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Ulrich Batzdorf, David L. McArthur and John R. Bentson

Object

This study aims to show the relationship between clinical outcome in patients who underwent surgical decompression for Chiari malformation (CM) and postoperative imaging studies, with particular emphasis on the subarachnoid cisterns of the posterior fossa.

Methods

One hundred seventy-seven patients with CM, including 97 with syringomyelia, underwent posterior fossa decompressive surgery. Both the dura and arachnoid were opened in 150 of these patients, and 135 underwent reduction of the cerebellar tonsils. The patients' clinical signs and symptoms were evaluated at 2 time points after surgery. Their imaging studies were analyzed specifically for the size of the retrotonsillar and subtonsillar cisterns and the syringomyelic cavities. The authors evaluated the relationship between these imaging findings and clinical parameters.

Results

Clinical improvement correlated strongly with enlargement of the subarachnoid cisterns, and enlargement of the cisterns also correlated with reduction in size of the syrinx cavities. Symptoms related to syringomyelia responded to reduction in size of the syrinx cavities.

Conclusions

Surgical decompression of the posterior fossa should aim to create relatively large subarachnoid cisterns and reduce the size of the syrinx cavity. Reduction of the cerebellar tonsils by surgical means, together with duraplasty, achieves this goal and thereby improves the clinical outcome for patients with CM. An incidental observation of the study is that obesity increases the likelihood of headache in patients with CM.

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Langston T. Holly, Bonnie Freitas, David L. McArthur and Noriko Salamon

Object

Magnetic resonance spectroscopy is commonly used to provide cellular and metabolic information in the management of a variety of pathological processes that affect the brain, and its application recently has been expanded to the cervical spine. The majority of radiographic investigations into the pathophysiology of cervical spondylotic myelopathy (CSM) have been focused on the spinal cord macrostructure. The authors sought to determine the feasibility of using MR spectroscopy to analyze spinal cord biochemical function in patients with CSM.

Methods

Twenty-one patients with clinical and radiographic evidence of CSM were prospectively enrolled in this study. The patients underwent preoperative neurological examination, functional assessment, and cervical spine MR spectroscopy. Voxels were placed at the C-2 level, and the MR spectroscopy spectra peaks for N-acetylaspartate (NAA), choline, lactate (Lac), and creatine (Cr) were measured. Thirteen age-matched healthy volunteers served as controls.

Results

The NAA/Cr ratio was significantly lower in patients with CSM than in controls (1.27 vs 1.83, respectively, p < 0.0001). The choline/Cr ratio was not significantly different between the 2 groups. Seven of the patients with CSM had a Lac peak, whereas no peaks were noted in the control group (p < 0.05). There was no correlation between the severity of myelopathy and the NAA/Cr ratio in the CSM cohort.

Conclusions

Data in this study demonstrated the feasibility of using MR spectroscopy to evaluate the cellular biochemistry of the spinal cord in patients with CSM. Patients with CSM had a significantly lower NAA/Cr ratio than healthy controls, likely because of axonal and neuronal loss. The presence of Lac peaks in one-third of the patients in the CSM cohort further supports the role of ischemia in the pathophysiology of CSM.

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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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Langston T. Holly, Daniel F. Kelly, George J. Counelis, Thane Blinman, David L. McArthur and H. Gill Cryer

Object. Diagnosing and managing cervical spine trauma in head-injured patients is problematic due to an altered level of consciousness in such individuals. The reported incidence of cervical spine trauma in head-injured patients has generally ranged from 4 to 8%. In this retrospective study the authors sought to define the incidence of cervical injury in association with moderate or severe brain injury, emphasizing the identification of high-risk patients.

