Journal of Neuro-Ophthalmology, December 1988, Volume 8, Issue 4

Trochlear nerve palsy following minor head trauma. A sign of structural disorder.

Trauma-induced superior oblique palsy usually results from contusion or avulsion of the trochlear nerve or from decompensation of a congenital trochlear nerve palsy. Severe craniocerebral trauma is often associated with the former mechanism, whereas more minor closed-head injuries can decompensate a congenital phoria. We report a patient who developed an isolated trochlear nerve palsy following minor head trauma. Investigation revealed an unsuspected tentorial vascular malformation that was compressing the trochlear nerve in its subarachnoid course. In the absence of other features (e.g., documentation of old head tilt, large vertical fusion amplitudes) that support decompensation of a congenital phoria, compressive lesions should be sought in cases of fourth cranial nerve palsies that follow minor head trauma.

Journal of Clinical Neuro-aphthalmology 8(4): 263-268, 1988. Trochlear Nerve Palsy Following Minor Head Trauma A Sign of Structural Disorder Daniel M. Jacobson, M.D., John J. Warner, M.D., Ali K. Choucair, M.D., and Louis J. Ptacek, M.D. © 1988 Raven Press, Ltd., New York Trauma-induced superior oblique palsy usually results from contusion or avulsion of the trochlear nerve or from decompensation of a congenital trochlear nerve palsy. Severe craniocerebral trauma is often associated with the former mechanism, whereas more minor closed-head injuries can decompensate a congenital phoria. We report a patient who developed an isolated trochlear nerve palsy following minor head trauma. In­vestigation revealed an unsuspected tentorial vascular malformation that was compressing the trochlear nerve in its subarachnoid course. In the absence of other fea­tures (e.g., documentation of old head tilt, large vertical fusion amplitudes) that support decompensation of a congenital phoria, compressive lesions should be sought in cases of fourth cranial nerve palsies that follow minor head trauma. Key Words: Trochlear nerve palsy-Superior oblique palsy-Trauma-Arterial vascular malformation-MR!. From the Departments of Neurology (D.M.J., A.K.C., L.J.P.), Ophthalmology (D.M.J.), and Radiology a.].W.), Marshfield Clinic, Marshfield, Wisconsin, U.S.A. Address correspondence and reprint requests to Dr. Daniel M. Jacobson, Neuro-ophthalmology Unit (4F), Marshfield Clinic, 1000 North Oak Avenue, Marshfield, WI 54449, U.S.A. 263 Trauma is the most commonly identified cause of an isolated trochlear nerve palsy (1). In this set­ting, superior oblique palsy can result from direct orbital injury (2) or from extraorbital injury causing contusion or avulsion of the trochlear nerve as it exits from the dorsal brainstem or compression in its subarachnoid course. In most instances, trauma-induced extraorbital palsy of the trochlear nerve follows severe blows to the cranium and of­ten results in other intracranial injuries (3,4). Another mechanism of trauma-induced superior oblique palsy is decompensation of a congenital trochlear nerve palsy. In such cases, decompensa­tion of the phoria, with resultant diplopia, often follows minor closed head injuries (3,5). Finding a compensatory head tilt on old photographs (e.g., driver's license) or demonstrating large vertical fu­sion amplitudes supports decompensation as the mechanism of trochlear nerve palsy. An infrequently considered mechanism of iso­lated trauma-induced trochlear nerve palsy is com­pression from a preexisting, but unrecognized, structural disorder, as illustrated by the following case. CASE REPORT A 54-year-old man tripped and fell, striking his left temple against the ground. He suffered no loss of consciousness or any other immediate symp­toms. He was well until 3 days later, when he noted constant vertical diplopia. Four days later, he developed a severe constant right-sided tem­poroparietal headache that was not associated with nausea or vomiting. He was admitted for evaluation 4 weeks after he fell. He had suffered from moderately well-con- FIG. 1. Initial unenhanced computed to­mography scan demonstrating hyper­dense lesion in the region of the right­sided quadrigeminal cistern (white arrow­head). FIG. 2. Postcontrast