Search

Supplemental Digital Content is available in the text., Objectives: To describe the risk factors for and outcomes after myoclonus in a cohort of patients with coronavirus disease 2019. Design: Multicenter case series. Setting: Three tertiary care hospitals in Massachusetts, Georgia, and Virginia. Patients: Eight patients with clinical myoclonus in the setting of coronavirus disease 2019. Interventions & Measurements and Main Results: Outcomes in patients with myoclonus were variable, with one patient who died during the study period and five who were successfully extubated cognitively intact and without focal neurologic deficits. In five cases, the myoclonus completely resolved within 2 days of onset, while in three cases, it persisted for 10 days or longer. Seven patients experienced significant metabolic derangements, hypoxemia, or exposure to sedating medications that may have contributed to the development of myoclonus. One patient presented with encephalopathy and developed prolonged myoclonus in the absence of clear systemic provoking factors. Conclusions: Our findings suggest that myoclonus may be observed in severe acute respiratory syndrome coronavirus 2 infected patients, even in the absence of hypoxia. This association warrants further evaluation in larger cohorts to determine whether the presence of myoclonus may aid in the assessment of disease severity, neurologic involvement, or prognostication.

Extracorporeal membrane oxygenation is considered a relative contraindication for patients with severe neurological injury manifested by fixed and dilated pupils. The inability to provide adequate cardiopulmonary support while attempting to treat the underlying neurologic disease results in a fatal outcome. The impairment of cerebral perfusion, compounded by the underlying neurologic condition, results in signs of brainstem dysfunction often equated with a fatal prognosis. As a result, these patients are not considered to be candidates for initiation of extracorporeal membrane oxygenation. We present a case series of three patients with complex neurologic conditions with fixed and dilated pupils, who received extracorporeal membrane oxygenation. All three patients achieved a significant neurologic recovery. Two survived with a cerebral performance category scale of 1, and the third succumbed to multi-organ failure after achieving a Glasgow Coma Scale of 11T. The decision to initiate extracorporeal membrane oxygenation should be based upon the pathophysiology of the underlying neurologic condition and not solely upon isolated clinical findings. Extracorporeal membrane oxygenation use is normally reserved for patients with reversible underlying processes, and a neurologic exam with fixed and dilated pupils is often interpreted as an irreversible neurologic injury. The implementation and success of extracorporeal membrane oxygenation in this patient population require understanding of complex neurologic diseases, rapid recognition of neurocardiogenic shock, and expeditious initiation of cardiopulmonary support in carefully selected patients. The patients described demonstrate that fixed and dilated pupils are not a contraindication for extracorporeal support in select patients.

Prompt treatment of acute intracranial hypertension is vital to preserving neurological function and frequently includes administration of 23.4% NaCl. However, 23.4% NaCl administration requires central venous catheterization that can delay treatment. Intraosseous catheterization is an alternative route of venous access that may result in more rapid administration of 23.4% NaCl. Single-center retrospective analysis of 76 consecutive patients, between January 2015 and January 2018, with clinical signs of intracranial hypertension received 23.4% NaCl through either central venous catheter or intraosseous access. Intraosseous cannulation was successful on the first attempt in 97% of patients. No immediate untoward effects were seen with intraosseous cannulation. Time to treatment with 23.4% NaCl was significantly shorter in patients with intraosseous access compared to central venous catheter (p

Bauxite mining is not known to most Malaysian except recently due to environmental pollution issues in Kuantan, Pahang. Potential impacts are expected to go beyond physical environment and physical illness if the situation is not controlled. Loss of economic potentials, and the presence of unpleasant red dust causing mental distress, anger and community outrage. More studies are needed to associate it with chronic physical illness. While evidences are vital for action, merely waiting for a disease to occur is a sign of failure in prevention. All responsible agencies should focus on a wider aspect of health determinants rather than merely on the occurrence of diseases to act and the need to emphasize on sustainable mining to ensure health of people is not compromised.

