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Dementia In Ayurveda

Dementia In Ayurveda

Dementia is characterized by multiple cognitive defects that include impairment in memory, without impairment in consciousness.The cognitive functions that can be affected in dementia include general intelligence, learning and memory, language, problem solving, orientation, perception, attention and concentration, judgement and social abilities.

Dementia In Ayurveda

In the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) dementia is characterized by multiple cognitive defects that include impairment in memory, without impairment in consciousness.
The cognitive functions that can be affected in dementia include general intelligence, learning and memory, language, problem solving, orientation, perception, attention and concentration, judgement and social abilities. The personality is also affected. In addition, diagnosis of dementia, according to DSM-IV, requires the symptoms that result in a significant impairment in social or occupational functioning and that they present a significant decline from a previous level of functioning. The critical clinical points of dementia are the identification of the syndrome and the clinical workup of its cause. The disorder may be progressive or static, permanent or reversible. An underlying cause is always assumed, although in rare cases it is impossible to determine a specific cause. The potential reversibility of dementia is related to the underlying pathological condition and to the availability and application of effective treatment. Approximately 15 percent of people with dementia have reversible illnesses if treatment is initiated before irreversible damage takes place.

          The prevalence of dementia rises exponentially with age. It is believed that 50% to 70% of dementia is caused by Alzheimer's disease. The world's population is aging. There are currently 18 million people in the world with dementia. 66% of people with dementia live in developing countries. Numbers are increasing, especially in rapidly developing and heavily populated regions such as China, India and Latin America. Although more women than men have Alzheimer's disease, this may reflect womens longer life spans because studies do not show marked gender differences in incidence rates. Alzheimer's disease is a prominent disorder of old age; 8 to 15% of people over age 65 have Alzheimer's disease. The prevalence of dementia nearly doubles with every 5 years of age after the age of 60 years. 1% of those aged 60 to 64 are affected with dementia, 2% of those aged 65 to 69 years, 4% of those aged 70 to 74 years, 8% those aged 75 to 79 years; 16% of those aged 80 to 84, and 30 to 45% of those aged 85 and above. According to the 1997 American Psychiatric Association Practice guideline for the treatment of patients with Alzheimer's disease and the Dementia of late life, the onset of the disease generally occurs in late life, most commonly in the 60s, 70s and 80s and beyond, but in some instances the disorder appears in the 40s and 50s known as early
onset dementia. The second most common type of dementia is vascular dementia, which is usually related to cerebrovascular diseases. Hypertension predisposes a person to the disease. Vascular dementias account for 15 to 30% of all dementia cases. Vascular dementia is most common in people between the ages of 60 and 70 years and is more common in men than in women. Approximately 10 to 15% of patients have co-existing Vascular dementia and dementia of the Alzheimer's type.

          Dementia has many causes, but dementia of the Alzheimer's type and vascular dementia together represent as many as 75% of all cases.
 Most common causes of Dementia:
 Alzheimer's disease  Alcoholism
 Vascular dementia  Parkinson's disease
 Varieties : Multiple infarct (called Drug/medication multiple infarct   
 dementia) intoxication Binswanger's disease
Cortical microinfarction
 Less common causes of Dementia :
 Intracranial masses and Nutritional disorders
tumors, subdural masses, brain Wernic - Korsakoff syndrome abscess Vit.B12 deficiency  Anoxia Folate deficiency  Trauma Pellagra Head injury Marchiafava Bignami disease Dementia pugilistica (punch- ? Zinc deficiency drunk syndrome)
 Metabolic disorders
 Normal pressure hydrocephalus Metachromatic leukodystrophy
 Neurodegenerative disorders Adrenal leukodystrophy
Huntington's disease Dialysis dementia Progressive supranuclear palsy Hypothyroidism & hyperthyroidism Pick's disease Renal insufficiency severe Amyotrophic lateral sclerosis Cushing's syndrome Spinocerebellar degeneration Hepatic insufficiency Ophthalmoplegia plus Parathyroid disease Metachromatic leukodystrophy
 Chronic inflammatory
Hallevorden Spatz disease disorders Wilson's disease Lupus and other
Infections collagen vascular
Creutzfelt - Jakob disease disorders with intracranial AIDS vasculitis
Viral encephalitis Multiple sclerosis Progressive multifocal Whipple's disease leukodystrophy Behcet's syndrome Neurosyphilis Chronic bacterial meningitis Cryptococcal meningitis Other fungal meningitides
In 1907, Alois Alzheimer first described the condition that later
assumed his name. He described a 51 year old woman with a 4.5 year course of progressive dementia. The final diagnosis of Alzheimer's disease is based on a neuropathological examination of the brain; nevertheless, dementia of the Alzheimer's type is commonly diagnosed in the clinical setting after other causes of dementia have been excluded from diagnostic consideration. According to DSM-IV classification, Alzheimer's disease (AD) is defined as a dementia syndrome, that is gradual in onset and progression and without other identified and sometimes treatable
Risk factors Aggravating factors
Age Drugs and alcohol
Gender Problems of eyes and ears
Education Metabolic, endocrine and nutritional deficiencies
Family history Emotional disorders
Down syndrome
Neurological disorders, tumours and space occupying lesions in the skull, infections,complication of atherosclerosis Head Injury
Although the cause of dementia of the Alzheimer's type remains
unknown, progress has been made in understanding the molecular
basis of the amyloid deposits that are a hallmark of the disorder's
neuropathology. 40% of patients have a family history of dementia of the Alzheimer's type.
The gene for amyloid precursor protein is on the long arm of
chromosome 21. Through the process of differential splicing, there are 4 forms of amyloid precursor proteins. The B/A4 protein, the major constituent of senile plaques, is a 42 amino acid peptide that is a breakdown product of amyloid precursor protein. Whether the
processing of abnormal amyloid precursor protein. The processing of
abnormal amyloid precursor protein is of primary causative significance in AD remain unknown.
Tangles are made up of neuronal proteins known as TAU proteins that play an essential structural role in holding the neurons together. In Alzheimer's patients, the protein break loose from the
neurons and form twisted tangles. After the protein breaks loose, the neurons begin to wither and eventually die. It is not clear why the tangles form. The amyloid plaques may set off a cascade of chemical reactions that lead to the tau tangling, or there may be some other biochemical abnormality that sets off the cascade.
(1) Diffuse atrophy (mainly of temporal lobes and hippocampus)
(2) Flattened cortical sulci
(3) Enlarged cerebral ventricles
(1) Neurofibrillary tangles (composed mainly of phosphorylated TAU
(2) Senile / Amyloid plaques (composed of B/A4 protein, astrocytes,
dystrophic neuronal process and microglia found in neocortex, hippocampus and amygdala.
(3) Neuronal and synaptic loss.

