Saturday, November 6, 2010

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

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."


Wednesday, October 13, 2010

Behavioral approaches to toluene intoxication.

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]

Tuesday, September 7, 2010

Corticosteroid-Induced Psychotic and Mood Disorders

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





Friday, August 20, 2010

Behavioral approaches to toluene intoxication

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.

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]

Sunday, May 23, 2010

Arsenic Induced Delirium

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.

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

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]

Insomnia Related to Chemical Exposure

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]

Thursday, March 4, 2010

Shingles and Manic Symptoms

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

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.

Saturday, February 6, 2010

What Makes us Mad? Amazon Bookstore

What Makes us Mad? Amazon Bookstore

ANTIBIOMANIA - antibiotic-induced manic episodes

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.

© 2002 Lippincott Williams & Wilkins, Inc.




Wednesday, February 3, 2010

PSYCHIATRIC ONSET OF MS

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

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

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

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


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.

Monday, February 1, 2010

Calcification of the basal ganglia presenting as a schizophreniform psychosis

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

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

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

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

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

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

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

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.

Sunday, January 31, 2010

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

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

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

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

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

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

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

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

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

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

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)

Saturday, January 30, 2010

TOXOPLASMOSIS MASQUERADING AS A PSYCHOTROPIC SIDE EFFECT

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

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

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

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

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

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

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

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

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]