• Open Access

Lumbar Cerebrospinal Fluid in Dogs with Type I Intervertebral Disc Herniation

Authors


  • Presented in part at the 25th American College of Veterinary Internal Medicine (ACVIM) Forum, Seattle, WA, June 6–9, 2007.

Corresponding author: Karen M. Vernau, Department of Surgical and Radiological Sciences, School of Veterinary Medicine, University of California Davis, 1 Shields Avenue, Davis, CA 95616; e-mail: kmvernau@ucdavis.edu

Abstract

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 (≥ 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.

Characteristics of cerebrospinal fluid (CSF) in dogs with type I IVDH are sparsely reported. In 1 report, pleocytosis was identified in <20% of samples, and 4% of CSF samples had a total nucleated cell count (TNCC) ≥ 20 cells/μL. The majority of dogs had a large mononuclear or mixed pleocytosis, but lymphocytes predominated in a small number of dogs. CSF neutrophilic pleocytosis was noted in some dogs with acute or clinically severe disease. Protein concentration increases correlated with acuteness and disease severity better than the TNCC.1

Lumbar CSF analysis is routine in dogs before surgery for type I IVDH at the authors' institution. Many dogs at our institution have moderate to marked inflammation in the CSF, often with a lymphocytic pleocytosis, suggesting the possibility of concurrent infectious or inflammatory disease such as granulomatous meningoencephalomyelitis. The purpose of this study was to characterize lumbar CSF in a large cohort of dogs with type I IVDH. We hypothesized that the majority of dogs with type I IVDH would have inflammatory CSF and that a predominance of lymphocytes would be the most common cellular inflammatory CSF change. We also hypothesized that dogs with a more chronic progressive history or AOC type I IVDH would be more likely to have a lymphocytic pleocytosis than would dogs with acute disc herniation, with no prior historical or intraoperative evidence of chronicity.

Materials and Methods

Medical records of the William R. Pritchard Veterinary Medical Teaching Hospital (VMTH) at University of California, Davis from 1996 to 2005 were searched for dogs with surgically confirmed type I IVDH for which lumbar CSF analysis with TNCC and differential cell count (DCC) were available. Dogs were excluded from the study if they had historical evidence of or concurrent neurologic disease not consistent with IVDH, or previous spinal cord surgery.

Lumbar CSF samples were collected into sterile evacuated glass red top tubes. Within 60 minutes of collection, the TNCC, red blood cell (RBC) count, cytocentrifuge slide preparation, and DCC were performed, and protein concentration was measured. The TNCC and RBC counts were determined with a hemacytometer and the mean value of counts from both sides of the hemacytometer chamber for TNCC (TNCC =mean × 1.11) and from 1 side of the chamber for RBC counts (RBC count=total number counted on 1 side [9 squares] × 1.11). Slides for the DCC and morphologic evaluation were prepared by cytocentrifugationa of 500 μL of CSF (without the addition of protein) for 5 minutes at 1,000 rpm using reusable chambersb and glass slidesc with subsequent Wright's Giemsa staining. The DCC was based on a 100-cell count. The protein concentration of 100 μL aliquots of the CSF samples was measured using a pyrogallol red microprotein assay.d

Dogs with iatrogenic hemorrhage severe enough to preclude accurate spinal fluid analysis were excluded. The upper limit for blood contamination was defined as 13,000 cells/μL because iatrogenic blood contamination <13,200 cells/μL does not alter CSF TNCC or protein concentration.2 Normal lumbar CSF was classified as having TNCC ≤ 5 cells/μL and protein concentration ≤ 35 mg/dL. Differential distribution was considered normal if it contained 60–70% macrophages, 30–40% lymphocytes, and 0% neutrophils.3

Time from onset of signs to examination at the VMTH, neurologic exam findings, steroid usage before presentation, and location of the IVDH were recorded in all dogs. Dogs were divided into 6 groups: those presenting within 1 day, and 2, 3, 4 days, from 5 to 7 days, and > 7 days after onset of clinical signs. Dogs were divided into 5 groups based on severity of neurologic dysfunction: 1 = ambulatory with hyperesthesia only; 2 = ambulatory tetra/paraparetic; 3 = nonambulatory tetra/paraparetic; 4 = tetra/paraplegic; and 5 = paraplegic with loss of deep pain sensation in one or both pelvic limbs or tail. The site of IVDH and spinal cord compression was identified by myelography and/or computed tomography and was confirmed intraoperatively.

