WHAT MAKES US MAD?

Relocation of Information on this Site

2011-04-15T06:00:00.001-07:00

The information on this site is being relocated to http://www.psychoticdisorders.wordpress.com/

Visual hallucinations from retinal detachment misdiagnosed as psychosis.

2011-03-27T08:51:00.000-07:00

J Psychiatr Pract. 2011 Mar;17(2):133-6.

Brda D, Tang EC.

*New York State Psychiatric Institute and Columbia University Department of Psychiatry †Columbia University College of Physicians & Surgeons.

Abstract

Hallucinations are a common presenting symptom in schizophrenia and other psychotic disorders. In particular, auditory hallucinations, such as hearing voices, are the most common type of hallucination described in schizophrenia, while visual hallucinations are less frequently seen. Hallucinations are also present in disorders that are not primarily psychotic in nature, including mood disorders, substance-induced disorders, and psychosis due to a general medical condition. However, it is extremely important to rule out general medical causes of hallucinations, as they are often treatable and reversible, and if left untreated, the underlying non-psychiatric disorders causing them can lead to irreversible damage. We present a case in which a 48-year-old woman with schizophrenia began to complain of visual disturbances. Because of her delusional interpretation of these disturbances, they were initially attributed to psychosis, but the disturbances were in fact found to be the result of a retinal detachment. (Journal of Psychiatric Practice. 2011;17:133-136).

PMID: 21430493 [PubMed - in process

Cough mixture misuse in Hong Kong--an emerging psychiatric problem?

2011-03-27T08:44:00.000-07:00

Addiction. 1996 Sep;91(9):1375-8.

Lam LC, Lee DT, Shum PP, Chen CN.

Department of Psychiatry, Chinese University of Hong Kong, Shatin, Hong Kong.

Abstract

Cough mixture misuse has become a focus of concern in Hong Kong since the late 1980s. Psychiatric admissions related to cough mixture misuse have been reported with increasing frequency during the past 5 years. A retrospective chart review of psychiatric admissions related to cough mixture misuse for a 54-month period was conducted in two psychiatric units in Hong Kong. Twenty-seven subjects were identified. The main psychiatric presentations included acute organic brain syndrome, schizophreniform psychosis and affective episode. They appeared to be associated with the pharmacological activities of opiates, antihistamines and sympathomimetics, the main ingredients of most cough mixtures.

PMID: 8854373 [PubMed - indexed for MEDLINE

Cough mixture induced psychosis.

2011-03-27T08:37:00.000-07:00

Br J Clin Pract. 1996 Oct-Nov;50(7):400-1.

Lee DT, Lam LC, Chan KP, Leung HC.
Department of Psychiatry, Chinese University of Hong Kong, Hong Kong.

Abstract

Cough mixture is the third most commonly abused substance in Hong Kong. Over the last two years, ten cases of cough mixture-induced psychosis were admitted to a University hospital. All of them were clinically indistinguishable from paranoid schizophrenia, but the psychotic symptoms often resolved promptly with the cessation of cough mixture use or a small dose of haloperidol. A representative case is described. The possible underlying aetiological mechanism and the treatment principle are discussed.

PMID: 9015916 [PubMed - indexed for MEDLINE]

Mania following head trauma.

2011-03-26T09:32:00.000-07:00

Am J Psychiatry. 1987 Jan;144(1):93-6.

Shukla S, Cook BL, Mukherjee S, Godwin C, Miller MG.

Abstract

The authors present psychiatric and neurologic data on 20 patients who developed mania after closed head trauma. An association was seen between severity of head trauma (based on length of posttraumatic amnesia), posttraumatic seizure disorder, and type of bipolar disorder. The manic episodes were characterized by irritable mood rather than euphoria and by assaultiveness. Psychosis occurred in only 15% of the sample, and 70% had no depressive episodes. Bipolar disorders were absent among 85 first-degree relatives. The authors suggest that posttraumatic seizures may be a predisposing factor in posttraumatic mania.

PMID: 3799847 [PubMed - indexed for MEDLINE]

Manic syndrome following head injury: another form of secondary mania.

2011-03-26T09:30:00.000-07:00

J Clin Psychiatry. 1987 Jan;48(1):29-30.

Riess H, Schwartz CE, Klerman GL.

Abstract

Two cases of mania secondary to head injury are reported. Only four well-documented reports of head trauma as a cause of secondary mania were found in an English and foreign literature search, although such a search is made difficult by the paucity of cases meeting modern diagnostic criteria for mania. Previous reviews of the causes of secondary mania have not included head injury, but the two case reports confirm that head injury may be an additional cause. A diagnosis of mania secondary to head trauma should be considered in manic patients with atypical age of onset, absence of previous psychiatric illness, negative family history for bipolar illness, and close temporal proximity of head trauma to subsequent mania.

PMID: 3804982 [PubMed - indexed for MEDLINE]

Mania in neurologic disorders.

2011-03-26T09:28:00.000-07:00

Curr Psychiatry Rep. 2000 Oct;2(5):440-5.

Mendez MF.

Neurobehavior Unit (116AF), Veterans Affairs Greater Los Angeles Healthcare System, 11301 Wilshire Boulevard, Los Angeles, CA 90073, USA. MMendez@ucla.edu

Abstract

Neurologic disorders can produce "secondary" mania. Clinicians must distinguish secondary mania from primary, idiopathic manic-depressive illness (MBI). In addition to medical and drug-induced causes of secondary mania, neurologic causes usually develop in older patients who may lack a strong family history of MDI. Neurologic causes of mania include focal strokes in the right basotemporal or inferofrontal region, strokes or tumors in the perihypothalamic region, Huntington's disease and other movement disorders, multiple sclerosis and other white matter diseases, head trauma, infections such as neurosyphilis and Creutzfeldt-Jakob disease, and frontotemporal dementia. Patients with new-onset mania require an evaluation that includes a thorough history, a neurologic examination, neuroimaging, and other selected tests. The management of patients with neurologic mania involving correcting the underlying disorder when possible and the judicious use of drugs such as the anticonvulsant medications.

PMID: 11122994 [PubMed - indexed for MEDLINE]

Organic causes of mania.

2011-03-26T09:25:00.000-07:00

Mayo Clin Proc. 1988 Sep;63(9):906-12.

Larson EW, Richelson E.
Department of Psychiatry and Psychology, Mayo Clinic, Rochester, MN 55905.

Comment in:
Mayo Clin Proc. 1989 Jan;64(1):129-30.

Abstract

Manic syndromes have many neurologic, toxic, and metabolic causes. It is important for clinicians to be able to distinguish these organic disorders from primary idiopathic mania (bipolar disorder). The cardinal symptom of organic mania is an abnormally and persistently elevated or irritable mood. Organic mania usually develops in patients who are older than 35 years of age, whereas bipolar disorder generally has its onset between late adolescence and age 25 years. In patients with the first episode of mania, the clinician should thoroughly elicit information about current symptoms, recent infections, use of drugs, and past or family history of psychiatric disorders. In addition, a complete medical examination, computed tomography of the head, electroencephalography, and screening for drugs and toxins should be done. Treatment of organic mania includes correcting the underlying disorder when possible.

PMID: 3137394 [PubMed - indexed for MEDLINE]

Suspected antidepressant-induced switch to mania in unipolar depression: a first-person narrative.

2011-03-26T08:31:00.000-07:00

J Affect Disord. 2010 Sep;125(1-3):111-5. Epub 2010 Jun 8.

Amey C.

catherine@redgraphite.co.uk

Abstract

BACKGROUND: Antidepressant-induced switch to mania has not been thoroughly characterized in bipolar disorder and is even less well understood in unipolar depression.

METHOD AND RESULTS: I describe, as a first-person narrative, my own experience of psychotic mania, which was suspected to have been induced by the tricyclic antidepressant, dosulepin. I have had a 16-year history of depression and was receiving sertraline 50 mg od when I was prescribed, off licence, dosulepin 25 mg 1-2 nocte for insomnia. Within days, I developed mild hypomanic symptoms and returned to my GP, who discontinued dosulepin but continued treatment with sertraline. I was also referred for psychiatric assessment. Two months later, I was detained under Section II of the Mental Health Act 1983 and admitted to hospital with psychotic manic symptoms.

CONCLUSION: More understanding of antidepressant-induced switch to mania is needed in unipolar depression. My case study highlights the need for prompt specialist care for patients with depression reporting even mild, sub-threshold symptoms of mania.

2010 Elsevier B.V. All rights reserved.

PMID: 20570368 [PubMed - indexed for MEDLINE]

Cough syrup psychosis.

2011-03-26T08:23:00.000-07:00

CJEM. 2011 Jan;13(1):53-6.

Amaladoss A, O'Brien S.

Department of Psychiatry, Queen's University, Kingston, ON, Canada. alfiamaladoss@yahoo.ca
Abstract

Over-the-counter medications are widely accessible and used. Cough suppressant syrups contain dextromethorphan (DM), which has the potential to be abused, with resultant psychiatric symptoms. This case report describes a young woman presenting with psychotic mania secondary to DM abuse. We also describe the treatment of this toxidrome and include the results of a literature search on this topic. The recognition of cough syrup as an agent of abuse and its toxidrome is important. This will facilitate early diagnostic clarification and promote efficient treatment strategies.

PMID: 21324299 [PubMed - in process]

Herpes zoster ophthalmicus and syndrome of inappropriate antidiuretic hormone secretion.

2011-03-26T08:21:00.000-07:00

Intern Med. 2008;47(5):463-5. Epub 2008 Mar 3.

Kucukardali Y, Solmazgul E, Terekeci H, Oncul O, Turhan V.

Department of Internal Medicine, Gulhane School of Medicine, Haydarpasa Training Hospital, Istanbul, Turkey.

Abstract

The syndrome of inappropriate antidiuretic hormone (SIADH) secretion is a common consequence of neurologic and pulmonary infections as well as drug intake and many other clinical situations. This report describes SIADH that developed in an elderly woman with single dermatomal herpes varicella zoster ophthalmicus without evidence of varicella zoster encephalitis or dissemination. A 76-year-old woman was admitted to our department for evaluation of left facial pain, confusion and disorientation. Further investigation revealed hyponatremia 112 mEq/L, low serum osmolality, high urine osmolality, normal renal function, normal adrenal and thyroid hormones, and high plasma vasopressin 40 pg/mL. These results indicate that the hyponatremia in this case was due to SIADH and that SIADH was caused by an increased release of vasopressin probably because of the antiviral drug (acyclovir) or infection of varicella zoster virus (VZV) in a single dermatome.

PMID: 18310984 [PubMed - indexed for MEDLINE]

Hyponatremia-induced change in mood mimicking late-onset bipolar disorder.

2011-03-26T08:17:00.000-07:00

Gen Hosp Psychiatry. 2011 Jan-Feb;33(1):83.e5-7. Epub 2010 Oct 27.

McKnight RF, Hampson S.
Department of Psychiatry, Warneford Hospital, University of Oxford, Warneford Lane, OX3 7JX Oxford, UK.

Abstract
OBJECTIVE: Hyponatremia and bipolar disorder are rarely considered to have common features. This report describes a case of hyponatremia secondary to syndrome of inappropriate antidiuretic hormone secretion (SIADH) presenting as late-onset bipolar disorder and discusses the evidence linking hyponatremia to mood disorders.

METHOD: Case report and review of published literature.

RESULTS: This case provides evidence that mood changes identical to those seen in bipolar disorder may be caused by hyponatremia at a variety of concentrations.

CONCLUSIONS: Further research is required to determine causes of SIADH in psychiatric patients with symptomatic hyponatremia and to elucidate the mechanism by which hyponatremia causes changes in mood. In older patients presenting with new-onset bipolar disorder, a physical etiology must always be excluded.

Copyright © 2011 Elsevier Inc. All rights reserved.

PMID: 21353139 [PubMed - in process]

Risk of herpes zoster among patients with psychiatric diseases: a population-based study.

2011-03-26T08:07:00.000-07:00

J Eur Acad Dermatol Venereol. 2011 Apr;25(4):447-53. doi: 10.1111/j.1468-3083.2010.03811.x.

Yang YW, Chen YH, Lin HW.

Department of Dermatology, Taipei Medical University Hospital, Taipei, Taiwan Department of Dermatology, College of Medicine, Taipei Medical University, Taipei, Taiwan School of Public Health, Taipei Medical University, Taipei, Taiwan Biostatistic Research and Consulting Center, Taipei Medical University, Taipei, Taiwan.

Abstract

Background: Psychiatric disorders have been shown to be associated with impaired immune response, including decreased cellular immunity to varicella-zoster virus. However, the risk of herpes zoster (HZ) in psychiatric patients is, to date, unknown.

Objective The aim of this study was to determine the risk of herpes zoster (HZ) in psychiatric patients compared with the general population. Methods We used data from the Taiwan Longitudinal Health Insurance Database from 2004 to 2006. Our study cohort consisted of patients aged 18 years and older diagnosed with psychiatric disorders in 2004 (N = 42 340). The comparison cohort (N = 169 360) consisted of four age- and gender-matched controls randomly selected for every patient in the study cohort. All subjects were followed from the date of cohort entry until they developed HZ or the end of 2006, whichever was earliest. Stratified Cox proportional hazard regressions were performed to compute the 2-year HZ-free survival rates. Results After adjusting for potential confounders, we found patients with psychiatric disorders were more likely to have an episode of HZ than the control population [adjusted hazard ratio (HR), 1.29; 95% confidence interval (CI), 1.18-1.38]. When stratified by age and psychiatric diagnostic categories, in patients aged ≤60 years, the adjusted HRs for HZ were 1.34 (P = 0.026) for patients with affective psychoses, 1.42 (P < 0.001) for those with neurotic illness or personality disorders and 1.53 (P < 0.001) for patients with other mental disorders. However, in patients aged >60 years, only neurotic illness or personality disorders were significantly associated with an increased risk of HZ (adjusted HR, 1.26; P = 0.003).

Conclusions: Our analysis suggests that patients with psychiatric disorders are at increased risk of HZ, especially those aged ≤60 years. Further study is required to elucidate the nature of this association.

© 2010 The Authors. Journal of the European Academy of Dermatology and Venereology © 2010 European Academy of Dermatology and Venereology.

Herpes simplex type 2 virus encephalitis presenting as psychosis

2011-03-26T07:39:00.000-07:00

Kalarickal J. Oommen, M.D.,

Peter C. Johnson, M.D.

C. George Ray, M.D.
Kalarickal J. Oommen, M.D.

Affiliations

Requests for reprints should be addressed to Dr. Peter C. Johnson, Department of Pathology, Arizona Health Sciences Center, Tucson, Arizona 85724.

From the Departments of Neurology, Pathology and Pediatrics, Arizona Health Sciences Center, Tucson, Arizona.

Accepted 20 January 1982.

