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PubMed1997

Psychiatric manifestations accompanying interferon therapy for patients with chronic hepatitis C: an overview of cases in Japan.

Thirty case reports published in Japan that refer to psychiatric symptoms accompanying interferon (IFN) therapy were examined. These papers covered a total of 49 cases. We categorized these 49 cases into 35 cases of mood disorder, 10 of delirium and four of psychotic disorder. The key findings of our study of these cases are as follows: (i) in total, 11 patients had psychiatric past histories: five patients in the mood disorders group were susceptible to the influence of social or psychological factors; (ii) whereas the symptoms of mood disorder or delirium appeared soon after IFN was administered, the symptoms of psychotic disorders appeared later. The patients with delirium displayed many neurological abnormalities, which were reduced by suspending IFN therapy. This suggests the neurological toxicity of IFN; (iii) the outcome of most patients was good; and (iv) we suspect that IFN-induced psychiatric symptoms other than delirium are connected with psychoneuroimmunological functions.

Delirium↗
PubMed1996

Acute psychosis associated with abrupt withdrawal of carbamazepine following intoxication.

Carbamazepine is regularly used in the treatment of trigeminal neuralgia. Although exacerbation of psychosis has been described following abrupt discontinuation of carbamazepine in chronic schizophrenics, a withdrawal syndrome has not been reported previously in patients treated for trigeminal neuralgia. The case presented here suggests that abrupt withdrawal of toxic concentrations of carbamazepine may precipitate a withdrawal reaction, which is manifest some days after discontinuation of the drug. Therefore it may be advisable to withdraw therapy slowly in these situations.

Acute Disease↗
PubMed2000

[Visual hallucinations in Parkinson and Charles Bonnet Syndrome patients. A phenomenological and pathogenetic comparison].

UNLABELLED: Visual hallucinations (VH) are seen in about a third of all patients with Parkinson's disease (PD) and are usually considered to be an early marker or clinical component of a dopaminergic psychosis. Their peculiar phenomenology has not yet been studied in a systematic manner. METHODS: A semi-structured interview was performed twice in 62 PD patients. Different motoric and cognitive disease scales were used. The patients were not demented or depressed and had no other psychotic features other than hallucinations. Their visions was at least 0.6. RESULTS: 22 patients (36%) reported complex visual hallucinations or illusions in both interviews. These patients were not different from the non-hallucinating patients in terms of age, duration and stage of the disease, dosage and type of medication and frequency of cataracts. VH were diurnal in 41% of the patients, nocturnal in 18% of the patients and mixed in 41 patients. They were seen at least once weekly in 67% and they lasted always less than an hour. VH most frequently involved adults, children and pets. They were often mobile and had normal size and physiognomy. Notable emotional reactions were only reported by 18% of the patients. DISCUSSION: The phenomenology of VH in PD differs from VH in exogenous or endogenous psychoses, but is similar to the Charles Bonnet-syndrome (CBS), appearing in elderly patients with different visual deficits. As PD patients suffer regularly from visual deficits of contrast and color perception, a similar pathogenesis to CBS can be hypothesized, with these "minor" and benign VH being due to "release phenomena" in relation to partial visual deprivation. The lack of multimodality hallucinations and of secondary paranoia as well as the clear sensorium are helpful features in distinguishing them from toxic psychosis.

Aged↗
PubMed2001

[Interferon alpha-associated agranulocytosis during clozapine treatment. Case report and status of current knowledge].

Little is known about possibilities of chronic hepatitis C treatment with interferon-alpha (IFN-alpha) in psychiatric patients continuously taking antipsychotics. We report on a 28-year-old hepatitis C-positive man with paranoid psychosis. He was successfully treated with clozapine, an atypical antipsychotic drug which is known for the risk of granulocytopenia and agranulocytosis. With doses up to 200 mg/day over 3 years, he showed no remarkable changes in WBC. Because of the chronic hepatitis C with genotype 3a, additional treatment was started with IFN-alpha (s.c., 3 x 6 million IU/week). After 2 months of therapy he developed a severe agranulocytosis. Both clozapine and IFN-alpha were discontinued, and his WBC returned to normal. Results from bone marrow examination were compatible with a toxic reaction possibly caused by either or both medications. We discuss possible problems with IFN-alpha during the treatment of psychiatric patients, interactions with psychiatric medication, and hematotoxic side effects like those from clozapine. We recommend combining IFN-alpha with less "toxic" antipsychotics and weekly checks of WBC.

Adult↗
PubMed1976

[Clinico-morphologic characteristics of cases of alcoholic delirium with lethal outcome].

The authors conducted a clinico-morphogicaly analysis of 12 cases (10 males and 2 females) of alcoholic delirium with a lethal outcome. All 12 patients were alcohol abusers (from 5--22 years). Pathoanatomical changes of the brain and internal organs were characterized by traits of chronic alcoholic encephalopathy accompanied by elements of toxic damage of the nervous tissue. The main factor in the genesis of this severe disorder is a diffuse acute toxic damage of the minor vessels of the cortex and white brain matter (more expressed in the frontal areas of the hemispheres). The authors discuss the pathogenetical role of hepatic lesions in alcoholic delirium.

