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PubMed2002

Three cases of angel's trumpet tea-induced psychosis in adolescent substance abusers.

An increase of intoxications in persons using alkaloid-containing ornamental plants (mainly angel's trumpet) for their hallucinogenic effects and easy and cheap availability is registered. It is mainly adolescents who are experimenting with these plants. In addition to severe vegetative anticholinergic symptoms, the clinical picture is often dominated by a toxic psychosis with hallucinations, disturbances of orientation, and psychomotoric agitation, aggression, or anxiety. Three cases of severe psychotic pictures with only mild or completely missing vegetative symptoms after ingestion of angel's trumpet tea are reported. Caused by the increasing spreading of angel's trumpet shrubberies in Europe and North America, intoxications with large numbers of fatalities have to be expected in the future. The taxonomical, pharmacological, and clinical aspects of angel's trumpet-induced disorders are discussed. Knowledge of the clinical picture is important for correct diagnosis and treatment. Prevention by mass media should mainly focus on the medical fatalities of abuse and not emphasize the hallucinogenic effects, presumably increasing unwanted interest for these plants among youths.

Adolescent↗

PubMed1983

Relationship between nutrition and dementia in the elderly.

The complexities of physiologic interactions between the nutritional status of the aged and the incidence of dementia in the elderly should be obvious from this partial survey of the field. Investigations aimed at delineating the role of individual nutrients in mentation among the elderly are extremely difficult to design and perform. However, the potential for practical applications of the results is indeed very high. The studies discussed in this article permit the following conclusions. Although many attempts have been made to enhance average life expectancy through nutritional manipulation, no such panacea currently exists. There is a well-documented decrease in caloric intake among the elderly. However, this does not seem to put them at any higher risk of developing overt deficiencies of specific nutrients. The elderly population in this country has a strong tendency to consume nutritional supplements, with vitamins C and E being the most popular. It is unknown at present whether this practice has any health value. Several attempts have been made to alter the course of dementia in the elderly through nutritional means. Attempts to ameliorate the symptoms of Alzheimer's disease through use of choline and lecithin have been overwhelmingly unsuccessful. The postulate that aluminum toxicity is an etiologic factor in this disease remains unproven, and therapies with chelating agents are not now advisable. Vitamin B12 has to be seriously considered as a causative factor in dementia; it is hoped that methods to test vitamin B12 nutriture in humans that are both more reliable and more capable of revealing marginal deficiency states will emerge. Although folic acid is intimately related biochemically and nutritionally to vitamin B12, its potential role in normal mental function remains largely unknown. Clearly, when considering nutrition and dementia in the elderly, there are many areas that still require thorough scientific investigation. Hopefully, the future will see an increase in research activity, resulting in answers to many of the questions posed in this paper.

Acetylcholine↗

PubMed1985

Comparison of carbamazepine, phenobarbital, phenytoin, and primidone in partial and secondarily generalized tonic-clonic seizures.

We conducted a 10-center, double-blind trial to compare the efficacy and toxicity of four antiepileptic drugs in the treatment of partial and secondarily generalized tonic-clonic seizures in 622 adults. Patients were randomly assigned to treatment with carbamazepine, phenobarbital, phenytoin, or primidone and were followed for two years or until the drug failed to control seizures or caused unacceptable side effects. Overall treatment success was highest with carbamazepine or phenytoin, intermediate with phenobarbital, and lowest with primidone (P less than 0.002). Differences in failure rates of the drugs were explained primarily by the fact that primidone caused more intolerable acute toxic effects, such as nausea, vomiting, dizziness, and sedation. Decreased libido and impotence were more common in patients given primidone. Phenytoin caused more dysmorphic effects and hypersensitivity. Control of tonic-clonic seizures did not differ significantly with the various drugs. Carbamazepine provided complete control of partial seizures more often than primidone or phenobarbital (P less than 0.03). Overall, carbamazepine and phenytoin are recommended drugs of first choice for single-drug therapy of adults with partial or generalized tonic-clonic seizures or with both.

Adolescent↗

PubMed2006

[Schizophrenia and cannabis consumption: epidemiology and clinical symptoms].

