NM - CVA

• CVA aka Stroke/brain attack
• To be classified as stroke, neurologic deficits must persists for at least 24 hours
• Paralysis, hemiplegia
• Weakness, hemiparesis
• CVA

  Definition: sudden loss of neurologic function due to an interruption of blood flow to the brain
• CVA

  Classification: base on etiology, management categories, and vascular territory/syndrome
• CVA

  Epidemiology:

  • 5th leading cause of death
  • leading cause of long term disability among adults
  • Men > women; if beyond 85 y/o, women > men
• CVA

  Mortality rate:

  • Hemorrhagic stroke - 37-38% (after onset)
  • Ischemic stroke - 14.7%
• CVA

  Atherosclerosis:

  • major contributory factor
  • plaque formation on arterial walls that leads to progressive narrowing of blood vessels
  • Most common sites: common carotid, middle cerebral, & vertebrobasilar
• Ischemic stroke - interruption of cerebral blood flow & O2 supply to the brain leading to tissue death
• Lesion to the extracranial (carotid/vertebral) arteries can also produce symptoms of stroke
• Ischemic Stroke - Thrombus

  • positive blood clot within the cerebral arteries (cerebral thrombosis)
  • cerebral infarction/tissue death (antherothrombotic brain infarction ABI)
• Ischemic Stroke - Embolus

  • dislodged thrombus formed elsewhere & has traveled to the cerebral arteries producing occlusion & infarction
  • Most common source: Cardiovascular system
  • other sources: systemic (septic, fat, air)
• Hemorrhagic Stroke

  • abnormal bleeding into the extravascular areas of brain due to ruptured blood vessels or trauma
  • closely linked to chronic hypertension
• Hemorrhagic Stroke - Intracerebral Hemorrhagic

  • bleeding into the brain due to a rupture of a cerebral vessel
  • Primary ICH - non-traumatic/spontaneous; usually in small blood vessels (atherosclerosis=aneurysm)
  • Secondary ICH - associated with trauma
• Hemorrhagic Stroke - Subarachnoid Hemorrhagic

  • bleeding into the subarachnoid space
  • results in sudden, severe headche, "worst headache of my life" (thunderclap headache)
• Subarachnoid Hemorrhagic

  • Saccular/Berry Aneurysm - congenital abnormal distention of large blood vessel at a bifurcation
  • Arteriovenous Malformation - congenital defect characterized by direct artery to vein communication without capillaries (tangled arteries & vein causes rupture)
• Non Modifiable RF

  • Family history
  • Age
  • Gender
  • Race
• Modifiable

  • Cigarette smoking
  • Physical inactivity
  • Obesity
  • Diet
• Major RF

  • Hypertension
  • Diabetes mellitus (due to heart rhythm, high blood cholesterol, heart disease)
• Early Warning Signs "FAST" bc "time is brain"

  • F - face dropping
  • A - arm weakness
  • S - speech difficulty
  • T - time to call 911
• Pathophysiology

  1. Sudden cessation of blood flow
  2. Ischemic core (all tissues) - region of cell death; neurons die
  3. Penumbra (damage tissue) - surrounding area with damaged tissue; needs 20-25% of blood flow to survive; cell may die if untreated
• Pathophysiology

  Ischemic cascade

  1. Release of neurotransmitters (glutamate & aspartate)
  2. Produces a progressive disturbance of energy metabolism and anoxic depolarization
  3. Inability of brain cells to produce energy, adenosine triphosphate (ATP)
  4. Excess influx of calcium ions & pump failureof the neuronal membrane
  5. Excess calcium reacts with intracellular phospholipids to form free radicals
  6. Calcium influx also stimulates the release of nitroc oxide and cytokines
• Cerebral edema

  • accumulation of fluids within the brain that begins from minute of insult - max. 3-4 days
  • swelling gradually subsides and generally disappears by 2-3 weeks
• Transient Ischemic Attack

  • temporary interruption of blood supply
  • symptoms lasts for <24 hours: few minutes - hours
  • positive residual brain damage after attack
  • precursor to cerebral and myocardial infarction
• Major Stroke

  • positive stable, severe impairments
• Deteriorating Stroke

  • refers to patients whose neurologic status deteriorates after admission
  • may be due to cerebral edema, progressing thrombosis
• Young stroke

  • stroke <45 years old
• ACA - Supplies

  • medial frontal lobe
  • medial parietal lobe
  • corpus callosum
  • basal ganglia (anterior internal capsule & inferior caudate nucles)
• Deficits are minimal with proximal ACA occlusion due to collateral supple of anterior communicating artery
• In ACA, more distal lesions produce more significant deficits
• ACA Affectation: LE > UE
• Common deficit in ACA: Apraxia

  • Ideomotor - cannot perform the task upon command
  • Ideational - cannot perform the task at all
• ACA S/Sx

  Contralateral hemiparesis LE - Primary motor area (Area 4), medial aspect of cortex, internal capsule
• ACA S/Sx

  Contralateral hemisensory loss LE - Primary sensory area (Area 3,1,2), medial aspect of cortex
• ACA S/Sx

  Urinary incontinence - Posteromedial aspect of superior frontal gyrus
• ACA S/Sx

  Problems with imitation and bimanual tasks, apraxia - Corpus callosum
• ACA S/Sx

  • Abulia, slowness, delay, lack of spontaneity, motor inaction
  • Contralateral grasp reflex, sucking reflex
• MCA Supplies:

  • lateral frontal lobe
  • lateral temporal lobe
  • lateral parietal lobe
  • basal ganglia
  • internal capsule
• MCA most common site of occlusion in stroke