Clinical and topographic magnetic resonance characteristics of suspected brain infarction in 40 dogs

Medical records of 40 dogs presented for evaluation of acute-onset, nonprogressive, intracranial dysfunction by means of magnetic resonance imaging (MRI) diagnosis of brain infarction were reviewed. Location of the brain infarcts was: 11 of 38, telencephalic; 8 of 38, thalamic/midbrain; 18 of 38, cerebellar; and 3 of 38, multifocal. Telencephalic infarcts developed within the territory of the middle cerebral (4/11), rostral cerebral (2/11), and striate (5/11) arteries. Thalamic/midbrain infarcts developed within the territory of perforating arteries of the caudal portion of the thalamus and rostral portion of the brainstem (8/8). All cerebellar infarcts (18/38) were within the territory of the rostral cerebellar artery or one of its branches. All infarcts appeared nonhemorrhagic, with marked contrast enhancement observed in only 3 of 38 dogs, all of which were imaged more than 7 days after the onset of signs of neurologic dysfunction. Diffusion-weighted imaging (DWI) sequences were available from 6 dogs, all imaged within 5 days of the onset of signs of neurologic dysfunction. Suspected infarcts were hyperintense on DWI sequences and were hypointense on the apparent diffusion coefficient map. Telencephalic infarcts caused abnormal mental status, contralateral postural reaction deficit, contralateral nasal hypalgesia, contralateral menace deficit, and ipsilateral circling. Thalamic/midbrain infarcts caused contralateral or ipsilateral postural reaction deficit, contralateral menace deficit, ipsilateral head tilt or turn, nystagmus, ventrolateral strabismus, and anisocoria. Cerebellar infarcts caused ipsilateral asymmetric cerebellar quality ataxia, head tilt, intermittent opisthotonus, nystagmus, and ipsilateral menace deficit with apparent normal vision.     

Cerebellar infarcts in two dogs diagnosed with magnetic resonance imaging

Two dogs presented with severe, peracute-onset, neurological signs. Neuroanatomical localization was cerebellovestibular. Magnetic resonance imaging (MRI) was performed and revealed focal, wedge-shaped lesions in the cerebellum. Diagnosis of cerebellar infarctions was made based on peracute-onset, clinical signs, MRI, and outcome as well as ancillary diagnostic information. Both dogs recovered completely. Cerebellar infarction should be included in the differential of any dog with peracute-onset, central cerebellovestibular signs regardless of severity of clinical signs. Outcome was excellent in these dogs.     

Presumptive caudal cerebellar artery infarct in a dog: clinical and MRI findings

Clinical signs and magnetic resonance imaging findings of a caudal cerebellar artery infarct are reported for the first time in a dog. Clinical signs were characterised by a peracute, non-progressive, right-sided central vestibular syndrome with paradoxical right-sided head tilt. Magnetic resonance images were consistent with a territorial, non-haemorrhagic, ischaemic lesion affecting the caudo-ventral part of the right cerebellar hemisphere, mainly involving the right paramedian lobe, the ansiform lobe and the caudal cerebellar peduncle. Bloodwork results were suggestive of an underlying hypercoagulable state, although the concomitant presence of a histologically confirmed mammary gland adenocarcinoma could have also been related to the cerebellar vascular obstruction through metastatic emboli formation. Posterior-inferior cerebellar artery infarction is the human equivalent of caudal cerebellar artery infarct in dogs.     

Presentation,clinical pathological and post‐mortem findings in three related Scottish terriers with ligneous membranitis

Ligneous conjunctivitis and gingivitis were diagnosed in three related Scottish terrier dogs presented for investigation of severe conjunctivitis and respiratory signs. Hypoplasminogenaemia was confirmed in one of the three affected dogs. Supportive treatment was not effective, and the dogs died or were euthanased because of the disease. Post‐mortem analysis of two of the dogs revealed multiple abnormalities including severe proliferative fibrinous lesions affecting the conjunctiva, gingiva, trachea, larynx and epicardium and multiple fibrous adhesions throughout the thoracic and abdominal cavities. One dog had internal hydrocephalus and lacked a cerebellar vermis. Ligneous membranitis was confirmed on histopathology. This is a rare condition in dogs but an important differential diagnosis for severe conjunctivitis and gingivitis.     

