Conventional and functional magnetic resonance imaging features of late subacute cortical laminar necrosis in a dog

Cerebral cortical laminar necrosis (CLN) is a consequence of severe hypoxic, ischemic, or hypoglycemic events. In humans, these cortical lesions show characteristic linear T1‐weighted (T1W) hyperintensity in the late subacute stage. Limited information reporting magnetic resonance imaging (MRI) findings in dogs affected by CLN is available. A 3‐year‐old Belgian Shepherd dog was referred 8 days after sudden onset of blindness after general anesthesia. Neurological examination showed central blindness and mild ataxia. Three‐Tesla MRI examination of the brain revealed bilateral asymmetrical areas of T2‐weighted hyperintensity within the occipital, parietal, temporal, and frontal cortex, involving gray and white matter. Furthermore, linear T1W‐hyperintense lesions were found in the cerebral cortex of the same areas and showed heterogeneous contrast enhancement. Perfusion‐weighted images revealed hyperperfusion in the affected regions. Lesions were compatible with subacute CLN with corresponding edema suspected to be secondary to anesthesia‐related brain hypoxia. Three‐Tesla MRI enabled identification of the laminar pattern of the cortical lesions.     

IMAGING DIAGNOSIS—TRANSCRANIAL COLOR‐CODED DUPLEX SONOGRAPHY IN A DOG WITH HEPATIC ENCEPHALOPATHY

We report the use of transcranial Doppler ultrasonography in a dog with hepatic encephalopathy secondary to a congenital portosystemic shunt. A severe increase in the pulsatility index was measured in the right middle cerebral artery, left middle cerebral artery, and basilar artery. These values returned to normal following medical stabilization of the patient and resolution of the neurologic signs. Transcranial Doppler ultrasonography appears to have value for monitoring the status of intracranial hypertension in patients with hepatic encephalopathy.     

Sequential magnetic resonance imaging changes after suspected global brain ischaemia in a dog

Sequential magnetic resonance imaging studies over a period of 18 months were performed in a two-year-old pug dog after suspected global brain ischaemia following an anaesthetic accident. The dog was presented with seizures and neurological deficits consistent with a left brainstem and multifocal/diffuse forebrain lesion after an asymptomatic interval of 72 hours following the ischaemic event. Magnetic resonance imaging scans were performed three hours, six weeks, seven and 18 months after the incident. In the acute stage, signal hyperintensity was evident in the occipital and parietal regions of the cerebral cortex and in both rostral caudate nuclei. Slight involvement of the white matter was also noticed. In the chronic phase, the signal hyperintensity in the affected areas of the cortex was diminished and smaller in size, whereas the white matter did not appear to be compromised anymore.     

Magnetic resonance imaging findings of hepatic encephalopathy in a dog with a portosystemic shunt

A 6-year-old ShihTzu presented with tonic-clonic cluster seizure. T2-weighted magnetic resonance (MR) images showed bilateral diffuse hyperintense lesions at the cerebral cortex with enlarged sulci. Computed tomography revealed a portosystemic shunt (PSS) and azygos continuation. Based on the clinical signs, blood examinations and diagnostic images, the dog was diagnosed with hepatic encephalopathy secondary to PSS. The neurologic signs were gradually improved after medical therapy for hyperammonemia. This is the first report of hyperintensity of the cerebral cortex on T2-weighted MR images associated with acute hepatic encephalopathy in a dog.     

