6. Neuro (Brain - Misc, Neuro-degenerative, Metabolic, Infections) Flashcards

1
Q

Monro-Kellie Doctrine (2)

A

This is the idea that the head is a clsoed shell, and that the 3 major components (brain, blood, CSF) are in a state of dynamic equillibtium.
As volume of one goes up, another must go down

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2
Q

Intracranial hypotension (3)

A

Leaking CSF will decrease the overall fixed volume, the volume of venous blood will increase to maintain equilibrium.
This results in meningeal engorgement (enhancement), distension of durial venous sinuses, predominance of the intracranial vessels and engorgement of the pituitary.
Development of subdural hygroma and haematomas is also classic here.

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3
Q

Idiopathic intracranial hypertension (pseudotumour cerebri). (5)

A

Classically fat, middle aged woman with headache.
Cause isn’t well understood.
Associated with hypothroid, Cushings, vit A toxicity.
Increased CSF causes slit like ventricles, shrinking pituitary (partially empty sella) and venous sinuses appear compressed.
Vertical tortuosity of the optic nerves and flattening of posterior sclera can also occur.

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4
Q

Cytotoxic oedema (3)

A

Can be thought of as intracellular swelling, due to malfunction of Na/K pump.
Tends to occur in grey matter, looks like loss of grey-white differentiation.
Classically seen in stroke or trauma.

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5
Q

Vasogenic oedema (4)

A

Extracellular, due to blood brain barrier disruption.
Looks like oedema tracking through the white matter, less tightly packed than grey matter.
Seen in tumour and infection.
Response to steroids is classic for vasigenit oedema.

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6
Q

Communicating oedema (3)

A

Obstruction at the level of the villi/granulation, blocking reabsorption.
All ventricles dilated (25% have normal 4th ventricle).
Caused by Normal Pressure Hydrocephalus, Blood, Pus, Cancer.

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7
Q

Normal pressure hydrocephalus (6)

A

Idiopathic.
“Ventricular size out of proportion to atrophy”
Frontal and temporal horns of lateral ventricles are most affected.
Upward bowing of the corpus callosum is another buzzword.
MRI: transependymal flow and or flow void in the aqueduct and 3rd ventricle.
Clinical triad of urinary incontinence, confusion and ataxia.
Rx: Surgical shunting

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8
Q

Blood, pus, cancer (communicating oedema) (2)

A

Anything causing plugging of the villi, most commonly SAH, meningitis, Carcinomatous meningiits

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9
Q

Non-obstructive hydrocephalus (2)

A

Anything that produces more CSF.
Choroid plexus papilloma is usually the answer.

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10
Q

Transependymal flow

A

Seeen more with acute rather than chronic hydrocephalus.

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11
Q

Subfalcine herniation (2)

A

aka midline shift.
ACA may be compressed, causing infarct.

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12
Q

Descending transtentorial herniation (8)

A

Uncus and hippocampus herniate through the tentorial incisura.
Effacement of ipsilateral suprasellar cistern occurs first.
Perforating basilar artery branches get compressed, causing Duret Haemorrhages (classically midline at pontomesencephalic junction)
CN3 compressed between PCA and Superior Cerebellar artery, causing ipsilateral pupil dilatation and ptosis.
Kernohan’s notch/phenomenon: Midbrain on the tentoriun forming an indentation/notch.
- Clinically: Ipsilateral hemiparesis “false localising sign”

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13
Q

Ascendng transtentorial herniation (4)

A

Posterior fossa mass. Vermis will herniate upward through tentoral incisura, often causing severe obstructive hydrocephalus.
“smile” of quadrigeminal cistern is flattened or reversed.
“spinning top” is buzzword for the appearance of the midbrain from bilateral compression along its posterior aspect.
Severe hydrocephalus (at the level of the aqueduct)

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14
Q

Cerebellar tonsil herniation (2)

A

Can be from severe herniation after downward transtentorial herniation.
In isolation, could be Chiari malformtion (Chairi 1 = 1 tonsil 5mm or both 3mm)

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15
Q

Multiple sclerosis (10)

A

Commonest demyelinating disease.
Usually women 20-40. No difference in gender in kids.
Multiple types, relapsing-remitting (85%) is comonest.
Clinical Hx of separated by time and space.
Classic T2/FLAIR oval and periventricular perpendicularly orientated lesions.
Involvement of calloso-septal interface is 98% specific in MS, helps differentiate from vascular lesions and ADEM.
In kids, posterior fossa is more commonly involved.
Acute demyelinating plaques should enhance and restric diffusion.
Brain atrophy is accellerated in MS.
Can get big MS plaque like a tumour, will ring enhance but classically incomplete (horseshoe), with leading demyelinating edge.
Solitary spinal cord involvement can be seen, but is usually in addition to brain lesions.
Cervical spine is most common spinal location. Cord lesions tend to be peripherally located.

