Imaging diagnosis--polioencephalomalacia in a calf.

A 2-month-old mix-breed calf developed acute blindness and ataxia. Serum thiamine concentration was deficient. In antemortem magnetic resonance imaging there were laminar T2-hyperintense regions extending along the cerebral cortex that primarily affected the gray matter. The lesions were relatively symmetric between the left and right hemispheres but no abnormalities were present at the frontal lobes. At necropsy, laminar autofluorescence of the cerebral cortex was observed under ultraviolet exposure at 365 nm, consistent with a diagnosis of polioencephalomalacia. Polioencephalomalacia in the bovine species is compared with that in other species, namely humans, dogs, and cats.     

Ultrastructural study of experimental cerebrocortical necrosis in calves (author's transl)

Cerebrocortical necrosis (CCN) was experimentally induced in three calves with the thiamine antagonist Amprolium. The calves were followed clinically. At the time of development of typical clinical signs of CCN the calves were killed and necropsied and a complete histopathologic examination was performed. The light microscopic lesions of the cerebral cortex were those of middle laminar necrosis and deep laminar edema. The necrotic zone consisted of fine vesicles and differed only slightly from the edema zone. In the former some neurons were morphologically normal, others showed signs of injury, while in the latter all neurons were injured. The lesions are consistent with those found in natural cases of CCN. Biopsies from the cerebral cortex were taken at the time of early clinical signs. Ultrastructural studies of these biopsies showed no clear difference between the zones of necrosis and edema observed light microscopically. The ultrastructural changes were characterized by dilatations in the neuropil. The cytoplasm and foot plates of the astrocytes had a "watery" appearance and contained dilated mitochondria and large vesicles. The vesicles were continuous with the granular endoplasmic reticulum. It was concluded that the initial morphologic changes in CCN in calves were indicative of a cytotoxic edema of the astrocytes. This may be due to a cytotoxic edema with subsequent loss of cell volume control. The primary astrocytic changes could then lead to neuronal injury.     

Oligodendroglial vacuolar degeneration in the bilateral motor cortices and astrocytosis in epileptic beagle dogs

We performed a pathologic examination of the brains of three dogs in an epileptic beagle colony. Histologically, all the cases had diffuse astrocytosis in the cerebral cortex and basal ganglia as well as the hippocampus, whereas they showed acute nerve cell change in the hippocampus and some other areas of the cerebrum. One of these animals showed laminar myelin pallor associated with the presence of many vacuoles in the IV to VI layers of the bilateral motor cortices. Most of the vacuoles contained fine granules stained with luxol-fast-blue stain. Ultrastructural examination revealed that some oligodendrocytes and perineuronal satellite oligodendrocytes in the bilateral cerebral motor cortices of the two affected dogs had many vacuoles surrounded by myelin-like lamellar structures. These findings suggest a possibility that astrocytosis in the cerebrum and vacuolar degeneration of oligodendrocytes in the cerebral motor cortex may be, at least in part, related to the occurrence or development of seizures.     

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.     

Cortical laminar necrosis detected by diffusion-weighted imaging in a dog suspected of having hypoglycemic encephalopathy

We describe a 5-year-old castrated male dog suspected hypoglycemic encephalopathy that was evaluated by using diffusion-weighted imaging (DWI). The dog experienced hypoglycemia after prolonged generalized and continued partial seizures. In the acute phase, DWI showed hyperintensity in the left temporal lobe. After about a month, DWI maintained hyperintensity, and left middle cerebral artery dilation was noted on magnetic resonance angiography (MRA). In the chronic phase, the left temporal lobe lesion was replaced by cerebrospinal fluid. In humans, it was reported that cortical laminar necrosis (CLN) with hypoglycemic encephalopathy presents hyperintensity in the cerebral cortex on DWI and increased vascularity of the middle cerebral artery branches on MRA. In conclusion, DWI has detected CLN in a dog suspected hypoglycemic encephalopathy.     

Gross and microscopic lesions of polioencephalomalacia in a llama (Lama glama).

A 14-wk-old female llama (Lama glama) developed progressive neurologic disease characterized by stiff gait, circling, decreased mentation, and seizures. At necropsy, lesions were limited to the brain and consisted of bilateral necrosis of the cortical gray matter of the occipital lobes of the cerebral cortex. The primary microscopic alteration was bilateral laminar cerebrocortical necrosis, affecting mainly the deep laminae. Clinical disease, and gross and microscopic lesions were consistent with those of polioencephalomalacia.     

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.     

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.     

