The Experts below are selected from a list of 315 Experts worldwide ranked by ideXlab platform
John W Dunne - One of the best experts on this subject based on the ideXlab platform.
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cephalosporin related neurotoxicity Metabolic Encephalopathy or non convulsive status epilepticus
Journal of Clinical Neuroscience, 2019Co-Authors: James D Triplett, Nicholas Lawn, John W Dunne, Josephine ChanAbstract:Abstract Metabolic Encephalopathy and Non-Convulsive Status Epilepticus (NCSE) have been reported with cephalosporin use, particularly cefepime. We aimed to analyze the clinical and EEG findings in patients with cephalosporin-related neurotoxicity (CRN) at our hospital identified via the hospital EEG database, and to critically review CRN case reports in the literature. A Medline search was performed to identify CRN cases where a representative sample of EEG was provided. EEGs were analyzed using published criteria differentiating NCSE from triphasic waves (TW). Eleven patients at our hospital were identified with CRN (9 cefepime, 2 ceftriaxone): all had an Encephalopathy with decreased consciousness and/or confusion. One patient had clinical seizures and 6 had multifocal myoclonus. All patients had abnormal EEGs, all with moderate to severe generalized slowing and 10 also with TW. Recovery was related to cephalosporin withdrawal rather than antiepileptic therapy. Analysis of 37 EEG samples of CRN patients reported in the literature as NCSE (30) or TW (7) revealed that most did not meet criteria for NCSE, with 33 showing TW, 1 showing generalised epileptiform discharges and 3 being uninterpretable. CRN usually produces a toxic Encephalopathy rather than NCSE, and is commonly associated with triphasic waves on EEG. In most patients anti-epileptic and/or sedative drugs do not hasten clinical improvement.
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baclofen neurotoxicity a Metabolic Encephalopathy susceptible to exacerbation by benzodiazepine therapy
Journal of Clinical Neurophysiology, 2019Co-Authors: James D Triplett, Nicholas Lawn, John W DunneAbstract:Purpose:Baclofen has been reported to cause both a Metabolic Encephalopathy and nonconvulsive status epilepticus. Baclofen is typically used in the management of muscle spasticity but is being increasingly used to manage alcohol withdrawal and opiate dependency. Given the increasing use of baclofen
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baclofen neurotoxicity a Metabolic Encephalopathy susceptible to exacerbation by benzodiazepine therapy p6 356
Neurology, 2016Co-Authors: James D Triplett, Nicholas Lawn, John W DunneAbstract:Background: Baclofen, a gamma-aminobutyric acid derivative, is commonly used in the treatment of spasticity. Baclofen toxicity can produce an Encephalopathy sometimes associated with myoclonus and seizures. Associated EEG abnormalities include generalized slowing, and periodic triphasic complexes and sharp waves that have been reported as non-convulsive status epilepticus (NCSE). Methods: Baclofen toxicity was defined as an Encephalopathy in the setting of baclofen use and without other identifiable cause. Patients with baclofen toxicity were identified from an EEG database, and their clinical and EEG findings analysed. Results: 13 patients were identified, aged 29 to 81 years. All were receiving oral baclofen in doses ranging from 10mg to 200mg daily, most commonly for spasticity (10 patients). All patients were confused, 11 with reduced consciousness and 4 requiring intubation. 5 patients had myoclonus, 2 of whom also had tonic-clonic seizures. All patients had abnormal EEGs. 12 patients had moderate-to-severe generalized slowing. 8 patients had generalized, bisynchronous triphasic sharp waves occurring at 1-2 Hz , sometimes with an anterior to posterior phase lag. Three patients received small doses of intravenous midazolam or diazepam, in all cases resulting in marked depression of consciousness and respiration, and without any subsequent improvement in the conscious state. Suppression of periodic complexes and all EEG activity following intravenous midazolam was confirmed in one patient, having continuous EEG monitoring. Baclofen was discontinued in all patients. Serial plasma Baclofen levels were measured in 2 patients. Falling levels mirrored clinical and electrophysiological improvement. Conclusions: Baclofen toxicity can produce an acute Encephalopathy even at modest doses. When present, periodic sharp triphasic complexes on EEG are a manifestation of a toxic Encephalopathy rather than NCSE. These patients exhibit a marked vulnerability to the depressant effects of benzodiazepines, even at small doses. Improvement follows a time course consistent with the period required for baclofen clearance. Disclosure: Dr. Triplett has nothing to disclose. Dr. Lawn has nothing to disclose. Dr. Dunne has nothing to disclose.
