Alzheimer’s disease is a neuropathic disorder which is an age-related condition. This is a primary degenerative cerebral disorder with a characteristic neuropathology. Its onset is insidious in middle life but the incidence is higher in later life. Genetic factors are more important in the presenilevariety which has a more rapid course and prominent focal cortical signs such as aphasia or apraxia. In case of a senile onset, the course is slower and there is a more general impairment of higher intellectual functions. Patients with Down syndrome appear to be at high risk of developing Alzheimer’s disease. The pathological changes result in widespread cerebral atrophy (degeneration of brain tissue) particularly involving the cortex and hippocampus.
On pathological investigations what is seen in microscopy is marked reduction of neurons, neurofibrillary tangles and neuritic plaques with an amyloid core; aluminum silicate is present in the cores of mature plaques. Several neurochemical changes occur, including a reduction in acetylcholine and choline acetyltransferase.
Alzheimer’s disease is the most common form of dementia. Itincreases in prevalence with age and is rare in people under45 years.1
Genetic factors play an important role and about 15% of cases are familial. These cases fall into two main groups: early-on set disease with autosomal dominant inheritance and a later-on set group where the inheritance is polygenic. Mutations in several genes have been described but most are rare and/or of small effect. The inheritance of one of the alleles of apolipo protein is associated with an increased risk of developing the disease (2–4 times higher in heterozygotes and 6–8 times higher in homo zygotes). Its presence is, however, neither necessary nor sufficient for the development of the disease and so genetic testing for ApoE4 is not clinically useful. The brain in Alzheimer’s disease is macroscopically atrophic, particularly the cerebral cortex and hippocampus. Histo logically, the disease is characterized bythe presence of senile plaques and neurofibrillary tangles in the cerebral cortex. Histo chemical staining demonstrates significant quantities of amyloid in the plaques; these typicallystain positive for the protein ubiquity in, which normally is involved in targeting unwanted or damaged proteins for degradation. This has led to the suggestion that the disease may be due to defects in the ability of neuronal cells to degrade unwanted proteins. Many different neurotransmitter abnormalities have also been described. In particular, there is impairment of cholinergic transmission, although abnormalities of noradrenaline (norepinephrine), 5-HT, glutamate and substance P have also been described.1
Risk factors for AD: old age, positive family history, and a history of head traumawith concussion. Pathology: neuritic plaques composed in part of Aβ amyloid,derived from amyloid precursor protein (APP); neurofibrillary tangles composed ofabnormally phosphorylated tau protein. The apolipo protein E (apoE) ε4 allele accelerates age of onset of AD and is associated with sporadic and late-onset familial cases. ApoE testing is not indicated as a predictive test. Rare genetic causes of AD are Downsyndrome and mutations in APP, presenilin-1, and presenilin-2 genes; all increaseproduction of Aβ amyloid. Genetic testing available for presenilin mutations; likelyto be revealing only in early-age-of-onset familial AD.2
The key clinical feature is:
- Impairment of the ability to remember new information.
- Hence, patients present with gradual impairment of memory, usually in association with disorders of other cortical functions.
- Short- and long-term memory is both affected but defects in the former are usually more obvious.
Later inthe course of the disease, typical features include:
- Visuo-spatial impairment and aphasia.
- As the disease progresses it is common for patients to deny that there is anything wrong (anosognosia).
In this situation, patients are often brought to medical attention by their attendants.
- Depression is commonly present.
- Occasionally, patients become aggressive, and the clinical features can be made acutely worse by intercurrent
- Patients typically present with subjective memory loss, sometimes getting lost in familiar locations.
- A history of progressive memory loss and associated functional impairment, corroborated by an informant, is the key to making the diagnosis.
Cognitive testing and neuroimaging can be helpful but in them is not diagnostic.1
Cognitive changes follow a characteristic pattern beginning with memory impairmentand spreading to language and visuospatial deficits, although 20% present with nonmemorycomplaints such as word-finding, organizational, or navigational difficulty.
Memory loss is often not recognized initially, in part due to preservation of socialappointments) draw attention of friends/family.
