Neuroradiology Flashcards
Which vessels cause this
Bridging veins. Subdural haemorrhage assumes a crescent shape. Acute looks bright, chronic looks same as brain. Most commonly from bridging veins in origin
Headache with previous falls
Subacute suburals –On the right there is a right subacute subdural and a left chronic subdural
Headahce
Sagital sinus thrombosis
Headache
Sagital sinus thrombosis
In the sagittal T1-weighted image, the normal flow void (low signal) is replaced by intraluminal high signal related to thrombosed superior sagittal sinus. The signal intensity of the thrombus over time has the same evolution pattern as intracerebral hematomas
Confusion
Alzheimers - temporal parietal atrophy
Confusion
FTD atrophy (used multiple times)
Frontotemporal dementia is the correct response. Frontotemporal dementia often is familial. Frontal and temporal atrophy as seen in the patient images are supportive features for diagnosis of frontotemporal dementia, though absence of atrophy does not exclude the diagnosis. Frontotemporal dementia is characterized by a strong gradient of atrophy from anterior to posterior along the temporal lobe, as seen in the patient images. In Alzheimer disease, atrophy occurs throughout the temporal lobe. Binswanger disease is characterized by subcortical foci of patchy T2 hyperintensities in white matter, a finding not seen in the patient images. Infarction typically has an acute onset of neurologic deficit and on imaging there will be a focal cortical defect. This patient had gradual dementia onset and no focal full thickness cortical loss. Herpes encephalitis is an acute febrile illness. Common early symptoms include change in consciousness (confusion, then stupor, then coma), fever, headache, and seizures. Inferior frontal lobe and medial temporal lobe involvement with edema, restricted diffusion and contrast enhancement in the acute phase, and tissue destruction later are usual findings. These are not features of the patient and her images.
Falls
PSP with hummingbird sign
Parkinsonism
MSA - hot cross bun sign
MSA
Discussion:
The MRI findings show the “Hot Cross Bun” sign in the pons, as well as hyperintensity in the cerebellar peduncles. These findings are most suggestive of multiple system atrophy, a neurodegenerative disorder. Parkinson disease, postencephalitic parkinsonism, and prolonged metoclopramide exposure typically would not have characteristic MRI findings. NPH would demonstrate enlargement of the ventricles along with transependymal flow.
Parkinsonism
MSA – C – pons, cerebellum, hot cross buns sign, big 4th vent
Parkinsonism
MSA - olivopontocerebellar atrophy
Child with Rett’s syndrome:
FT atrophy in kid – Rett syndrome
2017 RITE 50, headache, leg weakness
Vasculitis: beading of the vessels
Discussion:
The diffusion-weighted views demonstrate multiple focal areas of acute infarction. These involve both the deep gray and white matter along with scattered cortical areas of infarction. These regions of infarction are in a multifocal vascular distribution atypical for branch large vessel disease and similarly atypical for small vessel infarctions or a cardioembolic etiology, which tend to be cortical. An MRA scan of the head performed concomitant with the study illustrated demonstrated marked beading along numerous arterial structures typical of vasculitis. This is best seen and illustrated in Figure 3 on the conventional cerebral angiogram.
Arterial thrombus: Left vertebral artery Thrombus
Discussion:
The CT of the head demonstrates a hypo dense segment in the left cerebellum typical of an acute infarction, and the CTA axial view demonstrates a segment of decreased density within the left vertebral artery typical of a thrombus. The carotid and right vertebral artery are well demonstrated and are normal. A thrombus can occur due to atrial fibrillation, that would not be the only etiology. Similarly, trauma can result in a vertebral dissection, but again, that would not be the only possible etiology. The study demonstrates normal appearance on CT of the sigmoid sinus bilaterally and does not suggest a sigmoid sinus thrombosis. Similarly, subclavian steal is associated with posterior circulation symptoms or infarction; however, a segment of decreased density within the left vertebral artery is not the appearance seen with reversal of vertebral arterial flow.
DWI in HIV IVDU with 2/7 hx unwell. 52
Most likely dx bacterial abscess. High signal DWI with hypointense ADC shown =. This means – infarct or abscess.
