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PubMed1998

Glutamate antagonism during secondary deafferentation enhances cognition and axo-dendritic integrity after traumatic brain injury.

The combination of central fluid percussion traumatic brain injury (TBI) followed 24 h later by a bilateral entorhinal cortical deafferentation (BEC) produces profound cognitive morbidity. We recently showed that MK-801 given prior to TBI in this insult improved spatial memory for up to 15 days. In the present study we examine whether MK-801 treatment of the BEC component in the combined insult model affects cognitive recovery. Two strategies for drug treatment were tested. Fifteen minutes prior to the BEC lesion in the combined insult, rats were given i.p. doses of either 3 mg/kg (acute group) or 1 mg/kg (chronic group) MK-801. The acute group received no further injections, whereas the chronic group received 1 mg/kg MK-801 i.p. twice a day for 2 days post-BEC lesion. Two additional groups of animals received BEC lesion alone and either acute or chronic MK-801 treatment identical with the combined insult cases. Each group was then assessed for spatial memory deficits with the Morris water maze at days 11-15 and 60-64 postinjury. Both acute and chronic MK-801 treatment in the combined insult group significantly reduced spatial memory deficits at 15 days postinjury relative to untreated injured cases (P < .01). This reduction appeared more robust at 15 days and persisted for up to 64 days in the chronically treated group (P < .05). By contrast, neither acute nor chronic MK-801 treatment affected memory performance with the BEC insult alone. Immunocytochemical localization of parvalbumin showed that chronic administration of MK-801 in the combined insult cases attenuated the injury-induced dendritic atrophy of inhibitory neurons in the dentate gyrus and area CA1. Synaptophysin immunobinding revealed that chronic MK-801 treatment of the BEC component of the combined insult normalized the distribution of presynaptic terminals within the dentate gyrus. These results suggest that cognitive deficits produced by head trauma involving both neuroexcitation and deafferentation can be attenuated with chronic application of glutamatergic antagonists during the period of deafferentation injury and that this attenuation is correlated with axo-dendritic integrity.

Afferent Pathways↗
PubMed2001

Preoxygenation for tracheal suctioning in intubated, ventilated newborn infants.

BACKGROUND: Endotracheal suctioning for mechanically ventilated infants is routine practice in neonatal intensive care. However, this practice is associated with serious complications including lobar collapse, pneumothorax, bradycardia and hypoxemia. Increasing the inspired oxygen immediately prior to suction (preoxygenation) has been proposed as an intervention to minimise the risk of complications. OBJECTIVES: To compare the effects of preoxygenation with no preoxygenation for endotracheal suctioning on ventilated newborn infants. To conduct sub group analyses by i) different populations of newborn infants; by gestational age <30 weeks, <34 weeks and <37 weeks and by disease; infants with chronic lung disease compared to those without and; ii) by different techniques of endotracheal suctioning; with or without disconnection from the ventilator, increased mechanical ventilation, use of manual ventilation and chest wall vibrations or percussion. SEARCH STRATEGY: The standard search strategy of the Neonatal Review Group was used. This included searches of electronic databases; Oxford Database of Perinatal Trials; Cochrane Controlled Trials Register (Cochrane Library Issue 1 2001); MEDLINE (1966 - April 2001); and CINAHL (1982-2001) using MeSH term infant-newborn and text terms oxygen* and suction*, preoxygenation, pre-oxygenation and premature and also previous reviews including cross references, abstracts in conferences and symposia proceedings, expert informants, journal hand searching in the English language. SELECTION CRITERIA: Random or quasi random controlled trials of mechanically ventilated neonates in which endotracheal suctioning with preoxygenation was compared to suctioning without preoxygenation. DATA COLLECTION AND ANALYSIS: Standard methods of the Cochrane Collaboration and its Neonatal Review Group were used, including independent assessment of trial quality and extraction of data by the authors. Data were analysed using relative risk (RR) for dichotomous outcomes and mean difference (MD) for data measured on a continuous scale with the use of 95% confidence intervals. Meta-analysis was conducted using a fixed effects model. MAIN RESULTS: One cross-over trial involving outcomes for 16 preterm neonates was included in this review. Preoxygenation, prior to an endotracheal suctioning procedure involving two suctions, resulted in a statistically significant reduction in infants with hypoxemia (TcPO2 <40 mmHg) at the end of the first suction (RR 0.18, 95% CI 0.05, 0.69), at the end of the second suction (RR 0.23, 95% CI 0.08, 0.66) and also at 120 seconds after the second suction (RR 0.10, 95% CI 0.01, 0.69). Mean TcPO2 was statistically significantly higher in the preoxygenation group at the end of the first suction (MD 25.00 mmHg, 95%CI 14.20, 35.80), second suction (MD 24.80, 95% CI 14.80, 34.80) and also at 120 seconds after the second suction (MD 29.10, 95% CI 14.96, 43.24). The time taken to return to baseline oxygenation status was shorter than the group not receiving preoxygenation (MD -2.12 minutes, 95% CI -3.82, -0.42). REVIEWER'S CONCLUSIONS: No recommendations for practice can be confidently made from the results of this review. Although preoxygenation was shown to decrease hypoxemia at the time of suctioning, other clinically important short and longer-term outcomes including adverse effects were unable to be assessed. Further studies are needed to adequately assess the effects of this widely practiced procedure.