Once the memory loss becomesnoticeable to the pt and spouse and falls 1.5 standard deviations below normal onstandardized memory tests, the term mild cognitive impairment (MCI) is applied; roughly 50% will progress to AD over 4 years. Disorientation, poor judgment, poorconcentration, aphasia, and apraxia are increasingly evident as the disease progresses.Pts may be frustrated or unaware of deficit. In end-stage AD, pts become rigid, mute,incontinent, and bedridden. Help may be needed with the simplest tasks, such as eating,dressing, and toilet function. Often, death results from malnutrition, secondaryinfections, pulmonary emboli, heart disease, or, most commonly, aspiration. Typicalduration is 8–10 years, but the course can range from 1 to 25 years.2
- Memory loss that disrupts daily life
- Face difficulty in planning or solving problems
- Difficulty in understanding visual images
- Confusion with time or place
- Confusion in the evening hours
- Inability to create new memories
- Difficulty concentrating
- Difficulty with self care
- Meaningless repetition of own words
- Personality changes
- Mood swings
- In conventional therapy, AD cannot be managed but no highly effective drug exists. The focus is on judicioususe of cholinesterase inhibitor drugs; symptomatic management ofbehavioral problems; and building rapport with the patient, family members, andother caregivers and follow up with ones physician is a must as many drug combinations are used and its for physician to decide on same.
- Depression, common in early stages of AD, may respond to antidepressantsor cholinesterase inhibitors.
- Notebooks and posted daily reminders can function as memory aids in earlystages. Kitchens, bathrooms, and bedrooms need evaluation for safety. patients musteventually stop driving. Caregiver burnout is common; nursing home placementmay be necessary. Local and national support groups are valuable resources.2
History by a reliable informant of a patient shall be provided.Detecting focal neurological signs. Test of intellectual function. MRI, CT brain scan & PETshall be done. Conventional treatment includes management by drugs which are known to help reduce symptoms due to Alzheimer’s disease.
Homeopathic management includes giving drugs/remedies based on symptomatic presentation as per each case. Therefore, every next patient of Alzheimer’s disease will receive a different remedy based on his/her presentation. Homeopathic remedies if given rightly, not only reduces intensity of symptoms but also slow down progression of disease.
It is advisable to contact a registered homeopathic practitioner and seek homeopathic treatment in person consultation.
Do not self medicate.
Medicines for Alzheimer’s disease3
- Old people, with lack of vital heat, or prematurely old, with debility.
- Sluggish functions, heaviness, numbness, and staggering, and the characteristic
- constipation find an excellent remedy in Alumina
- Low-spirited; fears loss of reason.
- Confused as to personal identity.
- Hasty, hurried.
- Time passes slowly.
- Variable mood.
- Better as day advances.
- Suicidal tendency when seeing knife or blood.
- Thin, inactive; inclines to lie down.
- Paretic effects.
- Talking is exhausting.
- Illusions of being larger, numb, smooth, heavy, time passing too slowly, etc.
- Hasty, but slow of execution, hence mistakes in speaking, writing, etc.
- Depressive mental states.
- Depressed, on awaking.
- Timorous; fears his own impulses; the sight of knives; loss of reason, etc.
- Bad memory.
- Dusky wrinkled, old look.
- As of white of egg or a cobweb on face.
- Teeth feel long; pain extends to other parts (Kali-bi.).
- Twitching lower jaw (Gel.).
- Uvula hangs down.
- Throat feels full of sticks or constricted.
- Loss of memory, mental weakness.
- Lost confidence in him.
- Senile dementia.
- Aversion to strangers.
- Childish; grief over trifles.
- Weak memory.
- Very sensitive to noise.
- Averse to work, to talk.
- Child repeats everything said to it.
- Fears arrest on account of a supposed crime.
- Lethargic, stupid.
- Fixed ideas.
- Hallucinations; thinks he is possessed of two persons or wills.
- Anxiety when walking, as if pursued.
- Profound melancholy and hypochondriasis, with tendency to use violent language. Brain-fag.
- Impaired memory. Absent mindedness. Very easily offended.
