Acute Pain Management: Cryotherapy

OVERVIEW OF PAIN[edit | edit source]

According to the International Association for the Study of Pain (IASP), pain is defined as “An unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage,”[1] and is expanded upon by the addition of six key Notes and the etymology of the word pain for further valuable context. • Pain is always a personal experience that is influenced to varying degrees by biological, psychological, and social factors. • Pain and nociception are different phenomena. Pain cannot be inferred solely from activity in sensory neurons. • Through their life experiences, individuals learn the concept of pain. • A person’s report of an experience of pain should be respected. • Although pain usually serves an adaptive role, it may have adverse effects on function and social and psychological well-being. • Verbal description is only one of several behaviours to express pain; the inability to communicate does not negate the possibility that a human or a nonhuman animal experiences pain

The subjective experience of pain has two complementing components: a localized feeling in a specific body area and an unpleasant character of varying degrees that are frequently linked to actions used to lessen or end the experience. There are particular pain receptors, to start with. The majority of body tissues have these nerve endings, which only react to stimuli that are harmful or have the potential to be harmful. Second, the spinal cord receives the messages sent by these painful sensations via particular, identifiable nerves. The primary afferent nociceptor is made up of the sensitive nerve ending in the tissue and the nerve that connects to it. Second-order pain-transmission neurons in the spinal cord are in touch with the primary afferent nociceptor. The limbic system, brain stem reticular formation, thalamus, somatosensory cortex, and other higher centers get the message from the second-order cells via clearly defined channels. The thalamus and cortex are thought to play a major role in the mechanisms underpinning pain perception.

PAIN PROCESSES[edit | edit source]

The four main steps are transduction, transmission, modulation, and perception. When tissue-damaging stimuli activate nerve endings, this process is referred to as transduction. When we talk about transmission, we're talking about the relay processes that move the message from the location of tissue damage to the parts of the brain that underlie perception. Specifically designed to lessen activity in the transmission system, modulation is a recently discovered brain function. The subjective awareness brought on by sensory signals is known as perception, and it entails the synthesis of a large number of sensory signals into a single, cohesive idea. The processes of attention, expectancy, and interpretation together form the complicated process of perception. It is possible to objectively study the brain processes of transduction, transmission, and modulation by adopting techniques that include close observation. The consciousness of pain, on the other hand, is a perception and, thus, subjective, so it cannot be directly and objectively evaluated, even though it has an undeniably neurological basis. Even if we were able to observe the activity of pain-transmission neurons in a different individual, we would still need to draw an inference based on circumstantial evidence to say whether or not that individual experiences pain. Mechanical (pressure, pinch), thermal, and chemical stimulation can all cause pain receptors in peripheral tissues to become active. Chemical stimuli typically linger for a long time whereas mechanical and heat stimuli are typically transient. Regarding how these stimuli cause nociceptors to respond, little is known. Finding and studying the nociceptive nerve terminals is challenging due to their tiny size and dispersed location. Nevertheless, some research has been done on how chemicals affect the main afferent nociceptors' firing rate.

TRANSDUCTION[edit | edit source]

Primary afferent nociceptors are activated or sensitized by several pain-inducing substances Some of them, including potassium, histamine, and serotonin, may be released by harmed tissue cells or by blood cells in the circulatory system that move from blood arteries into the area of tissue damage. Enzymes that are activated by tissue injury produce other substances such as bradykinin, prostaglandins, and leukotrienes. In areas of inflammation as well as discomfort, all of these pain-inducing substances are present in higher concentrations. To activate the main afferent nociceptor, the transduction process undoubtedly involves a variety of chemical reactions. Any of these compounds may theoretically be tested to provide a calculation of the peripheral stimulation for pain. In reality, no such tests are accessible. It should be noted that studies of cutaneous nerves have provided the majority of our knowledge about primary afferent nociceptors. Despite the broad significance of this work, deep musculoskeletal or visceral processes in the body are what primarily cause clinically significant pain. The stimuli that trigger nociceptors in these deep tissues are being studied by researchers. Primary afferent nociceptors within muscle react to pressure, muscle contraction, and irritant substances. Some of these nociceptors respond particularly strongly to muscle contraction in ischemia-induced situations.