In dogs with CSF pleocytosis (> 5 cells/μL), the DCC was characterized as predominantly lymphocytic, neutrophilic, or histiocytic if (a) the percentage of lymphocytes, neutrophils, or macrophages, respectively, was ≥60% of the total or (b) the percentage of lymphocytes, neutrophils, or macrophages, respectively, was ≥ 40% of the total with no other cell type ≥33% of the total. The CSF was characterized as a mixed pleocytosis if (a) no cell type was ≥40% of the total or (b) 2 cell types were each >33% of the total.

Additional information obtained from the medical records of dogs with inflammatory spinal fluid included breed, sex, age, prior history of spinal hyperesthesia or paresis consistent with chronic IVDH, and intraoperative findings. Dogs were separated into groups of chondrodystrophic breeds (Dachshund, Basset Hound, Pembroke Welsh Corgi, Cardigan Welsh Corgi, Pekinese, Beagle, Cocker Spaniel, Shih Tzu, Lhasa Apso, Miniature Poodle, Toy Poodle, Bichon Frise) and nonchondrodystrophic breeds (all other breeds) for analysis. Information abstracted from surgery reports included evidence of a chronic component to the IVDH (fibrous attachments of herniated NP to the dura, bridging fibrous attachments over disc causing protrusion) and evidence of spinal cord injury, including hemorrhage, bruising, and malacia. Dogs with historical and/or intraoperative evidence of chronicity were determined to have acute-on-chronic (AOC) IVDH.

Statistics

Statistical analysis was performed by a statistical software program.e The Jonckheere-Terpstra test was used to compare CSF TNCC with day of presentation and neurologic grade and to compare inflammatory cell type predominance with day of presentation and neurologic grade. The Mann-Whitney test was used to compare TNCC with presence or absence of spinal cord injury noted intraoperatively. The χ2 test of homogeneity was used to compare the inflammatory cell types present in CSF with chronicity (ie, acute versus acute-on-chronic), breed, and history of steroid administration. A log-rank test was used to compare the time from onset of signs with presentation in dogs with cervical versus thoracolumbar IVDH. Linear correlation was used to test for a relationship between protein concentration and TNCC in dogs with cervical and thoracolumbar IVDH. The Fisher exact test was used to compare the percentage of dogs with elevation in protein concentration in cervical IVDH versus thoracolumbar IVDH and the percentage of dogs with albuminocytologic dissociation in cervical IVDH versus thoracolumbar IVDH. Significance for all statistical tests was set at P < .05.

Results

CSF Analysis

Four hundred fifty-seven dogs with surgically confirmed type I IVDH had CSF analyses with TNCC and DCCs. Thirty-four dogs were excluded because of markedly hemorrhagic CSF that precluded accurate interpretation. Of the remaining 423 dogs, 216 (51%) had a CSF pleocytosis. Data regarding the TNCC and type of cellular inflammation in dogs with cervical and thoracolumbar IVDH are listed in Table 1. Data listing the severity of inflammation in dogs with IVDH (cervical and thoracolumbar combined) with the 4 types of pleocytosis are listed in Table 2.

Table 1.   TNCC and distribution of inflammatory cell type in CSF of dogs with type I IVDH.
 Cervical
IVDH
Thoracolumbar
IVDH
Total
  1. TNCC, total nucleated cell count; IVDH, intervertebral disc herniation.

