1. Extracranial blood supply to brain
   1. • Extracranial blood supply to brain = provided by R & L ICAs & R & L vertebral arteries • I internal carotid artery begins at bifurcation of common carotid artery & ascends and the deep portions of neck two carotid canal • Turns rosteromedially & ascends into cranial cavity • Then pierces Dura mater & gives off ophthalmic & anterior choroidal arteries b4 bifurcating into middle & anterior cerebral arteries • Anterior communicating artery communicates with anterior cerebral arteries of either side, giving rise to the rostral portion of circle of Willis • Vertebral artery arises as branch off subclavian artery & enters ventral foramen of v-bra C6 & travels through foramina of TVP of upper 6 C-v-bra to foramen Magnum & into brain • Travels and posterior cranial fossa ventrally & medially & unites with vertebral artery from other side to form basilar artery at upper border of Medulla • At upper border of pons, basilar a. bifurcates to form posterior cerebral arteries & posterior portion of a circle of Willis • Posterior communicating arteries connect the posterior cerebral arteries with internal carotid arteries & complete the circle of Willis
2. Etiology (3)
3. Location
   1. ACA Syndrome
      1. supplies medial aspect of cerebral hemisphere & subcortical structures
      2. b/c anterior communicating a. allows perfusion of prox ACA from either side, occlusion proximal to this=min deficit
      3. Common characteristics: contralateral hemiparesis & sensory loss w/greater involvement of LE b/c the somatotopic org of the medial aspect of the cortex inclds the fnxal area for LE. P. 710 table 18.1
      4. LE INVOLVEMENT
   2. MCA Syndrome
      1. supplies entire lateral aspect of cerebral hemisphere & subcortical structures
      2. Occlusion of proximal MCA=extensive neurological damage w/signif cerebral edema
      3. Common characteristics: Contralateral spastic hemiparesis & sensory loss of face, UE, & LE, w/face & UE > LE; Table 18.2 p. 712
      4. Lesions:
         1. Parieto-occipital cortex of dominant hemisphere (L hem) typically produce Aphasia
         2. R Parietal Lobe of nondominant Hemisphere (R hem) typically produce perceptual deficits: unilat neglect, anosognosia, apraxia, spatial disorg
      5. Homonymous Hemianopsia=common
      6. MOST COMMON SITE OF OCCLUSION IN STROKE
      7. UE INVOLVEMENT
   3. PCA Syndrome
      1. each of the 2 supply the corresponding occipital love; supplies upper brainstem, midbrain, posterior diencephalon
      2. Occlusion proximal to posterior communicating a. typically results in min deficit owing to collateral blood supply from posterior communicating a (sim to ACA syndrome)
      3. Occlusion of thalamic branches may produce hemianesthesia (contralat sensory loss) or central post-stroke (thalamic) pain
      4. Occipital infarction=Homonymous Hemianopsia, visual agnosia, Prosopagnosia or if bilat, cortical blindness
      5. Temporal lobe ischemia=amnesia; Subthalmic branches involvement=wide variety deficits;
      6. Contralat Hemiplegia occurs w/involvement of cerebral peduncle
   4. Internal Carotid Artery Syndrome
      1. supplies both MCA & ACA
      2. Occlusion typically produces massive infarction in region of brain supplied by MCA
      3. Common: signif edema w/possible uncal herniation, coma, & death
   5. Lacunar Syndromes
      1. caused by small vessel disease deep in cerebral white matter
      2. strongly assoc w/hypertensive hemorrhage & diabetic microvascular disease
         1. hypertensive hemorrhage affecting thalamus can produce central post-stroke pain
      3. Specific to anatomic sites:
         1. Pure Motor Lacunar Stroke
            1. involvement of posterior limb of internal capsule, pons & pyramids
         2. Pure Sensory Lacunar Stroke
            1. involvement of ventrolateral thalamus or thalamocortical projections
         3. Dysarthrial Clumsy Hand Syndrome
         4. Ataxic Hemiparesis
         5. Sensory/Motor Stroke
         6. Dystonial/Involuntary movements
      4. Deficits in consciousness, lang, or visual fields aren't seen here as higher cortical areas are preserved
   6. Vertebrobasilar Artery Syndrome
      1. vertebral aa: supply the cerebellum and medulla
      2. basilar a: supplies the pons, internal ear, & cerebellum
         1. Locked-in Syndrome-occurs w/basilar a. thrombosis & bilat infarction of ventral pons p.713
            1. pt. can't move or speak but remains alert & oriented; horizontal eye movements=impaired but vertical eye movements & blinking=intact
      3. Occlusions of this syst =wide variety of sx w/ipsilat & contralat signs
      4. numerous cerebellar & CN abnormalities are present Table 18.4 p. 714-715
4. Management
   1. TIA
      1. Precursor to susceptibility for both cerebral infarction & myocardial infarction
   2. Minor or Major Stroke
      1. Major: in presence of stable, usually severe, impairments
   3. Deteriorating Stroke
      1. Pt whose neurological stat is deteriorating after admission to hosp; may be due to cerebral or systemic causes
   4. Young Stroke
      1. stroke affected ppl younger than 45