Stroke (main)

Background
  • Vascular injury that reduces cerebral blood flow to specific region of brain causing neuro impairment
  • Accurate determination of last known time when patient was at baseline is essential
  • In-hospital mortality of 5-10% for ischemic stroke and 40-60% for hemorrhagic stroke
  • Only 10% of stroke survivors will recover completely
Sensory Homonculus - courtesy AnatomyZone.com

Ischemic stroke causes (87% of all strokes)
  • Thrombotic (80% of ischemic CVA)
  • Embolic (20% of ischemic CVA)
    • Valvular vegetations
    • Mural thrombi
    • Arterial-arterial emboli from proximal source (ex. amaurosis fugax -> emboli from a proximal carotid artery plaque embolizes to the ophthalmic artery, causing transient monocular blindness)
    • Fat emboli
    • Septic emboli
  • Hypoperfusion
    • Cardiac failure resulting in systemic hypotension

Hemorrhagic stroke causes (13% of all strokes)

Stroke Types

Clinical Features

Anterior Circulation
  • Blood supply via internal carotid system
  • Includes ACA and MCA

Internal Carotid Artery
  • Tonic gaze deviation towards lesion
  • Global aphasia, dysgraphia, dyslexia, dyscalculia, disorientation (dominant lesion)
  • Spatial or visual neglect (non-dominant lesion)

Anterior Cerebral Artery (ACA)

Signs and Symptoms:

  • Contralateral sensory and motor symptoms in the lower extremity (sparing hands/face)
  • Urinary and bowel incontinence
  • Left sided lesion: akinetic mutism, transcortical motor aphasia
  • Right sided lesion: Confusion, motor hemineglect
  • Presence of primitive grasp and suck reflexes
  • May manifest gait apraxia

Middle Cerebral Artery (MCA)
Patient with stroke (forehead sparing).

Signs and Symptoms:

  • Hemiparesis, facial plegia, sensory loss contralateral to affected cortex
  • Motor deficits found more commonly in face and upper extremity than lower extremity
  • Dominant hemisphere involved: aphasia
    • Wernicke's aphasia (receptive aphasia) -> patient unable to process sensory input and don't understand verbal communication
    • Broca's aphasia (expressive aphasia) -> patient unable to communicate verbally, even though understanding may be intact
  • Nondominant hemisphere involved: dysarthria (motor deficit of the mouth and speech muscles; understanding intact) w/o aphasia, inattention and neglect side opposite to infarct
  • Contralateral homonymous hemianopsia
  • Gaze preference toward side of infarct
  • Agnosia (inability to recognize previously known subjects)

Posterior circulation

Signs and Symptoms:

Basilar artery

Signs and Symptoms:

  • Quadriplegia, coma, locked-in syndrome
  • "Crossed signs" in which a patient has unilateral cranial nerve deficits but contralateral hemiparesis and hemisensory loss suggest brainstem infarction
    • Millard-Gubler syndrome (ventral pontine syndrome) -- ipsilateral CN VI and VII palsy with contralateral hemiplegia of extremities
  • Sparing of vertical eye movements (CN III exits brainstem just above lesion)
    • Thus, may also have miosis b/l
  • One and a half syndrome (seen in a variety of brainstem infarctions)
    • "Half" - INO (internuclear ophthalmoplegia) in one direction
    • "One" - inability for conjugate gaze in other direction
    • Convergence and vertical EOM intact
  • Medial inferior pontine syndrome (paramedian basilar artery branch)
    • Ipsilateral conjugate gaze towards lesion (PPRF), nystagmus (CN VIII), ataxia, diplopia on lateral gaze (CN VI)
    • Contralateral face/arm/leg paralysis and decreased proprioception
  • Medial midpontine syndrome (paramedian midbasilar artery branch)
    • Ipsilateral ataxia
    • Contralateral face/arm/leg paralysis and decreased proprioception
  • Medial superior pontine syndrome (paramedian upper basilar artery branches)
    • Ipsilateral ataxia, INO, myoclonus of pharynx/vocal cords/face
    • Contralateral face/arm/leg paralysis and decreased proprioception

Superior Cerebellar Artery (SCA)

Posterior Cerebral Artery (PCA)

Signs and Symptoms:

