Case Vignettes in Neurology

PATIENT CASE STUDIES

Case 25 3/8/99 Cerebrovascular disease
Case discussion This 60 year old male with a history of hypertension for many years, suffered a stroke two years previously that had caused a sudden onset of left sided weakness that had progressed over a few hours. H subsequently recovered well and was left with only moderate residual weakness. Three months previously he developed further weakness of the left side beginning in the leg, progressing to his arm and eventually involving the left side of the face. He recovered slowly and incompletely but was able to walk with a cane upon discharge. On the day of the present admission, the patient arose from a nap, appeared confused and fell to the floor. He was taken to the hospital where he had a seizure on arrival. On admission the blood pressure was 180/105. He was unresponsive to verbal commands and responded to pain by movement of the left arm only. There was increased tone of the left with an extensor plantar reflex. The pupils were equal but miotic. Ophthalmoscopic examination showed no papilledema. Serum glucose was 320 mg/dl.
Summarize the Case in 1-2 sentences. Pt is a 60 yo male is brought to the ER following acute onset of confusion and unconsiousness. He was unresponsive to verbal commands showed increased tone and extensor plantar reflex on left. PMH is positive for stroke 2 yrs ago wth residual left sided weakness which worsened 3 months ago. spell out what the stroke was 2 yrs ago and 3 mos ago (eg prior strokes with a left hemiparesis 2 years ago and a new left hemiparesis 3 months previously, now with a new right hemiparesis); also hypertensive, hyperglycemic Discuss lesion localization on the basis of the physical examination. Motor: seizure -- cortex L side incr tone, extensor plantar reflex -- SC, cortex, brainstem Pupils equal but miotic -- CN III, brainstem (midbrain) , cortex not moving right side Sensory: not given Cognitive: confusion PMH: positive for HTN prev hx of stroke 2 yrs ago with sudden onset L sided weakness. 3 mo ago further weakness of L side Based on the pt's signs and symptoms, the lesion can be localized to a large area of the cerebral cortex on the R side, probably due to a block in the R internal carotid. pmh does not belong in this section; however you should try to localize the old physical signs eg left hemiparesis; lesion right corticospinal tracts above mid pons if face was invovled. Discuss underlying pathogenesis on the basis of clinical course. This patients disorder is acute in onset and the time course suggests a vascular or trauma etiology. good Indicate one likely clinical diagnosis. List (or classify) alternative diagnoses. Thrombosis of large cerebral vessel for which event? you need to develop a hypothesis for each event! Alternative Diagnoses: Hemorrhagic stroke (intracerebral or subarachnoid) Embolus to large cerebral vessel Indicate 2 ancillary tests that would assist in confirming or refuting the clinical diagnosis. Indicate the test results that would confirm the clinical diagnosis. MRI: pathological changes due to ischemia. Ultrasound: to detect stenosis, plaques or occlusion of the carotid artery. good; note seizures at onset suggests embolism Indicate complications of the disease and ancillary tests that would help evaluate them. Another stroke, brain damage, loss of motor or sensory function, loss of speech, herniation of brain due to increased ICP. good Discuss how the underlying pathophysiology is relevant in the management of this patient. 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 intracellular 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. It is importance to maintainin cerebral perfusion pressure by keeping BP elevated (up to 220/120) and correcting hyperglycemia (a mitochondrial toxin). very good; if you deem the cause to be embolic than anticoagulation to prevent further embolization. Another Version: >br>
Summarize the Case in 1-2 sentences. This 60 y/o male with a history of long-standing hypertension and questionable diabetes presents with progressively altered state of consciousness from confusion to coma, and a seizure. He has a blood pressure of 108/105 mmHg, apparent right sided and left leg paralysis, left sided hypertonia with Babinski sign, bilateral miosis but no papilledema, and serum glucose of 320 mg/dl. In the last 2 years, the patient has had 2 episodes of progressive left sided weakness which has resolved incompletely. good; weakness is worse on the right; left sided weakness may be recent or from prior weakness Discuss lesion localization on the basis of the physical examination. The most likely location of the lesion is the base of pons because a lesion there would disrupt: - the reticular activating system which is resposible for maintaining consciousness (symptoms: altered state of consciousness - confusion, coma) - the cortical spinal tracts which mediate motor activity ( symptoms: contralateral paralysis) - the desending sympathetic pathways which control pupillary dilatation (symptoms: ipsilateral miosis) The lesion would be in the base of pons bilaterally because the patient has the symptoms mentioned above bilaterally. In addition, stroke in the pons is common in the setting of hypertension and diabetes. The upper motor neuron syndrome present on the left side is most likely resulted from the last stroke in the base of the pons on the right (symptoms: pure left sided motor weakness). The time course is too short for the right side to develop symptoms of upper motor neuron syndrome. good Discuss underlying pathogenesis on the basis of clinical course. Acute, progressive (over a few hours) time course suggests a vascular lesion of either lacunar infarction or intraparenchymal hemorrhage. Because of no papilledema, lacunar infarction is a more likely underlying pathogenesis good; note that the question does not ask you what the likely pathogenesis is on the basis of the physical signs or presentation, rather it asks what is the likely pathogenesis is on the basis of the time course. infarct or hemorrhage are two possibilities (also note hemorrhage does not necessarily have to cause raised icp, for instance if it happens in the pons) Indicate one likely clinical diagnosis. List (or classify) alternative diagnoses. Dx: thrombosis of pontine blood vessels bilaterally DDx: pontine hemorrhage seizure disorder diabetic acidosis good; the scenario for the likely cause of your principal hypothesis would be basilar artery occlusion Indicate 2 ancillary tests that would assist in confirming or refuting the clinical diagnosis. Indicate the test results that would confirm the clinical diagnosis. CT scan of the head woud help rule out (or rule in) a pontine hemorrhage Serial EEG would help differentiate a seizure disorder from a pontine stroke. Blood pH would decrease and blood ketones would increase in the case of diabetic acidosis. try to stay clear of the expressions rule in or rule out; what you are actually doing is confirming or refuting your principal hypothesis. Indicate complications of the disease and ancillary tests that would help evaluate them. Expansion of the infarcted area to cause greater damage to the brain Recurrent strokes ok Discuss how the underlying pathophysiology is relevant in the management of this patient. Treatment: Reverse occlusion with thrombolysis therapy Salvage the penumbra (minimize the infarcted area) by: Maintain BP high to maximize collateral flow Prevent systemic hypoxia, acidosis, hyper or hypoglycemia Prevent recurrences by controlling hypertension and diabetes the reason to maintain the high BP is also to maintain the cerebral perfusion pressure (systemic BP - ICP); your answer is scanty on the pathophysiology (note the question is how does understanding the pathophysiology allow you to manage the patient); pathophysiology is covered well in Collins CVA chapter.