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16
Q

ADEM (5)

A

MS variant, Acute Disseminated Encephalomyelitis.
Presents in childhood or adolescents after viral illness or vaccination.
Multiple, large T2 bright lesions, enhancing in a nodular or ring pattern (open ring).
Lesions do not involve the calloso-septal interface.

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17
Q

Acute haemorrhagic leukoencephalitis (3)

A

Aka Hurst Disease
Fulminant form of ADEM with massive brain swelling and death.
Haemorrhagic part only seen on autopsy.

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18
Q

Devics (neuromyelitis optica) (2)

A

Transverse myelitis + optic neuritis.
Lesions in the cord and the optic nerve

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19
Q

Marburg variant (2)

A

Childhood variant that is fulminant and leads to rapid death.
Usually febrile prodrome

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20
Q

PRES (Posterior Reversible Encephalopathy Syndrome) (3)

A

Seen in HTN or chemotherapy.
Asymmetric cortical and subcortical white matter oedema, usually in parietal occupital regions.
Does NOT restrict diffusion, can differentiate from stroke

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21
Q

Radiation induced demyelination (3)

A

Seen as T2 bright areas and atrophy corresponding to radiation portal.
Can be seen with haemosiderin deposition and mineralising microangiopathy (calcifications involving the basal ganglia and subcortical white matter)

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22
Q

Osmotic demyelination syndrome (CPM) (3)

A

Seen with rapid correction of sodium.
T2 bright in the central pons, spares the periphery.
Can also have extra-pontine presentation involving the basal ganglia, external capsule, amygdala and cerebellum.

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23
Q

Wernicke encephalopathy (3)

A

Caused by thiamine deficiency.
Contrast enhancement of mammillary bodies (seen more in alcoholics).
Increased T2/FLAIR signal in bilateral medial thalamus and periaqueductal grey matter.

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24
Q

Carbon monoxide poisoning (2)

A

CT: hypodensity. MRI: T2 bright globus pallidus

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25
Q

Alcohol poisoning

A

Brain atrophy, especially cerebellar vermis

26
Q

Marchiafava-Bignami (3)

A

Seen in drunks.
Swelling and T2 bright signal affecting the corpus callosum (typically beginning in the body, then genu, then splenium).
Involves the central fibres and spare the dorsal and ventral fibres, called sandwich sign on sagittal imaging

27
Q

Methanol poisoning (2)

A

Optic nerve atrophy, haemorrhagic putaminal and subcortical white matter necrosis.

28
Q

Post-radiation changes (5)

A

Latent period in which imaging findings don’t show up for 2 mmonths.
Whole brain radiation: T2 bright in periventricular white matter, sparing subcortical regions early on.
Peripheral extension to subcortical regions occurs later.
Localised ratiation: Usually severe focal oedema with mass effect and enhancement.
Differentiation from residual tumour can be difficult, MR perfusion is useful here

29
Q

Post chemotherapy (3)

A

T2 effects acutely in the white matter, can progress to atrophy.
Enhancement or mass effect is rare, unless very severe.
Children recieving radiation and chemo sometimes develop calcifications “mineralising microangiopathy”

30
Q

Disseminated necrotising leukoencephalopathy (3)

A

Severe white matter changes, which demonstrate ring enhancement, classically with leukaemia patients undergoing radiation and chemo.
Can be fatal.

31
Q

PET in dementia

A

On FDG PET, the motor strip is always preserved in dementia

32
Q

Alzheimer disease (3)

A

Commonest cause of dementia.
Hippocampal atrophy occurs first, and out of proportion to rest of brain atrophy.
Tempral horn atrophy (>3mm) seen in more than 65% of cases.

33
Q

Multi-infarct dementia (3)

A

Second commonest cause of dementia.
Cortical infarcts and lacunar infarcts seen on MRI.
PET-FDG shows multiple scattered areas of decreased activity.

