Demence - poznámky o diagnostice a léčbě (IChE, nootropika, fytoterapeutika -EGb ) Loss of hippocampal volumes and memory impairment are typical findings in AD. FronTemp D is dg according to the clinical criteria of Lund and Manchester groups including symmetrical anterior temporal lobe and frontal lobe atrophy. Adults with Down sy have neuropathol.changes typical for AD by 40 yrs. In the general population, the greater frequency of AD in women than in men may be related to a relative estrogen deficiency in older women compared with men. In addition, the effect of gender may be modified by factors such as APOE genotype. N. Schupf, 1998 The neuropathology of PD modifies the clinical dementia of AD. Patients with AD and brainstem LB+ND are part of the spectrum of dementia. There is a genetic component for PD. M.F. Mendez,1998

Demence - poznámky o diagnostice a léčbě (IChE, nootropika, fytoterapeutika -EGb ) Donepezil may improve cognitive and neuropsychiatric symptoms in AD; the latter changes are robustly associated with caregiver distress. 25% subjects had significant lowering of neuropsychiatric symptoms without measured cognitive improvement. Expy signs in AD may reflect dementia with Lewy bodies and be associated with concomitant improvement in cognitive and neuropsychiatric symptoms. D.I.Kaufer,1998 AD is associated with a significant decline in functional brain activity as measured by CMR-glu. Donepezil (10 mg/day) for 24-w. reduced the decline in CMR-glu by approx.77%, suggesting a preservation of functional brain activity in these patients (L. E. Tun)

Demence -Pickova choroba. J.E.Galvin,1998, PD is a neurodegenerative dementing illness of unknown etiology, classified as one of Fronto-Temporal dementias (FTD) with characteristic clinical features. Pathologically - atrophy of the F&T lobes. Microscopically- swollen achromatic or "ballooned" neurons (BN) containing fibrillar inclusions known as PBs, which are. immunoreactive for hyperphosphorylated tau protein, the same protein found in the neurofibrillary tangles of Alzheimer's disease PB - an intense inflammatory response that is predominantly cell mediated (activated astros, microglia& T-lympho) affects vulnerable neurons. The most intense inflammation is associated with B- lymphocyte IR-a humoral response may play a role as well. This may contribute to neuronal dysfunction in PD by functionally isolating the affected neurons within a robust gliosis. Disconnection, cell death.

Demence. Vaskulár.demence. Nálezy u zdravých osob. A.Salviati, M and 11 F mean age 85.6 yrs (77-96 y). All were judged to be normal. The mean duration from last clinical evaluation to death was 10.2 months ( m.) 1)none non-neuritic plaques in neocortex (10/28; 36%); 2)sparse neuritic plaques&sparse neurofibrillary tangles in neocortex (11/28; 39%); 3) moderate neuritic plaques and neurofibrillary tangles in neocortex (7/28; 25%).4) 4 subj. showed neuropil threads and tau-positive plaques in neocortex. In some vascular lesions: 43% single infarct, 3.6% multiple lacunes, 7.1% lacunar&large infarctions.

Demence. Parkinsonova choroba. J.H.Bower, Incidence of PD in Olmsted County The incidence of PD -10.9/ in the general population and 49.7 in subjects over 50 yrs. Incidence increased with age in both M&F, higher in M. When combining PD and unspecified parkinsonism, incidence rates continue to increase after age 85 years. These findings have important implications for etiologic research. Survival is similar between M&F (overall med. survival 12.3 yrs). PD is very rare before age 40. Diabetes mellitus, atrial fibrillation, current smoking and atherosclerosis (as measured by plaques in the carotid arteries) at baseline were all significantly and independently associated with an increased risk of total dementia and Alzheimer's disease. The relative risks for the various vascular factors ranged from 1.4 to 2.6. A.Hofmann, 1998

Demence. Parkinsonova choroba. In healthy elderly followed for up to 5 years, there is minimal brain volume loss observed over time. Healthy oldest (over 84y) who maintain cognitive function, do not show greater rates of brain loss compared to younger elderly, suggesting that changes seen in cross sectional samples reflect the presence of preclinical dementia patients in older groups. J.A.Kaye, 1998 WMSH volume associated with severity of dementia. Lesions of cerebral cortex: preF (initiation-perseveration and conceptualization), T-P (receptive language and memory) association areas. CC connectivity. L.Willis, 98

Demence. Parkinsonova choroba. E.Kokmen, Rochester, ,320 records and identified 486 cases of dementia. 356 (73%) AD, 28 (6%) VaD,22 (5%) mixed AD and VaD. 66 (14%) had dementia due to other conditions (PD, brain tumors, alcoholism...), 14 (3%) could not be classified. The average annual incidence (/100,000 pers.-yrs) increased from 4.9 at to 6,584.4 at yrs for dementia and from 4.9 at to 5,349.8 at yrs for AD. For both dementia and AD the incidence increased exponentially with age and was similar in men and women.

AD - diagnostika-CT,MRI. M.D. Mattson, 1998 ? Does the omission of a head imaging study from the work-up of AD result in missed neuropathol. dg. (significant concomitant pathology such as infarcts, tumors, subdural hematomas, or hydrocephalus)? All 796 cases were reviewed. AD Res. Center ( ) AD was the neuropathol.dg. in all 31 cases without CT or MRI. Results: 1-multiple macroscopic infarcts-responsible for the dementia. 5- two or more macroscopic infarcts.

AD - diagnostika-CT,MRI. M.D. Mattson, single macroscopic infarcts. 3- incidental small Tu unrelated to the dementia. No other treatable pathology. None of multiple infarcts subj. had early infarcts recognized, and none were ever treated for infarcts. !!Many different physicians diagnosed the 31 cases, none of whom were neurologists.!! 7 (23%) - concomitant multiple infarcts contributed to the dem.. Since the early dg.of an infarct may lead to the prevention of additional infarcts, a CT or MRI can be beneficial in the work-up of similar cases. CT,MRI may be useful in the work-up of AD.

Demence. Parkinsonova choroba. In degenerative dementia patients (AD n=131, 67 y, PD n=54, 64y, HD n=43, 44 y)), institutional care costs account for the largest proportion of total, direct health care costs. However, unique patterns of costs and payers are seen in specific neurodegenerative dementias (70% in AD, 63% inPD, 42% in HD). Interventions that decrease the need for institutional care have the greatest impact on total direct costs, but must account for the unique DD subtypes and be justifiable to multiple payers. D.L.Murman, 1998