The responses of animals and humans to spinal cord injury (SCI) illustrate the integration of reflexes at the spinal level. The deficits seen after SCI vary, of course, depending on the level of the injury. Clinical Box 1 provides information on long-term problems related to SCI and recent advancements in treatment options.
Clinical Box 1
In all vertebrates, transection of the spinal cord is followed by a period of spinal shock during which all spinal reflex responses are profoundly depressed. Subsequently, reflex responses return and become hyperactive. The duration of spinal shock is proportional to the degree of encephalization of motor function in the various species. In frogs and rats it lasts for minutes; in dogs and cats it lasts for 1–2 h; in monkeys it lasts for days; and in humans it usually lasts for a minimum of 2 weeks.
Cessation of tonic bombardment of spinal neurons by excitatory impulses in descending pathways (see below) undoubtedly plays a role in development of spinal shock. In addition, spinal inhibitory interneurons that normally are themselves inhibited may be released from this descending inhibition to become disinhibited. This, in turn, would inhibit motor neurons. The recovery of reflex excitability may be due to the development of denervation hypersensitivity to the mediators released by the remaining spinal excitatory endings. Another contributing factor may be sprouting of collaterals from existing neurons, with the formation of additional excitatory endings on interneurons and motor neurons.
The first reflex response to appear as spinal shock wears off in humans is often a slight contraction of the leg flexors and adductors in response to a noxious stimulus (ie, the withdrawal reflex). In some patients, the knee jerk reflex recovers first. The interval between cord transection and the return of reflex activity is about 2 weeks in the absence of any complications, but if complications are present it is much longer. Once the spinal reflexes begin to reappear after spinal shock, their threshold steadily drops.
Circuits intrinsic to the spinal cord can produce walking movements when stimulated in a suitable manner even after spinal cord transection in cats and dogs. There are two locomotor pattern generators in the spinal cord: one in the cervical region and one in the lumbar region. However, this does not mean that spinal animals or humans can walk with out stimulation; the pattern generator has to be turned on by tonic discharge of a discrete area in the midbrain, the mesencephalic locomotor region, and, of course, this is only possible in patients with incomplete spinal cord transection. Interestingly, the generators can also be turned on in experimental animals by administration of the norepinephrine pre cursor L-dopa (levodopa) after complete section of the spinal cord. Progress is being made in teaching humans with SCI to take a few steps by placing them, with support, on a treadmill.
