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Show Journal of Neuro- Ophthalmology 14( 1): 21- 23, 1994. © 1994 Raven Press, Ltd., New York Inferior Branch Oculomotor Nerve Palsy A Case Report Emmett T. Cunningham, Jr., M. D., Ph. D., M. P. H. and William V. Good, M. D. We describe a 34- year- old man with acute, nontraumatic inferior branch oculomotor nerve palsy. Complete ophthalmologic, neurologic, and systemic examinations were otherwise normal. The oculomotor nerve palsy resolved, but the patient subsequently developed bilateral upper extremity numbness and painful dysesthesias in the distribution of the median nerves. These observations suggest that inferior branch oculomotor nerve palsy, although uncommon, may occur as part of a more generalized neurologic disorder, presumed in our patient to be either vasculitic or demyelinating in nature. Key Words: Oculomotor branch nerve palsy- MRI- CT scans. Oculomotor nerve palsies account for u p to one-third of all paretic ocular misalignment syndromes ( 1- 4). Incomplete involvement of the oculomotor nerve is common, particularly with regard to pupillary involvement in the setting of an ischemic vasculopathy ( 5,6). However, pure branch palsies of the oculomotor nerve are rare ( 6,7). Ten cases of isolated inferior branch oculomotor nerve paresis have been reported in the literature ( 6,8- 10) ( Table 1). Of these, six have been posttraumatic ( 8,9), while only four have occurred in the absence of trauma ( 6,10). We present here a fifth case of acute, nontraumatic inferior branch oculomotor nerve palsy. Our patient subsequently developed a second, temporally dissociated neurologic deficit, suggesting a generalized vasculitic or demyelinating etiology. From the Department of Ophthalmology, School of Medicine, University of California, San Francisco, U. S. A. Address correspondence and reprint requests to Dr. William V. Good, Department of Ophthalmology, K301, School of Medicine, University of California, San Francisco, 10 Kirkham Street, San Francisco, California 94143, U. S. A. CASE REPORT A 34- year- old man was seen in consultation at the Department of Ophthalmology of the University of California, San Francisco, for acute onset of right- sided periocular pain and horizontal diplopia. He had no history of diabetes mellitus, hypertension, systemic vasculopathy, migraine, or recent viral illness. The general physical examination was normal. Ophthalmologic examination showed vision of 20/ 20 in each eye. The right pupil was 6 mm and unreactive to light. The left pupil was 4 mm and reactive to light. In primary gaze he showed 30 prism diopters of right exotropia and 10 prism diopters of right hypertropia. The right eye also showed poor adduction and infraduction. Extraocular motility in the left eye was normal ( Fig. 1). The remainder of the ophthalmologic, neurologic, and systemic examination was unremarkable. Magnetic resonance imaging ( MRI) of the central 21 22 E. T. CUNNINGHAM JR AND W. V. GOOD Case 1 2 3 4 5 6 7 8 9 10 11 TABLE 1. Reported cases Age/ sex - - - 30/ M 5/ F 8/ F -/ M - - - 34/ M Etiology Orbital trauma Orbital trauma Orbital trauma Undetermined Undetermined Undetermined Undetermined Orbital trauma Orbital trauma Occipital trauma Undetermined of isolated inferior branch oculomotor nerve paresis Associated findings - - - None None None None Trigeminal Trigeminal nerve damage nerve damage Optic nerve damage Upper extremity numbness/ dysesthesias Author/ year ( ref.) Cross/ 1948 ( 8) Cross/ 1948 ( 8) Cross/ 1948 ( 8) Susac and Hoyt/ 1977 ( 10) Susacand Hoyt/ 1977 ( 10) Susac and Hoyt/ 1977 ( 10); Miller/ 1977 ( 11) Miller/ 1985 ( 6) Saul et al./ 1986 ( 9) Saul et al./ 1986 ( 9) Saul et al./ 1986 ( 9) Present case report nervous system ( CNS), MRI- cerebral angiography, and intravenous contrast cerebral angiography revealed no localizing lesions. Urinalysis and