More and more young people consume cannabis in sometimes high dosage at an age when their brain is not yet fully developed and reacts particularly sensitive to toxic influences. Cannabis can induce and exacerbate psychotic symptoms and it can deteriorate the disease process in schizophrenic patients. First-episode schizophrenic patients with long-term cannabis consumption were significantly younger at disease-onset, mostly male and suffered more often from paranoid schizophrenia (with a better prognosis) than those without cannabis consumption in our investigation. The significance of higher serum neurotrophin levels in cannabis consuming schizophrenics as compared to those without cannabis consumption remains equivocal so far. The cognitive functions of this patient group are at least not worse than in those with schizophrenia alone. Taken together, the effect of cannabis on the brain vulnerable to schizophrenia is not yet completely understood; besides the undoubtedly deleterious effects, there may also be some neuroprotective effects.

Adolescent↗

PubMed1994

Clinical spectrum of secondary parkinsonism in childhood: a reversible disorder.

Parkinsonism is an uncommon movement disorder in childhood. Six unusual cases of acquired parkinsonism in hospitalized children are described. Clinical manifestations included an akinetic-rigid syndrome with and without tremor, the combination of parkinsonism and dystonia, and a parkinsonism-plus syndrome. Altered mental status, mutism, dysphagia, and sialorrhea were frequent associations. Etiologies included hypoxic-ischemic encephalopathy; haloperidol treatment with and without neuroleptic malignant syndrome; toxicity of cytosine arabinoside, cyclophosphamide, amphotericin B, and methotrexate; St. Louis encephalitis and other encephalitides; and a pineal tumor with hydrocephalus. Cranial magnetic resonance imaging results ranged from normal to profound cerebral and cerebellar atrophy with chemotherapeutic toxicity. The illnesses usually were severe enough to require pharmacotherapy. Incorrect diagnoses of depression or catatonia delayed treatment or aggravated the problem. Acute treatment included amantadine, levodopa/carbidopa with or without selegiline, diphenhydramine, or benztropine. The concentration of CSF homovanillic acid was normal in a neuroleptic-associated patient, but the level was low in an encephalitic patient. All patients demonstrated dramatic improvement, including two who were not treated; some had complete resolution of symptoms and none required continued antiparkinsonian drugs despite poor scores on the Unified Parkinson's Disease Rating Scale and the Modified Hoehn and Yahr Rating Scales. The causes of parkinsonism described are more common in a general pediatric hospital than the parkinsonism associated with the popularized Segawa syndrome.

Adolescent↗

PubMed2004

[An auto-iatrogenic disease].

A 55-year-old practitioner from an island in the northern sea felt an increasing hypersensitivity of his entire body to various ambient and nutritional allergens and toxics. He started to treat himself with increasing doses of glucocorticoids and moved to a southern climate in Lanzarote and later on to the Swiss mountains in the grisons. On admission to our hospital in December he was in a disastrous psychotic condition, trying to cool down his body by laying naked on his bed at ambient temperatures around the freezing point. He had consumed on average 250 mg prednisone daily over weeks. As we found out later his personal assistant travelling with him was giving him glucocorticoids through the infusion during his hospital stay. He developed a necrotizing septic phlebitis at the infusion site followed by a Pseudomonas aeruginosa sepsis with fatal multiorgan failure. This case illustrates the dangers of self-treatment by doctors and the difficulties in treating a physician.

Anti-Inflammatory Agents↗

PubMed1994

Hepatic disease and psychiatric illness: relationships and treatment.

A relationship between hepatic diseases and psychiatric symptoms has long been speculated. While liver detoxication makes the exogenous substances harmless for the body, there are occasions where the liver may convert a harmless substance into a more toxic substance. With such an important role, the liver protects all the organs of the body. When liver is malfunctioning, toxic metabolites injurious to the brain may be produced. As the brain receives a high blood supply, a large amount of metabolites reach this organ. Hence, the metabolic function of the liver keeps a delicate reciprocal relationship between the two organs. In addition, a number of psychiatric medications affect liver functions. Another perplexing clinical problem is the difficulty in treating psychiatric symptoms in patients with liver disease. For example, benzodiazepines which do not affect the liver function in physically healthy psychiatric patients, may induce hepatic coma in patients with liver disease. Benzodiazepine antagonists produce dramatic and temporary improvement in patients with hepatic coma. Clinically, many psychoactive drugs produce hepatic complications. The very same drugs which produce hepatic side effects are required for the treatment of psychiatric symptoms in patients with hepatic disorders. To appropriately handle these situations, a thorough knowledge of the side effects of these drugs is necessary.

