From these observations one would suspect that the ultimate posture of the legs—flexion or extension—does not depend solely on the completeness or incompleteness of the spinal cord lesion, as originally postulated by Riddoch. The development of paraplegia in flexion (extreme flexion of the hips and knees, as in a fetal position) relates also to the level of the lesion, being seen most often with cervical lesions and progressively less often with more caudal ones. Greatly troubling to the spinal patient are repeated flexor spasms, which are more frequent with higher lesions of the cord, and the ensuing contractures ultimately produce a fixed flexor posture. Furthermore, reduction of flexor spasms by elimination of nociceptive stimuli (infected bladder, decubitus, etc.) favors an extensor posture of the legs (paraplegia in extension). According to Guttmann, the positioning of the limbs during the early stages of paraplegia influences their ultimate posture. Thus, prolonged fixation of the paralyzed limbs in adduction and semiflexion favors subsequent paraplegia in flexion. Placing the patient prone or placing the limbs in abduction and extension facilitates the development of predominantly extensor postures. Nevertheless, strong and persistent extensor postures are usually observed only with partial lesions of the spinal cord.
A number of sensory phenomena are expected after functional cord transection. The main one, of course, is the loss of all sensibility below the lesion, that is, the sensory level. Of some interest is the fact that many patients report sensory symptoms in segments of the body below the level of their transection. Thus, a tactile stimulus above the level of the lesion may be felt below the transection (a type of synesthesia). Patients describe a variety of paresthesias, the most common being a dull, burning pain in the lower back and abdomen, buttocks, and perineum. We have encountered several patients in whom aching testicular or rectal pain was a very distressing problem. The pain may be intense and last for a year or longer, after which it gradually subsides. It persists after rhizotomy but can be abolished by anesthetizing the stump of the proximal (upper) segment of the spinal cord, according to Pollock and coworkers. Transmission of sensation over splanchnic afferents to levels of the spinal cord above the lesion, the conventional explanation, is therefore not the most plausible one.
The overactivity of sensory systems in the isolated segments of the spinal cord has several explanations. One assumes that suprasegmental inhibitory influences have been removed by the transection, so that afferent sensory impulses evoke exaggerated nocifensive and phasic and tonic myotatic reflexes. But isolated neurons also become hypersensitive to neurotransmitters. Since the early experiments of Cannon and Rosenblueth, it has been known that section of sympathetic motor fibers leaves the denervated structures hypersensitive to epinephrine and to acetylcholine.
Various combinations of residual deficits (of lower and upper motor neurons and sensory neurons) are to be expected. High cervical lesions, for example, may result in extreme and prolonged tonic spasms of the legs as a result of release of tonic myotatic reflexes. Under these circumstances, attempted voluntary movement may excite intense contraction of all flexor and extensor muscles lasting for several minutes. Segmental damage in the low cervical or lumbar gray matter, destroying inhibitory Renshaw neurons, may release activity of remaining anterior horn cells, leading to spinal segmental spasticity.
Any residual symptoms persisting after 6 months are likely to be permanent, although in a small proportion of patients some return of function (particularly sensation) is possible after this time. Loss of motor and sensory function above the lesion, coming on years after the trauma, is the result of an enlarging cavity in the proximal segment of the cord (see further on, under “Syringomyelia [Syrinx]”).