Original Text from Spencer Gay, MD, UVA)
POSTERIOR FOSSA MASS – CHILD
Cerebellum/IVth Ventricle
- Medulloblastoma – midline, vermian or roof – usually hyperdense on plain CT -
often enhance homogeneously – Astrocytoma
- usually PILOCYTIC ASTROCYTOMA – 2/3 are cystic with mural nodule – cyst fluid
denser than CSF due to protein
- Ependymoma – INTRA-ventricular – “cast” of lumen – 50% are calcified
Brainstem – Brainstem glioma – expands brainstem (infiltration w/o destruction)
- hydrocephalus (may be late)
Extraaxial fluid collection
- Large cisterna magna (“Mega Cisterna Magna”)
- Epidermoid inclusion cyst
- Arachnoid cyst (may bevel inner table of skull) – Dandy Walker cyst of 4th
ventricle (look for vermian abnormalities)
- Vermian agenesis
- Chronic subdural hematoma
COMMENT: For a posterior fossa mass one should consider the direction of
displacement of the 4th ventricle to assess from which compartment it arises
POSTERIOR FOSSA MASS – ADULT
Extraaxial:
- Vestibular Schwannoma (CPA)
- Meningioma
- Ependymoma
Intraaxial:
Metastasis – most common intraaxial neoplastic post fossa mass in adult
Hemangioblastoma – cystic or solid – angio shows hypervascularity & stain
Astrocytoma – usually not vascular on angio
Medulloblastoma – often more lateral in adults Lymphoma Abscess Infarct
CEREBELLAR ATROPHY
Drugs
- Alcohol (vermis)
- Dilantin (hemispheres)
- Chemotherapeutic agents
Vascular process (incl. infarction)
Trauma
Hyperthyroidism
Paraneoplastic – lung, breast, lymphoma, ovary
Olivopontocerebellar degeneration
COMMENT: Cerebellar sulci > 1 mm, enlarged 4th ventricle, enlarged cisterns
MASS IN CLIVUS
Chordoma – bone destruction
Meningioma – hyperostosis
Local invasion
- nasopharyngeal cancer
- pituitary tumor
Metastasis
Chondrosarcoma (more often paramedian)
COMMENT: A basilar artery aneurysm may appear to arise from the clivus – look
for pulsationartifact in the phase encoding direction
BRAINSTEM LESION
Brainstem glioma
- present with cranial nerve palsies
- hydrocephalus less common
Infarction
Hemorrhage – often hypertensive
Pontine myelinolysis (“central”, aka. “Osmotic Myelinolysis”)
Multiple sclerosis
Metastasis
Basilar artery aneursym/dolichoectasia may displace brainstem
CEREBELLOPONTINE ANGLE TUMOR
Vestibular Schwannoma (aka. “Acoustic neuroma”)
- enlarges IAC, rounded mass in cistern
- enhances with IV contrast and Gadolinium DTPA
- large (>2.5 cm) schwannomas heterogeneous
- bilateral lesions in NF-2
Meningioma
- does not enlarge IAC
- enhances homogeneously
Epidermoid
- hypodense
- enlarges cistern
- serpentine margin
- FLAIR sequence may distinguish from CSF (arachnoid cyst)
Exophytic brainstem glioma
- progressive cranial nerve palsies
Acquired Epidermoid (“Cholesteatoma”)
-erupts from middle ear
- signs of mastoiditis, Hx of ear infection
Metastasis
Basilar artery aneurysm
Glomus jugulare
Trigeminal schwannoma (may “dumbell” into middle fossa)
Arachnoid cyst (homogeneous CSF density and signal)
CT PROGRESSION OF INTRACRANIAL HEMATOMA
(change from HYPER- to HYPO- dense over time)
Initially – 60 – 90 Hounsfield Units (HU)
2 days – 70 HU
3 weeks – 30 HU
>5 weeks –
MRI APPEARANCE OF INTRAPARENCHYMAL HEMATOMA
(T1/T2: II, ID, BD, BB, DD (I-iso, D-dark, B-bright)
Hyperacute – minutes to hours (DD => II)
- T1WI – hematoma hypointense (deoxyHb) => isointense
- T2WI – hematoma hypointense (deoxyHb) => isointense
Acute – 0-2 days (ID => BD)
- deoxyhemoglobin in intact RBCs with surrounding edema
- T1WI – hematoma isointense, low signal intensity (SI) edema
- T2WI – hematoma decreased SI at center, high SI edema
Subacute – 2-14 days (BB)
- deoxyhemoglobin changes to methemoglobin from outer to inner
- T1WI – outer core shows increased SI
- T2WI – Outer core shows increased SI due to shortened T1, longer T2
Chronic – 14 days (BB => DD)
- hemosiderin laden macrophages at periphery
- T1WI – inner core now also increased SI, rim has low SI
- T2WI – inner core also has increased SI, rim has low SI
Chronic – months later (DD)
- hemosiderin laden macrophages at periphery
- T1WI – mostly iso-/decreased SI, rim has lower SI
- T2WI – markedly hypointense rim has low SI – “blooms” with greater
T2-weighting
COMMENT: T1WI = T 1 weighted image T2WI = T 2 weighted image SI = signal
intensity
CT PROGRESSION OF ISCHEMIC INFARCT
Initially – 30 HU
1 day – CAUSES OF SUBARACHNOID HEMORRHAGE
Trauma (most common, but different clinical presentation)
* Ruptured aneurysm (classic “Worst HA of my life!”)
* Arteriovenous malformation
Neoplasm
Hypertensive hemorrhage (after rupture through brain or ventricle)
COMMENT: CT identifies a subarachnoid hemorrhage in upto 80 – 95% of cases.
A negative CT does not rule out a small subarachnoid hemorrhage – therefore LP
needed with classiscHx.
SAH => angiogram. If 1st angio negative (spasm, clot, etc) then follow-up angio
in 2-4 wks.
After 2 normal angio => workup spine for source of blood (e.g. spinal AVM,
spinal neoplasm (ependymoma)).
SUBDURAL vs. EPIDURAL
Subdural
- Crescentic shape
- Can layer along falx or tentorium
- Acute 1-7 d
- dense on CT
- MRI isointense on T1WI, decreased on T2W
- Subacute 7-21 d
- isodense on CT
- MRI increased on T1WI and T2WI
- Chronic >21 d
- hypodense on CT, may have enhancing rim
- MRI decreased intensity on T1WI, isointense on T2WI
Epidural
- Biconcave (lenticular)
- Does not cross cranial sutures (unless Fx crosses or previous surgery)
- OUTSIDE (external) to dural sinus
- middle fossa common (laceration of middle meningeal artery)
- may occur in posterior fossa after Fx lacerates transverse sinus
INTRAVENTRICULAR TUMOR
Colloid cyst
- often at foramen of Munro (3rd ventricle)
- hyperdense and enhancing
Choroid plexus papilloma
- usually in lateral ventricles in infants
- more often in 4th ventricle in adults
Meningioma
- uncommonly
Ependymoma
- 4th ventricle
Metastasis – to choroid plexus
Subependymal Giant Cell Astrocytoma (f. of Monro, attach to caudate, 90% have
Tuberous Sclerosis)
Astrocytoma
Central Neurocytoma (usually attached to septum pellucidum)
COMMENT: Both CPP and Meningioma arise within choroid, and derive blood supply
from choroid vessels.
3rd VENTRICULAR MASS
Anterior
- Colloid cyst
- Meningioma
- Ependymoma
- Choroid plexus papilloma (least common location)
- AVM (unusual)
- Basilar artery aneurysm (exotic)
Posterior
- Pineal region tumors (see below)
- Tectal glioma
- Epidermoid
- Meningioma
COMMENT: The 3rd ventricle is least common location for ependymoma and CPP.
PINEAL REGION TUMOR
Germ cell origin (about 60%)
- Germinoma
- 40 – 50% of ALL pineal region tumors
- 2/3 of all Germ-cell origin tumors
- tumor surrounds calcified gland
- homogeneous, dense on plain CT
- Teratoma
- heterogeneous
- may have fat/lipid
- Teratocarcinoma
- Embryonal cell/yolk sac/choriocarcinoma
Pineal parenchymal tumors
- exploded calcification
- radiosensitive
- Pineocytoma
- hyperdense
- Pineoblastoma – very malignant, a type of PNET
Tectal glioma
Meningioma (falx, tentorium)
Metastasis
Vein of Galen Malformation (including aneurysmal dilatation of vein of Galen)
EXTRA-AXIAL TUMORS
Meningioma
- parasagittal > convexities > sphenoid ridge > subfrontal > juxtasellar >
tentorial > posterior fossa > floor of middle cranial fossa
Epidermoid
- Dermoid
- Lipoma (midline, ALL fat, may have callosal agenesis)
Arachnoid cyst
Bony lesion
Meningeal infiltration by lymphoma or leukemia (may look epidural/subdural in
shape) Carcinomatous meningitis
SUPRATENTORIAL TUMOR
Glioma (30-40%)
- Glioblastoma (astro grade IV)
- Astrocytoma
- Oligodendroglioma
- Ependymoma
Metastasis (20-30%)
Meningioma (16%)
Pineal gland tumors
Lymphoma
BASAL GANGLIA CALCIFICATIONS
Birth anoxia
Idiopathic (most common) bilateral and symmetrical
Radiation TX
Toxoplasmosis / CMV – usually not limited to basal ganglia
Hypoparathyroidism / pseudohypoparathyroidism
Infarct
COMMENT: * BIRTH *
SUPRASELLAR MASS
(“SATCHMOE” – nickname for Louis Armstrong, deceased jazz musician
extraordinaire)
Sellar/Parasellar neoplasm
- pituitary adenoma
Aneurysm – sharply marginated – densely enhancing on CT, “pulsation artifact” on
MR
Germ Cell tumor (“ectopic pinealoma” – a misnomer)
Teratoma – heterogeneosu,iso-/lipid – small – solid
Craniopharyngioma – children>adults – calcified 75% – cystic 75%
Hypothalamic glioma – children /
Histiocytosis (Diabetes Insipidus)
Meningioma / metastasis
Optic glioma – erodes sphenoid – visual loss
Epidermoid/Dermoid inclusion cyst
COMMENT: For parasellar mass, add carotid-cavernous fistula and cavernous or
other carotid aneurysm
SELLAR MASS
Pituitary adenoma
Craniopharyngioma
Meningioma
Metastasis
Epidermoid
Abscess
Aneurysm
Pituitary bleed – apoplexy (post-partum or into adenoma)
Pituitary sarcoid
Rathke cleft cyst (usually intrasellar, may extend out)
Germinoma
RING ENHANCING LESION (CT)
Primary brain tumor (glioblastoma) – irregular thick ring
Metastasis (especially if on ChemTx)
Abscess
- ring is more smooth and regula
r – thinner on medial (WM) side
Multiple sclerosis – in white matter
Resolving hematoma – 10-21 days – usually has perilesional lucency
Tuberculoma – associated extracranial TB often found – irregular ring
Infarct
Radiation necrosis – 9 months-3 years after Rtx > 4000 rads
Postoperative change (at edges of resection)
Aneurysm – due to intraluminal thrombus
LOW DENSITY MASS LESION (CT)
Lipoma – (-) CT # (- 60 -90 HU, not merely low, but very low)
Epidermoid – due to inclusion of ectoderm
- often lateral, occasional midline
Arachnoid cyst – CSF density/intensity
- most at temporal tip/ middle fossa P
orencephalic cyst (brain defect)
Infarct (acute from edema, chronic from encephalomalacia)
Pilocytic astrocytoma (cyst fluid)
Ventricle/cistern
Chronic subdural
HYPERDENSE LESION WITHOUT CONTRAST
Meningioma
- 20% also show hyperostosis
- 2/3 show peritumoral edema
Lymphoma (small round blue-cell tumor – densely cellular)
- primary is usually intraaxial
- secondary is often extraaxial
Metastasis – * MRCT * Melanoma/Renal cell Ca/Choriocarcinoma/Thyroid
Medulloblastoma (small round blue-cell tumor – densely cellular)
Glioblastoma
Ependymoma
Colloid cyst (inspissated mucus)
Hemorrhage (acute) / hemorrhagic infarct
Craniopharyngioma
Germinoma (pineal and suprasellar)
MULTIPLE ENHANCING LESIONS
Hematogenous:
Metastases
- 45 -55% of CNS mets multiple
- >2cm often cavitate
- usually near gray-white junction (peripheral > central)
Lymphoma
- usually deeper, periventricular, may be rings in
AIDS Disseminated infection (multiple abscesses)
Multifocal infarction
Inflammatory/Unknown Etiology:
Multiple Sclerosis (white matter lesions)
Vasculitis
Hypertensive Crisis/Ecclampsia
Inherited Mass Lesions/Neoplasms:
Hemangioblastoma (von Hippel-Lindau)
Arteriovenous malformations (cavernous hemangioma >> AVM) Meningiomas – 4% are
multiple (some with NF-2, most without)
Multicentric gliomas – 5% of all gliomas
Tuberous sclerosis
Neurofibromatosis (both types – NF1 (von Recklinhausen) and NF2 (MISME)
GYRAL ENHANCEMENT:
* Ischemia/Infarction (incl. seizures, migraines, etc.)
* Cerebritis/Encephalitis (e.g. Herpes)
Meningeal carcinomatosis (carcinomatous meningitis)
Meningitis – chronic > acute
AVM
Cortical vein thrombosis
Lymphoma
Meningioangiomatosis (NF2)
COMMENT: Sturge-Weber will be dense without contrast due to tram track
calcification in cortex underlying a meningeal venous angioma
CAUSES OF HYDROCEPHALUS (literally “water on the HEAD”)
Communicating (decreased reabsorption)
- Normal pressure hydrocephalus
- prominent temporal horns
- s/p infection – meningitis
- s/p subarachnoid hemorrhage
- Dural vein thrombosis
Non-communicating (mechanical obstruction to flow)
- Aqueductal stenosis
- postinflammatory or congenital
- Tumors – especially colloid cyst
- Congenital anomalies
- Dandy-Walker cyst of 4th ventricle
- Arnold-Chiari malformation
Overproduction (increased production)
- Choroid plexus papilloma
COMMENT: Mimicked by atrophy – “hydrocephalus ex vacuo”
MIDLINE SHIFT
Intracranial mass
- Tumor
- Large infarct with edema
- Intracerebral bleed
Extracerebral collection
- Epidural hematoma
- Subdural hematoma
- Empyema
Unilateral atrophy
HYDROCEPHALUS vs. ATROPHY (CT)
Hydrocephalus (ventricles >> sulci)
- Ballooned and tight frontal horns – Dilated temporal horns
- Dilated 3rd (hourglass shape) with flow void on MR
- decreased mammillopontine measurement (expanded 3rd pushes mammillary bodies
post./inf.
- Dilated 4th ventricle
- Periventricular abnormal signal/density
Atrophy (sulci and ventricles dilate proportionately)
- Large cortical sulci
- Less 3rd ventricular dilatation (with parallel sides NOT hourglass shape)
- Increased with age
COMMENT: Normal pressure hydrocephalus evaluated by nuclear cisternogram. No
migration of activity over convexities/persistent intraventricular activity …
50% aided by shunt (“shunt responsive NPH”)
APPROACH TO INTERPRETATION OF ANGIOGRAPHY
What view (lateral, frontal, oblique, submental-vertex, etc)?