TRANSMISSION[edit | edit source]

Peripheral nervous system The main afferent nociceptor's axon carries the nociceptive signals from the peripheral area to the brain. The dorsal root ganglion houses the neuron's cell body, which is connected to the spinal cord via a lengthy process called the axon that separates into two branches. The primary afferent nociceptors' axons are slender and carry impulses slowly. It is feasible to insert an electrode into a human peripheral nerve and monitor the primary afferent nociceptors' activity. The nociceptor's reaction to noxious heat, pressure or chemical stimuli defines it. The primary afferent nociceptors' axons encode the "pain" information using the pattern and frequency of their impulses. The frequency of nociceptor discharge is directly correlated with the stimulus's strength. Additionally, investigations using neurophysiological and psychophysical techniques on people have revealed a direct link between the frequency of discharge in a primary afferent nociceptor and the subjective level of pain. blocking the nociceptors' small-diameter axons' ability to transmit. A potential approach for assessing certain forms of clinical pain is monitoring activity in identified main afferent nociceptors. In reality, this technique has been applied in clinical settings to show pain-producing neuronal activity resulting from injured nerves. Currently, this approach should only be used as a research tool, although it is theoretically possible and has a lot of potential for assessing pain patients. It increases the likelihood of really showing nociceptor activity originating from a painful region. The fact that this methodology evaluates the supposed noxious input or the brain activity that typically causes pain, makes it a potential improvement over existing correlative techniques for evaluating pain. The majority of the other metrics evaluate behaviours that may or may not be triggered by noxious stimuli. It is crucial to note that 1) pain can exist without primary afferent nociceptors being activated and (2) primary afferent nociceptors can be active without experiencing pain. When the central or peripheral neural systems have been damaged, several occurrences take place. The modulating system can also prevent activity triggered by nociceptor input from being sent centrally. As a result, the relationship between nociceptor input and perceived pain intensity is complex. Because of this, the technique of recording primary afferent nociceptors might be used to verify the existence of input but not to disprove the absence of pain. The measurement of either pain-producing chemicals or primary afferent nociceptor activity presents significant practical challenges in addition to the theoretical limits of attempting to gauge subjective pain intensity by recording nociceptors. One is that the majority of patients with pain that renders them incapacitated focus on the lower back's musculoskeletal systems. These structures' innervating nerves are difficult to locate since they are far from the skin. Another issue is that pain from deep structures is frequently felt far from the location of the tissue damage. The pain that results from deep tissue injury is typically painful, dull, and poorly localized, in contrast to the pain caused by skin damage, which is acute or searing and well localized to the site of injury. When deep tissue injury is severe or long-lasting, the sensation it causes could be mistakenly believed to originate from a location other than the actual site of damage. Referred pain is a phenomenon that helps to explain why patient symptoms and physical findings frequently conflict. For each unique occurrence, the cause of transferred pain is unknown. When patients are examined for pain-related complaints, referred pain can be a significant cause of uncertainty. Physicians are aware of this phenomenon and frequently use it to treat patients. Pain is directed from visceral interior organs to somatic bodily tissues. As an illustration, the pain associated with a heart attack is frequently diffuse and felt in the chest, left arm, and occasionally the upper abdomen rather than being always concentrated in the area around the heart. It's less well known that painful areas, like myofascial trigger points, can cause pain to radiate from the painful area to other parts of the skeletal muscle. The late 1930s saw Kellgren experimentally demonstrate this in muscle and fascia (Kellgren, 1938). patterns of pain that are specific and refer to certain muscles clinically.

3. The convergence-projection hypothesis states that a single nerve cell in the spinal cord gets nociceptive input from the internal organs as well as from nociceptors originating from the skin and muscles. The brain is unable to distinguish between somatic structures and visceral organs as the source of the stimulation. According to theory, the brain interprets any such signals as coming from the skin and muscular nerves rather than an interior organ. It has been shown that pain projection neurons in the spinal cord receive both somatic and visceral sensory signals. 4. The convergence-facilitation theory states that the activity of pain projection neurons in the spinal cord that receives input from one somatic region is increased (facilitated) by the background (resting) activity of these neurons occurring in nociceptors coming from a different part of the body. According to this hypothesis, the nociceptors that cause the background activity come from the area of perceived pain and tenderness, whereas the nerve activity that causes the facilitation comes from somewhere else, like a myofascial trigger point. Because suppressing sensory input in the reference zone with cold or a local anaesthetic should temporarily relieve pain, this convergence-facilitation mechanism is of clinical importance. The convergence-projection theory predicts that such relief would not occur. Both types of responses have been seen in clinical studies. When referred pain goes undiagnosed, it can pose a major concern for both patients and doctors. Considering that the pain's source is hidden and far away, the absence of any visible lesion at the location of pain or tenderness frequently raises questions about the pain's strong psychological component. Patients sometimes start to question whether the pain is "all in their brain" when medical specialists state categorically that there is no cause for it. This can aggravate psychological reactions to pain, such as worry, and is likely to frustrate both the patient and the doctor. It can also result in "doctor shopping". central nervous system pathways for pain

