Classification of Stroke Based on Arterial Distribution

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Classification of Stroke based on Arterial
distribution.

• By
• Dr. Edinen Santhus Asuka

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Introduction

• According to data provided by World Health
  Organization, stroke was shown to be the second
  most common cause of death worldwide in 2019 and
  is predominant even in developing countries. It
  accounted for about 11 of total deaths recorded.
• Stroke is simply an acute neurological deficit
  due to poor blood supply to the brain tissues.
  Confirmation of infarct can be done through
  imaging (Cranial CT scan and/or MRI). It is also
  termed as Cerebrovascular Accident.
• Transient ischemic attack is a brief, reversible
  episode of neurologic deficit without evidence of
  acute infarction on imaging. Most resolve within
  15 minutes of onset. Several risk factors have
  been linked to stroke, some of which are
  non-modifiable such as age, sex, race, and
  genetics while some are modifiable like
  hypertension, dyslipidemia, smoking and the rest
  not mentioned here.
• It is diagnosed clinically and confirmed with the
  use of imaging modalities such as Cranial CT-scan
  and MRI.

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Types of stroke

• Stroke can be ischemic (most common) or
  hemorrhagic.
• Ischemic sources
• Thrombosis
• Embolism
• Cerebral hypoperfusion

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Types of stroke contd.

• Hemorrhagic stroke
• Intracerebral hemorrhage
• Subarachnoid hemorrhage

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Cellular changes in stroke (Pathophysiology)

• Decreased blood perfusion of brain tissues leads
  to a dysfunction in Sodium-potassium ATP pump
  thereby causing the accumulation of sodium within
  cells. Water entry into the cells occurs, cell
  swelling and brain edema with increased
  intracranial pressure subsequently ensues leading
  to decreased cerebral blood flow. Due to sodium
  accumulation within the cells, increased
  excitotoxicity occurs via continual
  depolarization of cells. Influx of calcium takes
  place leading to necrosis and inflammation of
  cells.
• Cells with cerebral blood flow of lt10ml/100g of
  tissue/min tend to die within minutes of a
  Cerebrovascular accident or are irrevocably prone
  to undergo infarction. This part is termed the
  Infarct core.
• Otherwise, cells with cerebral blood of
  lt25ml/100g of tissue/min are salvageable if
  reperfusion occurs. This part is known as the
  ischemic Penumbra.

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Timeline of ischemic event in stroke

• It is pertinent to note that irreversible
  neuronal injury occurs after 5 minutes of
  hypoxia, with the most vulnerable tissues being
  the Hippocampus, Neocortex, purkinje cells of the
  cerebellum, and the watershed areas (regions of
  the brain bordering vascular territories supplied
  by the distal branches of cerebral arteries).
• 12-24 hours Eosinophilic cytoplasm and pyknosis
  of the cell nuclei
• 24-72 hours Necrosis and neutrophil infiltration
• 3-5 days Macrophage (microglia) infiltration
• 1-2 weeks Reactive gliosis via Astrocytes with
  vascular proliferation
• gt2 weeks Glial scar formation.

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Division of Neural pathways (Tracts)

• Ascending tracts
• Spinothalamic tracts (Anterior and lateral)
• Dorsal column medial lemniscus tract
• Spinocerebellar tracts (Anterior, posterior,
  cuneocerebellar and Rostral cerebellar)
• Spino-Olivary tract
• Descending tracts
• Corticospinal tracts (Anterior and lateral)
• Corticobulbar tract
• Rubrospinal tract
• Reticulospinal tract
• Vestibulospinal tract
• Olivo-spinal tract

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Clinical presentation based on Arterial
distribution

