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ULY CLINIC

10 Septemba 2025, 11:20:34

Gait, Scissors [Spastic diplegic gait]

Scissors gait arises from bilateral spastic paresis, predominantly affecting the lower limbs while sparing the upper limbs. The patient exhibits flexed hips and knees, thighs adducting with each step so that the knees hit or cross in a scissors-like motion. Steps are short, regular, and laborious, resembling wading through water. Plantarflexed and inward-turned feet, due to Achilles tendon shortening, often cause toe-walking or ball-of-foot ambulation.

Pathophysiology of Scissors Gait

Scissors gait results primarily from bilateral spastic paresis, which is caused by upper motor neuron (UMN) lesions affecting the corticospinal tract or other descending motor pathways. These lesions lead to spasticity, hypertonia, and impaired voluntary motor control in the lower extremities while often sparing upper limbs.

Spasticity and Hypertonia:
- Lesions of the UMN cause loss of inhibitory supraspinal input to spinal motor neurons.
- This results in increased excitability of alpha motor neurons, leading to persistent muscle contraction, especially in adductor, hamstring, and calf muscles.
- Thigh adduction produces the characteristic “scissoring” movement during ambulation.
Contractures and Musculoskeletal Changes:
- Chronic spasticity leads to shortening of tendons (e.g., Achilles tendon) and joint contractures.
- These structural changes reinforce abnormal gait mechanics, such as toe-walking or crouched posture.
Impaired Reciprocal Inhibition:
- Normally, agonist and antagonist muscles coordinate via reciprocal inhibition.
- In scissors gait, impaired inhibition causes co-contraction of antagonistic muscles, limiting knee extension and hip abduction.
Sensory and Proprioceptive Impairment (in some cases):
- In conditions like cerebral palsy or syringomyelia, sensory deficits further disrupt balance and gait control, increasing risk of falls.
Secondary Compensatory Mechanisms:
- Patients adopt a crouched posture with shortened stride to maintain balance.
- Muscle fatigue and energy inefficiency develop due to persistent contraction and increased effort during walking.

History and Physical Examination

Elicit onset, progression, and history of trauma, including birth trauma.
Assess for previous neurological disorders, developmental delays, or musculoskeletal abnormalities.
Conduct thorough motor, sensory, and reflex evaluation (especially deep tendon reflexes in lower limbs).
Identify contractures, limb underdevelopment, or musculoskeletal deformities.
Assess gait characteristics: step length, cadence, foot positioning, and balance.

Detailed history and examination findings

Domain	What to Check / Observe	Significance / Interpretation	Underlying Pathophysiology
History: Onset & Progression	Age of onset, gradual vs sudden, worsening or stable	Gradual onset → congenital/spastic CP; sudden → spinal cord tumor or trauma	Early brain injury or corticospinal tract damage leads to bilateral spastic paresis
Birth History	Premature birth, perinatal asphyxia, birth trauma	Suggests neonatal CNS insult	Hypoxic-ischemic injury damages upper motor neurons
Developmental Milestones	Delays in sitting, crawling, walking	Indicates neuromotor impairment	Impaired corticospinal tract development affects voluntary movement
Family History	Hereditary spastic paraplegia or neurodegenerative disorders	Supports genetic cause	Mutations affecting motor neuron pathways
Associated Symptoms	Weakness, spasticity, urinary/bowel issues, sensory deficits	Suggests extent and location of neurologic involvement	Upper motor neuron lesions or spinal cord pathology
Gait Observation	Short steps, thigh adduction, knee crossing, toe-walking, crouched posture	Confirms bilateral lower limb spasticity	Spasticity leads to abnormal coordination, contractures, and postural adaptation
Muscle Tone	Hypertonia/spasticity in hip adductors, hamstrings, calves	Indicates UMN lesion	Damage to corticospinal tract reduces inhibitory signals, causing sustained contraction
Reflex Testing	Deep tendon reflexes, Babinski sign	Hyperactive reflexes → UMN involvement	Loss of inhibitory modulation from CNS → exaggerated reflexes
Range of Motion & Contractures	Limited hip abduction, knee extension, ankle dorsiflexion	Chronic spasticity → joint contractures	Persistent muscle overactivity shortens muscles and tendons
Sensory Testing	Proprioception, vibration, pain, temperature	Sensory deficits can worsen gait instability	Spinal cord or peripheral nerve involvement
Strength Testing	Lower limb strength	Weakness may coexist with spasticity	Combination of UMN spasticity and secondary muscle disuse
Postural Assessment	Crouched posture, forward trunk lean	Compensatory mechanism to maintain balance	Altered center of gravity due to spasticity and contractures

