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Alzheimer Dementia

It is a insidious onset dementia responsible for most common cause of irreversible dementia.

Gene responsible
  1. APO E4 gene on chromosome 19
  2. Presenilin-1 gene on Chromosome 14
  3. Presenilin-2 Gene on chromosome 1
  4. APP (Amyloid precursor protein) on Chromosome 21
  5. Ubiquitin 1 on chromosome 9 is a newly implicated gene.
Clinical Features:
  1. Memory impairment esp. recent memory or learning of new information.
  2. Impairment in judgment and thinking
  3. Aphasia (language disturbance)
  4. Apraxia (impaired ability to carry out motor activities despite intact motor functions)
  5. Disturbance in executive functions, Personality decline
  6. May have Psychotic features (suspiciousness, hallucinations).
  7. MMSE score £ 23 (impairment), <20 (definite impairment).
  8. Agnosia (failure to identify object despite intact sensory functions) is, a feature of cortical dementia, not seen in             
  1. Senile / plaques, amyloid deposits
  2. Neuro-fibrillary tangles,
  3. Neuronal loss (particularly in cortex and hippocampus*)
  4. Neurochemically -  decrease brain choline acetyltransferase with decrease brain Ach. (esp. in nucleus basalis of Meynert).
  5. CT – diffuse atrophy, flattened sulci & enlarged cerebral ventricle.
    Hippocampus is specifically implicated for memory storage parieto-occipital involvement
The cerebroactive drugs may be grouped into:
  1. Cholinergic activators:
  2. Glutamate (NMDA) antagonist:
A. Cholinergic activators Since brain Ach levels are markedly reduced and cholinergic neurotransmission is the major sufferer in AD, various approaches to augment brain ACh have been tried.
  1. Tacrine It is the first centrally acting anti-ChE to be introduced for AD. In clinical trials tacrine produced significant improvement in memory, attention, praxis, reason and language. However, it does not alter course of the underlying disease process. Frequent side effects and hepatotoxicity have restricted its use and currently no more used.
  2. Rivastigmine This carbamate derivative of physostigmine inhibits both AChE and BuChE, but is more selective for the G1 isoform of AChE that predominates in certain areas of the brain. Rivastigmine is highly lipid-soluble-enters brain easily. Greater augmentation of cholinergic transmission in brain is obtained with mild peripheral effect.
  3. Donepezil This cerebroselective and reversible anti-AChE produces measurable improvement in several cognitive as well as non-cognitive (activities of daily living) scores in AD, which is maintained at least upto 2 years. The benefit is ascribed to elevation of ACh level in the cortex, especially in the surviving neurones that project from basal forebrain to cerebral cortex and hippocampus.
  4. Galantamine It is a natural alkaloid which selectively inhibits cerebral AChE and has some direct agonistic action on nicotinic receptors as well. Galantamine has produced cognitive and behavioural benefits in AD which are compa­rable to rivastigmine and donepezil.
B. Glutamate (NMDA) antagonist:
Memantine This new NMDA receptor antagonist, related to amantadine (also a NMDA antagonist),
  1. It slows the functional decline in moderate-to-severe AD, but benefit in milder disease are unclear.
  2. It appears to block excitotoxicity of the transmitter glutamate in a noncompetitive and independent manner.

Vascular dementia or Multi-infarct dementia
  1. CF same as above +
  2. Clinical evidence of focal brain damage. Eg. U/L spastic weakness of limb, U/L tendon reflexes,
  3. Sudden onset and Step-ladder pattern of dementia
  4. Extensor plantar, Pseudobulbar palsy
  5. Evidence of significant cerebro-vascular disease.

Binswanger ’s disease
It is subcortical (white matter) arteriosclerotic encephalopathy

Lewy body dementia
It is Extreme sensitivity to neuroleptics
  1. CF as of Alz dementia     
  2. Visual Hallucinations      
  3. Parkinsonian features                    
  4. Extra pyramidal signs     
  5. Repeated falls                
  6. Syncope            
  7. Sensitive to neuroleptics

Pick’s disease
Clinical Feature: as of Alzheimer’s dementia, chromosome involved is 21q
Predominance of frontal and temporal lobe:  i.e. Disinhibition / emotional blunting

Kluver-Bucy syndrome:
Klüver–Bucy syndrome is a syndrome resulting from bilateral lesions of the anterior temporal lobe (including amygdaloid nucleus). Characterized by Hypersexuality, Hyperorality, Placidity.

Normal Pressure Hydrocephalus (NPH)
Triad of dementia, ataxia & urinary incontinence

Creutzfeldt Jakob disease (Prion - Disease)
Infective, prion disease, Very rapid progression
Neurological symptoms – Pyramidal, extra pyramidal, cerebellar , aphasia , visual impairment Myoclonic seizures
Diffuse slow waves in EEG: triphasic EEG, Death within 2 years

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