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Christopher E. Louie, Jennifer Hong and David F. Bauer

Suboccipital craniectomy with duraplasty is a commonly performed procedure for children with symptomatic Chiari malformation type I (CM-I). Several dural substitutes are used for duraplasty, ranging from pericranium to synthetic materials. When available, autologous pericranium is often preferred due to its low cost, performance in obtaining a watertight closure, ease of suturing, and absence of immune reaction. Long-term follow-up data on the durability of various dural substitutes are lacking. The authors report a rare, long-term complication of duraplasty performed using an autologous pericranial graft, and they conduct a literature review of similar complications. Heterotopic ossification of an autologous pericranial graft is a rare complication of duraplasty. This dystrophic bone growth can be symptomatic due to compression of neural structures, and it requires reoperation for removal. Surgeons should consider this rare long-term complication in patients presenting with unusual symptoms after duraplasty with pericranium.

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Jennifer Hong, Atman Desai, Vijay M. Thadani and David W. Roberts

OBJECTIVE

Vagal nerve stimulation (VNS) and corpus callosotomy (CC) have both been shown to be of benefit in the treatment of medically refractory epilepsy. Recent case series have reviewed the efficacy of VNS in patients who have undergone CC, with encouraging results. There are few data, however, on the use of CC following VNS therapy.

METHODS

The records of all patients at the authors' center who underwent CC following VNS between 1998 and 2015 were reviewed. Patient baseline characteristics, operative details, and postoperative outcomes were analyzed.

RESULTS

Ten patients met inclusion criteria. The median follow-up was 72 months, with a minimum follow-up of 12 months (range 12–109 months). The mean time between VNS and CC was 53.7 months. The most common reason for CC was progression of seizures after VNS. Seven patients had anterior CC, and 3 patients returned to the operating room for a completion of the procedure. All patients had a decrease in the rate of falls and drop seizures; 7 patients experienced elimination of drop seizures. Nine patients had an Engel Class III outcome, and 1 patient had a Class IV outcome. There were 3 immediate postoperative complications and 1 delayed complication. One patient developed pneumonia, 1 developed transient mutism, and 1 had persistent weakness in the nondominant foot. One patient presented with a wound infection.

CONCLUSIONS

The authors demonstrate that CC can help reduce seizures in patients with medically refractory epilepsy following VNS, particularly with respect to drop attacks.

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Jae Hong Lee, Neil A. Martin, George Alsina, David L. McArthur, Ken Zaucha, David A. Hovda and Donald P. Becker

✓ The authors prospectively investigated cerebral hemodynamic changes in 152 patients with head injuries to clarify the relationship between cerebral vasospasm and outcome. They also sought to determine the most clinically meaningful criteria for diagnosing cerebral vasospasm. Patients with varying degrees of moderate-to-severe head injury were monitored using transcranial Doppler (TCD) ultrasonography and intravenous 133Xe—cerebral blood flow (CBF) measurements. Outcome was determined at 6 months. Using TCD ultrasonography, mean flow velocities were determined for the middle cerebral artery (VMCA, 149 patients) and basilar artery (VBA, 126 patients). Recordings of the mean extracranial internal carotid artery velocity (VEC-ICA) were also performed to determine the hemispheric ratio (VMCA/VEC-ICA, 147 patients). Cerebral blood flow measurements were obtained in 91 patients. Concurrent TCD and CBF data from 85 patients were used to calculate a “spasm index” (the VMCA or VBA, respectively, divided by the hemispheric or global CBF). The authors investigated the clinical significance of elevated flow velocity, hemispheric ratio, and spasm index. Patients diagnosed as having MCA or BA vasospasm on the basis of TCD-derived criteria alone had a significantly worse outcome than patients without vasospasm. When CBF was considered, hemodynamically significant vasospasm, as defined by an elevated spasm index, was even more strongly associated with poor outcome. Stepwise logistic regression analysis confirmed that hemodynamically significant vasospasm was a significant predictor of poor outcome, independent of the effects of admission Glasgow Coma Scale score and age. On the basis of the results of this study, the authors suggest that the important factor impacting on outcome is not vasospasm per se, but hemodynamically significant vasospasm with low CBF. These findings show that vasospasm is a pathophysiologically important posttraumatic secondary insult, which is best diagnosed by the combined use of TCD and CBF measurements.

