key: cord-0039695-3l76satg authors: Luttgen, Patricia J.; Cuddon, Paul A. title: Disorders of the Spinal Cord date: 2009-05-15 journal: Saunders Manual of Small Animal Practice DOI: 10.1016/b0-72-160422-6/50130-3 sha: 8ab1163c77ac263ff9579921fa87f4faea6c0feb doc_id: 39695 cord_uid: 3l76satg nan The term spinal cord disorders (see Table 128 -1 for classification and examples) broadly refers to all diseases affecting the spinal cord. Clinically, spinal cord disorders may cause dysfunction in one or more limbs. Urinary and fecal incontinence and tail dysfunction may also be seen. M Key Point Disorders of the spinal cord do not cause signs referable to diseases above the foramen magnum, such as mentation changes, cranial nerve deficits, and vestibular ataxia. Spinal cord disorders can arise from numerous insults and may be associated with particular signalments (breed, age, sex) and neuroanatomic localizations. Many of these disorders cause relatively predictable patterns of onset (acute versus chronic) and clinical signs (progressive versus nonprogressive). Anomalies of the spinal cord usually are first recognized when ambulation begins and are nonprogressive. Examples include spinal dysraphism in Weimaraners and sacrocaudal dysgenesis with spina bifida in English bulldogs and Manx cats. • For some anomalies, traumatically induced "decompensation" may be required for minor lesions to be recognized clinically. An example is atlantoaxial subluxation of toy breeds in which ligamentous and dens malformations create C1-C2 instability and an increased risk of C1-C2 luxation. • Some anomalies slowly worsen over the life of the animal to cause progressive worsening of signs. Dogs with congenital arachnoid cysts show slowly progressive spinal cord signs as the cavitating lesion expands in size. In dogs with caudal occipital malformation syndrome (COMS), progressive foramen magnum compression causes disruption of cerebrospinal fluid (CSF) flow and syringohydromyelia formation. Signs of slowly progressive spinal cord dysfunction can be seen at almost any age. • Vertebral anomalies that compromise the stability of the vertebral column or the canal size may cause spinal cord dysfunction secondary to compression. For example, hemivertebra may lead to vertebral body luxation, and malarticulation/malformation of articular facets may lead to spinal canal stenosis. Degenerative conditions are usually insidious in onset and chronically progressive. • Many of these conditions are inherited and are seen in young animals. Examples include lysosomal storage disorders such as globoid cell leukodystrophy and Niemann-Pick disease, spinal muscular atrophy of Brittany spaniels, and hereditary ataxia of Jack Russell and smooth-haired fox terriers. • Other neurodegenerative disorders are age-related and may be familial. Examples include degenerative myelopathy seen in older, large-breed dogs, particularly the German shepherd. In this disorder, white matter degeneration is most severe in the T3-L3 region. • Some age-related degenerative disorders affect bony and soft tissues surrounding the spinal cord and result in spinal cord compression. Examples include cervical spondylomyelopathy in Doberman pinschers, intervertebral disc disease (discussed under spinal cord trauma below), lumbosacral spondylopathy/stenosis of German shepherd dogs, and mucopolysaccharidosis in cats. • Trauma can arise from external sources (e.g., being hit by a car or a bullet) or from internal sources (e.g., disc herniation or a pathologically collapsed vertebra). • Clinical signs are usually acute and nonprogressive. However, progressive signs may be seen. • Pathologic vertebral body fractures can occur secondary to vertebral body neoplasia or osteomyelitis. Chapter 128 / Disorders of the Spinal Cord 1295 • Type I intervertebral disc disease is characterized by sudden disc extrusion. Signs of spinal cord compression are usually acute and may progress over a few hours or days. • Type II intervertebral disc disease is characterized by slow protrusion of a slowly degenerating disc. Signs are usually gradual in onset and progression. Numerous infectious agents can affect the spinal cord and surrounding structures of animals of all breeds and ages. Clinical signs vary depending on the inciting agent, the location of the lesion, and the degree of spinal cord involvement. Signs are usually rapid in onset and progression. Often inflammatory disease of the central nervous system (CNS) is not confined to the spinal cord, and clinical signs of brain involvement will also be present (see Chapter 126). • Primary bacterial