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Paul M. Foreman, Christoph J. Griessenauer, Michelle Chua, Mark N. Hadley and Mark R. Harrigan

OBJECT

Approximately 10% of patients with blunt traumatic extracranial cerebrovascular injury have a complete occlusion of the vertebral artery (VA). Ischemic stroke due to embolization of thrombus from an occluded VA following cervical spine surgery has been observed. The risk of ischemic stroke with cervical spine surgery in the presence of an occluded VA, however, has never been determined.

METHODS

A retrospective chart review of 52 patients with a VA occlusion following a blunt trauma was performed. Clinical and radiographic characteristics were collected and analyzed.

RESULTS

Ten patients (19.2%) suffered an ischemic stroke attributable to a traumatic VA occlusion. Univariate analysis demonstrated that patients with ischemic stroke were significantly older (p = 0.042) and had a lower rate of cervical spine surgery (p < 0.005). Multivariate analysis found cervical spine surgery to be protective against ischemic stroke (OR 0.049 [95% CI 0.014–0.167], p = 0.014); increasing age and bilateral VA injury (bilateral occlusion or unilateral occlusion with contralateral dissection) were risk factors for ischemic stroke (OR 1.05 [95% CI1.02–1.07], p = 0.065 and OR 13.2 [95% CI 2.98–58.9], p = 0.084, respectively).

CONCLUSIONS

Traumatic VA occlusion is associated with a risk of ischemic stroke and mortality. Corrective cervical spine surgery potentially decreases the risk of ischemic stroke by stabilizing the spine and thereby reducing motion across the occluded segment of the VA and preventing embolization of thrombus. While a high stoke risk may be inherent to the disease, novel therapies should be investigated.

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Joffre E. Olaya, Michelle Ghostine, Mark Rowe and Alexander Zouros

Cerebellopontine angle arachnoid cysts are usually asymptomatic, but are frequently found incidentally because of increased use of neuroimaging. Nevertheless, as these cysts enlarge, they may compress surrounding structures and cause neurological symptoms. Patients may present with vague, nonspecific symptoms such as headache, nausea, vomiting, and vertigo. Cranial nerve palsies, including sensorineural hearing loss and facial weakness, although rare, have also been reported in association with posterior fossa arachnoid cysts. Although surgery for these entities is controversial, arachnoid cysts can be treated surgically with open craniotomy for cyst removal, fenestration into adjacent arachnoid spaces, shunting of cyst contents, or endoscopic fenestration. Reversal of sensorineural hearing loss following open craniotomy treatment has been described in the literature in only 1 adult and 1 pediatric case. Improvement in facial weakness has also been reported after open craniotomy and arachnoid cyst fenestration. The authors report the first case of complete recovery from sensorineural hearing loss and facial weakness following endoscopic fenestration in a patient with a cerebellopontine angle arachnoid cyst.

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Paul C. McCormick

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Albert H. Kim, Manish K. Kasliwal, Brendan McNeish, V. Michelle Silvera, Mark R. Proctor and Edward R. Smith

Object

Spinal cord tethering due to a thickened filum terminale is a well-described entity that can be treated surgically. Postoperative MR imaging of the lumbar spine is performed for unrelated issues or for the development of new symptoms suggestive of cord retethering. A lack of radiological criteria for successful detethering makes interpretation of postoperative MR images challenging. The delineation of postoperative radiological characteristics of a sectioned filum terminale is therefore valuable to clinicians managing these often complex cases.

Methods

The clinical data for 16 patients who underwent sectioning of a fatty and thickened filum between 2001 and 2010 and in whom pre- and postoperative MR imaging studies were available were analyzed. Medical records were interrogated for preoperative neurological examination, operative details, and postoperative follow-up. The MR images were examined by both a neurosurgeon and a neuroradiologist to assess postoperative radiological characteristics.

Results

The patients' age at time of surgery ranged from 0.3 to 19.8 years (mean 7.5 years). Postoperative MR imaging was performed between 0.03 and 7.36 years after the procedure (mean 2.5 years). Indications for postoperative imaging included new neurological symptoms (11 of 16 patients), routine interval imaging (3 of 16), and possible development of pseudomeningocele (2 of 16). Filum discontinuity was confirmed in 79% of cases postoperatively. Filum remnants appeared thicker after surgery in most cases (80%), a phenomenon most often appreciated in the cephalad end of the sectioned filum. Postoperatively, the conus was elevated in 5 cases (31%) and was found to be more ventrally located in 7 cases (44%).

Conclusions

Discontinuity, along with thickening of the upper and lower remnants of a sectioned filum, may constitute important radiological features of a detethered filum. Radiological signs of conus relaxation, signified by elevation or a more ventral position, although reassuring, were less reliably observed postoperatively. Because it may be difficult to know if the goals of surgery were met on purely clinical grounds in this patient population, knowledge of the postoperative characteristics of a sectioned filum may aid the practicing neurosurgeon in the management of these complex cases.