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Michael K.-Y. Hong, Matthew K.-H. Hong, Wei-Ren Pan, David Wallace, Mark W. Ashton and G. Ian Taylor

Object

The angiosome concept has been the subject of extensive research by the senior author (G.I.T.), but its specific applicability to the spinal cord was hitherto unknown. The aim of this study was to see if the spinal cord vasculature followed the angiosome concept and to review the usefulness of preoperative spinal angiography in surgery for spinal disorders. Spinal cord infarction and permanent paraplegia may result from inadvertent interruption of the artery of Adamkiewicz. Spinal angiography, which may enable avoidance of this catastrophic complication, is still not commonly used.

Methods

Two fresh cadavers were injected with a gelatin–lead oxide mixture for detailed comparative study of spinal cord vasculature. One cadaver had insignificant vascular disease, whereas the other had extensive aortic atherosclerosis, presenting a unique opportunity for study. After removal from each cadaver, radiographs of the spinal cords were obtained, then photographed, and the vascular territories of the cords were defined.

Results

Four angiosome territories were defined: vertebral, subclavian, posterior intercostal, and lumbar. These vascular territories were joined longitudinally by true anastomotic channels along the anterior and posterior spinal cord. Anastomosis between the anterior and posterior vasculature was poor in the thoracolumbar region. The anterior cord relied on fewer feeder arteries than the posterior, and the anterior thoracolumbar cord depended on the artery of Adamkiewicz for its supply. In chronic aortic disease with intercostal artery occlusion at multiple levels, a rich collateral circulation supporting the spinal cord was found.

Conclusions

The arterial supply of the spinal cord follows the angiosome concept. The atherosclerotic specimen supports the suggestion that the blood supply is able to adapt to gradual vascular occlusion through development of a collateral circulation. Nevertheless, the spinal cord is susceptible to ischemia when faced with acute vascular occlusion. This includes inadvertent interruption of the artery of Adamkiewicz. The authors recommend the use of preoperative spinal angiography to prevent possible paraplegia in removal of thoracolumbar spinal tumors.

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Neil A. Martin, Ravish V. Patwardhan, Michael J. Alexander, Cynthia Zane Africk, Jae Hong Lee, Ehud Shalmon, David A. Hovda and Donald P. Becker

The extent and timing of posttraumatic cerebral hemodynamic disturbances have significant implications for the monitoring and treatment of patients with head injury. This prospective study of cerebral blood flow (CBF) (measured using 133Xe clearance) and transcranial Doppler (TCD) measurements in 125 patients with severe head trauma has defined three distinct hemodynamic phases during the first 2 weeks after injury. The phases are further characterized by measurements of cerebral arteriovenous oxygen difference (AVDO2) and cerebral metabolic rate of oxygen (CMRO2). Phase I (hypoperfusion phase) occurs on the day of injury (Day 0) and is defined by a low CBF15 calculated from cerebral clearance curves integrated to 15 minutes (mean CBF15 32.3 ± 2 ml/100 g/minute), normal middle cerebral artery (MCA) velocity (mean VMCA 56.7 ± 2.9 cm/second), normal hemispheric index (mean HI 1.67 ± 0.11), and normal AVDO2 (mean AVDO2 5.4 ± 0.5 vol%). The CMRO2 is approximately 50% of normal (mean CMRO2 1.77 ± 0.18 ml/100 g/minute) during this phase and remains depressed during the second and third phases. In Phase II (hyperemia phase, Days 1-3), CBF increases (46.8 ± 3 ml/100 g/minute), AVDO2 falls (3.8 ± 0.1 vol%), VMCA velocity rises (86 ± 3.7 cm/second), and the HI remains less than 3 (2.41 ± 0.1). In Phase III (vasospasm phase, Days 4-15), there is a fall in CBF (35.7 ± 3.8 ml/100 g/minute), a further increase in VMCA (96.7 ± 6.3 cm/second), and a pronounced rise in the HI (2.87 ± 0.22).

This is the first study in which CBF, metabolic, and TCD measurements are combined to define the characteristics and time courses of, and to suggest etiological factors for, the distinct cerebral hemodynamic phases that occur after severe craniocerebral trauma. This research is consistent with and builds on the findings of previous investigations and may provide a useful temporal framework for the organization of existing knowledge regarding posttraumatic cerebrovascular and metabolic pathophysiology.

