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Electroconvulsive therapy for severe depression, psychosis and chorea in a patient with Huntington's disease: case report and review of the literature.

ABSTRACT:

Aims and method

The psychiatric manifestations of Huntington's disease are myriad and difficult to control. The use of electroconvulsive therapy (ECT) is not commonly considered for this condition. We describe a patient with severe depression, psychomotor retardation, delusions and weight loss who responded to ECT with good control of her symptoms.

Results

Both our case and the literature appear to confirm the efficacy of ECT in the treatment of depression in Huntington's disease and suggest that other psychiatric manifestations of Huntington's are also responsive.

Clinical implications

ECT is an effective and safe treatment that should be considered earlier in the course of the disease in cases that show limited response to pharmacological therapy. It should also be considered as an adjunct to medical therapy that may simplify polypharmacy and allow better control in patients with debilitating psychiatric manifestations of the disease. There is limited and conflicting evidence for its efficacy in chorea.

SUBMITTER: Mowafi W

PROVIDER: S-EPMC8111993 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:IntroductionGitelman syndrome(GS) is a rare inherited tubular disorder which is characterized by hypokalemia, metabolic alkalosis, hypomagnesemia, and hypocalciuria. Here, we report a case of schizophrenia-like psychosis concomitant with GS and related literatures are reviewed.Case descriptionAn 18-year-old male patient with 1-week history of auditory hallucinations, sense of insecurity, delusions of reference and feelings of being followed and controlled by others unknown, insomnia was admitted to Psychiatry department in December, 2013. Hypokalemia and hypomagnesemia were noted. He was diagnosed as schizophrenia-like psychosis. Treatment with paliperidone at the dose of 6 mg/day and magnesium and potassium supplementations was commenced. However, electrolyte disturbances failed to improve following psychosis remission. Therefore, other underlying diseases resulting in electrolyte disturbances were suspected. Along with hypokalemia and hypomagnesemia, additional investigation showing metabolic alkalosis, hypocalciuria, renal loss of potassium, were consistent with GS. Gene analysis revealed this patient carried out c. 2687 G > A homozygous mutation of exon 23 in the SLC12A3 gene which led to p.Arg896Gln. Eventually, GS was identified. Thus, additional spironolactone (40 mg/day) combined with increased doses of oral potassium chloride sustained-release tablets (3.0 g/day) and potassium magnesium aspartate (0.3 g/day) were administered. During next half a year, fatigue resolved, paliperidone gradually tapered and eventually discontinued while psychosis maintained complete remission. His serum potassium was near normal (3.2-3.5 mmol/L), hypomagnesemia significantly improved (0.57-0.67 mmol/L).Discussion and evaluationElectrolyte abnormalities secondary to GS might cause or contribute to development of neuropsychiatric symptoms. In turn, hypokalemia was common among acute psychiatric inpatients. As a consequence, when concomitant with psychosis, GS was readily concealed.ConclusionElectrolyte disturbances are common in acute psychiatric patients. However, when electrolyte disturbances are not improved following psychosis remission, other underlying diseases such as GS should be considered.