The examination of cranial nerves is described in Chapters 6 and 7. When presented with a patient that exhibits clinical signs of spinal cord disease, the cranial nerve examination is important for determining whether the spinal cord signs are part of a multifocal disease process. It is also important to determine whether the spinal cord lesion is at a level where it can interfere with the sympathetic pathway to the head and cause Horner syndrome. That syndrome is observed when the cranial nerves are examined.

SUMMARY OF POSSIBLE CLINICAL SIGNS RELATED TO SPINAL CORD LESIONS

The spinal cord is divided into four regions on the basis of the clinical signs that are exhibited when any one of these four regions is affected (Fig. 10-1).

Figure 10-1 Regional neurologic signs in spinal cord disease. GP, General proprioceptive; GSA, general somatic afferent; LMN, lower motor neuron; UMN, upper motor neuron.

Lumbosacral: Fourth Lumbar to Fifth Caudal Spinal Cord Segments

Thoracolumbar: Third Thoracic to Third Lumbar Spinal Cord Segments

A Complete necrosis at a focal site between the third thoracic and third lumbar spinal cord segments

1 Spastic paraplegia: normal reflex weight support if held up in a standing posture but no voluntary movement of the pelvic limbs or tail; normal thoracic limbs. With peracute transverse lesions, the thoracic limbs may be hypertonic and held in extension (Schiff-Sherrington syndrome). With cranial thoracic spinal cord lesions, it may be difficult for the patient to stand up on its thoracic limbs from a recumbent position, and there may be loss of trunk support when the patient is suspended by the base of the tail and made to walk on the thoracic limbs. The trunk may abnormally sway to the side.

2 No neurogenic atrophy

3 Normal tone or hypertonia (spasticity) in the pelvic limbs

4 No postural reactions in the pelvic limbs

5 Reflexes are normal or hyperactive: patellar (+2 or +3) and flexor

6 Crossed extension may be observed with the flexor reflex

7 Analgesia caudal to the level of the lesion by about two spinal cord segments

8 Absent cutaneous trunci reflex caudal to the level of the lesion by about two spinal cord segments

Caudocervical: Sixth Cervical to Second Thoracic Spinal Cord Segments

Complete necrosis of these segments may cause death due to loss of respirations. Partial necrosis of gray and white matter between the sixth cervical and second thoracic spinal cord segments.

1 Tetraparesis and ataxia of all four limbs or nonambulatory tetraparesis and ataxia or tetraplegia

2 Thoracic limb deficits that may be worse due to the loss of ability to support weight

3 Short strides in the thoracic limbs with long paretic and ataxic strides in the pelvic limbs: a “two-engine gait”

4 Thoracic limb neurogenic atrophy with nonacute lesions

5 Postural reactions attempted if not tetraplegic and are abnormal in all four limbs; thoracic limb responses may be worse

6 Reflexes depressed or absent in the thoracic limbs and normal or hyperactive in the pelvic limbs; lesions confined to the white matter at this level have normal to hyperactive thoracic limb reflexes

7 Crossed extension may occur with the pelvic limb flexor reflexes

8 Hypalgesia or normal nociception in all four limbs or only hypalgesia in the thoracic limbs

9 Miosis, ptosis, protruded third eyelid, and enophthalmos with lesions between T1 and T3

Craniocervical: First Cervical to Fifth Cervical Spinal Cord Segments

Complete necrosis of these segments causes death due to loss of respirations. Partial necrosis of gray and white matter at a focal site between the first and fifth cervical spinal cord segments.

1 Spastic tetraparesis and ataxia of all four limbs or nonambulatory spastic tetraparesis and ataxia or spastic tetraplegia; recumbent patients, when held up, exhibit hypertonia and support their weight by hyperactive extensor tone. This differentiates them from patients that are tetraplegic due to neuromuscular disorders that cause flaccid paralysis and that are atonic in all their muscles.

2 No neurogenic muscle atrophy in chronic lesions.

3 Postural reactions abnormal in all four limbs if they can be performed at all.

4 Reflexes in all four limbs are normal or hyperactive.

5 Crossed extension may occur with the flexor reflexes.

6 Hypalgesia is possible caudal to the level of the lesion but is rarely determined; most cranial cervical lesions that are severe enough to cause analgesia caudal to the lesion cause death due to the loss of respirations.

