Dementia cognitive dysfunction

Dementia with Lewy bodies (DLB) is a common neurodegenerative dementia, which mainly occurs in late life (McKeith et al., 1996). The main clinical symptoms include visual hallucinations, parkinsonism and disturbances of consciousness, in the context of a global cognitive dysfunction with prominent... 

The deficit of cortico-striatal innervation that is presumably responsible for reported losses of striatal glutamate uptake sites (Aparicio-Legarza et al., 1997 Simpson et al., 1992), is likely to contribute to the cognitive dysfunction of schizophrenia. These have been described as having similarities to the subcortical dementia (Pantelis et al., 1992) seen in a variety of neurodegenerative disorders disturbances of corticostriatal function are thought to underlie this pattern of cognitive deficits that include disturbances of attention, executive function and short-term memory. 

Schizophrenia is certainly not the only disorder with such impairments in cognition. Autism, poststroke dementia, Alzheimer s disease, and many other organic dementias (parkinsonian/Lewy body dementia, frontotemporal/Pick s dementia, etc.) are also associated with some cognitive dysfunctions similar to those seen in schizophrenia (Fig. 10—4). 

Overall, in relatively young and healthy patients, the cumulative risk of contracting TD when exposed to neuroleptics ranges from 4% to 7% per year during the first several years of treatment. Approximately one-third of the patients will develop this largely irreversible disorder within the first 5 years of treatment. This represents an astronomical risk for patients and should become part of the awareness of all mental health professionals, their patients, and their patients families. Furthermore, we shall find that TD brings with it the additional risk of irreversible cognitive dysfunction and dementia (chapter 5). 

Persistent cognitive dysfunction, persistent amnestic syndrome, and persistent dementia... 

A number of studies have demonstrated that long-term exposure to BZs can produce persistent memory and cognitive dysfunction, including dementia (e.g., Ashton, 1984, 1995 Barker et al., 2004 Bergman et al., 1989 Berzele, 1992 Golombok et al., 1988 Lagnaoui et al., 2002 Petursson et al., 1983 Rickels et al., 1999 Tata et al., 1994). 

Drug-induced disruption of dopamine neurotransmission is known to produce a variety of neurological side effects (see chapters 3 and 5). The neuroleptics suppress dopamine neurotransmission, causing a reactive hyperactivity of the system that produces a high rate of irreversible dyskinesias, cognitive dysfunction, and dementia. 

Breggin, P. (1990). Brain damage, dementia and persistent cognitive dysfunction associated with neuroleptic drugs Evidence, etiology, implications. Journal of Mind and... 

It was suggested that cognitive dysfunction in PD, similarly to AD results from loss of cholinergic neurons in the nucleus basalis Meynert (Whitehouse, 1981). However, it was reported by Perry et al. (1985) that dementia in this disease usually occurs in the absence of substantial Alzheimer type changes in the cortex and may be related to abnormalities in the cortical cholinergic system. 

Xiong H, Zeng YC, Zheng J, Thyhn M, Gendelman HE (1999) Soluble HlV-1 infected macrophage secretory products mediate blockade of long-term potentiation A mechanism for cognitive dysfunction in HIV-1-associated dementia [In Process Citation]. J Neurovirol 5 519-528. 

AD is the most common cause of dementia, accounting for over 60% of cases of late-life cognitive dysfunction. Table 63-1 lists etiology-based subclasses of dementia. This chapter focuses exclusively on dementia of the Alzheimer s type. However, the reader is encouraged... 

Nordberg, A. (1996). Pharmacological of cognitive dysfunction in dementia disorders. Acta Neurologica Scandanavia Supplementum, 168, 87-92. 

Since many articles have recently appeared summarizing cholinergic approaches to the treatment of dementia,22-26 will only briefly review this active research area and then discuss other chemotherapeutic approaches which show promise In the treatment of cognitive dysfunction. 

III. Clinical presentation. Mild to moderate intoxication results in lethargy, muscular weakness, slurred speech, ataxia, tremor, and myoclonic jerks. Rigidity and ex-trapyramidal effects may be seen. Severe intoxication may result in agitated delirium, coma, convulsions, and hyperthermia. Recovery is often very slow, and patients may remain confused or obtunded for several days to weeks. Rarely, cerebellar and cognitive dysfunction are persistent. Cases of rapidly progressive dementia, similar to Jacob-Creutzfeldt disease, have occurred and are usually reversible. The ECG commonly shows T-wave inversions less commonly, bradycardia and sinus node arrest may occur. The white cell count is often elevated (15-20,000/mm ). 

Observational studies Donepezil improved cognitive dysfunction in patients with Alzheimer s disease, but also ameliorated behavioral and psychological symptoms of dementia (BPSD), including hallucinations/ delusions, wandering, and aggression [123 ]. Donepezil also alleviated the burden on care-givers for about 60% of patients. There were 30 reports of adverse drug... 

Although it might be expected that the incidence of the primary sleep disorders would increase in demented patients relative to age-matched controls because of the CNS dysfunction underlying these disorders, studies comparing the rates of sleep apnea in dementia patients and aged controls have not found consistent differences. Nevertheless, these conditions may interact with the dementia syndrome to further worsen sleep quality as well as cognitive and functional abilities. For example, some studies have shown that sleep apnea is associated with increased morning confusion in AD patients. 

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