Management of complex pediatric and adolescent spinal deformity.

OBJECT: The authors sought to analyze prospectively the outcome of surgery for complex spinal deformity in the pediatric and young adult populations. METHODS: The authors evaluate all pediatric and adolescent patients undergoing operative correction of complex spinal deformity from December 1997 through July 1999. No patient was lost to follow-up review (average 21.1 months). There were 27 consecutive pediatric and adolescent patients (3-20 years of age) who underwent 32 operations. Diagnoses included scoliosis (18 idiopathic, five nonidiopathic) and four severe kyphoscoliosis. Operative correction and arthrodesis were achieved via 21 posterior approaches (Cotrel-Dubousset-Horizon), seven anterior approaches (Isola or Kaneda Scoliosis System), and two combined approaches. Operative time averaged 358 minutes (range 115-620 minutes). Blood loss averaged 807 ml (range 100-2,000 ml). Levels treated averaged 9.1 (range three-16 levels). There was a 54% average Cobb angle correction (range 6-82%). No case was complicated by the patient's neurological deterioration, loss of somatosensory evoked potential monitoring, cardiopulmonary disease, donor-site complication, or wound breakdown. There was one case of hook failure and one progression of deformity beyond the site of surgical instrumentation that required reoperation. There were 10 minor complications that did not significantly affect patient outcome. No patient received undirected banked blood products. There was a significant improvement in cosmesis, and no patient experienced continued pain postoperatively. All patients have been able to return to their preoperative activities. CONCLUSIONS: Compared with other major neurosurgical operations, segmental instrumentation for pediatric and adolescent spinal deformity is a safe procedure with minimal morbidity and there is a low risk of needing to use allogeneic blood products.

Multilevel thoracic pedicle aplasia causing congenital thoracic kyphosis: case report.

OBJECTIVE AND IMPORTANCE: Congenital thoracic kyphosis is a rare cause of treatable myelopathy. Multilevel thoracic pedicle aplasia as a cause of this deformity has not been previously reported in the literature. We report a case and describe the surgical management and outcome. CLINICAL PRESENTATION: A 14-year-old boy presented to us with a 4-month history of back pain and slowly progressive spastic paraparesis. Radiographic studies revealed thoracic kyphosis and bilateral aplasia of the pedicles of T4-T8. INTERVENTION: The patient underwent surgical treatment via a posterior approach for decompression of T4-T8, followed by arthrodesis from T2 to T12, using a hook claw construct with multiple points of fixation and autologous bone grafting. CONCLUSION: Congenital vertebral anomalies may be clinically occult, and delayed presentation may occur in adolescence or adulthood. Aplasia of multiple thoracic pedicles can produce kyphotic deformities with neurological compromise. A posterior approach with multiple points of segmental instrumentation can be effective in treating kyphotic deformities that are flexible and of moderate severity (<75 degrees).

Postconcussive symptoms in children with mild closed head injuries.

OBJECTIVE: To examine the incidence and neuropsychological, behavioral, and neuroimaging correlates of postconcussive symptoms (PCS) in children with mild closed head injuries (CHI). DESIGN: 26 Children with mild CHI and 8 of their uninjured siblings, from 8 to 15 years old, were recruited prospectively and assessed at baseline (ie, within 7 days of injury) and at 3 months postinjury. Parents rated PCS, motivation and affective lability, and behavioral adjustment. Baseline ratings assessed premorbid functioning retrospectively, and follow-up ratings assessed postinjury status. On both occasions, children completed neuropsychological testing, and those with mild CHI also underwent magnetic resonance imaging (MRI). RESULTS: Children with mild CHI did not differ from siblings in baseline ratings of premorbid PCS but displayed higher ratings on several PCS at 3 months postinjury. Thirty-five percent of children with mild CHI showed increases in PCS, compared with baseline premorbid ratings, but none of the siblings did so. Children with mild CHI whose PCS increased from premorbid levels showed poorer neuropsychological functioning at baseline than did children whose PCS did not increase, although the differences had partially resolved by 3 months. They also displayed decreased motivation over time. Their behavioral adjustment was poorer and they had smaller white matter volumes on MRI, but the latter differences were present at baseline and did not change over time, suggesting that they existed prior to the injury. CONCLUSION: Postinjury increases in PCS occur in a sizable minority of children with mild CHI and more often than among uninjured siblings. Increases in PCS following mild CHI are associated with premorbid neurological and psychosocial vulnerability, but also with postinjury decrements in neuropsychological and neurobehavioral functioning.