Unwell, IVT for hyponatremia
Central pontine myelinolysis – concentrated, symmetric, noninflammatory demyelination within central basis pontis. CMP predisposition – alcoholism, liver disease, malnutrition hyponatremia. Na < 120 then aggressive IVT
8 year old. ALL. Acute mental state change. Given MTX 10 days prior. And now has recurrent pulmonary infections. What is going on? What is the implications?
MTX causes acute neurotoxicity with diffusion abnormalities indicating cerebral dysfunction but not necessarily overt structural injury to the cerebrum. Secondary demyelination or gliosis cannot be predicted on imaging. A single episode with DWI abnormalities should not necessarily prompt modification of chemo.
- R arm and leg weakness. DWI – Cause?
Left ACA stroke
Incidental finding
Epidermoid cyst – isointense T1, non-enhancing, but restricts like WOAH – looks like CSF on everything other than DWI where it restrics
Incidental finding
Epidermoid cyst
Young, headache, fever
Restricted fluid levels in ventricles, enhancement, pyogenic meningitis!
On the diffusion-weighted views, there are fluid levels within the cortical sulci and within the posterior horns of the lateral ventricles with increased signal and on the T1-weighted postcontrast views, there is a perimeter of dural enhancement. Intracranial hypotension can produce a similar appearance of the postcontrast T1 views of pachymeningeal enhancement. However, fluid with increased diffusion signal as seen in this study is not seen in conjunction with intracranial hypotension nor would would it occur in neurosarcoid or subarachnoid hemorrhage. The appearence is typical of pus as seen with a pyogenic meningitis, ventriculitis, or an empyema.
Post MI arrest
Diffuse cortical ischaemia
Post Asthma in ICCU what does it show
DWI MRI sequence shows (day 3) acute anoxic damage. It is hyperintense signal which follows the cortical convolutions, suggestive of cortical laminar necrosis, a hallmark of diffuse hypoxic injury. This can occur because of hypotension, CCF (generally watershed areas),
Diffuse hypoxic injury
The CT study demonstrates near complete loss of cortical sulcation and diffuse decreased density in all hemispheres including the cerebellum along with generalized edema. These changes are in no specific vascular distribution and are typical of a severe hypoxic insult. The relative increased density within the fissures is a manifestation of contrast to the severe hypodensity of the remainder of the brain. Petechial hemorrhage due to necrosis may also be present. There were, however, no imaging findings to suggest a primary subarachnoid hemorrhage. Lissencephaly would not be associated with marked mass effect and edema as seen in this study; nor would hypertension encephalopathy.
Homless and confused
Wernicke’s – bilateral medial thalami
Progressive confusion FI (2017 exam) but may not have been this exact picture
CJD – cortical ribboning
Discussion:
The correct answer is prion disease. There is restricted diffusion involving the left occipital and left lateral temporal cortices. This patient had sporadic Creutzfeldt-Jakob disease, a progressive neurodegenerative disorder resulting from misfolded prion proteins. The imaging abnormality does not respect vascular territories, making ischemic infarction unlikely. Hypoxic brain injury typically causes symmetric abnormalities. The limbic, or medial temporal, structures appear normal. Hashimoto’s encephalopathy more commonly results in lesions in the white matter and/or brain stem.
Progressive confusion
CJD
Progressive confusion
CJD – hockey stick sign
Young female, hearing loss and encephalopathy
Susacs: young to middle-age women that is clinically characterised by the triad of acute or subacute encephalopathy, bilateral sensorineural hearing loss, and branch retinal arterial occlusions. – if get this clinical stem think SUSACS!
There tend to be multiple, small white matter lesions which have a predilection for the corpus callosum
the roof of the corpus callosum is also frequently involved, rather than the callososeptal interface (which is more typical of multiple sclerosis), resulting in ‘icicle’ or linear ‘spoke’ lesions that look to hang from the roof of the corpus callosum 11
- Multiple sclerosis flare
Discussion:
Multiple, supratentorial and infratentorial lesions are seen, with 2 acute enhancing lesions. This is most consistent with an acute exacerbation of multiple sclerosis. Vasculitic and other autoimmune conditions may also have similar imaging features and further clinical and laboratory information would be needed to make this distinction. These images are not consistent with either ischemic or hemorrhagic stroke. No leptomeningeal enhancement is present in this study. Variant Creutzfeldt-Jakob disease (vCJD) is a rare prion disease typically seen in younger patients who present with rapidly progressive cognitive decline, visual disturbance and may have increased signal intensity lesions on FLAIR views in the bilateral posterior thalami (“pulvinar sign”).