Abstract

The current literature recognizes two antigenic types of herpes simplex virus, type 1 and 2. Type 1 is the most common cause of sporadic necrotizing encephalitis in the United States, with a mortality rate of 30 to 70 percent, and leaves various neurologic sequelae in the survivors. Herpes simplex virus type 2 has been recognized as an etiologic agent in fatal infections in neonates and a mild meningitis in adults, but its role in encephalitis in adults is less well known. We report a case of herpes simplex virus type 2 encephalitis with an analysis of four additional cases previously documented in the literature. Herpes simplex virus type 2 may cause more infections than is presently recognized, and we suggest that some cases of acute psychosis may, like in our case, represent herpes simplex virus type 2 encephalitis.

Click here for full article.

[Mania following the use of a decongestant].

2011-03-24T13:11:00.000-07:00

Tijdschr Psychiatr. 2007;49(2):125-9.

[Article in Dutch]

Stuer K, Claes S.

Psychiatrisch Ziekenhuis Heilig Hart, Ieper, België. katrien.stuer@gmail.com

Abstract

We report on the case of a 56-year-old woman with no psychiatric history who had a manic episode after taking a decongestant containing pseudoephedrine (a secondary or organic mania). The aetiology, differential diagnosis, treatment and risk factors for a manic episode are discussed. In addition, we review published articles on the subject of mania induced by pseudoephedrine.

PMID: 17290343 [PubMed - indexed for MEDLINE]

Mania as a presentation of primary hypothyroidism.

2011-03-24T13:09:00.000-07:00

Singapore Med J. 2009 Feb;50(2):e65-7.

Sathya A, Radhika R, Mahadevan S, Sriram U.

Associates in Clinical Endocrinology, Education and Research, Geo Towers, 3rd floor, Apollo Speciality Hospital Annexe, Chennai 35, India. anjalisathyab@yahoo.co.in

Abstract

Hypothyroidism is a common problem in clinical practice, with diverse manifestations. Neuropsychiatric problems include affective disorders, disturbances in cognition and psychosis. Mania is commonly associated with hyperthyroidism. Only a few selected case reports mention mania as a presenting feature of hypothyroidism. We report a case of mania with psychotic symptoms in a 47-year-old woman who had no previous history of psychiatric disorder. She had signs of florid hypothyroidism. She required both antipsychotic drugs and thyroxine replacement for the amelioration of her symptoms. The report is followed by a brief review of the literature on mania as a clinical presentation of hypothyroidism and its probable pathogenesis. One has to have a high index of suspicion of underlying organic causes in patients presenting with depression, psychosis or cognitive disorders.

PMID: 19296014 [PubMed - indexed for MEDLINE]

Human exposure assessment and relief from neuropsychiatric symptoms: case study of a hairdresser.

2011-03-24T13:04:00.000-07:00

J Am Board Fam Pract. 2004 Mar-Apr;17(2):136-41.

Genuis SJ, Genuis SK.

Department of Obstetrics and Gynecology, University of Alberta, Canada. sgenuis@incentre.net

Abstract

Human exposure assessment and the results of implementing 'precautionary avoidance' suggested a relationship between a hairdresser's neuropsychiatric symptoms and occupational exposure to potentially hazardous chemicals. A variety of investigations in response to patient complaints of depression, emotional instability and various physical symptoms revealed no objective abnormality; the CH2OPD2 mnemonic (community, home, hobbies, occupation, personal habits, diet and drugs) recommended by the Ontario College of Family Physicians was used as a first-line screening tool to assess potential environmental exposure to toxins. After occupational leave of absence, the patient reported cessation of symptoms. Environmental causes for familiar medical problems are frequently undiagnosed; it is recommended that, where appropriate, a screening tool for evaluation of environmental exposure to toxics be incorporated into primary care assessment and management of patients.

PMID: 15082673 [PubMed - indexed for MEDLINE]

Organic affective illness associated with lead intoxication.

2011-03-24T13:02:00.000-07:00

Am J Psychiatry. 1984 Nov;141(11):1423-6.

Schottenfeld RS, Cullen MR.

Abstract

Psychiatrists treating patients with depression or nonspecific somatic complaints seldom think of lead intoxication as a possible cause. Because occupational exposure to lead is so common, these disturbances may often be associated with lead intoxication. To facilitate earlier clinical recognition and proper treatment among the many individuals at risk, the authors describe four cases of organic affective disturbance associated with lead intoxication, review the neuropsychiatric disturbances that have been reported with chronic exposure to lead, and report the results of their experience evaluating the psychiatric aspects of lead intoxication among individuals exposed in their work.

PMID: 6496787 [PubMed - indexed for MEDLINE]

Sydenham chorea and psychosis

2011-01-25T20:04:00.000-08:00

Tijdschr Psychiatr. 2010;52(4):265-9.

[Article in Dutch]

Mengde W, Jessurun AY.

Caprileskliniek, Willemstad, Curacao. W.Mengde@ggzbreburggroep.nl

Abstract

Sydenham chorea (SC) is a complication of a group A beta-haemolytic streptococcal infection which is characterised by involuntary, choreatic movements. There is a definitive link between SC and psychoses. Furthermore, patients with SC seem to run a greater risk of developing neuroleptic-induced movement disorders. In this case-study of a 19-year-old psychotic male with a history of SC, the authors illustrate that this complicates the treatment of a psychotic episode.

PMID: 20503168 [PubMed - indexed for MEDLINE]

Promethazine-Induced Psychosis in a 16-Year-Old Girl

2011-01-25T19:58:00.000-08:00

Charles Timnak, M.D., and Ondria Gleason, M.D., Tulsa, Okla.

TO THE EDITOR: Promethazine is a phenothiazine derivative and an H1 receptor antagonist that is commonly used for symptomatic relief of nausea and vomiting and for allergic conditions. Some clinicians also use promethazine as a cough suppressant. Promethazine is known to cause CNS side effects, including confusion, nervousness, disorientation, and hallucinations.1

There are currently few case reports of promethazine-induced psychosis. A report in the Medical Journal of Australia indicated two cases involving promethazine-induced psychosis in children.2 A case study of a 3-year-old patient reported severe visual hallucinations and agitation after treatment with promethazine.3 One case involved a middle-aged woman, who overdosed on promethazine and was disoriented and agitated and experienced hallucinations.4 A geriatric patient also developed psychosis after intramuscular administration of promethazine.5 We now report on a 16-year-old African American girl who developed psychotic symptoms after receiving treatment with promethazine.

Case Report

Alice, a 16-year-old African American girl with no prior psychiatric history, came to the emergency room with a chief complaint of hallucinations. Her symptoms had developed 5 days previously and included fever and a cough. She was taken to a local emergency room, diagnosed with an upper respiratory infection, and given azithromycin. Her condition worsened over the next 2 days. She was again taken to the emergency room, given an injection of promethazine, and discharged with a prescription for oral promethazine with codeine.

Click here to read full article

[Acute psychotic disorders related to bupropion: review of the literature].

2011-01-25T19:42:00.000-08:00

Encephale. 2010 Dec;36(6):461-71. Epub 2010 Mar 15.

[Article in French]
Javelot T, Javelot H, Baratta A, Weiner L, Messaoudi M, Lemoine P.

Service "Les Hortensias", centre psychothérapique Nord Dauphiné, 100, avenue du Médipôle, 38307 Bourgoin-Jallieu cedex, France. javelot.thierry@cp-nord-dauphine.fr

Abstract

RATIONALE AND OBJECTIVES: Bupropion, or amfebutamone, is an atypical antidepressant also used during tobacco cessation. From a structural standpoint, it resembles amphetamine drugs with psychostimulant effects, and endogenous monoamines. From a pharmacological standpoint, bupropion, and two of its most important active metabolites, inhibit dopamine and norepinephrine reuptake. It has recently been discovered that bupropion may act as a non-competitive cholinergic nicotinic receptor antagonist, and that it may inhibit the activation of reward systems triggered by nicotine. Buproprion's efficacy as a smoking cessation aid has been demonstrated by numerous clinical trials that have compared its effects with those of placebo and other nicotinic substitutes. In 2001, buproprion SR received marketing authorization in France as a smoking cessation aid, under the name ZYBAN®. Tobacco addiction indeed remains a major public health issue. Among patients with psychiatric conditions, chronic tobacco consumption is frequent. The development of non-nicotinic drugs may therefore enhance therapeutic possibilities. However, the psychotropic effects of these molecules should be taken into account. We have recently reported the case of a patient with schizoaffective disorder, who presented two acute bupropion-induced psychotic episodes. We have also undertaken an exhaustive bibliographical research on this subject. The aim of the present study is to present the information available to us, in order to suggest aetiopathogenic hypotheses and therapeutic proposals.

DATA SOURCES: The following databases were consulted on a regular basis, with no date restriction: Medline, Cochrane and Elsevier. The present study identified 22 cases of psychotic conditions associated with buproprion, as well as randomized and pharmacovigilance studies published in English, from December 1985 to November 2008. Since 2002, there have been three published case-reports on patients who underwent a tobacco cessation program.

DATA SYNTHESIS: Psychotic disorders associated with buproprion appear after an average of 10 days of 300 mg/d bupropion intake. In about two third of cases, the patients have no history of psychiatric conditions. In one third of cases, they have a history of thymic disorders. In our review, auditory, visual or cenaesthetic hallucinations frequently occur (85% of the reported cases), and are sometimes characterized by single episodes and/or are rationalized. Some of them occur along with delusional episodes (mystical, paranoid, etc.). The patients are restless, confused, but seldom exhibit dissociative and thymic symptoms.

DISCUSSION AND CONCLUSIONS: From an aetiopathogenic, clinical and evolutive standpoint, buproprion-induced psychotic episodes share many similarities with acute organic or toxic psychosis (notably induced by amphetamines). The hypothesis of a dopaminergic hyper-reactivity should be analyzed. Moreover, most of these patients were taking other medication, and the possibility of a dopaminergic potentialization prior to buproprion intake could be suggested. In such cases, bupropion should be discontinued and complete remission is expected within an average of 10 days. Even though neuroleptic drugs are still frequently used in these cases, benzodiazepines could become a valid alternative, according to the model of amphetamine-induced acute psychosis.

Copyright © 2010 L'Encéphale, Paris. Published by Elsevier Masson SAS. All rights reserved.

PMID: 21130229 [PubMed - in process

Acute psychosis due to the interaction of legal compounds--ephedra alkaloids in 'vigueur fit' tablets, caffeine in 'red bull' and alcohol.

2011-01-25T19:38:00.000-08:00

Med Sci Law. 2001 Oct;41(4):331-6.

Tormey WP, Bruzzi A.

Department of Chemical Pathology, Beaumont Hospital, Dublin, Ireland.

Abstract

A short-lasting episode of acute psychosis in a 32-year-old male which followed the consumption of alcohol, caffeine and 'vigueur fit' tablets containing ephedra alkaloids is reported. Less than two days after the event, a urine sample contained 22 microg/ml of ephedrine and 5 microg/ml of pseudoephedrine. Despite detailed pharmacological evidence being given at a jury trial, he was convicted of assault and trespass and was fined pounds sterling 16,000. An earlier incident involving misbehaviour on an aircraft again involving alcohol and ephedrine resulted in a conviction and a court order to provide twice weekly urine tests for alcohol for a period of six months. He stopped taking the alkaloid tablets after the second incident. There was no history of aberrant behaviour in this man outwith the period when taking these tablets. Ephedra alkaloids may cause psychosis and their effects can be exaggerated by interaction with caffeine and ethanol. To protect the public, the use of stimulant drugs in over-the-counter weight control programmes should be prescription only and the package insert should include a warning on the dangers of concomitant use of ethanol.

PMID: 11693229 [PubMed - indexed for MEDLINE]

Caffeine and psychiatric symptoms: a review.

2011-01-25T19:35:00.000-08:00

J Okla State Med Assoc. 2004 Dec;97(12):538-42.

Broderick P, Benjamin AB.

University of Oklahoma, 2312 North Indiana Avenue, Oklahoma City, Oklahoma 73106, USA.

Abstract

Caffeine is a widely used psychoactive substance that has the potential to contribute to many psychiatric symptoms. This review article aims to address the specific research studies and case reports that relate caffeine to psychiatric symptoms. Caffeine can cause anxiety symptoms in normal individuals, especially in vulnerable patients, like those with pre-existing anxiety disorders. Caffeine use is also associated with symptoms of depression due to either a self-medication theory, or a theory that caffeine itself causes changes in mood. Psychosis can be induced in normal individuals ingesting caffeine at toxic doses, and psychotic symptoms can also be worsened in schizophrenic patients using caffeine. Sleep and symptoms of ADHD may be altered by caffeine as well. Prevention of caffeine-induced psychiatric symptoms is possible by recognizing, educating, and treating patients using a tapering approach.

PMID: 15732884 [PubMed - indexed for MEDLINE]

Caffeine-induced psychosis.

2011-01-25T19:32:00.000-08:00

CNS Spectr. 2009 Mar;14(3):127-9.

Hedges DW, Woon FL, Hoopes SP.

Department of Psychology, Neuroscience Center, Brigham Young University, Provo, UT, USA. dawson_hedges@byu.edu

Abstract

As a competitive adenosine antagonist, caffeine affects dopamine transmission and has been reported to worsen psychosis in people with schizophrenia and to cause psychosis in otherwise healthy people. We report of case of apparent chronic caffeine-induced psychosis characterized by delusions and paranoia in a 47-year-old man with high caffeine intake. The psychosis resolved within 7 weeks after lowering caffeine intake without use of antipsychotic medication. Clinicians might consider the possibility of caffeinism when evaluating chronic psychosis.

PMID: 19407709 [PubMed - indexed for MEDLINE]

Psychiatric side effects attributed to phenylpropanolamine.

2011-01-25T19:27:00.000-08:00

Pharmacopsychiatry. 1988 Jul;21(4):171-81.

Lake CR, Masson EB, Quirk RS.

Dept. of Psychiatry, F. Edward Hebert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland.

Abstract

Phenylpropanolamine (PPA) is a sympathomimetic drug similar in structure to amphetamine which, in the United States, is present in over 130 medications, primarily decongestants, cough/cold remedies, and anorectic agents. We have reviewed 37 cases (published in North America and Europe since 1960) that received diagnoses of acute mania, paranoid schizophrenia, and organic psychosis and that were attributed to PPA product ingestion. Of the 27 North American case reports, more reactions followed the ingestion of combination products than preparations containing PPA alone; more occurred after ingestion of over-the-counter products than those obtained by prescription or on-the-street; and more of the cases followed ingestion of recommended doses than overdoses. Groups at particular risk appear to be those with a past or family psychiatric history, children under the age of 6 and post-partum women. Failure to recognize PPA as an etiological agent in the onset of symptoms usually led to a diagnosis of schizophrenia or mania, lengthy hospitalization, and treatment with substantial doses of neuroleptics or lithium. While generally safe at recommended doses, PPA can be hazardous to susceptible individuals and we urge physicians to be alert to the potential for PPA related psychiatric reactions. We have compiled an alphabetized table (Table 1: Prescription and Over-the-Counter Products Containing Phenylpropanolamine) allowing busy clinicians quick access to those drugs containing PPA.