Introduction We discuss two cases of occipital seizures after neurological intervention presenting initially as complete or partial blindness and subsequently hallucinations. Methods The patients underwent continuous EEG monitoring in the ICU as part of their workup. Results Seizures arising from the occipital lobes were identified. Blindness resolved as seizure frequency decreased. The patients developed various forms of visual hallucinations with associated ictal EEG patterns after resolution of blindness. Conclusion Post ictal blindness is analogous to Todd’s paralysis after motor seizures and may represent ongoing ictal activity in the post neurosurgical patient. Reports of hallucinations as well as blindness may be attributed to delirium and patients may go untreated for prolonged periods of time if undiagnosed. A high index of suspicion is needed if these symptoms are present in conjunction, and CEEG should be employed early in the workup. Ongoing neurological injury, worsening morbidity, unnecessary testing and prolonged LOS can be avoided with timely diagnosis and treatment.

Background Magnesium (Mg) is an essential element for the body's normal physiological functioning. It has a major role in modulating vascular smooth muscle tone and peripheral arterial resistance. A low serum Mg level on admission (HMg 0 ) has been associated with more severe presentation in patients with subarachnoid hemorrhage. However, data on HMg 0 specifically in relation to intracerebral hemorrhage (ICH) are scarce. We sought to determine the incidence and clinical significance of HMg 0 in patients with ICH. Methods We reviewed the records of consecutive patients with ICH over a 2-year period. Data collected included initial Mg levels (Mg 0 ), clinical and radiologic characteristics on presentation, and discharge outcomes. Regression analysis was performed to look for any association of low Mg 0 with admission blood pressure (BP) and Glasgow Coma Scale (GCS) scores. We also examined the correlation of HMg 0 with clinical/radiologic features, admission severity (based on the ICH score), and poor outcome on discharge. Results In all, 33.6% presented with HMg 0 . Mg0 levels were negatively associated with systolic BP presentation ( P P = 0.01). Multivariate logistic regression showed an association between HMg 0 and severity at presentation ( P = 0.03), but not with poor outcome on discharge ( P = 0.26). Conclusions HMg 0 occurs in one third of patients with ICH and is associated with more severe presentation and intraventricular hemorrhage. Mg levels on admission correlate inversely with systolic BP and directly with GCS scores at presentation. HMg 0 does not influence outcomes at discharge.

Basilar meningovasculitis causing diffuse vasospasm is an under recognized complication of CNS cryptococcal infection. We report the case of cryptococcal meningitis causing severe vasospasm and its successful treatment with intraventricular (IVT) nicardipine.

We report a case of heparin-induced thrombocytopenia (HIT) that was complicated by acute intracerebral hemorrhage (ICH) and bilateral adrenal hemorrhage. In the setting of worsening thrombocytopenia, the risk of expansion of ICH and additional thrombotic events is concerning; hence, we employed plasmapheresis to reduce thrombotic risk. We followed serial daily heparin antibody enzyme-linked immunosorbent assay (ELISA) optical density measurements as well as heparin-induced platelet aggregation (HIPA) assays on both pre- and post-pheresis samples in order to objectively determine when thrombotic risk was sufficiently decreased. After four cycles of plasmapheresis, both heparin antibody ELISA and HIPA assays became negative. This case helps illustrate the utility of plasmapheresis in management of HIT when anticoagulation is contraindicated.

Acute hypokalemic paralysis is characterized by muscle weakness or paralysis secondary to low serum potassium levels. Neurogenic diabetes insipidus (DI) is a condition where the patient excretes large volume of dilute urine due to low levels of antidiuretic hormone. Here, we describe a patient with neurogenic DI who developed hypokalemic paralysis without a prior history of periodic paralysis. A 30-year-old right-handed Hispanic male was admitted for refractory seizures and acute DI after developing a dental abscess. He had a history of pituitary adenoma resection at the age of 13 with subsequent pan-hypopituitarism and was noncompliant with hormonal supplementation. On hospital day 3, he developed sudden onset of quadriplegia with motor strength of 0 of 5 in the upper extremities bilaterally and 1 of 5 in both lower extremities with absent deep tendon reflexes. His routine laboratory studies revealed severe hypokalemia of 1.6 mEq/dL. Nerve Conduction Study (NCS) revealed absent compound motor action potentials (CMAPs) with normal sensory potentials. Electromyography (EMG) did not reveal any abnormal insertional or spontaneous activity. He regained full strength within 36 hours following aggressive correction of the hypokalemia. Repeat NCS showed return of CMAPs in all nerves tested and EMG revealed normal motor units and normal recruitment without myotonic discharges. In patients with central DI with polyuria, hypokalemia can result in sudden paralysis. Hypokalemic paralysis remains an important differential in an acute case of paralysis and early recognition and appropriate management is key.

