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PubMed1999

Experimental animal models of traumatic brain injury: medical and biomechanical mechanism.

The numerous traumatic brain injury models were designed to study the nature of the human brain injury. The properties of six experimental injury models were reviewed in this article. Weight-drop models with or without skull protection were compared in terms of experimental setup, possible error source, and biomechanical prospect. The modified percussion models with or without rigid cortical impact were contrasted with regard to reliability, histopathological production, and deformation. The focal contusion model by mechanical suction force represented isolated cortical injury without compression brain injury. As a class of traumatic brain injury, brain retraction damage was reviewed in this article.

Journal Article↗
PubMed2002

Quantitative structural changes in white and gray matter 1 year following traumatic brain injury in rats.

There is evidence for chronic atrophy after human head trauma, which may be associated with long-term functional deficits. However, using established models of traumatic brain injury (TBI) only limited data are available for clarifying the extent of progressive gray and white matter atrophy. In the present study, male Sprague-Dawley rats underwent moderate (2.01-2.21 atm) parasagittal fluid percussion brain injury ( n=7) or sham ( n=3) surgery and were killed at 1 year post TBI. Semiserial sections were obtained through the neuraxis and double stained with hematoxylin and eosin to demarcate gray matter structures and Luxol fast blue for white matter visualization. Both ipsilateral and contralateral volume measurements were obtained for the following structures: cerebral cortex, hippocampus, dentate gyrus, thalamus, lateral ventricle, external capsule, internal capsule, cerebral peduncle and corpus callosum. Quantitative assessment of ipsilateral gray matter structures from TBI rats revealed significant reductions in cerebral cortical area measurements posterior from the trauma epicenter compared to sham animals. Importantly, several white matter tracts exhibited dramatic atrophy. A comparison of TBI and sham groups demonstrated a significant ( P<0.05) decrease in the external capsule and cerebral peduncle volumes ( P<0.007). In addition, there was a significant volume expansion (533% of control) of the ipsilateral lateral ventricle ( P<0.03). These novel data emphasize the need to clarify the pathophysiology of progressive white matter damage after TBI and the development of therapeutic strategies to target white matter pathology.

Animals↗
PubMed2005

Light and electron microscopic assessment of progressive atrophy following moderate traumatic brain injury in the rat.

The presence of progressive white matter atrophy following traumatic brain injury (TBI) has been reported in humans as well as in animal models. However, a quantitative analysis of progressive alterations in myelinated axons and other cellular responses to trauma has not been conducted. This study examined quantitative differences in myelinated axons from several white and gray matter structures between non-traumatized and traumatized areas at several time points up to 1 year. We hypothesize that axonal numbers decrease over time within the structures analyzed, based on our previous work demonstrating shrinkage of tissue in these vulnerable areas. Intubated, anesthetized male Sprague-Dawley rats were subjected to moderate (1.8-2.2 atm) parasagittal fluid-percussion brain injury, and perfused at various intervals after surgery. Sections from the fimbria, external capsule, thalamus and cerebral cortex from the ipsilateral hemisphere of traumatized and sham-operated animals were prepared and. estimated total numbers of myelinated axons were determined by systematic random sampling. Electron micrographs were obtained for ultrastructural analysis. A significant (P<0.05) reduction in the number of myelinated axons in the traumatized hemisphere compared to control in all structures was observed. In addition, thalamic and cortical axonal counts decreased significantly (P<0.05) over time. Swollen axons and macrophage/microglia infiltration were present as late as 6 months post-TBI in various structures. This study is the first to describe quantitatively chronic axonal changes in vulnerable brains regions after injury. Based on these data, a time-dependent decrease in the number of myelinated axons is seen to occur in vulnerable gray matter regions including the cerebral cortex and thalamus along with distinct morphological changes within white matter tracts after TBI. Although this progressive axonal response to TBI may include Wallerian degeneration, other potential mechanisms underlying this progressive pathological response within the white matter are discussed.