The spinal cord receives impulses from primary afferent nociceptors (or if they arise from the head, into the medulla oblongata of the brain stem). Primary afferent nociceptors in the spinal cord finish close second-order nerve cells in the grey matter's dorsal horn. From their spinal terminals, the major afferent nociceptors emit chemical transmitter molecules. The second-order pain-transmission cells are activated by these transmitters. Although their identities are unknown, candidates for these transmitters include tiny polypeptides like substance P and somatostatin as well as amino acids like glutamic or aspartic acid.

Some of these second-order cells cross over to the opposing side of the spinal cord and extend their axons to the brain stem and thalamus over considerable distances. The anterolateral quadrant of the spinal cord is where the pain is transmitted. The majority of the knowledge we have on the structure and function of pain-transmission channels in the central nervous sysHowever, it is understood that electrical stimulation of this anterolateral circuit in humans causes pain and that lesions of this pathway permanently impair pain perception. The thalamus and the medial reticular formation of the brain stem are the two primary targets for ascending nociceptive axons in the anterolateral quadrant of the spinal cord. The spinothalamic tract cells, or spinal cells with direct axon projections to the thalamus, are those about which we know the most. Because spinothalamic injuries at any level result in long-lasting pain sensitivity abnormalities, this route is thought to play a role in how humans perceive pain.

Numerous species have been studied to learn more about the characteristics of spinothalamic tract cells. In most of these species, spinothalamic neurons react to noxious stimuli at their maximum potential. Additionally, there is a direct correlation between stimulus intensities in the noxious range for human individuals and the frequency of firing in spinothalamic tract cells. These findings, along with years of meticulous clinical research, firmly suggest that the spinothalamic tract is a key mechanism for human pain. The spinoreticular tract is the other significant ascending nociceptive channel in the anterolateral quadrant. A significant portion of the spinal cord's direct projections to the medullary reticular formation as well as branches of some spinal neurons that project to the thalamus is received by this structure. There are two main places where pain pathways terminate in the thalamus: ventrocaudal and medial. Projecting spinal neurons deliver nociceptive information straight to the ventrocaudal thalamus. Direct connections between ventrocaudal thalamic neurons and the somatosensory cortex exist. The region of the brain stem reticular formation where the nociceptive spinoreticular neurons are projected provides the medial thalamus with significant input in addition to some indirect input from the spinal cord. Numerous forebrain regions, including the somatosensory cortex, are connected to the medial thalamus by projections. In light of this, there are two main ascending pain pathways: a direct lateral spinothalamic pathway and an indirect medial spinoreticulothalamic pathway. Sharp, well-localized aches that start close to the surface of the body are believed to be mostly brought on by the lateral pathway from the spinal cord to the ventrocaudal thalamus and the cortex. In contrast, the medial thalamus receives a large input from the region of the brain stem reticular formation where the nociceptive spinoreticular neurons are projected, in addition to some indirect input from the spinal cord. The somatosensory cortex is one of many forebrain regions that have connections to the medial thalamus. A direct lateral spinothalamic pathway and an indirect medial spinoreticulothalamic pathway are the two main ascending pain pathways a result. The lateral pathway from the spinal cord to the ventrocaudal thalamus and the cortex is thought to be primarily responsible for sharp, localized pains that begin close to the body's surface. On the other hand, the medial spinoreticulothalamic circuit responds more strongly to deep somatic and visceral structural stimuli. pinoreticulothalamic circuit reacts to deep somatic and visceral structural cues more strongly.

