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PubMedDate not supplied

Somatosensory evoked potentials in prolonged postcomatose unawareness state following traumatic brain injury.

Somatosensory evoked potentials (SEPs) were found by several authors to have a prognostic value in traumatically brain-injured (TBI) patients and can serve for monitoring changes in the state of TBI patients. Most of the studies were performed in the acute phase of trauma and most of reports have dealt with the short-latency components. The present study reports on seven patients (mean age 26.2 years) who suffered severe blunt TBI and were in prolonged post-comatose unawareness (PCU) state, in whom early and late SEP components were recorded at least 5 weeks after sustaining trauma. The SEPs studied could not reveal a uniform pattern apart from prolonged central conduction time (CCT), which was common to all patients. This may be due to individual non-homogeneous patterns of brain damage in our severe TBI patients. Meaningful late recovery of consciousness occurred in one patient and correlated with shortening of CCT. We suggest that the prolonged CCT found in our patients is related to diffuse subcortical axonal injury and that the shortened CCT found during the second examination in this patient actually reflects late partial recovery--either structural or functional--of affected brain regions. This patient is also an example of the possible relationship between reduction of CCT and recovery of consciousness a long time after injury.

Activities of Daily Living↗
PubMed2001

Studies on the mechanisms responsible for the formation of focal swellings on neuronal processes using a novel in vitro model of axonal injury.

A novel in vitro model of axonal injury using PC12 cells was designed to introduce traumatic alterations on neuronal processes and to identify mechanisms responsible for the formation of focal swellings by observation with phase-contrast and transmission electron microscopes. The injury on the processes was produced by one-dimensional, horizontal oscillation. The fluid shear stress applied by the oscillation did not exceed 380 dyne/cm2. The injured processes showed two forms. One involved an increase in the terminal diameter of the processes and the other entailed beading along the injured portions. Long-term observation of cellular responses to the mechanical insult disclosed that the terminal swelling coincided with the detachment of growth cones from the culture plate. The finding suggests that the detachment of the growth cone destroys the cytoskeletal network, which determines and maintains the cell shape, resulting in spherical deformation of the processes. When the cytoskeletal destruction occurred at non-terminal sites along the processes, spherical deformations developed slowly, and these appeared as beads. The beading also caused the detachment of the growth cones. As the most proximal bead grew, they absorbed the distal segment and their growth cones were pulled proximally with the spreading cytoskeletal destruction. The processes with terminal swellings as well as the bead segments showed regeneration with time evidence of and growth cone formation.

Animals↗
PubMed2006

Metabotropic glutamate receptor antagonists and agonists: potential neuroprotectors in diffuse brain injury.

Our previous study has suggested that metabotropic glutamate receptors (mGluRs) were significantly involved in the secondary processes after diffuse brain injury (DBI) and that mGluRs antagonists or agonists may be used for the treatment of DBI. In the present study, the neuroprotective effects of antagonists or agonists of mGluRs on DBI were further investigated. Sprague-Dawly rats were randomized into the following six groups: (i) normal control; (ii) sham-operated control; (iii) DBI; (iv) DBI treated with normal saline (NS); (v) DBI treated with alpha-methyl-4-carboxy-phenylglycine (MCPG); and (vi) DBI treated with (2S,1'R,2'R,3'R)-2-(2,3-dicarboxycyclopropyl)glycine (DCG-IV). Animals were injected intracerebroventricularly (icv) with 10 microL MCPG (100mmol/L), DCG-IV (10nmol/L) or the equivalent volume of normal saline 1 h after injury. The neurological severity score (NSS), brain water content and the number of damaged neurons were determined 6, 12, 24, 72 and 168 h after injury. In rats with DBI, it was found that the NSS was improved and the water content in the frontal cortex and the number of damaged neurons in the parietal cortex were significantly reduced following icv injection of either MCPG or DCG-IV. This suggests that icv injection of the mGluR group I antagonist MCPG or the mGluR group II agonist DCG-IV may exert neuroprotective effects in the early stage after DBI.

Animals↗
PubMed1996

Susceptibility of the injured rat brain to CNS oxygen toxicity.

