Status epilepticus.

Status epilepticus is a life-threatening cerebral event. Within 1-2 minutes of seizure onset, massive recurrent cerebral discharges cause autonomic and endocrine dysfunction and loss of normal brain homeostasis. Intracerebral abnormalities become progressively worse and self-perpetuating the longer seizures continue. Seizures lasting 90 minutes or more may cause irreversible injury to selectively vulnerable neurons in the brain and permanent impairment of neurologic function. In addition, status epilepticus is associated with cumulative anoxia that affects almost every major organ system of the body and leads to progressive organ failure. To prevent permanent neurologic injury, the treatment of status epilepticus must be prompt, aggressive, and rational. Stop the seizures, restore homeostasis, perform a thorough diagnostic evaluation to determine the cause of status, and treat definitively.

A quantitative morphological assessment of the effect of lidoflazine and deferoxamine therapy on global brain ischaemia.

The effect of the combination of two drugs, i.e. lidoflazine (a calcium antagonist), and deferoxamine (an iron chelator) was evaluated following 15 min global brain ischaemia (GBI) and reperfusion in dogs in a randomized blind study. GBI was produced by complete cardiac arrest of 15 min duration. Histopathological analysis performed on in situ fixed brains 40 h post-resuscitation revealed diffuse microhaemorrhages in the control group. These were noted rarely in the treatment group, the mean value of foci of microhaemorrhages/20 low power fields (LPF) being 5.2 in the treatment group versus 28 in the control group (p less than 0.001). Diffuse coagulative necrosis of neurons (ischaemic cell change) in the cerebral cortex, especially lamina 3, hippocampus, striatum, brain stem and cerebellum was present in all cases. Quantitation of the degree of cellular damage obtained by counting the number of anoxic neurons (in consistent regions of the brain) with the use of an image analysis system, revealed no significant difference between the 2 groups. The mean percentages of the ischaemic neurons in the control group in the various areas studied were: parietal cortex, 22.25; hippocampus, 50.37 and cerebellum (Purkinje cells), 66.75; and in the treatment group 25.3, 55.04 and 70.6 respectively. Thus, the lidoflazine-deferoxamine regimen significantly reduced the incidence of microhaemorrhages in the brain, but it did not have any protective effect against anoxic neuronal injury 40 h post-ischaemia in this experimental model of GBI of 15 min duration.

Lumbosacral stenosis and injury of the cauda equina.

Idiopathic (congenital) L/S stenosis, acquired (degenerative) L/S stenosis, and traumatic injury to the vertebral column caudal to L6 often produce signs of neurologic dysfunction attributed to compression, displacement, entrapment, or trauma of the cauda equina. Clinical signs vary from animal to animal and depend upon which roots of the cauda equina are involved and the nature of the compromise. An understanding of the anatomy of the area and an appreciation for the functional relationship between the cauda equina and structures innervated are essential for accurate evaluation, workup, diagnosis, treatment, and outcome.

Use of pentobarbital sodium to reduce seizures in dogs after cervical myelography with metrizamide.

We conducted a prospective study to examine the effect of pentobarbital administration on the development of seizures in dogs that had undergone cervical myelography with metrizamide while anesthetized with halothane. Thirty dogs scheduled for cervical myelography were assigned to 3 groups. Dogs in group 1 received no pentobarbital. Those in group 2 were administered pentobarbital (5 mg/kg, IM) before induction of anesthesia, and those in group 3 received pentobarbital at the end of the procedure when the anesthetic vaporizer was turned off. Anesthesia was induced with thiamylal sodium in all dogs and was maintained with halothane. Dogs that underwent surgery immediately after the myelography were not included in the study. A significant difference was not found among the 3 groups in terms of number of dogs that had seizures, mean body weight of the dogs, duration of anesthesia after injection of metrizamide, time from extubation to first seizure, volume of metrizamide injected, or clinician performing the myelography.

Influence of anesthetic regimen on the frequency of seizures after cervical myelography in the dog.

We examined the influence of various anesthetic drug combinations on the frequency of seizures in dogs after cervical myelography with metrizamide. Over a 12-month period, 78 dogs admitted to the teaching hospital for cervical myelography were assigned randomly to 1 of 6 anesthetic protocols. Myelography was performed, and the dogs were observed for signs of seizure activity after recovery from anesthesia. The person making the decision as to whether or not a dog had had a seizure was unaware of the anesthetic protocol that had been used. Preanesthetic treatment with pentobarbital (5.0 mg/kg) and maintenance of anesthesia with methoxyflurane significantly reduced the frequency of seizures (P less than 0.05). No reduction in seizure frequency was seen with any anesthetic protocol using halothane as the maintenance agent.

