Clinical signs, magnetic resonance imaging features, and outcome after surgical and medical treatment of otogenic intracranial infection in 11 cats and 4 dogs

Brainstem dysfunction resulting from central extension of infection is a life-threatening complication of otitis media/interna (OMI) that has been described infrequently in dogs and cats. We review the clinical signs of disease, diagnostic findings, and results of surgical and medical treatments of brainstem disease attributable to otogenic intracranial infection in cats and dogs. Eleven cats and 4 dogs were examined because of acute, subacute, or chronic clinical signs of brain disease including central vestibular signs, altered mentation, abnormal posture/gait, cranial nerve deficits, and seizures. Results of a minimal database (CBC, serum biochemical panel, urinalysis, thoracic radiographs, and abdominal ultrasonographic images or radiographs) were within reference intervals in all animals. Magnetic resonance (MR) images of the head were acquired for all animals, and cisternal cerebrospinal fluid (CSF) from 9 of 11 cats and 3 of 4 dogs was examined. Surgical exploration and ventral bulla osteotomy were done for 12 of 15 animals, followed by 1–3 months of antibiotic therapy; the remaining animals were euthanized before treatment. In all animals, MR imaging was effective in characterizing the location and extent of the pathologic changes intracranially as well as within middle/inner ear structures. Results of CSF analysis were characteristic of bacterial infection in most of the animals with acute or subacute disease. Since long-term outcome in all treated animals was very good to excellent, it was concluded that dogs and cats with intracranial disease secondary to extension of otitis media/interna have a good-to-excellent prognosis when the condition was diagnosed and was treated by surgical exploration and appropriate antibiotic therapy.     

SPINAL SUB ARACHNOID CYSTS IN 13 DOGS

Thirteen dogs, including 6 Rottweiler dogs, exhibiting clinical signs of spinal cord dysfunction and myelographically confirmed subarachnoid space enlargement were investigated. To characterize the lesions and to get a better understanding of their pathogenesis, different imaging techniques were used in association with explorative surgical procedures (12 dogs) and histopathologic techniques (5 dogs). All subjects underwent preoperative myelography, five of which were examined by computed tomography (CT) scanning and one by magnetic resonance imaging (MRI) as well as cerebrospinal fluid (CSF) flow measurement (velocimetry). Most animals were <12 months old (7/13 dogs) and Rottweilers were over-represented (6/13 dogs). The lesions were mainly located dorsally with respect to the spinal cord (10/13 dogs) and in the cranial cervical area (8/13 dogs). MRI suggested spinal cord deviation with signs of ventral leptomeningeal adhesion opposite the enlarged space. In one dog, velocimetry confirmed that the "cyst" was freely communicating with the surrounding CSF space. Surgical investigation confirmed leptomeninges-induced ventral adhesion in 4/5 dogs. Follow-up studies, carried out from 6 months to 2.5 years postoperatively, showed there was full recovery in 8/13 dogs. This study suggests that the compression of the spinal cord is possibly not caused by a cyst. Adhesion resulting from a combination of microtrauma and chronic inflammatory processes induces a secondary enlargement of the subarachnoid space and may be a significant causative factor in spinal cord compression and dysfunction. The over-representation of Rottweilers and the young age of the animals in the study suggest a possible genetic predisposition and an inherited etiology.     

INTRACRANIAL INTRA-ARACHNOID CYST WITH INTRACYSTIC HEMORRHAGE IN TWO DOGS

Clinical signs, magnetic resonance imaging (MRI) features, treatment, and outcome of two adult dogs with neurologic dysfunction resulting from hemorrhage into a quadrigeminal intracranial intra-arachnoid cyst are described. In dog 1, the cyst was hyperintense to cerebrospinal fluid (CSF) on T1-weighted MRI and hypointense to CSF on T2-weighted images. In dog 2, the cyst was isointense to CSF on T1- and T2-weighted images. Both dogs were treated with craniotomy and cyst fenestration. A large blood clot was removed from the lumen of the cyst in each dog. Dog 1 is clinically normal 3.5 years post-surgery and has a persistent cyst. Dog 2 had a good initial response to therapy but was euthanized 2.5 years post-operatively due to generalized seizures. The late onset of clinical signs in these dogs most likely resulted from hemorrhage into the cyst. Surgical fenestration and hematoma removal appear to provide a satisfactory treatment for adult dogs with an intracranial intra-arachnoid cyst and intracystic hemorrhage. Persistence of the cyst may occur in some dogs.     