Intranasal melanoma treated with radiation therapy in three dogs

Three dogs were investigated for chronic unilateral nasal discharge. In all cases CT imaging showed an intranasal mass causing turbinate lysis and no evidence of metastasis. Cytology in cases 1 (a 14-year-old neutered male crossbreed dog) and 2 (a five-year-old neutered male German Shepherd dog) demonstrated a pleomorphic cell population with variable intracellular pigment suspicious of melanocytic neoplasia. Histopathology with immunohistochemistry (Melan-A and vimentin, plus PNL-2 in one case) confirmed the diagnosis of melanoma in all dogs. All dogs were treated with megavoltage radiotherapy using linear accelerators. Cases 1 and 3 (a nine-year-old neutered female beagle dog) received a hypofractionated (4 × 8 Gy) protocol and case 2 received a definitive (12 × 4 Gy) protocol. Complete remission was demonstrated on repeat CT scan five months after diagnosis in case 1 and seven months in case 2. Stable disease was documented on CT at four months for case 3; however, clinical signs in this dog remained controlled for 10 months in total. Case 1 died of unrelated causes five months after diagnosis, case 2 was euthanased due to the development of seizures 13 months after diagnosis, and case 3 was lost to follow-up 12 months after diagnosis. Melanoma should be considered as a rare differential diagnosis for primary nasal neoplasia in the dog and radiation therapy can be used as effective local therapy.     

Magnetic resonance imaging in two dogs with central nervous system disease

Accurate localization of the lesions in two dogs with progressive neurological disease was demonstrated with magnetic resonance imaging (MRI). The first dog had unilateral cerebellar signs with associated paradoxical vestibular symptoms. The CSF tap and clinical localization suggested a right-sided cerebellar tumour and this was confirmed with MRI scanning. The second dog had predominantly asymmetrical fore-brain signs with circling, personality changes, seizures and contralateral proprioceptive deficits. CSF analysis suggested an inflammatory or neoplastic condition. MRI showed a diffuse oedematous lesion of the left cerebral hemisphere which corresponded exactly with the lesions seen at necropsy. The advantages of MRI over CT scans are discussed.     

Optimal placement of the region of interest for bolus tracking on brain computed tomography angiography in Beagle dogs

This study aimed to determine the optimal placement of the region of interest (ROI) among four anatomical sites—pulmonary artery (PA), pulmonary vein (PV), aortic arch (AA), and carotid artery (CA)—in computed tomography (CT) brain angiography with automatic bolus tracking in healthy beagle dogs. Six beagles were included, and CT brain angiography was performed four times for each dog, to cover each ROI. The scan parameters, amount, and injection rate of the contrast medium were the same. The major intracranial arteries were selected for quantitative and qualitative evaluation: caudal cerebellar artery (CcA), basilar artery (BA), rostral cerebellar artery (RcA), caudal cerebral artery (CCA), middle cerebral artery (MCA), and rostral cerebral artery (RCA). Quantitative evaluation showed significantly higher CT attenuation values for the RcA, CCA, and MCA in the PA group and RcA and MCA in the PV group than in the CA group. Qualitative analysis revealed significantly higher scores for the BA, CCA, and MCA in the PA and PV groups than in the CA group. Venous contamination did not differ significantly among the ROIs, but the mean scores of the AA and CA groups were higher than those of the PA and PV groups. CT brain angiography using bolus tracking in the beagle dogs showed that the ROI should be placed at the PA or PV rather than at the CA for optimal images with strong contrast enhancement of the BA, RcA, CCA, and MCA and minimal venous contamination.     

Results of diagnostic investigations and long-term outcome of 33 dogs with brain infarction (2000-2004)

