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Objective Our epilepsy population recently experienced the acute effects of the COVID‐19 pandemic in New York City. Herein, we aimed to determine patient‐perceived seizure control during the surge, specific variables associated with worsened seizures, the prevalence of specific barriers to care, and patient‐perceived efficacy of epilepsy care delivered via telephone and live video visits during the pandemic. Methods We performed a cross‐sectional questionnaire study of adult epilepsy patients who had a scheduled appointment at a single urban Comprehensive Epilepsy Center (Montefiore Medical Center) between March 1, 2020 and May 31, 2020 during the peak of the COVID‐19 pandemic in the Bronx. Subjects able to answer the questionnaire themselves in English or Spanish were eligible to complete a one‐time survey via telephone or secure online platform (REDCap). Results Of 1212 subjects screened, 675 were eligible, and 177 adequately completed the questionnaire. During the COVID‐19 pandemic, 75.1% of patients reported no change in seizure control, whereas 17.5% reported that their seizure control had worsened, and 7.3% reported improvement. Subjects who reported worsened seizure control had more frequent seizures at baseline, were more likely to identify stress and headaches/migraines as their typical seizure precipitants, and were significantly more likely to report increased stress related to the pandemic. Subjects with confirmed or suspected COVID‐19 did not report worsened seizure control. Nearly 17% of subjects reported poorer epilepsy care, and 9.6% had difficulty obtaining their antiseizure medications; these subjects were significantly more likely to report worse seizure control. Significance Of the nearly 20% of subjects who reported worsened seizure control during the COVID‐19 pandemic, stress and barriers to care appear to have posed the greatest challenge. This unprecedented pandemic exacerbated existing and created new barriers to epilepsy care, which must be addressed.

Purpose The reliability of somatosensory evoked potentials (SSEPs) in predicting outcome in comatose survivors of cardiac arrest treated with therapeutic hypothermia (TH) has been questioned. We investigated whether the absence of cortical (N20) responses was a reliable predictor of a nonawakening in the setting of TH. Methods A retrospective review was conducted in cardiac arrest survivors treated with TH admitted to a single tertiary care hospital from April, 2010 to March, 2013 who underwent SSEP testing at various time points after cardiac arrest. N20 responses were categorized as normal, present but abnormal, bilaterally absent, or inadequate for interpretation. Neurologic outcome was assessed at discharge by the Cerebral Performance Category Scale (CPC). Results Ninety-three SSEP studies were performed in 73 patients. Fourteen patients had absent N20 responses; all had poor outcome (CPC 4-5). Eleven patients had absent N20 s during hypothermia, three of whom had follow-up SSEPs after rewarming and cortical responses remained absent. Fifty-seven patients had N20 peaks identified and had variable outcomes. Evaluation of 1 or more N20 peaks was limited or inadequate in 11.4% of SSEPs performed during the cooling because of artifact. Conclusions Somatosensory evoked potentials remain a reliable prognostic indicator in patients undergoing TH. The limited sample size of patients who had SSEP performed during TH and repeated after normothermia added to the effect of self-fulfilling prophecy limit the interpretation of the reliability of this testing when performed during cooling. Further prospective, multicenter, large scale studies correlating cortical responses in SSEPs during and after TH are warranted. Technical challenges are commonplace during TH and caution is advised in the interpretation of suboptimal recordings.

Fibrodysplasia ossificans progressiva (FOP) is a rare genetic disorder characterized by heterotopic ossification of soft connective and muscle tissues, often as the result of minor trauma. The sequelae include joint fusion, accumulation of calcified foci within soft tissues, thoracic insufficiency syndrome, and progressive immobility. The authors report on a patient with FOP who developed severe spinal canal stenosis in the thoracic spine causing substantial myelopathy. He underwent a thoracic laminectomy and resection of a large posterior osteophyte. Unique considerations are required in treating patients with FOP, including steroid administration to prevent ossification and anesthetic technique. The nuances of neurosurgical and medical management as they pertain to this disease are discussed.

