Results suggest that PTM is associated with cognitive impairments and protracted recovery and that headache alone is not a good predictor of recovery.

HighlightsMyoclonus status epilepticus may be reflected by generalized epileptiform discharges and burst suppression on EEG.Patients with Lance-Adams syndrome often demonstrate focal epileptiform activity at the vertex on EEG.EEG is vital in evaluating post-hypoxic myoclonus; studies are needed to assess its utility in predicting outcomes.

Acute posthypoxic myoclonus portends a poor prognosis. Another form of posthypoxic myoclonus, Lance-Adams syndrome, is associated with a better outcome. Differentiating these two entities is important in prognostication and guiding further medical intervention. This can be difficult in the acute setting after hypoxic brain injury but the use of neurophysiologic studies may be helpful. In this article, we present a case of a patient who presented after pulseless electrical activity arrest, underwent targeted temperature management and subsequently developed Lance-Adams syndrome. The neurologic and electroencephalographic findings in Lance-Adams syndrome are discussed with an updated review.

Rationale The cytosolic protease calpain has been recently implicated in the vascular remodeling of angiotensin II (AngII) type-1 receptor (AT1r) signaling. The role of AngII/AT1r/calpain signaling on endothelial function, an important and early determinant of vascular pathology, remains though totally unknown. Accordingly, we investigated the role of calpain in the endothelial dysfunction of AngII. Objective To demonstrate a mechanistic role for calpain in the endothelial dysfunction induced by AngII/AT1r signaling. To establish endothelial-expressed calpains as an important target of AT1r signaling. Methods and Results Subchronic administration of nonpressor doses of AngII to rats and mice significantly increased vascular calpain activity via AT1r signaling. Intravital microscopy studies revealed that activation of vascular expressed calpains causes endothelial dysfunction with increased leukocyte-endothelium interactions and albumin permeability in the microcirculation. Western blot and immunohistochemistry studies confirmed that AngII/AT1r signaling preferentially activates the constitutively expressed μ-calpain isoform and demonstrated a calpain-dependent degradation of IκBα, along with upregulation of NF-κB-regulated endothelial cell adhesion molecules (eCAMs). These physiological and biochemical parameters were nearly normalized following inhibition of AT1r or calpain in vivo. Antisense depletion studies in microvascular endothelial cells along with knockout and transgenic mouse studies further confirmed the role of μ-calpain in the endothelial adhesiveness induced by AngII. Conclusions This study uncovers a novel role for calpain in the endothelial dysfunction of AngII/AT1r signaling and establishes the calpain system as a novel molecular target of the vascular protective action of RAS inhibition. Our results may have significant clinical implications in vascular disease.

No abstract

OBJECTIVEDelay in diagnosis and subsequent treatment of nonconvulsive seizures can lead to worsened outcomes. The gold standard in detecting nonconvulsive seizures is continuous video-electroencephalography (cEEG). Compared to routine, 30-minute EEG, the use of cEEG increases the likelihood of capturing intermittent nonconvulsive seizures. Studies of critically ill patients in intensive care units demonstrate a particularly high rate of nonconvulsive seizures. Some of these studies included postneurosurgical patients, but often subanalyses of specific populations were not done. In particular, few studies have specifically evaluated postneurosurgical patients by using cEEG in the acute postoperative setting. Therefore, the incidence and predictors of acute postneurosurgical seizures are unclear.METHODSIn this study, the authors focused on patients who were admitted to the neurological critical care unit following neurosurgery and who underwent cEEG monitoring within 72 hours of surgery.RESULTSA total of 105 cEEG studies were performed in 102 patients. Twenty-nine patients demonstrated electrographic (subclinical) seizures, of whom 10 had clinical seizures clearly documented either before or during cEEG monitoring. Twenty-two patients had subclinical seizures only detected on cEEG, 19 of whom did not have clinical seizure activity at any point during hospitalization. Those with seizures were more likely to have had a history of epilepsy (p = 0.006). The EEG studies of patients with seizures were more likely to show lateralized periodic discharges (p = 0.012) and lateralized rhythmic delta activity (p = 0.012). The underlying neuropathological disorders most associated with seizure risk were lobar tumor on presentation (p = 0.048), subdural hematoma (SDH) requiring craniotomy for evacuation (p = 0.002), subarachnoid hemorrhage (SAH) (p = 0.026), and perioperative SAH (p = 0.019). In those undergoing craniotomy, the presence of SDH (p = 0.032), particularly if requiring evacuation (p = 0.003), increased the risk of seizures. In those without preoperative intracranial bleeding, perioperative SAH after craniotomy was associated with a higher incidence of seizures (p = 0.014). There was an additive effect on seizure incidence when perioperative SAH as well as concomitant intraparenchymal hemorrhage and/or stroke were present. The clinical examination of the patient, including the presence or absence of altered mental status and the presence or absence of repetitive movements, was not predictive of subclinical seizures.CONCLUSIONSIn postneurosurgical patients referred for cEEG monitoring, there is a high rate of both clinical and subclinical seizures in the early postoperative period. Seizures are particularly common in patients with SDH or lobar tumor and perioperative SAH. There was an additive effect on seizure incidence when more extensive brain injury was present. As expected, those with a history of epilepsy also demonstrated higher seizure rates. Further studies are needed to evaluate the time period of maximum seizure incidence after surgery, and the effects acute postneurosurgical seizures have on long-term outcomes.

Prognostication after cardiac arrest often depends primarily on neurological function, and characterizing the extent of neurological injury hinges on neurophysiological testing and clinical neurological examination. The presence of early posthypoxic myoclonus (PHM) following cardiac arrest had been invariably associated with poor outcome, but more recent studies have shown that those with early PHM may survive with good neurological function. Electroencephalographic patterns suggestive of severe brain injury may be more valuable than the presence of PHM itself in portending poor functional status, and phenotyping PHM may also be useful in delineating benign and malignant forms. Patients with early PHM should be evaluated similarly to others who suffer cardiac arrest by using a multimodal approach in determining prognosis until further studies are performed that better characterize early PHM subtypes and their outcomes.

& AbstractBackground: Botulinum toxin is approved to treat chronic migraine and has been shown to confer significant benefit in refractory cases. Due to its effect on pain by sensory modulation, there may also be efficacy in its use in chronic tension-type headache (CTTH). Methods: A systematic review of the literature was performed using our predefined inclusion and exclusion criteria. We targeted prospective trials, randomized or nonrandomized, studying botulinum toxin in tension-type headaches (TTHs) in adults. Results: Twenty-two studies were included, including 9 nonrandomized, uncontrolled studies, 8 randomized, placebo-controlled and double-blinded trials (RCTs), 3 RCTs with a crossover, open-label period, 1 comparative, randomized, single-blinded evaluation, and 1 retrospective study with prospective evaluation of headache response to cosmetic botulinum toxin. Studies included 11 to 300 subjects, with duration typically less than 6 months and with only 1 treatment period. Results were mixed, likely due to variable study design, including toxin dosing, injection paradigms, duration/frequency of treatment, and outcome measures. There was moderate-quality evidence that botulinum toxin improved VAS scoring, and some studies demonstrated efficacy based on improved frequency/severity. Conclusion:This systematic review demonstrates variable study designs contributing to the low quality of evidence available regarding botulinum toxin in TTH, but some data suggest efficacy. There does not appear to be irrefutable evidence of a lack of efficacy of botulinum toxin in TTH. Using the paradigm for botulinum toxin in chronic migraine may prove fruitful in treating CTTH. Further studies are warranted to evaluate the utility of botulinum toxin in this common debilitating condition. &