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)

Inositol is a simple polyol precursor in a second messenger system important in the brain. Cerebrospinal fluid inositol has been reported as decreased in depression. A double-blind controlled trial of 12 g daily of inositol in 28 depressed patients for four weeks was performed. Significant overall benefit for inositol compared to placebo was found at week 4 on the Hamilton Depression Scale. No changes were noted in hematology, kidney or liver function. Since many antidepressants are effective in panic disorder, twenty-one patients with panic disorder with or without agoraphobia completed a double-blind, placebo-controlled, four week, random-assignment crossover treatment trial of inositol 12 g per day. Frequency and severity of panic attacks and severity of agoraphobia declined significantly with inositol compared to placebo. Side-effects were minimal. Since serotonin re-uptake inhibitors benefit obsessive compulsive disorder (OCD) and inositol is reported to reverse desensitization of serotonin receptors, thirteen patients with OCD completed a double-blind controlled crossover trial of 18 g inositol or placebo for six weeks each. Inositol significantly reduced scores of OCD symptoms compared with placebo. A controlled double-blind crossover trial of 12 g daily of inositol for a month in twelve anergic schizophrenic patients, did not show any beneficial effects. A double-blind controlled crossover trial of 6 g of inositol daily vs. glucose for one month each was carried out in eleven Alzheimer patients, with on clearly significant therapeutic effects. Antidepressant drugs have been reported to improve attention deficit disorder (ADDH) with hyperactivity symptomatology. We studied oral inositol in children with ADDH in a double-blind, crossover, placebo-controlled manner. Eleven children, mean age 8.9 +/- 3.6 years were enrolled in an eight week trial of inositol or placebo at a dose of 200 mg/kg body weight. Results show a trend for aggravation of the syndrome with myo-inositol as compared to placebo. Recent studies suggest that serotonin re-uptake inhibitors are helpful in at least some symptoms of autism. However a controlled double-blind crossover trial of inositol 200 mg/kg per day showed no benefit in nine children with autism. Cholinergic agonists have been reported to ameliorate electroconvulsive therapy (ECT)-induced memory impairment. Inositol metabolism is involved in the second messenger system for several muscarinic cholinergic receptors. Inositol 6 g daily was given in a crossover-double-blind manner for five days before the fifth or sixth ECT to a series of twelve patients, without effect. These results suggest that inositol has therapeutic effects in the spectrum of illness responsive to serotonin selective re-uptake inhibitors, including depression, panic and OCD, and is not beneficial in schizophrenia, Alzheimer's ADDH, autism or ECT-induced cognitive impairment.
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PMID:Controlled trials of inositol in psychiatry. 916 2

Klein's (1993: Arch Gen Psychiatry 50:306-317) "false suffocation alarm" theory of spontaneous panic attacks posits that central receptors compare CO2, O2, and lactate levels and trigger panic when an impending "false" state of suffocation is detected. Several investigators have found abnormalities of respiratory physiology in subjects with panic disorder. Twin and family studies have suggested that both panic disorder and tidal volume response to CO2 are inherited. We hypothesized that, if smothering symptoms are a marker for a hypersensitive suffocation detector and if this hypersensitivity is familial, then relatives of panic subjects with smothering symptoms would have higher rates of panic with smothering than relatives of panic subjects without smothering. We conducted a family study involving 104 panic disorder probands and 247 of their interviewed first-degree relatives. Probands and their relatives were interviewed using the Schedule for Affective Disorders and Schizophrenia--Lifetime Version for Anxiety Disorders to determine their panic disorder and smothering symptom status. Relatives of panic probands with smothering symptoms had an almost threefold higher risk for panic and an almost sixfold higher risk for panic with smothering symptoms when compared with relatives of panic probands without smothering. We conclude that panic disorder with smothering symptoms may be a subtype of panic disorder associated with increased familial risk and may be a group of interest to genetic investigators. These findings provide the first empiric evidence from a family study in support of Klein's false suffocation alarm theory of spontaneous panics.
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PMID:Panic disorder with smothering symptoms: evidence for increased risk in first-degree relatives. 955 84

To date, the quantitative psychopathology of panic disorder (PD) has been less well studied than that of other psychiatric conditions such as schizophrenia or major depression. The aim of the present study was to assess the frequency and factorial grouping of symptoms in a naturalistic sample of PD patients. A total of 274 consecutive cases of PD who contacted an out-patient clinic in Barcelona, Spain were assessed by two experienced interviewers. The assessment instruments included the Structured Clinical Interview for DSM-III-R Upjohn version (SCID-UP-R) and an inventory of panic attack symptoms based on DSM-III-R. Of the patients who presented at the unit during the assessment period, 8.5% presented with PD. Palpitations, shortness of breath, fear of dying and dizziness were the most frequent and intense symptoms reported by the PD patients. Principal-component analysis revealed four factors which accounted for 57% of the variance, including 'cardiorespiratory' (26.1%) and 'vestibular' (15.1%) factors, and two additional factors with mixed symptoms. The frequency of presentation of symptoms was similar to that reported in other studies. However, some discrepancies were observed that may be attributed to transcultural differences as well as to terminological problems and the range of symptoms assessed. These factors may also explain some of the differences found in factor analysis groupings in previous studies. Our findings support the symptom subtyping of PD.
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PMID:Semiology and subtyping of panic disorders. 957 Apr 87

