Clinical Vignette

History

Sadie, an 18-month-old female boxer residing in eastern Kansas, is presented for 48-hour duration of depression, anorexia, stiff short-strided gait, and crying out when the head is touched or bumped. She is appropriately vaccinated and has access to large pastures and wooded areas. Ticks have been a problem over the summer and into the early fall.

Physical Examination

On physical examination, the temperature is 104.5°F. Sadie walks with her head down and has a stiff gait. She has severe neck pain and pain in several levels of the thoracolumbar (TL) spinal cord.

Using the problem-oriented approach described in Chapter 1, please identify the problems and write an initial plan for each.

Problem Definition and Recognition

Pain is difficult to define. According to the International Association for the Study of Pain, it is “an unpleasant sensory and emotional experience, associated with actual or potential tissue damage, or described in terms of such damage.” Animals are unable to verbally communicate their pain experience, but inability to communicate pain does not negate its presence and effects. Consequently, a more specific definition of animal pain has been suggested as “an aversive sensory and emotional experience representing awareness by the animal of damage or threat to the integrity of its tissues… producing a change in physiology and behavior directed to reduce or avoid the damage, reduce the likelihood of recurrence, and promote recovery” (Molony and Kent 1997). Awareness implies a conscious patient with a perception of events giving rise to pain. Because it involves perception, pain will always be subjective, and has led to the following observation in people: “Pain is whatever the experiencing person says it is, existing whenever the experiencing person says it does” (McCaffrey and Pasero 1999). In addition, the subjective experience of pain may also be accompanied by feelings of fear, anxiety, or panic (Hellyer et al. 2007).

Acute pain is characterized by an abrupt beginning with a relatively brief duration, and generally may be alleviated by analgesic drugs; pain is considered to be chronic when it persists beyond the course of a disease process or appropriate healing time, or is associated with persistent or recurring conditions (Hellyer et al. 2007). Typically, chronic pain does not respond well to analgesics, but may respond to a combination of treatment modalities, including analgesics, sedative/tranquilizers, physical therapy, manipulation ofenvironment, or behavioral modification (Hellyer et al. 2007).Acute pain is considered to serve abiological function in that it provides a warning that something is wrong, which leads to protective behavioral modifications; chronic pain, however, is not considered to serve a biological function in that it imposes deleterious stresses on the patient (Hellyer et al. 2007). Some of the definitions commonly utilized in discussions of pain are included in Table 40-1. For a comprehensive listing of pain terminology and definitions, see references (Hellyer et al. 2007; Muir and Gaynor 2009).

TABLE 40-1. Some common definitions of pain (Hellyer et al. 2007; Muir and Gaynor 2009).

Agology	The science and study of pain phenomena
Allodynia	Pain caused by a stimulus that does not normally provoke pain
Analgesia	The absence of pain in the presence of stimuli that would normally be painful
Anesthesia	The absence of all sensory modalities
Causalgia	A syndrome of prolonged burning pain, allodynia, and hyperpathia after a traumatic nerve lesion, often combined with vasomotor and sudomotor (sweating) dysfunction and later trophic changes
Dysesthesia	An unpleasant abnormal sensation, whether spontaneous or evoked
Hyperalgesia	An increased response to a stimulation that is normally painful
Hyperesthesia	An increased sensitivity to stimulation
Hyperpathia	A painful syndrome characterized by an increased reaction to a stimulus, especially if repetitive
Hypoalgesia	A diminished sensitivity to noxious stimulation
Hypoesthesia	A diminished sensitivity to stimulation
Neuralgia	Pain in the distribution pathway of a nerve or nerves
Neuritis	An inflammation of a nerve or nerves
Neuropathic pain	Spontaneous pain and hypersensitivity to pain in association with damage to or a lesion of the nervous system
Neuropathy	A disturbance of function or a pathological change in a nerve
Nociception	The reception, conduction, and central nervous processing of nerve signals generated by the stimulation of nociceptors; it is a physiological process that when carried to completion results in the conscious perception of pain
Paresthesia	An abnormal sensation, whether spontaneous or evoked; paresthesias are not painful (as opposed to dysesthesias)
Tolerance	A shortened duration and decreased intensity of the analgesic, euphorigenic, sedative, and other central nervous system depressant effects, as well as considerable increase in the average dose required to achieve a given effect
Windup	Sensitization of nociceptors and peripheral and central pain pathways in response to a barrage of afferent nociceptive impulses resulting in expanded receptive fields and an increased rate of discharge

Pain assessment is difficult in animals. Because mammals possess the components and mechanisms necessary for transduction, transmission, and perception of noxious stimuli, it has been commonly assumed that animals experience pain even if they cannot verbally communicate it (Hellyer et al. 2007). It has been suggested that if something is painful to a human, it is reasonable to assume that it is also painful for an animal (Rowan and Tannenbaum 1986; Kitchell 1987).