Medical Causes

Cause	Key Features / Distinguishing Signs & Symptoms
Cerebral palsy (spastic type)	Hyperactive DTRs, increased muscle tone, rapid alternating contraction/relaxation, limb weakness, underdeveloped lower limbs, contractures, toe-walking, delayed motor milestones.
Hereditary spastic paraplegia	Slowly progressive spasticity in lower limbs, gait stiffness, increased DTRs, weakness without sensory loss, family history of similar gait abnormalities.
Cervical spondylosis with myelopathy	Late-onset scissors gait, back/neck pain radiating to lower limbs, sensory deficits, weakness, muscle atrophy, hyperreflexia, possible urinary dysfunction.
Multiple sclerosis	Gradual lower-limb weakness, spasticity, paraparesis, urinary urgency, constipation, vision disturbances, paresthesia, incoordination, impaired proprioception and vibration sense.
Spinal cord tumor (thoracic/lumbar)	Gait disturbance, radicular pain, spasticity, hyperactive DTRs, bilateral Babinski, muscle atrophy, sensory deficits in dermatomal pattern, spastic bladder, possible sexual dysfunction.
Syringomyelia	Late-onset scissors gait, analgesia/thermanesthesia, muscle atrophy, Charcot joints, scoliosis, clubfoot, nail/finger/toe loss, Dupuytren contracture, dry and grooved skin.
Traumatic spinal cord injury	Acute or chronic spasticity, limb weakness, contractures, sensory deficits below lesion, bladder/bowel dysfunction, impaired ambulation.
Stroke or perinatal hypoxic injury	Hemiparetic features with spasticity, delayed motor milestones in pediatric patients, abnormal gait pattern with scissoring in lower limbs.

Special Considerations

Prevent pressure ulcers through meticulous skin care due to sensory deficits.
Implement bladder and bowel retraining if indicated.
Encourage daily active and passive range-of-motion exercises.
Consider physical therapy for gait retraining, corrective orthoses, or in-shoe splints to maintain foot alignment and prevent contractures.
Monitor nutritional status and musculoskeletal integrity in patients with chronic immobility.

Patient Counseling

Educate patient and caregivers on proper skin care, safe ambulation, and use of orthotic devices.
Emphasize adherence to rehabilitation exercises and range-of-motion activities.
Reinforce bladder and bowel management strategies when needed.
Provide psychosocial support, particularly in pediatric patients with congenital causes.

Pediatric Pointers

Major pediatric causes: cerebral palsy (spastic type), hereditary spastic paraplegia, and birth-related spinal injuries.
Gait typically manifests when the child begins walking, often later than typical developmental milestones.
Early intervention with physiotherapy and orthotic management improves functional mobility and reduces complications.

References

Callisaya, M. L., Blizzard, L., Schmidt, M. D., McGinley, J. L., & Srikanth, V. K. (2010). Ageing and gait variability—a population-based study of older people. Age and Ageing, 39(2), 191–197.
de Laat, K. F., van Norden, A. G., Gons, R. A., van Oudheusden, L. J., van Uden, I. W., Bloem, B. R., & de Leeuw, F. E. (2010). Gait in elderly with cerebral small vessel disease. Stroke, 41(8), 1652–1658.
Damiano, D. L., & Abel, M. F. (1998). Functional outcomes of strength training in spastic cerebral palsy. Archives of Physical Medicine and Rehabilitation, 79(2), 119–125.
Rose, J., & Gamble, J. G. (2006). Human Walking (3rd ed.). Lippincott Williams & Wilkins.
Novak, I., McIntyre, S., Morgan, C., Campbell, L., Dark, L., Morton, N., … Goldsmith, S. (2013). A systematic review of interventions for children with cerebral palsy: state of the evidence. Developmental Medicine & Child Neurology, 55(10), 885–910.
Hadders-Algra, M. (2014). Development of postural control during the first 18 months of life. Neural Plasticity, 2014, 1–12.
Engsberg, J. R., & Ross, S. A. (2002). Functional strength training in children with cerebral palsy. Journal of Pediatric Rehabilitation Medicine, 1(1), 3–13.
Kernohan, W. G., & Moore, R. (2010). Neurological Rehabilitation: A Problem-Solving Approach. Churchill Livingstone.