The diagnostic value of intravenous contrast computed tomography in addition to plain computed tomography in dogs with head trauma.

BACKGROUND: The aim of this study is to evaluate additional findings which can be detected by post-contrast computed tomography (CCT) in relation to plain CT (PCT) findings in patients presented with head trauma. Medical records of canine patients with the history of head trauma from three institutions were reviewed. PCT- and CCT-anonymized images were evaluated by a veterinary radiologist separately. From the categorized findings the following conclusions were drawn as: abnormalities were identified on (A) PCT but missed on CCT, (B) CCT but missed on PCT, (C) both PCT and CCT. RESULTS: Thirty-two patients were included. The results showed that findings identified on CCT or PCT (category A and B) but missed on the other series were limited to mild soft tissue and sinus changes. Overall, 61 different fracture areas, 6 injuries of the temporomandibular joint (TMJ), 4 orbital injuries, 14 nasal cavities with soft tissue density filling, 13 areas of emphysema, 4 symphysis separations, 12 intracranial hemorrhages, 6 cerebral edema, 5 cerebral midline shifts, 3 intracranial aeroceles, 3 brain herniations and 6 intraparenchymal foreign bodies (defined as an abnormal structure located within the brain: e.g. bony fragments, bullet, teeth,..) were identified on both PCT and CCT separately (category C). Severity grading was different in 50% (3/6) of the reported cerebral edema using PCT and CCT images. CONCLUSION: The results showed that PCT is valuable to identify the presence of intracranial traumatic injuries and CCT is not always essential to evaluate vital traumatic changes.

Water intoxication in adult cattle.

Water intoxication is a common disorder in calves and is usually characterized by transient hemoglobinuria. In contrast, the condition is very rare in adult cattle, with few reports on naturally occurring cases. In the present report, four female Japanese Black cattle, aged 16-25 months, showed neurological signs when they drank water following a water outage. Hemoglobinuria was not grossly observed, while severe hyponatremia was revealed by laboratory tests. Autopsy indicated cerebral edema with accumulation of serous fluid in expanded Virchow-Robin spaces. These results indicate the possibility of water intoxication associated with cerebral edema due to severe dilutional hyponatremia in adult cattle.

Magnetic resonance imaging characteristics of equine head disorders: 84 cases (2000-2013).

The equine head is an anatomically complex area, therefore advanced tomographic imaging techniques, such as computed tomography or magnetic resonance imaging (MRI), are often required for diagnosis and treatment planning. The purpose of this multicenter retrospective study was to describe MRI characteristics for a large sample of horses with head disorders. Horses imaged over a period of 13 years were recruited. Eighty-four horses met the inclusion criteria, having neurological (n = 65), sinonasal (n = 14), and soft tissue (n = 5) disorders. Magnetic resonance imaging accurately depicted the anatomy and allowed identification of the primary lesion and associated changes. There were good correlations between MRI findings and intraoperative or postmortem results. Magnetic resonance imaging showed the exact localization of the lesions, their size, and relation to surrounding structures. However, in the neurological group, there were 45 horses with no MRI abnormalities, 29 of which had a history of recurrent seizures, related to cryptogenic epilepsy. Magnetic resonance imaging was otherwise a valuable diagnostic tool, and can be used for studying a broad range of head disorders using either low-field or high-field magnets.

Hypotonic induction of aquaporin5 expression in rat astrocytes through p38 MAPK pathway.

Brain oedema is a common pathological phenomenon following many diseases and may lead to severe secondary damage. Astrocytes are the most numerous cells in the brain. Five aquaporins (AQPs) have been found in mature astrocytes, which play crucial roles in water transportation. However, most studies have focused on AQP4 or AQP9 and whether another aquaporin such as AQP5 involved in brain oedema is unclear. Here, we addressed the issue that the expression pattern of AQP5 in rat astrocytes in vitro was altered in the hypotonic condition through some mitogen-activated protein kinases (MAPK) pathways. Primary astrocytes were randomly divided into the control group and the hypotonic group. Cell viability was evaluated by MTT test. Immunofluorescence, Western blotting and real-time PCR were used to detect the expression of AQP5. Western blotting was used to detect the variation of MAPK pathway. The present study demonstrated that incubation of astrocytes in the hypotonic medium produced an increase inAQP5 expression, and AQP5 peaked at 6-12 h after hypotension solution exposure. In addition, MAPK pathways were set in motion under hypotension, but not all branches. Only the p38 inhibitor can inhibit AQP5 expression in cultured astrocytes. AQP5 is directly related to the extracellular hypotonic stimuli in astrocytes, which could be regulated through the p38 MAPK pathway.

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.

Hemolytic-uremic syndrome in a postpartum mare concurrent with encephalopathy in the neonatal foal.

