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Biomedical subjects

P David Adelson

Publications and source records attributed to P David Adelson.

At least 37 records · Page 2Linked to original sources

End-to-side neurorrhaphies in a rodent model of peripheral nerve injury: a preliminary report of a novel technique.

OBJECT: The standard techniques for repair of peripheral nerve injuries with neuroma formation are typically suboptimal. To begin to explore alternative techniques, the authors used an established model in rodents by using end-to-side "terminolateral" neurorrhaphies (TLNs) to study alternative grafting techniques. The TLN "jump grafts" bypass a neuromain-continuity, hypothetically maintaining functional units within the neuroma to facilitate functional regeneration. Evaluation of the extent and origin of the regenerating fibers within the grafts was also undertaken. METHODS: The right tibial nerve in four adult Sprague-Dawley rats was injured using either a crush or transection technique and compared with four uninjured controls. The contralateral peroneal nerve was immediately harvested for microsurgical repair by using TLN jump grafts in all animals. Following a 3-month recovery, the repaired nerves were evaluated electrophysiologically by using evoked electromyography (EMG). Histological preparation was then performed using dual-fluorescent labeling to study axonal regeneration and origins. Evoked EMG evaluation confirmed healthy electrical conduction across the repair, which was unchanged after transection of the neuroma, but was abolished after transection of the jump graft, indicating functional neural regeneration across both the proximal and distal TLNs of the jump grafts. Fluorescent tracing analysis confirmed regeneration across both the proximal and distal portion of the jump grafts, demonstrated both motor and sensory neurons as the source of the regenerating fibers, and demonstrated significant numbers of double-labeled cell bodies, indicating that collateral sprouting was the primary source of regenerating fibers. CONCLUSIONS: The authors have preliminarily shown that regeneration occurs both electrophysiologically and histologically with a double-TLN jump graft. Clinically, this method could offer an alternative strategy for the technique and timing of neuroma repair.

Animals↗

Development of a novel method to predict disability after head trauma in children.

BACKGROUND/PURPOSE: Although analysis of functional independence measures (FIM) at discharge are useful for assessing extent of disability in head-injured children, there is no reliable method to predict the severity of disability at the time of admission. The authors developed a novel method to predict severe disability after head trauma on admission. METHODS: Head-injured patients, 2 to 16 years old, with FIM recorded at discharge (n = 3,491) were identified in our state trauma database for the period from 1993 through 1996. Patients categorized as completely dependent by one or more of the FIM (Feeding, Locomotion, Expression, Transfer Mobility, Social Interaction) were classified as disabled. Probability of disability (P(D)) was estimated based on regression weights for Glasgow Coma Scale (GCS), Injury Severity Score (ISS), age, and number of anatomic regions injured. Observed to expected disability rates were compared using a test data set of 2,553 patients entered in the database between 1997 through 1999. RESULTS: There was no statistically significant difference between observed and expected disability across all P(D) intervals, which suggests that the P(D) accurately predicted disability. CONCLUSIONS: P(D) offers a novel and reliable method for early prediction of likelihood of disability in children who sustain head trauma. Routine use of the P(D) may lead to earlier intervention to improve long-term results in head-injured children.

Activities of Daily Living↗

F2-isoprostane and neuron-specific enolase in cerebrospinal fluid after severe traumatic brain injury in infants and children.

It has been hypothesized that oxidative stress plays an important role in mediating secondary damage after traumatic brain injury (TBI). To study the relationship between lipid peroxidation, clinical variables, and neuronal damage in pediatric TBI, we measured levels of F2-isoprostane, a marker of lipid peroxidation, and neuron-specific enolase (NSE), a marker of neuronal damage, in serial cerebrospinal fluid (CSF) samples from 23 infants and children with severe TBI (Glasgow Coma Scale score <8). These were compared to CSF samples from 10 uninjured pediatric controls. On d1 after injury, F2-isoprostane was increased 6-fold vs. control (36.59+/-8.96 pg/ml vs. 5.64+/-8.08 pg/ml, p=0.0035) and NSE was increased 10-fold (100.62+/-17.34 ng/ml vs. 8.63+/-2.76 ng/ml, p=0.0002). Multivariate analysis of F2-isoprostane levels and selected clinical variables showed a trend toward an inverse association with time after injury (p=0.0708). Multivariate analysis of NSE levels and selected variables showed a positive association between d1 NSE and F2-isoprostane (p=0.0426). CSF F2-isoprostane increases early after TBI in infants and children and is correlated with NSE, supporting a role for oxidative stress in the evolution of secondary damage early after severe TBI in infants and children.

Adolescent↗

Increased S-nitrosothiols and S-nitrosoalbumin in cerebrospinal fluid after severe traumatic brain injury in infants and children: indirect association with intracranial pressure.

Nitric oxide (NO) is implicated in both secondary damage and recovery after traumatic brain injury (TBI). Transfer of NO groups to cysteine sulfhydryls on proteins produces S-nitrosothiols (RSNO). S-nitrosothiols may be neuroprotective after TBI by nitrosylation of N-methyl-D-aspartate receptor and caspases. S-nitrosothiols release NO on decomposition for which endogenous reductants (i.e., ascorbate) are essential, and ascorbate is depleted in cerebrospinal fluid (CSF) after pediatric TBI. This study examined the presence and decomposition of RSNO in CSF and the association between CSF RSNO level and physiologic parameters after severe TBI. Cerebrospinal fluid samples (n = 72) were obtained from 18 infants and children on days 1 to 3 after severe TBI (Glasgow Coma Scale score < 8) and 18 controls. Cerebrospinal fluid RSNO levels assessed by fluorometric assay peaked on day 3 versus control (1.42 +/- 0.11 micromol/L vs. 0.86 +/- 0.04, P< 0.05). S-nitrosoalbumin levels were also higher after TBI (n = 8, 0.99 +/- 0.09 micromol/L on day 3 vs. n = 6, 0.42 +/- 0.02 in controls, P< 0.05). S-nitrosoalbumin decomposition was decreased after TBI. Multivariate analysis showed an inverse relation between CSF RSNO and intracranial pressure and a direct relation with barbiturate treatment. Using a novel assay, the presence of RSNO and S-nitrosoalbumin in human CSF, an approximately 1.7-fold increase after TBI, and an association with low intracranial pressure are reported, supporting a possible neuroprotective role for RSNO. The increase in RSNO may result from increased NO production and/or decreased RSNO decomposition.

Adolescent↗