Humans↗
PubMed2006

Drug treatment for myotonia.

BACKGROUND: Abnormal delayed relaxation of skeletal muscles, known as myotonia, can cause disability in myotonic disorders. Sodium channel blockers, tricyclic antidepressive drugs, benzodiazepines, calcium-antagonists, taurine and prednisone may be of use in reducing myotonia. OBJECTIVES: To consider the evidence from randomised controlled trials on the efficacy and tolerability of drug treatment in patients with clinical myotonia due to a myotonic disorder. SEARCH STRATEGY: We searched the Cochrane Neuromuscular Disease Group trials register (April 2004), MEDLINE (January 1966 to December 2003) and EMBASE (January 1980 to December 2003). Grey literature was handsearched and reference lists of identified studies and reviews were examined. Authors, disease experts and manufacturers of anti-myotonic drugs were contacted. SELECTION CRITERIA: We considered all (quasi) randomised trials of participants with myotonia treated with any drug treatment versus no therapy, placebo or any other active drug treatment. The primary outcome measure was:reduced clinical myotonia using two categories: (1) no residual myotonia or improvement of myotonia or (2) No change or worsening of myotonia. Secondary outcome measures were:(1) clinical relaxation time; (2) electromyographic relaxation time; (3) stair test; (4) presence of percussion myotonia; and (5) proportion of adverse events. DATA COLLECTION AND ANALYSIS: Two authors extracted the data independently onto standardised extraction forms and disagreements were resolved by discussion. MAIN RESULTS: Nine randomised controlled trials were found comparing active drug treatment versus placebo or another active drug treatment in patients with myotonia due to a myotonic disorder. Included trials were double-blind or single-blind crossover studies involving a total of 137 patients of which 109 had myotonic dystrophy type 1 and 28 had myotonia congenita. The studies were of poor quality. Therefore, we were not able to analyse the results of all identified studies. Two small crossover studies without a washout period demonstrated a significant effect of imipramine and taurine in myotonic dystrophy. One small crossover study with a washout period demonstrated a significant effect of clomipramine in myotonic dystrophy. Meta-analysis was not possible. AUTHORS' CONCLUSIONS: Due to insufficient good quality data and lack of randomised studies, it is impossible to determine whether drug treatment is safe and effective in the treatment of myotonia. Small single studies give an indication that clomipramine and imipramine have a short-term beneficial effect and that taurine has a long-term beneficial effect on myotonia. Larger, well-designed randomised controlled trials are needed to assess the efficacy and tolerability of drug treatment for myotonia.

Humans↗
PubMed2005

Antibiotic use for irreversible pulpitis.