A postpartum mare and foal were presented for evaluation of fever and lethargy in the mare. The mare was diagnosed with endometritis and initially responded well to treatment. On the second day of hospitalization, the mare developed renal insufficiency characterized by oliguria, azotemia, hemolysis, and thrombocytopenia. Concurrently, the foal developed rapidly progressive central nervous system signs culminating in refractory seizures. Both animals failed to respond to treatment and were euthanized. Thrombotic microangiopathy involving glomeruli was evident on microscopic examination of the mare's kidneys. Microscopic evidence of brain edema was the principal postmortem finding in the foal. No specific etiology was confirmed in either case. Notably, Escherichia coli 0103:H2 was isolated from the mare's uterus and the gastrointestinal tracts of both animals. To the authors' knowledge, this is the first report in which an organism implicated as a cause of hemolytic-uremic syndrome was isolated from an animal with clinical signs and postmortem findings consistent with the disease.

Hereditary neuraxial edema in Polled Hereford calves.

Two newborn Polled Hereford calves with hereditary neuraxial edema were available for clinical and pathological examination. The affected animals showed extensor spasms and were unable to rise. Pathologic lesions were microscopic and consisted of widespread vacuolation of the neuraxis, chiefly in white matter and less markedly in grey matter. The lesions were most severe in the brain stem and cerebellar white matter. Examination of the breeding record indicated sire-daughters matings and thus a probably autosomal recessive mode of inheritance.

Facial cellulitis associated with fowl cholera in commercial turkeys.

Severe cephalic swelling and facial cellulitis in turkeys associated with fowl cholera were present in seven accessions submitted to two laboratories in a 2-year period. Flocks ranged in age from 6 to 18 weeks and included both toms and hens. Interestingly, turkeys with facial cellulitis had no gross internal lesions of fowl cholera, whereas birds with gross lung, liver, and air-sac lesions did not have swollen heads. Histologically, the facial cellulitis was characterized by extensive fibrinonecrotic inflammation of the deep dermis with heterophilic perivasculitis and thrombosis. Additional characterization of Pasteurella multocida isolates from these cases was conducted retrospectively from lyophilized cultures. Serogrouping, serotyping, and an enzyme-linked immunosorbent assay (ELISA) for dermonecrotic factor were performed. All isolates were serogroup A or unencapsulated. Serotype 1 was the most prevalent serotype isolated in association with facial cellulitis. ELISA results for dermonecrotic toxin were inconclusive.

Histopathological changes in the brain of mice given Clostridium perfringens type D epsilon toxin.

The distribution, severity and frequency of brain lesions produced in mice by the administration of Clostridium perfringens Type D epsilon toxin were examined by light microscopy. The granular layer of the cerebellum was the area most frequently affected in mice given single doses of toxin. Sequential changes in brain morphology were examined from 1 h to 7 days after injection of toxin. Lesions progressed from an initial vasogenic oedema to malacic foci which commonly were focal and bilaterally symmetrical, with a predilection for white matter. The topographical distribution of these malacic areas is discussed.

Effects of intravenous injection of Clostridium perfringens type D epsilon toxin in calves.

In cattle, a neurological lesion similar to that produced in sheep and goats by Clostridium perfringens type D enterotoxaemia has been reported. However, no causal relationship has been established between this disease and the lesion in cattle. The effects of single and multiple intravenous injections of epsilon toxin in three calves aged 6 months were studied. A further calf was inoculated intravenously with saline solution and used as a control. Epsilon toxin invariably produced neurological signs within 2-60 min of the end of the injection process. Clinical signs consisted of loss of consciousness, recumbency, convulsions, paddling, opisthotonus, hyperaesthesia and dyspnoea. Gross changes consisted of severe acute pulmonary oedema, which was particularly marked in the interlobular septa. The histological lesions consisted of intra-alveolar and interstitial oedema of the lung and variable degrees of perivascular proteinaceous oedema in the internal capsule, thalamus and cerebellar white matter. No clinical or post-mortem changes were observed in the control calf. These results show that calves are susceptible to the intravenous injection of epsilon toxin, and that they can show at least some of the histological lesions produced in sheep and goats by this toxin.

Histochemical characterization of cytotoxic brain edema. Potassium concentrations after cerebral ischemia and during the postmortem interval.

