Stroke

• ct can detect stroke within 6-24 hours
• mri can detect stroke within 3-30 mins
• irreversible brain injury occurs after 5 mins of hypoxia

  most affected hippocampus purkinje neocortex watershed areas
• 6-24 hours: eosinophilic cytoplasm pukynotic nucleus ( red neuron)

  24-72 hours : necrosis and neutrophil

  3 - 5 days : microglia

  1-2 weeks : reactive gliosis astrocytes vascular proliferation

  more than 2 weeks glial scar
• ischemia leads to infarction leads to liquefactive necrosis
• thrombotic type is due to occlusion of vessel at site of infarction usually ruptured atherosclerotic plaque in mca
• embolic due to emboli affects several vascular sites
• hypoxic due to hypoxemia or hypoperfusion often during cardiovascular surgeries affects watershed areas
• treatment of strok : TPA within 3-4.5 of onset with no hemorrhagic risk

  prophylaxis : aspirin clopidogrel smoking cessation blood pressure sugar and lipid managment and treat other risk factors like atrial fibirllation Carotid artery stenosis
• Transient ischemic attack reversible focal neurologic deficit negative mri resolves in less than 15 mins usually due to thrombi or small vessel occlusion presents as transient loss of vision ( amaurosis fugax) due to retinal artery emboli from CAD
• cerebral edema causes increased ICP
• cytotoxic edema due to osmotic shift Na/K atpase dysfunction causing increased intracellular Na+ caused by early stroke SIADH hyperammonemia
• vasogenic edema is due to increased permeability of the BB usually due to late stroke inflammation tumor hemorrhage
• anterior cerebral artery stroke: contralateral sensory and motor paralysis of lower limb and urinary incontinence
• middle cerebral artery stroke contralateral motor and sensory paralysis of upper limb broca and wernicke areas affected leading to aphasia if left hemisphere hemineglect if right hemisphere

  wernicke’s aphasia right upper quadrant visual field defect due to temporal lobe involvement
• Lenticulosstriate artery stroke lesion in striatum or internal capsule causes contralateral moto paralysis and absence of cortical signs neglect aphasia and visual field loss
• basillar artery stroke : loss of pons medulla lower midbrain corticospinal and corticobulbar tract ocular cranial nerve nuclei and pontine reticular paramedian formation

  presents as quadriplegia loss of voluntary facial movements only blinks and eyes move only vertically if RAS spared he is awake
• AICA stroke affect facial vestibular spinothalamic tract and spinal trigeminal sympathetic middle inferior cerebellar peduncle inner ear

  presents as facial paralysis decreased lacrimation salivation taste from anterior 2/3 tongue vomitting vertigp nustagmus. decreased pain sensation from contralateral side of body

  ipsilateral horner ipsilateral ataxia dysmetria ipsilateral sensorineural deafness

  lateral pontine syndrome facial nuclei effects are specific to AICA
• inner ear is supplied by labrynthine branch of AICA
• Epidural hematoma due to rupture of middle meningeal artery branch of maxillary due to skull fracture involving pterior ( thinnest part of lateral skull)

  presents as transient loss of conciousness - recovery - rapid deterioration due to Hematoma expansion

  scapl hematoma and rapid intracranial expansion under systemic arterial pressure leads to transtentorial herniation and facial nerve palsy

  ct shows lenitform biconvex hyperdense blood collection not crossing suture lines