BACKGROUND: Irreversible pulpitis, which is characterised by acute and intense pain, is one of the most frequent reasons that patients attend for emergency dental care. Apart from removal of the tooth the customary way of relieving the pain of irreversible pulpitis is by drilling into the tooth, removing the inflamed pulp (nerve) and cleaning the root canal. However, a significant minority of dentists continue to prescribe antibiotics to stop the pain of irreversible pulpitis. OBJECTIVES: The objective of this review was to provide reliable evidence regarding the effectiveness of prescribing systemic antibiotics for irreversible pulpitis by comparing clinical outcomes expressed as pain relief. SEARCH STRATEGY: We searched the following databases: Cochrane Oral Health Group Trials Register and Pain, Palliative Care and Supportive (PaPaS) Care Group Trials Register to 6th September 2004; the Cochrane Central Register of Controlled Trials (CENTRAL) The Cochrane Library Issue 3 2004; MEDLINE (1966 to 6th September 2004); EMBASE (1980 to week 36 2004). SELECTION CRITERIA: This review includes one randomised controlled trial which compared pain relief with systemic antibiotics and analgesics, against placebo and analgesics in the acute preoperative phase of irreversible pulpitis. DATA COLLECTION AND ANALYSIS: Only one trial is included in this review, therefore pooling of data from studies was not possible and a descriptive summary is presented. MAIN RESULTS: One trial involving 40 participants was included in this review. There was a close parallel distribution of the pain ratings in both the intervention and placebo groups over the 7 day study period. The between-group differences in sum pain intensity differences (SPID) for the penicillin group were (6.0+/-10.5), and for placebo (6.0+/-9.5) P = 0.776. The sum pain percussion intensity differences (SPPID) for the penicillin group were (3.5+/-7.5) and placebo (2.0+/-7.0) P = 0.290, with differences as assessed by the Mann-Whitney-Wilcoxon test considered to be statistically significant at P < 0.05. There was no significant difference in the mean total number of ibuprofen tablets (P = 0.839) and Tylenol tablets (P = 0.325), in either group over the study period. The administration of penicillin over placebo did not appear to significantly reduce the quantity of analgesic medication taken (P > 0.05) for irreversible pulpitis. AUTHORS' CONCLUSIONS: This review which was based on one methodologically sound but low powered small sample trial provided some evidence that there is no significant difference in pain relief for patients with untreated irreversible pulpitis who did or did not receive antibiotics in addition to analgesics.

Analgesics↗
PubMed2000

Effect of sonic driving on maximal aerobic performance.

The study purpose was to evaluate antecedent binaural stimulation (ABS) on maximal aerobic physical performance. Twenty-two healthy, physically active subjects, 21-34 years, randomly received one of two preparations for each session: 15 min of quiet (BLANK) or percussive sonic driving at 200+ beats per minute (bpm) using a recorded compact disc (FSS, Mill Valley, CA) with headphones (ABS). Baseline HR, blood pressure (BP), and breathing frequency (f(br)) were obtained. During each condition, HR and f(br) were recorded at 3-min intervals. The graded maximal treadmill testing was administered immediately postpreparation session on separate days, with at least 48 h rest between sessions. There were significant differences in the antecedent period means between the two conditions, ABS (HR: 70.2 +/- 10.7 bpm; f(br): 18.5 +/- 3.3 br min(-1); BP: 134.5/87.9 +/- 13.6/9.2 mm Hg) and BLANK (HR: 64.6 +/- 7.9; f(br): 14.3 +/- 2.9; BP: 126.7/80.3 +/- 12.1/8.6). Differences were noted for each 3-min interval and pre- postantecedent period. The maximal graded exercise test (GXT) results showed that there was a small but significant (P < 0.05), increase in maximal VO(2) in the ABS (49.8 +/- 6.8 ml. kg(-1). min(-1)) vs. BLANK (46.7 +/- 8.7) conditions. Related to that finding was a slight increase (0.5 min) in time to exhaustion (P < 0.05). There were no significant differences in HR or RPE (P > 0.05). There may be a latency to ABS related to entrainment or imagery-enhanced warm-up. Am. J. Hum. Biol. 12:558-565, 2000. Copyright 2000 Wiley-Liss, Inc.

Journal Article↗
PubMed1999

Apoptotic neurodegeneration following trauma is markedly enhanced in the immature brain.

Age dependency of apoptotic neurodegeneration was studied in the developing rat brain after percussion head trauma. In 7-day-old rats, mechanical trauma, applied by means of a weight drop device, was shown to trigger widespread cell death in the hemisphere ipsilateral to the trauma site, which first appeared at 6 hours, peaked at 24 hours, and subsided by 5 days after trauma. Ultrastructurally, degenerating neurons displayed features consistent with apoptosis. A decrease of bcl-2 in conjunction with an increase of c-jun mRNA levels, which were evident at 1 hour after trauma and were accompanied by elevation of CPP 32-like proteolytic activity and oligonucleosomes in vulnerable brain regions, confirmed the apoptotic nature of this process. Severity of trauma-triggered apoptosis in the brains of 3- to 30-day-old rats was age dependent, was highest in 3- and 7-day-old animals, and demonstrated a subsequent rapid decline. Adjusting the mechanical force in accordance with age-specific brain weights revealed a similar vulnerability profile. Thus, apoptotic neurodegeneration contributes in an age-dependent fashion to neuropathological outcome after head trauma, with the immature brain being exceedingly vulnerable. These results help explain unfavorable outcomes of very young pediatric head trauma patients and imply that, in this group, an antiapoptotic regimen may constitute a successful neuroprotective approach.

