Mayo Clin Proc. 1988 Sep;63(9):906-12.
Larson EW, Richelson E.
Department of Psychiatry and Psychology, Mayo Clinic, Rochester, MN 55905.
Comment in:
Mayo Clin Proc. 1989 Jan;64(1):129-30.
Abstract
Manic syndromes have many neurologic, toxic, and metabolic causes. It is important for clinicians to be able to distinguish these organic disorders from primary idiopathic mania (bipolar disorder). The cardinal symptom of organic mania is an abnormally and persistently elevated or irritable mood. Organic mania usually develops in patients who are older than 35 years of age, whereas bipolar disorder generally has its onset between late adolescence and age 25 years. In patients with the first episode of mania, the clinician should thoroughly elicit information about current symptoms, recent infections, use of drugs, and past or family history of psychiatric disorders. In addition, a complete medical examination, computed tomography of the head, electroencephalography, and screening for drugs and toxins should be done. Treatment of organic mania includes correcting the underlying disorder when possible.
PMID: 3137394 [PubMed - indexed for MEDLINE]
Showing posts with label Bipolar disorder. Show all posts
Showing posts with label Bipolar disorder. Show all posts
Saturday, March 26, 2011
Hyponatremia-induced change in mood mimicking late-onset bipolar disorder.
Gen Hosp Psychiatry. 2011 Jan-Feb;33(1):83.e5-7. Epub 2010 Oct 27.
McKnight RF, Hampson S.
Department of Psychiatry, Warneford Hospital, University of Oxford, Warneford Lane, OX3 7JX Oxford, UK.
Abstract
OBJECTIVE: Hyponatremia and bipolar disorder are rarely considered to have common features. This report describes a case of hyponatremia secondary to syndrome of inappropriate antidiuretic hormone secretion (SIADH) presenting as late-onset bipolar disorder and discusses the evidence linking hyponatremia to mood disorders.
METHOD: Case report and review of published literature.
RESULTS: This case provides evidence that mood changes identical to those seen in bipolar disorder may be caused by hyponatremia at a variety of concentrations.
CONCLUSIONS: Further research is required to determine causes of SIADH in psychiatric patients with symptomatic hyponatremia and to elucidate the mechanism by which hyponatremia causes changes in mood. In older patients presenting with new-onset bipolar disorder, a physical etiology must always be excluded.
Copyright © 2011 Elsevier Inc. All rights reserved.
PMID: 21353139 [PubMed - in process]
McKnight RF, Hampson S.
Department of Psychiatry, Warneford Hospital, University of Oxford, Warneford Lane, OX3 7JX Oxford, UK.
Abstract
OBJECTIVE: Hyponatremia and bipolar disorder are rarely considered to have common features. This report describes a case of hyponatremia secondary to syndrome of inappropriate antidiuretic hormone secretion (SIADH) presenting as late-onset bipolar disorder and discusses the evidence linking hyponatremia to mood disorders.
METHOD: Case report and review of published literature.
RESULTS: This case provides evidence that mood changes identical to those seen in bipolar disorder may be caused by hyponatremia at a variety of concentrations.
CONCLUSIONS: Further research is required to determine causes of SIADH in psychiatric patients with symptomatic hyponatremia and to elucidate the mechanism by which hyponatremia causes changes in mood. In older patients presenting with new-onset bipolar disorder, a physical etiology must always be excluded.
Copyright © 2011 Elsevier Inc. All rights reserved.
PMID: 21353139 [PubMed - in process]
Tuesday, January 25, 2011
Caffeine and psychiatric symptoms: a review.
J Okla State Med Assoc. 2004 Dec;97(12):538-42.
Broderick P, Benjamin AB.
University of Oklahoma, 2312 North Indiana Avenue, Oklahoma City, Oklahoma 73106, USA.
Abstract
Caffeine is a widely used psychoactive substance that has the potential to contribute to many psychiatric symptoms. This review article aims to address the specific research studies and case reports that relate caffeine to psychiatric symptoms. Caffeine can cause anxiety symptoms in normal individuals, especially in vulnerable patients, like those with pre-existing anxiety disorders. Caffeine use is also associated with symptoms of depression due to either a self-medication theory, or a theory that caffeine itself causes changes in mood. Psychosis can be induced in normal individuals ingesting caffeine at toxic doses, and psychotic symptoms can also be worsened in schizophrenic patients using caffeine. Sleep and symptoms of ADHD may be altered by caffeine as well. Prevention of caffeine-induced psychiatric symptoms is possible by recognizing, educating, and treating patients using a tapering approach.
