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Show Journal of ClilliC111 Neuro-(' l'hthnlmology 9( 2J: 112- 115, 1989. © 1989 Raven Press, Ltd., New York Bilateral Internuclear Ophthalmoplegia Due to Acute Cervical Hyperextension Without Head Trauma Juan L. Jammes, M. D. A 58- year- old woman developed bilateral internuclear ophthalmoplegia, probable right oculosympathetic paresis ( Homer's syndrome), and right facial dysesthesias with acute cervical hyperextension upon sustaining a rear- end automobile collision. There was no head trauma. A nuclear magnetic resonance scan revealed a discrete area of increased signal in the tegmentum of the pons to the left. Extensive recovery was noted 1 year later. The acute cervical hyperextension suggested acute shearing and stretching ofaxons from brain stem deceleration rather than transient vertebral artery ischemia. Internuclear ophthalmoplegia representing intracranial pathology without direct head trauma has not previously been described with acute cervical hyperextension injury. Key Words: Internuclear ophthalmoplegia- Homer's syndrome- Cervical injury- Axonal injury- Brainstem- Pons. From the Alexandria Hospital, Alexandria, Virginia, and Yakovlev Collection, Armed Forces Institute of Pathology, Washington, D. C., USA. Address correspnndencc and reprint requests to Dr. J. L. iMnm.:'. " t 19~ 1 ",(' minac-' rl,,,], I. SUile 117, Alexandria, VA 112 Gay and Abbot ( 1) described " whiplash injury" as an acute cervical hyperextension usually resulting from a rear- end automobile collision. Ocular manifestations following acute cervical hyperextension injury include amaurotic episodes, decreased accommodation and convergence, decreased prism vergence power, anisocoria, diplopia, blurred vision, photophobia, hyperphoria, hypertropia, exotropia, ptosis, tearing and inability to focus ( 2,3), and vitreous detachment including vitreomacular separation ( 4). Internuclear ophthalmoplegia is characterized by paralysis of the ipsilateral medial rectus muscle on conjugate gaze to the opposite side with nystagmus of the abducting eye, although the medial rectus muscle usually functions in convergence. Internuclear ophthalmoplegia is due to involvement of the medial longitudinal fasciculus between the nuclei of the sixth and third cranial nerves. Bilateral internuclear ophthalmoplegia is often a manifestation of multiple sclerosis. It also occurs after brain stern infarction. Unilateral internuclear ophthalmoplegia may be seen with head injuries and vascular or infectious diseases. Bilateral internuclear ophthalmoplegia has not been reported with acute cervical hyperextension injuries without any direct trauma to the head, but such a case is described here. My patient did not sustain head trauma or direct injury to the neck, but still demonstrated brainstem dysfunction. CASE SUMMARY A 58- year- old white woman, a college professor, was originally examined on May 1, 1986, presenting with tingling in the right side of the face and right anterior head, and horizontal diplopia on lateral gaze to either side. Symptoms began after a rear- end collision automobile accident on April 17, BILATERAL INTERNUCLEAR OPHTHALMOPLEGIA 113 1986. At the time of impact, she was thrown forward, hitting the steering wheel with her chest, and then was thrown backward, remaining fully awake afterward. There was no trauma to the head or direct injury to her neck. The collision was severe enough to demolish her car. She was wearing seatbelts: a lap belt and a shoulder harness. A physician at the scene happened to witness the accident, reporting no head trauma or loss of consciousness. She was admitted to National Orthopedic Hospital where she was found to have a fracture of the posterior arch of the sixth cervical vertebra, although not exclusively the spinous process, and this was treated with immobilization, initially with a Philadelphia collar and later with a Denison brace. Two days later, her physician found a difference in palpebral fissures but no asymmetry of her face. She also complained of soreness in both knees, right rib pains accentuated by respiratory movements, midsternal pains apparently where her seatbelt was, posterior midline cervical pains, accentuated by defecation, and occasional headaches. For the previous 10 years, the patient had suffered from depression and since December 1985 took desipramine as per her psychiatrist. Since 1972, she had been on estrogen and progesterone. The positive neurological findings on examination included slight anisocoria, with the left pupil slightly