CENTRAL PROJECTIONS OF THE SOMATIC SENSORY SYSTEM:

Small Diameter Afferents

The centrally directed, small-diameter axons of the non-discriminative sensory receptors, enter the cord laterally to the large axons of the discriminative afferents which enter the dorsal columns. Before entering the grey matter of the dorsal horn, they bifurcate rostro-caudally, to run for a few segments, in a thin tract of small axons capping the dorsal horn (Lissauer's tract), giving off branches into the grey matter at different levels. Lissauer's tract is not shown here, but lies just outside lamina I. The A afferents tend to synapse on second order cells in the: posterior marginal nucleus (Lamina I); C type afferents, in the substantia gelatinosa (Lamina II); and both types may terminate on cells in the nucleus proprius (Laminae III-VI). Some synapse on cells which project into the ipsilateral spino-cervical pathway (see sheets on Large Diameter Afferents). Posterior marginal cells give rise to the more discriminative neospinothalamic pathway; nucleus proprius cells, to the paleospinothalamic pathway.

Second order cells of the posterior marginal nucleus and nucleus proprius give off axons which cross obliquely in the anterior white commissure, ventral to the central canal, to enter, and ascend in the contralateral anterolateral white column. Inputs from successively more rostral levels, layer medial to fibres ascending from below, so that in the upper levels of the cord, this tract has superficial fibres from the lowest segments, with rostral levels being represented more deeply in the tract. Sixty percent of the fibres in the anterolateral column produced the sensation of pain when stimulated; 30% evoked warmth; 7% evoked cold (none produced tactile sensations), all sensations being felt on the contralateral side.

A cyst (syrinx) developing within the central canal (syringomyelia) may compress the anterolateral tract fibres as they cross from right and left, in the anterior commissure at the level of the cyst. This can produce a bilateral, girdle-like band with reduced pain and temperature sensitivity in the affected dermatomes. These sensations may be tested with pin-pricks and test-tubes with hot and cold water at different temperatures.

Axons of the anterolateral column terminate in three main sites:

(1) The majority terminate in the reticular formations of the medulla (spino-reticular tract) relaying from here via a polysynaptic pathway, to the hypothalamus and to diverse areas of cerebral cortex - both limbic and neocortical. These produce widespread arousal in response to noxious (and cold) stimuli, and elicit appropriate reflex responses to both thermal and noxious stimuli.

(2) Others terminate in the mesencephalon in the peri-aqueductal grey matter (PAG) and related areas (spinomesencephalic tract). Some of these excite enkephalinergic cells in the PAG, which activate important descending feedback pathways e.g. the serotonergic raphespinal pathway) which project back to the substantia gelatinosa in the cord, to regulate nociceptive inputs.

(3) The remainder terminate in the thalamus: in the ventrobasal and intralaminar thalamic nuclei (spinothalamic tract).

If the fibres of the anterolateral system are sectioned and allowed to degenerate, special stains can be used to trace the path of the degenerating fibres. This has been done in the figure to the left, and shows the extensive projections of the anterolateral system to the medulla (raphe nuclei), mid-brain (tectum; peri-aqueductal grey matter), and thalamus (ventral posterior and intralaminar nuclei).

From the ventral thalamus, axons project, along with the dorsal column fibres, to the SI and SII cortical areas. This pathway (the neo-spino-thalamic pathway) mediates temperature sense and the sense of sharp, prickling, localisable pain. From the intralaminar nuclei, axons project to the basal ganglia, notably to the mesolimbic area which projects to the limbic system, and thence to the prefrontal cortex. This pathway (the paleo-spino-thalamic pathway) mediates slow, burning, aching pain, and is responsible for much of the anguish associated with pain. This would explain why ablation of SI doesn't abolish pain, ablation of SII attenuates, while pre-frontal lobotomy abolishes the agony of pain (the affective response) without abolishing the conscious realisation (gnostic response) of its presence.

The Gate Control Mechanism explains why counter-stimulation (rubbing) helps to alleviate pain. It is through this mechanism also that morphine which mimics the action of enkephalin, induces analgesia. It may also explain why transcutaneous electrical nerve stimulation of the dorsal column axons (TENS) can cause analgesia (by antidromically exciting large diameter afferent axons, which excite the SG cells). And it gives insight into how events taking place in the brain, may feedback on the grey matter of the dorsal horn to produce analgesia (stress induced analgesia). We have already seen how it could explain the presence of excessive pain in diabetic neuropathy, neurosyphilis and herpes zoster.

Non-discriminative afferents from the facial region run in the spinal tract of the trigeminal nerve, synapse in the spinal nucleus, then decussate and project to the contralateral ventrobasal and intralaminar thalamic nuclei. Nociceptive inputs here include afferents from the teeth, which can produce intense pain. Excruciating facial pain of unknown origin (trigeminal neuralgia) can be alleviated by destruction of cells in the trigeminal ganglion, or sectioning of the spinal tract. The pain may have central origin however, and frequently returns post surgically. The central tract cells may develop epileptiform characteristics. Anti-epileptic drugs are now the treatment of choice.

Visceral pain originates from C type nociceptors in the viscera. It is poorly localised (large receptive fields; sparse innervation) and may be triggered by distention, inflammation or ischaemia of the viscera. Afferents reach the cord via the sympathetic nerves in the thoracolumbar region (T7 to L1) and via the parasympathetics from areas above and below this region. Visceral pain can sometimes be alleviated by sympathectomy - although the basis for the effectiveness is disputed.

There are more nociceptive afferents than tract cells at any spinal level. Convergence is a necessity. Visceral nociceptors sometimes converge onto the same tract cells as somatic nociceptors when they innervate structures derived from the same embryonic segment. When this happens the brain cannot distinguish between nociceptive activity originating in the viscus and that originating in the somatic structure. The brain then often "refers" pain from a viscus to the related somatic dermatomal area (the dermatomal rule). It is important to recognise the existence of referred pain, and be familiar with its standard pattern.

Commonly recognised referrals include cardiac pain to the region of the left shoulder and down the iner aspect of the left arm (between the shoulde blades in now accepted as an alternative site - common in women); appendix and small intestine, to the region of the umbilicus; ureteral pain to the groin.

Pain associated with headaches are also referred according to known patterns, to some extent dependent upon history. Persons who have had a history to problems with their teeth, often refer nasal sinus pain to the teeth. Inflammation or distention of the meninges or vessels of the cerebral vault tend to be referred to the frontal areas; of the cerebellar vault and brainstem, to the posterior areas. The brain parenchyma itself is devoid of nociceptors, and may be surgically managed in the awake patient.

Read: GANONG, Review of Medical Physiology, Chapter 7.

SOMJEN, Neurophysiology - the essentials, Chapter 7.3 & 7.9.