Ischemic Stroke - Neurology - Medbullets Step 1

Snapshot

A 60-year-old woman is immediately brought to the emergency department due to slurred speech and right arm and leg weakness. The patient was eating breakfast with her husband prior to developing these symptoms. Her husband denies his wife having any head trauma or recent surgeries. It has been one hour since her symptoms began. Medical history is significant for hypertension and type II diabetes mellitus. On physical exam, the patient can comprehend but speech is impaired. There is 0/5 strength in both right upper and lower extremities. Non-constrast computerized tomography (CT) of the head does not show any intracranial bleeds. After further evaluation, she was started on intravenous tPA.

Introduction

Clinical definition
- a sudden loss of blood supply to an area of the brain leading to
  - a neurologic deficit
    - the deficit depends on which area of the brain is affected
Epidemiology
- incidence
  - 3rd leading cause of death in the United States
- risk factors
  - hypertension
  - diabetes
  - smoking
  - atrial fibrillation
  - mechanical valves
  - valvular abnormalities
  - patent foramen ovale
  - significant decreased ejection fraction
  - hypercoagulable state
  - family history
  - prior history of
    - stroke
    - vascular disease
Pathogenesis
- ↓ blood supply to a region of the brain for enough time to result in infarcted (liquefactive necrosis) cerebral tissue
  - the most vulnerable to ischemic hypoxia is the
    - hippocampus
  - after 5 minutes, irreversible neuronal damage occurs
  - causes of this ↓ blood supply include
    - embolic infarction
      - a clot (typically) from one region of the body travels in the blood stream and occludes a vessel supplying the brain
      - consider in cases of sudden neurologic deficit
        
        maximal neurologic deficit occurs at onset
      - large vessel infarcts are commoly due to an embolism
    - thrombotic infarction
      - a clot is locally formed in the wall of the blood vessel usually
        
        where an atherosclerotic plaque is found
      - typically has a stuttering course

Large vs. Small Vessel Infarcts
Type	Comments
Large vessel	Occlusion of the major blood vessels such as the middle cerebral artery Occlusion is most often caused by emboli
Small vessel	Occlusion of the small penetrating arteries that supply the deep cerebral structures such as basal ganglia thalamus internal capsule Sometimes called lacunar infarcts

Ischemic Stroke Syndromes

Ischemic Stroke Syndromes
Anterior Circulation Stroke	Findings
Middle cerebral artery (MCA) stroke	Symptoms contralateral weakness and sensory loss in the face and upper limb hemineglect if the non-dominant hemisphere is involved aphasia Broca's aphasia if the superior division of the MCA is involved in the dominant hemisphere Wernicke's aphasia if the inferior division of the MCA is involved in the dominant hemisphere may also result in a right superior quadrant visual field defect Lesion localization motor and sensory cortices distributed by the MCA Wernicke's or Broca's area
Anterior cerebral artery (ACA) stroke	Symptoms contralateral weakness and sensory loss in the lower extremity Lesion localization motor and sensory cortices supplied by the ACA
Lenticulostriate artery stroke	Symptoms contralateral weakness and sensory loss in the face and body in the absence of cortical signs (e.g., neglect) Comments a common site of lacunar infarcts secondary to chronic hypertension leading to lipohyalinosis
Posterior Circulation Stroke	Findings
Medial medullary (Dejerine) syndrome	Secondary to occlusion of the paramedian branches of the anterior spinal artery and/or vertebral artery Symptoms triad ipsilateral hypoglossal palsy contralateral hemiparesis contralateral lemniscal sensory loss (e.g., proprioception) Lesion localization lateral corticospinal tract caudal medulla medial lemniscus
Lateral medullary (Wallenberg) syndrome	Secondary to occlusion of the posterior inferior cerebellar artery (PICA) or vertebral artery Symptoms dysphagia hoarsness ↓ gag reflex vertigo ↓ pain and temperature sensation of the ipsilateral face contralateral body Horner's syndrome ataxia Lesion localization lateral medulla involving the nucleus ambiguus vestibular nuclei lateral spinothalamic tract spinal trigeminal nucleus sympathetic fibers inferior cerebellar peduncle
Lateral pontine syndrome	Secondary to anterior inferior cerebellar artery Symptoms facial paralysis ↓ salivation, lacrimation, and taste from the anterior tongue (2/3rd) vertigo ↓ pain and temperature sensation of the ipsilateral face contralateral body ipsilateral Horner's ataxia Lesion localization Lateral pons involving the facial nucleus vestibular nuclei spinothalamic tract spinal trigeminal nucleus sympathetic fibers middle and inferior cerebellar peduncle
Locked-in syndrome	Secondary to occlusion of the basilar artery Symptoms quadraplegia bulbar manifestations able to perform vertical eye movements preserved conciousness Lesion localization ventral pons, lower midbrain, and medulla affecting the corticospinal and corticobulbar tracts oculomotor nerve nuclei paramedian pontine reticular formation
Posterior cerebral artery (PCA) occlusion	Symptoms contralateral hemianopsia with macular sparing Lesion localization occipital lobe

Presentation

Symptoms
- dependent on which area of the brain is involved
  - review chart above
Physical exam
- dependent on which area of the brain is involved
  - review chart above

Imaging

Computerized tomography (CT)
- indications
  - a non-contrast head CT should be performed in patients presenting with symptoms concerning for stroke and
    - to exclude intracerebral hemorrhage
  - CT angiography should be performed to assess for a thrombus and to evaluate the carotid and vertebral neck arteries
Magnetic resonance imaging (MRI)
- indications
  - MRI/MRA can aid in assessing infarct volume for further management

Studies

Labs
- complete blood count
- basal metabolic panel
- prothrombin time
- partial thromboplastin time
- cardiac enzymes
Histology

Histology
Time after Ischemic Event	Histologic findings
12-24 hours	Red neuron the cytoplasm is eosinophilic the nuclei is pyknotic cell body shrinkage loss of Nissl substance
1-3 days	Tissue necrosis Neutrophillic infiltration
3-5 days	Macrophage (microglial) infiltration
1-2 weeks	Reactive gliosis Vascular proliferation
> 2 weeks	Glial scar

Differential

Transient ischemic attack
- key distinguishing factors
  - no evidence of infarction on brain imaging
  - symptoms are transient and completely resolve after the event
  - major risk factor for ischemic stroke in the future
- treatment
  - lifestyle modification and medical treatment (aspirin, statins, antihypertensives, and glycemic control) to reduce future ischemic stroke risk
Hemorrhagic stroke

Treatment

Medical
- intravenous tPA
  - indication
    - used in patients presenting with
      - stroke symptoms, excluded to have an intracranial hemorrhage, and time since symptom onset is within the last 3-4.5 hours
Operative
- mechanical thrombectomy
  - indication
    - used in patients presenting with
      - stroke symptoms, excluded to have an intracerebral hemorrhage, and a proximal large artery occlusion involving the anterior circulation whether or not the patient received tPA
    - time since symptom onset within the last 8 hours

Complications

Intracerebral hemorrhage
Seizures
Aspiration pneumoniae