  2. Normal TNCC ≤ 5 cells/μL.

Total # dogs111312423
Median (cells/μL)286
Range (cells/μL)< 1–54< 1–428< 1–428
Normal CSF (# dogs)85 (77%)122 (39%)207 (49%)
CSF pleocytosis (# dogs)26 (23%)190 (61%)216 (51%)
 6–19 cells (# dogs)19 (17%)93 (30%)112 (26%)
 20–49 cells (# dogs)5 (4.5%)53 (17%)58 (14%)
 50–99 cells (# dogs)2 (1.8%)21 (6.7%)23 (5.4%)
 ≥ 100 cells (# dogs)023 (7.3%)23 (5.4%)
 Lymphocytic (# dogs)11 (42%)78 (41%)89 (41%)
 Neutrophilic (# dogs)8 (31%)60 (32%)68 (31%)
 Histiocytic (# dogs)2 (7.7%)14 (7%)16 (7.4%)
 Mixed (# dogs)5 (19%)38 (20%)43 (20%)
Table 2.   Severity of inflammation in dogs with lymphocytic, neutrophilic, histiocytic, or mixed pleocytosis.
 LymphocyticNeutrophilicHistiocyticMixed
Total # dogs81591957
Median (cells/μL)16241616
Range (cells/μL)6–1816–2006–2336–428
6–19 cells (# dogs)45 (56%)22 (37%)11 (58%)32 (56%)
20–49 cells (# dogs)23 (28%)22 (37%)4 (21%)10 (18%)
50–99 cells (# dogs)9 (11%)6 (10%)2 (10.5%)7 (12%)
≥ 100 cells (# dogs)4 (5%)9 (15%)2 (10.5%)8 (14%)

Three hundred and thirty-six dogs with surgically confirmed type I IVDH has CSF analysis that included measurement of protein concentration. Increase in protein concentration was more common in dogs with cervical IVDH (85 of 104; 82%) than dogs with thoracolumbar IVDH (152 of 232; 66%) (P= .0028). Sixty-two of 104 (60%) dogs with cervical IVDH had an increase in protein concentration with a normal TNCC (albuminocytologic dissociation) compared with 37 of 232 (16%) of dogs with thoracolumbar IVDH (P < .0001). There was a significant relationship between TNCC and increased protein concentration in dogs with cervical (P < .001, correlation coefficient 0.38) and thoracolumbar (P < .001, correlation coefficient 0.32) IVDH (Table 3).

Table 3.   Protein concentration in the CSF of dogs with type I IVDH.
 Cervical
IVDH
Thoracolumbar
IVDH
Total
  1. CSF, cerebrospinal fluid; IVDH, intervertebral disc herniation.

  2. Normal lumbar protein concentration ≤ 35 mg/dL.

Total # dogs104232336
Median (mg/dL)605758
Range (mg/dL)10–3063–1,9203–1,920
Normal (# dogs)19 (18%)80 (34%)99 (29%)
Elevated (# dogs)85 (82%)152 (66%)237 (71%)
 35–49 mg/dL (# dogs)15 (14%)26 (11%)41 (12%)
 50–100 mg/dL (# dogs)48 (46%)58 (25%)106 (32%)
 101–499 mg/dL (# dogs)22 (22%)57 (25%)79 (24%)
 500–999 mg/dL (# dogs)07 (3%)7 (2%)
 > 1,000 mg/dL (# dogs)04 (1.7%)4 (1.2%)

In dogs without CSF pleocytosis, RBC count was significantly different from that of dogs with pleocytosis (85 RBC/μL [range, 0–13,000 RBC/μL] versus 503 RBC/μL [range, 1–12,625 RBC/μL] [P < .0001]).