computed to­mography showing mild enhancement of the lesion (white arrowhead). TRAUMATIC TROCHLEAR NERVE PALSY 265 trolled generalized seizures since the age of 7 years. One of us (L.J.P.) had followed him for this problem for 20 years and had never observed any head tilt. His anticonvulsant medications (admis­sion serum level, normal value) included Tegretol 800 mg daily (3 j.Lg/ml, 4-12 j.Lg/ml), Dilantin 400 mg daily (17.5 j.Lg/ml, 10-20 j.Lglml), phenobarbital 120 mg daily (41 j.Lg/ml, 15-40 j.Lg/ml), and Myso­line 675 mg daily (6.6 j.Lg/ml, 7-11 j.Lg/ml). One year prior to admission, a left-sided lung mass was de­tected and he underwent a left thoracotomy for removal of an adenocarcinoma. There was no ev­idence of disease at the time of his current evalu­ation. He had also experienced recurrent deep vein thrombosis with pulmonary embolism since 1973 and was receiving Coumadin. Admission prothrombin time was 25.6 s (control value 11.5-­13.0 s). He was alert and fully oriented. His neck was stiff. Other abnormal findings were restricted to the neuro-ophthalmic examination. His ocular ductions were full, but he had a 7-prism diopter right hypertropia in forward gaze that increased to 12 diopters in left gaze and decreased to 3 diopters in right gaze. Right head tilt produced a 6-prism diopter right hypertropia, and left head tilt pro­duced a 2-prism diopter right hypertropia. Vertical fusion amplitude was 2-3-prism diopters. An anomalous head posture was not observed. Visual acuity, pupil size and reactions, ophthalmoscopy, lids, and orbital examination were all normal. Old photographs were not available for inspection of a previous head tilt. Computed tomography performed the day after admission revealed a small irregular mass of high density in the area of the right tentorium and quadrigeminal cistern (Fig. 1). There was mild en­hancement of the lesion after contrast adminis­tration (Fig. 2). A cerebral angiogram performed 3 days later revealed very faint staining posterior and to the right of the basilar artery bifurcation during injections of the vertebral arteries (Fig. 3). These radiographic abnormalities were felt to be most consistent with a tentorial meningioma. Ce­rebrospinal fluid examination performed 17 days after admission revealed xanthochromia, 11,280 erythrocytes/ml3 , 10 leukocytes/ml3 , protein 73 mg/dl, and negative cytology. The patient was eventually discharged after con­servative management. The subarachnoid hemor- FIG. 3. Digital subtraction arterio­gram following vertebral artery injec­tion (lateral view) demonstrating ab­normal vascular pattern (black ar­row) posterior to basilar artery (b) and inferior to posterior cerebral ar­teries (p). J Clin Neuro-ophthalmol. Vol. 8, No.4, 1988 266 D. M. JACOBSON ET AL. rhage and compressive trochlear nerve palsy were thought to result from trauma-induced intratumor hemorrhage. Magnetic resonance imaging per­formed 3 weeks after the initial computed tomog­raphy scan was consistent with a resolving he­matoma (Figs. H). Repeat computed tomography performed 4 weeks after the initial scan was nor­mal, before (Fig. 7) and after (Fig. 8) contrast ad­ministration. DISCUSSION The absence of findings on this patient's follow­up computed tomography scan was felt to be in­consistent with an underlying meningioma or me­tastasis. Although his anticoagulated state most certainly predisposed him to hemorrhagic compli­cations following head trauma, the focal location of his hematoma was unusual for trauma in the ab­sence of an underlying structural disorder. A dural vascular malformation that underwent thrombosis following hemorrhage was felt to be the most likely underlying structural disorder. Vascular malformations in this location comprise a relatively FIG. 4. Axial magnetic resonance image using T2­weighted sequence (TR = 2,500 ms, TE = 70 ms) showing lesion of high signal intensity surrounded by ring of absent signal, consistent with a resolving he­matoma (black arrow). The bright signal represents methemoglobin and the rim of low signal represents hemosiderin. The low intensity signal seen in the left temporal lobe is due to partial volume averaging of the left petrous bone. ','" 4, 1988 FIG. 5. Coronal magnetic resonance image using in­termediate