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Show ORIGINAL CONTRIBUTION Third, Fourth, and Sixth Cranial Nerve Palsies Following Closed Head Injury Avninder Dhaliwal, MD, Adrienne L. West, MD, Jonathan D. Trobe, MD, and David C. Musch, PhD Background: The relationship between the circumstances and severity of closed head injury ( CHI) and the clinical and imaging features of cranial nerve 3, 4, and 6 palsies has not been rigorously addressed in a large study. Methods: Retrospective chart review of 210 consecutive patients with CHI examined at a single tertiary care center from 1987 to 2002. Patients were located by searching the ophthalmology inpatient consultation and neuro- ophthalmology outpatient databases and hospital emergency room billing codes for a diagnosis of traumatic 3, 4, or 6 cranial nerve palsy ( Cranial Nerve Injury Group) and a diagnosis of CHI without traumatic 3, 4, or 6 nerve palsy ( Control Group). The Cranial Nerve Injury Group was then subdivided into two groups: those with injuries to an individual cranial nerve and those with multiple ( including bilateral) cranial nerve injuries. Comparisons between groups were based on age, gender, type of accident, Glasgow Coma Scale ( GCS), documented loss of consciousness ( LOC), type of ocular injury, presence of systemic injury, need for rehabilitation, physical therapy and cognitive scores, and imaging features. Results: The Cranial Nerve Injury Group had a significantly higher severity of head injury, more CT abnormalities, and worse short- term neurologic outcomes as compared with the Control Group. These trends were also found when each cranial nerve injury subgroup was compared with the Control Group. Those with cranial nerve 3 palsy had the most severe head injury; those with cranial nerve 4 palsy had an intermediate level of head injury; and those with cranial nerve 6 palsy had the lowest level of head injury. There were no consistent associations between the location of the imaging abnormalities and which cranial nerve was damaged. Departments of Ophthalmology and Visual Sciences ( AD, ALW, JDT, DCM), and Neurology ( JDT), University ofMichigan Medical Center, and Department of Epidemiology ( DCM), University of Michigan School of Public Health, Ann Arbor, Michigan. Address correspondence to Jonathan D. Trobe, MD, Department of Ophthalmology and Visual Sciences, University ofMichigan Medical Center, 1000 Wall Street, Ann Arbor, MI 48105; E- mail: jdtrobe@ umich. edu Conclusions: CHI with palsy of an ocular motor nerve was more severe than CHI without ocular motor nerve palsy, as measured by the GCS, intracranial and skull imaging abnormalities, and a greater frequency of inpatient rehabilitation. Palsy of cranial nerve 3 was associated with relatively more severe CHI than was palsy of cranial nerves 4 or 6. The location of the imaging abnormalities did not correlate with a particular cranial nerve injury. (/ Neuro- Ophthalmol 2006; 26: 4- 10) Damage to cranial nerves 3, 4, and 6 is a common accompaniment of closed head injury ( CHI) in adults ( 1- 3) and children ( 4,5). The relationship between damage to these ocular motor nerves and other clinical manifestations and imaging abnormalities is not well known, largely because previous reports have been limited to individual cases or small series. In these studies, there is sparse information about imaging and no information about neurological outcomes. In a retrospective chart review of 210 cases, we gathered information about the nature of the head injury, neuro- ophthalmic features, pertinent imaging findings, physical medicine assessment, and clinical outcome. Our aim was to determine if there were any features of CHI that predicted whether there would be ocular motor nerve damage, and if so, whether these features would predict which ocular motor nerve( s) would be damaged. Finally, we sought to determine if the presence of ocular motor nerve damage predicted neurological outcome. METHODS Patient Accrual After obtaining approval from the institutional review board, we performed a retrospective review of 210 consecutive charts of patients examined between 1987 and 2002 in the neuro- ophthalmology outpatient clinics, inpatient consultation unit, and emergency department of the University of Michigan Medical Center. Patients were located by searching the database of patients seen in the 4 J Neuro- Ophthalmol, Vol. 26, No. 1, 2006 Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. Traumatic