Hemiparetic gait is formed as a result of organic lesions of the central nervous system, is detected after a stroke, TBI, encephalitis, purulent lesions of the brain. It develops with tumors, parasitosis, toxic, demyelinating and degenerative-atrophic processes. The cause of the occurrence is established according to the anamnesis, general and neurological examination, echoencephalography, CT, MRI, laboratory tests, and other studies. At the initial stage of development of hemiparesis, pathogenetic and symptomatic measures are taken, followed by rehabilitation.
The gait has a "squinting" character. The arm is bent at the elbow joint, pressed to the body. The leg does not move in a straight line, but deviates to the side and describes a semicircle. At the moment of separation from the surface, the knee joint is extended, the foot is in the position of slight plantar flexion. The patient deviates the torso to the healthy side and raises the pelvis, the leg makes a circular motion, with difficulty moving forward. Instead of resting on the heel, the foot hits the surface.
Minor spasticity and partial preservation of the functions of the muscles of the thigh and lower leg allow some patients, instead of lifting the pelvis, to compensate for an extended knee and a drooping foot by increasing hip flexion. When using a cane, a person holds it with a healthy hand, while walking with a sore leg, he transfers his weight to it. Less commonly, there is three-joint extension (hip, knee, ankle) with typical vertical pelvic movements with each step.
The most common cause of hemiparetic gait is stroke. Walking disorders occur in both hemorrhagic and ischemic forms of the disease, develop as a result of stable hemiparesis. They can be combined with facial distortion, aphasia, dysarthria, visual-spatial agnosia, and other neurological disorders. The severity of symptoms varies depending on the volume of the affected area in the brain, the time of the start of therapeutic measures.
Hemiparetic gait is detected in some patients with traumatic brain injury. The cause of hemiparesis can be the direct destruction of the medulla by bone fragments in case of fractures of the vault and base of the skull, contusion and crushing of the brain substance, compression of the brain structures by epidural, subdural and intracerebral hematomas. The clinical picture and the severity of residual effects differ significantly, correlate with the severity of the injury.
Brain abscesses develop as a result of open TBI, otogenic complications, infection of wounds after neurosurgical operations, the spread of suppuration in osteomyelitis of the skull bones. The most severe neurological consequences, including hemiparesis with the occurrence of hemiparetic gait, are detected in patients with subdural empyema. After epidural purulent foci, changes in gait are less common.
Hemiparetic gait is not mandatory, but a possible consequence of the transferred encephalitis. The likelihood of residual movement disorders depends on the type and form of the disease. A symptom can be observed in people who have undergone the following pathology options:
Rasmussen's encephalitis is considered a special type of disease with frequent hemiparetic gait - a condition with an unexplained etiology (presumably viral or autoimmune). There is a chronic course with damage to one hemisphere of the brain.
Hemiparetic gait is characteristic of cerebral aspergillosis, since this pathology often causes cerebrovascular accidents and hemiparesis, resembling those of strokes. For other parasitoses, epileptic seizures are more typical, weakness of half of the body is rare, sometimes observed with echinococcosis.
Hemiparetic gait in a child
Mechanical damage during childbirth, especially against the background of previous fetal hypoxia, can lead to the development of intracranial hemorrhages. With damage to the corresponding parts of the brain and pathways, a hemiparetic gait is formed as a result. The symptom comes to light with the beginning of walking, motive stereotypes are initially formed according to the vicious principle caused by a hemiparesis.
Movement disorders, including hemiparesis, are observed in more than half of patients with cerebral tumors. Symptoms develop gradually, occur against the background of headaches, systemic dizziness, vomiting not associated with food intake, and focal disorders. Convulsions and mental disorders are possible. Hemiparetic gait can be formed in neoplasias of the cortex and subcortical structures, tumors of the brain stem and craniospinal neoplasms.
The symptom is determined in astrocytomas, meningiomas, medulloblastomas and other primary oncological processes. It is detected in cerebral gliomatosis with a predominant lesion of one hemisphere. In some patients, hemiparesis is found in tumors of other localizations, as a result of brain metastasis. Sometimes hemiparetic gait is provoked by neuroleukemia, which has arisen against the background of acute leukemia, less often - chronic leukemia.
The symptom is observed in demyelinating diseases of the brain, for example, progressive multifocal leukoencephalopathy. Sturge-Weber syndrome is among the congenital diseases accompanied by hemiparetic gait. A similar gait disorder can be observed in severe toxic brain damage. Sometimes the cause of cerebral ischemia with subsequent hemiparesis is a dissecting aortic aneurysm and tetralogy of Fallot.
A neurologist is engaged in determining the cause of hemiparetic gait. During the conversation with the patient, the specialist determines the time of the onset of the symptom, finds out against the background of which diseases and acute conditions neurological disorders have arisen. An important part of the examination is the study of the dynamics of the disease to confirm the stable or progressive nature of the disorders. The survey involves the following procedures:
Exercise therapy for hemiparesis
In the acute period, patients are shown pathogenetic and symptomatic therapy. Since hemiparetic gait develops as a result of hemiparesis and is considered as part of the long-term consequences of brain damage, restorative techniques play a leading role in eliminating or minimizing the symptom.
At an early stage, measures are taken to prevent contractures, provide a functionally advantageous position of the paretic limbs. The highest efficiency of rehabilitation is observed during the first year after the onset of neurological disorders. The following methods apply:
Surgical interventions on nerve structures are carried out in the acute phase of the disease; in the long-term period, methods aimed at correcting orthopedic disorders are more often used. Drainage or removal of abscesses and hematomas, excision of tumors and parasitic cysts are possible. In the early period of ischemic stroke, thrombolysis is effective.
In cerebrovascular insufficiency, vertebral artery reconstruction or carotid endarterectomy may be indicated. Patients with secondary disorders of the musculoskeletal system are operated on to eliminate contractures, move muscles and tendons, arthrodesis and other interventions.