Zur Feinstruktur der normalen Kapillaren in der grauen Substanz der Großhirnrinde beim Schwein1

Fine structure of normal capillaries in the gray matter of the cerebral cortex of the pig The capillaries in the cerebral cortex over the Ammon's horn were studied with the electron microscope in 8 specific pathogen-free pigs. The capillaries had a thin continuous endothelium without perivascular space and their lumina on the average measured 5.8 ± 1.23 μm. in diameter. Their fine structure was by and large similar to that described for the capillaries of other species.     

Complementary distributions of amyloid-beta and neprilysin in the brains of dogs and cats

Neprilysin is an amyloid-beta-degrading enzyme localized in the brain parenchyma. The involvement of neprilysin in the pathogenesis of Alzheimer's disease has recently received much attention. We examined the localization of neprilysin and amyloid-beta, as well as the activity of neprilysin, in the brains of dogs and cats of various ages to clarify the relationship between neprilysin activity and amyloid-beta deposition. The distribution of neprilysin was almost identical in dogs and cats, being high in the striatum, globus pallidus, and substantia nigra, but very low in the cerebral cortex. The white matter and hippocampus were negative. Neprilysin activity in the brain regions in dogs and cats was ranked from high to low as follows: thalamus/striatum > cerebral cortex > hippocampus > white matter. Amyloid-beta deposition was first detected at 7 and 10 years of age in dogs and cats, respectively, and both the quantity and frequency of deposition increased with age. In both species, amyloid-beta deposition appeared in the cerebral cortex and the hippocampus. In summary, the localization of neprilysin and neprilysin activity, and that of amyloid-beta, were complementary in the brains of dogs and cats.     

Postanaesthetic cerebral necrosis in five horses

After being anaesthetised for between one hour 40 minutes and seven hours, five adult horses developed acute neurological signs and extensive cerebrocortical necrosis. Four of them had had abdominal surgery for colic and one had had repeated orthopaedic interventions. Between five hours and seven days after the surgery, all five horses suddenly developed severe signs of a predominantly prosencephalic disturbance: bilateral blindness with normal pupillary light responses, abnormal behaviour varying from propulsive pacing to head pressing profound lethargy and generalised seizures. They were euthanased between 24 hours and three weeks after the onset of these signs. In three of the cases a gross examination of the brain revealed patchy malacia of the cerebral grey matter and some discolouration of the adjacent white matter. Microscopical examination revealed lesions that varied from laminar neuronal necrosis in the grey matter of the cerebral cortex to more diffuse necrosis of the cortex and underlying white matter. Four of the five cases had had a period of hypercapnea while anaesthetised, and two of them (and possibly a third) had also had hypoxaemia.     

Fas对镉暴露致大鼠大脑皮质自噬体形成的影响

为探究死亡受体Fas在镉暴露致大鼠大脑皮质自噬体形成中的作用,将24只21日龄雄性SD大鼠随机分为4组,分别为对照组、镉组、镉与对照病毒共处理组、镉与Fas基因沉默病毒共处理组。试验期间,对照组大鼠自由饮用纯净水,病毒处理组大鼠于第1天以每只1.4×10¹¹vg的剂量通过尾静脉注射相应病毒,4周后镉染毒组大鼠自由饮用镉水(50 mg·L^-1),持续90 d。试验结束后,透射电镜观察大脑皮质中自噬体数量,Western blot检测大脑皮质细胞外信号调节激酶1/2(Erk1/2)、p-Erk1/2、自噬相关蛋白7(ATG7)、自噬相关基因(Beclin-1)、微管相关蛋白1轻链3(LC3)蛋白表达水平,免疫荧光染色检测LC3表达水平。结果显示,镉暴露增加大脑皮质中自噬体数量,极显著激活Erk1/2并上调ATG7、Beclin-1、LC3蛋白表达水平(P<0.01);Fas基因沉默抑制镉引起的自噬体数量增加,极显著抑制镉致Erk1/2激活及ATG7、Beclin-1、LC3蛋白表达水平升高(P<0.01)。结果表明,Fas通过激活Erk1/2参与镉致大鼠大脑皮质自噬体形成。     

鹿特异性复合麻醉剂对大鼠不同脑区ATP酶活性的影响

为研究鹿特异性复合麻醉剂麻醉与大鼠各脑区突触体ATP酶活性的关系,探讨其麻醉机理。将20只SD大鼠分为对照组和麻醉组,对照组大鼠腹腔注射30mL/kg生理盐水,试验组腹腔注射30mg/kg鹿特异性复合麻醉剂,采集大鼠各脑区,利用比色法测定脑区内Na＋-K＋-ATP、Ca2＋-AT P和Mg2＋-ATP酶活性。结果显示,药物作用后大鼠大脑皮层和脑干Na＋、K＋-ATP酶活性与对照组比较降低显著（P〈0.05或P〈0.01）,小脑、脑干和海马Ca2＋-ATP酶活性与对照组比较显著降低（P〈0.05或P〈0.01）,大脑Mg2＋-AT P酶活性低于对照组（P〈0.05或P〈0.01）。结果表明,麻醉引起大鼠大脑皮层、脑干中Na＋-K＋-ATP酶活性降低,大脑皮层中Mg2＋-ATP酶活性低,小脑、脑干和海马脑区中Ca2＋-ATP酶活性降低可能是鹿特异性复合麻醉剂麻醉作用的机理之一。     

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.     

