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PubMed1997

Hemodynamic depression and microthrombosis in the peripheral areas of cortical contusion in the rat: role of platelet activating factor.

Cerebrovascular damages leading to subsequent reductions in regional cerebral blood flow (rCBF) may play an important role in secondary cell damages following traumatic brain injury (TBI). Recent studies have demonstrated that rCBF markedly decrease in experimental model of TBI (e.g. fluid percussion injury, acute subdural hematoma, contusion). However, precise mechanisms underlying post-traumatic CBF reduction remain unclear. In the present study, the rCBF changes and microthrombosis formation were investigated in a cortical contusional model in rats, and the effects of etizolam (platelet activating factor antagonist) on microthrombosis were tested. The rCBF in the peripheral areas increased transiently, and decreased to ischemic level 3 hours post- injury. The histological examinations revealed microthrombosis formation in the contused area, extending from the center to the peripheral areas within 6 hours post-injury. The rCBF decrease and the contusion necrosis volume were significantly attenuated by etizolam administration. These results indicate that platelet activating factor is involved in microthrombosis formation and hemodynamic depression, and resultant ischemic damages within areas surrounding the contusion.

Animals↗
PubMed1990

Effect of THAM on brain oedema in experimental brain injury.

The metabolic brain acidosis after trauma has been thought to increase brain oedema and contribute to neurologic deterioration. Amelioration of the brain acidosis either by systemic buffering agents or by hyperventilation has been proposed as a method of treatment. The objective of this study was to explore brain oedema and the metabolic changes in brain that occur with the use of hyperventilation. Tromethamine and combination (THAM and hyperventilation) therapy in experimental fluid-percussion brain injury. Brain lactate, brain pH, inorganic phosphate (Pi) and ATP were measured by 1H and 31P magnetic resonance spectroscopy. Also Water content in brain tissue using the specific gravimetric technique were determined in 32 cats. Prolonged hyperventilation provided relative ischaemia in brain tissue and promoted more production of brain lactate, no recovery of PCr/Pi ratio, and no decrease in brain oedema. On the other hand the administration of THAM served to decrease production of brain lactate and brain oedema and promoted the recovery of cerebral energy dysfunction. THAM ameliorates the deleterious effects of hyperventilation by minimizing energy disturbance and also decreases brain oedema. We conclude that THAM may be effective in reducing brain tissue acidosis and helpful as a metabolic stabilizing agent following severe head injury.

Animals↗
PubMed1990

The novel 21-aminosteroid U-74006F attenuates cerebral oedema and improves survival after brain injury in the rat.

The present study evaluated the effect of the non-glucocorticoid 21-aminosteroid U74006F on the development of regional cerebral oedema after lateral fluid-percussion (FP) brain injury in the rat. Male Sprague-Dawley rats (n = 20) were anaesthetized and subjected to lateral FP brain injury of moderate severity (2.5-2.6 atmospheres). Fifteen minutes after brain injury, animals randomly received an i.v. bolus of either U74006F (3 mg/kg, n = 11) followed by a second bolus (3 mg/kg) at 3 hours vs buffered saline vehicle (equal volume, n = 9). At 48 hours postinjury, animals were sacrificed and brains tissue assayed for water content using wet weight/dry weight methodology. Administration of U74006F significantly attenuated the increase in water content observed in control animals in the ipsilateral hippocampus (adjacent to the site of maximal injury, p less than 0.05). Administration of U74006F also significantly reduced post-injury mortality from 28% in control animals to zero in treated animals (p less than 0.001). These results suggest that lipid peroxidation may be involved in the pathophysiological sequelae of brain injury and that 21-aminosteroids may be beneficial in the treatment of brain injury.

Animals↗
PubMed1990

Brain oedema in experimental closed head injury in the rat.

Development of brain oedema was studied in a new closed head injury (CHI) model of the rat. This acceleration impact models does not produce the dramatic blood pressure surge seen with fluid percussion injury. Sixteen Sprague Dawley rats were separated into 4 groups; 8 survivors sacrified at 4 and 24 hours post injury; and 8 Sham treated animals sacrified at the same time intervals. Brains were analyzed using gravimetric technique. Despite absence of the high post traumatic blood pressure surge, mild oedema was observed in 4 of 5 slices at 4 hours post injury. At 24 hours post injury, significant oedema was observed throughout the brain tissue. The study demonstrates that traumatic oedema develops following acceleration impact within a 24 hour period of CHI. The oedema occurs in the absence of significant brain stem damage and blood pressure rise characteristic of this new CHI model.