Systematization, distribution and territory of the middle cerebral artery on the brain surface in chinchilla (Chinchilla lanigera)

The aim of the present study was to analyse thirty chinchilla ( Chinchilla lanigera ) brains, injected with latex, and to systematize and describe the distribution and the vascularization territories of the middle cerebral artery. This long vessel, after it has originated from the terminal branch of the basilar artery, formed the following collateral branches: rostral, caudal and striated (perforating) central branches. After crossing the lateral rhinal sulcus, the middle cerebral artery emitted a sequence of rostral and caudal convex hemispheric cortical collateral branches on the convex surface of the cerebral hemisphere to the frontal, parietal, temporal and occipital lobes. Among the rostral convex hemispheric branches, a trunk was observed, which reached the frontal and parietal lobes and, in a few cases, the occipital lobe. The vascular territory of the chinchilla's middle cerebral artery included, in the cerebral hemisphere basis, the lateral cerebral fossa, the caudal third of the olfactory trigone, the rostral two-thirds of the piriform lobe, the lateral olfactory tract, and most of the convex surface of the cerebral hemisphere, except for a strip between the cerebral longitudinal fissure and the vallecula, which extended from the rostral to the caudal poles bordering the cerebral transverse fissure.     

Successive torsion of the right middle and left cranial lung lobes in a dog

This case report describes the torsion of two lung lobes in a dog. The animal was first presented for a torsion of the right middle lung lobe. Following the surgical resection of that lobe, the dog suffered another torsion of the left cranial lung lobe (cranial and caudal segments).     

MAGNETIC RESONANCE IMAGING OF CEREBRAL CORTICAL NECROSIS (POLIOENCEPHALOMALACIA) IN A DOG

A 3-year-old neutered female mixed breed dog was examined because of severe, generalized seizure activity, tetraparesis, and encephalopathic signs. Cerebrospinal fluid (CSF) evaluation was unremarkable except for a mild increase in protein. Serum and CSF titers for infectious diseases were negative. Magnetic resonance (MR) imaging examination of the brain was performed and lesions were found within the cerebral gray matter of the temporal and parietal lobes. The lesions had increased signal intensity on T1, T2, and proton density-weighted images. There was mild inhomogeneous enhancement following intravenous contrast medium administration. Neurologic status improved and the seizures were well controlled, but the dog never regained normal mentation and euthanasia was performed 10 weeks after initial evaluation. At necropsy, severe cerebral cortical necrosis was found in the regions corresponding to the lesions seen on MR imaging examination. Large numbers of fat-containing macrophages (gitter cells) were found within these areas, and are thought to be responsible for the characteristic hyperintensity seen on the MR images.     

CONTRAST‐ENHANCED PORTAL MAGNETIC RESONANCE ANGIOGRAPHY IN DOGS WITH SUSPECTED CONGENITAL PORTAL VASCULAR ANOMALIES

Contrast‐enhanced multiphase magnetic resonance angiography (CE‐MRA) was used in 17 dogs with a suspected congenital portal vascular anomaly. Portal vascular anomalies were identified in 16 of the 17 dogs. Eleven had a single intrahepatic portocaval shunt (two central divisional, three right divisional, and six left divisional), one dog had a double intrahepatic portocaval shunt, one dog had a hepatic arteriovenous malformation, one dog had a complex intrahepatic porto‐caval shunt. Two dogs had an extrahepatic portosystemic shunt and no shunt was identified in one dog. Total imaging time was <10 min and image quality was good to excellent in all dogs. Portal CE‐MRA is a feasible, fast and non invasive technique to diagnose portal vascular anomalies in dogs, with a large field‐of‐view and good anatomic depiction of the abnormal vessels. Based on these results, CE‐MRA is an efficient imaging technique for the diagnosis of portal vascular anomalies in dogs.     