Animals↗
PubMed2006

The fate of Nissl-stained dark neurons following traumatic brain injury in rats: difference between neocortex and hippocampus regarding survival rate.

We studied the fate of Nissl-stained dark neurons (N-DNs) following traumatic brain injury (TBI). N-DNs were investigated in the cerebral neocortex and the hippocampus using a rat lateral fluid percussion injury model. Nissl stain, acid fuchsin stain and immunohistochemistry with phosphorylated extracellular signal-regulated protein kinase (pERK) antibody were used in order to assess posttraumatic neurons. In the neocortex, the number of dead neurons at 24 h postinjury was significantly less than that of the observed N-DNs in the earlier phase. Only a few N-DNs increased their pERK immunoreactivity. On the other hand, in the hippocampus the number of dead neurons was approximately the same number as that of the N-DNs, and most N-DNs showed an increased pERK immunoreactivity. These data suggest that not all N-DNs inevitably die especially in the neocortex after TBI. The fate of N-DNs is thus considered to differ depending on brain subfields.

Analysis of Variance↗
PubMed1997

Characterization of a prolonged regenerative attempt by diffusely injured axons following traumatic brain injury in adult cat: a light and electron microscopic immunocytochemical study.

Traumatic brain injury in animals and humans is well known to cause axonal damage diffusely scattered throughout the brain without evidence of other brain parenchymal change. This observation has prompted some to posit that such damaged axons are well positioned to mount a regenerative attempt. The present study uses an immunocytochemical marker specific for regenerating neurites to explore this issue. Further, in an attempt to expedite and enhance any potential regenerative effort, this study evaluates the efficacy of intrathecally applied nerve growth factor. Three sets of experiments were performed in adult cats. One group of animals was subjected to moderate fluid percussion brain injury and followed for 7 or 14 days post injury, with the continuous intraventricular infusion of nerve growth factor delivered by implanted osmotic pumps. These animals were compared to a second group of time-matched, sham-operated animals receiving artificial cerebrospinal fluid infusion. To assess axonal damage immunohistochemical staining for the low molecular weight neurofilament subunit (NF-L) was carried out using an NR4 monoclonal antibody. To localize axons exhibiting a regenerative response immunohistochemical staining for the growth associated protein GAP43 was employed. In sham controls, at the light microscopic level NF-L-immunoreactive axonal swellings were numerous at 7 days, but by 14 days post injury their frequency declined markedly. In contrast, GAP43-immunoreactive, disconnected reactive axonal swellings were rarely observed at 7 days but were numerous at 14 days. Ultrastructural analysis at 14 days post injury of carefully matched sections revealed reactive axons demonstrating sprouting consistent with a regenerative effort. Analysis of tissue from animals of 14 days of survival indicated that supplementation with nerve growth factor did not appear to enhance the capacity of damaged brain axons to mount a regenerative attempt. Rather, it appears that regenerative efforts seen reflect a spontaneous response. A third group of adult cats, subjected to the same injury but not subjected to osmotic pump implantation, was allowed to survive for 22-28 days. Animals in this group also demonstrated GAP43 immunoreactivity in reactive axonal swellings in the brain stem. This study demonstrates that diffusely injured axons can mount a sustained regenerative attempt that is associated with a reorganization of their cytoskeleton and accompanied by an up-regulation of growth-associated proteins.

Animals↗
PubMed1999

Regional and temporal characterization of neuronal, glial, and axonal response after traumatic brain injury in the mouse.

