As discussed in greater detail in Chap. 42, the initial effect of an acute cervical cord transection is abolition of all sensorimotor reflex, and autonomic functions of the isolated spinal cord. The autonomic changes include hypotension, loss of sweating and piloerection, paralytic ileus and gastric atony, and paralysis of the bladder. The flare component of the axon reflex may be lost. Plasma epinephrine and NE are reduced. This state, known as spinal shock, usually lasts for several weeks as described in Chap. 42. The basic mechanisms are not known, but changes in neurotransmitters (catecholamines, enkephalins, endorphins, substance P, and 5-hydroxytryptamine) and their inhibitory activities are considered to play a role. Naloxone mitigates some of the aspects of spinal shock; this may be, at least in part, the result of release of preformed endogenous opioids from the distal axons that are separated from their cells of origin in the periaqueductal gray region. Once these endogenous substances are exhausted, the phenomenon of spinal shock ends (see Chap. 42).
After spinal shock dissipates, reflex sympathetic and parasympathetic functions return because the afferent and efferent autonomic connections within the isolated segments of the spinal cord are intact, although no longer under the control of higher centers. With cervical cord lesions, there is a loss of the sympathetically mediated cardiovascular changes in response to stimuli reaching the medulla. However, cutaneous stimuli (pinprick or cold) in segments of the body below the transection will raise the blood pressure. However, a fall in blood pressure is not compensated by sympathetic vasoconstriction. Hence tetraplegics are almost obligatorily prone to orthostatic hypotension. Pinching the skin below the lesion causes gooseflesh in adjacent segments. Heating the body results in flushing and sweating over the face and neck, but not in the trunk and legs, because of the loss of connections from the hypothalamus. Bladder and bowel, including their sphincters, which are at first flaccid, become automatic as spinal reflex control returns. There may be reflex penile erection or priapism and even rarely ejaculation. With lesions in the upper thoracic cord, similar but lesser degrees of labile blood pressure are seen; in several of our patients with destructive myelitis, a viral infection of fever brought out episodes of a drop in blood pressure to approximately 80/60 mm Hg and a subsequent rapid rise to 190/110 mm Hg.
After a time, the tetraplegic patient may develop a mass reflex in which flexor spasms of the legs and involuntary emptying of the bladder are associated with a marked rise in blood pressure, bradycardia, and sweating and pilomotor reactions in parts below the cervical segments (autonomic dysreflexia). These reactions may also be evoked by pinprick, passive movement, contactual stimuli of the limbs and abdomen, and pressure on the bladder. An exaggerated vasopressor reaction also occurs in response to injected NE. In such attacks, the patient experiences paresthesias of the neck, shoulders, and arms; tightness in the chest and dyspnea; pupillary dilatation; pallor followed by flushing of the face; sensation of fullness in the head and ears; and a throbbing headache. Plasma NE and dopamine rise slowly during the autonomic discharge. When such an attack is severe and prolonged, electrocardiographic changes may appear, sometimes with evidence of myocardial injury that has been attributed to direct catecholamine toxicity or, alternatively, to myocardial ischemia caused by increased afterload or to coronary vasospasm. Seizures and visual defects have also been observed, related to cerebral dysautoregulation. Clonidine, up to 0.2 mg tid, has been useful in preventing the hypertensive crises.