Hemiplegic Gait - an overview (2023)

1 Hemiplegic Gait

This gait is the result of poor control of the flexor muscles during swing phase and spasticity of the extensor muscles acting to lengthen the affected leg (compared to the healthy side). The ankleis abnormally flexed downward and inward (equinovarus deformity), and initial contact during stance is abnormal, along the lateral edge of the foot or forefoot. The knee is stiff, hyperextends during stance, and does not flex normally during swing. The contralateral step often advances just to meet the position of the paralyzed limb, instead of advancing normally beyond it.

Because the paralyzed leg is hyperextended, and therefore longer than the sound leg, the patient may drag the toe of the affected leg during swing or adopt abnormal movements to clear that limb during the swing phase. These movements include contralateral trunk lean, which raises the ipsilateral pelvis to clear the paralyzed leg, and circumduction, an abnormal movement in which the toe traces a semicircle on the floor, first moving outward and then inward as it advances, instead of the normal straightforward movement (Fig. 7.4).

According to classic teachings, the clinician should suspect mild hemiplegia if a patient swings his or her arms asymmetrically while walking, although this finding appears in 11% to 70% of normal persons^22,23 and the sign did not accurately detect focal cerebral disease in one study (sensitivity 22%, specificity 89%, positive and negative LRs not significant).²²

Case Study 10

Spastic Hemiplegic Gait

Disruption of the corticospinal tract above the medulla results in contralateral abnormal tone, posture, and hemiplegic gait. The ipsilateral side is involved if the lesion occurs below the decussation of fibers in the medulla. Tone is often increased. Posture is characterized by leg extension or slight knee flexion. Hemiplegic gait includes impaired natural swing at the hip and knee with leg circumduction. The pelvis is often tilted upward on the involved side to permit adequate circumduction. With ambulation, the leg moves forward and then swings back toward the midline in a circular movement. The heel-walking exercise is impaired as the patient scuffs the lateral sole and the toe of the shoe while dragging the foot. With more severe involvement, the movements are markedly slow and require great effort. Some children with modest spasticity of the knee may assume a position of mild flexion at the knee and hip, keep the foot held in the equinovarus position, and show reduced foot scuffing.

The affected leg bears weight for decidedly less time than the normal leg during ambulation. Involvement of the upper extremity leads to the arm being held in an awkward posture, usually close to the body, flexed at the elbow and wrist, and with a closed fist (i.e., cortical thumb). The expected rhythmic reciprocal swing of the arm with the stance phase of the opposite leg is absent. Dystonia rather than spasticity should be considered if the arm is held behind the plane of the body on a routine basis.

The etiology of hemiplegic gait cannot always be determined, but one should look for focal brain lesions such as porencephalic cysts, subdural hematomas, cerebral masses, and cerebrovascular accidents.

MOTOR/REFLEXES/CEREBELLAR/GAIT

Patients with frontal lobe lesions associated with apraxia may have contralateral hemiparesis due to involvement of the motor cortex (Video 11, Hemiplegic Gait). Crural weakness without involvement of the arm and face suggests involvement of the medial frontal lobe; when acute, this suggests infarction in the territory of the anterior cerebral artery. These patients may also show evidence of callosal disconnection (see later discussion). Brachial‐facial weakness suggests involvement of the distribution of the middle cerebral artery. Evaluation of tone and evaluation for the presence of abnormalities of movement is also important. Patients with apraxia as part of corticobasal degeneration may have rigidity, bradykinesia, and tremor or myoclonus and alien hand (Video 39, Alien Hand Syndrome).

Spastic Hemiplegic Gait

Hemiplegia typically results from disruption of the corticospinal tract above the medulla. Tone is often increased, and posture is characterized by leg extension or slight knee flexion. Hemiplegic gait includes impaired natural swing at the hip and knee with leg circumduction. The pelvis is often tilted upward on the involved side to permit adequate circumduction. With ambulation, the leg moves forward and then swings back toward the midline in a circular movement. The heel-walking exercise is impaired as the patient scuffs the lateral sole and the toe of the shoe while dragging the foot.

The affected leg bears weight for less time than the normal leg during ambulation. The expected rhythmic reciprocal swing of the arm with the stance phase of the opposite leg is absent. Dystonia rather than spasticity should be considered if the arm is held behind the plane of the body on a routine basis.

The etiology of hemiplegic gait cannot always be determined, but one should look for focal brain lesions such as porencephalic cysts, subdural hematomas, cerebral masses, and cerebrovascular accidents.

MOTOR/REFLEXES/CEREBELLAR/GAIT

Changes in muscle tone can be indicative of neurological disease involving cranial nerves IX and X. Cerebral lesions causing pseudobulbar palsy with alteration of speech and dysphagia may be associated with limb spasticity due to corticospinal tract injury (Video 11, Hemiplegic Gait). Parkinsonism caused by various etiologies is frequently associated with difficulties in speech and swallowing (Video 49, Hypophonia). No specific lesions exist of the cranial nerves but, rather, the subcortical control is affected bilaterally. Patients with progressive supranuclear palsy particularly have prominent difficulty with speech and dysphagia (Video 206, Postural Instability). In patients with suspected cranial nerve IX or X lesions, the presence of abnormal reflexes, such as an extensor plantar response, or the emergence of rudimentary reflexes such as the suck or snout are indicators of CNS pathology. Disorders of the neuromuscular junction also produce dysarthria and dysphagia. Repetitive testing of ocular or limb muscle power may produce an inordinate amount of fatigue and weakness pointing to a diagnosis of myasthenia (Video 225, Myasthenia Gravis).

A brain stem lesion producing impairment of speech and swallow may also include ataxia of ipsilateral limbs and gait by injury to the inferior cerebellar peduncle that lies adjacent to the nuclei of nerves IX and X (Video 95, Brain Stem Infarction).

Acute Encephalitis

As discussed in the preceding section on pathogenesis, HSV encephalitis typically involves the temporal lobe or lobes, the orbital‐frontal cortex, and the limbic structures. The clinical presentation is that of a focal encephalitis characterized by focal neurological deficits (hemiparesis in approximately one third of patients) (Video 11, Hemiplegic Gait), focal seizure activity often involving the temporal lobe, headache, altered behavior, personality changes, fever, and altered levels of consciousness (Video 248, Complex‐Partial Seizures with Automatisms). The classic paper on diseases that mimic herpes simplex encephalitis appeared in the Journal of the American Medical Association in 1989.¹¹⁵ This study, which included a total of 432 patients who underwent brain biopsy for presumptive herpes simplex encephalitis, predated the routine use of MRI and the availability of CSF PCR. Today, the differential diagnosis of acute focal encephalitis with fever, after neuroimaging and CSF analysis, is that of a focal viral encephalitic process. The causes of a focal viral encephalitic process are listed in Table 41‐4.

Gait analysis

On watching a patient walk, the disturbance can be broadly subdivided into symmetrical and asymmetrical gait disturbances (Fig. 1).