  • Common after CPR, as occipital cortex is a watershed area
  • Unilateral headache (most common presenting complaint)
  • Visual field defects (contralateral homonymous hemianopsia, unilateral blindness)
  • Visual agnosia - can't recognize objects
  • Possible macular sparing if MCA unaffected
  • Motor function is typically minimally affected
  • Lateral midbrain syndrome (penetrating arteries from PCA)
    • Ipsilateral CN III - eye down and out, pupil dilated
    • Contralateral hemiataxia, tremor, hyperkinesis (red nucleus)
  • Medial midbrain syndrome (upper basilar and proximal PCA)
    • Ipsilateral CN III - eye down and out, pupil dilated
    • Contralateral paralysis of face, arm, leg (corticospinal)

Anterior Inferior Cerebellar Artery (AICA)

Posterior Inferior Cerebellar Artery (PICA)

Signs and Symptoms:

  • Lateral medullary/Wallenberg syndrome
  • Ipsilateral cerebellar signs, ipsilateral loss of pain/temperature of face, ipsilateral Horner syndrome, ipsilateral dysphagia and hoarseness, dysarthria, vertigo/nystagmus
  • Contralateral loss of pain/temp over body
  • Also caused by vertebral artery occlusion (most cases)

Internal Capsule and Lacunar Infarcts
  • May present with either lacunar c/l pure motor or c/l pure sensory (of face and body)[4]
    • Pure c/l motor - posterior limb of internal capsule infarct
    • Pure c/l sensory - thalamic infarct (Dejerine and Roussy syndrome)
  • C/l motor plus sensory if large enough
  • Clinically to cortical large ACA + MCA stroke - the following signs suggest cortical rather than internal capsule[5]:
    • Gaze preference
    • Visual field defects
    • Aphasia (dominant lesion, MCA)
    • Spatial neglect (non-dominant lesion)
  • Others
    • Ipsilateral ataxic hemiparesis, with legs worse than arms - posterior limb of internal capsule infarct
    • Dysarthria/Clumsy Hand Syndrome - basilar pons or anterior limb of internal capsule infarct

Anterior Spinal Artery (ASA)

Superior ASA
  • Medial medullary syndrome - displays alternating pattern of sidedness of symptoms below
  • Contralateral arm/leg weakness and proprioception/vibration
  • Tongue deviation towards lesion

Inferior ASA
  • ASA syndrome
  • Watershed area of hypoperfusion in T4-T8
  • Bilateral pain/temp loss in trunk and extremities (spinothalamic)
  • Bilateral weakness in trunk and extremities (corticospinal)
  • Preservation of dorsal columns

Differential Diagnosis

Stroke-like Symptoms

Weakness

Evaluation
Ischemic stroke with CT showing early signs of a middle cerebral artery stroke with loss of definition of the gyri and grey white boundary.
Hemorrhagic stroke (i.e. spontaneous intracranial hemorrhage).
Hemorrhagic stroke in the posterior fossa.
12-lead ECG of a patient with acute stroke, showing large deeply inverted T-waves.

Always obtain blood glucose, which is commonly overlooked (more embarrassing if you give tPA) Find out last known normal of affected deficit and write it down in chart

Stroke Work-Up
  • Labs
    • POC glucose
    • CBC
    • Chemistry
    • Coags
    • Troponin
    • T&S
  • ECG
    • In large ICH or stroke, may see deep TWI and prolong QT, occ ST changes
  • Head CT (non-contrast)
    • In ischemia stroke CT has sensitivity 42%, specificity 91%[6]
    • In acute ICH the sensitivity is 95-100%[7]
    • The goal of CTH is to identify stroke mimics (ICH, mass lesions, etc .)[8]
  • Also consider:
    • CTA brain and neck
      • To check for large vessel occlusion for potential thrombectomy
      • Determine if there is carotid stenosis that warrants endarterectomy urgently
    • Pregnancy test
    • CXR (if infection suspected)
    • UA (if infection suspected)
    • Utox (if ingestion suspected)

MR Imaging (for Rule-Out CVA or TIA)
  • MRI Brain with DWI, ADC (without contrast) AND
  • Cervical vascular imaging (ACEP Level B in patients with high short-term risk for stroke):[9]
    • MRA brain (without contrast) AND
    • MRA neck (without contrast)
      • May instead use Carotid CTA or US (Carotid US slightly less sensitive than MRA)[10] (ACEP Level C)

Large Vessel Occlusion - Thrombectomy
  • "Cortical strokes" of ICA, MCA, and some ACA occlusions are most likely to benefit from thrombectomy
  • CT perfusion study is the key factor in determining brain tissue salvageability from symptom onset to thrombectomy of 6-24 hours[11]
  • If CT perfusion unavailable, use ASPECT score[12]