Neuromuscular abnormalities associated with hypothyroidism and lymphocytic thyroiditis in three dogs.

Various degrees of persistent or paroxysmal paresis involving only the hindlimbs or all four limbs were observed in 3 dogs with hypothyroidism and lymphocytic thyroiditis. Clinical features included lethargy, obesity, alopecia, insidious and progressive paresis, hypotonia, and slow segmental reflexes in 2 dogs. Obesity, alopecia, paroxysmal paresis, and behavior change were observed in the third dog. Laboratory tests indicated that thyroid function was less than normal in all 3 dogs. Abnormal electromyographic potentials and slow motor nerve conduction velocities were found in each dog. Muscle biopsy specimen abnormalities included selective type-II myofiber atrophy in all dogs, whereas one dog had angular atrophy of type-I and type-II myofibers indicative of denervation. A substance that stained with para-aminosalicylic acid was observed within vacuoles of type-I myofibers in one dog. Lymphocytic thyroiditis characterized by lymphocytic infiltration of excised thyroid glands was observed in all dogs.

Brain iron delocalization and lipid peroxidation following cardiac arrest.

Brain injury after cardiac arrest and resuscitation may occur, in part, by oxygen radical mechanisms. The availability of a transition metal, such as iron, is essential for in vitro initiation of this type of reaction. The brain has significant stores of iron bound in large proteins. We conducted this study to determine whether iron availability is enhanced in the canine brain following resuscitation from 15 minutes of cardiac arrest, and whether this iron is associated with the appearance of products of radical-mediated lipid peroxidation (LP) after two hours of reperfusion. Examination of the data by the method of multivariate analysis revealed significant increases in the low molecular weight species (LMWS) iron (300% of nonischemic controls, P less than .01), malondialdehyde (MDA), a lipid peroxidation degradation product (145% of nonischemic controls, P less than .01), and conjugated dienes (CD) (204% of nonischemic controls, P = .07). Therapy with deferoxamine (50 mg/kg IV immediately post resuscitation) produced a reduction in MDA and CD to levels statistically indistinguishable from nonischemic controls. We conclude that brain tissue iron is delocalized from normal storage forms to a LMWS pool after two hours of reperfusion following resuscitation from a 15-minute cardiac arrest, and that this is associated with increased products of LP. The increase in LP products is blocked by treatment with deferoxamine.

Prolonged cardiac arrest and resuscitation in dogs: brain mitochondrial function with different artificial perfusion methods.

Clinical techniques for artificial perfusion have not previously been examined directly for their effects on brain high-energy metabolism. Our study involved 24 large mongrel dogs that were anesthetized, instrumented for central venous intravenous access, and subjected to craniotomy to expose the dura and underlying parietal cortex. The animals were divided into the following six experimental groups of four animals each: nonischemic controls; 15-minute cardiac arrest without resuscitation; 45-minute cardiac arrest without resuscitation; 15-minute cardiac arrest plus 30 minutes resuscitation with conventional cardiopulmonary resuscitation (CPR); 15-minute cardiac arrest plus 30 minutes resuscitation with interposed abdominal compression (IAC) CPR; and 15-minute cardiac arrest plus 30 minutes resuscitation with internal cardiac massage. Cardiac arrest was induced by central venous injection of KCl 0.6 mEq/kg, and it was confirmed by continuous ECG monitoring. The three active resuscitation models included administration of NaHCO3 and epinephrine, but no attempt was made to restart the heart by defibrillation during resuscitation. At the indicated time in each group, a 4- to 5-g sample of brain was removed through the craniotomy, immediately cooled to 0 C and processed for isolation of mitochondria. The mitochondria were studied for their content of superoxide dismutase and for quantitative oxygen consumption with glutamate/malate substrate during resting and ADP-stimulated respiration. Our results show a significant drop in brain mitochondrial superoxide dismutase activity during the first 15 minutes of cardiac arrest. There is minimal injury to brain mitochondrial oxygen consumption during both 15 and 45 minutes of complete ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Post resuscitation iron delocalization and malondialdehyde production in the brain following prolonged cardiac arrest.

