Lesions in the brains of three cattle resembling the lesions of enterotoxaemia in lambs

CASE HISTORY: A 3-month-old female Angus calf was found dead, and two adult Friesian dairy cows died soon after developing nervous signs. PATHOLOGICAL FINDINGS: Grossly, bilateral and mostly symmetrical areas of haemorrhage were evident that mainly involved areas of grey matter in the brainstem from the level of the caudal colliculi to the thalamus and, in one, the internal capsule and caudate nucleus. In the occipital and caudal parietal cortex, there was extensive oedema of white matter. Histologically, in addition to haemorrhage, there was protein-rich oedema around arterioles and venules in the cerebrum, hippocampus, internal capsule, thalamus, midbrain, dorsal medulla, and central cerebellar and cerebellar folial white matter. The calf 's brain had bilateral and symmetrical oedema and necrosis affecting several brainstem nuclei and the occipital grey matter overlying areas of oedema of the corona radiata. DIAGNOSIS: Although the cause was not established, the perivascular lesions resembled those produced in calves by the intravenous administration of epsilon toxin. CLINICAL RELEVANCE: It is possible that epsilon toxin-induced enterotoxaemia occurs naturally in cattle, and where bilateral haemorrhage is recognised in the brains of cattle, small intestinal contents should be collected for analysis of epsilon toxin.     

Hypertensive encephalopathy in cats with reduced renal function

The clinical, hemodynamic, and pathologic features of hypertensive encephalopathy in two cats with reduced renal mass are described. The cats developed a progressive syndrome of lethargy, ataxia, blindness, stupor, and seizures following an abrupt increase in blood pressure associated with a surgical reduction in renal mass. The cats had severe gross brain edema, evidenced by cerebellar changes of caudal coning and cranial displacement over the corpora quadrigemina and cerebral changes of widening and flattening of the gyri. Histologically, interstitial edema was most pronounced in the cerebral white matter. Hypertensive vascular lesions were present as hyaline arteriolosclerosis in one cat and hyperplastic arteriolosclerosis in the other. Rare foci of parenchymal microhemorrhages and necrosis were also observed. Systemic hypertension (especially severe or rapidly developing) accompanied by neurologic signs and the pathologic findings of diffuse brain edema with cerebral arteriolosclerosis are consistent with an etiologic diagnosis of hypertensive encephalopathy.     

Lesions in the brains of three cattle resembling the lesions of enterotoxaemia in lambs

CASE HISTORY: A 3-month-old female Angus calf was found dead, and two adult Friesian dairy cows died soon after developing nervous signs.

PATHOLOGICAL FINDINGS: Grossly, bilateral and mostly symmetrical areas of haemorrhage were evident that mainly involved areas of grey matter in the brainstem from the level of the caudal colliculi to the thalamus and, in one, the internal capsule and caudate nucleus. In the occipital and caudal parietal cortex, there was extensive oedema of white matter. Histologically, in addition to haemorrhage, there was protein-rich oedema around arterioles and venules in the cerebrum, hippocampus, internal capsule, thalamus, midbrain, dorsal medulla, and central cerebellar and cerebellar folial white matter. The calf's brain had bilateral and symmetrical oedema and necrosis affecting several brainstem nuclei and the occipital grey matter overlying areas of oedema of the corona radiata.

DIAGNOSIS: Although the cause was not established, the perivascular lesions resembled those produced in calves by the intravenous administration of epsilon toxin.

CLINICAL RELEVANCE: It is possible that epsilon toxin-induced enterotoxaemia occurs naturally in cattle, and where bilateral haemorrhage is recognised in the brains of cattle, small intestinal contents should be collected for analysis of epsilon toxin.     

Spongiform neurodegenerative disease in a Persian kitten

A congenital encephalopathy with spongiform degeneration and prominent neuronal apoptosis was observed in a 4-month-old Persian male cat with a history of depressed mental status and ataxia. On clinical examination, signs included right head tilt, ventroflexion of the head and neck, and tetraparesis. Histological examination of the central nervous system revealed multifocal, bilateral and symmetrical vacuolar degeneration of the neuropil, mainly involving the cerebellar and vestibular nuclei area, the caudal colliculi, the mesencephalic nuclei, the tegmental area and the deeper layer of the cerebral cortex. Accumulation of phosphorylated neurofilaments was detected in neuronal perikarya of the deep cortical layers, hippocampus and thalamus. Numerous pyknotic and apoptotic neurons were also observed in the cerebral cortex. These neuropathological changes differ from those observed in previous reports of spongiform degeneration of the grey matter in cats and were suggestive of a congenital neurodegenerative disease.     