Cerebrospinal Fluid Myelin Basic Protein as a Prognostic Biomarker in Dogs with Thoracolumbar Intervertebral Disk Herniation

Background: Release of myelin basic protein (MBP) into the cerebrospinal fluid (CSF) is associated with active demyelination and correlates with outcome in various neurological diseases. Hypothesis/Objectives: To describe associations among CSF MBP concentration, initial neurological dysfunction, and long‐term ambulatory outcome in dogs with acute thoracolumbar intervertebral disk herniation (IVDH). Animals: Five hundred and seventy‐four dogs with acute thoracolumbar IVDH and 16 clinically normal dogs. Methods: Prospective case series clinical study. Signalment, initial neurological dysfunction as determined by a modified Frankel score (MFS), and ambulatory outcome at >3‐month follow‐up were recorded. Cisternal CSF MBP concentration was determined by an ELISA. Associations were estimated between CSF MBP concentration and various clinical parameters. Results: Dogs with thoracolumbar IVDH that did not ambulate at follow‐up had a higher CSF MBP concentration (median, 3.56 ng/mL; range, 0.59–51.2 ng/mL) compared with control dogs (median, 2.22 ng/mL; range, 0–3.82 ng/mL) (P= .032). A CSF MBP concentration of ≥3 ng/mL had a sensitivity of 78% and specificity of 76% to predict an unsuccessful outcome based on receiver‐operating characteristics curve analysis (area under the curve =0.688, P= .079). Affected dogs with a CSF MBP concentration ≥3 ng/mL had 0.09 times the odds of ambulation at follow‐up compared with affected dogs with CSF MBP concentration <3 ng/mL when adjusted for initial MFS (95% confidence interval 0.01–0.66, P= .018). Conclusions and Clinical Importance: These results would suggest that CSF MBP concentration may be useful as an independent prognostic indicator in dogs with thoracolumbar IVDH.     

Evaluation of immunomodulatory effect of recombinant human granulocyte‐macrophage colony‐stimulating factor on polymorphonuclear cell from dogs with cancer in vitro

The objective of this in vitro study was to evaluate the immunomodulatory effects of recombinant human granulocyte‐macrophage colony‐stimulating factor (rhGM‐CSF) on polymorphonuclear cell (PMN) function in dogs with cancer. PMNs were harvested from dogs with naturally developing cancer as a pre‐clinical model to evaluate the immunomodulatory effects of rhGM‐CSF on PMN phagocytic and cytotoxic functions, cytokine production and receptor expression. Some aspects of cancer‐related PMN dysfunction in dogs with cancer were restored following incubation with rhGM‐CSF including PMN phagocytosis, respiratory burst and LPS‐induced TNF‐α production. In addition, rhGM‐CSF increased surface HLA‐DR expression on the PMNs of dogs with cancer. These data suggests that dysfunction of innate immune response in dogs with cancer may be improved by rhGM‐CSF. The results of this study provided a pathophysiologic rationale for the initiation of clinical trials to continue evaluating rhGM‐CSF as an immunomodulatory therapy in dogs with cancer.     

