Step 1: Neuro Awill's deck Flashcards
(157 cards)
Anterior spinal artery deficit
medial medullary syndrome - contralateral hemiparesis (lower extremities), medial leminscus (↓ contralateral proprioception), ipsilateral paralysis of hypoglossal nerve
PICA deficit
(lateral medullary syndrome, wallenberg’s) contralateral loss of pain and temperature, ipsilateral dysphagia, hoarsness, ↓ gag reflex, vertigo, diplopia, nystagymus, vomiting, ipsilateral horner’s, ipsilateral facial pain and temperature, trigeminal nucleus, ipsilateral ataxia
AICA deficit
(lateral inferior pontine syndrome) - Ipsilateral facial paralysis, ipsilateral cochlear ucleus, vestibular (nystagmus), ipsilateral facial pain and temperature, ipsilateral dystaxia (MCP, ICP)
Posterior cerebral artery deficit
contralateral homonymous hemianopia w/ macular sparing; supplie occipital cortex
Anterior cerebral artery defect
supplies medial surface of the brain, leg-foot area of motor and sensory cortices
Middle cerebral artery defect
Contralateral face and arm paralysis and sensory loss, aphasia (dominant sphere), left-sided neglect
Anterior communicating artery deficit
most common site of circle of Willis aneurysm; lesions may causes visual field defects
PCA deficit
common area of aneurysm, causes CNIII palsy
Lateral striate deficit
Divisions of MCA - supply internal capsule, caudate, putamen, globus pallidus. “arteries of stroke”; infarct of the posterior limb of the internal capsule causes pure motor hemiparesis
Watershed zones
between ACA/MCA, PCA/MCA. Damage in severe hypotension→ upper leg/upper arm weakness, defects in higher order visual processing
Basilar artery defect
infarct causes “locked-in syndrome” (CN III is typically intact)
Damage of stroke of anterior circle
general sensory and motor dysfunction, aphasia
Damage from stroke of posterior circle
cranial nerve deficits (vertigo, visual deficits), coma, cerebellar deficits (ataxia) dominant hemisphere (ataxia), nondominant (neglect)
Berry aneurysms
occur at bifurcations in circle of willis (most common ACA) 2. Rupture leads to hemorrhagic stroke/SAH 3. Assoc w/ adult polycystic kidney disease, Ehlers-Danlos syndrome and marfan’s. 4. Risk factors: advanced age, HTN, smoking, race (higher risk in blacks)
Charcol-Bouchard microaneurysms
associated with chronic hypertension, affects small vessels (in basal ganglia, thalamus)
Epidural hematoma CT
shows biconvex disk - not crossing suture lines - can cross falx, tentorium
Epidural hematoma
rupture of middle meningeal artery - often secondary to fracture of temporal bone. Lucid interval. Rapid expansion under systemic arterial pressure→ transtentorial herniation. CNIII palsy
Subdural haematoma imaging
crescent-shaped hemorrhage that crosses suture lines, Gyri are preserved since pressure is distributed equally. Cannot cross falx, tentorium
Subdural haematoma
rupture of bridging veins - slow venous bleeding. Delayed onset of symptoms. Seen in elderly individuals, alcoholics, blunt trauma, shaken baby
SAH
- rupture of an aneurysm or an AVM 2. patients complain of “worst headache of my life” 3. Bloody or yellow spinal tap 4. 2-3 days afterward there is a risk of vaspospasm due to blood breakdown products which irritate vessels (treat w/Ca channel blockers)
Parenchymal haematoma
caused by HTN, amyloid angiopathy. Lobar strokes all over the brain. DM and tumor. Typically occurs in basal ganglia and internal capsule.
Most vulnerable parts to ischaemic brain
hippocampus, neocortex, cerebellum, watershed areas
Irreversible neuronal injury
red neurons (12-48 hours), necrosis+neutrophils (24-72 hours), macrophages (3-5 days), reactive gliosis+ vasc proliferation (1-2 weeks), glial scar (> 2 weeks)
Atherosclerosis (re: stroke)
thrombi lead to ischemic stroke with subsequent necrosis (red neurons) - forms cystic cavity w/reactive gliosis