Panic Control Treatment (PCT) is a widely used, empirically validated cognitive-behavioral treatment for panic disorder. Initially developed for the treatment of panic disorder with limited agoraphobic avoidance, PCT more recently has been finding broader applications. It has been used as an aid to pharmacotherapy discontinuation in panic disorder; in the treatment of panic attacks associated with other disorders such as schizophrenia; and, in combination with a situational exposure component, in the treatment of patients with moderate to severe agoraphobia. The authors critically review the evidence for the clinical efficacy of PCT and recent work directed at further enhancing the long-term efficacy and cost-effectiveness of treatment.
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PMID:Panic control treatment and its applications. 988 3

Childhood parental loss has been associated with a number of psychiatric disorders in adulthood. The present article aims to examine, firstly, the etiologic relationship between early parental loss and later development of schizophrenia and, secondly, the pathoplastic effect of the former on the symptomatology of the latter. We have administered semi-structured interviews inquiring into psychopathology and early separation experiences to a representative sample of first-visit patients to the 31 hospitals and clinics all over Japan (n=1963) and also to a community sample in a small city in Japan (n=218). When 225 patients diagnosed with schizophrenia according to DSM-III-R criteria were compared with 122 healthy control subjects without any lifetime psychiatric disorder, controlled for sex and age, there was no statistically significant difference in the rates of childhood parental loss (death or separation). As regards the pathoplastic effects, it was found that schizophrenic men were less likely to present with negative symptoms if they had experienced separation from the father, and were more likely to show panic attacks if they had experienced separation from the mother. Schizophrenic women were more likely to present with hallucinations if they had suffered any loss of the father. Childhood parental loss is not pathogenic of schizophrenia but appears to exert some pathoplastic influences on its presenting symptoms.
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PMID:Childhood parental loss and schizophrenia: evidence against pathogenic but for some pathoplastic effects. 992 86

A combination of nefazodone with a conventional neuroleptic would lead to a serotonin (5-HT)2 and D2 receptor blockade resembling that of an atypical neuroleptic, with an additional increase of 5-HT (and noradrenaline) turnover. This may be of benefit in some cases of schizophrenia. In this study, eight patients with schizophrenia with predominantly negative and/or depressive symptoms underwent an open prospective 26-week trial with nefazodone, added to conventional neuroleptics. The total Positive and Negative Syndrome Scale (PANSS) and the Montgomery-Asberg Depression Rating Scale (MADRS) scores (the last observations carried forward, LOCF) significantly (P < 0.05) decreased in these eight patients by a mean of 31% and 63%, respectively, mainly within the first 6 weeks. Positive symptoms, observed in three patients and panic attacks in two patients disappeared entirely. The doses of neuroleptics, stable during the first 6 weeks of the trial, subsequently were able to be decreased by 28%. Extrapyramidal symptoms noticeably improved during the phase of stable neuroleptic dose regimen. Of the three patients who discontinued the trial prematurely (after 14 weeks or more), only one evidenced a nefazodone-related adverse event. Adjunctive nefazodone may be a useful treatment option in this patient population, but additional studies are recommended.
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PMID:Adjunctive nefazodone in neuroleptic-treated schizophrenic patients with predominantly negative symptoms: an open prospective pilot study. 1046 16

A study on the biology of 'panic disorder,' which I have classified under the category of 'anxiety disorder,' made progress recently. In a genetic study, the hereditary of panic disorder was checked by a 'linkage and twins' study, and the anticipation of panic disorder was recognized as being the same as that which is also found in the psychiatric conditions known as schizophrenia and manic depression. A panic disorder patient regards the anxious sign of a model as ruinous, and this weakness in recognition has been duly noted. Therefore, I studied a patient showing a continuance state of 'hyper-sensitivity,' and compared this to a patient showing a 'sleep disorder.' Noradrenaline plays an important role in anxiety as suppression of the locus ceruleus (LN), the major NE-containing nucleus of the noradrenaline nervous system, brings on a calming effect. Yohimbine, however, which is an alpha 2 antagonist, is found to induce panic attacks. The fact that selective serotonin reuptake inhibitor (SSRI) suppresses panic attacks suggests that serotonin is connected with panic disorders. It is also thought that the 'raphe nucleus' is the site of origin of the serotonin nervous system, which participates in the control of anxiety. This suggests the participation of a gamma-aminobutyric acid (GABA) nervous system in which the administration of benzodiazepine at a high potency would be an effective agent against panic disorder. Cholecystokinin (CCK) is also suggested to have a connection with panic disorder as CCK-4 causes panic attacks. There has been no CCK antagonist found effective for an object- or time-oriented panic disorder at the present. It is thought that corticotropin-releasing factor (CRF) is released during a panic attack. The development of a new CRF receptor antagonist is needed. In addition to the studies on the neurotransmitters of the traditional type, such as noradrenaline, serotonin and GABA, studies on the neuropeptides, such as CCK and CRF have become important for future consideration. Understanding this, image studies such as MRI, SPECT, fMRI and PET have become highly desirable.
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PMID:[Neuropharmacological and genetic study of panic disorder]. 1049 83