• Anterior Cerebral artery infarct
• Area of lesion Motor and sensory cortices-
  affecting the lower limb.
• Clinical presentation Contralateral paralysis
  and sensory loss of the lower limb with urinary
  incontinence.
• Middle cerebral artery infarct
• Area of lesion Motor and sensory cortices-
  affecting the upper limb Temporal lobe- Wernicke
  area (Receptive aphasia), and Frontal lobe- Broca
  area (Expressive aphasia).
• Clinical presentation Contralateral paralysis
  and sensory deficit of the upper limb and face,
  Aphasia (Expressive and/or Receptive), Right
  superior quadrantanopia due to involvement of the
  temporal lobe (ventral optic radiation), and Left
  Hemineglect if Non-dominant hemisphere (Right
  hemisphere-specifically right parietal lobe) is
  affected.
• Gerstmann syndrome presenting as agraphia,
  acalculia, finger agnosia and left-right
  disorientation when left parietal lobe (Dominant
  hemisphere) is affected.

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Lacunar infarcts (Lenticulostriate artery,
thalamoperforating arteries, and recurrent
artery of heubner, a branch of anterior cerebral
artery)

• Commonly, lacunar infarcts occur due to
  lipohyalinosis and microatheroma of small
  perforating arteries that supply deep brain
  structures.
• Area of lesion Striatum, internal capsule,
  thalamus, basis pontis, corona radiata and Globus
  pallidus.
• Clinical presentation Cortical signs like
  neglect, aphasia, and visual field defects are
  usually absent.
• Can present as
• pure motor deficit/hemiparesis on contralateral
  side-face, arm and leg (More common as compared
  to other types).
• Ataxic hemiparesis- contralateral cerebellar and
  pyramidal hemiparesis (with crural paresis more
  prominent than the hand and arm involvement).
• Pure sensory deficit on the contralateral side
  (face, arm and leg). In Dejerine-Roussy syndrome
  patient experiences contralateral dysesthesia
  weeks to months after thalamic infarct.
• Dysarthria-clumsy hand syndrome- contralateral
  hand clumsiness more noticeable when writing and
  dysarthria.
• Mixed sensory and motor deficit.

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Anterior choroid artery infarct

• Area of lesion Anterior choroidal artery
  territory as it has some anastomosis with deep
  perforating branches of the middle cerebral,
  posterior communicating and posterior cerebral
  artery.
• Clinical presentation Contralateral motor loss,
  Contralateral sensory loss with or without
  contralateral hemianopia.

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Posterior cerebral artery infarct

• Area of lesion occipital lobe
• Clinical presentation Contralateral hemianopia
  with macular sparing.
• Alexia without agraphia if on dominant hemisphere
  versus Prosopagnosia if on Non-dominant
  hemisphere.
• Associated syndromes
• Anton-Babinski syndrome Bilateral cortical
  blindness with visual anosognosia and visual
  confabulation.
• Riddoch syndrome Perception of light and objects
  in motion preserved with the hemianopic field.
• Dide-Botcazo syndrome Features of Anton-Babinski
  with memory impairment.
• Balint syndrome A constellation of
  simultagnosia, oculomotor apraxia, and optic
  ataxia.

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• Top of Basilar artery syndrome
• Area of lesion Bilateral thalamic infarction due
  to occlusion of the blood flow through the
  perforating arteries.
• -Occurs secondary to thromboembolic occlusion of
  the top of the basilar artery.
• Clinical presentation Visual and occulomotor
  nerve deficits, behavioural disturbances,
  hallucinations with absence of motor deficits.
• Artery of percheron infarct
• Solitary arterial trunk supply to the paramedian
  thalami and rostral midbrain bilaterally.
• Area of lesion Paramedian thalamic regions and
  rostral midbrain.
• Clinical presentation (Paramedian thalamic
  syndrome) Vertical conjugate gaze palsy, Altered
  mental status, memory impairment with rostal
  midbrain infarct signs such as contralateral
  hemiparesis, contralateral cerebellar ataxia, and
  occulomotor nerve deficit.

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• Superior cerebellar artery infarct
• Areas affected Superior cerebellar hemispheres,
  cerebellar vermis and parts of the midbrain.
• Clinical presentation Ipsilateral cerebellar
  signs and occasionally Horners syndrome.

