The Safety and Effectiveness of Intravenous Lacosamide for Refractory Status Epilepticus in the Critically Ill.

BACKGROUND: Status epilepticus (SE) often does not respond to initial treatment. A second-line agent with a less established safety and efficacy profile is then required. This study examined the safety of intravenous (IV) lacosamide (LCM) in a critically ill population and obtained an estimate of effectiveness in patients with refractory SE on continuous video EEG monitoring (cEEG). METHODS: Retrospective review of critically ill patients in SE on cEEG treated with IV LCM from June 2009 to April 2011. RESULTS: Eighty-four patients in SE (43 F/41 M), mean age 59.6 years, were identified; and 59.5 % had nonconvulsive SE. The most common etiologies were ischemic and hemorrhagic strokes. There were no significant changes in serial blood pressure monitoring, PR prolongation, aspartate aminotransferase (AST), or creatinine pre- and post-LCM. There was a significant increase in alanine aminotransferase (ALT) from days 1-7 (p = 0.031). Fifty-one patients were LCM-naïve. In these patients, cessation of SE on cEEG after LCM occurred in 15.7, 25.5, 58.8, and 82.4 % by 4, 12, 24, and 48 h, respectively. CONCLUSION: IV LCM appears safe short term in critically ill patients with SE. The retrospective estimate of effectiveness for LCM appears promising for management in SE. Prospective, randomized controlled studies are needed to better determine the role of LCM in treating SE.

Continuous electroencephalography (cEEG) changes precede clinical changes in a case of progressive cerebral edema.

BACKGROUND: Continuous electroencephalogram (cEEG) is tightly linked to cerebral metabolism and is sensitive to cerebral ischemia and hypoxia. The severity of cerebral ischemia can be seen on cEEG as changes in morphology, amplitude, or frequency, and cEEG may detect neuronal dysfunction at a reversible stage. METHODS: Case report and imaging. RESULTS: We present a case of focal cerebral edema with changes seen on cEEG 24 h before clinical signs of increased intracranial pressure. cEEG showed developing asymmetry in the left hemisphere followed by burst suppression. The right hemisphere showed similar progression to burst suppression. Complete suppression of both hemispheres was noted 6 h before clinical signs of herniation. Computed tomography (CT) head confirmed a large left parietal intracerebral hematoma with mass effect. CONCLUSIONS: cEEG has applications in monitoring cerebral dysfunction in addition to detecting seizure activity in the intensive care unit. It may serve a vital role in multi-modality monitoring for early recognition of neurological complications from brain injuries that may not be noticed clinically, which is paramount to early intervention.

Central Hyperthermia Treated with Bromocriptine.

Introduction. Central hyperthermia is common in patients with brain injury. It typically has a rapid onset with high temperatures and marked fluctuations and responds poorly to antibiotics and antipyretics. It is also associated with worse outcomes in the brain injured patient. Recognizing this, it is important to aggressively manage it. Case Report. We report a 34-year-old male with a right thalamic hemorrhage extending to the midbrain and into the ventricles. During his admission, he developed intractable fevers with core temperatures as high as 39.3°C. Infectious workup was unremarkable. The fever persisted despite empiric antibiotics, antipyretics, and cooling wraps. Bromocriptine was started resulting in control of the central hyperthermia. The fever spikes were reduced to minor fluctuations that significantly worsened with any attempt to wean off the bromocriptine. Conclusion. Diagnosing and managing central hyperthermia can be challenging. The use of bromocriptine can be beneficial as we have reported.

Increase in sensitivity of the baroreceptor reflex following microinjection of carbachol into the posterior hypothalamic nucleus of awake rats.

In a rat model, the baroreceptor reflex can be assessed by graded infusions of either phenylephrine or sodium nitroprusside with continuous hemodynamic monitoring. Microinjection of the cholinergic agonist carbachol (CCh) into the posterior hypothalamic nucleus (PHN) evokes an increase in mean arterial pressure and a change in heart rate. Lower doses of CCh evoke only tachycardia, whereas middle and higher doses evoke a biphasic change in heart rate of tachycardia followed by bradycardia. The bradycardia following the microinjection of CCh into the PHN can be attenuated by the previous administration of the vasopressin V1 receptor antagonist [d(CH2 )5 Tyr(Me)] arginine vasopressin (AVPX). Circulating arginine vasopressin (AVP) has been shown to increase the sensitivity of the baroreceptor reflex by stimulating vasopressin V1 receptors in the area postrema. The attenuation by AVPX of the bradycardia that results following the high doses of CCh suggests that AVP is released into the circulation following stimulation of cholinergic systems within the PHN. Thus, microinjection of a high dose of CCh (11 nmol) into the PHN alters the sensitivity of the baroreceptor reflex by increasing peripheral levels of AVP.

