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Show CT Demonstration of Dorsal Midbrain Hemorrhage in Traumatic Fourth Cranial Nerve Palsy Padmaja Sudhakar, MD, J.Rajiv Bapuraj, MD Abstract: A 21-year-old man who suffered a traumatic brain injury from a motor vehicle accident recovered brain function except for an isolated left fourth cranial nerve palsy. Brain CT showed a focal hemorrhage in the right dorsal midbrain, directly in the brainstem path of what would become the left fourth cranial nerve. Although there has been previous imaging documentation of midbrain and cisternal hemorrhage in patients with isolated post-traumatic fourth cranial nerve palsy, this is the first report to show a large midbrain hemorrhage on CT. The mechanism is likely to be concussive impact of the dorsal midbrain on the tentorium cerebelli. Journal of Neuro-Ophthalmology 2010;30:59-63 doi: 10.1097/WNO.0b013e3181ce1b1d 2010 by North American Neuro-Ophthalmology Society A21-year-old man had a traumatic brain injury in a motor vehicle accident in which he was struck from behind as a belted front seat passenger by a semi truck. He was unresponsive at the scene and taken to the hospital where he was intubated. Precontrast head CT revealed a right dorsal midbrain hemorrhage with surrounding edema. (Fig. 1A) There were also multiple small hemor-rhages in the frontal lobes, posterior horn of the left lateral ventricle, and corpus callosum. He required ventriculostomy and intracranial pressure monitoring. Over the next week, he gradually regained consciousness and was discharged after 2 weeks without focal neurologic deficits but with a percutaneous gastro-stomy tube. At discharge, he reported that he had binocular vertical diplopia with 1 tilted image especially in downward gaze to the right. He had been entirely healthy before the accident. Six weeks after the accident, best-corrected visual acuity was 20/20 in each eye. Pupils measured 5 mm in dim illumination and constricted normally to light without an afferent defect. Results of the ocular adnexal examination was normal. Eye movements were full, smooth, and without nystagmus. In primary gaze position, the patient had a 2 prism-diopter left hyperphoria, which became an 8 prism-diopter left hyperdeviation on right gaze. In down and right FIG. 1. Our patient with left fourth cranial nerve palsy. A. Precontrast head CT performed at presentation shows hemorrhage in the right dorsal midbrain contralateral to the fourth cranial nerve palsy. B. Precontrast CT performed 9 weeks later no longer shows the hemorrhage. Departments of Ophthalmology and Visual Sciences (PS), Kellogg Eye Center, and Department of Radiology (Neuroradiology) (JRB), University of Michigan, Ann Arbor, Michigan. Address correspondence to Padmaja Sudhakar, MD, Kellogg Eye Center, 1000 Wall Street, Ann Arbor, MI 48105; E-mail: padmajas@ med.umich.edu Sudhakar and Bapuraj: J Neuro-Ophthalmol 2010; 30: 59-63 59 Photo Essay FIG. 2. Reported cases of traumatic fourth cranial nerve palsy with imaging evidence of intracranial hemorrhage in the path of the fourth cranial nerve. A. Precontrast T1 axial MRI shows hemorrhage in the left dorsal midbrain with pontine extension (arrow). (Modified from Burgerman et al [1].) B. Gradient echo MRI exposes hemosiderin (black) in a small dorsal midbrain hemorrhage at the level of the left inferior colliculus. (Modified from Prosst and Majetschak [2].) C. Precontrast brain CT shows a large hemorrhage in the rostral left superior cerebellar cistern (Modified from Lavin and Troost [3].) D. Precontrast brain CT shows a hemorrhage in the right superior cerebellar cistern (Modified from Arbarbanel et al [4].) E. Precontrast axial brain CT shows hemorrhage in the left quadrigeminal cistern. (Modified from Ishizaki and Kurokawa [5].) F. Precontrast axial T1 shows high signal in the right ambient cistern consistent with methemoglobin (Modified from Hara et al [6].) G. Axial FLAIR study shows hyperintense signal in the right ambient cistern (Modified from Hara et al [6]). H. Precontrast axial brain CT shows a hyperdense focus in the collicular region in a patient with bilateral fourth nerve palsies. (Modified from Keane [7].) I. Precontrast brain CT shows bullet fragments in the collicular region in a patient with a left fourth cranial nerve palsy. (Modified from Keane [7].) Photo Essay 60 Sudhakar and Bapuraj: J Neuro-Ophthalmol 2010; 30: 59-63 FIG. 3. Axial schematic illustrations to demonstrate the postulated mechanisms of damage to the fourth cranial nerve in closed head trauma. A. Normal anatomy of the brainstem at a cross-sectional level immediately caudal to the inferior colliculus in the tentorial incisura. B. Lateral displacement of the midbrain and collision with the tentorial edge causes dorsal midbrain hemorrhage and damage to the intra-axial segment of the contralateral fourth cranial nerve, as in our patient. C. Lateral displacement of the midbrain and collision with the tentorial edge causes damage to the ipsilateral extra-axial (cisternal) segment of the fourth cranial nerve. D. Posterior displacement of the midbrain and collision with the tentorial edge causes damage to both fourth cranial nerves in the region of the anterior medullary velum. Photo Essay Sudhakar and Bapuraj: J Neuro-Ophthalmol 2010; 30: 59-63 61 gaze, he had a 20 prism-diopter left hypertropia. In left head tilt, he had a 6 prism-diopter left hypertropia. In right head tilt, his eyes were aligned as they were in all upgaze positions. With the double Maddox rod test, he had 10 of excyclotorsion. The results of the rest of the neuro-ophthalmologic examination were normal as were the results of the neurologic examination. Three weeks later, precontrast head CT (Fig. 1B) demonstrated resolution of the midbrain hemorrhage. The location of injury to the fourth cranial nerve in closed head trauma is uncertain. In most cases, brain imaging, whether by CT or MRI, fails to show a lesion. However, there are 7 reports demonstrating radiologic evidence of a causative hemorrhage (1-7). In 2 patients (1,2), the hemorrhage was in the dorsal midbrain contralateral to the side of the fourth cranial nerve palsy as in our patient, but unlike our patient, the hemorrhage was seen only on MRI and not on CT. In the first of these reported patients, Burgerman et al (1) documented a small dorsal midbrain hemorrhage on MRI in a patient who had residual truncal and left extremity ataxia (Fig. 2A), unlike our patient, who had no focal neurologic deficits apart from the fourth cranial nerve palsy. The lesion had a bright signal on T1 and T2, indicating the presence of methemoglobin in a late subacute hematoma. In the second patient, Prosst and Majetschak (2) demonstrated low signal in a dorsal midbrain hemorrhage on gradient echo (T2*) MRI (Fig. 2B), indicating hemosiderin at the level of the inferior colliculus in a patient with an isolated unilateral fourth cranial nerve palsy. Four reports (of 5 patients) have documented damage in the brainstem cerebrospinal fluid cisterns along the course of the extra-axial portion of the fourth cranial nerve. In 2 reports, the hemorrhage was located in the superior cerebellar cistern; in 1 report, it was in the quadrigeminal cistern; and in 1 report (2 patients), it was in the ambient cistern. In 1 of these 4 reports (3), the lesion was demonstrated on precontrast CT (MRI was not done) in the superior cerebellar cistern (Fig. 2C) in a 59-year-old patient who had fallen in the shower. He was being treated with warfarin after mitral valve replacement. That patient had had previous episodes of spontaneous extracranial bleeding. The fourth cranial nerve palsy in that patient was unilateral, isolated, and ipsilateral to the side of the hemorrhage. Another case was that of a 10- year-old child who struck his head in a fall from a swing. Precontrast CT (MRI was not performed) demonstrated hemorrhage in the superior cerebellar cistern on the side of an isolated fourth cranial nerve palsy (Fig. 2D) (4). In a further