Dementia

Reduction in the intellect (dementia) can be acquired (dementia) or as consequence of the mental
underdevelopment (oligophrenia), caused by the brain lesion of in perinatal period (perinatal encephalopathy)
or early childhood (to the formation of intellect). Dementia considerably more frequently appears in elderly and
senile age, its prevalence among the people of older than 65 years is 5-10%.
Dementia - loss previously the acquired intellectual abilities, is manifested by the defects of thinking, memory,
attention, speech, gnosis, praxis and leading to the everyday and social dysadaptation. In mild degree of
dementia, patient is capable to attend itself; however, in severe degree, they need a constant outsider care and
watch. Diagnosis is based on clinical data, in which large significance with results of a neuropsychological
investigation.
In examination of patient with suspected dementia, detailed analysis of the history of disease is very important.
The purpose of the somatic examination is to reveal the diseases and states, which can cause dementia. In the
cases of the organic damage of the brain, neurological investigation, besides for cognitive disorders, makes it
possible to reveal the symptoms of the focus of brain lesion (paresis, ataxia, sensory disorder, coordination and
others), which indicate the localization of lesion. An investigation of mental status can reveal depression and
other mental disorders in patients with dementia.
In the majority of cases, symptoms of dementia manifest gradually. At first, symptoms are frequently easily
expressed as forgetting of the names and objects. Reduction in the mental activity, certain decrease of initiative,
decrease circle of interests and unwillingness to communicate with public can be noted. Patient himself begins
having difficulties to count, to conduct professional activity and financial matters, domestic housework. In some
cases, tearfulness and irritability, flashes of anger are noted. All components of intellect are gradually disrupted,
memory especially suffers; speech, reading, letter, gnosis and praxis are disrupted; patient forgets the names of
well-known objects, it is complicated to him to correctly construct sentences; therefore he uses stereotype
phrases. More severe patient needs outside aid to fulfill not only certain works, but also elementary self-care.
Patient begin having difficulties to walk in late stages, he prefers to sit without doing anything, and then to lie
down. Later, patient it becomes riveted to bed and death begins from concomitant somatic or infectious
diseases.
Timely diagnostics of dementia and pre-dementia stages of cognitive disorders gives us the possibility to stop or
to slow down the heavy incurable disturbances of intellect.

Reasons of disturbances of higher cerebral functions and their treatment

Acute development of aphasia and disturbances of others highest psychological functions (apraxia, agnosia and
other) more frequently is caused by stroke or craniocerebral injury, while its gradual development maybe caused by
degenerative disease (such as Alzheimer, Dementia with Lewy bodies (DLB) and others), cerebrovascular disease,
tumor of brain, chronic exogenous intoxication (alcoholism, narcotics use), encephalopathy in HIV- infection or
other illnesses.
Treatment is directed toward the therapy of basic disease, if this is possible, and the elimination basic symptoms
and syndromes (symptomatic therapy). In aphasia, it is necessary to do logopedic classes, which should be begun
how it is possible faster and to continue with need long time. The social and family adaptation has great significance,
which allows patient even with the rough degree of vocal disturbances completely itself to attend and even to conduct
the active means of life.
Most common reason for dementia, which constitutes half of all the cases is Alzheimer's disease and others
degenerative disease (Dementia with Lewy bodies). About 10-15% dementia cases are caused by cerebrovascular
diseases, and 10-20% more cases are caused by their combination with Alzheimer's disease. Dementia is developed
also with other neurologic illnesses: craniocerebral injury, brain tumor, Parkinsonism, multiple sclerosis, herpetic
encephalitis, epilepsy, encephalopathy with the HIV- infection, neurosyphilis and others. Dementia can appear in
hereditary diseases, depression (pseudo-dementia), intake of the medicinal drugs (anti-psychotics, tranquilizers,
hypnotics, anticholinergic and antispileptics), alcoholism and other intoxications, metabolic disturbances
(hypoglycaemia, hypothyroidism, deficiency of vitamins B, and B12, hypoparathyroidism, liver disease).

Practically, it is very importantly that in circumstance that 10-15% of dementia recovers completely or partially.
these dementia, which developed as a result of medicine-induced intoxication, depressions, metabolic
disturbance, caused by the somatic disorders and sometimes by other reason (for example, by brain tumor or
chronic subdural hematoma, which can be removed surgically). Earliest diagnostics of dementia is extremely desirable.
In reversible form of dementia, makes it is possible begin timely treatment, in the case of the irreversible form, larger
effectiveness if pathogenetic and symptomatic therapy are carried out, and to organize medical and social aid.