PMID: 3060884 [PubMed - indexed for MEDLINE]

Organic affective psychosis associated with the routine use of non-prescription cold preparations

2011-01-25T19:24:00.001-08:00

Br J Psychiatry. 1990 Apr;156:572-5.

Brown TM, Golden RN, Evans DL.

Department of Psychiatry, University of North Carolina, School of Medicine, Chapel Hill 27599.

Abstract

A patient experienced an organic affective psychosis on three separate occasions after taking recommended doses of non-prescription cold/sinus preparations. The possible underlying pharmacological mechanisms of this clinical reaction lend support to the cholinergic-adrenergic balance hypothesis of affective disorders. Recognition of this acute drug-induced state can lead to appropriate short-term pharmacotherapy and can prevent misdiagnosis of a major affective disorder or schizophrenia.

PMID: 2386871 [PubMed - indexed for MEDLINE]

Dextromethorphan- and pseudoephedrine-induced agitated psychosis and ataxia: case report.

2011-01-25T19:23:00.000-08:00

J Emerg Med. 1999 Mar-Apr;17(2):285-8.

Roberge RJ, Hirani KH, Rowland PL 3rd, Berkeley R, Krenzelok EP.

Department of Emergency Medicine, Western Pennsylvania Hospital, Pittsburgh 15224, USA.

Abstract

Pseudoephedrine and dextromethorphan are therapeutic constituents of numerous commonly used, over-the-counter cough and cold preparations. Although this drug combination is generally considered quite safe if utilized in recommended doses, overmedication or overdose can result in serious neurologic and cardiovascular abnormalities that occasionally can be life-threatening. We present a case of a 2-year-old child who developed hyperirritability, psychosis, and ataxia after being overmedicated with a pseudoephedrine/dextromethorphan combination cough preparation, and discuss probable mechanisms of toxicity and risk factors for adverse events.

PMID: 10195488 [PubMed - indexed for MEDLINE]

Should Violent Criminal Offenders Be Tested for Past Exposure to Lead? and is treatment possible?

2010-11-06T07:34:00.000-07:00

Fairfax economist Rick Nevin has spent more than a decade researching and writing about the relationship between early childhood lead exposure and criminal behavior later in life. (By Lois Raimondo -- The Washington Post)

Research Links Lead Exposure, Criminal Activity

Data May Undermine Giuliani's Claims

By Shankar Vedantam

Washington Post Staff Writer

Sunday, July 8, 2007; Page A02

Rudy Giuliani never misses an opportunity to remind people about his track record in fighting crime as mayor of New York City from 1994 to 2001.

"I began with the city that was the crime capital of America," Giuliani, now a candidate for president, recently told Fox's Chris Wallace. "When I left, it was the safest large city in America. I reduced homicides by 67 percent. I reduced overall crime by 57 percent."

Although crime did fall dramatically in New York during Giuliani's tenure, a broad range of scientific research has emerged in recent years to show that the mayor deserves only a fraction of the credit that he claims. The most compelling information has come from an economist in Fairfax who has argued in a series of little-noticed papers that the "New York miracle" was caused by local and federal efforts decades earlier to reduce lead poisoning.

The theory offered by the economist, Rick Nevin, is that lead poisoning accounts for much of the variation in violent crime in the United States. It offers a unifying new neurochemical theory for fluctuations in the crime rate, and it is based on studies linking children's exposure to lead with violent behavior later in their lives.

What makes Nevin's work persuasive is that he has shown an identical, decades-long association between lead poisoning and crime rates in nine countries.

"It is stunning how strong the association is," Nevin said in an interview. "Sixty-five to ninety percent or more of the substantial variation in violent crime in all these countries was explained by lead."

Through much of the 20th century, lead in U.S. paint and gasoline fumes poisoned toddlers as they put contaminated hands in their mouths. The consequences on crime, Nevin found, occurred when poisoning victims became adolescents. Nevin does not say that lead is the only factor behind crime, but he says it is the biggest factor.

Richard Nevin has updated his graphs for crime, unwed teen pregnancy and mental retardation trends in a non-academic overview called “The Answer is Lead Poisoning”, with links to related academic research, at http://www.ricknevin.com/

To view full article click here.

Behavioral approaches to toluene intoxication.

2010-10-13T17:43:00.000-07:00

Environ Res. 1993 Jul;62(1):53-62.

Behavioral approaches to toluene intoxication.

Saito K, Wada H.

Department of Hygiene and Preventive Medicine, Hokkaido University, School of Medicine, Sapporo, Japan.

Abstract

Toluene is a chemical that is very useful in our lives but harmful to our health. Behavioral toxicology has the merit of providing an accurate indication of functional toxicity to the CNS through the analysis of learned behavior and use of behavioral analysis techniques that give us various learning paradigms for investigating the effects of chemicals on memory, stimulus discrimination, attention, time perception, etc. Learning is a common ability among various species and it is possible to predict toxicity to human health from animals. Behavioral toxicology is assumed to play an important role in occupational and environmental health. Using typical test batteries such as shuttle, Sidman, and pole-climb avoidance, and FI, FR, DRL, and DMS tasks, the effects of toluene were investigated and the results were reviewed. One important objective of a test battery is to be able to detect already-known toxicity. Behavioral toxicology research indicated such effects of toluene toxicity as hyperactivity, ataxia, addiction, insomnia, and memory disturbances. Some excellent results which might indicate clinically unknown effects of toluene such as hearing loss, impairments of time discrimination, and improvements of STM were also demonstrated. Introduction of blood and brain toluene levels as an index of toluene exposure and more sophisticated learning tasks which reflect specific higher nervous functions of the CNS has been proposed.

PMID: 8325266 [PubMed - indexed for MEDLINE]

Corticosteroid-Induced Psychotic and Mood Disorders

2010-09-07T20:30:00.000-07:00

Psychosomatics 42:461-466, December 2001

© 2001 The Academy of Psychosomatic Medicine

Corticosteroid-Induced Psychotic and Mood Disorders

Diagnosis Defined by DSM-IV and Clinical Pictures

Ken Wada, M.D., Norihito Yamada, M.D., Toshiki Sato, M.D., Hiroshi Suzuki, M.D., Masahito Miki, M.D., Yomei Lee, M.D., Kazufumi Akiyama, M.D., and Shigetoshi Kuroda, M.D.

Received November 15, 2000; revised March 23, 2001; accepted March 12, 2001. From the Department of Neuropsychiatry, Okayama University Medical School 2-5-1, Shikata-cho, Okayama 700-8558, Japan, Department of Psychiatry, Hiroshima City Hospital, 7-33, Moto-machi, Naka-ku, Hiroshima 730-8518, Japan. Address correspondence and reprint requests to Dr. Wada Department of Psychiatry, Hiroshima City Hospital, 7-33, Moto-machi, Naka-ku, Hiroshima 730-8518, Japan. E-mail: kenwada@do3.enjoy.ne.jp

The authors investigated long-term outcome and treatment strategy of corticosteroid-induced psychotic and mood disorders as defined by DSM-IV. Review of medical records of 2,069 referral patients revealed 18 applicable patients. Their clinical characteristics, longitudinal courses, and treatments were studied. The authors identified 15 patients with mood disorder and 3 patients with psychotic disorder. Increasing doses or resumption of corticosteroids had the strongest influence on the psychiatric course. These two corticosteroid-induced psychiatric disorders may have different pathophysiological substrates closely related to patient vulnerability. Effective psychopharmacological treatment options were indicated with consideration being given to the underlying diseases.

Key Words: Cortiscosteroid • Mood Disorder • Psychotic Disorder

Behavioral approaches to toluene intoxication

2010-08-20T17:04:00.001-07:00

Environ Res. 1993 Jul;62(1):53-62.

Behavioral approaches to toluene intoxication.

Saito K, Wada H.
Department of Hygiene and Preventive Medicine, Hokkaido University, School of Medicine, Sapporo, Japan.

Abstract

Toluene is a chemical that is very useful in our lives but harmful to our health. Behavioral toxicology has the merit of providing an accurate indication of functional toxicity to the CNS through the analysis of learned behavior and use of behavioral analysis techniques that give us various learning paradigms for investigating the effects of chemicals on memory, stimulus discrimination, attention, time perception, etc. Learning is a common ability among various species and it is possible to predict toxicity to human health from animals. Behavioral toxicology is assumed to play an important role in occupational and environmental health. Using typical test batteries such as shuttle, Sidman, and pole-climb avoidance, and FI, FR, DRL, and DMS tasks, the effects of toluene were investigated and the results were reviewed. One important objective of a test battery is to be able to detect already-known toxicity. Behavioral toxicology research indicated such effects of toluene toxicity as hyperactivity, ataxia, addiction, insomnia, and memory disturbances. Some excellent results which might indicate clinically unknown effects of toluene such as hearing loss, impairments of time discrimination, and improvements of STM were also demonstrated. Introduction of blood and brain toluene levels as an index of toluene exposure and more sophisticated learning tasks which reflect specific higher nervous functions of the CNS has been proposed.

PMID: 8325266 [PubMed - indexed for MEDLINE]

Toxicant exposure and mental health--individual, social, and public health considerations.

2010-08-20T16:56:00.001-07:00

J Forensic Sci. 2009 Mar;54(2):474-7. Epub 2009 Jan 31.

Toxicant exposure and mental health--individual, social, and public health considerations.

Genuis SJ.

Faculty of Medicine, University of Alberta, 2935-66 Street, Edmonton, AB, Canada. sgenuis@ualberta.ca

Abstract

Thoughts and moods are the result of biological processes; disordered thoughts and moods may be the result of disordered biological processes. As brain dysfunction can manifest with emotional symptoms or behavioral signs, the etiology of some mental health afflictions and some abnormal conduct is pathophysiological rather than pathopsychological. Various studies confirm that some chemical toxicants which modify brain physiology have the potential to affect mood, cognitive function, and to provoke socially undesirable outcomes. With pervasive concern about myriad chemical agents in the environment and resultant toxicant bioaccumulation, human exposure assessment has become a clinically relevant area of medical investigation. Adverse exposure and toxicant body burden should routinely be explored as an etiological determinant in assorted health afflictions including disordered thinking, moods, and behavior. The impact of toxicant bioaccumulation in a patient with neuropsychiatric symptoms is presented for consideration as an example of the potential benefit of recognizing and implementing exposure assessment.

PMID: 19187449 [PubMed - indexed for MEDLINE]

Hyperbaric Oxygen Therapy and TBI

2010-07-31T14:23:00.000-07:00

Arsenic Induced Delirium

2010-05-23T07:25:00.000-07:00

J Occup Med. 1987 Jun;29(6):500-3.

Neuropsychological impairment following inorganic arsenic exposure.

Bolla-Wilson K, Bleecker ML.

Abstract

A 50-year-old chemical engineer, routinely screened for occupational arsenic exposure, was admitted with a delirium for which no known etiology was found. Elevated levels of arsenic were found in the urine and hair. The patient received chelation treatment with British anti-Lewisite; substantial amounts of arsenic were excreted and the toxic encephalopathy improved gradually over the 8-month follow-up period. The patient was tested at 6 weeks, 4 months, and 8 months postdelirium with a battery of neuropsychological tasks. The pattern of results showed verbal learning and memory to be severely impaired while tests of general intellectual abilities and language remained unaffected. Follow-up examinations with no subsequent reexposure revealed improvements on specific cognitive tasks. It is unclear whether recovery of cortical functions occurred or if compensatory strategies were developed. It is proposed that a subacute exposure to arsenic may have contributed to the neuropsychological deficits.

PMID: 3612324 [PubMed - indexed for MEDLINE]

PANDAS: Pediatric Autoimmune Neuropsychiatric Disease Associated with Streptococcal Infection.

2010-05-23T07:06:00.000-07:00

J Pediatr (Rio J). 2007 May-Jun;83(3):201-8. Epub 2007 May 4.

PANDAS: a new disease?

de Oliveira SK.

Faculdade de Medicina, Universidade Federal do Rio de Janeiro (UFRJ), Rio de Janeiro, RJ, Brazil. sheila_knupp@hotmail.com

Abstract

OBJECTIVE: To establish the diagnostic criteria for PANDAS and to analyze the existing evidence regarding its etiopathogenesis, treatment and prophylaxis. SOURCES: Review of the scientific literature through a MEDLINE search carried out between 1989 and 2006. SUMMARY OF THE FINDINGS: The diagnostic criteria for PANDAS were established nearly 10 years ago, but a lot of controversy still exists over the actual existence of this new pediatric disease. The name of this new disease, supposedly of poststreptococcal etiology, derives from an acronym that stands for pediatric autoimmune neuropsychiatric disease associated with streptococcal infection. Tics and obsessive-compulsive symptoms are the major clinical signs of the disease, which develop after streptococcal infections, probably through autoimmune mechanisms. Even though these neuropsychiatric symptoms are common in rheumatic chorea, whose etiology is also poststreptococcal, the classic choreiform movements and other symptoms of rheumatic fevers are absent in PANDAS. The use of antimicrobial and immunologic therapy has been investigated and considered feasible in some cases. CONCLUSIONS: Further research is still necessary in order to answer the question posed in the title of this article. In the meantime, the identification of tic disorders and obsessive-compulsive disorders in children should include the possibility of PANDAS, seeking to provide evidence of previous streptococcal infection.

PMID: 17486197 [PubMed - indexed for MEDLINE]

Toxicant Exposure and Mental Health

2010-05-23T06:52:00.000-07:00

J Forensic Sci. 2009 Mar;54(2):474-7. Epub 2009 Jan 31.

Toxicant exposure and mental health--individual, social, and public health considerations.

Genuis SJ.

Faculty of Medicine, University of Alberta, 2935-66 Street, Edmonton, AB, Canada. sgenuis@ualberta.ca

Abstract

PMID: 19187449 [PubMed - indexed for MEDLINE]

Insomnia Related to Chemical Exposure

2010-05-23T06:49:00.000-07:00

Sleep Med Rev. 2009 Jun;13(3):235-43. Epub 2009 Feb 7.

Sleep disturbances and occupational exposure to solvents.

Viaene M, Vermeir G, Godderis L.

Department of Occupational, Environmental and Insurance Medicine, Catholic University of Leuven, UZ St. Rafaël, Leuven, Belgium. m.k.viaene@opzgeel.be

Abstract

A solvent can be defined as "a liquid that has the ability to dissolve, suspend or extract other materials, without chemical change to the material or solvent". Numerous chemical or technical processes rely on these specific properties of organic solvents in industry. Occupational exposure to solvents is not rare and some activities may cause substantial exposure to these substances in the workforce. Short-term or acute exposures cause a prenarcotic syndrome, and long lasting exposure conditions have been associated with various neurological and neuropsychiatric disorders, e.g., anosmia, hearing loss, colour vision dysfunctions, peripheral polyneuropathy and depression, but most significantly with the gradual development of an irreversible toxic encephalopathy. For the last 3 decades reports and epidemiological studies have been published reporting sleep disturbances among other complaints, related to long-term exposure to these compounds. In addition, the question has been posed if solvents can be the cause of a sleep apnoea syndrome in exposed workers, or on the contrary, if these workers are misdiagnosed and 'common' sleep apnoea syndromes are the cause of their chronic symptoms of fatigue and memory and attentional disturbances.