Confusion
PRES: posterior predominant, bilateral and symmetric confluent white matter changes
Young adult, TIA presentation
CADASIL: Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL)
- AD
- mutation on chromosome 19q12 involving the NOTCH3 gene,
- widespread confluent white matter hyperintensities 2
- relative sparing of the occipital and orbitofrontal subcortical white matter 2, subcortical U-fibersand cortex 3.
Leg weakness
ACA stroke
Frontal seizure
Focal cortical dysplasia
General features of focal cortical dysplasia include 4:
cortical thickening
blurring of white matter–grey matter junction with abnormal architecture of subcortical layer
T2/FLAIR signal hyperintensity of white matter with or without the transmantle sign
T2/FLAIR signal hyperintensity of grey matter
abnormal sulcal or gyral pattern
segmental and/or lobar hypoplasia/atrophy
Seizure
Focal cortical dysplasia
HIV patient, low CD4 count, unwell
PML, JC virus reactivation – confluent white matter change
HIV confused
FLAIR shows white matter hyperintense abnormal signal which is suggestive of PML. Rare, usually fatal virus, exclusively with severe immune deficiency.
Young, acute confusion
HSV encephalitits – temporal lobe prediliction
Confusion
HSV 1
Discussion:
The images show bilateral mesial temporal and hippocampal edema, and this and the clinical history supports diagnosis of herpes simplex encephalitis. This disease often leads to elevated RBC count in CSF due to hemorrhagic changes. JC Virus is seen in PML, a white matter disease. HTLV antibodies are seen in HTLV-associated Myelopathy/TSP. Elevated spirochete IgM levels can be seen in CNS Lyme Disease, which causes multifocal white matter lesions. Toxoplasmosis causes focal cerebritis rather than diffuse edema in the temporal lobes.
headache
Pineal tumor causing obstructive hydro with transependymal flow
35, visual defect, R sided loss, sleepy, weight gain, thirst. Enhancing meningeal thickening in the suprasellar area involving the left optic tract. CXR shows hilar lymphadenopathy. ? diagnosis
Sarcoid.
Suprastellar mass differentials SATCHMO
Sarcoid, aneurysm/ adenoma, teratoma / dermoid cyst, craniopharyngioma, hamartoma of tuber cinereum, meningioma and optifc nerve glioma.
Child to adult progressive motor and cognitive
Adrenoleukodystrophy:
X-linked inherited metabolic peroxisomal disorder characterised by a lack of oxidation of very long chain fatty acids (VLCFAs)
severe inflammatory demyelination of the periventricular deep white matter
posterior-predominant pattern and early involvement of the splenium of the corpus callosum
Infant to young adult psych and dementia
Metachromatic leukodystrophy: AR, lysosomal storage disorders,
Periatrial and frontal horns leukodystrophy with periventricular sparing resulting in tigroid pattern (stripe pattern)
Metachromatic leukodystrophy: stripe formation
Jewish infant, blind, mental retardation, big head
Canavan disease: Spongiform degeneration of white matter – or aspartoacylase deficiency – characterised by megalencephaly, severe mental and neurological deficits and blindness
MRI confirms the megalencephalic appearance and provides more detail of the white matter disease, which is typically diffuse, bilateral, and involving the subcortical U-fibers 4-8:
Jewish infant, blind, mental retardation, big head
Canavan
Infant, big head, seizures and neuro deterioration
Alexander disease: frontal predominance to white matter disease, big head
Infantile or adult: myoclonus, nystagmus, opsiclonus
Krabbe’s: globoid cells (hence the name) is characteristic of the disease.
The corticospinal tracts are typically most involved
It is caused by a deficiency of galactocerebroside ß-galactosidase, an enzyme that degrades cerebroside, a normal constituent of myelin. Cerebrosides accumulate in the lysosomes of macrophages within the white matter. This results in demyelination
Infantile or adult: myoclonus, nystagmus, opsiclonus
Krabbe’s – classic halo alternating hyper/hypo intensities
Early infancy: pendular eye movements, hypotonia, pyramidal weakness
Pelizaeus Merzbacher: near complete absence of expected low signal in supratentorial region- abnormal signal can either be diffuse or patchy
if there is patchy involvement, a characteristic tigroid appearance may be seen 5
may also show cortical sulcal prominence due to atrophy 4
white matter volume may be decreased 4
may also involve cerebellum and brainstem 4
Typically young childhood – ataxia, opthalmoplegia
Leigh disease: bilateral T2hyperintensity in brainstem, midbrain, medulla, thalami – involvement of cerebellum or cerebral cortex unusual.