larger than the right one, measuring under ordinary illumination 2 mm on the right and 2.8 mm on the left, and both reacted well to direct and consensual light illumination and convergence. The left palpebral fissure was larger than the right one. There was abducting nystagmus with conjugate gaze either to the right or left. The amplitude of the nystagmus was symmetrical and was accompanied by horizontal diplopia. There was also slight vertical nystagmus on upward gaze. There was a mild exotropia on forward primary gaze. There was a mild limitation of either adducting eye. The corneal reflex was depressed on the right. There was hypalgesia on the right side of her face. There was a minimal flatness of the right rhinolabial fold. The rest of her neurological examination was normal except for symmetrically depressed to absent deep tendon reflexes in both lower extremities. The range of motion of the cervical spine was markedly limited due to painful muscle spasms. A computed axial tomography ( CAT) scan of the brain with contrast, an electromyogram, nerve conduction velocities, an electroencephalogram, and visual and brainstem auditory evoked potentials were normal. Magnetic resonance imaging ( MRI) done May 25, 1986 revealed a small discrete area of abnormal increased signal in the tegmentum of the pons on the left side ( Figs. 1 and 2). No associated mass effect was seen, and no other abnormalities noted. Abnormal blink reflex responses and trigeminal evoked potentials were obtained, and this demonstrated a prolonged blink ( Rl) reflex response for the trigeminal nerve, being 27 ms on the right and 18 ms on the left ( normal Rl reflex latencies up to 13 ms). Cerebrospinal fluid ( CSF) examination was normal, including protein electrophoresis. Cerebral and aortic arch digital subtraction angiography were normal except for minimal atherosclerotic changes at the carotid bifurcations without evidence of high- grade stenosis or ulcerated plaques. Desipramine blood levels on June 17, 1986 were 177 ng with a therapeutic range between 100 and 300 ng. Other chemistries were normal, including glucose studies. Her course was one of gradual improvement, and 1 year after her accident she only complained of very slight left posterior cervical pains upon rotation of her neck to the right. There was still minimal pupillary asymmetry, with the left pupil larger than the right one, and horizontal nystagmus on lateral gaze to either side. She still had absent deep tendon reflexes of both lower extrem- FIG. 1. MRI scan revealing small discrete area of increased signal intensity in the tElgmentum on the left side of the pons near the origin of the brachium pontis. The MRI used was a Picker Vista 0.5- T with a TR of 2,200 ms and a TE of 80 ms. I Gin Neuro- ophlhalmol, Vol. 9, No. 2, 1989 114 f. L. JAMMES FIG. 2. MAl ( as in Fig. 1) revealing a closer view of the pons, as described. ities. The rest of her examination was neurologically normal. DISCUSSION Bilateral internuclear ophthalmoplegia, right oculosympathetic paresis ( Horner's syndrome), and sensory trigeminal involvement occurred in this patient following sudden cervical extension from a read- end automobile collision, and correlated with a small area of increased signal in the pons, as shown by MRI. Although a coincidental bilateral internuclear ophthalmoplegia due to demyelination is possible, there was no history of previous neurological or demyelinative symptomatology. Also, CSF examination, evoked potentials, and MRI did not demonstrate any abnormality indicative of multiple sclerosis. The differential diagnosis of the left- sided pontine lesion as shown by MRI also includes a traumatic contusion, an infarct, and, less likely, edema from a very small intraaxial neoplasm. However, the patient did not sustain direct head trauma. An intraaxial neoplasma is excluded by the clinical presentation and improvement, and by repeatedly normal neurological tests, including evoked potentials. All other studies, as well as the MRI, did not reveal lesions elsewhere consistent with multiple sclerosis. The MRI shows the medial longitudinal fasciculus slightly dorsal to the lesion. The area of hypersensitivity surrounding the aqueduct of C " h IV;, · ' l( A - ' rr~ l,, 1 finding in MRI. It is accentuated by the low- intensity signal within the aqueduct, which represents CSF flow secondary to the arterial pulse wave. This pattern is commonly identified and is felt to be normal. Although her MRI showed a discrete abnormality limited to the tegmentum of the pons on the left, clinically