Anatomy and Physiology

Sensory Transduction

Activation of sensory end organs produces a generator potential in the afferent neurons. If the generator potential reaches threshold, an action potential is produced that is conducted to the spinal cord by the sensory axons.

Sensory transducers are seldom directly affected by neuropathic conditions, although peripheral vascular disease can produce dysfunction of the skin sensory axons, and systemic sclerosis can damage skin sufficiently to produce a primary deficit of sensory transduction (Table 28.1).

Table 28.1 Sensory Receptors

Sensory Afferents

The rate of action potential propagation differs according to the diameter of the axons and depending on whether the fibers are myelinated or unmyelinated. In general, nociceptive afferents are small myelinated and unmyelinated axons. Non-nociceptive afferents are large-diameter myelinated axons. Afferent fiber characteristics are shown in Table 28.2.

Table 28.2 Sensory Afferents

Spinal Cord Pathways

Sensory afferent information passes through the dorsal root ganglia to the dorsal horn of the spinal cord. Some of the axons pass through the dorsal horn without synapsing and ascend in the ipsilateral dorsal columns; these serve mainly joint position and touch sensations. Other axons synapse in the dorsal horns, and the second-order sensory neurons cross in the anterior white commissure of the spinal cord to ascend in the contralateral spinothalamic tract. Although this tract is best known for conduction of pain and temperature information, some non-nociceptive tactile sensation is conducted as well.

The dorsal column tracts ascend to the cervicomedullary junction, where axons from the leg synapse in the nucleus gracilis and axons from the arms synapse in the nucleus cuneatus. Fig. 28.1 shows the ascending pathways through the spinal cord to the brain.

Fig. 28.1 Axial section of the spinal cord, showing dorsal and ventral roots forming a spinal nerve. Sensory afferents give rise to two major ascending pathways: the anterolateral system (nociceptive, serving thermal sensation primarily) and posterior columns (serving large-fiber modalities primarily including touch, vibration, and proprioception). Inhibitory input derives from descending fibers as well as collaterals, via interneurons, from mechanoreceptive fibers. Dashed circle indicates the anterior white commissure. DRG, Dorsal root ganglion.

(Modified with permission from Rizzo, M.A., Kocsis, J.D., Waxman, S.G., 1996. Mechanisms of paresthesiae, dysesthesiae, and hyperesthesiae: role of Na⁺ channel heterogeneity. Eur Neurol 36, 3-12.)

Brain Pathways

Sensory Abnormalities

Sensory perception abnormalities are varied, and the pattern of symptoms often is a clue to diagnosis:

Loss of sensation (numbness)

Dysesthesia and paresthesia

Neuropathic pain

Sensory ataxia

Patients often use the term numbness to mean any of a variety of symptoms. Strictly speaking, numbness is loss of sensation usually manifested as decreased sensory discrimination and elevated sensory threshold; these are negative symptoms. Some patients use the term numbness to mean weakness; others are referring to positive sensory symptoms such as dysesthesia and paresthesia.

Dysesthesia is an abnormal perception of a sensory stimulus, such as when pressure produces a feeling of tingling or pain. If large-diameter axons are mainly involved, the perception typically is tingling; if small-diameter axons are involved, the perception commonly is pain. Paresthesia is an abnormal spontaneous sensation similar in quality to dysesthesia. Dysesthesias and paresthesias usually are seen in localized regions of the skin affected by peripheral neuropathic processes such as polyneuropathy or mononeuropathy. These perceptual abnormalities also can be seen in patients with central conditions such as myelopathy or cerebral sensory tract dysfunction.

Neuropathic pain can result from damage of any cause to the sensory nerves. Peripheral neuropathic conditions result in failure of conduction of the sensory fibers, giving decreased sensory function plus pain from discharge of damaged nociceptive axons. The pathophysiology of neuropathic pain is interesting. Part of its basis is lowering of the membrane potential of the axons so that minor deformation of the nerve can produce repetitive action-potential discharges (Zimmermann, 2001). An additional feature with neuropathic conditions appears to be membrane potential instability, so that the crests of fluctuations of membrane potential can produce action potentials. Finally, cross-talk (ephaptic transmission) between damaged axons allows an action potential in one nerve fiber to be abnormally transmitted to an adjacent nerve fiber. These pathophysiological changes also produce exaggerated sensory symptoms including hyperesthesia and hyperpathia. Hyperesthesia is increased sensory experience with a stimulus. Hyperpathia is augmented painful sensation.