Neuronal-Visceral GM1 Gangliosidosis in Portuguese Water Dogs

Three female siblings in a litter of seven Portuguese Water dogs (PWDs) showed clinical signs of ataxia and/or lameness at 5 months of age. Signs of cerebellar dysfunction (intention tremors, ataxia, widebased stance, dysmetria, and/or nystagmus) and mild limb weakness developed rapidly. Results of hemograms (three dogs), blood chemistry profiles (two dogs), urinalyses (two dogs), electroencephalograms (two dogs), and radiographs of the limbs or pelvis (three dogs), vertebrae (two dogs), and skull (one dog) were unremarkable except for an absolute lymphocytosis in one dog. Routine cerebrospinal fluid (CSF) analyses were normal in all three dogs. However, the CSF creatine kinase concentration was elevated in the one dog in which it was measured. Mucopolysacchariduria was present in all three dogs. Due to the rapid progression of clinical signs and a poor prognosis, all three dogs were euthanatized between 6 and 7 months of age. Histopathologic and electron microscopic studies showed neuronal cytoplasmic inclusions, vacuolated hepatocytes, and vacuolated renal tubular epithelial cells, compatible with the diagnosis of a storage disease. Beta-galactosidase activities in leukocytes, serum, and brain homogenates were reduced when compared with that in normal dogs and the stored product was identified as GM1 ganglioside, confirming GM1 gangliosidosis.     

MAGNETIC RESONANCE IMAGING FINDINGS IN 25 DOGS WITH INFLAMMATORY CEREBROSPINAL FLUID

To describe the signs that may be associated with intracranial inflammatory conditions, magnetic resonance (MR) images of 25 dogs that had inflammatory cerebrospinal fluid (CSF) were mixed with those of a control group of 40 dogs that had CSF negative for inflammatory disease and reviewed without knowledge of the clinical signs or diagnosis. CSF was considered inflammatory if the protein level was > 0.25 g/l and the white cell count was > 5 mm(-3). Abnormalities were found by MR imaging in 19 (76%) dogs with inflammatory CSF. Two dogs had focal lesions, 10 had multifocal lesions, and seven had diffuse lesions. Lesions affected all divisions of the brain. Mass effect was identified in seven (28%) dogs, including one that had a choroid plexus carcinoma. Lesions were hyperintense in T2-weighted images in 18 dogs and hypointense in T1-weighted images in six dogs. Multifocal or diffuse intraaxial lesions that were hyperintense in T2-weighted images were observed in 17 (68%) dogs with inflammatory CSF. Administration of gadolinium resulted in enhancement of intraaxial lesions in nine (36%) dogs and enhancement of meninges in seven (28%) dogs. Six (24%) dogs with inflammatory CSF had images interpreted as normal.     

Oxytocin Content of the Cerebrospinal Fluid of Dogs and Its Relationship to Pain Induced by Spinal Cord Compression

Objectives —To determine whether oxytocin exists in the cerebrospinal fluid (CSF) of dogs and whether the amount of oxytocin in the CSF of dogs with neck or back pain caused by spinal cord compression is significantly different than that in the CSF of clinically normal dogs.
Study Design —Prospective controlled study.
Animal Population —A total of 15 purpose-bred beagles and 17 client-owned dogs.
Methods —CSF was collected by needle puncture of the cerebellar medullary cistern after induction of general anesthesia. Oxytocin levels within the samples were determined through radioimmunoassay.
Results —Dogs with spinal cord compression had significantly more oxytocin in their CSF than the clinically normal dogs (13.76 ± 2.0 pg/mL and 3.61 ± 0.63 pg/mL, respectively; P < .0001). Dogs with chronic signs (>7 days) had significantly more oxytocin in their CSF than dogs with acute signs (<7 days) (21.60 ± 0.86 pg/mL and 6.80 ± 0.81 pg/mL, respectively; P < .0001). Both acutely and chronically affected dogs had significantly more oxytocin in their CSF than the controls ( P < .005 and P < .0001 respectively).
Conclusions —Dogs with neck and back pain caused by spinal cord compression have significantly more oxytocin in their CSF than clinically normal dogs. Dogs with chronic clinical signs have significantly more oxytocin in their CSF than dogs with acute clinical signs.
Clinical Relevance —In humans, intrathecal injection of oxytocin is effective in treating low back pain for up to 5 hours. Intrathecal oxytocin may be a logical choice for perioperative analgesia in dogs undergoing myelography because the intrathecal space is accessed for injection of contrast agent.     