Hepatic Encephalopathy↗

PubMed2004

Cannabis-associated psychosis: current status of research.

Cannabis has been used for recreational, medicinal and religious purposes in different cultures since ancient times. There have been various reports of adverse effects due to or associated with cannabis consumption, including psychotic episodes. Historically, our understanding of these clinical observations has been significantly hindered by a lack of knowledge regarding their underlying neurobiological and pharmacological processes. However, the discovery of the endogenous cannabinoid system has allowed a greater understanding of these adverse effects to develop. From a clinical perspective, toxic or transient psychotic reactions to the administration of herbal cannabis preparations or specific cannabinoid compounds have to be differentiated from longer-lasting, persistent schizophrenia-like disorders associated with the use of cannabis/cannabinoids. The latter are most likely to be associated with a predisposition or vulnerability to schizophrenia. Interestingly, the recently suggested role of the endogenous cannabinoid system in schizophrenia not related to previous cannabinoid consumption introduces an additional perspective on the mechanism underlying cannabis-associated schizophrenia-like disorders, as well as on the effects of cannabis consumption in schizophrenia. At present, acute psychopharmacological treatment options for cannabis-associated transient and persistent schizophrenia-like psychotic episodes are similar and are based on the use of benzodiazepines and antipsychotics. However, new pharmacological strategies using the endogenous cannabinoid system as a primary target are under development. Long-term psychotherapeutic treatment options involve case management strategies and are mainly based on specialised psychotherapeutic programmes to encourage cannabis users to stop their use of the drug.

Animals↗

PubMed2002

Phenytoin/isradipine interaction causing severe neurologic toxicity.

OBJECTIVE: To report a young man on phenytoin who developed acute neurologic symptoms after isradipine was introduced to his treatment regimen and discuss the possible causes of this drug interaction. CASE SUMMARY: A 21-year-old white man, with propionic acidemia and seizures treated with phenytoin and carbamazepine, was started on isradipine for essential hypertension. Soon thereafter, he developed acute and severe lethargy, ataxia, dysarthria, and weakness that resolved once isradipine was withheld. Phenytoin concentrations were within normal limits or elevated, despite sequential reductions of phenytoin dosage, during concomitant isradipine administration. DISCUSSION: Isradipine is a known inhibitor of the CYP450 isoenzyme family. Although the daily dose of phenytoin was decreased significantly, phenytoin blood concentrations remained high, suggesting a pharmacokinetic interaction. Previously, the patient had never had neurologic symptoms associated with increased phenytoin concentrations. This also indicates a likely pharmacodynamic interaction between phenytoin and the calcium-channel blocker. Both phenytoin and isradipine have been shown to bind to calcium channels and to inhibit calcium entry into the cells. Binding of isradipine to the brain has been described in humans and animals, and calcium-channel blockers have been shown to cause potentiation of anticonvulsant action of phenytoin. CONCLUSIONS: Acute pharmacokinetic and pharmacodynamic interactions between phenytoin and isradipine were probably responsible for the lethargy, dysarthria, ataxia, and weakness our patient developed. The combination of phenytoin and calcium-channel blockers should be used with caution.

Acidosis↗

PubMed1996

Criminal responsibility and solvent exposure.

This case report contains the history of a man's exposure to benzene, trichloroethylene, and toluene. J suffered acutely from classic symptoms of toxic exposure to these compounds, such as fatigue, clumsiness, staggering, and hematopoietic depression. During his medical hospitalization, he was exposed to further organic insults, such as being treated with medications like Cytoxan and medications to treat an abscess in his right parietal lobe. After the acute exposure and after the abscess had resolved, his functioning on neuropsychological testing was still depressed, as he had a Full Scale IQ of 105, whereas at the time of the forensic evaluation he had a Full Scale IQ of 114. It would therefore appear that he did have some mild deficits when originally discharged from the hospital. While he reported having continual mental status changes at the time of the offense and even at the time of the forensic evaluation, it was not felt that these played a significant role in the commission of the offense. Comprehensive forensic evaluation suggested that psychological reactions to his illness and an underlying personality disorder were more direct contributors to the criminal acts. J was therefore recommended and ultimately found to be responsible for his behavior, according to the law.