Animals↗
PubMed1990

Early cellular swelling in experimental traumatic brain injury: a phenomenon mediated by excitatory amino acids.

Early cellular swelling following fluid-percussion brain injury was demonstrated in vivo by means of microdialysis in the rat. When rapid cellular swelling occurs, water moves from the extracellular space (ECS) into the cells and the extracellular concentration of ECS marker which does not move into the cells increases. Cellular swelling was therefore demonstrated in vivo as an increase in the dialysate concentration of 14C-sucrose ([14C-sucrose]d) pre-perfused as an ECS marker. The increase in [14C-sucrose]d occurred concomitantly with an increase in the dialysate concentration of K+ ([K+]d) representing large ionic fluxes. The increases in [K+]d and [14C-sucrose]d were both inhibited by kynurenic acid, a broad spectrum antagonist of excitatory amino acids (EAAs), which was administered through the dialysis probe. These findings suggest that early cellular swelling following traumatic brain injury is a result of ionic fluxes mediated by EAAs.

Amino Acids↗
PubMed1993

Traumatic brain tissue acidosis: experimental and clinical studies.

We have been focusing on potential metabolic derangement associated with severe head injury and a clinical trail directed toward treating brain tissue acidosis is currently underway. More specifically, we based this study on the hypothesis that following brain trauma brain tissue acidosis develops which may contribute to the prolongation of coma and neurologic deficit. Tromethamine (THAM), a safe and low toxicity agent which buffers in major part by causing a hypocapnic alkalosis, was selected for trial. Patients admitted with GCS < 8 were randomized into one of three arms: control: THAM plus hyperventilation; hyperventilation alone. Each regimen was maintained for 5 days post injury. Our analysis of 3 and 6 months Glasgow outcome score showed that prophylactic hyperventilation retards recovery, and the use of THAM overcomes the apparent deleterious effects of hyperventilation. One explanation is that the reduced ICP instability observed in THAM treated patients may account for this improvement. Is THAM effective in buffering traumatized brain tissue? What factors account for improvement in ICP stability? We addressed these questions in experimental studies utilizing MR spectroscopy to measure brain lactate production and tissue pH in fluid percussed anaesthetized cats. The protocol was designed to match our clinical trial, and brain injured animals were randomized into control, THAM, and hyperventilated groups. We observed that brain lactate production increased with trauma and remained above control at 8 hrs post injury. Lactate production in THAM treated animals was not elevated. Highest lactate production was associated with injured animals treated with sustained hyperventilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1994

Administration of an omega-conopeptide one hour following traumatic brain injury reduces 45calcium accumulation.

The omega-conopeptide, SNX-111 (NEUREX Corporation) was administered to rats 1 hour following a lateral fluid percussion brain injury to determine if the drug could reduced the extent and duration of trauma-induced calcium accumulation. Administration at doses of 3 or 5 mg/kg (i.v.) markedly reduced the extent of calcium accumulation as determined using 45calcium autoradiography primarily within the cerebral cortex and hippocampus. The reduction of calcium accumulation was particularly event within the parietal cortex beginning as early as 6 hours and lasting out to 48 hours following injury. Although not as effective as in the cerebral cortex, SNX-111 did exhibit a reduction of calcium accumulation within the dorsal hippocampus especially at 24 and 48 hours after the insult. These preliminary results demonstrate that SNX-111 can reduce the injury-induced accumulation of calcium even when administered 1 hour after the insult and offers this compound as a potential therapeutic treatment for traumatic brain injury.

Animals↗
PubMed1993

Ubiquitin marks the reactive swellings of diffuse axonal injury.

