Symptoms of Intervertebral Disk Disease

Any breed of dog can have a disk herniation, especially when external trauma is involved. However, because of the unique metabolic differences of their disks, the chondrodystrophoid breeds are far more likely to develop significant intervertebral disk disease in their lifetimes. Analysis of the frequency of occurrence of disk disease within particular breeds shows that standard and miniature dachshunds are at the highest risk of all dog breeds followed by Pekingese. Approximately one in every four dachshunds will have some degree of disk related problems in their lifetimes. The age of incidence for chondrodystrophoid breeds is highest between three and seven years, as opposed to eight to ten years for nonchondrodystrophoid breeds. No sex predilection has been identified. Clinical signs seen in dogs with intervertebral disk disease vary highly depending on which disk herniates, the amount and speed at which disk material actually protrudes, and which nervous system structures become involved and to what extent.

When increasing pressure is applied to the spinal cord, as occurs with a type II herniation, clinical symptom develop in a very predictable manner. This is because the different nerve fibers in the spinal cord vary in sensitivity to pressure based on their size. The largest nerve fibers are the most sensitive to pressure and the smallest the least sensitive. When a neurologic examination is performed, the knowledge gained is used to make accurate assessments (prognosis) of the degree of spinal cord and/or nerve root compression present, the possible reversibility of the damage, and how aggressively to instigate therapy.

Proprioceptive (position sense) nerve fibers are the largest and therefore the most susceptible to pressure. Proprioceptive losses can be seen with only slight amounts of pressure applied to the spinal cord. Clinically proprioceptive deficits are recognized as incoordination (ataxia). If proprioceptive losses are the only ones identified on the neurologic examination, the prognosis is usually good and less aggressive therapy is usually adequate.

Motor fibers are the next smallest size of nerve fiber and therefore require more pressure to become dysfunctional than do proprioceptive fibers. Moderate damage to these fibers causes decreased muscle strength and function resulting in clinical signs called paresis. In general, paresis holds a guarded to good prognosis and indicates the need for more aggressive medical, and often surgical, therapy if normal function is to return. More severe damage to motor fibers can result in an absence of muscle strength and function called paralysis. The presence of paralysis is accompanied by a fair to guarded prognosis and indicates the need for fairly rapid and aggressive medical and surgical therapy if the spinal cord is to regain reasonable function.

Superficially or cutaneous sensory nerve fibers are small and therefore require a great deal of pressure to become dysfunctional. Unfortunately this neurologic modality can be hard to evaluate because dogs can not talk to tell what they can or can not feel on their skin. If a lack of conscious perception of pain sensation in corresponding cutaneous sensory zones is identified, the prognosis is guarded to poor. Aggressive medical and surgical therapy must be initiated immediately if the animal is ever to function reasonably normally again.

The smallest nerve fibers transmit deep pain sensation and are the most resistant to pressure. Deep pain is pain perceived when hard pressure is applied to bones or joints. Lack of deep pain perception is the gravest of clinical signs but must be considered in light of how long it has been lost before deciding if the spinal cord is irreversibly damaged.

In acute type I disk herniations, spinal cord nerve fibers are sensitive to externally applied pressure in the same manner as in type II disk herniation. However, type II disk herniations do not cause as much of the acute internal damage to the spinal cord described above. Even so, the neurologic examination findings should be interpreted in basically the same way following an acute spinal cord trauma: only ataxia indicates a relatively good prognosis, additional motor deficits indicate the need for more aggressive therapy and loss of deep pain sensation is a grave sign.