Adult↗
PubMedDate not supplied

[A case of toxic psychosis caused by trichloroethylene].

A case of chronic intoxication by trichloroethylene--it is a liquid generally used as a fat solvent--is described in a young man aged eighteen who had been inhaling it for months while he was doing his military service. Hallucinatory symptoms--visual as well as verbal ones--appear over a slightly confusional basis but he also suffers from several psychotic symptoms like the feeling of a threat to his ego, depersonalization and some others. He is explored and evaluated by means of specific tests for psychotics--such as the Frankfurt psychopathological inventory which was introduced in Spain by these very authors. Structural and psychopathological relations among different types of psychoses--mainly those which are purely hallucinatory and the schizophreniform ones--are discussed based on their our doctrinal theories quoted in the bibliography.

Adolescent↗
PubMed1987

"Doom anxiety" and delirium in lidocaine toxicity.

Of 15 patients with psychiatric reactions to lidocaine, 12 (80%) had mood changes, 11 (73%) had "doom anxiety," eight (53%) had overt confusional states, and six (40%) had hallucinations and delusions. The authors contend that morbid fears of impending doom or the belief that death has occurred are specific manifestations of lidocaine toxicity and may be mistakenly attributed to "understandable" fears about death during the course of recovery from a myocardial infarction on the coronary care unit.

Aged↗
PubMedDate not supplied

Neurological and behavioral toxicity of kryptopyrrole in the rat.

Ten rats were given 9.1 to 82 mg/kg of 2,4-dimethyl-3-ethylpyrrole (kryptopyrrole) and the behavioral and electroencephalographic effects were studied. Kryptopyrrole was found to decrease EEG voltage, disrupt synchronization and induce abnormal spiking at a variety of cortical sites. Intermittent periods of low frequency hypersynchronous EEG activity was consistently elicited by kryptopyrrole. These waves bear a resemblance to the hypersynchronous EEG patterns associated with hallucinatory agents such as LSD-25. Marked behavioral alterations were observed following the initial injection including ataxia, hyperventilation, locomotor depression and catelepsy. Kryptopyrrole causes major central nervous system dysfunction, and these findings are discussed in the context of a drug-induced model of psychoses.

Animals↗
PubMed1993

Dissimilar patterns of degeneration in brain following four different addictive stimulants.

Patterns of neural degeneration were compared following continuous administration of four drugs of addiction, each of which induces model psychoses in chronic addicts. D-amphetamine (D-Amph), cocaine (Coc), or phencyclidine (PCP) were administered continuously over a 5-day period. Both D-Amph and Coc induced pronounced degeneration in fasciculus retroflexus, but only D-Amph further induced substantial degeneration in striatum. Continuous PCP produced entirely different degeneration largely confined to the posterior entorhinal cortex, ventral dentate gyrus, and cingulate cortex. Methamphetamine (Meth) administered in the very high dose but less prolonged drug regimen often employed in studies of dopamine toxicity induced pronounced degeneration in striatum, but widespread degeneration in many other regions as well. These results indicate that drugs of abuse with psychotomimetic properties induce distinctively different patterns of neural degeneration, a finding with implications for theories of addiction and psychosis. They predict two different anatomical loci for alterations in psychosis: fasciculus retroflexus and ventral parahippocampus and hippocampus.

Animals↗
PubMed1981

Toxic psychosis following use of quinacrine.

Toxic psychosis due to quinacrine treatment represents an infrequent, but serious psychiatric complication. Psychiatrists should be familiar with this side effect as quinacrine continues to be used as an antimalarial, as an antihelmintic and as an antineoplastic agent. A case of a young male is presented who developed an acute toxic psychosis which necessitated psychiatric hospitalization. The case is discussed in light of previously published clinical reports and experimental studies. It appears that quinacrine acts as a cortical stimulant, but the exact mechanism of its action on the CNS is not clear at this point.

Adolescent↗
PubMed1984

Phencyclidine (PCP): some human studies.

Studies on the effects of PCP have been conducted in volunteers in the Army Laboratories and elsewhere and in illicit users. The present review has summarized the observations of many investigators which showed that the acute effects of PCP following several routes of administration were shown to be dose-related. High doses of PCP produce disturbing manifestations including psychosis, numbness, light-headedness, vertigo, ataxia, and nystagmus due to acute intoxication. Furthermore, some subjects became irritable, argumentative or negative under the conditions of social stress and demanding tasks. In addition to a variety of central action, PCP has also been shown to affect cardiovascular function, heat storage, and exercise performance. PCP can also induce, although rarely, prolonged toxic psychosis in chronic abusers and precipitate psychotic episodes in psychotic and prepsychotic personalities. Tolerance, but not physical dependence, develops to the effects of PCP. Psychologic dependence as indicated by craving for the drug has however been reported.