Typically young childhood – ataxia, opthalmoplegia
Leigh: bilateral T2 enhanacement, symmetric
Stroke sounding presentation
MELAS: MELAS (mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes) is one of many mitochondrial disorders.
multifocal stroke-like cortical lesions in different stages of evolution (“shifting spread” pattern), crossing the cerebral vascular territories, and showing a certain predilection to the posterior parietal and occipital lobes.
MRI : chronic and acute infarcts involving multiple territories. Parieto occipital most common.
What is this?
Amyloid angiopathy
Recurrent presentations of Neuro dysfunction
MS
IVDU
Septic Emboli
Returned traveller: seizure
Neurocysticercosis: The disease is endemic in Central and South America, Asia and Africa. The perpetuation of this parasitic disease is related to poor sanitation and hygiene.
Vesicular: viable parasite with intact membrane and therefore no host reaction.
Colloidal vesicular: parasite dies within 4-5 years 1 untreated, or earlier with treatment and the cyst fluid becomes turbid. As the membrane becomes leaky oedema surrounds the cyst. This is the most symptomatic stage.
Granular nodular: oedema decreases as the cyst retracts further; enhancement persists.
Nodular calcified: end-stage quiescent calcified cyst remnant; no oedema.
Neurocysticercosis: The disease is endemic in Central and South America, Asia and Africa. The perpetuation of this parasitic disease is related to poor sanitation and hygiene.
Discussion:
Cysticercosis is the best response. Initial noncontrast CT shows small calcifications in cortex without edema. Two contrast enhanced CT images show intense ring enhancement with prominent surrounding edema. Thigh muscles have diffuse calcifications from dead Taenia solium (pork tapeworm) larval calcifications. Cryptococcosis does not produce calcified lesions
in the brain. Metastases which may cause multifocal involvement in brain is not best response because the patient has no primary neoplasm diagnosis and metastasis does not cause brain and muscular calcifications. D. (septic emboli) is not best response because brain and muscle calfication is not explained by this entity. E. (toxoplasmosis) is not best response because it doesn’t
cause the calcifications in brain and muscle, and in adults, it affects those who are immunocompromised.
NCC cyst causing hydro:
Subarachnoid/intraventricular
When in the subarachnoid space/interventricular, the the cysts typically do not have a visible scolex. In the basal cisterns they can be grape-like (racemose). The cysts are typically 1-2 cm in diameter 2. Usually the cysts are similar in signal intensity to CSF, although occasionally cyst fluid may somewhat differ 2.
In the ventricles, there is often (79%) 2 associated ventriculitis often leading to aqueductal stenosisand hydrocephalus 2.
Seizure
Hyperintense Scolex w/ NCC
HIV, unwell, fever and headache
Toxoplasmosis (used multiple times) – surrounding oedema, ring enhancement, isointense / difficult to see on T1
he infection most likely occurs once the CD4+ count has dropped below 200 cells/mm 3,6.
HIV, unwell, fever and headache
Toxo – surrounding oedema, ring enhancement
HIV - The infection most likely occurs once the CD4+ count has dropped below 200 cells/mm 3,6.
Discussion: sulfadiazone and pyrimethamine
Toxoplasmosis is caused by an obligate intracellular parasite Toxoplasma gondii. Patients who develop AIDS are at particularly
high risk of disseminated toxoplasmosis which most frequently involves the CNS. Toxoplasmosis is the most common focal mass
lesion in AIDS and it most commonly involves the basal ganglia.
80yr old. Hx cancer
Mets
- Hx breast Ca
Hemorrhagic mets – melanoma, renal cell, choriocarcinoma, thyroid, bronchogenic, breast
DDx? Most likely dx in 80 yr old with Bkgd Ca
Ring enhancing lesions. DDx tumour, abscess, metastasis, toxoplasmosis and lymphoma (in immunocompromised). Given hx ca = metastasis.
Young female, headache
Sarcoid- homogenous enhancement – leptomeningeal???