Type I disk herniations tend to occur explosively with large amounts of nucleus pulposus escaping into the spinal canal at one time. The spinal cord is damaged first by impactive forces when nuclear material strikes it, and then by compressive forces when nuclear material occupies the extradural space. When this occurs, major physiologic disruptions of nerve transmission occur which are not always permanent if aggressive medical therapy is instigated immediately. It is not unusual for dogs presented shortly after severe spinal cord trauma to show no signs of conscious perception of deep painful stimuli. The veterinarian is left with the task of trying to differentiate if the dog's failure to show that it feels the clamp on its toe indicates 1) a true lack of deep pain sensation from irreversible destruction of the ascending pain pathways which can not be altered by any amount of therapy, 2) severe physiologic interference with signal transmission in an otherwise viable nerve fiber which could return to normal function if immediately and aggressively treated, or 3) if so many painful stimuli are bombarding the dog's brain that it simply doesn't show behavioral acknowledgment of this one additional painful stimulus and deep pain sensation is actually intact. Unfortunately, there is no way to clinically differentiate these different states of "no deep pain" perception. With the goal of preserving the maximum amount of neurologic tissue and regaining the maximum amount of clinical function possible, the best course it always to treat these dogs as aggressively as possible (medical and surgical therapy) and wait to see if deep pain perception returns. In most cases it will and these dogs will be saved. However, sometimes owners are unable or unwilling to spend money for surgery on a gamble that deep pain function will return. In that case, the best course of action is aggressive medical therapy and reevaluation of the neurologic examination in a few hours to see if deep pain perception has returned. If it does, surgery should then be performed immediately. In this case, the owner understand that this delayed surgical intervention probably won't be as effective as if surgery had been performed earlier. In general the longer the state of no deep pain perception exists, the poorer the prognosis. In most case of acute spinal cord trauma, well documented lack of deep pain perception for 24 or more hours is most often indicative of functional transection (transverse malacia) of the spinal cord. However, due to the subjective nature of the interpretation of the presence or absence of deep pain perception, it is probably wise to extend the "window" of time in which aggressive medical and surgical therapy is attempted to 48 hours.

The pain suffered with intervertebral disk disease arises from several sources. The spinal cord has no sensory nerve fibers. However, the peripheral layers of the annulus fibrosus do. So called diskogenic pain arises from abnormal stresses being placed on the annulus fibrosus or physical tearing of fibers. Herniation of the nucleus pulposus is not necessary for diskogenic pain to occur. Another source of pain arises from the sensory nerves in the the meningeal coverings. When the spinal cord, and therefore the meningeal coverings, are compressed or when nuclear material contacts the meninges resulting in a "foreign body" inflammatory process, these sensory nerves are activated and meningeal pain occurs. A third source of pain from intervertebral disk disease arises when nerve roots are entrapped by herniated disk material. The resulting pain is referred to as radicular pain and the clinical signs called a "root signature."

In dogs, cervical and thoracolumbar disks are the most commonly herniated, but the degree of clinical dysfunction seen can vary remarkably. As mentioned previously, there is a great amount of extradural space in the cervical area. Large quantities of disk material may herniate without causing significant impact on or compression of the spinal cord leaving little to moderate clinical dysfunction. In comparison, the thoracolumbar area has almost no extradural space around the spinal cord. Consequently, a comparable amount of herniated disk material at this level may significantly impact and/or compress the thoracolumbar spinal cord resulting in major clinical dysfunction. The spinal cord has a great ability to compensate if compression is applied slowly over a long period of time, such as occurs with type II disk herniation. In comparison, it has little ability to compensate for the acutely applied compression that occurs in type I disk herniation. Unfortunately, thoracolumbar disks herniate more frequently than cervical disks.

One of the cardinal signs of cervical disk disease is neck pain. Dogs display this pain by tightened neck muscles, reluctance to move the neck, inability to lower the head to eat or drink, and painful cries when the neck is manipulated or touched. Their posture reminds you of a turtle with its head partially pulled into its shell. They may also walk with the back in an arched position to try to straighten and lower the neck to avoid pain. Unfortunately this posture is often misinterpreted as a sign of back pain. Probably all three types of pain (diskogenic, meningeal and radicular) are involved. Nagging neck pain that responds to appropriate medications and then recurs when medications are withdrawn is a very typical history. Large quantities of herniated disk material can lie on the floor of the spinal canal without proprioceptive or motor deficits ever being observed because there simply isn't enough pressure on the spinal cord. However the irritation causing the pain remains and surgical removal of the herniated material is the only solution. If enough disk material herniates, ataxia and perhaps motor deficits may be seen. Classically all four limbs will be affect but this can be highly variable. If disk material herniates mainly to one side, only the limbs on that side of the body may be affected. Low cervical disk herniations may cause only forelimb or only hind limb involvement. Luckily there is seldom enough pressure on the spinal cord in cervical disk herniation to cause a loss of deep pain sensation.

