Spasticity in spinal cord injury

Introduction

Spasticity is a common complication after spinal cord injury (SCI) that occurs in the context of an upper motor neuron injury syndrome, and may develop even years after the acute injury leading to further loss of function ( ; ).

Spasticity was defined by as “a motor disorder characterized by a velocity dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyper excitability of the stretch reflex, as one component of the upper motoneuron syndrome.” Dynamic phenomena were not included, so the Ability Network (an international panel of clinical experts to develop management algorithms to guide and standardize assessment, treatment and outcomes in SCI people with disabling spasticity) recommends Pandyan definition ( ): “Disordered sensorimotor control, resulting from an upper motor neuron injury, presenting as intermittent or sustained involuntary activation of muscles.”

Considering every SCI people regardless of the time of evolution, neurological level or extent, the prevalence of spasticity is approximately 65% according to the studies of . Some studies have been conducted on SCI complications; demonstrated an incidence of 25%–37% in acute traumatic SCI, showed an incidence of 15%–36% in acute nontraumatic SCI, and in papers by or , incidence of chronic SCI is estimated about 65%–93%. There is no significant correlation among neurological level, ASIA Impairment Scale (AIS) grade, and spasticity, but related severe spasticity with cervical levels and grade A, and a highest prevalence of spasticity among people with grade C.

Pathophysiology of spasticity

The stretch reflex is a monosynaptic reflex that originates in the muscle spindles with any stimulus (not just stretch) and travels through an afferent pathway to the spinal cord (SC) where it synapses with the corresponding alpha motor neuron and contracts the muscle fibers where it is has produced the stimulus. If the stimulus is prolonged, the Golgi tendon organs are activated, and via interneurons Ib, the previous contraction can be relaxed. Studies by show that spasticity is generally due to a lowered threshold of phasic or tonic stretch reflexes; when inhibitory signals are lost due to spinal cord damage, the segmental reflexes are released and become hyperactive. In addition, other spinal mechanisms are postulated, such as fusimotor hyperexcitability, axonal sprouting, reduction of presynaptic inhibition, and reduction of reciprocal inhibition.

described that clinical features of spasticity depend on the greater or lesser loss of the ability to voluntarily modulate the level of activity of a given motor pool and the capacity of the interneurons that project to these motor pools to recruit the appropriate combination of them.

Besides, there are plastic alterations in affected muscles. Basically, spasticity causes fibrosis, atrophy of muscle fibers, decrease in the elastic properties, decrease in the number of sarcomeres, accumulation of connective tissue, and alteration of contractile properties toward tonic muscle characteristics.

Manifestations of spasticity in spinal injuries

According to , two classification criteria can be used: the place where the stimulus for spasticity is located, which differentiates between intrinsic if the stimulus emerges within the central nervous system, and extrinsic if the afferences come from other structures such as the skin, muscles, and joints; also if there is no resultant movement, a tonic or static component is described, and if there is any movement, a phasic or dynamic component is described. So, we can distinguish three main types of spasticity:

• (a)

  Intrinsic tonic spasticity: hypertonia.

• (b)

  Intrinsic phasic spasticity: clonus and osteotendinous hyperreflexia.

• (c)

  Extrinsic spasticity: spasms.

The presence of triggers was described by ; these exacerbating factors can cause a patient with a SCI and a normal or decreased tone to present intense or frequent spasms. The most important triggers are neurogenic bowel (constipation) and bladder problems (hyperreflexia). The supine position is associated with more intense hypertonia and increased likelihood to provoke spasms, and according with , the most frequent clinical sign is usually spasms when making any transfer. Other factors such as pregnancy, cold, circadian rhythm, pressure ulcers, menstrual cycle, stress, and even tight clothing also increase spasticity, while acute and severe infections (sepsis) and syringomyelia can cause both an increase of spasticity as a sudden absence of spasticity.

The ability to achieve functional goals may be impaired due to spasticity and can even make the length of hospital stay last longer, according to .

Assessment of spasticity and its consequences