Pediatric atlantoaxial instability: management with screw fixation.

Sixteen pediatric patients (age range 3-15 years; mean 9.4 years) with atlantoaxial instability underwent screw fixation at Columbus Children's Hospital between 1992 and 1998. Three patients with type II odontoid fractures underwent odontoid screw fixation. The remaining group of 13 patients had posterior C1-2 transarticular screw fixation and Sonntag C1-2 fusion. The group included 3 patients with rotatory C1-2 fixation, 4 patients with os odontoideum, 4 patients with congenital atlantoaxial instability and 2 patients with traumatic C1-2 instability. Postoperatively, all patients were placed in a Miami-J collar only. At 3 months follow-up, all patients achieved fusion. Bony fusion across the fracture line was clearly evident in patients with odontoid screws. The only complications in this series were a transient swallowing difficulty that resolved spontaneously in 2 weeks, and another patient's C1-2 fusion had extended to C2-3 at 9 months follow-up. This study demonstrates that children at 3 years of age and older, who sustain a type II odontoid fracture with an intact transverse ligament, can be safely managed with odontoid screws if the fracture is less than 4 weeks old. Posterior C1-2 transarticular screw fixation can be done safely and results in a high fusion rate in children older than 4 years of age. The technical difficulties of screw fixation in children are discussed.

Cerebellar infarction from a traumatic vertebral artery dissection in a child.

Infarction due to vertebral dissection is a rarely reported event in children. We describe the clinical presentation, radiological findings and surgical treatment of a child with cerebellar infarction resulting from a traumatic vertebral artery dissection. Review of the literature on stroke due to a vertebral artery dissection in the pediatric population shows that trauma is a common preceding event. Although the most common site of traumatic vertebral artery dissection is at C1-2 level, our case illustrates that the vertebral artery dissection may also involve the lower cervical segment. We emphasize that vertebral artery dissection should be considered in a child with acute symptoms and signs of posterior circulation ischemia and that MRI and MR angiography may be helpful in the diagnosis of infarction and vertebral artery dissection.

Early onset of leptomeningeal cyst with severe brain herniation: report of two cases.

Leptomeningeal cyst as a rare complication of skull fracture in children is well documented. Most cases occur months or years after the original skull fracture, with characteristic roentgenogram findings. The authors report two cases of leptomeningeal cysts in children less than two years old. The association of hygroma, severe brain injury, increased ICP, and early development of leptomeningeal cyst are discussed. Both patients sustained parietal diastatic skull fracture and developed external brain herniation within 10 days after motor vehicle accidents. Clinically they presented with seizure, hemiparesis, and an enlarging subgaleal mass over the skull fracture. MRI demonstrated severe underlying brain contusion, hygroma around the fracture site, and brain herniation through the skull fracture. Surgical repair of dural laceration and cranioplasty produced good results. The development of hygroma and increased intracranial pressure might account for the early development of leptomeningeal cysts in these two cases.

Pediatric cervical spine fractures: predominantly subtle presentation.