What Vessel Was Injected?
What phase (arterial, capillary, venous) of injection?
Localize lesion (hypervascular/hypovascular, mass effect?, shift?)
Check vessels for displacement
- don’t forget extracerebral lesions
AP – Anterior cerebral arteries, pericallosal
- Internal cerebral veins
- Sylvian point
LAT – Sylvian triangle
POSTERIOR CIRCULATION (verterbral injection)
- Precentral cerebellar vein
- PICA
Characterize vascularity – increased (Hyper) or decreased (Hypo)
BRANCHES OF INTERNAL CAROTID
Meningohypophyseal trunk (that “Italian artery” Bernasconi-Casanari)
Ophthalmic
Superior hypophyseal
Posterior communicating (infundibulum, connects to PCA)
Anterior choroidal (AChoA – marker for temporal lobe herniation)
Anterior cerebral (ACA)
- Frontopolar
- Callosomarginal
- Pericallosal
Middle cerebral (MCA)
- Lenticulostriate (perforators to basal ganglia)
Internal Carotid (ICA)
- Cervical-Petrous-Cavernous-Supraclinoidsegments
POSTERIOR CIRCULATION BRANCHES
Vertebral
- Muscular (occipital) branches
- Meningeal branch
- PICA Basilar
- AICA
- Superior cerebellar (SCA)
- Posterior cerebral (PCA)
- Posterior communicating
- Posterior choroidal (medial/ and lateral branches)
- Parietoccipital
- Posterior temporal
- Calcarine
EXTERNAL CAROTID BRANCHES
Superior thyroid
Lingual
Facial
Ascending pharyngeal
Occipital
Posterior auricular
Superficial temporal
Internal maxillary
- Middle meningeal (f. spinosum)
DEEP VENOUS DRAINAGE
Anterior septal
Thalamostriate
Internal cerebral veins (paired)
Basal vein(s) of Rosenthal (medial temporal lobe)
Great vein of Galen
Inferior sagittal sinus (free edge of Falx)
Straight sinus
Superior sagittal sinus (don’t forget the “Torcular Herophilus”)
Transverse sinus
Sigmoid sinus
Internal jugular
COMMENT: Superficial drainage is superficial middle cerebral vein, vein of
Trolard and vein of Labbe to superior sagittal sinus
CAUSES OF EARLY DRAINING VEIN – (rapid or short “transit time”)
* Neoplasms – primary or secondary
* AVM Inflammatory lesion
Trauma (hyperemia)
Ischemia
Epileptic focus
Toxic encephalopathy
COMMENT: Definition is vein seen CRANIAL FORAMINA AND CONTENTS
Cribiform plate – CNN-I – Olfactory nerve twigs to nasal vault
Optic canal – CNN-II – Optic nerve and ophthalmic artery
Superior orbital fissure
- III – Oculomotor, IV – Trochlear, V1 – Ophthalmic , VI – Abducens, superior
ophthalmic vein
f. Rotundum – V2 Maxillary
f. Ovale – V3 Mandibular and accessory meningeal artery
f. Spinosum – Middle meningeal artery
f. Internal auditory canal – VII (Facial), VIII (Vestibulo-Cochlear)
f. Jugular – Jugular vein, IX — Glossopharyngeal, X – Vagus, XI- Accessory
f. Hypoglossal – XII Hypoglossal
f. Magnum – Spinal cord, XI Accessory, vertebral arteries, spinal arteries
APPROACH TO INTERPRETATION OF MYELOGRAPHY
Check plain films – for bone destruction, previous surgery, trauma, dysraphism
Contrast used – water-soluble, oily
Filling defects, displacement of sac, cord ?
Compartment involved:
CLASSIC:
Intramedullary (cord lesion)
Extramedullary/Intradural (subarachnoid space)
Extradural (outside the thecal sac)
Conus (How low?)
Roots (Thickend, clumped, displaced?)
Thecal sac (Narrowed? Stenosis?)
INTRAMEDULLARY LESION
Tumors
- Ependymoma (most common, esp in adults)
- Astrocytoma (more common in children/Cx location)
- Medulloblastoma (CSF seeding)
- Lipoma/Dermoid/Epidermoid – especially in dysraphism
- Hemangioblastoma (Von Hippel-Lindau syndrome)
- Metastasis – breast/lung/melanoma
- Syringomyelia/Hydromyelia
- Hematoma Inflammation – myelitis
- AVM-Angioma
Cervical – usually glioma or syrinx
Thoracic – consider teratoma, dermoid, astrocytoma?
EXTRAMEDULLARY/INTRADURAL LESION
Meningioma (most thoracic)
Schwannoma (more common than neurofibroma)
Neurofibroma (erodes bone while extending through neural foramen, usually NF-1)
Drop metastasis – medulloblastoma/ependymoma/pineal dysgerminoma/glioma
Dermoid-Epidermoid (associated with dysraphism ?)
Lipoma – most common location is caudal (also “fatty filum”)
COMMENT: Most tumors in this location are benign
EXTRADURAL LESION
Herniated disc (90% at L4-5 and L5-S1)
Osteophyte
Metastasis (Breast-Lung)
Lymphoma
Meningioma
Primary Bone tumor:
- Chordoma
- Osteosarcoma/blastoma
- Myeloma
- Aneurysmal bone cyst
- Giant cell tumor
Neurofibroma (often w/intradural component)
Dermoid-Epidermoid/Lipoma
SACRAL EXPANSILE LESION
Sacrococcygeal Teratoma (often presents in newborn)
Epidermoid cyst
Chordoma (bulky, lobulated mass with bone destruction)
Dural ectasia – meningocele
Dermoid
Lipoma
Giant cell tumor
Aneurysmal bone cyst
OPTIC NERVE THICKENING
Optic nerve glioma (usually pilocytic, often with NF1)
Optic nerve sheath meningioma (tram track lesion outlines normal size nerve)
Papilledema (dilations of SAS that surrounds nerve)
Optic neuritis (MS-Sarcoid)
Orbital pseudotumor
- near globe
- responds to steroid therapy
- thickens muscles AND tendons
Graves’ disease
- thickens extraocular muscles
- no tendon involvement
Vascular malformations
- cavernous hemangioma > AVM
- carotid-cavernous fistula
Orbital cellulitis – may be 2nd to ethmoid sinusitis Leukemia Perineuritis Optic
nerve hemorrhage
COMMENT: Check optic chiasm for intracranial extension
OCULAR MASS
Child
- Retinoblastoma
- 2/3 “heritable”, 1/3 w/Family Hx
- multiple/bilateral if “heritable”
- 90% Ca++
- staging (vitreous, choroidal, scleral, extension?)
Adult
- Choroidal melanoma
- older patient, enhance
- Metastasis – breast, lung, extra-ocular melanoma
- Intraocular lymphoma
- Choroidal hemangioma
RETRO-OCULAR MASS (Intraconal)
Hemangioma
- enhance – phleboliths seen in 10%
Optic nerve glioma
Optic nerve meningioma
Angioma
Lymphangioma
AVM
CONAL MASS
Rhabdomyosarcoma
- bone destruction
- calcification
Thyrotoxic ophthalmopathy
- 88% bilateral
- 80 % medial, inferior rectus muscles
Myositic pseudotumor
EXTRACONAL MASS
Dermoid Mucocele
- occurrence frontal > ethmoid > maxillary > sphenoid
* FEMS
* Lymphoma
Pseudotumor
LACRIMAL GLAND MASS
Unilateral
- Pleomorphic adenoma (histo similar to minor salivary gland tumors)
- benign
- Malignant epithelial cell tumors
- Adenoid cystic carcinoma
- bone destruction
- Pseudotumor – Dacroadenitis
Bilateral (systemic diseases)
- Lymphoma
- Sarcoid
- Collagen vascular disease
RADIOLUCENT SKULL LESION
Metastasis
Normal variant
Epidermoid (intradiploic)
Eosinophilic granuloma (“beveled” margins)
Plasmacytoma
Paget’s (widened diploic space)
Burr hole
Fibrous dysplasia (widened diploic space)
Hemangioma (widened diploic space, radial or starburst trabeculae)
Brown tumor of hyperparathyroidism
Osteomyelitis
Erosion from intracranial tumor (usu slow-growing, e.g. meningioma,
oligodendroglioma)
OPAQUE PARANASAL SINUS
Acute sinusitis – FLUID
Fracture (blood)
Chronic sinusitis – MUCOSAL THICKENING
Mucocele (obstructed sinus ostium => expanded sinus)
Retention cyst (obstructed mucus gland => round mass)
Polyp
Normal hypoplastic
- OTHER
Cystic fibrosis
Inverting papilloma (bone destruction)
Malignant tumor
EXPANSILE LESION OF SINUS
Fibrous dysplasia
Mucocele
Ossifying fibroma
Extensive polyposis (allergic history?)
PHAKOMATOSES
Tuberous sclerosis
- Autosomal dominant
- Adenoma sebaceum, seizures, mental retardation
- Hamartomas involving many organs, angiomyolipomas of kidneys
- Brain – periventricular subependymal nodules
- Cortical tubers
- 15% develop subependymal giant cell astrocytoma
Sturge-Weber (Encephalotrigeminal angiomatosis )
- No inheritance pattern, congenital malformation
- Port wine nevus of face
- V1 distribution
- Seizures, mental retardation, glaucoma
- CT – gyral calcification and cerebral atrophy
- MR – gyriform enhancement – mass-like choroid plexus
- calvarial/facial thickening
- hemiatrophy and hemiparesis
Von Hippel-Lindau
- Hemangioblastomas – cerebellum, retina, medulla, spinal cord
- Pheochromocytoma (NIH Type 2a or 2b)
- Renal cysts 60%
- Renal cell carcinoma 45%
- Pancreatic cysts, Islet cell tumors, serous adenomas
Von Recklinghausen (Neurofibromatosis Type 1, NF1)
- Autosomal dominant
- Cafe-au-lait spots 6 or more, 15mmm in adult
- fibroma molluscum (multiple cutaneous neurofibromas) – Sphenoid dysplasia -
Acute kyphotic scoliosis
- Lateral thoracic meningocele
Type I – chromosome 17 – “peripheral” type (misnomer)
- Peripheral neurofibromas – Other CNS tumors – glioma, optic glioma
Wishart Neurofibromatosis (Bilateral Vestibular Schwannomas) Type II
- chromosome 22 – “central” type (misnomer)
(aka MISME Syndrome: Multiple Inherited Schwannomas, Meningiomas, and
Ependymomas)
- Bilateral vestibular schwannomas in “all” patients
- Other CNS tumors – meningioma, spinal cord ependymoma, other cranial and
spinal schwannomas
COMMENT: The gliomas of NF-2 are ependymoma, those in NF-1 are astrocytoma
(both pilocytic and glioblastoma)
D/D ‘s IN CHEST DISEASES
Differential diagnoses in Chest diseases
NEONATAL LUNG DISEASES:
Hyaline Membrane Disease
Bronchopulmonary Dysplasia
Meconium Aspiration
Neonatal Pnuemonia – strep B, HSV, CMV
Premi Acclerated Lung Maturation – stress, glucocorticoids
Transient Tachypnea of the Newborn
Congenital Lobar Emphysema
Pulmonary Interstitial Emphysema
Pulmonary Lymphangiectasia
DIFFERENTIAL Dx FOR NEONATAL LUNG
Decreased Lung Vol – HMD
Plueral Effusion – pneumonia, mec aspiration, TTN
Pneumothorax – HMD, mec aspiration
Normal Heart Size w edema – TAPVR III, TTN, pulmonary lymphagiectasia
CHEST WALL DENSITY
Skin – nipple, mole
Soft Tisssue Noplasm – lipoma, neural, askin
Bone Neoplasm – myeloma, chondrosarcoma, ewings
Trauma – hematoma, fractures
Infection – actinomycosis, TB
PLUERAL DENSITIES
Loculated Effusion – CHF, infection
Mets – multiple, thymoma
Mesothelioma – benign has pedicle, malig no plaques assoc
Lipoma
Splenosis – assoc with trauma
PNEUMOTHORAX
Trauma
Ventilator
Eosinophilic Granuloma
Lymphangiomyomatosis
Alveolar Protienosis
Pneumocystis Carini
Osteosarcoma Mets
PLEURAL EFFUSIONS
CHF
PE
Pneumonia – TB
Trauma – chylous, boerhaave’s, aorta
Neoplasm – meig’s
Pericarditis – dressler’s, post-pericardotomy
Abdominal Pathology – pancreatitis, post-surg
Collagen Vascular Diseases – rheumatoid, SLE, wegener’s
Low Colloid Pressure
DIAPHRAGM ELEVATION
Subpulmonic
Pulmonary Volume Loss – atelectasis, venolobar
Nerve Paralysis – phrenic, ALS, myasthenia
Diaphragmatic Abnormality – hernia, eventration
Abdominal Process – abscess, chiliditi
WIDE MEDIASTINUM
Technique
Vascular – ectasia, dissection, coarctation, left SVC
Trauma
Neoplasm
Pneumomediastinum
Mediastinitis – histo
Lipomatosis
Achalasia – look for AF levels
SHIFT OF THE MEDIASTINUM
Decreased Lung Volume
Increased Lung Volume – FB, bronchogenic cyst, CAM, swyer-james
Plueral Space Abnormality – effusion, pneumo, diaphragmatic hernia
Partial Absent Pericardium
ANTERIOR MEDIASTINAL MASS
Thymus
Germ Cell – teratoma, seminoma, choriocarcinoma
Thyroid
Lymphoma
Cardiovascular – aneurysm, pericardial cyst, epicardial fat pad
Cystic Hygroma
MIDDLE MEDIASTINAL MASS
Lymphadenopathy – mets, castleman’s
Neoplasm
Vascular
Achalasia
Duplications – bronchogenic cyst, sequestration
POSTERIOR MEDIASTINAL MASS
Neural – nerve root tumors, gangliomas, paragangliomas, lat meningocele
Duplication – enteric, neurenteric cysts
Inflammation – paraspinous abcess, sarcoid
Hematoma – trauma
Extramedullary Hematopoesis
HILAR ENLARGEMENT
Bronchogenic Carcinoma
Lymphoma
Sarcoid
TB
Histo
Pneumoconiosis
TRACHEAL MASSES
Squamous Cell
Adenoid Cystic – cylindroma
Carcinoid – “iceberg”
Chondroma
Fibroma
Papilloma – aquired at birth
Hemangioma – children
TRACHEAL NARROWING
Saber Sheath
Postintubation Stenosis
Relapsing Polychondritis
Amyloidosis
Tracheobronchopathia Osteochondroplastica – benign calc nodules
TRACHEAL DILATION
Mounier-Kuhn Syn
Tracheobronchomalacia
Ehler’s-Danlos Syn
ATELECTASIS
Obstructive – bronchial neoplasm, inflammatory, FB
Passive – plueral process
Compressive – intraparenchymal mass, air trapping
Adhesive – PE, hyaline membrane Dz
Cicatrization
AIRSPACE CONSOLIDATION
Blood – trauma, DIC, PE, vasculitis, hemosiderosis
Pus – bacteria, PCP, fungus, TB
Fluid – CHF, renal failure, toxic inhalation, ARDS
Cells – bronchoalveolar Ca, lymphoma
Protien – alveolar portienosis, mucus plug
SEGMENTAL CONSOLIDATION
Lobar Pneumonia
Bronchopneumonia
Interstitial Pneumonia – viral, mycoplasm
Aspiration
TB & Atypical Mycobacterium
Trauma
Pulmonary Embolism
Obstructing Neoplasm
Mitral Regurgitation
ADULT RESPIRATORY DISTRESS SYNDROME
Event
White Out
Loss of Compliance
Refractory Hypoxemia
Shunt – precapillary
PULMONARY VASCULITIS
Infectious – RM spotted fever, mucormycosis
Wegener’s – diffuse, cavitate, nasal, 40+yrs, 2:1 male
Goodpasture’s – perihilar, hemoptysis, 25yrs, 7:1 male
SLE
PATTERNS OF INTERSTITIAL DISEASE
Septal Lines – CHF, lyphangitic Ca
Reticular (irregular lines) – UIP, sarcoid, asbestos, drug
Air Cysts (round) – UIP, PCP, LAM, EG, bronchiectasis
Nodules – sarcoid, silicosis, EG, EAA (extrinsic allergic alveolitis)
Ground Glass Opacities – DIP, PCP, EAA, alveolar proteinosis
Hyperinflation – LAM, EG, CF, or any w COPD
LOWER LOBE INTERSTITIAL DISEASES (mnemonic: badd lass rf)
Bronchiectasis
Aspiration
DIP – desquamative interstitial pneumonitis
Dermatomyositis
Lymphangitic spread
Asbestosis
Scleroderma
Sarcoid
Rheumatoid Lung
Furadantin
UPPER LOBE INTERSTITIAL DISEASES (casset)
Cystic Fibrosis
Ankylosing Spondylitis
Silicosis
Sarcoid
Eosinophilic Granuloma
TB
BRONCHIECTASIS (saccular & cylindrical types)
Infectious – aspergilla, TB, Sweyer-James
Congenital – cystic fibrosis, Kartagner syn, agammaglobulinemia
Obstructive – neoplasm, nodes
Chemical – aspiration, inhalation
Fibrotic – COPD
SOLITARY PULMONARY NODULE
Bronchogenic Ca
Hamartoma
Granuloma
AVM
Abcess
CAVITATING PULMONARY NODULES
Infection – staph, klebsiella, TB, coccidiomycosis, septic emboli, PCP
Neoplasm – squamous cell ca, osteosarcoma
Vasculitis – wegener’s, rheumatoid
Trauma – pneumatoceles
Bronchogenic Cyst
Pulmonary Embolism
PULMONARY CALCIFICATION
TB
Histo
Silicosis
Alveolar Microlithiasis
Hyperparathyroidism
Chronic Venous Congestion – mitral stenosis
Treated Lymphoma
Idiopathic Pulmonary Osteopathy
UNILATERAL HYPERLUCENT LUNG
Chest wall defect – mastectomy, absent pectoralis
PE – westmarks sign
FB – obstuctive emphysema
Pulmonary hypoplasia
Sweyer-James
AORTIC ANEURYSMS
Atherosclerosis – abd
Marfan’s
Vasculitis – Syphilis, Takayasu, Kawasaki, fungal, TB, polyarteritis nodosa
Aortic Valve Stenosis – asc dilation
CAUSES OF RIB NOTCHING
Coarctation
Aortic Thrombosis
Subclavian Obs – Blalock shunt for tricuspid atresia
Pulmonary Oligemia – any cause of dec flow
CARDIOMEGALY
Highoutput Failure – vein of Galen aneurysm, AVM etc
Outflow Obstruction Failure
Cardiomyopathy
Pericardial Effusion – always rule out
PULMONARY ARTERIAL HYPERTENSION
Primary
Lung Disease – COPD
Multiple PE
Eisenmienger
EMPHYSEMA TYPES
Centrilobular – #1, smoker, upper
Panacinar – alpha-1-antitrypsin, diffuse
Paraseptal – peripheral blebs
RADIOLOGICAL TERMS IN DEGENERATIVE DISC DISEASE:
RADIOLOGICAL TERMS IN DEGENERATIVE DISC DISEASE:
Aging disc: Disc demonstrating the features of normal aging. Spondylosis deformans possibly represents the normal aging process.
