This study aimed to find cut-off scores for the Montgomery-Asberg rating scale (MADRS) and the Beck depression inventory (BDI) that can relate to specific clinical diagnoses of depression in Parkinson s disease (PD). Mild and moderate PD patients (n=46) were evaluated for depression according to the DSM IV criteria. All patients were assessed with the MADRS and the BDI. A "receiver operating characteristics" (ROC) curve was obtained and the sensibility, specificity, positive and the negative predictive values were calculated for different cut-off scores of the MADRS and the BDI. The Kappa statistic was calculated for different cut-off scores to assess the agreement between the clinical judgment and both scales. Depression was present in 18 patients. MADRS cut-off scores of 6 and 10 showed Kappa 0.5 and 0.56, respectively. Specificity of cut-off score of 6 was 78.6% and of cut-off score of 10 was 96.4%. Kappa agreement of BDI cut-off scores of 10 and 18 were 0.36 and 0.62, respectively. Specificity was 60.7% for 10 and 92.9% for 18. Both rating scales show similar accuracy within the ROC curves (84.3% for MADRS and 79.7% for BDI). The MADRS and the BDI show a good accuracy and correlation to the clinical diagnosis when a cut-off score of 10 is used to MADRS and a cut-off score of 18 is used to BDI to recognize depression in mild to moderate PD patients. This may help clinicians to recognize depression in PD.
Pantothenate kinase-associated neurodegeneration (PKAN) is an autosomal recessive disorder caused by mutation in the PANK2 gene. It is characterized by abnormal brain iron accumulation, mainly in the globus pallidus. PKAN is included in a group of disorders known as neurodegeneration with brain iron accumulation (NBIA). We report a case of atypical PKAN with its most characteristic presentation, exhibiting marked psychiatric symptoms, speech disorder and focal dystonia. Brain MRI has great diagnostic importance in this group of disorders and, in this case, disclosed the eye-of-the-tiger sign. Genetic testing confirmed the diagnosis.
-Previous reports on the use of olanzapine in Huntington's disease (HD) used doses ranging from 10-30 mg. We report a case of HD with marked delusions and behavioral impairment assessed by the Unified Huntington's Disease Rating Scale at baseline and four months later treated with a low dose of olanzapine. The patient improved in motor, psychiatric and activity of daily living symptoms after four months of treatment. The response to a low dose of olanzapine in HD may be an indicator of efficacy in similar cases. Further randomized controlled trials can properly assess these findings.KEY WORDS: Huntington's disease, olanzapine, behavioral abnormalities, functional capacity.Resposta funcional e motora a doses baixas de olanzapina na doença de Huntington: relato de caso RESUMO -Relatos de casos sobre o uso de olanzapina na doença de Huntington (DH) usaram doses variando de 10-30 mg. Este é um relato de caso de DH avaliado pela Unified Huntington Rating Scale no iní-cio e quatro meses depois com uma dose baixa de olanzapina. A paciente melhorou dos sintomas motores, psiquiátricos e nas atividades de vida diária após os quatro meses de tratamento. A resposta a baixas doses de olanzapina na DH pode ser um indicador de eficácia em casos similares. Mais estudos controlados randomizados podem avaliar apropriadamente esses achados. PALAVRAS-CHAVE: doença de huntington, olanzapina, transtornos de comportamento, capacidade funcional.Huntington's disease (HD) is a heredodegenerative disorder of the central nervous system, transmitted as dominant autosomic inheritance with a 100% penetrance. It is caused by a three nucleotide basis (CAG) repetition at the IT15 gene, which resides in the short arm of chromosome 4 [1][2] . HD is characterized by insidious onset of neurological manifestations including choreic movements, dysarthria, dysphagia, ideomotor and eyelid apraxia, postural instability, dystonia, dysfunction of eye movements and rarely myoclonus. Incontinence of urinary and anal sphincters (common in the terminal stage of HD), autonomic dysfunction including hyperhydrosis, and pressure lability are other signs and symptoms of the disease. Seizures may occur in 3% of adult HD patients. Neuropsychiatric signs and symptoms may occur before, during or after neurological manifestations. They are present in 35 to 73%, and a wide range of disturbances are reported: affective, behavioral, personality changes which include depression, bipolar disorder, manic episodes, agitation, impulsiveness, aggressiveness. Cognitive symptoms are present in all HD patients at some stage of the disease, characterized by a subcortical dementia profile 3 . The neuroimage shows atrophy of caudate nuclei as the typical feature. The genetic testing is able to confirm the presence of the disease and polymerase chain reaction (PCR) shows an expanded trinucleotide (CAG) repeat sequence.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.