Sources of Pain
Somatic Pain
Somatic pain can be classified as either: 1) cutaneous, superficial or peripheral pain and 2) deep pain.
- Cutaneous, Superficial or Peripheral Pain. Pain that arises from the skin and muscles or peripheral nerves themselves. In general, this pain has two components, the initial response (a) followed by later response (b). These signals are transmitted via different pathway.
- Pricking pain reaches the CNS via neospinothalamic tract (i.e., LST) to the VPL (or VPM) and to the SCI.
- Burning and soreness pain resulting from tissue damage reaches the CNS via the paleospinothalamic tract (AST) and archispinothalamic tract to brain stem nuclei and to PF-CM complex, etc.
- Deep pain. This pain arises from joint receptors tendons and fascia (i.e., deep structures). The quality of deep pain is dull, aching or burning. Deep pain is accompanied by a definite autonomic response associated with sweating and nausea, changes in blood pressure and heart rate. Somatic deep pain reaches the CNS mainly via the paleospinothalamic (Figure 7.3) and archispinothalamic tract (Figure 7.4).
Reaction to Somatic Pain. Sudden, unexpected damage to the skin is followed by three responses:
- Startle response. This is a complex psychosomatic response to a sudden unexpected stimulus which includes: A flexion reflex, postural readjustment and orientation of the head and eyes to examine the damaged area.
- Autonomic response. This response includes: NE and E release, ACTH and/or cortisol release, and vasoconstriction and piloerection.
- Behavioral response. This response includes: Vocalization, rubbing designed to diminish pain, learning to respond to sudden pain and psychosomatic pain.
Visceral Pain
In the visceral organs, nociceptors respond to mechanical stimulation such as pressure, tissue damage, and chemical stimulation.
Most noxious information carried by visceral afferents does not give rise to conscious sensation. Visceral pain is diffuse, less precisely graded and typically accompanied by slowing of the heart, lowered blood pressure, cold sweats and nausea. It conveys also hunger, thirst, electrolyte balance, irregulation in the respiratory and circulatory systems. Many of these signals reach the CNS bilaterally (Figure 7.6) by the following three channels:
In the visceral organs, free nerve endings are scattered, and any stimulus that excites these nerve endings causes visceral pain (Figure 7.6). Such stimuli include spasm of the smooth muscle in a hollow viscus, or distention or stretching of the ligament, such as a stone blocking the ureter or the gall ducts. Stretching of the tissues such as intestinal obstruction can also provoke visceral pain. Visceral pain is also caused by chemical means as a result of gastrointestinal lesions, and tumors as well as thrombosis of an artery. In many cases, visceral pain is not localized to the site of its cause, rather in a distant site.
Figure 7.6 |
Thalamic Pain
Lesions in the spinothalamic tract and its targets of termination as well as local manifestations of diencephalic lesions are usually complex. They can induce alteration of sensory, motor and endocrine components because of the functional diversity of the thalamus. This condition is known also as thalamic pain syndrome or Dejerive-Roussy syndrome. Subjects with this syndrome experience spontaneous aching and burning pain in body regions where sensory stimuli normally do not lead to pain. Because the brain and the spinal cord do not contain nociceptors, the pathological process presumably directly stimulates nociceptive pathways, or it prevents the activation of the pain suppression pathways.
Stroke or occlusion in the thalamogeniculate artery (a branch of the posterior cerebral artery), which supplies the lateroposterior half of the thalamus, can result in a thalamic lesion, which is often accompanied by neurologic conditions several months after the initial event. The condition is associated with a devastating intracranial pain in the contralateral side of the thalamic lesion and sensory loss. In some cases, severe facial pain is experienced without any sensory loss. The pain resulting from an intracranial lesion is also termed "central pain."
Neuropathic Pain
Neuropathic pain is a sharp, shooting and devastating pain. It is a persistent pain that arises from functional changes occurring in the CNS secondary to peripheral nerve injury. Once the nerve is damaged, the damaged nerve elicits sustained activation of nociceptors and/or nociceptive afferents. The neuropathic pain is due to an abnormal activation of the nociceptive system without specifically stimulating the nociceptors. Neuroplastic changes occurring in the CNS secondary to the afferent barrage are believed to culminate in CNS neuronal hyperexcitability. Many scientists suggest that “sensitization” of the nervous system following injury is a factor in neuropathic pain. Neuropathic pain can usually be controlled by anti-inflammatory drugs and opioids. In some cases, such as in diabetics, AIDS, cancer, etc., no treatment or relief is available to neuropathic pain. Neuropathic pain should not be confused with neurogenic pain, a term used to describe pain resulting from injury to a peripheral nerve but without necessarily implying any neuropathy.
Psychosomatic Pain
Psychic reaction to pain includes all the well-known responses to pain such as anguish, anxiety, crying, depression, nausea and excess muscular excitability through the body. These reactions vary tremendously from one person to another following a comparable degree of pain stimuli. The sensation of pain can be influenced by emotions, past experiences and suggestions. The same stimulus can elicit different responses in different subjects under the same conditions.
Recently, Positron Emission Tomography (PET) has been used to study pain pathways and psychosomatic pain centers. For example, volunteers had their hands dipped in hot water (50° C) while they were conscious. They then dipped their hand again in hot water (50° C) after a post-hypnotic suggestion that the pain would be either more or less unpleasant than the first time. The PET scans of their brains showed that activity in the anterior cingulate cortex changed in accordance with how unpleasant they expected the pain to be. However, the intensity in the primary somatosensory cortex remained constant (i.e., the emotional component of pain is independent of its sensation).