Anterior displacement: Displacement of disc tissues beyond the disc space into the anterior zone.
Annulus, (abbreviated form of annulus fibrosus): A multilaminated ligament surrounding the periphery of each disc space, attaching, craniad and caudad, to end-plate cartilage and ring apophyseal bone and blending centrally with nucleus pulposus. Note: Either anulus or annulus is correct spelling. Nomina Anatomica uses both forms whereas Terminologia Anatomica states “annulus fibrosus.” Fibrosus, has no correct alternative spelling; fibrosis has a different meaning and is incorrect in this context.
Asymmetric bulge: Presence of outer annulus beyond the plane of the disc space, more evident in one section of the periphery of the disc than another, but not sufficiently focal to be characterized as a protrusion. Note: Asymmetric bulge is a morphologic observation of various potential causes and is not a diagnosis. See: bulge.
Balloon disc (colloquial): Diffuse displacement of nucleus through the vertebral end plate, commonly seen in severe osteoporosis.
Base (of displaced disc): The cross sectional area of disc material at the outer margin of the disc space of origin, where disc material displaced beyond the disc space is continuous with disc material within the disc space. In the cranio-caudal direction, the length of the base cannot exceed, by definition, the height of the intervertebral space.
Broad-based protrusion: Herniation of disc material extending beyond the outer edges of the vertebral body apophyses over an area greater than 25% (90 degrees) and less than 50% (180 degrees) of the circumference of the disc. See protrusion. Note: Broad based protrusion refers only to discs in which disc material has displaced in association with localized disruption of the annulus and not to generalized (over 50% or 180 degrees) apparent extension of disc tissues beyond the edges of the apophyses. If the base is less than 25%, it is called “focal protrusion.” Apparent extension of disc material, formation of additional connective tissue between osteophytes, or overlapping of non-disrupted tissue beyond the edges of the apophyses of over 50% of the circumference of the disc may be described as bulging. See: bulging disc, focal protrusion.
Bulging disc, bulge (n), bulge (v): 1. A disc in which the contour of the outer anulus extends, or appears to extend, in the horizontal (axial) plane beyond the edges of the disc space, over greater than 50% (180 degrees) of the circumference of the disc and usually less than 3mm beyond the edges of the vertebral body apophyses. 2. (Non-Standard) [A disc in which the outer margin extends over a broad base beyond the edges of the disc space.] 3. (Non-Standard) [Mild, smooth displacement of disc, whether focal or diffuse.] 4. (Non-Standard) [Any disc displacement at the discal level.] >Note: Bulging is an observation of the contour of the outer disc and is not a specific diagnosis. Bulging has been variously ascribed to redundancy of annulus secondary to loss of disc space height, ligamentous laxity, response to loading or angular motion, remodeling in response to adjacent pathology, unrecognized and atypical herniation, and illusion from volume averaging on CT axial images. Bulging may or may not represent pathologic change, physiologic variant, or normalcy. Bulging is not a form of herniation; discs known to be herniated should be diagnosed as herniation or, when appropriate, as specific types of herniation. See: herniated disc, protruded disc, extruded disc.
Capsule: Combined fibers of annulus and posterior longitudinal ligament. Note: The interface between outer annulus and posterior longitudinal ligament can be indistinguishable, making useful the term “capsule” and the derivative “sub-capsular,” which refers to disc tissue beneath the capsule.
Central zone: Zone within the vertebral canal between sagittal planes through the medial edges of each facet. Note: The center of the central zone is a sagittal plane through the center of the vertebral body. The zones to either side of the center plane are right central and left central, which are preferred terms when the side is known, as when reporting imaging results of a specific disc. When the side is unspecified, or grouped with both right and left represented, the term paracentral is appropriate.
Chronic disc herniation: 1. Disc herniation with presence of calcification, ossification, or gas accumulation within the displaced disc material, suggesting that the herniation is not of recent origin. Note: The term implies the presence of calcification, ossification, or gas accumulation and should not be used for herniations of soft disc material, regardless of the duration of displacement. See: degenerated disc, hard disc.
Claw osteophyte: Bony outgrowth arising very close to the disc margin, from the vertebral body apophysis, directed, with a sweeping configuration, toward the corresponding part of the vertebral body opposite the disc.
Communicating disc, communication (n), communicate (v): Interruption in the periphery of the disc, so that fluid injected into the disc space could flow into the vertebral canal and thus into contact with displaced disc material. Note: Communication refers to the status of displaced disc tissues with reference to the parent disc. Containment refers to the integrity of the annulus as container of disc tissues. Uncontained, displaced disc tissues could be noncommunicating if the displaced tissue is sealed off by peridural membrane or by healing of the tear in the annulus.
concentric tear: Tear or fissure of the annulus characterized by separation, or break, of anular fibers, in a plane roughly parallel to the curve of the periphery of the disc, creating fluid-filled spaces between adjacent anular lamellae. See: radial tears, transverse tears.
Contained herniation, containment (n), contain (v): 1. Displaced disc tissue that is wholly within an outer perimeter of uninterrupted outer annulus or capsule. 2. (Non-standard) [A disc with its contents mostly, but not wholly, within annulus or capsule.] 3. (Non-Standard) [A disc with displaced elements contained within any investiture of the vertebral canal.] Note: The preferred meaning encompasses disc tissues that are enclosed by distended portions of the outer annulus or composite of fibers of the annulus and posterior longitudinal ligament. A disc whose substance is less than wholly contained by annulus is uncontained, as is a disc outside of anular fibers but under a distinct posterior longitudinal ligament or peridural membrane. Designation of a disc as contained, or uncontained, should define the integrity of the annulus enclosing the disc, though such distinction may not be possible with currently available imaging modalities.
Continuity: 1. Connection of displaced disc tissue by a bridge of disc tissue, however thin, to tissue within the disc of origin. 2. (Non-Standard) [Connection of displaced displaced disc tissue by a substantial bridge of disc tissue to disc within the disc of origin]. 3. (Non-Standard) [Connection of displaced disc tissue by any tissue to disc tissue within the disc or origin.] Note: Tenuous attachments, beyond recognition by most imaging methods, may have significance to the surgeon or endoscopist. Bridges of peridural membrane, or scar, do not represent continuity. See sequestration.
degenerated disc, degeneration (n), degenerate (v): 1. Changes in a disc characterized by desiccation, fibrosis and cleft formation in the nucleus, fissuring and mucinous degeneration of the annulus, defects and sclerosis of end-plates, and/or osteophytes at the vertebral apophyses. 2. Imaging manifestations commonly associated with such changes. 3. (Non-Standard) [Changes in a disc related to aging.] Note: Either of the first two definitions may be correct, depending upon context. Clinical features must be considered to determine whether degenerative changes are pathologic and what may or may not have contributed to their development. The term degenerated disc, in itself, does not infer knowledge of cause, relationship to aging, presence of symptoms, or need for treatment. See intervertebral osteochondrosis, spondylosis, spondylosis deformans.
Degenerative disc disease(DDD): 1. A clinical syndrome characterized by manifestations of disc degeneration and symptoms thought to be related to those changes. 2. (Non-Standard) [Abnormal disc degeneration.] 3. (Non-Standard) [Imaging manifestations of degeneration greater than expected, considering the age of the patient]. Note: Causal connections between degenerative changes and symptoms are often difficult clinical distinctions. The term carries implications of illness that may not be appropriate if the only manifestations are from imaging. The preferred term for description of imaging manifestations alone, or imaging manifestations of uncertain relationship to symptoms, is degenerated disc rather than degenerative disc disease.
Delamination: Separation of anular fibers along planes parallel to the periphery of the disc, thought to represent separation of laminated layers of the outer anulus fibrosus.
Desiccated disc: 1. Disc with reduced water content, usually primarily of nuclear tissues. 2. Imaging manifestations of reduced water content of the disc; or apparent reduced water content, as from alterations in the concentration of hydrophilic glycosaminoglycans.
Disc (disk): Complex structure composed of nucleus, anulus, cartilaginous end-plates, and vertebral body ring apophyseal attachments of anulus. Note: Most English language publications use the spelling disc more often than disk.12 Nomina Anatomica designates the structures as “Disci intervertebrales” and Terminologia Anatomica as “discus intervertebralis/Intervertebral disc.”18,21
Disc of origin: Disc from which a displaced fragment originated. Syn: parent disc. Note: Since displaced fragments often contain tissues other than nucleus, disc of origin is preferred to nucleus of origin. “Parent disc” is synonymous, but more colloquial.
Disc space: 1. Space limited, craniad and caudad, by the end-plates of the vertebrae and peripherally by the edges of the vertebral body ring apophyses exclusive of osteophytes. Syn: intervertebral disc space.
Discogenic vertebral sclerosis: Increased bone density and calcification adjacent to the end-plates of the vertebrae craniad and caudad to a degenerated disc, usually a manifestation of intervertebral osteochondrosis.
Displaced disc: A disc in which disc material is beyond the outer edges of the vertebral body ring apophyses (exclusive of osteophytes) of the craniad and caudad vertebrae, or, as in the case of intravertebral herniation, penetrated through the vertebral body end-plate. Note: Displaced disc is a general term that does not imply knowledge of the underlying pathology, cause, relationship to symptoms, or need for treatment. The term includes, but is not limited to, disc herniation and disc migration.See: herniated disc, migrated disc.
Extra-foraminal zone: The zone beyond the sagittal plane of the lateral edges of the pedicles, having no well-defined lateral border. Syn: far lateral zone, far-out zone.
Extra-ligamentous: Posterior or lateral to the posterior longitudinal ligament. Note: Extra-ligamentous disc refers to displaced disc tissue that is located lateral, or posterior to the posterior longitudinal ligament. If the disc has extruded through the posterior longitudinal ligament it is sometimes called “trans-ligamentous” or “perforated,” and if through the peridural membrane, it is sometimes refined to as “trans-membranous.”
Extruded disc, extrusion (n), extrude (v): A herniated disc in which, in at least one plane, any one distance between the edges of the disc material beyond the disc space is greater than the distance between the edges of the base in the same plane, or when no continuity exists between the disc material beyond the disc space and that within the disc space. Note: The preferred definition is consistent with the common language image of extrusion as an expulsion of material from a container through and beyond an aperture. Displacement beyond the outer anulus of disc material with any distance between its edges greater than the distance between the edges of the base distinguishes extrusion from protrusion. Distinguishing extrusion from protrusion by imaging is best done by measuring the edges of the displaced material and remaining continuity with the disc of origin, whereas relationship of the displaced disc material to the aperture through which it has passed is more readily observed surgically. Characteristics of protrusion and extrusion may co-exist, in which case the disc should be subcategorized as extruded. Extruded discs in which all continuity with the disc of origin is lost may be further characterized as sequestrated. Disc material displaced away from the site of extrusion may be characterized as migrated. See: herniated disc, migrated disc, protruded disc.
