ALZHEIMER’S DISEASE IN OLD AGE - homeopathy360
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ALZHEIMER’S DISEASE IN OLD AGE

 Abstract: Alzheimer’s disease is going to be an important psycho-geriatric problem of modern era. In the said article a bird’s eye view of its causation, pathology, clinical picture, progress, and homoeopathic management is discussed.
Introduction
Alzheimer’s disease is a progressive neurodegenerative disease resulting in decline in cognitive functions together with declining activities of daily living and behavioral disturbances. Clinically there is subtle onset of memory loss followed by a slowly progressive dementia and pathologically there is gross, diffuse atrophy of the cerebral cortex with secondary enlargement of the ventricular system.
It is the most common cause of cognitive impairment in elderly persons, from the age of 60 onwards up to 80 years, incidence and prevalence of AD increases exponentially with age, doubling every 5 years. . It is the most common cause of dementia in the elderly.
It was first described by Professor Alois Alzheimer in Germany in 1907
Pathology
•  Earliest metabolic changes occur in Parietal cortex.  Pathological changes occur in Hippocampus, temporal cortex, and nucleus basalis.
•  The pathological process consists mainly of neuronal loss, principally in the temporoparietal cortex but also in the frontal cortex, together with an inflammatory response to the deposition of senile and neurofibrillary tangles.
•  Senile plaques and neurofibrillary tangles are regarded as hallmark of alzheimer’s disease though they may also be present with normal aging.
•  Senile plaques consist of extracellur deposition of congophilic, insoluble material which is amyloid-B (AB). It is derived from the enzymatic cleavage of a larger membrane protein, the amyloid precursor protein (APP).
•  Neurofibrillary tangles represent intracellulare paired helical filaments of hyperphosphorylated protein known as tau protein. Tau protein is expressed in neurons and normally acts to stabilize microtubules in the cells.
•  Accumulate in small numbers during normal aging but occur in quantitative excess in the dementia of AD.
•  The neuritic plaques contain a central core that includes Ab amyloid, proteoglycans, Apo E,a1 antichymotrypsin
•  Plaque core is surrounded by the debris of degenerating neurons, microglia, and macrophages.
• AMYLOID ANGIOPATHY – Accumulation of Ab amyloid in cerebral arterioles
Biochemically
↓↓ Cerebral cortical levels of several proteins and neurotransmitters

  • Acetylcholine- Due to degeneration of neurons in the nucleus basalis of Meynert that project to many areas of cortex.
  • ↓↓ Norepinephrine levels in brainstem nuclei

RISK FACTORS:
•  Old age , female
•  F/H
•  Head trauma with concussion
•  Lower education group
•  Aluminium, mercury, viruses
•  Inflammation
•  Genetic factors – defective genes on chromosomes 1,14,19,21
•  The apoE4 variant brings forward age of onset
• Insulin resistance
CLINICAL MANIFESTATIONS
•  EARLY STAGES-

  • Subtle Memory loss
  • Slowly Cognitive problems begin to interfere with daily Activities – Job, driving, shopping, and housekeeping.
  • Insight- Absent or present → Frustration and anxiety
  • Change of environment ,bewildering- lost on walks or while driving an automobile

• MIDDLE STAGES-
Patient is unable to work, is easily lost and confused, and requires                                                                                   daily supervision

  • Social graces, routine behavior, and superficial conversation may be surprisingly retained. Language may be impaired, especially comprehension and naming of objects
  • Word-finding difficulties.  Impairments in fluency, comprehension, and repetition
  • In some, aphasia is an early and prominent feature.
  •  Deficits in performing sequential motor tasks – Dressing, eating,                    solving simple puzzles, and copying geometric figures, simple calculations or tell time
  • •  LATE STAGES OF THE DISEASE
  • Ø   Complete loss of judgment, reason, and cognitive abilities.
    Ø  Hallucinations and delusions are common
  • Ø  Loss of inhibitions

Ø  Disturbed Sleep – wake patterns and nighttime wandering
Ø  Some patients look Parkinsonian but rarely have a rapid, rhythmic, resting tremor
•      IN END-STAGE –
Ø  Rigid, mute, incontinent, and bedridden
Ø  Help needed with the simplest tasks – Eating, dressing, and toilet function.
Ø  Hyperactive tendon reflexes
Ø  Myoclonic jerks
Ø  Generalized seizures
Ø  Death – From malnutrition, secondary infections, or heart disease
 
COURSE OF THE DISEASE:
•      EARLY –  CT and MRI are not specific and may be normal
•      LATER –  Diffuse cortical atrophy
•      Detailed MRI scans show atrophy of hippocampus
•      MRI (Midbrain)
•         ↓↓ volume of hippocampus
•      Positron emission tomographic scans
•       ↓↓ Activity in parietal lobes bilaterally , a typical finding in this condition
Differential Diagnosis
•      Resting tremor with stooped posture, bradykinesia, and masked face suggests Parkinson’s disease.
•       Early prominent gait disturbance with only mild memory loss suggests Normal-pressure hydrocephalus
•      Early onset of a seizure suggests a metastatic or primary brain Neoplasm
•      A past history of long-term severe depression suggests Pseudodementia
•      A history of treatment for insomnia, anxiety, psychiatric disturbance, or epilepsy suggests chronic drug intoxication
•      Prominent behavioral changes with intact memory and lobar atrophy on brain imaging suggests fronto-temporal dementia (FTD)
•      Loss of sensibility to position and vibration + Babinski responses suggests Vitamin B12 deficiency
•      +Ve  F/h  of dementia suggests either one of the familial forms of ad or other genetic disorders associated with dementia – Huntington’s disease , familial prion diseases, or rare forms of hereditary ataxias
•      Thyroid Disease
Management: Ancillary measures
Education: Education of caregiver is very important in patients with Alzheimer’s disease.
Behavioral problems:  Associated behavioral problems should be managed carefully by both medicine and psychotherapy.
Homoeopathic Management
Homoeopathy removes the sickness of the patient by stimulating the vital dynamis which at the same time increases the power of resistance of the sick person. But if the power of resistance is weakened by morbific (damaging) influences of toxic and parasitic agents or by chronic miasms, Dr Hahnemann has advised to remove these obstructions or chronic miasmatic taint or tendency to produce degenerative diseases in the future.
The scope of homoeopathy is subject to research once severe pathological damage started. If the said disease process is identified  earlier before the gross destruction have taken place homoeopathy may definitely check further progression of pathology by minimizing disease process and development of complications. Here comes the importance of constitutional medicine, if used along with supportive therapy, it is expected that many of the complications or further deterioration may be avoided.  The quality and longevity of life can be improved. Constitutional treatment will help to stimulate the system as a whole at the same time will act as a palliative in incurable cases.  We must know our scope and limitation in the treatment of incurable and malignant diseases. We can not cure the incurable diseases but we can give supportive treatment like other system of medicine keeping in view the 7th observation of Kent which he arrived at the conclusion after going through the several cases of such incurable diseases. More over homoeopathic constitutional medicine will help to halt the progress of disease to other direction or other system by encapsulating the disease process in one plane which is lacking in other system of medicine.  
References
1.Harrison’sPrinciples of Internal Medicine”, 16th edition, Mc Graw- Hill, Medical publishing division.
2. Kent J. T., “Lectures on Homoeopathic Philosophy”, Calcutta, National Homoeo Laboratory, 1975.
3. Hahnemann, Samuel. “The Chronic Diseases, Their Peculiar Nature and Their Homoeopathic Cure.” B. Jain publishers PVT. LTD. Reprint Ed

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