Mild Head Trauma (mild + head_trauma)

Distribution by Scientific Domains


Selected Abstracts


Peripheral blood picture following mild head trauma in children

PEDIATRICS INTERNATIONAL, Issue 3 2008
Bulent Alioglu
Abstract Background: The aim of the present study was to investigate changes in peripheral white blood cell, and differential counts following mild head trauma in a pediatric population. Methods: Fifty-one patients (mean age, 79 ± 62 months) with mild head trauma (Glasgow Coma Scale [GCS] score 15) who were admitted to the emergency department, were studied. Two blood specimens were collected from each patient, one on arrival and one after 24 h at the emergency department. Complete blood count was performed using a hemocytometer and the absolute cell counts for each sample were calculated after examination of peripheral smear. Results: No patient developed any complication during the hospital stay or after discharge. Significant differences were found for white blood cell, neutrophil, and immature cell counts just after and 24 h after trauma (P = 0.047, 0.039 and 0.009, respectively). Conclusions: Mild head trauma may cause an increase in white blood cell, neutrophil and band counts in children just after trauma. In a child with a mild head trauma, who is asymptomatic, with GCS score of 15 and absence of risk factors, and without clinical deterioration, complete blood cell count may be omitted from laboratory workup. But a prospective randomized study comparing mild head trauma patients with good and bad clinical outcome is needed to draw a definite conclusion. [source]


Bilateral basal ganglia infarction after mild head trauma

PEDIATRICS INTERNATIONAL, Issue 6 2009
Chie Ishihara
First page of article [source]


Peripheral blood picture following mild head trauma in children

PEDIATRICS INTERNATIONAL, Issue 3 2008
Bulent Alioglu
Abstract Background: The aim of the present study was to investigate changes in peripheral white blood cell, and differential counts following mild head trauma in a pediatric population. Methods: Fifty-one patients (mean age, 79 ± 62 months) with mild head trauma (Glasgow Coma Scale [GCS] score 15) who were admitted to the emergency department, were studied. Two blood specimens were collected from each patient, one on arrival and one after 24 h at the emergency department. Complete blood count was performed using a hemocytometer and the absolute cell counts for each sample were calculated after examination of peripheral smear. Results: No patient developed any complication during the hospital stay or after discharge. Significant differences were found for white blood cell, neutrophil, and immature cell counts just after and 24 h after trauma (P = 0.047, 0.039 and 0.009, respectively). Conclusions: Mild head trauma may cause an increase in white blood cell, neutrophil and band counts in children just after trauma. In a child with a mild head trauma, who is asymptomatic, with GCS score of 15 and absence of risk factors, and without clinical deterioration, complete blood cell count may be omitted from laboratory workup. But a prospective randomized study comparing mild head trauma patients with good and bad clinical outcome is needed to draw a definite conclusion. [source]


High cortical spreading depression susceptibility and migraine-associated symptoms in Cav2.1 S218L mice

ANNALS OF NEUROLOGY, Issue 1 2010
Arn M. J. M. van den Maagdenberg PhD
Objective The CACNA1A gene encodes the pore-forming subunit of neuronal CaV2.1 Ca2+ channels. In patients, the S218L CACNA1A mutation causes a dramatic hemiplegic migraine syndrome that is associated with ataxia, seizures, and severe, sometimes fatal, brain edema often triggered by only a mild head trauma. Methods We introduced the S218L mutation into the mouse Cacna1a gene and studied the mechanisms for the S218L syndrome by analyzing the phenotypic, molecular, and electrophysiological consequences. Results Cacna1aS218L mice faithfully mimic the associated clinical features of the human S218L syndrome. S218L neurons exhibit a gene dosage,dependent negative shift in voltage dependence of CaV2.1 channel activation, resulting in enhanced neurotransmitter release at the neuromuscular junction. Cacna1aS218L mice also display an exquisite sensitivity to cortical spreading depression (CSD), with a vastly reduced triggering threshold, an increased propagation velocity, and frequently multiple CSD events after a single stimulus. In contrast, mice bearing the R192Q CACNA1A mutation, which in humans causes a milder form of hemiplegic migraine, typically exhibit only a single CSD event after one triggering stimulus. Interpretation The particularly low CSD threshold and the strong tendency to respond with multiple CSD events make the S218L cortex highly vulnerable to weak stimuli and may provide a mechanistic basis for the dramatic phenotype seen in S218L mice and patients. Thus, the S218L mouse model may prove a valuable tool to further elucidate mechanisms underlying migraine, seizures, ataxia, and trauma-triggered cerebral edema. ANN NEUROL 2010;67:85,98 [source]