Cerebrospinal fluid monoamine metabolism in a case of neuroleptic malignant syndrome improved by electroconvulsive therapy

Nisijima, Koichi; Oyafuso, Katumi; Shimada, Tatuhiro; Hosino, Hitoshi; Ishiguro, Takeo

doi:10.1016/0006-3223(95)00389-4

Cited by 10 publications

(1 citation statement)

References 3 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Predisposition to exaggerated sympathetic nervous system activity in response to emotional or psychological stress, along with variables such as psychotic distress or excessive dopamine antagonism, could pave the way to the induction of NMS [ 28 ]. This is supported by markedly elevated catecholamines in cerebral spinal fluid in patients with NMS; norepinephrine concentration was two times greater during acute illness in these patients than in matched controls during convalescence [ 30 ]. Similar findings have been reported for serotonin [ 31 ].…”

Section: Pathology Of Toxin Induced Temperature Disturbances and Theimentioning

confidence: 99%

Bench-to-bedside review: Mechanisms and management of hyperthermia due to toxicity

Eyer

Zilker

2007

Crit Care

View full text Add to dashboard Cite

Body temperature can be severely disturbed by drugs capable of altering the balance between heat production and dissipation. If not treated aggressively, these events may become rapidly fatal. Several toxins can induce such non-infection-based temperature disturbances through different underlying mechanisms. The drugs involved in the eruption of these syndromes include sympathomimetics and monoamine oxidase inhibitors, antidopaminergic agents, anticholinergic compounds, serotonergic agents, medicaments with the capability of uncoupling oxidative phosphorylation, inhalation anesthetics, and unspecific agents causing drug fever. Besides centrally disturbed regulation disorders, hyperthermia often results as a consequence of intense skeletal muscle hypermetabolic reaction. This leads mostly to rapidly evolving muscle rigidity, extensive rhabdomyolysis, electrolyte disorders, and renal failure and may be fatal. The goal of treatment is to reduce body core temperature with both symptomatic supportive care, including active cooling, and specific treatment options. IntroductionBody temperature regulation is complex and requires a balance between heat production and dissipation. Hyperthermia occurs when metabolic heat production exceeds heat dissipation. Many exogenously administered drugs are capable of altering the body's ability to maintain a constant temperature.Normal body temperature is approximately 37.0°C, although this varies with the time of day. The Society of Critical Care Medicine has defined fever as a body temperature of ≥38.3°C, which has gained wide acceptance [1]. Adaptive thermogenesis by heat production is controlled through hypothalamic regulation of the sympathetic nervous system [2]. The preoptic nucleus of the anterior hypothalamus responds to core temperature changes and regulates the autonomic nervous system, inducing either cutaneous vasodilatation, which dissipates heat, or vasoconstriction, which conserves heat [3]. Norepinephrine, dopamine and serotonin have all been suggested to play major roles in regulating hypothalamic control of body temperature [4]. Sympathetic nervous system activation contributes to effects on thermogenesis through cutaneous vasoconstriction and nonshivering thermogenesis [5]. Thus, drugs altering the hypothalamic levels of these neurotransmitters are capable of altering body temperature regulation [6]. Activation of the hypothalamic-pituitary-thyroid and the hypothalamic-pituitaryadrenal axes are adjacent mechanisms in regulating body core temperature that can be influenced by drugs that affect them. Nonshivering thermogenesis occurs primarily by uncoupling of oxidative phosphorylation through the activity of a group of mitochondrial proteins known as uncoupling proteins.Uncontrolled hyperthermia is independently associated with increased morbidity and mortality [7]. Hyperthermia may cause rhabdomyolysis, liver failure, disseminated intravasal coagulation and multi-organ failure [8]. It accentuates excitotoxic neurotransmitter release, increases production ...

show abstract

Section: Pathology Of Toxin Induced Temperature Disturbances and Theimentioning

confidence: 99%