Most compressive lesions that affect the cranial cervical spinal cord segments cause more obvious clinical signs in the pelvic limbs than in the thoracic limbs. Explanations for this include the following: lesions that compress from the periphery of the spinal cord affect primarily the superficial tracts, which contain cranially coursing GP pathways from the pelvic limbs (Fig. 10-2); the pelvic limbs are further removed from the center of gravity, which is just caudal to the thoracic limbs; more UMN pathways terminate in the cervical intumescence than in the lumbosacral intumescence. Occasionally a cervical spinal cord lesion causes more obvious clinical signs in the thoracic limbs. This is seen with caudocervical lesions that affect the gray matter in the intumescence, causing LMN signs in the thoracic limbs. With more craniocervical lesions, this occurs when the spinal cord lesion affects the tracts closer to the gray matter and spares the more superficial tracts. These are predominantly UMN pathways to the cervical intumescence. A glial neoplasm that arises in the gray matter and grows peripherally toward the surface of the spinal cord will do this as will a midline intervertebral disk protrusion that compresses the spinal cord dorsally and laterally, making the spinal cord form a tent shape over the compressing mass. This disparity in clinical signs is also seen in many dogs with an atlantoaxial subluxation.

Figure 10-2 Transverse section of cervical spinal cord. The more superficial location of pelvic limb spinocerebellar tracts may explain the more profound pelvic limb ataxia that is often observed with compressive lesions. CCB, Cuneocerebellar tract; FC, fasciculus cuneatus; FG, fasciculus gracilis; SCB, spinocerebellar tracts; UMN, upper motor neuron.

Be aware that lesions that affect the first two or possibly three cervical spinal cord segments may also cause clinical signs of vestibular system dysfunction. This presumably results from the interruption of the spinovestibular tracts that carry GP impulses from the first three cervical spinal nerves, which are important in the orientation of the head to the neck.

There are two additional important concepts to remember when dealing with spinal cord lesions. First, lesions in the intumescences that affect the gray matter as well as the white matter present with the clinical signs of loss of the gray matter; that is, LMN clinical signs. You cannot observe UMN or GP clinical signs unless the LMN is intact. Second, a focal lesion between the C1 and C5 or T3 and L3 spinal cord segments that affects both the white matter and the gray matter causes clinical signs referable only to the white matter lesion; that is, UMN and GP clinical signs. Loss of the gray matter in a segment that innervates only the axial muscles cannot be determined by a physical neurologic examination. Only a careful electromyographic study may reveal the denervation of a segment of axial muscles.

Bladder and occasionally rectal dysfunction commonly accompanies spinal cord lesions. These lesions were described, along with the anatomy involved, in Chapter 7. Lesions in the sacral segments result in LMN incontinence in urine and feces; UMN incontinence is common with severe lesions of the cervical and thoracolumbar spinal cord segments. This incontinence is a primary concern in your treatment of the patient.

Schiff-Sherrington Syndrome and Spinal Shock

These two separate clinical disorders often present at the same time in a patient and appear to be exceptions to the rules that we have established for UMN and LMN disorders. They occur only with peracute, usually transverse, spinal cord lesions between the T3 and L3 spinal cord segments. Fractures of the vertebral column are the most common cause of such lesions. Others include infarction caused by fibrocartilaginous emboli and the myelopathy associated with peracute intervertebral disk extrusions. These patients exhibit persistent severe extension of the thoracic limbs in most postures because of disinhibition of the extensor motor neurons in the cervical intumescence. However, when these patients are held up, the thoracic limb gait is normal except for a mild stiffness. These clinical signs represent the Schiff-Sherrington syndrome.⁷⁹ The disinhibition is not the result of dysfunction in a UMN pathway, which is why these patients can walk so well with the thoracic limbs when the trunk and pelvic limbs are supported. The disinhibition is the result of a sudden loss of the axons in a long interneuronal pathway that originates from neuronal cell bodies primarily in the gray matter of the L1 to L5 spinal cord segments. These interneurons are referred to as border cells because they are located in the dorsolateral border of the ventral gray column of the lumbar spinal cord segments.⁸⁹ Their axons course cranially in the fasciculus proprius and terminate by synapsing on thoracic limb extensor LMNs in the cervical intumescence (Fig. 10-3). Their normal function is to inhibit these extensor motor neurons. This extensor release phenomenon is observed only with peracute severe lesions, and it spontaneously resolves in about 10 to 14 days. The presence of the Schiff-Sherrington syndrome indicates a severe lesion and a guarded prognosis but does not indicate that recovery cannot occur.

