PHYSICAL EXAMINATION

LABORATORY STUDIES

DIAGNOSIS

Carpal tunnel syndrome

PATHOPHYSIOLOGY OF KEY SYMPTOMS

The patient’s complaint is primarily due to pain in the hand, accompanied by minor sensory and motor defects. The simultaneous appearances of both sensory and motor defects that are limited to a discrete dermatome suggest damage to one of the spinal nerves.

Pain receptors are free nerve endings distributed throughout the skin and, to a lesser degree, in visceral organs and spaces. Pain receptors are activated by mechanical, thermal, and chemical stimuli. Mechanical activation is generally sensed as fast pain, and thermal and chemical activation is generally sensed as slow pain.

Fast pain is carried along myelinated Aδ fibers that synapse in the dorsal horn and ascend through the neospinothalamic tract to the thalamus and then on to the somatosensory cortex (Fig. 51-1). Within the spinal cord, glutamate is a neurotransmitter secreted at Aδ synapses. Slow pain is carried along the unmyelinated C fibers, which make polysynaptic connections in the spinal cord and ascend through the paleospinothalamic tract to the brain stem and thalamus. Within the spinal cord, substance P is the neurotransmitter released at C fiber synapses. The multiple synaptic connections transmitting slow pain mean that slow pain is very poorly localized on a somatotopic map.

FIGURE 51–1 Transmission of pain signals into the brain stem, thalamus, and cerebral cortex by way of the fast pricking pain pathway and slow burning pain pathway.