REHABILITATION OF MODERATE TO SEVERE TBI: MOVEMENT DISORDERS: SPASTICITY AND CONTRACTURES  

  • Due to loss of cortical control over spinal reflex centers following an upper motor lesion, which results in increased input to or output from the spinal cord. This can cause unwanted and involuntary motor phenomena when the limbs are moved actively or passively, usually an increase in flexor tone in the upper limbs, a tendency toward extensor tone in the lower limbs, and hypertonicity in the torso, face, mouth, and pharynx. Common terms include "spastic gait", "spastic elbow flexion", "spastic hand", spastic equinovarus", and "spastic dystonia". Risk factors for early spasticity include immobilization, motor dysfunction (hemiplegia or tetraplegia), associated hypoxic ischemic injury, spinal cord injury, and age (Zafonte, et al 2004).

  • The 13 clinical patterns of motor dysfunction following TBI are:

    1. Adducted/internally rotated shoulder - The humerus is held tightly against the chest wall. Frequently, the elbow is flexed and the forearm is pronated due to shoulder internal rotation, and the pectoralis major muscle is prominent. ROM into abduction and external rotation are limited and may be painful (Keenan & Mehta, 2004)

    2. Bent elbow - Due to more spasticity in the three major elbow flexors (the biceps, brachialis, and brachioradialis) than in the elbow extensors. Frequently, there is relatively fixed elbow flexion posturing, with either voluntary flexion and some extension, or, less commonly, little voluntary flexion or extension

    3. Pronated forearm - More common than supination, although many patients have some degree of active pronation and active supination. May be due to spasticity of the pronator teres and/or pronator quadratus.

    4. Bent wrist - Wrist flexion posturing is more common than wrist extension. Frequently, passive motion is severely restricted, but there may be slight wrist extension and flexion as recovery occurs

    5. Clenched fist - The fingers are clasped tightly into the palm, due to spasticity, separately, in part, or in their entirety of the flexor digitorum sublimis and the flexor digitorum profundus, and, possibly, weakness in the extrinsic finger extensors, contracture of the palmer skin and joint capsule, collateral ligament tightness at various finger joints, and fixed contracture of the intrinsic muscles. The metacarpophalangeal and proximal interphalangeal joints are flexed to 90 degrees, and finger tightness is enhanced with wrist extension. Frequently, the distal interphalangeal joints are fully extended or flexed into the palm

    6. Thumb-in-palm deformity - The thumb is pulled into the palm and unable to function due to spasticity in many different muscles, including the flexor pollicus longus, flexor pollicus brevis, abductor pollicis brevis, opponens pollicus, adductor pollicis, and first dorsal and palmer interossei muscles. Frequently, thumb-in-palm deformity is accompanied by clenched fist deformity

    7. Excessively flexed hip - Hip flexion predominates over hip extension, causes hip flexor posturing, and may cause knee flexion deformities as well. Excessively flexed hip is due to spasticity in the iliopsoas, rectus femoris, and/or pectineus, and may be exacerbated by spasticity in the adductor longus and brevis. When adductor spasticity is also present, pelvic obliquity frequently develops

    8. Scissoring thighs - Spasticity of the adductor longus and brevis, adductor magnus, and gracilis results in "kissing" thighs during sitting or a scissoring gait. Severe adductor spasticity can lead to hip subluxion or dislocation or pelvic obliquity. If hip flexor spasticity is also present, the thigh of the involved side almost "sits atop" the opposite thigh

    9. Stiff knee - Knee is maintained in extension, during the swing phase or throughout the gait cycle, due to contracture of the rectus femoris, vastus medialis, vastus lateralis, vastus intermedius, and/or the hamstrings. May also be caused by hip flexor weakness or calf muscle spasticity. Toe drag is likely during the early swing phase. Circumduction of the involved limb, hiking of the pelvis, and/or contralateral limb vaulting may occur as a result.  An algorithm can evaluate stiff-legged gait, identify the specific etiology, and thereby serve as the basis of a treatment plan (Kerrigan, et al 1999)

    10. Bent knee - Persistent bent knee posturing and knee flexor contractures occur when hamstring spasticity is severe

    11. Equinovarus foot with curl or claw toes -
      • Equinovarus posturing is demonstrated in terminal swing; weight is applied to the lateral border of the foot in the stance phase; and the knee is hyperextended, due to spasticity of the heads of the gastrocnemius, the soleus, tibialis anterior, tibialis posterior, extensor hallucis longus, extensor digitorum, flexor digitorum, foot intrinsics, and peroneus longus
      • Treatment includes split anterial tibial transfer, which can result in definite improvement and increased autonomy (Vogt, 1998) and serial plaster casting (Singer, et al 2001). Physiotherapy alone can remediate reduced dorsiflexion range, with serial casting +/- botulinum to correct persistent or worsening contracture (Sunger, et al 2004)
      • Curled toes may also be present due to contracture of the long toe flexors
      • Claw toes may also be present due to exaggerated activity in the toe extensors and flexors and the intrinsic muscles of the foot