meningitis or meningomyelitis is infrequently diagnosed in dogs and cats. Bacterial infection is most commonly introduced secondary to infection of surrounding tissues or to trauma. • For example, bacterial discospondylitis causes discomfort from disc and vertebral body infection and may cause neurologic deficits if secondary compression of the spinal cord occurs. Viral myelitis is a relatively common problem in dogs and cats. Clinical presentation and neuroanatomic localization vary. • Typically, encephalitic signs are associated with rabies infection, but this virus may also cause signs of myelitis (see Chapter 15). • All ages of dogs are susceptible to canine distemper virus (CDV; see Chapter 13). Previous vaccination does not preclude "breaks" in immunocompetency due to other illnesses or disease states. Signs of spinal cord disorder without associated encephalitic signs may occur. • In cats, coronavirus (feline infectious peritonitis) and retrovirus (feline leukemia virus and feline immunodeficiency virus) infections may cause signs of spinal cord dysfunction with or without signs of brain involvement (see Chapters 8, 9, and 10). • Fungal myelitis has been reported in patients with cryptococcosis, blastomycosis, histoplasmosis, and coccidioidomycosis. • Multiple levels of the nervous system usually are involved simultaneously (e.g., eyes, brain, spinal cord); however, signs are limited to the spinal cord in some patients. • Systemic mycoses are discussed in Chapter 20. • In addition to other clinical signs, tickborne rickettsial diseases such as ehrlichiosis and Rocky Mountain spotted fever may cause myelitis, meningitis, and encephalitis (see Chapter 17). • Neospora caninum may cause pelvic limb rigidity followed by a rapid ascending tetraparesis/tetraplegia due to a severe myelitis (see Chapter 21). • This is believed to be an immune-mediated disorder of the brain and spinal cord. • Signs of spinal cord myelitis and meningitis may predominate. The cervical area seems to be the preferred site of involvement in the spinal cord. • GME primarily affects the white matter of the CNS and consists of perivascular accumulations of lymphocytes, plasma cells, and reticuloendothelial cells. Perivascular cuffs can coalesce to produce granulomas. • The disease is invariably progressive in nature (see Chapter 126). • Immune-mediated steroid-responsive meningitis and/or meningeal-vasculitis have been reported in young dogs of many breeds. Boxers are commonly affected with this disorder. A more severe form of this syndrome (necrotizing vasculitis) has been reported in beagles, Bernese Mountain dogs, and German short-haired pointers. • Clinical signs are typical of spinal meningitis including neck stiffness, hyperesthesia, and fever. • Strychnine and tetanus directly affect the spinal cord in dogs and cats. These toxins act in a similar manner. • Tetanus toxin decreases the release of the inhibitory neurotransmitters, g-aminobutyric acid and glycine in the spinal cord, whereas strychnine competitively blocks the inhibitory effect of glycine. • Clinical onset is usually acute, and the disease progresses to a state of severe tetany. • Vascular conditions resulting in ischemia of the spinal cord most often cause peracute to acute nonprogressive spinal cord dysfunction. Intramedullary spinal cord lesions are nonpainful. • The lesion may affect any area of the spinal cord. M Key Point In adult large-breed dogs, fibrocartilaginous embolization is the most common cause of vascular injury to the spinal cord. Lesions are often asymmetrical and may affect several spinal cord segments in a continuous or discontinuous distribution. • In cats, caudal aortic embolization secondary to cardiomyopathy is a common cause of spinal cord vascular injury. • Neoplasia of the spinal cord can affect animals of all ages and breeds. Initial clinical signs vary, depending on the type and location of the tumor. Signs usually are progressive over weeks to months. Two major types of tumors affect the spinal cord: intramedullary and extramedullary. • Intramedullary tumors such as astrocytoma and ependymoma arise from the spinal cord itself, causing damage by derangement of the normal anatomy. Hemangiosarcoma, lymphoma, and other tumors may metastasize to intramedullary sites in the spinal cord. • Extramedullary tumors arise from tissues surrounding the spinal cord and cause damage by compression. Extramedullary tumors can be located intradurally (e.g., meningiomas and nerve root tumors) or extradurally (e.g., vertebral osteosarcomas and multiple myeloma). Extradural lymphoma is a common cause of caudal