Decreased Range Of Motion (Oligokinesia) : Causes, Symptoms, Diagnosis & Treatment

Last Updated: 29/09/2022

A decrease in the number of movements (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 a neurological examination and additional diagnostic procedures. Treatment includes dopaminomimetics, symptomatic agents. Surgical interventions are carried out according to indications.

general information

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 range of motion develops against the background of the following disorders:

  • difficulties in the initial phase of the motor act (at the stage of initiation);
  • problems when performing sequential movements;
  • rapid decrease in speed and amplitude;
  • the disappearance of natural synkinesis (simultaneous movements within the framework of a complex motor act);
  • fragmentation, loss of motor automatisms.

Oligokinesia in combination with bradykinesia cause impoverishment of facial expressions, a decrease in the volume of the voice, a change in handwriting, a shuffling gait and the absence of normal hand movements during walking, and difficulty in moving from a sitting 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. Often they become the main cause of disability in patients. A decrease in the number of movements in other pathologies has more variable symptoms, depending on the nature of the process.

Why the number of movements decreases

Primary parkinsonism

Parkinson's disease develops under the influence of several factors, including hereditary predisposition. Manifests in the elderly, rarely middle age. Oligokinesia increases gradually, at first it is detected only during special tests, subsequently it makes everyday activities difficult, becomes the cause of impoverishment of facial expressions and gestures, and changes in walking. The hallmarks are asymmetry of symptoms and resting tremor.

Juvenile parkinsonism is inherited, debuting before the age of 25. The number of movements decreases already at the initial stage, interferes with children's games, makes self-service difficult. The stage of hemiparkinsonism is absent, the disorders are symmetrical from the very beginning. Resting tremor is possible, but a more typical variant is statokinetic tremor (during movements, muscle tension).

Symptomatic parkinsonism

It develops against the background of injuries, intoxications, some diseases. It is characterized by the rapid formation and progression of the clinical picture, the symmetry of manifestations. There are the following variants of symptomatic parkinsonism:

  • Drug. The most common form. It occurs subacutely, in 90% of cases - in the first three months of therapy, mainly in people older than 6 years. It is caused by sympatholytics, neuroleptics, metoclopramide, calcium antagonists, anticonvulsants. Oligokinesia is considered the most frequent, sometimes the only manifestation.
  • Post-traumatic. In severe traumatic brain injury (compression, brain contusion) develops acutely or subacutely. With frequent repeated concussions, a gradual formation and slow progression of a decrease in the number of movements are noted.
  • Toxic. It is determined in the absence of timely treatment in patients with poisoning with methanol, hydrocyanic acid, carbon monoxide. In people with drug dependence, the cause is the toxic effects of manganese, which enters the body with ecstasy or synthetic heroin.
  • Vascular. It is observed after ischemic and hemorrhagic strokes against the background of cerebral atherosclerosis, angiopathy of medium and large arteries, arteriovenous malformations. It is potentiated by chronic ischemia in hypertension, antiphospholipid syndrome, systemic lupus erythematosus. Usually subacute. Oligokinesia is more pronounced in the lower extremities. Resting tremor is uncommon.
  • With hydrocephalus. A decrease in the number of movements in hydrocephalus occurs after a period of intense cephalalgia, nausea and vomiting. Depending on the nature of the underlying disease, the course can be acute or chronic. Parkinsonian manifestations are combined with dementia, urinary incontinence, frontal dysbasia, vestibular ataxia. Possibly decreased vision.



sporadic parkinsonism plus

It develops with degenerative lesions of the central nervous system, which are predominantly not hereditary in nature (some 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 autonomic disorders are noted. The presence of cerebellar ataxia and pyramidal signs is typical. The head is tilted forward (anterocollis), breathing is noisy, wheezing (stridor).
  • Progressive supranuclear palsy. Oligokinesia, muscle rigidity and other symptoms are more pronounced in the trunk area. The extensor posture, severe dysphagia, early development of postural instability, gaze paresis are determined.
  • Diffuse Lewy body disease. 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 come to light. Psychotic symptoms are unstable, their severity fluctuates.
  • Corticobasal degeneration. It belongs to 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, myoclonus, 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, with damage to the extrapyramidal system, it includes hypokinesia, tremor, rigidity, and postural disorders.
  • Creutzfeldt-Jakob disease. Rare prion disease. The clinical picture is formed from bradykinesia, trembling of the extremities, athetosis, epileptic seizures, progressive spastic paralysis, myoclonus, and increasing dementia.