(4) Granulovascular degeneration of neurons.
(5) Amyloid angiopathy.
(6) Involvement of nucleus Basalis of Meynert.

Acetylcholine and norepinephrine are hypothesized to be hypoactive in AD. Several studies show that a specific degeneration of cholinergic neurons is present in nucleus basalis of Meynert in people with AD. Other data in support of a cholinergic deficit in AD are those that demonstrate decreases in acetylcholine and choline
Acetyl transferase concentrations in the brain. Choline acetyl transferase is the key enzyme for the synthesis of Ach, and a
reduction in choline acetyl transferase concentrations suggests a decrease in the number of cholinergic neurons present. The decrease in norepinephrine activity in AD is suggested by the decrease in norepinephrine containing neurons in the locus ceruleus found in some pathological examinations of brains from people with AD. Two other neurotransmitters, Somatostatin and Corticotropin have been reported to be decreased in AD. Neurotransmitters are important in developing strategies for symptomatic treatment based on neurotransmitter replacement.
Many physicians and researchers have categorized Alzheimer's
into 2 types :
(1) Presenile or early onset Alzheimer's
(2) Senile or late onset dementia
Young people who develop Alzheimer's have greater
neurochemical impairment. It is likely thought that younger brains
simply need to be more damaged before a person starts to show
symptoms, so the difference may not reflect a true difference in the
nature of the disease. It may be genetic, to which late onset
Alzheimer's is not linked.
The onset of mental changes is usually so insidious that neither
the family nor the patient can date the time of its beginning.
Occasionally, however, it is brought to attention by an unusual degree of confusion in relation to a febrile illness, an operation, mild head injury, or the taking of medication. The gradual development of forget fullness is the major symptom, small day to day happenings are not remembered. Seldom used names are particularly illusive. Little used words from an earlier period of life also tend to be lost. Appointments are forgotten and possessions misplaced. Questions are repeated again and again the patient having forgotten what was just discussed. Once the memory disorder has become pronounced, other failures in cerebral function become increasingly apparent. The patient speech is halting because of failure to recall the needed word. The same difficulty interrupts writing. Almost imperceptible at first, all these disturbances of language became more apparent as the disease progresses. Finally, there is a failure to speak in a full sentence; to find words requires a continuous search; and little that is said or written is fully comprehended. Occasionally, there is a rather dramatic repletion of every spoken phrase (echolalia). The deterioration of verbal skills has by then progressed to an obvious dysphasia.Skill in arithmetic calculation suffers a similar deterioration. Faults in balancing the checkbook, mistakes in figuring the price of items and in making the correct change - all these and other progress to a point where the patient can no longer carry out the simplest business affairs. This type of conceptual loss is called accalculia or dyscalculia. Visuospatual orientation becomes defective. The car cannot be parked, the arms do not find the correct sleeves of the dressing gain, the patient turns in the wrong direction on the way home or becomes lost. The route from one place to another cannot be described nor can given directions be understood. As this state worsens, the simplest of geometric forms and patterns cannot be copied.Eventually the patient forgets how to use common objects and tools while retaining the necessary motor pathways and coordination for these activities. Finally, only the most habitual and virtually automatic actions are preserved. Tests of commanded and demonstrated actions cannot be executed or initiated. Ideomotor apraxia is the term applied to the advanced forms of this motor incapacity.
As the disease progresses, restlessness and agitation or their
opposites - hypokinesia and placidity - becomes evident. Dressing,
shaving and bathing are neglected. The patient becomes more
egocentric and indifferent to the feelings and reactions of others. There is gradual weight loss. Difficulty in locomotion, a kind of unsteadiness, with shortened steps but without motor weakness and rigidity, frequently supervenes. later, elements of parkinsonian akinesia and rigidity, and tremor can be perceived in the motor disability. Ultimately the patient loses the ability to stand and walk, being forced to lie inert in bed, having to be fed and bathed.
Memory impairment is typically an early and prominent feature in
dementia, especially in dementias involving the cortex such as
dementia of the Alzheimer's type. Early in the course of dementia,
memory impairment is mild and is usually most marked for recent
events; people forget telephone numbers, conversations and events of the day. As the course of dementia progresses, memory impairment becomes severe and only the earliest learned information such as a person's place of birth is retained.