paresis in cats. • See Chapter 101 for discussion of neoplasia of the axial skeleton. Characteristic clinical signs of spinal cord injury include spinal pain or hyperpathia, proprioceptive deficits, paresis or plegia, and nociceptive (pain) loss. • Involvement of nerve roots, dura, and other extradural structures adjacent to the spinal cord will result in hyperpathia (exaggerated response to a painful stimulus). • Spinal hyperpathia can be assessed by observing for pain on spinal palpation, neck guarding or stiffness, or signs of a root signature (holding/favoring the limb at rest). • Extradural and extramedullary lesions are often painful. This can be helpful in lesion localization. • Ascending sensory tracts in cord white matter convey proprioceptive information from the limbs to the brain. • Conscious proprioceptive (CP) tracts convey signals concerning limb position at rest to the cerebral cortex. • Unconscious proprioception (UP) tracts convey signals concerning limb position during locomotion to the cerebellum. • Injury to CP tracts causes knuckling and slow postural reactions (as during the hopping test). • Injury to UP tracts causes ataxia ("drunken" gait with crossing over, wide-based posture, truncal sway, circumduction, and, occasionally, hypermetria). Ataxia is usually observed in the limbs caudal to the lesion. M Key Point Ascending proprioceptive fibers in the spinal cord are the most sensitive to compressive lesions. Therefore, CP deficits and incoordination (sensory ataxia) of one or more limbs is commonly the initial sign of spinal cord disease. • Descending upper motor neuron (UMN) tracts in cord white matter originate in brain and terminate in the spinal cord. The UMN system modulates functions of the thoracic and pelvic limb lower motor neurons (LMNs) located in the gray matter of cord segments C6-T2 and L4-S2, respectively. • UMN inputs facilitate limb strength and motor abilities and inhibit some spinal reflexes and limb extensor muscle tone. • LMNs also facilitate strength, relay locomotor signals from the UMN system, are part of the reflex arc for spinal reflexes, and provide trophic support to limb muscles. • Injury to either UMN or LMN pathways will cause varying degrees of paresis (weakness) or plegia (weakness with loss of locomotor abilities) of the limbs. M Key Point UMN injury results in paresis to limbs caudal to the level of the lesion, and LMN injury results in paresis to limbs at the level of the lesion. • Injury to UMN pathways results in retention of spinal reflexes and increased extensor muscle tone when animals are recumbent. • Injury to LMN pathways results in depression of spinal reflexes, decreased muscle tone, and muscle atrophy. • C1-C5 injuries can potentially cause signs of UMN tetraparesis or tetraplegia if damage to UMN pathways occurs. • C6-T2 injuries can cause signs of LMN paresis in the thoracic limbs and signs of UMN paresis in the pelvic limbs. • T3-L3 injuries can cause signs of UMN paresis in the pelvic limbs. • L4-S3 lesions can cause signs of LMN paresis in the pelvic limbs, incontinence due to urinary bladder, urethral sphincter, and anal sphincter dysfunction. • Ascending nociceptive tracts in the spinal cord white matter convey nociceptive (pain) signals from the limbs to the cerebral cortex. • Injury to these tracts results in depressed or absent detection of noxious stimuli. • Nociceptive perception is usually assessed by testing the digits for superficial and deep pain sensation. • Nociceptive tracts in cord white matter are very resistant to injury and are affected by only very severe spinal cord injuries. M Key Point The ascending spinal cord pain fibers are the most resistant to compressive lesions. Therefore, lack of deep pain perception as demonstrated by no visible response to a noxious stimulus (i.e., the animal does not appear to be consciously aware of the pain) applied to a limb or tail caudal to a compressive lesion indicates severe damage to the spinal cord. • As compressive (extradural or extramedullary) lesions worsen, CP, UP, UMN (limbs and then bladder/sphincter), and then nociceptive functions are lost in that order. Examples include intervertebral disc disease, discospondylitis, vertebral body tumors, and vertebral malformations. Predictable and sequential signs of CP deficits, sensory ataxia, and then paresis are observed. • Neurologic deficits are ipsilateral to the lesion. • Extramedullary lesions that "lateralize" cause asymmetrical signs. • Intramedullary lesions such as some spinal cord tumors, degenerative conditions, myelitis, and some spinal cord anomalies tend to