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]

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.

What Makes us Mad? Amazon Bookstore

What Makes us Mad? Amazon Bookstore