Katrin Beckmann

Evaluation of intracranial neoplasia and noninfectious meningoencephalitis in dogs by use of short echo time, single voxel proton magnetic resonance spectroscopy at 3.0 Tesla

OBJECTIVE To investigate metabolite concentrations of the brains of dogs with intracranial neoplasia or noninfectious meningoencephalitis by use of short echo time, single voxel proton magnetic resonance spectroscopy ((1)H MRS) at 3.0 T. ANIMALS 29 dogs with intracranial lesions (14 with neoplasia [3 oligodendromas, 3 glioblastomas multiformes, 3 astrocytomas, 2 lymphomas, and 3 meningiomas] and 15 is with noninfectious meningoencephalitis) and 10 healthy control dogs. PROCEDURES Short echo time, single voxel (1)H-MRS at 3.0 T was performed on neoplastic and noninfectious inflammatory intracranial lesions identified with conventional MRI. Metabolites of interest included N-acetyl aspartate (NAA), total choline, creatine, myoinositol, the glutamine-glutamate complex (Glx), glutathione, taurine, lactate, and lipids. Data were analyzed with postprocessing fitting algorithm software. Metabolite concentrations relative to brain water content were calculated and compared with results for the healthy control dogs, which had been previously evaluated with the same (1)H MRS technique. RESULTS NAA, creatine, and Glx concentrations were reduced in the brains of dogs with neoplasia and noninfectious meningoencephalitis, whereas choline concentration was increased. Concentrations of these metabolites differed significantly between dogs with neoplasia and dogs with noninfectious meningoencephalitis. Concentrations of NAA, creatine, and Glx were significantly lower in dogs with neoplasia, whereas the concentration of choline was significantly higher in dogs with neoplasia. Lipids were predominantly found in dogs with high-grade intra-axial neoplasia, meningioma, and necrotizing meningoencephalitis. A high concentration of taurine was found in 10 of 15 dogs with noninfectious meningoencephalitis. CONCLUSIONS AND CLINICAL RELEVANCE (1)H MRS provided additional metabolic information about intracranial neoplasia and noninfectious meningoencephalitis in dogs.

Unexplained bleeding as primary clinical complaint in dogs infected with Angiostrongylus vasorum.

INTRODUCTION Unexplained bleeding was the primary clinical complaint in 15 dogs diagnosed with A. vasorum and was observed in the mouth, as external bleeding, as large subcutaneous hematoma, as hemoptysis, in the brain, post ovariectomy, as epistaxis, in the anterior ocular chamber and on a tracheal intubation tube. In 8 dogs the cause of bleeding initially was suspected to be a minor trauma or a surgical complication, and various surgical approaches had been undertaken to eliminate the problem. In only 3 dogs respiratory signs were observed before the bleeding prompted referral. The median time elapsed between the first recognized clinical signs attributed to A. vasorum until diagnosis was 2 weeks (range1 day to 4 months). Four dogs died, 3 on the day of admission and 1 dog 4 days after admission. Suspected causes of death were respiratory failure and cerebral hemorrhage in 2 dogs each. Four dogs had been pre-treated with NSAIDs; of these, 2 dogs developed severe hemoptysis (1 died), 1 dog developed brain hemorrhage (and died), and 1 dog developed a large subcutaneous hematoma with marked anemia. Bleeding at various sites may be the only recognized abnormality in A. vasorum infection. Without a high index of suspicion, the diagnosis and appropriate therapy may be delayed to the point of a fatal outcome. Tests of coagulation were quite variable and the cause of bleeding likely multifactorial.

