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Kelly D. Flemming, David O. Wiebers, Robert D. Brown Jr., Michael J. Link, Hirofumi Nakatomi, John Huston III, Robyn McClelland, and Teresa J. H. Christianson

Object. Nonsaccular intracranial aneurysms (NIAs) are characterized by dilation, elongation, and tortuosity of intracranial arteries. Dilemmas in management exist due to the limited regarding the natural history of this disease entity. The objective of this study was to determine the prospective risk of subarachnoid hemorrhage (SAH) in patients with vertebrobasilar NIAs.

Methods. All patients with vertebrobasilar fusiform or dolichoectatic aneurysms that had been radiographically demonstrated between 1989 and 2001 were identified. These patients' medical records were retrospectively reviewed. A prospective follow-up survey was sent and death certificates were requested. Based on results of neuroimaging studies, the maximal diameter of the involved artery, presence of SAH, and measurements of arterial tortuosity were recorded. Nonsaccular intracranial aneurysms were classified according to their radiographic appearance: fusiform, dolichoectatic, and transitional. Dissecting aneurysms were excluded. The aneurysm rupture rate was calculated based on person-years of follow up. Predictive factors for rupture were evaluated using univariate analysis (p < 0.05). One hundred fifty-nine patients, 74% of whom were men, were identified. The mean age at diagnosis was 64 years (range 20–87 years). Five patients (3%) initially presented with hemorrhage; four of these patients died during follow up. The mean duration of follow up was 4.4 years (692 person-years). Nine patients (6%) experienced hemorrhage after presentation; six hemorrhages were definitely related to the NIA. The prospective annual rupture rate was 0.9% (six patients/692 person-years) overall and 2.3% in those with transitional or fusiform aneurysm subtypes. Evidence of aneurysm enlargement or transitional type of NIA was a significant predictor of lesion rupture. Six patients died within 1 week of experiencing lesion rupture.

Conclusions. Risk of hemorrhage in patients harboring vertebrobasilar NIAs is more common in those with evidence of aneurysm enlargement or a transitional type of aneurysm and carries a significant risk of death.

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Wells I. Mangrum, John Huston III, Michael J. Link, David O. Wiebers, Robyn L. McClelland, Teresa J. H. Christianson, and Kelly D. Flemming

Object. Vertebrobasilar nonsaccular intracranial aneurysms (NIAs) are characterized by elongation, dilation, and tortuosity of the vertebrobasilar arteries. The goal of this study was to define the frequency, predictors, and clinical outcome of the enlargement of vertebrobasilar NIAs.

Methods. Patients with vertebrobasilar fusiform or dolichoectatic aneurysms demonstrated on imaging studies between 1989 and 2001 were identified. In particular, patients who had undergone serial imaging were included in this study and their medical records were retrospectively reviewed. Prospective information was collected from medical records or death certificates when available. Both initial and serial imaging studies were reviewed. The authors defined NIA enlargement as a change in lesion diameter greater than 2 mm or noted on the neuroradiologist's report. A Cox proportional hazards regression was used to model time from diagnosis of the vertebrobasilar NIA to the first documented enlargement as a function of various predictors. The Kaplan-Meier method was used to study patient death as a function of aneurysm growth.

Of the 159 patients with a diagnosis of vertebrobasilar NIA, 52 had undergone serial imaging studies including 25 patients with aneurysm enlargement. Lesion growth significantly correlated with symptomatic compression at the initial diagnosis (p = 0.0028), lesion type (p < 0.001), and the initial maximal lesion diameter (median 15 mm in patients whose aneurysm enlarged compared with median 8 mm in patients whose aneurysm did not enlarge; p < 0.001). The mortality rate was 5.7 times higher in patients with aneurysm growth than in those with no enlargement after adjustment for patient age (p = 0.002).

Conclusions. Forty-eight percent of vertebrobasilar NIAs demonstrated on serial imaging enlarged, and this growth was associated with significant morbidity and death. Significant risk factors for aneurysm enlargement included symptomatic compression at the initial diagnosis, transitional or fusiform vertebrobasilar NIAs, and initial lesion diameter. Further studies are necessary to determine appropriate treatments of this disease entity once enlargement has been predicted or occurs.

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Brian J. Park, Colin J. Gold, David Christianson, Nicole A. DeVries Watson, Kirill V. Nourski, Royce W. Woodroffe, and Patrick W. Hitchon


Adjacent-segment disease (ASD) proximal to lumbosacral fusion is assumed to result from increased stress and motion that extends above or below the fusion construct. Sublaminar bands (SBs) have been shown to potentially mitigate stresses in deformity constructs. A similar application of SBs in lumbar fusions is not well described yet may potentially mitigate against ASD.


Eight fresh-frozen human cadaveric spine specimens were instrumented with transforaminal lumbar interbody fusion (TLIF) cages at L3–4 and L4–5, and pedicle screws from L3 to S1. Bilateral SBs were applied at L2 and tightened around the rods extending above the L3 pedicle screws. After being mounted on a testing frame, the spines were loaded at L1 to 6 Nm in all 3 planes, i.e., flexion/extension, right and left lateral bending, and right and left axial rotation. Motion and intradiscal pressures (IDPs) at L2–3 were measured for 5 conditions: intact, instrumentation (L3–S1), band tension (BT) 30%, BT 50%, and BT 100%.


There was significant increase in motion at L2–3 with L3–S1 instrumentation compared with the intact spine in flexion/extension (median 8.78°, range 4.07°–10.81°, vs median 7.27°, range 1.63°–9.66°; p = 0.016). When compared with instrumentation, BT 100% reduced motion at L2–3 in flexion/extension (median 8.78°, range 4.07°–10.81°, vs median 3.61°, range 1.11°–9.39°; p < 0.001) and lateral bending (median 6.58°, range 3.67°–8.59°, vs median 5.62°, range 3.28°–6.74°; p = 0.001). BT 50% reduced motion at L2–3 only in flexion/extension when compared with instrumentation (median 8.78°, range 4.07°–10.81°, vs median 5.91°, range 2.54°–10.59°; p = 0.027). There was no significant increase of motion at L1–2 with banding when compared with instrumentation, although an increase was seen from the intact spine with BT 100% in flexion/extension (median 5.14°, range 2.47°–9.73°, vs median 7.34°, range 4.22°–9.89°; p = 0.005). BT 100% significantly reduced IDP at L2–3 from 25.07 psi (range 2.41–48.08 psi) before tensioning to 19.46 psi (range −2.35 to 29.55 psi) after tensioning (p = 0.016).


In this model, the addition of L2 SBs reduced motion and IDP at L2–3 after the L3–S1 instrumentation. There was no significant increase in motion at L1–2 in response to band tensioning compared with instrumentation alone. The application of SBs may have a clinical application in reducing the incidence of ASD.