Oligokinesia is a typical manifestation of various forms of Parkinsonism: primary or symptomatic, parkinsonism-plus. It occurs in temporal lobe epilepsy, some encephalopathies and mental disorders. The cause is established on the basis of complaints, anamnesis data, results of neurological examination and additional diagnostic procedures. Treatment includes dopaminomimetics, symptomatic agents. According to the indications, surgical interventions are performed.
Oligokinesia and bradykinesia are two symptoms on the basis of which hypokinesia is formed, which is one of the main signs of primary and secondary parkinsonism. A decrease in the volume of movements develops against the background of the following disorders:
- difficulties in the initial phase of the motor act (at the initiation stage);
- problems when performing sequential movements;
- rapid decrease in speed and amplitude;
- disappearance of natural synkinesias (simultaneous movements within a complex motor act);
- fragmentation, loss of motor automatism.
Oligokinesia in combination with bradykinesia causes impoverishment of facial expressions, a decrease in voice volume, a change in handwriting, shuffling gait and lack of normal hand movements while walking, difficulties in moving from a sitting position to a standing position.
At a certain stage, they are found in almost all patients with Parkinson’s disease and secondary lesions of extrapyramidal structures. They often become the main cause of disability of patients. A decrease in the number of movements in other pathologies has more variable symptoms, depending on the nature of the process.
Causes of oligokinesia
Parkinson’s disease develops under the influence of several factors, including hereditary predisposition. Manifests in the elderly, less often in middle age. Oligokinesia increases gradually, at first it is detected only during special tests, subsequently complicates everyday actions, causes impoverishment of facial expressions and gestures, changes in walking. Distinctive features are asymmetry of symptoms and tremor of rest.
Juvenile parkinsonism is inherited, debuts before the age of 25. The number of movements decreases already at the initial stage, hinders children’s games, makes self-service difficult. There is no stage of hemiparkinsonism, the disorders are symmetrical from the very beginning. Rest tremor is possible, but a more typical option is statokinetic tremor (during movements, muscle tension).
Develops against the background of injuries, intoxication, some diseases. It is characterized by rapid formation and progression of the clinical picture, symmetry of manifestations. The following variants of symptomatic parkinsonism are distinguished:
- Medicinal. The most common form. It occurs subacute, in 90% of cases – in the first three months of therapy, mainly in people over 60 years old. It is caused by sympatholytics, neuroleptics, metoclopramide, calcium antagonists, anticonvulsants. Oligokinesia is considered the most frequent, sometimes the only manifestation.
- Post-traumatic. With severe traumatic brain injuries (compression, bruising of the brain), it develops acutely or subacutely. With frequent repeated concussions, there is a gradual formation and slow progression of a decrease in the number of movements.
- Toxic. It is determined in the absence of timely treatment in patients with poisoning with methanol, prussic acid, carbon monoxide. In people with drug addiction, the cause is the toxic effect of manganese, which enters the body with ecstasy or synthetic heroin.
- Vascular. It is observed after ischemic and hemorrhagic strokes on the background of cerebral atherosclerosis, angiopathies of medium and large arteries, arteriovenous malformations. It is potentiated by chronic ischemia in hypertension, antiphospholipid syndrome, systemic lupus erythematosus. As a rule, it is subacute. Oligokinesia is more pronounced in the lower extremities. Rest tremor is uncharacteristic.
- With hydrocephalus. A decrease in the number of movements in hydrocephalus occurs after a period of intense cephalgia, nausea and vomiting. Depending on the nature of the underlying disease, the course may be acute or chronic. Parkinsonian manifestations are combined with dementia, urinary incontinence, frontal dysbasia, vestibular ataxia. There may be a decrease in vision.
Sporadic parkinsonism plus
It develops with degenerative lesions of the central nervous system, mostly of a non-hereditary nature (individual cases of occurrence in several generations are possible). It is found in the following pathologies:
- Multisystem atrophy. Along with a decrease in the number and slowing down of movements, orthostatic hypotension and pronounced vegetative disorders are noted. The presence of cerebellar ataxia and pyramidal signs is typical. The head is tilted forward (anterocollis), breathing is noisy, whistling (stridor).
- Progressive supranuclear paralysis. Oligokinesia, muscle rigidity and other symptoms are more pronounced in the trunk area. Extensor posture, severe dysphagia, early development of postural instability, paresis of the eye are determined.
- Disease of diffuse Levi’s bodies. In some patients, the onset of dementia is observed even before the appearance of motor disorders, in others, changes in the mental and motor spheres are aggravated in parallel. At the initial stage, visual hallucinations are detected. Psychotic symptoms are unstable, their severity fluctuates.
- Corticobasal degeneration. It is part of the group of taupathies. Oligokinesia and other manifestations are found in all patients, have an asymmetric character. The akinetic-rigid form prevails. Possible muscular dystonia, myoclonia, cerebellar ataxia, sometimes – athetosis, chorea.
- Alzheimer’s disease. The decrease in the number of movements is due not only to the involvement of the extrapyramidal system, but also to a pronounced cognitive decline. Clumsiness appears already at the stage of early dementia, when the extrapyramidal system is affected, it includes hypokinesia, tremor, rigidity, postural disorders.
- Creutzfeldt-Jakob disease. A rare prion disease. The clinical picture is formed from bradykinesia, limb trembling, athetosis, epipripadki, progressive spastic paralysis, myoclonia, increasing dementia.