A newly designed radiation therapy protocol in combination with prednisolone as treatment for meningoencephalitis of unknown origin in dogs: a prospective pilot study introducing magnetic resonance spectroscopy as monitor tool

BackgroundA plethora of treatment options have been described for canine meningoencephalitis of unknown origin (MUO), yet a gold standard has not been established. The aim of this prospective pilot study was to document the effect of a newly designed 30 Gray (Gy) radiation therapy (RT) protocol plus corticosteroids as treatment for focal and multifocal MUO, to monitor clinical and imaging changes during the course of the disease with conventional magnetic resonance imaging (MRI) and proton MR Spectroscopy (H-1 MRS) and to detect the occurrence of radiation related side effects.ResultsSix dogs (3 with focal and 3 with multifocal lesions) were included in the study. The RT protocol used consisted of 30 Gy in 10 fractions. The neurological status of all six dogs improved during RT, with 3 of 6 cases returning to a normal condition. One dog was euthanized early during follow-up (<3 weeks after end of RT). Three month follow up MRI was normal in one dog and improved in 3 dogs and H-1 MRS normalized in 4. In the dog without improvement of the MRI lesions, the N-acetyl aspartate continued to decrease, while choline and creatine concentrations remained stable during that time. This dog was euthanized 18 month after the end of RT due to relapse. One dog was lost to follow up 12 month after completion of RT. The other 3 dogs are still alive at the time of writing.ConclusionsRT with 30 Gy in 10 fractions can provide an additional option for anti-inflammatory treatment of focal and multifocal MUO. The protocol used for treatment monitoring was feasible while no side effects of RT could be observed during the follow up period. Moreover, H-1 MRS could represent a new and non-invasive tool to control the progression of the disease during the treatment course.

IMAGING DIAGNOSIS—CONVENTIONAL AND FUNCTIONAL MAGNETIC RESONANCE IMAGING OF A BRAIN ABSCESS IN A GOAT

A 2-month-old female goat was presented for depressed mental status and multifocal central neurologic signs 3 weeks after hot-iron disbudding. Conventional magnetic resonance imaging (MRI) findings included a large intra axial mass in the left frontal lobe that was T2 hyperintense and T1 hypointense centrally with a contrast-enhancing peripheral capsule and perilesional T2 hyperintensity. A restrictive pattern was present in diffusion-weighted imaging. Magnetic resonance spectroscopy demonstrated an increased amount of succinate, acetate, amino acids, lipids; minimal amounts of lactate; and decreased amounts of N-acetyl aspartate and choline. A cerebral abscess due to Trueperella pyogenes was confirmed from necropsy and tissue culture.

Comparison between proton magnetic resonance spectroscopy findings in dogs with tick-borne encephalitis and clinically normal dogs

In vivo diagnosis of tick-borne encephalitis is difficult due to high seroprevalence and rapid viral clearance, limiting detection of antibodies in blood and cerebrospinal fluid. Magnetic resonance imaging (MRI) characteristics of tick-borne encephalitis have been reported, however MRI studies can also be negative despite the presence of neurologic signs. Magnetic resonance spectroscopy (1 H MRS) is an imaging method that provides additional information about the metabolic characteristics of brain tissues. The purpose of this retrospective cross-sectional study was to describe brain metabolites using short echo time single-voxel 1 H MRS in dogs with confirmed tick-borne encephalitis and compare them with healthy dogs. Inclusion criteria for the affected dogs were neurological symptoms suggestive of tick-borne encephalitis, previous endemic stay and tick-bite, diagnostic quality brain MRI and 1 H MRS studies, and positive antibody titers or confirmation of tick-borne encephalitis with necropsy. Control dogs were 10, clinically normal beagles that had been used in a previous study. A total of six affected dogs met inclusion criteria. All dogs affected with tick-borne encephalitis had 1 H MRS metabolite concentration alterations versus control dogs. These changes included mild to moderate decreases in N-acetyl aspartate and creatine peaks, and mild increases in glutamate/glutamine peaks. No lactate or lipid signal was detected in any dog. Myoinositol and choline signals did not differ between affected and control dogs. In conclusion, findings supported the use of 1 H MRS as an adjunctive imaging method for dogs with suspected tick-borne encephalitis and inconclusive conventional MRI findings.

