Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Insomnia is a common feature in schizophrenia. However, it seldom is the predominant complaint. Nevertheless, severe insomnia is often seen during exacerbations of schizophrenia, and may actually precede the appearance of other symptoms of relapse. The sleep disturbances of either never-medicated or previously treated schizophrenia patients are characterized by a sleep-onset and maintenance insomnia. In addition, stage 4 sleep, slow wave sleep (stages 3 and 4), non-REM (NREM) sleep in minutes and REM latency are decreased. The atypical antipsychotics olanzapine, risperidone, and clozapine significantly increase total sleep time and stage 2 sleep. Moreover, olanzapine and risperidone enhance slow wave sleep. On the other hand, the typical antipsychotics haloperidol, thiothixene, and flupentixol significantly reduce stage 2 sleep latency and increase sleep efficiency. Future research should address: (1) the sleep patterns in subtypes of schizophrenia patients; (2) the role of neurotransmitters other than dopamine in the disruption of sleep in schizophrenia; (3) the functional alterations in CNS areas related to the pathophysiology of schizophrenia during NREM sleep and REM sleep (brain imaging studies); (4) the short-term, intermediate-term, and long-term effects of atypical antisychotics on sleep variables.
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PMID:Sleep in schizophrenia patients and the effects of antipsychotic drugs. 1503 52

This short-term, single-blind, pilot trial was initiated to investigate the usefulness of quetiapine therapy in the treatment of schizophrenic patients refractory to first-generation antipsychotics. Following a neuroleptic-free period prior to study entry (at least 1 week for oral formulations and 6 weeks for depot formulations), quetiapine was started at 50 mg/day and titrated up to 500 mg/day by Day 6. This 500 mg daily dose was then maintained or increased up to a maximum of 750 mg/day, at the discretion of the treating physician, who was aware of the antipsychotic prescribed. Efficacy measures were represented by changes in total and component PANSS score from baseline to different intervals. Safety and tolerability were evaluated by monitoring the spontaneously referred moderate-to-severe adverse events, changes from baseline in SAS, BARS, and AIMS scores, supplementary use of flurazepam, lorazepam, and benztropine, clinically relevant physical changes, abnormalities in vital signs, blood chemistry, and hematology, and modifications in QTc interval and body weight. Rating scale assessments, categorization of adverse events, determination of physical examination, vital signs, and body weight were performed by a qualified physician blind to the particular antipsychotic under investigation and the aims of the study. All 12 patients completed the 4-week quetiapine treatment course. Mean total PANSS scores were significantly reduced between baseline and study endpoint (p=0.006). Five out of six PANSS subcomponent scores also showed significant decreases (p < 0.05). Six patients showed a reduction of > or = 20% in PANSS total score by the final day of quetiapine treatment, so were classified as responders. There were responders in all schizophrenia diagnostic subgroups (undifferentiated, paranoid, and disorganized). Two patients reported moderate adverse events. One patient received 3 days of benztropine therapy for EPS and five received flurazepam for insomnia. Weight change was minimal and mean SAS, BARS, and AIMS scores all showed nonsignificant decreases between baseline and endpoint. The 50% quetiapine response rate reported here in refractory patients is comparable with those previously reported for other atypical antipsychotics in populations of both refractory and intolerant patients.
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PMID:Quetiapine in hospitalized patients with schizophrenia refractory to treatment with first-generation antipsychotics: a 4-week, flexible-dose, single-blind, exploratory, pilot trial. 1546 4