image sequence (TR = 2,500 ms, TE = 30 ms) revealing that the high signal intensity lesion originates from the medial edge of the tentorium (black arrow). small proportion of intracranial dural arteriove­nous malformations (6). Patients harboring such lesions usually present with spontaneous sub­arachnoid hemorrhage or with symptoms caused by progressive posterior fossa mass effect (7,8). A case similar to ours was reported by Lavin and Troost (9). A 59-year-old man receiving warfarin suffered minor head trauma, resulting in an iso­lated trochlear nerve palsy that became symptom­atic the following day. Computed tomography showed a hematoma involving the midbrain tec­tum and the adjacent subarachnoid space. Either the fourth nerve nucleus, fascicle, or subarachnoid portion could have been damaged from the lesion shown in their article. Neetens and Van Aerde (10) described three pa­tients who developed trochlear nerve palsies fol­lowing minor head trauma. Subsequent investiga­tion uncovered tumors at the base of the brain. However, two of their three cases had other find­ings, so that the trochlear nerve palsy was not truly isolated. In most cases, an isolated trochlear nerve palsy following head trauma represents a benign condi­tion that only requires careful exclusion of orbital restriction and close follow-up to ensure that no other neurologic signs develop. The presence of a head tilt on old photographs and large vertical fu­sion amplitudes supports decompensation of a FIG. 6. Sagittal magnetic reso­nance image using T1-weighted se­quence (TR = 600 ms, TE = 20 ms) showing bright signal lesion with thin rim of low signal intensity, which is consistent with a subacute resolving hemorrhage (black ar­row). FIG. 7. Follow-up computed to­mography scan, without con­trast, showing resolution of the previously seen hyperdense le­sion. I Gin Neuro-ophthalmol, Vol. 8, No.4, 1988 268 FIG. 8. After contrast adminis­tration, the follow-up com­puted tomography scan shows no abnormal enhancement. D. M. JACOBSON ET AL. congenital trochlear nerve palsy as the mechanism of diplopia. In the absence of these two ancillary findings, we recommend computed tomography of the base of the brain and posterior fossa in cases that follow seemingly minor head trauma to ex­clude a previously unrecognized underlying struc­tural disorder. A similar strategy has been advo­cated for the evaluation of an oculomotor nerve palsy following minor head trauma (11). REFERENCES 1. Rush JA, Younge BR. Paralysis of cranial nerves III, IV, and VI. Cause and prognosis in 1,000 cases. Arch Ophthalmol 1981;99:76-9. 2. Wojno TH. The incidence of extraocular muscle and cranial nerve palsy in orbital floor blow-out fractures. Ophthalmol­ogy 1987;94:682-7. 3. Burger LJ, Kalvin NH, Smith JL. Acquired lesions of the fourth cranial nerve. Brain 1970;93:567-74. 4. Younge BR, Sutula F. Analysis of trochlear nerve palsies. , ;,r,}. 4, 1988 Diagnosis, etiology, and treatment. Mayo Clin Proc 1977;52:11-18. 5. Miller NR. Topical diagnosis of neuropathic ocular motility disorders. In: Clinical neuro-ophthaImoIogy, 4th ed, vol 2. Bal­timore: Williams & Wilkins, 1985:683-4. 6. Lasjaunias P, Chiu M, Brugge KT, Tolia A, Hurth M, Bern­stein M. Neurological manifestations of intracranial dural arteriovenous malformations. I Neurosurg 1986;64:724-30. 7. Grisoli F, Vincentelli F, Fuchs 5, Baldini M, Raybaud C, Leclercq TA, Vigouroux RP. Surgical treatment of tentorial arteriovenous malformations draining into the subarach­noid space. Report of four cases. I Neurosurg 1984;60:1059­66. 8. Lasjaunias P, Halimi P, Lopez-Ibor L, Sichez jP, Hurth M, De Tribolet N. Traitement endovasculaire des malforma­tions vasculaires durales (MVD) pures "spontanees." Re­vue de 23 cas explores et traites entre mai 1980 et Octobre 1983. Neurochirurgie 1983;30:207-23. 9. Lavin PJM, Troost BT. Traumatic fourth nerve palsy. aini­coanatomic correlations with computed tomographic scan. Arch Neurol 1984;41:679-80. 10. Neetens A, Van Aerde F. Extra-ocular muscle palsy from minor head trauma. Initial sign of intracranial tumour. Bull Soc BeIge OphtaI 1981;193:161-7. 11. Eyster EF, Hoyt WF, Wilson CB. Oculomotor palsy from minor head trauma. An initial sign of basal intracranial tu­mor. lAMA 1972;220:1083-6.