Medical records of 33 dogs presented for acute onset, nonprogressive, intracranial dysfunction that had a magnetic resonance imaging diagnosis of brain infarction were reviewed. Postmortem confirmation of brain infarction was available in 10 dogs. All dogs were evaluated by CBC, serum biochemistry, thyroid and adrenal testing, urinalysis, thoracic and abdominal imaging, and cerebrospinal fluid analysis. Results of coagulation profile and arterial blood pressure were available in 32/33 and 28/33 dogs, respectively. On the basis of the imaging findings, infarcts were classified depending on their type (territorial or lacunar) and location within the brain (telencephalic, 10/33; thalamic/midbrain, 8/33; cerebellar, 15/33). No marked associations among location or type of infarct and patient age and sex, occurrence of systemic hypertension, and the presence or absence of a concurrent medical condition were identified. Small breed dogs (< or =15 kg) were significantly more likely to have territorial cerebellar infarcts, whereas large breed dogs (>15 kg) were significantly more likely to have lacunar thalamic or midbrain infarcts. A concurrent medical condition was detected in 18/33 dogs with brain infarcts, with chronic kidney disease (8/33) and hyperadrenocorticism (6/ 33) being most commonly encountered. Of 33 dogs, 10 were euthanized because of the severity and lack of improvement of their neurologic status or the severity of their concurrent medical condition. No association was identified between type or location of infarct and patient outcome. Dogs with concurrent medical conditions had significantly shorter survival times than those with no identifiable medical condition and were significantly more likely to suffer from recurrent neurologic signs because of subsequent infarcts.     

Presumed and confirmed striatocapsular brain infarctions in six dogs

OBJECTIVE: To describe the clinical and diagnostic features of the canine sensorimotor syndrome caused by striatocapsular brain infarctions (SCI). ANIMALS STUDIED: Six dogs with diagnostic imaging or postmortem evidence of SCI. PROCEDURES: Medical records of dogs with SCI were retrospectively reviewed and the signalment, history, clinical signs, antemortem clinicopathologic test results, diagnostic imaging findings, case outcomes, and pathologic findings recorded. RESULTS: All dogs had an acute onset of nonprogressive homonymous visual field deficits and contralateral general proprioceptive (GP) deficits. Contralateral hemiparesis and facial hypalgesia were noted in 5/6 dogs. CT scans were normal in 2/4 dogs, and revealed poorly defined hypoattenuating lesions in the subcortical white matter in two dogs. MRI exams were performed in 5/6 dogs and revealed unilateral, variably sized, striatocapsular lesions consistent with nonhemorrhagic infarctions. Diagnostic imaging (6/6) and postmortem examinations (2/6) suggested that SCI resulted from lesions in the vascular territories of the rostral choriodal (6/6) and lenticulostriate arteries (2/6). Diseases predisposing to infarction were not identified in 5/6 dogs. Improvements in mentation, behavior, proprioceptive deficits, and hemiparesis were seen in surviving dogs, but persistent, symptomatic sensory deficits were noted during the follow-up period. CONCLUSIONS: SCI should be considered as a differential diagnosis for dogs with acute onset, nonprogressive homonymous hemianopia, contralateral GP deficits or hemiparesis, and facial hypalgesia. MRI is the preferred modality for the antemortem imaging diagnosis of SCI. Although partial recovery occurred in all surviving dogs, visual and facial sensory disturbances persisted.     

The Effect of Acute, Unilateral Transverse Venous Sinus Occlusion on Intracranial Pressure in Normal Dogs

Lateral rostrotentorial and caudal suboccipital approaches to the brain were performed on six beagles. Intracranial pressure (ICP) was measured as the two craniectomies were connected by removing the bone of the nuchal crest and occluding the transverse venous sinus. Intracranial pressure remained constant after acute occlusion of the sinus with bone wax and there was no gross evidence of brain edema. All six dogs survived the surgery and five dogs survived for a minimum of 3 months. One dog died acutely during the postoperative period. The exact cause of the cerebellar hemorrhage and infarction found at necropsy in the latter dog was not evident. Anemia occurred in three of the six dogs as a result of intraoperative hemorrhage. All dogs surviving the perioperative period had mild, transient hypermetria and conscious proprioceptive deficits, but were neurologically normal 72 hours after surgery. Results of this study indicate that acute, unilateral transverse sinus occlusion is possible without an increase in ICP. The ability to do this allows access to the rostral aspect of the ipsilateral cerebellum and brain stem.     

Five cases of canine dysautonomia in England (2004 to 2006)

Canine dysautonomia was diagnosed definitively in five dogs by histopathology. All dogs were seen between June 2004 and July 2006 and originated from south-east England; four dogs originated from an urban area and one from a rural area. Of the urban dogs, one had recently visited Scotland and one had visited a kennel in a rural area nearby. Acute-onset but progressive vomiting, diarrhoea, depression and inappetence were the most common presenting clinical signs. Reduced or absent anal tone, dysuria, absence of pupillary light reflexes with intact vision, mydriasis, decreased corneal sensitivity and nictitating membrane protrusion were among the most frequent neurological findings. Abnormalities in pharmacological autonomic and physiological function testing (including orthostatic hypotension in two dogs) and diagnostic imaging studies were detected in some of the animals. All dogs failed to respond adequately to treatment, and given the poor prognosis, they were eventually euthanased. Histopathology identified marked chromatolysis of ganglion cell bodies. This case series emphasises that dysautonomia should be considered when a dog is presented in the UK with acute- or subacute-onset gastrointestinal signs and compatible physical and neurological abnormalities.     