Cytotoxic edema is a phenomenon of the ischemically damaged brain. In the present study we tested a histochemical method that detects this phenomenon based on potassium (K+) levels in the brain. In a first series focal cerebral ischemia was induced by arterial occlusion in 23 gerbils (Meriones unguiculatus). After survival times of 30, 60 and 120 min, the animals were killed and brain section histochemically stained for potassium and quantitatively evaluated with a morphometric method. The results were compared with those using physicochemical techniques. A distinct K+ depletion could be demonstrated in the area of the focal ischemia within a survival time of 30 min, the depletion growing thereafter with increasing survival time. In a second series histochemical and chemical methods were used to study the stability of K+ levels in undamaged brains of 15 healthy rats during postmortem intervals of 2.5 and 5 h. Within these intervals K+ levels were clearly depleted, apparently as a result of cerebral spinal fluid (CSF) diffusion. Even if neuronal injury can be demonstrated histochemically after very brief survival times of about 30 min, postmortem storage of the cadavers rendered detection impossible due to electrolyte and water diffusion. In autoptic human cases, therefore, this technique is of no practical utility in detecting cytotoxic brain edema in postmortem tissue.

Computed tomography and magnetic resonance findings in two dogs and a cat with intracranial lesions.

Two dogs and a cat with intracranial lesions were evaluated by both computed tomography (CT) and magnetic resonance (MR) imaging. In a dog with vestibular syndrome, better quality images of the medulla oblongata surrounded by thick bones were obtained by MR than by CT, on which the appearance of artifacts impeded the clear image of the area. In a dog with multiple brain metastases of lymphoma, contrast CT delineated lesions more clearly than MR, which was performed one week after CT. During that week dexamethasone which might affect the clarity of MR images of the lesion was administered to reduce brain edema. In a cat with meningeal syndrome of lymphocytic leukemia, only contrast MR imaging identified the width and site of the lesion. These results indicate that it is necessary to select either one of these imaging methods according to the type and site of lesions that are suspected in a particular case.

Effects of an extract of Gingko biloba on bromethalin-induced cerebral lipid peroxidation and edema in rats.

The effects of administration of a commercially available extract of Gingko biloba (EGB) on bromethalin-induced brain lipid peroxidation and cerebral edema in adult male Sprague-Dawley rats was determined. Gingko biloba extract was given (100 mg/kg) by gavage immediately after bromethalin (1.0 mg/kg) administration. Rats were euthanatized at 24 hours after dosing. Brain lipid peroxidation was determined by measurement of brain malonaldehyde-thiobarbituric acid chromophore (MDA-TBA) concentration, brain sodium concentration, and brain water content. Treatment of bromethalin-dosed rats (10/group) with EGB was associated with a statistically significant (P less than 0.05) decrease in clinical sign severity, compared with bromethalin-dosed saline solution-treated rats. All rats given bromethalin and saline solution developed clinical signs of toxicosis including CNS depression, hind limb weakness, ataxia, paralysis, and coma. Some rats given bromethalin and EGB developed clinical signs, however, none developed hind limb paralysis. The brain MDA-TBA concentration (2.4 +/- 0.5 delta MDA-TBA concentration/mg of protein), percentage of water in brain tissue (80.3 +/- 0.30%), and brain sodium concentration (6.68 +/- 0.21 mg/g of dry weight) were significantly increased in rats given bromethalin and saline solution, compared with control rats given saline solution (1.0 +/- 0.1 delta MDA-TBA concentration/mg of protein; 78.1 +/- 0.33% water in brain tissue; 4.83 +/- 0.30 mg of brain Na+/g of dry weight) and rats given bromethalin and EGB (1.6 +/- 0.2 delta MDA-TBA concentration/mg of protein; 79.3 +/- 0.31% water in brain tissue; 5.37 +/- 0.34 mg of brain Na+/g of dry weight).(ABSTRACT TRUNCATED AT 250 WORDS)

Brain edema and gliopathy induced by 6-aminonicotinamide intoxication in the central nervous system of rats.

Brain edema was produced by 6-aminonicotinamide (6-AN) in the rat with accompanying metabolic disturbance due to the accumulation of an antimetabolite of nicotinamide in the CNS. Twenty-four hours after intraperitoneal administration of 6-AN, significant (P less than 0.01) increases of sodium and water in the medulla oblongata were observed. By electron microscopy, the lesion was characterized by swelling of the perivascular neuroglial processes, producing disturbances of the active transport in the cell membrane and increased pinocytosis in the endothelial cells, especially of the arterioles and venules. The metabolic inhibitor was shown to produce not only an increased water and sodium uptake in neuroglias, which is characteristic of cytotoxic brain edema, but also produced protein-rich edema in the extracellular space, ie, vasogenic brain edema. The protein transport in the metabolic disturbance caused by 6-AN was traced, using horseradish peroxidase, revealing that it occurred from the vasculature into the extracellular spaces via pinocytotic vesicles due to the change in the cerebrovascular permeability.

Treatment of hypernatremia in an acidotic neonatal calf.