Objective To determine whether hypothermia modulates acquisition of sleep-wake cycling in term neonates with moderate to severe hypoxic-ischemic encephalopathy (HIE) and the relationship to outcome. Study design Twenty-nine term infants with moderate to severe HIE treated with selective head cooling were evaluated. All were monitored with amplitude-integrated electroencephalography during and video electroencephalography immediately after hypothermia for ≥72 hours. Electroencephalograpic data were analyzed for background and sleep-wake cycling. Abnormal outcome included death or severe global neurodevelopmental disability ≥18 months. Results Acquisition of sleep-wake cycling was noted in nine infants by 72 hours, in 13 by 96 hours, 19 by 120 hours, and 22 by 144 hours. Presence of sleep-wake cycling was associated with normal outcome, that is, 14 of 22 (64%), versus abnormal outcome, that is, none of seven without sleep-wake cycling (P = .006). The presence of sleep-wake cycling by 120 hours had a positive predictive value of 68% and negative predictive value of 90%. Magnetic resonance imaging abnormalities were related to onset of sleep-wake cycling. Conclusions Although onset of sleep-wake cycling is markedly delayed in term neonates with moderate to severe HIE treated with hypothermia, approximately 65% with acquisition of cycling have a normal outcome. Sleep-wake cycling is an important additional tool for assessing recovery in term infants with moderate to severe HIE treated with hypothermia.

The role of surgical resection in temporal lobe epilepsy (TLE) is well-established (Wiebe et al., 2001; Jutila et al., 2002; Spencer et al., 2003; Yoon et al., 2003; McIntosh et al., 2004; Spencer et al., 2005). Although historically patients with TLE have been categorized as a single group, recent work has shown subclassifications based on clinical features, imaging, histology, and electroencephalography (EEG) (Du et al., 1993; Burgerman et al., 1995; Gil-Nagel & Risinger, 1997; Bertram & Scott, 2000; Bertram, 2009; Ogren et al., 2009; Stefan et al., 2009). One of the main challenges facing clinicians is the patient with presumed TLE but a normal magnetic resonance imaging (MRI) scan. Unlike patients with hippocampal atrophy, who have a seizure-free rate after surgery approaching 70–80%, TLE with normal MRI has a 40–60% rate of surgical cure (Berkovic et al., 1995; Holmes et al., 2000; Ozkara et al., 2000; Cohen-Gadol et al., 2005; Alarcon et al., 2006; Tatum et al., 2008; Bell et al., 2009). Ambiguities about seizure focus localization pose a challenge to resection, since onsets may be either neocortical or mesial and be clinically indistinguishable (Sylaja et al., 2004; Chapman et al., 2005; Bell et al., 2009). For these patients, chronic intracranial electrocorticography (ECoG) is often employed to acquire ictal data to guide temporal lobe resection (Cascino et al., 1995; Siegel et al., 2001; Kuruvilla & Flink, 2003; Cohen-Gadol et al., 2005; Oliveira et al., 2006). Although relatively safe, electrode implantation significantly increases length of stay and is associated with a 10–26% rate of complications, including hematoma and infection (Van Gompel et al., 2008; Wong et al., 2009). The risks and costs are higher than a single-stage surgery (Hamer et al., 2002). For this reason, techniques to localize seizure foci such as positron emission tomography (PET), ictal single-photon emission computed tomography (SPECT), functional (f)MRI, and magnetoencephalography (MEG) have been pursued (Assaf et al., 2003, 2004; Stephen et al., 2005; Willmann et al., 2007; Boling et al., 2008; Chassagnon et al., 2009; la Fougere et al., 2009; Kobayashi et al., 2009). Clinical history, neuropsychological, and Wada testing can also assist in this distinction (Loring et al., 1994; Sperling et al., 1994; Sylaja et al., 2004). However, none of these adjuncts have high enough sensitivity and specificity to completely obviate the need for ECoG in these patients. Another useful technique for localizing epileptogenic cortex is acute (intraoperative) ECoG. The main limitation of acute ECoG is that usually only interictal data is recorded. Acute ECoG has been proven helpful in defining the limits of neocortical lesional epilepsy surgery; however, its use in TLE is controversial (Schwartz et al., 1997; Holmes et al., 2000; Oliveira et al., 2006). Studies have evaluated the predictive value of postresection spikes or preresection spike-tailored resections (Schwartz et al., 1997; McKhann et al., 2000; Chen et al., 2006; Oliveira et al., 2006), but few have correlated the results of acute ECoG with chronic ECoG. Likewise, there are few data on the utility of intraoperative ECoG in MRI-negative TLE. A recent report showing a strong correlation between the distribution of intracranially recorded interictal spikes and ictal onsets in TLE supports an interest in evaluating acute ECoG efficacy in MRI-negative TLE (Goncharova et al., 2009). The purpose of this study was to determine if acute ECoG could screen patients with MRI-negative TLE to select who would require chronic implantation of electrodes and who could move directly to a standard anteromedial resection (SAMR) (Spencer et al., 1984). We also hypothesized that these patients might have better outcomes with respect to seizure control.