PMID: 15732884 [PubMed - indexed for MEDLINE]
Wednesday, February 3, 2010
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.
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
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
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.
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.
Saturday, January 30, 2010
GLUTATHIONE IN THE PATHOPHSIOLOGY OF BIPOLAR DISORDER AND SCHIZOPHRENIA?
Curr Med Chem. 2009;16(23):2965-76.
A role for glutathione in the pathophysiology of bipolar disorder and schizophrenia? Animal models and relevance to clinical practice.
The Mental Health Research Institute of Victoria, Parkville, Victoria, Australia. oliviad@barwonhealth.org.au
The tripeptide, glutathione (gamma-glutamylcysteinylglycine) is the primary endogenous free radical scavenger in the human body. When glutathione (GSH) levels are reduced there is an increased potential for cellular oxidative stress, characterised by an increase and accruement of reactive oxygen species (ROS). Oxidative stress has been implicated in the pathology of schizophrenia and bipolar disorder. This could partly be caused by alterations in dopaminergic and glutamatergic activity that are implicated in these illnesses. Glutamate and dopamine are highly redox reactive molecules and produce ROS during normal neurotransmission. Alterations to these neurotransmitter pathways may therefore increase the oxidative burden in the brain. Furthermore, mitochondrial dysfunction, as a source of oxidative stress, has been documented in both schizophrenia and bipolar disorder. The combination of altered neurotransmission and this mitochondrial dysfunction leading to oxidative damage may ultimately contribute to illness symptoms. Animal models have been established to investigate the involvement of glutathione depletion in aspects of schizophrenia and bipolar disorder to further characterise the role of oxidative stress in psychopathology. Stemming from preclinical evidence, clinical studies have recently shown antioxidant precursor treatment to be effective in schizophrenia and bipolar disorder, providing a novel clinical angle to augment often suboptimal conventional treatments.
PMID: 19689277 [PubMed - indexed for MEDLINE]
Friday, January 29, 2010
TOXIC CAUSES OF MENTAL ILLENSS ARE OVERLOOKED
Neurotoxicology. 2008 Nov;29(6):1147-9. Epub 2008 Jun 24.
While proper brain function requires the complex interaction of chemicals perpetually occupied in purposeful biochemistry, it is well established that certain toxic substances have the potential to disrupt normal brain physiology and to impair neurological homeostasis. As well as headache, cognitive dysfunction, memory disturbance, and other neurological signs and symptoms, disruption of brain function may also manifest as subtle or overt alteration in thoughts, moods, or behaviors. Over the last four decades, there has been the unprecedented development and release of a swelling repertoire of potentially toxic chemicals which have the capability to inflict brain compromise. Although the ability of xenobiotics to induce clinical illness is well established, the expanding public health problem of widespread toxicant exposure in the general population is a relatively new phenomenon that has spawned escalating concern. The emerging area of clinical care involving the assessment and management of accrued toxic substances such as heavy metals, pesticides, plasticizers and other endocrine disrupting or neurotoxic compounds has not been fully appreciated by the medical community and has yet to be incorporated into the clinical practice of many consultants or primary care practitioners.
PMID: 18621076 [PubMed - indexed for MEDLINE]
PMID: 18621076 [PubMed - indexed for MEDLINE]
Thursday, January 28, 2010
PAST EXPOSURE TO LEAD LINKED TO SYMPTOMS OF BIPOLAR DISORDER
Lead Levels in the Hair of Bipolar Patients and Normal Controls
Med Hypotheses. 1986 Jun;20(2):151-5.
Lead levels in the hair of bipolar patients and normal controls.
Kanofsky JD, Rosen WA, Ryan PB, Decina P, Fieve RR, Kanofsky PB.
The analysis of hair samples taken from ten symptomatic bipolar patients and from ten normal controls matched for age, sex and race suggest that a relatively high body burden of lead may be associated with episodes of bipolar illness.
PMID: 3637615 [PubMed - indexed for MEDLINE]
Med Hypotheses. 1986 Jun;20(2):151-5.
Lead levels in the hair of bipolar patients and normal controls.
Kanofsky JD, Rosen WA, Ryan PB, Decina P, Fieve RR, Kanofsky PB.
The analysis of hair samples taken from ten symptomatic bipolar patients and from ten normal controls matched for age, sex and race suggest that a relatively high body burden of lead may be associated with episodes of bipolar illness.
PMID: 3637615 [PubMed - indexed for MEDLINE]
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