Canine granulomatous meningoencephalomyelitis.

In 27 adult dogs with a distinctive chronic granulomatous meningoencephalomyelitis there were locomotor problems, cervical meningitis and blindness. Lesions were widespread, but most severe in cerebral and cerebellar white substance and in the cervical spinal cord. Lesions were characterized by the development of epithelioid cell granulomas arising from mononuclear cuffs. There were secondary edema and necrosis in severe cases and eventual fibroplastic repair in chronic cases. The cause is unknown.     

Pathology of sarcocystis neurona in interferon-gamma gene knockout mice

Pathologic changes were studied in 27 interferon-gamma gene knockout mice 34-54 days after being fed graded doses of Sarcocystis neurona sporocysts derived from a naturally infected opossum. The target tissue for S. neurona infection was the central nervous system. Characteristic histopathologic changes present in all mice consisted of an inflammatory infiltrate consisting of mostly neutrophils and macrophages, fewer eosinophils, and rare multinucleated giant cells. Intralesional protozoa and scattered subacute perivascular cuffs were present. Where the infiltrates were extensive, neuropil rarefaction was frequent. Pathologic changes were much more frequent and severe in the caudal portion of the brain, especially in the cerebellum, than in the middle and cranial portions. Changes were present in all spinal cords examined (10 of 10). Lesions were equally distributed in white and gray matter of the brain and spinal cord and their meningeal linings.     

Lesions in the central nervous system associated with perinatal lamb mortality

OBJECTIVE: To identify and describe the occurrence of neurological lesions that could have an effect on lamb mortality. PROCEDURE: The central nervous system was investigated macroscopically (n = 92) and microscopically (n = 72) in lambs dying in the perinatal period during 3 years in flocks of adult Corriedale ewes. The central nervous system was removed intact and samples of cerebral cortex, basal ganglia, thalamus, hippocampus, mesencephalon, cerebellar cortex, medulla oblongata, and cervical spinal cord were scored microscopically for the severity of neuronal dead, cytotoxic and perivascular oedema, and haemorrhage. RESULTS: Neurologic findings between birth and 6 days included haemorrhages in meninges, brain congestion and oedema, neuronal ischemic necrosis, intraparenchymal haemorrhages in medulla oblongata and cervical spinal cord, parasagittal cerebral necrosis, and periventricular leukomalacia. No significant lesions were found in anteparturient deaths or in those aged between 7 and 16 days. Oedema was more severe in the brain than in other regions of the central nervous system. Ischaemic neurons first appeared 24 hours post partum, increased linearly in number between 48 hours and 5 days post partum, and had a laminar distribution in the cerebral cortex, indicating a hypoxic-ischemic encephalopathy. Haemorrhages were most severe in the gray matter of medulla oblongata and cervical spinal cord, suggesting trauma due to instability of atlantoaxialis joint. CONCLUSION: Lesions in the central nervous system can explain most deaths at birth and within 6 days of birth. The lesions were hypoxic-ischemic and appeared to be related to birth injury.     

Severe involvement of cerebral neopallidum in a dog with hepatic encephalopathy

This report describes a unique distribution of cerebral cortical necrotic lesion, which was diagnosed as hepatic encephalopathy in a 2-year-old Maltese dog. The dog showed splenocaval shunt and small liver with marked hepatocellular fatty degeneration. Histopathologic examination revealed that diffuse laminar cortical necrosis composed of neuronal necrosis, marked infiltration of gitter macrophages, and astrogliosis were found bilaterally in the dorsolateral area of the cerebrum. No necrotic lesions were observed in the cerebral paleopallium and archipallium, the central gray matter, cerebellum, and brain stem. Astrocytes with large and pale nuclei (Alzheimer type II astrocytes) were apparent throughout the brain. Immunohistochemically, a decrease of immunostains for glutamine synthetase and glutamate transporter antibodies was seen in Alzheimer type II astrocytes and neuropil. This is, to our knowledge, the first report of extensive involvement of cerebral neopallidum in canine hepatic encephalopathy.     

Cerebellar vermian hypoplasia in dogs

Six dogs with cerebellar dysplasia, in which the cerebellar vermis was hypoplastic, are described. Clinical signs in these dogs were noted around 2 weeks of age and included ataxia, dysmetria, and intention tremors. A variable portion of the caudal cerebellar vermis was absent in each dog; portions of the cerebellar hemispheres and flocculus also were absent in some of them. Neurons in certain brain stem nuclei that project to the cerebellum were either chromatolytic or vacuolated. Cerebellar vermian hypoplasia of dogs is analogous to the Dandy-Walker syndrome of human beings.     

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.     