Signalment

The median age of dogs with IVDH and CSF pleocytosis was 6 years (range, 1–17 years). The group included 11 intact females, 102 spayed females, 30 intact males, and 73 castrated males. The most common breeds were Dachshunds (89/216), Pembroke Welsh or Cardigan Welsh Corgis (10/216), Cocker Spaniels (9/216), Beagles (8/216), Basset Hounds (6/216), and Pekinese (5/216). Of 216 dogs, 155 (72%) were chondrodystrophic whereas 61 (28%) were nonchondrodystrophic. Of the 155 chondrodystrophic dogs, 93 (60%) were Dachshunds or Dachshund crosses.

Lymphocyte predominance was more common in chondrodystrophic (63 of 155; 41%) than nonchondrodystrophic dogs (17 of 61; 28%); however, the difference was not statistically significant (P= .13). In Dachshunds and Dachshund crosses (44 of 93; 47%), lymphocyte predominance was significantly more common than in non-Dachshunds/Dachshund crosses (36 of 123; 30%) (P= .048).

Time from Onset of Signs to Examination

The time from onset of signs to examination in dogs with cervical IVDH (median, 7 days; range, 1–60 days) was significantly longer than in dogs with thoracolumbar IVDH (median 3 days; range, 1–60 days) (P < .001). The majority of dogs with CSF pleocytosis were examined within 1–2 days from onset of signs (Fig 1). In dogs with CSF pleocytosis, TNCC decreased significantly with increased time from the onset of clinical signs (P < .001) (Fig 1). There was no significant difference in predominant inflammatory cell type among dogs that presented ≤ 7 days from onset of signs; however, dogs presenting > 7 days after onset of clinical signs were more likely to have a predominance of lymphocytes (P= .032) (Fig 2).

Figure 1.

 The time examined after onset of clinical signs and cerebrospinal fluid (CSF) total nucleated cell count (TNCC) in dogs with type I intervertebral disc herniation. In dogs with CSF pleocytosis, TNCC decreased significantly with increased time from the onset of clinical signs (P < .001).

Figure 2.

 The percentage of lymphocytic, neutrophilic, histiocytic, or mixed pleocytosis in dogs examined from 1 day to >7 days from onset of clinical signs. There was no significant difference in predominant inflammatory cell type among dogs that presented ≤7 days from onset of signs; however, dogs presenting >7 days after onset of clinical signs were more likely to have a predominance of lymphocytes (P= .032).

Steroid Administration before Presentation

There was no statistical difference between the number of dogs with normal TNCC that received intravenous or oral corticosteroids before presentation (118 of 207) and the number of dogs with CSF pleocytosis that received steroids before presentation (105 of 216) (P= .098). The median cell count for dogs that had received steroids was 16 cells/μL (range, 6–428 cells/μL) compared with a median of 23 cells/μL (range, 6–351 cells/μL) in dogs that did not receive steroids. Lymphocyte predominance was significantly less common in dogs that received steroids (30/105) than in dogs that did not receive steroids (51/111) (P= .025).

Neurologic Grade

The distribution of neurologic grade in dogs with normal and pleocytotic CSF is listed in Table 4. Data regarding TNCC and protein concentration among dogs based on grade of neurologic dysfunction are listed in Table 5 (cervical) and Table 6 (thoracolumbar).

Table 4.   Distribution of neurologic grade in dogs with cervical and thoracolumbar IVDH with normal CSF and CSF pleocytosis.
 Cervical NormalCervical InflammatoryThoracolumbar NormalThoracolumbar Inflammatory
  1. IVDH, intervertebral disc herniation.

Total # dogs8526122190
Grade 127 (32%)6 (23%)7 (6%)5 (2.6%)
Grade 236 (42%)8 (31%)44 (36%)64 (34%)
Grade 317 (20%)12 (46%)29 (24%)61 (32%)
Grade 45 (9%)042 (34%)49 (26%)
Grade 500011 (6%)
Table 5.   CSF TNCC and protein concentration in dogs with cervical IVDH with Grades 1–5 neurologic score.
 Grade
12345
  1. TNCC, total nucleated cell count; IVDH, intervertebral disc herniation; NA, not available . Normal TNCC ≤ 5 cells/μL . Normal lumbar protein concentration ≤ 35 mg/dL.