Association of cerebrospinal fluid analysis findings with clinical signs and outcome in acute nonambulatory thoracolumbar disc disease in dogs

Background: Cerebrospinal fluid (CSF) pleocytosis recently was associated with the severity of neurologic signs in dogs with intervertebral disc disease (IVDD). Hypothesis/Objectives: To look for an association among CSF cell counts, total protein concentration, and severity of neurologic signs at presentation with outcome in dogs with acute thoracolumbar IVDD. Our hypothesis was that CSF total nucleated cell count (TNCC) and percentage cell types would be associated with the severity of spinal cord damage and therefore with both the presenting clinical signs and the prognosis of affected dogs. Animals: Fifty‐four dogs with acute nonambulatory thoracolumbar IVDD were evaluated. Methods: Retrospective study. Signalment, neurologic grade, CSF TNCC, protein concentration, red blood cells count and differential cell percentages, and short‐ and long‐term outcomes were evaluated. Results: CSF pleocytosis (>5 cells/μL) was present in 54% of dogs and was positively associated with neurologic grade at presentation and with postoperative time to regaining ambulation. Neutrophils were observed most frequently. The percentage of CSF macrophages and macrophage to monocyte ratio were higher (P= .001, for both) in dogs presented without deep pain sensation (DPS) that did not regain ambulation. Receiver operator characteristics curve analysis yielded a cut‐off point of 13% macrophages with a sensitivity and specificity of 100 and 83%, respectively, for prediction of a negative outcome. Conclusions and Clinical Importance: CSF pleocytosis is positively associated with the severity of spinal cord damage in dogs with thoracolumbar IVDD. The percentage of CSF macrophages can be used as a prognostic indicator for regaining ambulation in dogs that have lost DPS.     

Bacterial meningoencephalomyelitis in dogs: a retrospective study of 23 cases (1990-1999)

The clinical records of 23 dogs (1990-1999) with histopathologically confirmed bacterial meningoencephalomyelitis were evaluated retrospectively. No breed, age, sex, or weight predisposition was found. All the dogs presented with clinical signs of a brain lesion, whereas 5 of 23 had neck pain. Pyrexia was detected in 11 of 23 dogs on admission. CBCs revealed neutrophilic leucocytosis in 7 of 21 dogs and thrombocytopenia in 3 of 21 dogs. The serum chemistry profiles were abnormal in 15 of 21 dogs. The results of cerebrospinal fluid (CSF) analysis were abnormal in 13 of 14 dogs and aerobic CSF culture was positive for bacteria in 1of 8 samples. At postmortem examination, the lesions were localized to the central nervous system. Escherichia coli, Streptococcus, and Klebsiella spp were the most frequently isolated bacteria from cultures collected at postmortem examination. Twelve papers reporting 51 total clinical cases of canine bacterial meningoencephalomyelitis were reviewed. The clinical signs and results of the CBC, serum chemistry, blood culture, and CSF analysis were collated and compared with those of this study. The results of the CSF analysis in this study were similar to those in the literature. CSF cultures documented in the literature were positive for Staphylococcus, Pasteurella. Actinomyces, Nocardia spp, and various anaerobic species including Peptostreptococcus, Eubacterium, and Bacteroides spp.     

