Acta Neurochir (2009) 151:999–1000 DOI 10.1007/s00701-009-0337-y
BRIEF REPORT OF A SPECIAL CASE
Isolated contralateral post-ictal oculomotor nerve palsy following supratentorial craniotomy. Case report Manish Singh Sharma & Karanjit Singh Narang & Bhawani Shankar Sharma
Received: 27 November 2008 / Accepted: 31 January 2009 / Published online: 16 May 2009 # Springer-Verlag 2009
Abstract The authors report the unique occurrence of an isolated post-ictal contralateral oculomotor nerve (OCN) palsy following excision of a medial frontal oligoastrocytoma. A 45-year-old male presented with a history of generalized tonic clonic seizures (GTCS) for 8 years. His neurological examination was unremarkable. Magnetic resonance imaging (MRI) of the brain revealed a left frontopolar low grade glioma. Nine hours after an uneventful near total microsurgical excision, the patient had a GTCS, following which he was noted to have an isolated right-sided OCN palsy. The immediate post-ictal computed tomographic scan and magnetic resonance images acquired 2 weeks after surgery failed to reveal any abnormality. The palsy had recovered completely by the 9-month follow-up. Keywords Astrocytoma . Craniotomy . Oculomotor nerve . Palsy . Post-ictal . Supratentorial neoplasm
Introduction Seizures may occur in up to 19% of patients undergoing a supratentorial craniotomy and cause varied neurological deficits [1]. The authors report the unique occurrence of an isolated post-ictal contralateral oculomotor nerve (OCN) palsy following excision of a left medial frontal oligoastrocytoma.
M. Singh Sharma (*) : K. Singh Narang : B. Shankar Sharma Department of Neurosurgery, Neurosciences Centre, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, 110029, India e-mail:
[email protected]
Case report A 45-year old male presented with a history of generalized tonic clonic seizures (GTCS) for the past 8 years. He had no neurological deficits or co-morbid conditions, and was seizure free with oral diphenylhydantoin (DPH). Magnetic resonance imaging (MRI) of the brain revealed a left frontopolar low-grade glioma. Histopathological examination after an uneventful near total excision revealed an oligoastrocytoma. The patient was extubated prior to transfer to the intensive care unit, where he was noted to be alert, oriented and free of any neurological deficits. Nine hours after surgery, he had a GTCS lasting about 2 min, which was controlled with 4 mg of midazolam and a 15 mg/kg loading dose of DPH. Immediately after the seizure, a complete right-sided OCN palsy was detected (Fig. 1a). An urgent computed tomographic (CT) scan revealed a good operative cavity, no intracerebral hematomas and open ambient cisterns. After regaining consciousness, he was noted to have normal fourth and sixth cranial nerve function, no motor weakness, symmetrical reflexes and downgoing plantars. A 2-week follow-up MRI and MR angiogram revealed normal OCNs with no evidence of a midbrain infarct or a posterior communicating arterial aneurysm (Fig. 1b). The right OCN palsy resolved completely after 9 months.
Discussion Postoperative seizures may produce a spectrum of deficits ranging from drowsiness to transtentorial herniation and death, yet a review of literature has failed to reveal a similar case.
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Fig. 1 a Clinical photograph of the patient revealing right-sided ptosis. The right eye is abducted and depressed, suggesting a complete OCN palsy. b T2weighted MR axial images acquired 2 weeks after the ictus revealing normal oculomotor nerves and cerebral peduncles
Though OCN palsy may occur after transtentorial herniation with ipsilateral hemiparesis because of the Kernohan’s notch, this cannot be a possible explanation in this case as the palsy was contralateral, and no motor weakness developed [3]. DPH toxicity can also produce ophthalmoplegia, but this is external, bilateral and temporary; our patient had an isolated OCN palsy that took 9 months to resolve [5]. In the presence of a dilated pupil, we favored a compressive hypothesis [2]. Perhaps a powerful surge in ictal intracranial pressure may have produced transient central transtentorial herniation with a contusing effect on the contralateral OCN alone as the ipsilateral operative cavity provided a buffer for expansion. A normal CT supported this hypothesis. MRI may have failed to detect OCN contusion because of the time lapse of 2 weeks. A vascular insult seems unlikely, though atherosclerosed mesencephalic arteries have been implicated as a cause of isolated OCN palsy following midbrain infarction, as our patient had no comorbid conditions, normal postoperative MR images and a dilated pupil, which classically has been associated with a compressive rather than an ischemic injury [4]. Though the etiology may have been multifactorial, it has to be recognized that postoperative seizures can produce de novo neurological deficits despite adequate preoperative seizure control, uneventful surgery and normal postoperative imaging.
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Comment This is an interesting report of a contralateral third nerve palsy coming on in the postoperative period following left frontal intrinsic tumor resection. The various possibilities for this development have been considered by the authors, who ultimately decided that the cause was likely to be trans-tentorial herniation. If this is so, it is unusual that it has not been reported before. Why do we not see it more frequently in individuals in status epilepticus? Is the location of the tumor relevant in some way, with the potential for rapid spread of any seizure to the temporal lobes? The patient was described as being normotensive, and random blood sugar was within normal limits. Other risk factors for vascular disease, including smoking and hypercholesterolemia, would be relevant in a vascular etiology. Although uncommon, complete palsy can occur from an ischemic etiology. Brian Brophy Royal Adelaide Hospital, Australia
