P. Kenny

Evaluation of brain tissue or cerebrospinal fluid with broadly reactive polymerase chain reaction for Ehrlichia, Anaplasma, spotted fever group Rickettsia, Bartonella, and Borrelia species in canine neurological diseases (109 cases).

BACKGROUND Vector-transmitted microorganisms in the genera Ehrlichia, Anaplasma, Rickettsia, Bartonella, and Borrelia are commonly suspected in dogs with meningoencephalomyelitis (MEM), but the prevalence of these pathogens in brain tissue and cerebrospinal fluid (CSF) of dogs with MEM is unknown. HYPOTHESIS/OBJECTIVES To determine if DNA from these genera is present in brain tissue and CSF of dogs with MEM, including those with meningoencephalitis of unknown etiology (MUE) and histopathologically confirmed cases of granulomatous (GME) and necrotizing meningoencephalomyelitis (NME). ANIMALS Hundred and nine dogs examined for neurological signs at 3 university referral hospitals. METHODS Brain tissue and CSF were collected prospectively from dogs with neurological disease and evaluated by broadly reactive polymerase chain reaction (PCR) for Ehrlichia, Anaplasma, Spotted Fever Group Rickettsia, Bartonella, and Borrelia species. Medical records were evaluated retrospectively to identify MEM and control cases. RESULTS Seventy-five cases of MUE, GME, or NME, including brain tissue from 31 and CSF from 44 cases, were evaluated. Brain tissue from 4 cases and inflammatory CSF from 30 cases with infectious, neoplastic, compressive, vascular, or malformative disease were evaluated as controls. Pathogen nucleic acids were detected in 1 of 109 cases evaluated. Specifically, Bartonella vinsonii subsp. berkhoffii DNA was amplified from 1/6 dogs with histopathologically confirmed GME. CONCLUSION AND CLINICAL IMPORTANCE The results of this investigation suggest that microorganisms in the genera Ehrlichia, Anaplasma, Rickettsia, and Borrelia are unlikely to be directly associated with canine MEM in the geographic regions evaluated. The role of Bartonella in the pathogenesis of GME warrants further investigation.

Migraine‐like Episodic Pain Behavior in a Dog: Can Dogs Suffer from Migraines?

Migraines and other primary headache disorders commonly affect people. There is evidence to suggest that migraines can occur in dogs. In this review, we present a dog with paroxysmal episodes that have a striking resemblance to human migraine, and we give an overview of migraine in people. The current classification, clinical signs, and diagnosis in people are discussed, as well as the anatomy of head pain, pathophysiology, pharmacology, and treatment options.

Clinical reasoning in canine spinal disease: what combination of clinical information is useful?

Spinal disease in dogs is commonly encountered in veterinary practice. Numerous diseases may cause similar clinical signs and presenting histories. The study objective was to use statistical models to identify combinations of discrete parameters from the patient signalment, history and neurological examination that could suggest the most likely diagnoses with statistical significance. A retrospective study of 500 dogs referred to the Queen Mother Hospital for Animals before June 2012 for the investigation of spinal disease was performed. Details regarding signalment, history, physical and neurological examinations, neuroanatomical localisation and imaging data were obtained. Univariate analyses of variables (breed, age, weight, onset, deterioration, pain, asymmetry, neuroanatomical localisation) were performed, and variables were retained in a multivariate logistic regression model if P<0.05. Leading diagnoses were intervertebral disc extrusion (IVDE, n=149), intervertebral disc protrusion (n=149), ischaemic myelopathy (IM, n=48) and neoplasms (n=44). Multivariate logistic regression characterised IM and acute non-compressive nucleus pulposus extrusions as the only peracute onset, non-progressive, non-painful and asymmetrical T3-L3 myelopathies. IVDE was most commonly characterised as acute onset, often deteriorating, painful and largely symmetrical T3-L3 myelopathy. This study suggests that most spinal diseases cause distinctive combinations of presenting clinical parameters (signalment, onset, deterioration, pain, asymmetry, neuroanatomical localisation). Taking particular account of these parameters may aid decision making in a clinical setting.