Ocular Motor Palsies J Neuro- Ophthalmol, Vol. 26, No. 1, 2006 outpatient neuro- ophthalmology clinics and ophthalmology inpatient consultation service with a diagnosis of CHI and traumatic ocular motor palsy, as well as the hospital billing codes for patients examined in the emergency room with a diagnosis of CHI. The CHI patients were then subdivided into those who had a diagnosis of cranial nerve 3, 4, or 6 palsy ( Cranial Nerve Injury Group) and those who did not ( Control Group). The Control Group was drawn entirely from patients examined in the emergency room. The Cranial Nerve Injury Group was divided into four subgroups, three with injuries to a single cranial nerve ( Cranial Nerve 3 Injury Subgroup, Cranial Nerve 4 Injury Subgroup, and Cranial Nerve 6 Injury Subgroup), and one with multiple ( including bilateral) cranial nerve injuries ( Multiple Cranial Nerve Injury Subgroup). We compared the Cranial Nerve Injury Group as a whole to the Control Group and each of the four cranial nerve injury subgroups to the Control Group. Then we compared the four cranial nerve injury subgroups to each other. Because the Control Group had a significantly greater number of patients with a fall as the cause of the accident, patients with this mode of injury were excluded from the evaluation to remove bias. We examined the following variables: age, gender, type of accident, Glasgow Coma Scale ( GCS), documented loss of consciousness ( LOC), type of ocular injury, presence of systemic injury, need for rehabilitation, physical therapy and cognitive scores, and imaging features. Statistical Analysis Pearson's x2 test or Fisher exact test was used to compare proportions between the Cranial Nerve Injury Group and the Control Group. Contingency table analysis using 2 X 4 x2 tests was used for comparison of the relative frequencies between the four subgroups. All P values less than 0.15 in the four- way comparisons were then evaluated using Pearson's x2 test to evaluate differences between each pair within the four subgroups. Analysis of variance and the Student t test was used for comparison of means. A P value of less than 0.05 was deemed statistically significant, except in the multiple comparisons of imaging results in individual cranial nerve injury groups and controls, wherein Bonfer-roni's adjustment was used. RESULTS Cranial Nerve Injury Group versus Control Group The Cranial Nerve Injury Group had a significantly lower GCS than did the Control Group ( Table 1). The Cranial Nerve Injury Group also had a higher rate of ocular adnexal, optic nerve, and chest injuries. On imaging, the Cranial Nerve Injury Group more often had manifestations of intracranial injury ( particularly in the frontal, temporal, parietal, and interpeduncular regions) and more frequent craniofacial fractures. Craniofacial fractures were present in 46 ( 49%) of 93 patients in the Cranial Nerve Injury Group but only in 9 ( 13%) of 71 patients in the Control Group. Intracranial injury was present in 62 ( 67%) of 93 patients in the Cranial Nerve Injury Group but only in 3 ( 4%) of 71 patients in the Control Group. Cranial Nerve Injury Subgroups versus Control Group When the cranial nerve injury subgroups were compared individually to the control group, each subgroup was associated with a higher degree of severity of injury as measured by a lower GCS, a greater frequency of intracranial and craniofacial imaging abnormalities, and a more frequent need for inpatient rehabilitation ( Table 2). Four- Way Comparison of Cranial Nerve Injury Subgroups Cranial Nerve 3. Damage to cranial nerve 3 alone was associated with a relatively low GCS, particularly as compared with damage to cranial nerve 6 or to multiple cranial nerves. The subgroup with cranial nerve 3 injury also had higher ( worse) physical therapy scores for gait and bed mobility as compared with all other subgroups. Cranial nerve 3- injured patients were also more likely to have been involved in a motor vehicle accident and to have had temporal lobe region imaging abnormalities ( Table 3). Cranial Nerve 4. Injury to cranial nerve 4 appeared to be of intermediate severity between injury to cranial nerves 3 and 6, but not significantly different from either subgroup, as judged by the GCS. Cranial Nerve 6. Injury to cranial nerve 6 was significantly less severe than to cranial nerve 3, but not significantly less severe than injury to cranial nerve 4, as measured by the