Idiopathic detrusor-urethral dyssynergia in dogs: a retrospective analysis of 22 cases

Results of a retrospective study of 22 dogs with signs of dysuria and/or stranguria in which a diagnosis of idiopathic detrusorurethral dyssynergia was made are presented. The diagnosis was based on the exclusion of detectable pathological conditions which could also cause urine outflow obstruction. The affected cases were 22 middle-aged male dogs (mean age 4·9 years) of large and giant breeds (mean bodyweight 36·7 kg). Nine dogs had had periodic clinical signs for longer than one year, one for seven months and eight for two to five weeks, while in four dogs signs had begun four to five days before referral. All dogs received the α-sympatholytic agent prazosin as an initial treatment and in 11 it remained the only therapy. There was a good effect in seven and a moderate response in the other four dogs. In one dog, prazosin was ineffective and was replaced by diazepam, which markedly reduced the signs. Three other dogs required frequent catheterisation and antibiotics were administered. These dogs responded favourably. Another three dogs with evidence of impaired bladder contractility were also treated with the parasympathomimetic agent carbachol. One did not improve and was euthanased. Four dogs developed bladder paralysis and severe infectious cystitis. Only one of these could be managed satisfactorily by long-term administration of prazosin, carbachol and antibiotics, and the others had to be euthanased.     

Porencephaly and hydranencephaly in six dogs

A retrospective study was performed to identify dogs with cerebrospinal fluid-filled cavitatory lesions on MRI. Six dogs were included and the lesions were classified. In the three dogs in the present study with hydranencephaly, unilateral but complete loss of the temporal and parietal lobes was noted and had almost complete loss of the occipital and frontal lobes of a cerebral hemisphere. In the three dogs with porencephaly, there was unilateral incomplete loss of the parietal lobe and one dog had additional partial loss of the temporal and frontal lobes. Two of the dogs with porencephaly had seizures; the third showed no associated clinical signs. The dogs with hydranencephaly had mentation changes and circled compulsively. The two porencephalic dogs with seizures were treated with phenobarbitone. One of the dogs with hydranencephaly showed increased frequency and duration of circling; one dog's clinical signs did not progress and the third dog was euthanased due to increasing aggression. The dog with increased circling had ventriculoperitoneal shunt placement and the circling frequency reduced.     

Cerebral Computed Tomography Scan Demonstrating Ischemic Stroke in a Filly After Intravenous Antibiotic Administration

Performing a brain computerized tomography scan (CT scan) on a foal requires specific equipment and anesthesia for large animals. However, the information obtained may demonstrate lesions responsible for the neurological deficits. Especially, CT scan findings may help to understand a mechanism of cerebral ischemia. Indeed, categories of cerebral ischemia are divided in three types: territorial infarctions (downstream of the territory of an artery), watershed infarctions (slow-flow at the junction of two arterial territories), and lacunar infarctions (small-vessel occlusions). Hypersensitivity reactions and type I anaphylactic IgE antibody reactions are severe potential adverse effects of sulfonamide administration, which occur in about three percent of cases. In horses, anaphylaxis is often clinically expressed as hypotension and collapse. Cardiovascular collapse may lead to multiorgan slow-flow leading to infarction with multiorgan failure and death. We report the case of a filly that suffered a presumed watershed cerebral infarction after antibiotic injection, indicated on a brain CT scan. This was attributed to a cerebral slow-flow during cardiovascular collapse, at the posterior junction of the right cerebral arteries. No abnormalities were initially identified on the CT scan; however, a review of the imaging by a radiologist specialized in cerebrovascular diseases detected a limited right occipital cortico-subcortical lesion in the visual cortex, interpreted as an ischemic scar in the watershed area related to hemodynamic infarction. This case highlights that detection of brain lesions by CT scan might require specialized knowledge and careful reading for interpretation particularly in the case of limited lesions.     