A 7-day-old Jersey calf was evaluated because of diarrhea and pneumonia. The calf was hypernatremic, hypoproteinemic, and acidemic, and was treated initially with i.v. administration of fluids with sodium concentration (175 mEq/L) similar to the calf's serum sodium concentration. Sodium concentration of the administered fluids was gradually decreased over the following days, but the calf's serum sodium concentration decreased too rapidly, and the calf developed neurologic signs attributed to cerebral edema. Treatment with mannitol and i.v. administration of fluids with a higher concentration of sodium resulted in abatement of clinical signs. In calves, hypernatremia may develop over several days. Prescribing traditional isotonic or hypotonic fluids in such cases will be harmful, because during chronic hypernatremia, the brain's adaptive mechanisms involve accumulation of organic osmoles that may take several days to equilibrate across cell membranes, and cerebral edema may result. Administration of fluids containing sodium concentration approximately equal to the patient's measured serum sodium concentration is required to decrease serum sodium concentration more slowly than is possible with traditional isotonic fluids.

Hypovolemic hyponatremia and signs of neurologic disease associated with diarrhea in a foal.

Hypovolemic hyponatremia attributable to severe fluid and electrolyte alterations was diagnosed in a foal with diarrhea. Subsequent consumption of water resulted in rapid reduction of serum sodium concentration and serum osmolar depression. Clinical signs of neurologic disease developed including blindness, loss of menace response, and seizures. Treatment of this condition with IV administered fluids included hypertonic saline solution (7.2%; 2 ml/kg of body weight), and frequent monitoring of serum electrolyte concentrations and osmolality resulted in gradual correction of the fluid and electrolyte imbalance and resolution of the neurologic signs. Hyponatremia has been recognized in foals with renal failure, ruptured urinary bladder, and iatrogenic water overload. The key to diagnosis and management of profound hyponatremia is accurate diagnosis of the status of plasma volume and association of the electrolyte imbalance with clinical signs of neurologic disease. This report describes an unusual complication of a commonly encountered problem in equine practice and documents that the severe metabolic and electrolyte abnormalities associated with diarrhea can result in clinical neurologic disease. The differential diagnosis also should include bacterial sepsis, parasitism, thoracic mass, acute renal failure, congenital neurologic deficit, or seizure syndrome. Serum electrolyte disorders should be considered as a potential cause of signs of neurologic disease in foals with diarrhea.

High-sodium crystalloid solution for treatment of hypernatremia in a Vietnamese pot-bellied pig.

An 11-month-old female Vietnamese pot-bellied pig was examined for severe dehydration and neurologic signs including disorientation, ataxia, blindness, and involuntary twitching of the muscles of the neck and head. Biochemical analyses of serum revealed hypernatremia, hyperchloremia, hyperkalemia, azotemia, hyperphosphatemia, hyperalbuminemia, and high activities of aspartate transaminase and creatine kinase. A diagnosis of salt toxicosis/water deprivation was made. Medical management consisted of intravenous administration of a high-sodium crystalloid solution, anti-inflammatory drugs, and other supportive care. Sodium concentration of fluids administered intravenously was adjusted to be slightly less than the pig's serum sodium concentration so that the serum sodium concentration was reduced gradually over 48 hours. Resolution of clinical signs was rapid and the pig was discharged after 8 days of hospitalization. Fourteen days after the initial examination, the pig appeared healthy except for visual deficits. Historically, prognosis with conventional treatment of salt toxicosis/water deprivation is poor; however, this alternative approach to treating this condition appears promising.

Evaluation of autofluorescence as an aid to diagnosis of cerebrocortical necrosis.

A series of brains from sheep, cattle, goats and pigs was examined histopathologically and illuminated by ultraviolet light to test the specificity of autofluorescence in the diagnosis of cerebrocortical necrosis. Fluorescence was seen in only four cases of porcine encephalopathy. In the ruminant brains it occurred in seven out of eight cases of cerebral oedema of lambs; otherwise it was confined to cases of cerebrocortical necrosis, although a few false negative cases were encountered. Ovine cerebral oedema is a disease of unweaned lambs which is unlikely to be confused with cerebrocortical necrosis. Thus bright cerebrocortical autofluorescence in a naturally occurring disease of cattle, sheep and goats is a likely indicator of cerebrocortical necrosis; however, a small proportion of cases will escape detection by this method.

Bovine citrullinaemia: a clinical, pathological, biochemical and genetic study.

Calves affected with citrullinaemia are clinically normal immediately after birth. In the majority of calves the clinical course of the disease was similar. Within 24 hours of birth they become depressed; then within 3 to 4 days were observed to wander aimlessly or stand with their head pressed against a wall or fence. By day 4 to 5 they become recumbent, developed convulsions, followed by collapse and death. Oedema of the cerebral cortex is a consistent histological lesion. Citrulline concentration in blood, cerebrospinal fluid, eye fluid and cerebral tissue is greatly elevated. Information gathered from pedigrees of affected calves indicate that the defect is widely disseminated throughout the Australian Friesian population.