Spasticity



Spasticity





Spasticity is a disorder characterized by a velocity-dependent increased resistance to passive stretch, associated with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex. Spasticity is part of the UMN syndrome, which includes the positive symptoms of spasticity and uninhibited flexor reflexes in the lower limbs and the negative symptoms of weakness and poor dexterity. Commonly used clinical scales are listed in Table 26-1.




PHYSICAL MODALITIES

A stretching program should be the cornerstone for most spasticity treatment programs. Splints, casting, or bracing can help preserve ROM by “resetting the muscle spindles.” Contractures can be reduced by serially casting a joint (i.e., increasing the stretch stepwise for 1 to 2 days at a time), although this technique is not always well-tolerated and may lead
to skin breakdown. Cryotherapy (>15 minutes) may be helpful transiently by reducing the hyperexcitability of the muscle stretch reflex and reducing nerve conduction velocities. Functional electrical stimulation (>15 minutes) can improve function and reduce tone for hours after the stimulation (thought to be due to neurotransmitter modulation at the spinal cord level). Hippotherapy, which involves rhythmic movements, is found useful in spasticity reduction in lower limbs. Other modalities include application of tendon pressure, cold, warmth, vibration, massage, low-power laser, and acupuncture.1


PHARMACEUTICAL OPTIONS

Oral Medications – These may be indicated for nonfocal spasticity. Efficacy is often limited by side effects. FDA-approved medications include baclofen, diazepam, dantrolene (clonidine), and tizanidine. Recently, offlabel use of gabapentin has shown promising results in the treatment of spasticity in a small group of MS patients undergoing a crossover study.2

Botulinum Toxin-A (BTX-A)BTX irreversibly blocks NMJ transmission by inhibiting presynaptic ACh release. BTX-A (Fig. 26-2; Botox and Allergan) is FDA-approved for blepharospasm, strabismus, and cervical dystonia and most recently for severe glabellar (between the eyebrows) frown lines. It is also widely used for spasticity and myofascial pain with favorable results. Onset of effect is typically 24 to 72 hours. Peak effect is at 2 to 6 weeks. Clinical efficacy is typically up to 3 to 4 months. Recovery is due to axonal sprouting.

The theoretical parenteral LD50 for a 75-kg adult is 3,000 U; the recommended maximum dose is 10 U/kg IM (up to 400 U) per visit. At least 3 months of interval between sessions is recommended to decrease the potential for antibody formation. BTX-A is contraindicated in pregnancy, lactation, NMJ disease, and concomitant aminoglycoside use and with human albumin USP allergy. BTX-A should be stored at -5° to -20°C and should be reconstituted with 0.9% preservative-free saline only. It is available for use for up to 4 hours if refrigerated (2° to 8°C).

Only gold members can continue reading. Log In or Register to continue

Stay updated, free articles. Join our Telegram channel

Jun 19, 2016 | Posted by in PHYSICAL MEDICINE & REHABILITATION | Comments Off on Spasticity

Full access? Get Clinical Tree

Get Clinical Tree app for offline access