Neurological manifestations in dogs naturally infected by Leishmania infantum: descriptions of 10 cases and a review of the literature

In order to evaluate possible nervous system involvement in canine leishmaniasis, retrospective evaluation of all medical records of leishmaniotic dogs exhibiting neurological signs referred to our hospital over a 5‐year period was performed. The records of 10 dogs were reviewed. Depending on the neuroanatomical localisation, the dogs underwent advanced diagnostic imaging, cerebrospinal fluid analysis, electrodiagnostic testing and histopathologic evaluations. The final neurological diagnosis was: meningoencephalitis (n=2), brain haemorrhagic stroke (n=1), haemorrhagic choroiditis (n=1), meningomyelitis (n=2), ischaemic myelopathy (n=1), polymyositis (n=2) and peripheral neuropathy (n=1). This study confirms that both central and peripheral nervous systems can be affected by leishmaniasis and provides an overview on the possible etiopathogenetic mechanisms. In addition, clinical and diagnostic findings, therapy and follow‐up of affected dogs are described.     

Cellophane banding of congenital intrahepatic portosystemic shunts in two Irish wolfhounds

Two three-month-old, male Irish wolfhound siblings were diagnosed with breed-typical left divisional congenital intrahepatic portosystemic shunts consistent with patent ductus venosus. The shunts were amenable to surgical dissection at a posthepatic location. Both dogs had cellophane banding for shunt attenuation. One dog was euthanased after developing post-ligation neurological dysfunction, which was refractory to treatment. The other dog survived and demonstrated shunt attenuation. Successful surgical management using cellophane banding of a patent ductus venosus has not been previously described in a large-breed dog.     

Femoral medullary infarction secondary to canine total hip arthroplasty

OBJECTIVE: To evaluate the prevalence of femoral intramedullary infarction after total hip arthroplasty (THA) and to determine whether any specific femoral morphology predisposes to bone infarction. STUDY DESIGN: Retrospective clinical study. SAMPLE POPULATION: All dogs from our hospital population undergoing THA between 1984 and 1997 with radiographic follow-up available at 1 year or more postoperatively. METHODS: A case control study was conducted within the THA group to determine risk factors predisposing to femoral infarction after THA. Medical records and radiographs were reviewed. Data were collected on clinical parameters, femoral morphology, prosthesis, and bone changes. Radiographic diagnosis was confirmed using histopathology in 11 femora. Radiographs of 50 age-matched control dogs weighing more than 20 kg with coxofemoral degenerative joint disease were randomly chosen to determine the prevalence of bone infarction in nonoperated dogs. RESULTS: Ninety-one dogs with 110 THA were included in the study. Fifteen of the 110 femora with THA had radiographic evidence of infarction (14%). Infarction was not present in any femora in the control group. There was no significant difference in the prevalence of infarction between dogs that received cemented or uncemented prostheses. Clinical signs were not reported in any patient that developed femoral infarction. Young age (P = .03) and a distance between the greater trochanter and nutrient foramen greater than 79 mm (P = .008) predisposed dogs to femoral infarction. Over time, three infarcts decreased in size radiographically, five remained unchanged, and three expanded. An osteosarcoma developed at the site of a bone infarct in one dog. CONCLUSION: Femoral intramedullary infarction occurred in 15 of 110 THA. Young age at the time of THA and a greater distance between the greater trochanter and the nutrient foramen predisposed to infarction. CLINICAL RELEVANCE: Intramedullary infarction occurs after canine THA. These bone infarcts do not appear to cause clinical signs; however, they may present a diagnostic challenge. Malignant transformation could potentially result from medullary infarction.     

Fibrocartilaginous embolism in the dog

Eighteen dogs with acute neurological symptoms suggestive of ischaemic myelopathy are described. A presumptive diagnosis of spinal parenchymal infarction, due to fibrocartilaginous embolism (FCE), was made in 16 cases. This was confirmed by histological examination post mortem in the remainder. Clinical neurological parameters were the most reliable prognostic indicators following FCE. High dose corticosteroid therapy should be administered as soon as possible to influence the secondary pathophysiological reaction in such cases. Only one dog made a complete neurological recovery, however nine returned to normal activity with-out regaining normal neurological function. Eight dogs required euthanasia.