Aripiprazole treatment for psychosis associated with Friedreich's ataxia

Chan, Yiu-Chung

doi:10.1016/j.genhosppsych.2005.05.004

Cited by 8 publications

(4 citation statements)

References 3 publications

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“…High MAOA activity is associated with schizophrenia, psychosis and bipolar disorders, and MAOA inhibitors have been used as antidepressants [51]. Friedreich ataxia has been reported to be associated with a number of psychiatric manifestations including cognitive impairment, depression, emotional lability and schizophrenia-like psychosis [52][53][54]. The association of neuropsychiatric signs with porphyrias has also been long-recognized [55,56], but never understood, and we propose that defects in the heme pathway feed back to stimulate ALAS1, (and thus necessarily MAOA through the heme shunt) to cause the neuropsychiatric symptoms.…”

Section: Induction Of the Heme Pathway Is A Late Consequence Of Fratamentioning

confidence: 99%

Frataxin knockdown causes loss of cytoplasmic iron–sulfur cluster functions, redox alterations and induction of heme transcripts

Cortopassi

2007

Archives of Biochemistry and Biophysics

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Frataxin protein deficiency causes the neurodegenerative disease Friedreich ataxia. We used inducible siRNA to order the consequences of frataxin deficiency that we and others have previously observed. The earliest consequence of frataxin deficiency was a defect in cytoplasmic iron-sulfur proteins. In the second phase, protein oxidative damage increased, and CuZnSOD was induced, as was the unfolded protein response (UPR), long before any decline in mitochondrial aconitase activity. In the third phase, mitochondrial aconitase activity declined. And in the fourth phase, coincident with the decrease in heme-containing cytochrome c protein, a transcriptional induction of the heme-dependent transcripts ALAS1 and MAOA occurred. These observations suggest that the earliest consequences of frataxin deficiency occur in ISC proteins of the cytoplasm, resulting in oxidative damage and stress and activation of the unfolded protein response which has been associated with neurological disease, and that later consequences involve mitochondrial iron-sulfur cluster deficiency, heme deficiency, and then increased heme biosynthesis.

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Section: Induction Of the Heme Pathway Is A Late Consequence Of Fratamentioning

confidence: 99%

Frataxin knockdown causes loss of cytoplasmic iron–sulfur cluster functions, redox alterations and induction of heme transcripts

Cortopassi

2007

Archives of Biochemistry and Biophysics

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“…In Friedreich's ataxia, the most common autosomal‐recessive cerebellar ataxia worldwide, psychosis is rare, usually occurring after years or during the final stages of disease and responding in most cases to antipsychotics, such as risperidone, quetiapine, and aripiprazole . In cerebrotendinous xanthomatosis (ATX‐CYP27A1), 7 patients developed delusions and hallucinations during the disease, responding partially to antipsychotics and chenodeoxycholic acid .…”

Section: Resultsmentioning

confidence: 99%

Nosology and Phenomenology of Psychosis in Movement Disorders

Rossi

Farcy

Starkstein

et al. 2020

Movement Disord Clin Pract

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Background Background: Psychotic symptoms, such as delusions and hallucinations, are part of the clinical picture of several conditions presenting movement disorders. Phenomenology and epidemiology of psychosis in Parkinson's disease have received wide attention; however, the presence of psychosis in other movement disorders is, comparatively, less well known. Objectives Objectives: To review psychotic symptoms present in different movement disorders. Methods Methods: A comprehensive and structured literature search was performed to identify and analyze data on patients with movement disorders and comorbid psychosis.

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“…Structural and functional changes of the cerebello‐thalamo‐cortical circuits have been suggested as the neuroanatomical correlates of these neuropsychiatric problems . This notwithstanding, psychotic symptoms associated with FA have only been rarely reported . Although there is no definite proof of a causal relation between FA and psychosis, the latter has been viewed as a complication in end‐stage disease .…”

Section: Discussionmentioning

confidence: 99%

“…Although there is no definite proof of a causal relation between FA and psychosis, the latter has been viewed as a complication in end‐stage disease . Proposed treatments include atypical antipsychotics, such as aripiprazole, risperidone, and quetiapine …”

Section: Discussionmentioning

confidence: 99%

Psychosis Complicating Friedreich Ataxia

Ganos

Schöttle

Zühlke

et al. 2014

Movement Disord Clin Pract

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Psychotic symptoms have only rarely been reported in Friedreich ataxia (FA) and do not constitute core features of the disorder. Here, we report on the case of a 29-year-old patient with FA who, over the course of his illness, developed psychotic symptoms shortly upon administration of intravenous (IV) amiodarone. They were difficult to manage and ultimately led to psychomotor regression and death within 6 months after symptom onset. We suggest that treating physicians regularly enquire for the presence of psychotic symptoms in patients with FA given that the outcome can be fatal. CaseA 29-year-old patient with FA (compound heterozygous for the [GAA] expansion [800 repeats] and a mutation of the ATG start codon, Met1Ile), 1 who was a former chess tournament champion, presented to our department with a 1-week history of irritability, dysphoria, perseverations, derailment, paranoid delusions (fear of being poisoned or castrated by his family), auditory hallucinations (men whispering to his ear), and somatic sensations (feeling of being raped). He had become suspicious, and at times hostile, refusing to take his medication. Four days before symptom onset, he had been treated with IV amiodarone in an emergency department because of an episode of paroxysmal tachyarrhythmia, presumably resulting from dilated cardiomyopathy. The wheelchair-bound patient presented with a classic FA phenotype, in particular, severe visual impairment resulting from optic atrophy, saccadic hypermetria, square-wave jerks, saccadic pursuit, dysarthria, tetraparesis with distal amyotrophy, absent tendon reflexes, bilateral Babinski signs, and abolished joint position and vibration sense distally. Thyroid function was normal. He was diagnosed with a psychotic episode and admitted. Aripiprazole (5 mg) was commenced. At that time, the patient also received aspirin, metoprolol, insulin, and idebenone. Symptoms subsided within 4 days, and he was discharged. One month later, he was readmitted because his initial symptoms had recurred. He was then taking 30 mg of aripiprazole daily, albeit irregularly. He was aggressive and refused insulin treatment, causing hyperglycemia (310 mg/dL) and metabolic acidosis. Risperidone (2 mg mane) was introduced. Three days later, his introspection, affect, psychotic symptoms, and thought disorder had improved. Considering the difficulties of daily administration and lack of compliance, paliperidone palmitate (PP) was introduced (first intramuscular dose: 150 mg) and risperidone stopped. Initially, the patient became somnolent, but then improved over the course of the subsequent days with remission of psychiatric symptoms for approximately 2 months. Over the ensuing period, however, recurrent relapse of psychotic symptoms led to repeated emergency admissions. Risperidone (2 mg mane) was reintroduced, parallel to PP. Though psychotic symptoms improved, the patient was severely sedated for most of the day. He did not present to the clinic again, but we were informed that he had become lethargic, apathetic, and refused...

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Aripiprazole treatment for psychosis associated with Friedreich's ataxia

Cited by 8 publications

References 3 publications

Frataxin knockdown causes loss of cytoplasmic iron–sulfur cluster functions, redox alterations and induction of heme transcripts

Frataxin knockdown causes loss of cytoplasmic iron–sulfur cluster functions, redox alterations and induction of heme transcripts

Nosology and Phenomenology of Psychosis in Movement Disorders

Psychosis Complicating Friedreich Ataxia

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