Elevated intracranial pressure is one of the most common causes of death and disability following severe traumatic brain injury and ischemic stroke. Unfortunately, there have been no new medical treatments for cerebral edema and elevated intracranial pressure in more than 80 years. Decompressive craniectomy may be an appropriate surgical option in the face of elevated intracranial pressure that is refractory to medical treatment. When performed correctly, this procedure can reduce intracranial pressure and prevent cerebral herniation and death. The last decade has seen a renewed interest in the use of decompressive craniectomy, but many questions remain regarding patient selection, timing of surgery, surgical technique, timing of cranioplasty, and complications.
Shirley I. Stiver and Geoffrey T. Manley
The aim of this study was to review the current protocols of prehospital practice and their impact on outcome in the management of traumatic brain injury. A literature review of the National Library of Medicine encompassing the years 1980 to May 2008 was performed. The primary impact of a head injury sets in motion a cascade of secondary events that can worsen neurological injury and outcome. The goals of care during prehospital triage, stabilization, and transport are to recognize life-threatening raised intracranial pressure and to circumvent cerebral herniation. In that process, prevention of secondary injury and secondary insults is a major determinant of both short- and longterm outcome. Management of brain oxygenation, blood pressure, cerebral perfusion pressure, and raised intracranial pressure in the prehospital setting are discussed. Patient outcomes are dependent upon an organized trauma response system. Dispatch and transport timing, field stabilization, modes of transport, and destination levels of care are addressed. In addition, special considerations for mass casualty and disaster planning are outlined and recommendations are made regarding early response efforts and the ethical impact of aggressive prehospital resuscitation. The most sophisticated of emergency, operative, or intensive care units cannot reverse damage that has been set in motion by suboptimal protocols of triage and resuscitation, either at the injury scene or en route to the hospital. The quality of prehospital care is a major determinant of long-term outcome for patients with traumatic brain injury.
Geoffrey T. Manley and William Dillon
✓ The authors report on a series of patients who underwent lumbar drainage of cerebrospinal fluid (CSF) for treatment of posterior fossa pseudomeningoceles and who subsequently developed an acute posterior fossa syndrome. These patients were found to have similar radiological findings demonstrating acute mass effect secondary to movement of CSF from the pseudomeningocele into the cerebellar parenchyma. Discontinuation of lumbar drainage resulted in symptomatic and radiological improvement in all patients. From these cases the authors infer that not all pseudomeningoceles communicate directly with the subarachnoid space. A readily recognizable appearance on magnetic resonance imaging that is useful in diagnosing this reversible complication of treatment for posterior fossa pseudomeningocele is also illustrated.
Orin Bloch and Geoffrey T. Manley
✓Despite decades of research into the pathogenesis of cerebral edema, nonsurgical therapy for brain swelling has advanced very little after more than half a century. Recent advancements in our understanding of molecular water transport have generated interest in new targets for edema therapy. Aquaporin-4 (AQP4) is the primary cellular water channel in the brain, localized to astrocytic foot processes along the blood–brain barrier and brain–cerebrospinal fluid interface. Multiple studies of transgenic mice with a complete deficiency or altered expression of AQP4 suggest a prominent role for AQP4 in cerebral water transport. In models of cellular (cytotoxic) edema, AQP4 deletion or alteration has been shown to be protective, reducing edema burden and improving overall survival. In contrast, AQP4 deletion in extra-cellular (vasogenic) edema results in decreased edema clearance and greater progression of disease. The data strongly support the conclusion that AQP4 plays a pivotal role in cerebral water transport and is an essential mediator in the formation and resorption of edema fluid from the brain parenchyma. These findings also suggest that drug therapy targeting AQP4 function and expression may dramatically alter our ability to treat cerebral edema.
Case report, review of the literature, and management algorithm
John H. Chi, Geoffrey T. Manley and Dean Chou
Pregnancy is a recognized risk factor for quiescent vertebral hemangiomas becoming symptomatic; this usually occurs during the 3rd month of gestation. The natural history of these lesions is poorly understood, and treatment practices must consider the overall safety of the mother and fetus. The authors report a case of cervical vertebral hemangioma presenting during the 24th week of pregnancy and review the current literature.
A 26-year-old woman in her 24th week of pregnancy presented with upper-back pain and progressive spastic paresis in the legs. Neuroimaging studies revealed a diffuse C-7 vertebral body lesion with extradural extension and compression of the spinal cord consistent with a vertebral hemangioma. Successful decompression was accomplished, and the fetus experienced no adverse effects from the surgery.
In a review of the literature, 23 cases of pregnancy-related vertebral hemangioma dating back to 1927 were identified. Prepartum surgical decompression was performed in eight patients, postpartum surgery was performed in 12, and surgery was not performed in four. Overall, patients experienced excellent neurological recovery, regardless of the severity and duration of spastic paresis.