Lumbar cerebrospinal fluid in dogs with type I intervertebral disc herniation

BACKGROUND: Cerebrospinal fluid (CSF) in dogs with Hansen type I intervertebral disc herniation (IVDH) is classically described as normal or mildly inflammatory with a predominance of large mononuclear cells or neutrophils in severe acute herniations. However, we have observed a moderate to marked pleocytosis with a predominance of lymphocytes in some dogs with IVDH. HYPOTHESIS: Moderate to marked CSF pleocytosis occurs more commonly in dogs with type I IVDH than is reported in the literature. Lymphocytic predominance is more common than nonlymphocytic pleocytosis in dogs with chronic IVDH. ANIMALS: Four hundred twenty-three client-owned dogs with type I IVDH. METHODS: Retrospective study. Lumbar CSF of dogs with surgically confirmed type I IVDH was evaluated cytologically. Information obtained from medical records included signalment, prior clinical history, time from onset of signs to presentation, neurologic status, and intraoperative findings. Dogs with prior history and/or intraoperative evidence consistent with chronic IVDH before an acute herniation were termed acute-on-chronic (AOC). RESULTS: Pleocytosis (> 5 cells/uL) was present in 51% of dogs, including 23% with cervical IVDH and 61% with thoracolumbar IVDH. Moderate or marked inflammation (> or = 20 cells/uL) was identified in the CSF of 51% of dogs with thoracolumbar IVDH and pleocytosis. A predominance of lymphocytes was significantly more common in dogs examined > 7 days from onset of signs (P= .032) and in dogs with AOC IVDH (P= .0013). CONCLUSIONS AND CLINICAL IMPORTANCE: Moderate to marked CSF pleocytosis in dogs with type I IVDH is more common than previously reported. Lymphocytic pleocytosis is most common in dogs with chronic progression or AOC IVDH. Lymphocytic inflammation in the CSF of some dogs might suggest an immune-mediated response to chronically herniated disc material.     

Determination of homovanillic acid, 5-hydroxyindoleacetic acid and pressure in the cerebrospinal fluid of Collie dogs following administration of ivermectin

Twelve adult Collie dogs were studied to determine the effects of ivermectin on neurotransmitter metabolites released from the brain into the cerebrospinal fluid (CSF) and on CSF pressure. Ten of the 12 Collies were given ivermectin orally at a concentration of 200 g/kg body weight. Three of these 10 Collies showed clinical signs of ivermectin-induced toxicosis which progressed into a state of unresponsive recumbency in 2 dogs.Cerebrospinal fluid pressures and neurotransmitter metabolite concentrations in cisterna magna CSF were analysed 49 to 50 hours after administration of ivermectin in 6 of the 10 treated dogs, and in the 2 untreated control Collies. Cerebrospinal fluid pressures were within normal limits in all dogs. However, compared to the CSF concentrations in the 2 untreated and 3 non-reactive Collies, the 2 ivermectin-reactive Collies still in recumbency had elevated CSF concentrations of homovanillic acid (HVA), a metabolite of dopamine, and 5-hydroxyindoleacetic acid (5-HIAA), a metabolite of serotonin. These findings suggest an association between altered neurotransmission and severe ivermectin-induced neurological abnormalities. No evidence of elevated intracranial pressure was found.     

Matrix metalloproteinase-9 activity in the cerebrospinal fluid and serum of dogs with acute spinal cord trauma from intervertebral disk disease

OBJECTIVE: To detect matrix metalloproteinase (MMP)-9 in serum and CSF and determine relationships between MMP activity and severity of disease, duration of clinical signs, and duration of hospitalization in dogs with acute intervertebral disk disease (IVDD). ANIMALS: 35 dogs with acute IVDD and 8 clinically normal control dogs. PROCEDURE: CSF and serum were collected from affected and control dogs. Zymography was used to detect MMP-9. RESULTS: Activity of MMP-9 in CSF was detected in 6 of 35 dogs with IVDD; activity was significantly more common in dogs with duration of signs < 24 hours. Paraplegic dogs were more likely to have MMP-9 activity in the CSF than non-paraplegic dogs. No significant difference in hospitalization time was detected in dogs with IVDD between those with and without activity of MMP-9 in the CSF. Serum MMP-9 was detected more frequently in dogs with IVDD than in control dogs. CONCLUSIONS AND CLINICAL RELEVANCE: Data were consistent with results of experimental rodent spinal cord injury studies that indicate that MMP-9 is expressed early during secondary injury.     