The enhancing, nodular, patchy, diffuse abnormalities shown are most characteristic of neurosarcoidosis. Toxoplasmosis produces inflammatory lesions, which may enhance but are rarely restricted to the gray matter, as in this case. Cerebrotendinous xanthomatosis is a white matter disease. Hemorrhagic encephalopathy typically shows areas of both low and high signal intensity and is not uniformly enhancing. The patient’s age and race are also suggestive of neurosarcoidosis
Young female, headache, seizure
Sarcoid – leptomeningeal enhancement
65, low grade fever, general headache (CT Contrast)
Abscess (ring enhancing lesion, most likely abscess given background history) DDx tumour, abscess, metastasis, toxoplasmosis, lymphoma
T1 (L), T2(R) -46, homeless, confused
Acute and subacute haemorrhage. MRI shows haemorrhage of blood at different stages with perihematomal oedema – main component is isointense – with some more hyperintense specks. Acute hemorrhage appears isointense on T1 and hypointense on T2. early subacute are hyperintense on T1 and hypointense on T2
Male, headache, better lying
Intracranial hypotension sagging penis
Extra line along dural edge
headache
Intracranial hypotension
Leptomeningeal carcinomatosis
Pilocytic astrocytoma
Cerebellar hemangioblastoma
The images depict a large mass within the right cerebellum. This is cystic, with a markedly enhancing nidus or mural nodule. The enhancement is predominately confined to the mural nodule and spares most of the perimeter. There is very mild adjacent vasogenic edema. A metastatic lesion or abscess would be unlikely to demonstrate a mural nodule, and they generally demonstrate a complete ring pattern of enhancement. This appearance can be seen in a setting of a pilocystic astrocytoma; however, this lesion is a frequent finding in youth and highly unlikely in a patient of this age. Medulloblastomas tend to arise in the midline along the margin of the fourth ventricle between the brain stem and cerebellum and not laterally as in this instance and would not have the cystic appearance with a mural nodule. An arteriovenous malformation frequently demonstrates an enhancing nidus with multiple vascular structures. The vessels in an AVM however, are significantly larger as compared to the capillary size vessels seen here. This lesion is also known as a capillary hemangioblastoma as was confirmed on pathologic examination.
Cerebellar hemangioblastoma
The images depict a large mass within the right cerebellum. This is cystic, with a markedly enhancing nidus or mural nodule. The enhancement is predominately confined to the mural nodule and spares most of the perimeter. There is very mild adjacent vasogenic edema. A metastatic lesion or abscess would be unlikely to demonstrate a mural nodule, and they generally demonstrate a complete ring pattern of enhancement. This appearance can be seen in a setting of a pilocystic astrocytoma; however, this lesion is a frequent finding in youth and highly unlikely in a patient of this age. Medulloblastomas tend to arise in the midline along the margin of the fourth ventricle between the brain stem and cerebellum and not laterally as in this instance and would not have the cystic appearance with a mural nodule. An arteriovenous malformation frequently demonstrates an enhancing nidus with multiple vascular structures. The vessels in an AVM however, are significantly larger as compared to the capillary size vessels seen here. This lesion is also known as a capillary hemangioblastoma as was confirmed on pathologic examination.
Ganglioglioma
GBM
Discussion:
There is a single, large infiltrative multicystic enhancing mass with vasogenic edema. This appearance is most frequently seen with a glioblastoma multiforme. No vascular structures are seen as expected in an arteriovenous malformation (AVM). An infectious process, such as toxoplasmosis and a metastasis, would more likely have a ring pattern of enhancement and not the large complex multicystic pattern seen here.
Headache
GBM
Headache
GBM
Lymphoma
Lymphoma
There is an ovoid homogeneously enhancing mass with adjacent vasogenic edema. A hemorrhage, hemorrhagic infarction or demyelinating lesion would not have this pattern of homogeneous enhancement. A giant aneurysm would not show this degree of edema. This pattern is most frequently seen with lymphoma.
