Week 31: Neuro Part 1

The correct answer is immediate reversal of the anticoagulation (whether with fresh frozen plasma, prothrombin complex concentrate, recombinant factor VIIa). High dose vitamin K intravenously should be administered, however its reversal mechanism takes approximately 12 to 24 hours, during which time the intracerebral hemorrhage may continue to enlarge. Plasma, prothrombin complex concentrate, or recombinant factor VIIa are more appropriate choices for immediate reversal of warfarin’s anticoagulant action. Protamine sulfate is the reversal agent for heparin, not coumadin. The 2010 AHA/ASA guidelines recommend against the use of prophylactic antiepileptic drugs. However, if a seizure occurs, then antiepileptic drugs would be appropriate to administer, in order to prevent recurrent seizures.

Transient ischemic attack is defined as a transient neurologic deficit that has complete resolution within 24 hours. The ABCD2 score can be used to predict likelihood of subsequent stroke within 2 days. Low risk patients (scores of 0-3) may be discharged home if they have reliable follow-up within two days, whereas moderate risk (4-5 points) and high risk (6-7 points) patients should be admitted for echocardiography, carotid dopplers, and likely carotid endarterectomy.

The scoring system is as follows:

Age of 60 years or greater = 1 point
Initial SBP of 140 or greater OR DBP of 90 or greater = 1 point
Clinical features (Unilateral weakness = 2 points; Speech disturbance without weakness = 1 point; Other symptoms = 0 points)
Duration of symptoms (<10 minutes = 0 points; 10-59 minutes = 1 point; 60 minutes or greater = 2 points)
History of diabetes = 1 point

This patient’s score = 4. He receives 1 point for age and 2 points for unilateral weakness as well as 1 point for history of diabetes.

The correct answer is internal capsule (likely posterior limb) or thalamus. This patient has a pure motor lacunar stroke syndrome, manifested by: pure motor contralateral hemiparesis without any sensory deficits. Lateral frontoparietal, superior temporal is a complete middle cerebral artery distribution, which is manifested by: contralateral hemianesthesia, hemiparesis, hemianopia with gaze preference; If dominant hemisphere: aphasia and apraxia; if nondominant hemisphere: aprosodia, hemineglect. Lateral medulla also known as Wallenberg syndrome, this is a brainstem syndrome manifested by: ipsilateral facial sensory loss, Horner’s syndrome, palatal weakness, dysphagia and ataxia, contralateral body pain and temperature loss. Medial frontoparietal lobes is descriptive of anterior cerebral artery distribution stroke, which is manifested by: contralateral anesthesia, leg > arm hemiparesis, abulia. If dominant hemisphere: mutism; if nondominant hemi- sphere: acute confusional state.

The patient had a transient ischemic attack. Two interventions that reduce mortality in patients with TIA are anticoagulation for patients with atrial fibrillation or LV thrombus, and carotid endarterectomy for carotid stenosis > 70%.  The patient only has 65% stenosis, thus anticoagulation is the better answer choice. While long-term blood pressure control is important in decreasing morbidity and mortality for this patient, emergent blood pressure control has not been shown to decrease the immediate morbidity of this patient. Long-term blood glucose control is also important in decreasing morbidity and mortality for this patient, emergent blood glucose control has not been shown to decrease the immediate morbidity of this patient

The indications for tPA include age at least 18 years, clinical diagnosis of ischemic stroke (no finding on noncontrast Head CT), and time of symptoms onset <4.5 hours.

There are multiple contraindications to systemic thrombolysis (tPA) including: significant stroke/head trauma in prior 3months, prior intracranial hemorrhage, intracranial neoplasm/AVM/aneurysm, recent intracranial/intraspinal surgery, arterial puncture at noncompressible site in past 1 week, sustained SBP at least 185 or DBP at least 110 mmHg, serum glucose <50 mg/dL (<2.8 mmol/L), active internal bleeding or acute bleeding diatheses, current use of anticoagulants or INR > 1.7 and platelet count < 100,000/μL.

The patient has a subarachnoid hemorrhage, of which there are 3 major causes: ruptured aneurysm, leaking AVM, or a peri-mesencephalic bleed. Of ruptured aneurysms, the most common blood vessel affected is the anterior communicating artery in the circle of Willis.

Several historical clues in this scenario point to tuberculosis being the “bad lung infection” in this patient. In patients with seizures that are refractory to benzodiazepines, isoniazid (a common medication for tuberculosis) overdose is a possibility and should be considered. Pyridoxine is the only fully effective pharmacologic treatment for toxic isoniazid seizures, although benzodiazepines have been shown to suppress seizure activity in some cases.

Early, aggressive benzodiazepine administration is associated with decreased morbidity and mortality in status epilepticus. Intramuscular midazolam is superior to intravenous lorazepam; in addition, the dose of lorazepam is inadequate. Endotracheal intubation may ultimately be required, but is a secondary priority; use of a long-acting neuromuscular blockade agent, such as vecuronium, should be avoided. Cranial computed tomography may or may not be needed in this patient, depending on the response to benzodiazepine therapy. Bedside electroencephalograms are most useful in diagnosing nonconvulsive status epilepticus.

Cerebral venous thrombosis may present with headache, lethargy, cranial nerve deficits, seizures, or even psychiatric complaints. CT scan and/or MRI/magnetic resonance angiography (MRA) are likely to reveal the diagnosis. Treatment includes heparin. Neurosurgical consultation is not useful. Subarachnoid hemorrhage would not be expected to cause a focal neurologic deficit. Eclampsia and meningitis would be expected to give characteristic findings on history and examination.

Seizure activity may occur when the serum glucose concentration is less than 45 mg/dL. Although cation derangements may also cause seizures (hyponatremia, hypocalcemia, and hypomagnesemia), sodium levels less than 120 mEq/L are typically seen, with these levels having been achieved rapidly rather than slowly. This level of hypocalcemia is appropriate for the decreased albumin level, likely rendering ionized calcium levels normal. Hyperkalemia does not cause seizures. Uremia may cause status epilepticus, but only at higher levels in cases of a more rapid onset of untreated renal failure or during rapid fluid shifts such as during dialysis.