Fluid percussion injury (FPI) is a commonly used and clinically relevant model of traumatic brain injury (TBI) in the rat. Recently, our lab successfully adapted FPI to mice. To account for differences in response to injury between mice and rats and provide a foundation for further use of FPI in gene-targeting studies, we sought to characterize the temporal and regional response to FPI in male C57BL/6 mice. Animals were killed at 10 min, 24 h, and 4, 7, 14, and 35 days (n = 3 for each group) after a very severe parasagittal FPI (> 4.0 atm) or sham injury (n = 3). Extensive numbers of damaged neurons were consistently found in the ipsilateral cortex, thalamus, and hippocampus by 10 min. This damage was nearly identical at 24 h, but quickly declined at subsequent time points. Activated microglia were found only in regions of neuronal injury at the earliest time points. Glial fibrillary acidic protein immunoreactivity reached significantly higher levels compared with controls at 7 days (P < 0. 05) in the cortex, thalamus, and hippocampus and remained elevated for 35 days. White matter degeneration was present in all regions examined. This damage did not appear until at least day 4, but progressed up to day 35. The spatial pattern of damage we observed in mice after FPI is similar to that seen in rats. However, the temporal progression of neuronal injury in mice is comparatively abbreviated in the hippocampus and thalamus. In conclusion, these results suggest that FPI in mice may be a particularly useful tool for studying mechanisms of TBI in gene-targeting studies.

Animals↗
PubMed2005

Paroxysmal positional vertigo as a complication of osteotome sinus floor elevation.

Paroxysmal positional vertigo (PPV) is a high prevalence, vestibular end organ disorder due to the detachment of the utricular otoconia floating in the posterior or lateral semicircular canal. Even though in the majority of cases the etiology of PPV is unknown, it may follow viral infection, vascular disorders and head trauma after different surgical procedures. The aim of this study was to investigate the correlation between PPV and the surgical trauma induced by the vibratory and percussive forces on the upper maxilla during the osteotome sinus floor elevation procedure. We performed a complete otoneurological examination on 146 patients affected by atrophic ridges before and after upper maxilla surgery. Four patients showed a PPV of the posterior semicircular canal controlateral to the implanted side 1 or 2 days after the surgical procedure, which promptly was solved with the Epley re-positioning maneuver. We hypothesize that the surgical trauma, and specifically the pressure exerted by the osteotomes, determines the detachment of the otoliths from the utricular macula while the patient head position, hyper-extended and tilted opposite to the side where the surgeon is working, favors the entry of these free-floating particles in the posterior semicircular canal of the implanted side. Although this disease is rather frequent in the normal population and it is a benign, self-limiting peripheral disorder, it should be considered by the oral surgeon as a possible complication of pre-prosthetic upper maxilla surgery, and the patient should be informed before undergoing surgery.

Aged↗
PubMed1998

Exposure-response relationship in the hand-arm vibration syndrome: an overview of current epidemiology research.

The complex of vascular, neurologic, and osteoarticular disorders occurring in the upper limbs of vibration-exposed workers is called hand-arm vibration syndrome. There is epidemiologic evidence for an increased occurrence of peripheral sensorineural disorders in occupational groups working with vibrating tools. An excess risk for wrist osteoarthrosis and for elbow arthrosis and osteophytosis has been reported in workers exposed to shocks and low-frequency vibration of high magnitude from percussive tools. However, there are too few epidemiology data to enable reliable conclusions to be drawn about exposure-response relationships for both sensorineural disturbances and bone and joint disorders caused by hand-transmitted vibration. Cross-sectional and longitudinal epidemiology studies have shown that occupational exposure to hand-transmitted vibration from a great variety of hand-held tools is significantly associated with an increased occurrence of digital vasospastic disorders called vibration-induced white finger (VWF). The proposal of an exposure-response relationship for VWF has been included in an annex to the international standard ISO 5349. The findings of several epidemiology studies have shown a poor agreement between the risk for VWF observed in various occupational groups and that predicted by the ISO 5349 model. Both overestimation and underestimation of the occurrence of VWF have been reported by investigators. It has been argued that the current ISO frequency-weighting curve for hand-transmitted vibration may be inappropriate for the assessment of vibration-induced adverse vascular effects. Alternative exposure-response relationships for VWF have been suggested in recent epidemiology studies. The epidemiology data used to construct current exposure-response relationships for vibration-induced injuries are primarily derived from cross-sectional studies. Future epidemiology research should be based on prospective cohort studies because the design characteristics of such studies permit the study of cause-effect relationships and the formulation of etiologic hypotheses.

