EpistemisSpastic gait
Specialty: Neurology.
Why it occurs
- Old cerebrovascular accident with pyramidal sequelae (spastic hemi-gaiter/unilateral reaper)
- Multiple sclerosis (bilateral spastic gait due to involvement of the pyramidal tract in the spinal cord or brain)
- Familial spastic paraparesis (bilateral retrograde axonal degeneration of long tracts)
- Severe obstructive cervical spondylotic myelopathy
- Spastic cerebral palsy (neonatal history)
Initial workup
Observation of the gait pattern characterized by lower limb rigidity, thigh adduction (scissor gait), dragging of the toes and hyperextension of the knees; MRI of the complete cervical and dorsal spine, as well as brain MRI; electroneuromyogram; Somatosensory evoked potentials and motor pathways.
red flags
Acute and severe worsening of bilateral spastic gait in a previously stable patient, associated with sudden loss of tactile proprioceptive sensitivity starting from the navel or inguinal region, suggesting acute spinal cord compression or extensive demyelinating flare requiring methylprednisolone or emergency decompressive surgery.
Standard management
- Baclofen — 10-80 mg/day orally
- Tizanidine — 2-16 mg/day
- Local infiltration of botulinum toxin in hip adductors and triceps surae to improve gait pattern
- Physiotherapy focused on progressive muscle stretching and gait re-education with technical aids.
Educational guidance for study. It is NOT a prescription recommendation. The actual choice depends on the cause, the patient, and current guidelines.
- Area
- Neurology
- Listed causes
- 5
- Treatment options
- 4