Observation should be considered for symptomatic patients at greater than 32 weeks gestation. Surgery should be considered for patients with severe neurological deficits at less than 32 weeks of gestation.
Marco D. Sorani and Geoffrey T. Manley
Brain edema can increase intracranial pressure (ICP), potentially leading to ischemia, herniation, and death. Edema and elevated ICP are often treated with osmotic agents to remove water from brain tissue. Mannitol is the osmotic diuretic most commonly used in the intensive care unit; however, despite its clinical importance, treatment protocols vary from center to center, and the dose–response relationship is not understood. The goal of this metaanalysis was to aggregate and analyze data from studies in which authors have described the dose–response relationship between mannitol and ICP.
The authors identified 18 studies that quantitatively characterized the dose–response relationship of mannitol and ICP. We also examined study designs and mannitol administration protocols.
Meta-regression found a weak linear relationship between change in ICP (ΔICP) and dose (ΔICP = 6.6 × dose − 1.1; p = 0.27, R2 = 0.05). The lack of statistical significance could reflect the variation in protocols among studies and the variation in patients both within and among studies. However, the authors found a highly significant difference (p < 0.001) in decrease in ICP when the initial ICP was higher or lower than 30 mm Hg. Nonlinear regression suggested that ICP decrease is greatest shortly after mannitol is given (R2 = 0.63). Finally, the authors found that recent studies tend to include fewer patients and set a lower ICP threshold for mannitol administration but report more parameters of interest; the duration of mannitol's effect was the most frequently unreported parameter.
Despite its clinical importance, the determination of the mannitol dose–response curve continues to be challenging for many reasons. This metaanalysis highlights the need for a consensus of methods and results required to determine this important relationship.
Shirley I. Stiver, Alisa D. Gean and Geoffrey T. Manley
Brainstem hemorrhage can occur as a primary or secondary event in traumatic brain injury (TBI). Secondary brainstem hemorrhage that evolves from raised intracranial pressure and transtentorial herniation is referred to as Duret hemorrhage. Duret hemorrhage following TBI has been considered an irreversible and terminal event. The authors report on the case of a young adult patient with TBI who presented with a low Glasgow Coma Scale score and advanced signs of cerebral herniation. She underwent an urgent decompressive hemicraniectomy for evacuation of an acute epidural hematoma and developed a Duret hemorrhage postoperatively. In accordance with the family's wishes, aggressive TBI monitoring and treatment in the intensive care unit was continued even though the anticipated outcome was poor. After a lengthy hospital course, the patient improved dramatically and was discharged ambulatory, with good cognitive functioning and a Glasgow Outcome Scale score of 4. Duret hemorrhage secondary to raised intracranial pressure is not always a terminal event, and by itself should not trigger a decision to withdraw care. Aggressive intracranial monitoring and treatment of a Duret hemorrhage arising secondary to cerebral herniation may enable a good recovery in selected patients after severe TBI.
Shirley I. Stiver, Max Wintermark and Geoffrey T. Manley
The “syndrome of the trephined” is an uncommon and poorly understood disorder of delayed neurological deficit following craniectomy. From the authors' extensive experience with decompressive hemicraniectomy for traumatic brain injury (TBI), they have encountered a number of patients who developed delayed motor deficits, also called “motor trephine syndrome,” and reversal of the weakness following cranioplasty repair. The authors set out to study motor function systematically in this patient population to define the incidence, contributing factors, and outcome of patients with motor trephine syndrome.
The authors evaluated patient demographics, injury characteristics, detailed motor examinations, and CT scans in 38 patients with long-term follow-up after decompressive hemicraniectomy for TBI.
Ten patients (26%) experienced delayed contralateral upper-extremity weakness, beginning 4.9 ± 0.4 months (mean ± standard error) after decompressive hemicraniectomy. Motor deficits improved markedly within 72 hours of cranioplasty repair, and all patients recovered full motor function. The CT perfusion scans, performed in 2 patients, demonstrated improvements in cerebral blood flow commensurate with resolution of cerebrospinal fluid flow disturbances on CT scanning and return of motor strength. Comparisons between 10 patients with and 20 patients (53%) without delayed motor deficits identified 3 factors—ipsilateral contusions, abnormal cerebrospinal fluid circulation, and longer intervals to cranioplasty repair—to be strongly associated with delayed, reversible monoparesis following decompressive hemicraniectomy.
Delayed, reversible monoparesis, also called motor trephine syndrome, is common following decompressive hemicraniectomy for TBI. The results of this study suggest that close follow-up of motor strength with early cranioplasty repair may prevent delayed motor complications of decompressive hemicraniectomy.