PMID: 19201227 [PubMed - indexed for MEDLINE]

Shingles and Manic Symptoms

2010-03-04T11:59:00.000-08:00

Can J Psychiatry. 1992 May;37(4):271-3.

Encephalitis associated with herpes zoster: a case report and review.

McKenna KF, Warneke LB.

Alberta Heritage Foundation for Medical Research; Edmonton.
Comment in:
Can J Psychiatry. 1993 Nov;38(9):631.

This paper describes the case of a patient with a history of affective disorder who developed encephalitis associated with herpes zoster which presented as a delirium with prominent manic symptoms. Published reports of encephalitis following herpes zoster infections are reviewed. The diagnosis of herpes zoster-associated encephalitis should be suspected in individuals with changes in his or her mental state, an abnormal electroencephalogram and an abnormal cerebrospinal fluid examination which closely follow a cutaneous herpes zoster lesion.

PMID: 1611590 [PubMed - indexed for MEDLINE]

Vitamin D Deficiency and Schizophrenia

2010-03-04T11:47:00.000-08:00

Psychoneuroendocrinology. 2009 Dec;34 Suppl 1:S247-57.

Developmental vitamin D deficiency causes abnormal brain development.

Eyles DW, Feron F, Cui X, Kesby JP, Harms LH, Ko P, McGrath JJ, Burne TH.

Queensland Brain Institute, The University of Queensland, Brisbane, Qld 4072, Australia. Eyles@uq.edu.au

There is now clear evidence that vitamin D is involved in brain development. Our group is interested in environmental factors that shape brain development and how this may be relevant to neuropsychiatric diseases including schizophrenia. The origins of schizophrenia are considered developmental. We hypothesised that developmental vitamin D (DVD) deficiency may be the plausible neurobiological explanation for several important epidemiological correlates of schizophrenia namely: (1) the excess winter/spring birth rate, (2) increased incidence of the disease in 2nd generation Afro-Caribbean migrants and (3) increased urban birth rate. Moreover we have published two pieces of direct epidemiological support for this hypothesis in patients. In order to establish the "Biological Plausibility" of this hypothesis we have developed an animal model to study the effect of DVD deficiency on brain development. We do this by removing vitamin D from the diet of female rats prior to breeding. At birth we return all dams to a vitamin D containing diet. Using this procedure we impose a transient, gestational vitamin D deficiency, while maintaining normal calcium levels throughout. The brains of offspring from DVD-deficient dams are characterised by (1) a mild distortion in brain shape, (2) increased lateral ventricle volumes, (3) reduced differentiation and (4) diminished expression of neurotrophic factors. As adults, the alterations in ventricular volume persist and alterations in brain gene and protein expression emerge. Adult DVD-deficient rats also display behavioural sensitivity to agents that induce psychosis (the NMDA antagonist MK-801) and have impairments in attentional processing. In this review we summarise the literature addressing the function of vitamin D on neuronal and non-neuronal cells as well as in vivo results from DVD-deficient animals. Our conclusions from these data are that vitamin D is a plausible biological risk factor for neuropsychiatric disorders and that vitamin D acts as a neurosteroid with direct effects on brain development.

What Makes us Mad? Amazon Bookstore

2010-02-06T08:25:00.000-08:00

What Makes us Mad? Amazon Bookstore

ANTIBIOMANIA - antibiotic-induced manic episodes

2010-02-06T06:03:00.000-08:00

Journal of Clinical Psychopharmacology:
February 2002 - Volume 22 - Issue 1 - pp 71-81
Review Article

Antimicrobial-Induced Mania (Antibiomania): A Review of Spontaneous Reports
Abouesh, Ahmed MD; Stone, Chip DO; Hobbs, William R. MD

Abstract
The authors reviewed reported cases of antibiotic-induced manic episodes by means of a MEDLINE and PsychLit search for reports of antibiotic-induced mania. Unpublished reports were requested from the World Health Organization (WHO) and the Food and Drug Administration (FDA). Twenty-one reports of antimicrobial-induced mania were found in the literature. There were 6 cases implicating clarithromycin, 13 implicating isoniazid, and 1 case each implicating erythromycin and amoxicillin. The WHO reported 82 cases. Of these, clarithromycin was implicated in 23 (27.6%) cases, ciprofloxacin in 12 (14.4%) cases, and ofloxacin in 10 (12%) cases. Cotrimoxazole, metronidazole, and erythromycin were involved in 15 reported manic episodes. Cases reported by the FDA showed clarithromycin and ciprofloxacin to be the most frequently associated with the development of mania. Statistical analysis of the data would not have demonstrated a significant statistical correlative risk and was therefore not undertaken. Patients have an increased risk of developing mania while being treated with antimicrobials. Although this is not a statistically significant risk, physicians must be aware of the effect and reversibility. Further research clearly is required to determine the incidence of antimicrobial-induced mania, the rela-tive risk factors of developing an antimicrobialinduced manic episode among various demographic populations, and the incidence of patients who continue to have persistent affective disorders once the initial episode, which occurs while the patient is taking antibiotics, subsides. The authors elected to name this syndrome antibiomania.

PSYCHIATRIC ONSET OF MS

2010-02-03T20:22:00.000-08:00

J Neurol Sci. 2006 Jun 15;245(1-2):59-62. Epub 2006 Apr 24.

Psychiatric onset of multiple sclerosis.
Jongen PJ.
Multiple Sclerosis Centre Nijmegen, Heiweg 97, 6533 PA Nijmegen, The Netherlands. p.jongen@mscentrumnijmegen.nl

We present a patient with psychotic disorder as onset of relapsing-remitting multiple sclerosis (MS). In this patient, a 26-year-old female, neurological examination revealed only minor abnormalities. As cranial CT scan was normal, her psychosis was diagnosed as psychogenic. Literature on psychiatric onset of MS is reviewed paying special attention to clinical and MRI aspects. It is concluded that psychiatric onset of MS may occur in up to 1% of patients, and that in previously healthy persons with acute psychotic disorder even the slightest neurological abnormality justifies a cranial MRI examination.

PMID: 16631798 [PubMed - indexed for MEDLINE]

MANIC-DEPRESSIVE PSYCHOSIS AS PREVALENT MANIFESTATION OF MS

2010-02-03T20:19:00.000-08:00

Rev Neurol (Paris). 2008 May;164(5):472-6. Epub 2008 Apr 24.
[Manic-depressive psychosis as prevalent manifestation of multiple sclerosis]
[Article in French]
El Moutawakil B, Sibai M, Bourezgui M, Boulaajaj FZ, Rafai MA, Gam I, Slassi I.
Service de neurologie-explorations fonctionnelles, CHU Ibn-Rochd, 9, rue Ahmed-Naciri, quartier Palmier, Casablanca, Maroc. elmoutawakilb@yahoo.fr

INTRODUCTION: Manic-depressive psychosis (MDP) and multiple sclerosis (MS) coexistence is unusual but well-proven.

OBSERVATIONS: We report two cases observed in two women aged 30 and 31, who were followed up for neurological episodes associated with concomitant or deferred manic or depressive fits. Brain magnetic resonance imaging revealed multiple zones of high intensity signals in the white matter. Biological balance was normal. The diagnosis of multiple sclerosis (MS) was established. Given to treat acute episodes, high-dose corticosteroids enabled regression of the psychological fits. Similarly, long-term treatment in one patient enabled significant regression of fits, which became less frequent and less severe.

DISCUSSION/CONCLUSION: The MDP-MS association may be due to local MS-related brain damage or to common genetic susceptibility. The positive effect of corticosteroids against psychological fits is another finding favouring an organic cause of these disorders.

PMID: 18555881 [PubMed - indexed for MEDLINE]

COMMON INFECTIOUS AETIOLOGIES FOR MULTIPLE SCLEROSIS, SCHIZOPHRENIA AND CHRONIC FATIGUE SYNDROME

2010-02-03T20:12:00.000-08:00

Med Hypotheses. 2009 Jun;72(6):736-9. Epub 2009 Mar 6.

On the question of infectious aetiologies for multiple sclerosis, schizophrenia and the chronic fatigue syndrome and their treatment with antibiotics.
Frykholm BO.
aion.terapi@yahoo.com

Close similarities in the courses of multiple sclerosis and schizophrenia laid the theoretical ground for attempting to find a common infectious aetiology for the two diseases. Chlamydia pneumoniae, which belongs to the rickettsial family of microorganisms has been linked to both diseases. It is postulated that since rickettsial microorganisms are ubiquitous in human populations they and the human species normally live in peaceful coexistence. In rare cases, for unknown reasons, varieties of them may become aggressive and pathogenic. The kynurenic acid hypothesis of schizophrenia has attracted much attention. It also seems to have initiated a paradigmatic shift from the hitherto prevailing serological research approach to one which focuses on immunological factors. An open clinical pilot study in which, during 2006, eight female and five male patients with psychotic symptoms were treated with a combination of antibiotics is presented, to which, in the beginning of 2007 two female patients suffering from severe and long standing chronic fatigue syndrome were added. On one year follow-up, six out of the eight female patients showed stable excellent treatment results, whereas two were rated as showing significant treatment results. Four of the five men who entered the study were suffering from chronic schizophrenia, whereas the fifth, was a case of severe acute catatonic schizophrenia. Two of the male patients showed significant treatment results, whereas three of them were rated as having had a slight to moderate improvement. No less than three of the women had suffered their first episode of psychosis after giving birth to their first (and only) child. This finding, as these women all responded excellently to treatment with antibiotics, indicates that post partum psychosis could be regarded as an infectious complication of childbirth of, as to the causative agent, unknown aetiology. High priority ought therefore be given to initiate controlled clinical trials with antibiotic treatment of this serious condition. The otherwise promising results of the pilot study seem to warrant further and controlled clinical trials with treatment with antibiotics of patients with psychotic symptoms. As the second patient with psychotic symptoms to enter the study, had a long standing history of chronic fatigue, where an initial treatment with the antidepressant fluoxetine had only worsened her condition, whereas ninety days of treatment with antibiotics, combined with vitamin B injections, effected a complete recovery, the author decided, when two patients with long standing and incapacitating chronic fatigue syndromes sought the clinic in February and March 2007, to include them in the study. The first of them, after sixty days of treatment with antibiotics showed excellent treatment results on follow-up one year later, whereas the second, who also took the combination of antibiotics for sixty days, was rated as having shown a significant improvement.

PMID: 19269110 [PubMed - indexed for MEDLINE]

RECOGNIZING OCCUPATIONAL DISEASE--TAKING AN EFFECTIVE OCCUPATIONAL HISTORY

2010-02-03T06:57:00.001-08:00

Recognizing Occupational Disease -- Taking an Effective Occupational History

MICHAEL B. LAX, M.D., M.P.H., and WILLIAM D. GRANT, ED.D.,
Central New York Occupational Health Clinical Center,
State University of New York Health Science Center at Syracuse, Syracuse, New York
FEDERICA A. MANETTI, M.D., M.S.,
Syracuse, New York
ROSEMARY KLEIN, M.S., C-ANP, COHN-S,
Central New York Occupational Health Clinical Center,
State University of New York Health Science Center at Syracuse, Syracuse, New York

Occupational exposures contribute to the morbidity and mortality of many diseases. However, occupational diseases continue to be underrecognized even though they are responsible for an estimated 860,000 illnesses and 60,300 deaths each year. Family physicians can play an important role in improving the recognition of occupational disease, preventing progressive illness and disability in their own patients, and contributing to the protection of other workers similarly exposed. This role can be maximized if physicians raise their level of suspicion for workplace disease, develop skills in taking occupational histories and establish routine access to occupational health resources.

The patient with a possibly work-related illness frequently seeks care initially from a family physician. The physician's recognition of a possible link between work and disease often determines the diagnostic tests that are performed and the treatment that is recommended. Early diagnosis of an occupational illness may prevent progressive morbidity and disability from conditions such as occupational asthma and may facilitate the reversal of adverse effects from exposures to substances such as lead.1 The identification of an occupational illness in one patient also provides the physician with an opportunity to protect other patients with similar exposures.2 Since much remains to be learned about the effects of toxins on health, the family physician is in a crucial position to contribute new information about occupational disease.

To read full article go here.

OCCUPATIONAL DISEASE THOUGHT TO BE BIPOLAR DISORDER

2010-02-03T06:04:00.000-08:00

CASE REPORT: 33 year old female experienced acute, full-blown manic episode, diagnosed as manic-depression with psychotic features. Subsequent treatment included various psychiatric medications from which she suffered numerous severe side effects including involuntary movements and a weight gain of 80lbs. Despite pharmaceutical management, she continued to have manic episodes and required recurrent psychiatric hospitalization.

Two years after the initial onset of mania the patient was seen by a physician trained in environmental health sciences and had various investigations confirming she had bioaccumulated high levels of lead. Patient had been employed for 15 years in an industry that uses chemical processes and was diagnosed with Substance Induced Neuropsychiatric and Cognitive Disorders (292.11, 292.12, 294.9). Substances included Toluent, Heavy Metals (lead, silver, mercury), Sulfuric Acid, Xylene, Propyl Alcohol, n-Hexane, and other organic solvents.

Patient sought treatment from complimentary medicine for detoxification. Chemical detoxification of lead was undertaken with a heavy metal chelator and values of lead progressively diminished. Chelation treatments were initially covered by the patients primary insurance company. Concomitant with the decline in accumulated lead, all of her psychiatric symptoms gradually subsided and all medication was discontinued.

Patient received supportive depositions in worker’s compensation proceeding of the diagnosis toxic encephalopathy and was awarded a worker’s compensation settlement in New York State.

Patient was unable to continue maintenance chelation treatments and over the course of 10 years has experienced two incidents exacerbating symptoms of mania. A detoxing protocol quickly relieved symptoms of the first incident. The second incident was a result of a bacterial infection from an abscessed tooth, patient reported both visual and auditory hallucinations, that of schizophrenic nature. Treatment with the anti-biotic Flagyl, and a root canal quickly abated all symptoms.

This case represents the importance of taking an effective work history and recognizing visual hallucinations as part of organic brain disease.

Calcification of the basal ganglia presenting as a schizophreniform psychosis

2010-02-01T09:12:00.000-08:00

Postgrad Med J 1972;48:636-639 doi:10.1136/pgmj.48.564.636
Case report
Calcification of the basal ganglia apparently presenting as a schizophreniform psychosis
Peter Hall

Abstract
A patient with gross basal ganglia calcification is described, whose condition was associated with severe psychotic symptoms and in whom the clinical picture was not typical of hypoparathyroidism, pseudohypoparathyroidism or pseudo-pseudohypoparathyroidism.
Calcification of the basal ganglia may occur in a variety of infections, toxic and metabolic disorders, particularly hypoparathyroidism, pseudohypoparathyroidism, toxoplasmosis and some anoxic conditions (Moskowitz, Winickoff & Heinz, 1971).

