Haloperidol decanoate is a first generation antipsychotic drug used to treat patients with schizophrenic disorder who require prolonged parenteral antipsychotic therapy. Cases of oral haloperidol decanoate are rare, and only one has been reported in foreign literature. In this report, we present a case of an oral ingestion of haloperidol decanoate of a male with schizophrenic disorder who presented to the emergency department following an oral ingestion of 1 ampoule of haloperidol decanoate 100 mg. At presentation he was hemodynamically stable. He was maintained on vigilance for 12 hours after what was discharged to the outpatient unit for psychiatric follow-up. The bioavailability and pharmacokinetic of oral intake of haloperidol decanoate are unknown. Although there is a report of treatment with oral activated charcoal in this case there was no need of intervention.
IntroductionCorticosteroids have either somatic and psychiatric side effects. Somatic adverse effects are well described while neuropsychiatric have received less attention. Psychiatric symptoms such as depression, psychosis and especially mania are common side effects of corticotherapy.Aims and objectivesDescribe a case of a 53 year old female patient, with no psychiatric history, who developed psychiatric symptoms during the treatment of an acute exacerbation of multiple sclerosis with large parenteral doses of corticosteroids. Three days after the onset of corticotherapy she developed increased energy, elevated mood, increased motor activity, racing thoughts, and diminished need for sleep. She subsequently developed grandiose and persecutory ideation and then feared her grandson was going to die. This lead to her admission to psychiatric unit of our hospital to address this behavioral problems. Her husband noticed that she had become “hyper” in the past when she received pulse corticosteroid therapy, but the most recent episode was by far the worst.MethodsRevision of the scientific literature through Pubmed, Embase and Psychinfo using search terms including corticosteroids, mania, depression, psychosis and mood.ResultsPrednisone was suspended and Risperidone 2 mg was begun for presumed steroid-induced mood disorder, and the patient became calmer and much less guarded over the next 2-3 days. After a week she recovered complete euthymic mood and reverted to normal functioning.ConclusionsThese data suggest that Risperidone is well tolerated and appears to be useful for mood disturbances associated with corticosteroid therapy. Controlled trials seem warranted to confirm these observations.
IntroductionThe clinical syndromes related to fronto-temporal lobar degeneration are the second most common cause of pre-senile primary dementia. There are three distinct clinical variants: behavioral-variant fronto-temporal dementia (BvFTD), semantic dementia and progressive non-fluent aphasia. BvFTD is characterized by a significant change in the patients personality and social behavior, and impaired executive function.ObjectivesReview the current literature on both the pharmacologic and nonphar- macologic management of fronto-temporal dementia.AimsBrief literature review.MethodsCase report and literature review.ResultsWe describe case of a 65-years-old male with hyperactivity, desinhibition, aggressive, stereotyped and persevering behaviors with continuous walking and changes in eating habits (hyperphagia). He also presented distractibility, poor speech with loss of spontaneity, an indifferent attitude, mental rigidity, inflexibility, and lack of insight for his condition. This condition developed within one year, with a change in his personality and the appearance of an inadequate social conduct, with an insidious onset and gradual progression. He has family history of dementia. Computerized Tomography scan shows lobar fronto-temporal atrophy. During hospitalization no drugs has had effect, apart from paroxetine (partial response).ConclusionConcerning therapy, several drugs were used without proved effect in controlling the symptoms, highlighting the difficulty in the psychopharmacological approach of this disorder. The selective serotonin reuptake inhibitors have shown some effect on behavior.
IntroductionIntricate interactions between the immune system and the brain might have important etiological and therapeutic implications for neuropsychiatric brain disorders. A probable association between schizophrenia and the immune system was postulated over a century ago, and is supported by epidemiological and genetic studies pointing to links with infection and inflammation.ObjectiveTo describe some important areas of research regarding immune response in schizophrenia and related psychotic disorders and discuss potential mechanisms and therapeutic implications of these findings.AimsAssociations between immune response, inflammation and schizophrenia and related psychotic disorders are reviewed.MethodsA literature review of the theme is surveyed. Several articles were search on MEDLINE with the keywords: schizophrenia, psychosis, inflammation, immunity, infection.ResultsSchizophrenia is a multifactorial disease. It is associated with multiple genetic loci that confer risk, in addition to developmental and postnatal risk factors. Antipsychotic-naive first-episode psychosis and acute psychotic relapse seems to be associated with increased serum concentrations of interleukin 6 and other proinflammatory cytokines, which are normalized after remission of symptoms with antipsychotic treatment.ConclusionsInflammation and immune dysfunction might contribute to cognitive, negative, and positive symptoms in schizophrenia. Identification of specific inflammatory pathways for neuropsychiatric symptoms would provide novel targets for therapeutic intervention.Disclosure of interestThe authors have not supplied their declaration of competing interest.
IntroductionThe comorbidity between obsessive-compulsive disorder (OCD) and attention deficit/hyperactivity disorder (ADHD) has been discussed for a couple of decades. Reported co-occurrence rates are highly inconsistent in the literature.ObjectiveTo review phenomenological and theoretical issues concerning concomitant OCD-ADHD.AimsPhenomenological and theoretical issues regarding OCD-ADHD comorbidity are reviewed.ResultsAlthough numerous studies suggest an OCD-ADHD comorbidity, thus far etiological (i.e., genetic) background has been provided only for a pediatric comorbidity. High rates of co-occurrence may be mediated by the existence of tic disorders, and evidence of impaired neuronal maturational processes in OCD pediatric population may lead to probably transitory phenotypical expressions that look like ADHD symptomatology. Thus, it is possible that ADHD-like symptoms resulting from OCD-specific symptomatology may be misdiagnosed as ADHD. This may explain the lower co-occurrence rates reported in adolescents and adults.ConclusionOCD and ADHD are very different disorders in terms of pathophysiology, phenomenology, and treatment strategies. Several methodological concerns have been identified in our review. Future studies on OCD-ADHD comorbidity should try to mitigate these biases.Disclosure of interestThe authors have not supplied their declaration of competing interest.
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