Age Distribution↗
PubMed2002

Heterogeneity for congenital generalized lipodystrophy in seventeen patients from Oman.

Seventeen children with congenital generalized lipodystrophy or Berardinelli-Seip Congenital Lipodystrophy (BSCL) from 12 consanguineous sibships were observed in Oman. All children had widespread absence of adipose tissue from infancy together with apparent muscle hypertrophy and hepatomegaly. They did not appear to represent a single homogenous entity, and it was possible to subclassify the cases into two distinct groups. In the first group of seven cases, the features were similar to other published cases with acanthosis nigricans, raised insulin levels, and insulin resistance. In this group, there was an association between the degree of acanthosis nigricans and the severity of the disorder. Molecular analysis of these cases showed homozygosity at the BSCL2 locus on chromosome 11q13 in four of the seven cases. In the second group of ten cases, there were striking abnormalities in both skeletal and nonskeletal muscle. Reduced exercise tolerance and percussion myoxedema were observed in skeletal muscle, while infantile hypertrophic pyloric stenosis, prominent veins (phlebomegaly), disturbance of cardiac rhythm, and cardiomyopathy were observed in nonskeletal muscle. There was evidence against homozygosity in some cases for the known loci for BSCL, and this group may represent a new clinical syndrome with lipodystrophy at a different genetic location.

Adolescent↗
PubMed2001

Long-term hyperexcitability in the hippocampus after experimental head trauma.

Head injury is a causative factor in the development of temporal lobe epilepsy. However, whether a single episode of concussive head trauma causes a persistent increase in neuronal excitability in the limbic system has not been unequivocally determined. This study used the rodent fluid percussion injury (FPI) model, in combination with electrophysiological and histochemical techniques, to investigate the early (1 week) and long-term (1 month or longer) changes in the hippocampus after head trauma. Low-frequency, single-shock stimulation of the perforant path revealed an early granule cell hyperexcitability in head-injured animals that returned to control levels by 1 month. However, there was a persistent decrease in threshold to induction of seizure-like electrical activity in response to high-frequency tetanic stimulation in the hippocampus after head injury. Timm staining revealed both early- and long-term mossy fiber sprouting at low to moderate levels in the dentate gyrus of animals that experienced FPI. There was a long-lasting increase in the frequency of spontaneous inhibitory postsynaptic currents in dentate granule cells after FPI, and ionotropic glutamate receptor antagonists selectively decreased the spontaneous inhibitory postsynaptic current frequency in the head-injured animals. These results demonstrate that a single episode of experimental closed head trauma induces long-lasting alterations in the hippocampus. These persistent structural and functional alterations in inhibitory and excitatory circuits are likely to influence the development of hyperexcitable foci in posttraumatic limbic circuits.

Animals↗
PubMed1979

Ontogeny of spontaneous blinking and of habituation of the blink reflex.

Habituation of the blink reflex to glabellar percussion was examined in 164 infants and children from ages 2 days to 18 years and in 18 adults aged 18 to 50 years. Spontaneous blink rates were measured in 269 children and 179 adults. The mean number of glabellar taps required for habituation of the blink reflex increased from 2.7 (SD 1.2) at 0 to 2 months of age to a peak of 13.3 (SD 5.6) at age 3 to 4, remained at more than 10 until age 6, after which a rapid decline occurred, reaching the adult level of 2 to 5 blinks to habituation at age 12 years. The mean rate of spontaneous blinking was less than 2 per minute in early infancy and increased steadily during childhood up to age 14 or 15. The inverse relationship of spontaneous blink rate and number of blink reflexes to habituation in early childhood and in disorders of dopamine transmission suggests that spontaneous blink rate and habituation of the blink reflex reflect maturation and integrity of dopaminergic circuits in the brain.

Adolescent↗
PubMed1980

Cylindrical spirals in a familial neuromuscular disorder.