    12. Valgus foot - Occurs in stance phase and leads to abnormal base of support, valgus force on the knee which leads to genuvalgum deformity, and hind-foot valgus or pronation deformity. Due to an overactive peroneus longus muscle and possibly to a preexisting pes planus or congenital flat feet, weakness of the gastrocsoleus muscle, leg-length discrepancy, and contralateral hip abductor weakness, knee valgus deformity, and/or ankle valgus deformity

    13. Hitchhiker's great toe - A persistent extension of the great toe, due to a hyperactive extensor hallucis longus muscle

  • Diagnosis, which is still somewhat problematic (Elovic, et al 2004), involves:
    • Ashworth Scale (Zafonte, et al 2004)
    • EMG recordings of involved muscles to distinguish voluntary capacity from spastic reaction; dynamic EMG to determine which muscle(s) contribute to the dynamic dysfunction present and to provide guidelines for distinguishing local from referred motion errors (Perry, 1999)
    • Inspection, palpation, and measurement of the area to determine deformity, swelling, tenderness, atrophy, weakness, leg-length discrepancy, skinfold markings, nailbed infection or indentation, ROM, and pain on motion; passive ROM at slow, intermediate, and rapid speeds of stretch may help distinguish among hypertonicity, rigidity, and contracture
    • X-rays to rule out bony deformity, such as congenital deformities, heterotopic ossification, fractures, dislocations, or ankylosis
    • Anesthetic block of the nerves to the affected area, with short-acting local anesthetics such as lidocaine or bupivacaine, to determine if a fixed myostatic contraction of the affected joint is responsible for the limited ROM, dynamic movement, or muscle stiffness
    • Anesthetic blocks of individual muscles to determine if surgical release will improve function in the potentially functional area
    • Thomas test to determine hip flexor tone
    • Three-dimensional motion analysis to quantify amount of hip adduction, knee flexion, and ankle motion
    • Medication use which can mask the severity of the spasticity, e.g., neuroparalytic agents, opioids, benzodiazepines, and propofol (Zafonte, et al 2004)

  • Requires intervention when spasticity interferes with rehab goals:
    • Range of motion and exercise
    • Cryotherapy and/or application of casts, if necessary. Serial casting may be beneficial to treat pressure ulcers at the extremities of patients with severe cerebral spasticity (Pohl, et al 2002)
    • Cutaneous electrical stimulation for transient relief (Seib, et al 1994)
    • Medication, if spasticity persists and the decrease in spasticity outweighs potential side effects:
      • Dantrolene sodium
        • Reduces the force of the muscle contraction, thereby reducing tension in spastic muscles
        • Useful for short-duration, low-frequency, mild-to-moderate spasticity, such as clonus or brief spasms
        • Has low cognitive side effects, but may be sedating to patients with arousal dysfunction and may be hepatotoxic

      • Baclofen
        • Acts as a GABA antagonist, thereby reducing muscle tone and spasticity in skeletal muscles by inhibiting transmission of specific synapses within the spinal cord
        • Useful for flexor spasms
        • Significant side effects, including cognitive and arousal effects, drowsiness, confusion, and hallucinations
        • Intrathecal administration
          • Both bolus and continuous infusion have been found effective (Meythaler, et al 1996; 1997; 1999)
          • May reduce cognitive and arousal side effects, but continue to include drowsiness, dizziness, and weakness
          • Useful for diffuse spasticity in the limbs, particularly hip flexor and hamstring spasticity
          • Intrathecal overdose due to pump failure or other technical problems may cause seizures, coma, and respiratory depression

      • Botulinum toxin
      • Clonidine or the benzodiapines may be effective (Dall, et al 1996), but may need to be monitored for cognitive side effects

      • Tizandine is effective in decreasing spastic hypertonia, but there are limitations on its use due to side effects related to drowsiness (Meythaler, et al 2001)

    • Motor point blocks and nerve blocks during early recovery, when increased muscle tone is the most severe, if medication fails
      • Reduce spastic tension for 3-5 months (or possibly years) produced by a contracting spastic muscle or muscle group
      • Allow compensatory behaviors during functional activities and passive limb mobilization (Botte, et al 1995) and prevent an impingement syndrome.
      • Primarily phenol blocks, injected in or near a nerve bundle identified by electrical stimulation prior to injection
      • Used cautiously in patients taking anticoagulants
      • Injection into a mixed sensory-motor nerve may produce dysesthesia

    • Surgery
      • Surgical release of offending muscles, surgical lengthening of flexor muscles , or neurectomy during late recovery, if spasticity persists and when it has become static, for patients with functional potential
      • Carpectomy and fusion, alone or following surgical release or lengthening, for patients with functional control (Pinzur, 1996)

Based on information in Medical Rehabilitation of Traumatic Brain Injury, L.J. Horn and N.D. Zasler, eds. St. Louis, MO, Mosby, 1996, except for information where other papers are cited.