THREE TESLA MAGNETIC RESONANCE IMAGING FINDINGS IN 12 CASES OF CANINE CENTRAL EUROPEAN TICK-BORNE MENINGOENCEPHALOMYELITIS

Central European tick-borne encephalomyelitis can be challenging to diagnose in dogs because the virus may not be detected in blood and cerebrospinal fluid (CSF) after the first viremic stage of the disease. The purpose of this retrospective case series study was to describe 3 Tesla magnetic resonance imaging (3T MRI) findings in a sample of dogs with a confirmed diagnosis of tick-borne encephalomyelitis. Dogs were included if they had neurological signs consistent with tick-borne encephalomyelitis, history of a stay in endemic areas for tick-borne encephalomyelitis virus, 3T MRI of the brain and/or spinal cord, cerebrospinal fluid changes compatible with viral infection and positive antibody titers in cerebrospinal fluid or pathologic confirmation of tick-borne encephalomyelitis. Twelve dogs met inclusion criteria. Ten out of 12 patients had 3T MRI lesions at the time of presentation. One patient had persistent lesions in follow-up MRI. The 3T MRI findings included bilateral and symmetrical gray matter distributed lesions involving the thalamus, hippocampus, brain stem, basal nuclei, and ventral horn on the spinal cord. All lesions were hyperintense in T2-weighted sequences compared to white matter, iso- to hypointense in T1-weighted, nonenhancing, and had minimal or no mass effect or perilesional edema. Six patients survived while the remaining six dogs were euthanized. Necropsy revealed neuronophagia and gliosis of the gray matter of the affected regions seen in 3T MRI, in addition to the cerebellum. Findings from the current study indicated that tick-borne encephalomyelitis should be included in the differential diagnosis list for dogs with the above described 3T MRI characteristics.

MRI findings in a case of canine tick born meningoencephalomyelitis

Tick borne encephalitis virus (TBE) is an endemic infectious agent in northeastern Switzerland causing mainly meningoencephalomyelitis in dogs. We report a canine case of tick born meningoencephalomyelitis resulting in flaccid tetraplegia and, subsequently, fatal respiratory failure. Magnetic resonance imaging (MRI) demonstrated intra-axial bilateral, symmetric, and hyperintense lesions in T2-weighted and Fluid Attenuated Inversion Recovery (FLAIR) sequences affecting thalamus, basal nuclei, cerebral white matter and ventral horns of the caudal cervical spine. These radiological findings overlap those described during flavivirus encephalitis affecting human beings. These lesions in MRI and diffusion weighted images correlated with areas of vasogenic edema detected histopathologically. In endemic regions, clinicians should be aware that bilateral, symmetrical hyperintense thalamic lesions in T2WI can be suggestive of flavivirus infection in dogs with encephalitis.