Fissure of anulus: Separations between anular fibers, avulsion of fibers from their vertebral body insertions, or breaks through fibers that extend radially, transversely, or concentrically, involving one or more layers of the anular lamellae. Syn: tear of anulus, torn anulus. Note: The terms fissure and tear are commonly used synonymously. Neither term implies any knowledge of etiology, relationship to symptoms, or need for treatment. Tear or fissure are both used to represent separations of anular fibers from causes other than sudden violent injury to a previously normal anulus, which can be appropriately termed “rupture of the anulus,” which, in turn, contrasts to the colloquial, non-standard, use of the term “ruptured disc,” referring to herniation.
Focal protrusion: Protrusion of disc material so that the base of the displaced material is less than 25% (90 degrees) of the circumference of the disc. Note: Focal protrusion refers only to herniated discs that are not extruded and do not have a base greater than 25% of the disc circumference. Herniated discs with a base greater than 25% are “broad-based protrusions.”
Foraminal zone: The zone between planes passing through the medial and lateral edges of the pedicles. Note: The foraminal zone is sometimes called the “pedicle zone,” which can be confusing because pedicle zone might also refer to measurements in the sagittal plane between the upper and lower surface of a given pedicle, which is properly called the “pedicle level.” The foraminal zone is also sometimes called “lateral zone,” which can be confusing because lateral zone can also mean extra-foraminal zone or an area including both the foraminal and extra-foraminal zones.
Free fragment: 1. A fragment of disc that has separated from the disc of origin and has no continuous bridge of disc tissue with disc tissue within the disc of origin. Syn: sequestrated disc . 2. (Non-Standard) [A fragment that is not contained within the outer perimeter of the anulus.] 3. (Non-Standard) [A fragment that is not contained within anulus, posterior longitudinal ligament, or peridural membrane.] Note: Sequestrated disc and free fragment are virtually synonymous. When referring to the condition of the disc, categorization as extruded with sub-categorization as sequestrated is preferred, whereas free fragment or sequestrum is appropriate when referring specifically to the fragment.
Hard disc: Disc displacement in which the displaced portion has undergone calcification or ossification and may be intimately associated with apophyseal osteophytes. Note: The term hard disc is most often used in reference to the cervical spine to distinguish chronic hypertrophic and reactive changes in the periphery of the disc from acute extrusion of soft, predominantly nuclear tissue. See: chronic disc herniation.
Herniated disc, herniation (n), herniate (v): 1. Localized displacement of disc material beyond the normal margins of the intervertebral disc space. 2. (Non-Standard) [Any displacement of disc tissue beyond the disc space]. Note: Localized means, by way of convention, less than 50% (180 degrees) of the circumference of the disc. Disc material may include nucleus, cartilage, fragmented apophyseal bone, or fragmented anular tissue. The normal margins of the intervertebral disc space are defined, craniad and caudad, by the vertebral body end-plates and peripherally by the edges of the vertebral body ring apophyses, exclusive of osteophytic formations. Herniated disc generally refers to displacement of disc tissues through a disruption in the anulus, the exception being intravertebral herniations (Schmorl’s nodes) in which the displacement is through vertebral end-plate. Herniated discs in the horizontal (axial) plane may be further subcategorized as protruded or extruded. Herniated disc is sometimes referred to as “herniated nucleus pulposus,” but the term herniated disc is preferred because displaced disc tissues often include cartilage, bone fragments, or anular tissues. The term “ruptured disc” is used synonymously with herniated disc, but is more colloquial and can be easily confused with violent, traumatic rupture of the anulus or end-plate. The term “prolapse” has also been used as a general term for disc displacement, but its use has been inconsistent. The term herniated disc does not infer knowledge of cause, relation to injury or activity, concordance with symptoms, or need for treatment.
High intensity zone (HIZ): Area of high signal intensity on T2-weighted magnetic resonance images of the disc, usually referring to the outer anulus. Note: High intensity zones within the posterior anular substance may reflect fissure or tear of the anulus, but do not imply knowledge of etiology, concordance with symptoms, or need for treatment.
infra-pedicular level: The level between the axial planes of the inferior edge of the pedicle craniad to the disc in question and the inferior end-plate of the vertebral body above. Syn: superior vertebral notch.
Internal disc disruption syndrome: Internal disc disruption associated with symptoms, which are thought, on clinical grounds, to be caused by the disruption. Syn: Crock disc.
Intervertebral osteochondrosis: Degenerative process of the spine involving the vertebral body end-plates, the nucleus pulposus, and the anulus fibrosus, which is characterized by disc space narrowing, vacuum phenomenon, and vertebral body reactive changes. Syn: deteriorated disc, chronic discopathy, osteochondrosis.
Intra-anular displacement: Displacement of central, predominantly nuclear, tissue to a more peripheral site within the disc space, usually into a fissure in the anulus. Syn: (Non-Standard) [intra-anular herniation], [intra-discal herniation]. Note: Intra-anular displacement is distinguished from disc herniation, in that herniation of disc refers to displacement of disc tissues beyond the disc space. Intra-anular displacement is a form of internal disruption. When referring to intra-anular displacement, it is best not to use the term “herniation” in order to avoid confusion with disc herniation.
Intra-dural herniation: A disc from which displaced tissue has penetrated, or become enclosed by, the dura so that it lies within the thecal sac.
Intra-vertebral herniation: A disc in which a portion of the disc is displaced through the end-plate into the centrum of the vertebral body. Syn: Schmorl’s node.
limbus fracture: Traumatic separation of a segment of bone from the edge of the vertebral ring apophysis at the site of anular attachment. Note: Limbus fractures of various types may be accompanied by disc herniation, usually by either focal or broad-based protrusion. They may occur into the anterior zone or posteriorly into the zones where they may compress neural tissues.
Limbus vertebrae: Separation of a segment of rim of vertebral body ring apophysis. Note: Limbus vertebrae may result from fracture or from developmental abnormalities. Limbus vertebrae is commonly seen in patients who have had Scheuermann’s Disease. The lesions may be called “rim lesions.” The term is derived from the Latin nominative limbus and genitive modifier vertebrae, thus is singular.
Marginal osteophyte: Osteophyte that protrudes from and beyond the outer perimeter of the vertebral end-plate apophysis.
Migrated disc, migration (n), migrate (v): 1. Herniated disc in which a portion of extruded disc material is displaced away from the tear in the outer anulus through which it has extruded. 2. (Non-Standard) [A herniated disc with a free fragment or sequestrum beyond the disc level.] Note: Migration refers to the position of the displaced disc material, rather than to its continuity with disc tissue within the disc of origin; therefore, it is not synonymous with sequestration.
non-marginal osteophyte: Osteophyte the occurs at sites other than the vertebral end-plate apophysis. See: marginal osteophyte.
Normal disc: 1. A fully and normally developed disc with no changes attributable to trauma, disease, degeneration, or aging. The bilocular appearance of the adult nucleus is considered a sign of normal maturation. 2. (Non-Standard) [A disc that may contain one or more morphologic variants which would be considered normal given the clinical circumstances of the patient.]. Note: Many congenital and developmental variations may be normal in that they are not associated with symptoms; certain adaptive changes in the disc may be normal considering adjacent pathology, and certain degenerative phenomena may be normal given the patient’s age; however, classification and reporting for medical purposes is best served if such discs are not considered normal. What is clinically normal for a given patient is a clinical judgment independent of the need to describe any variation in the disc itself.
Osteophytes: Focal hypertrophy of bone surface and/or ossification of soft tissue attachments to the bone.
TELERADIOLOGY
TELE-RADIOLOGY:
Teleradiology is a method of distributing digital diagnostic images such as, X-rays, ultrasonography, magnetic resonance and radioisotopes, and other related information through local area or wide area networks between remotely located facilities.
A well planned teleradiology system can be a cost effective and time efficient method that allows users to capture, transmit, store, and review patient studies. In design and implementation of a successful teleradiology system the following categories play a significant role:
Storage Systems And Databases (PACS)
Picture Archiving and Communication System (PACS) is an image-based information system for the acquisition, storage, communication, archiving, display, and manipulation of medical digital images, and other relevant data. The PACS archive is expected to replace radiology film library.
Imaging Standards (DICOM)
A practical archive system must be capable of moving the data off onto its successor system. DICOM (Digital Imaging Communication) is an imaging standard that allows the exchange of data between different hosts and equipment across the network in a heterogeneous environment.
HIS/RIS:
The concepts of PACS and HIS/RIS (Hospital and Radiology Information Systems) are the same; only the data types are different. PACS applications manage images, and HIS/RIS applications manage patients, studies, and results. The coupling of PACS and HIS/ RIS has been repressed due to incompatibility of data definitions and standards. Triggered by user needs, recent developments aim at high level integration of PACS and HIS/RIS.
High Speed Networks
High speed data transmission and data security are crucial prerequisites for the clinical acceptance of distributed medical services. It is widely believed that Asynchronous Transfer Mode (ATM) is a type of networking technology that will make transmission of digital medical images practical and affordable. ATM has the ability to handle large amounts of traffic simultaneously, bandwidth scalability and integration with existing network protocols such as Ethernet, and FDDI.
Video Networks And Multimedia Systems
Providing “real-time interactive” video transfer of ultrasound images can improve efficiency and faster turnaround time for radiographic reports, while maintaining the quality of care. Implementation of the real-time ultrasound video transfer has become possible because of the availability of ATM technology and Advanced Communications Technology Satellite (ACTS). These technologies allow remote real time monitoring of invasive procedures, and remote clinical diagnosis of multiple disease and pathology states which in turn make subspecialty consultation and education at a distance feasible.
MR CASE: DERMATOMYOSITIS
MRI of thighs was performed by T1 and T2 weighted images in multiple planes. T2 weighted Fat suppressed sequence was obtained in coronal plane.
Present study reveals areas of increased signal intensity noted involving all the muscle groups in the coronal fat suppressed sections under review namely the adductor group, hamstrings, gluteal muscles and bilateral psoas muscles.
These muscles appear normal in size and shape. These muscles appear isointense on T1 weighted images (not shown) with preservation of the intermuscular cleavage planes. Overlying subcutaneous fat show normal signal intensity. The visualized bones under review show normal signal intensity. Both the hip joint spaces are intact.
IMP: INFLAMMATORY MYOSITIS - DERMATOMYOSISTIS
v
ulcerative colitis
Mandibular osteosarcoma
nuclear medicine
What is Nuclear Medicine ?
Nuclear Medicine involves the use of radioactive materials (isotopes , radioisotopes or radio pharmaceuticals) to diagnose or treat medical conditions. Very small amounts of radioactive materials (which have no harmful effect) allow “pictures” or “scans” of the area of the body that doctor needs to know more about. Sometimes larger amounts are used to treat cancer or certain thyroid disorders.
Safety :-
Used in proper amounts, radioactive materials have been shown to be extremely safe in adults and children and may even be used in pregnant women. The overall safety of Nuclear Medicine is unmatched by any other medical field. Studies of over 100,000 patients showed no ill effects after 15-20 years following treatment utilizing radioactive materials.
PET AND SPECT
PET : Positron Emission Topography.
SPECT : Single Photo Emission Computed Topography.
PET & SPECT :-
Shows blood flow by imaging trace amounts of radioisotopes. PET however can measure metabolism revealing how well the body is working. Use of radioactive tracer is well suited to studies of epilepsy, schizophrenia, Parkinson disease and stroke. Both PET and SPECT depict the distribution of blood into tissues, but PET does so with grater accuracy.
PET scanner watches the way tissue cells (eg brain cells) consume substances such a sugar (glucose). The substance is tagged with radioisotopes and brewed in a small low energy cyclotron. The isotope has a short half-life meaning it loses half of its radioactivity only within minutes or hours of being created. After injecting into the body, the radioactive solution emits positions 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 direction and strike crystals in a ring of detectors located around the patient’s head or body causing the crystal to light up. A computer records the location of each flash and plots the source of radiation, translating that 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.
Nuclear Medicine Procedures
Most common scans a doctor might order and what they can do:
· Thyroid Uptakes and Scans are used to find over and under-active thyroid gland and to determine if lumps might be cancerous.
· Bone Scans find problems such as a tumor, infection and trauma sooner than x-rays and used to evaluate bone pain, injuries and many cancers.
· Heart scans are most often used to determine if chest pain is a result of heart disease and are also used to monitor the pumping function of the heart and detect recent heart attacks.
· Lung scans find blood clots in the lungs.
· Kidney scans find blockages to drainage or blood flow, tumor and infections of the kidney and can tell if high blood pressure is because of a kidney problem. Scans can also check for bladder reflux.
· Gallbladder scans help decide the need for surgery for abdominal pain.
· Stomach/Bowel bleeding can be located with nuclear medicine scans.
· Tumor/Abscess localization leads the way to finding the problem in difficult cases.
· Scintimammograms offer another way to look for cancers in the breast.
· Nuclear Medicine Therapy is the quickest, easiest, cheapest and most importantly the safest of all ways to treat overactive thyroid glands (hyperthyroidism). It is the best form of treatment for most cancers of the thyroid and may also be used for other cancers.