褪黑素对镉致鸭大脑皮质毒性损伤的保护作用

为探究褪黑素对镉致鸭大脑皮质毒性损伤的保护作用,本试验将16只20日龄高邮鸭随机分为4组,分别为对照组、褪黑素组、镉组、镉与褪黑素共处理组。对照组鸭自由采食饮水;褪黑素组鸭自由饮用含有0.2 mg·L^-1褪黑素的水;镉组鸭自由采食拌有2 mg·kg^-1氯化镉的饲料;镉与褪黑素共处理组鸭自由饮用含有0.2 mg·L^-1褪黑素水的同时自由采食拌有2 mg·kg^-1氯化镉的饲料。60 d后,剖检并采集鸭大脑皮质。比色法检测大脑皮质中丙二醛（MDA）和总抗氧化能力（T-AOC）的水平,ELISA法检测肿瘤坏死因子（TNF-α）、白介素-1β（IL-1β）的含量,免疫组化染色观察Nrf2核转位,免疫印迹法检测Nrf2、HO-1的蛋白表达。结果显示,与对照组相比,镉组鸭大脑皮质发生明显Nrf2核转位,T-AOC水平极显著降低（P<0.01）,MDA、TNF-α、IL-1β含量和Nrf2、HO-1蛋白表达量极显著升高（P<0.01）;与镉组相比,镉与褪黑素共处理组鸭大脑皮质Nrf2核转位减少,T-AOC水平显著升高（P<0.05）,MDA、TNF-α、IL-1β含量和Nrf2、HO-1蛋白表达量显著或极显著降低（P<0.05或P<0.01）。综上,褪黑素对镉所致的鸭大脑皮质毒性损伤具有一定的保护作用。     

Estrogen modulates Bcl-2 family proteins in ischemic brain injury

Estradiol acts as a neuroprotective factor against brain injury. This study investigated whether estradiol modulates the Bcl-2 family proteins in ischemic brain injury. Adult female rats were ovariectomized and treated with estradiol prior to middle cerebral artery occlusion (MCAO). Brains were collected 24 hr after MCAO, and infarct volumes were analyzed. Estradiol significantly reduces the infarct volume and decreases the positive cells of TUNEL staining in cerebral cortex. In ischemic cerebral cortex, the level of Bcl-2 was decreased, and the level of Bax was significantly increased. Estradiol prevents the injury-induced decrease of Bcl-2 and increase of Bax. In conclusion, our findings suggest that estradiol plays a potent protective role in brain injury through the regulation of Bcl-2 family proteins.     

Canine model of ischemic stroke with permanent middle cerebral artery occlusion: clinical and histopathological findings

The aim of the present study was to assess the clinical and histopathological findings in a canine model of ischemic stroke. Cerebral ischemic stroke was induced by middle cerebral artery occlusion in four healthy beagle dogs using silicone plugs. They showed neurological signs of forebrain dysfunction such as reduced responsiveness, head turning, circling, postural reaction deficits, perceptual deficits, and hemianopsia. These signs gradually regressed within 4 weeks without therapy. On magnetic resonance imaging, T2 hyperintensity and T1 hypointensity were found in the cerebral cortex and basal ganglia. These lesions were well-defined and sharply demarcated from adjacent brain parenchyma with a homogenous appearance. No abnormalities of the cerebrospinal fluid were observed. At necropsy, atrophic and necrotic lesions were observed in the cerebral cortex. The cerebral cortex, basal ganglia, and thalamus were partially unstained with triphenyl-tetrazolium chloride. Histopathologically, typical features of infarction were identified in cortical and thalamic lesions. This study demonstrates that our canine model resembles the conditions of real stroke patients.     

