However, a multicenter registry and two recent cohort registries have largely reduced this concern, by showing sudden death rates lower than that observed from the disease itself.These concerns about the drug must be viewed from the clinical perspective that disopyramide is generally the last agent that is tried for patients before they are referred for invasive septal reduction with surgical septal myectomy (an open-heart operation) or alcohol septal ablation (a controlled heart attack). Both of these invasive procedures have risk of morbidity and mortality. For selected patients, a trial of oral disopyramide is a reasonable approach before proceeding to invasive septal reduction. Patients who respond to disopyramide are continued on the drug. Those who continue to have disabling symptoms or who experience side effects are promptly referred for septal reduction. Using such a stepped strategy, investigators have reported that survival does not differ from that observed in the age-matched normal United States population. Cardiac adverse effects
Acute heart failure – Disopyramide should not be given to patients with impaired LV systolic function and low ejection fraction. Heart failure is not seen when disopyramide is used in patients with normal or supernormal LV systolic function. Severe hypotension – Disopyramide should not be given to patients with impaired LV systolic function and low ejection fraction. Hypotension is not seen in patients with normal or supernormal LV systolic function. Extracardiac effects
Atropine like effects (anticholinergic)
Dry mouth
Constipation
Urinary retention – Disopyramide should not be given to patients with symptomatic prostatism. Blurred vision
Glaucoma
Rash
AgranulocytosisAdditionally, disopyramide may enhance the hypoglycaemic effect of gliclazide, insulin, and metformin.
In most cases, it is preceded by extreme stress and followed by amnesia for the period of psychosis. In addition to approximate answers, other symptoms include a clouding of consciousness, somatic conversion disorder symptoms, confusion, stress, loss of personal identity, echolalia, and echopraxia. Cause
To date, no definitive cause or reason of the disorder has been established. The sources that classify the syndrome as a dissociative disorder or a factitious disorder conflict in their proposed aetiologies. As a result, there are differing theories as to why the syndrome develops. Ganser syndrome was previously classified as a factitious disorder, explaining the symptoms as mimicking of what patients who do not experience psychosis believe is typical of the experience. However, the DSM-IV placed the syndrome under "Dissociative Disorders Not Otherwise Specified". There has been evidence of a strong correlation between approximate answers and amnesia, suggesting that these have an underlying dissociative mechanism.Both Gansers syndrome and the broader category of dissociative disorders have been linked to histories of hysteria, psychosis, conversion, multiple personality and possible feigning. Despite this, the conditions aetiology remains under question due to associations with established psychiatric disorders, as well as organic states. According to Stern and Whiles (1942), Ganser syndrome is a fundamentally psychotic illness.