1/68. The coincidence of schizophrenia and Parkinsonism: some neurochemical implications.The hypothesis has recently been advanced that increased activity of central dopaminergic mechanisms underlies the symptomatology of the schizophrenias. The evidence that dopaminergic transmission in the corpus striatum is impaired in Parkinson's disease suggests that observations on the relationship between Parkinson's disease and schizophrenia may illuminate the patholophysiology of the latter disease. Four cases are reported in which an illness with schizophrenic features developed in the setting of longstanding Parkinson's disease; attention is drawn to earlier reports of schizophrenic illnesses occurring as postencephalitic sequelae in the presence of a parkinsonian syndrome. These observations appear to conflict with the view that increased dopamine release in the striatum is necessary for the expression of schizophrenic psychopathology, but do not exclude the possibility that increased transmission may occur at other dopaminergic sites in the brain, for example the nucleus accumbens, tuberculum olfactorium or cerebral cortex. Similarly the dopamine receptor blockade hypothesis of the therapeutic effects of neuroleptic drugs cannot be maintained with respect to an action in the striatum in view of the differences between the actions of thioridazine and chlorpromazine in this structure, but may be tenable for actions at extra-straital sites.- - - - - - - - - - ranking = 1keywords = parkinson (Clic here for more details about this article) |
2/68. Asymptomatic pancreatitis associated with clozapine.Besides the well-known adverse effects of clozapine, such as granulocytopenia, tiredness and hypersalivation, acute pancreatitis is known to be a very rare complication of the drug. In the literature a total of five case reports have been published so far. We report a case of asymptomatic pancreatitis subsequent to clozapine treatment at therapeutic doses in a 38-year-old male patient with chronic paranoid-hallucinatory schizophrenia. The patient was rehospitalized after an acute exacerbation of the psychosis subsequent to an attempt to change medication on an outpatient basis. Treatment with clozapine was initiated again. During phases of progressively increasing the clozapine dose, serum levels of amylase and lipase were increased; after maintaining daily doses of clozapine of 300 mg and/or 600 mg the pancreatic enzymes normalized quickly within a few days. The patient did not report any pancreas-related complaints, nor did specific diagnostic studies produce any indicative result, only a minor thickening of the head and body of the pancreas in the ultrasound. It is assumed that the phenomenon of subclinical, asymptomatic pancreatitis during increasing dosage of clozapine occurs more often than previously supposed. The monitoring of serum amylase levels during slow increase in clozapine is recommended; if leukocytosis or eosinophilia is present, the possibility of even a subclinical and asymptomatic pancreatitis should be considered.- - - - - - - - - - ranking = 7.3583816255121E-5keywords = body (Clic here for more details about this article) |
3/68. schizophrenia - A disturbance of signal interaction between the entorhinal cortex and the dentate gyrus? The contribution of experimental dibenamine psychosis to the pathogenesis of schizophrenia: A hypothesis.In addition to the existence of complex memory (similar to the implicit nondeclarative memory of Squire), the existence of a phylogenetically old apparatus of a memory of situations (SMA) is supposed, which is to some extent comparable with the declarative memory of Squire. During actual sensory information the SMA generates a general frame and forms a general 'mark', indicating whether a given information has its origin inside or outside the body, and whether it is new or known. The procedure of this marking process can be explained as the time-depending arrest of a copy of the actual original information-transporting signal 'shower'; this copy must last until the feedback from thalamocortical centers indicates the termination of the processing of the original signal showers. The arrest of the shower copies is the performance of neuronal networks of the entorhinal cortex (EC) and the gyrus dentatus (GD). The psychopathological and biochemical analyses of experimental dibenamine psychosis show a different effect of dibenamine on the noradrenaline (NA) receptors of the EC and GD, respectively: these effects are responsible for the