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Steven W. Hwang, Amer F. Samdani, Baron S. Lonner, Michelle C. Marks, Tracey P. Bastrom, Randal R. Betz and Patrick J. Cahill

Object

In the surgical management of adolescent idiopathic scoliosis (AIS), patients are often preoperatively informed that they will gain height as a result of their surgery. However, current estimations conflict significantly and do not have any clinical correlation. The authors developed a formula that would predict postoperative gains in height after deformity correction in AIS.

Methods

A large, multicenter, prospective database was retrospectively queried for AIS patients with Lenke Type 1, 2, or 3 curves having undergone posterior spinal fusion alone. A univariate and multivariate analysis was performed to identify which factors contributed significantly to changes in height.

Results

Four hundred forty-seven patients were included in the series. Factors correlating with changes in postoperative height included: upper thoracic curve magnitude, main thoracic curve magnitude, lumbar curve magnitude, T2–12 kyphosis, T5–12 kyphosis, curve flexibility, number of levels fused, presence of Ponte osteotomies, total preoperative coronal Cobb angle, change in coronal curve magnitude, total preoperative sagittal curvature, change in sagittal curvature, and thoracic curve correction.

When combined in a multivariate regression analysis the following variables remained significant: thoracic curve magnitude (p < 0.01), number of levels fused (p < 0.01), change in total sagittal curvature (p < 0.01), and the presence of osteotomies (p = 0.03). The contribution from the thoracic curve magnitude was significantly greater than any of the other parameters identified (R2 = 0.140). Change in height (in cm) = ([thoracic curve magnitude × 0.039] + [number of levels fused × 0.193] − [change in sagittal curvature × 0.033] + [x × 0.375]) − 1.858, where x = 1 if 1 or more osteotomies were performed and x = 0 if no osteotomy was performed.

Conclusions

The authors' results suggest that changes in the coronal plane contribute more significantly to height changes than those in the sagittal plane and approximately 0.39 cm of height gain can be expected for each 10° of coronal curve preoperatively. Unfortunately, a significant fraction of the postoperative height changes cannot be predicted by currently measured parameters.

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Paul M. Foreman, Michelle H. Chua, Mark R. Harrigan, Winfield S. Fisher III, R. Shane Tubbs, Mohammadali M. Shoja and Christoph J. Griessenauer

OBJECTIVE

Delayed cerebral ischemia (DCI) following aneurysmal subarachnoid hemorrhage (aSAH) occurs in approximately 30% of patients. The Practical Risk Chart was developed to predict DCI based on admission characteristics; the authors seek to externally validate and critically appraise this prediction tool.

METHODS

A prospective cohort of aSAH patients was used to externally validate the previously published Practical Risk Chart. The model consists of 4 variables: clinical condition on admission, amount of cisternal and intraventricular blood on CT, and age. External validity was assessed using logistic regression. Model discrimination was evaluated using the area under the receiver operating characteristic curve (AUC).

RESULTS

In a cohort of 125 patients with aSAH, the Practical Risk Chart adequately predicted DCI, with an AUC of 0.66 (95% CI 0.55–0.77). Clinical grade on admission and amount of intracranial blood on CT were the strongest predictors of DCI and clinical vasospasm. The best-fit model used a combination of the Hunt and Hess grade and the modified Fisher scale to yield an AUC of 0.76 (95% CI 0.675–0.85) and 0.70 (95% CI 0.602–0.8) for the prediction of DCI and clinical vasospasm, respectively.

CONCLUSIONS

The Practical Risk Chart adequately predicts the risk of DCI following aSAH. However, the best-fit model represents a simpler stratification scheme, using only the Hunt and Hess grade and the modified Fisher scale, and produces a comparable AUC.

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Michelle J. Clarke, Robert D. Ecker, William E. Krauss, Robyn L. McClelland and Mark B. Dekutoski

Object

The cervical foraminotomy was pioneered in the 1940s to address radicular symptoms via a posterior approach, but the long-term outcome has not been adequately studied.

Methods

The authors retrospectively analyzed data obtained from 303 patients (188 male and 115 female, mean age 49.2 years) who had consecutively undergone a single-level posterior foraminotomy for cervical radiculopathy between 1972 and 1992. The median follow-up duration was 7.1 years. The major end point studied was the development of symptomatic adjacent- or same-segment disease. Incidence rates per 1000 person-years were calculated, and the natural history of the disease was predicted using Kaplan–Meier survivorship analysis.

In 15 (4.9%) of 303 patients, symptomatic adjacent-segment disease developed, yielding a rate of 6.4/1000 person-years at risk. This included nine (2.9%) of 303 patients requiring reoperation, yielding a rate of 3.8/1000 person-years. Kaplan–Meier survivorship analysis suggested a relatively stable annual 0.7% rate for developing adjacent-segment disease, with a 10-year rate of 6.7%. Ten patients developed same-segment disease, yielding a risk rate of 3.9/1000 person-years.

Kaplan–Meier survivorship analysis demonstrated a 5- and 10-year risk rate of developing same-segment disease of 3.2 and 5.0%, respectively.

