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CT Demonstration of Dorsal Midbrain Hemorrhage in Traumatic Fourth Cranial Nerve Palsy

Sudhakar, Padmaja MD; Bapuraj, J Rajiv MD

Journal of Neuro-Ophthalmology: March 2010 - Volume 30 - Issue 1 - p 59-63
doi: 10.1097/WNO.0b013e3181ce1b1d
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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.

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:

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 hemorrhages in the frontal lobes, posterior horn of the left lateral ventricle, and corpus callosum.

FIG. 1

FIG. 1

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 gastrostomy 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 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.

FIG. 2

FIG. 2

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 hemorrhage (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).

FIG. 3

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.

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We thank David Murrel for drawing Figure 3.

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