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  • Title: [Bilateral traumatic abducens nerve palsy without skull fracture or intracranial hematoma-a report of 3 cases and consideration of the mechanism of injury (author's transl)].
    Author: Takagi H, Miyasaka Y, Kuramae T, Ohwada T, Tsunoda M.
    Journal: No Shinkei Geka; 1976 Oct; 4(10):963-9. PubMed ID: 1033472.
    Abstract:
    Three cases of bilateral traumatic abducens nerve palsy were presented and the mechanism of damage to the abducens nerve was discussed in relation to the analysis of traumatic force at the time of impact and topographical anatomy of the abducens nerve in detail. Case 1. A 70 year old man sustained a traffic accident with one hour loss of consciousness. Physical examination revealed a contused area on the medial side of his right forehead. Neurological examination revealed bilateral abducens nerve palsy (Fig. 1). There were no ther cranial nerve abnormalities. Roentgenograms of the skull, including views of the base and orbit showed no fracture. At follow up examination 12 months later, bilateral Duane's retraction syndrome could be noticed with slight increase in size of the pupil on each side of lateral gaze (Fig. 2). Case 2. A 32 year old women sustained a traffic accident with 31 days of loss of consciousness. At the time of admission, bilateral abducens nerve palsy and slight left hemiparesis were noticed in semicomatose condition. Right carotid angiogtam showed no evidence of intracranial hematoma. One month later, the right eye began to abduct and 2 months later, the left eye began to abduct. Three months after the injury, bilateral abducens nerve palsy could no longer be demonstrated. No retraction syndrome was observed during this period. Case 3. A 3 year old boy sustained a traffic accident with 32 days of loss of consciousness. At the time of admission, neurological examination showed bilateral abducens palsy and left sided decerebrate posture in comatose condition. At the time of discharge 3 months after admission, bilateral abducens palsy, right hemiataxia, left spastic hemiparesis and scanning speach were noticed. Three months later, right eye began to abduct and 4 months later, the left eye began to abduct. At follow up examination 6 months later, there was no evidence of abducens nerve palsy. Topographical details of anatomy of the abducens nerve are shown in Fig. 3, 4. It is greatly speculated that both abducens nerves are streched by the lineal accerelated force on mid sagittal plane at the time of impact, then the apex of petrous pyramid acts as the fulculum, so that the abducens nerves are compressed, contused and streched at this point (Fig. 5-a). The authors pointed out that the abducens nerve are impossible to be damaged at the petroclinoid ligament (Grüber's lig.) by the upward movement of the brainstem, because the abducens nerve is fixed downward below this ligament by the dura and apex of the petrous pyramid (Fig. 4-b, c). One case showed bilateral acquired retraction syndrome with slight increase in size of the pupil on each side of lateral gaze, the fact greatly suggesting that the sympathetic nerve have intimate relationship to the miss direction during the recovery stage of abducens nerve palsy.
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