Howard E Gendelman - One of the best experts on this subject based on the ideXlab platform.
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hiv 1 associated dementia a Metabolic Encephalopathy perpetrated by virus infected and immune competent mononuclear phagocytes
Journal of Acquired Immune Deficiency Syndromes, 2002Co-Authors: Eric R Anderson, Walter E Zink, Huangui Xiong, Howard E GendelmanAbstract:Infection of the nervous system by HIV-1 commonly causes a broad range of cognitive, behavioral, and motor abnormalities called, in its most severe form, HIV-1-associated dementia (HAD). HAD is a Metabolic Encephalopathy caused by productive viral infection of brain mononuclear phagocytes (MPs) (perivascular and parenchymal brain macrophages and microglia) and sustained by paracrine-amplified, inflammatory, neurotoxic responses. MP neurotoxins are, in large measure, homeostatic secretory products that can have a negative effect on neuronal cell function when produced in abundance. Proinflammatory cytokines, chemokines, platelet-activating factor, arachidonic acid and its metabolites, nitric oxide, quinolinic acid, progeny virions, and viral structural and regulatory proteins are all included as part of these cellular and viral toxic elements. In addition, neuronal damage can occur directly by engaging specific receptors or through inducing widespread inflammatory activities in brain tissue that ultimately induce neuronal demise. The mechanisms for immune- and viral-mediated neural injury in HAD are made more striking by the effects of abused drugs on cognitive function. Ultimately, linkages between neuronal function and disordered MP immunity will provide insights into how HIV-1 infection of the brain leads to compromised mental function as well as providing clues into the pathogenesis of other neurodegenerative disorders.
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the hiv 1 associated dementia complex a Metabolic Encephalopathy fueled by viral replication in mononuclear phagocytes
Current Opinion in Neurology, 1997Co-Authors: Jialin C Zheng, Howard E GendelmanAbstract:: HIV enters the brain soon after virus exposure but elicits profound neurological deficits in infected humans years later usually during progressive immunosuppression and the development of the acquired immune deficiency syndrome. The neurological disease complex associated with virus infection occurs in a large proportion of infected patients and is commonly referred to as HIV-1 associated dementia complex. The neuropathogenesis of central nervous system/viral infection revolves around mononuclear phagocytes (brain macrophage/microglial) infection and immune activation in brain. Macrophages secrete neurotoxic factors that elicit neuronal injury and inevitably death leading to the constellation of cognitive and motor impairments common during progressive disease. Neurotoxic factor production requires virus entry and replication, the evolution/selection of neurovirulent HIV-1 strains and the production of viral and cellular immune factors injurious to human neurons. Interestingly, neurological deficits, the HIV-1 associated neuropathology and viral replication disease are not always associated. This has led to the notion that viral replication induces the autocrine/paracrine production of cellular/viral factors leading to a Metabolic Encephalopathy. Anti-retroviral and anti-inflammatory therapies should prove increasingly beneficial for treatment and, ultimately, reversal of HIV-1 associated dementia complex in the affected human host.
James D Triplett - One of the best experts on this subject based on the ideXlab platform.
