Dementia

From Ganfyd

Introduction

Dementia (Chronic cognitive dysfunction, neurocognitive disorder) is a clinical syndrome characterised by a chronic (and usually progressive) deterioration of memory, concentration, and judgment and sometimes accompanied by emotional disturbance and personality changes. It's effects are devastating to the patient and those around the patient, especially the carers. The increased care is costly, and is largely borne by families and the tax-payer. Do not confuse with delirium. Be aware that the semantic choice of the term can cause anxiety and has been a subject of controversy so that there is a move with DSM-V due in 2013 to retire it.

• Guidelines and pathway for dementia recommended for British geriatricians and old age psychiatrists (2006)
• NICE clinical guideline 42:Dementia Nov. 2006

Aetiology

The list of causes is long but Alzheimer's disease and vascular dementia top the bill. A prime role of the physician is to look for treatable and reversible causes of dementia and exclude things that look like dementia but aren't. Once this is done the role is to support the patient and family. The use of drugs for Alzheimer's disease is possible. Other drugs are being developed.

Associations

Dementia is not one disease so these associations being indirect are likely to be markers for risk factors for the underlying disease or common pathways involved in neuroprotection and degeneration. The association is usually evaluated in context of later development of cognitive impairment. It is important to note that public perceptions of possible associations with dementia in Western society is different from the objective evidence base^[1] and many health professionals may be exposed to the same biasing factors as the public. Some associations are:

• Social class and education - lower the more likely^[2]
• Pre-morbid IQ - lower the more likely^[3]
• Lower motor function^[4] and past physical activity ^[5] increase risk
• Obesity - there is a J shaped relationship with marked leaness and more importantly with changes in most Western populations with visceral adipose tissue correlating reasonably well with risk. The relationship with BMI^[6] is not consistent^[7].
• Metabolic syndrome up to age 75^[8]
• HDL - increased levels seem protective for this^[9] and is a general predictor of longevity
• Smoking - increases risk of cognitive impairment^[10], but protective for those who later meet the diagnostic criteria for Alzheimer's disease
• Diet - multiple potential correlations as would be expected by underlying aetiologies. The role of cyanobacteria is a current flavour of the month^[11]
• Head trauma - especially if repetitive or severe^[12].
• Hormone status eg HRT^[13]
• Alcohol exposure - U shaped curve ! ^[14]
• Drugs. A wide spectrum of drugs might be expected to influence cognition, and the confounding with the underlying disease can make the associations particularly challenging. Some associations such as prior exposure to NSAIDs^[15] and simvastatin^[16] being protective and antipsychotics possibly enhancing progression have been analyzed in some detail in models relating to the known increased risk with earlier major psychiatric illness^[17].

History

It is important to obtain a collateral history as well as assessing the patient. Indeed the history independent of the patient's own perceptions is often the key to early diagnosis and is likely to benefit the patient which can help resolve potential conflicts where capacity to give consent for assessment is an issue, as can occasionally arise. Enquire about rate of intellectual decline, ADLs, social interaction, nutritional status, general health PMH e.g. stroke, any previous head injury, drug history, FHx of dementia, and look for confabulation.

Examination

Examination should include a brief mental state examination to screen for depressive pseudodementia and a MMSE. Neurological examination may identify focal signs, involuntary movements, pseudobulbar signs, primitive reflexes or ataxia.

Does this patient have dementia?

Investigations

All patients nowadays should have some basic investigations. If the onset has been rapid and associated with idiosyncratic signs eg Myoclonic jerks as seen in CJD then further tests should be done.

• FBC and ESR
• VDRL/FTA to exclude neurosyphilis
• B12 and folate
• Give Thiamine especially in alcoholics
• TFTs - exclude Hypothyroidism
• Assess mood - Depression ?
• CT Head - exclude space occupying lesions, stroke disease. Usually find cerebral atrophy
• MRI scan may be indicated in some
• Lumbar puncture and CSF analysis where encephalitis, meningitis or CJD suspected

Causes

• Alzheimer's disease
• Vascular dementia
• Dementia with Lewy Bodies
• Progressive supranuclear palsy
• Creutzfeldt-Jakob disease
• HIV dementia
• Hashimoto's encephalopathy
• Post encephalitis
• Cerebral Hypoxia
  • Carbon monoxide poisoning

Also see Pseudodementia

Prognosis

Survival times for dementia (as opposed to a specific underlying cause) are now available prospectively for up to 14 years follow up^[18]. A graphical view of this data is on the web.

External links

• Mental Health Foundation, publishers of a variety of reports and support material for people with mental health problems, including dementia, and their carers, including Getting on with living.^[19]

References