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Posterior cerebral artery infarcts affecting the
midbrain

• -Usually occurs due to occlusion of the
  penetrating branches of the posterior cerebral
  artery.
• Weber syndrome
• Areas affected cerebral peduncle, ipsilateral
  fascicles of CN III with/without substantia
  nigra.
• Ipsilateral CN III palsy (Oculomotor nerve)
• diplopia
• ptosis 
• afferent pupillary defect
• Contralateral hemiplegia or hemiparesis
• involvement of the corticospinal and/or
  corticobulbar tract
• contralateral parkinsonian rigidity when
  substantia nigra is involved.

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• Benedikt syndrome
• Area of lesion Cerebral peduncle, superior
  cerebellar peduncle, CN III, Red nucleus, Medial
  longitudinal fasciculus, Edinger-Westphal
  Nucleus, substantia nigra.
• Clinical presentation
• Ipsilateral oculomotor nerve palsy with loss of
  visual accommodation.
• Contralateral hemiparesis
• Contralateral cerebellar ataxia and/or Holmes
  tremor and/or choreoathetosis.
• Internuclear ophthalmoplegia
• Contralateral parkinsonism

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• Claude syndrome
• Areas affected Red nucleus, Superior cerebellar
  peduncle, and CN III.
• Clinical presentation Ipsilateral oculomotor
  nerve palsy and contralateral upper and lower
  limb ataxia.
• Claude syndrome tend to have more ataxic
  manifestation than Benedikt while Benedikt tend
  to produce more tremors and chereoathetosis.

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• Nothnagel syndrome
• Areas affected Tectum (quadrigeminal plate),
  superior cerebellar peduncle and CNIII fascicles.
• Clinical presentation Ipsilateral CN III palsy
  and contralateral cerebellar ataxia.
• Parinauds syndrome
• Areas affected Midbrain tectum, Edinger-westphal
  nuclei, Adjacent CNIII, and the vertical
  conjugate gaze center in the Rostral interstitial
  nucleus of the Medial longitudinal fasciculus.
  Can also occur due to compression by tumors such
  as pinealoma.
• Clinical presentation vertical conjugate gaze
  palsy, sun-setting of the eyes,
  Convergence-retraction nystagmus, colliers sign
  (lid retraction)

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Basilar artery infarct

• Areas affected Pons, medulla, lower midbrain,
  crticospinal tracts, corticobulbar tracts, CN VI
  nucleus, Paramedian pontine reticular formation,
  Reticular activating system (RAS) and medial
  lemniscus.
• Clinical presentation Ipsilateral CN VI deficit,
  loss of horizontal conjugate gaze (vertical gaze
  preserved), quadriplegia, loss of tongue, facial,
  and mouth movement.

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Anterior inferior cerebellar artery infarct

• Areas affected Facial nucleus, vestibular nucei,
  spinthalamic tract, spinal trigeminal
  nucleus-motor and sensory, sympathetic fibers,
  middle and inferior cerebellar peduncles, and the
  labyrinthine artery.
• Clinical presentation ipsilateral vertigo and
  sensorineural hearing loss, ipsilateral horner
  syndrome, ipsilateral ataxia and dysmetria,
  decreased lacrimation and salivation (Facial
  nerve supplies the submandibular and sublingual
  salivary glands), decreased taste from anterior
  2/3 of the tongue, contralateral decrease in pain
  and temperature sensation, Ipsilateral facial
  paresis.

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Stroke syndromes associated with pontine
infarction

• Brissaud-Sicard syndrome
• Facial colliculus syndrome
• Marie-Foix syndrome
• Gasperini syndrome
• Foville syndrome
• Locked-in-syndrome
• Millard-Gubler syndrome
• Raymond-cestan syndrome
• Grenet syndrome
• Gelle syndrome

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Posterior inferior cerebellar artery infarct