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Neuro-Radiology Differentials
CONGENITAL INFECTIONS
CMV – central calc
Toxoplasmosis – peripheral calc
Ruebella – both
Herpes – none
VaricellaH. flu – subdural hygroma
AIDS RELATED CNS DZ
Toxoplasmosis
HIV Encephalopathy
Progressive Multifocal Leukoencephalopathy – papova virusI’
CNS Lymphoma
DEMYELINATING DISEASES
Multiple Sclerosis
Aquired Disseminated Encephalomyelitis
Progressive Multifocal Leukoencephalopathy – papova virus
Toxic – Etoh,
Wernicke’s,
osmotic myelinosis
TraumaVascular – PVL,
necrotizing leukoencephalopathy,
Binswanger’s, SLE
DYSMYELINATION DISORDERS
Metachromatic Leukodystrophy – lysosomal, deep confluent, hypo thalami
Krabbe Dz – lysosomal, deep confluent, hyper thalami, rapid
Adrenoleukodystrophy – post to ant
Alexander’s Dz – inclusions, ant to post
Canavan’s Dz – spongy degen, U fibers 1st
Amino Acid Deficiency – phenylketonuria, maple syrup urine, homocystinuria
DIFFUSE AXONAL INJURY
Corticomedullary Junction – frontal, temporal
Corpus Callosum – post body & spenium
Pons & Dorsal Midbrain
VASCULAR COLLATERALS
Circle of Willis
Ophthalmic
Meningeal
MRI STAGES OF HEMORRHAGE
T1 T2Hyperacute 4wks Dark Dark Hemosiderin
CT STAGES OF HEMORRHAGE
Hyperacute – 2-3hrs, i
sodenseAcute – 3hrs to 2wks,
hyperdense (60-100HU, dec by 1.5HU/d)
Subacute – 2-4wks, isodense
Chronic – >4wks, hypodense
PARENCHYMAL HEMATOMA
Trauma
Hypertention
Infarct
Aneurysm
AVM
TumorBleeding Diathesis
Amyloid
SKULL BASE LESIONS
Chordoma
Chondrosarcoma
Squamous Cell
Schwannoma
Meningioma
Mets
Glomus
POSTERIOR FOSSA MASS IN A CHILD
Medulloblastoma – hyperdense, no calc
Ependymoma – plastic, calc
Pilocytic Astrocytoma – cyst & nodule
Brainstem Glioma
POSTERIOR FOSSA MASS IN AN ADULT
Mets
Hemangioblastoma – 20% w VHL
Subependymoma
Infarct/HemorrhageAbcess
CEREBELLOPONTINE ANGLE MASS
Schwannoma – 7/8,
vest of VIII 75%,
facial 4%
Epidermoid
Arachnoid Cyst
Meningioma
CEREBELLAR DYSPLASIA’S
Cebellar atrophy
Chiari IV Malformation
Joubert’s Syndrome – split vermis
Rhomboencephalosynapsis – absent vermis
Tectocerebellar Dysraphia – hypoplastic vermis, cb rotated ant lat to stem
Lhermitte-Duclos Dz – gangliocytoma
PINEAL TUMORS
Germinoma – 60%, dense, placental alk phos
Teratoma – bothChoriocarcinoma – B-hcg
Endodermal Sin
CHEST Differentials
DIFFERENTIAL DIAGNOSES:
FOR NEONATAL LUNG DISEASES
Decreased Lung Vol – HMD
Plueral Effusion – pneumonia, meconium aspiration, TTN
Pneumothorax – HMD, mec aspiration
Normal Heart Size w edema – TAPVR III, TTN, pulmonary lymphagiectasia
CHEST WALL DENSITY
Skin – nipple, mole
Soft Tisssue Noplasm – lipoma, neural, askin
Bone Neoplasm – myeloma, chondrosarc, ewings
Trauma – hematoma, fx
Infection – actinomycosis, TB
PLUERAL DENSITIES
Loculated Effusion – CHF, infection
Mets – #1 multiple, thymoma
Mesothelioma – benign has pedicle, malig no plaques assoc
Lipoma
Splenosis – assoc w trauma
PNEUMOTHORAX
Trauma
Ventilator
Eosinophilic Granuloma
Lymphangiomyomatosis
Alveolar Protienosis
Pneumocystis Carini
Osteosarcoma Mets
PLEURAL EFFUSIONS
CHF
PE
Pneumonia – TB
Trauma – chylous, boerhaave’s, aorta
Neoplasm – meig’s
Pericarditis – dressler’s, post-pericardotomy
Abdominal Pathology – pancreatitis, post-surg
Collagen Vascular Dz – rheumatoid, SLE, wegener’s
Low Colloid Pressure
DIAPHRAGM ELEVATION
Subpulmonic
Pulmonary Volume Loss – atelectasis, venolobar
Nerve Paralysis – phrenic, ALS, myasthenia
Diaphragmatic Abnormality – hernia, eventration
Abdominal Process – abscess, chiliditi
WIDE MEDIASTINUM
Technique
Vascular – ectasia, dissection, coarctation, left SVC
Trauma
Neoplasm
Pneumomediastinum
Mediastinitis – histo
Lipomatosis
Achalasia – look for AF levels
SHIFT OF THE MEDIASTINUM
Decreased Lung Volume
Increased Lung Volume – FB, bronchogenic cyst, CAM, swyer-james
Plueral Space Abnormality – effusion, pneumo, diaphragmatic hernia
Partial Absent Pericardium
ANTERIOR MEDIASTINAL MASS
Thymus
Germ Cell – teratoma, seminoma, choriocarcinoma
Thyroid
Lymphoma
Cardiovascular – aneurysm, pericardial cyst, epicardial fat pad
Cystic Hygroma
MIDDLE MEDIASTINAL MASS
Lymphadenopathy – met, castleman’s
Neoplasm
Vascular
Achalasia
Duplications – bronchogenic cyst, sequestration
POSTERIOR MEDIASTINAL MASS
Neural – nerve root tumors, gangliomas, paragangliomas, lat meningocele
Duplication – enteric, neurenteric cysts
Inflammation – paraspinous abcess, sarcoid
Hematoma – trauma
Extramedullary Hematopoesis
HILAR ENLARGEMENT
TB,Bronchogenic Carcinoma
Lymphoma
Sarcoid
Histo
Pneumoconiosis
TRACHEAL MASSES
Squamous Cell
Adenoid Cystic – cylindroma
Carcinoid – “iceberg”
Chondroma
Fibroma
Papilloma – aquired at birth
Hemangioma – children only
TRACHEAL NARROWING
Saber Sheath
Postintubation Stenosis
Relapsing Polychondritis
Amyloidosis
Tracheobronchopathia Osteochondroplastica – benign calc nodules
TRACHEAL DILATION
Mounier-Kuhn Syn
Tracheobronchomalacia
Ehler’s-Danlos Syn
ATELECTASIS
Obstructive – bronchial neoplasm, inflammatory, FB
Passive – plueral process
Compressive – intraparenchymal mass, air trapping
Adhesive – PE, hyaline membrane Dz
Cicatrization
AIRSPACE CONSOLIDATION
Blood – trauma, DIC, PE, vasculitis, hemosiderosis
Pus – bacteria, PCP, fungus, TB
Fluid – CHF, renal failure, toxic inhalation, ARDS
Cells – bronchoalveolar Ca, lymphoma
Protien – alveolar portienosis, mucus plug
SEGMENTAL CONSOLIDATION
Lobar Pneumonia
Bronchopneumonia
Interstitial Pneumonia – viral, mycoplasm
Aspiration
TB & Atypical Mycobacterium
Trauma
Pulmonary Embolism
Obstructing Neoplasm
Mitral Regurgitation
ADULT RESPIRATORY DISTRESS SYNDROME
Event
White Out
Loss of Compliance
Refractory Hypoxemia
Shunt – precapillary
PULMONARY VASCULITIS 4
Infectious – RM spotted fever, mucormycosis
Wegener’s – diffuse, cavitate, nasal, 40+yrs, 2:1 male
Goodpasture’s – perihilar, hemoptysis, 25yrs, 7:1 male
SLE
PATTERNS OF INTERSTITIAL DISEASE
Septal Lines – CHF, lyphangitic Ca
Reticular (irregular lines) – UIP, sarcoid, asbestos, drug
Air Cysts (round) – UIP, PCP, LAM, EG, bronchiectasis
Nodules – sarcoid, silicosis, EG, EAA (extrinsic allergic alveolitis)
Ground Glass Opacities – DIP, PCP, EAA, alveolar proteinosis
Hyperinflation – LAM, EG, CF, or any w COPD
LOWER LOBE INTERSTITIAL DZ
Bronchiectasis
Aspiration
DIP – desquamative interstitial pneumonitis
Dermatomyositis
Lymphangitic spread
Asbestosis
Scleroderma
Sarcoid
Rheumatoid Lung
Furadantin
UPPER LOBE INTERSTITIAL DZ
Cystic Fibrosis
Ankylosing Spondylitis
Silicosis
Sarcoid
Eosinophilic Granuloma
TB
BRONCHIECTASIS (saccular & cylindrical types)
Infectious – aspergilla, TB, Sweyer-James
Congenital – cystic fibrosis, Kartagner syn, agammaglobulinemia
Obstructive – neoplasm, nodes
Chemical – aspiration, inhalation
Fibrotic – COPD
SOLITARY PULMONARY NODULE
Bronchogenic Ca
Hamartoma
Granuloma
AVM
Abcess
CAVITATING PULMONARY NODULES 6
Infection – staph, klebsiella, TB, coccidiomycosis, septic emboli, PCP
Neoplasm – squamous cell ca, osteosarcoma
Vasculitis – wegener’s, rheumatoid
Trauma – pneumatoceles
Bronchogenic Cyst
Pulmonary Embolism
PULMONARY CALCIFICATION
TB
Histo
Silicosis
Alveolar Microlithiasis
Hyperparathyroidism
Chronic Venous Congestion – mitral stenosis
Treated Lymphoma
Idiopathic Pulmonary Osteopathy
UNILATERAL HYPERLUCENT LUNG
Chest wall defect – mastectomy, absent pectoralis
PE – westmarks sign
FB – obstuctive emphysema
Pulmonary hypoplasia
Sweyer-James
AORTIC ANEURYSMS
Atherosclerosis – abd
Marfan’s
Vasculitis – Syphilis, Takayasu, Kawasaki, fungal, TB, polyarteritis nodosa
Aortic Valve Stenosis – asc dilation
CAUSES OF RIB NOTCHING
Coarctation
Aortic Thrombosis
Subclavian Obs – Blalock shunt for tricuspid atresia
Pulmonary Oligemia – any cause of dec flow
CARDIOMEGALY
Highoutput Failure – vein of Galen aneurysm, AVM etc
Outflow Obstruction Failure
Cardiomyopathy
Pericardial Effusion – always rule out
PULMONARY ARTERIAL HYPERTENSION
Primary
Lung Disease – COPD
Multiple PE
Eisenmienger
EMPHYSEMA TYPES
Centrilobular – #1, smoker, upper
Panacinar – alpha-1-antitrypsin, diffuse
Paraseptal – peripheral blebs
D/D Adrenal masses
D/D of Adrenal Masses :
Adenoma
· Smooth contour and well marginated, diameter less than 5 cm.
· May appear heterogeneous due to cystic degeneration or hemorrhage.
· If a functioning adenoma, may have report of hypersecretion of cortisol (Cushing’s syndrome), aldosterone (Conn’s syndrome), or androgens (adrenal virilization). Correlate clinically.
Cushing’s syndrome
· Unilateral mass with decrease in size of contralateral gland.
· Usually 2-4 cm diameter lesion.
Conn’s syndrome
Hypoattenuating lesion in gland with average diameter less than 2 cm (need thinner cuts to visualize).
· Hyperplasia
o Have diffuse enlargement bilaterally.
o A variant called macronodular hyperplasia shows not only thickened adrenals but multiple nodules.
o Clinically will have hyperfunctioning gland.
· Carcinoma
o Rare
o Size is often greater than 5 cm with central areas of necrosis, may have tumor calcification.
o Tumor may demonstrate spread into the lever, nodal system or venous system.
· Metastasis
o The adrenals are the fourth most common location for metastatic disease. In most cases, patients are asymptomatic.
o Appearance on CT is widely variable, but there are five patterns commonly seen :
o Mass less than 5 cm in diameter.
o Mass greater than 5 cm in diameter.
o Multiple masses.
o Diffuse enlargement.
o Normal appearing glands.
o It is frequently difficult to distinguish a nonhyperfunctioning adenoma from a metastasis in cancer patients.
o In non-cancer patients, an adrenal mass less than 5 cm in size with no features consistent with malignancy should be followed with serial CT scans. If after 18 months the lesion is stable, it can be considered benign.
Pheochromocytoma
· Typically greater than 3 cm, and if large, may be cystic due to necrosis.
· Because of hypervascular nature, will enhance brightly with contrast.
· May contain calcification.
· Clinically will have hyperfunction, with increased urinary levels of catecholamines.
· If associated with MEN syndrome or von Hippel-Lindau disease, may have lesions in pancreas, kidney and spinal cord.
· If difficult to differentiate from adenoma, perform T2-weighted MR. Pheochromocytoma will have significantly higher signal intensity.
Hematoma
· Round to oval adrenal mass.
· In adults, is typically related to blunt abdominal trauma, and if so is usually right sided.
· Acute to subacute hematomas have attenuation values between 50 and 90 HU. Follow up studies will demonstrate decrease in size and attenuation.
Cyst
· Unilateral and solitary hypoattenuating mass.
· Usually round or ovoid with thin, smooth wall.
· Inferior wall may be flat or even concave.
· May see peripheral, curvilinear calcification.
Infections
· Granulomatous infection
o The most common infectious cause of Addison disease is tuberculosis.
o Early adrenal findings include bilateral enlargement with a hypoattenuated center & an enhancing rim. Later the adrenal atrophies with calcification
o With disseminated histoplasmosis, CT demonstrates bilateral enlargement again with central hypoattenuation and a peripheral rim. Diagnosis can be made with FNA biopsy and special staining.
· Pneumocysitis carinii infection
o Consider in immunocompromised patient population.
o On unenhanced CT will see either punctate or coarse calcifications in multiple abdominal structures including the adrenals, liver, spleen, kidneys and lymph nodes.
· Abscess
o Most adrenal abscesses are found in neonates who have had a prior adrenal hemorrhage.
o On contrast-enhanced CT will see thick-walled cystic mass.
Myelolipoma
· Usually asymptomatic unless hemorrhage within the mass causes symptoms.
· Consist of mature fat and bone marrow. Appearance ranges from nonfatty soft tissue mass to a fat predominated mass. Typically unilateral, may be calcified, especially if had previous hemorrhage.
· Most commonly has a well-defined capsule surrounding fat. Attenuation ranges especially if had previous hemorrhage.
· With contrast, the soft-tissue areas will enhance, potentially masking the areas of fat.
Hemangioma
· Rare benign tumor that is a well-defined hypoattenuating or heterogeneously attenuating mass, often containing calcifications.
· A characteristic finding is phleboliths within the haemangioma.
Ganglioneuroma
· Homogeneous hypoattenuating lesions in comparison to muscle on both enhanced and unenhanced CT, may have calcification.
· CT-guided biopsy or surgical resection necessary to confirm diagnosis.
radio image- pyogenic infection MRI
multiphasic helical CT in HCC
Abstract of paper presented in Asia Pacific Congress for Study of Liver (APASL,2004,N.Delhi)
HEPATO CELULLAR CARCINOMA : MULTIPHASIC CT EVALUATION IN 27 PATIENTS
H. S. Das, N. Medhi, P. K. Sarma, P. Goswami, P. Hazarika, B. Sarma
Primus Imaging, G. S. Road
Hepato cellular carcinoma ( HCC) is the eight most common malignancy worldwide and represents 6 % of all tumors. It is also the most common primary hepatic malignancy. Increased incidence of HCC is seen in the Far East, Southeast Asia and sub-Saharan Africa ( 90 cases per 1,00,000 population versus 2.4 cases per 100,000 in the United States.
Risk factors for developing HCC includes cirrhosis, hepatitis B and C viruses. Additional risk factors include haemochromatosis, excessive androgens, ∞ 1 antitrypsin deficiency, exposure to oral contraceptives, Thorotrast, aflatoxins and vinyl chloride. Hepatitis B is considered to be the primary cause in 80% of cases worldwide. Peak age of incidence is 50 to 70 yrs with a male predominance of 4:1.
Objective :- To evaluate clinical and multiphasic helical CT findings in 27 patients of hepato cellular carcinomas.
Materials and Methods :- Multiphasic helical CT scans were performed in 27 patients of HCC’s. Non ehanced scans were obtained in all patients, along with hepatic arterial dominant phase ( HAP) and portal venous dominant phase (PVP) images at 25-28 and 60-70 seconds after intravenous infusion of 60 to 80 ml of contrast. Delayed sections were also obtained in all the patients after 5 to 10 minutes. We reviewed age, gender, tumor risk factor, serum tumor markers, and tumor morphology with degree and type of enhancement on helical multiphasic CT.
