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.     

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.     

Polioencephalomalacia associated with canine distemper virus infection

Eight dogs with severe neurologic signs, including seizures, had polioencephalomalacia of the pyriform cortex, Ammon's horn and deep structures in the temporal lobe. The polioencephalomalacia was considered to be a consequence of canine distemper virus infection based on clinical signs, typical inclusions, the demonstration of viral antigens in the lesions and of characteristic paramyxovirus nucleocapsids by electron microscopy. Little evidence for neuronal destruction by direct viral activity was found. Selective nerve cell necrosis was attributed to ischemia (vascular lesions and seizure induced consumptive anoxia) and immune mechanisms. The selective involvement of the rhinencephalic structures was thought to be related to the mode of entry and spread of the virus.     

Polioencephalomalacia in a llama

A 5-year-old, female llama (Lama glama) developed acute, progressive neurological disease, characterized by recumbency, muscle fasciculations, intermittent convulsions/opisthotonos, and absent menace responses. Postmortem histopathologic lesions, limited to the cerebral cortex, consisted of necrosis of the superficial and deep laminae. The clinical disease and microscopic lesions were consistent with polioencephalomalacia.     

Apparent thiamin status of cattle and its relationship to polioencephalomalacia.

The thiamin status (thiamin concentration in whole blood, plasma, and erythrocytes; erythrocyte transketolase activity) of normal cattle consuming varying diets did not differ from that of cattle with polioencephalomalacia or lead poisoning. Dairy cattle had higher ruminal content of thiamin and lower thiamin destroying activity than did beef cattle. Renal oxalosis was no more frequent in cattle which had polioencephalomalacia than in postnatal calves. In normal beef cattle, approximately 75% of total blood thiamin is in erythrocytes and the remainder in plasma.     

Red neurons in ovine polioencephalomalacia (cerebrocortical necrosis) are strongly amyloid precursor protein immunopositive

The signature pathological feature of the pseudolaminar cerebrocortical necrosis found in polioencephalomalacia (PEM) of ruminants is the development of red (eosinophilic) neurons. These neurons are generally considered to be irredeemably injured but we have shown, for the first time, in ovine PEM cases, that most strongly express amyloid precursor protein (APP), which has a neuroprotective role in the brain. By contrast, neurons in unaffected cerebral cortices from control sheep were APP immunonegative. This finding suggests that, rather than being inevitably destined to die, some of these APP immunoreactive cortical neurons may survive and regain structural and functional integrity.

     

Epinephrine induced hyperglycemia in bulls and its relationship to polioencephalomalacia.

Data on blood glucose concentration in bulls affected with molasses associated polioencephalomalacia are controversial. It has been suggested that the brain lesions are related to a "hypoglycemic state" during the development of polioencephalomalacia. This paper reports the mobilization of glucose by means of the epinephrine test in three bulls fed two diets, one forage based and the other molasses based. The results showed significantly greater hyperglycemic responses in the animals during the molasses diet than during the forage one. This probably means that glucose stores (as glycogen) are higher in cattle consuming molasses than those consuming forage. Such hepatic glucose output is in disagreement with the hypoglycemia theory as the cause of the early stages of brain lesions and focuses the probable cause as being related to glucose utilization.     

A review of heat stroke and its complications in the canine

Thiamine deficiency diseases are briefly reviewed with particular attention to the use of blood thiamine levels in their diagnosis. Blood thiamine levels below 50 nmol/1 are considered significant with levels as low as 6–12 nmol/1 often being found in suspected cases 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.     

Polioencephalomalacia (cerebrocortical necrosis) induced by experimental thiamine deficiency in lambs

Lesions of polioencephalomalacia (PEM, cerebrocortical necrosis) have been demonstrated in pre-ruminant lambs fed on synthetic, thiamine-free milk. Thiamine deficiency in these lambs was confirmed by transketolase assay.     

A review of thiamine deficiency and its diagnosis, especially in ruminants

Thiamine deficiency diseases are briefly reviewed with particular attention to the use of blood thiamine levels in their diagnosis. Blood thiamine levels below 50 nmol/l are considered significant with levels as low as 6-12 nmol/l often being found in suspected cases of polioencephalomalacia.     

