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Dynamics of subdural hygroma following decompressive craniectomy: a comparative study

Bizhan Aarabi, David Chesler, Christopher Maulucci, Tiffany Blacklock, and Melvin Alexander


This retrospective comparative cohort study was aimed at discovering the risk factors associated with subdural hygroma (SDG) following decompressive craniectomy (DC) to relieve intracranial hypertension in severe head injury.


Sixty-eight of 104 patients who had undergone DC during a 48-month period and survived > 30 days were eligible for this study. To assess the dynamics of subdural fluid collections, the authors compared CT scanning data from and the characteristics of 39 patients who had SDGs with the data in 29 patients who did not have hygromas. Variables significant in the appearance, evolution, and resolution of this complication were analyzed in a 36-week longitudinal study.


The earliest imaging evidence of SDG was seen during the 1st week after DC. The SDG volume peaked between Weeks 3 and 4 post-DC and was gradually resolved by the 17th week. Among the mechanisms of injury, motor vehicle accidents were most often linked to the development of an SDG after DC (p < 0.0007), and falls were least often associated (p < 0.005). Moreover, patients with diffuse brain injury were more prone to this complication (p < 0.0299) than those with an evacuated mass (p < 0.0001). There were no statistically significant differences between patients with and without hygromas in terms of age, sex, Glasgow Coma Scale score, intraventricular and subarachnoid hemorrhage, levels of intracranial pressure and cerebral perfusion pressure, timing of decompression, and the need for CSF diversion. More than 90% of the SDGs were ipsilateral to the side of the craniectomy, and 3 (8%) of 39 SDGs showed evidence of internal bleeding at ~ 8 weeks postinjury. Surgical evacuation was needed in 4 patients with SDGs.


High dynamic accidents and patients with diffuse injury were more prone to SDGs. Close to 8% of SDGs converted themselves into subdural hematomas at ~ 2 months postinjury. Although SDGs developed in 39 (~ 60%) of 68 post-DC patients, surgical evacuation was needed in only 4.

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Hyperextension cervical spine injuries and traumatic central cord syndrome

Bizhan Aarabi, Michael Koltz, and David Ibrahimi

Traumatic central cord syndrome (TCCS), regardless of its biomechanics, is the most frequently encountered incomplete spinal cord injury. Patients with TCCS present with disproportionate weakness of the upper extremities, and variable sensory loss and bladder dysfunction. Fractures and/or subluxations, forced hyperextension, and herniated nucleus pulposus are the main pathogenetic mechanisms of TCCS. Nearly 50% of patients with TCCS suffer from congenital or degenerative spinal stenosis and sustained their injuries during hyperextension as originally described by Schneider in 1954. Immunohistochemical and imaging studies indicate mild to moderate insult to axons and their ensheathing myelin in the lateral funiculi culminating in cytoskeletal injury and impaired conduction. More than one-half of these patients enjoy spontaneous recovery of motor weakness; however, as time goes on, lack of manual dexterity, neuropathic pain, spasticity, bladder dysfunction, and imbalance of gait render their activities of daily living nearly impossible. Based on the current level of evidence, there is no clear indication of the timing of decompression for relief of sustained spinal cord compression in hyperextension injuries. Future research, taking advantage of validated digital imaging data such as maximum canal compromise, maximum spinal cord compression, and lesion length on the CT and MR images, as well as more sensitive measures of bladder and hand function, spasticity, and neuropathic pain may help tailor surgery for a specific group of these patients.

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Decompressive Craniectomy

Anthony A. Figaji, A. Graham Fieggen, and Jonathan C. Peter

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Outcome following decompressive craniectomy for malignant swelling due to severe head injury

Bizhan Aarabi, Dale C. Hesdorffer, Edward S. Ahn, Carla Aresco, Thomas M. Scalea, and Howard M. Eisenberg


The aim of this study was to assess outcome following decompressive craniectomy for malignant brain swelling due to closed traumatic brain injury (TBI).


During a 48-month period (March 2000–March 2004), 50 of 967 consecutive patients with closed TBI experienced diffuse brain swelling and underwent decompressive craniectomy, without removal of clots or contusion, to control intracranial pressure (ICP) or to reverse dangerous brain shifts. Diffuse injury was demonstrated in 44 patients, an evacuated mass lesion in four in whom decompressive craniectomy had been performed as a separate procedure, and a nonevacuated mass lesion in two. Decompressive craniectomy was performed urgently in 10 patients before ICP monitoring; in 40 patients the procedure was performed after ICP had become unresponsive to conventional medical management as outlined in the American Association of Neurological Surgeons guidelines. Survivors were followed up for at least 3 months posttreatment to determine their Glasgow Outcome Scale (GOS) score.

Decompressive craniectomy lowered ICP to less than 20 mm Hg in 85% of patients. In the 40 patients who had undergone ICP monitoring before decompression, ICP decreased from a mean of 23.9 to 14.4 mm Hg (p < 0.001). Fourteen of 50 patients died, and 16 either remained in a vegetative state (seven patients) or were severely disabled (nine patients). Twenty patients had a good outcome (GOS Score 4–5). Among 30-day survivors, good outcome occurred in 17, 67, and 67% of patients with postresuscitation Glasgow Coma Scale scores of 3 to 5, 6 to 8, and 9 to 15, respectively (p < 0.05). Outcome was unaffected by abnormal pupillary response to light, timing of decompressive craniectomy, brain shift as demonstrated on computerized tomography scanning, and patient age, possibly because of the small number of patients in each of the subsets. Complications included hydrocephalus (five patients), hemorrhagic swelling ipsilateral to the craniectomy site (eight patients), and subdural hygroma (25 patients).