cause symmetrical neurologic deficits (exception is asymmetrical fibrocartilagenous infarction) that may progress in a less predictable fashion. • Intramedullary lesions without concurrent extramedullary involvement are nonpainful. • Intramedullary cervical cord lesions may lead to cervical torticollis (lateral deviation of the neck). • The ratio of spinal canal to spinal cord diameter is much greater in the cervical region than in the thoracolumbar region. For this reason, extramedullary lesions in the cervical region can be quite large without causing severe neurologic deficits. Conversely, smaller extramedullary lesions in the thoracolumbar area can be associated with severe neurologic deficits due to the small amount of space around the spinal cord. • In spinal cord disorders, key aspects of the history are signalment, nature of onset, and progression of clinical signs. Knowledge of breed, age, and progression of signs can usually aid in narrowing down the list of most likely differential diagnoses. • For example, chronic progressive disease in an older German shepherd suggests degenerative myelopathy, neoplasia, or chronic type II disc herniation. • Acute nonprogressive disease in a young dog suggests trauma, acute type I disc herniation, or fibrocartilaginous embolization. • The neurologic examination establishes the presence or absence of neurologic dysfunction (see Chapter 125). • See previous discussion under "Clinical Signs" for localizing lesions in animals with paresis and/or plegia. • Many of the diseases described above (myelitis, tumors, fibrocartilagenous infarction, degenerative disorders) can affect any segment of the spinal cord. • Other diseases target specific areas of the spinal cord. Examples include atlantoaxial subluxation (C1-C2), hemivertebrae (thoracic spinal cord), degenerative myelopathy (T3-L3), spina bifida (lumbosacral area), and cervical spondylomyelopathy (C5-C7). Knowledge of these predilection sites can aid in choosing appropriate diagnostic tests to perform. • As discussed above, spinal hyperpathia usually suggests an extramedullary lesion while absence of hyperpathia suggests an intramedullary lesion. This information may influence choice of imaging modality (magnetic resonance imaging [MRI] versus myelography). • Establishing a minimum database (MDB) is essential for assessment of the animal's overall health prior to general anesthesia for neurologic testing. The MDB also aids in ruling out systemic inflammatory, metabolic, and endocrine disorders that may be contributing to the neurologic state. M Key Point The MDB for neurologic patients consists of a complete physical examination (including neurologic, otic, and ophthalmic evaluation), complete blood count (CBC), serum biochemical analysis, urinalysis, fecal analysis, thyroid panel (T4, free T4, thyroid-stimulating hormone) and electrocardiogram. Routinely test for heartworm in endemic areas. • Epaxial and limb EMG is useful for localizing areas of denervation secondary to a lower motor neuron lesion (see Chapter 125). • MNCV and SNCV studies of peripheral nerves, and nerve root evaluation (CDPs and F waves), help to rule out peripheral nerve, nerve root, and muscle diseases that present with many of the same clinical signs as spinal cord disease (see Chapters 129 and 130 for discussion of peripheral nerve and muscle disorders, respectively). • SCEPs and SSEPs evaluate the integrity of the ascending spinal cord tracts to determine the extent of functional damage. • Plain radiography is often sufficient to diagnose problems such as atlantoaxial subluxation, vertebral fracture/luxation, vertebral neoplasia, vertebral anomalies such as spina bifida and hemivertebrae, and discospondylitis. • Discospondylitis is characterized by lytic, irregular end plates with sclerosis of adjacent vertebral bone. Avoid causing further injury to the animal during these procedures. • Refer to Chapter 4 for positioning and technique. • When plain radiographs are inconclusive, use specialized procedures. • Myelography remains a useful diagnostic procedure in small animals (see Chapter 4). • Disadvantages compared to MRI include greater invasiveness (intrathecal contrast injection), longer anesthetic times, lack of imaging of intramedullary lesions, and inability to image in the axial plane. • Myelography has certain advantages for imaging extradural lesions, especially those involving bony structures or those that may dynamically compress the spinal cord. Post-myelogram computed tomography allows excellent imaging of the axial spinal canal and bony structures and provides accurate information