Figure 10-3 Schematic diagram depicting the cranial projecting pathway that, when interrupted, results in the Schiff-Sherrington syndrome.

The severe peracute thoracolumbar spinal cord lesion that is responsible for the Schiff-Sherrington syndrome usually causes paraplegia because of the complete interruption in function of the UMN pathways, and it usually causes analgesia caudal to the lesion because of interruption of the nociceptive pathways. As a rule, with progressive transverse spinal cord lesions, paraplegia occurs before analgesia, suggesting that the nociceptive pathways are the most resistant to spinal cord compression and ischemia. However, in these severe peracute transverse thoracolumbar spinal cord lesions in which the Schiff-Sherrington syndrome is present, there usually is severe pelvic limb hypotonia. If you examine this patient within a few hours of the onset of the paraplegia, there may be absent or very depressed pelvic limb tone and spinal reflexes. These paradoxical LMN-like pelvic limb signs in a patient with a UMN pathway interruption represent what is called spinal shock.⁸⁸ In primates, spinal shock causes areflexia and atonia for 2 to 3 weeks. In domestic animals, the areflexia is observed for only a few hours after the onset of the lesion, but the hypotonia persists for 10 to 14 days, when it is replaced by normal tone at first and then by hypertonia. The reasons a UMN lesion causes LMN signs are poorly understood. One explanation is that the sudden loss of the UMN synapses, indirectly via interneurons or directly on the dendritic zones or the cell bodies of the alpha motor neurons, causes such a disruption to that LMN cell body that it cannot function for a variable period of time. In primates, more of these UMN pyramidal system synapses are directly on the LMN, which may explain the difference in reaction among species that is observed here. Some studies have found an excessive accumulation of the inhibitory neurotransmitter glycine in the lumbosacral intumescence in these patients.⁸⁶ The basis for the release of glycine is unknown. It is important to understand this unique combination of clinical signs that results from a focal lesion in the UMN and GP systems and not make an anatomic diagnosis of a multifocal disorder.

In a recumbent patient that has a fracture and should not be manipulated, the basis for these clinical signs can be determined through minimal handling of the patient. With the patient lying on the floor, a table, or a stretcher, provide a rigorous noxious stimulus to a digit of a pelvic limb; no movement occurs or there is just a mild reflex flexion if it is a few hours after the onset of clinical signs. Note the bilateral pelvic limb hypotonia. Provide very minimal compression of a digit of one of the hyperextended thoracic limbs or just a light squeeze of that forepaw with your hand, and note the immediate vigorous voluntary withdrawal of the limb. This tells you that you have a transverse thoracolumbar spinal cord lesion with Schiff-Sherrington syndrome in the thoracic limbs and spinal shock in the pelvic limbs. By providing forceps compression of the skin on the midline of the back as a noxious stimulus, starting in the caudal lumbar region and progressing cranially, a line of analgesia and/or a cutaneous trunci reflex can be found that locates the focal lesion, and imaging studies can be pursued with no further manipulation of the patient. If the patient does not have a fracture, its ability to walk with the thoracic limbs when supported differentiates the Schiff-Sherrington syndrome from a severe cervical spinal cord lesion.

(For a complete description of disorders that affect the lumbosacral spinal cord segments or the peripheral nerves associated with these segments, see the case examples of neuromuscular disease in Chapter 5.)

SMALL ANIMAL THORACOLUMBAR SPINAL CORD DISEASES

Paraplegia

CASE EXAMPLE 10-1

Signalment: 8-year-old spayed female boxer, Brittney

Chief Complaint: Unable to use the pelvic limbs

History: The day before this dog was videoed, the owner left her home at 11 AM, leaving Brittney in the house. On returning at 3 pm, she found Brittney unable to stand on her pelvic limbs.

Examination: Video 10-1 shows the flaccid paraplegia and the hyperextended thoracic limbs but normal voluntary use of these limbs. Note the atonia and areflexia in the left pelvic limb and the mild hypotonia and hyporeflexia in the right pelvic limb. Note the analgesia of the left pelvic limb except for the proximal medial thigh area. Not shown are the normal tail, anal tone, and perineal reflex.