There is no consistently reliable objective measure for pain, although attempts have been made in animals with limited success. Pain assessment in animals has typically been subjective, sporadic observation of animal behavior, which is not optimal for revealing signs of pain (Hellyer et al. 2007). Correlation of pain with plasma cortisol and β-endorphins is unreliable (Fox et al. 1998; Smith et al. 1999; Cambridge et al. 2000). Force plate gait analyses have been widely used to assess lameness in dogs, and possibly in cats (Conzemius et al. 2003). Scoring methods that include physiological variables and behavioral variables have been suggested. In addition, pain assessment can be particularly complex due to differences in gender, age, species, breed, strain, and environment (Hellyer et al. 2007). It is currently accepted that quantitative measurements of behavior are the most reliable methods for assessing pain in animals (Hansen 1997). Table 40-2 lists the common indicators of pain in cats and dogs. For a comprehensive discussion of pain indicators and behaviors, see reference (Muir and Gaynor 2009).

Table 40-2. Common pain indicators in dogs and cats (Muir and Gaynor 2009).

Dogs

Decreased social interaction

Anxious expression

Submissive behavior

Refusal to move

Whimpering

Howling

Growling

Guarding behavior

Aggression; biting

Loss of appetite

Self-mutilation

Cats

Reduced activity

Loss of appetite

Quiet/loss of curiosity

Hiding

Hissing or spitting

Excessive licking/grooming

Stiff posture/gait

Guarding behavior

Attempts to escape

Cessation of grooming

Tail flicking

The Neuroanatomy of Pain

Nociception is a component of the general somatic afferent system (GSA). This system contains receptors in the skin for touch, temperature, chemicals, pressure, and pain. Stimuli are transmitted to the central nervous system via axons contained in peripheral and cranial nerves. For spinal nerves, GSA neurons are located in dorsal root ganglia. Axons enter the spinal cord and synapse on neurons in the dorsal horn (gray matter). Noxious stimuli are processed, integrated, and relayed to the thalamus where sensory information is relayed to the parietal lobes of the cerebral cortex. Axons in the dorsal horn also project to the motor neurons in the ventral horn as the sensory arc of the withdrawal and crossed extensor reflexes.

Pain receptors in skin of the trunk and limbs are organized in dermatomes. A dermatome is that area of skin innervated by a pair of spinal nerves. The cutaneous trunci reflex is useful in localizing lesions affecting TL spinal cord segments (T3–L3). Pain receptors in the skin are stimulated by gently pin pricking or pinching the skin. The sensory component of the reflex includes skin receptors, TL spinal nerves, and the spinothalamic tract. Sensory fibers synapse on motor nuclei of the lateral thoracic nerve located in the caudal cervical spinal cord segments. The lateral thoracic nerve innervates the cutaneous trunci muscle and a positive reflex is twitching of the skin. Each dermatome is tested from caudal to cranial.

The long tracts responsible for transmitting noxious stimuli to the brain are the spinothalamic and spinoreticular tracts. Nociceptive pathways from the skin, also called superficial pain, are located in the spinothalamic tracts. In primates, fibers in this pathway immediately cross to the opposite side and ascend on the contralateral side. The spinothalamic tracts are bilateral in dogs and cats. Nociceptive fibers from deeper structures (tendons, joint capsule), also called deep pain, and are incorporated in bilateral multisynaptic pathways that ascend to the thalamus and cerebral cortex. Deep pain pathways contain sparsely myelinated, slow-conducting fibers that are more resistant to compressive injuries of the spinal cord than are proprioceptive and motor fibers. In dogs and cats, it may be difficult to differentiate superficial and deep pain responses, and this is of little consequence in localizing neurologic lesions. In spinal cord compression, the absence of cerebral responses to stimuli that normally elicit deep pain indicates a severe and bilateral injury. The prognosis for recovery from such compressive injuries is guarded to poor.

The trigeminal nerve (CN V) provides for perception of noxious stimuli from the face via its maxillary, ophthalmic, and mandibular branches. It is the afferent (sensory) arc of the palpebral and corneal reflexes.