Previous description of cervical spine fractures in children have emphasized high mortality injuries to the upper cervical vertebra. Our experience suggests a much wider spectrum of injury. The medical records of all children with cervical spine fractures admitted to Children's Hospital between January 1, 1985 and December 31, 1989 were reviewed. The average age of the 50 patients was 11 years (range, 2.7 to 18.8 years) and 62% were boys. Motor vehicle-related accidents (54%), sports injuries (18%), and falls (12%) accounted for the majority of the fractures. Twenty-nine patients (58%) had an associated head injury. Fifty percent of the patients were transported from the accident scene and 44% were interhospital transfers. All patients receiving medical care prior to referral had appropriate cervical spine stabilization. On admission 30% of the patients were unresponsive. Thirty-one children were alert and verbal at the time of evaluation and 30 complained of neck pain and tenderness (97%). Twenty-five of the 31 patients (83%) had no demonstrable neurological deficit on initial physical examination. Lateral cervical spine radiographs were diagnostic in 49 children (98%). A relatively even distribution of fractures occurred at all levels of the cervical spine. The anatomic site of the injury did not correlate with age. Sixteen patients (32%) died. Of the 34 who survived, only 6 had a persistent neurological deficit. Children with cervical spine fractures have two distinct patterns of presentation: lethal or intact. The majority of children with cervical spine fractures presented with no complaints of neck pain and/or tenderness need a complete radiographic evaluation of their cervical spine.

Pharmacokinetics, cerebrospinal fluid concentration, and safety of intravenous rifampin in pediatric patients undergoing shunt placements.

The objectives of this study were to characterize the pharmacokinetics and determine the cerebrospinal fluid concentrations and safety of intravenous rifampin in pediatric patients undergoing shunt placement. Nine patients (mean age 5.6 y) received a single dose of rifampin, 20 mg.kg-1, administered intravenously 1 h prior to surgery. The peak serum concentrations ranged from 13.5-26.7 micrograms.ml-1; cerebrospinal fluid concentrations ranged from 0.12-3.0 (mean: 1.4) micrograms.ml-1. The mean total clearance, apparent distribution volume, and elimination half-life were 0.29 l.kg-1.h-1, 1.11.kg-1, and 2.8 h. The concentrations of rifampin achieved in the cerebrospinal fluid exceeded the minimum inhibitory concentrations by 100- to 1000-fold against Staphylococcus epidermidis. However, 5 of 9 patients developed cutaneous reactions during intravenous rifampin prophylactic therapy. Because of the high frequency of adverse effects and more than adequate rifampin concentrations achieved in the cerebrospinal fluid, rifampin doses lower than that used in this study may be evaluated in future studies.

The specific NMDA receptor antagonist AP-7 attenuates focal ischemic brain injury.

Pharmacologic blockade of excitatory amino acid receptors, especially the N-methyl-D-aspartate-preferring subclass of glutamate receptors, has been shown to reduce neuronal damage in models of global cerebral ischemia followed by reperfusion. The pharmacologic blockade at the NMDA receptor attenuates infarct size following permanent focal vascular occlusion in brain. Functional recovery is improved as well. These effects were seen with treatment begun 15 min following the stroke.

Kynurenate inhibition of cell excitation decreases stroke size and deficits.

Pharmacological inhibition of excitatory neurotransmission attenuates cell death in models of global ischemia/reperfusion and hypoglycemia. The current investigations extend these observations to a model of focal ischemia. Kynurenic acid, a broad-spectrum antagonist at excitatory amino acid receptors, was used as treatment (300 mg/kg; 3 doses at 4-hour intervals) before and after focal cerebral ischemia in rats (n = 54). Preischemia but not 1 hour postischemia treatment with kynurenate attenuated infarction size (p less than 0.001) and improved neurological outcome (p less than 0.001) studied at 24 hours after injury. These data support the role of excitatory neurotransmission in acute neuronal injury and support pharmacological inhibition of cell excitation as a potential therapy for stroke.

The therapeutic value of nimodipine in experimental focal cerebral ischemia. Neurological outcome and histopathological findings.

