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1/13. Gamma-hydroxybutyrate withdrawal syndrome.

    STUDY OBJECTIVE: Gamma-hydroxybutyrate (GHB) withdrawal syndrome is increasingly encountered in emergency departments among patients presenting for health care after discontinuing frequent GHB use. This report describes the characteristics, course, and symptoms of this syndrome. methods: A retrospective review of poison center records identified 7 consecutive cases in which patients reporting excessive GHB use were admitted for symptoms consistent with a sedative withdrawal syndrome. One additional case identified by a medical examiner was brought to our attention. These medical records were reviewed extracting demographic information, reason for presentation and use, concurrent drug use, toxicology screenings, and the onset and duration of clinical signs and symptoms. RESULTS: Eight patients had a prolonged withdrawal course after discontinuing chronic use of GHB. All patients in this series were psychotic and severely agitated, requiring physical restraint and sedation. Cardiovascular effects included mild tachycardia and hypertension. Neurologic effects of prolonged delirium with auditory and visual hallucinations became episodic as the syndrome waned. Diaphoresis, nausea, and vomiting occurred less frequently. The onset of withdrawal symptoms in these patients was rapid (1 to 6 hours after the last dose) and symptoms were prolonged (5 to 15 days). One death occurred on hospital day 13 as withdrawal symptoms were resolving. CONCLUSION: In our patients, severe GHB dependence followed frequent ingestion every 1 to 3 hours around-the-clock. The withdrawal syndrome was accompanied initially by symptoms of anxiety, insomnia, and tremor that developed soon after GHB discontinuation. These initial symptoms may progress to severe delirium with autonomic instability.
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2/13. confusion and dysphoria with low-dose topiramate in a patient with bipolar disorder.

    BACKGROUND: Topiramate, a newer antiepileptic agent, may benefit several neurological and psychiatric states, including bipolar disorder. CASE REPORT: A physically healthy, stockily built, 47-year-old, hypomanic Asian male with a >20-year history of uneventful use of psychotropic agents received topiramate in a dose that was stepped up to 100 mg/day across 10 days. He developed dysphoria, confusion, word-finding difficulties, and difficulties in maintaining a train of thought; the symptoms vanished within a week of drug discontinuation, and reappeared 1-2 days after rechallenge at a dose of 25 mg/day. CONCLUSION: It appears that, while confusion is usually a dose-dependent adverse effect of topiramate, certain patients may idiosyncratically develop this adverse effect at very low doses.
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3/13. Bizarre behavior during intracarotid sodium amytal testing (Wada test): are they predictable?

    The intracarotid sodium amytal test (ISAT or Wada Test) is a commonly performed procedure in the evaluation of patients with clinically refractory epilepsy candidates to epilepsy surgery. Its goal is to promote selective and temporary interruption of hemispheric functioning, seeking to define language lateralization and risk for memory compromise following surgery. Behavioral modification is expected during the procedure. Even though it may last several minutes, in most cases it is subtle and easily manageable. We report a series of patients in whom those reactions were unusually bizarre, including agitation and aggression. Apart of the obvious technical difficulties (patients required physical restraining) those behaviors potentially promote testing delay or abortion and more importantly, inaccurate data. We reviewed those cases, seeking for features that might have predicted their occurrence. overall, reactions are rare, seen in less than 5% of the ISAT procedures. The barbiturate effect, patients' psychiatric profiles, hemisphere dominance or selectiveness of the injection were not validated as predictors. Thorough explanation, repetition and simulation may be of help in lessening the risk of those reactions.
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4/13. risperidone-induced psychosis and depression in a child with a mitochondrial disorder.

    OBJECTIVE: To our knowledge, this is the first published case report of an adolescent girl with a mitochondrial disorder and depression who displayed both new-onset psychotic and increased mood symptoms during treatment with risperidone. DATA: A 16-year-old girl was treated with risperidone for mood lability and impulsivity at a community hospital. Within days, she developed paranoid ideation, profound psychomotor retardation, increased depression, and fatigue. She was transferred to an inpatient psychiatric hospital, where she was taken off risperidone. Within 48 hours after discontinuation of the medication, she had complete resolution of psychotic symptoms, fatigue, and psychomotor retardation, and her depression improved. CONCLUSIONS: This observation of "on-off" risperidone treatment suggests that risperidone may have worsened both psychiatric and physical manifestations of the mitochondrial disorder in this adolescent. These findings are consistent with recent in vitro literature, which implicate a series of neuroleptic medications with mitochondrial dysfunction. Furthermore, the authors provide diagnostic and treatment options that are available for mitochondrial disorders, which are of interest to child psychiatrists due to the central nervous system manifestations of these disorders.
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5/13. dextromethorphan psychosis, dependence and physical withdrawal.