concerning localization of lateralized lesions. • Myelography is contraindicated in the presence of CNS inflammation (encephalitis, myelitis, meningitis) or if increased intracranial pressure is suspected. • MRI is a very useful and effective technique to image the spinal cord (see Chapter 4). • MRI provides excellent soft tissue resolution and is the imaging modality of choice for characterizing intramedullary spinal cord lesions, nerve sheath tumors, and lumbosacral spondylopathy in the German shepherd. • MRI has increased our awareness of the prevalence of syringohydromyelia in certain breeds. It also provides imaging in the sagittal, axial, and horizontal planes for improved lesion localization. • If the goal is to evaluate a suspected bony lesion, CT is the preferred imaging modality (see Chapter 4). M Key Point CSF analysis is the test of choice for establishing an inflammatory cause of spinal cord disease; furthermore, it provides nonspecific information that is helpful in the diagnosis of degenerative, neoplastic, and vascular conditions, including the following: • Degenerative, neoplastic, and occasionally vascular problems may cause increased protein levels in the presence of normal cell counts in CSF. • Inflammatory conditions of the spinal cord cause increases in CSF protein and variable increases in cell numbers and type, depending on the specific etiologic agent causing the insult. • Sterile suppurative or steroid responsive meningitis is characterized by a predominance of neutrophils in CSF. • GME is characterized by increased numbers of lymphocytes, monocytes, and macrophages in CSF. • Etiologic agents (e.g., bacteria, rickettsiae, protozoa, fungi) are sometimes identified in CSF by culture (bacteria) or cytology. • Comparative titers on simultaneously collected CSF and serum are also helpful for identifying active CNS infection by canine distemper virus and toxoplasmosis. • Neoplastic cells are rarely seen in the CSF of patients with CNS neoplasia. However, globoid cells may be identified in cases of globoid cell leukodystrophy. • For further details concerning CSF collection technique and abnormalities in specific infectious and inflammatory conditions of the CNS, see Chapters 125 and 126. The management of spinal cord disorders depends on the etiology and the severity of the spinal cord injury. Medical treatment, surgery, radiation therapy, or a combination of these treatment modalities may be indicated. • Glucocorticosteroids at anti-inflammatory doses are recommended for degenerative conditions that cause secondary compression of the spinal cord. These disorders include cervical spondylomyelopathy, type II intervertebral disc disease, and lumbosacral spondylopathy. In each of these disorders, avoid long-term corticosteroid therapy. Surgical intervention is usually indicated due to the progressive nature of these conditions. • For most of the neurodegenerative diseases, no specific therapy is available and only supportive treatment can be provided. Various treatments have been attempted in degenerative myelopathy, all without proven effect. Bone marrow transplantation has shown some efficacy is some lysosomal storage diseases (see Chapter 126). • Medical therapy to combat the effects of acute spinal cord trauma (e.g., edema, ischemia) is based on the use of glucocorticosteroids. • Best results in spinal cord trauma are obtained when large doses of corticosteroids are administered immediately after injury, followed by rapid dosage tapering. • Base the total dosage and tapering of dosage on the patient's response to therapy. Evaluate the patient's neurologic function at least every 8 hours to determine if another dose is necessary. • The maximum amount of time that glucocorticosteroids are beneficial following spinal cord injury appears to be 2 to 3 days; longer administration is of little benefit and enhances the likelihood of gastric ulcers, gastroenteritis, and pancreatitis. Use a concurrent H 2 -blocker and sucralfate therapy to reduce the potential for gastric ulceration (see Chapter 67 for dosages). M Key Point The most beneficial glucocorticosteroid for acute spinal cord trauma, including that from acute intervertebral disc herniation, is methylprednisolone sodium succinate (MPSS or Solu-Medrol, Upjohn). • In experimental studies, MPSS administered intravenously during the first 8 hours following injury has shown remarkable sparing action on the spinal cord compared with dexamethasone, mannitol, dimethyl sulfoxide (DMSO), naloxone, and thyrotropinreleasing hormone. • Give an initial dose of 30 mg/kg IV followed by dosages of 