Depression is a frequent symptom in psychiatry, either isolated (major depression) or entangled with other psychiatric symptoms (psychotic depression, depression of bipolar disorders). Many antidepressant drugs are available with different pharmacological profiles from different classes: tricyclic antidepressants, monoamine oxydase inhibitors, selective serotonin reuptake inhibitors (SSRI). However, there are some limitations with these drugs because there is a long delay before relief for symptoms, some patients with major depression are resistant to treatment, there is a risk to induce manic symptoms in patients with bipolar disorders and these drugs have no effect on the psychotic symptoms frequently associated to major depression. The leading hypothesis for the search of more efficient new antidepressants has been the amine deficit hypothesis: noradrenaline and/or serotonin deficit and more recently dopamine deficit. Moreover, a dopamine deficit has been also hypothesized as the central mechanism explaining the negative symptoms of schizophrenia. These symptoms are the consequence of a deficit of normal behaviours and include affective flattening, alogia, apathy, avolition and social withdrawal. There is thus a great overlap between symptoms of depression and negative symptoms of schizophrenia. Atypical antipsychotics, in contrast with conventional neuroleptics, have been shown to decrease negative symptoms, most probably through the release of dopamine in prefrontal cortex, thus improving psychomotor activity, motivation, pleasure, appetite, etc. The dopamine deficit in cortical prefrontal areas was thus an unifying hypothesis to explain both some symptoms of depression and negative symptoms of schizophrenia. Studies in animal confirm this view and show that the association of an atypical antipsychotic drug and an SSRI (olanzapine plus fluoxetine) increases synergistically the release of dopamine in prefrontal areas. Moreover, most of the atypical antipsychotics have a large action spectrum, beyond the only dopamine receptors: their effects on the serotonin receptors--particularly the 5-HT2A and 5-HT2C receptors--suggest that their association to SSRI could be a promising treatment for depression. Indeed, SSRI act mainly by increasing the serotonin level in the synapse, thus leading to a non specific activation of all pre- and post-synaptic serotonin receptors. Among them, 5-HT2A/2C receptors have been involved in some of the unwanted effects of SSRI: agitation, anxiety, insomnia, sexual disorders, etc. The inhibition of these receptors could be thus beneficial for patients treated with SSRI. Amisulpride is an unique atypical antipsychotic that selectively blocks dopamine receptors presynaptically in the frontal cortex, possibly enhancing dopaminergic transmission. The antidepressant effect of amisulpride was shown in dysthymia in many clinical studies versus placebo, tricyclic antidepressants, SSRI or others. However, a shorter delay for symptom relief was not demonstrated for amisulpride as compared to comparative antidepressants. Other atypical antipsychotics (clozapine, olanzapine), which act on a large variety of receptors, have shown antidepressant effects--mainly in association with SSRI--in different psychiatric diseases: treatment-resistant major depression, major depression with psychotic symptoms and depression of bipolar disorders, with no increase of manic symptoms in this latter case. Moreover, the delay for symptom relief was greatly shortened. More comparative double-blind studies are required to confirm and to precise the antidepressant effects of atypical antipsychotics. Nevertheless, these studies suggest that atypical anti-psychotics could be of great value in depressive conditions reputed for their resistance to treatment with usual antidepressants. Particularly, new strategies emerge that combine atypical antipsychotics and antidepressants for greater efficacy and more rapid relief of depression symptoms.
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PMID:[Efficacy of atypical antipsychotics in depressive syndromes]. 1573 62

It is acknowledged that a considerable proportion of patients who have an episode of acute and transient psychotic disorder (ATPD), will develop schizophrenia after the episode is remitted. If features discriminating the patients who later developed schizophrenia from those who underwent a monomorphous ATPD-only course are discerned, they may be useful for predicting the prognosis. The authors performed a chart review study of those who were hospitalized with the diagnosis of ATPD and followed up thereafter for >5 years and compared two subject groups: 10 later-schizophrenia-developing (SD) patients and 15 non-schizophrenia-developing (non-SD) patients. Assessment of the subjects, conducted by two psychiatrist raters blind to the subject groups, included frequency of ATPD episodes, adaptation levels and life events before admission, and psychiatric symptoms before and after admission. The interrater reliability of the assessment proved to be favorable. As a result, early recurrence of psychotic episodes in the follow-up period, lack of acute upsurge of insomnia in an early phase of the episode and poor premorbid heterosexual relations characterized the SD patients. The result indicated heterogeneity of ATPD episodes.
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PMID:Predicting features of later development of schizophrenia among patients with acute and transient psychotic disorder. 1582 59

Cognitive deficits are a fundamental feature of the schizophrenic disorder, but the effect of antipsychotic treatment is still debated. The study assesses the effect of olanzapine on neurocognitive functioning and symptomatology of patients with schizophrenic disorder residual type. Executive function evaluation by the Wisconsin card sorting test (WCST) was performed on 39 patients treated with olanzapine (5-20 mg/day); the efficacy of drug in improving symptomatology, safety and quality of life was also evaluated. After 7 months of treatment, the mean number of WCST categories tended to increase. Correct responses increased with a statistically significant change from the baseline. The total and unique errors decreased significantly. At all post-baseline visits a decrease from baseline in the PANSS total, positive and negative scores was seen. The proportion of patients with less severe illness (CGI), increased over the course of the study with a corresponding decrease of patients with more severe illness. The quality of life scores also tended to improve during treatment. The Simpson Angus scale, Barnes-akathisia and abnormal involuntary movement scale scores decreased consistently. The most common treatment emergent drug related adverse events were weight gain, insomnia, agitation and anxiety. Neurocognitive functioning in terms of executive performance and symptomatology improved in people with schizophrenia residual type.
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PMID:Executive function assessment of patients with schizophrenic disorder residual type in olanzapine treatment: an open study. 1599 Dec 59

Because of their better side-effect profile, atypical antipsychotic agents have replaced conventional antipsychotic agents as the first-line treatment for schizophrenia. Although atypical agents are less likely to be associated with extrapyramidal symptoms, such symptoms sometimes do occur in patients treated with atypical agents. The authors report the cases of two patients who developed akathisia after treatment with quetiapine for insomnia, consider previously reported cases of akathisia induced by atypical antipsychotic agents, discuss other medications that can induce similar symptoms, discuss treatments for akathisia, and examine issues in the use of quetiapine as a soporific agent.
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PMID:Acute akathisia associated with quetiapine use. 1600 Jun 72