Cylindrical spirals are unique membranous structures that were detected in skeletal muscle of a mother and one of her two children; all three have percussion myotonia but no evidence of weak or wasted skeletal muscles. Muscle cramps, stiffness, posteffort muscle tightness, myotonic lid lag, and the cylinders appear or progress with age, but the disorder is asymptomatic in the children and only mildly incapacitating in the mother. The cylinders are 8 mu long and 1 mu wide, are composed of spiraling double-laminate membrane resembling myelin, and are derived from abnormal subsarcolemmal tubulovesicular structures that are interpreted as pathological T-tubes.

Adult↗
PubMed1992

The importance of the T cell in initiating and maintaining the chronic synovitis of rheumatoid arthritis.

We hope that this short review has produced convincing, although indirect, evidence that in the case of rheumatoid synovitis, the T cell is the conductor of an orchestra playing a tune written by an antigen-presenting cell. The tune develops and becomes modified with time, so that it is difficult to discern with clarity much of the original melody. We believe that it may be possible to substitute a new score that will bring this symphony to a harmonious end. We also strongly believe that this is preferable to augmenting the string section or suppressing the percussion section of the orchestra in the vain hope that in the end harmony can be achieved. The final musical analogy must be the hope that the first page of the score can be found, so that we may discover the main theme, the leitmotif, of the rheumatoid-specific antigenic peptide.

Animals↗
PubMed2004

Meta-analysis of the clinical and laboratory diagnosis of appendicitis.

BACKGROUND: The importance of specific elements in the clinical diagnosis of appendicitis is controversial. This review analyses the diagnostic value of elements of disease history, clinical findings and laboratory test results in suspected appendicitis. METHODS: A systematic Medline search was made of all published studies on the clinical and laboratory diagnosis of appendicitis in patients admitted to hospital with suspected disease. Meta-analyses of receiver-operator characteristic (ROC) areas, and positive and negative likelihood ratios, of 28 diagnostic variables described in 24 studies are presented. RESULTS: Inflammatory response variables (granulocyte count, proportion of polymorphonuclear blood cells, white blood cell count and C-reactive protein concentration), descriptors of peritoneal irritation (rebound and percussion tenderness, guarding and rigidity) and migration of pain were the strongest discriminators, with ROC areas of 0.78 to 0.68. The discriminatory power of the inflammatory variables was particularly strong for perforated appendicitis, with ROC areas of 0.85 to 0.87. Appendicitis was likely when two or more inflammatory variables were increased and unlikely when all were normal. CONCLUSION: Although all clinical and laboratory variables are weak discriminators individually, they achieve a high discriminatory power when combined. Laboratory examination of the inflammatory response, clinical descriptors of peritoneal irritation, and a history of migration of pain yield the most important diagnostic information and should be included in any diagnostic assessment.

Appendicitis↗
PubMed2002

Clinical anatomy as the basis for clinical examination: development and evaluation of an Introduction to Clinical Examination in a problem-oriented medical curriculum.

Clinical anatomy is usually defined as anatomy applied to patient care. The question is asked whether students of a new horizontally and vertically integrated medical curriculum recognize the subject as the basis for clinical examination. A clinical anatomy practicum was developed in the special activity, "Introduction to Clinical Medicine," held in the second year of the Pretoria medical curriculum. The practicum was conducted on a station basis to anatomically prepare the student for the inspection, palpation, percussion, and auscultation of the cardiovascular, respiratory, abdominal, and urogenital systems. A total of 23 stations consisting of eight cardiovascular, seven respiratory, and eight abdominal/urogenital stations were designed. Standardized patients, cadavers, skeletons, prosected specimens, x-rays, computed tomography (CT) scans, magnetic resonance imaging (MRI), multimedia programs, and clinical case studies were used as resources. A Likert-type questionnaire was used for student evaluation of the practicum. Most students realized the importance of surface anatomy for a family physician. More than two-thirds thought the practicum improved their understanding of the anatomical basis for clinical examination. The minority of students were stimulated to do further reading on clinical examination. The students' response to their ability to integrate the clinical examination with the radiological anatomy was average. Most students were continuously aware of the appropriateness of the practicum for their future career. We conclude that medical students recognize the importance of anatomy as the basis for clinical examination when exposed to an appropriate integrated presentation format.

Anatomy↗
PubMed2003

Early loss of astrocytes after experimental traumatic brain injury.

