Parkinson’s Disease

What is Parkinson’s Disease?

The disease was first described by an English doctor, James Parkinson, who called it a trembling paralysis. In 1877, Jean-Martin Charcot supplemented the clinical characteristics of the disease. The disease occurs in 60–140 per 100,000 population; its frequency increases dramatically with age. According to statistics, shivering paralysis occurs in 1% of the population under 60 years old and in 5% of older people. Men get sick more often than women.

Causes of Parkinson’s Disease

Clinical manifestations of trembling paralysis and parkinsonism syndrome result from acute and chronic infections of the nervous system (epidemic encephalitis Economo, tick-borne, viral and other types of encephalitis). The causes of the disease are cerebral atherosclerosis, vascular diseases of the brain, tumors, injuries of the nervous system, long-term use of drugs of the phenothiazine series (aminazin, triftazin), rauwolfia derivatives, methyldof — drug parkinsonism. Parkinsonism can develop with acute or chronic intoxication with carbon monoxide and manganese. In the occurrence of akinetic-rigid syndrome, hereditary impaired catecholamine metabolism in the brain or the inadequacy of the enzyme systems that control this metabolism can be important. Often revealed the familial nature of the disease in an autosomal dominant mode of inheritance. Such cases are attributed to Parkinson’s disease. Various exo– and endogenous factors (atherosclerosis, infections, intoxication, injuries) contribute to the manifestation of genuinic defects in the mechanisms of the exchange of catecholamines in the subcortical nuclei and the occurrence of the disease.

Pathogenesis during Parkinson’s Disease

The main pathogenetic link of trembling paralysis and Parkinson’s syndrome is a metabolic catecholamine (dopamine, noradrenaline) in the extrapyramidal system. Dopamine performs an independent mediator function in the implementation of motor acts. Normally, the concentration of dopamine in the basal nodes is many times higher than its content in other structures of the nervous system. Acetylcholine is a mediator of excitation between the striatum, the pale ball and the black substance. Dopamine is its antagonist, acting inhibitingly. With the defeat of the black substance and the pale ball decreases the level of dopamine in the caudate nucleus and the shell, the ratio between dopamine and noradrenaline is disturbed, a disorder of the functions of the extrapyramidal system occurs. Normally, impulsation is modulated in the direction of suppressing the caudate nucleus, the shell, the black substance, and stimulation of the pale ball. When the black substance function is turned off, a blockade of impulses from the extrapyramidal zones of the cerebral cortex and striatum to the front horns of the spinal cord occurs. At the same time, pathological impulses come from the pale ball and the black substance to the cells of the front horns. As a result, the circulation of impulses in the system of alpha and gamma motoneurons of the spinal cord with a predominance of alpha activity increases, which leads to the appearance of pallidarno-nigral rigidity of muscle fibers and tremor.

Symptoms of Parkinson’s Disease

The main clinical syndrome is akinetic-rigid or hypertonic-hypokinetic. Hypo- and akinesia are characteristic of trembling paralysis and parkinsonism. A kind of flexion pose appears: the head and torso are bent forward, the arms are semi-bent at the elbow, wrist and phalangeal joints, often tightly attached to the lateral surfaces of the chest, torso, and the legs are bent at the knee joints. Poor facial expressions. The rate of voluntary movements with the development of the disease gradually slows down, sometimes quite immobilized quite early. Gait is characterized by small shuffling steps. Often there is a tendency to involuntarily run ahead (propulsions). If you push the patient forward, he runs so as not to fall, as if “catching up with his center of gravity.” Often tolcho to the chest leads to running back (retropulsions), to the side (laterpulsion). These movements are also observed when trying to sit down, stand, tilt the head back. Often with a pronounced syndrome, the posture of the patient resembles cataleptic. Akinesis and plastic hypertension are particularly pronounced in the muscles of the face, chewing and occipital muscles, muscles of the limbs. When walking there are no friendly movements of the hands (achaeurokinesis). Speech is quiet, monotonous, without modulations, with a tendency to fade out at the end of a phrase.

