Bradykinesia is a slowing down of movements. As a rule, it occurs with a simultaneous increase in muscle tone, provoked by the defeat of the extrapyramidal system in Parkinson’s disease, secondary Parkinsonism of various etiologies, some degenerative diseases. In mental disorders, hypothyroidism is not associated with pathology of intracerebral structures, occurs with a decrease in muscle tone. The cause of bradykinesia is established according to anamnesis, neurological examination, additional studies. Treatment includes dopaminomimetics, medications to correct the underlying pathology, symptomatic remedies, physical therapy, massage, surgical interventions.
Causes of bradykinesia
Parkinson’s disease
Bradykinesia is a mandatory sign of Parkinson’s disease, combined with rigidity, tremor, postural disorders. At the initial stages, it is poorly expressed, special tests are required for detection, for example, rapid clenching and unclenching of the fist. Then it becomes noticeable to the patient himself during self-care: during shaving, buttoning, etc. Subsequently progresses, has a significant impact on speech, facial expressions, gestures and plasticity.
Children with juvenile Parkinsonism have violations of fine motor skills: problems with buttoning and tying shoelaces, collecting constructors and mosaics. Movements are stiff, slow, shuffling gait with a decrease in the length of the step. The speech is slow, expressionless, the face is amimic. Statokinetic tremor and muscle rigidity are revealed. Symptoms decrease in the morning and increase throughout the day.
Secondary parkinsonism
Patients show the same manifestations as in Parkinson’s disease. A distinctive feature is the initial symmetry of violations. The etiofactors of secondary Parkinsonism are:
- Traumatic brain injuries: compression or bruising of the brain, repeated concussions.
- Infectious diseases: viral encephalitis, measles, herpes, mumps, HIV.
- Exogenous intoxication: poisoning with methanol, carbon monoxide, heavy metals, prussic acid, manganese (with drug dependence on ecstasy and heroin).
- Taking medications: anticonvulsants, antipsychotics, antiemetics, antispasmodics.
- Damage to cerebral vessels: cerebral atherosclerosis, multiple lacunar infarcts, chronic ischemia, ischemic strokes.
- Neoplasms: benign tumors and malignant neoplasia of the brain.
- Degenerative diseases: multiple sclerosis, multisystem atrophy, neuroacanthocytosis, dementia with Lewy bodies, Wilson’s disease.
- Other causes: hydrocephalus, Farah’s disease, posthypoxic syndrome of various genesis, frequent hypoglycemia.
Depending on the nature of the underlying pathology, bradykinesia and other signs may be supplemented by cerebellar ataxia, early dementia, pyramidal syndrome, and other neurological symptoms. After encephalitis, there are bright vegetative disorders, pronounced rigidity, absence of tremor. In vascular diseases, cognitive disorders, minor tremor are noted.
Shay-Dreijer syndrome
The main manifestation of this variant of multisystem atrophy at the initial stage are dressed-up vegetative disorders, frequent fainting and pre-fainting states. Bradykinesia usually appears after a few months. It is complemented by muscle rigidity, hypomimia, trembling of the hands, anhidrosis, frequent urination, urinary incontinence. In 40% of patients, cerebellar ataxia is detected, in 20 – corticobulbar disorders.
Olivopontocerebellar degeneration
The main manifestation of olivopontocerebellar degeneration is progressive cerebellar ataxia. Minor instability gradually transforms into falls when walking, inability to maintain a static posture. Bradykinesia, hyperkinesis, dysphagia, pyramidal disorders, urinary incontinence are added. Phobias, depressions, hallucinations, attacks of psychomotor agitation, cognitive disorders are found in the mental sphere. In the later stages, patients cannot walk, independently change the position of the body. Bradykinesia is increasing, supplemented by rigidity.
Steele-Richardson syndrome
A nonspecific debut is characteristic, including a decrease in working capacity, headaches, dizziness, insomnia, increased fatigue. After some time, the clinical picture expands due to bradykinesia, back stiffness, ataxia. Subsequently, patients with progressive supranuclear palsy develop ophthalmoplegia, pseudobulbar syndrome, emotional and cognitive disorders. More than half of the patients have dementia 3 years after the onset of the disease.
Spinocerebellar ataxia
This group of hereditary pathologies is characterized by cerebellar disorders. The clinical manifestations of all spinocerebellar ataxias are similar, only the age of onset and individual symptoms differ. The first sign is the clumsiness of movements, which is subsequently supplemented by gait disorders, hand trembling, ophthalmoplegia, bradykinesia, muscle rigidity. In some forms, dysphagia occurs.