GCS. Patients with cranial nerve 6 injury required significantly less frequent inpatient rehabilitation than all other subgroups. Multiple Cranial Nerves. Patients with multiple cranial nerve injuries had a significantly higher GCS than did those with damage to cranial nerve 3. They had less frequent need for inpatient rehabilitation than did those with cranial nerve 6 injury. On the other hand, they had more frequent extremity injuries than did all subgroups. DISCUSSION This study generally supports the findings gleaned from smaller, uncontrolled studies of ocular motor palsies in CHI. 5 Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. J Neuro- Ophthalmol, Vol. 26, No. 1, 2006 Dhaliwal et al TABLE 1. Comparison of Cranial Age Men Loss of consciousness Glasgow Coma Scale Type of injury Fall Collision Motor vehicle accident Car versus pedestrian Ocular injury Globe Adnexal Optic nerve Pupil Systemic injury Soft tissue Chest Abdominal Extremity Intracranial injury ( any) Frontal Temporal Parietal Tentorial Interpeduncular Occipital Cervical spine injury Other spine injury Craniofacial fracture ( any) Orbital Facial Calvarial Skull base Inpatient rehabilitation Outpatient rehabilitation Nerve Injury Group i Closed head to Control Group Injury with Cranial Nerve Injury ( Cranial Nerve Injury Group) 31.4( 19.6), n = 51/ 95 53/ 63 9.39 ( 4.7), n = N/ A 9/ 87 72/ 87 6/ 87 2/ 95 11/ 95 7/ 95 3/ 95 46/ 95 32/ 95 12/ 95 32/ 95 62/ 93 18/ 93 18/ 93 9/ 93 5/ 93 6/ 93 0/ 93 6/ 93 9/ 93 46/ 93 19/ 93 25/ 93 35/ 93 33/ 93 59/ 95 14/ 95 95 74 Numbers in parentheses represent one standard deviation from the mean. N/ A, not applicable. Closed Head Injury without Cranial Nerve Injury ( Control Group) 27.66 ( 18.2), n = 48/ 71 46/ 63 13.00 ( 3.93), n = N/ A 11/ 71 54/ 71 6/ 71 1/ 71 2/ 71 0/ 71 0/ 71 40/ 71 9/ 71 12/ 71 21/ 71 3/ 71 1/ 71 1/ 71 0/ 71 1/ 71 0/ 71 1/ 71 3/ 71 4/ 71 9/ 71 4/ 71 8/ 71 1/ 71 2/ 71 13/ 71 7/ 71 71 71 P values < 0.15 0.07 0.13 < 0.0001 0.04 0.02 < 0.01 0.0002 0.0002 0.0055 0.04 < 0.0001 0.007 0.01 < 0.0001 < 0.0001 < 0.0001 We found that patients with CHI and ocular motor cranial nerve palsy had sustained more severe head trauma than had patients without ocular motor cranial nerve palsy, as judged by a relatively low initial GCS, higher rates of intracranial and craniofacial imaging abnormalities, and worse short- term neurological outcomes, as judged by the relatively greater frequency of inpatient rehabilitation. Our Cranial Nerve Injury Group tended to have poorer physical therapy scores, which suggests a worse clinical outcome than in the Control Group. In the comparison between the subgroups of cranial nerve palsy patients, those with cranial nerve 3 palsy had suffered relatively severe head trauma ( as measured by GCS), worse clinical outcomes ( as measured by bed mobility and gait scores), and higher rates of temporal 6 © 2006 Lippincott Williams & Wilkins Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. Traumatic Ocular Motor Palsies J Neuro- Ophthalmol, Vol. 26, No. 1, 2006 TABLE 2. Cranial Nerve Injury Subgroups versus Control Group Loss of consciousness* Glasgow Coma Scalef Any intracranial injury^ Any craniofacial fracture* Inpatient rehabilitation* Outpatient rehabilitation^ Cranial Nerve 3 Subgroup vs Control Group 0.14 < 0.0001 < 0.0001 < 0.0001 < 0.0001 1.0 Cranial Nerve 4 Subgroup vs Control Group 0.24 0.0020 < 0.0001 0.0038 < 0.0001 0.74 Cranial Nerve 6 Subgroup vs Control Group 0.68 0.04 < 0.0001 0.0001 0.07 0.29 Multiple Cranial Nerve Subgroup vs Control Group 0.95 0.02 < 0.0001 0.0030 < 0.0001 0.50 * Pearson's x test for a 2 X 2 contingency table. tStudent t test ( 2- sided). ifFisher exact test ( 2- sided). region intracranial imaging abnormalities. Those with cranial nerve 4 palsy had an intermediate level of head trauma, and those with cranial nerve 6 palsy had the lowest severity of head trauma. Surprisingly, those with multiple ocular motor cranial nerve palsies had a relatively low severity of head injury ( as measured by GCS) but the highest frequency of extremity injuries. Although ocular motor cranial nerve palsy was associated with a relatively low GCS and more craniofacial imaging abnormalities, these patients did not have a greater rate of LOC, the rates being over 80% in CHI patients with and without ocular motor cranial nerve palsy. An earlier study ( 6) had found that LOC is relatively common in CHI patients with various neuro- ophthalmic manifestations