Sensory ataxia is the difficulty in coordination of a limb that results from loss of sensory input, particularly proprioceptive input. The resulting deficit may resemble cerebellar ataxia, but other signs of cerebellar dysfunction are seen on neurological examination.

Localization of Sensory Abnormalities

A general guide to sensory localization is presented in Table 28.3. Guidelines for diagnosis of these sensory abnormalities are summarized in Table 28.4. Details of specific sensory levels of dysfunction are discussed next.

Table 28.3 Sensory Localization

Level of Lesion	Features and Location of Sensory Loss
Cortical	Sensory loss in contralateral body restricted to portion of the homunculus affected by lesion. If entire side is affected (with large lesions), either the face and arm or the leg tends to be affected to a greater extent.
Internal capsule	Sensory symptoms in contralateral body which usually involve head, arm, and leg to an equal extent. Motor findings common, although not always present.
Thalamus	Sensory symptoms in contralateral body including head. May split midline. Sensory dysfunction without weakness highly suggestive of lesion of the thalamus.
Spinal transaction	Sensory loss at or below a segmental level, which may be slightly different for each side. Motor examination also key to localization.
Spinal hemisection	Sensory loss ipsilateral for vibration and proprioception (dorsal columns), contralateral for pain and temperature (spinothalamic tract).
Nerve root	Sensory symptoms follow dermatomal distribution.
Plexus	Sensory symptoms span two or more adjacent root distributions, corresponding to anatomy of plexus divisions.
Peripheral nerve	Distribution follows peripheral nerve anatomy or involves nerves symmetrically.

Table 28.4 Diagnosis of Sensory Abnormalities

Peripheral Sensory Lesions

Lesions of peripheral nerves and the plexuses produce sensory loss that follows their peripheral anatomical distribution. Exact mapping of sensory deficit is commonly difficult because sensory testing is subjective. Also recognized are interindividual differences in sensory peripheral anatomy including distribution and overlap of sensory fields. Peripheral sensory loss produces a multitude of potential complaints. Clues to localization are as follows:

Distal sensory loss and/or pain in more than one limb suggests peripheral neuropathy.

Sensory loss in a restricted portion of one limb suggests a peripheral nerve or plexus lesion, and mapping of the deficit should make the diagnosis.

Sensory loss affecting an entire limb seldom is due to a peripheral lesion, because even proximal plexus lesions rarely affect the entire limb. A central lesion should be sought.

Unfortunately, especially with peripheral lesions, a discrepancy between the complaint and the examination findings is common. The patient may complain of sensory loss affecting an entire limb when the examination shows a median or ulnar distribution of sensory loss. Alternatively, the patient may complain of sensory loss, but examination fails to reveal a sensory deficit. This discrepancy is more likely to be due to limitations of the examination than to malingering. Also, patients may have significant sensory complaints as a result of pathophysiological dysfunction of the afferent axons while the integrity and conducting function of the axons are still intact, so the examination will show no loss of sensory function.

Fig. 28.2 summarizes the peripheral nerve anatomy of the body, and Fig. 28.3 shows the dermatomal distribution.

Fig. 28.2 Cutaneous (cut.) fields of peripheral nerves (n.). Note that thoracic dermatomes are innervated by primary anterior and posterior rami of spinal nerves from the respective level. Spinous processes of T1, L1, and S1 are indicated. inf., Inferior; lat., lateral; med., median.

(Reprinted with permission from Haymaker, W., Woodall, B., 1953. Peripheral Nerve Injuries: Principles of Diagnosis. W.B. Saunders, Philadelphia.)

Fig. 28.3 Dermatomes: cervical (C), thoracic (T), lumbar (L), and sacral (S). Boundaries are not quite as distinct as shown here because of overlapping innervation and variability among individuals.

(Reprinted with permission from Martin, J.H., Jessell, T.M., 1991. Anatomy of the somatic sensory system. In: Kandel, E.R. (Ed.), Principles of Neural Science. Appleton & Lange, Norwalk, Conn.)

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