• Areas affected Nucleus ambigus (CN IX, X and
  XI)-motor components, vestibular nuclei, lateral
  spinothalamic tract, spinal trigeminal nucleus,
  sympathetic fibers, inferior cerebellar peduncle.
• Clinical presentation Dysphagia, hoarseness,
  decreased gag reflex, hiccups, vertigo,
  nystagmus, ipsilateral horner syndrome,
  ipsilateral loss of sensation on the face,
  ipsilateral ataxia and dysmetria, contralateral
  decrease in pain and temperature sensation on the
  body.
• Associated syndromes
• Wallenberg syndrome (Lateral medullary syndrome)
• Babinski-Nageotte syndrome
• Reinhold syndrome (Hemimedullary syndrome)

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Anterior spinal artery infarct

• Areas affected Corticospinal tract, Medial
  lemniscus, Hypoglossal nerve.
• Clinical presentation Ipsilateral hypoglossal
  nerve palsy, contralateral hemiparesis and
  contralateral decrease in proprioception.
• Associated syndromes
• Jackson stroke syndrome ( Medial medullary
  syndrome without medial lemniscus involvement)
• Dejerine syndrome (Medial medullary syndrome with
  medial lemniscus involvement)

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Acute spinal cord ischemia syndromes

• Anterior spinal artery syndrome
• Posterior spinal artery syndrome
• Sulcal artery syndrome (Partial or Hemi-Brown
  sequard syndrome)

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Investigations

• Non-contrast cranial CT-scan and/or MRI/
  CT-angiogram when indicated. Cranial CT-scan can
  detect ischemic changes in 6-24 hours while
  Diffusion-weighted MRI can detect similar changes
  in 3-30 minutes.
• Full blood count and/or urgent PCV
• ECG
• Transthoracic echocardiography in patients with
  suspected structural heart abnormalities like
  dilated cardiomyopathy, valvular defects and
  ventricular aneurysm which may serve as a source
  of embolism.
• Random blood sugar and fasting blood sugar.
• Fasting lipid profile
• Electrolyte, Urea, creatinine.
• Swallow assessment
• Lumbar puncture if infectious process need to be
  ruled out or is Subarachnoid hemorrhage is highly
  suspected and Cranial CT scan is negative.

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Complications

• Decubitus ulcer
• Deep venous thrombosis
• Pulmonary embolism
• Cerebral salt wasting
• Aspiration pneumonitis
• Pneumonia
• Limb contractures
• Depression
• Joint pains
• Constipation
• Vascular dementia
• Recurrent seizures
• Urinary and fecal incontinence
• Urinary tract infection (prolonged
  catheterization)

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Brief summary on treatment

• Blood pressure control
• tPA if within 3-4.5 hours of onset and patient is
  not at risk of hemorrhage or hemorrhagic stroke
  is excluded.
• Lipid-lowering medications such as statins.
• Anti-oxidants like vitamin A and Vitamin E.
• Blood sugar control with anti-glycemic agents.
• ASA if hemorrhagic stroke is excluded and
  ischemic stroke is confirmed.
• Sc clexane if hemorrhagic stroke is excluded.
• Tabs Nimodipine (neuroprotective) to prevent
  vasospasm.
• Compression stockings
• Carotid endarterectomy if indicated.
• I.V mannitol when indicated and in the absence of
  contraindications (Anuria).
• Endovascular treatment if available.
• Hemicraniectomy as a temporary option for
  malignant cerebral infarction with significant
  brain swelling.
• NG-tube feeding till patient can tolerate orally.
• Speech therapy
• Physical and occupational therapy
• Treatment of co-morbid cardiac conditions such as
  valvular defects, atrial fibrillation, dilated
  cardiomyopathy and Patent foramen ovale.

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Differentials

• CNS tumors
• Subdural hemorrhage
• Seizure (Todds paralysis)
• Hyperglycemia
• Hypoglycemia
• Cerebral abscess
• Multiple Sclerosis
• Meningitis
• Migraine
• Substance intoxication

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References

• Mastering the Boards- Neurology
• Radiopedia website- https//radiopaedia.org/articl
  es/stroke
• Clinical Neuroanatomy by Richard S. Snell 7th
  Edition
• First aid for USMLE step 1-2020 edition
• Wikipedia

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