In cooperation with
What Is Your Neurologic Diagnosis? A
6-year-old 2-kg (4.4-lb) sexually intact female Yorkshire Terrier was referred to the Dallas Veterinary Surgical Center because of pelvic limb paresis. The owners first noticed a sudden decrease in activity 2 days earlier; clinical signs progressed until the dog was unable to rise the morning of evaluation. Three years prior, the dog had been treated because of sudden onset of pelvic limb paralysis; at that time, a CT examination revealed intervertebral disk herniation with pronounced spinal cord compression at the L2-3 and L3-4 intervertebral spaces. A right-sided hemilaminectomy spanning the L1 through L4 vertebrae was performed, and a moderate amount of disk material was successfully removed from within the spinal canal. Functional neurologic recovery was achieved as determined by an in-hospital follow-up examination,
which revealed that the dog was fully ambulatory with only residual pelvic limb proprioceptive deficits. At the referral neurologic examination, the dog was nonambulatory with severe pelvic limb paresis and absent proprioception bilaterally. Overt signs of pain were not elicited during palpation of the cervical or thoracolumbar region of the vertebral column. Cranial nerve examination findings and forelimb proprioceptive reactions were considered normal. Withdrawal and myotactic reflexes were considered appropriate in all 4 limbs. Other abnormalities detected during a general physical examination included a large urinary bladder, bilateral medial patella luxation (grade 3/4), and a left-sided systolic heart murmur (grade 2/6).
Neurologic examination Observation Mental Posture Gait Paresis Other
Alert X Normal X Normal Pelvic limbs X
Depressed Head tilt Ataxia X Tetra
Disoriented Tremor Pelvic limbs X Hemi
Stupor Falling All 4 Mono
Coma Circling
Key: 4=exaggerated, clonus; 3=exaggerated; 2=normal; 1=diminished; 0=none; NE = not evaluated
Postural reactions Wheelbarrow Hopping Ext postural thrust Proprioceptive pos Hemistand/walk Placing–tactile Placing–visual
Spinal reflexes Quadriceps Extensor carpi Flexion Crossed extensor Perineal
Cranial nerves
LF
RF
NE 2
NE 2
2 NE NE NE
2 NE NE NE
LF
RF
2 2 0
II, VII–Vision menace II, III–Pupils resting Stim L Stim R II–Fundus III, IV, VI–Strabismus, resting III, IV, VI, VIII–Strabismus, position
LR
RR
0 0 0 NE
0 0 0 NE
LR
RR
2
2
2 0 2
2 0 2
2 2 0 L
R
2 2 2 2 2 2 2
2 2 2 2 2 2 2
VIII–Nystagmus, resting VIII–Nystagmus, change V–Sensation VII–Facial mm V, VII–Palpebral flex IX, X–Gag XII–Tongue
L
R
2 2 2 2 2 2 2
2 2 2 2 2 2 2
Comments CN
Sensation (Locate and describe abnormal) Hyperesthesia 0 No signs of pain elicited during palpation of the thoracolumbar portion of the vertebral column Superficial pain 2 Cutaneous reflex 1 Absent at the mid-lumbar region of the vertebral column Deep pain 2
What is the problem? Where is the lesion? What are the most probable causes of this problem? What is your plan to establish a diagnosis? Please turn the page. JAVMA, Vol 243, No. 11, December 1, 2013
Vet Med Today: What Is Your Neurologic Diagnosis?
1537
Assessment Anatomic diagnosis Rule out location
Problem Nonambulatory paraparesis with bilateral absence of pelvic limb proprioception
Myelopathy at the T3 through L3 vertebrae
Likely location of one lesion Myelopathy at the region of the vertebral column from T3 through L3.
