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

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 Unpublished reports were requested from the World Health Organization (WHO) and the Food and Drug Administration (FDA).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


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.

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]


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.

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]


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.
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

Central New York Occupational Health Clinical Center,
State University of New York Health Science Center at Syracuse, Syracuse, New York
Syracuse, New York
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.


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

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


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.
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.


Mario F. Mendez1

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


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.


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 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:

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.

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.


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.


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.


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.