SUMMARYDose-dependent PR interval prolongation has been reported in preclinical studies of lacosamide (LCM), a recently U.S. Food and Drug Administration (FDA)-approved antiepileptic drug (AED). Here we report a case of second-degree atrioventricular block (AV) block caused by the addition of LCM to other AEDs known to prolong the PR interval, resulting in hypotension and bradycardia, with consequent seizure exacerbation. The patient recovered completely after withdrawal of LCM. This case demonstrates the need for caution and interval cardiac testing when adding LCM to other AEDs known to prolong the PR interval. KEY WORDS: Lacosamide, Heart block, Arrhythmia. Case ReportA 45-year-old man with frontal lobe epilepsy, seizurefree for 1 year, developed palpitations, dyspnea, and exercise intolerance 1 week prior to hospitalization for recurrent seizure. En route to the hospital, he was noted to have bradycardia (44 bpm) with hypotension (83/64 mm Hg).His medical history included craniopharyngioma at age 6, treated with right frontal craniotomy, resection, radiation, and ventriculoatrial shunting. His course was complicated by right eye blindness and panhypopituitarism with diabetes insipidus, hypothyroidism, and adrenal insufficiency. At age 21, he developed acute lymphocytic leukemia, treated with chemotherapy. At age 23, he developed frontal lobe epilepsy featuring generalized tonic-clonic seizures beginning with stereotyped right arm extension. There was no personal or family history of cardiac conduction disorders.His medications included desmopressin, hydrocortisone, levothyroxine, somatropin, alfuzosin, risedronate, Carbatrol 100 mg po qAM and 200 mg po qPM, oxcarbazepine 600 mg po qAM, 600 mg po qPM, and 1200 mg po qHS, and LCM 200 mg nightly. His only medication change over the last year was LCM replacing zonisamide (ZNS) for unclear reasons 3 months previously, reaching 200 mg 2 months prior to presentation.Initial laboratory evaluation with blood counts, electrolytes, and hepatic enzymes was unremarkable; carbamazepine (CBZ) level was 3.8 lg/ml. Head computerized tomography showed stable right frontal encephalomalacia. Electrocardiography (ECG) showed second-degree AV block (Mobitz I/Wenckebach) with frequent dropped beats and bradycardia. A transvenous pacemaker was placed. After three further seizures, Carbatrol was increased to 200 mg twice daily, continuous intravenous lorazepam was added, and he was transferred to our institution.At our institution, physical examination revealed prior craniotomy, depressed consciousness, and right afferent pupillary defect. Echocardiography, urinalysis, urine toxicology, and endocrine evaluation [including sodium, thyroxine, and morning cortisol] were unremarkable. Thyroid-stimulating hormone was undetectable, as expected. His antiepileptic drugs (AEDs) were continued except for ZNS replacing LCM. Initial cardiac monitoring showed a markedly prolonged PR interval, frequent Mobitz I AV block, and right bundle branch block. Continuous videoelectroencephalography (EEG) ...
Acute oculomotor nerve palsies with pupillary involvement warrant thorough investigation. When routine work-up fails to elucidate an etiology, extracranial carotid pathology should be considered.
The κBEST metric can measure significant interrater reliability differences between any number of EEG readers and reports, retrospectively, and is generalizable to other domains (e.g., pathology or radiology reporting). We suggest using this metric as a guide or starting point for focused quality control efforts.
Introduction: Reversible cerebral vasoconstriction syndrome (RCVS) is a cerebrovascular disorder associated with multifocal intracranial arterial constriction and dilation that occurs spontaneously or as a result of a stimulant. The authors present a case of RCVS in a patient who presented with a new-onset thunderclap headache a day after carotid endarterectomy (CEA). RCVS has been rarely reported after CEA. Case Report: A 65-year-old woman was evaluated for a new-onset thunderclap headache a day after left-sided CEA. Computed tomography (CT) of the head revealed left frontal and parietal subarachnoid hemorrhage (SAH). CT angiography did not show any saccular aneurysms or vessel stenosis. The initial impression was SAH related to reperfusion injury after carotid revascularization. Seven days postoperatively, the patient returned to the hospital with a persistent headache. CT revealed SAH in the vertex of the frontal region bilaterally. Magnetic resonance angiogram (MRA) of the head revealed multifocal stenosis of the intracranial circulation bilaterally. A follow-up MRA 9 weeks postoperatively showed interval improvement of the caliber of the circle of Willis branches and significant improvement of the multifocal stenosis. The patient was diagnosed with RCVS as a result of CEA. Conclusion: The authors advise clinicians to consider RCVS as a cause of thunderclap headache or recurrence of a severe headache shortly after CEA—particularly with the presence of a nonaneurysmal convexity SAH.
Introduction: Froin syndrome is a rare condition that is defined as marked coagulability, elevated protein level, and xanthochromia of the cerebrospinal fluid (CSF). Froin syndrome more commonly occurs because of obstruction of CSF flow due to underlying inflammatory or neoplastic conditions. Case Report: We present a case of a 38-year-old man who was found to have Froin syndrome a year after he was diagnosed with multiple myeloma (MM). CSF analysis, laboratory work-up, and magnetic resonance imaging of the neuroaxis supported the diagnosis of Froin syndrome related to leptomeningeal myelomatosis. To our knowledge, this is the first reported case of FS due to MM. Conclusion: Leptomeningeal myelomatosis associated with MM can cause blockage of CSF circulation leading to Froin syndrome. Inflammatory or neoplastic conditions should be considered as an underlying etiology.
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