Assays for brain tissue malondialdehyde (MDA) and low molecular weight chelated (LMWC) iron were used to examine samples of the cerebral cortex obtained from dogs 2 h after resuscitation from a 15-min cardiac arrest. The effect of post-resuscitation treatment with lidoflazine and/or desferrioxamine was similarly examined. Non-ischemic brain samples had LMWC iron levels (in nmol/100 mg tissue) of 12.32 + 2.60 and MDA levels (in nmol/100 mg tissue) of 8.46 + 1.35. Animals subjected to cardiac arrest and resuscitation and standard intensive care (SIC) had LMWC iron levels of 37.04 + 4.58 (p less than .01 against non-ischemic controls) and MDA levels of 12.24 + 1.9 (p less than .05 against non-ischemic controls). All treatment interventions significantly reduced the LMWC iron (p less than .05), but only treatment with desferrioxamine alone significantly reduced MDA (p less than .05), although a trend toward reduction of the MDA was also evident in animals treated with both desferrioxamine and lidoflazine. LMWC iron levels are increased in the post-ischemic brain, and this increase may be related to lipid peroxidation in the brain following resuscitation from cardiac arrest. These changes are probably pathologic and are amenable to pharmacologic intervention.

Spinal cord medulloepithelioma in a dog.

Medulloepithelioma, an embryonal neural tumor, was diagnosed in a 6-month-old Bullmastiff. Clinical signs of incomplete, upper motor neuron, transverse myelopathy involving the hindlimbs were observed on examination. Myelography was required to identify the cause of clinical abnormality. The tumor involved the L1 spinal cord segment.

Peripheral neuropathy and hypotension in a diabetic dog.

Peripheral neuropathy and hypotension were found in a diabetic dog with profound weakness. Insulin therapy controlled the diabetes mellitus. As the blood glucose was normalized, the neurologic signs and hypotension resolved, suggesting a causal relationship.

Myasthenia gravis in two cats.

A case of the autoimmune form of myasthenia gravis and a case of what is probably a congenital form of myasthenia gravis were diagnosed in 2 unrelated cats. Neuromuscular weakness exacerbated by exercise was a prominent feature in both cats. Weakness was eliminated temporarily by administration of anticholinesterase drugs. Serum autoantibodies to acetylcholine receptors of skeletal muscle were present in the 1st cat and were not detected in the 2nd cat. A characteristic decrement in the amplitude of the compound muscle action potential during repetitive stimulation of the motor nerve was elicited in the 2nd cat. There was marked electromyographic improvement in response to anticholinesterase drugs. Electromyography was not performed in the 1st cat.

Threonine imbalance, deficiency and neurologic dysfunction in the kitten.

The effect of feeding threonine-imbalanced and threonine-deficient purified diets (containing L-amino acids as the only source of dietary nitrogen on food intake, weight gain and blood plasma amino acid pattern has been examined in growing kittens. The imbalance was created by adding 17.5% of amino acid mixture lacking threonine to a low amino acid basal diet comtaining 17.5% amino acid mixture including 0.4% threonine. A depression in food intake and weight gain occurred while feeding the imbalanced diet which was corrected by adding an additional 0.2% threonine to the imbalanced diet. There was no adaptation with time in the form of increased food intake or weight gain while feeding the imbalanced diet. Plasma threonine was consistently and similarly depressed (10 to 35% of normal) while feeding the basal, imbalanced and corrected diets and increased to normal when the standard diet with 1.4% threonine was fed. Plasma threonine and total amino acid concentrations of kittens fed the imbalanced diet did not differ from those observed in kittens fed the basal diet. Signs of neurologic dysfunction and/or lameness developed in 14 of the 17 kittens fed threonine-imbalanced or deficient diets, which resolved as dietary threonine was increased.

Critical evaluation of creatine phosphokinase in cerebrospinal fluid of dogs with neurologic disease.

Creatine phosphokinase (CPK) concentrations in CSF and in serum of dogs with a variety of neurologic diseases were evaluated. Concentrations of CPK in CSF and serum were diagnostically nonspecific. Although a diagnostic advantage was not found in measurement of CPK concentrations in CSF and serum, it appeared that increased CPK concentration in CSF was associated more frequently with a guarded-to-poor prognosis. The concentration of CPK in CSF was statistically independent of CPK concentration in serum. Cerebrospinal fluid CPK concentration was significantly (P = 0.01) correlated to the number of RBC in CSF. However, CSF concentration of CPK was not significantly correlated to serum, blood, or CSF variables evaluated.