Though there is doubt as to the precise diagnosis in the present case, familial calcification appears to be the most probable.

Basal ganglia calcification, idiopathic 1: Abnormal calcium deposits in the part of the brain called the basal ganglia. Type 1 results in psychiatric, cognitive or neurological problems associated with the calcification

CARBON MONOXIDE INTOXICATION INDUCED MANIA

2010-02-01T07:46:00.000-08:00

Secondary mania in a patient with delayed anoxic encephalopathy after carbon monoxide intoxication

Department of Neurology, Kwandong University College of Medicine, Myongji Hospital, Gyeonggi, Korea

Received 6 July 2005;
accepted 19 October 2005.
Available online 28 August 2006.

Abstract
Mania is a rare clinical manifestation of delayed anoxic encephalopathy (DAE). Prior case reports on mania after hypoxic injury involved patients with a previous history of mania or depression, potentially reflecting a recurrence of premorbid mood disorders after hypoxia rather than pure secondary mania. Herein, we report a 55-year-old woman with no past history of neurological or psychiatric illness, who developed mania as a symptom of DAE after carbon monoxide intoxication. Brain magnetic resonance imaging showed diffuse white matter lesions, particularly visible in the frontal white matter. This frontal lesion may have prevented frontal inhibition from being transmitted to the basotemporal limbic area, resulting in mania manifested as a burst of limbic activity.

ACUTE MANIA AND NEUROLOGICAL DISORDERS

2010-02-01T07:41:00.000-08:00

Mario F. Mendez1

Neurobehavior Unit (116AF), Veterans Affairs Greater Los Angeles Healthcare System, 11301 Wilshire Boulevard, 90073 Los Angeles, CA, USA

Abstract

Neurologic disorders can produce “secondary” mania. Clinicians must distinguish secondary mania from primary, idiopathic manic-depressive illness (MBI). In addition to medical and drug-induced causes of secondary mania, neurologic causes usually develop in older patients who may lack a strong family history of MDI. Neurologic causes of mania include focal strokes in the right basotemporal or inferofrontal region, strokes or tumors in the perihypothalamic region, Huntington’s disease and other movement disorders, multiple sclerosis and other white matter diseases, head trauma, infections such as neurosyphilis and Creutzfeldt-Jakob disease, and frontotemporal dementia. Patients with new-onset mania require an evaluation that includes a thorough history, a neurologic examination, neuroimaging, and other selected tests. The management of patients with neurologic mania involving correcting the underlying disorder when possible and the judicious use of drugs such as the anticonvulsant medications.

To read full article go here.

PSYCHIATRIC PRESENTATION OF CREUTZFELDT-JAKOB DISEASE

2010-02-01T07:38:00.000-08:00

The British Journal of Psychiatry 151: 260-263 (1987)© 1987 The Royal College of Psychiatrists
Psychiatric presentation of Creutzfeldt-Jakob disease. A case report
MS Keshavan, WA Lishman and JT Hughes Maudsley Hospital.

A patient with Creutzfeldt-Jakob disease is described. Many alternative psychiatric diagnoses were considered, and the true situation only became apparent late in the clinical course.

MULTIPLE MYELOMA WITH MANIC FEATURES

2010-02-01T07:20:00.000-08:00

Multiple Myeloma Presenting as Secondary Mania

Donald J. Kushon, MD, Sunil Verma, MD, Mahmoud Elfatah, MD, Scott F. Allen, MD, Kehinde Ogundipe, MD, Renata Angelini, MD, and Amy Mackenzie, MD
Primary Psychiatry. 2009;16(11):22-24

Disclosure: The authors report no affiliation with or financial interest in any organization that may pose a conflict of interest.

Off-label disclosure: This article includes discussion of the following unapproved medications for mood disorder due to multiple myeloma with manic features: risperidone, quetiapine fumarate, and valproic acid.

Please direct all correspondence to: Kehinde Ogundipe, MD, Drexel University College of Medicine, Department of Adult Psychiatry, 1427 Vine Street, 8th Floor, Philadelphia, PA, 19102; Tel: 215-762-6660; Fax: 215-762-6673; E-mail: Kehinde.Ogundipe@DrexelMed.edu.

Focus Points
• Psychosomatic manifestations of multiple myeloma have been described in the literature.• Multiple myeloma can be a cause of secondary mania and mania can be one of the first presenting symptoms.• Causes of mental status changes in patients with multiple myeloma include hypercalcemia, renal failure, infections, hyperammonemia, and hyperviscosity syndrome.• Multiple myeloma should be included in the differential diagnosis in patients presenting for the first time with recent onset of mania.• Recognition of multiple myeloma as a cause of secondary mania will facilitate proper treatment and prevent advancement of the disease.

Abstract
Medical conditions that can cause new onset of mania may be overlooked, leading to treatment delays. The authors seek to increase awareness of multiple myeloma as a possible cause of secondary mania. The authors report on new-onset mania in a 59-year-old woman who after further medical investigation was found to have stage III multiple myeloma. Palliative treatment for multiple myeloma resulted in a decrease in the patient’s manic symptoms and stabilization of the medical condition. Recognition of multiple myeloma as a cause of secondary mania will facilitate proper treatment and prevent advancement of the disease.

To read full article go here.

ORGANIC MANIC DISORDERS

2010-02-01T07:17:00.000-08:00

Psychosomatics 26: 394-402, 1985Copyright © 1985 Academy of Psychosomatic Medicine

Organic manic disorders CHRIS STASIEK M.A.1, and MARK ZETIN M.D.1

From the department of psychiatry and human behavior of the University of California, Irvine
Using specified criteria, Krauthammer and Klerman's review of the literature for causes for manic symptoms found cases of secondary mania owing to drugs, infection, neoplasm, epilepsy, and metabolic disturbances. We reviewed publications subsequent to their 1978 report for additional cases of secondary mania occurring in the absence of delirium and of prior affective illness. Our review reemphasizes the importance of the medical and neurologic history and examination, of a medication history, and of appropriate laboratory studies (electrolytes, thyroid function, syphilis serology) in evaluating manic patients for underlying medical conditions. Attention to the diagnosis of secondary mania is especially important in patients presenting with a first episode in later life and with a negative family history for mania.

45 YEAR OLD FEMALE WITH A FATAL DISEASE THOUGHT TO BE BIPOLAR DISORDER

2010-02-01T07:11:00.000-08:00

Creutzfeldt-Jakob Disease Presenting as Secondary Mania Ivan Lendvai , M.D., Stephen M. Saravay , M.D., and Maurice D. Steinberg , M.D.

Received October 15, 1998; revised May 3, 1999; accepted May 20, 1999. From the Long Island Jewish Medical Center, Consultation-Liaison Psychiatry, New Hyde Park, New York. Address correspondence and reprint requests to Dr. Lendvai, Staten Island University Hospital, Department of Psychiatry, 375 Seguine Avenue, Staten Island, NY 10309.
Key Words: Creutzfeldt-Jakob Disease • Mania

Ours is a report of a patient with Creutzfeldt-Jakob disease who presented with mania and was initiallly diagnosed and treated for Bipolar I Disorder, manic type. Psychiatric disturbances constitute the prodromal manifestations in 18%–39% of those with Creutzfeldt-Jakob disease.1 Dementia occurs in all patients and progresses rapidly. Patients may complain of fatigue and appear apathetic; personal hygiene suffers early; in some cases irritability may be prominent.2,3 Depression has been found in more than 30% of patients with Creutzfeldt-Jakob disease, and 10% of patients with Creutzfeldt-Jakob disease need psychiatric hospitalization for depression.1,2 We were unable to find any report of mania as a prominent presenting symptom.

Case Report
The patient, a 45-year-old, married mother of two, was in her usual state of health, working as a secretary until about 8 weeks before admission to a short-term psychiatric inpatient facility. At that time, the patient began to have pressured, incoherent speech, with thoughtracing, and abrupt shifts of thoughts. She went on spending sprees and built up considerable credit card debt, buying unnecessary things. She had severe insomnia, sleeping only a few hours each night. She also complained of blurred vision and gait difficulty, the latter also noted by her family. After evaluation of these complaints and a normal magnetic resonance imaging (MRI) of the brain, she was given a diagnosis of Bipolar I Disorder, manic type. After 2 weeks, she was discharged on Haldol (haloperidol: 15 mg/day), Cogentin (benztropine: 0.5 mg bid), and Depakote (divalproex sodium: 750 mg bid). During the first week at home, she became less spontaneous, increasingly lethargic, and less interpersonally responsive, and her gait problems worsened. She spent much of her time staring into space, not speaking. During the second week at home, the patient became increasingly agitated. Her medications were stopped; Klonopin (clonazepam) was started without improvement, and the patient was hospitalized at another acute psychiatric hospital, again diagnosed as Bipolar I Disorder, manic type.

To read full article go here.

CASE REPORT OF A 75 YEAR OLD FEMALE: FATAL PSYCHOSIS FROM CJD

2010-02-01T07:02:00.000-08:00

Of Illusions, Hallucinations and Creutzfeldt-Jakob Disease (Heidenhain’s Variant)

J Neuropsychiatry Clin Neurosci 17:1, Winter 2005

SIR: Sporadic Creutzfeldt–Jakob disease (CJD), a rare progressive neurodegenerative disorder whose classic features include dementia, ataxia, and myoclonus can initially present with nonspecific psychiatric symptomatology such as fatigue, anxiety or a change in personality in about one third of cases, sometimes leading to erroneous diagnoses of depression or psychosis, as has been described in single patient reports. 1 In contrast to the above psychiatric symptoms, the presence of visual perceptual abnormalities such as illusions and hallucinations observed at the onset of a patient’s clinical course is usually more likely to be viewed as indicative of a medical, ophthalmologic or neurologic illness rather than of psychiatric etiology.2 We present a case of an elderly female with an initial presentation notable for the acute manifestation of visual illusions followed by visual hallucinations, but whose complicated medical course led to a variety of psychiatric diagnoses prior to her ultimate diagnosis of CJD.

MY MYSTERIOUS LOST MONTH OF MADNESS: a case of Anti-nmdar Encephalitis Acute Psychosis

2010-01-31T20:36:00.000-08:00

My mysterious lost month of madness

I was a happy 24-year-old suddenly stricken by paranoia & seizures. Was I going crazy?

By SUSANNAH CAHALAN
To read Susannah's article go here.

Susannah's story was featured on MSNBC's Medical Mysteries Series.

Dr. Souhel Najjar is the Neurologist who determined the underlying cause to Susannah's psychosis was anti-NMDAR Encephalitis.

Street: 223 East 34th Street
City/state/zip: New York NY 10016
Country: US
Email: Souhel.Najjar@nyumc.org
Phone: +1 646 558 0807
Fax: +1 646 358 7166

ANTI-NMDA RECEPTOR ENCEPHALITIS

2010-01-31T20:04:00.000-08:00

Epileptic Disord. 2009 Sep;11(3):267-9. Epub 2009 Aug 28.

Anti-NMDA receptor encephalitis: a video case report.
Labate A, Irani SR, Vincent A, Gambardella A, Piane EL, Cianci V, Aguglia U.

Institute of Neurology, University Magna Graecia, Catanzaro, Italy. a.labate@isn.cnr.it
This report concerns a 26-year-old Italian woman who was given the diagnosis of anti-NMDAR encephalitis after the incidental identification of an ovarian tumour. Neuropsychiatric symptoms and hyperkinetic movements are very commonly seen as initial symptoms of paraneoplastic encephalitis. Interestingly, our patient showed stereotypical movements predominantly located to lower limbs, mimicking a psychogenic seizure. This latter feature further extends the clinical spectrum of dyskinetic movements of anti-NMDAR encephalitis.

PMID: 19713171 [PubMed - indexed for MEDLINE]

ANTI-NMDA RECEPTOR ENCEPHALITIS

2010-01-31T20:01:00.000-08:00

Epileptic Disord. 2009 Sep;11(3):261-5. Epub 2009 Sep 7.
Complex partial status epilepticus revealing anti-NMDA receptor encephalitis.

Bayreuther C, Bourg V, Dellamonica J, Borg M, Bernardin G, Thomas P.

Department of Neurology, University of Nice Sophia-Antipolis, Pasteur Hospital, Nice, France.
Encephalitis with anti-NMDA receptor antibodies is a recently-recognised form of paraneoplastic encephalitis characterized by a prodromal phase of unspecific illness with fever resembling viral disease, followed by memory loss, psychiatric features, seizures, disturbed consciousness, prominent abnormal movements and autonomic imbalance. Association with ovarian teratoma is common. Neurological outcome can be good, especially when surgery is performed at an early stage. Here, we report a case of anti-NMDA receptor encephalitis associated with ovarian teratoma presenting with inaugural complex partial status epilepticus. The nature of abnormal movements at early stages was unclear and abnormal movements were misinterpreted as the recurrence of partial epileptic seizures. Despite its rarity, all clinicians treating epilepsy and movement disorders should be familiar with anti-NMDA receptor encephalitis, that appears to be a very severe but curable disease.

PMID: 19736168 [PubMed - indexed for MEDLINE]

ACUTE PSYCHOTIC MANIA: ANTI-NMDA ENCEPHALOPATHY

2010-01-31T19:58:00.000-08:00

Med J Aust. 2009 Sep 7;191(5):284-6.
Acute psychiatric illness in a young woman: an unusual form of encephalitis.

Parratt KL, Allan M, Lewis SJ, Dalmau J, Halmagyi GM, Spies JM.
Department of Neurology, Royal Prince Alfred Hospital, Sydney, NSW. drksharp@bigpond.net.au

A 21-year-old woman was admitted to hospital with a diagnosis of acute psychotic mania, but developed, over approximately 6 weeks, seizures, delirium, catatonia, movement disorder and autonomic dysfunction. She was found to have antibodies to N-methyl-D-aspartate (NMDA) NR1-NR2 receptors in both serum and cerebrospinal fluid, consistent with anti-NMDA-receptor encephalitis, a severe, potentially lethal but treatment-responsive encephalitis often associated with ovarian tumour. With aggressive immunotherapy and bilateral oophorectomy, she recovered over a period of 14 months from her initial presentation. No ovarian tumour was identified.

PMID: 19740054 [PubMed - indexed for MEDLINE]

ANTI-NMDA ENCEPHALITIS

2010-01-31T19:53:00.000-08:00

Med Mal Infect. 2009 Nov 24. [Epub ahead of print]

[Anti-NMDA-receptor encephalitis.]
[Article in French]
de Broucker T, Martinez-Almoyna L.

Service de neurologie, hôpital Delafontaine, 2, rue du Dr-Delafontaine, 93200 Saint-Denis, France.