repeated perception cycles of a single situation. N,N-Dibencylamine blocks the postsynaptic alpha(1)-receptors of the EC without influencing the beta-receptors of the GD. Thus the interaction between EC and GD is changed: instead of new scenes, perceptions that have just been experienced get repeated presence and the quality of familiarity. The prolonged arrest of shower copies simultaneously blocks the entrance of new signal showers from the EC to the GD. No information-transporting signal showers can come in as long as the arrest lasts. In case of a disturbance in NA-dependent actions within the EC and the GD, the duration of arrest of information-transporting signal showers is shortened. Thus the formal frame of experience receives the quality of novelty instead of familiarity, and in addition the qualities of uncertainty, vagueness, and alienity. These very changes in perception and experience represent the basic disturbance of schizophrenia. All the symptoms of schizophrenia may be explained by this basic disturbance. The analysis of biochemical aspects turns attention to the energetic situation of NA and N-methyl-D-aspartate systems. These considerations suggest a genetic background of the basic disturbance of schizophrenia: transmitter effects on membranes of neurons and possibly also on glial cells, and energy supply of these effects may be predetermined genetically. It may be assumed that the compensation of such membrane-dependent disturbances will be possible within wide areas of the neural network, except for the 'bottleneck' of the overlapping region of the iso- and allocortex.- - - - - - - - - - ranking = 7.3583816255121E-5keywords = body (Clic here for more details about this article) |
4/68. Deterioration of parkinsonian symptoms following treatment of dopaminergic hallucinosis with olanzapine.The atypical antipsychotic drug olanzapine has been proposed for treatment of dopaminergic psychosis in Parkinson's disease (PD). We report on a 68-year-old patient who developed a severe akinetic-rigid extrapyramidal syndrome, accompanied by additional paranoid symptoms, following olanzapine treatment of optic hallucinosis in PD. Olanzapine may also induce clinically relevant extrapyramidal side effects in PD patients.- - - - - - - - - - ranking = 4keywords = parkinson (Clic here for more details about this article) |
5/68. hallucinations in Parkinson's disease: prevalence, phenomenology and risk factors.hallucinations, mainly of a visual nature, are considered to affect about one-quarter of patients with Parkinson's disease. They are commonly viewed as a side-effect of antiparkinsonian treatment, but other factors may be involved. The aim of this study was to determine the phenomenology, prevalence and risk factors of hallucinations in Parkinson's disease. Two-hundred and sixteen consecutive patients fulfilling clinical criteria for Parkinson's disease were studied. Demographic and clinical variables were recorded, including motor and cognitive status, depressive symptoms and sleep-wake disturbances. patients with and without hallucinations were compared using non-parametric tests, and logistic regression was applied to significant data. hallucinations had been present during the previous 3 months in 39.8% of the patients, and fell into three categories: minor forms, consisting of a sensation of a presence (person), a sideways passage (commonly of an animal) or illusions were present in 25.5% of the patients (an isolated occurrence in 14.3%), formed visual hallucinations were present in 22.2% (isolated in 9.3%) and auditory hallucinations were present in 9.7% (isolated in 2.3%). patients with minor hallucinations had a higher depression score than non-hallucinators but did not differ in other respects. Logistic regression analysis identified three factors independently predictive of formed visual hallucinations: severe cognitive disorders, daytime somnolence and a long duration of Parkinson's disease. These findings indicate that, when minor hallucinations are included, the total prevalence is much higher than previously reported. A simple side-effect of dopaminergic treatment is not sufficient to explain the occurrence of all visual hallucinations. The main risk factor in treated patients is cognitive impairment, although sleep-wake cycle disturbances, and possibly other factors related to the duration of the disease, act as cofactors.- - - - - - - - - - ranking = 1keywords = parkinson (Clic here for more details about this article) |