Clinical signs of thoracolumbar disk herniation unfortunately are usually more profound than in the cervical area. With almost no extradural space for herniated disk material to occupy, the spinal cord can be severely compressed. These dogs have normal forelimb function with one exception. If the disk is just starting to protrude but has not actually herniated, dogs will walk with an arched stiff back due to pain. They often cry out when picked up or their back muscles are squeezed. They are usually reluctant to move around as usual. If more pressure is present on the spinal cord, ataxia and paresis of the hindlimbs is usually evidenced by the dog dragging its toes and walking with a wobbly gait. At this point immediate surgical intervention can provide excellent results. Further pressure causes hindlimb paralysis and eventually loss of deep pain sensation if therapy is not instigated. The greatest value of surgery is in the earliest stages of disk herniation. The longer clinical signs exist without surgical intervention, the less value the surgery can provide and the more permanent damage the spinal cord sustains.

Occasionally injury to the thoracolumbar spinal cord can cause clinical signs in the forelimbs. Almost invariably the injury is extremely acute and severe, such as a spinal fracture or profound type I disk herniation. There are motor fibers in the upper lumbar spinal cord segments that run forward to the cervicothoracic area to influence the nerves exiting to the muscles of the forelimbs and neck. When these motor fibers are damaged, the forelimbs become rigidly extended and the dog holds its head back. Also, deep pain perception is often not recognizable. This is called Schiff-Sherrington syndrome and, in the past, was said to always be an indication of irreversible spinal cord malacia. Unfortunately that is not true because many dogs that display this syndrome can recover if immediate aggressive medical and surgical therapy is instigated. Unfortunately, many dogs have been needlessly euthanized due to failure to understand that this syndrome can be reversible. However, if signs of Schiff-Sherrington syndrome persist after aggressive therapy has been administered, or persist when therapy has been delayed for whatever reason, then the prognosis is grave.

Diagnostics

 

Intervertebral disk herniation is usually suspected based on the signalmen(breed, age, sex), history of appropriate clinical dysfunction, and a neurologic localization of the cervical or thoracolumbar areas. To make a positive diagnosis, spinal radiographs or Xrays will need to be taken. It is absolutely imperative that no movement occur and that the muscles along the spinal column be relaxed if an accurate assessment of vertebral relationships and disk spaces is to be made. Consequently, the only way to get good quality spinal radiographs is by administering a general anesthetic to the affected dog. The only exception would be if some other physical abnormality, such as severe heart disease, precludes this being done safely. In that event, surgical intervention is probably also not an option and specifically locating the offending disk is not necessary to carry out good medical therapy.

Once the dog is anesthetized, a series of plain radiographs will be taken with the dog lying on its side (lateral view). The veterinarian will be looking for changes in the normal relationships and density of the vertebrae and the disks. Those changes include narrowed or wedged disk spaces, displaced calcified disk material in the intervertebral disk space or intervertebral foramina, narrowed articular joint spaces, and/or many other suggestive signs. However, calcification of the nucleus pulposus does not necessarily mean that a disk will herniate. Unfortunately, most herniated disk material is not calcified enough to be seen on Xray. Therefore the exact position of the herniated material most often can not be determined on plain Xrays and a specialized study called a myelogram must be performed. Risks are involved and the possibility of worsening a delicately balanced situation exists. However, the manufacture of new less irritative dyes has removed a great deal of the risk and myelograms are now routinely performed without the great concern of the past.

In a myelogram, radioopaque dye is injected into the cerebrospinal fluid in the subarachnoid space. In a normal study, two lines of dye will be seen running on each side of the spinal cord more or less like railroad tracks running parallel to one another. When a disk has herniated, nuclear material and torn annular fibers can occupy the extradural space compressing the spinal cord. The normal parallel configuration of the two dye lines will be disrupted by either pushing them closer together or farther apart depending on the particular radiographic view examined. Additional oblique views can be taken to help identify which side of the spinal cord is more affected. By examining all views carefully, the amount of herniated material, and therefore the amount of pressure on the spinal cord, can be estimated. Also the preferred side to enter surgically can be determined.