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 and delta -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- threedimensional 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 -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 Clinical picture Dementia with progressive amnesia and accompanied by aphasia, agnosia, apraxia and disorders others higher mental functions Dementia with Lewy Bodies Progressive dementia as Alzheimer disease, confused state, hallucination and paranoiac mania, parkinsonism symptoms Diffuse cerebral atrophy Frontal -Temporal dementia Progressive dementia in combination with apathy, reduction of mental and motor activity, progressive disturbance of possiblities of speech Expressed atrophy in frontal and temporal portion

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

Sign up to vote on this title
UsefulNot useful