REVERSIBLE MAGNETIC RESONANCE IMAGING ABNORMALITIES IN DOGS FOLLOWING SEIZURES

Reversible magnetic resonance (MR) imaging lesions have been described in humans following seizures. This condition has not yet been reported in animals. This paper describes reversible abnormalities identified in 3 dogs using MR imaging that was performed initially within 14 days of the last seizure and follow-up imaging that was performed after 10 to 16 weeks of anticonvulsant therapy. All three dogs had lesions in the piriform/temporal lobes, characterized by varying degrees of hyperintensity on T2-weighted images and hypointensity on T1-weighted images. In one dog, contrast enhancement was evident. On reevaluation, partial resolution occurred in all 3 dogs. In a fourth animal with an olfactory meningioma, similar appearing lesions in the temporal cortex and right and left piriform lobes were identified after seizure activity. A surgical biopsy of the temporal cortex and hippocampus was performed and edema, neovascularization, reactive astrocytosis, and acute neuronal necrosis were evident. These histologic findings are similar to those reported in humans with seizures. Recognizing the potential occurrence of reversible abnormalities in MR images is important in developing a diagnostic and therapeutic plan in canine patients with seizures. Repeat imaging after seizure control may help differentiate between seizure-induced changes and primary multifocal parenchymal abnormalities.     

Use of computed tomography and minimum intensity projection in the detection of lobar pneumonia mimicking lung lobe torsion in a dog

A 10‐year‐old female spayed Dachshund was referred with progressive coughing for 1 month. The dog was tentatively diagnosed with right middle lung torsion based on pleural effusion, vesicular emphysema, abruptly ending bronchus in consolidated right middle lung, and no contrast enhancement of the affected lobe on radiography and computed tomography (CT). There was no evidence of torsion upon thoracotomy, and histological examination confirmed lobar pneumonia. The CT images were reevaluated using minimum intensity projection and revealed normal bronchial courses. The minimum intensity projection technique can be to assist in evaluation of the bronchial tree for dogs with suspected lung lobe torsion and other pulmonary diseases.     

Ischaemic encephalopathy and focal granulomatous meningoencephalitis in the cat

Three cats were presented with neurological deficits compatible with cerebral disease. Two of the cats had temporal lobe infarction diagnosed as ischaemic encephalopathy; one cat had granulomatous inflammation, diagnosed as focal granulomatous meningoencephalitis. In all three cases the lesions were characterized by necrotic, cavitated areas. Vascular insult was the cause of the ischaemic encephalopathy and the focal granulomatous meningoencephalitis may have been caused by feline infectious peritonitis (FIP) virus. An infectious aetiology, possibly FIP virus, is proposed for the ischaemic encephalopathy. A relationship between these two neurological diseases may exist.     

DIFFUSION‐WEIGHTED MAGNETIC RESONANCE IMAGING OF THE NORMAL CANINE BRAIN

Diffusion‐weighted imaging (DWI) MRI has been primarily reported as a method for diagnosing cerebrovascular disease in veterinary patients. In humans, clinical applications for diffusion‐weighted MRI have also included epilepsy, Alzheimer's, and Creutzfeld–Jakob disease. Before these applications can be developed in veterinary patients, more data on brain diffusion characteristics are needed. Therefore, the aim of this study was to evaluate the distribution of diffusion in the normal canine brain. Magnetic resonance imaging of the brain was performed in ten, clinically normal, purpose‐bred beagle dogs. On apparent diffusion coefficient maps, regions of interest were drawn around the caudate nucleus, thalamus, piriform lobe, hippocampus, semioval center, and cerebral cortex. Statistically significant differences in mean apparent diffusion coefficient were found for the internal capsule, hippocampus, and thalamus. The highest apparent diffusion coefficient (1044.29 ± 165.21 μm²/s (mean ± SD (standard deviation)) was detected in the hippocampus. The lowest apparent diffusion coefficient was measured in the semioval center (721.39 ± 126.28 μm²/s (mean ± SD)). Significant differences in mean apparent diffusion coefficients of the caudate nucleus, thalamus, and piriform lobe were found by comparing right and left sides. Differences between brain regions may occur due to differences in myelination, neural density, or fiber orientation. The reason for the differences between right and left sides remains unclear. Data from the current study provide background for further studies of diffusion changes in dogs with brain disease.     

