Pain.
No pain, no gain.
Pain is the most common of all symptoms, requires treatment before its cause is known. Pain is an emotional and a physical experience, difficult to compare from one person to another.
One patient may have a high pain threshold and complain only after the disease process has progressed beyond its early stage, while another with a low pain threshold may complain about pain that would be ignored or tolerated by most people.
Pain from any cause can be increased by anxiety, fear, depression, loneliness, and frustration or anger. Acute pain serves a useful function as a protective mechanism that leads to the removal of the source of the pain, whether it be localized injury or infection.
Chronic pain serves a less useful function and is often more difficult to treat. Although acute pain requires immediate attention, its cause is usually easily found, whereas chronic pain complaints may be more vague and difficult to isolate. The ideal method for treating pain is to eliminate the cause, such as to surgically remove an inflamed structure, to apply hot compresses to a muscle spasm, or to set a fractured bone in a cast. Alternatives to drug therapy, such as physical therapy, should be relied on whenever possible.
The analgesic drugs most often used to alleviate mild and moderate pain are the non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin, ibuprofen, acetaminophen, or indomethacin. If these are ineffective, a weak opiate such as codeine, hydrocodone, or oxycodone would be the next choice.
Severe pain not controlled by these agents requires a strong opiate such as morphine or meperidine. Because opiates are addictive, their use is controlled by the Controlled Substances Act, and individuals prescribing or dispensing these drugs must register annually with the Drug Enforcement Administration.
Each drug is assigned to one of five groups, from schedule I, which includes drugs that have the highest potential for abuse, to schedule V, which includes drugs with a limited dependence-causing potential.
In spite of its subjective nature, most pain is associated with tissue damage and has a physiological basis. Not all tissues, however, are sensitive to the same type of injury.
For example, although skin is sensitive to burning and cutting, the viscera (internal organs) can be incised with a knife or laser without pain being generated. Over-distension of a hollow viscus or chemical irritation of the visceral surface, however, induce pain.
Some tissues do not give rise to pain, no matter what the stimulus; the parenchyma of the liver and the alveoli of the lungs are insensitive to almost any stimulus. Thus tissues respond only to the specific stimuli they are likely to encounter and are not generally receptive to all types of damage.
Pain receptors, found in the skin and other tissues, are nerve fibres with free endings that lack specialized characteristics. They can be excited by three types of stimuli--mechanical, thermal, and chemical; some endings respond primarily to one type of stimulation, while other endings can detect all types. The chemical substances that are produced by the body and excite pain receptors include bradykinin, serotonin, and histamine. Prostaglandins (cyclic fatty acids), which can heighten the pain sensation, are released by the body when inflammation occurs and sensitize, but do not directly stimulate, the free nerve endings.
This increase in sensitivity is called hyper-algesia. Two types of primary afferent nerve fibres transmit electrical impulses from the tissues to the spinal cord, called the ascending pathways because they rise from lower to higher centres, and correspond to the dual-phase pain experienced described above. The A delta fibres are larger and conduct impulses more quickly; hence, they are associated with the sharp, well-localized pain that first occurs. They are thinly myelinated (covered by a fatty sheath) and are activated by mechanical and thermal stimuli. The smaller, unmyelinated C fibres respond to chemical, mechanical, and thermal stimuli and are associated with the burning, lingering, poorly localized sensation that follows the first quick sting.
Pain impulses enter the spinal cord and synapse (connect) primarily on the dorsal horn neurons in the marginal zone and substantia gelatinosa of the gray matter of the spinal cord.
This area is responsible for regulating and modulating the incoming impulses. Two different pathways, the spinothalamic and spinoreticular tracts, transmit impulses to the brain stem and thalamus.
Spinothalamic input is believed to effect the conscious sensation of pain, including its components, and the spinoreticular tract is thought to effect the arousal and emotional aspects of pain.
Pain signals can be selectively inhibited in the spinal cord through a descending pathway (progressing from higher to lower centres), which originates in the midbrain and ends in the dorsal horn.
This analgesic (pain-relieving) response is controlled by neuro-chemicals called endorphins, opioid peptides such as enkephalins that are produced by the body.
These substances block reception of stimuli by binding to neural receptors that activate the descending, pain-inhibiting neural pathway.
This system can be activated by stress or shock and is probably responsible for the absence of pain associated with extremely severe injury. It may also help to explain the differing abilities among individuals to perceive pain.
The origin of pain signals can be unclear to the sufferer. Pain arising from the deep tissues but "felt" in the superficial tissues is called referred pain. This phenomenon results from the proximity of visceral nerve fibres to neural fibres from the skin and musculature, which allows nerve impulses from one pathway to accidentally pass to the other pathway. Another type of confused pain is phantom limb pain--that which is suffered by an amputee who experiences pain in a severed limb.
This occurs because the nerve trunks that connected the now absent limb to the brain still exist and are capable of being excited. The brain interprets stimuli from these fibres as coming from that which it learned to be the limb.
The theory of pain that most accurately accounts for the physical and psychological aspects of pain is the gate-control theory. According to this model, the perception of pain depends on a neural mechanism in the substantia gelatinosa layer of the dorsal horn.
This mechanism acts as a synaptic gate that modulates the pain sensation from myelinated and unmyelinated peripheral nerve fibres and the activity of inhibitory neurons.
Thus stimulation of nearby nerve endings can inhibit the nerve fibres transmitting pain signals, which explains the relief that can occur when an injured area is stimulated by pressure or rubbing.