Risk factors for early post-operative neurological deterioration in dogs undergoing a cervical dorsal laminectomy or hemilaminectomy: 100 cases (2002–2014)

Early post-operative neurological deterioration is a well-known complication following dorsal cervical laminectomies and hemilaminectomies in dogs. This study aimed to evaluate potential risk factors for early post-operative neurological deterioration following these surgical procedures. Medical records of 100 dogs that had undergone a cervical dorsal laminectomy or hemilaminectomy between 2002 and 2014 were assessed retrospectively. Assessed variables included signalment, bodyweight, duration of clinical signs, neurological status before surgery, diagnosis, surgical site, type and extent of surgery and duration of procedure. Outcome measures were neurological status immediately following surgery and duration of hospitalisation. Univariate statistical analysis was performed to identify variables to be included in a multivariate model. Diagnoses included osseous associated cervical spondylomyelopathy (OACSM; n = 41), acute intervertebral disk extrusion (IVDE; 31), meningioma (11), spinal arachnoid diverticulum (10) and vertebral arch anomalies (7). Overall 54% (95% CI 45.25-64.75) of dogs were neurologically worse 48 h post-operatively. Multivariate statistical analysis identified four factors significantly related to early post-operative neurological outcome. Diagnoses of OACSM or meningioma were considered the strongest variables to predict early post-operative neurological deterioration, followed by higher (more severely affected) neurological grade before surgery and longer surgery time. This information can aid in the management of expectations of clinical staff and owners with dogs undergoing these surgical procedures.

Cervical Vertebral Stenosis Associated with a Vertebral Arch Anomaly in the Basset Hound

OBJECTIVES To report the clinical presentation, imaging characteristics, treatment results, and histopathological findings of a previously undescribed vertebral malformation in the Basset Hound. ANIMALS AND METHODS Retrospective case series study. Eighteen Basset Hounds presented for evaluation of a suspected cervical spinal cord problem. All dogs underwent computed tomography myelography or magnetic resonance imaging of the cervical region. RESULTS Thirteen male and 5 female Basset Hounds between 6 months and 10.8 years of age (median: 1.4 years) were studied. Clinical signs varied from cervical hyperesthesia to nonambulatory tetraparesis. Imaging demonstrated a well-defined and smooth hypertrophy of the dorsal lamina and spinous process of ≥ 2 adjacent vertebrae. Although this bony abnormality could decrease the ventrodorsal vertebral canal diameter, dorsal midline spinal cord compression was predominantly caused by ligamentum flavum hypertrophy. The articulation between C4 and C5 was most commonly affected. Three dogs were lost to follow-up, 10 dogs underwent dorsal laminectomy, and medical management was initiated in 5 dogs. Surgery resulted in a good outcome with short hospitalization times (median: 4.5 days) in all dogs, whereas medical management produced more variable results. Histopathology confirmed ligamentum flavum hypertrophy and demonstrated the fibrocartilaginous nature of this anomaly. CONCLUSIONS AND CLINICAL IMPORTANCE Dorsal lamina and spinous process hypertrophy leading to ligamentum flavum hypertrophy should be included in the differential diagnosis of Basset Hounds with cervical hyperesthesia or myelopathy. Prognosis after decompressive surgery is favorable. Although a genetic component is suspected, additional studies are needed to determine the specific etiology of this disorder.