EFFECT OF DEPENDENCY VERSUS NONDEPENDENCY ON LUNG LESION VISUALIZATION

Paraffin blocks and mineral oil were used as a model to determine the effect of dependency versus nondependency on radiographic visualization of lung lesions in lateral thoracic radiographs. It was concluded that the increased opacity of the material surrounding the lesion, not contact between the heart and the lesion, was responsible for the inability to detect lung disease in the dependent lung. The results were tested in dogs with pneumonia in the right middle lung lobe. When the dog was in right lateral recumbency, the dependent right lung was increased in opacity and decreased in volume and the pulmonary lesion was difficult to detect. When the dog was in left lateral recumbency, the nondependent right lung was increased in volume and decreased in opacity and the pulmonary disease was clearly visible. A single recumbent lateral radiograph must not be used to assess a dog with suspected lung disease because lesions in the dependent lung lobes may not be detected.     

CONTRAST‐ENHANCED MAGNETIC RESONANCE ANGIOGRAPHY FOR DIAGNOSIS OF PORTOSYSTEMIC SHUNTS IN 10 DOGS

Computed tomography angiography, sonography, scintigraphy, and portography can be used to evaluate the portal vasculature to evaluate for a portosystemic shunt (PSS). Time‐of‐flight magnetic resonance angiography (TOF‐MRA) and contrast‐enhanced MRA (CE‐MRA) are other potentially useful techniques. The aim of this study was to evaluate CE‐MRA in 10 dogs suspected of having a PSS. Noncontrast MR images of the abdomen were obtained using a Siemens Symphony MR‐scanner (1.5 T) and a T1‐weighted FLASH‐3D sequence with a very short scan time (about 20 s). After injection of contrast medium, the initial sequence was repeated five times. The sequence with the best contrast medium filling of the portal vasculature was selected subjectively, subtracted from the initial survey image series, and a maximum intensity projection (MIP) of the subtraction data, in multiple views, was created. The cross‐sectional and MIP images were evaluated for abnormal portosystemic vasculature. A single PSS was identified and confirmed at surgery in all dogs. A portocaval shunt was found in five dogs, a portophrenic shunt in three dogs, a portoazygos shunt in one, and a central divisional intrahepatic shunt in one other dog. Based on our results, CE‐MRA is a useful tool for imaging abdominal and portal vasculature and for the diagnosis of a PSS.     

Systematization and distribution of the middle cerebral artery on the brain surface in pampas fox (Pseudalopex gymnocercus)

The present study has analysed 30 pampas fox brains (Pseudalopex gymnocercus), injected with latex, aiming to systematize and describe the distribution and vascularization territories of the middle cerebral artery. After being originated from the rostral branch of the internal carotid artery this vessel formed the following collateral branches: rostral choroidal artery, rostral and caudal central branches and cortical branches. Before crossing the lateral rhinal sulcus, the common trunk of the middle cerebral artery frequently bifurcated in a rostral and a caudal branch. In a smaller amount, the common trunk did not show any bifurcation, ramifying in arborescence. The vascular territory of the pampas fox middle cerebral artery included the lateral cerebral fossa, the lateral third of the olfactory trigone, the two rostral thirds of the piriform lobe, the lateral olfactory tract and most of the convex surface of the cerebral hemisphere, except for the more rostromedial areas of the frontal lobe bordering the endomarginal sulcus in the parietal and occipital lobes as well as the transverse fissure at the caudal pole of the cerebral hemisphere.     

Brain and ocular metastases from a transmissible venereal tumour in a dog

A five-year-old crossbred dog was referred with rapidly growing masses over its penis and right popliteal lymph node. The dog had severe blepharospasm, congestion of episcleral vessels and rubeosis iridis of the left eye. A presumptive diagnosis of transmissible venereal tumour (TVT) and iridocyclitis was made based on the results of fine needle aspiration. Chemotherapy with vincristine and prednisolone was initiated and after four months the dog made a complete recovery. However, the dog subsequently relapsed, showing miosis, blepharospasm and a well defined mass within the anterior chamber of the left eye. In addition, the dog exhibited generalised 'grand mal' type seizures. Computed tomographic (CT) examination of the brain revealed two distinct masses in the left frontal lobe. Because of the poor prognosis, the owners elected to have the dog euthanased. On histopathology, metastases of TVT in the left eye and left cerebral hemisphere were found, showing no specific staining for CD3, immunoglobulin (Ig) G, IgM and lambda light chains. It was therefore concluded that the tumour growth was progressive, and that there was an absence of local humoral immune response against TVT in this case.     