Adult↗

PubMed1983

Organic cerebral reactions in alcoholism: psychobiological aspects of treatment.

The paper considers the rational biological basis for treatment of alcohol withdrawal reactions, alcoholic hallucinosis and the Wernicke-Korsakoff syndrome. Both clinical and experimental data indicate that the alcohol withdrawal reaction reflects a state of hyper-reactivity of the central nervous system. The evidence comprises physiological, electrophysiological and biochemical findings. Magnesium, vitamins and antipsychotics are not specific in the treatment of the alcohol withdrawal reactions per se; rational treatment comprises drugs that may substitute for the suppressive effects of alcohol in the CNS during readaptation to the alcohol free condition (e.g. barbiturates or benzodiazepines). Alcoholic hallucinosis is characterised by acutely developed auditory hallucinations of an evil or reproachful nature. The condition may develop during or shortly after excessive alcohol consumption in chronic alcoholics. Suggestibility and unclear consciousness is not part of the condition. Tentatively three subgroups are suggested to occur: a) a withdrawal reaction; treatment with sedatives is recommended; the prognosis is good, b) a toxic reaction occurring during the drinking bout; this condition should be treated with antipsychotics until symptoms have disappeared. The prognosis is fairly good, c) a schizophreniform condition. Long-term treatment with antipsychotics must be applied. The Wernicke-Korsakoff syndrome is described. The condition often occurs during or shortly after an acute withdrawal reaction. The biochemical role of the etiological factor thiamine in glucose metabolism suggests that precautions (thiamine treatment) must be taken when giving a glucose load to alcoholics. Finally focus is set on the recent suggestion that the syndrome may in some cases result from an inborn enzymatic abnormality comprising low binding of thiamine pyrophosphate to transketolase. Psychobiological aspects of treatment in alcoholism may apply to a very large spectrum of conditions involving symptoms of cerebral, hepatic, gastrointestinal, cardial and peripheral nervous system origin. In the present expose we shall concentrate on organic cerebral reactions partly or exclusively presenting with psychiatric symptoms and signs. Thus the review will consider the rational biological basis for treatment of alcohol withdrawal reactions (including delirium tremens), alcoholic hallucinosis and the Wernicke-Korsakoff syndrome.

Alcohol Amnestic Disorder↗

PubMed1997

[Experimental study of methamphetamine psychosis--role of glutamate and nitric oxide in methamphetamine-induced dopaminergic and serotonergic neurotoxicity in the rat brain].

The present study examined effects of a high dose of methamphetamine (MA) (5mg/kg, s.c., x 4) on extracellular concentrations of dopamine (DA), dihydroxyphenylacetic acid (DOPAC), 5-hydroxyindoleacetic acid (5-HIAA) and glutamate in rat striatum (ST) and nucleus accumbens (NA) using microdialysis. The toxic dose of MA markedly increased extracellular DA, and decreased DOPAC and 5-HIAA in both ST and NA. The increase in DA release was not different in magnitude between ST and NA. Extracellular glutamate showed a delayed increase in ST, but not in NA. Tissue contents of serotonin (5-HT) and 5-HIAA significantly decreased in both ST and NA, whereas those of DA, DOPAC and HVA decreased in ST but did not change in NA. These data suggest that the marked increase of DA release is not directly related to the MA-induced dopaminergic neurotoxicity. The increase in glutamate release found only in ST may be related to the dopaminergic damage in ST. However, enhancement in glutamate release did not appear to be essential for the serotonergic neurotoxicity. Nitric oxide (NO) has recently been recognized as a novel neuronal messenger. Taking into account the relationship between NMDA receptor activation and NO formation, the present study examined effects of a NO synthesis inhibitor, N omega-nitro-L-arginine methyl ester (LNAME) on MA-induced decreases in contents of the monoamines and their metabolites, in order to clarify whether the MA-induced dopaminergic and serotonergic neurotoxicity would be mediated by NO synthesis. Coadministration with LNAME (30 mg/kg, i.p., x2), reduced the MA-induced decreases in contents of DA, DOPAC and HVA in ST, but not reduced the MA-induced decreases in contents of 5-HT in ST and NA. These findings suggest that the MA-induced dopaminergic, but not serotonergic neurotoxicity, may be related to the neural process such as NO formation caused by the activation of postsynaptic DA receptor.

3,4-Dihydroxyphenylacetic Acid↗