Recent studies suggest that nimodipine, a potent calcium-channel antagonist that causes significant cerebrovascular dilatation, may improve neurological outcome after acute experimental permanent focal cerebral ischemia when given before or immediately after occlusion of the middle cerebral artery (MCA) in various animals. The authors describe the effect of nimodipine on cerebral ischemia in a rat model. At 1, 4, or 6 hours after occlusion of the MCA, rats were treated in a double-blind technique with either nimodipine, placebo, or saline. Neurological and neuropathological evaluation was performed at 24 hours. Neurological outcome was better in rats treated with nimodipine 1, 4, or 6 hours after occlusion (p less than 0.001, p less than 0.01, p less than 0.05 respectively), and the size of areas of infarction was statistically smaller in nimodipine-treated groups (p less than 0.01, p less than 0.01, p less than 0.05, respectively) when compared with control rats treated with saline or placebo. The best neurological outcome and the smallest area of infarction were found in nimodipine-treated rats 1 hour after occlusion. Compared with controls, the size of the periphery of the infarcted area was smaller in nimodipine-treated rats. The results show that nimodipine improves neurological outcome and decreases the size of infarction when administered up to 6 hours after ischemic insult. These results suggest a possible mechanism of action of nimodipine on the "penumbra" of the ischemic area.

Effect of hypoxia on traumatic brain injury in rats: Part 1. Changes in neurological function, electroencephalograms, and histopathology.

The effect of hypoxia on neurological function, compressed spectral array electroencephalography, and histopathology in head-injured rats was evaluated. By itself, an hypoxic insult (PaO2, 40 mm Hg for 30 minutes) caused no neurological deficit. Twenty per cent of rats injured by a 5-atmosphere temporal fluid percussion impact were hemiparetic contralateral to the side of impact, whereas 80% had no deficit 24 hours after injury. Seventy per cent of rats with both fluid impact injury and hypoxic insult, however, either had a definite hemiparesis, showed no spontaneous movement, or died (P less than 0.02). Impact alone produced an initial depression in electroencephalogram power that was prolonged in rats with hypoxic insult; the most dramatic effect was found in the injured hemisphere, with shorter and less profound effects in the contralateral hemisphere. Perfusion staining of injured cerebral tissue in vivo with 2,3,5-triphenyltetrazolium chloride showed an area of extensive ischemia around the impact site in rats with hypoxic insult. This ischemic area was not present in rats with either impact injury or hypoxia alone. We conclude that posttraumatic hypoxia clearly increases the severity of impact injury in this rat model. These findings suggest that hypoxia, which is common in head-injured patients, very likely worsens the effect of impact injury and may account for much of the diffuse neurological dysfunction in patients with severe craniocerebral trauma.

Effect of hypoxia on traumatic brain injury in rats: Part 2. Changes in high energy phosphate metabolism.

The effect of different degrees of hypoxia on phosphate metabolism in the brains of impact-injured rats was studied using in vivo phosphorus-31 magnetic resonance (P-31 MR) spectroscopy. Sequential changes in P-31 MR spectra within 60 minutes of insult were compared among rats with hypoxia alone, impact injury alone, or a combined impact-hypoxic insult. Hypoxia alone (PaO2 of 40 mm Hg for 30 minutes) caused no remarkable changes in phosphorus spectra except a decrease in intracellular pH. In impact-injured rats, the concentration of inorganic phosphate (Pi) increased, but signals for phosphocreatine (PCr) and beta-adenosine triphosphate (beta-ATP) did not change, and the ratio of PCr/Pi changed only slightly to 7% below control value. When rats with a fluid percussion impact injury of 5 atm were subjected to hypoxic conditions of a PaO2 of 40 mm Hg for 15 minutes, the PCr/Pi ratio decreased by 14%, a value significantly below that of the impact alone group (P less than 0.05). After longer periods of hypoxia (PaO2 of 40 mm Hg for 30 minutes) in impact-injured rats, there were marked increases of Pi and significant decreases in signals for PCr and beta-ATP, which caused a marked decrease in the PCr/Pi ratio to 39% below control values (P less than 0.001). Milder hypoxia (PaO2 of 50 mm Hg for 30 minutes) plus impact injury caused smaller changes in high energy metabolite concentrations, and the PCr/Pi ratio decreased to 15% below control values.(ABSTRACT TRUNCATED AT 250 WORDS)

Evaluation of 2,3,5-triphenyltetrazolium chloride as a stain for detection and quantification of experimental cerebral infarction in rats.