In Alzheimer's disease, anticholinesterases (rivastigmine, galantamine and others), acatinol and memantin are
used. In vascular dementia, besides the use of these drugs, treatment is directed toward the prevention of
progression of cerebrovascular disease, (reaching the optimum level of arterial pressure, anti-aggregant, if
indicated - anticoagulants, statins). In case with dysmetabolic disturbances and the intoxications, it is indicated to
eliminate them. In the quality of preparations, to increase cognitive functions, at the early stage of dementia it is
possible to use Piracetam (nootropil), vinpocetin (Cavinton), Cerebrolizin, tanakan, pentoxiphillin and other.
Improvement of cognitive abilities can be achieved by systematic exercises and training of memory and
attention, active participation of patients in the daily life of family, support of the existing daily habits.

The reasons for the acute development of amnesia are craniocerebral injury, stroke, encephalitis, hypoglycaemia,
metabolic encephalopathy, acute alcoholism, or other intoxication. Transient amnesia can be due to epilepsy,
migraine, transitory ischemic attack (transitory global amnesia). Korsakov syndrome most often is caused by chronic
alcoholism. Other reasons are stroke, injury, tumor and hypoxic encephalopathy with the lesion of hypocampus.
Progressive amnesia more frequently appears in Alzheimer disease or vascular dementia, being combined
usually with the disturbance of speech, and reduction of intellect.

The treatment of memory disturbances is directed to basic disease, if it is possible. It is possible to recommend
neuropsychological training, to correct of memory disturbances in the daily life of patient, and also drugs, which
improve the memory: akatinola of memantin, Piracetam (nootropil), vinpotsetin (Cavinton), cerebrolizin,
tanakan, pentoxipillin and other

Degenerative disease of the brain causing dementia

Alzheimer ’s disease
Alzheimer Disease is the most frequent degenerative diseases of brain, which lead to dementia. Disease appears
predominantly in the elderly and old age. Alzheimer's disease is encountered in 5% of people older than 60 year old and in
20% people older than 85 years. The disease is encountered more frequently among the women than in men.

Pathogenesis. The etiology of disease is not known, in 15% of the cases, it is hereditary. In the present time,
several genetic versions of Alzheimer disease are established, and they are connected with the anomaly of
chromosome 14 or, rarely chromosomes 1, 19 and 21.

Atrophic process develops in greatest degree in the associative zones of temporal, occipital and frontal portion. In the
pathogenesis of disease, its important role is assigned to reduction in the activity of cholinoacetyltransferase and
content of acetylcholine in the hippocampus and neocortex. In pathomorphological investigation, besides the loss of
neurons, they reveal the deposit of amyloid in the senile plague and in many preserved neurons thinning and
densifying of neurofibrillary structures (neurofibrilary depositon/tangle), which contain that pathologically changed
protein - tau-protein. Deposit of amyloid in the senile plague and neurofibrillary deposits in the neurons of brain
are revealed in insignificant quantity in all elderly persons; however, these changes they do not achieve this large
prevalence as with Alzheimer disease.
Clinical picture. Disease is developed unnoticeably, most frequently observed as disturbance of memory,
predominantly short-term (on the events of previous day). The aggravation of this defect leads to decrease of
memorization, forgetting names of close people, titles of objects and events of past years. Speech is hesitated,
difficulties in selection of words, understanding speech becomes slow, frequently appear errors in calculation;
disrupted visual three-dimensional orientation; therefore the patients they can easily stray in the unknown places. They
[percept read idea with diffuculty, loss of previously acquired habits (apraxia), behavior it becomes cliché and
stereotypic. Preservation of some professional habits can allow patients to have some time to work, in spite of
noticeable manifestations of disease. Frequently they have instable mood, irritability, episodes of the psycho-motor
excitation; and considerably less frequent - psychotic disturbance (delirium and hallucination).

Approximately in 25% of patients, stroke appears, which leads to exaggeration of symptoms, and in some cases
it allows for the first time with the detailed investigation of the highest mental functions in the patient with
stroke to suspect the combination of Alzheimer disease (mixed nature of dementia).

In the late stages of disease, patient loses the capability of reading, writing, calculating, marked disturbed
speech, patients lose capability of elementary self-care, control of urination and defecation, they are disoriented
in place and time, they are in need a constant care. Patients have symptoms of oral automatism; grasp and
suckling reflexes, gait changes as result of the shortening of step, moderate rigidity and deceleration of motions.
However, towards the final stages of disease, patient preserves arbitrary motions in the extremities, sensory,
hearing, fields of view, motion of eyes and other functions of the brain stem and cranial nerves. In the final
stage, patient is apathetic; patient sits or motionlessly lies at the bed. The duration of disease on the average is
about 5-10 years, death more frequently begins due to combination of infectious or complication of somatic
diseases (pneumonia, heart insufficiency, kidney deficiency and other).

Diagnosis is based on the typical clinical picture, the exception of other reasons for dementia (cerebrovascular
diseases, brain tumor, craniocerebral injury, hypovitaminosis B1, insufficiency of folic acid, depression and
others), the gradual development of disease and its constant progression. MRI and CT of head reveal atrophic
changes in the temporal, occipital and frontal portions of brain, most explicit in the medial divisions of temporal
portions, which make it possible to exclude many other illnesses (vascular lesion of brain, tumor, and subdural
hematoma). Electroencephalogram is used only in the last stages of disease to show the diffuse slow activity
(theta θ and delta δ-wave).
When examining patients with suspected Alzheimer's disease, it is important to exclude curable reasons for
dementia (subdural hematoma, depression, encephalopathy with some somatic illnesses and others).