Orientation can be progressively affected during the course of a
dementing illness. For example, patients with dementia may forget
how to get back to their rooms after going to the bathroom. No matter how severe the disorientation seems, however, patients show no impairment in their level of consciousness.
Dementing processes that affect the cortex, primarily dementia
of the Alzheimer's type and Vascular dementia, can affect patients'
language abilities. DSM-IV includes aphasia as one of the diagnostic
criteria. The language difficulty may be characterized by a vague,
stereotyped, imprecise, or circumstantial locution and patients may
also have difficulty in naming objects.
Changes in the personality of a person with dementia are especially disturbing for the families of affected patients. Pre-existing personality traits may be accentuated during the development of
dementia. Patients with dementia may also seem to be less concerned than they previously were about the effects of their behaviour on others. People with dementia who have paranoid delusions are generally hostile to family members and caretakers. Patients with frontal and temporal involvement are likely to have marked personality changes and may be irritable and explosive.
An estimated 20 to 30 percent of patients with dementia, primarily patients with dementia of the Alzheimer's type, have hallucinations and 30 to 40 percent have delusions, primarily of a paranoid or persecutory and unsystematized nature, although complex, sustained and well-systematized delusions are also reported by these patients. Physical aggression and other forms of violence are
common in demented patients who also have psychotic symptoms.
􀂧 PSYCHIATRIC : In addition to psychosis and personality changes, depression and anxiety are major symptoms in an estimated 40 to 50 percent of patients with dementia, although the full syndrome of depressive disorder may be present in only 10 to 20 percent. Patients with dementia may also exhibit pathological laughter or crying i.e., extremes of emotions with no apparent provocation.
􀂧 NEUROLOGICAL : In addition to the aphasias in patients with dementia, apraxias and agnosias are common, and they are included as potential diagnostic criteria in DSM-IV. Other neurological signs that can be associated with dementia are seizures, seen in approximately 10 percent of patients with dementia of the Alzheimer's type and in 20 percent of patients with vascular dementia and atypical neurological presentations, such as nondominant parietal lobe syndromes. Primitive reflexes, such as the grasp, snout, tonic-foot, and palmomental reflexes - may be present on neurological examination and myoclonic jerks are present in 5 to 10 percent of patients.
Patients with vascular dementia may have additional neurological symptoms, such as headaches, dizziness, faintness, weakness, focal neurological signs and sleep disturbances, possibly attributable to the location of the cerebrovascular disease. Pseudobulbar palsy, dysarthria and dysphagia are also more common in vascular dementia than in other dementing conditions.
􀂧 CATASTROPHIC REACTION : Patients with dementia also exhibit a reduced ability to apply what Kurt Goldstein called the abstract attitude. Patients have difficulty in generalizing from a single instance, in forming concepts and in grasping similarities and differences among concept. Furthermore, the ability to solve problems, to reason logically and to make sound judgement is compromised. Goldstein also described a catastrophic reaction, marked by agitation secondary to the subjective awareness of intellectual deficits under stressful circumstances. People usually attempt to compensate for defects by using strategies to avoid demonstrating failures in intellectual performance; they may change the subject, make jokes, or otherwise divert the interviewer. Lack of judgement and poor impulse control commonly appear, particularly in dementias that primarily affect the frontal lobe. Examples of these impairments include coarse language, inappropriate jokes, the neglect of personal appearance and hygiene and a general disregard for the conventional rules of social conduct.

(1) Malnutrition
(2) Secondary infections
(3) Heart disease
Microscopic examination of brain tissue (at autopsy) can only make a final definite diagnosis of AD. Without this examination a diagnosis of only probable AD can be made. Traditionally, clinicians have made this diagnosis by adopting a process of exclusion :
The diagnostic process include :
(1) Review of clinical history
(2) Cognitive assessment
(3) Physical examination
(4) Laboratory tests
(5) Neuroimaging
􀃉 Meticulous history from patient and informant preferably a collateral observes is mandatory.
􀃉 Assess change from previous level of performance, personality and cognition.
􀃉 Confirm temporal course of disease..
􀃉 Inquire about stroke, sleep wake cycle, gait, incontinence hallucinations, movement disorder.
􀃉 Inquire into family history of dementia and other neurologic diseases.
 The AD assessment begins with a comprehensive clinical history.
􀃉 Mini mental screening (MMSE, Folstein et al. 1975) on a scale of 30 is used to survey cognitive functions considering patients education and previous strengths and weaknesses.
􀃉 Evaluate attention, learning, recall, language, visuospatial skills,
calculations and obstructions.
AD has certain characteristic clinical features, which differentiate
it from other conditions associated with memory impairment or
cognitive deficits. These characteristic features include :
􀃉 Memory impairment interfering with the patients daily activities.
􀃉 Global memory impairment : Memory deficit seen in patients with AD is global and affects important as well as trivial matters. For instance, a patient with benign forgetfulness may forget to pay a bill, form, return a phone call, but will not forget to cases a check, or that a bill has already been paid. In contrast, patients with AD may forget to pay bills and to cash checks they may even forget that they have paid a bill and may pay the same bill repeatedly.
􀃉 Cognitive deficit symptoms : Initially, these deficits may be so small as to escape the notice of most clinicians, and can only be diagnosed by specialized neuropsychological testing. In AD, these deficits become more pronounced and readily noticeable. Common deficits include;
(i) Anomia : Anomia is an inability to find the correct word and name objects. As the disease progresses, the patient is unable to name even the common objects that are being used everyday.
(ii) Agnosia : Agnosia is an inability to recognize objects. This is a much more serious condition than anemia and may even put the patient at risk of injury.
(iii) Apraxia : Apraxia is an inability to carryout voluntary activities in the absence of any muscle weakness of in coordination. The patient for instance may not be able to get dressed or undressed or even to faced. A very early manifestation of apraxia is the inability to adjust to
changes in the work place such as changes in the operating system, or changes in the work environment.
(iv) Aphasia : Patients with AD tend to have a mixture
receptive and expressive aphasia and are unable to
sustain a conversation. It also prevents the patient from
following instructions and expressing his needs.
(v) Behavioural symptoms and personality changes :
They are useful to identify patients affected by AD.
􀃉 Give special attention to :
(1) Focal UMN findings (5) Peripheral neuropathy
(2) Abnormal muscle tone (6) Sensory deprivation
(3) Involuntary movements (7) Agnesia, Apraxia
(4) Raised intracranial tension (8) Soft signs
􀃉 Conduct general medical examination to look for signs of
nutritional deficiency, systemic diseases etc.
􀃉 The examination should include blood pressure, pulse, vision
and hearing, cardiac and respiratory function, mobility and
Suggested tests Optional tests
Hematology group HIV
Biochemistry group Toxicology screen
S. TSH Lymph Serology
Vitamin B12 level Urinary heavy metals
Folic acid level Thyroid antibodies
Syphilis serology CSF

It is important for
􀃉 Precise quantitative of cognitive deficits
􀃉 Pattern and severity of cognitive deficits
􀃉 Baseline for future assessments
For the mental state assessment to be valid, the patients state of
consciousness should be clear and the patient should not be under the effect of any medication that may interfere with the cognitive functions.

It is useful in the diagnosis of AD. The principle reason for conducting brain imaging is to eliminate other causes of dementia, such as tumors and ischaemic lesions. It includes -
(a) (CT) Computed Tomography
(b) (MRI) Magnetic Resonance Imaging
(c) (SPECT) Single Photon Emission Computed Tomography
Though these are not specific for AD, these are accurate at differentiating AD from normal aging.
􀃉 Neural Thread Protein (NTP) : This is a nonspecific breakdown product of neuronal degeneration in the brain and can be detected on spinal fluid testing. There is ongoing research on role of CSF tan, AB-42, NTP and other biomarkers of AD.
􀃉 Genetic testing : Genetic proveness to AD in the typical late life
onset patient, in the majority, rests on the type of apolipoprotein present; apolipoprotein E2 is protective and apolipoprotein E4 is a risk factor. Both can be readily detected on a simple test. It should be used only when there is a strong family history or other special reason, and then only in the context of expert genetic counseling. It may have some use for increasing diagnostic certainty in a symptomatic patient, but it is unlikely to change therapeutic planning.