Leptomeningeal spread of cancer can have protean presentations, increasing the difficulty of making this diagnosis. We present the case of a 77-year-old man with prior metastatic melanoma who presented with spontaneous headache that worsened over several days, and was found to have both intraventricular and cortical subarachnoid hemorrhage on CT head. His neurological exam was unremarkable. MRI of the brain with contrast confirmed the CT findings and did not reveal any evidence of parenchymal or leptomeningeal metastases. MR angiogram followed by a conventional angiogram did not demonstrate any vascular abnormalities. Cerebrospinal fluid examination revealed 110 white blood cells, 34000 red blood cells, and protein of 160. Cytology returned positive for malignant melanoma cells. No additional sites of disease were found on further evaluation with MRI spine and CT of the chest, abdomen and pelvis. In retrospect, the patient had endorsed some fluctuating nausea and fatigue three months prior to presentation, as well as positional vertigo two weeks prior to presentation. His oncologic history was notable for prior immunotherapy with ipilimumab, as well as diagnosis of dural-based brain metastases two years earlier, for which he underwent surgical resection and radiation therapy. He had no evidence of disease for one year prior to this new diagnosis of leptomeningeal involvement. This case highlights an unusual presentation of leptomeningeal metastasis and underscores the importance of maintaining heightened suspicion for this diagnosis when evaluating subarachnoid hemorrhage in a cancer patient, especially in the case of melanoma. It raises the question of whether this particular cancer type or the patient’s prior immunotherapy contributed to his presentation, and emphasizes the need for further elucidation of the biology of leptomeningeal metastasis.

Despite concerns about the adverse effects of second-generation antipsychotics on weight regulation and glucose and lipid metabolism, little is known about the relationship between these agents and the metabolic syndrome. Because the metabolic syndrome is more strongly associated with cardiovascular morbidity and mortality than its individual components, attention to the full syndrome is important. The authors' goal was to explore the relationship between second-generation antipsychotics and the metabolic syndrome.They assessed the prevalence of metabolic syndrome in a nearly consecutive group of 89 acutely admitted psychiatric inpatients treated with at least one second-generation antipsychotic for different psychiatric disorders. Patients' waist circumference and blood pressure were measured as well as their fasting blood glucose and lipid levels.Twenty-six (29.2%) of the 89 patients fulfilled criteria for the metabolic syndrome. Presence of the syndrome was associated with older age, higher body mass index, and higher values for each individual criterion of the metabolic syndrome but not with specific diagnoses or antipsychotic treatment regimens. Presence of abdominal obesity was most sensitive (92.0%), while fasting glucose110 mg/dl was most specific (95.2%) in correctly identifying the presence of metabolic syndrome. Combining abdominal obesity and elevated fasting blood glucose had 100% sensitivity.The measurement of both abdominal obesity and fasting blood glucose is a simple, cost-effective screening test to detect patients at high risk for future cardiovascular morbidity.