History Of Psychotic Symptoms Research Articles

The Neurocognitive Signature of Psychotic Bipolar Disorder

Psychotic bipolar disorder may represent a neurobiologically distinct subgroup of bipolar affective illness. We sought to ascertain the profile of cognitive impairment in patients with bipolar disorder and to determine whether a distinct profile of cognitive deficits characterizes bipolar patients with a history of psychosis. Sixty-nine outpatients with bipolar I disorder (34 with a history of psychotic symptoms and 35 with no history of psychosis) and 35 healthy comparison subjects underwent a comprehensive neurocognitive battery. All three groups were demographically matched. Despite preserved general intellectual function, bipolar I patients overall showed moderate impairments on tests of episodic memory and specific executive measures (average effect size = .58), and moderate to severe deficits on attentional and processing speed tasks (average effect size = .82). Bipolar I patients with a history of psychosis were impaired on measures of executive functioning and spatial working memory compared with bipolar patients without history of psychosis. Psychotic bipolar disorder was associated with differential impairment on tasks requiring frontal/executive processing, suggesting that psychotic symptoms may have neural correlates that are at least partially independent of those associated with bipolar I disorder more generally. However, deficits in attention, psychomotor speed, and memory appear to be part of the broader disease phenotype in patients with bipolar disorder.

Bipolar I patients with and without a history of psychotic symptoms: Do they differ in their cognitive functioning?

Recently, many reports have consistently demonstrated cognitive deficits in patients with bipolar disorder (BD), but their relationship with symptomatology, specifically psychotic symptoms, remains unclear. Our main hypothesis was that a history of hallucinations and/or delusions in the course of BD-I is associated with severe cognitive deficits. We investigated several cognitive functions (memory, attention, verbal fluency and executive functions) in 18 BD-I patients with a history of psychotic symptoms (HPS+), 17 BD-I patients without a history of psychotic symptoms (HPS−), 33 schizophrenic patients and 26 healthy control subjects. Both groups of BD-I patients were more impaired than the normal controls in attention, verbal memory, verbal fluency and executive functions. Only HPS+ BD-I patients showed more difficulties in completing the Stroop test than nonpsychotic bipolar patients. Nevertheless, after adjustment for the effects of current psychopathology, this difference disappeared. Schizophrenic subjects showed worse performance than BD-I subjects in verbal memory and verbal fluency. These results suggest that a history of psychotic symptoms in bipolar I disorder may not be associated with more cognitive deficits. Further research on euthymic bipolar patients with and without HPS is required to confirm these findings.

Clinical correlates of first-episode polarity in bipolar disorder

Objective To determine the clinical and long-term implications of mood polarity at illness onset. Methods During a 10-year follow-up prospective study, systematic clinical and outcome data were collected from 300 bipolar I and II patients. The sample was split into 2 groups according to the polarity of the onset episode (depressive onset [DO] vs manic/hypomanic onset [MO]). Clinical features and social functioning were compared between the 2 groups of patients. Results In our sample, 67% of the patients experienced a depressive onset. Depressive onset patients were more chronic than MO patients, with a higher number of total episodes and a longer duration of illness. Depressive onset patients experienced a higher number of depressive episodes than MO patients, who in turn had more manic episodes. Depressive onset patients made more suicide attempts, had a later illness onset, were less often hospitalized, and were less likely to develop psychotic symptoms. Depressive onset was more prevalent among bipolar II patients. Bipolar I patients with DO had more axis II comorbidity and were more susceptible to have a history of psychotic symptoms than bipolar II patients with DO. Conclusion The polarity at onset is a good predictor of the polarity of subsequent episodes over time. A depressive onset is twice as frequent as MO and carries more chronicity and cyclicity.

