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 Specifically, CA1 pyramidal neurons of 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 thedominant 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 Ischemic Stroke Syndromes Posterior Circulation Stroke Findings Medial medullary (Dejerine) syndrome Secondary to occlusion of the paramedian branches of the anterior spinal artery and/orvertebral 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 consciousness 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 Weber syndrome Secondary to occlusion of the peduncular perforating branches of the posterior cerebral artery Symptoms ipsilateral ptosis ipsilateral oculomotor palsy contralateral hemiparesis Lesion localization ventral midbrain involving the cerebral peduncles that contain the corticospinal and corticobulbar tracts oculomotor fibers 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