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cephalosporin related neurotoxicity Metabolic Encephalopathy or non convulsive status epilepticus
Journal of Clinical Neuroscience, 2019Co-Authors: James D Triplett, Nicholas Lawn, John W Dunne, Josephine ChanAbstract:Abstract Metabolic Encephalopathy and Non-Convulsive Status Epilepticus (NCSE) have been reported with cephalosporin use, particularly cefepime. We aimed to analyze the clinical and EEG findings in patients with cephalosporin-related neurotoxicity (CRN) at our hospital identified via the hospital EEG database, and to critically review CRN case reports in the literature. A Medline search was performed to identify CRN cases where a representative sample of EEG was provided. EEGs were analyzed using published criteria differentiating NCSE from triphasic waves (TW). Eleven patients at our hospital were identified with CRN (9 cefepime, 2 ceftriaxone): all had an Encephalopathy with decreased consciousness and/or confusion. One patient had clinical seizures and 6 had multifocal myoclonus. All patients had abnormal EEGs, all with moderate to severe generalized slowing and 10 also with TW. Recovery was related to cephalosporin withdrawal rather than antiepileptic therapy. Analysis of 37 EEG samples of CRN patients reported in the literature as NCSE (30) or TW (7) revealed that most did not meet criteria for NCSE, with 33 showing TW, 1 showing generalised epileptiform discharges and 3 being uninterpretable. CRN usually produces a toxic Encephalopathy rather than NCSE, and is commonly associated with triphasic waves on EEG. In most patients anti-epileptic and/or sedative drugs do not hasten clinical improvement.
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baclofen neurotoxicity a Metabolic Encephalopathy susceptible to exacerbation by benzodiazepine therapy
Journal of Clinical Neurophysiology, 2019Co-Authors: James D Triplett, Nicholas Lawn, John W DunneAbstract:Purpose:Baclofen has been reported to cause both a Metabolic Encephalopathy and nonconvulsive status epilepticus. Baclofen is typically used in the management of muscle spasticity but is being increasingly used to manage alcohol withdrawal and opiate dependency. Given the increasing use of baclofen
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baclofen neurotoxicity a Metabolic Encephalopathy susceptible to exacerbation by benzodiazepine therapy p6 356
Neurology, 2016Co-Authors: James D Triplett, Nicholas Lawn, John W DunneAbstract:Background: Baclofen, a gamma-aminobutyric acid derivative, is commonly used in the treatment of spasticity. Baclofen toxicity can produce an Encephalopathy sometimes associated with myoclonus and seizures. Associated EEG abnormalities include generalized slowing, and periodic triphasic complexes and sharp waves that have been reported as non-convulsive status epilepticus (NCSE). Methods: Baclofen toxicity was defined as an Encephalopathy in the setting of baclofen use and without other identifiable cause. Patients with baclofen toxicity were identified from an EEG database, and their clinical and EEG findings analysed. Results: 13 patients were identified, aged 29 to 81 years. All were receiving oral baclofen in doses ranging from 10mg to 200mg daily, most commonly for spasticity (10 patients). All patients were confused, 11 with reduced consciousness and 4 requiring intubation. 5 patients had myoclonus, 2 of whom also had tonic-clonic seizures. All patients had abnormal EEGs. 12 patients had moderate-to-severe generalized slowing. 8 patients had generalized, bisynchronous triphasic sharp waves occurring at 1-2 Hz , sometimes with an anterior to posterior phase lag. Three patients received small doses of intravenous midazolam or diazepam, in all cases resulting in marked depression of consciousness and respiration, and without any subsequent improvement in the conscious state. Suppression of periodic complexes and all EEG activity following intravenous midazolam was confirmed in one patient, having continuous EEG monitoring. Baclofen was discontinued in all patients. Serial plasma Baclofen levels were measured in 2 patients. Falling levels mirrored clinical and electrophysiological improvement. Conclusions: Baclofen toxicity can produce an acute Encephalopathy even at modest doses. When present, periodic sharp triphasic complexes on EEG are a manifestation of a toxic Encephalopathy rather than NCSE. These patients exhibit a marked vulnerability to the depressant effects of benzodiazepines, even at small doses. Improvement follows a time course consistent with the period required for baclofen clearance. Disclosure: Dr. Triplett has nothing to disclose. Dr. Lawn has nothing to disclose. Dr. Dunne has nothing to disclose.