Anti-NMDA-receptor encephalitis has been described only recently among other causes of paraneoplastic and auto-immune limbic encephalitis. Its frequency is probably underestimated. The very characteristic clinical presentation, the severity of symptoms frequently leading to the intensive care unit, the therapeutic implications of the diagnosis whatever the cause, paraneoplastic or not and, once treated, the possibility of a full recovery or mild sequels in the majority of cases justify a surveillance either in neurology wards or in infectious, psychiatric, intensive care, or pediatric units. The authors review the history of this disease, the available epidemiological data, the characteristic clinical presentation of patients, the differential diagnosis, and the suggested treatment according to an up-to-date literature review.

PMID: 19942390 [PubMed - as supplied by publisher]

SEVERE CHILDHOOD ENCEPHALOPATHY

2010-01-31T19:50:00.000-08:00

Dev Med Child Neurol. 2009 Dec 23. [Epub ahead of print]
Severe childhood encephalopathy with dyskinesia and prolonged cognitive disturbances: evidence for anti-N-methyl-d-aspartate receptor encephalitis.
Poloni C, Korff CM, Ricotti V, King MD, Perez ER, Mayor-Dubois C, Haenggeli CA, Deonna T.

Department of Paediatrics, Child Neurology, University Hospital Lausanne, Lausanne, Switzerland.

Aim We report four cases of acquired severe encephalopathy with massive hyperkinesia, marked neurological and cognitive regression, sleep disturbance, prolonged mutism, and a remarkably delayed recovery (time to full recovery between 5 and 18mo) with an overall good outcome, and its association with anti-N-methyl-d-aspartate (anti-NMDA) receptor antibodies. Method We reviewed the four cases retrospectively and we also reviewed the literature. Results Anti-NMDA receptor antibodies (without ovarian teratoma detected so far) were found in the two children tested in this study. Interpretation The clinical features are similar to those first reported in 1992 by Sebire et al.,(1) and rarely recognized since. Sleep disturbance was not emphasized as part of the disorder, but appears to be an important feature, whereas coma is less certain and difficult to evaluate in this setting. The combination of symptoms, evolution (mainly seizures at onset), severity, paucity of abnormal laboratory findings, very slow recovery, and difficult management justify its recognition as a specific entity. The neuropathological substrate may be anatomically close to that involved in encephalitis lethargica, in which the same target functions (sleep and movement) are affected but in reverse, with hypersomnolence and bradykinesia. This syndrome closely resembles anti-NMDA receptor encephalitis, which has been reported in adults and is often paraneoplastic.

PMID: 20041934 [PubMed - as supplied by publisher]

PROMINENT PSYCHIATRIC SYMPTOMS IN ANTI-NMDAR ENCEPHALITIS

2010-01-31T19:44:00.000-08:00

Eur J Clin Microbiol Infect Dis. 2009 Dec;28(12):1421-9. Epub 2009 Aug 29.

Anti-NMDA receptor encephalitis: report of ten cases and comparison with viral encephalitis.
Gable MS, Gavali S, Radner A, Tilley DH, Lee B, Dyner L, Collins A, Dengel A, Dalmau J, Glaser CA.

Department of Psychiatry, University of California San Francisco, Fresno, CA, USA. ms2gable@yahoo.com

The California Encephalitis Project (CEP), established in 1998 to explore encephalitic etiologies, has identified patients with N-methyl-D-aspartate receptor (NMDAR) antibodies, the likely etiology of their encephalitis. This study compares the presentation of such patients to those with viral encephalitis, so that infectious disease clinicians may identify individuals with this treatable disorder. Patients were physician-referred, and standardized forms were used to gather demographic, clinical, and laboratory data. Features of anti-NMDAR+ patients were compared with the viral encephalitides of enteroviral (EV), rabies, and herpes simplex-1 (HSV-1) origins. Sixteen cases with confirmed viral etiologies were all negative on NMDAR antibody testing. Ten anti-NMDAR+ patients were profiled with a median age of 18.5 years (range 11-31 years). None were Caucasian. They had a characteristic progression with prominent psychiatric symptoms, autonomic instability, significant neurologic abnormalities, and seizures. Two had a teratoma, and, of the remaining eight, four had serologic evidence of acute Mycoplasma infection. The clinical and imaging features of anti-NMDAR+ patients served to differentiate this autoimmune disorder from HSV-1, EV, and rabies. Unlike classic paraneoplastic encephalitis, anti-NMDAR encephalitis affects younger patients and is often treatable. The association of NMDAR antibodies in patients with possible Mycoplasma pneumoniae infection warrants further study.

PMID: 19718525 [PubMed - in process]

PSYCHOTIC MANIA IN G6PD SUBJECTS

2010-01-31T19:14:00.000-08:00

Ann Gen Hosp Psychiatry. 2003 Jun 13;2(1):6.

Psychotic mania in glucose-6-phosphate-dehydrogenase-deficient subjects.
Bocchetta A.
Bernard B, Brodie Department of Neurosciences, University of Cagliari, Italy. bocchett@unica.it

BACKGROUND: Glucose-6-phosphate dehydrogenase (G6PD) deficiency has been associated with acute psychosis, catatonic schizophrenia, and bipolar disorders by previous inconclusive reports. A particularly disproportionate rate of enzyme deficiency was found in manic schizoaffective patients from 662 lithium patients surveyed in Sardinia. The purpose of this study was to describe clinical characteristics which may be potentially associated with G6PD deficiency.

METHODS: Characteristics of episodes, course of illness, family pattern of illness, laboratory tests, and treatment response of 29 G6PD-deficient subjects with a Research Diagnostic Criteria diagnosis of manic schizoaffective disorder were abstracted from available records. RESULTS: The most peculiar pattern was that of acute recurrent psychotic manic episodes, mostly characterized by loosening of associations, agitation, catatonic symptoms, and/or transient confusion, concurrent hyperbilirubinemia, positive psychiatric family history, and partial response to long-term lithium treatment.

CONCLUSIONS: A relationship between psychiatric disorder and G6PD deficiency is to be searched in the bipolar spectrum, particularly among patients with a history of acute episodes with psychotic and/or catatonic symptoms or with transient confusion.

PMID: 12844366 [PubMed - as supplied by publisher]

CIPROFLOXACIN-INDUCED MANIA

2010-01-31T19:01:00.000-08:00

Ciprofloxacin-Induced Mania in an Elderly Male

ISSN: 1524-7929 VOLUME: 17 PUBLICATION DATE: Jan 08 2009
Issue Number: 1 Jan 09
author: Linda Sohn, MD, MPH

Author Affiliations: Dr. Sohn is Associate Director, Sepulveda VA Nursing Home Care Unit, VA Greater Los Angeles Health Care System, and Assistant Clinical Professor, UCLA School of Medicine/Geriatrics, CA.

Ciprofloxacin is a broad-spectrum fluoroquinolone antibiotic. The newer drugs in this class differ from earlier agents with increased potency, broader spectrum of antibacterial activity, and pharmacokinetics that permit treatment of systemic bacterial infections. The fluoroquinolone antibiotics have a relatively benign side-effect profile, but there have been case reports of behavioral changes in patients after initiation of this class of antibiotics.

We present a case of mania after ciprofloxacin antibiotic use. Elderly patients are especially at risk for adverse effects of medications. Multiple medical comorbidities, polypharmacy, and the potential of drug-drug interactions all increase the risk. Changes in mood or behavior such as mania are a serious adverse effect that can occur. Adverse drug reactions after the addition of a new medication always need to be considered.

ACUTE MANIC PYSCHOSIS FOLLOWING THE DERMAL APPLICATION OF DEET

2010-01-31T15:59:00.000-08:00

Summary: Clinical Toxicology
1986, Vol. 24, No. 5, Pages 429-439 , DOI 10.3109/15563658608992605

Acute Manic Psychosis Following the Dermal Application of N,N-Diethyl-M-Toluamide (deet) in an Adult

J. W. Snyder‌, R. O. Poe‌, J. F. Stubbins‌ and L. K. Garrettson‌
Departments of Pharmacology and Toxicology, Eastern Virginia Medical School, Norfolk, Virginia, 23501
Department of Psychiatry and Behavioral Sciences, Eastern Virginia Medical School, Norfolk, Virginia, 23501
Medicinal Chemistry Medical College of Virginia Virginia Commonwealth University, Richmond, Virginia, 23298
Pediatrics and Pharmaceutics Medical College of Virginia Virginia Commonwealth University, Richmond, Virginia, 23298

Abstract
Extensive animal testing and 30 years of human experience have established the general safety of DEET when applied episodically to skin or bedclothes. Local and systemic toxic and allergic reactions to DEET have been observed in man. Three weeks prior to admission, for the purpose of self-medication, a 30 year old man began daily applications of the insect repellant, DEET followed by a 1-2 hour period in a light-bulb heated box. Sedation and incoherence were noted for short periods following each application session. Aggressiveness and psychotic ideation led to hospital admission where he displayed psychomotor hyperactivity, rapid and pressured speech, tangentiality, flight of ideas, and grandiose delusions. Treatment was begun with haloperidol. Clinical improvement was complete within 6 days, atypical for classic endogenous mania. Drug and metabolites were identified in the urine more than 2 weeks after the last drug application.
References PDF (437 KB) PDF Plus (201 KB)

TOXOPLASMOSIS MASQUERADING AS A PSYCHOTROPIC SIDE EFFECT

2010-01-30T19:16:00.000-08:00

J Clin Psychiatry. 1978 Jul;39(7):631-2.

Toxoplasmosis masquerading as a psychotropic side effect.
Pariser SF, Zunich J, Pinta ER.

When treating a patient with neuroleptics or tricyclic antidepressants, it is usually assumed that complaints of blurred vision can be ascribed to the anticholinergic side effects of these drugs. The authors present a patient treated with imipramine and trifluoperazine whose complaints of blurred vision led to the diagnosis of toxoplasma chorioretinitis.

PMID: 681294 [PubMed - indexed for MEDLINE]

INFECTIOUS AGENTS AND RISK OF SCHIZOPHRENIA AMONG U.S. MILITARY PERSONNEL

2010-01-30T19:13:00.000-08:00

Am J Psychiatry. 2008 Jan;165(1):99-106. Epub 2007 Dec 17.

Selected infectious agents and risk of schizophrenia among U.S. military personnel.
Niebuhr DW, Millikan AM, Cowan DN, Yolken R, Li Y, Weber NS.

Department of Epidemiology, Division of Preventive Medicine, Walter Reed Army Institute of Research, 503 Robert Grant Ave., Silver Spring, MD 20901. David.Niebuhr@us.army.mil.

OBJECTIVE: A number of studies have reported associations between Toxoplasma gondii (T. gondii) infection and the risk of schizophrenia. Most existing studies have used small populations and postdiagnosis specimens. As part of a larger research program, the authors conducted a hypothesis-generating case control study of T. gondii antibodies among individuals discharged from the U.S. military with a diagnosis of schizophrenia and serum specimens available from both before and after diagnosis.

METHOD: The patients (N=180) were military members who had been hospitalized and discharged from military service with a diagnosis of schizophrenia. Healthy comparison subjects (3:1 matched on several factors) were members of the military who were not discharged. The U.S. military routinely collects and stores serum specimens of military service members. The authors used microplate-enzyme immunoassay to measure immunoglobulin G (IgG) antibody levels to T. gondii, six herpes viruses, and influenza A and B viruses and immunoglobulin M (IgM) antibody levels to T. gondii in pre- and postdiagnosis serum specimens.

RESULTS: A significant positive association between the T. gondii IgG antibody and schizophrenia was found; the overall hazard ratio was 1.24. The association between IgG and schizophrenia varied by the time between the serum specimen collection and onset of illness.

CONCLUSION: The authors found significant associations between increased levels of scaled T. gondii IgG antibodies and schizophrenia for antibodies measured both prior to and after diagnosis.

PMID: 18086751 [PubMed - indexed for MEDLINE]

THE SCHIZOPHRENIA AND TOXOPLASMA GONDIII CONNECTION

2010-01-30T19:09:00.000-08:00

Adv Ther. 2008 Jul;25(7):703-9.

The schizophrenia and Toxoplasma gondii connection: infectious, immune or both?
Tamer GS, Dundar D, Yalug I, Caliskan S, Yazar S, Aker A.

Kocaeli University, Medical Faculty, Department of Clinical Microbiology, Kocaeli, Turkey. guldensonmez@hotmail.com

INTRODUCTION: Recent research has suggested a possible link between toxoplasmic agents and schizophrenia. We aimed to assess this by measuring Toxoplasma gondii-associated antibodies in schizophrenia patients and controls

METHODS: We used a commercially available enzyme-linked immunosorbent assay (ELISA) kit to measure the level of immunoglobulin G (IgG) and IgM antibodies in serum samples from schizophrenia patients (n=40) and from a group of non-schizophrenic control subjects (n=37)

RESULTS: Among schizophrenic patients, 16 (40%) showed IgG seropositivity and two (5%) showed IgM seropositivity. Among the control group, five (13.5%) were found have IgG seropositivity and one (2.7%) showed IgM seropositivity. In our study we found that IgG T gondii antibodies were significantly higher in schizophrenia patients compared with controls

CONCLUSIONS: This study supports the theory that toxoplasmic agents may have a role in the aetiology of schizophrenia.

PMID: 18563312 [PubMed - indexed for MEDLINE]

VIRUS ASSOCIATION TO COGNITIVE FUNCTION IN SCHIZOPHRENIA

2010-01-30T19:05:00.000-08:00

Schizophr Res. 2008 Dec;106(2-3):268-74. Epub 2008 Sep 17.
Antibodies to cytomegalovirus and Herpes Simplex Virus 1 associated with cognitive function in schizophrenia.

Shirts BH, Prasad KM, Pogue-Geile MF, Dickerson F, Yolken RH, Nimgaonkar VL.
Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States.

BACKGROUND: Cognitive impairment in the form of decreased working memory and executive functions has been recognized as a key deficit in schizophrenia. Neurotropic viruses have been associated with focal gray matter deficits in patients with schizophrenia. We evaluated whether such agents alter cognitive function in schizophrenia.

METHODS: The sample consisted of 329 patients diagnosed with schizophrenia or schizoaffective disorder. We evaluated associations between exposure to selected agents (Herpes Simplex Viruses 1 and 2 (HSV1, HSV2 respectively) cytomegalovirus (CMV) and Toxoplasma gondii) and scores on the Trail Making Test (TMT), controlling for relevant variables.

RESULTS: Serological evidence of exposure to CMV was associated with impaired performance on TMT part A time to completion (p=0.044), a measure of visual search, working memory, and psychomotor speed. Both CMV and HSV1 were significantly associated with increased errors on TMT part B

PARASITIC BRAIN INFECTION, ENDOCANNABINOIDS, AND SCHIZOPHRENIA

2010-01-30T19:02:00.001-08:00

Med Hypotheses. 2009 Feb;72(2):220-2. Epub 2008 Nov 7.

