Head's Zones

Visceral pain is not felt in the internal organ where it originates, but is rather referred to a cutaneous zone (of Head) specific to that organ.

This phenomenon is explained by the arrival of sensory impulses from both the internal organ and its related zone of Head at the posterior horn at the same level of the spinal cord; the brain thus (mis)interprets the visceral pain as originating in the related cutaneous zone. The

pain may be described as urning, pulling, pressure, or soreness, and there may be cutaneous hyperesthesia to light touch. Certain etiologies (e. g., angina pectoris, cholecystitis, gastric ulcer, intestinal disease) can produce ipsilateral mydriasis. In addition to the zones of Head, referred pain may also be felt in muscles and connective tissue (pressure points, as in Blumberg's sign or

McBurney's point). Physicians should beware ofmistaking referred for local pain. Spinal Autonomic Reflexes The afferent arm of these reflexes originates in the internal organs and terminates on the sympathetic preganglionic neurons in the intermediolateral and intermediomedial cell columns of the spinal cord at levels T1 through L2 (p. 140).

Typical examples are the viscerovisceral reflex

(causing meteorism in colic and anuria in myocardial infarction), the viscerocutaneous reflex (a

visceral stimulus leads to sweating and hyperemia in the corresponding zone of Head), the cutivisceral reflex (reduction of colic,myogelosis,etc., by warm compresses or massage), the visceromotor reflex (defensive muscle contraction in response to visceral stimulus), and the vasodilatory axon reflex (dermographism). Any abnormality of these reflexes may be an important sign of impaired autonomic function (cardiovascular, gastrointestinal, thermoregulatory,

or urogenital), particularly in patients with spinal cord disorders.

Complex Regional Pain Syndrome (CRPS)

The International Association for the Study of Pain (IASP) recommends the term CRPS for a set of painful disorders of apparently related pathophysiology, which are further classifiedinto CRPS type I (reflex sympathetic dystrophy;

without peripheral nerve injury) and CRPS type II (causalgia; with peripheral nerve injury).

CRPS usually results from a traumatic or other injury to a limb, often in conjunction with prolonged disuse. The pain is persistent and diffuse, and of burning, stabbing, or throbbing quality, often in association with allodynia (pain evoked by a normally nonpainful stimulus) and hyperpathia (abnormally intense pain evoked by a normally painful stimulus). It is generally not in a radicular or peripheral nerve distribution. It

may be accompanied by motor disturbances (paresis, disuse of limb), autonomic disturbances (sweat secretion or circulatory disturbances), trophic changes (edema, muscle atrophy, joint swelling, bone destruction), and reactive mental changes (depression, anxiety). The

diagnosis of CRPS is based on criteria defined by the IASP and requires the exclusion of other disease processes such as fracture, vasculitis, thrombosis, radicular lesion, rheumatoid ar-

thritis, etc. Its pathogenetic mechanism is un-known