Cerebrospinal Fluid Analysis and Clinical Outcome of Eight Dogs With Eosinophilic Meningoencephalomyelitis

Eight dogs, 14 weeks to 5.5 years of age, had signs of diffuse or multifocal meningoencephalomyelitis. The total white cell counts of the cerebrospinal fluid (CSF) ranged from 11 to 5,550 cells/microliters; the percentage of eosinophils ranged from 21% to 98%. The total CSF protein content range was 19 to 1,430 mg/dl. On necropsy, two dogs had granulomatous encephalomyelitis due to protozoan infection. The other six dogs, of which three were Golden Retriever dogs, appeared to have an idiopathic eosinophilic meningoencephalitis; four of these dogs recovered. The significance of eosinophils in CSF and the possible emergence of a new encephalitic syndrome of dogs involving a hypersensitivity to an unknown agent is also discussed.     

Cerebrospinal Fluid Eosinophilia in Dogs

Background: Marked eosinophilic meningitis or meningoencephalomyelitis (EME) is rarely reported in dogs and the cause is usually undetermined. Long-term prognosis for dogs with cerebrospinal fluid (CSF) eosinophilia is variable.
Animals: Twenty-three client-owned dogs.
Methods: Retrospective case series. Dogs with eosinophilic CSF, defined as total nucleated cell count (TNCC) >3 cells/μL with >20% eosinophils, were identified by a computerized search of all dogs having cisternal and/or lumbar CSF analyzed as part of the diagnostic workup between 1992 and 2007.
Results: TNCC in CSF ranged from 4 to 4,740 cells/μL (median 84 cells/μL, reference range ≤3 cells/μL), with 22 to 95% (median 78%) eosinophils in the differential count. An infectious agent was identified on necropsy in 4 of 23 (17%) dogs ( Cryptococcus neoformans [n = 2], Neospora caninum [n = 1], and Baylisascaris procyonis [n = 1]). Each of these dogs had progressive neurologic deterioration. Sixteen dogs had idiopathic EME. Magnetic resonance imaging (MRI) findings were abnormal in 7 of 13 dogs with EME; 2 dogs had focal lesions and 5 dogs had multifocal lesions. Clinical signs in 12 of 16 (75%) dogs with idiopathic EME resolved with prednisone treatment. Three dogs with acute intervertebral disc herniations recovered after decompressive surgery alone.
Conclusions: Idiopathic EME is a common cause of eosinophilic pleocytosis in dogs. MRI findings are variable. Infectious causes of EME were less common and had a poor prognosis.     

Blood–brain‐barrier disruption in chronic canine hypothyroidism

Background: Central nervous system (CNS) manifestations of hypothyroidism have been associated with cerebrovascular complications. Reports of cerebrospinal fluid (CSF) abnormalities are rare in hypothyroid dogs. Objective: The aim of this study was to determine if chronic hypothyroidism causes blood–brain‐barrier (BBB) abnormalities that are detectable using indirect CSF biomarkers. Methods: The study included 18 normal, euthyroid, female mixed‐breed dogs. Hypothyroidism was induced by ¹³¹iodine administration in 9 dogs; 9 served as untreated controls. Evaluations included physical and neurologic examination, complete CSF analysis, serum and CSF protein electrophoresis, measurement of plasma vascular endothelial growth factor (VEGF) and serum S‐100B concentrations, and calculation of CSF albumin quota (AQ) and were conducted at baseline and 6, 12, and 18 months after induction of hypothyroidism. Data were analyzed using repeated measures ANOVA. Results: At baseline, differences between groups were not detected for any variable. Throughout the study, controls dogs remained free of neurologic disease and had test variables that remained within reference intervals. Two hypothyroid dogs developed CNS signs during the study, and evidence of cerebrovascular disease was found at necropsy. At 12 and 18 months, the CSF total protein, VEGF, S‐100B, and fractional albumin concentrations, and AQ were significantly higher (P<.04) in hypothyroid dogs than controls. Among test variables assayed in serum or plasma, the only significant difference was a higher S‐100B concentration in hypothyroid dogs (P=.003) at 18 months. Conclusions: BBB integrity is disrupted in chronic hypothyroidism. Significant increases in CSF concentrations of VEGF and S100‐B in hypothyroid dogs indicate dysfunction in both endothelial and glial elements of the BBB.     