Achalasia‐Like Disease with Esophageal Pressurization in a Myasthenic Dog

An 8-year-old, intact male Pug was examined for a 7-day history of progressive weakness, progressive decline in food intake, dysuria, and dysphonia. The dysuria was described as an inability to void when being walked as the dog could not lift its leg and did not urinate although there was evidence of urine leakage in the dog’s blankets. When initially examined, the dog was alert with a BCS of 5/9. The physical examination did not reveal abnormalities. Results of hematology, serum biochemistry, and urinalysis as well as abdominal ultrasound did not reveal abnormalities. Upon owners’ request, the dog was discharged without further work-up, and gabapentin (5 mg/kg, PO q12h) were prescribed for suspected lumbosacral pain. Because of increasing weakness over the next 2 days, the dog was presented at an emergency clinic, where urinary retention caused by lumbosacral disease was suspected and treated with a single dose of dexamethasone (10 mg IM). Three days later, the dog was again examined for anorexia and progressive weakness. Physical examination revealed an alert dog able to walk 2–3 m with a stiff gate and kyphotic posture before finally lying down. Laboratory work revealed a CK (111 U/L; reference range, 51–191) within reference range and no abnormalities were detected on urinalysis. A bacterial culture of urine showed no growth. Thoracic radiographs revealed moderate esophageal dilatation and a markedly dilated stomach (Fig 1). Results of a neurologic examination were consistent with a neuromuscular junction disorder, and an edrophonium chloride challenge (0.2 mg/kg IV) showed a dramatic positive response. At the time of electromyographic testing, an upper gastrointestinal endoscopy was also performed because of concerns about steroid-induced gastric ulceration. Before anesthesia, esophageal high-resolution manometry (HRM) was used to evaluate esophageal function (Fig 2). A manometric catheter was lubricated with 2% lidocaine gel and carefully inserted intranasally. It was passed through the nasopharynx into the esophagus and finally positioned so that it recorded the pressure profile of the entire esophagus from the pharynx to the stomach. Real-time pressure imaging enabled accurate placement, and 3–4 pressure sensors were positioned intragastrically to rule out artifacts caused by breathing-related movements of the esophagogastric junction. HRM examination revealed an abnormal swallowing mechanism: after normal upper esophageal sphincter (UES) relaxation (UES residual pressure 0.4 mmHg [ 10.5 to 0.3 mmHg], UES relaxation time to nadir 138 mmHg (58–140 mmHg), relaxation duration 300 ms [145–305 ms]) the aborally propagating peristaltic waves of the tubular esophagus, as well as lower esophageal sphincter (LES) relaxations [LES baseline pressure 37.3 mmHg (14.6–45.1 mmHg), LES residual pressure 27 mmHg (1.9–19.1 mmHg)] were completely absent throughout the study. The peristaltic waves were discontinued by simultaneous contractions of the tubular esophagus beginning at a point just past the first third of the tubular esophagus (Fig 3). The subsequent esophagogastroduodenoscopy did not reveal abnormalities except for a dilated and flaccid esophagus. Biopsies were taken from the middle and lower esophagus, stomach, and duodenum. Histopathologically, all esophageal, gastric, and duodenal biopsies did not reveal abnormalities. Electromyographic examination of the limbs and epaxial muscles did not reveal abnormalities. Supramaximal repetitive nerve stimulation of the tibial and ulnar nerve at a frequency of 3 Hz produced a decrement of 30% (reference <10%). At this point, myasthenia gravis (MG) was suspected on the basis of clinical, electromyographic, and pharmacologic testing results. After treatment with pyridostigmin (1.5 mg/kg PO, q8h), the dog had progressive improvement of all clinical findings. By the time the AChR titer came back negative (0.22 nmol/L; normal <0.6 nmol/L) on day 14, the dog had already fully recovered. Upon recheck on day 21, the dog’s owners had already stopped pyridostigmin 4 days From the Clinic for Small Animal Internal Medicine (Kempf, Kook), and the Division of Neurology, Clinic for Small Animal Surgery (Beckmann), Vetsuisse Faculty, University of Zurich, Zurich, Switzerland (Beckmann). Corresponding author: Dr Peter Hendrik Kook, Clinic for Small Animal Internal Medicine, Vetsuisse Faculty, University of Zurich, Winterthurerstrasse 260, Zurich 8057, Switzerland; e-mail: peterhen drikkook@gmail.com. Submitted June 20, 2013; Revised January 2, 2014; Accepted January 14, 2014. Copyright

Presence of Probst Bundles Indicate White Matter Remodeling in a Dog with Corpus Callosum Hypoplasia and Dysplasia

Corpus callosum abnormalities (CCA) rarely occur in dogs and are related to hypo/adypsic hypernatremia and seizures. Hypoplasia and dysplasia of the corpus callosum (CC) with concomitant lobar holoprosencephaly is the most common variant. It is currently uncertain using conventional MRI if canine CCA reflects the failure of commissural fibers to develop or the failure of the commissural fibers to cross hemispheres. Diffusion tensor imaging was performed in a 4-year-old Staffordshire mix breed dog with CCA and an age-matched healthy Beagle. In comparison to the control dog, CC tractography of the affected dog depicted only axonal tracts corresponding to the temporal CC fibers. The cingulum bundles appeared supernumerary with unorganized architecture, extending into the ipsilateral cerebral cortex, and therefore strongly suggested homology to Probst bundles reported in humans with CCA. The presence of Probst bundles in canine CCA could represent compensatory neuroplasticity-mediated networking and may contribute the fair prognosis reported in affected dogs.