Amyloid angiopathy with cerebral hemorrhage and senile plaque in aged dogs

Amyloid angiopathy with cerebral hemorrhage and senile plaques was found in the brain of aged dogs. In all 9 cases examined, 13 to 19 years old, 6 males and 3 females, amyloid deposits were observed mostly in the wall of cerebral arterioles and capillaries showed hyaline degeneration. The accumulation of amyloid fibrils measuring about 10 nm in diameter was seen in the cerebral vessel wall by electron microscopy. The cerebral hemorrhage was observed in 6 of 9 dogs and 2 of them showed massive hemorrhage. The hemorrhagic foci were sometimes closely contact with the vessels involved in amyloid angiopathy. In addition, senile plaques being classified into 2 types were found in the cerebral cortex of 3 dogs. The first type was characterized by the accumulation of degenerative neurites and often contained granular argyrophilic material. The second type had a well-defined amyloid core with neuritic halo. Amyloid deposits were also found in or around intestinal vessel walls of 3 dogs. The amyloid deposited in the cerebral vessels, senile plaques and intestinal vessels showed characteristic green birefringence under the polarized light even after potassium permanganate treatment.     

Pathological studies on cerebral amyloid angiopathy, senile plaques and amyloid deposition in visceral organs in aged dogs.

The relationship between cerebral lesions such as amyloid angiopathy or senile plaques and amyloid deposition in the visceral organs were studied in 90 autopsy cases of dogs, 0 to 19-year-old. Cerebral amyloid angiopathy was detected in 28 aged dogs (mean age: 13.7-year-old) and was found mostly in or around the wall of cerebral meningeal arterioles and capillaries of the neocortex. That condition was often accompanied by cerebral hemorrhage in dogs more than 9 years of age. Senile plaques were detected in the neocortex of the brain of 12 dogs (mean age: 13.2-year-old) and classified into 3 subtypes, i.e., "diffuse plaque", "primitive plaque" and "classical plaque". Among those 3 subtypes of senile plaques, amyloid containing plaques were small in number. In the visceral organs of dogs with cerebral amyloid angiopathy, amyloid deposition was found in the vascular walls or connective tissues of small intestines at a high frequency and sometimes in the vascular walls of the heart, lung, liver and thyroid gland as well as in atrioventricular valves. Amyloid in both cerebral and visceral organs was congophilic and showed green birefringence under poralized light even after potassium permanganate oxidation.     

Sulfur-induced polioencephalomalacia in a herd of rotationally grazed beef cattle

Central nervous system disease occurred in a herd of rotationally grazed beef cattle consuming water containing 3400 ppm sulfate. Clinical signs, pathologic findings, and high water sulfate levels confirmed the diagnosis of sulfur-induced polioencephalomalacia. The incidence of disease reduced when the herd was switched to a low sulfate water source.     

Immunohistochemical studies on canine cerebral amyloid angiopathy and senile plaques.

Amyloid protein was isolated from the cerebral meninges of 4 aged dogs with cerebral amyloid angiopathy. By immunoblot analysis, antiserum against synthetic oligo-peptide consisting of 1-28 amino acid of amyloid beta protein recognized prominent wide band ranging from 14 to 18 kilodalton (kd). When amyloid samples were solubilized by formic acid, the antiserum recognized lower molecular weight band ranging from 3 to 4 kd. Immunohistochemical studies on cerebral amyloid angiopathy and senile plaques were performed in 17 aged dogs. Anti-amyloid beta protein serum labeled amyloid deposits in cerebral vessel walls and senile plaques. Compact deposits of beta protein were detected in primitive or classical plaques. After using formic acid pretreatment, diffuse deposits of beta protein in the neuropil representing diffuse plaques were detectable. Classical and primitive plaques reacted with antiserum against glial fibrillary acidic protein, while not with antisera against alpha 1-antichymotrypsin, IgG and IgM. Amyloid deposits in the intestines of aged dogs examined, did not react with anti-amyloid beta protein serum.     