Psychotic Symptoms With Underlying Graves Disease

Psychotic Symptoms With Underlying Graves Disease

38-Year-Old Man With Priapism and a History of Paranoid Schizophrenia

38-year-old man with a 20-year history of paranoid schizophrenia presented to the hospital with a prolonged, painful erection of the penis (priapism) occurring for 48 hours. The patient denied previous events of priapism, substance abuse, genital trauma, erectile dysfunction, or history of a prior hypercoagulable state. Physical examination revealed engorgement of both the corpora cavernosa and the corpus spongiosa but no evidence of genital trauma. The patient had a history of psychotic symptoms. During the first 10 years of treatment, the patient had been given various traditional neuroleptics such as trifluoperazine, haloperidol, thiothixene, and fluphenazine. However, his psychotic symptoms continued to be poorly controlled. The patient was hospitalized numerous times for paranoia and auditory and visual hallucinations; a trial of clozapine was initiated, with considerable improvement in the patient’s symptoms. Clozapine and phenytoin therapy was continued for at least 8 years until the occurrence of priapism. Results of the patient’s physical examination were otherwise normal. His only medications at the time were clozapine, 800 mg at bedtime and 100 mg every morning, and phenytoin, 200 mg orally per day.

38-Year-Old Man With Priapism and a History of Paranoid Schizophrenia

38-Year-Old Man With Priapism and a History of Paranoid Schizophrenia

Cannabis use and psychotic disorders: an update

This paper evaluates three hypotheses about the relationship between cannabis use and psychosis in the light of recent evidence from prospective epidemiological studies. These are that: (1) cannabis use causes a psychotic disorder that would not have occurred in the absence of cannabis use; (2) that cannabis use may precipitate schizophrenia or exacerbate its symptoms; and (3) that cannabis use may exacerbate the symptoms of psychosis. There is limited support for the first hypothesis. As a consequence of recent prospective studies, there is now stronger support for the second hypothesis. Four recent prospective studies in three countries have found relationships between the frequency with which cannabis had been used and the risk of receiving a diagnosis of schizophrenia or of reporting psychotic symptoms. These relationships are stronger in people with a history of psychotic symptoms and they have persisted after adjustment for potentially confounding variables. The absence of any change in the incidence of schizophrenia during the three decades in which cannabis use in Australia has increased makes it unlikely that cannabis use can produce psychoses that would not have occurred in its absence. It seems more likely that cannabis use can precipitate schizophrenia in vulnerable individuals. There is also reasonable evidence for the third hypothesis that cannabis use exacerbates psychosis.

Psychosis in Alzheimer disease: postmortem magnetic resonance spectroscopy evidence of excess neuronal and membrane phospholipid pathology.

The presence of psychotic symptoms in Alzheimer Disease subjects (AD+psychosis, AD+P) is a marker for a phenotype characterized by more severe cognitive impairment and a more rapidly deteriorating course. Although AD+P has been inconsistently associated with more severe neuropathology, no prior studies have examined measures of neuronal and synaptic integrity. To determine whether AD+P is associated with evidence of disrupted neuronal and synaptic integrity, as indicated by magnetic resonance spectroscopy (MRS) measurement of N-acetyl-L-aspartate and the membrane breakdown products, glycerophosphocholine and glycerophosphoethanolamine. 31P and 1H MRS studies of perchloric acid extract from postmortem brain of AD subjects with and without a history of psychotic symptoms. All subjects were characterized for the presence of comorbid cortical Lewy body pathology and for history of neuroleptic use. Brain tissue from dorsolateral prefrontal, superior temporal, inferior parietal, and occipital cortex, amygdala, and cerebellum were examined in all subjects. Statistical analysis accounted for correlated observations across brain regions within-subjects. AD+P subjects demonstrated significant elevations of glycerophosphoethanolamine and significant reductions of N-acetyl-L-aspartate. Between group differences were greatest in neocortical brain regions. Excess impairment of neocortical neuronal and synaptic integrity may provide the structural substrate underlying AD+P. Confirmation of these findings using in vivo MRS measures is indicated.

Age onset of psychotic versus non-psychotic bipolar illness in men and in women

Objective: To investigate the relationship between psychotic symptoms and age at onset of bipolar illness. Method: The charts of bipolar patients treated at the Massachusetts General Hospital Bipolar Clinic were reviewed for age of first affective episode, demographics and history of psychotic symptoms. Results: Data was obtained for 328 bipolar patients (56.7% females) of whom 42% had psychotic symptoms sometime through the course of their illness. Overall, there was no significant difference in age of onset between the psychotic and non-psychotic groups. Additional analysis carried out separately by gender found significant difference for males but not for females. Age at onset for psychotic males was significantly lower than non-psychotic males. Psychosis was less common in males than females. The mean age of onset for psychotic males was significantly lower than psychotic females. Conclusion: This result implies that developmental physiology underlying psychosis in bipolar illness may differ for men and women. The different proportions of males and females in the study samples may account for conflicting results reported in the literature for age of onset of psychotic bipolar illness.