Medial insertion of the patent ductus arteriosus characterized by computed tomography angiography in a cat and dog

Surgical ligation of a left-to-right shunting patent ductus arteriosus was attempted in two animals. In both cases, a young cat and dog, ligation was complicated by poor visualization of the ductus resulting in unsuccessful ligation. Post-operatively, both the cat and dog underwent computed tomography angiography to characterize the location and morphology of the patent ductus arteriosus. In both cases, computed tomography angiography revealed a left-to-right shunting patent ductus arteriosus with an insertion location medial to the left pulmonary artery branch compared to the typical location. We hypothesize that this atypical location resulted in a difficult surgical visualization from the left thoracotomy approach. Transvenous coil embolization of the duct from the external jugular vein was performed in both cases and resulted in successful occlusion. Variations in the medial-lateral insertion of the ductus arteriosus may have consequences for surgical intervention. If an atypical location of a patent ductus arteriosus is suspected on transthoracic echocardiography, computed tomography angiography prior to ligation may be useful to further define ductal location and help guide the surgical approach.     

Diagnosis and treatment of a cerebral infarct in a chimpanzee (Pan troglodytes).

A 29-yr-old chimpanzee (Pan troglodytes) presented after an acute onset of right facial and forearm paresis that progressed to paralysis within 24 hr, with subsequent development of right leg paresis. Magnetic resonance imaging (MRI) of the head revealed an abnormal region of increased signal intensity in the left frontal, parietal, and temporal cerebral hemispheres, corresponding to the vascular territory of the middle cerebral artery, with resultant compression of the left lateral ventricle. The findings were consistent with a cerebral infarct (stroke). MRI is the most sensitive test for early detection of cerebral changes due to ischemia and was essential in obtaining a diagnosis in this case. The chimpanzee responded well to treatment with long-term anticoagulant aspirin and a short, tapered course of prednisone and regained full gross motor function.     

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.     

Ataxia and weakness as uncommon primary manifestations of hepatic encephalopathy in a 15‐year‐old trotter gelding

A 15‐year‐old trotter gelding was evaluated because of an acute onset of ataxia in all 4 limbs. There was no known history of trauma. The gelding showed grade 2/5 ataxia in all 4 limbs, which was localised after clinical neurological examination to the cervical vertebral spinal cord. Initial therapy consisted of oral anti‐inflammatory doses of prednisolone and antimicrobial treatment with potentiated sulphonamides. The ataxia progressed to grade 3/5 at Day 10 of hospitalisation. Additionally, the horse was slightly depressed and showed spontaneous yawning during examination. Facial sensation was blunted. Blood chemistry revealed a marked elevation of liver specific enzymes and blood ammonia levels. Transcutaneous abdominal ultrasonography revealed hepatomegaly. Due to a guarded prognosis, the horse was subjected to euthanasia. At necropsy the left lateral liver lobe was markedly enlarged and showed a firm texture, whereas the cranial part and the right and quadratic liver lobe displayed a severe and diffuse atrophy. Histopathologically, the left lateral liver lobe revealed a moderate to severe cirrhosis with a severe, diffuse hepatocellular iron‐accumulation. Increased numbers of Alzheimer type II astrocytes in the cerebral cortex and cerebral white matter vacuolisation were indicative for encephalopathy. These findings were interpreted as haemosiderosis and cirrhosis of the liver with consecutive hepatic encephalopathy. Aetiologically, haemosiderosis should be considered as a cause of liver cirrhosis with consecutive hepatic encephalopathy. Although hepatic encephalopathy in horses usually presents with predominating cerebral signs, it has to be taken into account as a differential diagnosis in cases of acute onset generalised ataxia.