6. Neuro (Brain - Misc, Neuro-degenerative, Metabolic, Infections) Flashcards
Monro-Kellie Doctrine (2)
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
Intracranial hypotension (3)
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.
Idiopathic intracranial hypertension (pseudotumour cerebri). (5)
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.
Cytotoxic oedema (3)
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.
Vasogenic oedema (4)
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.
Communicating oedema (3)
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.
Normal pressure hydrocephalus (6)
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
Blood, pus, cancer (communicating oedema) (2)
Anything causing plugging of the villi, most commonly SAH, meningitis, Carcinomatous meningiits
Non-obstructive hydrocephalus (2)
Anything that produces more CSF.
Choroid plexus papilloma is usually the answer.
Transependymal flow
Seeen more with acute rather than chronic hydrocephalus.
Subfalcine herniation (2)
aka midline shift.
ACA may be compressed, causing infarct.
Descending transtentorial herniation (8)
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”
Ascendng transtentorial herniation (4)
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)
Cerebellar tonsil herniation (2)
Can be from severe herniation after downward transtentorial herniation.
In isolation, could be Chiari malformtion (Chairi 1 = 1 tonsil 5mm or both 3mm)
Multiple sclerosis (10)
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.
ADEM (5)
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.
Acute haemorrhagic leukoencephalitis (3)
Aka Hurst Disease
Fulminant form of ADEM with massive brain swelling and death.
Haemorrhagic part only seen on autopsy.
Devics (neuromyelitis optica) (2)
Transverse myelitis + optic neuritis.
Lesions in the cord and the optic nerve
Marburg variant (2)
Childhood variant that is fulminant and leads to rapid death.
Usually febrile prodrome
PRES (Posterior Reversible Encephalopathy Syndrome) (3)
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
Radiation induced demyelination (3)
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)
Osmotic demyelination syndrome (CPM) (3)
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.
Wernicke encephalopathy (3)
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.
Carbon monoxide poisoning (2)
CT: hypodensity. MRI: T2 bright globus pallidus