Bradykinesia is slow movement. As a rule, it occurs with a simultaneous increase in muscle tone, provoked by a lesion of the extrapyramidal system in Parkinson's disease, secondary parkinsonism of various etiologies, and some degenerative diseases. In mental disorders, hypothyroidism is not associated with pathology of intracerebral structures, it proceeds with a decrease in muscle tone. The cause of bradykinesia is established according to the anamnesis, neurological examination, and additional studies. Treatment includes dopaminomimetics, drugs to correct the underlying pathology, symptomatic agents, exercise therapy, massage, and surgical interventions.
Bradykinesia is an obligatory symptom of Parkinson's disease, combined with rigidity, tremor, and postural disorders. In the initial stages, it is weakly expressed; special tests are required for detection, for example, rapid clenching and unclenching of the fist. Then it becomes noticeable to the patient during self-service: during shaving, fastening buttons, etc. Subsequently, it progresses, has a significant impact on speech, facial expressions, gestures and plasticity.
In children with juvenile parkinsonism, fine motor disorders are observed: problems when fastening buttons and tying shoelaces, collecting constructors and mosaics. The movements are constrained, slowed down, the gait is shuffling with a decrease in the length of the step. The speech is slow, inexpressive, the face is amimic. Statokinetic tremor, muscle rigidity are detected. The symptoms improve in the morning and increase during the day.
Patients show the same manifestations as in Parkinson's disease. A distinctive feature is the initial symmetry of the disturbances. The etiofactors of secondary parkinsonism are:
Depending on the nature of the underlying pathology, bradykinesia and other signs may be accompanied by cerebellar ataxia, dementia praecox, pyramidal syndrome, and other neurological symptoms. After encephalitis, bright vegetative disturbances, pronounced rigidity, and the absence of tremor are observed. In vascular diseases, cognitive disorders, slight tremor are noted.
The main manifestation of this variant of multisystem atrophy at the initial stage is pronounced vegetative disorders, frequent fainting and pre-syncope states. Bradykinesia usually appears after a few months. Complemented by muscle rigidity, hypomimia, trembling of the hands, anhidrosis, frequent urination, urinary incontinence. In 40% of patients, cerebellar ataxia is found, in 2 - corticobulbar disorders.
The main manifestation of olivopontocerebellar degeneration is progressive cerebellar ataxia. Minor unsteadiness gradually transforms into falls when walking, inability to maintain a static posture. Join bradykinesia, hyperkinesis, dysphagia, pyramidal disorders, urinary incontinence. 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 increases, complemented by rigidity.
A nonspecific debut is characteristic, including a decrease in working capacity, headaches, dizziness, insomnia, and 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 impairment. More than half of patients develop dementia 3 years after the onset of the disease.
This group of hereditary pathologies is characterized by cerebellar disorders. Clinical manifestations in all spinocerebellar ataxias are similar, only the age of onset and individual symptoms differ. The first sign is clumsiness of movements, which is subsequently supplemented by gait disturbances, hand tremors, ophthalmoplegia, bradykinesia, and muscle rigidity. In some forms, dysphagia occurs.
This hereditary disease manifests itself at the age of 20-5 years. At the onset in adults, as a rule, there is a choreic syndrome, half of the adolescents develop convulsions, rigidity and bradykinesia. Most patients with Huntington's chorea have oculomotor disorders in the early stages. Progressive speech disorders are revealed.
Psychogenic bradykinesia is not associated with the pathology of the extrapyramidal system, but with disorders that develop against the background of severe mental illness. There is no increase in muscle tone. The symptom accompanies major depression, is detected in the later stages of epilepsy and schizophrenia. Another possible cause of bradykinesia with reduced muscle tone is hypothyroidism.
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 has changed over time. Observation and conducting special tests as part of a neurological examination make it possible to detect characteristic motor disorders and establish their severity. Reflexes are assessed, muscle tone is determined.
An important step in the diagnosis is to distinguish Parkinson's disease from 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 (presence of encephalitis, repeated traumatic brain injury or stroke in anamnesis, cerebellar disorders, dementia praecox, and some other signs).
Then apply the criteria confirming the presence of this pathology (effectiveness of levodopa, asymmetry of symptoms, rest tremor). As part of an additional examination, the following diagnostic procedures are carried out:
In addition, the examination plan may include electroencephalography, rheoencephalography and other techniques. Patients with olivopontocerebellar degeneration should consult an ophthalmologist.
Therapeutic exercise for bradykinesia
In the early stages of Parkinson's disease, dopamine receptor agonists and selective MAO inhibitors in the form of monotherapy or in various combinations are the best option. This approach makes it possible to delay the use of levodopa preparations, which are more often prescribed after 6 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 development of the disease. Patients with poisoning are detoxified, with the consequences of hypoxia, infections and TBI, neurometabolites and oxygen therapy are used. In vascular lesions, 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 anticholinergics are effective. With spinocerebellar ataxia, nootropics, vitamins, and metabolic stimulants are used. Patients with Huntington's chorea require drugs to reduce the activity of the dopaminergic system.
All patients with bradykinesia are recommended massage, special physical therapy complexes to improve the motor sphere, increase the ability to self-service. In some cases, electrical stimulation is useful. In the terminal stage, constant care, prevention of bedsores is required.
In patients with Parkinson's disease, the presence of severe symptoms with insufficient effectiveness of drug therapy or the development of severe adverse reactions is considered as an indication for surgery. Deep brain stimulation, stereotaxic pallidotomy or cryothalamotomy is performed. With akinetic-rigid syndrome, electrical stimulation of the globus pallidus is sometimes performed.
Patients with chronic cerebral ischemia due to damage to the main vessels are recommended carotid stenting or carotid endarterectomy. Intracerebral tumors are excised. With hydrocephalus, endoscopic ventriculocisternostomy and external ventricular drainage are performed. Also possible are cystoperitoneal, lumboperitoneal, or ventriculoperitoneal shunts.