Classification of Stroke Based on Arterial Distribution - PowerPoint PPT Presentation

About This Presentation
Title:

Classification of Stroke Based on Arterial Distribution

Description:

For educational purposes only. – PowerPoint PPT presentation

Number of Views:31
Updated: 6 November 2021
Slides: 29
Provided by: EdinenAsuka
Tags:

less

Transcript and Presenter's Notes

Title: Classification of Stroke Based on Arterial Distribution


1
Classification of Stroke based on Arterial
distribution.
  • By
  • Dr. Edinen Santhus Asuka

2
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.

3
Types of stroke
  • Stroke can be ischemic (most common) or
    hemorrhagic.
  • Ischemic sources
  • Thrombosis
  • Embolism
  • Cerebral hypoperfusion

4
Types of stroke contd.
  • Hemorrhagic stroke
  • Intracerebral hemorrhage
  • Subarachnoid hemorrhage

5
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.

6
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.

7
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

8
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.

9
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.

10
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.

11
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.

12
  • 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.

13
  • 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.

14
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.

15
  • 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

16
  • 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.

17
  • 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)

18
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.

19
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.

20
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

21
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)

22
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)

23
Acute spinal cord ischemia syndromes
  • Anterior spinal artery syndrome
  • Posterior spinal artery syndrome
  • Sulcal artery syndrome (Partial or Hemi-Brown
    sequard syndrome)

24
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.

25
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)

26
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.

27
Differentials
  • CNS tumors
  • Subdural hemorrhage
  • Seizure (Todds paralysis)
  • Hyperglycemia
  • Hypoglycemia
  • Cerebral abscess
  • Multiple Sclerosis
  • Meningitis
  • Migraine
  • Substance intoxication

28
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
User Comments (0)
About PowerShow.com