15 mg/kg IV at 2 hours and then every 6 hours for a minimum of 24 hours. Alternatively, give the initial 30 mg/kg dose followed by a continuous infusion of 5.4 mg/kg/hr IV for 24 to 48 hours. The above protocols have been shown to be effective in human and experimental animal models of spinal cord injury if provided within 1 to 6 hours of the injury. Controlled clinical trials in veterinary medicine have not been performed. • If additional glucocorticosteroid therapy is necessary, substitute with dexamethasone, prednisolone, or prednisone. • Hyperosmotic solutions, such as mannitol, have been widely used to combat post-traumatic brain edema, but their use in cases of spinal cord trauma is ineffective. • Other investigated drugs for adjunctive therapy of spinal cord trauma, such as antioxidants, calcium channel blockers, and vasodilators, are not routinely recommended at this time. Antimicrobial Drugs • Antimicrobial drugs may be indicated if specific infectious agents are identified or suspected. Treatment of systemic mycoses, protozoal, and rickettsial infections are discussed in detail in Chapters 20, 21, and 17, respectively. Also, see Chapter 126 for treatment of CNS infections. • In cases of meningitis or myelitis, select antimicrobials that are known to cross the blood-brain barrier readily (i.e., highly lipid soluble in the non-ionized state, such as trimethoprim-sulfonamide combinations, rifampin, metronidazole, chloramphenicol, and certain imidazoles such as fluconazole). • Drugs with intermediate penetrating abilities in the normal CNS may have improved penetrating abilities when the CNS is inflamed. These include the penicillin family (e.g., amoxicillin, carbenicillin), quinolones (e.g., enrofloxacin), the newer-generation tetracyclines (e.g., doxycycline, minocycline), clindamycin, and certain cephalosporins. • Avoid drugs that penetrate poorly such as the aminoglycosides, amphotericin B, and ketoconazole. • Treatment of discospondylitis presents a unique challenge because of the difficulty of presenting sufficient antimicrobial concentrations to the affected disc space and vertebral bodies. • Staphylococcus is the organism most frequently reported. Brucella canis, Nocardia, Streptococcus canis, Corynebacterium diphtheroides, and various fungi also have been isolated. • If possible, base selection of antimicrobial drugs on positive culture results (blood, urine, or the affected disc space) or a positive Brucella agglutination test. Otherwise, assume that the causative organism is coagulase-positive Staphylococcus and administer betalactamase-resistant antibiotics that reach sufficient therapeutic levels in bone and purulent exudates. • Clinical signs may improve within a few days, but long-term therapy of several months is usually required to prevent relapses. • In some cases, antimicrobials alone are not effective, and surgical intervention is required. When surgery is required, remove the infected vertebral end plates and associated disc structures. Use a vertebral body bone plate to stabilize the area and fill in the defect with cancellous bone. (See Chapter 100 for more information on spinal surgery.) Administer intralesional antibiotics. • Both GME and immune-mediated meningitis syndromes are treated via immunosuppression. Initially give prednisone (1.0-2.0 mg/kg q12h) and consider using it in combination with other immunosuppressive agents (cytosine arabinoside, azathioprine, procarbazine, lomustine). With combination therapy, the prednisone dosage often can be decreased to once daily or every other day therapy. In some dogs, prednisone therapy can be eliminated over time. • Radiation therapy has been shown to have a beneficial effect on encephalitis caused by GME. • For tetanus, initially administer penicillin G (20,000-100,000 IU/kg q6-12h IV or IM). Tetracycline (22 mg/kg q8h PO or IV) is recommended as an alternative because of the variable effect of penicillins on vegetative forms of the organism. Metronidazole (dog, 15 mg/kg q8h PO; cat, 250 mg total, q12-24h, PO) has shown excellent efficacy. It is bactericidal against most anaerobes and reaches effective levels in necrotic tissues. • Equine tetanus antitoxin (100-1000 IU/kg IV, usually administered only once) may combat the neurotoxin if given early enough. However, anaphylactic reactions are common, necessitating an initial test dose (0.1-0.2 ml) given SC or intradermally (ID) 15 to 30 minutes prior to IV dosing. • Chlorpromazine (0.5-2.0 mg/kg q8-12h, given IM, IV, or PO) is effective against the hyperexcitability sometimes observed. • Diazepam (dog, 5-10 mg total, q2-4h, given