The possibility of an altered susceptibility of the injured brain to central nervous system (CNS) oxygen toxicity was examined in awake rats. Moderate to severe closed head injury with diffuse axonal damage was produced in anesthetized rats by the fluid percussion method (2-2.5 atm), after which chronic EEG electrodes were implanted. Twenty-four hours later, the rats were exposed to 5 atm abs (506.5 kPa) oxygen and the time to appearance of paroxysmal EEG patterns was noted. The difference between the 19 minute median latency of this group and 16 minute of a control group which underwent a sham operation did not reach statistical significance. Some injured animals convulsed with minimal or no EEG changes. The clinical implication could be that brain injured patients are not at higher risk of CNS oxygen toxicity but the EEG alterations that could potentially be used to forecast incipient convulsions, or be the indication of actual convulsions in the intact brain of a paralyzed patient, may not always be present.

Analysis of Variance↗
PubMed2004

Traumatic axonal injury is exacerbated following repetitive closed head injury in the neonatal pig.

Inflicted brain injury is associated with widespread traumatic axonal injury (TAI) and subdural hematoma and is the leading cause of death in infants and children. Anesthetized 3-5-day-old piglets were subjected to either a single (n = 5) or double (n = 6, 15 min apart) rapid (<15 msec), non-impact, axial rotations of the head. Peak rotational velocities (averaging 172 rad/sec for single and 138 rad/sec for double loads) were lower than those utilized to induce severe injuries (240-260 rad/sec; Raghupathi and Margulies, 2002). At 6 h post-injury, brains were evaluated for the presence TAI using immunohistochemistry for the 200-kDa neurofilament protein (NF200). Accumulation of NF200 was observed in both contiguous (swellings) and in disconnected axons (axon bulbs) predominantly in central deep and peripheral subcortical white matter regions in the frontal, temporal, and parietal lobes of all injured piglets. Although the density of injured axons did not significantly increase after two rotational loads, the distribution of injured axons shifted from a few foci (2.2 +/- 2.3 per animal) with 1-2 swellings/bulbs following a single rotation to significantly more foci (14.7 +/- 11.9), and additional foci (2.5 +/- 1.9) containing 3 or more axon swellings/bulbs following two rotational loads. The density and distribution of injured axons following a single mild rotation were significantly reduced compared with those obtained previously following a single more severe rotational load. Collectively, these data are indicative of the graded response of the immature brain to rotational load magnitude, and importantly, the vulnerability to repeated, mild, non-impact loading conditions.

Animals↗
PubMed2005

[Lesion mechanism dependent, differential changes in neurofilaments and microtubules: a pathological and experimental study].

INTRODUCTION: The consequences of axonal or demyelinating injuries on the axonal cytoskeleton have rarely been described. METHODS: We have compared the density of fibers labeled by anti-neurofilaments (NF) and -beta tubulin (TUB) to the density of total fibers in nine patients with axonal neuropathies of undetermined etiology (AUE), six with necrotizing angeitis with neuropathy (NAN), seven with chronic inflammatory demyelinating neuropathy (CIDP) and in five controls, as well as in six patients with chronic multiple sclerosis (MS). We also studied demyelinated rat corpus callosum after lysophosphatidyl (LPC) microinjection. RESULTS: In AUE and NAN NF positive fibers decreased together with total fiber density, whereas TUB increased. In demyelinating lesions TUB was not altered (CIDP) or strongly decreased (MS, LPC); NF were strongly reduced in MS (where axon loss was prominent) and in LPC lesions (despite the lack of fiber degeneration) and for fiber densities<3900/mm2 in CIDP. CONCLUSION: The initial mechanism of a disease, either axonal degeneration or demyelination, could result into a specific pattern of axonal cytoskeleton alterations.

Aged↗
PubMed2006

Proximity of lesioning determines response of facial motoneurons to peripheral axotomy.

We recently found that rubrospinal (RS) neurons, which typify central neurons projecting within the central nervous system (CNS), exhibited different neuronal and glial reactions to axotomy at proximal as opposed to distal sites. To determine whether distance also determines the reaction to axonal injury of central neurons projecting to the periphery, we studied the temporal expression of four free-radical-related enzymes as well as the severity of cell loss, perineuronal astrocytic and microglial reactions, and degeneration of the proximal central axons of facial motoneurons after axotomies performed at various sites on the brainstem surface and in the stylomastoid foramen, respectively. Distal lesions resulted in upregulation of these neurons' expression of nitric oxide synthase (NOS) and persistent downregulation of their expression of the NOS-activating enzyme calcineurin. It also led to transient upregulation of their expression of manganese-dependent superoxide dismutase (Mn-SOD), and resulted in a mild neuronal loss. Proximal axotomy led to an upregulation of NOS but a transient downregulation in the expression of calcineurin and Mn-SOD at 4 weeks after injury. This was accompanied by severe cell loss and swelling of mitochondria at 2-4 weeks postinjury. However, neither proximal nor distal axonal lesioning led to nuclear fragmentation or TUNEL staining of neurons. Proximal as opposed to distal axotomy produced an earlier transformation of glial morphology, including the hypertrophy of astrocytic processes and metamorphosis of ramified microglia to amoeboid cells. We unexpectedly found that unlike RS neurons, whose central axons degenerated slowly and in an anterograde manner only after the severe cell loss induced by proximal axotomy, the central axons of facial motoneurons degenerated rapidly and in a retrograde manner independently of the severity of loss of these neurons after axotomy. However, degeneration began sooner after proximal than after distal axotomy. Since the central axons of both rubrospinal neurons and facial motoneurons lie within the CNS, the differences in whether and how they degenerated after axotomy suggests that central neurons that project within and outside the CNS are inherently different. The significance of these and also the free radical environment regulation differences between these two types of neurons following close and distant axotomies remains to be explored.