Well
Meningioma
Fever
Abscess
- Abscess
Discussion:
The images demonstrate a multi-ring enhancing mass lesion within the left occipital lobe with marked adjacent vasogenic edema. The multi-ring masses have narrow, homogenously enhancing margins. There is marked increased diffusion signal within the masses. Marked increased signal on diffusion is more likely in an abscess as compared to a tumor. The extent of vasogenic edema and patterns of ring enhancement would also favor an infectious etiology. A subacute infarction can show luxury enhancement, which generally involves the cortical ribbon. The pattern of edema in an infarction is cytotoxic edema, not vasogenic as seen in this case. A cerebral abscess is the more likely consideration in this instance. The pathology confirmed Nocardia in this patient with diabetes.
Headache
Pituitary macroadenoma
The study demonstrates increased density within the pituitary fossa extending to the cavernous sinuses bilaterally with an expansive lesion, which is demonstrated on the FLAIR and T1 view areas of both increased and decreased signal. There is an ovoid mass throughout the suprasellar cistern compressing the optic chiasm. It appears as that of a large pituitary mass, likely a pituitary macro adenoma. There is a perimeter of increased T1 weighted signal in the non-contrast view. A compilation of these features would be that of hemorrhagic transformation i.e. pituitary apoplexy of the pituitary tumor mass. A pituitary tumor of this size can be expected to result in bitemporal hemianopia. However, in the absence of hemorrhagic transformation, one would not expect to the tumor’s presence to result in coma as seen with this patient. A colloid cyst would not be expected in this location and generally arises as an intraventricular lesion adjacent to the foramen of Monro in the third ventricle. A metastatic lesion within the sella would be in the differential of a tumor mass; however, again, it would not be the best clinical explanation for the patient’s clinical presentation of sudden coma.
Metastatic mass
What is it
Mucocele
On the coronal and axial CT views, there is a complete opacification of the right maxillary sinus. The lesion appears expansile. There is marked thinning and a dehiscence of the lateral wall of the right maxillary sinus. A posterior wall of the right maxillary sinus and upper right lateral wall appears thickened. These changes are consistent with an indolent, expansile mass typical of a mucocele. Mucoceles can become infected and result in an abscess.
Lytic lesions, from mets, not pagets
The bone density images depict multiple lytic lesions within both the inner and outer tables, resulting in a somewhat moth-eaten appearance throughout the calvarium. The tissue density views demonstrate a hyperdense tissues within the lytic lesions. Paget disease is a disorder with lytic and sclerotic changes. However, there is generally a widening of the trabeculae and relative bone enlargement within the skull. In addition, the lytic lesions would not be filled with a more homogenous tissue density as seen in this study.
Fibrous dysplasia results in a ground-glass appearance to the bone, often expansile, but can show homogenous sclerotic areas or cystic areas, none of which is present in this study. A focus of eosinophilic granuloma is a solitary lytic lesion seen in children and young adults. The pattern of these lytic lesions is typical of a metastatic malignancy, and in this case breast carcinoma
SAH
Mixed bleeds – trauma
The CT provided demonstrates hematomas within the right frontal region, along with subarachnoid hemorrhage overlying the right hemisphere. The pattern is typical of contusions which arise in the interface between the bone surfaces. In addition, there is an obvious right parietal soft tissue hematoma. This pattern of hemorrhage with contusion is not typical of an aneurysmal rupture, nor would encephalitis present with this pattern of intracranial hemorrhages and subarachnoid hemorrhage. There is evidence of subdural hemorrhage; however, no epidural hematoma is seen in this view.
Severe hypoxic insult
Hemimegalencephaly is a congenital anomaly in which one hemisphere shows thickened or duplicated cortex, myelination is excessive. Severe epilepsy and hemiparesis are commonly found. If epilepsy is uncontrollable, hemispherectomy may be indicated
Diffuse calcifications – congenital infection
- Suependymal giant cell astrocytoma
Calcifications and hamartomas from tuberous sclerosis
Discussion:
Subependymal giant cell astrocytoma is the best response. The calcifications are at the medial aspect of head of caudate nucleus
at foramen of Monro, the site where calcified subependymal giant cell astrocytomas arise in TS. Low attenuation cortical hamartomas also are visible at left frontal and both parietal lobes; this is very typical tuberous sclerosis. Cysticercosis forms cystic lesions. Fahr’s disease is not associated with cortical hamartomas. CO poisoning does not produce calcified basal ganglia lesions. Cryptococcus does not produce calcified lesions or cortical hamartomas.
headache
Venous thrombosis with bleed
Wilsons
There is symmetric high signal intensity involvement of the putamen and thalami bilaterally. The globus pallidus is also involved but not exclusively as it is in many patients with carbon monoxide poisoning. The heads of the caudate and nuclei appear normal, and there is no significant overall atrophy of the brain. These are findings that tend to exclude Huntington disease while the high signal intensity within the globus pallidus and putamen is atypical for Parkinson disease. Gliomatosis cerebri, an infiltrating astrocytoma of the white matter, is excluded by the fact that the disease process spares the white matter where the tumor occurs. The correct response is Wilson disease.