    As part of a synthesis of evidence regarding the abuse and addiction liability of dextromethorphan (DM), an over-the-counter cough medicine available in over 140 preparations, an uncommonly published case of dextromethorphan dependence (addiction) is described, with specific, rarely published complications. The individual was interviewed and several medical databases were also reviewed (medline, 1966-present; pubmed) for all content relating to the Keywords: dextromethorphan, abuse, dependence, cough medicine, addiction, withdrawal, psychosis. The patient evidenced history suggesting substance dependence, substance-induced psychosis and substance withdrawal in relation to DM. A literature review revealed that DM has specific serotonergic and sigma-1 opioidergic properties. dextrorphan (DOR), the active metabolite of DM, has similar properties; however, DOR is a weaker sigma opioid receptor agonist, and a stronger NMDA receptor antagonist. DM and DOR display specific biological features of addiction, and are capable of inducing specific psychiatric sequelae. A specific, reproducible toxidrome with significant psychiatric effects occurred, when DM was abused at greater than indicated doses, with more profound and potentially life-threatening effects at even higher doses. DM withdrawal appears evident. DM's active metabolite, DOR, has pharmacodynamic properties and intoxication effects similar to dissociatives, and may be more responsible for the dissociative effect that this DM abuser sought. However, it is this same metabolite that may be fraught with the potentially life-threatening psychoses and dissociative-induced accidents, as well as addiction. While DM has been hypothesized as the most commonly abused dissociative, health-care providers seem largely unaware of its toxidrome and addiction liability.
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6/13. cimetidine-induced psychosis in a 14-year-old girl.

    A 14-year-old girl presented with hallucinations and bizarre behaviour 3 days following the institution of cimetidine therapy for acute gastritis. She had no history of drug abuse or psychiatric disorders, and physical examination and laboratory investigations yielded no abnormalities. Within 24 hours after cimetidine therapy was discontinued her behaviour returned to normal and the hallucinations stopped.
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7/13. Anticholinergic psychosis.

    A case of anticholinergic psychossis in a 17-year-old male following suspected ingestion of an unknown amount of benztropine mesylate is discussed. The borderline mentally retarded patient exhibited acute psychosis and physical signs common to anticholinergic and amphetamine intoxications such as mydriasis, tachycardia and hypertension. Intramuscular chlorpromazine hydrochloride and oral haloperidol were administered to sedate the patient. The differential diagnosis of anticholinergic intoxication was based on the patient's physical and mental symptoms, the short duration of the psychosis and a negative urine assay for amphetamine. The neuropsychiatric signs of and treatment for anticholinergic psychosis are discussed. physostigmine salicylate is the drug of choice for reversing the signs and symptoms of anticholinergic poisoning. benzodiazepines may be used if sedation is indicated, but use of phenothiazines for this purpose should be avoided.
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8/13. hyponatremia and rhabdomyolysis: a possible relationship.

    A 40-year-old schizophrenic presenting with an acute toxic psychosis was found to be severely hyponatremic with a serum osmolality of 217 mOsm/kg. The patient was combative and required physical restraints. Shortly after admission the patient's serum transaminase level was elevated, and the next day the CPK value was 175,000 IU. In addition, his serum and urinary myoglobin levels were markedly raised. Shortly after rhabdomyolysis was diagnosed, the patient developed reversible acute renal failure presumably secondary to the myoglobinuria. This report examines the possibility that the severe hyponatremia and hypoosmolality caused his skeletal muscles to become potassium depleted, leading to rhabdomyolysis during the stenuous exercise involved in his battling the restraints.
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9/13. LSD 'flashback' as a cause of diagnostic error.

    An emaciated, but otherwise physically normal young man presented with an acute psychosis resembling hallucinogenic drug abuse. His behaviour was so strange that the underlying pathology of severe pyloric stenosis was only detected when a chance measurement of urea and electrolytes was made, revealing gross biochemical abnormalities. His abnormal mental state persisted for more than one week and an LSD 'flashback' was postulated as the cause of the prolonged psychosis
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10/13. Benzodiazepine administration induces exogenic psychosis: a case of child abuse.

    An 11-year-old boy with psychiatric symptoms was brought to the pediatric clinic by his father. The boy exhibited anxiety, sometimes exaggerating to panic reactions, rage, and disorientation. Because of the boy's behavior it was presumed he was having delusions. Careful physical examination revealed evidence of physical abuse. This article alerts readers to the possible combination of physical abuse and purposeful drug administration.
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