Tethered Cord Syndrome Associated with a Thickened Filum Terminale in a Dog

A1-year-old female neutered English Cocker Spaniel was presented with a 9 months history of progressive right pelvic limb lameness. Survey radiographs, computed tomography (CT), magnetic resonance imaging (MRI), and joint taps of the pelvis, stifles, hock joints and tarsi, performed before referral, were within normal limits. Medical management with meloxicam did not result in clinical improvement. Treatment with gabapentin, initiated 7 days before presentation, resulted in improvement. General physical examination did not reveal any abnormalities. Neurological examination revealed paraparesis, right pelvic limb lameness, a low tail carriage, proprioceptive deficits expressed by delayed hopping, but intact paw placement in both pelvic limbs, a reduced withdrawal reflex in the right pelvic limb and decreased tail tone. Pain was elicited on lumbosacral palpation, dorsal extension of the tail and extension of both hips. The remainder of the neurological examination was within normal limits. Her neurological lesion was localized to the L4-S3 spinal cord segments. A complete blood count and biochemistry panel were within normal limits. After premedication with methadone (0.2 mg/kg IM) and acepromazine (0.0 1mg/kg IM), anesthesia was induced with propofol (4–6 mg/kg, IV), and maintained with sevoflurane in oxygen. MRI of the lumbar and lumbosacral vertebral column was performed with the dog in dorsal recumbency with flexed limbs (ie, frog-leg position). The imaging protocol included sagittal and transverse plane T2-weighted (repetition time (ms) (TR), echo time (ms) (TE), 3000/120), sagittal and dorsal plane T2-weighted short-tau inversion recovery (TR/TE, 3612/80), and transverse plane T2-weighted BAL TGRAD (TR/TE, 7.9/3.9) sequences. Sagittal and transverse plane T1-weighted (T1W TSE) (TR/TE, 400/8) images were acquired before and after IV injection with gadolinium contrast. MRI demonstrated possible caudodorsal displacement of the conus medullaris. Mild lumbosacral intervertebral disk protrusion was also seen (Fig 1). After MRI, a CT examination of the lumbosacral vertebral column was performed using a 16-slice scanner. After completion of the transverse CT study, sagittal and dorsal reconstructions were made. CT imaging (Fig 2) confirmed the MRI findings and did not reveal any other vertebral or spinal abnormalities. Differential diagnoses included tethered cord syndrome and dynamic lumbosacral vertebral canal stenosis. Given her initial positive response, medical management was continued with gabapentin (10mg/kg, q8h, PO), carprofen (2mg/kg, q12h, PO) and restricted exercise for 4 weeks. A re-examination 4 weeks later demonstrated progression of her clinical signs characterized by more pronounced paraparesis and right pelvic limb lameness. General anesthesia was induced and maintained with the aforementioned protocol. A standard dorsal lumbosacral laminectomy, from L7 to S2 was performed. After opening the vertebral canal, a ligamentous structure was identified between the conus medullaris and the dorsal lamina of S2, which caused caudodorsal displacement and traction of the conus medullaris (Fig 3A,B). After sectioning and sampling the distal aspect of this ligamentous structure, the conus medullaris regained a more cranial position. The wound was closed routinely. Intraoperative analgesia was provided with ketamine (loading dose of 0.5 mg/kg IV followed by a CRI at 10 lg/kg/min IV) and methadone (0.1 mg/kg q4h, IV). Postoperative analgesia consisted of a combination of methadone (0.2 mg/kg, q4h, IV), carprofen (2 mg/kg, q12h, PO) and gabapentin (10 mg/kg, q8h, PO). The dog was discharged from hospitalization 4 days after surgery. The owner was advised to provide strict rest for 4 weeks in combination with gabapentin and carprofen for 2 more weeks. From the Department of Veterinary Clinical Science and Services, (De Decker, Gregori, Kenny, Hoy, Volk); Department of Pathology and Pathogen Biology, The Royal Veterinary College, University of London, North Mymms, Hertfordshire England (Erles). Department of Veterinary Clinical Science and Services, The Royal Veterinary College, University of London, Hawkshead Lane, North Mymms, Hertfordshire AL97TA, England. This case report was presented in abstract form (poster) at the 27 Symposium of the European College of Veterinary Neurology (ECVN), 18–20 September 2014, Madrid, Spain. Corresponding author: S. De Decker, Department of Veterinary Clinical Science and Services, The Royal Veterinary College, University of London, Hawkshead Lane, North Mymms, Hertfordshire AL97TA, England; e-mail: sdedecker@rvc.ac.uk. Submitted September 15, 2014; Revised October 28, 2014; Accepted November 11, 2014. Copyright