Parasitic brain infection, endocannabinoids, and schizophrenia.
Melamede R.
Biology Department, University of Colorado at Colorado, Springs, Colorado Springs, CO 80918, USA. rmelamed@uccs.edu

Cannabis use has often been associated with various forms of psychosis. Today it is well established that everyone produces marijuana-like compounds known as endocannabinoids. The endocannabinoid system is a homeostatic regulator of all body systems including the nervous system. As a result, imbalances in the endocannabinoid system have been considered as possible causes of various forms of mental illness and abnormal behavior. In this paper, a novel hypothesis is presented that suggests that an as yet undefined subset of schizophrenia is caused by an excess of endocannabinoids that are produced to protect the brain in response to infections by agents such as Toxoplasma gondii.

PMID: 18995970 [PubMed - indexed for MEDLINE]

NEUROPSYCHIATRIC DISEASE AND TOXOPLASMA GONDII INFECTION

2010-01-30T18:57:00.000-08:00

Neuroimmunomodulation. 2009;16(2):122-33. Epub 2009 Feb 11.
Neuropsychiatric disease and Toxoplasma gondii infection.

Henriquez SA, Brett R, Alexander J, Pratt J, Roberts CW.
Strathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, 27 Taylor Street, Glasgow, UK.

Toxoplasma gondii infects approximately 30% of the world's population, but causes overt clinical symptoms in only a small proportion of people. In recent years, the ability of the parasite to manipulate the behaviour of infected mice and rats and alter personality attributes of humans has been reported. Furthermore, a number of studies have now suggested T. gondii infection as a risk factor for the development of schizophrenia and depression in humans. As T. gondii forms cysts that are located in various anatomical sites including the brain during a chronic infection, it is well placed anatomically to mediate these effects directly. The T. gondii genome is known to contain 2 aromatic amino acid hydroxylases that potentially could directly affect dopamine and/or serotonin biosynthesis. However, stimulation of the immune response has also recently been associated with mood and behavioural alterations in humans, and compounds designed to alter mood, such as fluoxetine, have been demonstrated to alter aspects of immune function. Herein, the evidence for T.-gondii-induced behavioural changes relevant to schizophrenia and depression is reviewed. Potential mechanisms responsible for these changes in behaviour including the role of tryptophan metabolism and the hypothalamic-pituitary-adrenal axis are discussed. Copyright (c) 2009 S. Karger AG, Basel.

PMID: 19212132 [PubMed - indexed for MEDLINE]

TOXOPLASMA GONDII INFECTION

2010-01-30T18:52:00.000-08:00

Korean J Parasitol. 2009 Jun;47(2):125-30. Epub 2009 May 27.

Seroprevalence of Toxoplasma gondii infection and characteristics of seropositive patients in general hospitals in Daejeon, Korea.

Shin DW, Cha DY, Hua QJ, Cha GH, Lee YH.
Department of Infection Biology, Research Institute for Medical Science, College of Medicine, Chungnam National University, Daejeon, Korea.

To figure out the epidemiological status and relevance with other diseases in toxoplasmosis, we checked serum IgG antibody titers of 1,265 patients and medical records of seropositive patients. Seropositive rates were 6.6% by latex agglutination test (LAT) and 6.7% by ELISA. No significant differences were detected between sexes and age groups. The peak seroprevalence was detected in the 40-49-year-old age group. According to clinical department, Toxoplasma-positive rates were high in patients in psychiatry, ophthalmology, health management, emergency medicine, and thoracic surgery. Major coincidental diseases in seropositive cases were malignant neoplasms, diabetes mellitus, arthritis, chronic hepatitis B, chronic renal diseases, schizophrenia, and acute lymphadenitis, in the order of frequency. In particular, some patients with chronic hepatitis B and malignant neoplasms had high antibody titers. These results revealed that the seroprevalence of toxoplasmosis in a general hospital-based study was similar to that in a community-based study, and T. gondii seropositivity may be associated with neoplasms, diabetes, and other chronic infections.

PMID: 19488418 [PubMed - indexed for MEDLINE]

SCHIZOPHRENIA AND EPILEPSY REPORTED TO AFFECT HUMANS COINFECTED WITH T. GONDII

2010-01-30T18:48:00.000-08:00

Parasitol Res. 2009 Oct;105(4):893-8. Epub 2009 Jun 23.

Toxoplasma gondii: host-parasite interaction and behavior manipulation.

da Silva RC, Langoni H.
Department of Veterinary Hygiene and Animal Science, College of Veterinary Medicine and Animal Science, São Paulo State University, Campus of Botucatu, Botucatu, São Paulo, Brazil. silva_rcd@yahoo.com.br

Toxoplasma gondii is an obligate intracellular parasite that causes different lesions in men and other warm-blooded animals. Humoral and cellular immune response of the host against the parasite keeps the protozoan in a latent stage, and clinical disease ensues when immunological response is compromised. Brain parasitism benefits the parasite causing behavioral changes in the host, not only in animals but also in humans. Schizophrenia and epilepsy are two neurological disorders that have recently been reported to affect humans coinfected with T. gondii. Further studies based on host-parasite interaction in several wild or domestic warm-blooded species are still necessary in order to better understand parasitism and behavioral changes caused by T. gondii.

PMID: 19548003 [PubMed - indexed for MEDLINE]

TOXOPLASMA GONDI IN MOTHERS AND RISK OF PSYCHOSIS AMONG ADULT OFFSPRING

2010-01-30T18:45:00.000-08:00

Microbes Infect. 2009 Nov;11(13):1011-8. Epub 2009 Jul 26.

Serological pattern consistent with infection with type I Toxoplasma gondii in mothers and risk of psychosis among adult offspring.
Xiao J, Buka SL, Cannon TD, Suzuki Y, Viscidi RP, Torrey EF, Yolken RH.

The Stanley Division of Developmental Neurovirology, Johns Hopkins School of Medicine, 600 N. Wolfe Street, 1105 Blalock, Baltimore, MD 21287-4933, USA.

Previous studies have shown that maternal antibodies to Toxoplasma measured during pregnancy are associated with an increased risk of schizophrenia and other psychoses in adult offspring. Recently, it has been recognized that different genotypes of Toxoplasma have distinct neuropathogenic potential. The objective of this study was to investigate whether parasite genotype is a contributing factor to disease risk. We have developed an enzyme-linked immunosorbent assay (ELISA) that uses polymorphic polypeptides specific to the three clonal parasite lineages and derived from three dense granule antigens, GRA5, GRA6 and GRA7. We used this assay to measure type-specific antibodies in the sera from 219 pregnant women whose children developed schizophrenia and affective psychotic illnesses in adult life, and 618 matched unaffected control mothers from three cohorts of the Collaborative Perinatal Project. We found that the offspring of mothers with a serological pattern consistent with Toxoplasma type capital I, Ukrainian infection were at significantly increased risk for the development of psychoses as compared with the matched unaffected control mothers (odds ratio=1.94; 95% confidence interval=1.08-3.46; p=0.03). The risk was particularly elevated for affective psychoses (OR=5.24; 95% CI=1.67-16.5; p=0.005). In contrast, we did not find an association between maternal antibodies to other genotypes and risk of psychoses in the offspring. These findings suggest an influence of the parasite genotype on increased risk of psychosis and provide further support for a substantive role of Toxoplasma in the etiology of psychosis.

PMID: 19638313 [PubMed - in process]

SCHIZOPHRENIA AND TOXOPLASMOSIS

2010-01-30T18:35:00.000-08:00

Med Sci (Paris). 2009 Aug-Sep;25(8-9):687-91.

[Schizophrenia and toxoplasmosis]
[Article in French]
Dion S, Barbe PG, Leman S, Camus V, Dimier-Poisson I.

Université François Rabelais de Tours, INRA , France. sarah.dion@univ-tours.fr

Schizophrenia is one of the most severe and disabling psychiatric disease that affects about 1 % of the adult worldwide population. Aetiology of schizophrenia is still unknown but genetic and environmental factors are suspected to play a major role in its onset. Recent epidemiologic studies indicate that infectious agents may contribute to some cases of schizophrenia. In particular, several epidemiological, behavioural and neurochemical studies suggested the existence of an association between schizophrenia and past history of primo-infection by the Toxoplasma gondii. However, they are some limitations for this hypothesis among which the lack of correlation between the geographic distribution of both diseases and of direct evidence for the presence of the parasite in schizophrenic patients. Nevertheless the identification of physiopathological mechanisms related to the parasite could provide a better comprehension to the outcome of schizophrenia. Studies on the link between toxoplasmosis and schizophrenia may provide interesting data for the diagnosis and the development of new treatments for this disorder.

PMID: 19765381 [PubMed - indexed for MEDLINE]

TOXOPLASMA GONDI AND SCHIZOPHRENIA

2010-01-30T18:25:00.000-08:00

Toxoplasma gondii and Schizophrenia

E. Fuller Torrey* and Robert H. Yolken†*Stanley Medical Research Institute, Bethesda, Maryland, USA; and †Johns Hopkins University Medical Center, Baltimore, Maryland, USA

Suggested citation for this article: Torrey EF, Yolken RH. Toxoplasma gondii and schizophrenia.

Emerg Infect Dis [serial online] Nov 2003 [date cited]. Available from: URL: http://www.cdc.gov/ncidod/EID/vol9no11/03-0143.htm

Recent epidemiologic studies indicate that infectious agents may contribute to some cases of schizophrenia. In animals, infection with Toxoplasma gondii can alter behavior and neurotransmitter function. In humans, acute infection with T. gondii can produce psychotic symptoms similar to those displayed by persons with schizophrenia. Since 1953, a total of 19 studies of T. gondii antibodies in persons with schizophrenia and other severe psychiatric disorders and in controls have been reported; 18 reported a higher percentage of antibodies in the affected persons; in 11 studies the difference was statistically significant. Two other studies found that exposure to cats in childhood was a risk factor for the development of schizophrenia. Some medications used to treat schizophrenia inhibit the replication of T. gondii in cell culture. Establishing the role of T. gondii in the etiopathogenesis of schizophrenia might lead to new medications for its prevention and treatment.

Schizophrenia is a pervasive neuropsychiatric disease of uncertain cause that affects approximately 1% of the adult population in the United States and Europe. An increased occurrence of schizophrenia in family members of affected persons suggests that genetic factors play a role in its etiology, and some candidate predisposing genes have been identified. Environmental factors are also important. Epidemiologic studies, for example, have established that winter-spring birth, urban birth, and perinatal and postnatal infection are all risk factors for the disease developing in later life. These studies have rekindled an interest in the role of infectious agents in schizophrenia, a concept first proposed in 1896 (1). This review focuses on evidence specifically linking infection with Toxoplasma gondii to the etiology of some cases of schizophrenia.

T. gondii is an intracellular parasite in the phylum Apicomplexa. Its life cycle can be completed only in cats and other felids, which are the definitive hosts. However, T. gondii also infects a wide variety of intermediate hosts, including humans. In many mammals, T. gondii is known to be an important cause of abortions and stillbirths and to selectively infect muscle and brain tissue. A variety of neurologic symptoms, including incoordination, tremors, head-shaking, and seizures, have been described in sheep, pigs, cattle, rabbits, and monkeys infected with T. gondii (2).
Humans may become infected by contact with cat feces or by eating undercooked meat. The importance of these modes of transmission may vary in different populations (3). Individual response to Toxoplasma infection is determined by immune status, timing of infection, and the genetic composition of the host and the organism (4).

To read full article go here.

GLUTATHIONE IN THE PATHOPHSIOLOGY OF BIPOLAR DISORDER AND SCHIZOPHRENIA?

2010-01-30T18:21:00.000-08:00

Curr Med Chem. 2009;16(23):2965-76.

A role for glutathione in the pathophysiology of bipolar disorder and schizophrenia? Animal models and relevance to clinical practice.

Dean OM, van den Buuse M, Bush AI, Copolov DL, Ng F, Dodd S, Berk M.

The Mental Health Research Institute of Victoria, Parkville, Victoria, Australia. oliviad@barwonhealth.org.au

The tripeptide, glutathione (gamma-glutamylcysteinylglycine) is the primary endogenous free radical scavenger in the human body. When glutathione (GSH) levels are reduced there is an increased potential for cellular oxidative stress, characterised by an increase and accruement of reactive oxygen species (ROS). Oxidative stress has been implicated in the pathology of schizophrenia and bipolar disorder. This could partly be caused by alterations in dopaminergic and glutamatergic activity that are implicated in these illnesses. Glutamate and dopamine are highly redox reactive molecules and produce ROS during normal neurotransmission. Alterations to these neurotransmitter pathways may therefore increase the oxidative burden in the brain. Furthermore, mitochondrial dysfunction, as a source of oxidative stress, has been documented in both schizophrenia and bipolar disorder. The combination of altered neurotransmission and this mitochondrial dysfunction leading to oxidative damage may ultimately contribute to illness symptoms. Animal models have been established to investigate the involvement of glutathione depletion in aspects of schizophrenia and bipolar disorder to further characterise the role of oxidative stress in psychopathology. Stemming from preclinical evidence, clinical studies have recently shown antioxidant precursor treatment to be effective in schizophrenia and bipolar disorder, providing a novel clinical angle to augment often suboptimal conventional treatments.

PMID: 19689277 [PubMed - indexed for MEDLINE]

BIPOLAR DISORDER AND ENDOCRINE DISORDERS

2010-01-29T20:06:00.000-08:00

Nippon Rinsho. 1994 May;52(5):1311-7.

[Manic-depressive symptom associated with endocrine and metabolic disorders]
[Article in Japanese]
Yamada T.
Kashiwa City Hospital.

In an attempt to study "manic-depressive" affairs associated with endocrine and mental disorders, our clinical data are analyzed before and after appropriate treatment in Cushing's disease, Cushing's syndrome, hyperthyroid Graves' disease and primary hypothyroidism. Although our data do not provide definite findings on manic-depressive affairs associated with Cushing's disease and syndrome, review data by others indicated a high incidence of depression under untreated condition and its disappearance after appropriate treatment. In contrast, patients with adrenocortical insufficiency did have a depression but this was cleared after supplemental therapy. In hyperthyroid Graves' disease, a number of emotional and mental instability and irritability were noticed before the treatment, but these abnormalities all disappeared after appropriate treatment for 3-6 months. In contrast, patients with primary hypothyroidism did show lethargy and apathy, and these abnormalities disappeared after appropriate treatment. From the data accumulated, it is concluded that adrenal steroid and thyroid hormone do affect the functions of nervous system and, as a result, cause a number of clinical symptoms. The exact biochemical processes underlying these abnormalities are not known and remains for further investigations.

PMID: 8007407 [PubMed - indexed for MEDLINE]

MOOD AND ANXIETY DISORDERS CAUSED BY GRAVE'S DISEASE

2010-01-29T20:01:00.001-08:00

Gen Hosp Psychiatry. 2005 Mar-Apr;27(2):133-9.

Mood and anxiety disorders in women with treated hyperthyroidism and ophthalmopathy caused by Graves' disease.

Bunevicius R, Velickiene D, Prange AJ Jr.

Department of Psychiatry, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7160, USA. robertas_bunevicius@med.unc.edu

OBJECTIVE: To evaluate the prevalence of mood and anxiety disorders in women with treated hyperthyroidism caused by Graves' disease and to compare them with the prevalence of such findings in women without past or present thyroid disease.