Adult↗
PubMed2005

Congenital hyperekplexia: five sporadic cases.

UNLABELLED: We report fives sporadic cases of hyperekplexia or startle disease characterized by a highly exaggerated startle reflex and tonic attacks. Affected neonates suffer from prolonged periods of stiffness and are at risk for sudden death from apnea. An early diagnosis is needed. Sudden loud sounds, unexpected tactile stimuli or percussion at the base of the nose can also elicit excessive jerking or tonic attack. The diagnosis of hyperekplexia is a purely clinical one. A defect of the alpha1 subunit of inhibitory glycine receptor (GLRA1) has been observed in the dominant form with a mutation in the chromosome 5. Clonazepam is effective and decreases the severity of the symptoms. The disease tends to improve after infancy and the psychomotor development is normal. The major form of "hyperekplexia" should be considered whenever one is confronted with neonatal hypertonicity associated with paroxysmal tonic manifestations (without electroencephalography anomalies). CONCLUSION: the diagnosis of hyperekplexia should be evaluated in any neonate with tonic attacks without evident cause.

Anticonvulsants↗
PubMed2004

Air-mattress motion therapy for respiratory failure after cardiothoracic surgery.

PURPOSE: The standard management of respiratory failure after cardiothoracic surgery involves prolonged mechanical ventilation, drug support, and chest physiotherapy. We report the effectiveness of a novel type of respiratory physiotherapy, the air mattress V-CUE unit, which utilizes a computerized automatic combination of three movements: rotation, percussion, and vibration. METHODS: Among 189 patients who underwent various cardiothoracic operations, 6 were eligible for V-CUE application, after the development of respiratory failure caused by early adult respiratory distress syndrome, massive atelectasis, or pulmonary infection. RESULTS: The V-CUE unit was used to treat six postsurgical patients, aged 58-73 years (mean, 65.8 years); four who had undergone coronary artery bypass grafting, one who had undergone mitral valve replacement, and one who had undergone a bilobectomy. The mean duration of supportive V-CUE was 3.9 days (range 2-6 days), and the mean duration of mechanical ventilation was 2.9 days. There was no need for reintubation or tracheotomy, and all six patients recovered uneventfully. CONCLUSION: Our preliminary results indicate that V-CUE dynamic air therapy is effective for managing postoperative respiratory failure, adjuvant to or complementary to standard therapy.

Aged↗
PubMed1978

Prediction of aortic valvular area and gradient by noninvasive techniques.

Sixty-two patients with isolated aortic valvular stenosis were analyzed by a series of common noninvasive procedures and by cardiac catheterization. The data from 50 of these were evaluated in a retrospective fashion by multiple regression methods to determine significant objectively obtained predictors of aortic-left ventricular gradient and valvular area. Formulae were derived from these analyses and an additional 12 patients were then studied prospectively to evaluate the validity of the predictive formulae. Forty-three of 50 patients (86 per cent) were correctly identified as to a gradient of greater or less than 50 mm. Hg in the initial group, and all those in the prospectively studied sample were correctly classified. Thiry-five of 43 patients (82 per cent) of those with valve area data in the first application were correctly classified as to valve area or greater or less than 0.8 cm.2, and all patients in the prospectively studied group were appropriately identified as to the same area. The combined application of the observations of calcification of the aortic valve, shudder waves on the anacrotic limb, prolonged time to peak of the percussion wave and alteration of the dicrotic notch of the carotid pulse tracing, left ventricular hypertrophy by electrocardiogram, and the altered duration of ventricular ejection time were reliable predictors of elevated aortic-left ventricular gradient and decreased aortic valvular size.

Adolescent↗
PubMed1975

Attempted orthodontic movement in the presence of suspected ankylosis.