During the passive movement of the limb, a kind of muscular resistance is observed due to an increase in the tone of the antagonist muscles, the phenomenon of a “gear wheel” (the impression arises that the articular surface consists of the coupling of two gear wheels). Increasing the tone of the antagonist muscles during passive movements can be determined by the following method: if you raise the head lying, and then abruptly release the hand, the head will not fall on the pillow, and will fall relatively smoothly. Sometimes the head in the supine position is somewhat elevated – the phenomenon of the “imaginary pillow”.

Tremor is a characteristic, though not mandatory, symptom for Parkinson’s syndrome. It is a rhythmic, regular, involuntary trembling of the limbs, facial muscles, head, lower jaw, tongue, more pronounced at rest, diminishing with active movements. The oscillation frequency is 4–8 per second. Fingers are sometimes marked as “rolling pills”, “coin counting”. Tremor increases with excitement, almost disappears in sleep.

Mental disorders are manifested by the loss of initiative, activity, narrowing of horizons and interests, a sharp decrease in various emotional reactions and affects, as well as a certain surface and slowness of thinking (bradyfrenia). Bradypsychia is observed – difficult active switching from one thought to another, Akairia – stickiness, viscosity, egocentrism. Other paralysis. There are sleep disorders, respiratory dyskinesias with bouts of yawning, coughing, adiposogenital disorders, vegetative paroxysms. Post-traumatic parkinsonism can be reliably diagnosed in young and middle-aged patients. The disease develops after a severe, sometimes repeated traumatic brain injury. For post-traumatic parkinsonism, anteropathy, gaze cramps, disorders of chewing, swallowing, breathing, cataleptoid phenomena are not typical. At the same time, vestibular disorders, impaired intelligence and memory, visual hallucinations (due to damage of the cerebral cortex) are common. Often marked regredient course or stabilization of the pathological process. For the diagnosis of manganese parkinsonism are important history (information about working in contact with manganese or its oxides), the detection of manganese in biological fluids. Diagnostics of oxy-carbon parkinsonism is based on the determination of carboxyhemoglobin in the blood.

In atherosclerotic parkinsonism, trembling and rigidity are combined with signs of cerebral atherosclerosis or occur after acute disorders of cerebral circulation. Focal neurological symptoms in the form of pyramidal insufficiency, pronounced pseudobulbar symptoms. The unilaterality of rigidity and stiffness is often determined. Dyslipidemia, characteristic of atherosclerosis, is found in the blood. Recorded certain changes in the REG in the form of flattening of the pulse waves.

A clinical picture resembling Parkinson’s disease can be observed in senile atherosclerotic dementia, for which severe mental disorders are most characteristic, including dementia. Rigidity and stiffness expressed moderately, tremor, as a rule, is absent. Separate clinical manifestations of parkinsonism can be found in other hereditary degenerative diseases of the nervous system: Friedreich’s ataxia, olivopontocerebellar atrophy, orthostatic hypokinesia, Creutzfeldt-Jakob disease. In these diseases, along with akinetic-rigid symptoms, there are progressive cerebellar ataxia.

Current and forecast. The disease is progressing steadily. The exception is made by some forms caused by medicinal intoxications (in case of drug withdrawal, the condition may improve). It is generally accepted that treatment in the initial stage can reduce the severity of symptoms, slow the progression of the disease. In the later stages, therapeutic measures are less effective. The disease leads to disability over several years. Even levodopa treatment is currently slowing down for a short time. This confirms the position that the basis of the disease is not only the primary biochemical defect, but also the neuropathological process that has not yet been studied.

