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.

Temporal Dysynchrony in brain connectivity gene expression following hypoxia.

BACKGROUND: Despite the fundamental biological importance and clinical relevance of characterizing the effects of chronic hypoxia exposure on central nervous system (CNS) development, the changes in gene expression from hypoxia are unknown. It is not known if there are unifying principles, properties, or logic in the response of the developing CNS to hypoxic exposure. Here, we use the small vertebrate zebrafish (Danio rerio) to study the effects of hypoxia on connectivity gene expression across development. We perform transcriptional profiling at high temporal resolution to systematically determine and then experimentally validate the response of CNS connectivity genes to hypoxia exposure. RESULTS: We characterized mRNA changes during development, comparing the effects of chronic hypoxia exposure at different time-points. We focused on changes in expression levels of a subset of 1270 genes selected for their roles in development of CNS connectivity, including axon pathfinding and synapse formation. We found that the majority of CNS connectivity genes were unaffected by hypoxia. However, for a small subset of genes hypoxia significantly affected their gene expression profiles. In particular, hypoxia appeared to affect both the timing and levels of expression, including altering expression of interacting gene pairs in a fashion that would potentially disrupt normal function. CONCLUSIONS: Overall, our study identifies the response of CNS connectivity genes to hypoxia exposure during development. While for most genes hypoxia did not significantly affect expression, for a subset of genes hypoxia changed both levels and timing of expression. Importantly, we identified that some genes with interacting proteins, for example receptor/ligand pairs, had dissimilar responses to hypoxia that would be expected to interfere with their function. The observed dysynchrony of gene expression could impair the development of normal CNS connectivity maps.

Consciousness, unconsciousness and death in the context of slaughter. Part I. Neurobiological mechanisms underlying stunning and killing.

This review describes the neurobiological mechanisms that are relevant for the stunning and killing process of animals in the abattoir. The mechanisms underlying the loss of consciousness depend on the technique used: mechanical, electrical or gas stunning. Direct exsanguination (without prior stun) causes also a loss of consciousness before inducing death. The underlying mechanisms may involve cerebral anoxia or ischemia, or the depolarisation, acidification and/or the destruction of brain neurons. These effects may be caused by shock waves, electrical fields, the reduction or arrest of the cerebral blood circulation, increased levels of CO2 or low levels of O2 in the inhaled air, or the mechanical destruction of neurons. The targeted brain structures are the reticular formation, the ascending reticular activating system or thalamus, or the cerebral hemispheres in a general manner. Some of the techniques, when properly used, induce an immediate loss of consciousness; other techniques a progressive loss of consciousness.

Neonatal diseases in llamas and alpacas.

This article attempts to cover the most common problems likely to present in neonatal crias and to give guidance on how to approach these cases, particularly how to stabilize the acute presentation of a sick neonate. It is impossible to cover every eventuality and it is important to keep an open mind when evaluating and treating sick neonatal camelids. Despite the often moribund presentation of sick neonatal crias, they may be highly rewarding to treat, although hospitalization and 24-hour care is recommended.

Perinatal asphyxia pathophysiology in pig and human: a review.

In utero fetuses are evidently exposed to several factors that cause an interruption of the oxygen flow through the umbilical cord causing asphyxia leading to hypoxia and metabolic acidosis. These conditions are important causes of intra-partum and neonatal mortality. The main objective of this review is to provide current information regarding the pathophysiology of asphyxia in piglets around parturition; the physiological mechanisms invoked by affected piglets to compensate perinatal hypoxemia are discussed. This review also addresses some similarities and differences of asphyxia between piglets and other mammals, including human neonates. Metabolic acidosis and hypoxia are sequela to asphyxia and can cause profound health effects in postnatal performance because of an abnormal suckling, a reduced absorption of colostrum and inadequate passive transfer of neonatal immunity. Acidosis also cause hypothermia, increased mortality and reduced survival in neonates. One of the first deleterious effects of intrauterine hypoxia is the expulsion of meconium into the amniotic sac leading to meconium staining of the skin, and in severe cases, meconium aspiration into the lungs. Even though there have been technological changes and improvements in husbandry, piglet mortality due to asphyxia remains a major problem. One potential alternative to reduce neonatal mortality in pigs is the monitoring of fetal stress during birth and the implemention of strategies such as the Apgar score, that is often used in human pediatrics. It is also important to consider the physiological, behavioral and biochemical changes that take place during parturition which subsequently impact the vitality, maturity and development of neonatal pigs. Understanding the pathophysiology of fetal hypoxia should help practitioners and farmers implement more effective delivery techniques aimed at reducing neonatal mortality and improving postnatal performance.

Model of cerebral palsy in the perinatal rabbit.