Sensory Versus Affective Aspects of Pain[edit | edit source]

Two major categories can be used to separate the processes that noxious stimuli set in action. The sensory procedures that result in the recognition and detection of the stimuli are on the one hand. On the other hand, aversive behavioral sequelae like withdrawal and escape can stop the stimulation and protect the organism, perhaps because of the noxious stimulus's potential for tissue damage. There are two subjective elements of pain: sensory and affective, which are correlated with these two kinds of reactions. The sensory parts include locating the stimuli, determining their location, gauging their intensity, and identifying them. When concentrating on the sensory components, a person may describe their pain as a slight burning sensation on the back of their hand. Contrarily, the affective or unpleasantness part of pain is not directly related to a sensory experience and is defined by phrases like nagging, uncomfortable, or excruciating. It correlates with the aversive impulse to stop the noxious stimuli. Anxiety and depression, which are typically categorized as psychological rather than sensory changes in mood, would accompany the affective features.

By separating between pain threshold and pain tolerance, it is possible to further highlight the differences between the sensory and affective elements of pain. For instance, most people will report that the sensation becomes uncomfortable during a specific temperature range (43–46 C) if calibrated thermal stimuli are applied to the skin. The pain detection or sensory threshold would be the temperature that is described as painful 50% of the time. Contrary to this highly repeatable pain-detection threshold, pain tolerance varies greatly between people. For instance, when individuals dip their hands in ice water, they are divided into two groups: those who remain submerged for more than five minutes and those who remove their hands after less than 90 seconds (Turk and Kerns, 1983-1984). The ability to tolerate pain is a complicated function that can be influenced by a person's personality, attitudes, past experiences, economic status, gender, and the specific situation in which the pain is felt. You could think of tolerance as a reaction threshold. A certain amount of pain can be tolerated, however, a little bit more severe discomfort may cause some people to seek medical attention, take medications, or take the day off work. The specific actions brought on by a certain amount of pain are highly individual and are significantly determined by the patient's perception of the severity of the situation and what they think will be beneficial. For instance, most individuals who experience headaches don't go to the doctor because they're not seen to be a sign of a serious illness (and usually are not). On the other hand, someone whose father recently passed away from a brain tumor would be extremely alarmed by even a minor headache and seek medical help. The cognitive and emotional components of pain are also related to tolerance. Pain in cancer patients may indicate that the tumor has returned or spread and that they are on the verge of passing away. Such patients experience pain that is both intense and meaningful, which causes them to suffer. Pain is frequently accompanied by suffering, anxiety, and anguish.

Many patients with significant cancer-related pain in the 1950s underwent frontal lobotomies. These procedures interfere with the medial spinoreticulothalamic pathway's frontal lobe projections. Pain threshold and severity were unaffected in these patients, but suffering and agony were eliminated. Unfortunately, this was an inappropriate approach to the problem since the drastic personality changes that came with the end of suffering. These medical observations, however, demonstrate that the affective aspect of pain has a distinct physical substrate from the sensory aspect.

MODULATION[edit | edit source]

When it was revealed that electrical activation of particular brain regions suppresses reactions to painful stimuli in lab animals, a theory for spontaneous analgesia was born. When it was demonstrated that stimulating homologous brain regions gave relief to people suffering from chronic pain, the phenomenon known as stimulation-produced analgesia (SPA) became more than a laboratory curiosity. Hundreds of people and a wide range of animals have both been used to illustrate SPA. From clearly identified brain stem locations, SPA can be induced. A growing body of evidence suggests that a distinct neural network that extends from the midbrain to the medulla and ultimately to the spinal cord mediates SPA. The spinal cord areas that contain pain-transmission neurons are served by this descending, pain-modulating route. The detected nociceptive spinothalamic tract neurons are selectively inhibited by stimulation at brain stem locations that provide behavioral analgesia. This inhibition may cause behavioral and clinical analgesia brought on by brain stem stimulation.

Morphine and other opiate analgesic medications, in addition to electrical stimulation, can activate the analgesia network (Yaksh, 1978). Directly applied opiates can cause pain in the spinal cord and the SPA sites in the brain stem. The overwhelming body of research suggests that opiates activate these pain-modulating networks to cause analgesia. The brain contains molecules with the same pharmacological qualities as opiates produced from plants and manufactured opioid medications were one of the most significant findings in pain research. These chemicals, known as endogenous opioid peptides, are found in the peripheral and central nervous systems' nerve cells. The existence of these peptides in high concentrations in the brain stem regions linked to pain suppression is very significant for our discussion, and these findings have generated some exciting new psychopharmacological possibilities. This endorphin-mediated analgesia mechanism can be triggered by a range of stressful manipulations, including painful stimuli, according to studies done on laboratory animals. According to clinical investigations, it becomes active during surgery and has a potent analgesic effect. The fact that there is a clearly defined network for regulating pain transmission is crucial. According to recent research, this network may be responsible for some of the startling differences in pain reports among individuals who have experienced seemingly equivalent noxious stimuli.