34
Q

Crossed cerebellary diaschisis (CCD) (2)

A

Depressed blood flow and metabolism affecting the cerebellar hemisphere after a contralateral supratentorial insult (infarct, tumour resection, radiation)

35
Q

Demential with Lewy bodies (3)

A

3rd commonest cause of dementia, similar picture to Parkinsons dementia (except here the dementia comes first).
Hippocampi remain normal.
Decreased FDG uptake in the lateral occipital cortex, with sparing of the mid posterior cingulate gyrus (cingulate island sign)

36
Q

Binswanger disease (3)

A

Subcortical leukoencephalopathy affecting older people, strongly associated with HTN.
Basically small vessel vascular dementia.
Classically spares subcortical U fibers

37
Q

FDG-PET in Brain DDx (4)

A

Alzheimer: low posterior temporoparietal cortical activity, identical to Parkinsons dementia
Multi-infarct: Scattered areas of decreased activity. Lyme, HIV and vasculitis are mimics.
Dementia with Lewy bodies: Low activity in lateral occipital cortex. Preservation of mid posterior cingulate gyrus (Cingulate island sign)
Picks/frontotemoral/depression: Decreased frontal lobe activity.
Huntingtons: low activity in caudate nucleus and putamen

38
Q

Torch infections (2)

A

Only clinically important in first 2 trimesters.
Calcifications and microcephaly seen in all of them

39
Q

CMV (4)

A

Commonest torch infection.
Likes to affect germinal matrix, causing periventricular tissue necrosis.
Periventricular calcifications also seen.
Highest association with polymicrogyria among TORCH infections

40
Q

Toxoplasmosis (4)

A

Second commonest TORCH.
Associated with cat faeces.
Calcifications are more random, and affet basal ganglia.
Frequency is increased in 3rd trimester (less clinically significant here).
Associated with hydrocephalus

41
Q

Rubella (3)

A

Less commoin due to vaccination.
Calcifications are less common.
MR: focal high T2 signal in white matter, related to vasculopathy and ischaemia

42
Q

HSV (3)

A

Usually HSV-2. Unlike adults, doesn’t primarily affect the limbic system, rather the endothelial cells, resulting in thrombus and harmorrhagic infarction, causing encephalomalacia and atrophy.

43
Q

HIV (3)

A

Not a TORCH, but occurs during pregnancy, at delivery or through breast feeding.
Brain atrophy in the frontal lobes predominantly.
Faint basal ganglia enhancement on CT and MRI preceeding the appearance of basal ganglia calcifications

44
Q

Opportunistic infections (4)

A

Most common opportunistic infection with AIDS patients is toxoplasmosis.
Commoinest fungal infection in AIDS is Cryptococcus.
JC virus and CMV are also notable

45
Q

HIV encephalitis (5)

A

Affects around 50% of people with AIDS.
CD4 <200.
Symmetric increased T2/FLAIR signal in deep white matter. Normal T1.
Lesions will not enhance.
May be associated brain atrophy.
Tends to spare subcortical U fibres (PML will involve them).

46
Q

Progressive Multifocal Leukoencephalopathy (PML) (4)

A

Caused by JC virus.
CD4 <50.
Imaging shows single or multiple scattered hypodensities with corresponding T1 hypointensity and T2/FLAIR hyperintensities out of proportion to mass effect.
Predilictions for subcortical U fibres.
Asymmetry helps differentiate from HIV.

47
Q

CMV (2)

A

Brain atrophy, periventricular hypodensities (T2/FLAIR bright) and ependymal enhancement.

48
Q

Cryptococcus (5)

A

Most common fungal infection in AIDS.
Usually meningitis affecting base of brain (leoptomeningeal enhancement).
Dilated perivascular spaces filled with mucoid gelatinous material which will not enhance.
Can also be seen as lesions in the basal ganglia (cryptococcomas), which are T1 dark, T2 bright and may ring enhance.