Results : - 22 of the 27 patients ( 81% ) were men. Patients had an age range of 30 to 87 yrs ( mean = 55.9 years ). Abdominal signs and symptoms were present in 25 out of 27 patients ( 92.5 %) and 11 of 27 patients( 40.7 %) had chronic liver disease ( CLD). Abdominal signs and symptoms were present in 24 of 27 patients HCC was proved on the basis of Biopsy (n= 16 ) and by levels of increased serum alpha feto-protein (n=19 ). 15 patients had solitary or dominant mass. At CT well defined tumor was demonstrated in all the patients with signs of malignancy with hepatic hypervascularity ( 96 %), biliary obstruction (10%),satellite lesions (45%) , lymphadenopathy ( 25 %), ascites (18 % ) and
portal venous thrombosis in 11 %. Portions of tumors were heterogeneously hyperattenuating at arterial phase in 27 (100%) and hypoattenuating in portal phase in 24 patients (88 %). Some of the larger tumors showed delayed persistent enhancement in the equilibrium phase (n= 6 ). Most of the tumors were hypoattenuating on the unenhanced images.
Conclusion: In our patients HCC was seen to develop in presence and absence of cirrhosis or known risk factors and typically appeared as large, symptomatic hepatic masses with clinical, laboratory and CT features that helps to identify these tumors from other hepatic masses.
MR IMAGING IN ORTHOPAEDICS
MR IMAGING OF THE SPINE AND CLINICAL APPLICATIONS :
MRI is the most useful imaging modality for evaluation of the spine. It can be routinely used in degenerative spinal diseases, spinal infections, marrow diseases, congenital anomalies, craniovertebral junction . This article gives an overview of the utilities of MRI in imaging of spinal pathologies as far as an orthopaedic surgeon is concerned.
DEGENERATIVE DISEASES OF THE SPINE
Degenerative diseases of the spine is the commonest condition causing backache, neck pain, radiculopathy and radiculo -myelopathy. Depending upon the location the symptoms vary. Degenerative spinal disease itself is an ill defined concept, better understanding has been possible due to advent of various newer imaging modalities specially MRI.
Indications for imaging:
# Failure of appropriate conservative therapy.
# When there is evidence of deficit.
# In patients having excruciating pain.
# When the diagnosis is in doubt.
# For follow up evaluation.
Choice of imaging modalities:
Plain X-ray still has a role in degenerative spinal diseases if it is properly done. Along
with AP and lateral views, the, oblique views are also very helpful sometimes in demonstrating the neural foraminae. It guides the clinician to choose the subsequent modalities. Conditions like infection, neoplasia, spondylolisthesis etc. can be excluded. Disc narrowing , vacuum phenomena or associated osteophytosis however does not rule out any cord or nerve root impingement and only reflects the consequences of disc degeneration.
Myelography with or without CT cuts is another helpful modality in the evaluation of the degenerative diseases.It is possible to evaluate any intrinsic or extrinsic pressure effect on the neural elements,though the morphology of the lesion can not be made with certainity.Still better information can be gathered with addition of CT cuts with the myelography.The greatest disadvantage of myelography is its invasive nature and associated side effects.
MRI is the best imaging modality as it removes all the disadvantages faced by the clinician in other imaging modalities.It is superior to other modalities because-
- It is totally noninvasive.
- Its multiplanar capability-axial,sagittal,coronal and oblique projection can be obtained.
- soft tissues and bony elements can be equally imaged
- Early detection of disease enabling the clinician to reduce the morbidity and mortality.
MRI of disc degeneration:
Normal disc is composed of two basic component-Nucleus pulposus and annulus fibrosus Central nucleus pulposus is composed of gelatinous material consisting of water and proteoglycans. Annulus fibrosus surrounds the nucleus and has two layers.Inner portion is composed of fibrocartilage whereas the outer fibre are composed of lamellated collagen fibres.The annulus is anchored to the adjacent vertebral bodies by sharpeys fibres
In a normal disc the nucleus pulposus is seen as hyperintense signal on T2 weighted images due to increased water content.There is a T2 hypointense cleft(intranuclear cleft) in the centre of the nucleus which represents residual notochordal remnant. The annulus is hypointense on T2 weighted images due to ligaments. Normal disc is well hydrated and with advancing age there is loss of hydration, the process is termed as desiccation. Abnormal desiccation may start at an early age also. Though it is not clearly known why disc desiccation starts with aging vartious theories have been put foroward.These include –decreased diffusion,cell viability and activity and proteoglycan synthesis. On MRI the desiccated discs are hypointense on T2 weighted images and there is loss of biconvex contour of the disc. The intranuclear cleft becomes prominent.
Disc degeneration can be divided into two types-
- Intervertebral osteochondrosis(chondrosis)-When the degenerative process involves the nucleus pulposus the process is called intervertebral chondrosis and osteochondrosis when it involves the adjacent bone also. This is reflected in MRI by disc desiccation,end plate changes,intervertebral disc herniation(schmorls node),vacuuming and reduced disc height.There are three types of end plate changes depending upon the MR morphology.Type I change reflect water,type II change reflects fatty change and type III change signifies sclerotic change.
-
- Spondylosis deformans :- When the degenerative process involves the annulus fibrosus the process is called spondylosis deformans. Here there is abnormal traction in the osseous attachment of the annular fibres leading to osteophytic lipping. Disc space and end plates are preserved here.
Disc herniation:
Disc herniation means displacement of the intervertebral disc from its normal position.Disc may herniate in any direction-anterior,lateral ,posterior and in craniocaudal direction. Various names have been applied and classifications have been made for different entities by different authorities in the comminuted method. Disc herniation has been subdivided into three main groups. Protrusion, extrusion(including sequestration) and intravertebral herniation. In conventional teaching this classification is based on the integrity of the annular/posterior longitudinal ligament complex.A herniated disc is called protruded when the ligaments are intact.When there is break in the ligament complex in a herniated disc it is termed as disc extrusion.However the ligament complex may not be possible to visualize,hence various authorities try to use various names for these entities.Sometimes these terms become confusing .To obviate these confusions a consensus has been made in the nemenclature (after P.Milette). This has been endorsed by –American Society of Spine Radiology,American Society of Neuroradiology,North American Society Spine Society,American Association of Neurological Surgeons,Congress of Neurological Surgeons and American Academy of Orthopaedic Surgeon. A simplified version of the terminology has been discussed here :-
According to the morphology (based on the shape of the displaced disc material) a herniated disc is called
1. Protrusion: If the greatest distance in any plane ,between the edges of the disc material is less than the distance between the edges of the base in the same plane than this called protrusion.
2. Extrusion: If the greatest distance in any plane,between the edges of the herniated disc is more than the distance between the edges at the base is called extrusion.Sequestration is a type of extrusion where the extruded fragment looses its contact with the parent disc.
3. Intravertebral: It means craniocaudal herniation of the disc material through the break in the end plates(Schmorls node).
According to the location a herniated disc may be Central,right/left central,lateral recess(subarticular zone),foraminal(pedicule zone) and extraforaminal (far lateral zone).
Spinal infections:
Infection of the spine may be broadly classified into two main groups-tubercular and non-tubercular. Non-tubercular infections may be due to pyogenic,fungal,parasitic and viral infecting agents.
Tubercular infection:
Lower thoracic and upper lumbar region is the commonest site for tubercular infection follwed by cervicodorsal region.Tubercular infection can involve the vertebral body,disc,epidural space,cord parenchyma,posterior elements and paraspinal soft tissues in combined or isolated form.
MR features of tubercular spinal infections:
MRI can detect the ongoing tubercular infection in the spine at a stage when it is not appreciable in plain X-ray or CT scan. The vertebral involvement may not show any abnormal signal intensity in T2 weighted images. On T1 weighted images the vertebral lesion becomes hypointense. The disc height is relatively maintained so that sometimes it mimics neoplasia. There may be skip lesion, epidural soft tissue lesion, paraspinal muscle involvement ect. Reduction of disc height, reactive sclerosis, vertebral body destruction, gibbus formation are found in advanced cases. In the spinal cord it may produce cord tuberculoma or in early cases myelitis. Involvment of the posterior elements favours the diagnosis of tubercular infection.
Pyogenic spondylodiscitis:
Pyogenic infection of the spine or disc can occur by haematogenous route or by direct inoculation of the disc or the vertebral body. In pyogenic spinal infection ,infection centres around the disc. Disc is vascular in children and in haematogenous infections the disc is first to be involved and the endplates and vertebra are secondarily involved. As in adult the disc gets supply from the endplates thus the disc is involved after the end plates.
On MRI there is irregulartities in the end plates with altered signal in the end plates.The disc height is invariably reduced with strong hyperintense signal in the disc.The vertebral body shows increased signal on T2 and reduced signal on T1 weighted images.There is inhomogenous soft tissue extension.
Brucella spondylitis:
In brucella there is destruction of the anterior aspect of superior end plate of the vertebral body.Healing starts simultaneously in the form of sclerosis and in typical cases there is spillage of healing bones forming large anterior osteophytes.Then the sclerosis extends to the body.Another typical finding of brucella is the peripheral vacuum phenomena.Here there is collection of aerocele in between the disc and superior end plate anteriorly.
Fungal spondilytis:
Fungal spondylitis may be caused by various organisms like blastomycosis, cryptococcosis and coccidiodomycosis. Destructive lesions associated with sclerotic margins, paraspinal masses, multiple sites of involvement with preservation of the disc space are the hallmark of fungal spondylitis.
MRI of failed back surgery syndrome:
Intractable pain and chronic disability after surgery is referred to as failed back surgery syndrome. It is a major cause for increased morbidity and mortality in patients with lumbar disc surgery.The main causes can be divided into two groups-immediate and delayed.
Immediate causes:
Haemorrhage: Onset of symptoms in haematoma occurs within few days.The haematoma occurs in the epidural space and compresses the thecal sac.The severity of symptoms will depend on the size of the haematoma. On MRI the haematoma is bright on T1 weighted images and dark on T2 weighted images.
Disc space infection: Disc space infection(discitis) is the most difficult situation for the surgeons. as there is severe pain and it takes long time to control. The symptoms starts as early as first week and as long as 2 years. On MRI the disc become hyperintense, there is T1 hypointensity in the end plates. These hypointensities my extend to entire vertebral body. On T2 weighted images these are moderately hyperintense. There is T2 hyperintense lesions extending to the epidural space compressing the thecal sac .Soft tissue lesions may be seen in the paraspinal soft tissues.
Pseudomeningocele: may result from dural tear during surgery.It protrudes posteriorly .The sac is hyperintense on T2 and hypointense on T1 weighted images.
Delayed causes:
Disc related causes: The simple cause of persistant pain after surgery may be due to operation in a wrong level. The main disc causing symptoms may be left untreated.There may be recurrent disc at the same level or in a different disc level causing symptoms. Lastly a portion of the disc(residual) may be left during surgery which may cause recurrence of symptoms.
Canal stenosis: There may be congenital canal stenosis associated with herniated disc so that even after removal of the disc patient may not impoove .Again there may be stenotic changes in the central,foramina or recess due to bony overgrowth after facetectomy,late spur formation and post-operative spondylolisthesis.
Epidural fibrosis :Epidural scarring/fibrosis is of uncertain clinical significance, when it is present it may or may not produce any symptoms. On MRI most of the it can be demonstrated easily. In difficult cases intravenous contrast study may be necessary.
Arachnoiditis: Spinal arachnoiditis is a nonspecific response to a variety of stimulus .It is chracterisized by root adhesion, clumping and sometimes cord swelling. There may be deformity of the thecal sac in late cases.
MRI of marrow disease:
MRI is the best imaging modality in the study of structural and morphological anatomy of bone marrow.Earliest changes in the marrow can be detected which are not picked up in X-ray or CT scan so that early intervention can be made.
MRI of normal marrow: Bone marrow has three components. Trabecular bone, Red marrow and Yellow marrow. Trabecular bone acts as a support to the red and yellow marrow. Red marrow is responsible for haemopoiesis and yellow marrow gives nutritional support to red marrow. On T1weighted images yellow marrow appears bright as subcutaneous fat and T2 weighted images it is hyperintense but less than T1.Red marrow is of intermediate signal intensity in both T1 and T2 weighted images.
Marrow pathology:. Abnormalities in the bone marrow can be divided into –
Marrow proliferative disease.
Marrow replacement disorders
Marrow depletion
Vascular
Miscellaneous diseases.
Marrow proliferative diseases:
In this group of diseases there is abnormal proliferation of the cells that exists normally in the bone marrow. Marrow proliferative diseases may be benign or malignant.Common conditions causing marrow proliferation are leukaemia, multiple myeloma, primary amyloidosis, myelodysplasia, mastocytosis and sometimes reconversion of yellow marrow.
MRI findings:
If the changes are very less or the density of the abnormal cells are less MR may be normal.
Signal intensity varies with the disease pattern.In leukaemia the marrow becomes slightly hyperintense on T2 and hypointense of T1 weighted images.In multiple myeloma T1 images will be hypointense and in 50% of patients T2 images may be hypointense.In mastocytosis and myelofibrosis ,it stimulates fibrosis and marrow show reduced signal on both T1 and T2 weighted images.In all these conditions as the haemopoiesis is hampered due to reduction in the affective red marrow ,there is associated reconversion of the existing yellow marrow.
In haemolytic anaemia there is reconversion of yellow marrow.There may deposition of haemosiderin in the bone marrow causing reduced signal in spin echo images.
Marrow replacement diseases:
In this group of diseases there is replacement of the existing normal bone marrow by cells not present normally in the bone marrow.The conditions include metastases,lymphoma,,infectionand primary bone tumours. MRI can be used as screening modality and frequently used to monitor the response to therapy.
MRI features : On T1 weighted images the marrow will be hyperintense,On T2 weighted images it gives variable signal depending upon the infiltrates.Lyphoma and other sclerotic metastases gives hypointense signal on T2 weighted images.
Marrow depletion:
Marrow depletion can occur in aplastic anaemia, post radiation and chemotherapy. The red marrow will replaced by yellow marrow. These changes are observed when MRI is performed for different purpose.Focal areas of red marrow can be seen if there is patchy marrow regeneration.
Marrow oedema:
Various conditions produce marrow oedema. Examples are osteoporosis, trauma (bone contusion)transient osteoporosis, ischaemia, infection, tumour and degenerative joint abnormalities. On T2 weighted images it is very hyperintense and on T1 weighted images these of are intermediate signal intensity.
OsteoporoticVs Pathological frature :
In osteoporotic collapse marrow signal aleteration involves only the vertebral body. The posterior elements are relatively spared. In pathological collapse the posterior elements may also show altered signal intensity.
In osteoporotic collapes no soft tissue involvement is seen. But in pathological collapse the soft tissue involvement is usually seen.
In pathological compression the posterior margin of the involved vertebra is convex.
Fracture line(s) may be seen in osteoporotic collapse.
Spinal dysraphism:
Spinal dysraphism refers to a group of diseases where there is incomplete closure of the spine involving skin, bones, cartilage and neural elements. It is of two types-spina bifida aperta when the spinal contents come out through the osseous defect and produces a visible swelling. Examples-meningocele and meningomyelocele. Second type is spina bifida occulta(occult spinal dysraphism).In this type the malformationis not visible from outside as it dose not produce any swelling. Examples of this condition are-meningocele, dorsal dermal sinus, spinal lipomas, tethered cord ,diastematomyelia, neuroenteric cyst etc. With the advent of MRI there has been better understanding and early detection of these conditions followed by early intervention and hence better prognosis.
