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Anthony C. Wang, Joseph J. Gemmete, Catherine E. Keegan, Cordelie E. Witt, Karin M. Muraszko, Khoi D. Than, and Cormac O. Maher

Roberts/SC phocomelia syndrome (RBS) is a rare but distinct genetic disorder with an autosomal recessive inheritance pattern. It has been associated with microcephaly, craniofacial malformation, cavernous hemangioma, encephalocele, and hydrocephalus. There are no previously reported cases of RBS with intracranial aneurysms. The authors report on a patient with a history of RBS who presented with a spontaneous posterior fossa hemorrhage. Multiple small intracranial aneurysms were noted on a preoperative CT angiogram. The patient underwent emergency craniotomy for evacuation of the hemorrhage. A postoperative angiogram confirmed the presence of multiple, distal small intracranial aneurysms.

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Cordelie E. Witt, Anthony C. Wang, Cormac O. Maher, Khoi D. Than, Hugh J. L. Garton, and Karin M. Muraszko

In this report, the authors describe the first known case of inducible hemifacial weakness in a patient with Chiari malformation Type I (CM-I). The patient was a 14-year-old girl with a 1-year history of right facial paresis induced by sustained leftward head rotation. These episodes were characterized by weak activation of her right facial muscles with preserved eye opening and closure. Additionally, she had hypernasal speech, persistent headaches, and intermittent left arm twitching. Magnetic resonance imaging demonstrated a CM-I. A suboccipital craniectomy and C-1 laminectomy were performed for decompression of the CM-I, with duraplasty and coagulation of the pial surface of the cerebellar tonsils. At the 9-month follow-up, the patient's inducible hemifacial weakness had completely resolved. Her symptoms were thought to have resulted from the CM-I, perhaps due to traction on the right facial nerve by the ectopic tonsils with head rotation.

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Ik-Seong Park, Joseph R. Meno, Cordelie E. Witt, Abhineet Chowdhary, Thien-Son Nguyen, H. Richard Winn, Al C. Ngai, and Gavin W. Britz


Cerebrovascular dysfunction after subarachnoid hemorrhage (SAH) may contribute to ischemia, but little is known about the contribution of intracerebral arterioles. In this study, the authors tested the hypothesis that SAH inhibits the vascular reactivity of intracerebral arterioles and documented the time course of this dysfunction.


Subarachnoid hemorrhage was induced using an endovascular filament model in halothane-anesthetized male Sprague-Dawley rats. Penetrating intracerebral arterioles were harvested 2, 4, 7, or 14 days postinsult, cannulated using a micropipette system that allowed luminal perfusion and control of luminal pressure, and evaluated for reactivity to vasodilator agents.


Spontaneous tone developed in all pressurized (60 mm Hg) intracerebral arterioles harvested in this study (from 66 rats), with similar results in the sham and SAH groups. Subarachnoid hemorrhage did not affect dilation responses to acidic pH (6.8) but led to a persistent impairment of endothelium-dependent dilation responses to adenosine triphosphate (p < 0.01), as well as a transient attenuation (p < 0.05) of vascular smooth muscle–dependent dilation responses to adenosine, sodium nitroprusside, and 8-Br-cyclic guanosine monophosphate (cGMP). Impairment of NO-mediated dilation was more sustained than adenosine- and 8-Br-cGMP–induced responses (up to 7 days postinsult compared with 2 days). All smooth muscle–dependent responses returned to sham levels by 14 days after SAH.


Subarachnoid hemorrhage led to a persistent impairment of endothelium-dependent dilation and a transient attenuation of vascular smooth muscle–dependent dilation responses to adenosine. Impairment of NOmediated dilation occurred when the response to cGMP was intact, suggesting a change in cGMP levels rather than an alteration in intracellular mechanisms downstream from cGMP.

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Robert H. Bonow, Cordelie E. Witt, Mahmud Mossa-Basha, Joseph Cuschieri, Saman Arbabi, Monica S. Vavilala, Frederick P. Rivara, and Randall M. Chesnut


The goal of this study was to compare the odds of stroke 24 hours or more after hospital arrival among patients with blunt cerebrovascular injury (BCVI) who were treated with therapeutic anticoagulation versus aspirin.


The authors conducted a retrospective cohort study at a regional level I trauma center including all patients with BCVI who were treated over a span of 10 years. Individuals with stroke on arrival or within the first 24 hours were excluded, as were those receiving alternative antithrombotic drugs or procedural treatment. Exact logistic regression was used to examine the association between treatment and stroke, adjusting for injury grade. To account for the possibility of residual confounding, propensity scores for the likelihood of receiving anticoagulation were determined and used to match patients from each treatment group; the difference in the probability of stroke between the two groups was then calculated.


A total of 677 patients with BCVI receiving aspirin or anticoagulation were identified. A total of 3.8% (n = 23) of 600 patients treated with aspirin sustained a stroke, compared to 11.7% (n = 9) of 77 receiving anticoagulation. After adjusting for injury grade with exact regression, anticoagulation was associated with higher likelihood of stroke (OR 3.01, 95% CI 1.00–8.21). In the propensity-matched analysis, patients who received anticoagulation had a 15.0% (95% CI 3.7%–26.3%) higher probability of sustaining a stroke compared to those receiving aspirin.


Therapeutic anticoagulation may be inferior to aspirin for stroke prevention in BCVI. Prospective research is warranted to definitively compare these treatment strategies.