Gabapentin-Associated Aggression

Back to table of contents Previous article Next article LetterFull AccessGabapentin-Associated AggressionNarsimha R. Pinninti, M.D., , and Deepak S. Mahajan, M.D., Narsimha R. PinnintiSearch for more papers by this author, M.D., Department of Psychiatry, SOM-UMDNJ, Cherry Hill, NJ, and Deepak S. MahajanSearch for more papers by this author, M.D., Philadelphia, PAPublished Online:1 Aug 2001AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail SIR: Gabapentin is an effective adjunctive mood stabilizer.1 There are case reports of aggression and hyperactivity when gabapentin was added to existing antiepileptic medication2 or used as a monotherapy in children.3 In adults, hostility, but not aggressive behavior, is reported to occur in at least 1% of patients treated with gabapentin.4 We report two cases where introduction of gabapentin was associated with aggressive behavior.Case ReportsCase 1. A 38-year-old man was admitted for the third time to our facility with a diagnosis of bipolar disorder, manic phase with psychotic symptoms. There was no history of rapid cycling, comorbid substance abuse, or physical aggression. His symptoms were partially responsive to a combination of lithium carbonate 1,650 mg/day (level of 0.7 mEq/l), olanzapine 25 mg/day, and lorazepam 2 mg bid. Gabapentin was started in a dose of 300 mg tid and increased to 1,200 mg/day by day 3. By day 4, the patient became very irritable and physically aggressive. He attacked a nurse, and mechanical restraints were used to control his behavior. He did not receive any additional medication at this time. The patient later recognized this behavior as out of character for him. Gabapentin was stopped while all other medications were continued. Within a day, his irritability decreased and aggressive behavior stopped completely. No further incidents of aggression were noted throughout the rest of his hospital stay.Case 2. A 51-year-old man with a diagnosis of bipolar disorder was admitted for the fourth time to our facility in a manic phase with mixed affective features. He had no history of psychotic symptoms, substance abuse, or aggression. On a combination of sodium valproate 2 g/day and risperidone 4 mg/day (to which the patient had responded well on previous admission) he became very withdrawn, spending 12 hours a day in bed, but denied depressive symptoms. When a reduction in sodium valproate to 1 g did not improve his condition, a decision was made to switch mood stabilizers. Gabapentin was started in a dose of 300 mg bid, and sodium valproate was stopped. Within 48 hours, the patient developed new symptoms of hostility, verbal aggression, and command auditory hallucinations and destroyed property by breaking the commode in his room. The patient clearly attributed these new symptoms to gabapentin. Gabapentin was stopped and sodium valproate reinstated in a dose of 1g per day. Within 48 hours, hostility, aggressive behavior, and hallucinations stopped. No further aggressive behavior was noted throughout his hospital stay.CommentAggression in the above two cases could be an aspect of mania, or it could be gabapentin-related. The absence of prior aggression, the temporal relation to instituting gabapentin, the cessation of aggression soon after stopping gabapentin, and the ego-dystonic nature of the aggressive behavior indicate an association between gabapentin and aggression. To our knowledge, there are no published case reports of aggression with gabapentin in adult patients. More than 100 cases of hostility and aggression have been reported to the manufacturer in the past 5 years (personal communication, Parke-Davis, 2000). With increasing use of gabapentin in psychiatry, this possible adverse effect should be kept in mind.References1 Ferrier IN: Lamotrigine and gabapentin: alternative in treatment of bipolar disorder. Neuropsychobiology 1998; 38:192-197Crossref, Medline, Google Scholar2 Wolf SM, Shinnar S, Kang H, et al: Gabapentin toxicity in children manifesting as behavioral changes. Epilepsia 1996: 36:1203-1205Google Scholar3 Tallian KB, Nahata MC, Lo W, et al: Gabapentin-associated aggressive behavior in pediatric patients with seizures. Epilepsia 1996; 37(suppl):501-502Google Scholar4 Neurontin (gabapentin). Physician's Desk Reference, 55th edition. Montvale, NJ, Medical Economics Co, 2001, p 2460Google Scholar FiguresReferencesCited byDetailsCited byEffect of gabapentin on sleep-deprivation-induced disruption of prepulse inhibition27 June 2020 | Psychopharmacology, Vol. 63BMJThe Psychopharmacology of Aggressive BehaviorJournal of Clinical Psychopharmacology, Vol. 32, No. 2The Consultant Pharmacist, Vol. 22, No. 12Gabapentin-Induced Paradoxical Exacerbation of Psychosis in a Patient with Schizophrenia1 December 2002 | The Canadian Journal of Psychiatry, Vol. 47, No. 10 Volume 13Issue 3 August 2001Pages 424-424 Metrics PDF download History Published online 1 August 2001 Published in print 1 August 2001