Administration, Oral↗
PubMed2000

Disulfiram revisited.

Disulfiram can be important in helping motivated alcoholics to remain abstinent. Prescribers should be aware of disulfiram's toxicity, and how to recognize and manage reactions. A number of other agents are available to help alcoholics remain sober, although these do not necessarily obviate use of disulfiram. Also, disulfiram may have a wider role in the management of the addictions, e.g. in cocaine use.

Alcohol Deterrents↗
PubMed2000

Neurotoxicity of calcineurin inhibitors: impact and clinical management.

Between 10%-28% of patients who receive the immunosuppressant cyclosporine (CsA) experience some form of neurotoxic adverse event. Both sensorial motoric functions may be adversely affected, and thus patients present with a wide range of neurological and psychiatrical disorders. Mild symptoms are common and include tremor, neuralgia, and peripheral neuropathy. Severe symptoms affect up to 5 % of patients and include psychoses, hallucinations, blindness, seizures, cerebellar ataxia, motoric weakness, or leukoencephalopathy. Tacrolimus is associated with similar neurotoxic adverse events. Neurotoxicity may result in serious complications for some patients, particularly recipients of orthotopic liver transplants. Factors that may promote the development of serious complications include advanced liver failure, hypertension, hypocholesterolemia, elevated CsA or tacrolimus blood levels, hypomagnesemia, and methylprednisolone. Occipital white matter appears to be uniquely susceptible to the neurotoxic effects of CsA; injury to both the major and minor vasculature may cause hypoperfusion or ischemia and local secondary toxicity in the white matter. Calcineurin inhibition by CsA and tacrolimus alters sympathetic outflow, which may play a role in the mediation of neurotoxic and hypertensive adverse events. The symptoms of CsA- and tacrolimus-associated neurotoxicity may be reversed in most patients by substantially reducing the dosage of immunosuppressant or discontinuing these drugs. However, some patients have experienced permanent or even fatal neurological damage even after dose reduction or discontinuation. CsA-sparing and tacroli-mus-sparing drug regimens that use the immunosuppressant mycophenolate mofetil, which has no neurotoxic effects, may reduce the incidence and severity of neurotoxic adverse events while maintaining an adequate level of immunoisuppression.

Calcineurin Inhibitors↗
PubMed2000

Agony and ecstasy: a review of MDMA effects and toxicity.

BACKGROUND: Ecstasy is a recreational drug with an anecdotal reputation for safety. However, reports of adverse effects and fatalities have increased in the medical and popular press. METHOD: Literature search and review. RESULTS: Acute Ecstasy toxicity does not appear to be due to overdose and cannot be solely attributed to the nature of the usual ambient environment. Adverse effects include hyperthermia, seizures, cardiac arrhythmias, hepatotoxicity, hyponatraemia and many psychiatric disorders. Ecstasy causes serotonergic neurotoxicity in the brains of animals at doses close to those used by humans, but its long-term effect on the human brain is unknown. CONCLUSION: Ecstasy toxicity should be considered in the differential diagnosis of a variety of medical and psychiatric conditions. Given its popularity, both the acute and the potential long-term effects are a cause for concern.

Acute Disease↗
PubMed1991

Considerations on "organic" exclusion criteria for schizophrenia.

Given the variety of "organic" or "toxic" conditions that may produce, precipitate, or exacerbate psychotic disorders, it is important to attempt to clarify existing nosologies and to highlight the need for research strategies that may help to validate relevant distinctions. This review provides a brief discussion of some of those issues.

Humans↗
PubMed1999

Psychiatric aspects of alcohol misuse.

Alcohol and psychiatric disorder have a complicated relationship. Certain important psychiatric syndromes arise from the toxic effects of alcohol and thiamine deficiency. Liver disease and hypoglycaemia are also associated with their own psychiatric syndromes. Many psychiatric patients also turn to alcohol as an easily available 'medication'.

Alcohol Amnestic Disorder↗
PubMed1987

The twilight zone between scientific certainty and legal sufficiency: should a jury determine the causation of schizophrenia?

In lawsuits involving complex scientific issues of causation, dispute resolution requires that a final decision be reached in each case, regardless of whether science is able to provide definitive answers to the questions of causation raised at trial. Proving causation before science has is a concept that scientists may find disconcerting and foreign to some of their basic assumptions. This paper explores the foregoing issues, discusses medical versus legal concepts of causation, outlines the legal tests for admissibility of novel scientific evidence (including Federal Rule of Evidence 702 and the Frye test of general acceptance by the relevant scientific community), and presents a toxic tort case in which expert psychiatric testimony addressed the issue of causation of schizophrenia. The paper articulates concerns about the "misleading aura of certainty" posed by scientific evidence and the burden of decision making that is cast upon the legal system in such scientific issue cases.

Adult↗