A systematic study of brain base arteries in the wild boar (Sus scrofa scrofa)

This study aimed at describing and systematizing the arteries of the base of the brain of the wild boar (Sus scrofa scrofa). Thirty-three heads were used, of which 30 were injected with latex, and three with acrylic dental resin through the common carotid arteries. The brain carotid artery arose from the rostral epidural rete mirabile, and divided into a rostral and a caudal branch. The rostral branch gave off the middle cerebral artery and then continued as rostral cerebral artery. The latter branched into lateral rhinal, internal ethmoidal and medial rhinal arteries. The rostral cerebral artery joined its contralateral homologue, becoming the single rostral inter-hemispheric artery. The caudal branch emitted the caudal cerebral artery and the tectal arteries, and then fused with the branch of the opposite antimere, joining the basilar artery. The rostral cerebellar arteries derived from this point. The basilar artery originated from the anastomosis between the arteries derived from the caudal epidural rete mirabile of each antimere. The basilar artery extended rostrally, giving off as main collateral branch the caudal cerebellar artery. The basilar artery presented a significant decrease in diameter before joining the caudal branches of the brain carotid arteries. The cerebral arterial circle was rostrally and caudally closed.     

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.     

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.     

FAMILIAL CEREBELLAR ATAXIA WITH HYDROCEPHALUS IN BULL MASTIFFS

Familial cerebellar ataxia with concurrent hydrocephalus has previously been described in a family of bull mastiff pups, and recently has been identified in a litter from Louisiana. The 4 affected pups had ataxia, hypermetria, conscious proprioceptive deficits, behavioral abnormalities, and a visual deficit. In magnetic resonance imaging of the brain of two of the pups, there were symmetric hydrocephalus and two focal areas of increased signal intensity within the central nuclei of the cerebellum. Histopathologically there was vacuolization and mild astrogliosis within the deep cerebellar nuclei (dentate, interpositus, fastigial), caudal colliculi, and lateral vestibular nuclei. Although the postmortem results were not exactly the same as in the previously published report, the clinical features and histopathologic findings strongly support the diagnosis. This disorder is most likely inherited in an autosomal recessive manner.     

PREPUBIC AND TRANSRECTAL ULTRASONOGRAPHY OF THE CANINE PROSTATE: A COMPARATIVE STUDY

A comparative study was conducted in ten dogs with signs of prostatic disease in order to evaluate the usefulness of the prepubic and transrectal ultrasonography for the examination of the prostate gland and for prostate biopsy guidance. Both techniques were adequate to identify the prostate gland and prostatic urethra. Transrectal ultrasound found 5 occurrencies of parenchymal echogenicity changes whereas the prepubic technique found only 2. Lesions in the cranial prostatic margin (two dogs) were detected only by prepubic ultrasound. Lesions of the caudal prostatic margin (six dogs), prostatic urethra disruption (two dogs) and prostatic capsule abnormalities (five dogs) were only recognized by the transrectal approach. Prepubic ultrasonography was useful for biopsy guidance of cranial prostatic lesions and transrectal ultrasonography was a good means for biopsy guidance of caudal lesions.     

Neuronal migration defect: a case of subcortical heterotopia in a California sea lion

A 2 and a half-year-old male California sea lion (Zalophus californianus) presented with a history of intermittent generalized seizures. Magnetic resonance imaging revealed a large focal mass occupying the right cerebral hemisphere with moderate dilatation of the contralateral lateral ventricle. At necropsy, the right cerebral hemispheric white matter was expanded by numerous irregularly shaped, pale pink nodules up to 10 mm in diameter. The overlying cortex was characterized by increased numbers of small, poorly developed gyri with shallow, often indistinct, sulci (polymicrogyria). Microscopically, nodules were composed of neurons, oligodendroglia, microglia, and supporting neuropil and were well delineated from the surrounding white matter. The gross, histological, and immunohistochemical features of this lesion are consistent with a neuronal migration defect resulting in unilateral subcortical heterotopia.     

Brain Stem Auditory-Evoked Response Abnormalities in 14 Dogs With Confirmed Central Nervous System Lesions

Abnormal brain stem auditory-evoked responses (BAER) were recorded on 14 dogs with brain lesions confirmed by necropsy (n = 13) or magnetic resonance imaging and surgical biopsy (n = 1). Lesions included brain stem or cerebellar tumors (6 dogs), brain stem trauma (1 dog), forebrain tumors (3 dogs), hydrocephalus (2 dogs), granulomatous meningoencephalitis (1 dog), and meningoencephalitis (1 dog). Five affected dogs were comatose at the time of recording. BAER abnormalities could be classified as (1) absence of some or all of waves I to V, (2) increased latencies, with wave V being most frequently affected, or (3) a reduction in the amplitude ratio of waves V/1.     

