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.

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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.

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