ACUTE PAIN[edit | edit source]

Acute pain is a type of pain that typically lasts less than 3 to 6 months. It is a type of pain that is directly related to soft tissue damage such as a sprained ankle or a paper cut. Acute pain is of short duration but it gradually resolves as the injured tissues heal. Acute pain is distinct from chronic pain and is relatively sharper and more severe.

Promoting the elimination of the underlying causes of pain while effectively numbing it is the main objective of acute pain management. Both pharmaceutical and nonpharmacologic methods physical which include physiotherapy can be used to treat acute pain, either separately or more frequently in combination. The World Health Organization's (WHO) Analgesic Ladder which was initially created to encourage continuous monitoring of pain management during the palliative care of cancer patients, provides the foundation for pharmacologic management of acute pain.
Step 1 of the WHO ladder is for patients with mild pain, in whom nonopioid analgesia is advised; step 2 is for patients with moderate pain, in whom the use of weak opioids with or without nonopioids is advised;
and step 3 is for patients with severe pain, in whom the use of strong opioids with or without nonopioids is advised.

In this article, we will be focusing on cryotherapy as a physiotherapy intervention for the management of acute pain. To cure acute inflammation following a soft tissue injury, cryotherapy is one of the most often employed electro-physical treatments. The majority of clinicians agree that cryotherapy has an "anti" inflammatory impact following injury, which forms the basis of much of the clinical justification for this. Recent developments have improved our knowledge of the inflammatory response to soft tissue injury in a variety of ways. For the treatment of the inflammatory stage of tissue repair, cryotherapy, a physical therapy method, is frequently used in clinical rehabilitation practices. It can lower the temperature of the tissue, which can then lessen inflammatory symptoms including pain and edema. The mechanisms behind the suppression of inflammatory symptoms by cryotherapy often involve a decrease in tissue temperature and a reduction in blood flow, nerve conduction velocity, vasopermiability, and cell metabolism. Cryotherapy has been shown to lessen edema and discomfort in earlier animal trials. Additionally, in earlier investigations on acute pain, freezing decreased discomfort in patients who had total hip arthroplasty, anterior cruciate ligament reconstruction, and delayed onset muscular soreness. Additionally, cryotherapy has been shown to lessen swelling in individuals with acute soft-tissue injuries and shoulder arthroscopies. Through central sensitization and synovium reduction, cryotherapy can reduce inflammatory pain. In the acute phase of inflammation, cryotherapy may be helpful as a physical therapy treatment method for managing pain and swelling. Additionally, the temperature at which the treatment is administered may affect its outcome. Temperature affects cell metabolism, and a 10°C drop in temperature results in a 50% reduction in metabolic enzymatic activity. As compared to normothermia (37°C), profound hypothermia (17°C) downregulated the production of inflammatory mediators and cytokines. However, continuous cryotherapy at 10°C can dramatically lessen pain, whereas continuous cryotherapy at 5°C had little effect on pain in patients who have had an anterior cruciate ligament replacement. Additionally, moderate cold (11°C–15°C) is more helpful than severe cold (5°C–10°C) for patients with delayed onset muscular pain. These results might imply that differing tissue fat/muscle ratios affect actual tissue temperature changes at the same ice bath temperature in different ways.

BENEFITS OF CRYOTHERAPY IN ACUTE PAIN MANAGEMENT: 1. Reduction of oedema, inflammation, local blood flow, and bleeding are all reduced when a soft tissue injury is directly treated locally with cryotherapy 2. Cryotherapy reduces spasticity during rehabilitation. 3. Cryotherapy also has a local anaesthetic effect. 4. Lower risk of frostbite due to the sporadic administration of cryotherapy to the skin for therapy for the first 36 hours following an injury. 5. It is more comfortable with intermittent application. PRECAUTION FOR CRYOTHERAPY:

Patients with the following disorders should not receive cryotherapy:

• collagen diseases, • vasospastic conditions, • unconsciousness or semiconsciousness

References[edit | edit source]

  1. Malik NA. Revised definition of pain by ‘International Association for the Study of Pain’: Concepts, challenges and compromises. Anaesthesia, Pain & Intensive Care. 2020 Jun 10;24(5):481-3.