FDG‐PET IN HEALTHY AND EPILEPTIC LAGOTTO ROMAGNOLO DOGS AND CHANGES IN BRAIN GLUCOSE UPTAKE WITH AGE

Regional cerebral metabolism and blood flow can be measured noninvasively with positron emission tomography (PET). 2‐[¹⁸F]fluoro‐2‐deoxy‐D‐glucose (FDG) widely serves as a PET tracer in human patients with epilepsy to identify the seizure focus. The goal of this prospective study was to determine whether juvenile or adult dogs with focal‐onset epilepsy exhibit abnormal cerebral glucose uptake interictally and whether glucose uptake changes with age. We used FDG‐PET to examine six Lagotto Romagnolo dogs with juvenile epilepsy, two dogs with adult‐onset epilepsy, and five control dogs of the same breed at different ages. Three researchers unaware of dog clinical status visually analyzed co‐registered PET and magnetic resonance imaging (MRI) images. Results of the visual PET analyses were compared with electroencephalography (EEG) results. In semiquantitative analysis, relative standard uptake values (SUV) of regions of interest (ROI) drawn to different brain regions were compared between epileptic and control dogs. Visual analysis revealed areas of hypometabolism interictally in five out of six dogs with juvenile epilepsy in the occipital, temporal, and parietal cortex. Changes in EEG occurred in three of these dogs in the same areas where PET showed cortical hypometabolism. Visual analysis showed no abnormalities in cerebral glucose uptake in dogs with adult‐onset epilepsy. Semiquantitative analysis detected no differences between epileptic and control dogs. This result emphasizes the importance of visual analysis in FDG‐PET studies of epileptic dogs. A change in glucose uptake was also detected with age. Glucose uptake values increased between dog ages of 8 and 28 weeks and then remained constant.     

Brain monitoring in dogs using the cerebral state index during the induction of anaesthesia via target-controlled infusion of propofol

The aim of this study was to evaluate the correlation between the cerebral state index (CSI) and the estimated propofol plasma concentrations in dogs during induction of anaesthesia. Fifteen healthy dogs undergoing scheduled routine surgical procedures were enrolled in this study. Target controlled infusion (TCI) software, based on the pharmacokinetic model for propofol, was used to control the syringe pump and to estimate plasma propofol concentrations (PropCp) and the CSI values every five-seconds. Three electrodes placed in the centre of the forehead, on the left side of the forehead and on the left mastoid were used to collect the electroencephalographic (EEG) signal converted by the cerebral state monitor into the CSI. The cerebral electrical changes induced by increasing propofol concentrations appear to be detected by CSI monitoring in dogs. The negative correlation between CSI and PropCp demonstrates that the CSI could be used to assess electrical brain activity in dogs during the induction of anaesthesia with propofol.     

Polioencephalomalacia in adult sheep grazing pastures with prostrate pigweed

Polioencephalomalacia was diagnosed in 2 animals from different farms. In apparently healthy animals from same farms, fecal thiaminase and a significant reduction in erythrocyte trans-ketolase activity was observed. The presence of thiaminase in Amaranthus blitoides could have contributed to the development of polioencephalomalacia in sheep grazing on natural pastures.     

Update on sulfur-related polioencephalomalacia.

Sulfur-related polioencephalomalacia is frequently associated with a high total sulfur intake by ruminants. The onset of clinical signs coincides with excessive ruminal sulfide production. Measurement of ruminal gas cap hydrogen sulfide makes it possible to identify cattle with potentially hazardous total sulfur intake. Evaluation of all potential sulfur sources is necessary to estimate total dietary sulfur concentration, which can lead to prevention strategies.     

Cerebrospinal fluid flow in normal beagle dogs analyzed using magnetic resonance imaging

BackgroundDiseases related to cerebrospinal fluid flow, such as hydrocephalus, syringomyelia, and Chiari malformation, are often found in small dogs. Although studies in human medicine have revealed a correlation with cerebrospinal fluid flow in these diseases by magnetic resonance imaging, there is little information and no standard data for normal dogs.ObjectivesThe purpose of this study was to obtain cerebrospinal fluid flow velocity data from the cerebral aqueduct and subarachnoid space at the foramen magnum in healthy beagle dogs.MethodsSix healthy beagle dogs were used in this experimental study. The dogs underwent phase-contrast and time-spatial labeling inversion pulse magnetic resonance imaging. Flow rate variations in the cerebrospinal fluid were observed using sagittal time-spatial labeling inversion pulse images. The pattern and velocity of cerebrospinal fluid flow were assessed using phase-contrast magnetic resonance imaging within the subarachnoid space at the foramen magnum level and the cerebral aqueduct.ResultsIn the ventral aspect of the subarachnoid space and cerebral aqueduct, the cerebrospinal fluid was characterized by a bidirectional flow throughout the cardiac cycle. The mean ± SD peak velocities through the ventral and dorsal aspects of the subarachnoid space and the cerebral aqueduct were 1.39 ± 0.13, 0.32 ± 0.12, and 0.76 ± 0.43 cm/s, respectively.ConclusionsNoninvasive visualization of cerebrospinal fluid flow movement with magnetic resonance imaging was feasible, and a reference dataset of cerebrospinal fluid flow peak velocities was obtained through the cervical subarachnoid space and cerebral aqueduct in healthy dogs.