Etiologic diagnosis—Differential diagnoses for pelvic limb paresis originating within the thoracolumbar portion of the vertebral column include intervertebral disk disease (protrusion or extrusion of disk material), fibrocartilaginous embolus, inflammatory disease, infectious diseases (eg, bacterial, viral, or protozoal infection), diskospondylitis, trauma, syrinx, and neoplasia (primary or metastatic). Despite an inability to incite a pain response during vertebral column palpation, the acute and progressive nature of the pelvic limb paresis coupled with the history of intervertebral disk disease increased the suspicion of intervertebral disk disease as the underlying cause of recurrent neurologic signs. Recommended diagnostic testing for the patient included a CBC and serum biochemical analysis (to assess general health status), radiography of the thoracic and lumbar regions of the vertebral column (to rule out spinal trauma or an osseous lesion), CT of the thoracolumbar portion of the vertebral column with and without contrast medium administration (to evaluate for disk herniation and other myelopathy), and, if no surgical lesion was identified via CT, analysis and microbial culture of a CSF sample (to evaluate for inflammatory, infectious, or neoplastic cause). Diagnostic test findings—Results of a CBC and serum biochemical analysis were provided for review by the referring veterinarian; all variables were within reference limits. Radiography failed to identify any vertebral column abnormalities to account for the dog’s neurologic signs. Findings of CT myelography included an accumulation of contrast medium within the arachnoid space at the L2-3 intervertebral disk space and corresponding atrophy of the spinal cord in this region (Figure 1). No other abnormalities affecting the thoracic or lumbar portions of the spinal cord were identified. A spinal arachnoid cyst was diagnosed. This cyst was anatomically located at the same disk space as the historical intervertebral disc herniation. A CSF sample was collected prior to myelography but was not submitted for analysis or microbial culture because a diagnosis was achieved on the basis of the diagnostic imaging findings. Comments Spinal arachnoid cysts (also referred to in the veterinary medical literature as subarachnoid cysts, meningeal cysts, or leptomeningeal cysts) are an uncommon cause of compression of the thoracolumbar portion of the spinal cord in dogs.1–4 Spinal arachnoid cysts result 1538
Vet Med Today: What Is Your Neurologic Diagnosis?
Figure 1—Image obtained during CT myelography of the L2-3 intervertebral disk space of a 6-year-old dog that was evaluated because of sudden-onset pelvic limb paresis that increased in severity over a 2-day period. Notice the dorsolateral accumulation of contrast medium in the subarachnoid space and corresponding atrophy of the spinal cord at this location. The right side of the dorsal lamina is absent as a result of a previous hemilaminectomy for treatment of intervertebral disk disease at the L2-3 disk space.
from an accumulation of CSF within the subarachnoid space between the pia mater and arachnoid. These cysts, which lack an epithelial membrane and thus are not considered to be true cysts, can be best described as intradural, extramedullary diverticula of the arachnoid. Intradural spinal arachnoid cysts are also described as a rare cause of spinal cord compression in humans.5,6 The typical clinical sign associated with cyst formation and spinal cord compression is progressive ataxia or paresis over a period of months. 2,3,7 Previous reports2–4 describing spinal arachnoid cysts in veterinary species often attribute these lesions to congenital anomalies within the arachnoid; however, acquired cysts have been reported to develop as a result of trauma. It has been postulated that intervertebral disk disease may traumatize the arachnoid and lead to spinal arachnoid cyst formation. To the authors’ knowledge, intervertebral disk disease has resulted in spinal arachnoid cyst formation in only 2 other dogs.2,4 In both of those cases as for the dog of the present report, the diagnosis of spinal arachnoid cyst was made years following the initial episode of disk herniation. For the JAVMA, Vol 243, No. 11, December 1, 2013