Magnetic Resonance Imaging Findings in a Dog with Sensory Neuronopathy

A 3-year-old, male neutered Miniature Dachshund was presented for investigation of an acute onset, slowly progressive ataxia of 2 months’ duration. Serum titers for Toxoplasma gondii and Neospora caninum evaluated before referral were negative. General physical examination was within normal limits. Neurological examination identified a “bouncy” generalized ataxia with exaggerated movements of all of the limbs, neck and head. No apparent paresis was present. The dog had proprioceptive deficits in all limbs manifested by a delay in hopping and paw placement. Clinical signs and neurological abnormalities were more severe in the pelvic limbs. The dog had bilaterally decreased menace responses and palpebral reflexes. The remainder of the neurologic examination was within normal limits. A diffuse or multifocal neuro-anatomic localization was considered most likely. Results of a CBC and serum biochemistry profile were within reference intervals. The dog was premedicated with butorphanol (0.2 mg/kg IV) and anesthesia was induced with propofol (3.5 mg/kg IV) and maintained with sevoflurane in oxygen. Magnetic resonance imaging (MRI) of the brain and cervical spinal cord included T2-weighted (repetition time, [TR] [ms], echo time [TE] [ms] 3333/110) sagittal and transverse images and transverse fluid attenuation inversion recovery (TR/TE, 6000/120) images. Sagittal and transverse plane T1-weighted images (TR/TE, 515/15) were acquired before and after IV injection of gadolinium contrast material. Slice thickness was 3.5 mm in all planes with an interslice gap of 0.9 mm in the sagittal and 1 mm in the transverse planes. No abnormalities were identified on MRI of the brain. In the cervical spinal cord, a linear, intra-parenchymal signal, hyperintense on T2-weighted images, delineated the dorsal funiculus (Fig 1). No contrast enhancement was observed. Differential diagnoses at this time included an inflammatory spinal cord disorder, a neurodegenerative disorder involving the cervical spinal cord, or a sensory neuronopathy. Analysis of cerebrospinal fluid, obtained by cisternal and lumbar punctures was within normal limits. Based on these findings, a sensory neuronopathy was considered the most likely diagnosis. Neurologic re-examination 1 month later identified worsening of the dog’s ataxia, decreased patellar reflexes and decreased nociception in the digits of all limbs. Electrodiagnostic evaluation and spinal ganglion biopsy were offered, but declined by the owner. The dog was presented 15 months after its initial clinical presentation for assessment of perceived vision loss and further worsening of clinical signs. There was a known familial history of progressive retinal atrophy. Neurologic examination identified severe deterioration of clinical signs. Although paresis still was not apparent, the severity of the dog’s ataxia impeded ambulation. Other findings included wide head and neck excursions, proprioceptive deficits in all limbs, absent bilateral menace responses, absent bilateral palpebral and corneal reflexes, bilaterally decreased responses after stimulation of the nasal mucosa, decreased pupillary light reflexes bilaterally (direct and indirect), absent patellar reflexes bilaterally and decreased nociception in the digits of all limbs. The remainder of the neurologic examination was within normal limits. A complete ophthalmic examination confirmed visual impairment and abnormalities of ocular reflexes as described above. Rudimentary corneal esthesiometry (ie, use of cottontipped applicator and the noncontact air-puff technique) indicated decreased corneal sensation. General anesthesia was induced and maintained by using the previously described protocol. A mixed rod-cone electroretinogram (ERG) disclosed no visible ERG in the right eye and a markedly diminished ERG in the left eye with barely discernible a and b waves. Findings of the ophthalmic and ERG examinations were in agreement with From the Department of Clinical Science and Services, Royal Veterinary College, University of London, North Mymms, Hatfield UK (Hamzianpour, Kenny, Sanchez, Volk, De Decker); and the Department of Pathology and Pathogen Biology, The Royal Veterinary College, University of London, North Mymms, Hertfordshire UK (Eley). This case report has been presented in part at the 26 Annual Symposium of the European Society of Veterinary Neurology – European College of Veterinary Neurology, 26-28 September 2013, Paris. Corresponding author: S. De Decker, Department of Clinical Science and Services, Royal Veterinary College, University of London, Hawkshead Lane, AL9 7TA North Mymms, Hatfield, UK; e-mail: SDeDecker@rvc.ac.uk. Submitted January 28, 2015; Revised May 14, 2015; Accepted June 17, 2015. Copyright