Treatment. In the present time, the most effective one are preparations of cholinomimetic action - inhibitors of
cholinoacetyltransferase (rivastigmine 1-12mg/day, galanthamine 5-30 mg/day) and acatinola memoitin (blocker
of glutamatergic receptors) 20 mg/day, to improve the state of patient and to slow down the progression of
disease. Other preparations with certain positive actions can also be used (nimodipine 90-120 mg/day,
selegeline 5-10 mg/day, tanakan 120-160 mg/day, cerebrolysine 20-30 ml/day, gidergin 6-9 mg/day).
In the case that need the use of neuroleptics (in case of delirium, hallucinations, psycho-motor excitation) and
antidepressants, preparations used should not be with expressed cholinolytic properties (Haloperidol,
nortryptiline). In patient with increased anxiety and sleep disturbance, the usage of barbiturates is undesirable,
if indicated is possible to use small doses of benzodiazepine (Diazepam , etc) and drugs to treat insomnia
(Imovan, Ivadal). If possible, it is necessary to stimulate to the feasible dailyand social activity, to avoid
premature and prolonged hospitalization.

Dementia with Lewy Bodies

In the present time, Dementia with Lewy bodies the second common according to frequency (after Alzheimer's
disease) degenerative disease, which leads to dementia.
Pathogenesis. Diffuse cerebral atrophy with the predominance in the temporal, occipital and frontal portions is
noted. In the preserved neurons reveal special inclusions (Levi's corpuscle) and rarely amyloid plaque and the
neurofibrillary tangle, which is characteristic for Alzheimer's disease.

Clinical picture and diagnosis. At the initial stages frequently are noted the same symptoms as with the
Alzheimer disease. The distinctive special feature of disease includes prominent fluctuations of behavior and
thinking: irregular augmentation of confusion, hallucination and paranoiac mania. Characteristically gradual
connection of Parkinsonism symptoms: hypokinesia, rigidity and tremor. The manifestations of Parkinsonism can
be seen as different degree of expression, sometimes they are the first symptoms of disease. In some patients
the symptoms of orthostatic hypotension are revealed: vertigo and instability with rapid getting up or prolonged
stay in the vertical position. In proportion to the progression of disease appear the similar disturbances of the
highest mental functions, that also with Alzheimer's disease: amnesia, aphasia, acalculia, visual- three-
dimensional disorientation, apraxia and agnosia. Hallucinations, predominantly visual, are the distinguishing
feature of disease.

Diagnosis is based on the clinical picture and the results CT or MRI of the heads, which reveal diffuse atrophic
process, in the brain and excluding other possible reasons for dementia. Differential diagnosis with Alzheimer's
disease frequently causes complexities.
Treatment is as Alzheimer's disease. Symptoms of Parkinsonism at the early stages of disease can be effective
using preparations such as levodopa (Madopar, Nakom) at the small doses.

Frontal-temporal dementia (Pick’s Disease)

Pathogenesis. In most cases, it is noted as autosomal dominant type of inheritance, the remaining cases -
sporadic. In frontotemporal dementia, the atrophy of frontal and temporal portions is more expressed than in
Alzheimer's disease. The loss of neurons is combined with the presence of the swelling in the preserved neurons
and inclusions (Pick’s bodies) in cytoplasm. In some cases, neurofibrilary deposits, which consist of tau τ-protein
is seen in the neurons.

Clinical picture and diagnosis. Disease is manifested by the increasing apathy, reduction in the mental and
motor activity, presence of symptoms of oral automatism, seizing and sucking reflexes (lesion of frontal portion)
or by progressive disturbance of speech (lesion of temporal portion). There can be the manifestations of
behavioral disinhibition, euphoria.
Diagnosis is based on clinical data, family anamnesis of disease, presence of expressed atrophy in frontal and
temporal portion in CT or MR.

Treatment symptomatic, as with Alzheimer's disease, but it is less effective.

Brief information about the degenerative disease, which are manifested by dementia

Alzheimer Disease Dementia with Lewy Bodies Frontal -Temporal dementia

Clinical Dementia with progressive
picture amnesia and accompanied
by aphasia, agnosia, apraxia
and disorders others higher
mental functions
CT or MRI Atrophy of temporal and
of head occipital portion
Diagnosis It is based on clinical picture, absence of another reason for dementia according to clinical data,
CT and MRI of head
Progressive dementia as Progressive dementia in
Alzheimer disease, confused combination with apathy,
state, hallucination and reduction of mental and motor
paranoiac mania, activity, progressive disturbance of
parkinsonism symptoms possiblities of speech
Expressed atrophy in frontal and
Diffuse cerebral atrophy
temporal portion