dog of this report, diagnostic imaging and intraoperative findings 3 years prior failed to identify the presence of a spinal arachnoid cyst at the L2-3 intervertebral space; thus, the cyst identified in this case was acquired and developed following disk herniation at the affected site. Resection is considered the treatment of choice for spinal arachnoid cysts in veterinary and human medicine.2,3,5 The dog of this report underwent surgery the day following the referral examination and a limited left-sided hemilaminectomy was performed at the articular facet of the L2-3 intervertebral disk space. The spinal cord at that location had a distended dura mater that was slightly discolored, compared with the appearance of the adjacent regions of the spinal cord. The dura and arachnoid membranes were each longitudinally incised, and approximately 2 to 3 mL of a clear, pressurized fluid was expelled. The morning following surgery, neurologic evaluation revealed the dog’s neurologic status to be similar to that before surgery. The dog remained hospitalized for 5 days during which time it was treated with tramadol (3 mg/kg [1.36 mg/lb], PO, q 8 h) and prednisone (0.5 mg/kg [0.23 mg/lb], PO, q 24 h). At the time of discharge from the hospital, the dog’s neurologic status had improved very little; the dog was still considered nonambulatory with a slight increase in motor function. At 2 months after surgery, a follow-up phone conversation with the owners revealed that the dog’s condition was considered vastly improved. The dog was described as being ambulatory with residual pelvic limb paresis. The owners were pleased with the surgical outcome and the dog’s improved quality of life at that time. Long-term data regarding resection of spinal arachnoid cysts among veterinary patients is limited. Overall, surgery is generally associated with improved neurologic function; however, the presence of residual neurologic deficits, such as paresis, ataxia, or proprioceptive deficits, is common.2,3 In 1 study3 in dogs, clinical factors associated with positive surgical outcome included age < 3 years at the time of diagnosis and duration of clinical signs < 4 months prior to surgery. The acute onset of neurologic signs (2-day history) in the dog of the present report was atypical, compared with most cases of spinal arachnoid cysts described in the veterinary medical literature. An explanation for the acute onset was not available but may be related to a sudden increase in cyst size for reasons such as formation of a unidirectional valve-like structure that prevented CSF outflow, pressure shifts resulting from motion of the thoracolumbar por-
JAVMA, Vol 243, No. 11, December 1, 2013
tion of the vertebral column, or abnormal distribution of arachnoid trabeculae causing intra-cystic shifts of CSF.3,5,6 It is also possible that clinical signs were actually present for a period longer than that described by the owners but were either unnoticed or attributed to the known deficits related to the historical intervertebral disk disease. On the basis of the case described in the present report, a spinal arachnoid cyst should be considered a differential diagnosis for any dog with a history of intervertebral disk disease and recurrent thoracolumbar myelopathy, even when clinical onset of recurrence is sudden. Resection of a spinal arachnoid cyst can improve neurologic function, but recovery is generally prolonged and more variable, compared with the outcome following surgical treatment of intervertebral disk disease. References 1. 2. 3. 4. 5. 6. 7.
Gage ED, Hoerlein BF, Bartels JE. Spinal cord compression resulting from a leptomeningeal cyst in the dog. J Am Vet Med Assoc 1968;152:1664–1670. Rylander H, Lipsitz D, Berry WL, et al. Retrospective analysis of spinal arachnoid cysts in 14 dogs. J Vet Intern Med 2002;16:690– 696. Skeen TM, Olby NJ, Muñana KR, et al. Spinal arachnoid cysts in 17 dogs. J Am Anim Hosp Assoc 2003;39:271–282. Galloway AM, Curtis NC, Sommerlad SF, et al. Correlative imaging findings in seven dogs and one cat with spinal arachnoid cysts. Vet Radiol Ultrasound 1999;40:445–452. Hughes G, Ugokwe K, Benzel EC. A review of spinal arachnoid cysts. Cleve Clin J Med 2008;75:311–315. Nabors MW, Pait TG, Byrd EB, et al. Updated assessment and current classification of spinal meningeal cysts. J Neurosurg 1988;68:366–377. Sessums KB, Ducote JM. What is your diagnosis? Spinal arachnoid cysts. J Am Vet Med Assoc 2006;228:1019–1020.
This report was submitted by Eric C. Hans, DVM, and Sarah K. Bisgard Chaudhari, DVM, DACVS; from the Dallas Veterinary Surgical Center, 4444 Trinity Mills Rd, Ste 203, Dallas, TX 75287. Dr. Hans’ present address is the Comparative Orthopaedic Research Laboratory, School of Veterinary Medicine, University of Wisconsin, Madison, WI 53706. Address correspondence to Dr. Hans ([email protected]).
This feature is published in coordination with the American College of Veterinary Internal Medicine on behalf of the specialty of neurology. Contributors to this feature should contact Dr. Helen L. Simons (800-2482862, ext 6692) for case submission forms. Submissions will be sent to Dr. Karen Kline, DVM, DACVIM, for her review, except when Dr. Kline is an author.
Vet Med Today: What Is Your Neurologic Diagnosis?
