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Flashcards in Neuro Deck (229)
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Perinatal Brain Injury

  • non-aggressive motor deficits from pre- and perinatal neurologic insults.
  • risk factor: prematurity.
  • can have brain injury without reactive gliosis.
  • intraparenchymal hemorrhage, periventricular leukomalacia, multicystic encephalopathy, ulegyria, status marmoratus.
  • presentation: depends on location but includes dystonia, spasticity, ataxia/athetosis, and/or paresis


Perinatal Intraparenchymal Hemorrhage

  • in germinal matrix btw thalamus and caudate nucleus.  can extend to ventricular system.


Periventricular Leukomalacia

  • ischemic infarcts in periventricular white matter.


Multicystic Encephalopathy

  • ischemic infarcts within the hemispheres.



  • thin, gliotic gyri from perinatal cortical ischemia.


Status Marmoratus

  • ischemic neuronal loss and gliosis in basal ganglia and thalamus with aberrant and irregular myelin formation.


Skull Fractures

  • fracture resistance varies with skull bone thickness.
  • displaced fracture = bone shifts into cranial vault by more than its thickness.
  • accidental falls = occiput.  2° basal skull involved with lower CN or cervicomedullary symptoms, CSF discharge, and/or meningitis.
  • syncope ⇒ frontal skull.
  • diastatic fractures = transverse sutures.



  • transient trauma-related clinical syndrome with loss of consciousness, temporary respiratory arrest, loss of reflexes, amnesia of event.


Direct Parenchymal Injury (Brain)

  • lacerations = penetrating injury causes tissue tearing.
  • contusions = CNS bruises.
    • gyral crest very susceptible.
    • coup contusion = at site of impact
    • contrecoup = on opposite side of cranium from impact
  • brain hemorrhage and edema resolves ⇒ depressed, yellow-brown glial scar going to pial surface = plaque jaune


Diffuse Axonal Injury

  • when mechanical forces (acceleration) disrupt axonal integrity and axoplasmic flow.
  • widespread axonal swelling and focal hemorrhage ⇒ degenerated fibers and gliosis.
  • 1/2 pts comatose after trauma have diffuse axonal injury even without contusions.


Epidural Hematoma

  • rupture of dural arteries (middle meningeal artery) ⇒ blood btw dura and skull ⇒ compress brain.
  • can have lucid period several hours after trauma


Subdural Hemorrhage

  • tearing of veins that stretch from cortical surface through subarachnoid and subdural spaces into draining veins (superior sagittal sinus).
  • after traumatic shifting of brain.
  • geriatric pts with cerebral atrophy susceptible.
  • presentation: non-localizing headache, confusion within 48hrs of injury.
  • chronic subdural hematoma = recurrent episodes of bleeding from hemorrhage of thin-walled vessels of granulation tissue.
  • tx: surgical drainage and remove granulation tissue.


Sequelae of Brain Trauma

  • epilepsy, meningiomas, infectious disease, psychiatric disorders.
  • post-traumatic hydrocephalus = hemorrhage into subarachnoid space obstructs CSF resorption
  • post-traumatic dementia = dementia pugilistica.  repeated head trauma ⇒ hydrocephalus, corpus callosum thinning, diffuse axonal injury, amyloid plaques, and neurofibrillary tangles.


Spinal Cord Trauma

  • displacement of spinal column. 
  • injury level:
    • thoracic vertebrae or below ⇒ paraplegia.
    • cervical vertebrae ⇒ quadriplegia.
      • C4 and above ⇒ respiratory compromise from diaphragm paralysis.
  • acute = hemorrhage, necrosis, white matter axonal swellings
  • later = cystic and gliotic.  ascending and descending white matter tracts do 2° degeneration.


Global Cerebral Ischemia

  • hypoxia from reduced blood flow or hypotension.
  • neurons more sensitive to hypoxia.
  • severe ⇒ widespread neuronal cell death, pt vegetative state or brain dead.
    • brain dead = flat EEG, absent reflexes/respiratory drive/cerebral perfusion
    • kept on ventilator ⇒ brain autolyzes.
  • watershed/border zone infarcts = oxygenation incompletely compromised.  interface between major vessels.
    • btw anterior and middle cerebral arteries most vulnerable.
  • morphology: edematous with widened gyri and narrowed sulci.  poor gray/white demarcation.
    • red neurons 12-24hrs post injury.  pyramidal neurons in hippocampus CA1 (Sommer sector), cerebellar Purkinje cells, cortical pyramidal neurons most susceptible.
    • then neutrophil infiltration ⇒ macrophage influx, neovascularization, reactive gliosis.
    • pseudolaminar necrosis = uneven cortical neuronal loss and gliosis alternating with preserved zones.



  • brain oxygen deprivation from global or focal ischemic necrosis.  
  • outcome depends on collateral circulation, duration of ischemia, magnitude and rapidity of flow reduction.