Animals↗
PubMed2001

Acquisition of skilled visual search performance following severe closed-head injury.

This study used a semantic-category visual search task to investigate skill acquisition and automatic process development in a severe closed-head injured (CHI) population. Eighteen severe CHI participants (> I year post injury) and 18 matched controls completed over 3600 trials of training in both consistent mapping (CM) and varied mapping (VM) training situations. Transfer conditions were also used to test for development of an automatic attention response (AAR) that was independent of general, task-related learning. For both the severe CHI and control group, CM training, where individuals always responded in the same way to a specific class of stimuli, resulted in dramatic performance improvements and the development of an AAR. In the VM training condition, where individuals could not respond in the same way to a class of stimuli from one stimulus exposure to the next, there was little performance improvement and continued reliance on controlled processes. The visual search rates of the CHI participants also remained slower than those of controls following extended VM but not extended CM practice. These results indicate that skill acquisition training guidelines can be used to teach severe CHI patients to develop a new automatic skill.

Adult↗
PubMed2003

Neurotrophic factors attenuate microvascular permeability disturbances and axonal injury following trauma to the rat spinal cord.

Alterations of the blood-spinal cord barrier (BSCB) following spinal cord injury (SCI) and leakage of serum proteins induce vasogenic edema and cell damage. The possibility that two members of the neurotrophin family, BDNF or IGF-1 induce neuroprotection by attenuating the BSCB permeability following trauma was examined in a rat model. Repeated topical application of BDNF or IGF-1 (0.1 1microg, 0.5 microg or 1 microg in 10 microl) onto the spinal cord 30 min before SCI or 2, 5, 10 or 30 min thereafter significantly attenuated BSCB permeability to Evans blue and iodine. In the neurotrophin treated rats. edema formation, degradation of MBP, and myelin vesiculation were much less frequent compared to the untreated traumatised rats. The protective effect of BDNF and IGF-1 was most pronounced at the high dose (1 microg in 10 microl) given either 30 min before or within 10 min after SCI. The observations suggest that early intervention with neurotrophins in high doses following trauma (within 10 min) attenuates disturbances of the fluid microenvironment of the spinal cord. This indicates that BSCB opening plays an important role in SCI induced myelin vesiculation and cord pathology.

Animals↗
PubMed2001

The effects of sevoflurane and isoflurane on intracranial pressure and cerebral perfusion pressure after diffuse brain injury in rats.

Twenty-four adult male Wistar rats, weighing 220 to 290 g, were anesthetized with 30 mg/kg intraperitoneal sodium thiopental, then underwent a tracheostomy. After diffuse impact-acceleration brain injury (BI) was induced, each rat was paralyzed and mechanically ventilated with 30% O2 in nitrous oxide (N2O). The rats were assigned randomly to two groups, each of which received one of the two volatile anesthetic agents, sevoflurane or isoflurane. The anesthetics were administered at 0.5, 0.75, 1.0, and 1.25 minimal alveolar concentration (MAC) for 30 minutes each, respectively, and anesthesia was maintained at 0.75 MAC during the last hour of the study period. Intracranial pressure (ICP), mean arterial pressure (MAP), rectal and intrahemispheric temperatures, and end-tidal volatile anesthetic concentrations were monitored continuously throughout the 3 hours, with measurements recorded every 15 minutes. At baseline, there were no significant differences between the two groups regarding the monitored physiologic values. In the sevoflurane group, MAP fell significantly after 45 minutes, and a similar change was observed in the isoflurane group after 30 minutes (P < .05, P < .01, and P < .001, respectively). Intracranial pressure increased significantly at 45 minutes in the sevoflurane group (P < .01) and remained elevated from 60 minutes until the end of the study period (P < .01, P < .001). Although ICP increased in the isoflurane group, the change was not significant. Cerebral perfusion pressure (CPP) decreased in parallel with MAP, with the reduction in the sevoflurane group being more pronounced than that in the isoflurane group. The results demonstrated that, under the conditions of diffuse BI, animals that were anesthetized with sevoflurane had higher ICP and lower CPP levels than those anesthetized with isoflurane.