including ocular motor nerve injury, but no comparison was made to head- injured patients without neuro- ophthalmic findings. We infer that the GCS and imaging studies are better predictors of the presence of an ocular motor palsy than LOC, which may occur at too mild a level of CHI to be a useful discriminator. With respect to craniofacial fractures, our study is consonant with three smaller studies ( 7- 9) that demonstrated a greater than 50% frequency of craniofacial fractures in head- injured patients with ocular motor cranial nerve palsies. However, a small series found a less than 50% frequency of orbital fractures ( 10) and another found a less than 50% frequency of craniofacial fractures of any region ( 11). Cranial Nerve 3 Palsy Our data confirm the suggestion from smaller reports that cranial nerve 3 palsy is associated with relatively severe CHI. A study by Elston ( 7) demonstrated that among 20 patients with traumatic cranial nerve 3 palsy, all had LOC. Ing ( 12) characterized all 20 of his patients with traumatic cranial nerve 3 palsy as having serious injury but presented no supportive data. These earlier reports had, unlike our study, dealt only with single cranial nerve injuries without comparison to other cranial nerve injuries or to head-injured patients without cranial nerve injury. Our study also confirms the findings of earlier small studies ( 7,11,12) that motor vehicle accidents account for most of the head injuries leading to traumatic cranial nerve 3 palsy. Cranial Nerve 4 Palsy We found that CHI patients with cranial nerve 4 palsy had an intermediate severity of head injury. Our findings are in line with the study of Younge ( 13) who reported that 14 of 16 patients had suffered coma or concussion. But our study differs from two studies suggesting that traumatic cranial nerve 4 is often associated with relatively mild CHI. Khawan ( 14) reported that only two of 27 patients had LOC lasting beyond 30 minutes. Teller ( 15) reported that only two of 24 patients had LOC and that 11 had suffered minor head trauma based on direct questioning. Cranial Nerve 6 Palsy Our finding that cranial nerve 6 palsy patients had the lowest degree of head injury is at variance with the common concept that, among injuries to the three ocular motor cranial nerves, injury to cranial nerve 6 injury is associated with relatively severe CHI. For example, Crouch ( 16) found that 18 of 20 patients with traumatic cranial 6 nerve palsy had suffered LOC. Multiple Ocular Motor Nerve Palsies Our study surprisingly found that patients with bilateral cranial nerve 4 injuries had a relatively minor degree of head injury, differing from the series of Sydnor ( 17) and Chapman ( 18) in which nearly all patients had suffered LOC. An earlier head trauma study ( 19) had found 7 Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. J Neuro- Ophthalmol, Vol. 26, No. 1, 2006 Dhaliwal et al TABLE 3. Comparison of Cranial Nerve Injury Subgroups Men Glasgow Coma Scale Type of injury Motor vehicle accident Systemic injury Extremity Intracranial injury ( any) Temporal region Cranial Nerve 3 Subgroup 8/ 21 7.7 ( 3.2), n= 16 19/ 21 4/ 21 16/ 21 9/ 21 Cranial Nerve 4 Subgroup 23/ 32 9.0 ( 5.6), n = 25 16/ 32 10/ 32 19/ 32 5/ 32 to each other* Cranial Nerve 6 Subgroup 12/ 25 10.9 ( 4.3), n = 22 17/ 25 5/ 25 14/ 25 2/ 25 Multiple Injury Subgroup 17/ 28 10.5 ( 5.3), n = 22 20/ 28 16/ 28 18/ 28 6/ 28 Significant 2- way comparisons CN 3 v CN 4, P = 0.01 CN 3 v CN 6, P = 0.01 CN 3 v Multiple, P = 0.05 CN 3 v CN 4, P = 0.0028 CN 3 v CN 6, P = 0.08 Multiple vCN 3, P = 0.007 Multiple v CN 4, P = 0.04 Multiple v CN 6, P = 0.006 CN 3 v CN 4, P = 0.05 Inpatient rehabilitation PT scores ( on admit) Bed mobility Gait 15/ 21 3.8 ( 0.4), n = 20 4.0 ( 0.2), n = 20 21/ 32 3.2 ( 1.1), n = 30 3.6 ( 0.9), n = 30 9/ 25 3.3 ( 1.1), n = 24 3.5 ( 0.9), n = 24 CN 3 v CN 6, P = 0.01 CN 3 v Multiple, P = 0.13 18/ 28 CN6 v C N 3 , P = 0.02 CN 6 v CN 4, P = 0.03 CN 6 v Multiple, P = 0.04 3.3 ( 0.9), CN 3 v CN 4, P = 0.02 n = 26 CN 3 v CN 6, P = 0.05 CN 3 v Multiple, P = 0.02 3.6 ( 0.7), CN 3 v CN 4, P = 0.02 n = 26 CN 3 v CN 6, P = 0.02 CN 3 v Multiple, P = 0.04 * A11 variables with P < 0.15 in the four- way comparisons between each of the cranial nerve injury subgroups were subjected to two- way comparisons. We report only the comparisons with P £ 0.05. Number in parentheses represents one standard deviation from the mean. PT, physical therapy. that a