| OCR Text |
Show Journal of Neuro- Ophthalmology 21( 3): 212- 213, 2001. © 2001 Lippincott Williams & Wilkins, Inc., Philadelphia Original Contribution Isolated Unilateral Post- traumatic Internuclear Ophthalmoplegia Jane W. Chan, MD A patient developed an isolated unilateral internuclear ophthalmoplegia ( INO) after head trauma. An uncommon complication of closed head trauma, INO usually occurs bilaterally and is often associated with other neurologic deficits. The mechanism may be shear injury caused by angular acceleration leading to downward displacement of the posterior brainstem downward, stretching of the nerve fibers of the medial longitudinal fasciculus, or compression and tearing of its arterial supply. Key Words: Internuclear ophthalmoplegia- Head trauma. Internuclear ophthalmoplegia ( INO) is characterized by paresis of adduction on lateral gaze with horizontal jerk nystagmus in the contralateral abducting eye. Vertical nystagmus during upward gaze may be present ( 1). Approximately 3 to 7% of patients with head injuries have ocular motor palsies, most commonly of the third, fourth, and sixth cranial nerves. Nystagmus, skew deviation, supranuclear palsy, conjugate deviation of the eyes, and impaired convergence are less frequently observed ( 1). INO is an uncommon complication of closed head trauma, with only 13 documented cases, four of which were unilateral. Of the four unilateral cases, two were associated with other neurologic findings ( 1,2). This case report describes a patient with isolated unilateral INO from a medial longitudinal fasciculus ( MLF) infarct immediately after blunt head trauma. CASE REPORT A 32- year- old man was assaulted, sustaining injury to the right side of his head that caused loss of consciousness for several hours. He had a right mandibular fracture and right periorbital edema. His corrected visual acuity Manuscript received April 12, 2001; accepted July 10, 2001. From the Division of Neurology, Department of Internal Medicine, University of Nevada, School of Medicine, Las Vegas, Nevada. Address correspondence and reprint requests to Jane W. Chan, MD, Department of Internal Medicine, Division of Neurology, University of Nevada School of Medicine, 2040 W. Charleston Blvd., Suite 300, Las Vegas, NV 89102. E- mail address: worjun@ aol. com was 20/ 20 in both eyes. Pupillary responses and Humphrey automated visual field testing were normal. Ocular motility examination demonstrated orthophoria in primary position. His right eye was unable to adduct and his left eye had abduction nystagmus during leftward gaze. The nystagmus had a vertical and rotary component in upgaze. Convergence was not spared. Forced duction testing revealed no restriction. He had no other neurologic abnormalities. Orbital computed tomography ( CT) revealed no orbital fractures. Magnetic resonance imaging ( MRI) of the brain with contrast revealed a right hyperintense MLF lesion on axial T2- weighted images ( Fig. 1). Gradient echo MRI showed no evidence of primary brainstem hemorrhages or secondary Duret hemorrhages. Diffusion- weighted imaging suggested that the MLF lesion was an acute infarct. Cerebrospinal fluid ( CSF) cell count, protein, and glucose were all within normal limits. CSF venereal disease research laboratories test, Gram stain, acid- fast bacilli stain, and bacterial antigens for Haemophilus influenzae, Neisseria meningitidis, and Streptococcus pneumoniae were all negative; routine bacterial, viral, and fungal cultures were also negative. A CSF multiple sclerosis panel, including immunoglobulin G ( IgG) index, CSF IgG synthesis rate, oligoclonal immunoglobulin bands, and myelin basic protein, was within normal limits. Three months later, he had a mild adduction deficit OD and residual horizontal diplopia in left gaze. Six months later, he had gained almost full recovery. DISCUSSION Bilateral INO resulting from head trauma is more commonly reported than is unilateral INO. Unilateral INO without any associated neurologic deficits, as in the patient described here, is a very rare complication of blunt head trauma. Our patient presented with slowed adducting saccades OD and abducting nystagmus OS. The vertical and rotary component of this abduction nystagmus on upgaze and the presence of a right MLF signal abnormality on MRI support a central rather than a peripheral cause such as a partial third nerve palsy. The 212 ISOLATED UNILATERAL POSTTRAUMATIC INO 213 FIG. 1. Axial T2- weighted MRI scan reveals a right medial longitudinal fasciculus infarct, as indicated by the arrow. absence of orbital fractures and restriction on forced duc-tion testing exclude an extraocular muscle