Understanding Psychosis: Can the Participatory Medicine movement help individuals with symptoms of psychosis?

By Maria Mangicaro

mangicaro829@aol.com

As an individual who has experienced psychotic episodes, I believe that the emergence of participatory concepts in mental health care can empower consumers to become engaged in recognizing symptoms, selecting treatment options, and working in partnership with providers to develop illness self-management recovery programs.[1][2] Patient empowerment is critically needed to strengthen the mental health care system. Innovative strategies targeting informed, safe decisions are needed in order to effectively involve mental health consumers in the prevention and recovery of psychotic disorders.

Psychosis results in loss of contact with reality, sometimes including delusions, insomnia, hallucinations or impaired cognitive functioning.[3] Psychotic behavior affects the ability to manage and maintain personal relationships, employment, medical care, and in some cases, housing.[4][5] A psychotic experience distorts an individual’s belief system and perceptions. Most individuals experiencing a psychosis have poor insight regarding their illness and refuse to acknowledge that a problem even exists.[6]

Click here to read more in the Journal of Participatory Medicine

Organic causes of mania.

Mayo Clin Proc. 1988 Sep;63(9):906-12.

Source

Department of Psychiatry and Psychology, Mayo Clinic, Rochester, MN 55905.

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.

Organic psychosis induced by ofloxacin and metronidazole.

Br J Hosp Med (Lond). 2009 Apr;70(4):236-7.

Source

Birmingham and Solibull Mental Health Foundation Trust, Birmingham.

PMID:
19357607
[PubMed – indexed for MEDLINE]

Organic psychosis induced by ofloxacin and metronidazole

Unknown or invalid date

CASE REPORT Organic psychosis induced by ofloxacin and metronidazole Introduction Antimicrobial agents are a recognized cause of psychopathological and neurological adverse drug reactions (Table 1) (Farrington et al, 1995). However, relatively few of these patients are seen by psychiatrists. This article presents an unusual case in a young woman. Discussion A catatonic, depressive or organic stupor was initially considered in the differential diagnosis. Subsequently, a schizophreniform psychotic picture emerged and then a gradual and spontaneous reduction of all symptoms without psychotropic medication. The patient described many symp-toms at different times during this episode, e.g. paranoid delusions, delusions of reference and control, third person auditory hallucinations, suicidal ideation, tearfulness, psychomotor retardation and psychomotor agitation. There was no identifiable stressor that could have triggered a disassociative stupor Case Report An 18-year-old black African woman was referred to the on-call medical team by her GP with a history of confusion and

stupor. Three weeks before admission she complained of abdominal pain and was treated for urinary tract infection with co-amoxiclav. After 1 week, as her pain persisted, co-amoxiclav was stopped and she was treated for presumed pelvic inflammatory disease with ofloxacin 400 mg twice daily and metronidazole 400 mg three times daily. After 2 days on this combination she started to develop confusion, so her mother stopped the ofloxacin. The next day her GP advised her to also stop the metronidazole. During the next 5 days she became increasingly confused, frightened, almost mute and at times immobile. She was referred urgently to the accident and emergency department from where she was admitted to the medical ward.

Continue reading “Organic psychosis induced by ofloxacin and metronidazole.”

Clinical experience and laboratory investigations in patients with anti-NMDAR encephalitis

The Lancet Neurology, Volume 10, Issue 1,  Pages 63 – 74, January 2011

Prof Josep Dalmau MD  , Eric Lancaster MD , Eugenia Martinez-Hernandez MD , Prof Myrna R Rosenfeld MD , Prof Rita Balice-Gordon PhD

Summary

Since its discovery in 2007, the encephalitis associated with antibodies against the N-methyl-D-aspartate receptor (NMDAR) has entered the mainstream of neurology and other disciplines. Most patients with anti-NMDAR encephalitis develop a multistage illness that progresses from psychosis, memory deficits, seizures, and language disintegration into a state of unresponsiveness with catatonic features often associated with abnormal movements, and autonomic and breathing instability.
The disorder predominantly affects children and young adults, occurs with or without tumour association, and responds to treatment but can relapse. The presence of a tumour (usually an ovarian teratoma) is dependent on age, sex, and ethnicity, being more frequent in women older than 18 years, and slightly more predominant in black women than it is in white women. Patients treated with tumour resection and immunotherapy (corticosteroids, intravenous immunoglobulin, or plasma exchange) respond faster to treatment and less frequently need second-line immunotherapy (cyclophosphamide or rituximab, or both) than do patients without a tumour who receive similar initial immunotherapy.
More than 75% of all patients have substantial recovery that occurs in inverse order of symptom development and is associated with a decline of antibody titres. Patients’ antibodies cause a titre-dependent, reversible decrease of synaptic NMDAR by a mechanism of crosslinking and internalisation. On the basis of models of pharmacological or genetic disruption of NMDAR, these antibody effects reveal a probable pathogenic relation between the depletion of receptors and the clinical features of anti-NMDAR encephalitis.