Vascular Dimentia is the second most frequent cause of
dementia, predominantly by causing ischemic brain injury.
Large artery syndromes Small artery syndromes
Multi infarct state Lacunar state, Apathy, Abulia, Dysexecutive syndrome Major hemispheral syndromes Strategic infarct dementia,
dysexecutive and frontal lobe syndrome Aphasia, Apraxia Binswarger disease, depression Constructional apraxia Gait, apraxia, incontinents
Clinical Diagnosis :
Owing to diversity of stroke mechanisms, there are no set diagnostic rules. However, look for :
􀂃Sudden onset, stepwise decline, fluctuation with transient or residual focal neurologic deficit.
􀂃Bilateral UMM signs or pseudobulbar palsy
􀂃Gait apraxia, incontinence, paratonic rigidity.
􀂃Patchy cognitive deficits
􀂃Family history and risk factors for stroke.
Other Common Disorders Encountered in Patients with Dementia :
Clinical features include :
􀂃Alteration in social and personal behaviour
􀂃Abnormalities of sensations
􀂃Alteration in eating and oral behaviour
􀂃Repetition and compulsion rituals
There is progressive cognitive decline interfering with social / occupational function, progressive memory impairment with deficits of
attention, front sub-cortical skills and visuospatial ability.
Clinical features include :
􀂃Fluctuating cognition
􀂃Recurrent visual hallucinations
􀂃Spontaneous motor features of Parkinsenism
􀂃Falls, syncope, transcendental loss of consciousness, delusions.
􀂃Precise diagnosis is problematic
􀂃Impairment in orientation, new learning
􀂃Dysphasia, dyspraxia
􀂃Subtle subcortical deficits
􀂃Levodopa induced confusion and poor verbal fluency should alert
It is a progressive neurodegenerative, autosomal dominant disorder with following features :
􀂃Chorea with insidious onset, gradual worsening
􀂃Deterioration in personality
􀂃Cognitive deficit
􀂃Psychiatric disturbance
􀂃Positive family history
􀂃It is rapidly progressive, fatal, spongiform encephalopathy.
􀂃Dementia with myoclonus
􀂃Pyramidal or extrapyramidal signs
􀂃Cerebellar signs
􀂃EEG shows brust suppression pattern
It is a chronic progressive adult occult hydrocephalus with
clinical features of dementia; gait apraxia; urinary incontinence.
A comprehensive laboratory workup must be performed when
evaluating a patient with dementia. The purposes of the workup are to
detect reversible causes of dementia and to provide the patient and
family with a definitive diagnosis. Magnetic resonance imaging (MRI) in some cases, have made the differentiation between AD and vascular
dementia somewhat more straightforward than in the past. Single Photen Emission Computed Tomography (SPECT) may help to detect
patterns of brain metabolism in various types of dementia, and it may
soon help in the clinical differential diagnosis of dementing illnesses.
Pseudodementia should be differentiated from dementia. Some major clinical features differentiating pseudodementia from Dementia are as follows :
Pseudodementia Dementia
Family always aware of dysfunction and its severity Family often unaware Onset can be dated with some precision Onset can be dated only within broad limits Symptoms of short duration before medical help is sought Symptoms usually of long duration before medical help is sought Rapid progression of symptoms after onset Slow progression throughout course H/O previous psychiatric dysfunction common
H/O previous psychiatric dysfunction unusual
Pseudodementia Dementia
Patients usually c/o cognitive loss c/o little cognitive loss
Detailed complaints Vague complaints
Patients emphasize disability Patients conceal disability
Patients highlight failures Patients delight in accomplishments
Loss of social skills often early andprominent
Social skills often retained
Behaviour often incongrvent with severity of cognitive dysfunction
Behaviour usually compatible with severity of cognitive dysfunction
Attention and concentration often
well preserved
Usually faulty
"Don't know" answers typical Near miss answers frequent Memory loss for recent and remote events usually severe
More severe
 Marked variability in performance on tasks of similar difficulty
Consistently poor performance on tasks of similar difficulty
The classic course of dementia is an onset in a patients 50s or
60s, with gradual deterioration over 5 to 10 years, leading eventually to death. The age of onset and the rapidity of deterioration vary among
different types of dementia and within individual diagnostic categories.
The mean survival expectation for patients with dementia of Alzheimer's type is approximately 8 years with a range of 1 to 20 years. Once dementia is diagnosed, patients must undergo a complete
medical and neurological workup, because 10 to 15% of all patients with dementia have a potentially reversible condition if treatment is initiated before permanent brain damage occurs. The most common course of dementia begins with a number of subtle signs that may, at first, be ignored by both the patient and the people closest to the patient. Although the symptoms of the early phase of dementia are subtle, the symptoms became conspicuous as the dementia progresses, and family members may then bring a patient to a physician's attention. In the terminal stages of dementia, patients became empty shells of their former selves – profoundly disoriented, incoherent, amnestic and incontinent of urine and faeces. With psychosocial and pharmacological treatments and possibly because of self healing properties of the brain, the symptoms of dementia may progress slowly for a time or may even recede somewhat. The regression symptoms is certainly a possibility in reversible dementias once treatment is initiated.
The severity and course of dementia can be affected by psychosocial factors. The greater a person's premorbid intelligence and education, that better the ability to compensate for intellectual deficits. Anxiety and depression may intensity and aggravate the symptoms. Pseudodementia occurs in depressed people who complain of impaired memory but are, in fact, suffering from a depressive disorder. When the depression is treated, the cognitive defects disappear.
The treatment of AD and related dementias is multimodal. It is guided by the stage of illness and is focussed on the specific symptoms manifested by the patient. This discussion begins with psychiatric management, the cornerstene of the treatment of the demented patient, and then goes on to review specific treatments, first the broad range of psychosocial interventions used with dementia and then the pharmacologic options organized by target symptom.
(A) Determining the site of treatment and frequency of visits.
(B) Psychiatric management, psychotherapy and other psychosocial
treatments :
(1) Establish and maintain an alliance with the patient and
(2) Perform a diagnostic evaluation and refer the patient for any needed general medical care.
(3) Assess and monitor psychiatric status.
(4) Monitor safety and intervene when required.
(5) Intervene to decrease the hazards of wandering.
(6) Advise the patient and family concerning driving and other activities that put other people at risk.
(7) Educate the patient and family regarding the illness and available treatments.
(8) Advise the family regarding sources of care and family support.
(9) Guide the family is financial and legal issues.
(C) Specific psychotherapies psychosocial treatments :
􀂧 Goals :
While these treatments differ in philosophy, focus and methods, they have the broadly overlapping goals of improving the quality of life and maximizing function in the context of existing deficits. Many have as an additional goal the improvement of cognitive skills, mood or behaviour.
􀀒 Types of psychotherapies / treatments and their efficacy :
(a) Behaviour - oriented approaches
(b) Emotion - oriented approaches
(c) Cognition - oriented approaches
(d) Stimulation - oriented approaches
(D) Somatic Treatments :
Consuming a low-fat, low-calorie diet may reduce the risk for AD. Higher intake of fatty, cold-water fish (such as tuna, salmon, and mackerel) has been associated with a lower risk of dementia.
This may be due to the high level of omega-3 fatty acids found in
such fish. Eating fish at least two to three times per week provides a healthy amount of omega-3 fatty acids.
