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This chapter presents the case of a 72-year-old man with a 10-year history of Parkinson's disease. He experienced visual hallucinations with preserved insight 2 years previously, subsiding on withdrawal of selegiline. Physical examination revealed a fairly symmetric and moderately severe parkinsonian syndrome, with akinetic-rigid features dominant and little in the way of rest tremor. The initial diagnostic impression was of a dementia syndrome relating to his Parkinson's disease, although the doctor was initially uncomfortable with what he regarded as a normal mini-mental state examination (MMSE) score of 27 out of 30. After 3 and 6 months, repeat MMSE scores were 23 and 25, respectively. Despite some initial diagnostic uncertainty, the patient was commenced on a cholinesterase inhibitor with considerable improvement in his psychotic features and lessening of his periods of confusion. Rationalization of anti-parkinsonian and other medications is an important first step in the management of PD-D.
This chapter presents a case of a 54 year old man Mr. H who had some neurotic personality features associated with some impulsivity. A majority of patients develop neuropsychiatric symptoms, also called behavioral and psychological symptoms of dementia (BPSD) during the course of their illnesses. Neuropsychiatrie symptoms are primary manifestations of the disease process, but other psychological and social factors also play a role in determining which patients will manifest behavioral symptoms. For Mr. H, irritability, anxiety, and delusion are related both to the personal history of the patient and his wife. They are also the consequences of the cognitive deficit and the patient psychological reaction to the perception of his memory loss. Mr. H. has a major loss of self-initiated behavior and interest. However, he is able to respond to external cognitive and emotional stimulation. This helps in choosing the best non-pharmacological strategies.
There is currently little information on the genetic epidemiology of Alzheimer disease (AD) among North American Aboriginal populations. No cases of familialAD (FAD) in these populations have been published to date.
Here, we describe a large North American Aboriginal kindred with early onset FAD (EOFAD) in which genetic testing was done.
Results and Conclusions:
A novel Presenilin 1 (PS1) gene mutation (L250F) has been identified. In contrast to the three previously reported families with PS1 codon 250 mutations, affected members of this kindred demonstrate neither myoclonus nor seizures. Furthermore, the identification of a PS1 mutation in a North American Aboriginal kindred presents several unique challenges with respect to knowledge transfer and continuity of care in a geographically remote and culturally distinct community.
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