Total # dogs33442950
Median TNCC (cells/μL)2241NA
Range TNCC (cells/μL)1–541–100–500–5NA
Total # dogs30442550
Median protein (mg/dL)46587369NA
Range protein (mg/dL)18–30615–24028–18658–108NA
Table 6.   TNCC and protein concentration in dogs with thoracolumbar IVDH with Grades 1–5 neurologic score.
 Grade
12345
  1. TNCC, total nucleated cell count; IVDH, intervertebral disc herniation. Normal TNCC ≤ 5 cells/μL.Normal lumbar protein concentration ≤ 35 mg/dL.

Total # dogs12108909111
Median TNCC (cells/μL)5813640
Range TNCC (cells/μL)1–230–1200–42810–35110–145
Total # dogs128365666
Median protein (mg/dL)42597838745
Range protein (mg/dL)16–15010–68211–5833–1,92042–1,734

Paraplegic dogs without deep pain sensation (Grade 5) had significantly higher median TNCC (P= .05) and protein concentration (P < .001) than dogs with intact deep pain sensation. There was no significant difference in median TNCC and protein concentration among dogs with intact deep pain sensation (Grades 1–4). Of the 23 dogs with TNCC ≥ 100 cells/μL, only 2 were Grade 5. Five of 11 (45%) dogs with Grade 5 neurologic status had a predominance of neutrophils in their CSF compared with 27% of all dogs with thoracolumbar lesions; however, there was no statistical correlation between neutrophilic predominance in CSF and severity of neurologic dysfunction.

Imaging and Intraoperative Findings

Of the 216 dogs with CSF pleocytosis, 157 (73%) had disc herniations between T11 and L2; the most common sites were T13 to L1 (27%) and T12 to 13 (23%). Forty-six (21%) dogs had extradural hemorrhage, spinal cord bruising, or malacia noted during surgery. Of these 46 dogs, the median TNCC was 30 cells/μL (range, 6–295 cells/μL) and median protein concentration was 138 mg/dL (range, 29–1,734 mg/dL) compared with a median TNCC of 16 cells/μL (range, < 1–428) and median protein concentration of 84 mg/dL (range, 13–1,920 g/dL) in dogs without gross evidence of spinal cord injury. Dogs with Grade 5 neurologic dysfunction were significantly more likely to have gross evidence of spinal cord injury noted intraoperatively (9/11) than dogs with neurologic Grades 1–4 (P= .0001).

Acute versus Acute-On-Chronic Disc Herniation

Of the 216 dogs with CSF pleocytosis, 70 (32%) had history of spinal hyperesthesia or paresis weeks to months previously that responded to conservative management (consisting of cage rest and/or corticosteroid administration or nonsteroidal anti-inflammatory medications), suggesting a history of chronic IVDH. In 58 of 216 dogs, evidence of chronic IVDH in addition to acutely herniated disc material was recorded in the surgery report. Twenty-four dogs had both historical and intraoperative evidence of chronic type I IVDH. Combining dogs with historical, or intraoperative evidence of chronicity or both, 103 (48%) dogs had CSF pleocytosis and evidence of AOC IVDH. A total of 113 (52%) dogs had CSF pleocytosis and no evidence of chronicity and were considered to have an acute IVDH.

Dogs with AOC IVDH (51/103) were more likely (P= .0013) to have a predominance of lymphocytes than were dogs with acute IVDH (30/113) (Fig 3, Table 7).

Figure 3.

 Percentage of dogs with acute or acute-on-chronic (AOC) intervertebral disc herniation (IVDH) with a lymphocytic, neutrophilic, histiocytic, or mixed pleocytosis. Dogs with AOC IVDH were more likely to have a predominance of lymphocytes than were dogs with acute IVDH (P= .0013).