1539
What Is Your Neurologic Diagnosis? A
6-year-old 2-kg (4.4-lb) sexually intact female Yorkshire Terrier was referred to the Dallas Veterinary Surgical Center because of pelvic limb paresis. The owners first noticed a sudden decrease in activity 2 days earlier; clinical signs progressed until the dog was unable to rise the morning of evaluation. Three years prior, the dog had been treated because of sudden onset of pelvic limb paralysis; at that time, a CT examination revealed intervertebral disk herniation with pronounced spinal cord compression at the L2-3 and L3-4 intervertebral spaces. A right-sided hemilaminectomy spanning the L1 through L4 vertebrae was performed, and a moderate amount of disk material was successfully removed from within the spinal canal. Functional neurologic recovery was achieved as determined by an in-hospital follow-up examination,
which revealed that the dog was fully ambulatory with only residual pelvic limb proprioceptive deficits. At the referral neurologic examination, the dog was nonambulatory with severe pelvic limb paresis and absent proprioception bilaterally. Overt signs of pain were not elicited during palpation of the cervical or thoracolumbar region of the vertebral column. Cranial nerve examination findings and forelimb proprioceptive reactions were considered normal. Withdrawal and myotactic reflexes were considered appropriate in all 4 limbs. Other abnormalities detected during a general physical examination included a large urinary bladder, bilateral medial patella luxation (grade 3/4), and a left-sided systolic heart murmur (grade 2/6).
Neurologic examination Observation Mental Posture Gait Paresis Other
Alert X Normal X Normal Pelvic limbs X
Depressed Head tilt Ataxia X Tetra
Disoriented Tremor Pelvic limbs X Hemi
Stupor Falling All 4 Mono
Coma Circling
Key: 4=exaggerated, clonus; 3=exaggerated; 2=normal; 1=diminished; 0=none; NE = not evaluated
Postural reactions Wheelbarrow Hopping Ext postural thrust Proprioceptive pos Hemistand/walk Placing–tactile Placing–visual
Spinal reflexes Quadriceps Extensor carpi Flexion Crossed extensor Perineal
Cranial nerves
LF
RF
NE 2
NE 2
2 NE NE NE
2 NE NE NE
LF
RF
2 2 0
II, VII–Vision menace II, III–Pupils resting Stim L Stim R II–Fundus III, IV, VI–Strabismus, resting III, IV, VI, VIII–Strabismus, position
LR
RR
0 0 0 NE
0 0 0 NE
LR
RR
2
2
2 0 2
2 0 2
2 2 0 L
R
2 2 2 2 2 2 2
2 2 2 2 2 2 2
VIII–Nystagmus, resting VIII–Nystagmus, change V–Sensation VII–Facial mm V, VII–Palpebral flex IX, X–Gag XII–Tongue
L
R
2 2 2 2 2 2 2
2 2 2 2 2 2 2
Comments CN
Sensation (Locate and describe abnormal) Hyperesthesia 0 No signs of pain elicited during palpation of the thoracolumbar portion of the vertebral column Superficial pain 2 Cutaneous reflex 1 Absent at the mid-lumbar region of the vertebral column Deep pain 2
What is the problem? Where is the lesion? What are the most probable causes of this problem? What is your plan to establish a diagnosis? Please turn the page. JAVMA, Vol 243, No. 11, December 1, 2013
Vet Med Today: What Is Your Neurologic Diagnosis?
1537
Assessment Anatomic diagnosis Rule out location
Problem Nonambulatory paraparesis with bilateral absence of pelvic limb proprioception
Myelopathy at the T3 through L3 vertebrae
Likely location of one lesion Myelopathy at the region of the vertebral column from T3 through L3.
