Stage of heightened reflex activity This is the more familiar condition of spasticity that emerges sometime  after spinal injury and is also typical of most of the nontraumatic subacute myelopathies that have developed more slowly than traumatic injuries and have not had a period of spinal shock. A few weeks after an acute traumatic injury, all reflex responses, which are initially minimal and unsustained, become stronger and more easily elicitable and as time passes, come to include additional and more proximal muscles. Gradually, the typical pattern of heightened flexion reflexes emerges: dorsiflexion of the big toe (Babinski sign); fanning of the other toes; and later, flexion or slow withdrawal movements of the foot, leg, and thigh with contraction of the tensor fascia lata muscle (the last several features referred to as “triple flexion”). Tactile stimulation of the foot may suffice as a stimulus, but a painful stimulus is more effective. The Achilles reflexes and then the patellar reflexes return. Retention of urine becomes less complete, and at irregular intervals urine is expelled by spontaneous contractions of the detrusor muscle. Reflex defecation also begins. After several months the withdrawal reflexes become greatly exaggerated, to the point of flexor spasms, and they may be accompanied by profuse sweating, piloerection, and automatic emptying of the bladder (occasionally of the rectum). This is the “mass reflex,” which can be evoked by stimulation of the skin of the legs or by some interoceptive stimulus, such as a full bladder. Varying degrees of heightened flexor reflex activity may last for years, or indefinitely. Heat-induced sweating is defective, but reflex-evoked (“spinal”) sweating may be profuse (see Kneisley). In such cases the lateral horn cells in much of the thoracic cord are still viable and have been disinhibited. Above the level of the lesion, thermoregulatory sweating may be exaggerated in order to compensate for the loss of evaporative cooling of lower segments, and there is cutaneous flushing, hypertension that causes pounding headache and reflex bradycardia. This syndrome (“autonomic dysreflexia”) is episodic and occurs in response to a certain stimuli, such as a distended bladder or rectum. It has been ascribed to the reflex release of adrenaline from the adrenal medulla and of norepinephrine from the disinhibited sympathetic terminals caudal to the lesion but is exaggerated by defective baroreceptor compensatory reflexes as discussed in Chap. 25.
Extensor reflexes and tone eventually develop in most cases (18 of 22 of Kuhn’s patients who survived more than 2 years), but their appearance does not lead to the abolition of the exaggerated flexor reflexes. The overactivity of extensor muscles may appear as early as 6 months after the injury, but this only happens, as a rule, after the flexor responses are fully developed. Extensor responses are at first manifest in certain muscles of the hip and thigh and later of the leg. In a few patients, extensor reflexes are organized into support reactions sufficient to permit spinal standing. Kuhn observed that extensor movements were at first provoked most readily by a sudden shift from a sitting to a supine position and later by proprioceptive stimuli (squeezing of the thigh muscles) and tactile stimuli from wide areas. Marshall, in a study of 44 patients with chronic spastic paraplegia of spinal origin, found all possible combinations of flexor and extensor reflexes; the type of reflex obtained was determined by the intensity and duration of the stimulus (a mild prolonged noxious stimulus evoked an ipsilateral extensor reflex; an intense brief stimulus, a flexor response).