In Kuwait, spasticity Management is managed by physical medicine & rehabilitations. Spasticity is a velocity-dependent increase in muscle tone caused by loss of upper-motor-neuron control after stroke, spinal cord injury, traumatic brain injury, cerebral palsy, multiple sclerosis, or anoxic brain injury. About 30-43% of stroke survivors develop persistent spasticity by 12 months, roughly 65-78% of people with spinal cord injury show clinically meaningful tone after one year, and 75-80% of children with cerebral palsy live with some form of spasticity.
Spasticity (ICD-10: R25.2 for muscle spasm; encoded under the primary upper-motor-neuron diagnosis) is one component of the upper-motor-neuron syndrome that follows damage to descending motor pathways anywhere from the motor cortex through the brainstem and spinal cord. Lance defined it in 1980 as a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex. The SPASM EU-COST consortium widened the definition in 2005 to include the broader phenomena of disordered sensorimotor control resulting in intermittent or sustained involuntary activation of muscles. The pathophysiology involves loss of supraspinal inhibition of alpha-motor neurons, sprouting of intraspinal afferents, and intrinsic muscle changes (sarcomere shortening, fibrosis, fatty infiltration).
The key symptoms of Spasticity Management are: Velocity-dependent stiffness in a limb — moved slowly the joint feels normal, moved quickly the muscle catches sharply, sometimes followed by sudden release (the clasp-knife phenomenon)., Clonus: rhythmic involuntary muscle contractions, typically four to seven beats per second at the ankle after a sudden dorsiflexion stretch., Painful flexor or extensor spasms triggered by movement, full bladder, constipation, infection, or pressure injuries, lasting seconds to minutes., Exaggerated deep-tendon reflexes (3+ or 4+) and an upgoing plantar response (Babinski sign) on the affected side., Loss of selective motor control: difficulty moving one joint without the rest of the limb moving together (synergy pattern after stroke)., Stereotyped postures — flexed elbow, wrist, and fingers and adducted shoulder in the upper limb; extended knee with plantarflexed and inverted foot in the lower limb after stroke and spinal cord injury., Progressive joint contracture and loss of range of motion if untreated, eventually requiring tenotomy or arthrodesis..
Diagnosis of spasticity is clinical: history, exam, and goal-setting decide who needs treatment more than any test. The clinician asks about onset, distribution, triggers, pain, hygiene difficulties, and function. Examination starts with passive limb movement at slow and fast velocities to feel the velocity-dependent catch, plus assessment of deep-tendon reflexes, clonus, plantar response, range of motion, and selective active movement. Two validated bedside scales document severity and track response: the Modified Ashworth Scale (0-4, scored on resistance to fast passive movement) and the Tardieu Scale (which separates dynamic tone from contracture by comparing slow and fast stretch). The Modified Tardieu is preferred for distinguishing fixed contracture from spasticity. Goal Attainment Scaling captures patient-centered outcomes. Differential diagnosis includes rigidity (Parkinson disease), paratonia (gegenhalten in dementia), dystonia, contracture, and rigidity from stiff-person syndrome. Investigations target the underlying cause: MRI of brain or spinal cord identifies new lesions; urinalysis and culture exclude infection; bladder ultrasound checks post-void residual; rectal exam excludes fecal impaction; and gait analysis with surface electromyography and three-dimensional motion capture refines decisions about botulinum toxin targets or surgery in ambulatory patients. Examination under anesthesia or diagnostic nerve blocks with short-acting local anesthetic are used selectively to separate spasticity from contracture before considering surgery.
Outlook depends on the underlying diagnosis and on how early team-based management begins. After stroke, two-thirds of patients with mild spasticity at 6 months remain at the same level or improve with treatment over the following year; severe contracture is largely preventable when therapy and focal injections start by 3 months. In cerebral palsy, the Gross Motor Function Measure typically plateaus by age 6-7; selective dorsal rhizotomy and intensive therapy can shift trajectories upward, but ambulatory status is set largely by initial GMFCS level. In multiple sclerosis and progressive hereditary spastic paraplegia, spasticity tends to worsen over years; symptomatic therapy slows but does not reverse the trajectory. Intrathecal baclofen patient-reported satisfaction remains above 75% at 5 years. Across diagnoses, the strongest predictors of good outcome are early specialist referral, attention to noxious triggers, and access to a multidisciplinary spasticity service.
Specialist input is needed once spasticity interferes with hygiene, function, sleep, or skin integrity, or when a focal injection or pump is being considered. Physiatrists (PMR) lead the assessment and oral therapy, perform botulinum toxin injections, and coordinate with neurosurgeons for SDR and intrathecal baclofen and with orthopedists for contracture surgery.
Find specialists →Botulinum toxin effect begins at 3-7 days, peaks at 4-6 weeks, and wanes by 12 weeks. Oral baclofen and tizanidine produce noticeable tone reduction within 1-2 weeks of titration. Intrathecal baclofen trials produce immediate response within 4-6 hours of test dose; permanent pump effect is stable within 2-4 weeks. Selective dorsal rhizotomy produces tone reduction within days, with functional gains accruing over 6-12 months of intensive postoperative therapy. Orthopedic surgery for fixed contracture requires 3-6 months of rehabilitation before maximum benefit is achieved.
Aerobic exercise (cycling, arm ergometry, adapted swimming) for 20-40 minutes most days improves cardiovascular fitness and may reduce tone transiently. Task-specific repetitive practice (constraint-induced movement therapy, locomotor training, treadmill walking with body-weight support) is the rehabilitation backbone. Resistance training of antagonist muscles is encouraged; classic concerns that strength training worsens spasticity have not been borne out by trials.
Look for a physiatrist or neurologist who runs a dedicated spasticity or spasticity-management clinic, performs at least 50 botulinum toxin injections a year under ultrasound or EMG guidance, and works in a multidisciplinary team with physical therapy, occupational therapy, orthotics, and neurosurgery. For children with cerebral palsy, prefer a pediatric rehabilitation team affiliated with a cerebral palsy registry.
Medically reviewed by AIHealz Medical Editorial Board · May 13, 2026
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