Neuronal-glial interactions are important for normal brain function and contribute to the maintenance of the brain's extracellular environment. Damage to glial cells following traumatic brain injury (TBI) could therefore be an important contributing factor to brain dysfunction and neuronal injury. We examined the early fate of astrocytes and neurons after TBI in rats. A total of 27 rats were euthanized at 0.5, 1, 2, 4, or 24 h after moderate lateral fluid percussion TBI or after sham TBI. Ipsilateral and contralateral hippocampi were examined in coronal sections from -2.12 to -4.80 mm relative to bregma. Adjacent sections were processed with markers for either astrocytes or degenerating neurons. Astrocytes were visualized using glial fibrillary acidic protein (GFAP) or glutamine synthetase immunohistochemistry. Neuronal degeneration was visualized using Fluoro-Jade (FJ) histofluorescence. At 30 min, there was a significant loss of GFAP immunoreactivity in ipsilateral hippocampal CA3 with some loss of normal astrocyte morphology in the remaining cells. The number of normal staining astrocytes decreased progressively over time with extensive astrocyte loss at 24 h. At 4 h, lightly stained FJ-positive neurons were scattered in the ipsilateral CA3. The intensity and number of FJ-positive neurons progressively increased over time with moderate numbers of degenerating neurons in the ipsilateral hippocampal CA3 evident at 24 h. We conclude that astrocyte loss occurs in the hippocampus early after TBI. The data suggest that loss of supporting glial cell may contribute to subsequent neuronal degeneration.

Animals↗
PubMed1996

Fulminant hepatitis in a tropical population: clinical course, cause, and early predictors of outcome.

The profiles of patients with fulminant hepatic failure (FHF) from developing countries have not been reported earlier. The current study was conducted prospectively, at a single tertiary care center in India, to document the demographic and clinical characteristics, natural course, and causative profile of patients with FHF as well as to define simple prognostic markers in these patients. Four hundred twenty-three consecutive patients with FHF admitted from January 1987 to June 1993 were included in the study. Each patient's serum was tested for various hepatotropic viruses. Univariate Cox's regression for 28 variables, multivariate Cox's proportional hazard regression, stepwise logistic regression, and Kaplan-Meier survival analysis were done to identify independent predictors of outcome at admission. All patients presented with encephalopathy within 4 weeks of onset of symptoms. Hepatotropic viruses were the likely cause in most of these patients. Hepatitis A (HAV), hepatitis B (HBV), hepatitis D (HDV) viruses, and antitubercular drugs could be implicated as the cause of FHF in 1.7% (n= 7), 28% (n= 117), 3.8% (n= 16), and 4.5% (n= 19) patients, respectively. In the remaining 62% (n= 264) of patients the serological evidence of HAV, HBV, or HDV infection was lacking, and none of them had ingested hepatotoxins. FHF was presumed to be caused by non-A, non-B virus(es) infection. Sera of 50 patients from the latter group were tested for hepatitis E virus (HEV) RNA and HCV RNA. In 31 (62%), HEV could be implicated as the causative agent, and isolated HCV RNA could be detected in 7 (19%). Two hundred eighty eight (66%) patients died. Approximately 75% of those who died did so within 72 hours of hospitalisation. One quarter of the female patients with FHF were pregnant. Mortality among pregnant females, nonpregnant females, and male patients with FHF was similar (P > .1). Univariate analysis showed that age, size of the liver assessed by percussion, grade of coma, presence of clinical features of cerebral edema, presence of infection, serum bilirubin, and prothrombin time prolongation over controls at admission were related to survival (P < .01). The rapidity of onset of encephalopathy and cause of FHF did not influence the outcome. Cox's proportional hazard regression showed age > or = 40 years, presence of cerebral edema, serum bilirubin > or = 15 mg/dL, and prothrombin time prolongation of 25 seconds or more over controls were independent predictors of outcome. Ninety-three percent of the patients with three or more of the above prognostic markers died. The sensitivity, specificity, positive predictive value, and the negative predictive value of the presence of three or more of these prognostic factors for mortality was 93%, 80%, 86%, and 89.5%, respectively, with a diagnostic accuracy of 87.3%. We conclude that most of our patients with FHF might have been caused by hepatotropic viral infection, and non-A, non-B virus(es) seems to be the dominant hepatotropic viral infection among these patients. They presented with encephalopathy within 4 weeks of the onset of symptoms. Pregnancy, cause, and rapidity of onset of encephalopathy did not influence survival. The prognostic model developed in the current study is simple and can be performed at admission.

Adolescent↗
PubMed2006

Mechanisms underlying the inability to induce area CA1 LTP in the mouse after traumatic brain injury.