Conclusions

Although additional study is needed, analysis of the present data suggests that posterior foraminotomy is associated with a low rate of same- and adjacent-segment disease.

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Ali Tayebi Meybodi, Leandro Borba Moreira, Michael T. Lawton, Jennifer M. Eschbacher, Evgenii G. Belykh, Michelle M. Felicella and Mark C. Preul

OBJECTIVE

In the current neurosurgical and anatomical literature, the intracanalicular segment of the ophthalmic artery (OphA) is usually described to be within the optic nerve dural sheath (ONDS), implying direct contact between the nerve and the artery inside the optic canal. In the present study, the authors sought to clarify the exact relationship between the OphA and ONDS.

METHODS

Ten cadaveric heads were subjected to endoscopic endonasal and transcranial exposures of the OphA in the optic canal (5 for each approach). The relationship between the OphA and ONDS was assessed. Histological examination of one specimen of the optic nerve and the accompanying OphA was also performed to confirm the relationship with the ONDS.

RESULTS

In all specimens, the OphA coursed between the two layers of the dura (endosteal and meningeal) and was not in direct contact with the optic nerve, except for the first few millimeters of the proximal optic canal before it pierced the ONDS. Upon reaching the orbit, the two layers of the dura separated and allowed the OphA to literally float within the orbital fat. The meningeal dura continued as the ONDS, whereas the endosteal dura became the periorbita.

CONCLUSIONS

This study clarifies the interdural course of the OphA within the optic canal. This anatomical nuance has important neurosurgical implications regarding safe exposure and manipulation of the OphA.

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Paul M. Foreman, Michelle Chua, Mark R. Harrigan, Winfield S. Fisher III, Nilesh A. Vyas, Robert H. Lipsky, Beverly C. Walters, R. Shane Tubbs, Mohammadali M. Shoja and Christoph J. Griessenauer

OBJECTIVE

Delayed cerebral ischemia (DCI) is a recognized complication of aneurysmal subarachnoid hemorrhage (aSAH) that contributes to poor outcome. This study seeks to determine the effect of nosocomial infection on the incidence of DCI and patient outcome.

METHODS

An exploratory analysis was performed on 156 patients with aSAH enrolled in the Cerebral Aneurysm Renin Angiotensin System study. Clinical and radiographic data were analyzed with univariate analysis to detect risk factors for the development of DCI and poor outcome. Multivariate logistic regression was performed to identify independent predictors of DCI.

RESULTS

One hundred fifty-three patients with aSAH were included. DCI was identified in 32 patients (20.9%). Nosocomial infection (odds ratio [OR] 3.5, 95% confidence interval [CI] 1.09–11.2, p = 0.04), ventriculitis (OR 25.3, 95% CI 1.39–458.7, p = 0.03), aneurysm re-rupture (OR 7.55, 95% CI 1.02–55.7, p = 0.05), and clinical vasospasm (OR 43.4, 95% CI 13.1–143.4, p < 0.01) were independently associated with the development of DCI. Diagnosis of nosocomial infection preceded the diagnosis of DCI in 15 (71.4%) of 21 patients. Patients diagnosed with nosocomial infection experienced significantly worse outcomes as measured by the modified Rankin Scale score at discharge and 1 year (p < 0.01 and p = 0.03, respectively).

CONCLUSIONS

Nosocomial infection is independently associated with DCI. This association is hypothesized to be partly causative through the exacerbation of systemic inflammation leading to thrombosis and subsequent ischemia.

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James P. McAllister II, Arcangela S. Wood, Martha J. Johnson, Robert W. Connelly, David J. Skarupa, Michelle Secic, Mark G. Luciano, Neil G. Harris and Hazel C. Jones

Although neonatal hydrocephalus often results in residual neurological impairments, little is known about the cellular mechanisms responsible for these deficits. The immediate early gene, fos (c-fos), functions as a “third messenger” to regulate protein synthesis and is a good marker for neuronal activation. To identify functional changes in neurons at the cellular level, the authors quantified fos RNA expression and localized fos protein in the H-Tx rat model of congenital hydrocephalus. Tissue samples from sensorimotor and auditory regions were obtained from hydrocephalic rats and age-matched, normal litter mates at 1, 6, 12, and 21 days of age (four-six animals in each group) and processed for immunohistochemical analysis of fos and Northern blot analysis of RNA. At 12 days of age, hydrocephalic animals exhibited significant decreases in the ratio of fos immunoreactive cells to Nissl-stained neurons from both cortical regions, but no statistical differences were noted in fos expression. At 21 days of age, both the ratio of fos immunoreactive cells to Nissl-stained neurons and fos expression decreased significantly. The number of fos-positive neurons decreased in all cortical layers but was most prominent in layers V through VI. This decrease did not appear to be caused by neuronal death because examination of Nissl-stained sections revealed many viable neurons within the areas where fos immunoreactivity was absent. These results suggest that progressive neonatal hydrocephalus reduces the capacity for neuronal activation in the cerebral cortex, primarily in those neurons that provide corticofugal projections, and that this impairment may begin during relatively early stages of ventriculomegaly.