Anatomic Diagnosis: L4 to S1 spinal cord segments, worse on the left side

The thoracic limbs exhibit the Schiff-Sherrington syndrome resulting from the sudden loss of function of the lumbar spinal cord neuronal cell bodies of the long interneurons that normally inhibit thoracic limb extensor motor neurons. However, the pelvic limbs’ clinical signs are not due to spinal shock because they are so asymmetric, and the left pelvic limb areflexia had persisted for 24 hours when this examination was done. The intact nociception from the proximomedial thigh area indicates sparing of the genitofemoral nerve, which arises from the L3 and L4 spinal cord segments. The right pelvic limb paralysis represents a mixture of loss of function of the UMN and GP systems in the white matter and mild loss of GSE LMN function, all of which could occur in these segments.

Differential Diagnosis: Fibrocartilaginous embolic myelopathy (FCEM); intervertebral disk extrusion; neoplasia

External injury was excluded by the history. Based on the acute onset of clinical signs and the signalment, FCEM and intervertebral disk extrusion are the two most presumptive diagnoses. The absence of any discomfort is more likely with FCEM, but exceptions are common. It is important to make this distinction in the clinical diagnosis because an extruded intervertebral disk commonly requires immediate surgery.

Ancillary Procedures: Radiographs of the lumbar and sacral vertebrae were normal. A myelogram and a computed tomography (CT) scan with a myelogram (see Video 10-1) showed a mild intramedullary swelling of the lumbosacral intumescence. The CT images are from the body of the L3 vertebra through the body of the L5 vertebra.

Because of the guarded prognosis, the owner of Brittney requested euthanasia. Necropsy confirmed extensive infarction scattered through the caudal lumbar and cranial sacral spinal cord segments. The gray matter was more extensively affected on the left side. There were numerous fibrocartilaginous emboli in spinal cord blood vessels associated with these lesions.

FIBROCARTILAGINOUS EMBOLIC MYELOPATHY

Because of the extensive collateral circulation to the spinal cord (Fig. 10-4), multiple blood vessels must be compromised to cause the degree of infarction and severe clinical signs seen in dogs similar to Brittney. This suggests that a sudden shower of emboli must occur at one time. At necropsy, these emboli can be found in many blood vessels in or near the lesions. Usually, this shower affects the blood vessels to a few adjacent spinal cord segments and the associated lesions often are scattered and asymmetric within these segments. Thus, the clinical signs are usually focal and often asymmetric, as seen in Brittney. FCEM may be much more common than we realize and not be extensive enough to cause clinical signs or cause only transient clinical signs. Most veterinarians have had the experience of being called by a distraught owner who has just found their pet dog collapsed and unable to stand, but by the time the dog arrives at the hospital for examination, the dog is walking normally. We believe that some of these transient episodes of collapse may be due to transient spinal cord ischemia caused by FCEM.

Figure 10-4 Arterial vasculature of the canine spinal cord. The lesion distribution following fibrocartilaginous embolism often reflects occlusion of multiple arteries.

Many dogs in which you make this clinical diagnosis will recover spontaneously. This is more common in dogs with paresis and ataxia due to interruption of the UMN and GP pathways. The more severe the involvement of the gray matter in the intumescences, the more guarded the prognosis. As a rule of thumb, if there are no signs of improvement in 10 to 14 days after the onset of clinical signs, it is unlikely that any recovery will occur. In a few patients, after an initial mild improvement, there may be a period of weeks before they rapidly regain the ability to walk. We usually tell owners that it may take up to 10 weeks before final improvement occurs.

An interesting observation is that FCEM is very rare in the chondrodystrophic breeds in which the chondroid metaplastic form of intervertebral disk degeneration is so common. FCEM also is observed in dogs as young as 3 months of age in which you do not expect intervertebral disk degeneration to occur. In these young dogs, the source of cartilage may be the vertebral growth plates. Often, there is an associated history of mild trauma such as a sudden fall or vigorous playing and jumping as with catching a frisbee. This relationship between young age and vigorous handling is associated with FCEM in young feeder pigs; it occurs during their transportation in crowded trucks.

The three primary disorders that can cause an acute onset of relatively nonprogressive spinal cord dysfunction are external injury by objects in the environment, most commonly vehicles; internal injury resulting from intervertebral disk extrusions; and vascular compromise resulting from FCEM. The history usually permits substantiation or exclusion of external injury. Lacking that, vertebral column radiographs should provide that answer. To differentiate between the other two causes of these clinical signs, evidence of discomfort by the patient is more suggestive of an intervertebral disk extrusion than of FCEM, but exceptions are common for both of these disorders. Ultimately, immediate imaging is necessary because a diagnosis of an intervertebral disk extrusion usually requires emergency surgery. Myelograms in dogs with FCEM are helpful only in the small percentage of dogs in which intramedullary swelling is extensive. MR imaging is much more reliable in detecting the spinal cord edema that accompanies the ischemia or infarction caused by the fibrocartilaginous emboli.²⁵ Be aware that MR imaging that is done in the first 24 to 48 hours after the embolic shower occurs may occasionally be normal.