hereditary parkinsonism plus

Pathologies are inherited, in most cases, genetic transmission mechanisms have been identified. The group includes:

  • Chorea of ​​Huntington. In adolescence and youth, in half of the cases it debuts with rigidity, a decrease in the amplitude, number and speed of movements. Seizures are possible. In adults, choreic syndrome usually comes to the fore.
  • Spinocerebellar ataxia. They begin with clumsiness, which subsequently turns into oligokinesia, shuffling gait and hand trembling. Cerebellar ataxia is detected, in some forms various ophthalmic disorders are found.
  • Hallervorden-Spatz disease. Clinical features include ataxia, postural tremor, muscle rigidity, and hypokinesia. Along with extrapyramidal disorders, hyperkinesias are observed. Some patients develop dementia.
  • Hepatolenticular degeneration. Oligokinesia is characteristic of a rare extrapyramidal-cortical form of pathology. Complemented by epileptic seizures, intellectual decline.
  • Neuroacanthocytosis. At the initial stages, mental disorders and hyperkinesis prevail. Subsequently, hypokinesia comes to replace the hyperkinetic syndrome. With an early debut, bradykinesia can be detected already at the stage of manifestation.

Other reasons

The number of movements may decrease with the following pathologies:

  • Encephalopathy: in severe renal and hepatic insufficiency, diseases of the respiratory system, accompanied by chronic hypoxia (COPD, obstructive bronchitis, etc.), severe hemolytic and B12 deficiency anemia.
  • Other neurological problems: Tourette syndrome, temporal lobe epilepsy.
  • Mental disorders: catatonia (more often with schizophrenia), major depression (endogenous, reactive, postpartum and others), bipolar disorder in the depressive phase, mental retardation, autism.

The manifestations of oligokinesia often differ from those in parkinsonism. More often, the usual impoverishment of movements is noted without the disappearance of synkinesis, the “cog wheel” symptom, changes in handwriting, and problems when standing up.


Determining the cause of a decrease in the number of motor acts is the responsibility of neurologists. Patients with mental disorders are referred for consultation with a psychiatrist. 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 the 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, it differentiates Parkinson's disease and various variants of secondary parkinsonism. Taking into account the results, it draws up a survey program, which may include methods such 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 scan of the brain, as a rule, is somewhat inferior to MRI. It is used for suspected stroke in history, hydrocephalus, and a number of other pathologies. Patients with vascular problems require duplex scanning or dopplerography of cerebral vessels to clarify the location, extent and severity of pathological changes.
  • Laboratory tests. In hereditary neurodegenerative processes, genetic tests are indicated to verify the pathology. In case of intoxication, toxicological studies are recommended. With atherosclerosis, a biochemical blood test is prescribed to determine the level of lipids. With encephalopathies, a comprehensive study is carried out to assess the degree of deterioration in the functions of the kidneys or liver, to establish the type of anemia.

If necessary, an EEG is performed, functional techniques are used. Patients with visual loss are referred for consultation with an ophthalmologist.

Exercise therapy for oligokinesia



Conservative therapy

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-induced dyskinesias occur.

The drug is chosen individually, taking into account age, concomitant diseases, personal characteristics, professional status and other factors. As a rule, monotherapy is used. With insufficient effect, a combination of drugs is selected. The time of initiation of therapy with levodopa is also determined individually, if possible trying to postpone this moment until the age of 60-7 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 eliminates or significantly reduces the severity of symptoms. In case of vascular pathology, vascular therapy is prescribed, in case of toxic effects, detoxification is carried out, etc.

Specific treatment for many "plus" syndromes has not been developed. They use vitamins, neurometabolites, nootropics. In dementia with Lewy bodies, cholinesterase inhibitors and NMDA antagonists are used. With severe psychotic problems, antipsychotics may be indicated. In patients with myoclonus and severe tremor due to corticobasal degeneration, beta-blockers are recommended.

With encephalopathies against the background of hematological and somatic diseases, treatment is carried out aimed at normalizing the blood count, restoring the functions of internal organs, and eliminating endogenous intoxication. Anticonvulsants are effective in temporal lobe epilepsy. Patients with psychiatric disorders are prescribed antipsychotics


With the ineffectiveness of conservative therapy for Parkinson's disease, it is possible to conduct electrical stimulation of the pale ball, cryotalamotomy, pallidotomy, deep brain stimulation. Patients with hydrocephalus undergo bypass surgery. In chronic ischemia against the background of damage to large cerebral vessels, reconstructive operations (stenting) are indicated.