Hereditary Parkinsonism plus
Pathologies are inherited, in most cases the genetic mechanisms of transmission are determined. The group includes:
- Huntington’s chorea. In adolescence and adolescence, in half of the cases, it debuts with rigidity, a decrease in the amplitude, number and speed of movements. Convulsions are possible. In adults, the choreic syndrome usually comes to the fore.
- Spinocerebellar ataxia. They begin with clumsiness, which later turns into oligokinesia, shuffling gait and hand trembling. Cerebellar ataxia is detected, and various ophthalmological disorders are detected in some forms.
- Gallervorden-Spatz disease. The clinic includes ataxia, postural tremor, muscle rigidity and hypokinesia. Along with extrapyramidal disorders, hyperkinesis is observed. Some patients develop dementia.
- Hepatolenticular degeneration. Oligokinesia is characteristic of a rare extrapyramidal-cortical form of pathology. Supplemented by epileptic seizures, intellectual decline.
- Neuroacanthocytosis. In the initial stages, mental disorders and hyperkinesis prevail. Subsequently, hyperkinetic syndrome is replaced by hypokinesia. With an early debut, bradykinesia can be detected already at the stage of manifestation.
The number of movements may decrease with the following pathologies:
- Encephalopathy: with severe renal and hepatic insufficiency, diseases of the respiratory system accompanied by chronic hypoxia (COPD, obstructive bronchitis, etc.), severe hemolytic and B12-deficient anemia.
- Other neurological problems: Tourette’s syndrome, temporal lobe epilepsy.
- Mental disorders: catatonia (more often – with schizophrenia), major depression (endogenous, reactive, postpartum and others), BAD in the depressive phase, oligophrenia, autism.
Manifestations of oligokinesia often differ from those in Parkinsonian syndrome. More often there is the usual impoverishment of movements without the disappearance of synkinesia, the symptom of a “gear wheel”, changes in handwriting, problems when getting up.
Determining the cause of the decrease in the number of motor acts is the responsibility of neurologists. Patients with mental disorders are referred to a psychiatrist for consultation. At the initial stage of the examination, the doctor finds out when oligokinesia first appeared, how it was expressed, how the symptom changed over time.
Based on complaints and anamnesis, the specialist forms a general idea of the clinical picture and dynamics of the disease. According to the neurological examination, it reveals extrapyramidal and cerebellar disorders, pyramidal signs, and other characteristic symptoms. Based on the data obtained, differentiates Parkinson’s disease and various variants of secondary Parkinsonism. Taking into account the results, he draws up a survey program, which may include such methods as:
- MRI of the brain. It is the most informative diagnostic procedure. Allows you to determine most of the causes of symptomatic forms, to detect signs characteristic of certain degenerative pathologies.
- Other visualization methods. CT of the brain, as a rule, is somewhat inferior to MRI. It is used for suspected stroke in anamnesis, hydrocephalus, and a number of other pathologies. Patients with vascular problems require duplex scanning or Dopplerography of cerebral vessels to clarify the localization, prevalence and severity of pathological changes.
- Laboratory tests. In hereditary neurodegenerative processes, genetic tests are shown to verify pathology. In case of intoxication, toxicological studies are recommended. With atherosclerosis, a biochemical blood test is prescribed to determine the level of lipids. In encephalopathies, a comprehensive study is carried out to assess the degree of deterioration of kidney or liver functions, to establish the type of anemia.
If necessary, EEG is performed, functional techniques are used. Patients with vision loss are referred to an ophthalmologist for consultation.
With parkinsonian manifestations of any genesis, dopaminomimetics are indicated. The drug is selected individually, taking into account the etiology of oligokinesia and the stage of the disease. Despite the effectiveness of levodopa in Parkinson’s disease, they try to delay the appointment of this drug, since with prolonged use its effectiveness decreases, drug dyskinesia occurs.
The medication is selected individually, taking into account age, concomitant diseases, personal characteristics, professional status and other factors. As a rule, monotherapy is used. If the effect is insufficient, a combination of drugs is selected. The start time of levodopa therapy is also determined individually, if possible, trying to postpone this moment until the age of 60-70 years.
In secondary parkinsonism, levodopa is usually ineffective. Preference is given to selective irreversible MAO inhibitors and dopamine receptor agonists. In symptomatic forms, etiopathogenetic treatment is carried out, which in some cases makes it possible to eliminate or significantly reduce the severity of symptoms. In case of vascular pathology, vascular therapy is prescribed, detoxification is carried out with toxic effects, etc.
Specific treatment for many “plus” syndromes has not been developed. Vitamins, neurometabolites, and nootropics are used. In dementia with Lewy bodies, cholinesterase inhibitors and NMDA antagonists are used. With pronounced psychotic problems, neuroleptics can be shown. Beta-blockers are recommended for patients with myoclonia and severe tremor due to corticobasal degeneration.
With encephalopathies on the background of hematological and somatic diseases, treatment is carried out aimed at normalizing the blood formula, restoring the functions of internal organs, eliminating endogenous intoxication. Anticonvulsants are effective in temporal lobe epilepsy. Patients with mental disorders are prescribed antipsychotics
If conservative therapy of Parkinson’s disease is ineffective, it is possible to perform electrostimulation of the pale globe, cryothalamotomy, pallidotomy, deep brain stimulation. Patients with hydrocephalus undergo bypass surgery. In chronic ischemia, reconstructive operations (stenting) are indicated against the background of damage to large cerebral vessels.