Neuropsychological aspects of Wilson’s disease.

Int J Neurosci. 1996 Apr;85(3-4):221-9.

Rathbun JK. SourceUniversity of Michigan, Department of Psychology, Ann Arbor 48103, USA.

Abstract: A consecutive series of 34 patients with confirmed diagnoses of Wilson’s disease (WD) was administered complete neuropsychological examinations upon admission to a university medical center for routine laboratory tests.

Twenty-five patients with neurological and/or hepatic symptoms (symptomatics) revealed frequent and severe motor deficits and infrequent and mild cognitive deficits in contrast to nine patients with genetic findings of Wilson’s disease but no symptomatic findings (asymptomatics). Somato-sensory tests were normal in all.

One of the most intriguing findings was the absence of a significant correlation between the level of copper toxicity and the degree, nature, and frequency of associated neurological deficits in both symptomatic and asymptomatic patients.

Fifty per cent of the present sample received psychiatric treatment, including hospitalization, for schizophrenia, depression, anxiety, and related disorders prior to confirmed diagnosis of WD.

The present findings provide additional evidence that patients with the initial presenting psychological symptoms may be easily misdiagnosed and mistreated if the possibilities of Wilson’s disease are not ruled out first. PMID: 8734560

[PubMed – indexed for MEDLINE]

Manganese and acute paranoid psychosis: a case report.

J Med Case Reports. 2011 Apr 12;5(1):146. [Epub ahead of print]

Verhoeven WM, Egger JI, Kuijpers HJ.

Abstract

ABSTRACT:

INTRODUCTION: Manganese regulates many enzymes and is essential for normal development and body function. Chronic manganese intoxication has an insidious and progressive course and usually starts with complaints of headache, fatigue, sleep disturbances, irritability and emotional instability.

Later, several organ systems may be affected and, due to neurotoxicity, an atypical parkinsonian syndrome may emerge. With regard to neuropsychiatry, an array of symptoms may develop up to 30 years after intoxication, of which gait and speech abnormalities, cognitive and motor slowing, mood changes and hallucinations are the most common. Psychotic phenomena are rarely reported.

CASE PRESENTATION: We describe the case of a 49-year-old Caucasian man working as a welder who was referred to our facility for evaluation of acute paranoid psychotic behavior. Our patient’s medical history made no mention of any somatic complaints or psychiatric symptoms, and he had been involved in a professional career as a metalworker. On magnetic resonance imaging scanning of his brain, a bilateral hyperdensity of the globus pallidus, suggestive for manganese intoxication, was found. His manganese serum level was 52 to 97nmol/L (range: 7 to 20nmol/L).

A diagnosis of organic psychotic disorder due to manganese overexposure was made. His psychotic symptoms disappeared within two weeks of treatment with low-dose risperidone. At three months later, serum manganese was decreased to slightly elevated levels and the magnetic resonance imaging T1 signal intensity was reduced. No signs of Parkinsonism were found and a definite diagnosis of manganese-induced apathy syndrome was made.

CONCLUSION: Although neuropsychiatric and neurological symptoms caused by (chronic) manganese exposure have been reported frequently in the past, in the present day the disorder is rarely diagnosed.

In this report we stress that manganese intoxication can still occur, in our case in a confined-space welder, and may present clinically with a paranoid psychotic state that necessitates a rapid diagnostic procedure in order to avoid the permanent structural brain damage that may occur with chronic exposure.

PMID: 21486469 [PubMed – as supplied by publisher]

Youtube Credit:  Uploaded by on Sep 22, 2010

Charlie Rose: The brain series part 1 The great mysteries of the human brain. ” The Charlie Rose Brain Series explores one of sciences final frontiers, the study of the human brain.
Over the next year Charlie will interview the most knowledgeable scientists and researchers in hopes of illuminating a new topic of study. Each monthly episode will examine different subjects of the brain, including perception, social interaction, aging and creativity.
We will also look at scientific discovery and advances in technology, in the hope that someday terrible illnesses such as depression, schizophrenia, and Alzheimer’s will be history.
Our special colleague on this journey is Dr. Eric Kandel. He is a psychiatrist and neuroscientist and professor at Columbia University. He’s also affiliated with the Howard Hughes Medical Institute.
He received the Nobel Prize in physiology or medicine in 2000 for his research into the biological mechanisms of learning and memory. ”
These videos are also available from the charlie rose website directly: http://www.charlierose.com/view/collection/10702

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