A 37-year-old man with suspected ankylosis ("submerged" teeth, radiographically obliterated periodontal membranes, and sharp or ringing percussion tests) was subjected to attempted orthodontic movement. The maxillary canine and posterior segments were chosen as treatment areas. While the terms "light" and "heavy" are relative, forces ranging from 6 to 24 ounces were variants great enough in the areas treated to have elicited movement if movement were possible. After continuous forces had been applied for 110 days, measurements showed no movement in either maxillary quadrant.

Adult↗
PubMed1987

Decrease in total and free magnesium concentration following traumatic brain injury in rats.

31P magnetic resonance spectroscopy was used to determine the intracellular free Mg2+ concentration prior to and following fluid percussion induced traumatic brain injury in rats. Prior to injury, cerebral intracellular free Mg2+ concentration in the rat was 0.93 +/- 0.19 mM (mean +/- SE; n = 5). Following injury, free Mg2+ in the injured cortex declined by 70% within the first hour, and did not recover over the next 3 hours. Total Mg2+ also declined by 10% over this time period; however, there were no changes in brain Na+ or tissue water content. Because of its primary role in cellular metabolism, the early decline in tissue Mg2+ following brain trauma may be a critical factor in the development of irreversible tissue injury.

Adenosine Triphosphate↗
PubMed1987

Alterations in regional concentrations of endogenous opioids following traumatic brain injury in the cat.

Delayed injury following trauma to the central nervous system (CNS) may be due to the release or activation of endogenous factors. Endogenous opioid peptides have been proposed as one such class of injury factors, based on pharmacological studies demonstrating a therapeutic effect of naloxone and other opiate receptor antagonists following CNS injury. However, changes in brain opioid concentrations following injury have not been evaluated. In the present study, we measured regional alterations in dynorphin (ir-Dyn), leucine-enkephalin (ir-Enk) and beta-endorphin immunoreactivity (ir-End) following low- (1.0-2.0 atmospheres (atm)) or high- (3.0-4.0 atm) level fluid-percussion brain injury in the cat. A significant decrease in ir-End was observed in the hypothalamus at 2 h following high- but not low-level injury. No changes were observed in tissue ir-Enk following either level of injury. Severe brain trauma but not low-level injury caused a significant increase in ir-Dyn in the striatum, frontal cortex, parietal cortex, pons and medulla. In the anterior pituitary, a significant increase in ir-End and a significant decrease in ir-Dyn was observed at 2 h following both levels of injury. Pathological damage to brain tissue after injury was most pronounced in those regions showing significant increases in ir-Dyn but not other opioids. In the medulla, the increase in ir-Dyn but not ir-End or ir-Enk was also significantly correlated with a fall in systemic mean arterial pressure (MAP) at 2 h following high- but not low-level injury.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Effects of scopolamine treatment on long-term behavioral deficits following concussive brain injury to the rat.

Scopolamine (0.1, 1.0, or 10.0 mg/kg) or saline was systemically (i.p.) administered to rats 15 min prior to concussive fluid percussion brain injury. Animals pretreated with the 1.0 mg/kg dose exhibited significantly (P less than 0.05) less motor deficits and less body weight loss and recovered to baseline performance sooner than saline-treated rats. Mortality and associated convulsions were significantly lower in rats pretreated with the 1.0 mg/kg dose of scopolamine. A 1.0 mg/kg dose of scopolamine administered (i.p.) 30 s after injury also significantly reduced behavioral deficits. No differences were observed between saline- and scopolamine-treated animals in either the incidence or duration of transient apnea following injury. A 1.0 mg/kg dose of scopolamine administered (i.p.) 15 min prior to epidural clip compression of the spinal cord had no effect on the severity of motor function deficits assessed by an inclined plane test. The data from these experiments suggest muscarinic cholinergic involvement in at least some of the long-term behavioral deficits following mild and moderate levels of brain injury. These results suggest that muscarinic cholinergic antagonists may prove beneficial in the treatment of human head injury.