The clinical syndrome of tuberculous (TB) meningitis leading to ischemic strokes is rarely seen today in immunocompetent adults native to North America. This entity is also notoriously difficult to diagnose because the presenting symptoms are often nonspecific. The authors describe a case of a man with TB meningitis which progressed to recurrent ischemic cerebral infarcts.

To examine patterns of use, efficacy, and safety of intravenous ketamine for the treatment of refractory status epilepticus (RSE).Multicenter retrospective review of medical records and electroencephalography (EEG) reports in 10 academic medical centers in North America and Europe, including 58 subjects, representing 60 episodes of RSE that were identified between 1999 and 2012. Seven episodes occurred after anoxic brain injury.Permanent control of RSE was achieved in 57% (34 of 60) of episodes. Ketamine was felt to have contributed to permanent control ("possible" or "likely" responses) in 32% (19 of 60) including seven (12%) in which ketamine was the last drug added (likely responses). Four of the seven likely responses, but none of the 12 possible ones, occurred in patients with postanoxic brain injury. No likely responses were observed when infusion rates were lower than 0.9 mg/kg/h, when ketamine was introduced at least 8 days after SE onset, or after failure of seven or more drugs. Ketamine was discontinued due to possible adverse events in five patients. Complications were mostly attributed to concurrent drugs, especially other anesthetics. Mortality rate was 43% (26 of 60), but was lower when SE was controlled within 24 h of ketamine initiation (16% vs. 56%, p = 0.0047).Ketamine appears to be a relatively effective and safe drug for the treatment of RSE. This retrospective series provides preliminary data on effective dose and appropriate time of intervention to aid in the design of a prospective trial to further define the role of ketamine in the treatment of RSE.

Importance Histoplasmosis, a systemic mycosis caused by the fungus Histoplasma capsulatum, primarily affects immune-suppressed patients and commonly involves the lung and rarely the central nervous system (CNS). Herein, we report a case of isolated CNS histoplasmosis presenting with pontine stroke and meningitis. Observations A 35-year-old, white, immune-competent man was transferred from an outside facility with worsening dysarthria and confusion after having presented 4 weeks prior with dysarthria, gait ataxia, and bilateral upper extremity weakness. Brain magnetic resonance imaging revealed bilateral pontine strokes, and the working diagnosis was ischemic infarctions, presumed secondary to small vessel vasculitis. Cerebral spinal fluid (CSF) examination showed marked abnormalities including an elevated protein level (320 mg/dL), low glucose level (2 mg/dL), and high white blood cell count (330/mm 3 ; 28% lymphocytes, 56% neutrophils, and 16% monocytes) suggestive of a bacterial, fungal, or tuberculosis meningitis. Empirical antibiotics and a second trial of intravenous steroids were started before infectious etiologies of meningitis were ultimately ruled out. Repeated magnetic resonance imaging of the brain revealed no evidence of new ischemic lesions. On hospital day 11, results of his CSF Histoplasma antigen and urine antigen tests were positive. His CSF culture also was positive for H capsulatum. The patient was treated initially with liposomal amphotericin B, 430 mg daily, but changed to voriconazole, 300 mg twice daily, secondary to renal insufficiency and eventually continued treatment with itraconazole cyclodextrin, 100 mg twice daily. Computed tomographic imaging revealed obstructive hydrocephalus, and a ventriculoperitoneal shunt was placed that successfully decompressed the ventricles. At 1 year, the patient demonstrated good clinical improvement and results of follow-up CSF cultures were negative. Conclusions and Relevance While pulmonary involvement of histoplasmosis in immune-suppressed patients is common, systemic presentation of this fungal infection in immune-competent patients is rare and self-limiting. Isolated CNS histoplasmosis is exceedingly rare. Clinicians should consider CNS histoplasmosis in the differential diagnosis in atypical stroke cases, particularly those presenting with meningitis.

