Memory complaints that do not qualify for a diagnosis of dementia are common in elderly people. All of the following are shown to predict conversion from mild cognitive impairment (MCI) to dementia except:
E. The presence of hippocampal atrophy in patients with amnestic MCI may predict the onset of later dementia. The risk of conversion to dementia is four times higher in 5 years when hippocampal atrophy is present. It is generally accepted that the closer one’s cognitive ability, brain imaging, and genetic susceptibility are to AD, the more likely is the progression to dementia from MCI. Other factors predicting conversion include older age, greater severity of baseline cognitive deficits, especially impaired episodic recall and hypoperfusion of multiple brain regions in neuroimaging studies. It is also noted that multi-domain amnestic MCI has a higher conversion rate than pure amnestic MCI. This conversion is more pronounced if the cognitive complaints are accompanied by carers’ reports of impaired daily function. Sensory impairment has no role in such predictions.
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The annual rate of progression from mild cognitive impairment (MCI) to dementia is estimated to be around:
A. It is very difficult to conclusively decide on epidemiological facts of mild cognitive impairment due to the variations in diagnostic terms and inclusion criteria used in epidemiological research. A prevalence between 3% and 19% has been reported in elderly people. The age-specific prevalence of MCI is greater than that of dementia. MCI is about four times more common than dementia when based on community assessment of noninstitutionalized individuals. An incidence of 8–58 per 1000 per year and a risk of developing dementia of 11–33% over 2 years have been quoted. The progression of amnestic MCI to dementia has been examined in various clinical populations. Generally a yearly incidence of dementia of 10–15% has been quoted for those with MCI attending memory clinics (compare this with general rates of 1–2% in elderly people). Community-based studies show slightly lower rates of conversion closer to 5–10% per year. A significant number of those with amnestic MCI actually improve their cognitive performance during follow up. Up to 44% of patients with mild cognitive impairment are estimated to return to normal a year later.
Median survival from the time of diagnosis for patients with Alzheimer’s dementia (AD) is:
C. It is important to note that AD by itself is not a fatal disease. The median survival time following a diagnosis of AD depends strongly on the patient’s age at diagnosis. The older the age at diagnosis, the higher the chances of death. For example, some studies have shown a difference in median survival time of around 5 years between those diagnosed with dementia at the age of 65 and those diagnosed at the age of 90. The median survival from initial diagnosis is higher for men than women in some studies but this is not consistently shown. The presence of frontal lobe release signs, extrapyramidal signs, and gait disturbance,history of falls, congestive heart failure, ischaemic heart disease,and diabetes at baseline may predict shorter survival. Based on numerous longitudinal studies, a median survival of 5–8 years has been estimated. A multicentre prospective population-based cohort study in England and Wales with 14 years’ follow-up reported median survival after the estimated onset of dementia as 4.6 years for women and 4.1 years for men. There was a difference of nearly 7 years in survival between the younger old and the oldest people with dementia:10.7 years for ages 65–69 vs. 3.8 years for ages ≥90. Significant factors that predicted mortality in the presence of dementia during the follow-up included sex, age of onset, and disability before the onset. Type of accommodation, marital status, and self-reported health were not associated with survival.
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Braak stages are used in neuropathological quantifi cation of brain changes in Alzheimer’s disease.
Which of the following is the basis of Braak’s stages?
D. Braak’s staging system has been used to grade pathologically the various degrees of dementia severity. It is based on the appearance of neurofibrillary tangles in brain. These tangles commence the transentorhinal and entorhinal cortex spreading to the hippocampus, and then extend across the remaining limbic system before involving other cortical regions, followed by the primary motor and somatosensory cortices, and finally the occipital cortex.This progression is the basis of the Braak’s staging. A decline in memory test performance and mental state of the demented patient correlate with the pathological progression through the neocortical Braak stages.
Many subtypes of vascular dementia have been identifi ed.
Which of the following refers to Binswanger’s disease?
A. The term Binswanger’s disease refers to a type of subcortical vascular dementia caused by widespread, microscopic atherosclerotic vascular damage to the deep white matter in the brain. As a result patients may have frontal executive dysfunction, short-term memory loss, and behavioural changes. The most characteristic feature is said to be the reduction of processing speed. An MRI scan of the brain can reveal the characteristic brain lesions essential for diagnosis. Single large infarcts or multiple cortical infarcts give rise to vascular dementia. Periventricular white matter lesions are non-specific and are commonly seen in Alzheimer’s dementia, extreme aging with vascular risk factors, and also in patients with frank vascular dementia.
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