Snapshot A 55-year-old man presents to the emergency department for difficulty with speech and weakness in the right upper extremity. He was last known to be neurologically normal 2 hours prior to presentation. He has a medical history of atrial fibrillation, hypertension, hyperlipidemia, and type 2 diabetes mellitus. He smokes approximately 1 pack of cigarettes daily for the past 15 years. Physical examination is notable for 2/5 power in the right upper extremity and word finding difficulty. A non-contrast head CT is performed, which does not demonstrate an intracranial hemorrhage. He is immediately started on alteplase. Introduction 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 significantly 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 the onset large vessel infarcts are commonly 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 byemboli 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 Presentation 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 pure, unilateral motor weakness face and body in the absence of cortical signs (e.g., neglect) pronator drift pure, unilateral sensory weakness ataxic hemiparesis dysarthria-clumsy hand syndrome proprioception remains intact (e.g., normal Romberg test). Comments branch arteries originating directly from larger arteries a common site of lacunar infarcts secondary to chronic hypertension Ischemic Stroke Syndromes 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 hoarseness ↓ 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 Paramedian midbrain (Benedikt) syndrome Symptoms Ipsilateral CN III palsy, contralateral hemiataxia, tremor/choreoathesois, hemiparesis Lesion localization Paramedian midbrain affecting the midbrain tegmentum, red nucleus, superior cerebellar penducle, and corticospinal tract 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 Echocardiography indications evaluates evidence of an intracardiac shunt or ventricular thrombus Studies Labs fingerstick blood glucose should be performed immediately in all suspected stroke patients complete blood count basal metabolic panel prothrombin time partial thromboplastin time cardiac enzymes Histology History the NIH stroke scale stratifies these patients level of consciousness ask month and age follows commands (blink eye and squeeze hands) horizontal eye movements visual fields facial palsy left arm motor drift right arm motor drift left leg motor drift right leg motor drift limb ataxia sensation language/aphasia dysarthria extinction/inattention Histology Time after Ischemic Event Histologic findings 12-24 hours Red neuron cytoplasm is eosinophilic nuclei are pyknotic cell body shrinkage loss of Nissl substance 1-3 days Tissue necrosis Neutrophilic infiltration 3-5 days Tissue necrosis Neutrophilic infiltration 1-2 weeks Reactive gliosis Vascular proliferation > 2 weeks Glial scar Differential Hemorrhagic stroke differentiating factor hyperdense lesion in a non-contrast head CT Transient ischemic attack differentiating factor normal MRI brain Posterior reversible encephalopathy syndrome (PRES) differentiating factor hypertension that can lead to confusion, visual changes, and seizures MRI demonstrating cerebral edema in the posterior hemispheres 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 contraindications history of stroke/head trauma in the past 3 months history of intracranial hemorrhage major surgery in the past 14 days GI or urinary tract bleeding in the past 21 days myocardial infarction in the previous 3 months arterial puncture at a non-compressible site in past 7 days resolving stroke symptoms very minor and isolated neurological symptoms seizure at the onset of stroke persistent hypertension SBP > 185 mmHg or DBP > 110 mmHg use of direct thrombin inhibitors (such as dabigatran or argatroban) use of factor Xa inhibitors (such as rivaroxaban or apixaban) active bleeding or acute trauma with fractures platelets < 100,000, serum glucose < 50 mg/dL or > 400 mg/dL INR > 1.7 or PT > 15 seconds if on warfarin elevated PTT if on heparin head CT showing hemorrhage or multilobular infarction > 33% of a cerebral hemisphere intracranial neoplasm, arteriovenous malformation, or aneurysm non-tPA candidate medical management aspirin statin clopidogrel blood pressure control most important management for hypertensive strokes and vascular dementia Operative mechanical thrombectomy indication in proximal large artery occlusion involving the anterior circulation whether or not the patient received tPA Complications Intracerebral hemorrhage Seizures Aspiration pneumonia Central post-stroke pain