Table 7.   Type of inflammation in dogs with CSF pleocytosis and acute and acute-on-chronic IVDH.
 Acute IVDDAcute-on-Chronic IVDD
  1. IVDH, intervertebral disc herniation.

Lymphocytic
 Total # dogs30 (27%)51 (50%)
 Median (cells/μL)2214
 Range (cells/μL)6–1816–79
Neutrophilic
 Total # dogs41 (36%)18 (17%)
 Median (cells/μL)2922
 Range (cells/μL)6–2006–100
Histiocytic
 Total # dogs11 (10%)8 (8%)
 Median (cells/μL)23.57
 Range (cells/μL)9–2336–20
Mixed
 Total # dogs31 (27%)26 (25%)
 Median (cells/μL)2011
 Range (cells/μL)8–4286–192

Discussion

Fifty-one percent of dogs with type I IVDH in this study had lumbar CSF pleocytosis. A smaller percentage of dogs with cervical IVDH in our study had lumbar CSF pleocytosis (23%) than dogs with thoracolumbar IVDH (61%), which might reflect the effect of distance from the CSF collection site to the location of the IVDH. This is in contrast to a previous report in which 19% of dogs with IVDH had CSF pleocytosis.1 CSF was sampled from the cerebellomedullary cistern in the majority of dogs in that report, which might not have accurately reflected the CSF abnormalities associated with thoracolumbar lesions.2,5 Additionally, in dogs with lumbar CSF analysis in that report, no dogs with cervical IVDH and 39% of dogs with thoracolumbar IVDH had CSF pleocytosis4; this compares with 23% of dogs with cervical IVDH and 61% of dogs with thoracolumbar IVDH in this study.

Fifty-one percent of all dogs with thoracolumbar IVDH and CSF pleocytosis in our study had lumbar CSF with ≥20 TNNC/μL. Additionally, 12% of dogs with thoracolumbar IVDH and CSF pleocytosis had CSF TNCC > 100/μL. Moderate to marked pleocytosis is classically associated with infectious or primary inflammatory diseases. However, because dogs in our study had surgically confirmed IVDH, did not receive postoperative steroids, and improved clinically following surgery, concurrent infectious or inflammatory disease is unlikely. Therefore, noting moderate to marked pleocytosis in some dogs with confirmed IVDH, including moderate to marked pleocytosis with a predominance of lymphocytes, should not necessarily mandate additional CNS imaging or infectious CNS disease testing. However, because many of the breeds predisposed to type I IVDH are also predisposed to primary inflammatory diseases such as granulomatous meningoencephalomyelitis, additional diagnostics might be warranted in dogs with a moderate to marked CSF pleocytosis that do not recover as expected from surgical treatment for type I IVDH.

Although there was a significant difference in RBC counts between dogs with CSF pleocytosis and dogs without CSF pleocytosis, the median RBC count was still low in dogs with CSF pleocytosis (503 RBC/μL). RBC counts <13,000 are considered unlikely to affect the nucleated cell count.5 Additionally, given that neutrophils are the predominant leukocyte in the peripheral blood of dogs, RBC contamination of CSF is most likely to increase the percentage of neutrophils in the DCC. Lymphocytic predominance was most common in dogs in this study (Table 2). Therefore, despite the statistical difference in RBC counts between these 2 groups, it is unlikely that RBC contamination affected the TNCC or leukocyte distribution.

Paraplegic dogs without deep pain sensation had a significantly higher median TNCC and protein concentration than those with intact pain sensation; however, there was no significant difference among dogs with intact deep pain sensation, regardless of degree of motor function loss. There does not appear to be a linear relationship between severity of CSF inflammation and degree of neurologic dysfunction. Dogs with gross evidence of spinal cord injury had higher median TNCC and protein concentrations than those without obvious gross pathology, indicating that TNCC and protein concentration may reflect both structural and functional severity of injury in some dogs.