Hypersomatotropism in 3 Cats without Concurrent Diabetes Mellitus

A 16-year-old, 6.8 kg, castrated male Domestic Short-haired cat was presented to Louisiana State University Veterinary Teaching Hospital with a 3-day history of progressive ataxia, tetraparesis, and altered mentation. The owner did not report having observed evidence of polyuria or polydipsia. The cat had been diagnosed with hypertrophic cardiomyopathy (HCM) 4 years earlier and was receiving atenolol, benazepril, and aspirin. Dull mentation, patchy truncal alopecia, and a grade III of VI systolic heart murmur were noted during the physical examination. The neurologic examination revealed ambulatory tetraparesis that was more severe in the pelvic limbs, plantigrade stance, proprioceptive deficits in all limbs, and positional vertical nystagmus. The CBC, biochemistry profile, and abdominal ultrasound were unremarkable. The blood glucose concentration measured with the chemistry analyzer was 130 mg/dL (7.2 mmol/L). Subsequent blood glucose measurements (n = 6) using a glucometer validated for use in cats ranged from 122 mg/dL (6.7 mmol/L) to 159 mg/dL (8.7 mmol/L) during the 5-day period the cat was hospitalized. These blood glucose concentrations combined with a normal serum fructosamine concentration (228 lmol/L, RI 192–288) ruled out overt diabetes mellitus (DM). Two-dimensional echocardiogram revealed severe asymmetric septal hypertrophy (8.7 mm in diastole). The left atrium was normal in size and all valves appeared normal. Continuous wave Doppler through the left ventricular outflow tract revealed dynamic outflow tract obstruction. Color Doppler demonstrated marked turbulence in the left ventricular outflow tract and a narrow eccentric jet of mitral regurgitation associated with systolic anterior motion of the mitral valve. Magnetic resonance imaging (MRI) images of the head were obtained in multiple planes prior to and following contrast administration at a dose of 0.1 mmol/kg. In the region of the pituitary gland, there was a T2 hyperintense, T1 hypointense nodule having marked uniform contrast enhancement (Fig 1). This nodule had moderate extension dorsal to the sella turcica and was increased in size compared to a normal pituitary gland: length (0.63 cm), width (0.83 cm), and height (0.85 cm). On T2* weighted (gradient recalled echo) images, some regions of reduced signal and small signal voids were present within the pituitary gland, mostly on the left side, consistent with magnetic susceptibility likely due to regions of hemorrhage within the nodule. Additionally, there was moderate dilation of the entire ventricular system with most severe ventricular enlargement occurring in the fourth ventricle, which caused dorsal elevation and compression of the cerebellum. Findings were most consistent with a pituitary macroadenoma, hydrocephalus, and hydrosyringomyelia. The degree of pituitary enlargement and severity of 4th ventricular dilation did not support obstruction due to the pituitary mass. A cystic accumulation of cerebrospinal fluid (CSF) within the 4th ventricle or obstructive hydrocephalus due to an additional lesion not visible on the MRI could not be ruled out. A clinical diagnosis of hypersomatotropism was supported by the presence of a pituitary mass and a total From the Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70810 (Fletcher, Pipe-Martin, Granger); Department of Clinical Science and Services, The Royal Veterinary College, University of London, North Mymms, AL9 7TA, Herts, UK(Scudder, Kenny, Mantis, Fenn, Niessen); Department of Pathobiology and Diagnostic Investigation, Diagnostic Center for Population and Animal Health, Michigan State University, Lansing, MI 48910 (Kiupel); Department of Pathology and Pathogen Biology, The Royal Veterinary College, University of London, North Mymms, AL9 7TA, Herts, UK(Smith); Department of Pathobiological Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70810(Blair). Corresponding author: J.M. Fletcher, Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70810; e-mail: jmfletcher@lsu.edu Submitted March 31, 2016; Revised May 12, 2016; Accepted May 16, 2016. Copyright