We have evaluated the use of 2,3,5-triphenyltetrazolium chloride (TTC) as an histopathologic stain for identification of infarcted rat brain tissue. The middle cerebral artery (MCA) of 35 normal adult rats was occluded surgically. At various times after surgical occlusion, rats were sacrificed and brain slices were obtained and stained with TTC or hematoxolin and eosin (H & E); the size of the area of infarcted tissue stained by each method was quantified. In rats sacrificed 24 hr after occlusion of the MCA, the size of the area of infarction was 21 +/- 2% of the coronal section for TTC, and 21 +/- 2% for H & E (mean +/- S.D., N = 13). The size of areas of infarction determined by either staining method was not significantly different in area by the paired test, and a significant correlation between sizes determined by each method was found by linear regression analysis (r = 0.91, slope = 0.89, and the y intercept = 4.4%). Staining with TTC is a rapid, convenient, inexpensive, and reliable method for the detection and quantification of cerebral infarction in rats 24 hr after the onset of ischemia.

Traumatic intracerebral hematomas: timing of appearance and indications for operative removal.

Immediate and delayed traumatic intracerebral hematomas (ICH) can produce devastating secondary brain damage after severe head injury. The relationship between the initial injury and eventual occurrence, size, and time of appearance of such hematomas is not well understood, but has great importance since delayed appearance may necessitate delayed surgical decompression of developing lesions not present on early CT scans. We reviewed the records of 35 consecutive patients with operated post-traumatic ICH to document when these lesions appeared on CT, what were the indications for surgery, and what was eventual outcome. Time between injury and ICH appearance was categorized as immediate (0-3 hours), intermediate (3-6), delayed (6-24) or very delayed (later than 24 hours). ICH appearance was immediate in 20%, intermediate in 6%, delayed in 29%, and very delayed in 46%. Half of the patients were not comatose at the time of admission (GCS greater than or equal to 8). Hematoma removal was prompted by clinical deterioration or failure to improve in half the patients and by uncontrolled intracranial hypertension in the other half. Half the patients died, generally those in traumatic coma immediately after injury although advanced age also was associated with poor outcome. Only about one quarter of patients who require surgical removal of ICH can be shown to have their lesions soon after injury. Most operable intraparenchymal clots develop after initial CT scanning and trauma surgeons must be prepared to recognize and treat this delayed complication of brain injury. Even with aggressive management, ICH contribute significantly to poor outcome and improved treatment must be sought.

Is computed tomographic scanning necessary in patients with tentorial herniation? Results of immediate surgical exploration without computed tomography in 100 patients.

Computed tomographic (CT) scans are performed on virtually all patients with severe head injury at the time of admission. Because of the time involved in obtaining these studies, the evacuation of significant intracranial mass lesions is delayed. To avoid such delays, the authors performed burr-hole exploration for the diagnosis of intracranial hematomas before CT scans were obtained in 100 consecutive head-injured patients with clinical signs of tentorial herniation or upper brain stem dysfunction upon admission to the emergency room. Patients in whom a hematoma was discovered had a craniotomy for evacuation of the clot; those in whom the exploration was negative had a CT brain scan immediately after operation. Burr-hole exploration revealed extracerebral mass lesions in 56 patients. In 38 patients, the exploration was negative, and postoperative CT scanning showed no significant hematoma. Of 6 patients in whom the CT scan demonstrated extraaxial hematomas requiring surgical evacuation, 4 had subdural hematomas that were missed because the exploration was incomplete; 1 patient had an epidural hematoma and 1 had a subdural hematoma contralateral to a craniotomy on the side of a positive initial burr-hole exploration. Our results indicate that the relatively small subgroup of head-injured patients with early tentorial herniation or upper brain stem compression have a high incidence of immediate extraaxial hematomas and a low incidence of intracerebral hematomas. This is particularly true of patients over 30 years of age and those who suffer low speed trauma, such as falls and vehicle-pedestrian accidents.