Using the techniques described in this report, microvascular decompression is an extremely safe and effective treatment for many cranial nerve rhizopathies.
To further describe the pathophysiologic processes that occur in infants and young children after severe traumatic brain injury (TBI), we retrospectively reviewed the cerebral blood flow (CBF) values and 6-month Glasgow Outcome Scores (GOS) in 30 children < 8 years old (25 were < 4 years old) with a Glasgow Coma Score (GCS) on admission of < 8. Twelve females and 18 males (mean age 2.1 years, range 1 month to 8 years) underwent 61 CBF studies using stable xenon computed tomography at variable times from admission to 9 days after TBI. In 12 patients, PaCO2 was manipulated an average of 8.4 torr (range 5–11 torr) and a second CBF study performed to determine CO2 vasoreactivity (CO2VR), defined as the percent change in CBF per torr change in PaCO2. CBF on admission (n = 13) was 25.1 ± 7.7 ml/100 g/min (mean ± SEM) and was < 20 ml/100 g/min in 10 of 13 patients (77%). By 24 h and for up to 6 days after TBI, the mean CBF increased to 55.3 ± 3.4 ml/100 g/min (range 2–95) which differed significantly from the admission CBF value (p < 0.05); a CBF of >70 ml/100 g/min tended to be associated with a good outcome. Poor outcome (GOS ≤ 3) was seen uniformly in children under the age of 1 year and in patients with a CBF of <20 ml/100 g/min any time after TBI. Poor outcome was seen in 85% of children under the age of 24 months, but in only 41% of children ≧ 24 months old. Mean CO2VR was 2.1 ± 0.6%/torr PaCO2 and ranged from 0.02 to 5.98%. Mean CO2VR tended to differ between good and poor outcome children (3.2 ± 0.9 and 1.17 ± 0.2%, respectively) and a CO2VR of <2% was significantly associated with a poor outcome. Younger age, low CBF in the early period after TBI, and a CO2VR of <2% was associated with a poor outcome in this subgroup of children. Young children (<24 months) may represent a particular high-risk group with early hypoperfusion after severe TBI. This finding may be a key factor in the pathophysiology and outcome in this age group, and may need to be addressed in our future therapeutic protocols.
The outcomes of 25 pediatric patients who underwent upper cervical or occipitocervical fusion at the authors' institution since 1983 were reviewed. At a mean age of 9 years, the patients presented with spinal instability that was associated with os odontoideum in 11 cases, rotatory subluxation in five cases, odontoid fracture in two cases, atlantooccipital dislocation in two cases, and congenital atlantoaxial instability in five patients, four of whom had Down's syndrome (trisomy 21). Ten children had abnormal findings on neurological examination preoperatively; however, nine experienced improvement or resolution of deficits as of their latest follow-up evaluation (mean 17 months). Fusion was achieved with the first operation in 21 of 25 patients; eventually it was attained in all but one. Four patients exhibited persistent spinal instability after an initial procedure. This was caused by erosion of a multistranded cable through the intact arch of C-2 in two cases, by pin site infection necessitating early halo removal in one case, and by slippage in a halo following a Gallie procedure, which was revised with a Brooks fusion in one case. This series, the largest yet published, shows that with appropriate surgical management, posterior upper cervical fusion in the pediatric population is highly successful. Careful attention to halo pin site care and caution in using multistranded cable in young patients may improve results.
The diagnosis of traumatic atlanto-occipital dislocation is often missed in the emergency department, and current methods for evaluating the integrity of the atlanto-occipital joint on cervical radiographs fail to identify all patients with this injury. Although infratentorial subarachnoid hemorrhage is uncommon in traumatic head injury, craniocervical junction subarachnoid hemorrhage is often associated with atlanto-occipital dislocation and should raise the suspicion of severe craniocervical ligamentous injury. Sagittal computed tomography reconstructions or sagittal magnetic resonance imaging can allow for the diagnosis when plain radiography is inconclusive.
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