MAGNETIC RESONANCE IMAGING FINDINGS ASSOCIATED WITH LATERAL CEREBRAL VENTRICULOMEGALY IN ENGLISH BULLDOGS

Multiple congenital or developmental anomalies associated with the central nervous system have been reported in English Bulldogs. The purpose of this retrospective study was to identify and describe the prevalence and MRI characteristics of these anomalies and their association with presence and degree of cerebral ventriculomegaly. Magnetic resonance imaging studies of 50 English Bulldogs were evaluated. Forty‐eight dogs had some degree of cerebral ventriculomegaly, 27 of which had an otherwise normal brain. Presence of lateral ventriculomegaly was not significantly associated with presence of another intracranial lesion. Appearance of the septum pellucidum was variable, ranging from intact to incomplete or completely absent. The corpus callosum was subjectively thinned in all but three dogs, two of which had normal lateral ventricles. Fusion of the rostral colliculi was not found in any dog. A persistent craniopharyngeal canal was identified in one dog. Aqueductal stenosis caused by fusion of the rostral colliculi was not identified in any dog. Findings indicated that cerebral ventriculomegaly is a common finding in English Bulldogs with or without other intracranial lesions, aqueductal stenosis caused by fusion of the rostral colliculi is unlikely to be a common etiology leading to obstructive hydrocephalus, and a large craniopharyngeal canal is a rare finding that has unknown clinical significance at this time.     

Effects of changes in power setting of an ultrasonic aspirator on amount of damage to the cerebral cortex of healthy dogs

OBJECTIVE: To determine the minimal ultrasonic aspirator pressure necessary to damage the cerebral cortex of healthy dogs. ANIMALS: 9 mixed-breed dogs. PROCEDURE: The study comprised 2 parts. In part A, 6 dogs were euthanatized immediately prior to the experiment. In part B, 3 dogs were anesthetized for recording of physiologic variables. In both parts, craniectomy and durotomy were performed to bilaterally expose the lateral aspect of the cerebral cortex. An ultrasonic aspirator was placed in contact with various areas of the cerebral cortex, and aspirator power was altered (10, 20, 30, and 40%). Duration of contact at each power was 5 and 10 seconds. Subsequently, gross morphologic and histologic damage was assessed in the cortex. RESULTS: Gross observations for all dogs were similar. At 10% power, visible or histologic damage was not evident in the cortex. At 20% power, the cortex was slightly indented from contact with the hand piece; however, cortical disruption was not evident. Cortical disruption was initially detectable at 30% power in some dogs and was consistently evident at 40% power in both sets of dogs. CONCLUSIONS AND CLINICAL RELEVANCE: Ultrasonic aspirator power of < 20% created minimal acute morphologic damage to the cortex. Power settings between 20 and 30% may superficially damage the cerebral cortex in healthy dogs, whereas 40% power consistently damages the cerebral cortex. Knowledge of the degree of damage to cerebral cortex caused by various amounts of power for ultrasonic aspirators will allow surgeons to avoid damaging normal brain tissues during surgery.     

Comparison of cerebral cranium volumes between cavalier King Charles spaniels with Chiari-like malformation, small breed dogs and Labradors

O bjectives : To ascertain whether cavalier King Charles spaniels (CKCSs) have a proportionately smaller caudal fossa compared with other small dogs and with Labradors. To evaluate if cerebellar herniation in CKCS correlates with caudal fossa volume.
M ethods : In this retrospective study, three-dimensional images were created from magnetic resonance imaging brain series of 117 dogs (split into three groups: CKCS, Labradors and small breeds) from which the volumes of the fossae and brain parenchyma were calculated. These volumes were transformed into percentages of total cranial cavity and parenchyma volumes, respectively. The percentages were statistically compared among the groups. The percentage of herniated cerebellum in the CKCS was compared using linear regression with the caudal fossa and parenchyma percentages.
R esults : Cavalier King Charles spaniels had a proportionately smaller caudal fossa compared with Labradors (P=0·002) but not to small breeds (P=0·103). Their caudal fossa parenchyma was proportionately the same volume as Labradors (P=0·976) but greater than small breeds (P=0·005). No relationship was found for the per cent of cerebellum herniated.
C linical S ignificance : The results support mesoderm insufficiency or craniosynostosis as the pathogenesis of Chiari-like malformation (CM) in CKCS. It presents evidence for overcrowding of the caudal fossa due to a mismatch of brain parenchyma and fossa volumes as to why CKCS and not other small dogs are affected.