Wilson’s disease
PKAN eye of the tiger
The basal globus pallidus lesions produce an “eye of the tiger” on MRI, seen with pantothenate kinase deficiency (PKAN). The globus pallidus lesions are from iron deposition. Huntington disease produces caudate atrophy; Niemann-Pick type C disease may have dystonia and rigidity but does not produce isolated globus pallidus lesions. Idiopathic torsion dystonia and Sandifer syndrome have normal MRI
Fahr’s syndrome
Fahr’s syndrome. Idiopathic basal ganglia calcification, also known as Fahr disease, is a rare, genetically dominant, inherited neurological disorder characterized by abnormal deposits of calcium in areas of the brain that control movement.
Carbon monoxide
Hypoxic ischaemic encephalopathy
Discussion:
The correct answer is hypoxic-ischemic injury. There is diffuse symmetric T2 hyperintensity and restricted diffusion involving
the cortex and deep gray matter structures, with diffuse edema. This patient had a cardiac arrest due to respiratory depression
from drug overdose. Meningitis, encephalitis, status epilepticus, and gliomatosis do not produce this pattern of brain injury.
confusion and abnormal movements
Huntingtons
Huntington’s
Discussion:
Huntington disease: Diffuse cerebral atrophy, Atrophy of caudate nucleus.
Hypoxic ischemic injury
Methanol toxicity
Confusion
Wernicke’s
Mesial temporal sclerosis
Headache and diplopia
Tolosa Hunt
MRI the enhancing lesion in right cavernous sinus and meninges present in this case
Tolosa–Hunt syndrome (THS) is a rare disorder characterized by severe and unilateral headaches with orbital pain, along with weakness and paralysis (ophthalmoplegia) of certain eye muscles (extraocular palsies).
Headache and diplopia
Tolosa Hunt
Visual disturbance
Optic neuritis (NMO)
Neuromyelitis Optica: Autoimmune inflammatory disorder involving myelin of neurons of optic nerves and spinal cord, with limited brain parenchymal involvement. 3 segments of T2 abnormality more likely in NMO or acute transverse myelitis than in classic MS.
Revised diagnostic criteria for definite neuromyelitis optica (NMO) require optic neuritis, myelitis, and at least two of three supportive criteria: MRI evidence of a contiguous spinal cord lesion 3 or more segments in length, onset brain MRI nondiagnostic for multiple sclerosis, or NMO-IgG seropositivity. CNS involvement beyond the optic nerves and spinal cord is compatible with NMO
Lymphoma
Diplopia
Ocular myositis or pseudotumor or thyroid
Pilocytic astrocytoma in NF1
NF1 with bilateral optic gliomas
MRI of the brain demonstrates markedly enlarged optic nerves, the left greater than the right, typical of optic nerve gliomas. The coronal plexus study demonstrates an ovoid homogeneous enhancing lesion typical of a nerve sheath tumor. The combination of peripheral nerve sheath tumors and optic nerve gliomas is seen in conjunction with neurofibromatosis type 1 and is not a feature of the other choices. NF type 2 and schwannomatosis are not associated with optic nerve gliomas.
Pineocytoma
pineoblastoma
Neurocytoma (multiple times)
Discussion:
Central neurocytoma is the best diagnosis, based on lesion morphology, location, signal intensity and contrast enhancement pattern. Central neurocytomas are located in the ventricles near the foramen of Monro and characteristically have attachment to the septum pellucidum, as shown in this case. Choroid plexus papillomas and meningiomas enhance intensely, and do not assume this morphology that is so characteristic of central neurocytoma. Subependymomas do not typically enhance. Lymphoma is not typically an intraventricular lesion, but instead infiltrates subependymal tissue and surrounds the ventricles, if involvement is near
the ventricles.
Neurocytoma
subependymoma