CASE EXAMPLE 10-2

Signalment: 3-year-old female Labrador retriever, Brandy

Chief Complaint: Unable to stand in the pelvic limbs

History: Brandy was an indoor dog in which the owner observed a sudden loss of the ability to walk with the left pelvic limb, followed in a few hours by collapse of the right pelvic limb.

Examination: Video 10-2 was made 12 hours after the onset of the pelvic limb dysfunction. Note the paraplegia with thoracic limb hyperextension but normal voluntary movements in the thoracic limbs. Note the pronounced pelvic limb hypotonia but intact spinal reflexes. Note the line of analgesia at about the thoracolumbar junction.

Anatomic Diagnosis: Focal caudal thoracic transverse spinal cord lesion with Schiff-Sherrington syndrome in the thoracic limbs and spinal shock in the pelvic limbs

Differential Diagnosis: FCEM, intervertebral disk extrusion, neoplasia

The owner’s history of this dog’s clinical signs is sufficient to deny any external injury. It was difficult to determine how much of this dog’s struggling was due to discomfort, frustration, or dislike of the examiners. An acute intervertebral disk extrusion is less likely than FCEM in a 3-year-old Labrador retriever, due to its young age.

No ancillary studies were performed in Brandy, and with no clinical signs of improvement after a few days, the owners elected euthanasia. Necropsy revealed extensive ischemic and hemorrhagic infarction in the caudal thoracic spinal cord segments, with numerous fibrocartilaginous emboli in both arteries and veins. No intervertebral disk material was found on opening the ventral internal vertebral venous plexus in the area of the involved spinal cord segments, and a median plane section of the vertebral column did not reveal any recognizable intervertebral disk material in the marrow of the vertebral bodies.

The following videos show two more examples of the Schiff-Sherrington syndrome.

Video 10-3 shows Spanky, an 11-year-old male mixed-breed dog that was riding in a car that skidded on ice and struck a guard rail. Radiographs (shown in the video) revealed a fracture in the spinous process of the T6 vertebra and a collapsed intervertebral disk space between the T5 and T6 vertebrae, with no displacement. The video was made 4 days after the injury. Note the pelvic limb hypertonia and hyperreflexia and therefore no evidence of any spinal shock. Note the presence of nociception in the pelvic limbs, indicating that the spinal cord lesion has not caused a complete transverse dysfunction. A body cast was applied and Spanky regained the ability to walk with his pelvic limbs in about 5 weeks.⁷²

Video 10-4 shows a 6-year-old Parson (Jack) Russell terrier that was struck by an automobile and suffered a moderately displaced fracture of the L3 vertebra. The video shows the radiographs. Note the clinical signs of Schiff-Sherrington syndrome but the absence of any spinal shock.

In our experience, Schiff-Sherrington syndrome and spinal shock are rare in cats. The following three videos show cats with thoracolumbar vertebral column fractures that caused a transverse spinal cord dysfunction with peracute paraplegia and analgesia caudal to the lesion.

Video 10-5 shows Poison, an 8-year-old castrated male domestic shorthair that was struck by a vehicle 2 days before the video was made. Note the crossed extension in the pelvic limbs and the pelvic limb flexion when the tail was compressed with forceps. The latter is referred to as a mass reflex, which is another manifestation of hyperreflexia. Radiographs (see the video) showed a fracture at the articulation between the L3 and L4 vertebrae, with at least 50% displacement. Poison was euthanized and the necropsy showed that at the site of the fracture and displacement, there was only a sleeve of dura remaining. The parenchyma of the spinal cord at this site had been completely crushed and displaced into the adjacent spinal cord segments (Fig. 10-5).

Figure 10-5 Lumbar spinal cord of the cat in Video 10-5, showing a crease in the dura at the level of the fracture site. At this site there is only a sleeve of dura, and the parenchyma has been entirely displaced into the adjacent spinal cord segments.