Traumatic brain injury (TBI) is a significant health issue that often causes enduring cognitive deficits, in particular memory dysfunction. The hippocampus, a structure crucial in learning and memory, is frequently damaged during TBI. Since long-term potentiation (LTP) is the leading cellular model underlying learning and memory, this study was undertaken to examine how injury affects area CA1 LTP in mice using lateral fluid percussion injury (FPI). Brain slices derived from FPI animals demonstrated an inability to induce LTP in area CA1 7 days postinjury. However, area CA1 long-term depression could be induced in neurons 7 days postinjury, demonstrating that some forms of synaptic plasticity can still be elicited. Using a multi-disciplined approach, potential mechanisms underlying the inability to induce and maintain area CA1 LTP were investigated. This study demonstrates that injury leads to significantly smaller N-methyl-D-aspartate potentials and glutamate-induced excitatory currents, increased dendritic spine size, and decreased expression of alpha-calcium calmodulin kinase II. These findings may underlie the injury-induced lack of LTP and thus, contribute to cognitive impairments often associated with TBI. Furthermore, these results provide attractive sites for potential therapeutic intervention directed toward alleviating the devastating consequences of human TBI.

Animals↗
PubMed2004

Acute treatment with MgSO4 attenuates long-term hippocampal tissue loss after brain trauma in the rat.

Previous studies have shown that magnesium salts and the noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist, NPS 1506, attenuated short-term cognitive deficits and histopathological changes associated with traumatic brain injury (TBI). We evaluated the long-term effects of both therapies after brain trauma. Young adult rats were subjected to parasagittal fluid-percussion brain injury and received either MgSO(4) (125 micromol/400 g rat; n = 12) 15 min post-injury, NPS 1506 (1.15 mg/kg; n = 12) 15 min and 4 hr post-injury, or vehicle (n = 9) 15 min post-injury. Uninjured animals (sham) received vehicle (n = 10). Learning function in these animals was evaluated using a water maze paradigm 8 months after injury or sham treatment, and the brains were examined for cortical and hippocampal tissue loss. Compared to sham animals, injured vehicle-treated animals displayed a substantial learning dysfunction, indicated by an increased latency to find a hidden platform in the water maze (P < 0.001). No improvements in learning, however, were found for injured animals treated with NPS 1506 or MgSO(4). Injury induced >30% loss of tissue in the ipsilateral cortex in vehicle-treated animals that was not reduced in animals treated with either NPS 1506 or MgSO(4). Treatment with MgSO(4) significantly reduced progressive tissue loss in the hippocampus (P < 0.001). These findings are the first to demonstrate long-term neuroprotection of hippocampal tissue by an acute treatment in a TBI model. These data also show that the previously reported broad efficacy of MgSO(4) or NPS 1506 observed shortly after brain trauma could not be detected 8 months post-injury.

Animals↗
PubMed2005

Traumatic brain injury induces biphasic upregulation of ApoE and ApoJ protein in rats.

Apolipoproteins play an important role in cell repair and have been found to increase shortly after traumatic brain injury (TBI). In addition, apolipoproteins reduce amyloid-beta (Abeta) accumulation in models of Alzheimer's disease. Considering that TBI induces progressive neurodegeneration including Abeta accumulation, we explored potential long-term changes in the gene and protein expression of apolipoproteins E and J (ApoE and J) over 6 months after injury. Anesthetized male Sprague-Dawley rats were subjected to parasagittal fluid-percussion brain injury and their brains were evaluated at 2, 4, 7, 14 days, and 1 and 6 months after TBI. In situ hybridization, Western blot, and immunohistochemical analysis demonstrated that although there was a prolonged upregulation in both the gene expression and protein concentration of ApoE and J after injury, these responses were uncoupled. Upregulation of ApoE and J mRNA expression lasted from 4 days to 1 month after injury. In contrast, a biphasic increase in protein concentration and number of immunoreactive cells for ApoE and ApoJ was observed, initially peaking at 2 days (i.e., before increased mRNA expression), returning to baseline by 2 weeks and then gradually increasing through 6 months postinjury. In addition, ApoE and J were found to colocalize with Abeta accumulation in neurons and astrocytes at 1-6 months after injury. Collectively, these data suggest that ApoE and J play a role in the acute sequelae of brain trauma and reemerge long after the initial insult, potentially to modulate progressive neurodegenerative changes.

Amyloid beta-Peptides↗