49
Q

Toxoplasmosis (4)

A

Commonest opportunistic infection in AIDS.
T1 dark, T2 bright, ring enhancing lesions without diffision restriction.
Lots of surrounding oedema.
Toxoplasmosis is thallium cold, lymphoma is thallium hot

50
Q

Toxoplasmosis vs lymphoma (4)

A

Both demonstrate
- Ring enhancement
Haemorrhage more common after treatment vs less common
Thallium hot vs cold
PET cold vs hot
MR perfusion: decreased CBV vs increased (or decreased) CBV

51
Q

Stroke vs Tumour vs Abscess vs MS plaque (8)

A

T2: All will have oedema so will all be bright.
DWI: Classically, Abscess and stroke will restrict diffusion, however hypercellular tumours like lymphoma and demyelinating lesions with acute features can also restrict diffusion
Enhancement: Each shoud have a different enhancement pattern
- Tumour: heterogenous or homogenous if high grade.
- Abscess with RING enhance
- MS will have Incomplete ring enhancement
- Stroke will have cortical ribbon (gyriform) type enhancement in subacute perior (around 1 week)

52
Q

TB meningitis (4)

A

Looksl ike regular meningitis, except prediliction for basal cisterns and may have dystrophic calcifications.
May be enhancement of the basilar meninges with minimal nodularity.
Complications include vasculitis (May result in infarct (more common in kids).
Obstructive hydrocephalus is common.

53
Q

HSV (4)

A

HSV 1 in adults and HSV 2 in kids.
Swollen (uni or bilateral) medial temporal lobe, will be T2 bright.
Earliest sign is restricted diffusion related to vasogenic oedema.
Blooming on gradient means bleeding (more common in adult form).
Spares the basal ganglia unlike MCA stroke.

54
Q

Limbic encephalitis (3)

A

Not infection, but common mimic.
Paraneoplastic syndrome, usualy small cell lung cancer, looks similar to HSV.
Ask for lung cancer screening.

55
Q

West Nile virus (4)

A

Several viruses characteristically involve the basal ganglia (Japanese Encephalitis, Murray Valley Fever, West Nile).
West nile causes T2 bright basal ganglia and thalamus, corresponding to restricted diffision.
Haemorrhage sometimes seen.

56
Q

CJD (7)

A

3 types
- Sporadic (80-90%), variant (rare) and familial (10%)
Characteristic appearance on EEG and 14-3-3 protein assay on CSF.
Imaging is variable, can be unilateral, bilateral, symmetric or asymmetric.
3 likely appearances
- DWI showing cortical gyriform restricted diffusion (diffusion is most sensitive sign, cortex is the most common, early site of manifestation)
- Hockey stick sign/Pulvinar sign: Restricted diffusion in the dorsal medial thalamus (which looks like hockey stick) or int he pulvinar.
- Series of MR or CT showing rapidly progressive atrophy

57
Q

Neurocysticercosis (7)

A

Caused by undercooked pork. Tinea solium is the pathogen.
Common locations are subarachnoid space overlying the cerebral hemispheres, basal cisterns, brain parenchyma and ventricles (in order).
Involvement of basal cisterns carries worst prognosis.
4 stages
- Vesicular: thin walled cysts, iso on T1/T2, no oedema
- Colloidal: hyperdense cyst, bright on T1/T2 and oedema
- Granular: Cyst shrinks, wall thickens, less oedema
- Nodular: small calcified lesion, no oedema.

58
Q

Meningitis and cerebral abscess (7)

A

4 main categories of meningitis:
- Bacterial (acute pyogenic)
- Viral (lymphocytic)
- Chronic (TB or fungal)
- Non infectious (Sarcoid)
Thick, leptomeningeal enhancement in the appropriate clinical setting.
Complications include thrombosis, vasospasm (leading to stroke), empyema, ventriculitis, hydrocephalus, abscess.
Infants often get sterile reactive subdurals (less common in adults).
Abscess imaging: DWI restricts, MRS - raised lactate, PET FDG - increased metabolic

59
Q

Empyema (4)

A

Subdural or epidural. Same rules as blood for crossing dural attachments (epidurals don’t) or crossing falx (subdurals don’t).
Subdural is more common and have more complications.
Most subdurals are due to frontal sinusitis, as are most epidurals.
Often T1 bright and restrict diffusion.

60
Q

Intraaxial infections (4)

A

Cerebritis, Abscess and Ventriculitis.
Lots of causes via direct or haematogenous spread.
Left to right shunts and pulmonary AVMs are important causes.
Cerebritis is early form of intra-axial infection, which can lead to abscess if not treated.

61
Q

Ventriculitis (3)

A

Usually due to shint placement or intrathecal chemo.
Ventricle will enhance and can sometimes seen ventricular fluid-fluid levels.
If septa start to develop, can get obstructive hydrocephalus.
Intraventricular extension of abscess is serious/ominous “pre terminal” event.