Ubiquitin is a protein that targets proteins for non-lysosomal degradation. It has been found to be present in a number of inclusions characteristic of neurodegenerative diseases. Using the fluid percussion model of closed head injury in the cat, a well-established model of diffuse axonal injury (DAI), we now report that the reactive axonal swellings and the retraction balls produced in this model stain positively with anti-ubiquitin immunohistochemistry. Furthermore, the affected axons become ubiquitin positive quickly (within the first 6 h after injury). Anti-ubiquitin immunohistochemistry compares well with the recently reported ability of antibodies to low molecular weight neurofilament proteins to demonstrate reactive axonal change in DAI, and it could provide additional clues to the pathogenesis of axonal transection.

Animals↗
PubMed1991

Neuroplasticity following traumatic brain injury: a study of GABAergic terminal loss and recovery in the cat dorsal lateral vestibular nucleus.

Terminal loss and recovery were assessed in the cat dorsal lateral vestibular nucleus (dLVN) following diffuse axonal damage caused by experimental traumatic brain injury. Using sterile technique, anesthetized adult cats received a moderate fluid-percussion traumatic brain injury. After predetermined survival periods of 7-368 days, the animals were perfused and the dLVN prepared for the immunocytochemical visualization of GABAergic puncta/terminals at the light (LM) and electron (EM) microscopic levels. In controls, the Deiters' neuronal somata within the dLVN were encompassed by numerous GABA-immunoreactive puncta/terminals. Within 7 days of injury, axonal damage was seen scattered throughout the dLVN, and associated with this, some neuronal somata demonstrated a dramatic loss of perisomatic GABA-immunoreactive puncta, while other somata appeared unchanged. Ultrastructural examination demonstrated that the loss of immunoreactive puncta observed with LM was directly correlated with the presence of degenerating GABAergic terminals. Overall, these neuronal somata showed a reduction of perisomatic puncta/terminals to values approximately 25% of controls. Over a thirty day posttraumatic course, this pattern of scattered perisomatic puncta/terminal loss persisted, with some puncta/terminal return by 60 days postinjury. During the next six months, a recovery of the immunoreactive puncta/terminals was observed in relation to the deafferented somata, with perisomatic terminal numbers now reaching 75% of control values. Over the 7 to 12 month postinjury period, recovery continued, with virtually complete recovery observed in the later phases of this period. Importantly, throughout this recovery period, there was a consistent correlation between the light and electron microscopic findings. The observed diffuse pattern of terminal loss, followed a prolonged adaptive recovery process, suggests that traumatic injury with its attendant diffuse axonal injury and related diffuse deafferentation creates a unique environment for rather complete and adaptive synaptic recovery. As diffuse axonal injury is a common feature of human traumatic brain injury, we believe that these studies, performed in cat, help explain some of the initial morbidity as well as some of the partial recovery seen in head-injured man.

Animals↗
PubMed1995

Long-term potentiation deficits and excitability changes following traumatic brain injury.

The effects of traumatic brain injury (TBI) on hippocampal long-term potentiation (LTP) and cellular excitability were assessed at postinjury days 2, 7, and 15. TBI was induced using a well-characterized central fluid-percussion model. LTP of the Schaffer collateral/commissural system was assessed in vivo in urethane-anesthetized rats. Significant LTP of the population excitatory postsynaptic potential (EPSP) slope was found only in controls, and no recovery to control levels was observed for any postinjury time point. Four measurement parameters reflecting pyramidal cell discharges (population spike) indicated that TBI significantly increased cellular excitability at postinjury day 2: (1) pretetanus baseline recording showed that TBI reduced population spike threshold and latency; (2) tetanic stimulation (400 Hz) increased population spike amplitudes to a greater degree in injured animals than in control animals; (3) tetanus-induced population spike latency shifts were greater in injured cases; and (4) tetanic stimulation elevated EPSP to spike ratios (E-S potentiation) to a greater degree in injured animals. These parameters returned to control levels, as measured on postinjury days 7 and 15. These results suggest that TBI-induced excitability changes persist at least through 2 days postinjury and involve a differential impairment of mechanisms subserving LTP of synaptic efficacy and mechanisms related to action potential generation.

Action Potentials↗
PubMed1990

Skeletal muscle changes associated with equine myotonic dystrophy.