Patients with schizophrenia often suffer from sleep disturbances such as excessive sleeping and insomnia. Common medications for schizophrenia can have a sedative effect on patients. Not all antipsychotic medications have the same sedative effect, which is related to dosage and affinity for histamine H1 receptors. Studies have shown that, compared with conventional antipsychotics, atypical antipsychotics such as risperidone, olanzapine, quetiapine, and ziprasidone generally cause less sedation yet are as effective in controlling psychosis and agitation. Sedation can be troublesome to patients who are trying to become re-integrated into society and interfere with their treatment regimen. Both persistent sedation and chronic insomnia can be managed by the physician.
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PMID:Atypical antipsychotics: sleep, sedation, and efficacy. 1600 Oct 94

Insomnia is a common symptom in schizophrenia, although it is seldom the predominant complaint. Sleep-onset and maintenance insomnia is a characteristic feature of schizophrenic patients regardless of either their medication status (drug-naive or previously treated) or the phase of the clinical course (acute or chronic). Regarding sleep architecture, the majority of studies indicate that stage 4 sleep and rapid eye movement (REM) latency are reduced in schizophrenia, whereas REM sleep duration tends to remain unchanged. Insomnia in schizophrenic patients could be partly related to the presumed over-activity of the dopaminergic system. However, there is a possibility that the GABAergic system is also involved in sleep disturbance in schizophrenia. Since many signal transmission systems within the CNS can be implicated in the reduction of REM latency in schizophrenia, the characterization of the neurotransmitter systems involved remains a challenging dilemma.
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PMID:Sleep disturbance in schizophrenia. 1619 96

Acute agitation is a common psychiatric emergency often treated with intramuscular (i.m.) medication when rapid control is necessary or the patient refuses to take an oral agent. Conventional i.m. antipsychotics are associated with side effects, particularly movement disorders, that may alarm patients and render them unreceptive to taking these medications again. Ziprasidone (Geodon) is the first second-generation, or atypical, antipsychotic to become available in an i.m. formulation. Ziprasidone IM was approved by the Food and Drug Administration in 2002 for the treatment of agitation in patients with schizophrenia. In October 2004, a roundtable panel of physicians with extensive experience in the management of acutely agitated patients met to review the first 2 years of experience with this agent. This monograph, a product of that meeting, discusses clinical experience to date with ziprasidone IM and offers recommendations on its use in various settings. In clinical trials, patients treated with ziprasidone IM demonstrated significant and rapid (within 15-30 minutes) reduction in agitation and improvement in psychotic symptoms, agitation, and hostility to an extent greater than or equal to that attained with haloperidol i.m. Tolerability of ziprasidone IM was superior to that of haloperidol IM, with a lower burden of movement disorders. Clinical trials have also shown that ziprasidone IM can be administered with benzodiazepines without adverse consequences. Transition from i.m. to oral ziprasidone has been well tolerated, with maintenance of symptom control. The most common adverse events associated with ziprasidone IM were insomnia, headache, and dizziness in fixed-dose trials and insomnia and hypertension in flexible-dose trials. No consistent pattern of escalating incidence of adverse events with escalating ziprasidone doses has been observed. Changes in QTc interval associated with ziprasidone at peak serum concentrations are modest and comparable to those seen with haloperidol IM. Results of randomized clinical trials of ziprasidone IM have been corroborated in studies in real-world treatment settings involving patients with extreme agitation or a recent history of alcohol or substance abuse. In these circumstances, clinically significant improvement was seen within 30 minutes of ziprasidone IM administration, without regard to the suspected underlying etiology of agitation. Agents with a good safety/tolerability profile, such as ziprasidone IM, may be more cost effective long term than older agents, due to reduced incidence of acute adverse effects (eg, acute dystonia) that often require extended periods of observation. Additional trials of ziprasidone IM in agitated patients in a variety of clinical setting are warranted to generate comparative risk/benefit data with conventional agents and other second-generation antipsychotics.
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PMID:Best clinical practice with ziprasidone IM: update after 2 years of experience. 1624 23

A 21-year-old female presented excitement, auditory hallucination, monologue, and insomnia. After 1 week of risperidone administration, she showed hyperthermia, salivation, and muscle rigidity. Risperidone was discontinued, but stupor, convulsions, and respiratory distress developed. In the intensive care unit where she was transferred, catatonic symptoms such as stupor or excitement, catalepsy, and negativism were prominent. In addition, severe bronchorrhea causing respiratory failure was observed. Her catatonic symptoms, hyperthermia, and bronchorrhea resolved by ECT. After recovery, affective flattening, alogia, and avolition remained. The final diagnosis was MC associated with schizophrenia. This report suggests that MC may be complicated by severe bronchorrhea, but this condition responds to ECT.
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PMID:Malignant catatonia with severe bronchorrhea and its response to electroconvulsive therapy. 1667 86


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