A higher percentage of dogs with cervical IVDH (82%) had an increased protein concentration than dogs with thoracolumbar IVDH (66%). Albuminocytologic dissociation was also more common in dogs with cervical IVDH (60%) compared with dogs with thoracolumbar IVDH (16%). These findings may be a function of both chronicity of disease and the effect of distance from the CSF collection site to the location of the IVDH resulting in increased likelihood of concurrent pleocytosis in dogs with thoracolumbar IVDH. Dogs with cervical IVDH had a significantly longer time from onset of signs to presentation compared with dogs with thoracolumbar IVDH. This may be because dogs with cervical IVDH often have less debilitating signs (ie, pain only or mild paresis) compared with dogs with thoracolumbar IVDH. Chronic spinal cord compression in some dogs with cervical IVDH could result in increased protein concentration relative to TNCC.5

Lymphocyte predominance was significantly more common in dogs with a chronic progression of signs (>7 days) or AOC presentation. Dachshund and Dachshund crosses were also significantly more likely to have a predominance of lymphocytes than other breeds, which can reflect a higher incidence of chronic type I IVDH in Dachshunds. Although lymphocytes can be more common with chronic inflammation in general, identifying predominantly lymphocytes in 30% of dogs in our study with acute herniations suggests that the presence of lymphocytes is more than just a temporal phenomenon.

The nucleus pulposus is avascular and therefore has no access to the systemic circulation to develop immunologic tolerance.6 Immunohistologic studies of IVDH in the human lumbar spine suggest that exposure of the immune-privileged nucleus pulposus induces a lymphocyte mediated autoimmune response which may contribute to chronic inflammation and pain.6–9 Subcutaneous injection of autologous nucleus pulposus in pigs has been shown to increase vascular permeability and attract significantly more leukocytes than fat and sham-injected controls.10 Immunohistochemical analysis of the leukocyte population has shown activated T and B cells, indicating a specific immune response against the herniated nucleus pulposus.11

Injection of autologous nucleus pulposus into the epidural space of dogs induced both gross and microscopic evidence of inflammation after 7 days, which was not observed in saline-injected controls.12 Inflammation associated with herniation of the nucleus pulposus results in both structural and functional damage. Analysis of ultrastructural changes in pig nerve roots exposed to autologous nucleus pulposus via epidural injection revealed axonal injury and Schwann cell damage, which became prominent 7 days after application of the nucleus pulposus.13 Epidural injection of nucleus pulposus cells in pigs resulted in decreased nerve conduction velocity in the adjacent nerve roots.14

The specific immune response to herniated disc material in dogs has not been described. Herniated nucleus pulposus can induce an immune-mediated inflammatory reaction in some dogs, which persists beyond surgical decompression. Persistent inflammation might explain why some dogs do not recover as quickly or completely as others. Further research is required to characterize the inflammatory reaction to herniated disc material in dogs and to determine whether the resultant inflammatory process is reflected in the CSF.

In conclusion, lumbar CSF pleocytosis is more common than previously reported in dogs with type I IVDH; this lumbar CSF pleocytosis is more frequent in dogs with thoracolumbar IVDH than cervical IVDH. Moderate to marked lumbar CSF pleocytosis occurs in many dogs with IVDH alone without concurrent infectious or inflammatory disease. Lymphocyte predominance is the most common cellular inflammatory change in the CSF of dogs with type I IVDH and occurs more frequently in dogs with acute-on-chronic disease.

Footnotes

aCytospin3, ThermoShandon, Pittsburgh, PA

bCytofunnel, ThermoShandon

cCytoslide, ThermoShandon

dTotal Protein [Micro] Assay, DCL, Oxford, CT

eStatXact Version 8, Cytel Software Corporation, Cambridge, MA

Ancillary