high degree of head injury was associated with multiple rather than single ocular motor cranial nerve injuries, but these conclusions were drawn from a comparison of the single, bilateral, and multiple cranial nerve injury groups to each other without a control group. A disappointing outcome of our study was the lack of correlation between the location of the imaging abnormalities and the type of cranial nerve injury. The closest correlation was the relatively high prevalence of temporal lobe imaging abnormalities in patients with cranial nerve 3 injuries. The lack of a correlation between imaging abnormalities and a particular cranial nerve palsy precludes any new insights into the mechanism of traumatic ocular motor nerve injury. There is experimental pathologic evidence of injury at three locations: in the brain stem, at the nerve exit from the brain stem, and at the point where the nerves pierce the dura. Epstein and Baker ( 20) hypothesized that shock waves from the impact site distort the skull, leading to calvarial and basilar skull fractures and movement of the brain. Shock waves or fractures might cause damage to the ocular motor cranial nerves as they pierce the dura to enter the cavernous sinus. Heinze ( 21) demonstrated injury to the ocular motor nerves at or near their exit from the brainstem in post- mortem examinations of motor vehicle accident victims. Cranial nerve injury inside the brainstem is suggested by post- mortem examinations of trauma patients by Lindenberg ( 22), who demonstrated that the midbrain is damaged as it is thrust against the stiff tentorium. Such injuries occurred in frontal blows to the head and falls onto the buttocks, but rarely in falls onto the occiput. However, none of the patients of Lindenberg ( 22) had clinical or pathologic evidence of damage to a cranial nerve. In another study by Lindenberg ( 23), a patient with traumatic hyperextension of the neck exhibited histopathologic evidence of injury to the brainstem fascicle of cranial nerve 6. Studies by Adams and Gennarelli ( 24- 26) in humans and primates have confirmed that head injury from rapid 8 © 2006 Lippincott Williams & Wilkins Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. Traumatic Ocular Motor Palsies J Neuro- Ophthalmol, Vol. 26, No. 1, 2006 deceleration causes diffuse axonal injury in the brain stem, particularly in the midbrain. Proposed Mechanisms of Traumatic Cranial Nerve 3 Injury Pathologic reports have demonstrated injury to cranial nerve 3 at its exit from the brainstem ( 21), from the superior orbital fissure ( 21), and at the tentorial shelf after herniation secondary to traumatic brain edema ( 27). Balcer ( 28) reported a case of traumatic cranial nerve 3 palsy with an MRI finding of hemorrhage at the midbrain exit site of cranial nerve 3. Hooper ( 10) reported that 11 of 12 patients with cranial nerve 3 injuries had suffered a blow to the central frontal region of the head. Our study failed to disclose midbrain imaging abnormalities, but CT was the standard modality, which is less sensitive than MRI to hemorrhagic contusion. The relatively common rate of temporal region imaging abnormalities in our study ( 43% of patients) may implicate this region in injury to cranial nerve 3. Proposed Mechanisms of Traumatic Cranial Nerve 4 Palsy Post- mortem examinations of patients in motor vehicle accidents have demonstrated injury to cranial nerve 4 at its exit from the brainstem in the dorsal midbrain ( 21). Coppeto ( 29) reported two patients with traumatic cranial nerve 4 palsy and contralateral Horner syndrome with CT evidence of parenchymal contusion of the dorsolateral midbrain at the ponto- mesencephalic junction. Lavin ( 30) reported a patient with cranial nerve 4 palsy who had CT evidence of a hematoma near the superior cerebellar cistern. He hypothesized that the hemorrhage was secondary to bleeding from a small vessel dashed against the tentorium, similar to the mechanism proposed by Linden-berg ( 22). Burgerman ( 31) reported a patient with traumatic cranial nerve 4 palsy and MRI evidence of a parenchymal contusion in the dorsal midbrain with a previously negative CT. In a study of 13 patients with cranial nerve 4 injury, Burger ( 32) found that those with unilateral cranial nerve 4 palsy had suffered frontolateral blows, whereas those with bilateral cranial nerve 4 injury had suffered midfrontal blows. We lacked the information about the site of the head blows in our study. We