Beneficial effect of donepezil augmentation for the management of comorbid schizophrenia and dementia.

Comorbid schizophrenia and dementia is a common clinical phenomenon; however, management of the coexisting illnesses remains incomplete. Donepezil, a cholinesterase inhibitor, may be beneficial for the management of symptoms of Alzheimer's disease, a disease in which cholinergic pathways in the cerebral cortex and basal forebrain are well known to be compromised. Furthermore, impaired cognition in elderly schizophrenic patients has been observed to be more than two thirds; however, there are no published controlled studies reporting the use of cholinesterase inhibitors in the management of schizophrenia in patients with associated dementia. In this study, six patients with chronic schizophrenia and comorbid dementia were administered donepezil, 5 mg, in single-blind fashion as augmentation to their standard antipsychotic medication for a 4-week period. Patients were evaluated with the Mini Mental State Examination (MMSE); Alzheimer's Disease Assessment Scale, Cognitive subscale; Positive and Negative Symptom Scale (PANSS); and the Clinical Global Impression (CGI) scales. A significant improvement was noted in MMSE scores (P < 0.01) and for CGI scores (P < 0.01). In addition, three patients demonstrated improvement on the PANSS. Donepezil appears to be an effective treatment for the management of symptoms of dementia accompanying patients with comorbid schizophrenia and dementia. Since cholinergic dysfunction may be present in some patients with schizophrenia, the authors' findings further demonstrate the possibility that this disorder may be managed with cholinergic medications as augmenting agents, at least in this specific subpopulation of patients with comorbid dementia. To confirm the findings of this preliminary trial, further investigation is mandated with a larger sample of subjects in the context of a double-blind medication trial.

Rivastigmine augmentation in the management of chronic schizophrenia with comorbid dementia: an open-label study investigating effects on cognition, behaviour and activities of daily living.

Comorbid schizophrenia and dementia is becoming an increasingly common phenomenon. Because rivastigmine, a reversible acetylcholinesterase inhibitor, appears to delay the progression of Alzheimer's disease, it may also improve or delay the cognitive and behavioural disturbances evident in elderly chronic schizophrenia patients with comorbid cognitive decline. The aim of this study was to investigate augmentative rivastigmine administration in this population and to determine any effect on cognition, behaviour and 'activity of daily living' (ADLs) capabilities. Thirteen subjects with comorbid schizophrenia and dementia were administered open-label oral rivastigmine (9 mg/day) for a period of 12 weeks. The results indicated improvement in Mini-Mental State Examination scores (P<0.01), Alzheimer's Disease Assessment Scale-cognitive subscale scores (P<0.001), ADL scores (P<0.01) and Positive and Negative Syndrome Scale scores (P<0.01). Study observations indicate beneficial effects of rivastigmine administration in this subpopulation of schizophrenia patients. Following on from other studies of cholinesterase inhibitor agents, clinical improvement in this patient subpopulation may extend to the class of cholinesterase inhibitor agents in general and not necessarily be a specific effect of any of the medications. The effects noted may be specific to the subpopulation of comorbid schizophrenia and dementia rather than schizophrenia in general. Although speculative, these effects may be related to cholinergic dysfunction, which has been hypothesized to be present in some patients with schizophrenia.

Phenotypic presentation of frontotemporal dementia with Parkinsonism-chromosome 17 type P301S in a patient of Jewish-Algerian origin.

A 39-year-old old Jewish woman of Algerian origin developed a rapidly progressive neurocognitive disorder characterized by asymmetric rigidity, spasticity with bilateral Babinski's sign, bradykinesia, altered speech that progressed to mutism, and severe bradyphrenia. She partially responded to levodopa. The family history revealed 4 affected first-degree relatives (3 had already died). Genetic studies carried out in the proband and her living affected sister showed a P301S mutation in chromosome 17.