Miscellaneous conditions: MRI is the best imaging modality for evaluation of Craniovertebral junction anomalies. Due to its multiplannar capability and better soft tissue contrast it is the modality of choice in evaluating such cases. The spinal intramedullary and extramedullary tumours are best assessed by MRI. Various cord lesions of the cord like syringomyelia, myelitis, pyogenic and tubercular infections are also easily assessed by MRI. . MRI is invaluable in spinal trauma especially when the bony elements are apparently normal. Haemorrhagic and non haemorrhagic contusions are only detected on MRI.
References:
1.Appeal.B: Nomenclature and classification of lumbar disc pathology.Rivista di Neurologica 14:147-152,2001.
2.Milette PC,Fontine S et al:Differenting lumbar disc protrusions,disc bulges and discs with normal contour but abnormal signal intensity.Spine 24:44-53,1999.
3.Kaplan,Helms,Dussault,Anderson and Major.Musculoskeletal MRI. W.B.Saunders company.2001.
4.Wilmink JT.Clinical and Radiological aspects of degenerative disc disease and spinal stenosis,Rivista di neurological 14:163-166,2001.
5.Osborn Anne G. Nonneoplastic disorders of the spine and spinal cord,Diagnostic Neuroradiology Mosby year book,Inc.1994.
6.Tali ET,Imaging of spinal infectious diseases,Rivista di neurological.14:177-187,2001.
CANCER OF THE LIVER
INCIDENCE
· Usually thought of as uncommon but although there is a low level of incidence in industrialised countries, worldwide it is one of the most common primary tumours.
WHO figures indicate 250,000 new cases of hepatocellular Ca annually
Highest incidence in Asian and Negro populations where it is believed to be linked to lifestyle rather than race.
North America & Australasia 0.1 – 0.6 % of Ca deaths West/South Africa 15 – 20% of Ca deaths
UK & USA 1.8 cases per 100,000 persons Japan 17.3 cases per 100,000 persons West Africa 58 cases per 100,000 persons
Highest known incidence in Mozambique 104 I 100,00
· Overall more common in men than women (figures vary between 4 and 11:1) Can occur in childhood
AETIOLOGY
In populations with increased incidence linked to malnutrition, poor diet
Associated with carcinogens – hepatoxins eg. Aflatoxin produced by
Aspergillius flavus mould which grows on stored grain
· Hepatitis B – present in 40% of cases
Parasitic infections – schistosomiasis in the gut chinese liver fluke
Haemochromatosis – uncommon disease where there is excessive
absorption of iron giving rise to cirrhosis, splenomegaly, skin pigmentation &diabetes mellitus
In Western populations cirrhosis evident in 80% of hepatocellular Ca, therefore associated with high alcohol intake.
Suggested increase in incidence of benign liver adenoma in women using high Oestrogen contraceptive pill (Rooks cited in Fielding 1986)
A suggested link has been made between exposure to polyvinylchloride (PVC) and the development of Angiosarcoma of the liver (Souhami & Tobias 1986).
PRESENTING SIGNS & SYMPTOMS
Symptoms may vary depending on whether the disease is accompanied by cirrhosis.
Generally:
· General malaise
· Localized pain – right hypchondriac /epigastric regions
· Signs of liver failure – progressive destructive jaundice
Ascites
Prolonged drug activity
Increased clotting times
· Hepatomegaly – palpable mass
· Nutritional imbalance – hypoglycaemia
Hypercalcaemia
Polycythaemia
INVESTIGATIONS
A differential diagnosis may be difficult – especially in the presence of cirrhosis, but also in cases of cysts, hepatic mets and cholangitis.
· History – predisposing factors
· Clinical examination
· Liver function tests – have no diagnostic pattern (ie. Always abnormal), however, blood tests may reveal abnormal levels in many of the metabolic indicators including:
- blood glucose & protein levels (hypoglycaemia etc)
- alkaline phosphatase & bilirubin levels
- alpha-feto protein
· Radionuclide imaging
· Ultrasound
· CT scan
· CXR (+lung tomos if +ve)
· Laporotomy
· Guided biopsy (if surgery not to be undertaken) – not recommended for vascular tumours due to life threatening risk of haemorrhage.
HISTOLOGY
Primary liver tumours are classified as benign or malignant.
Classification of Tumours
Benign Epithelial Adenoma (liver or bile ducts)- most
common of benign tumours
Focal nodular hyperplasia
Mesenchymal Angioma
Infantile haemangioendothelioma
Mesenchymal haematoma
Malignant
Primary Epithelial Hepatocellular (hepatoma)carcinoma
Hepatoblastoma
Cholangiocarcinoma
Mesenchymal Angiosarcoma
Embryonal sarcoma
Embryonal Rhabdomyosarcoma
Secondary Solitary
(most common) Multiple
Metastatic disease in the liver commonly originates from Ca Colon or Ca Breast.
BENIGN TUMOURS:
HAEMANGIOMA
The most common of benign liver tumours. Can range in size from small lesion to gigantic cavernous haemangioma. Tumours larger than 4cm are classified as ‘giant haemangioma’. These tend to develop more frequently in females with a ration of 6:1. Lesions smaller than 4cm seldom become symptomatic.
Surgery is the treatment option for symptomatic tumours. Procedure may range from minor wedge resection to an extended hepatectomy, depending on size and location of tumour. Contra-indication to surgery would be a result of size, multiplicity or operative risk. These cases are managed palliative with RT.
ADENOMAS
These tend to occur more frequently in young females with a history of long term use of oral contraceptive. Most of these tumours tend to be singular vascular , well circumscribed and sharply demarcated, although not necessarily encapsulated.
About 1/3 of patients have acute abdominal haemorrhage following rupture of the tumour.
Small tumours on the edge of liver is easily removed by surgery. Symptomatic patients who are not suitable for surgery should be advised against use of oral contraceptives and becoming pregnant. Association with oestrogens. These tumours do not show elevated levels of alpha-fetoproteins.
FOCAL NODULAR HYPERPLASIA
These tumours usually have a nodular surface and on gross examination may be confused with cirrhosis. Intratumoural haemorrhage may be present and lead to misdiagnosis of adenoma. The most characteristic feature is the proliferation of small bile ducts, usually accompanied by heavy infiltration of lymphocytes.
Emergency surgery is rarely needed since focal nodular hyperplasia seldom bleeds.. Operative management is usually reserved for those who present with pain or in whom there is diagnostic uncertainty.
MALIGNANT TUMOURS:
HEPATOCELLULAR CARCINOMA
Striking geographic variations can be seen. It is more common in males in high incidence and low incidence areas. In all populations, the incidence rises with age. However, high incidence areas show a shift towards the younger age group. This prevalence is maintained even when emigration to low incidence regions occurs, the increased risk is retained.
In the western world, hepatocellular carcinoma has a low incidence, occuring more frequently in males and generally on a background of cirrhosis. HCC occurs in two gross patterns; diffuse and focal form.
CHOLANGIOCARCINOMA
Intra-hepatic cholangiocarcinoma is an adenocarcinoma of the bile duct. It is distinguished from HCC by its mucin production. Surgery has been shown to be the most suitable treatment although many patients present with unresectable tumours, due to their multicentric nature. Short term surgical intubation provides good palliation. RT nor CT has been shown to be effective in controlling this lesion.
ANGIOSARCOMA
This multicentric tumour has variable differentiated endothelial cells which are associted with fibrosis. Factor VIII is usually present in the tumour, which helps to distinguish it. Tumours are usually large and clinically advanced on presentation. Survival is a matter of months following diagnosis. Little can be done in the way of treatment. Death usually results from liver failure, gastrointestinal bleeding or renal failure.
Approx 60% of cases have multiple lesions within the liver, most of these having a large mass accompanied by several smaller masses.
The remainder have diffuse disease -solitary masses are unusual. The presence of cirrhosis is very common.
STAGING
T1 Single tumour up to 2cms no vascular invasion
T2 Single tumour less than 2cms with vascular invasion
or Multiple tumours all less than 2cms with no vascular
or Single tumour invasion greater than 2cms with no vascular
invasion
T3 Single tumour greater than 2cms with vascular invasion
or Multiple tumours limited to one lobe all less than 2cms with vascular
invasion
or Multiple tumours limited to one lobe all greater than 2cms without
vascular invasion
T4 Multiple tumours in more than one lobe
orTumour(s) involve a major branch of portallhepatic veins
No
N1 Regional nodes positive
Spread
· Local invasion and spread within the liver is common as is venous
involvement.
· Lymphatic spread to local nodes at porta hepatis then to cisterna chyli.
· Blood borne spread to lungs & bones.
MANAGEMENT OPTIONS
1. First choice is SURGERY.
Resection of the tumour, particularly if it requires removal of only one lobe offers a chance of cure. The liver has the ability to regenerate (even after 75% removal) although this ability is reduced if cirrhosis is present – and surgery under these conditions may even lead to degeneration of liver function.
Surgery is more successful in children than in adults.
Resection usually follows laparotomy, undertaken to establish the full extent of the disease within the abdomen.
Resection may be:
Segmentectomy
Lobectomy
Triscgmentectomy
Resection offers:
good palliation
good control of solitary mets from other primaries
However, resection carries a high mortality rate and only offers a chance of cure in 5% of cases!
Palliation may also be achieved by Hepatic Artery Ligation or Embolizafion. Embolization is particularly attractive as it is a non surgical procedure performed without anaesthetic, with a low mortality rate and possible pain relief achieved.
Liver Transplantation is still being developed as a management option for patients with liver tumours although it was these patients on which it was first pioneered. Patient selection is clearly critical with the physical condition of most patients eliminating this as a management option. Availability and cost vs benefit issues also arise. Local recurrence rates are high.
2. CHEMOTHERAPY
Chemotherapy for primary and secondary liver tumours takes a variety of forms.
Both single agent (5FU and Doxorubicin) and combination regimes have been tried in the management of liver tumours. A selection of studies show differing results, although most conclude that there is no significant benefit to be gained from combination systemic chemotherapy as opposed to single agent regimes.
Both approaches appear to offer reasonable (approx 50%) response rates in early primary disease treatment and show increased survival rates and measurable palliation in later stage and rnetastatic cases.
Howcver, it should be noted that many studies have low patient numbers due to the rarity of the tumours and the poor physical condition of the patients.
lntra-arterial infusion of chemotherapeutic agents via the hepatic and superior rnesenteric arteries is an alternative management option (Halnan 1990 p. 445). A combination of 5 FU and Adriamycin or FUDR (5-flurodeoxyuridine), agents with a very short half-life have been shown to offer increased survival rates and achieve a measurable palliative response in up to 61% of cases.
3. RADIOTHERAPY
Due to the insensitivity of liver tumours to radiation and the low tolerance levels of normal liver tissue to radiation there is little role for radiotherapy in the management of these tumours. Radiation-induced hepatitis may occur after doses of 3OGy – eliminating the opportunity to apply radical tumouricidal doses.
Radiotherapy is occasionally used for symptom control in the case of painful metastases where large field sizes are used and small fractions of radiation are given. Careful monitoring of blood counts is required.
PROGNOSIS
Liver tumours are commonly fast growing and consequently offer a very bad prognosis -mean survival is 3 months if left untreated!!
Prognosis is particularly bad with cirrhotic livers with at best 50% 3 months survival with treatment, falling to zero at 12 months.
Patients with non cirrhotic livers fair better although only 10% of these will be alive at 2 years. However, patients who have a complete surgical resection or show a complete response to chemotherapy fair better as do children where surgical resection is more often possible.
Death is commonly due to either: hepatic failure; widespread metastatic disease; secondary infections (lung/liver) or portal hypertension.
Overall 5 year survival approx 1%.
MR IMAGING IN MALIGNANT & BENIGN NEOPLASTIC DISEASES OF THE UTERUS
MR imaging in malignant and benign neoplastic
pathologies of uterus
Dr.P. Goswami, Dr N Medhi , Dr P K Sarma, Dr H .S. Das, Dr P Hazarika Dr B J Sarma
Primus, GS Road, Guwahati –
Although ultrasound remains the initial modality for evaluating clinically suspected masses in female pelvis, ultrasound is limited in its ability to clearly differentiate between many pelvic pathologies. MR imaging is exceptionally well suited for study of female pelvis. MR imaging provides an excellent noninvasive means of evaluating uterine zonal anatomy. The superior contrast resolution of MRI and the capability for direct multiplanar imaging has made it a valuable tool in the evaluation of benign and malignant uterine tumors and staging of pelvic malignancies.
Clinical indications : MRI is often indicated in the patients in whom ultrasound findings are suboptimal. MRI is also indicated in the patients in whom the origin of the pelvic mass can not be determined by ultrasound, patients in whom further lesion characterization is required and in patients with pelvic malignancies.
Cervical diseases :
Carcinoma of cervix :
Carcinoma of cervix is the most common gynaecologic malignancy in woman under the age of 50. Widespread screening was made possible following introduction of papanicolau smear. Improved early detection of noninvasive cancer has led to an overall decrease in mortality over the past three decades. Unfortunately, there has been no significant change in the mortality of invasive cervical carcinoma over the same period, despite improved treatment. Carcinoma cervix can occur at any age from menarche onwards. The peak incidence is prenemopausal. The two major symptoms of cervical carcinoma are vaginal bleeding and discharge. However upto 20% of patients with invasive carcinoma are asymptomatic at the time of diagnosis. The majority of noninvasive or early stage disease is most likely to be discovered in asymptomatic females with abnormal cervical cytology. Approximately 90% of cervical malignancies are squamous cell carcinomas. The remaining 10% of cervical cancers consists of adenocarcinoma and sarcomas. The prognosis is determined primarily by the tumor stage, histological grade, size, location within the cervix, depth of stromal invasion, adjacent tissue extension and presence of lymphnode metastases. Stage of disease is one parameter influencing the choice of therapy. For stage l and limited stage lla disease the options are surgery, radiation therapy, or both. In the majority of the patients with more advanced disease (stage ll a or greater ) treatment consists of radiation only. Therefore accuracy of staging is important not only for prognosis but also for choice of optimal therapy. The clinical staging in a patient of cervical carcinoma is not very accurate because of limitations in assessment of tumor extension in the pelvis.