METHODS: Thirty inpatient women with treated hyperthyroidism and ophthalmopathy caused by Graves' disease and 45 women hospitalized for treatment of gynecologic disorders such as abnormal vaginal bleeding, benign tumors or infertility were evaluated for the prevalence of mood and anxiety diagnoses using a standard Mini-International Neuropsychiatric Interview and for mood and anxiety ratings using the Profile of Mood States (POMS). At the time of assessment, it was discovered that 14 of 30 women with treated hyperthyroidism caused by Graves' disease were still hyperthyroid, while 16 women were euthyroid.

RESULTS: Significantly greater prevalence of social anxiety disorder, generalized anxiety disorder, major depression and total mood and anxiety disorders, as well as higher symptom scores on the POMS, was found in hyperthyroid women with Graves' disease in comparison with the control group. A prevalence of total anxiety disorder, as well as history of mania or hypomania and lifetime bipolar disorder, but not lifetime unipolar depression, was more frequent in both the euthyroid and the hyperthyroid subgroups of study women in comparison with the control group.

CONCLUSIONS: These results confirm a high prevalence of mood and anxiety disorders in women with treated hyperthyroidism and ophthalmopathy caused by Graves' disease. Hyperthyroidism plays a major role in psychiatric morbidity in Graves' disease.
PMID: 15763125 [PubMed - indexed for MEDLINE]

Neuropsychiatric Symptoms and Occupational Exposure to Chemicals

2010-01-29T19:47:00.000-08:00

Human Exposure Assessment and Relief From Neuropsychiatric Symptoms: Case Study of a

Hairdresser

Stephen J. Genuis, MD, FRCSC, DABOG and Shelagh K. Genuis, BScOT, MLIS
From the Department of Obstetrics and Gynecology (SJG), University of Alberta, Canada (SKG)
Correspondence: Address correspondence to Dr. Stephen Genuis, 2935–66 Street, Edmonton Alberta, Canada T6K 4C1 (E-mail: sgenuis@incentre.net

Abstract

Human exposure assessment and the results of implementing ‘precautionary avoidance’ suggested a relationship between a hairdresser’s neuropsychiatric symptoms and occupational exposure to potentially hazardous chemicals. A variety of investigations in response to patient complaints of depression, emotional instability and various physical symptoms revealed no objective abnormality; the CH2OPD2 mnemonic (community, home, hobbies, occupation, personal habits, diet and drugs) recommended by the Ontario College of Family Physicians was used as a first-line screening tool to assess potential environmental exposure to toxins. After occupational leave of absence, the patient reported cessation of symptoms. Environmental causes for familiar medical problems are frequently undiagnosed; it is recommended that, where appropriate, a screening tool for evaluation of environmental exposure to toxics be incorporated into primary care assessment and management of patients.

PSYCHOSIS CAUSED BY MICROBIAL AGENTS?

2010-01-29T19:33:00.000-08:00

Mol Psychiatry. 2008 May;13(5):470-9. Epub 2008 Feb 12.

Are some cases of psychosis caused by microbial agents? A review of the evidence.

Yolken RH, Torrey EF.

The Stanley Laboratory of Developmental Neurovirology, Department of Pediatrics, Johns Hopkins University Medical Center, Baltimore, MD 21287-4933, USA. yolken@mail.jhmi.edu

The infectious theory of psychosis, prominent early in the twentieth century, has recently received renewed scientific support. Evidence has accumulated that schizophrenia and bipolar disorder are complex diseases in which many predisposing genes interact with one or more environmental agents to cause symptoms. The protozoan Toxoplasma gondii and cytomegalovirus are discussed as examples of infectious agents that have been linked to schizophrenia and in which genes and infectious agents interact. Such infections may occur early in life and are thus consistent with neurodevelopmental as well as genetic theories of psychosis. The outstanding questions regarding infectious theories concern timing and causality. Attempts are underway to address the former by examining sera of individuals prior to the onset of illness and to address the latter by using antiinfective medications to treat individuals with psychosis. The identification of infectious agents associated with the etiopathogenesis of schizophrenia might lead to new methods for the diagnosis, treatment and prevention of this disorder.

PMID: 18268502 [PubMed - indexed for MEDLINE]

TOXIC CAUSES OF MENTAL ILLENSS ARE OVERLOOKED

2010-01-29T08:40:00.000-08:00

Neurotoxicology. 2008 Nov;29(6):1147-9. Epub 2008 Jun 24.

Toxic causes of mental illness are overlooked.
sgenuis@ualberta.ca
Genuis SJ.

While proper brain function requires the complex interaction of chemicals perpetually occupied in purposeful biochemistry, it is well established that certain toxic substances have the potential to disrupt normal brain physiology and to impair neurological homeostasis. As well as headache, cognitive dysfunction, memory disturbance, and other neurological signs and symptoms, disruption of brain function may also manifest as subtle or overt alteration in thoughts, moods, or behaviors. Over the last four decades, there has been the unprecedented development and release of a swelling repertoire of potentially toxic chemicals which have the capability to inflict brain compromise. Although the ability of xenobiotics to induce clinical illness is well established, the expanding public health problem of widespread toxicant exposure in the general population is a relatively new phenomenon that has spawned escalating concern. The emerging area of clinical care involving the assessment and management of accrued toxic substances such as heavy metals, pesticides, plasticizers and other endocrine disrupting or neurotoxic compounds has not been fully appreciated by the medical community and has yet to be incorporated into the clinical practice of many consultants or primary care practitioners.
PMID: 18621076 [PubMed - indexed for MEDLINE]

LYME DISEASE AND NEUROPSYCHIARIC DISORDERS

2010-01-29T08:37:00.000-08:00

J Am Osteopath Assoc. 1998 Jul;98(7):373-8.

Neuropsychiatric manifestations of Lyme disease.

Paparone PW.

Lyme Disease Center for South Jersey, Absecon, NJ 08201, USA.

Lyme disease is a multisystem illness that may affect the central nervous system and subsequently produce mild to severe psychiatric disorders. Physicians who treat patient with Lyme disease need to be aware of its neuropsychiatric symptoms, which may emerge months to years after the initial infection. Prompt diagnosis and effective treatment are needed to avoid the debilitating and possibly irreversible mental illness associated with the neurologic involvement of this spirochetal infection. The author reviews the neuropsychiatric manifestations of Lyme disease and provides diagnostic and therapeutic approaches for the management of the central nervous system disease that may cause them.
PMID: 9695456 [PubMed - indexed for MEDLINE]

ACUTE MANIA IN THE SETTING OF SEVERE HYPOTHYROIDISM

2010-01-29T08:34:00.000-08:00

Psychosomatics. 2005 May-Jun;46(3):259-61.

Acute mania in the setting of severe hypothyroidism.

Stowell CP, Barnhill JW.

Department of Psychiatry, New York-Presbyterian Hospital, Weill-Cornell Medical Center, 525 East 68th St., New York, NY 10021, USA. chs9017@nyp.org

Although the associations between depression and hypothyroidism and between mania and hyperthyroidism are well described, mania in the setting of hypothyroidism is unusual. The authors present the case of a patient whose acute mania appears to have been precipitated by hypothyroidism secondary to postpartum thyroiditis. This case underscores the importance of thyroid screening in patients with mood and psychotic disorders, including patients who lack the classical psychiatric features of thyroid dysfunction. Further investigation is required on the nature of the relationship between thyroid function and bipolar disorder and any implications it may have for the diagnosis and treatment of this illness.
PMID: 15883148 [PubMed - indexed for MEDLINE]

PSYCHIATRIC MANIFESTATIONS OF VITAMIN B12 DEFICIENCY

2010-01-29T07:36:00.000-08:00

Encephale. 2003 Nov-Dec;29(6):560-5.

[Psychiatric manifestations of vitamin B12 deficiency: a case report]

[Article in French]

Durand C, Mary S, Brazo P, Dollfus S.

Centre Esquirol, Service du Professeur S. Dollfus, CHU de Caen, avenue Côte-de-Nacre, 14033 Caen.

Psychiatric manifestations are frequently associated with pernicious anemia including depression, mania, psychosis, dementia. We report a case of a patient with vitamin B12 deficiency, who has presented severe depression with delusion and Capgras' syndrome, delusion with lability of mood and hypomania successively, during a period of two Months. Case report - Mme V., a 64-Year-old woman, was admitted to the hospital because of confusion. She had no history of psychiatric problems. She had history of diabetes, hypertension and femoral prosthesis. The red blood count revealed a normocytosis with anemia (hemoglobin=11,4 g/dl). At admission she was uncooperative, disoriented in time and presented memory and attention impairment and sleep disorders. She seemed sad and older than her real age. Facial expression and spontaneous movements were reduced, her speech and movements were very slow. She had depressed mood, guilt complex, incurability and devaluation impressions. She had a Capgras' syndrome and delusion of persecution. Her neurologic examination, cerebral scanner and EEG were postponed because of uncooperation. Further investigations confirmed anemia (hemoglobin=11,4 g/dl) and revealed vitamin B12 deficiency (52 pmol/l) and normal folate level. Antibodies to parietal cells were positive in the serum and antibodies to intrinsic factor were negative. An iron deficiency was associated (serum iron=7 micromol/l; serum ferritin concentration=24 mg/l; serum transferrin concentration=3,16 g/l). This association explained normocytocis anemia. Thyroid function, hepatic and renal tests, glycemia, TP, TCA, VS, VDRL-TPHA were normal. Vitamin B12 replacement therapy was started with hydroxycobalamin 1 000 ng/day im for 10 days and iron replacement therapy. Her mental state improved dramatically within a few days. After one week of treatment the only remaining symptoms were lability of mood, delusion of persecution, Capgras' syndrome but disappeared totally 9 days after the beginning of the treatment. A neurologic examination was possible because of cooperation. All the tendon reflexes of inferior members were absent. The plantars were in flexion and there was a left inferior member hypoesthesia. The cerebral scan and EEG were normal. Fundic biopsy, realized by fibroscopy, revealed fundic atrophia and intestinal metaplasia compatible with Biermers' disease. The iron deficiency exploration concluded diet deficiency. Mme V. appeared euphoric, her speech was very rapid with play on words and overactivity. This hypomania state totally disappeared 3 days after. Six Months after her hospitalisation, she presented an hypothyroidism (TSH=3,780; T3=1,35; T4=1,08). A thyroid hormones replacement was started and she continued to receive Monthly B12 replacement. Discussion - This case report illustrates psychiatric manifestations of Biermers' disease. The clinical arguments in favour are: white woman, more than 60 Years old, no history of psychiatric problems, atypical symptoms (confusional state with psychiatric symptoms), fluctuation of symptoms (severe depression with confusional state, delusion of persecution and Capgras' syndrome; delusion with lability of mood and hypomania), dramatic improvement after 9 days of vitamin B12 replacement therapy. The biological arguments are: anemia, vitamin B12 deficiency, normal folate level, atrophia and fundic metaplasia, positive antibodies to parietal cells in the serum, association between Biermers' disease and autoimmune disease (Haschimoto thyroidite). Psychiatric manifestations can occur in the presence of low serum B12 levels but in the absence of the other well recognized neurological and haematological abnormalities of pernicious anemia. Mental or psychological changes may precede haematological signs by Months or Years. They can be the initial symptoms or the only ones. Verbank et al. described the case of a patient with vitamin B12 deficiency in whom hypomania, paranoia and depression had been successively presented during a period of 5 Years before anemia have been developed. The case of Mme V. is similar in the succession of severe depression with delusion of persecution and Capgras' syndrome, delusion with lability of mood and hypomania, during a period of two Months. This report seems to be the first one of a sequence of several psychiatric states with pernicious anemia during a period of two Months with normocytosis anemia. To illustrate this illness we reviewed the literature regarding psychopathology associated with B12 deficiency. The most common psychiatric symptoms were depression, mania, psychotic symptoms, cognitive impairment and obsessive compulsive disorder. The neuropsychiatric severity by vitamin B12 deficiency and the therapeutic efficacy depends on the duration of signs and symptoms. Conclusion - We recommend consideration of B12 deficiency and serum B12 determinations in all the patients with organic mental disorders, atypical psychiatric symptoms and fluctuation of symptomatology. B12 levels should be evaluated with treatment resistant depressive disorders, dementia, psychosis or risk factors for malnutrition such as alcoholism or advancing age associated with neurological symptoms, anemia, malabsorption, gastrointestinal surgery, parasite infestation or strict vegetarian diet. In first intention, B12 deficiency should be researched by serum B12 determination (normal 200-950 pg/ml). Studies of methylmalonic acid and homocysteine showed that they are very sensitive functional indicators of cobalamin status especially when other evidence of cobalamin (B12) deficiency was equivocal. Measurement of methylmalonic acid (normal 73-271 nmol/l) and homocysteine (normal 5,4-13,9 micromol/l) should not replace the measurement of serum cobalamin.

PMID: 15029091 [PubMed - indexed for MEDLINE]

DECREASED N-3 FATTY ACID LEVELS REPORTED IN PATIENTS WITH SYMPTOMS OF MENTAL ILLNESS

2010-01-29T07:28:00.000-08:00

Expert Opin Investig Drugs. 2007 Oct;16(10):1627-38.
Omega-3 fatty acid eicosapentaenoic acid. A new treatment for psychiatric and neurodegenerative diseases: a review of clinical investigations.
Song C, Zhao S.
University of Prince Edward Island, Department of Biomedical Sciences, AVC, 550 University Avenue, Charlottetown, PE, Canada. cai.song@nrc.gc.ca
Decreased n-3 fatty acid levels have been reported in patients with depression, schizophrenia or Alzheimer's disease. Recently, eicosapentaenoic acid (EPA) has been used to treat several psychiatric and neurodegenerative diseases due to its anti-inflammatory and neuroprotective effects. A total of six out of seven clinical trials have shown that EPA significantly improved depressive symptoms when compared with the placebo-treated populations. Several investigations have also reported that EPA could effectively treat schizophrenia. A case report and a clinical trial have shown that EPA was beneficial for the management of most symptoms of Huntington's disease, while a more extensive clinical investigation has demonstrated that EPA could only improve motor functions. Further clinical studies are required to fully explore the effects of EPA on other neurodegenerative diseases. The limitations of previous studies and further research directions have also been discussed.
PMID: 17922626 [PubMed - indexed for MEDLINE]

PAST EXPOSURE TO LEAD LINKED TO SYMPTOMS OF BIPOLAR DISORDER

2010-01-28T09:12:00.000-08:00

Lead Levels in the Hair of Bipolar Patients and Normal Controls

Med Hypotheses. 1986 Jun;20(2):151-5.

Lead levels in the hair of bipolar patients and normal controls.
Kanofsky JD, Rosen WA, Ryan PB, Decina P, Fieve RR, Kanofsky PB.

The analysis of hair samples taken from ten symptomatic bipolar patients and from ten normal controls matched for age, sex and race suggest that a relatively high body burden of lead may be associated with episodes of bipolar illness.

PMID: 3637615 [PubMed - indexed for MEDLINE]