Etiologic diagnosis—Differential diagnoses for pelvic limb paresis originating within the thoracolumbar portion of the vertebral column include intervertebral disk disease (protrusion or extrusion of disk material), fibrocartilaginous embolus, inflammatory disease, infectious diseases (eg, bacterial, viral, or protozoal infection), diskospondylitis, trauma, syrinx, and neoplasia (primary or metastatic). Despite an inability to incite a pain response during vertebral column palpation, the acute and progressive nature of the pelvic limb paresis coupled with the history of intervertebral disk disease increased the suspicion of intervertebral disk disease as the underlying cause of recurrent neurologic signs. Recommended diagnostic testing for the patient included a CBC and serum biochemical analysis (to assess general health status), radiography of the thoracic and lumbar regions of the vertebral column (to rule out spinal trauma or an osseous lesion), CT of the thoracolumbar portion of the vertebral column with and without contrast medium administration (to evaluate for disk herniation and other myelopathy), and, if no surgical lesion was identified via CT, analysis and microbial culture of a CSF sample (to evaluate for inflammatory, infectious, or neoplastic cause). Diagnostic test findings—Results of a CBC and serum biochemical analysis were provided for review by the referring veterinarian; all variables were within reference limits. Radiography failed to identify any vertebral column abnormalities to account for the dog’s neurologic signs. Findings of CT myelography included an accumulation of contrast medium within the arachnoid space at the L2-3 intervertebral disk space and corresponding atrophy of the spinal cord in this region (Figure 1). No other abnormalities affecting the thoracic or lumbar portions of the spinal cord were identified. A spinal arachnoid cyst was diagnosed. This cyst was anatomically located at the same disk space as the historical intervertebral disc herniation. A CSF sample was collected prior to myelography but was not submitted for analysis or microbial culture because a diagnosis was achieved on the basis of the diagnostic imaging findings. Comments Spinal arachnoid cysts (also referred to in the veterinary medical literature as subarachnoid cysts, meningeal cysts, or leptomeningeal cysts) are an uncommon cause of compression of the thoracolumbar portion of the spinal cord in dogs.1–4 Spinal arachnoid cysts result 1538
Vet Med Today: What Is Your Neurologic Diagnosis?
Figure 1—Image obtained during CT myelography of the L2-3 intervertebral disk space of a 6-year-old dog that was evaluated because of sudden-onset pelvic limb paresis that increased in severity over a 2-day period. Notice the dorsolateral accumulation of contrast medium in the subarachnoid space and corresponding atrophy of the spinal cord at this location. The right side of the dorsal lamina is absent as a result of a previous hemilaminectomy for treatment of intervertebral disk disease at the L2-3 disk space.
from an accumulation of CSF within the subarachnoid space between the pia mater and arachnoid. These cysts, which lack an epithelial membrane and thus are not considered to be true cysts, can be best described as intradural, extramedullary diverticula of the arachnoid. Intradural spinal arachnoid cysts are also described as a rare cause of spinal cord compression in humans.5,6 The typical clinical sign associated with cyst formation and spinal cord compression is progressive ataxia or paresis over a period of months. 2,3,7 Previous reports2–4 describing spinal arachnoid cysts in veterinary species often attribute these lesions to congenital anomalies within the arachnoid; however, acquired cysts have been reported to develop as a result of trauma. It has been postulated that intervertebral disk disease may traumatize the arachnoid and lead to spinal arachnoid cyst formation. To the authors’ knowledge, intervertebral disk disease has resulted in spinal arachnoid cyst formation in only 2 other dogs.2,4 In both of those cases as for the dog of the present report, the diagnosis of spinal arachnoid cyst was made years following the initial episode of disk herniation. For the JAVMA, Vol 243, No. 11, December 1, 2013