Reducing intake of linoleic acid (found in margarine, butter, and
dairy products) may prevent cognitive decline.
Antioxidants, such as vitamins A, E, and C (found in darkly colored fruits and vegetables) may help prevent damage caused by free radicals.
Maintaining normal blood pressure levels may reduce the risk for
Hormone-replacement therapy in postmenopausal women may
decrease production of chemicals that cause AD, stimulate growth of brain cells, and improve blood flow in the brain. However, the role of hormones in the prevention of AD is still controversial.
Keeping mentally and socially active may help delay the onset or
slow the progression of AD.
More research is necessary, however, to determine how
effective these medications are in reducing the risk of the
Research indicates that the following lifestyle modifications may
help improve behavior in people with AD.
A supervised walking program with a caregiver or other reliable
companion may improve communication skills and diminish the
risk of wandering.
Bright light therapy may control insomnia and wandering.
Calming music may reduce wandering and restlessness, boost
brain chemicals, and improve behavior. Pet dogs can increase appropriate social behaviors.
Relaxation training and other exercises that require focused
attention (often used with refreshments as rewards) can improve
social interaction and the ability to perform tasks.
The Safe Return Program, implemented by the Alzheimer's Association, requires that a person with AD wear an identification bracelet.
Individuals with AD may also have particular dietary concerns. They may require: Extra calories due to increased physical activity and restless wandering. Supervised meals and assistance with feeding. People with AD often forget to eat and drink, and, as a result, often become dehydrated.
􀂴 Communication strategies :
􀁹Identify and correct visual or hearing deficits
􀁹Communicate one thought or idea at a time
􀁹Use written notes
􀁹Speak slowly
􀁹Avoid distracting noise
􀁹Use gestures
􀁹Provide reassurance
􀁹Consider speech therapy evaluation
􀂴 Feeding Strategies :
􀁹Feed in non-distracting environment
􀁹Add flavor and spices to meals
􀁹Avoid plates with confusing patterns
􀁹Allow eating with hands
􀁹Verbal reminders
􀁹Consider nutritional supplements
(1) AD prevention
(2) Research
(3) Diagnostic truth telling
(4) Advance planning
(5) Cognition enhancing drugs
(6) Preventive medications and restrictions
(7) Respectful caring
(8) Distributive justice
(9) Mere natural dying
A review of currently available treatment suggests a number of areas for further study. Several of these are in the realm of evaluation and assessment. Several points are to be noted.
(1) Better detection and evaluation of dementia, especially in the
prodremal and early stages, when treatment that slows
progression would be more likely to be beneficial.
(2) Earlier and more accurate detection of non-cognitive problems,
so as to facilitate optimal intervention.
(3) Better assessment of dangerous symptoms, especially impaired
driving ability.
(4) Development of a consensus on clinically meaningful outcome
measures, including neuropsychological testing, functional assessment, and 'hard' end points, such as institutionalization and mortality.
(5) Promising leads to be actively studied for patients with AD including additional cholinergic agents, further work of vitamin E1 and other antioxidants, NSAIDS and estrogen supplement.
(6) Efforts to prevent stroke and to decrease its destructive effect on
brain tissue which are particularly important avenues for dementia prevention.
(7) There is a critical need for randomized controlled studies of upto-
date treatments for psychosis, agitation, depression and sleep disturbance in dementia.
(8) Research is also needed to identify which patients will benefit
from alternative forms of living environments and supplemental care giving.
Ayurveda View
It can be said that Smritibhramsha is a disease of the mind developed due to provoked Vata. The above mentioned etiological factors have polymodal effect in the pathogenesis. Heena Satva, Rajas predominant Prakriti and the person whose mind is weakened by all the stressful conditions are more prone to develop Smritibhramsha. Again, as discussed earlier in the Nidana, the regular consumption of diet dominant in Tamas and Rajas Gunas increase the Tama and Rajo Doshas in the mind. The increased Rajas supports the Tamas to develop Smritibhramsha. Moreover, the Rajas diet depreciates the Dhriti (Su. Sh. 1/18). To control the functions of the Manas is the main function of Dhriti. The mind depreciated or lacking in Dhriti cannot restrain itself (Svasyanigraha) and yet indulges in excess thinking, looses confidence, fails to achieve the decided goal and thus the person lags behind. At the biological level, Vata, Pitta and Kapha are stated to represent predominantly of Rajasika, Satvika and Tamasika nature. Hence, the factors provocating the respective Doshas also provocate the respective Manodosha Viz. the provoked
Vata will vitiate the Rajo Dosha and the provoked Kapha will vitiate the Tamo Dosha of the mind.
Due to the etiological factors, Prana, Udana and Vyana Vayu are vitiated first. This provoked Vata goes in the Hridaya and dislodges the Avalambaka Kapha therein. This dislodged Kapha further obstructs the channel of the Prana, Udana and Vyana Vayus and again vitiates them. This is the condition of Kaphavritt Prana, Udana and Vyana. Thus, Vayu may get vitiated by its own etiological factors or by the obstruction due to Kapha. The vitiated Vata as well as many other etiological factors depreciate the Sadhakagni resulting in the impairment of its functions. The Sadhaka Pitta makes available the objects of senses intended for Buddhi. It is responsible for good Medha and Utsaha also. Hence its impairment results in the impairment of Medha and consequently in the impairment of its faculties like Dhi, Dhriti etc. The control of Buddhi and Manas are the functions of Prana. (As. S.. Su. 20/2). The vitiated Prana looses this control and causes Upaghata of these factors (A. Hr. Ni. 16/20).
Likewise, Kaphavritt Prana results in Sada, Tandra, Daurbalya, Aruchi and Chhardi occasionally. Dhi, Dhriti and Smriti and Manobodhana are the functions of Udana (A. S. Su. 20/2). Therefore in the vitiation of Udana, Dhi as well as Dhriti are hampered. The perception of knowledge and the understanding by the Manas are also hampered to some extent. (As. H. Ni. 16/22). Its obstruction due to Kapha (Kaphavritt Udana) also hampers its functions like Prayatna, Urja and Vakpravriti. This condition leads to loss of interest, loss of energy and low intended speech respectively. It also develops Aharsha, Mandagni, Aruchi and Vaivarnya (Ch. Chi. 28/224). The vitiated Vyana causes disturbances in the function of the Manas upto some extent (Chittopaplava) and loss of enthusiasm as well as loss of interest in work. Likewise, the Kaphavritt Vyana causes aches and pains in different parts of the body (Ca. Chi. 28/228). The vitiated Udana and Vyana affect the functions of Ojas resulting in Utsahabhramsha. The obstruction of the three Vayu together causes
psychomotor retardation. Thus, a vitiation of any of the three Vayus and Sadhakagni results in vitiation of Rajas and Tamas which again results in the disturbances in the functions of Buddhi, Dhriti and Manas which ultimately results in gradual Smritibhramsha. The disturbances in the functions of Buddhi cause indecisiveness and a feeling of worthlessness. The disturbances in the functions of Dhriti hampers the concentration and increases irritability. Similarly an impairment of the Dhriti along with Buddhi leads to excessive feeling of guilt. Likewise, the disturbances in the function of Manas causes excessive thinking, social withdrawal and self-centeredness. The Manas alongwith the Buddhi develops poverty of ideas. When the deranged Dhriti also joints these factors, it ultimately develops suicidal tendency. In a nut shell the vitiated Prana, Udana and Vyana,
Sadhakapitta, Avalambaka and Tarpakakapha and Rajas and Tamo
Doshas are regarded as the factors involved in the pathogenesis of
Smritibhramsha and all the symptoms are produced due to these