VAN Score
  • NIHSS score ≥ 6 is nearly 100% sensitive for emergent large vessel occlusion, which may be amenable to thrombectomy[13]
  • VAN score is just as sensitive, but also may be more specific (~90%)
    • Weakness must be present, plus one or all of the VAN to be VAN positive
      • Weakness qualifying findings -- if no weakness, the pt is VAN negative
        • Mild (minor drift)
        • Moderate (severe drift—touches or nearly touches ground)
        • Severe (flaccid or no antigravity)
      • Visual disturbance qualifying findings
        • Field cut (which side) (4 quadrants)
        • Double vision (ask patient to look to right then left; evaluate for uneven eyes)
        • Blind new onset
      • Aphasia qualifying findings
        • Expressive (inability to speak or paraphasic errors); do not count slurring of words (repeat and name 2 objects)
        • Receptive (not understanding or following commands) (close eyes, make fist)
        • Mixed
      • Neglect qualifying findings
        • Forced gaze or inability to track to one side
        • Unable to feel both sides at the same time, or unable to identify own arm
        • Ignoring one side
    • If VAN positive, CT and CTA of the head should be ordered for consideration of thrombectomy plus/minus tPA

Management
  • Depends on type
    • Ischemic vs Hemorrhagic
    • Acute vs subacute vs old
    • Due to risk for hemorrhagic transformation, there is no role in acute completed stroke for:
      • Dual antiplatelet therapy (as opposed in select cases of TIA)
      • Anticoagulation, with or without atrial fibrillation

Disposition
  • Admit for acute or subacute stroke

See Also

References
  1. Itoh Y, Yamada M, Hayakawa M, Otomo E, Miyatake T. Cerebral amyloid angiopathy: a significant cause of cerebellar as well as lobar cerebral hemorrhage in the elderly. J Neurol Sci. 1993 Jun;116(2):135-41.
  2. Macdonell RA, Kalnins RM, Donnan GA. Cerebellar infarction: natural history, prognosis, and pathology. Stroke. 18 (5): 849-55.
  3. Lee H, Kim HA. Nystagmus in SCA territory cerebellar infarction: pattern and a possible mechanism. J Neurol Neurosurg Psychiatry. 2013 Apr;84(4):446-51.
  4. Rezaee A and Jones J et al. Lacunar stroke syndrome. Radiopaedia. http://radiopaedia.org/articles/lacunar-stroke-syndrome.
  5. Internal Capsule Stroke. Stanford Medicine Guide. http://stanfordmedicine25.stanford.edu/the25/ics.html
  6. Mullins ME, Schaefer PW, Sorensen AG, Halpern EF, Ay H, He J, Koroshetz WJ, Gonzalez RG. CT and conventional and diffusion-weighted MR imaging in acute stroke: study in 691 patients at presentation to the emergency department. Radiology. 2002 Aug;224(2):353-60.
  7. Suarez JI, Tarr RW, Selman WR. Aneurysmal subarachnoid hemorrhage. N Engl J Med. 2006; 354(4):387–396.
  8. Douglas VC, Johnston CM, Elkins J, et al. Head computed tomography findings predict short-term stroke risk after transient ischemic attack. Stroke. 2003;34:2894-2899.
  9. ACEP Clinical Policy: Suspected Transient Ischemic Attackfull text
  10. Nederkoorn PJ, Mali WP, Eikelboom BC, et al. Preoperative diagnosis of carotid artery stenosis. Accuracy of noninvasive testing. Stroke. 2002;33:2003-2008.
  11. Albers GW, Marks MP, Kemp S, et al. Thrombectomy for Stroke at 6 to 16 Hours with Selection by Perfusion Imaging. N Engl J Med. 2018;378(8):708-718.
  12. Barber PA, Demchuk AM, Zhang J, Buchan AM. Validity and reliability of a quantitative computed tomography score in predicting outcome of hyperacute stroke before thrombolytic therapy. ASPECTS Study Group. Alberta Stroke Programme Early CT Score. Lancet. 2000;355(9216):1670-4.
  13. Teleb MS, Ver Hage A, Carter J, et al Stroke vision, aphasia, neglect (VAN) assessment—a novel emergent large vessel occlusion screening tool: pilot study and comparison with current clinical severity indices Journal of NeuroInterventional Surgery 2017;9:122-126.
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