Focal Cerebral Ischemia

  • infarction from obstruction of local blood supply ⇒ thrombotic or embolic arterial occlusion.
  • thrombosis = from atherosclerosis.  affects extracerebral carotid system and basilar artery.
  • embolism = involves intracerebral arteries (middle cerebral).  comes from atheromatous cerebrovascular plaques, cardiac mural trhombi, valvular lesions, or paradoxical embolisms.
  • inflammatory lesions can ⇒ lumenal narrowing and cerebral infarct.
  • venous infarcts after occlusion of superior sagittal sinus or deep cerebral veins.  are hemorrhagic.
  • morphology: nonhemorrhagic infarcts = bland/anemic infarcts.  see at 48hrs as pale, soft regions of edematous brain with neutrophils.  then liquefies ⇒ fluid-filled cavity with macrophages lined by reactive glia.
    • hemorrhagic infarcts = embolic occlusion with reperfusion injury, have blood extravasation.


Lacunar Infarcts

  • small cystic infarcts from cerebral arteriolar sclerosis and occlusion.
  • lipid-laden macrophages and surrounding gliosis.
  • affects: lenticular nucleus, thalamus, internal capsule, deep white matter, caudate nucleus, and pons.


Slit Hemorrhages

  • when HTN causes small vessel rupture.  
  • they resorb leaving hemosiderin-laden macrophages and gliosis.


Acute Hypertensive Encephalopathy

  • ↑ ICP ⇒ diffuse cerebral dysfunction (headaches, confusion, vomiting, convulsions, coma).
  • need rapid intervention.
  • post mortem shows edematous brain with petechiae and arteriolar fibrinoid necrosis.  somtimes see herniation.


Chronic Hypertensive Injury

  • recurrent small infarcts ⇒ vascular (multi-infarct) dementia
    • dementia, gait abnormalities, pseudobulbar signs, focal neuro deficits.
  • Binswanger disease = pattern of recurrent ischemic injury involves subcortical white matter with myelin and axonal loss.


Intracerebral Hemorrhage

  • spontaneous rupture of small intraparenchymal vessel.  
  • age >60yrs.
  • causes:
    • HTN in 50%.  ⇒ hyaline arteriosclerosis and vessel weakening, focal vessel necrosis, Charcot-Bouchard aneurysms.  in putamen (50-60%), thalamus, pons, cerebellar hemispheres.
    • cerebral amyloid angiopathy (CAA): 2nd most common.  amyloidogenic peptides deposited in vessel walls ⇒ weakening.  lesions have stiff amyloid deposits in leptomeningeal and cerebral cortical vessels.
    • cerebral autosomal dominanty arteriopathy with subcortical infarcts (CADASIL): mutation in Notch3 receptor.  vessels have concentric medial and adventitial thickening with basophilic granular depostis and smooth muscle drop-out


Subarachnoid Hemorrhage

  • usually from berry (saccular) aneurysm rupture, traumatic hematomas, vascular malformations, HTN intracerebral hemorrhage, tumors, hematologic disturbances.
  • pathogenesis: 90% berry aneurysms in anterior circulation near arterial branch points.
    • can be with polycystic kidney disease (autosomal dominant), HTN, aortic coarctation, collagen disorders, neurofibromatosis type I, and fibromuscular dysplasia
  • morphology: small with red shiny translucent wall.  at aneurysm neck, the muscular wall and intimal elastic lamina are absent.  sac wall is only thickened hyalinized intima.
  • presentation: rupture from ↑ ICP.  excruciating headache, rapid loss of consciousness.  re-bleeding common with worse episode each time the aneurysm bleeds.
    • blood in subarachnoid ⇒ arterial vasospasm
    • blood resorption ⇒ meningeal fibrosis and hydrocephalus


Arteriovenous Malformation

  • tangles of abnormalled tortuous and misshapen vessels, shunting arterial blood into venous circulation.
    • usually MCA.
  • 2:1 m:f 
  • presentation: btw ages 10-30yrs as seizure disorder, intracerebral hemorrhage, or subarachnoid hemorrhage


Cavernous Hemangiomas

  • distended, loosely organized vascular channels with thin, collagenized walls.
  • usually cerebellum, pons, and subcortical regions.
  • low flow without arteriovenous shunting.


Capillary Telangiectasias

  • microscopic foci of dilated, thin-walled vascular channels separated by normal brain parenchyma.
  • in pons.


Venous Angiomas

  • aka varices
  • aggregates of ecstatic veins.


Foix-Alajouanine Disease

  • venous angiomatous malformation in lumbosacral region.
  • slowly progressive ischemia and neuro symptoms.


Acute Bacterial Meningitis

  • neonates = E. coli and group B strep
  • infants & kids = S. pneumoniae
  • adolescents & young adults = N. meningitidis
  • elderly = S. pneumoniae and L. monocytogenes
  • morphology: meningeal vessels engorged, purulent exudate.
    • neutrophils in subarachnoid space.  may have cerebritis.
    • phlebitis ⇒ venous thrombosis and hemorrhagic infarction.
    • resolution ⇒ leptomeningeal fibrosis and hydrocephalus
  • presentation: fever, headache, photophobia, irritability, clouded sensorium, neck stiffness.
    • CSF purulent with neutrophils and organisms, ↑ protein, and ↓ glucose.


Acute Viral Meningitis

  • meningeal irritation, CSF lymphocytic pleocytosis, mod ↑ protein, normal glucose.
  • self-limited.