Methods. The study included 447 consecutive moderately (209 cases) or severely (238 cases) head injured patients who underwent evaluation at two Level 1 trauma centers over a 40-month period. Of the 447 patients, 24 (5.4%) suffered a cervical spine injury (17 men and seven women; mean age 39 years; median Glasgow Coma Scale [GCS] score of 6, range 3–14). Of these 24 patients, 14 (58.3%) sustained spinal cord injuries (SCIs), 14 sustained injuries in the occiput—C3 region, and 10 underwent a stabilization procedure. Of the 14 patients with SCIs, nine experienced an early hypotensive and/or hypoxic insult. Regarding the mechanism of injury, cervical injuries occurred in 21 (8.2%) of 256 patients involved in motor vehicle accidents (MVAs), either as passengers or pedestrians, compared with three (1.6%) of 191 patients with non-MVA-associated trauma (p < 0.01). In the subset of 131 MVA passengers, 13 (9.9%) sustained cervical injuries. Patients with an initial GCS score less than or equal to 8 were more likely to sustain a cervical injury than those with a score higher than 8 (odds ratio [OR] 2.77, 95% confidence interval [CI] = 1.11–7.73) and were more likely to sustain a cervical SCI (OR 5.5, 95% CI 1.22–24.85). At 6 months or more postinjury, functional neurological recovery had occurred in nine patients (37.5%) and eight (33.3%) had died.

Conclusions. Head-injured patients sustaining MVA-related trauma and those with an initial GCS score less than or equal to 8 are at highest risk for concomitant cervical spine injury. A disproportionate number of these patients sustain high cervical injuries, the majority of which are mechanically unstable and involve an SCI. The development of safer and more rapid means of determining cervical spine integrity should remain a high priority in the care of head-injured patients.

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Daniel F. Kelly, Rouzbeh K. Kordestani, Neil A. Martin, Tien Nguyen, David A. Hovda, Marvin Bergsneider, David L. McArthur and Donald P. Becker

✓ The role of posttraumatic hyperemia in the development of raised intracranial pressure (ICP) has important pathophysiological and therapeutic implications. To determine the relationship between hyperemia (cerebral blood flow (CBF) > 55 ml/100 g/minute), intracranial hypertension (ICP > 20 mm Hg), and neurological outcome, 193 simultaneous measurements of ICP and CBF (xenon-133 method) were obtained in 59 patients with moderate and severe head injury.

Hyperemia was associated with an increased incidence of simultaneous intracranial hypertension compared to nonhyperemic CBF measurements (32.2% vs. 21.6%, respectively; p < 0.059). However, in 78% of blood flow studies in which ICP was greater than 20 mm Hg, CBF was less than or equal to 55 ml/100 g/minute. At least one episode of hyperemia was documented in 34% of patients, all of whom had a Glasgow Coma Scale (GCS) score of 9 or below. In 12 individuals with hyperemia without simultaneous intracranial hypertension, ICP was greater than 20 mm Hg for an average of 11 ± 16 hours and favorable outcomes were seen in 75% of patients. In contrast, in eight individuals with hyperemia and at least one episode of hyperemia-associated intracranial hypertension, ICP was greater than 20 mm Hg for an average of 148 ± 84 hours (p < 0.001), and a favorable outcome was seen in only one patient (p < 0.001). Compared to the remainder of the cohort, patients with hyperemia-associated intracranial hypertension were distinctive in being the youngest, exhibiting the lowest GCS scores (all ≤ 6), and having the highest incidence of effaced basilar cisterns and intractable intracranial hypertension.

In the majority of individuals with hyperemia-associated intracranial hypertension, their clinical profile suggests the occurrence of a severe initial insult with resultant gross impairment of metabolic vasoreactivity and pressure autoregulation. In a minority of these patients, however, high CBF may be coupled to a hypermetabolic state, given their responsiveness to metabolic suppressive therapy. In patients with hyperemia but without intracranial hypertension, elevated CBF is also likely to be a manifestation of appropriate coupling to increased metabolic demand consistent with a generally favorable outcome. This study supports the concept that there are multiple etiologies of both elevated blood flow and intracranial hypertension after head injury.