Video 10-6 shows George, an adult Siamese cat that was found beside the road unable to use his pelvic limbs. Radiographs (see the video) showed a fracture at the articulation between the T13 and L1 vertebrae, with slight displacement. Note the pelvic limb flexion when the tail was compressed with forceps. This is an example of a mass reflex. George was euthanized and necropsy revealed hemorrhage and necrosis that involved all of the transverse section of the spinal cord at the level of the fracture (Fig. 10-6).

Figure 10-6 Transverse sections of the spinal cord of the Siamese cat in Video 10-6, showing the hemorrhage and necrosis at the site of the displaced fracture.

The spinal cord lesions resulting from injury caused by external trauma include the physical disruption of the high-risk spinal cord parenchyma as compared with the more resistant dural layer of meninges. See Fig. 10-6, which shows this severe spinal cord lesion. A contused spinal cord exhibits hemorrhage, edema, and necrosis due to compromise of the spinal cord’s vasculature. Following the traumatic event, there is continued degeneration of the injured spinal cord that progresses for a few hours, usually less than 24 hours. The basis for this is the subject of intense research directed at determining ways to treat these patients to prevent this progressive spinal cord destruction. Areas of interest include the release of neurotransmitters, such as toxic levels of glutamate, excessive accumulation of calcium ions, free radical species, nitrous oxide, and the release of various amines that cause vasoconstriction and subsequent ischemia and infarction.

Video 10-7 shows an 8-week-old Siamese kitten that was found beside the road by Society for the Prevention of Cruelty to Animals employees. Radiographs (see the video) showed a fracture at the T8-T9 vertebral articulation, with complete displacement through the vertebral canal. No owner was located. Despite the peracute paraplegia and analgesia caudal to the lesion, there were no signs of the Schiff-Sherrington syndrome or spinal shock. A medicine resident adopted the kitten, knowing that there would be no improvement in the clinical signs. The fracture was reduced and stabilized and a cart was made for the kitten (see the video). When the resident took a permanent position in Alaska, the then young adult cat was doing fine and enjoying life in a larger cart.

Monoplegia

CASE EXAMPLE 10-3

Signalment: 3-year-old castrated male malamute, Drake

Chief Complaint: Unable to use the left pelvic limb

History: After a 5-mile run with his owners, Drake was in their home when he suddenly lost the ability to move his left pelvic limb. He was examined by a local veterinarian and then referred to Cornell University, where his disorder was filmed on the second day of the dysfunction, which had not changed since the onset.

Examination: Video 10-8 shows the spastic monoplegia limited to the left pelvic limb. The right pelvic limb gait was normal, but the limb showed some difficulty with the hopping response.

Anatomic Diagnosis: A focal lesion on the left side, between the T3 and L3 spinal cord segments

Do not confuse this anatomic diagnosis with sciatic nerve paralysis, which looks much different. Review Video 5-44 of the collie dog Keane, described with Case Example 5-15; Keane has a left sciatic nerve injury due to a pelvic fracture. Dogs with sciatic nerve deficits can always advance the limb by hip flexion, and there is hypotonia of the crural muscles.

Differential Diagnosis: FCEM, intervertebral disk extrusion, neoplasia

External injury was excluded based on the history and on the knowledge that such localized unilateral signs would be very unusual for an external spinal cord injury. The lack of any discomfort at the onset of the paralysis or during the examination is more suggestive of FCEM than of an intervertebral disk extrusion. An intervertebral disk extrusion would be unlikely in a 3-year-old nonchondrodystrophic breed. However, it can best be ruled down by imaging. Radiographs and a myelogram were normal, which supported a presumptive FCEM lesion.

On the video, you can follow the spontaneous recovery. The section of the video where Drake is walking indoors after you see his vigorous response to a noxious stimulus was made 1 week later, and the section outdoors was made 3 weeks after the initial filming.

CASE EXAMPLE 10-4

Signalment: A 6-year-old castrated male Labrador retriever, Penfield

Chief Complaint: Unable to use the right pelvic limb

History: The owners were playing ball with Penfield in a local park when he suddenly yelped and stopped using his right pelvic limb.

Examination: This examination took place the day after the onset of the clinical signs, which had not changed. Video 10-9 shows that this dog’s clinical signs are the mirror image of those observed in Drake in Case Example 10-3. Penfield exhibits a spastic monoplegia of his right pelvic limb.

