A typical dementia laboratory screen includes: • FBE. • Urea and electrolytes. • Thyroid function tests. • Lipids. • B12, folate. • Syphilis serology. • Brain CT scan.
It is unlikely that this screen will uncover treatable causes of demen-tia. These are rare. People with brain tumours or normal-pressure hydrocephalus usually present with localising signs and symptoms. With rare exceptions, a routine laboratory screen uncovers inci-dental pathology that cognitively impaired patients have failed to report (eg, hypothyroidism), together with pathology due to self-neglect (for example, iron-defi-ciency anaemia). Identifying and treating these conditions may not reverse the dementia but will improve functional capacity, lessen
carer burden and delay admission to residential care. A brief physical examination will reveal treatable vascular risk factors (eg, hypertension) and pointers to self-neglect (eg, poor hygiene and weight loss). Brain scans are often normal in cases of mild to moderate demen-tia. Eventually, people with demen-tia show generalised atrophy, irre-spective of cause. In earlier stages, medial temporal lobe atrophy is typical of Alzheimer's disease. Spe-cial views must be requested to see these changes clearly. In later cases, bilateral temporo-parietal deficits are characteristic (figure 2). Focal frontal and/or temporal atrophy is typical of frontotempo-ral dementia, while infarctions and deep white-matter ischaemia are typical of vascular dementia. Func-tional imaging using PET or single-photon emission computed tomog-raphy can be useful in cases of diagnostic uncertainty.
Pathology PATHOLOGICALLY, Al-zheimer's disease is charac-terised by the presence of amy-loid plaques and neurofibrillary tangles, initially in medial temporal lobe struc-tures and later more diffusely. Amyloid protein is ubiq-uitous in human tissues. Its role is unclear but in Alzheimer's disease its struc-ture is changed and it pre-cipitates in an insoluble form as extracellular plaques (figure 3). This toxic, abnormal form of amyloid results in cell death. Deposits are present within the brain at least 10 years before symptom onset. Amyloid can now be imaged
directly in selected research centres using radio-ligands (figure 4). Neurofibrillary tangles are intracellular inclusions com-posed of tau protein. Tau
gives structural support to channels transporting cellu-lar nutrients and neurotrans-mitters along axons In Alzheimer's disease, fibril hyperphosphorylation
results in a loss of structural rigidity and the formation of tangles. Neither tau nor amyloid pathology are unique to Alzheimer's disease. Amy-
loid changes are also associ-ated with vascular demen-tia and dementia with Lewy bodies, whilst tau pathology is seen in frontotemporal dementia.
Dementia versus normal ageing
Diagnosing dementia
Alzheimer's disease
fore be more impaired. Currently about 30% of residents of low-care facilities, and 80% of those in high care facilities, have significant degrees of dementia. These propor-tions will increase in the future. It is vital that GPs be familiar with the signs, symptoms and com-plications of dementia and with its treatment. In the past, doctors were reluctant to share diagnoses with families, let alone patients, on the grounds that dementia was an untreatable, progressive and thus unspeakably depressing condition. They feared that families would
react adversely to a diagnosis, but in fact most welcome a clear expla-nation for the changes in cognition, personality and behaviour that have so perplexed and frustrated them. Frank, sympathetic disclosure alerts spouses and children to the need to monitor personal care and safety more vigilantly. They will also respond less critically when con-fronted with memory lapses, self-neglect and challenging behavioural symptoms. There is now a trend to share information with patients, espe-cially those in the early stages of dementia, who have insig
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