Stroke Flashcards

1
Q

Blood supply to brain - origin

A
  • There are 2 paired arteries responsible for blood supply to the brain, each of which arise in the neck and ascend to the cranium.
    1. Vertebra arteries
    2. Internal carotid arteries
  • The terminal branches of these arteries anastomose to for the circle of willis. From the circle other arterial branches arise to supply the majority of the cerebrum. Other areas of the brain are supplied by smaller branches from veretebral arteries.
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2
Q

Internal Carotid Arteries (ICA)

A
  • Originate at bifurcation of left and right common carotid level at C4.
  • It enters the brain via carotid canal of temporal bone (does not give off any branches that supply the face or neck).
  • Once in the cranial cavity, the ICA pass anteriorly through the cavernous sinus. From here, each ICA gives rise to:
    • Ophthalamic artery - supplies the strucutres of the orbit
    • Posterior communicating artery - acts as an anastamotic connecting vessels in circle of willis
    • Anterior cerebral artery - supplies part of cerebrum
  • The internal carotids then continue as middle cerebral artery, which supplies the lateral portion of the cerebrum.
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3
Q

Vertebral Arteries

A
  • Vertebral arteries arise from the subclavian arteries, medial to anterior scalene muscle. From here, they ascend up the posterior side of the neck, through holes in the transverse process of the cervical vertebrae (foramen transversarium).
  • Vertebral arteries enter the cranial cacity via the foramen magnum. From here, the vertebral arteries divide into several branches:
    • Meningeal branch - suppli es the flax cerebelli (a sheet of dura mater).
    • Anterior and posterior spinal arteries - supplies spinal cord (spans entire length).
    • Posterior inferior cerebellar artery - supplies cerebellum
  • From here, the two vertebral arteries converge to form the basilar artery.
  • Branches from basilar artery go on to supply the cerebellum pons. Basilar artery terminates by bifurcating into posterior cerebral arteries.
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4
Q

Arterial Circle of Willis

A
  • Terminal branches of vertebral and internal carotid anastomsose to form the circle of willis
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5
Q

Regional Blood supply to cerebrum

A
  • There are 3 cerebral arteries - anterior, middle, and posterior each of which supply a different portion of cerebrum.
  1. Anterior cerebral arteries - supplies anteromedial portion
  2. Middle cerebra arteries - supplies majority of lateral part of brain
  3. Posterior cerebral arteries - supplies medial and lateral part of posterior cerebrum
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6
Q

Arterial Supply to Spinal Cord

A
  • Anterior spinal artery - arises from vertebral arteries. Gives rise to sulcal arteries, which enter the spinal cord.
  • 2 posterior spinal arteries - arise from veretebral or posteroinferior cerebellar arteries. Anastomose in pia mater.
    • Below cervical level these 3 arteries are insufficient to supply spinal cord - there is support via anastomosis with segmental medullary and radicular artery
  • Anterior and posterior segmental - derived from spinal branches of numerous arteries, before entering vertebral canal via intervetebral foramina.
  • Radicular arteries - supplies anterior and posterior nerve roots
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7
Q

Transient Ischemic Attack TIA

A
  • Transient episode of neuologic dysfunction caused by focal brain, spinal cord, or retinal ischemia without acute infarction. There must be an absence of end-organ injury as assessed by imaging or other techniques.
  • Symptom duration is not a realiable indication
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8
Q

Stroke

A
  • An acute neurologic injury as a result of eiter hemorrhage of ischemia
    1. Hemorrhagic - too much blood within closed cranial cavity
    2. Ischemic - too little blood to supply an adequate amount of O2 and nutrients
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9
Q

Etiology Stroke

Ischemia

A
  1. Thrombosis - local in situ obstruction of an artery. May be due to disease of arterial wall - arteriosclerosis, dissection, or fibromuscular dysplasia. Can be either large or small vessel.
    • Large vessel - includes extracranial (common and internal carotides, vertebral) and intracranial arterial system (circle of Willis and Proximal branches).
    • Small vessel - affects intracerebral arterial system, specifically penetrating arteries that arise from the distal veretebral artery, the basilar artery, the middle cerebral artery stem, and arteries of circle of willis. Due to liophyalinosis, fibrinoid degeneration, and atheroma formation.
  2. Embolism - when debris originating from somewhere else in the body block an artery of particular brain region - since the process is not local, local therapy only temproarily solves the problem. There are 4 categories:
    • Those with known sources that is cardiac
    • Those with a possbile cardiac or aortic source based upon transthoracic and/or transesophageal echocardiographic finding
    • Those with an arterial source (artery to artery embolism)
    • Those with a truly unknown source in which tests for embolic sources are negative
  3. Systemic hypoperfusion - A more general circulartory problem. Can manifest in brain (stroke) or other organs
    • Does not affect isolated regions.
    • Can be due to cardiac pump failure caused by cardiac arrest or arrhythmia or due to reduced cardiac output related to myocardical ischemica, PE, pericardial effusion, or bleeding.
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10
Q

