| Case 26 3/8/99 |
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| Case discussion A 65-year old female was brought to the emergency room by her daughter. While eating dinner with the family that evening the patient had suddenonset of "garbled" speech and appeared ‘confused’. Patient had a history of onset of atrial fibrillation two years ago that was found to be secondary to thyrotoxicosis. She had been started on propylthiouracil for this but this had been discontinued 6 months previously. She was not hypertensive or diabetic. She was not on any medication On examination the patient was awake. Heart rate was 120 and irregularly irregular. Blood pressure was 180/90. She was afebrile. She was verbose but her speech, though fluent was incoherent with several paraphasia. She did not appear to comprehend and failed to follow simple midline or appendicular commands. She could not repeat simple sentences such as “the boy ran away". She was unable to read or write. Visual fields were full to threat. Optic disks were sharp. Extraocular movments were full without nystagmus. Face was symmetric. Hearing was intact. Tongue movements were normal. Tone, bulk, and power were normal in all extremities. There was a mild right pronator drift. Sensory testing appeared intact and symmetric to pinprick. Finger to nose testing and gait were unremarkable. DTRs were 2+ and symmetric. Plantar reflexes were flexor. Pathologic Case Correlate: Neuropath Case 1 |
The 65 year old female patient, with a PMHx of atrial fibrillation secondary to thyrotoxicosis, complains of sudden onset garbled speech and confusion and presents with increased HR and high BP. Her cognitive function is primary affected, with incoherent speech, paraphrasia, and difficulties with comprehension, commands, repetition, reading and writing. Her sensory, motor, cerebellar, vestibular and CN functions appear intact, and her last medication taken 6 months ago was propylthiouracil. summary is too long Central nervous system - left hemisphere, notably involving Wernike's Area at the posterior superior temporal lobe and the motor area in the parietal precentral gyrus. good The acute onset suggests vascular, trauma or infectious etiology. good
Vascular ischemic event: embolism, secondary to atrial fibrillation and
intracardiac thrombus, in the MCA territory. good
MRI - pathological changes due to ischemia good another stroke, death, brain damage, loss of language, edema and increased ICP, hemorrhage, hypoventilation, pneumonia, DVT, PE, UTI, skin ulcer, depression good Decreased cerebral blood flow leads to an increase in pH, NO, CO2, O2 and glc extraction. The dendrites and axons are most vulnerable. Lack of ATP leads to failure of the cell pump, allowing K+ to leak out and Na+, Ca2+, and Cl- to leak in. Fluid follows the ions into the cell, resulting in cellular edema. The cell accumulates glutamate, Ca2+, enzymes and free radicals. Electrical failure, cell necrosis, extracellular edema and hemorrhage ensue. Restoring flow with antithrombic therapy is crucial in returning O2 and energy to the cells as soon as possible. Neurotransmitter antagonists, Ca blockers, NO blockers, proteolysis blockers, prostaglandin blockers, and anti-leukocyte and anti-adhesion treatments aim to reduce cellular damage and necrosis. Anti-coagulant therapy and risk factor reduction aim to reduce the risk of future embolism, while physical therapy improves function lost from the neuron cell death. Anti-arrythmic drugs to treat the atrial fibrillation will reduce the risk of a future intracardiac thrombus and resultant embolism. importance of maintaining cerebral perfusion pressure by keeping BP elevated (up to 220/120) and correcting hyperglycemia (hyperglycemia is a mitochondrial toxin); otherwise very good |
This is a 65-year-old woman with a history of atrial fibrillation with sudden onset of receptive aphasia and incoherent, fluent speech with normal hearing, and absence of motor or sensory changes. good inferior division of MCA, temporoparietal cortex (Wernicke’s aphasia indicates cortical involvement) good; you need to define what wernicke#146;s aphasia is. The sudden onset is consistent with trauma or a vascular lesion. good
Stroke due to cardiac embolus lodged in inferior division of MCA. good
* CT: determine extent of damage, edema, and assess for hemorrhage before
thrombolytics are administered. Infarct will appear as hypodense lesion in
vascular territory after 12-24hrs good
* brain edema and mass effect: CT good The sudden onset is consistent with an embolic cause of ischemia of parts of temporoparietal cortex. Management should be geared toward minimizing the duration of ischemia by giving thrombolytics to resolve the clot as soon as possible. In addition, the blood pressure should be maintained to maximize blood flow to the areas of the brain which are ischemic but have not yet necrosed, the penumbra region. Additionally, the patient should be anticoagulated to prevent further clotting, and her heart condition should be corrected in order to prevent further embolization. good |
A 65 year old woman with a history of atrial fibrillation secondary to thyrotoxicosis presented in the emergency room with sudden onset of garbled speech and confusion. Her heart rate was 120 and irregularly irregular, her blood pressure was 180/90, and she was experiencing paraphasias, apraxia, and right sided upper motor weakness. Sensory function and deep tendon reflexes are in tact. good; also likely poor comprehension misinterpreted as confusion 2) Lesion localized to CNS.
Problem list: good; what features of the language exam make it likely to be Wernicke's? (poor comprehension, poor repetition, paraphasias, fluent speech) Because this case is so acute, the cause is likely a vascular phenomenon leading to an ischemic attack. Other possibilities include trauma or infection. good Cardiogenic emboli in left middle cerebral artery secondary to atrial fibrillation secondary to thyrotoxicosis. The differential diagnosis includes intracerebral hemorrhage, aneurysm, or thrombotic stroke. good CT scan to rule out hemorrhage, echocardiogram of heart to visualize thrombus from atrial fibrillation. ok; rather than a ct scan to rule out hemorrhage I would say that ct evidence of a primary hemorrhagic stroke would refute the hypothesis that the patient had an embolic event. Recurrent stroke due to thrombus in left atrium, hemorrhage due to HTN if thrombolytic given as treatment, total right sided paralysis, permanent Wernicke’s aphasia good Pathophysiology related to management: Decreased cerebral blood flow due to a cardiogenic embolism leads to hypoxia and ischemia of temporal and parietal regions supplied by the left middle cerebral artery. Anoxia in these tissues leads to edema, which impairs connections between neurons and ultimately leads to tissue necrosis. It is therefore important to maintain blood pressure and correct hyperglycemia (a mitochondrial toxin) in this patient to preserve as much of the penumbrum as possible. Thrombolytic therapy within the first three hours should be considered to restore flow of O2 if this patient has no cerebral hemorrhage. However, due to her increased blood pressure, hemorrhage is a risk of treatment. Her embolus is most likely due to a thrombus in her left atrium due to atrial fibrillation resulting from her thyrotoxicosis. Therefore, we must treat the underlying thryrotoxicosis and atrial fibrillation, as well as consider anti-coagulant therapy to eliminate the clot in the atrium to minimize the risk of future emboli. good |