- Malicious; seems bent on wickedness.
- Lack of confidence in himself or others.
- Suspicious [Hyos.].
- Clairaudient, hears voices far away or of the dead.
- Senile dementia.
- Absence of all moral restraint.
- Profound, melancholic delusion; feeling of moral deficiency; religious depression; delusions of conspiracies against him.
- Imagines he is singled out as an object of divine wrath.
- Loss of memory.
- Must do something-move about; gets fidgety. [Tarant.]
- Fear of being poisoned. [Hyos.]
- Amnesic aphasia; can pronounce any word told, but cannot speak otherwise.
- Night terrors.
- Horrid illusions.
- Active delirium.
- Among these the all-prevailing debility, exhaustion, and restlessness
- Gives quiet and ease to the last moments of life when given in high potency.
- Fear fright and worry.
- Anaemia and chlorosis.
- Degenerative changes.
- Gradual loss of weight from impaired nutrition.
- Great anguish and restlessness. Changes place continually. Fears, of death, of being left alone.
- Great fear, with cold sweat.
- Thinks it useless to take medicine.
- Hallucinations of smell and sight.
- Despair drives him from place to place.
- Miserly, malicious, selfish, lacks courage.
- General sensibility increased.
- Sensitive to disorder and confusion.
- Sudden, intense effects.
- Restless, anxious and very weak.
- The weakness characteristic of all Potassium Salts is seen especially in this, with soft pulse, coldness, general depression, and very characteristic stitches, which may be felt in any part of the body, or in connection with any affection.
- Sensitive to every atmospheric change, and intolerance of cold weather.
- Early morning aggravation is very characteristic.
- Fleshy aged people, with dropsical and paretic tendencies.
- Sweat, backache, and weakness.
- Pains from within out, and of stinging character.
- Giving-out & quot; sensation.
- Fatty degenerations.
- Stinging pains in muscles and internal parts.
- Twitching of muscles.
- Alternating moods.
- Very irritable.
- Full of fear and imaginations.
- Anxiety felt in stomach.
- Sensation as if bed were sinking.
- Never wants to be left alone.
- Never quiet or contented.
- Obstinate and hypersensitive to pain, noise, touch.
- WEAKENING, intellection; muscles, heart, back, limbs, etc.
- Gives out, leans on something or lies down; with backache, profuse secretions, sweat, etc.
- Soft, thin blooded and cold.
- Old, fleshy, dropsical or paralytic.
- Sub-acute conditions.
- Parts lain on are painful and go to sleep.
- Easily startled; agg. Touch; on dropping to sleep.
- Anxious aversion to solitude.
- Headaches, into eyes; wake from sleep.
- Eyes weak.
- Vision, spotted; like drops before.
- Puffs over, inner angle of eyes or baggy upper lids.
- Stitches out of ears.
- General lameness, unreasonable fear with loquacity. Left supra-orbital pain, Muscular weakness
- Face pale and features drawn.
- Numbness, with shivering.
- Irrational fears, with rapid speech.
- Nebulous condition, with the impression of unreality.
- Needs to criticize others and him.
- Suppressed anger, with desire to tear up something.
- Psychological – Despite sensation of fatigue, mental work is more easily carried out.
- Insomnia between 2 a.m. and 3 a.m.:
- Sleep heavy, with nightmares (visions of corpses):
- Sensation of heat in the anus.
- General numbness, irrational fear, and volubility.
- Pain above the left orbital nerve.
- Pain in the pharynx and stomach.
- Ralston S.H., Penman I.D., Strachan M.W.J., Hobson R.P. Davidson’s, Principles and Practice of Medicine. 17thed. Edinburgh; New York: Churchill Livingstone; 1995. 1203p.
- Kasper D.L., Fauci A.S., Hauser S.L., Longo D.L., Jameson J.L., Loscalzo J. Harrison’s Manual of Medicine. 19th ed. United States: McGraw Hill; 2016, 1222p.
- Boericke W. Pocket Manual of Homoeopathic Materia Medica. New Delhi: B. Jain Publishers (P) Ltd.; 2011