Animals↗
PubMed1988

The effect of concussive head injury on central cholinergic neurons.

This study examined the effect of fluid percussion head injury on the activity of cholinergic neurons in specific brain areas of the rat 12 min, 4 h and 24 h following injury. Acetylcholine (ACh) turnover, used as an index of cholinergic neuronal activity, was determined using a gas chromatographic-mass spectrometric technique. The most striking changes in cholinergic activity were observed in the dorsal pontine tegmentum, where concussive head injury produced an increase in ACh turnover 12 min and 4 h following injury. This area has been previously associated with behavioral changes observed following concussive injury. ACh turnover in the thalamus, a region to which pontine cholinergic neurons project, also tended to increase 4 h following injury. On the other hand, ACh turnover tended to decrease in the amygdala 4 h following injury. Although there were no significant changes in hippocampal ACh content or turnover following injury. ACh content did tend to increase in that brain region 12 min following injury. There were no significant effects of injury on cholinergic neurons in the cingulate/frontal cortex. These changes in cholinergic neuronal activity may contribute to the neurological deficits following concussive injury. In particular, activation of cholinergic neurons in the pontine region may contribute to components of behavioral suppression associated with reversible traumatic unconsciousness. More generalized changes in cholinergic function may lead to the production of more chronic deficits.

Acetylcholine↗
PubMed1988

Effects of anticholinergic treatment on transient behavioral suppression and physiological responses following concussive brain injury to the rat.

Increasing doses (0.1, 1.0, 10.0 mg/kg) of scopolamine were systemically (i.p.) administered to rats subjected to moderate fluid percussion brain injury. Scopolamine treatment (1.0 mg/kg, i.p.) 15 min prior to trauma significantly reduced mortality and the duration of transient behavioral suppression assessed by a variety of measures. No differences were observed between saline- and scopolamine-treated animals in either the incidence or duration of transient apnea associated with injury. Preinjury treatment with methylscopolamine (1.04 mg/kg) or mecamylamine (1.0 mg/kg) had no effect on transient behavioral suppression. Except for increased heart rate, preinjury treatment with scopolamine (1.0 mg/kg) did not significantly alter systemic physiological responses to injury. Rats treated with scopolamine (1.0 mg/kg, i.p.) 30 s after injury tended to have shorter durations of reflex and response suppression. These experiments suggest that antimuscarinics can attenuate components of transient behavioral suppression associated with concussive brain injury. These findings are consistent with previous experimental and clinical observations and lend further support to the hypothesis that activation of a muscarinic system within the CNS mediates components of reversible traumatic unconsciousness following cerebral concussion.

Animals↗
PubMed1988

Treatment with the thyrotropin-releasing hormone analog CG3703 restores magnesium homeostasis following traumatic brain injury in rats.

Treatment with thyrotropin-releasing hormone (TRH) analogs following traumatic injury to the central nervous system (CNS) improves neurological outcome through mechanisms that remain unclear. Previous studies have shown that traumatic brain injury is associated with a profound decline in intracellular free magnesium (Mgf) and in total tissue magnesium (Mgt), the extent of Mgf decline being linearly correlated to the severity of injury and resultant neurological deficit. We have used 31P magnetic resonance spectroscopy and atomic absorption spectrophotometry, respectively, to measure cerebral Mgf concentration and Mgf content in rats following fluid percussion brain trauma and treatment with the TRH analog, CG3703. Treatment at 30 min postinjury with CG3703 significantly improved Mgf when compared to saline-treated controls. There were no significant changes in Mgt, Na+, K+ or water content following CG3703 treatment. Since a decline in intracellular free magnesium may affect cellular bioenergetic status, calcium flux, activity of excitatory amino acids, opiate receptors, and the release of eicosanoids, these results suggest that the beneficial effects of treatment with TRH analogs after CNS trauma may be mediated through magnesium-dependent mechanisms.

Animals↗