Kala, Satvabala, Rasakshaya-due to Atichintana (Ca. Vi. 5)
Prakrti, Beeja dusti Majjakshaya - due to injury, Triggering Viruddha Ahara, Pragnyaparadha factors Vatakara Ahara-Vihara
Manodosha (Rajas & Tamas) Manovaha Psychic Srotodusti phase
↑Vata (Prana, Udana, Vyana) Primary memory impairment(Ca. Sha.1) and other psychic symptoms Affect Sharirik Dosha Kaphakshaya Pitta
Psycho Neurotic phase
Satva Guna
Mana, Buddhi, Gyana, Smriti, Ahara, Bhakti, Chesta, Shila Vibhrama
Ojokshaya (As. Hri. 12) Psycho Somatic phase Srotas and Dhatus get involved Dhatukshaya, Smritibhramsha and other cognitive manifestations.

Dosha :
 Mano Dosha: Rajas and Tamas
Sharirika Dosha : Vata : Prana, Udana, Vyana
Pitta : Sadhaka
Kapha : Tarpaka
Dushya : Rasa, Rakta, Majja
Srotas : Manovaha, Rasavaha, Majjavaha
Agni : Manda, Vishama
Udbhava Sthana : Manas
Adhisthana : Sirohridaya
Vyaktisthana : Manas, Sarva Sarira, Indriya
Purvarupa : Alpa Vyakta laksana
Rupa : Udvega, Smritihrasa, Kampa, Bhaya etc.
Upashaya : Dhairya, Ashvasana, Medhya and Rasayana dravyas
Anupshaya : Klesa
Arista Lakshana : Sarva Sampurna Lakshana and chronicity
Sandhya Sadhyatva : Kricchrasadhya / Yapya / Asadhya depending
on Severity and chronicity
Upadrava : Can produce several psychosomatic symptoms and diseases.
Rogamarga : Madhyama

The symptom complex of Smritbhramsha may comprise both somatic and psychological symptoms. Hridaya is the Asraya of Manas. Along with Hridaya, the other Ashrayi of Hridaya viz. Prana, Udana, Vyana Vayu, Sadhaka Pitta and Avalambaka Kapha gets vitiated leading to vitiation of Sarira Dhatu, Mala and Srotamsi. The symptoms of Smritibhramsha are related to mind also. They are Krodha, Udvega, Moha, Chinta, Bhaya etc. Some of the psychological symptoms like Asahishnuta (irritability), Vishada (depression), Bhaya etc. will manifest early. When the disease runs for a chronic course, the above symptoms may get clustered together and other physical and mental disorders may manifest. The factors which disturb the Vatadosha especially the Prana, Vyana and Udana are the causative fctors of Smritibhramsha as per correlated references of Manobhramsha, Dhi, Visada, Cittoplava which are quoted in As.H.Ni. 15/23. Here, an attempt has been made to correlate the relevant Ayurvedic symptoms with the modern symptoms of dementia. Further, an effort has been made to deduct these symptoms according to the Samanyaja and Nanatmaja Doshic diseases. It is assumed that these Ayurvedic terms regarding the symptoms play a major role in the Vyakta Lakshanas of Smritibhramsha.