Decompressive craniectomy was associated with a better-than-expected functional outcome in patients with medically uncontrollable ICP and/or brain herniation, compared with outcomes in other control cohorts reported on in the literature.

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Prognostic factors in the occurrence of posttraumatic epilepsy after penetrating head injury suffered during military service

Bizhan Aarabi, Musa Taghipour, Ali Haghnegahdar, Majidreza Farokhi, and Lloyd Mobley

In this retrospective study, the authors evaluated confounding risk factors, which are allegedly influential in causing unprovoked posttraumatic epilepsy, in 489 patients from the frontlines of the Iran–Iraq War.

Four hundred eighty-nine patients were followed for 6 to154 months (mean 39.4 months, median 23 months), and important factors precipitating posttraumatic epilepsy were evaluated using uni- and multivariate regression analysis.

One hundred fifty-seven (32%) of 489 patients became epileptic during the study period. The results of univariate analysis indicated a significant relationship between epilepsy and Glasgow Outcome Scale (GOS) score (X2 = 76.49, p < 0.0001, df = 2), Glasgow Coma Scale score at admission (X2 = 19.48, p < 0.0001, df = 3), motor deficit (X2 = 11.79, p < 0.001, df = 1), mode of injury (X2 = 10.731, p < 0.05), transventricular injury (X2 = 6.9, p < 0.008, df = 1), dysphasia (X2 = 5.3, p < 0.02), central nervous system infections (X2 = 5.3, p < 0.02), and early-onset seizures (X2 = 4.1, p < 0.04, df = 1). The results of multivariate analysis, on the other hand, indicated that the GOS score and motor deficit were of greater statistical importance (X2 = 35.24, p < 0.0001; and X2 = 7.1, p < 0.07, respectively). Factors that did have much statistically significant bearing on posttraumatic epilepsy were the projectile type, site of injury on the skull, patient age, number of affected lobes, related hemorrhagic complications, and retained metallic or bone fragments.

Glasgow Outcome Scale score and focal motor neurological deficit are of particular importance in predicting posttraumatic epilepsy after missile head injury.

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Intradural extramedullary spinal metastasis

A report of 10 cases

Richard G. Perrin, Kenneth E. Livingston, and Bizhan Aarabi

✓ The management of 10 patients with symptomatic localized intradural extramedullary spinal metastasis is reviewed. The single most common primary source was carcinoma of the breast (four cases). The initial symptom in nine patients was pain, with five patients reporting a characteristically severe cramping discomfort with radicular distribution. All patients underwent laminectomy decompression. At the time of surgery, six of the patients were weak but ambulatory and four were bedridden. Following surgery, four patients enjoyed some measure of pain relief, seven patients became ambulatory, and three remained bedridden. Two patients achieved a “satisfactory” result, and were walking and continent 6 months after surgery. Secondary brain tumors were demonstrated or implicated in nine patients, supporting the concept that the spinal metastases represented tertiary deposits following dissemination via the cerebrospinal fluid.

Symptomatic intradural extramedullary spinal metastasis causes a virulent clinical syndrome with poor prognosis and disappointing outcome after treatment. Given the high incidence of associated cerebral metastatic involvement, total neuraxis radiation and/or chemotherapy should be considered when symptomatic spinal metastasis is discovered to be intradural and extramedullary.

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Dynamics of cerebral edema

The role of an intact vascular bed in the production and propagation of vasogenic brain edema

Bizhan Aarabi and Donlin M. Long

✓ Brain edema was produced in cats by a standardized cortical freezing lesion. With a careful microsurgical technique, the injured cortex was removed as a single piece, either immediately after induction or at 2, 4, or 8 hours after lesion production. The injured brain was either discarded or replaced in its bed. Brain edema and the defect in the blood-brain barrier were assessed by determining percent dry weight, increase in volume of white matter, and spread of Evans' blue by planimetry. The results indicate that 1) if the lesion is removed immediately after production, formation of the expected vasogenic brain edema is completely abolished; 2) replacement of the frozen brain is unable to induce significant increase in permeability of the surrounding blood-brain barrier or a significant amount of brain edema; and 3) if the lesion is removed at 2, 4, or 8 hours with or without replacement, advancement of the edema front and increase in the amount of edema is stopped. It appears that an intact vascular bed is necessary for the extracellular fluid component of brain edema, and that no edemagenic factors exist within the injured brain in this model that influence either the production or propagation of the increased extracellular fluid volume.

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Familial intradural arachnoid cysts

Report of two cases

Bizhan Aarabi, Gavril Pasternak, Orest Hurko, and Donlin M. Long

✓ Two cases of intradural arachnoid cysts are reported in one family. The propositus was a 27-year-old woman with right inframammillary radicular pain and subjective weakness of the lower extremities. Her 57-year-old father was admitted with a progressive, painless paraparesis of 6 years' duration. Intradural arachnoid cysts, at T8–9 and T5–6, respectively, were found in both patients at the time of exploration.

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Giant thrombosed aneurysm associated with an arteriovenous malformation

Case report

Bizhan Aarabi and John Chambers

✓ The authors describe a case of giant anterior cerebral artery aneurysm associated with an anatomically related arteriovenous malformation (AVM). The aneurysm was almost completely thrombosed and was resected along with the AVM.