Severe Systemic Calciphylaxis in a Young Cat

A 7-month-old female intact domestic shorthair/ British Blue crossbreed cat was referred to the Queen Mother Hospital for Animals (QMHA) of the Royal Veterinary College for further investigation of progressive lethargy preceded by 48 hours of mixed bowel diarrhea, moderate pyrexia (39.9°C; 103.8°F), and unproductive retching. Laboratory tests performed at the primary practice identified marked hypercalcemia (serum total calcium concentration). Despite treatment with IV fluids and potentiated amoxicillin, the cat deteriorated clinically, prompting referral. On presentation to the QMHA, the cat was dull but responsive with poor body condition (3.5/9) and pyrexia (39.2°C; 102.6°F). Firm white lingual plaques were observed (Fig 1). Both kidneys were subjectively mildly enlarged. The remainder of the physical examination was unremarkable. With the exception of the cat’s decreased mentation, neurologic examination was considered normal. No neurologic deficits suggesting a structural intracranial lesion were found at any point throughout the time the cat was hospitalized, but the level of obtundation would wax and wane. No association between the cat’s mentation and the treatments administered was apparent. Initial investigations confirmed marked total hypercalcemia (19.28 mg/dL; 4.82 mmol/L; reference interval [RI], 8.28–10.72 mg/dL) and ionized hypercalcemia (9.0 mg/dL; 2.25 mmol/L; RI, 4.52–5.32 mg/dL), with mild hyperphosphatemia (7.68 mg/dL; 2.48 mmol/L; RI, 2.85–6.69 mg/dL). Markedly increased serum CK activity was identified (21,322 U/L; RI, 52–506 U/L) increasing to 43,616 U/L upon repeated measurement after 3 days. Serum ALT activity was within normal limits. At the time of presentation, serum urea nitrogen concentration was moderately increased (49.0 mg/ dL; 17.5 mmol/L; RI, 17.1–33.6 mg/dL), whereas serum creatinine concentration was within normal limits (1.36 mg/dL; 118 lmol/L; RI, 0.84–2.1 mg/dL). Interpretation of complete blood cell count was consistent with a stress leukogram. Mild leukocytosis (26.2 9 10/L; RI, 5.5–19.5 9 10/L) with mild neutrophilia (23.8 9 10/L; RI, 2.5–12.5 9 10/L) and mild lymphopenia (0.58 9 10/L; RI, 1.5–7.0 9 10/L) were present. Urinalysis disclosed the presence of granular casts (10 per 81 high-power fields, 4009), but was otherwise unremarkable. Urine specific gravity was 1.015 (after IV fluid therapy). Venous blood gas, electrolyte, and metabolite analyses were performed throughout hospitalization to monitor plasma creatinine, urea, and ionized calcium concentrations. Plasma ionized calcium concentration gradually decreased from 9.0 mg/dL to 7.44 mg/dL 24 hours after admission, whereas blood urea nitrogen and creatinine concentration increased to 142.6 mg/dL (50.9 mmol/L) and 3.0 mg/dL (268 lmol/L), respectively. The azotemia was believed to be at least partly prerenal, because it gradually resolved over the next 48 hours, with concurrent decreases in packed cell volume and total protein concentration (from 30% and 6.4 g/dL to 20% and 5.4 g/dL, respectively). During the first 3 days of hospitalization, treatment included IV fluid therapy (up to 8 mL/kg/h by the second day), furosemide (0.5–1.0 mg/kg IV q6h), and salmon calcitonin (4 IU/kg SC q8h), all of which were initiated on the first day of hospitalization. Furosemide probably contributed to dehydration and development of azotemia, supported by a 100 g (4.8%) decrease in body weight over the first 24 hours. Owing to persistent hypercalcemia despite treatment, IV pamidronate infusion (1.75 mg/kg diluted in 16 mL 0.9% NaCl, infused at a rate of 4 mL/h) was administered on the third day of hospitalization, at which time salmon calcitonin was discontinued. These treatments failed to substantially alter the plasma ionized calcium concentration, but approximately 48 hours after initiating prednisolone treatment (0.5 mg/kg PO q12h) on day 6 of hospitalization, plasma ionized calcium conFrom the Department of Clinical Sciences and Services, Queen Mother Hospital for Animals (Anfinsen, Kenny, Garden); the Comparative Neuromuscular Diseases Laboratory, Department of Clinical Sciences and Services, Royal Veterinary College, University of London, London, UK (Piercy, Massey); and the Department of Pathology & Pathogen Biology (Smith), Royal Veterinary College, University of London, Hatfield, UK. Corresponding author: K.P. Anfinsen, Department of Companion Animal Clinical Sciences, NMBU School of Veterinary Science, N-0033 Oslo, Norway; e-mail: kristin.anfinsen@nmbu.no. Submitted November 5, 2013; Revised March 18, 2014; Accepted April 22, 2014. Copyright