Perinatal brain injury results in one of the highest burdens of disease in view of the lifelong consequences and is of enormous cost to society. This makes it imperative to develop better animal models that mimic the human condition. Many neurodevelopmental deficits, such as cerebral palsy, are believed to be a result of prenatal hypoxia-ischemia in humans. Fetal global hypoxia-ischemia is most commonly a consequence of acute placental insufficiency. Our laboratory has modeled in utero sustained and repetitive hypoxia-ischemia in the pregnant rabbit to mimic the insults of abruptio placenta and labor, respectively. Sustained hypoxia-ischemia at 70% (22 days' gestation) and 79% (25 days' gestation) and repetitive hypoxia-ischemia at 90% gestation (28 days' gestation) caused stillbirths and multiple deficits in the postnatal survivors. The deficits included impairment in multiple tests of spontaneous locomotion, reflex motor activity, motor responses to olfactory stimuli, and the coordination of suck and swallow. Hypertonia was observed in the 22 and 25 days' gestation survivors but not in the 28 days' gestation group. Hypertonic survivors were artificially fed and found to have the motor deficits persist for at least 11 postnatal days. A spectrum of brain abnormalities is found on magnetic resonance imaging. This is the first animal model to mimic cerebral palsy. The findings also suggest a window of vulnerability during brain development when the injury results in hypertonia in newborn pups.

Big cat scan: magnetic resonance imaging of the tiger.

In August 2002, we performed MRI scans on a female juvenile Bengal tiger. We present the clinical course, imaging and autopsy findings, and some comparative anatomy of the tiger brain and skull. Magnetic resonance images of a tiger have not previously been published.

Pathophysiologic sequelae of intracranial disease.

A variety of intracranial diseases affect dogs and cats. Clinical signs often result not only from mechanical destruction of normal brain but also from associated pathophysiologic alterations induced secondary to the primary disease process. Effective management of intracranial disease requires recognition and treatment of the primary as well as of many of these secondary pathophysiologic sequelae. This article discusses the evolution, ramifications, diagnosis, and treatment of these pathophysiologic sequelae.

Role of adenosine in NMDA receptor modulation in the cerebral cortex of an anoxia-tolerant turtle (Chrysemys picta belli).

Accumulation of the neuromodulator adenosine in the anoxia-tolerant turtle brain may play a key role in a protective decrease in excitatory neurotransmission during anoxia. Since excitatory neurotransmission is mediated largely by Ca2+ entry through N-methyl-D-aspartate (NMDA) receptors, we measured the effect of adenosine on NMDA-mediated Ca2+ transients in normoxic and anoxic turtle cerebrocortical sheets. Intracellular [Ca2+] was measured fluorometrically with the Ca2+-sensitive dye Fura-2. Baseline intracellular [Ca2+] and [ATP] were also measured to assess cortical sheet viability and potential toxic effects of NMDA. Baseline [Ca2+] did not change significantly under any condition, ranging from 109 +/- 22 to 187 +/- 26 nmoll-1. Throughout normoxic and 2h anoxic protocols, and after single and multiple NMDA exposures, [ATP] did not change significantly, ranging from 16.0 +/- 1.9 to 25.3 +/- 4.9 nmol ATP mg-1 protein. Adenosine caused a reduction in the normoxic NMDA-mediated increase in [Ca2+] from a control level of 287 +/- 35 to 103 +/- 22 nmoll-1 (64%). This effect is mediated by the A1 receptor since 8-phenyltheophylline (a specific A1 antagonist) effectively blocked the adenosine effect and N6-cyclopentyladenosine (a specific A1 agonist) elicited a similar decrease in the NMDA-mediated response. Cortical sheets exposed to anoxia alone exhibited a 52% decrease in the NMDA-mediated [Ca2+] rise, from 232 +/- 30 to 111 +/- 9 nmoll-1. The addition of adenosine had no further effect and 8-phenyltheophylline did not antagonize the observed decrease. Therefore, the observed down-regulation of NMDA receptor activity during anoxia must involve additional, as yet unknown, mechanisms.

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.

Differences in blood supply to the cerebral cortex between sheep and calves during slaughter.

Using methylene blue boli, injected via an intracardiac catheter, the blood supply to the brain in two one- to 10-day-old calves and three adult sheep was studied during and after severance of the common carotid arteries and jugular veins. Passage of dye through cerebral vessels could not be observed in the exposed cerebrum of sheep after bilateral severance of major blood vessels. When vessels were severed on one side only, the passage of dye was noted for at least 53 seconds. In calves, after bilateral severance, sequential boli of dye could be detected passing through the cerebral vessels for more than 100 seconds. These results provide an explanation and support for the belief that there are major differences in the onset of insensibility between sheep and calves subsequent to severance of the common carotid arteries and jugular veins. The differences in blood supply to the brain which were demonstrated could be accounted for by differences in the blood supply to the brain by the vertebral artery in sheep and cattle. The effects of slaughter on the blood supply to the eye are discussed as a possible explanation of the disparity between results of studies in this general field which have used retinal responses in their investigations and those which have not.