Diagnosis of Parkinson’s Disease

In post-traumatic parkinsonism, an increase in the pressure of cerebrospinal fluid is detected with normal cellular and protein composition. When parkinsonism occurs due to carbon monoxide poisoning, carboxyhemoglobin is found in the blood, while manganese parkinsonism shows traces of manganese in the blood, urine, and cerebrospinal fluid. Global electromyography in trembling paralysis and parkinsonism reveals a violation of muscle electrogenesis – an increase in muscle bioelectrical activity at rest and the presence of rhythmic group discharges of potentials. Electroencephalography reveals mainly diffuse, non-coarse changes in the bioelectrical activity of the brain.

Diagnosis and differential diagnosis. The first step is to differentiate Parkinson’s disease from Parkinson’s syndrome. Ocular symptoms are characteristic of post-encephalitic parkinsonism; torticollis, the phenomena of torsion dystonia can be observed.

Parkinson’s Disease Treatment

Treatment of patients with trembling paralysis and Parkinson’s syndrome should be complex, long-term and include specific anti-Parkinsonian drugs, sedatives, physiotherapy, physical therapy, psychotherapy, taking into account the etiological factor, age of patients, clinical form and stage of the disease, as well as the presence of concomitant diseases . In milder forms, amantadine (midantan) and parasympatholytics are prescribed first, as they cause fewer side effects. Apply central parasympatholytics (tsiklodol, narkopan), pyridoxine, amantadine, dopamine receptor agonists (bromocriptine, lizurid).

With marked clinical manifestations of parkinsonism, levodopa is currently the base drug, usually in combination with a decarboxylase inhibitor. Doses are increased slowly, over a period of several weeks, until a clinical effect is obtained. Side effects of the drug – dystonic disorders and psychosis. Levodopa, falling into the central nervous system, is decarboxylated to dopamine, which is necessary for the normal function of the basal ganglia. The drug affects primarily akinesia and, to a lesser extent, other symptoms. When combined with levodopa inhibitor decarboxylase, you can reduce the dose of levodopa and thereby reduce the risk of side effects.

In the arsenal of symptomatic antiparkinsonian drugs, an important place is occupied by cholinolytic drugs, which, by blocking the m-and n-cholinergic receptors, contribute to the relaxation of striated and smooth muscles, reduce violent movements and phenomena of bradykinesia. These are natural and synthetic atropine-like drugs: bellazon (omparkin), norakin, and kombipark. Also used drugs phenothiazine series: dinezin, deparkol, parsidol, diprazin. The main reason for the diversity of drugs used for the treatment of parkinsonism, in their insufficient therapeutic efficacy, the presence of side effects, individual intolerance and quick addiction to them.

Surgery. Despite the great successes achieved in the medical treatment of parkinsonism, its possibilities are in some cases limited.

The most widely used drug levodopa to a greater extent contributes to the elimination of such symptoms of the disease as akinesia, general stiffness, to a lesser extent, it affects muscle rigidity and tremor. In approximately 25% of patients, this drug is practically ineffective or poorly tolerated.

In these cases, there are indications for stereotactic surgery on subcortical nodes. Local destruction of the ventrolateral nucleus of the optic tubercle, subtalamic structures, or a pale ball is usually performed.

With the help of the operation, it is possible in most cases to achieve a positive effect – reduction of muscle tone, weakening or cessation of tremor, reduction of hypokinesia.

The operation is usually performed on the side opposite to the one on which the symptoms of parkinsonism predominate. When evidence is produced bilateral destruction of subcortical structures.

In recent years, implantation of the embryonic tissue of the adrenal gland into the striatum has also been used to treat parkinsonism. It is premature to speak of the clinical efficacy of such operations.

Stereotactic operations on subcortical structures are also used for other diseases accompanied by violent movements (hemiballism, choreoathetosis, torticollis, and some others).

The ability to work in Parkinson’s disease and parkinsonism depends on the severity of motor disorders, the type of professional activity. With mild and moderate impairments of motor functions, the patients for a long time retain their ability to work during various types of mental work, as well as works not related to physical exertion and performing precise and coordinated movements. When expressed manifestations of the disease patients are disabled and need assistance.

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