Anatomic Diagnosis: Focal lesion on the right side of the spinal cord between the T3 and L3 spinal cord segments

Differential Diagnosis: The diagnosis is the same as that described for Drake in Case Example 10-3. The indication of discomfort when the initial clinical signs occurred is suggestive of a possible intervertebral disk extrusion. Radiographs and a myelogram diagnosed a unilateral right-side intervertebral disk extrusion between the L3 and L4 vertebrae. This was removed via a hemilaminectomy, and Penfield was walking with the right pelvic limb after about 3 weeks.

The following two videos show the same two clinical disorders that are described in this case example and Case Example 10-3.

Video 10-10 shows Dude, a 3-year-old male miniature schnauzer that had been outdoors unconfined during the night and was found in the morning unable to use his left pelvic limb. From your study of this video you should make the anatomic diagnosis of a focal spinal cord lesion on the left side between the T3 and L3 spinal cord segments. The differential diagnosis is the same as in this case example and Case Example 10-3 but must include external injury because the history cannot rule it out. The absence of any reluctance to try to walk as well as of any discomfort when palpated and the presence of extensive unilateral signs all suggest that external injury is unlikely. The young age of this dog suggests that a unilateral intervertebral disk extrusion is also less likely. In addition, this breed is at some risk for the development of fibrocartilaginous emboli. Radiographs and a myelogram were normal, which made FCEM the most presumptive diagnosis. Within 2 to 3 weeks, without specific therapy, Dude was walking well in the left pelvic limb. Figure 10-7 shows the kind of FCEM lesion that explains these clinical signs but from which recovery would not occur.

Figure 10-7 Transverse section of the T13 spinal cord segment of a 3-year-old Saint Bernard with a left pelvic limb spastic monoplegia due to a fibrocartilaginous embolism that caused ischemic infarction of the left half of the spinal cord. A similar anatomic but less severe lesion was presumed to have occurred in Drake in Video 10-8 and in Dude in Video 10-10.

Video 10-11 shows Beaver Dam, an 8-year-old spayed female mixed-breed dog that was presented because of difficulty using the left pelvic limb. This dysfunction began when the dog fell down a flight of stairs and had not changed significantly since that time. From your study of the video, you should make the same anatomic and differential diagnosis as for Dude in the previous video. The video of Beaver Dam shows the radiographs, myelogram, and CT imaging, which diagnosed intervertebral disk extrusions at the L1-L2, and L3-L4 vertebral articulations. The owner elected to treat the dog medically, and no follow-up on its success is available.

Paraparesis and Ataxia

CASE EXAMPLE 10-5

Signalment: 5-month-old male Labrador retriever, Cassidy

Chief Complaint: Unable to walk normally with the pelvic limbs

History: About 4 weeks before examination at Cornell University, this dog was on a camping trip in the Adirondacks when the owners first noticed that Cassidy occasionally stumbled with his left pelvic limb. Within the next week he was also stumbling with the right pelvic limb. This pelvic limb dysfunction slowly progressed until the time of this examination.

Examination: Video 10-12 shows the monoplegia of the left pelvic limb and grade 2 monoparesis and ataxia of the right pelvic limb, with absent postural reactions. Cranial nerves and thoracic limb function were all normal. Note the mild hypertonia and normal spinal reflexes for the pelvic limbs and the normal nociception.

Anatomic Diagnosis: A focal or diffuse lesion between spinal cord segments T3 and L3, worse on the left side

With normal nociception, there is no reliable way to localize a focal lesion between these segments using the physical neurologic examination. Be aware that there could be multiple or diffuse lesions in this anatomic area that would explain the clinical signs that were observed in this dog.

Differential Diagnosis: The following diagnoses are limited to those spinal cord disorders that could cause a progressive lesion within these thoracolumbar spinal cord segments of a dog: neoplasm, vertebral malformation, myelitis, discospondylitis, multiple cartilaginous exostosis, intervertebral disk extrusion-protrusion, degenerative myelopathy.

NEPHROBLASTOMA

Although we tend to relegate neoplasia to older dogs, there are many exceptions to this, and one of them occurs at this location in dogs. Nephroblastoma is a unique intradural, extramedullary (extraaxial) neoplasm that occurs in young dogs, usually between spinal cord segments T10 and L2 (Figs. 10-8 through 10-10).⁹¹ Most of our experience and reports in the literature involve dogs younger than 3.5 years of age, many of them only a few months old. There are numerous reports, mostly in the European literature, that describe this neoplasm as an ependymoma.^58,^92,¹⁰⁹ In the first two editions of this text, I (AD) recognized that this was not intramedullary and therefore was not an ependymoma, and I called it a neuroepithelioma based on the morphology of the cells and the abundance of tubular elements in the neoplasm. Since then, we have recognized tubular structures that resemble renal glomeruli and have diagnosed this neoplasm as a presumptive nephroblastoma. It is an embryonic neoplasm that may arise from mesonephric tubules. This is supported by the positive immunocytochemical staining of the neoplastic cells for a polysialic acid marker of this tumor; the test was developed in children by Dr. J. Roth in Switzerland.⁷⁸

Figure 10-8 A nephroblastoma in a 5-month-old Labrador retriever at the level of the T13 spinal cord segment.