Etiology Stroke

Hemorrhage

A
  • Intracerebral hemorrhage (ICH) - bleeding directly into brain parenchyma. Usually derviced from arterioles or small arteries. Bleeding is directly into brain, forming a localized hematoma that spreads along white matter pathways. The hematoma grows over minutes to hours until the pressure surrounding it increases enough to limit its spread or until it decompresses by emptying into ventricle system or CSF. Most common causes - hypertension, trauma, bleeding, diathesis, amyloid angiopathy, illicit drug use, and vascular malformations. (Symptoms increase gradually over mins to hours)
  • Subarachnoid hemorrhage (SAH) - bleeding into CSF within subarachnoid space that surrounds the brain. Casued by rupture of arterial aneurysm that lie at the base of the brain and bleeding from vascular malformation that lie near the pial surface. Rupture of aneurysm releases blood directly into CSF under arterial pressure. Blood spreads quickly within CSF rapdily increasing ICP - death or deep coma occurs if bleeding continues. (Symptoms begin abruptly)
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11
Q

Anterior Cerebral Artery Stroke Symptoms

A
  • Contralateral leg paresis, sensory, cognitive deficits (e.g., apathy, confusion, and poor judgement)
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12
Q

Middle Cerebral Artery Stroke Symptoms

A
  • Contralateral weakness and sensory loss of face and arm
  • Cortical sensory loss
  • May have contralateral homonymous hemianopia or quadrantanopia
  • If dominant (usually left) hemisphere: aphasia
  • If non-dominatns (usually right) hemisphere: neglect ( a deficit in attention to and awareness of one side of the field of vision is observed)
  • Eye deviation towards the side of the lesion and away from weak side.
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13
Q

Posterior Cerebral Artery Stroke Symptoms

A
  • Contralateral hemianopia or quadrantanopia
  • Midbrain finding: CN III and IV palsay/pupillary changes, hemiparesis
  • Thalamic finding: Sensory loss, amnesia, decreased level of consciousness
  • If bilateral: Cortical blindess or progopagnosia
  • Hemiballisum
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14
Q

Basial Artery Stroke Symptoms

A
  • Proximal (usually thrombosis): impaireed extra-ocular muscle, vertical nystagmus, reactive miosis, hemi- or quadraplegia, dysarthria, locked-in syndrome, coma.
  • Distal (usually embolic): Somnolence (sleepiness), memory and behavioural abnormalities, oculomotor deficit.
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15
Q

Posterior Inferior Cerebellar Artery Stroke Symptoms

A
  • Ipsilaterial ataxia, ipsilateral Horner’s (miosis, partial upper eyelid ptosis, and facial anhidrosis), ipsilateral facial sensory loss, contralateral limb impairment of pain and temp sensation, nystagmus, N/V, dysphagia, dysarthria, hiccups.
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16
Q

Medial Medullary Infarct Stroke Symptoms

A
  • Anterial spinal artery, which can be associated with anterior cord infart: contralteral hemiparesis (facial sparing), contralteral imparied proprioception and vibration sensation, ipsilateral tongue weakness.
17
Q

Lacunar Infarcts Symptoms

A
  • Deep hemispheric white matter; involving deep penetrating arteries of MCA, Circle of Willis, basilar, and vertebral arteries.
    • Pure motor hemiparesis (posterior limb of internal capusle): contralateral arm, leg, and face.
    • Pure sensory loss (ventral thalamic): hemisensory loss
    • Ataxic hemiparesis (ventral pons or internal capsule): ipsilateral ataxia and leg paresis
    • Dysarthria-clumsy hand syndrome (ventral pons or genu of internal capule): Dysarthria, facial weakness, dysphagia, mild hand weakness, and clumsiness.
18
Q

Investigations Stroke

A
  • General Assessment
    • ABCs, full vital signs monitoring, capillary glucose, ugent CODE STROKE if <4.5hrs from symptom onset (for possible thrombolysis)
    • Level of consciousness, dysarthria (difficulty of unclear artciulation of speech that is otherwise lingusiticallt normal), dysnomia (can’t name objects).
    • Gase prefence, visual fields, facial palsy
    • Sensation to pinprick, extinction/neglect
  • History
    • Onset - time when last known to be awake and symptom free
    • Mimics to rule out - seizure/post-ictal, hypoglycemia, migraine, conversion disorder
  • Investigation
    • Non-contract CT head (STAT) to rule out hemorrage and assess extent or infract
    • EEG to rule of artical fibrillation
    • Cartoid doppler, echocardiogram
    • CBC, electrolyties, creatinine, PTT/INR, blood glucose, lipid profile
  • Imaging - CT +/- MRI or CT angiography
  • Additional investigtions for cerebral hemorrhage
    • LP - if suspect subarachnoid hemorrhage despite negative CT
    • May require cerebral angiogram if suspect aneurysm or AVM
    • If typical location for hypertensive hemorrhage, repeat CT head in $-6 weeks after hemorrhage ahs resolved to rule out an underlying lesion.
19
Q