did not find any midbrain hemorrhages. Proposed Mechanisms of Traumatic Cranial Nerve 6 Palsy There are two hypotheses as to the mechanism of injury in traumatic cranial nerve 6 palsies: petrous bone injury transmitted to the nerve in that region and neck hyperextension causing stretch of the nerve. Lateral crushing injuries to the skull have been shown in the laboratory ( 33) to cause fracture of the apex of the petrous portion of the temporal bone. A subsequent pathologic study ( 34) found traumatic injury to cranial nerve 6 as it passes over this region. Clinical reports of bilateral compression injuries in cranial nerve 6- injured patients support this mechanism ( 10,35). Lindenberg ( 23) described a patient with a traumatic neck hyperextension who had pathologic evidence of injury to the pontine segment of the sixth cranial nerve. Schneider ( 36) reported two cranial nerve 6- injured patients following traumatic neck hyperextension in a motor vehicle accident who had suffered cervical vertebral but no craniofacial fractures. He hypothesized that the injury was secondary to upward and posterior displacement of the brainstem causing stretch injury to the sixth cranial nerve as it passes through Dorello's canal under the rigid petrosphenoidal ligament. Neither of these studies ( 23,36) provides information as to the location of the blow. In two other reports, the mechanism is less clear. Rosa ( 37) described a patient with severe frontal trauma and neck hyperextension who suffered cranial nerve 6 injury. In Hooper's series ( 10) of six patients with traumatic cranial nerve 6 injury, four had a frontolateral blow, one had a midfrontal blow, and one had a lateral compression injury. We found no difference in the distribution of craniofacial fractures or intracranial injury on CT imaging to suggest a particular location of injury, nor did we find a difference in the rate of cervical spine injury in the cranial nerve- injured group, although this does not rule out traumatic neck hyperextension as a mechanism of injury. We are mystified at the finding that our patients with multiple or bilateral cranial nerve injuries had a relatively low level of severity of trauma as measured by the GCS. Interestingly, this group sustained the highest frequency of extremity injuries. The mechanism of injury in single and multiple cranial nerve damage may be different. Our study supports earlier reports that low levels of CHI, as determined by lack of LOC, are unlikely to cause cranial nerve palsy. Walter ( 38) reported two patients with head trauma and cranial nerve 3 injuries without LOC or associated injuries who were later found to have posterior communicating artery aneurysms. Eyster ( 39) reported three patients with cranial nerve 3 injuries in a setting of head trauma insufficient to cause LOC who were eventually found to have basal intracranial tumors. In another report ( 40), neoplasms were found at the base of the brain in a series of three patients with cranial nerve 4 palsy in the setting of minor head trauma. A patient with cranial nerve 4 palsy and minimal head trauma without LOC was found to have a tentorial arteriovenous malformation compressing the subarachnoid portion of the nerve ( 41). This information suggests that, in the setting of a cranial palsy following minimal head trauma, other etiologies should be sought. 9 Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. J Neuro- Ophthalmol, Vol. 26, No. 1, 2006 Dhaliwal et al We acknowledge two sources of accrual bias that might have affected our results: 1) all patients were drawn from a tertiary care medical center, which might have excluded patients with milder forms of CHI; and 2) the Cranial Nerve Injury and Control Groups were not drawn from identical sources. The Cranial Nerve Injury Groups included patients drawn from outpatient clinics and the emergency room whereas the Control Group patients were drawn entirely from the emergency room. We also recognize that many statistical comparisons were made between the case and control groups and subsets thereof, and that this practice can lead to falsely positive findings by chance alone. We have tried to avoid this trap by using the Bonferroni adjustment and by adhering to the clinical relevance of statistical findings. Having done so, we believe that our data have sufficient validity to provide useful information to the clinician. REFERENCES 1. 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