A progressive neuromuscular disorder in young horses, clinically apparent as early as 1 month of age, is characterized by generalized myotonia, muscle stiffness, muscle weakness and atrophy. Myotonia is identified by percussion dimpling and myotonic EMG discharges. Changes in one case included testicular hypoplasia, cataract formation, and glucose intolerance, indicating a systemic involvement. Pathologic changes in skeletal muscles from three affected foals were examined. Sarcoplasmic masses, ringed fibers, internal positioning of sarcolemmal nuclei, and nuclear rowing were among the primary histologic changes noted. Variation in fiber diameter size, especially atrophy, and type I predominance were also prominent changes. A neurogenic involvement was indicated by type grouping changes in several muscles.

Animals↗
PubMed1980

Treatment of myotonic dystrophy with acetazolamide.

This report describes a patient with myotonic dystrophy who had severe action and percussion myotonia. The patient was unresponsive to diphenylhydantoin therapy. Treatment with acetazolamide, 250 mg daily, decreased the myotonia markedly. A possible mechanism of the favorable effect of acetazolamide in myotonia is discussed.

Acetazolamide↗
PubMed1982

Peripheral neuropathy with a syndrome of continuous motor unit activity.

A chronic alcoholic who had also been submitted to partial gastrectomy developed a syndrome of continuous motor unit activity responsive to phenytoin therapy. There were signs of minimal distal sensorimotor polyneuropathy. Symptoms of the syndrome of continuous motor unit activity were fasciculation, muscle stiffness, myokymia, impaired muscular relaxation and percussion myotonia. Electromyography at rest showed fasciculation, doublets, triplets, multiplets, trains of repetitive discharges and myotonic discharges. Trousseau's and Chvostek's signs were absent. No abnormality of serum potassium, calcium, magnesium, creatine kinase, alkaline phosphatase, arterial blood gases and pH were demonstrated, but the serum Vitamin B12 level was reduced. The electrophysiological findings and muscle biopsy were compatible with a mixed sensorimotor polyneuropathy. Tests of neuromuscular transmission showed a significant decrement in the amplitude of the evoked muscle action potential in the abductor digiti minimi on repetitive nerve stimulation. These findings suggest that hyperexcitability and hyperactivity of the peripheral motor axons underlie the syndrome of continuous motor unit activity in the present case.

Alcoholism↗
PubMed1984

Muscle hypertrophy and a syndrome of continuous motor unit activity in prednisone-responsive Guillain-Barré polyneuropathy.

The clinical, electrophysiological and morphological findings (light and electron microscopy of the sural nerve and gastrocnemius muscle) are reported in an unusual case of Guillain-Barré polyneuropathy with an association of muscle hypertrophy and a syndrome of continuous motor unit activity. Fasciculation, muscle stiffness, cramps, myokymia, impaired muscle relaxation and percussion myotonia, with their electromyographic accompaniments, were abolished by peripheral nerve blocking, carbamazepine, valproic acid or prednisone therapy. Muscle hypertrophy, which was confirmed by morphometric data, diminished 2 months after the beginning of prednisone therapy. Electrophysiological and nerve biopsy findings revealed a mixed process of axonal degeneration and segmental demyelination. Muscle biopsy specimen showed a marked predominance and hypertrophy of type-I fibres and atrophy, especially of type-II fibres.

Electromyography↗
PubMed1979

Paramyotonia congenita. A clinical, electrophysiological and histological study of 12 patients.

The present paper describes the clinical, electrophysiological and histological findings made in 12 patients belonging to 2 genealogical lineages in Switzerland, suffering from paramyotonia congenita. This is the first report of this disease in Switzerland. The myopathy, transmitted by autosomal dominant inheritance, is characterized by a typical past medical history and by the persistent contraction of the muscles of the face, arms and legs provoked by exposure to cold. Also of diagnostic importance are the myotonic reactions inducible at room temperature, such as percussion myotonia, active myotonia and paradoxical myotonia. During paramyotonic episodes provoked by exposure of the subjects in a refrigeration chamber, serum potassium concentrations remained within normal limits. Potassium loading producing serum levels above 6 mEq/1 in 2 patients gave rise to stiffness and weakness of the arms and legs, but no signs of paralysis. Induced hypokalemia in 3 cases caused no paramyotonic symptoms. Electromyographic recordings in 5 patients showed myotonic discharges, which disappeared upon cooling of the limb, giving way to progressive muscular stiffness. Histological, histochemical and electronmicroscopical examination of the muscle tissue revealed only diagnostically unspecific myopathological changes.