serology, including tests of electrolytes, complete blood cell count, Westergren erythrocyte sedimentation rate, antinuclear antibody titer, and rapid plasma reagin test were normal. A lumbar puncture was performed under an opening pressure of 190 mmHg. The cerebral spinal fluid ( CSF) had no xanthochromic discoloration, no red blood cells, and 6 white blood cells per microliter, all of which were lymphocytes. The CSF glucose, total protein, quantitative venereal disease research laboratories test, and cryptococcal antigen titer were normal. Aerobic, anaerobic, and fungal cultures of CSF were negative. The patient was discharged and followed closely for 3 months, during which time he regained complete ocular realignment. More than 4 months after the onset of his oculomotor palsy, the patient experienced bilateral numbness and painful dysesthesias in the distribution of the median nerves. FIG. 1. Palsy of the inferior division of the oculomotor nerve. The inferior division of the oculomotor nerve provides innervation to the medial rectus ( adduction), inferior rectus ( depression), inferior oblique, and pupil, all of which are affected in this man's right eye. Note that he can elevate his right eye, and that there is no right ptosis, both functions subserved by the superior division of the oculomotor nerve. J Neuro- Ophthnlmol, Vol. 14, No. 1, 1994 OCULOMOTOR NERVE PALSY 23 Computed tomography ( CT) and MRI of the vertebral column and spinal cord were performed and revealed mild lumbar disc herniation but no evidence of cervical cord or root disease. DISCUSSION Isolated oculomotor branch palsies are uncommon. Superior branch palsies have been reported in patients with structural disorders of the subarachnoid space in the region of the oculomotor nerve ( 12), intrinsic midbrain disease ( 13), diabetes mellitus ( 14,15), migraine ( 16), and viral upper respiratory tract infections ( 11,17,18). Four cases of nontraumatic inferior branch oculomotor palsy have been described ( 6,10,11), each with undetermined etiology. A prodromal viral illness is often the presumed cause of idiopathic oculomotor nerve paresis ( 6,10,11,17- 24). Our patient subsequently developed bilateral numbness and painful dysesthesias in his upper extremities. Spinal CT scans and MRI failed to disclose localizing lesions. The occurrence of two temporally dissociated neurologic deficits is highly suggestive of a generalized neurologic illness, such as occurs with vasculitic or demyelinat-ing disease. Patients with inferior branch oculomotor nerve palsy have a good prognosis for spontaneous recovery, but they should be evaluated and followed closely for the possibility of a generalized systemic or neurologic disorder. REFERENCES 1. Rucker CW. Paralysis of the third, fourth and sixth cranial nerves. Am J Ophthalmol 1958; 46: 787- 94. 2. Rucker CW. The causes of paralysis of the third, fourth and sixth cranial nerves. Am J Ophthalmol 1966; 61: 1293- 8. 3. RushJA, Younge BR. Paralysis of cranial nerves III, IV, and VI: cause and prognosis in 1,000 cases. Arch Ophthalmol 1981; 99: 76- 9. 4. Richards BW, Joes FR, Younge BR. Causes and prognosis in 4,278 cases of paralysis of the oculomotor, trochlear, and abducens cranial nerves. 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Ocular paralysis following mumps. Br Med J 1937; 1: 752- 3. 21. Nelhaus G. Isolated oculomotor nerve palsy in infectious mononucleosis. Neurology 1966; 16: 221. 22. Scarf B, Hyama S. Oculomotor palsy following mumps. / Pediatr Ophthalmol 1972; 9: 245. 23. Hertenstein IR, Sarnat HB, O'Connor DM. Acute unilateral oculomotor palsy associated with ECHO 9 viral infection. / Pediatr 1976; 89: 79- 81. 24. Marzetti G, Midulla M, Balducci L. Monolateral paralysis of the third cranial nerve associated with A9 Coxsackie virus infection. Ann Neurol 1980; 7: 493. / Neuro- Ophthalmol, Vol. 14, No. 1, 1994 |