report, hemorrhage was present in the quadrigeminal cistern on CT and MRI (low signal on T2; T1 signal not reported) in an isolated ipsilateral fourth nerve palsy in a 72 year-old man who had fallen down the stairs (Fig. 2E) (5). In 2 other patients, an ambient cistern hemorrhage was demonstrated in association with isolated traumatic ipsilateral fourth cranial nerve palsy (6). One of these patients was 65 years old and had fallen intoxicated from his bicycle; the hemorrhage displayed a signal of high intensity on T1 and FLAIR and of isointensity on T2, indicating methemoglobin due to early subacute hemor-rhage (Fig. 2F). The second patient was a 16-year-old-boy who had fallen off his motorcycle; his lesion was visible only as a high intensity signal on FLAIR (Fig. 2G). In 2 additional reported patients, imaging resolution was too low to allow precise localization. In the first case, CT performed on a first-generation EMI1010 scanner appeared to show a collicular hemorrhage in a patient with bilateral traumatic fourth nerve palsies (7), upper extremity numbness, and contralateral truncal ataxia (Fig. 2H). The other patient, who had been shot in the head, had a unilateral fourth cranial nerve palsy, ataxia, and extremity sensory loss. CT showed a bullet fragment in the region of the inferior colliculus (Fig. 2I). Our patient and the reported literature indicate that intrinsic midbrain or perimesencephalic hemorrhages may occasionally be seen on imaging in traumatic fourth cranial nerve palsy. The hemorrhage may result from tearing of intrinsic nutrient blood vessels, thrombosis and subsequent infarction, or bruising by concussion against the tentorium (8,9). Interestingly, most of these hemorrhages have been present at the superolateral aspect of the midbrain near the intra-axial course of the fourth cranial nerve (7,9). Impact of the midbrain against the rigid tentorium would be the most plausible mechanism of injury. After head impact, the brainstem moves backwards, so that the tentorium collides with either the dorsal midbrain or the fourth cranial nerve exit zone in the anterior medullary velum (2,10) (Fig 3). The striking feature of our patient is that a large midbrain hemorrhage, so easily seen on CT, would cause lingering damage limited to the fourth cranial nerve. The explanation seems to be that in this dorsal location other critical brain stem pathways are spared because they are not near the lesion. ACKNOWLEDGMENT We thank David Murrel for drawing Figure 3. REFERENCES 1. Burgerman RS, Wolf AL, Kelman SE, et al. Traumatic trochlear nerve palsy diagnosed by magnetic resonance imaging: case report and review of the literature. Neurosurgery 1989;25:978-81. 2. Prosst RL, Majetschak M. Traumatic unilateral trochlear nerve palsy. J Trauma 2007;62:E1-E3. 3. Lavin PJ, Troost BT. Traumatic fourth nerve palsy. Clinicoanatomic correlations with computed tomographic scan. Arch Neurol 1984;41:679-80. 4. Abarbanel JM, Hertzanu Y, Herishanu Y. Traumatic trochlear-nerve palsy due to haematoma. Dev Med Child Neurol 1986;28:509-11. 5. Ishizaki E, Kurokawa Y. A case of solitary and unilateral trochlear nerve palsy due to a blunt head impact. Rinsho Shinkeigaku 2003;43:571-3. Photo Essay 62 Sudhakar and Bapuraj: J Neuro-Ophthalmol 2010; 30: 59-63 6. Hara N, Kan S, Simizu K. Localization of post-traumatic trochlear nerve palsy associated with hemorrhage at the subarachnoid space by magnetic resonance imaging. Am J Ophthalmol 2001;132: 443-5. 7. Keane JR. Trochlear nerve pareses with brainstem lesions. J Clin Neuroophthalmol 1986;6:242-6. 8. Lindenberg R. Significance of the tentorium in head injuries from blunt forces. Clin Neurosurg 1964;12:129-42. 9. Tomlinson BE. Brainstem lesions after head injury. J Clin Pathol Suppl (R Coll Pathol) 1970;4:154-65. 10. Hoya K, Kirino T. Traumatic trochlear nerve palsy following minor occipital impact-four case reports. Neurol Med Chir (Tokyo) 2000;40:358-60. Photo Essay Sudhakar and Bapuraj: J Neuro-Ophthalmol 2010; 30: 59-63 63 |