PO, IV, or IM; cat, 2.5-5 mg total, q2-4h, PO) blocks the effect of the toxin on the spinal cord but has a very short duration of action. • Barbiturates also may be used to combat the tetany. Phenobarbital (16-18 mg/kg, IV) can be given to immediately control seizure activity and generalized body stiffness, followed by oral maintenance therapy (2-4 mg/kg q12h PO). Pentobarbital therapy may be needed if muscle spasms are severe and nonresponsive to diazepam, methocarbamol, and phenobarbital therapy. • For strychnine intoxication, chlorpromazine, diazepam, and barbiturates are used as for tetanus above. In order to block further gastrointestinal absorption, perform gastric lavage followed by oral administration of binding agents, such as activated charcoal. • Most antineoplastic drugs do not cross the bloodbrain and blood-CSF barrier. • Lomustine does penetrate CNS tissues and, in conjunction with prednisone, can be useful for treatment of CNS lymphoma. Cytosine arabinoside penetrates into the CNS when given intravenously at high concentrations (up to 400 mg/m 2 ). Use of cytosine arabinoside at induction followed by long-term lomustine therapy can be used in conjunction with traditional chemotherapy protocols for multicentric lymphoma with CNS involvement (see Chapter 27). • Lomustine and glucocorticoid therapy can also be used effectively for malignant histiocytosis in the CNS. • Radiation therapy has been beneficial in the treatment of some types of neoplasia. Remission times of 1 to 2 years for tumors such as meningiomas, nerve sheath tumors, and lymphoma must be weighed against the significant risk of radiation-induced spinal cord injury. • The primary goals of neurosurgical intervention are to decompress the spinal cord and nerve roots and to stabilize the vertebral column. Surgical intervention is most frequently effective in cases of compressive extramedullary spinal cord disease such as intervertebral disc herniation. It is possible to debulk some intramedullary tumors, but surgery has no application in the majority of intramedullary diseases (i.e., degenerative, anomalous, and infectious disorders; traumatic lacerations; vascular accidents). • The decision for neurosurgical intervention is based on the historical progression of spinal cord signs, the localization and extent of neurologic deficits, and the likelihood that decompression and/or stabilization will be effective for the disorder diagnosed. • When indicated, surgical intervention is most valuable in the early stages of a problem, especially in acute compressive conditions such as acute type I disc herniation in which the functional outcome often parallels the speed with which surgical decompression is performed. • Prompt surgical decompression for acute compressive lesions is indicated if neurologic deficits are progressive over 24 hours or if the patient is plegic or has lost deep pain. See "Prognosis" (next page) for prognostic indicators of outcome. • In chronic progressive conditions, such as caudal cervical spondylomyelopathy and type II intervertebral disc disease, surgery performed in the early stages of disease is far more rewarding than surgery performed after significant dysfunction has been allowed to develop. Chronic compression causes irreversible damage to the spinal cord that surgery cannot correct and may even worsen by decompensating a chronically compensated condition. M Key Point When recommending spinal cord surgery for a paralyzed animal, warn the owner that extensive postoperative physiotherapy and nursing care may be necessary. • Cervical cord decompression for disc herniation usually is performed via a ventral slot procedure (through the vertebral body). Dorsal decompression of the cervical cord is used less frequently for cases of stenosis, malformation, malarticulation, dorsal ligamentous hypertrophy, and lateralized disc extrusion. • Surgical decompression of the thoracolumbar or lumbosacral spinal cord usually is performed via hemilaminectomy, foramenotomy, or dorsal laminectomy, depending on the site of the lesion. • Disc fenestration is routinely performed by some neurosurgeons as a prophylactic procedure to prevent recurrence of disc herniation. Disc fenestration does not decompress the spinal cord. • For COMS, a subtotal occipital craniectomy with durotomy decompresses the foramen magnum and has been shown to improve CSF flow in humans. • Give daily baths to prevent secondary dermatitis. • In general, the more severe the neurologic deficits, the more guarded the prognosis. • As discussed under Clinical Signs, severe clinical signs of compressive spinal cord