Anesthetics, Inhalation↗
PubMed2003

Lack of improvement in cerebral metabolism after hyperoxia in severe head injury: a microdialysis study.

OBJECT: The authors investigated the effects of hyperoxia on brain tissue PO2 and on glucose metabolism in cerebral and adipose tissue after traumatic brain injury (TBI). METHODS: After 3 hours of ventilation with pure O2, 18 tests were performed on different days in eight comatose patients with TBI. Lactate, pyruvate, glucose, glutamate, and brain tissue PO2 were measured in the cerebral extracellular fluid (ECF) by using microdialysis. Analytes were also measured in the ECF of abdominal adipose tissue. After 3 hours of increase in the fraction of inspired O2, brain tissue PO2 rose from the baseline value of 32.7 +/- 18 to 122.6 +/- 45.2 mm Hg (p < 0.0001), whereas brain lactate dropped from its baseline (3.21 +/- 2.77 mmol/L), reaching its lowest value (2.90 +/- 2.58 mmol/L) after 3 hours of hyperoxia (p < 0.01). Pyruvate dropped as well, from 153 +/- 56 to 141 +/- 56 micromol/L (p < 0.05), so the lactate/pyruvate ratio did not change. No significant changes were observed in glucose and glutamate. The arteriovenous difference in O2 content dropped, although not significantly, from a baseline of 4.52 +/- 1.22 to 4.15 +/- 0.76 m/100 ml. The mean concentration of lactate in adipose tissue fell significantly as well (p < 0.01), but the lactate/pyruvate ratio did not change. CONCLUSIONS: Hyperoxia slightly reduced lactate levels in brain tissue after TBI. The estimated redox status of the cells, however, did not change and cerebral O2 extraction seemed to be reduced. These data indicate that oxidation of glucose was not improved by hyperoxia in cerebral and adipose tissue, and might even be impaired.

Adolescent↗
PubMed2003

Axonal damage: a key predictor of outcome in human CNS diseases.

Axonal damage has recently been recognized to be a key predictor of outcome in a number of diverse human CNS diseases, including head and spinal cord trauma, metabolic encephalopathies, multiple sclerosis and other white-matter diseases (acute haemorrhagic leucoencephalitis, leucodystrophies and central pontine myelinolysis), infections [malaria, acquired immunodeficiency syndrome (AIDS) and infection with human lymphotropic virus type 1 (HTLV-I) causing HTLV-I-associated myelopathy (HAM)/tropical spastic paraparesis (TSP)] and subcortical ischaemic damage. The evidence for axonal damage and, where available, its correlation with neurological outcome in each of these conditions is reviewed. We consider the possible pathogenetic mechanisms involved and how increasing understanding of these may lead to more effective therapeutic or preventive interventions.

AIDS Dementia Complex↗
PubMed2004

Hereditary neuropathy with liability to pressure palsy: fulminant development with axonal loss during military training.

Hereditary neuropathy with liability to pressure palsy (HNPP) is characterised by recurrent mononeuropathies following minor trauma. We describe a case of fulminant HNPP beginning on the first day of military physical training. Protracted weakness, muscle atrophy, hand contractures, and multifocal sensory loss developed during a further three weeks of basic training. Nerve conduction changes were typical of HNPP, but without segmental slowing. Electromyographically, there was prominent acute denervation in muscles of the hands and right shoulder. Sural nerve biopsy demonstrated tomaculae and remyelination. Genetic testing revealed PMP-22 gene deletion. This case report demonstrates that HNPP can present with rapidly progressive peripheral nerve dysfunction and electrophysiological evidence of focal axonal loss.

Adult↗
PubMed2006

Multifocal axonal polyneuropathy in celiac disease.

The authors report six patients with multifocal axonal polyneuropathy and the subsequent diagnosis of celiac disease (CD). Five patients did not improve or had only modest improvement following dietary intervention or immune therapies; one patient with marked weakness and mild electrodiagnostic findings had complete resolution of the neuropathy following immunomodulatory therapy. CD may be a cause of multifocal axonal polyneuropathy.

Adult↗