MR findings
MRI plays a crucial role in the evaluation and staging of cervical carcinoma. On T2 weighted images, cervical carcinoma most often appears as a mass of high signal intensity, distinct from the normal lower signal intensity cervical stroma, with distortion or disruption of the normal zonal anatomy of the cervix (Fig : 1). There may be broadening of the central uterine high intensity zone caused by uterine secretions retained within the enlarged uterine cavity due to cervical stenosis. On T1 weighted images, the cervical mass is isointense with normal cervix and uterus and only gross parametrial or adnexal extension causing contoural abnormality can be seen. Although administration of intravenous Gd allows distinction between viable tumor and areas of necrosis, it has not been shown to increase diagnostic accuracy in tumor depiction. For the local staging of cervical carcinoma, MRI is superior to other available modalities. In evaluating stage of disease MRI has an accuracy of 90% compared with 65% for CT. MRI is more accurate than CT (94% versus 76%) in assessing parametrial infiltration. MRI assessment is useful for placement of radiation ports. CT can not evaluate the tumor size or stromal invasion because it can not distinguish cancer from surrounding normal cervical tissue due to similar densities. MRI can accurately determine the tumor size. Tumor staging based on MRI follows FIGO staging criteria. Cervical carcinoma in situ is considered as stage O. Cervical carcinoma is considered stage l, when the tumour is strictly confined to the cervix. Stage l carcinoma is again subdivided to (a) stage la – microinvasive carcinoma and (b) stage l b – all other cases of stage l. MRI is not applicable in stage O and stage la disease. Stage ll disease indicates extension of tumor beyond the cervix. This stage is further subdivided to (a) stage ll a – tumor extension into the upper two thirds of the vagina and there is no obvious parametrial involvement. On T2 weighted images there is loss of low signal intensity from the normal vaginal wall (b) stage ll b – obvious parametrial involvement. Parametrial involvement is diagnosed when, in addition to loss of the normal low signal intensity cervical stroma, there is irregularity of the lateral cervical margin on T1 weighted images and presence of parametrial soft tissue mass. On T2 weighted images, there is diffuse or localized abnormal signal intensity within the paracervical region. Encasement of uterine vessels is another important finding in diagnosing parametrial invasion. Disruption of the fibrous stroma is the earliest finding of parametrial invasion. The presence of an intact ring has a high true negative rate for absence of parametrial infiltration. A tumor is considered as stage lll when it involves the lower third of vagina. Stage lll disease is subdivided to (a) stage lll a – no extension to the pelvic side wall (b) stage lll b – extension to the pelvic side wall and /or hydronephrosis or nonfunctioning kidney. Stage IV disease indicates extension of the tumor beyond the true pelvis or involvement of the mucosa of the bladder or rectum. This stage is further subdivided to (a) stage lV a – spread to bladder or bowel wall, which appears on T2 weighted images as loss of the normal low signal intensity of the wall of the organ (b) stage lV b – spread to distant organs. Cervical carcinoma spreads to parametrial nodes, followed by obturator nodes and then the internal iliac and external iliac chain. MRI can accurately detect adenopathy when an axial diameter of greater than 1 cm is used as an indicator of lymphadenopathy.
Nabothian cysts :
Nabothian cysts are small nodules on the surface of the cervix caused by distension of the endocervical glands. They are often associated with healing chronic cervicitis. When small they are rarely symptomatic and require no treatment.
MR Findings :
A nabothian cyst demonstrates high signal intensity on T2 weighted images (Fig : 2). On T1 weighted images they exhibit medium to high signal intensity. The small size and well defined margins differentiate them from other cervical neoplasms.
Uterine tumors :
Endometrial Carcinoma :
Endometrial carcinoma is the most common invasive malignancy of the female genital tract. Approximately 70% of endometrial cancers are adenocarcinoma, 15% are adenoacanthoma, and 15% are adenosquamous carcinoma. Uterine sarcomas are rare. Patient most frequently present with postmenopausal bleeding. Tumors may be localized or diffuse. Localized tumors are polypoidal or exophytic in nature, with only superficial attachment to the endometrium. Diffuse tumors often demonstrate extensive invasion of entire endometrium. Intitial tumor spread through myometrium to involve both corpus and cervix, is followed by spread outside the uterus and then involvement of adjacent organs. The lymphatic spread is to pelvic, paraaortic and inguinal nodes. Distant metastases occur frequently in the peritoneum, lung, liver and supraclavicular nodes. The prognosis depends on the stage of the disease, tumor location, size, depth of myometrial involvement, lymphnode involvement, histological grade, cell type and age of the patient.
MR findings :
Endometrial carcinoma has a variable MRI appearance. On T1 weighted images, most endometrial carcinoma will be isointense to the uterus unless they contain haemorrhagic areas. On T2 weighted images, tumor nodules ranging from a few millimeters to a few centimeters in size can be identified within the endometrial cavity. They usually have a signal intensity intermediate between that of normal endometrium and that of myometrium. In some patient with endometrial carcinoma, MRI will show only show expansion of the central high signal intensity area of the uterus without discrete nodules (Fig :3). Because endometrial carcinoma occurs predominantly in postmenopausal woman, and because normal post menopausal uteri have a very thin central high signal intensity zone (< 5mm), expansion of the central high signal intensity zone in this age group should raise the suspicion of uterine malignancy. The appearance of endometrial carcinoma after intravenous administration of Gd is variable. Most tumors enhance less than myometrium on both dynamic and delayed post contrast images. However some may show early enhancement compared to the myometrium, and others may appear isointense or hyperintense to myometrium on delayed images. Although MR appearance of endometrial carcinoma is nonspecific, MRI can accurately stage the disease in histologically documented endometrial carcinoma. In stage l endometrial carcinoma the tumor is confined to uterine corpus. Stage l tumors are further subdivided depending on degree of myometrial penetration. – (a) Stage l A , tumor confined to the endometrium (b) Stage l B, invasion confined to the inner half of myometrium and (c) Stage l C, invasion of outer half of myometruim. Stage ll endometrial cancer indicates involvement of the cervix but does not extend beyond uterus. Stage ll tumors are subdivided to (a) stage ll A – cervical stroma not invaded (b) stage ll B – cervical stoma invaded. Endometrial carcinoma is stage lll when tumor extends outside uterus. Stage lll endometrial carcinomas are subdivided to (a) stage lll A – tumors invades serosa and / or adnexa. (b) stage lll B – vaginal metastases, (c) stage lll C regional lymphnode larger than 1 cm in diameter. Stage IV endometrial carcinoma indicates tumor extension outside true pelvis or involvement of bladder or rectal mucosa. This stage is further subdivided to (a) stage IV a – tumor involves bladder or rectum, (b) stage IV B – tumor extends outside true pelvis (distant metastases). MRI can not distinguish malignant from hyperplastic nodes.
Gestational Trophoblastic Neoplasia :
Gestational trophoblastic neoplasia (GTN) represents a spectrum of tumors ranging from the benign hydatidiform mole, to the invasive mole, to the highly malignant choriocarcinoma. Choriocarcinoma is a very aggressive tumour, growing rapidly and metastasizing to the lung, liver and the brain. With the development of combination chemotherapy, complete and permanent remission can be achieved in more than 90% of the patients.
MR Findings :
Uterine GTN appears on MR images as a heterogeneous hypervascular mass that obliterates uterine zonal anatomy. The distortion of uterine zonal anatomy and the presence of a mass are detected on T2 weighted images. On T1 weighted images tumor may demonstrate a signal intensity similar to that of myometrium or they may demonstrate a high signal intensity within the tumour. Intratumoral haemorrhage and necrosis are frequently findings in GTN and they produce high signal intensity within the tumour in MR images. Tortuous vessels are frequently seen traversing the tumour and through adjacent myometrium and adnexa. Engorgement of internal iliac vessels are often seen, exceeding the diameters of corresponding external iliac vessels. Prominence of main uterine arteries may also be seen. Associated adnexal cysts (theca lutein cysts) may exhibit medium to high signal intensity on T1 weighted images. Contrast enhanced scans show enhancement of the involved myometrium and identification of the vesicles suggest the diagnosis of molar pregnancy. MRI findings in persistent GTN, incomplete abortion and ectopic pregnancy are relatively nonspecific. In the setting of documented GTN, however MRI can diagnose invasive disease that may alter therapeutic management. MRI sensitivity in detecting GTN within the uterus is specially useful when the tumour deeply infiltrates the myometrium but does not extend to the endometrial surface, because uterine curettage specimen will be non diagnostic. MR imaging may play an important role in excluding a uterine source for elevated HCG in patient with extrauterine germ cell tumour or gestational, mammary, hepatic or pulmonary malignancies.
Leiomyoma :
Leiomyomas are the most common tumor in women of reproductive age. They may be solitary or multiple and most are found in submucosa, intramural or subserosal locations. Submucosal leiomyomas most often come to clinical attention because of infertility, recurrent abortion or hypermenorrhoea. Intramural leiomyomas may also be associated with infertility. Subserosal leiomyoma may undergo torsion causing acute abdominal pain. MRI accuracy for diagnosis of leiomyoma can have a significant clinical impact.
MR findings :
Most leiomyomas are round or oval, have clear margin and do not infiltrate the myometrium. The nondegenerative leiomyomas have intermediate signal intensity on T1 weighted images, and low signal intensity on T2 weighted images (Fig: 4). Calcified leiomyomas have low signal intensity on both T1 and T2 weighted images. Degenerative ( hyaline, myxomatous, fatty and cystic) leiomyomas show variable signal intensities. They may have medium or high signal intensity on T1 weighted images, and on T2 weighted images they demonstrate heterogeneous high signal intensities. Red degeneration leiomyomas demonstrate variable signal intensity on both T1 and T2 weighted images. There is no further benefit in the detection and chraracterization of leiomyomas after intravenous contrast. There is yet no reliable MRI feature for detecting malignant degeneration within a benign leiomyoma.
Adenomyosis :
Adenomyosis is defined as the presence of endometrial glands and stroma within the myometrium, at least 2.5 mm from the basal endometrial layer. Patient frequently present with hypermenorrhoea, anaemia, dysmenorrhoea, perimenstrual pelvic pain and enlarged uterus.
MR findings :
There are two types of adenomyosis, a diffuse and a focal type. In diffuse adenomyosis the fundus and body of uterus show diffuse enlargement. The thickness of low signal intensity junctional zone is increased on MR images (> 12 mm ). Tiny foci of high signal, which probably represent islands of endometrium, can be seen within the myometrium on T2 weighted images. When these high signal intensity foci are seen on both T1 and T2 weighted images, they possibly represent haemorrhage. Focal adenomyosis is seen as a mass of low signal intensity which may
appears similar to a leiomyoma. Distinction between focal adenomyosis and leiomyoma is of primary clinical importance. The interface between focal ademyosis and adjacent myometrium is ill defined, whereas leiomyomas are sharply defined. In extensive adenomyosis there may be distortion of endometrial canal. There may be multiple dilated veins accompanying a leiomyoma, which are not seen with adenomyosis.
Endometrial polyps :
Endometrial polyps are sessile or pedunculated hyperplastic endometrial projections. They arise in the fundus or cornual regions of the uterus. Malignant change is only rarely identified within endometrial polyp. Patient usually present with intramenstrual or post menopausal bleeding.
MR findings :
On T1 weighted images endometrial polyps show medium signal intensity similar to that of normal endometrium. On T2 weighted images, polyps demonstrate signal intensity similar to or slightly lower than that of endometrium. They may also cause apparent expansion of the endometrial cavity. Non contrast scans may not be able to detect them because of their similar signal intensity with the normal ebdometrium. Endometrial polyps show enhancement after Gd contrast, facilitating their detection. Polyps may degenerate and become heterogeneous in appearance.
FOCAL CT BRAIN LESIONS
RING ENHANCING LESIONS
(CT)
Primary brain tumor (glioblastoma) – irregular thick ring
Metastasis (especially if on ChemTx),
Abscess – ring is more smooth and regular – thinner on medial (WM) side ,
Multiple sclerosis – in white matter,
Resolving hematoma – 10-21 days – usually has perilesional lucency
Tuberculoma – associated extracranial TB often found – irregular ring
Radiation necrosis – 9 months-3 years after Rtx > 4000 rads
Postoperative change (at edges of resection)
Aneurysm – due to intraluminal thrombus
HYPERDENSE LESION WITHOUT CONTRAST
Meningioma – 20% also show hyperostosis – 2/3 show peritumoral edema
Lymphoma (small round blue-cell tumor – densely cellular) – primary is usually intraaxial – secondary is often extraaxial
Metastasis – Melanoma/Renal cell Ca/Choriocarcinoma/Thyroid Medulloblastoma (small round blue-cell tumor – densely cellular) Glioblastoma Ependymoma Colloid cyst (inspissated mucus)
Hemorrhage (acute) / hemorrhagic infarct
Craniopharyngioma
Germinoma (pineal and suprasellar)
MULTIPLE ENHANCING LESIONS
Hematogenous: Metastases – 45 -55% of CNS mets multiple – >2cm often cavitate – usually near gray-white junction (peripheral > central)
Lymphoma – usually deeper, periventricular, may be rings in AIDS Disseminated infection (multiple abscesses)
Multifocal infarction Inflammatory/Unknown Etiology: Multiple Sclerosis (white matter lesions)
Vasculitis Hypertensive Crisis/Ecclampsia Inherited Mass Lesions/Neoplasms: Hemangioblastoma (von Hippel-Lindau) Arteriovenous malformations (cavernous hemangioma >> AVM)
Meningiomas – 4% are multiple (some with NF-2, most without)
Multicentric gliomas – 5% of all gliomas Tuberous sclerosis Neurofibromatosis (both types – NF1 (von Recklinhausen) and NF2 (MISME)
GYRAL ENHANCEMENT: * Ischemia/Infarction (incl. seizures, migraines, etc.) * Cerebritis/Encephalitis (e.g. Herpes) Meningeal carcinomatosis (carcinomatous meningitis) Meningitis – chronic > acute AVM Cortical vein thrombosis Lymphoma Meningioangiomatosis (NF2)
CT/MRI INTRACRANIAL HAEMATOMA
CT PROGRESSION OF INTRACRANIAL HEMATOMA (change from HYPER- to HYPO- dense over time) Initially – 60 – 90 Hounsfield Units (HU) 2 days – 70 HU 3 weeks – 30 HU >5 weeks – <30 HU 20% show enhancing rim at 2-6 weeks
MRI APPEARANCE OF INTRAPARENCHYMAL HEMATOMA (T1/T2: II, ID, BD, BB, DD (I-iso, D-dark, B-bright) Hyperacute – minutes to hours (DD => II) – T1WI – hematoma hypointense (deoxyHb) => isointense – T2WI – hematoma hypointense (deoxyHb) => isointense Acute – 0-2 days (ID => BD) – deoxyhemoglobin in intact RBCs with surrounding edema – T1WI – hematoma isointense, low signal intensity (SI) edema – T2WI – hematoma decreased SI at center, high SI edema Subacute – 2-14 days (BB) – deoxyhemoglobin changes to methemoglobin from outer to inner – T1WI – outer core shows increased SI – T2WI – Outer core shows increased SI due to shortened T1, longer T2 Chronic – 14 days (BB => DD) – hemosiderin laden macrophages at periphery – T1WI – inner core now also increased SI, rim has low SI – T2WI – inner core also has increased SI, rim has low SI Chronic – months later (DD) – hemosiderin laden macrophages at periphery – T1WI – mostly iso-/decreased SI, rim has lower SI – T2WI – markedly hypointense rim has low SI – “blooms” with greater T2-weighting COMMENT: T1WI = T 1 weighted image T2WI = T 2 weighted image SI = signal intensity
CT PROGRESSION OF ISCHEMIC INFARCT Initially – 30 HU 1 day – <30 HU Enhance ~3 days till 6 weeks Mass effect peaks at 3-5 days – seen in 20 % of ischemic infarcts – a significant mass effect is a poor prognostic sign After 8th week – 50% have “negative mass effect” (atrophy)
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 Steal – occulusion 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
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 RINGdevelops 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.