Psychic Symptoms Somatic Symptoms Samanyaja :
Apraharsha (Gloomy) Su. Su. 15/9
Kampa (Tremor) A. H. Su. 11/6
Cittopaplava (Disturbed Sensorium) A. H. Ni. 16/24
Bhramsha (Loss of Libido) A. H. Ni. 16/24
Manobhramsha (Deorganisation) A. H. Ni. 16/23
Vakparusata (Hoarseness of voice) Su. Su. 15/14.
Pralap (Delirium) Ca. Su. 12/8
Soka (Melancholy) Ca. Su. 12/8
Utsaha Bhramsha (Loss of interest) A. H. Ni. 16/24
Nanatmaja :
Atipralapa (Delirium) Ca. Su. 20/11
Asabda Sravanam (Auditory Hallucinations) Ca. Su. 20/11
Bharma (Giddiness) Ca. Su. 20/11
Mukhasosa (Dryness of Mouth) Ca. Su. 20/11
Visada (Asthenia / Depression) Ca. Su. 20/11
Vepathu (Trembling) Ca. Su. 20/11
Psychic Symptoms Somatic Symptoms
Samanyaja :
Alpanidrata (Disturbed sleep) Su. Su. 15/14
Angamarda (Malaise) Ca. Su. 20/11
Amarsa (Intolerance) Ca. Chi. 9/12
Bhaya (Phobia) Ca. Su. 12/11
Krodha (Anger) Ca. Su. 12/11
Moha (Bewilderment) Ca. Su. 12/11
Nanatmaja :
Atripti (Dissatisfaction) Ca. Su. 20/14
Kapha Prakopa :
Psychic Symptoms Somatic Symptoms
Nanatmaja :
Alasya (Laziness) Ca. Su. 20/17
Apakti (Indigestion) Ca. Su. 20/11
Staimitya (Tiredness) Cu. Su. 20/17
Svetavabhasata (Pallor) Ca. Su. 20/11
Ojo Kshaya (Primary Stage)
Abhiksnam Dhyanam (Excessive Worry) A. Hr. Su. 11
Vyathitendriyatvam (Lack of pleasure) A. Hr. Su. 11
Durmana (Loss of Interest) A. Hr. Su. 11
Bibheti (Fearful anticipation) A. Hr. Su. 11
From the above, it is clear that majority of the symptoms are related to Vata Dosha. Hence, coming to a conclusion it can be suggested that these correlated symptoms of dementia might be those of Smritibhramsha, but since its incidence rates in ancient times might be low, the importance for its detailed description and treatment methods would not have been found essential by our Acharyas.

As Smritibhramsha occurs mainly due to old age and due to impairment of Buddhi. management by Rasayana drugs would be the
appropriate line of treatment. Furthermore, prior to Rasayana therapy,
Panchakarma is very essential for Deha Shuddhi. Also, as Smritibhramsha can be considered as an Urdhwajatrugata Vikara, Nasya Karma can be performed. Hence, the line of treatment comprises of Nasya and administration of Rasayana and Medhya drugs orally.
Charaka has classified all the drugs into the following 3 groups :
(1) Dosha Prashamana means that which pacifies the vitiated Doshas
(2) Dhatu Pradushana means that which vitiate Dhatus
(3) Svasthavritta means that which maintains the health.
Rasayana and Vajikarana may be classified under Svasthavritta.
Rasayana is concerned with the promotion of physical and mental
The different definitions of Rasayana given in the Ayurvedic texts are as follows :
(1) According to Charaka, Rasayana is a mean by which one gets
Rasa, Rakta etc Dhatu of optimum quality (Ca. Chi. 11/8).
(2) Sushruta, while defining the scope of Rasayana Tantra mentions
that the therapy which establishes the age (Vayasthapana),vincreases the life span (Ayushkaram), intelligence (Medha) and strength (Bala) and enables one to prevent the diseases (Rogapaharanam Smartham) is known as Rasayana (Su. Su.1/16).
Dalhana while commenting on the above definition of Sushruta gives two meanings of Vayasthapana. First meaning is enabling a person to live his normal span of life. For second meaning Dalhana quotes some other authority according to which Rasayana prevents the Jara, so that young age is established for a longer period. Ayushkaram means increasing the span of life (Su. Su. 1/15).
(3) Vagbhata has given the definition of Rasayana which is similar to that of Charaka Samhita (As. H. Utt. 39/1).
(4) According to Sharngdhara, the drug which alleviates aging and prevents disease is known as Rasayana (Sha. Pu. 4/14).
(5) Bhavaprakasha has defined Rasayana as the therapy which  alleviates Vyadhi and Jara and retard aging (Vayastambhakara) and (Chakshushyam, Brimhana and Vrishya have been included under it. (Bha. Utt. 79/1).
(6) Dalhana has described two types of definition as follows :
(i) Rasayana is a theapy which provides nourishment to Rasa, Rakta etc. Dhatu.
(ii) Rasayana is a way by which the Rasa, Virya, Vipaka and Prabhava of the used drug provides Ayu, Bala, Virya and firmness and causes prevention of aging (Su. Chi. 27/1).