dog of this report, diagnostic imaging and intraoperative findings 3 years prior failed to identify the presence of a spinal arachnoid cyst at the L2-3 intervertebral space; thus, the cyst identified in this case was acquired and developed following disk herniation at the affected site. Resection is considered the treatment of choice for spinal arachnoid cysts in veterinary and human medicine.2,3,5 The dog of this report underwent surgery the day following the referral examination and a limited left-sided hemilaminectomy was performed at the articular facet of the L2-3 intervertebral disk space. The spinal cord at that location had a distended dura mater that was slightly discolored, compared with the appearance of the adjacent regions of the spinal cord. The dura and arachnoid membranes were each longitudinally incised, and approximately 2 to 3 mL of a clear, pressurized fluid was expelled. The morning following surgery, neurologic evaluation revealed the dog’s neurologic status to be similar to that before surgery. The dog remained hospitalized for 5 days during which time it was treated with tramadol (3 mg/kg [1.36 mg/lb], PO, q 8 h) and prednisone (0.5 mg/kg [0.23 mg/lb], PO, q 24 h). At the time of discharge from the hospital, the dog’s neurologic status had improved very little; the dog was still considered nonambulatory with a slight increase in motor function. At 2 months after surgery, a follow-up phone conversation with the owners revealed that the dog’s condition was considered vastly improved. The dog was described as being ambulatory with residual pelvic limb paresis. The owners were pleased with the surgical outcome and the dog’s improved quality of life at that time. Long-term data regarding resection of spinal arachnoid cysts among veterinary patients is limited. Overall, surgery is generally associated with improved neurologic function; however, the presence of residual neurologic deficits, such as paresis, ataxia, or proprioceptive deficits, is common.2,3 In 1 study3 in dogs, clinical factors associated with positive surgical outcome included age < 3 years at the time of diagnosis and duration of clinical signs < 4 months prior to surgery. The acute onset of neurologic signs (2-day history) in the dog of the present report was atypical, compared with most cases of spinal arachnoid cysts described in the veterinary medical literature. An explanation for the acute onset was not available but may be related to a sudden increase in cyst size for reasons such as formation of a unidirectional valve-like structure that prevented CSF outflow, pressure shifts resulting from motion of the thoracolumbar por-
JAVMA, Vol 243, No. 11, December 1, 2013
tion of the vertebral column, or abnormal distribution of arachnoid trabeculae causing intra-cystic shifts of CSF.3,5,6 It is also possible that clinical signs were actually present for a period longer than that described by the owners but were either unnoticed or attributed to the known deficits related to the historical intervertebral disk disease. On the basis of the case described in the present report, a spinal arachnoid cyst should be considered a differential diagnosis for any dog with a history of intervertebral disk disease and recurrent thoracolumbar myelopathy, even when clinical onset of recurrence is sudden. Resection of a spinal arachnoid cyst can improve neurologic function, but recovery is generally prolonged and more variable, compared with the outcome following surgical treatment of intervertebral disk disease. References 1. 2. 3. 4. 5. 6. 7.
Gage ED, Hoerlein BF, Bartels JE. Spinal cord compression resulting from a leptomeningeal cyst in the dog. J Am Vet Med Assoc 1968;152:1664–1670. Rylander H, Lipsitz D, Berry WL, et al. Retrospective analysis of spinal arachnoid cysts in 14 dogs. J Vet Intern Med 2002;16:690– 696. Skeen TM, Olby NJ, Muñana KR, et al. Spinal arachnoid cysts in 17 dogs. J Am Anim Hosp Assoc 2003;39:271–282. Galloway AM, Curtis NC, Sommerlad SF, et al. Correlative imaging findings in seven dogs and one cat with spinal arachnoid cysts. Vet Radiol Ultrasound 1999;40:445–452. Hughes G, Ugokwe K, Benzel EC. A review of spinal arachnoid cysts. Cleve Clin J Med 2008;75:311–315. Nabors MW, Pait TG, Byrd EB, et al. Updated assessment and current classification of spinal meningeal cysts. J Neurosurg 1988;68:366–377. Sessums KB, Ducote JM. What is your diagnosis? Spinal arachnoid cysts. J Am Vet Med Assoc 2006;228:1019–1020.
This report was submitted by Eric C. Hans, DVM, and Sarah K. Bisgard Chaudhari, DVM, DACVS; from the Dallas Veterinary Surgical Center, 4444 Trinity Mills Rd, Ste 203, Dallas, TX 75287. Dr. Hans’ present address is the Comparative Orthopaedic Research Laboratory, School of Veterinary Medicine, University of Wisconsin, Madison, WI 53706. Address correspondence to Dr. Hans ([email protected]).
This feature is published in coordination with the American College of Veterinary Internal Medicine on behalf of the specialty of neurology. Contributors to this feature should contact Dr. Helen L. Simons (800-2482862, ext 6692) for case submission forms. Submissions will be sent to Dr. Karen Kline, DVM, DACVIM, for her review, except when Dr. Kline is an author.
Vet Med Today: What Is Your Neurologic Diagnosis?
1539