Acute Treatment Ischemia Stroke

A
  • Thrombolysis
    • rTPA (recombinant tissue plasminogen activator)
    • given within 4.5hr of acute ischemic stroke oset provided there are clinical indications and no contraindications
      • Contraindications - improving symptoms, minor symptoms, seizures at stroke onset major surgery within 14 days or trauma, recent LP or arterial puncture at noncompressible site, PMHx ICH, symptoms of subarachnoid hemorrhage/pericarditis/MI, pregnancy.
      • Indications - clinical diagnosis of ischemic stroke cuasing measurable neurologic deficit, onset of symptoms <4.5hrs, age 18+
  • Mechanical thrombectomy - indicated for those with acute ischemic stroke due to a large artery occlusion in anterior circulation who can be treated within 24hrs, regardless of whether they receied rTPA.
  • Anti-platelet therapy:
    • Give at presentation of TIA or stroke if rTPA is not received.
    • Antiplatelet agents - ASA 81mg chewed.
  • Statin therapy - starts as soon as oral medication can be used safely.
  • Bloos pressure control - Do NOT lower BP unless HYN is severe (sBP >220 or dBP >120). Acutely elevated BP is necessary to maintain brain persion. Most patients with acute cerebral infarct are initially hypertensive and their BP will fall spontaneousl within 1-2days.
20
Q

Acute Treamtnet Intracerebral Hemorrhage (ICH)

A
  • Reversal of anticoagulation - all anticolagulant and anti-platelet drugs should be discontinued. Aggressive use of vitamin K, unacitvated prothrombin complex concentrate, fresh frozen plasma, and other factors may be necessary for those taking warfin.
  • BP - BP elevation may predispose to hematoma expansion:
    • Acute ICH with sBP between 150-220 - lower to 150
    • Acute ICH with sBP > 220 - aggressive reduction of BP via continuous IV infusion
  • ICP management
    • Basic measures - elevation of head of bed to 300, mild sedation (for comfort), avoidance of devices that might constrict cervical veins, use of normal saline for maintenance and replacement of fluids (hypotonic are contraindicated)
    • CSF drainage - reasonable for patients with hydocephalus or trapped ventricle
    • Ostmotic therapy - hypertonic saline or mannitol
  • Surgery - indications depend on the site of the bleed.
21
Q

Subarachnoid Hemorrhage Acute Treatment

A
  • Antithrombic discontinuation
  • ICP management
  • BP control - no optimal target has been identified
  • Aneurysm repair should be preformed within 24-72 hours to prevent re-occurrance
  • Prevention of vasospams and delayed cerebral ischemia - administer nimodipine (60mg every 4hrs within 4 days of SAH) and euvolemia should be maintained
22
Q

Watershed Zone

A
  • Watershed infarcts occur at the border zones between major cerebral arterial terriotires as a result of hypoperfusion. There are 2 patterns of border zone infarcts
    1. Cortical border zone infarctions - infarctions of cortex and adjancent subcoritcal white matter located at border zone of ACA/MCA and MCA/PCA
    2. Internal border zone infarctions - infractions of the deep white matter between lentoculostriate perforators and deep penetrating cortical branches of MCA or at border zone of deep white matter branches of MCA and ACA
23
Q

Blood Supply of

  1. Basal ganglia
  2. Brain Stem
  3. Cerebellum
A

1.

  • Medial lenticulostriate - supplies globus pallidus and medial portion of putamen
  • Lateral lenticulostriate - lateral putamen
  • Recurrent artery of Heubner (arises as large branch for ACA) - supplies caudate

2.

  • Midbrain - small penetrating branches from basilar, superior cerebellar, posterior cerebellar
  • Pons - medial branches of superior cerebellar; pontine branches of basilar artery

3.

  • Superior, anterior inferior, and posterior inferior cerebellar artery.
24
Q

Neuroanatomy of Aphasia

A

An acquried disturbance of language characteized by errors in lanuage production, writing, comprehension, or reading.

  • Brocas area (posterior inferior frontal lobe) - involved in lanuage production (expressive). Innervated adjacent motor neruons suberving the month and larnyx and controls the output of spoken language
  • Wernicke’s aphsia (posterior surperior temporal lobe) involved in comprehension of language (receptive). Receives information from auditory cortex and accesses a network of cortical association to assign word meaning.
  • Angular gyrus (inferior perietal lobe) - responsbile for relaying wirrten visual stimuli to Wernicke’s area for reading comprehension
25
Q

Ventral vs. Dorsal Stream

A
  • Ventral - rooted in bilateral temporal lobes and is important for mapping from auditory input to memory. Integrity og this is crucial for normal audotry comprehension.
  • Dorsal - unilaterally organized and includes the frontal lobe areas associated with speech production and a region of the temproparietal junction. Integrity of this stream is essential for fluent speech as they provide auditory and proprioceptive feedback.