There were studied 2 groups of the patients with a diagnosis of agoraphobia (according to ICD = 10). The first group included 34 patients which didn't use a specialized psychiatric service; the second one included 25 patients which needed an active therapy under conditions of psychiatric hospital. Dynamics of a disease was investigated by the method of retrospective (3 years) and following prospective (3 years) evaluation. The first group was characterized by relatively favourable outcome of chronic anxious-phobic disorders (APD) with the phenomena of a stable agoraphobia (5.8% of patients with a decrease of social adaptation): a limited agoraphobic avoidance (2 cases in the average), a rare and only psychogenic exacerbation (23 cases). Comorbid disorders were presented as minor depression (53%), somatophormic disorders (single isolated cardialgias and the conversive disorders--28%), personal disorders of hyperthimic (53%) and hysteric (35.5%) type. The second group was characterised by relatively worse outcome of chronic APD with the phenomena of a stable agoraphobia (32.0% of the patients with a decrease of social adaptation), that was associated with more generalized avoidance behaviour (more than 2 cases), with a gradual increase of both the severity of panic attacks and agoraphobia in limits of either periodic long-term aggravations (46%) or a continuous progredient course (29%). As compared with the 1-st group the second group was also characterised by significantly higher average number in a month of the panic attacks (4.9 + 1.1 vs 2.4 + 0.4; p < 0.01) and hospitalization (2.5 + 0.6 vs 0.2 + 0.2 + 0.1; p < 0.05) during all period of prospective observation. More severe comorbid disorders were revealed: slow-progredient schizophrenia (20% vs 0% in the first group; p < 0.01), a major depressive disorder (28% vs 3%; p < 0.01), dysthymic disorder (32% vs 3%; p < 0.05); personal disorders were presented mostly by the deviations of schizoid type (59%).
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PMID:[Chronic anxiety and phobic disorders with persistent agoraphobia: clinical and follow-up study]. 1053 47

The relationship between epilepsy and behavioral disturbances has been a subject of controversy since the 19th century. Affective changes may occur prior, during, or after the ictal discharge. Depression is the most prevalent comorbidity. Anxiety, panic attacks, and pseudoseizures may resemble complex partial seizures, and their diagnosis and treatment may be confusing, even to experienced clinicians. Epilepsy-related psychosis is less common, manifesting occasionally with symptoms that are indistinguishable from schizophrenia. There is no clear evidence of a distinct "epileptoid" personality, and interictal violence is extremely rare. Pharmacologic treatment with anticonvulsants remains the cornerstone of treatment. In case of psychiatric comorbidities or refractory seizures, the diagnosis should be re-examined.
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PMID:The relationship of psychiatric illnesses and seizures. 1135 88

The aim of this study was to investigate the relationship between panic attacks and hostility in patients with chronic schizophrenia. Thirty-two patients with a minimum 2-year history of treatment for schizophrenia were interviewed. The patients took mood stablizers lithium, carbamazepine and valproate adjunctively for hostility and anger attacks. Panic attacks were defined by Structure Clinical Interview of DSM-IV. Severity of psychopathology was assessed by the Hamilton Depression Rating Scale (HDRS) and Brief Psychiatric Rating Scale (BPRS). Functional level was assessed by the Global Assessment of Functioning Scale (GAF). Eight (25%) patients met the diagnostic criteria for panic attacks (DSM-IV) with affective symptoms including hostility and sudden spells of anger. Their HDRS scores were significantly higher (P < 0.01), and GAF scores were significantly lower (P < 0.05) than those of patients without panic attacks. Patients with panic attacks displayed significantly higher hostility in the score of the BPRS (P = 0.01). Those who received higher doses of neuroleptics were more likely to be considered hostile. Multivariate analysis revealed that panic attacks were correlated with more severe depression, greater hostility and lower GAF scores. The results suggest that increased hostility and anger spells may be symptoms of panic attacks, which are overlooked by psychiatrists.
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PMID:Correlation of panic attacks and hostility in chronic schizophrenia. 1144 90


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