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Neil A. Martin, Ravish V. Patwardhan, Michael J. Alexander, Cynthia Zane Africk, Jae Hong Lee, Ehud Shalmon, David A. Hovda and Donald P. Becker

✓ The extent and timing of posttraumatic cerebral hemodynamic disturbances have significant implications for the monitoring and treatment of patients with head injury. This prospective study of cerebral blood flow (CBF) (measured using 133Xe clearance) and transcranial Doppler (TCD) measurements in 125 patients with severe head trauma has defined three distinct hemodynamic phases during the first 2 weeks after injury. The phases are further characterized by measurements of cerebral arteriovenous oxygen difference (AVDO2) and cerebral metabolic rate of oxygen (CMRO2). Phase I (hypoperfusion phase) occurs on the day of injury (Day 0) and is defined by a low CBF15 calculated from cerebral clearance curves integrated to 15 minutes (mean CBF15 32.3 ± 2 ml/100 g/minute), normal middle cerebral artery (MCA) velocity (mean VMCA 56.7 ± 2.9 cm/second), normal hemispheric index ([HI], mean HI 1.67 ± 0.11), and normal AVDO2 (mean AVDO2 5.4 ± 0.5 vol%). The CMRO2 is approximately 50% of normal (mean CMRO2 1.77 ± 0.18 ml/100 g/minute) during this phase and remains depressed during the second and third phases. In Phase II (hyperemia phase, Days 1–3), CBF increases (46.8 ± 3 ml/100 g/minute), AVDO2 falls (3.8 ± 0.1 vol%), VMCA rises (86 ± 3.7 cm/second), and the HI remains less than 3 (2.41 ± 0.1). In Phase III (vasospasm phase, Days 4–15), there is a fall in CBF (35.7 ± 3.8 ml/100 g/minute), a further increase in VMCA (96.7 ± 6.3 cm/second), and a pronounced rise in the HI (2.87 ± 0.22).

This is the first study in which CBF, metabolic, and TCD measurements are combined to define the characteristics and time courses of, and to suggest etiological factors for, the distinct cerebral hemodynamic phases that occur after severe craniocerebral trauma. This research is consistent with and builds on the findings of previous investigations and may provide a useful temporal framework for the organization of existing knowledge regarding posttraumatic cerebrovascular and metabolic pathophysiology.

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Matthias Oertel, Daniel F. Kelly, Jae Hong Lee, David L. McArthur, Thomas C. Glenn, Paul Vespa, W. John Boscardin, David A. Hovda and Neil A. Martin

Object. Hyperventilation therapy, blood pressure augmentation, and metabolic suppression therapy are often used to reduce intracranial pressure (ICP) and improve cerebral perfusion pressure (CPP) in intubated head-injured patients. In this study, as part of routine vasoreactivity testing, these three therapies were assessed in their effectiveness in reducing ICP.

Methods. Thirty-three patients with a mean age of 33 ± 13 years and a median Glasgow Coma Scale (GCS) score of 7 underwent a total of 70 vasoreactivity testing sessions from postinjury Days 0 to 13. After an initial 133Xe cerebral blood flow (CBF) assessment, transcranial Doppler ultrasonography recordings of the middle cerebral arteries were obtained to assess blood flow velocity changes resulting from transient hyperventilation (57 studies in 27 patients), phenylephrine-induced hypertension (55 studies in 26 patients), and propofol-induced metabolic suppression (43 studies in 21 patients). Changes in ICP, mean arterial blood pressure (MABP), CPP, PaCO2, and jugular venous oxygen saturation (SjvO2) were recorded. With hyperventilation therapy, patients experienced a mean decrease in PaCO2 from 35 ± 5 to 27 ± 5 mm Hg and in ICP from 20 ± 11 to 13 ± 8 mm Hg (p < 0.001). In no patient who underwent hyperventilation therapy did SjvO2 fall below 55%. With induced hypertension, MABP in patients increased by 14 ± 5 mm Hg and ICP increased from 16 ± 9 to 19 ± 9 mm Hg (p = 0.001). With the aid of metabolic suppression, MABP remained stable and ICP decreased from 20 ± 10 to 16 ± 11 mm Hg (p < 0.001). A decrease in ICP of more than 20% below the baseline value was observed in 77.2, 5.5, and 48.8% of hyperventilation, induced-hypertension, and metabolic suppression tests, respectively (p < 0.001 for all comparisons). Predictors of an effective reduction in ICP included a high PaCO2 for hyperventilation, a high study GCS score for induced hypertension, and a high PaCO2 and a high CBF for metabolic suppression.