Figure 10-9 A nephroblastoma in a 10-month-old German shepherd at the level of the T12 spinal cord segment, with the dura reflected.

Figure 10-10 A transverse section of the nephroblastoma in Fig. 10-9. The nephroblastoma is intradural but extramedullary. Note the marked spinal cord compression.

In children, this nephroblastoma occurs in the kidney and is called a Wilm tumor. A gene located on chromosome 11 has been identified for this tumor in children. Using antibodies developed for the protein product of this tumor gene, immunocytochemical staining has identified this protein product in the canine neoplasm.⁷⁶ The unique location of this neoplasm between spinal cord segments T10 and L2 correlates with the site of embryonic renal development from intermediate mesoderm. This is adjacent to the development of the somitic sclerotomes that envelope the neural tube that forms the thoracolumbar spinal cord. A Wilm tumor has three components, sheets of unorganized epithelial cells referred to as blastemal cells; tubular elements lined by epithelial cells that vary from squamous to cuboidal and some of which form glomerular structures; and a fibrous component that consists primarily of bundles of collagen. The canine neoplasm is made up primarily of the first two components (Figs. 10-11 through 10-15). A nephroblastoma in this spinal cord location is very rare in children. In dogs, this neoplasm does occur in the kidney but it is much more common adjacent to the spinal cord. There are no reports of this neoplasm being in both locations in the same patient.

Figure 10-11 A nephroblastoma in the T12 spinal cord segment of a 6-month-old German shepherd.

Figure 10-12 A microscopic section of the nephroblastoma in the dog in Fig. 10-11. The nephroblastoma is growing in the subarachnoid space, compressing the spinal cord to the right side.

Figure 10-13 A microscopic section of the diffuse blastemal epithelial cells of a nephroblastoma.

Figure 10-14 A microscopic section of the tubular elements of a nephroblastoma.

Figure 10-15 A microscopic section of a glomeruloid structure in a nephroblastoma.

Typically, the clinical signs occur in one pelvic limb prior to their occurrence in the other, which reflects the asymmetric location of the neoplasm. We suspect this is a very slowly growing neoplasm and recognize that the spinal cord can be slowly compressed by an extramedullary mass for a long time before the autoregulation of spinal cord vascular perfusion fails and clinical signs occur. Therefore, when these clinical signs occur, be aware that the spinal cord is already very compressed, and if surgery is to be considered it should be done as soon as possible. Often at necropsy, the spinal cord consists only of a thin 1- to 3-mm quarter-moon-shaped shell covering one side of the neoplasm (see Figs. 10-10 through 10-12). When surgeons remove this neoplasm they often see the severely compressed spinal cord slowly start to fill the space where the mass was removed. Postoperative radiation therapy should be done to avoid recurrence of the neoplasm.

Another neoplasm that is more common in cats and can occur at any level of the vertebral canal is lymphoma. In cats it commonly occurs before 1 year of age. Gliomas are less common in the spinal cord of all species and usually occur in older animals.

VERTEBRAL MALFORMATION

Vertebral malformation with kyphosis and secondary spinal cord compression is a realistic consideration in this dog. This vertebral malformation is usually in the midthoracic portion of the vertebral column.^49,⁶⁷ Although these dogs have the vertebral malformation at birth, the clinical signs of spinal cord compression usually do not occur until a few months of age but prior to 1 year of age. We believe that the kyphosis that causes the spinal cord compression develops at the site of the malformation as the dog grows, and this accounts for the age of onset of the progressive spastic paraparesis and ataxia of the pelvic limbs. Occasionally, on your physical examination of the patient, you can see and palpate the kyphosis. However, it is easy to overlook if you do not take the time to carefully examine the patient for it. This malformation is readily seen on radiographs. It was not visible or palpated in Cassidy. (See Videos 10-15 and 10-16.)

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