lesions include plegia and loss of deep pain. Loss of deep pain for greater than 24 hours indicates a poor prognosis for recovery of normal function. If deep pain is still present and surgery is done immediately, the prognosis is fair to good. M Key Point Accurately assess for deep pain sensation prior to recommending surgery on paralyzed animals. The animal must exhibit conscious perception of pain, not just a withdrawal reflex. • The presence of conscious proprioceptive deficits and sensory ataxia only in animals with non-neoplastic extramedullary compression is a favorable prognostic sign because it indicates compression affecting only the proprioceptive fibers. • In general, the longer the duration of spinal cord injury, the more guarded the prognosis. The spinal cord undergoes irreversible degenerative changes if compressed or inflamed for a long period of time. • Anomalous conditions usually have a nonprogressive course and thus their prognosis depends on the extent of spinal cord injury. • Anomalous conditions that either decompensate after minor trauma (atlantoaxial subluxation) or gradually worsen over time (COMS) may benefit from surgical decompressive procedures. • Neurodegenerative conditions often progress to severe disability and have a guarded to poor prognosis. Intervertebral Disc Disease • The prognosis for intervertebral disc disease and trauma will depend on the conditions outlined above for compressive lesions. • In general, extramedullary compressive lesions have a better prognosis than intramedullary destructive lesions. • In an animal with spinal fractures, if radiographs indicate severe vertebral displacement, it is likely that the neurologic deficit is irreversible; therefore, advise the owner that surgical intervention probably will not be beneficial. However, in cases in which MRI, or other imaging modalities, indicates that the spinal cord may be intact, a significant percentage will improve if surgery, combined with aggressive medical therapy, is performed within a few hours of injury. • Infectious myelitis has a guarded prognosis unless a specific causative agent can be identified and/or response to antimicrobial therapy occurs. Spinal cord infections for which no treatments are available (canine distemper, rabies, and feline infectious peritonitis) have a poor prognosis. • Discospondylitis has a fair to good prognosis if antimicrobial therapy is instituted before the onset of paresis or more severe neurologic deficits. If plegia is present, the prognosis is poor. • Immune-mediated meningitis generally has a good prognosis with appropriate immunosuppressive therapy. • Myelitis due to GME has a guarded prognosis, especially if immunosuppressive therapy is not started promptly. GME can progress rapidly resulting in irreversible cord damage. GME is treatable but is rarely curable. Remission times will vary depending on the severity of the CNS involvement (see Chapter 126). • The prognosis for fibrocartilagenous embolic myelopathy will depend on the severity of the neurologic deficit (see preceding page). For any vascular disorder of the spinal cord, it is advisable to monitor affected animals for at least 48 hours for signs of improvement. Early signs of recovery may change the long-term prognosis. • The prognosis for intramedullary tumors is usually poor because surgical removal is not possible and radiation therapy is often not effective. Glucocorticosteroids may slow progression but do not effect a cure. • The prognosis for extramedullary nerve sheath tumors is variable depending on their location and extent of involvement. The prognosis is poor when multiple nerve roots are involved, but can be good if only one nerve root is involved and surgical removal can be performed. Radiation therapy can increase remission times for nerve sheath tumors. Even in these cases, however, the tumor will eventually regrow and invade the spinal cord. • Extramedullary meningiomas can often be surgically debulked. They are also radiation sensitive. Survival times with combined therapy may be as long as 2 years. • Extradural lymphoma can be treated with chemotherapy and/or radiation therapy but recurrence usually occurs within 1 year. • Vertebral osteosarcomas are difficult to resect and often result in pathologic fractures (see Chapter 101). Multiple myeloma is chemotherapy responsive and has a fair to good prognosis if therapy is instituted before bony destruction has become severe. A Practical Guide to Canine and Feline Neurology Infectious Diseases of the Dog and Cat Diseases of the spinal cord Veterinary Neurology. Philadelphia: WB Saunders