Comparison of opioid receptor binding in horse, guinea pig, and rat cerebral cortex and cerebellum

OBJECTIVE: To compare the density and binding characteristics of opioid receptor subtypes in horse, rat, and guinea pig cerebral cortex and cerebellum. STUDY DESIGN: Prospective receptor binding study. ANIMALS: Whole brains were obtained from four neurologically normal adult horses during necropsy. Rat and guinea pig brains were obtained commercially. METHODS: The cerebellum and cerebral cortex were dissected from each brain, and tissue homogenates prepared. A radioligand binding technique with the highly selective ligands [(3)H]-DAMGO, [(3)H]-U69593, and [(3)H]-DPDPE was used to identify the mu- (mu), kappa- (kappa) and delta- (delta) opioid receptors, respectively. Competitive binding assays were performed with these ligands and varying concentrations of one of multiple unlabeled ligands. RESULTS: While there were marked species differences in relative densities of opioid receptors, all radioligands interacted with their binding sites with high, nanomolar affinity in both the cerebral cortex and cerebellum. In the horse cerebral cortex, the percentages of total opioid binding sites for the mu-, kappa- and delta-receptors were 71%, 14% and 15%, respectively. In the rat and guinea pig cerebral cortex, the corresponding values were 56% mu-, 4% kappa- and 40% delta-receptors, and 25% mu-, 37% kappa- and 38% delta-receptors, respectively. In horse and guinea pig cerebellum, the binding was 37% mu-, 59% kappa- and 4% delta-receptors, and 15% mu-, 76% kappa- and 10% delta-receptors, respectively. For competitive analysis, all competitors of the mu-, kappa- and delta-receptors completely displaced [(3)H]-DAMGO, [(3)H]-U69593, and [(3)H]-DPDPE and had inhibitory constants in the nanomolar range. CONCLUSION AND CLINICAL RELEVANCE: Horses used in this study had a greater density of mu-receptors in the cerebral cortex compared with rats and guinea pigs but without further characterization of the functional role of these receptors it is impossible to determine the clinical significance of these data.     

Preliminary study of histological comparison on the growth patterns of long-bone cortex in young calf, pig, and sheep

Some young large farm animals show a laminar bone formation in the long-bone cortex. Such a laminar bone is gradually replaced by Haversian bone with osteons during their growth periods. In this preliminary study, we observed the transverse ground samples of tibia cortex in young calves, pigs, and sheep by backscattered electron imaging. The cortex bones of all the newborn (NB) animals were basically formed with laminar bone structures. The NB and 1-month-old (1-M) calves had a typical concentric structure of laminar bone, whereas the NB and 1-M pigs showed a wire-netting bone with laminar-bone units. The NB sheep was similar to the calf rather than the pig. In the growth rate of bone volume, sheep was similar to calf up to 6 months after birth (6-M). Such calf and sheep showed a more rapid ratio of bone volume than pig. A few osteons had initially appeared in the innermost layer of the 6-M calf. A 1-year-old (1-Y) calf showed scattered osteons in the bone cortex, but many laminar-bone units were still retained in the outer layer. A 6-M pig had many osteons in the entire cortex but only a few osteons in the outermost layer. In the 6-M sheep, no osteons were observed, whereas a 1-Y sheep showed a relatively small number of osteons mainly in the middle layer but a higher osteon-volume than the 1-Y calf. In the 1-Y sheep, the more widely absorbed areas by bone-remodeling with osteons were observed as compared with the 1-Y calf, and the bone volume was decreased from the 6-M into the 1-Y sheep because of the remarkable bone-absorption. Thus, calf kept on possessing many laminar-bone units for a longer time in the growth period than sheep, while pig showed the earliest bone-remodeling with osteons. These results may be caused by their different body size and withers height in calf and sheep after growing and the difference of the dependence upon mother's body during juvenile period between pig and calf with sheep. The initial region of osteon formation may be distinguishable among their animals, respectively. However, further detailed investigations of their young animals at successive stages will be necessary.     

Acute pit gas (hydrogen sulfide) poisoning in confinement cattle.

Rapid deaths in confinement cattle caused by exposure to hydrogen sulfide (H2S) gas from manure pits has not been reported in the USA. In 1997, 158 cattle in 2 confinement pens were exposed to H2S gas as the manure in the pits under a slatted floor was agitated prior to pumping. Approximately 35 of the cattle were lying on the floor when the upper agitator was turned on. Within 5 minutes, many these cattle were down on their sides and paddling. Of these, 26 died within a few minutes. The survivors were treated and sent to slaughter. Cattle that did not show immediate signs of toxicosis remained clinically unaffected. Two steers that were near death were brought to the Purdue Animal Disease Diagnostic Laboratory for clinical evaluation, euthanasia, and necropsy. They were recumbent and unresponsive to visual and auditory stimuli. Necropsy examination yielded no significant gross lesions. No evidence of viral or bacterial infection was found. Ocular fluid nitrate concentrations were within normal limits, and no lead was detected in either animal. Microscopic examination revealed lesions consistent with H2S-induced central nervous system anoxia. Histologically, sections of brain demonstrated massive, diffuse cerebral cortical laminar necrosis and edema. Portions of the outer lamina contained hypereosinophilic and shrunken neurons. The subcortical white matter was vacuolated in some areas. The history, clinical signs, and histologic lesion of cerebral laminar necrosis led to a diagnosis of H2S toxicosis in these cattle.