Abnormal platelet function may complicate the assessment and treatment of continuing blood loss, hypotension, and coagulation disorders during adult donor care. Antiplatelet drugs, such as aspirin, nonsteroidal anti-inflammatory drugs, clopidogrel (Plavix), ticlopidine (Ticlid), prasugrel (Effient), abciximab (ReoPro), eptifibatide (Integrilin), and tirofiban (Aggrastat) are commonly prescribed for older patients. These medications may be part of home therapy or may be given during acute cardiac or cerebrovascular crises that may lead to brain death and organ donation. This discussion reviews normal platelet formation and function, drug actions, methods to evaluate medication effects, pharmacological characteristics, treatment recommendations for platelet transfusion, and risks attendant with those infusions.

Historically, neurology has been a primarily outpatient specialty.1 The advent of modern neurosurgical techniques, as well as more elegant means of artificial ventilation in the 1960s, brought increasing numbers of neurologic patients to the intensive care units (ICU). Although these patients were primarily managed by medical and surgical–anesthesiologist intensivists, occasional consults for neurophysiologic testing, management of neuromuscular failure, and, more commonly, prognostication, would bring neurologists to the ICU. In the 1980s and 1990s, the surge in new neurosurgical procedures and advances in cardiovascular disease spurred on the development of a newer, different subset of neurologist. Some developed an interest in cerebrovascular diseases, while others ventured into the ICUs and carved a niche for a new subspecialty: neurocritical care. A small number of neurologists, anesthesiologists, neurosurgeons, and medical intensivists aimed to identify and correct the factors that were contributing to the high mortality rates in neurologic intensive care units (NICUs). Through the 1980s and 1990s, four major centers of NICU training emerged. These centers were headed by Dr. Allan Ropper at Massachusetts General Hospital, Dr. Matthew Fink at Columbia University, Dr. Thomas Bleck at University of Virginia at Charlottesville, and Dr. Dan Hanley at Johns Hopkins.2 These “Four fathers”3 of neurocritical care in the United States have trained numerous fellows who …

To investigate the effect of malarial infection during pregnancy on the newborn.A retrospective cohort study was conducted at The Aga Khan University Hospital (AKUH), Karachi, using in-patient hospital records over an 11-year period from 1988 to 1999. The incidence of preterm delivery, low birth weight (LBW) and intrauterine growth retardation (IUGR) in 29 pregnant women with malaria, was compared with that in 66 selected pregnant women without malaria, who delivered at the AKUH during the same time period.Pregnant women with malaria had a 3.1 times greater risk of preterm labor (p=0.14). They were more likely to be anaemic compared to women without malaria (RR=2.9, 95% CI=1.6-5.4) and had a significantly lower mean haemoglobin level (p=0.0001). Maternal malaria was significantly associated with LBW babies (p=0.001). The mean birth weight of infants born to pregnant women with malaria was 461 g less (p=0.0005). No significant association was, however, found between malarial infection during pregnancy and IUGR (p=0.33).Malarial infection during pregnancy is associated with poor maternal and fetal outcome. It is significantly associated with maternal anaemia and LBW infants. Appropriate measures must, therefore, be taken to prevent malaria during pregnancy, especially in endemic areas.

There is a wide differential diagnosis for patients presenting with multiple cranial nerve palsies, including infectious, inflammatory, malignant, genetic, toxic, and metabolic conditions. This report describes the clinical features, neuroimaging findings, and response to surgical treatment in a patient with bilateral deafness and recurrent episodes of bilateral facial nerve palsy that were caused by renal osteodystrophy. It is suggested that renal osteodystrophy be considered in the differential diagnosis of multiple cranial nerve palsies in the appropriate clinical setting.