The combination of nefazodone and psychotherapy was more effective than either treatment alone in chronic depression

Keller MB, McCullough JP, Klein DN, et al. A comparison of nefazodone, the cognitive behavioral-analysis system of psychotherapy, and their combination for the treatment of chronic depression . N Engl...

Genetic associations with clinical characteristics in bipolar affective disorder and recurrent unipolar depressive disorder

Genetic factors may be associated with disease subtype as well as susceptibility. We have therefore typed polymorphisms at the serotonin transporter, dopamine receptor, tryptophan hydroxylase, tyrosine hydoxylase, and monoamine oxidase A (MAOA) loci in 139 unipolar and 131 bipolar patients and investigated associations with gender, number of episodes, age of onset, history of psychotic symptoms, history of suicidal behavior, and history of substance abuse. In bipolar subjects, the promoter variable number tandem repeat (VNTR) allele 132 of MAOA was associated with history of suicide attempts, P = 0.029, particularly in females, P = 0.006. The Fnu4HI allele 1 of MAOA was also associated with history of suicide attempts in females, P = 0.0162. The serotonin transporter promoter allele 2 was associated with increasing number of manic episodes, P = 0.02, and history of psychotic symptoms, P = 0.0243. One significant association was found in the unipolar group: dopamine D2 receptor promoter allele 2 with history of psychotic symptoms, P = 0. 0165. We have tested multiple loci for a variety of different clinical variables and performed 228 tests of significance in total. It is possible that these preliminary findings are type 1 errors, because one would expect 11 of the 228 tests to reach a nominal significance level of P < 0.05 by chance alone if all the tests were independent. The associations with the MAOA and serotonin transporter loci are consistent with previous data suggesting associations with susceptibility to bipolar affective disorder. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 96:36-42, 2000

DOPAMINE RECEPTOR CORRELATES OF PSYCHOSIS IN DEMENTIA

Psychotic symptoms are common in AD patients, causing substantial distress and premature institutionalization. Current pharmacotherapies are inadequate, with only modest efficacy and, in the case of typical neuroleptics, frequent intolerable side effects. The use of neuroleptics in elderly AD patients with psychotic symptoms has been based on the observed efficacy of these medications in schizophrenia, despite the obvious clinical and neurobiological differences in these disorders. To define a neuropharmacology specific to the psychosis of AD, the authors have been exploring selective dopamine receptor correlates of these symptoms. Using a candidate gene approach, the authors previously reported that psychotic symptoms in AD patients are associated with genetic variation in the dopamine1 (D1) and D3, but not D2 and D4 receptors (Sweet et al., Arch Neurol, 1998). The authors followed up this finding by conducting the first study to examine D1 and D3 receptor binding in postmortem brain from AD patients with and without psychotic symptoms. Twenty subjects with a final neuropathologic diagnosis of AD, without concurrent neurodegenerative disease were studied, thirteen of whom had a history of psychotic symptoms (AD+P). Selective D1 and D3 receptor saturation binding studies, using [3H]-SCH23390 and [125I]trans-7-OH-PIPAT were conducted on frozen tissue from the right rostral caudate. AD+P was associated with a 20% reduction in D1 density from 17.8 fmol/mg wet weight in nonpsychotic AD subjects to 14.0 fmol/mg wet weight in AD+P subjects. AD+P was also associated with a 40% increase in D3 receptor affinity, from a Kd of 2.2nM to 1.3nM, without a change in D3 receptor density. The differences between AD and AD+P patients in D3 affinity are determined, in part, by D3 receptor genotype. While confirmation in a larger sample is required, the preliminary receptor binding findings suggest leads to novel, selective pharmacotherapies for AD+P. Further exploration of the mechanisms underlying the genetic determination of receptor density and affinity are required.