Spinal epidural empyema in seven dogs

OBJECTIVE: To characterize the clinical signs, diagnostic and surgical findings, and outcome in dogs with spinal epidural empyema (SEE). STUDY DESIGN: Retrospective study. ANIMALS: Seven dogs. METHODS: Dogs with SEE between 1992 and 2001 were identified from a computerized medical record system. Inclusion criteria were: neurologic examination, vertebral column radiographs, myelography, antimicrobial culture and susceptibility of material collected surgically from the vertebral canal, a definitive diagnosis of SEE confirmed by surgery, and microscopic examination of tissue from the vertebral canal. RESULTS: Common signs were lethargy, fever, anorexia, apparent spinal pain, and paraparesis/plegia. Common laboratory abnormalities were peripheral neutrophilia, and neutrophilic pleocytosis in cerebrospinal fluid (CSF). Three dogs had concurrent discospondylitis and 1 of these had vertebral luxation. On myelography, extradural spinal cord compression was focal (2 dogs), multifocal (3), or diffuse (2). Bacteria were isolated not from CSF but from blood, surgical site, pleural fluid, or urine in 6 dogs. Dogs were administered antibiotics and had surgical decompression by hemilaminectomy. Five dogs improved neurologically and had a good long-term outcome. Two dogs were euthanatized, 1 because of worsening of neurologic signs and pneumonia, and the other because of herniation of a cervical intervertebral disc 1 month postoperatively, unrelated to the SEE. CONCLUSION: Dogs with SEE may have a good outcome when treated by surgical decompression and antibiotic administration. CLINICAL RELEVANCE: SEE should be included in a list of possible causes for dogs with fever, apparent spinal pain, and myelopathy.     

Canine intervertebral disc disease: Changes in the cerebrospinal fluid

Data was obtained from 118 cerebrospinal fluid (CSF) samples from dogs with intervertebral disc disease. The effect of lesion location and the severity and duration of clinical signs was studied. Ninety-seven samples were obtained from the cerebellomedullary cistern and 21 from the lumbar cistern. Changes in CSF were identified in 84.7 per cent of the lumbar samples, compared with only 37.1 per cent of the cerebellomedullary samples. More pronounced pleocytosis and protein level increases were seen in dogs with acute and clinically severe lesions. The protein concentration was more commonly elevated than the total white blood cell count. These results indicate that marked protein and white blood cell count elevations can occur in association with intervertebral disc extrusion. Such findings, therefore, should not necessarily preclude myelographic examination in dogs presented for paralysis.     

Analysis of cerebrospinal fluid from the cerebellomedullary and lumbar cisterns of dogs with focal neurologic disease: 145 cases (1985-1987)

Data were obtained from 158 CSF samples from 145 dogs with focal, noninfectious/noninflammatory neurologic disease. The effect of lesion location and the duration and severity of clinical signs were studied. One hundred and twenty-five samples were obtained from the cerebellomedullary cistern (CMC), and 33 were obtained from the lumbar cistern (LC). Intracranial and cervical disease affected the CSF from the CMC more often than did thoracolumbar disease. However, lumbar CSF was more frequently affected by disease anywhere along the neuraxis. For compressive spinal cord disease, the protein concentration at both cisterns was more often high in acute, clinically severe lesions. Intracranial lesions consistently caused abnormalities in CSF from both the CMC (7 of 7; 100%) and LC (2 of 2; 100%). Abnormalities were identified in 16 of 38 (42%) and 5 of 7 (71%) CMC and LC samples, respectively, in dogs with cervical disease. In dogs with thoracolumbar lesions, only 22 of 80 (27.5%) CMC samples were abnormal, compared with 21 of 24 (87.5%) LC samples. These findings suggest that CSF collected cranial to the lesion may be normal or only mildly altered by focal neurologic disease. Fluid obtained caudal to the lesion presumably is more substantially altered because of the predominant caudal flow of CSF. To maximize the yield of diagnostic information from CSF analysis, the fluid should preferably be obtained caudad to the disease site; however, because of problems associated with lumbar puncture, we suggest that CSF from the CMC also be obtained.