The finely graded, discriminative tactile, and kinesthetic senses are associated with large, myelinated A and A (Type I & II) axons, from larger somata in the dorsal root ganglia. The non-discriminative senses (thermoreceptive, crude tactile, sexual and nociceptive) are associated with small diameter A and C (Type II, IV) axons, from smaller cell bodies in the dorsal root ganglia. The axons of each dorsal root innervate a circumscribed area of skin, known as a dermatome.

The centrally directed axons of the discriminative sensory receptors, enter the cord dorsomedially and bifurcate into a short descending and a long ascending branch. The short branches project deeply into the grey matter of the spinal cord, making synapses in the dorsal horn, and in the motor nuclei of the ventral horn. The ascending collaterals enter the ipsilateral dorsal white column, where, axons entering at any spinal level, are overlaid laterally to the axons ascending from lower levels. This creates an orderly representation of the body in the dorsal column: inputs from the lowest segments being most medial (in the gracile bundle) and the upper segments (above T6) most lateral, in the cuneate fasciculus.

The axons in the dorsal column synapse in the dorsal column nuclei (gracile & cuneate nuclei) in the medulla. Only 25% of the dorsal column axons ever reach the dorsal column nuclei. Most of the proprioceptive afferents, particularly from the lower limbs, and many slowly adapting cutaneous afferents, leave the dorsal column after a few segments, to synapse on cells of Clarke's column (nucleus dorsalis- between C8/T1 and L2/L3) which give rise to the ipsilateral dorsal spino-cerebellar tract. Many of these will terminate in the ipsilateral cerebellum to mediate unconscious proprioceptive regulation. Many will synapse in medullary nuclei (cervical nucleus - see below), on cells whose axons will decussate into the contralateral medial lemniscus, and travel to the ventrobasal thalamus, then to the contralateral cerebral cortex to mediate conscious proprioception.

From the thalamus, following the orderly arrangement maintained (with minor reorganisation) throughout the whole pathway, axons project through the internal capsule to the post-central gyrus in the parietal lobe, where a somatotopic projection of inputs from the contralateral side of the body is formed (check diagrams in your text-books). The most densely innervated regions (fingers, lips, tongue) are disproportionately represented so that the map is somewhat distorted. The post-central gyrus is referred to as Somatic Sensory Area I or SI. Axons for different sensory modalities project to different columns of cortical cells, forming cylindrical arrays c. 1 mm² in cross-sectional area. Outputs from SI relay back to the parietal association area for more complex processing, and forward into the motor cortex.

 There is an almost exactly matching somatotopic map in the motor cortex of the precentral gyrus, just opposite the postcentral gyrus.

At the foot of the central sulcus, above the lateral cerebral sulcus, another, smaller, less detailed and bilaterally responding map is formed both from direct thalamic inputs and from SI and the parietal association area. This second map is referred to as the Somatic Sensory Area II or SII.

In both maps, the sensory inputs from the face and buccal cavity project to the SI and SII regions lying above the lateral fissure and extending into the upper bank of the insula. These facial inputs originate mainly from trigeminal afferents, which synapse in the main sensory and mesencephalic nuclei of the trigeminal nerve, and decussate to join the contralateral medial lemniscus, as the trigeminal lemniscus. These fibres terminate in the ventral posterior medial thalamus and then relay to the cerebral cortex. Proprioceptive facial afferents follow a similar path, but the cell bodies of these afferents are located in the ipsilateral mesencephalic nucleus of the trigeminal nerve.

Atypical large diameter afferent pathways: Large diameter afferents also may synapse in the dorsal horn on second order cells whose axons may ascend either in the dorsal column, or in the dorsolateral column. Axons in the dorsolateral white column (just lateral to the tip of the dorsal grey horn) synapse on cells in the lateral cervical nucleus, lateral to the dorsal horns at the C1/C2 level. Axons of these cells decussate into the contralateral medial lemniscus, along with the axons from the dorsal column nuclei, to synapse in the ventral posterior-lateral thalamus.

The large axons of the dorsal column/spinocervical system are more susceptible than the smaller, non-discriminative afferents, to mechanical (crush) or metabolic damage. Compression or entrapment syndromes (e.g. carpal tunnel syndrome) disturb discriminative tactile sensations: proprioceptive loss; paresthesias (numbness, pins & needles, prickling). Pain is a frequent concomitant. One hypothesis holds that this is due to loss of large diameter afferent input, which normally inhibits transmission in the nociceptive pathway. However, demyelination of peripheral axons can lead to formation of abnormal contacts between larger axons and unmyelinated nociceptive fibres. Thus, action potentials in non-nociceptive afferents may spread electrically to, and excite nociceptive pathways thus causing pain. In myelinated nerve fibres, there are Na⁺ but no K⁺ channels at the nodes. On the other hand, there are K⁺ but no Na⁺ channels in the internode under the myelin sheath. If the axon is demyelinated therefore, leakage of current from the exposed internode, may prevent adequate depolarisation of the next node, thereby slowing or completely blocking action potential transmission.

Metabolic compromise is seen in diseases such as diabetes mellitus, B1 or B12 deficiency, or in heavy metal poisoning. These conditions result in "dying back" of segments of large axons, which are most remote from the cell bodies, and therefore most susceptible to derangement of transport systems. Deficits are seen first in the extremities (hands and feet). Compromise of the vascular supply to peripheral nerves may contribute to metabolic nerve disorders in diabetes mellitus.

Lesions of SI lead to paresthesias, loss of two-point, texture and weight discrimination. Temperature and pain sensitivity are not lost but thresholds and quality of sensation may be altered. Lesions in SII have a greater influence on pain perception.

Lesions of the parietal association area may leave tactile sensation and proprioceptive reflexes intact, but produce astereognosis, agraphesthesia, and amorphosynthesis (neglect of contralateral body parts, disturbance of body image, and disturbed perception of contralateral spatial organisation). This area is responsible for processing the inputs from the primary projection area (postcentral gyrus) to produce higher order cognitive responses. This processing involves divergence and convergence of output from the from the cells in the primary projection area on to cells in the association area, producing cells with increasingly complex receptive fields and response profiles.

Read NEUROPHYSIOLOGY - the essentials (Somjen) Chapter 7

PHYSIOLOGY (Berne & Levy) Chapter 9