Byung Chul Shin - One of the best experts on this subject based on the ideXlab platform.
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severe hypophosphatemia induced acute toxic Metabolic Encephalopathy in continuous renal replacement therapy
Electrolyte & Blood Pressure, 2019Co-Authors: Ha Yeol Park, Jong In Choi, Da Yeong Kang, Jong Hoon Chung, Byung Chul ShinAbstract:: Acute toxic-Metabolic Encephalopathy (TME) is an acute condition of global cerebral dysfunction in the absence of primary structural brain disease. Severe hypophosphatemia leads to muscle weakness and involves the diaphragm but hypophosphatemia-induced TME is very rare. Herein, we report the case of a 43-year-old woman with Encephalopathy with severe hypophosphatemia during continuous renal replacement therapy. She presented with features of oliguric acute kidney injury on diabetic kidney disease due to volume depletion. At admission, her mental status was alert but gradually changed to stupor mentation during continuous renal replacement therapy. Her phosphate level was less than 0.41 mEq/L and Glasgow coma scale decreased from 15 to 5. After phosphate intravenous replacement and administration of phosphate-containing replacement solution, the phosphate level increased to 2.97 mEq/L and mental state returned to alert state. This case demonstrates that the level of phosphorus should be observed during continuous renal replacement therapy.
A I Arieff - One of the best experts on this subject based on the ideXlab platform.
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age gender and vasopressin affect survival and brain adaptation in rats with Metabolic Encephalopathy
American Journal of Physiology-regulatory Integrative and Comparative Physiology, 1995Co-Authors: A I Arieff, E Kozniewska, Timothy P L Roberts, Zinaida S Vexler, J C Ayus, J KucharczykAbstract:Children and menstruant women are far more likely than men to develop Metabolic brain damage from hyponatremia. We evaluated brain adaptation and mortality from hyponatremia in male and female rats of three different age groups. With acute hyponatremia, the mortality was 84% in prepubertal rats vs. 15% in adults and 0% in elderly rats. With chronic hyponatremia, mortality was 13% in adult males vs. 62% in females. Testosterone pretreatment significantly decreased mortality (from 62 to 9% in adult females, and from 100% to zero in prepubertal rats), but estrogen significantly increased mortality (from 13 to 44% in adult males). With acute hyponatremia in adult rats, brain sodium was significantly decreased (-17%), but in prepubertal rats it was actually increased (+ 37%). Cerebral perfusion during chronic hyponatremia was significantly impaired in adult females vs. males or controls (P < 0.01). Neither vasopressin administration nor chronic hyponatremia induced with desmopressin resulted in any mortality or decrement of cerebral perfusion. Thus age, gender, and the cerebral effects of vasopressin are major determinants of mortality in experimental Metabolic Encephalopathy.
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Metabolic Encephalopathy as a complication of renal failure mechanisms and mediators
New horizons (Baltimore Md.), 1994Co-Authors: C L Fraser, A I ArieffAbstract:Abstract Among patients with end-stage renal disease, nervous system dysfunction remains a major cause of disability. Patients with chronic renal failure who have not yet received dialysis may develop symptoms ranging from mild sensorial clouding to delirium and coma. Dialysis itself is associated with at least three distinct disorders of the CNS: dialysis disequilibrium syndrome; dialysis dementia; and progressive intellectual dysfunction. Peripheral neuropathy is also a major cause of disability in uremic subjects. It is believed that aluminum contributes to the pathogenesis of dialysis dementia. Biochemically, brain calcium is elevated in patients with renal failure, probably because of actions of parathyroid hormone on the brain. The diagnosis of dialysis disequilibrium syndrome, intellectual dysfunction, dialysis dementia, and uremic neuropathy can be made by the characteristic clinical pictures of these syndromes and the exclusion of other causes of nervous system dysfunction.