Since the action of Rasayana is in the whole body, changes occurs at both, physical and mental level. So these two changes should be considered separately.
(1) Improvement in mental qualities :
Charaka mentions that Rasayana improves intelligence, power of recollection, power of sense organs and perfection in speech. Moreover, Medhya Rasayana can specially act on Medha as it can cause improvement in mental capacity.
(2) Improvement in the physical qualities:
Rasayana also helps to regain youthfulness, longevity, strength, complexion, voice etc and cures excess sleep, fatigue and intolerance. Rasayana is Tridosha Shamaka, Agni Deepana and helps in the proper formation of bodily tissues (Ca. Chi. 1/ii/3).
:Rasayana by its action, removes the impurities (Malas) located in the tissue elements (Dhatus) causing the enhancement of Agni in each Dhatu. Enhanced Agni causes restoration of respective Dhatus in quality and their improved quality leads to perfect health and longevity
in the human being. There are mainly two opinions regarding the mode of action of Rasayana which are as follows :
Controlling the formation of tissue elements (Dhatupaka) by Rasayana and by removing the vitiation from different channels.
(1) Tissue formation :
The body is maintained by the continuous process of destruction of old elements and formation of new elements. This process mainly depends upon the amount of food one takes and the condition of Agni
of each tissue elements (Dhatus). Role of Agni is very important as the
bodily elements get deteriorated when the Agni is increased. During
the old age, this destructive process is very rapid, even if the subject
takes enough food leading to weakness of the body. At such a stage, if
a Rasayana drug is used, it controls the Dhatupaka. Thus, Rasayana
maintains the proper Dhatupaka and brings back the lost vitality of the body.
(2) Removing vitiation from different channels:
Two functions are attributed to Srotas :
(i) Absorbed food materials are carried to the site of metabolism
through Srotas.
(ii) Ejection of waste products resulted due to the process of
Through the two functions, Srotas play an important role in maintaining the proper health of the body, when it is not afflicted by vitiated Doshas (Ch. Vi. 5/7). In the process of Samprapti, aggravated Doshas are circulated in the body and produce the disease. When it gets obstructed by a vitiated Srotas (Viguna Srotas), then such an obstruction is also responsible for lowering the resistance power of the
body which leads to the improper formation of tissue elements and weakens the body. So in any disease, Srotovaigunya is common. Treatment should be done to remove this Srotovajgunya. This can be achieved by administering Rasayana therapy. The term 'Rasayana' itself indicates that it is a substance which helps in the free  circulation of Rasa through its channels without any obstruction i.e. Rasa + Ayana. Ayana here means Marga i.e. pathway. So it can be seen that Rasayana is doing a dual role in removing the obstructions in the pathways (Srotovaigunya) and taking the nutrient materials to the respected Dhatus leading to the regaining of the lost resistance power of the body. Strength, colour and longevity of the body can also be achieved by Rasayana, Charaka says that there are 3 main factors necessary to bring back the strength, colour etc. which are lost through the catabolic activities of the body. These are the equilibrium of Agni of Dhatu, Vayu and Srotas respectively (Ch. Su. 28/3). Charaka considers 8 factors responsible for the process of digestion and metabolism. There Vayu is also considered as a main factor. Rasayana has got the capacity to control Vayu. Hence, Rasayana therapy is also being prescribed specially in Vatika type of disorders.
Medha is a board term which comprises of all the three mental faculties i.e. Dhee, Dhriti and Smriti which are again interrelated with
each other and acordingly the Medha can be subdivided into the following faculties :
(1) Grahanshakti (Power of Grasping);
(2)Dharanashakti (Power of Retension);
(3) Vivekashakti (Power of Discrimination)
(4) Smriti (Power of recollection)
Medhya drugs have a definite role in the treatment of psychiatric and psychosomatic diseases, where chief aim of the treatment is to achieve a sedation, tranquility or a stimulation of the activities of the brain. Modern researches conducted so far on the Medhya drugs indicate that these drugs have varying degree of psychotropic action. Many drugs have been screened for antidepressant, sedative and tranquilizing effects both experimentally and clinically and have shown encouraging results. Hence it can be concluded that the Medhya Rasayana of Ayurveda has a broad concept having direct action of psychological functioning and they are beneficial in the promotion of the Medha.
The ancient scholars of Ayurveda have considered 'Nasa' as the passage to the head i.e. cranial organs. The drug given through nose  as Nasya, reaches the brain and eleminates only the morbid Doshas responsible for producing the diseases (Ca. Si. 2/22) Vagbhata, further clarifying the mode of action of Nasyakarma mentions that the drug administered in the nose, reaches Murdha (Brain) through Shringataka Marma and eleminates the morbid Doshas quickly through the Shriomukhani (Veins) of eye, ear, throat etc. (As. S. Su. 29/2). Sushruta has clarified Shringataka Marma as a Sira Marma formed by the union of Siras (blood vessels) which supplies the nose, ear and tongue. Further, he has pointed out that injury to this Marma will be fatal immediately. (Su. Sha. 6/27). Commenting on Ashtanga Samgraha, Indu has opined Shringataka as the inner side of middle part of the head. (Shiraso Antarmadhyam). After the drug spreads in the Murdha, it scrapes out the morbid Dosha like a sharp instrument and expels them out through the nose. The action of Nasya Karma can be understood in the following manner.
(1) Through the blood circulation
(2) Through the lymphatic channels including C.S.F.
(3) Through the neuroendocrinal and neurovascular stimulation.
Absorption of many drugs through the nasal mucosa is a well-established fact. Many drugs including hormones are administered through the nose for their effective therapeutic results. However, these drugs are believed to be rapidly absorbed through the mucous membrane and enter into the general blood circulation of the body. Specific circulation may probably be involved for which, the posturing
of the patient may be important. This includes the entry of the drugs absorbed into the facial vein, through which the back flow of the blood
occurs through the inferior opthalmic vein and to the venous sinuses of the brain.
The lipid soluble substances can easily and rapidly be transported across the epithelial membrane e.g. Taila, Kshara, Ghrita,
etc. These lipid soluble substances can also gain an assess into the lymphoid tissue. Thus, a rapid circulation through the lymphatic channels denotes a positive phenomenon. On the other hand, the  extended arachnoid sheath from the brain to the submucosal area ofthe nose is the other path for the absorption of drugs directly through the nose.
The stimulation of the olfactory system during the course of Nasya Karma is other possibility. The olfactory nerve functions by means of chemoreceptors. The chemical characteristic of the particle, that has reached into the nose will be identified by the nerves which carry the stimuli to the olfactory bulbs. Further, the stimuli will be carried to the high centres, probably involving the hippocampus, limbic system, hypothatamus, etc. there, the drug absorption deeper into the tissues will not be required. Nasya Karma, performed through the nasal drug delivery may influence certain enzymes and hormones in the body.
Charaka mentions that one who practices systemic Nasya at the proper time will keep his sight, smell and hearing unimpaired, his beard and hair will not turn grey or twanny, rigidity of neck, headache, facial paralysis, trismus, rhinitis, hemicrania and tremors will be alleviated. The vessels, joints, sinuses of his cranium will be well nourished by Nasya and will acquire great strength. The face will become cheerful and plump, the voice will become mellow, firm and stentorian, all the sense organs will be clarified and greatly strengthened. There will be no sudden invasion of disease occurring in
the upper parts (Urdhwajatrugata) of the body and though the man is aging, the effects of senility will be retarded. (Ch. Su. 5/57-60.)

A. Hr. = Astanga Hrdya
A.S. = Astanga Samgraha
Cha. Ka. = Caraka Kalpasthana
Cha.Chi. = Caraka Cikitsasthana
Cha. Su. = Caraka Sutrasthana
Cha. Vi. = Caraka Vimanasthana
Su. Sh. = Sushrut  Sharirsthan
 Su.Chi = Sushrut Chikitsasthan