Cold Temperature↗
PubMed1990

Ataxia in myxoedema: a neurophysiological reassessment.

In a long-standing case of myxoedema with ataxia and dysarthria, neurophysiological investigations were carried out to assess how much of the ataxic dysbasic syndrome depended on the slowness of mechanical contraction and how much resulted from primary cerebellar involvement. It was observed that the Achilles reflexogram showed a marked prolongation of contraction and relaxation time and that in both quadriceps and triceps surae mechanical percussion induced a marked myxoedema and prolonged relaxation time. The EMG of these muscles during voluntary contraction and stopping reaction detected an excessive recruitment of the antagonistic muscles, starting without any abnormal delay, a finding at variance with a typical cerebellar pattern. Post-urographic analysis gave a pattern of oscillations still within the normal range. These findings suggest that the gait alterations of our patient depended on the increase in muscle contraction time and the consequent excessive recruitment of the antagonists.

Achilles Tendon↗
PubMed1986

Facilitation and inhibition of synaptic transmission in the spinal cord: an electroneurographic study in humans.

The neurographic activity evoked either by stimulation of the tibial nerve at the popliteal fossa or by percussion of the Achilles tendon has been recorded at lumbar and thigh levels, in order to find out whether conduction time, temporal dispersion and central delay of the neural volleys underlying the monosynaptic reflex (H or T) may change as a function of stimulus intensity; under facilitatory or inhibitory experimental conditions; "spontaneously", i.e. during the steady state. The reflexly evoked ventral root discharge (VRD) decreases in latency with increasing stimulus intensity up to the maximum reflex response in the absence of changes in afferent (thigh to spine) or efferent (spine to thigh) conduction times. Reduction of the central delay was greater with mechanical than electrical stimulation, probably due to the combined effect of spatial and temporal summation under the former experimental condition. The latency of the VRD related to the maximal H response was not further modified by supramaximal stimulus strengths. The Jendrassik manoeuvre caused a significant decrease in latency of the VRD, the opposite effect being observed during calf muscle vibration. A significant relationship between amplitude and latency of single VRDs could be demonstrated during the "steady state". Our data point to the existence of a positive correlation between the size of the motoneuronal pool activated by an afferent volley and speed of transmission in the reflex pathway, both during the "steady state" and under either facilitatory or inhibitory experimental conditions, provided that the test stimulus strength does not exceed the maximum reflex response (H or T). No detectable signs of peripheral dispersion of the VRD could be demonstrated, irrespective of the stimulus employed: this suggests that the axon diameters of the motoneurones contributing to the monosynaptic reflex fall within a fairly narrow distribution.

Adolescent↗
PubMed1992

Epidemiological study of gastrointestinal and liver effects of carbon disulfide.

In the framework of an extensive health survey, 119 viscose rayon workers exposed to carbon disulfide (CS2) and 79 workers from other plants not exposed to any toxic agent in the working environment underwent a gastrointestinal examination including a self-administered questionnaire, abdominal palpation, percussion and a number of liver function tests. In the viscose rayon factory the working conditions have not changed since 1932. Personal monitoring performed in 17 jobs showed CS2 exposures varying from 4 to 112 mg.m-3. For each individual a cumulative CS2 exposure index (CS2 index) was calculated. Univariate analysis of the questionnaire findings showed significantly higher prevalences of anorexia (37.0% vs 11.4%, P less than 0.0001), vomiting (12.6% vs 3.8%, P = 0.04), and recent weight loss (10.9% vs 1.3%, P = 0.009) in the exposed than in the non-exposed workers. The exposed workers had a larger total number of gastrointestinal complaints and a larger proportion reported at least one complaint at least once a month than the non-exposed ones. Abdominal tenderness was very rare in both groups. In multiple logistic regression analysis, adjusting for alcohol intake, smoking, body mass index (BMI), coffee consumption, commuting time, stress at work, shift work, educational level, family history of ulcer disease and intake of medication, significant associations with exposure were found for anorexia (P = 0.0001), nausea (P = 0.009), vomiting (P = 0.002) and flatulence (P = 0.03). Stress at work was a determinant for quite a few digestive complaints, but shift work was not significantly associated with any of them.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