Huntington ‘s Chorea
This hereditary disease manifests itself at the age of 20-50 years. In the debut, adults, as a rule, have a choreic syndrome, half of adolescents develop seizures, rigidity and bradykinesia. Most patients with Huntington’s chorea have oculomotor disorders already in the early stages. Progressive speech disorders are revealed.
Other causes
Psychogenic bradykinesia is not associated with the pathology of the extrapyramidal system, but with disorders developing against the background of severe mental illnesses. There is no increase in muscle tone. The symptom accompanies major depression, is detected in the late stages of epilepsy and schizophrenia. Another possible cause of bradykinesia with reduced muscle tone is hypothyroidism.
Diagnostics
The etiology of bradykinesia is established by a neurologist. The specialist interviews the patient, finds out when the symptom first appeared, how the clinical picture of the disease changed over time. Observation and carrying out special tests within the framework of a neurological examination make it possible to detect characteristic motor disorders and establish their severity. Reflexes are evaluated, muscle tone is determined.
An important stage of diagnosis is the distinction of Parkinson’s disease with other neurological diseases and psychopathological syndromes accompanied by similar symptoms. It is carried out in two stages. Initially, criteria are used to exclude Parkinson’s disease (the presence of encephalitis, repeated TBI or strokes in the anamnesis, cerebellar disorders, early dementia and some other signs).
Then apply criteria confirming the presence of this pathology (effectiveness of levodopa, asymmetry of symptoms, rest tremor). As part of the additional examination , the following diagnostic procedures are performed:
- MRI of the brain. It is informative in determining the causes of secondary parkinsonism, olivopontocerebellar degeneration, spinocerebellar ataxia, Huntington’s chorea.
- CT scan of the brain. As a rule, it provides less data, is used for tumors, hydrocephalus, stroke and some other diseases that provoke bradykinesia.
- Laboratory tests. Verification of Huntington’s chorea, spinocerebellar ataxia, Wilson’s disease is performed by genetic diagnosis. With infectious pathologies, PCR tests may be required, with hypothyroidism – tests for thyroid hormones, with atherosclerosis – a biochemical blood test.
In addition, the examination plan may include electroencephalography, rheoencephalography and other techniques. Patients with olivopontocerebellar degeneration are advised to consult an ophthalmologist.
Treatment
Conservative therapy
In the early stages of Parkinson’s disease, dopamine receptor agonists and selective MAO inhibitors in the form of monotherapy or in different combinations are the best option. This approach makes it possible to delay the use of levodopa drugs, which are more often prescribed after 60 years. Subsequently, due to a decrease in the effectiveness of levodopa, an increase in medication intake or complex therapy with the use of several medications is required.
In secondary Parkinsonism, the effect of levodopa is relatively weak, although it can be used during treatment. The appointment of one or more dopaminomimetics is practiced. Therapeutic measures also include the impact on the cause of the disease. Patients with poisoning are detoxified, with the consequences of hypoxia, infections and TBI, neurometabolites and oxygen therapy are used. In case of vascular damage, vascular agents are indicated.
There is no specific treatment for olivopontocerebellar degeneration, Huntington’s chorea and spinocerebellar ataxia. Neurometabolites and vitamin preparations are recommended for OPCD. To reduce the severity of bradykinesia, central cholinolytics are effective. In spinocerebellar ataxia, nootropics, vitamins, and metabolic stimulants are used. Patients with Huntington’s chorea require medications to reduce the activity of the dopaminergic system.
All patients with bradykinesia are recommended massage, special complexes of physical therapy to improve the motor sphere, increase the ability to self-care. In some cases, electrical stimulation is useful. In the terminal stage, constant care is required, prevention of bedsores.
Surgical treatment
In patients with Parkinson’s disease, the presence of pronounced symptoms with insufficient effectiveness of drug therapy or the development of severe adverse reactions is considered as indications for surgery. Deep brain stimulation, stereotactic pallidotomy or cryothalamotomy is performed. With akinetic-rigid syndrome, electrical stimulation of the pale ball is sometimes performed.
Carotid artery stenting or carotid endarterectomy is recommended for patients with chronic cerebral ischemia due to damage to the main vessels. Intracerebral tumors are excised. In hydrocephalus, endoscopic ventriculocysternostomy and external ventricular drainage are performed. Cystoperitoneal, lumboperitoneal or ventriculoperitoneal bypass surgery is also possible.