6/68. Central anticholinergic syndrome from orphenadrine in a 3 year old.orphenadrine (N,N-dimethyl-2(o-methyl-alpha-phenylbenzyloxy)ethylamine) is an analog of diphenhydramine with central and peripheral anticholinergic properties. It is commonly prescribed both as a muscle relaxant and as an adjunct to antipsychotic medications to prevent parkinsonism. We report a case of orphenadrine poisoning in a 3-year-old boy following ingestion of no more than two 100-mg tablets. Central anticholinergic toxicity was prominent, manifested by hallucinations and severe agitation. orphenadrine can cause profound toxicity in children after ingestion of small doses, and should be considered as a potential cause for acute delirium in childhood.- - - - - - - - - - ranking = 1.005893052413keywords = parkinson, parkinsonism (Clic here for more details about this article) |
7/68. Visual hallucinations induced by deep brain stimulation in Parkinson's disease.We report a patient with idiopathic Parkinson's disease who underwent bilateral deep brain stimulation (DBS) of the nucleus subthalamicus (STN) and developed visual hallucinations (VH) while taking no medications only when the DBS was turned on. The hallucinations resolved when the stimulator was turned off. The phenomenology and the prompt response to clozapine suggest that DBS-induced VH mimic pharmacologically-induced VH.- - - - - - - - - - ranking = 0.00012218960385391keywords = idiopathic (Clic here for more details about this article) |
8/68. Successful management of prolonged gamma-hydroxybutyrate and alcohol withdrawal.A 27-year-old man was admitted with tremulousness, diaphoresis, tachypnea (28 breaths/min), full-body rigidity, irritability, paranoia, and auditory and visual hallucinations 2 days after stopping long-term gamma-hydroxybutyrate (GHB) and 8 hours after stopping alcohol intake. He received intravenous fluids and tapering dosages of lorazepam to control agitation and rigidity, and recovered with no significant sequelae after 8 days. Abrupt cessation of GHB after high-dosage abuse can precipitate a clinically significant withdrawal syndrome. lorazepam should be considered for treatment of GHB withdrawal. Concomitant alcohol abuse may mask early GHB withdrawal symptoms and exacerbate withdrawal.- - - - - - - - - - ranking = 7.3583816255121E-5keywords = body (Clic here for more details about this article) |
9/68. Leucopenia induced by low dose clozapine in Parkinson's disease recedes shortly after drug withdrawal. Clinical case descriptions with commentary on switch-over to olanzapine.Four patients affected by severe Parkinson's disease developed leucopenia (900-1200 WBC) during treatment of psychosis (3) or untreatable insomnia (1) with clozapine (37.5-75 mg/day). clozapine withdrawal was followed by recovery of leucopenia (4000-6000 WBC) in two weeks with no need for the administration of leucokines. After 1-6 months olanzapine was administered (increasing the dose from 2.5 to 10 mg/day) to treat persisting disturbances, but the drug induced severe worsening of parkinsonism and also this drug had to be withdrawn.- - - - - - - - - - ranking = 1.005893052413keywords = parkinson, parkinsonism (Clic here for more details about this article) |
10/68. poisoning with Boophane disticha: a forensic case.Scales from the bulb are traditionally used as wound dressing after circumcision and as general wound dressing. Concoctions of the bulb taken orally cause sedation, analgesia, visual hallucinations, irrational behaviour, coma or death. A man ingested 150 ml of a concoction to see who placed a spell on him. He started to hallucinate, thinking that somebody was attacking him. He pulled his gun and fired shots randomly, killing one person and injuring others. A gas chromatograph/mass spectrometer was used to analyze a sample of the concoction. The sample contained buphandrin, buphanine and crinamidine (alkaloids) and eugenol. Buphanine has a pharmacological action similar to that of hyoscine and, when ingested in toxic quantities, leads to excitement, agitation, hallucinations and coma. eugenol is a volatile oil with analgesic properties. Although itcould not be proved that the concoction was only from Boophane disticha, the components were similar to those found in Amaryllidaceae to which Boophane belongs. The man's behaviour could be ascribed to the ingestion of compounds found in B. disticha.- - - - - - - - - - ranking = 7.3583816255121E-5keywords = body (Clic here for more details about this article) |
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