[(18)F]-Fluoro-Deoxy-Glucose Positron Emission Tomography Scan Should Be Obtained Early in Cases of Autoimmune Encephalitis.

Introduction. Autoimmune encephalitis (AE) is a clinically challenging diagnosis with nonspecific neurological symptoms. Prompt diagnosis is important and often relies on neuroimaging. We present a case series of AE highlighting the importance of an early [(18)F]-fluoro-deoxy-glucose positron emission tomography (FDG-PET) scan. Methods. Retrospective review of seven consecutive cases of autoimmune encephalitis. Results. All patients had both magnetic resonance imaging (MRI) and FDG-PET scans. Initial clinical presentations included altered mental status and/or new onset seizures. Six cases had serum voltage-gated potassium channel (VGKC) antibody and one had serum N-methyl-D-aspartate (NMDA) antibody. MRI of brain showed mesial temporal lobe hyperintensity in five cases of VGKC. The other two patients with VGKC or NMDA AE had restiform body hyperintensity on MRI brain or a normal MRI, respectively. Mesial temporal lobe hypermetabolism was noted in three cases on FDG-PET, despite initial unremarkable MRI. Malignancy workup was negative in all patients. Conclusion. A high index of suspicion for AE should be maintained in patients presenting with cognitive symptoms, seizures, and limbic changes on neuroimaging. In cases with normal initial brain MRI, FDG-PET can be positive. Additionally, extralimbic hyperintensity on MRI may also be observed.

Variables That Best Differentiate In-Patient Acute Stroke from Stroke-Mimics with Acute Neurological Deficits.

Introduction. Strokes and stroke-mimics have been extensively studied in the emergency department setting. Although in-hospital strokes are less studied in comparison to strokes in the emergency department, they are a source of significant direct and indirect costs. Differentiating in-hospital strokes from stroke-mimics is important. Thus, our study aimed to identify variables that can differentiate in-hospital strokes from stroke-mimics. Methods. We present here a retrospective analysis of 93 patients over a one-year period (2009 to 2010), who were evaluated for a concern of in-hospital strokes. Results. About two-thirds (57) of these patients were determined to have a stroke, and the remaining (36) were stroke-mimics. Patients with in-hospital strokes were more likely to be obese (p = 0.03), have been admitted to the cardiology service (p = 0.01), have atrial fibrillation (p = 0.03), have a weak hand or hemiparesis (p = 0.03), and have a prior history of stroke (p = 0.05), whereas, when the consults were called for "altered mental status" but no other deficits (p < 0.0001), it is likely a stroke-mimic. Conclusion. This study demonstrates that in-hospital strokes are a common occurrence, and knowing the variables can aid in their timely diagnosis and treatment.

Variability in diagnosing Creutzfeldt-Jakob disease using standard and proposed diagnostic criteria.

INTRODUCTION: Creutzfeldt-Jakob disease (CJD) is a rapidly progressive dementia with a median survival of 2-14 months. The diagnosis can only be made accurately by biopsy/autopsy. However, this is not always feasible or desirable. Thus, diagnostic criteria have been proposed by UCSF, European MRI-CJD Consortium, and WHO. We will compare these criteria. PATIENTS AND METHODS: Retrospective study of 31 patients (average age of 69.2 years) between 2003 to 2010 by ICD9 codes 046.1, 046.11, and 046.19. RESULTS: All patients presented with rapidly progressive dementia (mean duration of 4.25 months). Pyramidal and extrapyramidal findings, myoclonus, cerebellar changes, akinetic mutism, and visual disturbances were observed in 6.5-48.4%. Five had periodic pattern on EEG. CSF biomarker 14-3-3 was positive in 11. Tau was positive in 6. Neuron specific enolase was positive in 9. By consensus (kappa = 0.62), MRI was "typical" of CJD in 23 with cortical ribboning (n = 16), basal ganglia hyperintensity (n = 15), or combination (n = 8). By WHO criteria, which does not include neuroimaging, CJD was diagnosed in 10, but 14 if any CSF biomarker was used (p = NS). The UCSF criteria, which does not include CSF biomarkers, diagnosed 18 cases, and the European MRI-CJD Consortium, which includes neuroimaging and CSF biomarkers but with less neurological signs, diagnosed 23 cases (p < 0.05 and p < 0.001, respectively). CJD-mimics included urosepsis, neurosarcoidosis, idiopathic left temporal lobe epilepsy, alcohol intoxication, central nervous system vasculitis, viral encephalitis, and non-Hodgkin's lymphoma. CONCLUSION: This study illustrates the variability in diagnosing CJD and emphasizes the diagnostic utility of neuroimaging. It also highlights false-positives that occur with neuroimaging.