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Marvin Bergsneider, David A. Hovda, Ehud Shalmon, Daniel F. Kelly, Paul M. Vespa, Neil A. Martin, Michael E. Phelps, David L. McArthur, Michael J. Caron, Jess F. Kraus and Donald P. Becker

✓ Experimental traumatic brain injury studies have shown that cerebral hyperglycolysis is a pathophysiological response to injury-induced ionic and neurochemical cascades. This finding has important implications regarding cellular viability, vulnerability to secondary insults, and the functional capability of affected regions. Prior to this study, posttraumatic hyperglycolysis had not been detected in humans.

The characteristics and incidence of cerebral hyperglycolysis were determined in 28 severely head injured patients using [18F]fluorodeoxyglucose—positron emission tomography (FDG-PET). The local cerebral metabolic rate of glucose (CMRG) was calculated using a standard compartmental model. In six of the 28 patients, the global cerebral metabolic rate of oxygen (CMRO2) was determined by the simultaneous measurements of arteriovenous differences of oxygen and cerebral blood flow (xenon-133). Hyperglycolysis, defined as an increase in glucose utilization that measures two standard deviations above expected levels, was documented in all six patients in whom both FDG-PET and CMRO2 determinations were made within 8 days of injury. Five additional patients were found to have localized areas of hyperglycolysis adjacent to focal mass lesions. Within the 1st week following the injury, 56% of patients studied had presumptive evidence of hyperglycolysis.

The results of this study indicate that the metabolic state of the traumatically injured brain should be defined differentially in terms of glucose and oxygen metabolism. The use of FDG-PET demonstrates that hyperglycolysis occurs both regionally and globally following severe head injury in humans. The results of this clinical study directly complement those previously reported in experimental brain-injury studies, indicating the capability of imaging a fundamental component of cellular pathophysiology characteristic of head injury.

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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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Paul M. Vespa, W. John Boscardin, David A. Hovda, David L. McArthur, Marc R. Nuwer, Neil A. Martin, Valeriy Nenov, Thomas C. Glenn, Marvin Bergsneider, Daniel F. Kelly and Donald P. Becker

Object. Early prediction of outcomes in patients after they suffer traumatic brain injury (TBI) is often nonspecific and based on initial imaging and clinical findings alone, without direct physiological testing. Improved outcome prediction is desirable for ethical, social, and financial reasons. The goal of this study was to determine the usefulness of continuous electroencephalography (EEG) monitoring in determining prognosis early after TBI, while the patient is in the intensive care unit.

Methods. The authors hypothesized that the reduced percentage of alpha variability (PAV) in continuous EEG tracings indicates a poor prognosis. Prospective continuous EEG monitoring was performed in 89 consecutive patients with moderate to severe TBI (Glasgow Coma Scale [GCS] Scores 3–12) from 0 to 10 days after injury. The PAV was calculated daily, and the time course and trends of the PAV were analyzed in comparison with the patient's Glasgow Outcome Scale (GOS) score at the time of discharge.

In patients with GCS scores of 8 or lower, a PAV value of 0.1 or lower is highly predictive of a poor outcome or death (positive predictive value 86%). The determinant PAV value was obtained by Day 3 after injury. Persistent PAV values of 0.1 or lower over several days or worsening of the PAV to a value of 0.1 or lower indicated a high likelihood of poor outcome (GOS Scores 1 and 2). In comparison with the combination of traditional initial clinical indicators of outcome (GCS score, pupillary response to light, patient age, results of computerized tomography scanning, and early hypotension or hypoxemia), the early PAV value during the initial 3 days after injury independently improved prognostic ability (p < 0.01).

Conclusions. Continuous EEG monitoring performed with particular attention paid to the PAV is a sensitive and specific method of prognosis that can indicate outcomes in patients with moderate to severe TBI within 3 days postinjury.