entrapment. The pathogenesis of isolated damage to the MLF in head trauma is unclear, but several mechanisms have been suggested to explain this phenomenon. Shearing forces from angular acceleration or deceleration of the head on impact can stretch the nerve fibers of the MLF ( 3). The shearing forces exert maximal effect where the difference in density between CSF and adjacent neural tissue is greatest ( 3). Because the MLF is situated near the aqueduct and the floor of the fourth ventricle, it is vulnerable to these shearing forces. The posterior portion of the brainstem is also downwardly displaced more than the anterior portion during rapid acceleration/ deceleration because the anterior portion is tethered by small penetrating arteries of the basilar artery, as reported in experimental angiographic studies ( 4). The shearing forces can therefore create a temporary downward displacement of the posterior brainstem, causing shear injury to the MLF. Furthermore, the shear forces within the brainstem could damage the perforating branches of the basilar artery, resulting in decreased blood flow or focal brainstem hemorrhage. MRI correlation of structural lesions with the described possible mechanisms has been shown in only a few previously documented cases of posttraumatic INO. In two cases, Strauss et al. ( 5) showed that a unilateral INO after head trauma could be a result of a pontomesencephalic hemorrhage as seen on MRI and CT. In this report, we demonstrate that an infarct of the right MLF was probably responsible for the unilateral INO immediately after head trauma. This lesion was seen as a bright signal on the T2- weighted image ( Fig. 1) and as a Tl- weighted dark signal with gadolinium enhancement. Diffusion- weighted imaging also helped to confirm this lesion to be an acute infarct. Other reported cases of posttraumatic INO in the literature either had no verification by neuroimaging or had no visible lesion on CT or MRI, suggesting that direct stretch injury to the MLF could cause a lesion too small to be detected by MRI ( 1,2,6,7). More extensive brainstem dysfunction accompanying a posttraumatic INO can include upper extremity ataxia, gait ataxia, and cranial nerve palsies, such as a third nerve palsy with a dilated pupil ( 8). The damage to the brainstem may result from a remote lesion such as a subdural hematoma, which may lead to transtentorial herniation, pyramidal tract signs, and various cranial nerve palsies ( 9). This patient had no neurologic abnormalities except an INO. Doslak et al. ( 10) showed that a unilateral posttraumatic INO could fully resolve in 18 weeks. This patient described here had residual horizontal diplopia and a mild adduction deficit after 3 months with almost full recovery after 6 months. As demonstrated by quantitative oculography, central nervous system plasticity, manifested as adaptive firing patterns in response to the MLF lesion, helps in this recovery by increasing and then later normalizing the saccadic pulse duration. As the firing frequency of the pulse and step increases and the conduction of MLF axons improves, greater saccadic gain and velocity are also attained for normal recovery ( 10). When an acute head trauma patient presents with an adduction deficit, an INO should be considered as a cause. REFERENCES 1. Constantoyannis C, Tzortzidis F, Papadakis N. Internuclear ophthalmoplegia following minor head injury: a case report. Br J Neurosurg 1998; 12: 377- 9. 2. Catalano RA, Sax RD, Krohel GB. Unilateral internuclear ophthalmoplegia after head trauma. Am J Ophthalmol 1986; 101: 491- 3. 3. Hardman JM. The pathology of traumatic brain injuries. Adv Neurol 1979; 22: 15- 50. 4. Johnson RT, Yates PO. Brainstem hemorrhages in expanding su-pra- tentorial conditions. Acta Radiol 1956; 46: 250- 6. 5. Strauss C, Ganslandt O, Huk WJ, et al. Isolated unilateral internuclear ophthalmoplegia following head injury: findings in magnetic resonance imaging. A'euro- ophthalmology 1995; 15: 15- 9. 6. Mueller C, Koch S, Toifl K. Transient bilateral internuclear ophthalmoplegia after minor head trauma. Ophthalmology 1993; 35: 158- 76. 7. Rosati G, Pinna L, Paolino E, et al. Reversible bilateral internuclear ophthalmoplegia due to head trauma: a case report. Eur Neurol 1981; 20: 80- 3. 8. Keane JR. Traumatic internuclear ophthalmoplegia. J Clin Neu-roophthalmol 1987; 7: 165- 6. 9. Beck RW, Meckler RJ. Internuclear ophthalmoplegia after head trauma. Ann Ophthalmol 1981; 13: 671- 5. 10. Doslak MJ, Kline LB, Dell'Osso LF, et al. Internuclear ophthalmoplegia: recovery and plasticity. Invest Ophthalmol Vis Sci 1980; 19: 1506- 11. J Neuro- Ophthalmol, Vol. 21, No. 3, 2001 |
