Dementia is a generalized decline of intellect, memory, also personality, without impairment of consciousness, leading to functional impairment. [1]
It is a clinical syndrome, rather than a diagnosis in itself, which may cause by a variety of pathologies. Dementia is an acquired disorder, as distinct from learning disability in which impairments are present from birth, although the onset may be at any age.
In either middle-aged or older person any social lapse that is out of character should always suggest dementia. [1]
Onset: Insidious
Course: Protracted, although may be reversible in some cases. [2]
Alzheimer’s disease, Pick’s disease, Parkinson’s disease, Huntington’s chorea, Lewy body dementia, Steel Richardson syndrome ( in other words, Progressive Supranuclear Palsy).
Multi-infarct dementia, subcortical vascular dementia ( in other word, Binswanger’s disease).
Bromide intoxication, drugs, heavy metals, alcohol, carbon monoxide, analgesics, anticonvulsants, benzodiazepines, also psychotropic drugs.
Chronic hepatic or uraemic encephalopathy, dialysis dementia, Wilson’s disease.
Chronic subdural haematoma, head injury.
Thyroid, parathyroid, pituitary, also adrenal dysfunction.
Pernicious anaemia, pellagra, folic acid deficiency, also thiamine deficiency.
Neoplasms and other intracranial space-occupying lesions.
Normal pressure hydrocephalus. [2]
This is the commonest cause of dementia, seen in about 70% of all cases of dementia in USA. It is more commonly seen in women. Earlier, it was differentiated into two forms: a presenile form and a senile
form. Autopsy shows macroscopic changes such as enlarged cerebral ventricles, widened cerebral sulci and shrinkage of cerebral cortex.
Neurochemically, there is a marked decrease in brain choline acetyltransferase (in other words, CAT) with a similar decrease in brain acetylcholinesterase (AchE).
Cholinesterase Inhibitors:
These elevate acetylcholine (Ach) concentrations in cerebral cortex by slowing the degradation of acetylcholine released by still intact cholinergic neurons in Alzheimer’s disease.
Memantine (5-20 mg/day), an N-methyl-D’Aspartate (NMDA) antagonist, is also available for the treatment of moderately severe to severe Alzheimer’s disease.
Multi-infarct dementia is the second commonest cause of dementia, seen in 10-15% of all cases, though it is probably more common in India. Occurrence of multiple cerebral infarctions can lead to a progressive disruption of brain function, leading to dementia.
The most typical form of multi-infarct dementia is characterised by the following features:
1. An abrupt onset.
2. Acute exacerbations (due to repeated infarct ions).
3. Stepwise clinical deterioration (especially, step-ladder pattern).
4. Fluctuating course.
5. Presence of hypertension (most commonly) or any other significant cardiovascular disease.
6. History of previous stroke or transient ischemic attacks (in other words, TIAs).
Diagnosis: Emotional lability is common. EEG (specifically, showing focal area of slowing) and brain imaging (either CT scan or MRI scan of brain showing multiple infarcts) help in diagnosis.
This has been considered one of the most important treatable also reversible causes of dementia, second only to toxic dementias.
Although it accounts for less than 1% of dementias, hypothyroidism should be suspected in every patient of dementia.
All in all, Prompt treatment can reverse the dementing process and can lead to complete recovery if the treatment is start within two years of the onset of dementia.
About 50-70% of patients suffering from AIDS exhibit a triad of cognitive, behavioural and motoric deficits of subcortical dementia type and this is known as the AIDS-dementia complex (in other words, ADC).
As the AIDS virus (a lentivirus, a type of retrovirus) is highly neurotropic and the virus crosses the blood-brain barrier early in the course of the disease cognitive impairment is nearly ubiquitous in AIDS.
Diagnosis: The diagnosis is established by ELISA (enzyme linked immunosorbent assay) showing anti-HIV antibodies, and the Western Blot test (blotting of antibody specificities to HIV-specific proteins).
A Cranial CT scan can show cortical atrophy 1-4 months before the onset of clinical dementia while MRI scan is helpful in detecting the white matter lesions.
Lewy body dementia is now believe to be the second most common cause of the degenerative dementias, accounting for about 4% of all dementias.
Typically, the clinical features of Lewy body dementia include:
i. Fluctuating cognitive impairment over weeks or months, with involvement of memory and higher cortical functions (such as language, visuo-spatial ability, praxis and reasoning). Lucid intervals can be present in between fl uctuations.
ii. Recurrent and detailed visual hallucinations.
iii. Spontaneous extrapyramidal or parkinsonian symptoms such as rigidity and tremors.
iv. Neuroleptic sensitivity syndrome, characterised by a marked sensitivity to the effects of typical doses of antipsychotic drugs (resulting in severe extrapyramidal side-effects with use of antipsychotics).
It may include repeated falls, autonomic dysfunction (e.g. orthostatic hypotension), urinary incontinence, delusions and depressive features.
Although Lewy bodies (intracytoplasmic inclusion bodies) are also present in Parkinson’s disease, the occurrence of Lewy bodies in Lewy body dementia is more widespread. Antipsychotic medication should be avoided (or used with extreme caution and in low doses) in patients with Lewy body dementia.
Diagnosis: A PET (Positron Emission Tomography) or SPECT (Single Photon Emission Computerised Tomography) scan of brain may show low dopamine transporter uptake in basal ganglia. [2]
According to ICD-10, the following features are required for diagnosis:
Decline in both memory and thinking, sufficient enough to impair personal activities of daily living
Memory impairment (typically affecting registration, storage, and retrieval of new information though previously learned material may also be lost particularly in later stages.
Impaired thinking, presence of clear consciousness (consciousness can be impaired if delirium is also present), and a duration of at least 6 months. [2]
A CT or MRI brain scan may be needed, as they are valuable in the diagnosis of both focal and diffuse cerebral pathology. [1]
Antipsychotics : Antipsychotics should generally be avoided whenever possible and only have a role in patients with severely distressing symptoms or agitation causing risk to self or others.
They should be avoided in those with mild to moderate dementia, as there is a slight increase in the risk of cerebrovascular events.
The recommended drugs are haloperidol also olanzapine. A few patients need long-term oral antipsychotics to manage their behaviour at home.
Benzodiazepines: Benzodiazepines should be avoided wherever possible, especially during the day.
Intramuscular lorazepam is a suitable alternative to an antipsychotic for extreme agitation, also should be tried if antipsychotics do not relieve the symptoms.
For instance; agaricus, anacardium, hyoscyamus, nux vomica, lilium tig, phosphorus.
e.g. aconite, belladonna, silica.
tarentula.
agnus castus, anacardium, conium, crotalus hor, lycopodium.
(a) Person once intellectually sharp and ambitious, now thin and withered, lacking in self-confidence, afraid of being alone, always using wrong words Lycopodium 30c.
(b) Degenerative changes in blood vessels, enlarged prostate gland, weakness and tiredness, problems exacerbated by cold Batuta 30c.
(c) Partial paralysis, blood vessels supplying brain affected by arteriosclerosis Auruti iod 30c.
(d) Atherosclerosis, craving for salt, person highly strung and very apprehensive Phosphorus 30c. [3]
Dementia is a generalized decline of intellect, memory, and personality, without impairment of consciousness, leading to functional impairment.
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