Lifetime comorbidity, lifetime history of psychosis and suicide attempts, and current symptoms of patients with deteriorated affective disorder

This study extends our prior research by examining the lifetime comorbidity, history of psychosis and suicide attempts, and current symptoms of an unusual group of patients with major affective disorders who have not only been symptomatic for prolonged periods but have also been so functionally impaired that they required years of care in psychiatric facilities or by family members. Twenty-seven of these deteriorated affective patients and 29 patients with deteriorated schizophrenia were recruited from a large state hospital; 27 patients with non-deteriorated affective disorder were recruited from an affiliated outpatient facility. Patients with deteriorated affective disorder, as compared to those with non-deteriorated affective disorder, were far more likely to have a history of psychotic symptoms with suicidal themes and a history of life-threatening suicide attempts and completed suicide. Deteriorated affective patients were also more likely to meet criteria for melancholia and to have attentional deficits, thought disorder and negative symptoms. The deteriorated and non-deteriorated affective groups had similar lifetime rates of psychotic symptoms (bizarre and non-bizarre) and lifetime psychiatric comorbidity. Functional deterioration in schizophrenia, as compared to functional deterioration in affective disorders, was distinguished by a virtual absence of psychotic symptoms with suicidal themes, lower lifetime rates of life-threatening suicide attempts, greater variety and severity of psychotic symptoms, and greater severity of current affective flattening, anhedonia-asociality and disorientation to time. The results of this study extend our previous research by demonstrating that patients with major mood disorders who have experienced extreme functional deterioration evidence a distinct constellation of symptoms that differentiates them from their better outcome peers with mood disorders, and from similarly functionally deteriorated patients with schizophrenia.

Patterns of response to neuroleptic treatment: factors influencing the amelioration of individual symptoms in psychotic patients.

Fifty-three patients with acute psychotic disorders (diagnosed according to DSM-III) were treated with thioridazine alone and observed during periods of up to 2 months. The amelioration of paranoid ideas and hallucinations (target symptoms) and of concentration difficulties, disorientation, reduced appetite, and reduced sleep (additional symptoms) was studied by repeated psychopathology ratings (CPRS). The patients were classified as "fast, slow or partial responders" according to the therapeutic effect registered on each target symptom. Paranoid ideas disappeared completely after less than 3 weeks of treatment in 28% of the patients (fast responders) and after more than 3 weeks in 32% (slow responders). Hallucinations disappeared significantly faster than paranoid ideas; 47% of the patients were completely free from hallucinations after less than 2 weeks of treatment (fast responders) and 38% after more than 2 weeks (slow responders). The following factors were significantly correlated to positive treatment effects of thioridazine: 1) diagnosis involving a brief history of psychotic symptoms before admission; 2) a low CPRS score for paranoid ideas on admission; 3) presence of disorientation on admission; 4) normal appetite on admission, and 5) rapidly reached optimal serum concentration of the drug.

Acute Psychosis Following Phenelzine Discontinuation

Most concern over the untoward effects of monoamine oxidase inhibitors (MAOIs) has concentrated on the hypertensive crises and recently on orthostatic hypotension, hypomania, and sexual dysfunction. However, little has been written about withdrawal effects when MAOIs are discontinued. This article reports an acute organic psychosis marked by visual, auditory, and tactile hallucinations after abrupt discontinuation of phenelzine in two young women without previous history of psychotic symptoms.