Conclusions Of the three modalities tested to reduce ICP, hyperventilation therapy was the most consistently effective, metabolic suppression therapy was variably effective, and induced hypertension was generally ineffective and in some instances significantly raised ICP. The results of this study suggest that hyperventilation may be used more aggressively to control ICP in head-injured patients, provided it is performed in conjunction with monitoring of SjvO2.

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Ivar Mendez, Alain Dagher, Murray Hong, Adam Hebb, Paula Gaudet, Adam Law, Swarna Weerasinghe, David King, Jacques Desrosiers, Sultan Darvesh, Tanya Acorn and Harold Robertson

✓ The authors have studied the ability of glial cell line—derived neurotrophic factor (GDNF) to promote survival of human fetal dopaminergic tissue after a storage period of 6 days and subsequent implantation into the human putamen. The results indicate that GDNF promotes survival of stored dopaminergic cells. Cells stored without GDNF had a 30.1% decrease in survival time compared with those exposed to GDNF. Two patients with Parkinson's disease received bilateral putaminal implants of fetal dopaminergic cells exposed to GDNF for 6 days and showed enhancement of graft survival as assessed by positron emission tomography scanning. A mean increase of 107% in putaminal fluorodopa uptake from baseline values was observed 12 months postgrafting.

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Matthias Oertel, W. John Boscardin, Walter D. Obrist, Thomas C. Glenn, David L. McArthur, Tooraj Gravori, Jae Hong Lee and Neil A. Martin

Object. The purpose of this prospective study was to evaluate the cumulative incidence, duration, and time course of cerebral vasospasm after traumatic brain injury (TBI) in a cohort of 299 patients.

Methods. Transcranial Doppler (TCD) ultrasonography studies of blood flow velocity in the middle cerebral and basilar arteries (VMCA and VBA, respectively) were performed at regular intervals during the first 2 weeks posttrauma in association with 133Xe cerebral blood flow (CBF) measurements. According to current definitions of vasospasm, five different criteria were used to classify the patients: A (VMCA > 120 cm/second); B (VMCA > 120 cm/second and a Lindegaard ratio [LR] > 3); C (spasm index [SI] in the anterior circulation > 3.4); D (VBA > 90 cm/second); and E (SI in the posterior circulation > 2.5). Criteria C and E were considered to represent hemodynamically significant vasospasm. Mixed-effects spline models were used to analyze the data of multiple measurements with an inconsistent sampling rate.

Overall 45.2% of the patients demonstrated at least one criterion for vasospasm. The patients in whom vasospasm developed were significantly younger and had lower Glasgow Coma Scale scores on admission. The normalized cumulative incidences were 36.9 and 36.2% for patients with Criteria A and B, respectively. Hemodynamically significant vasospasm in the anterior circulation (Criterion C) was found in 44.6% of the patients, whereas vasospasm in the BA—Criterion D or E—was found in only 19 and 22.5% of the patients, respectively. The most common day of onset for Criteria A, B, D, and E was postinjury Day 2. The highest risk of developing hemodynamically significant vasospasm in the anterior circulation was found on Day 3. The daily prevalence of vasospasm in patients in the intensive care unit was 30% from postinjury Day 2 to Day 13. Vasospasm resolved after a duration of 5 days in 50% of the patients with Criterion A or B and after a period of 3.5 days in 50% of those patients with Criterion D or E. Hemodynamically significant vasospasm in the anterior circulation resolved after 2.5 days in 50% of the patients. The time course of that vasospasm was primarily determined by a decrease in CBF.

Conclusions. The incidence of vasospasm after TBI is similar to that following aneurysmal subarachnoid hemorrhage. Because vasospasm is a significant event in a high proportion of patients after severe head injury, close TCD and CBF monitoring is recommended for the treatment of such patients.