the bilaterality of her internuclear ophthalmoplegia, her probable right oculosympathetic paresis ( Horner's syndrome), as well as the right sensory trigeminal involvement suggested more extensive brain stem involvement. The prolonged blink reflex latencies on both sides also implied more bilateral or diffuse abnormalities. Desipramine, which the patient was taking for treatment of depression, has not been reported to cause internuclear ophthalmoplegia or ophthalmoparesis and would have not been expected to produce abnormalities in her MRI. In considering an ischemic mechanism, compression of the vertebral arteries at the time of acute cervical hyperextension may limit blood supply to the brainstem ( 5). This could be a possible cause of the patient's transient bilateral internuclear ophthalmoplegia. The vertebral arteries may be temporarily occluded or injured during acute cervical hyperextension at the CI- C2 level where they are relatively fixed in the transverse foramen ( 6), but at the same time the CI- C2 joints being the most mobile levels of the cervical spine. Vertebral artery injuries leading to dissecting aneurysms and artery occlusion have taken place at this level ( 7). Transient brain stem ischemia, actual vascular occlusion, or dissection with distal embolization BILATERAL INTERNUCLEAR OPHTHALMOPLEGIA 115 have been described as complications from chiropractic neck manipulations consisting of cervical rotation, tilting, and extension ( 5,8). Internuclear ophthalmoplegia following chiropractic cervical manipulations has also been reported ( 9). Even in asymptomatic volunteers ( 10) and in patients with vascular disease ( 7), angiography during cervical rotation or extension may result in symptomatic vertebral artery compression at the C1 level ( 11). Following manipulations, patients may experience immediate ischemia, or delayed ( by minutes to several days) ( 6) or progressive infarction manifesting most commonly as infarction of the pons as in this case. An ill- defined period of several hours to 2 days is reported in our case for the onset of awareness of horizontal diplopia to either side. Sudden cervical extension as caused by the automobile rear- end collision in our patient is very similar to the acute cervical extension motions produced during manipulations. Usually, internuclear ophthalmoplegia from vascular disease is unilateral and not bilateral as described here clinically, although both may occur ( 12). Acute cervical hyperextension from rear- end automobile collisions, as in this case, occurs too briefly to result in vertebral ischemia of clinical significance. Diffuse axonal injury is a distinct form of head injury occurring at the time of impact, characterized by diffuse shearing to axons, particularly in the corpus callosum and posterolateral rostral brain stem ( 13- 15). All cases reported have followed direct head trauma. In this case, it is conceivable that stretching and shearing ofaxons in the brainstem occurred at the time of sudden cervical hyperextension. In cats, even minor head injuries have been demonstrated to be associated with axonal changes and this appears to be a consistent feature of minor head injury ( 16). Some few hours delay in noting asymmetry of palpebral fissures and facial dysesthesias in our case could be explained by a temporal evolution demonstrated in traumatically induced axonal changes ( 17). Axonallesions take place, however, at the moment of injury rather than as a secondary change caused by cerebral edema or by ischemia ( 13,16). In summary, this patient developed bilateral internuclear ophthalmoplegia, probably a right oculosympathetic paresis ( Horner's syndrome) and sensory trigeminal involvement following an acute cervical hyperextension without direct cervical or head trauma; conceivably, this may be due to stretching and shearing ofaxons in the brain stem. REFERENCES 1. Gay JR, Abbott KH. Common whiplash injuries in the neck. JAMA 1953; 152: 1698- 1704. 2. Roca PD. Ocular manifestations of whiplash injuries. Ann Ophthalmol 1972; 4: 6:>- 73. 3. Fite JD. Neuro- ophthalmologic syndromes in automobile accidents. South Med J 1970; 63: 567- 70. 4. Daily L. Macular and vitreal disturbances produced by traumatic vitreous rebound. South Med J 1970; 63: 1197-- 8. 5. Sheehan S, Bauer RB, Meyer JS. Vertebral artery compression in cervical spondylosis. Neurology 1960; 10: 968- 86. 6. Robertson JT. Neck manipulation as a cause of stroke. Stroke 1981; 12: 1. 7. Danesham TK, Langston Hewer R, Bradshaw JR. 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