Pathophysiology of Pain

Nociceptors are free nerve endings especially abundant in the skin, cornea, anus, periosteum, joint capsule, muscles, tendons, and meninges. There are three types of nociceptors; each is characterized by responsiveness to (1) extreme heat, (2) excessive mechanical stress, and (3) chemicals. Several chemicals (serotonin, bradykinin, histamine, prostaglandins, leukotrienes, and proteolytic enzymes) are released following injury or inflammation. Stimuli are transmitted to the spinal cord via fast-conducting small type A-δ fibers and slow-conducting type C fibers. Fast type A fibers conduct pain perceived as pricking sensation and type C fibers conduct impulses perceived as a slow burning sensation. Pain is a combination of both perceptions. Chronic pain is mostly the slow burning type.

Physiologic mechanisms exist to modulate pain. Enkephalins and endorphins are two morphine-like compounds found in areas of the brain associated with pain control. These compounds activate the brain’s analgesic system. This system acts in part through descending pathways to modulate neurons in the dorsal horn. In addition, there are inhibitory neurons in the dorsal horn that are activated to suppress pain.

Types of Pain

Acute or physiologic pain results from minimal tissue damage that activates high-threshold sensory nerve fibers. Pain is usually well localized, transient and activates reflex, physiologic and avoidance responses. It promotes healing and tissue repair.

Chronic or clinical pain results from intense or prolonged stimuli from tissue damage, extended discomfort, and abnormal sensitivity. Chronic pain has no protective value. It induces physiologic, metabolic, and immunologic alterations that promote illness and death. Chronic perception of noxious stimuli induces withdrawal, behavioral, autonomic nervous system, neuroendocrine, and suppresses immune system responses. Chronic pain can be localized or referred. In most cases, chronic pain is caused by tissue damage resulting in chronic inflammation or from peripheral or central nerve injury called neuropathic pain. Some diseases cause pain through both mechanisms.

There are several phenomena that occur to establish or enhance chronic pain (Muir and Woolf 2001). Sensitization of peripheral receptors results from the release of inflammatory mediators. This “inflammatory soup” activates sensory nerve endings and works to sensitize high-threshold nociceptors and activates silent nociceptors (such as those in joints). Central sensitization involves several events. Basically, excitability of sensory neurons in the dorsal horn is increased by constant bombardment of stimuli from afferent C fibers. This is known as windup. It is a major explanation for postinjury pain hypersensitivity.

Disinhibition results most often from peripheral nerve injuries. Normally, sensory information arriving in the dorsal horn is modulated by excitatory and inhibitory influences. In disinhibition, there is decreased activity of inhibitory interneurons and endogenous opiates.

Modification represents a change in neuronal phenotypes. Cytokines from spinal cord glial cells can change the way neurons respond to stimuli and induce hypersensitization. Along with disinhibition, modification promotes changes in the functional profile of sensory neurons and the development of chronic intractable pain syndromes.

Musculoskeletal Pain. Joint surfaces and periosteum contain abundant nociceptors, and focal stimulation may cause intense pain or a waxing and waning pain. Injuries to the joint capsule, ligaments, and synovium are very painful. Degenerative joint disease may episodically painful depending on concurrent inflammatory or mechanical conditions. Lameness is the primary consequence.

Visceral Pain. The viscera contains a lower density of nociceptors and more widespread tissue involvement is necessary to elicit pain. Stimuli include ischemia, distention of hollow viscus, chemical damage to visceral surfaces, spasm of smooth muscle, and stretching of ligaments. The parietal peritoneum, pleura, and pericardium can also be sources of visceral pain. The parietal surfaces of the thoracic and abdominal cavities are supplied by spinal nerves and contain abundant nerve endings. Stimuli to parietal surfaces cause a sharp pain. Disease of organs or structures that are located in the retroperitoneal space (kidneys, ureters) can result in very intense and “stabbing pain” due to the presence of parietal nerve fibers.

Neurologic Pain. The only nervous structure that has abundant nociceptors is the meninges. Diseases affecting the meninges (meningitis) are very painful and can result in severe neck or back pain. Compression or inflammation of spinal or peripheral nerves can also be very painful. Lesions affecting the spinal column can be very painful if the meninges, dorsal spinal root, vertebral periosteum, or disk annulus is affected. Typically, lesions within the spinal cord or brain are not painful unless they affect the meninges.

Ischemic Pain. Except for the spinal cord and brain, which do not contain nociceptors, ischemia of tissue is a potent and important cause of pain due to the production of lactic acid, bradykinin, and proteolytic enzymes that affect chemical receptors. A good example is the muscle pain associated with early ischemic myopathy or myositis.

Referred Pain. Pain that is manifested in a site considerable distance from the primary lesion is called referred pain. This is common in people whom associated pain with myocardial infarction and gallbladder disease is distant from the primary organ. It is much less common in dogs and cats but can occur with disease processes that affect viscera in the abdominal cavity with pain then being referred to body surfaces.