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Case Report: Oculomotor nerve palsy secondary to aberrant posterior cerebral artery

A sphenoid mucocele often presents late due to its deep seated anatomical site. BACKGROUND: Isolated nuclear oculomotor nerve palsy usually consists of complete ipsilateral third nerve palsy in addition to contralateral ptosis and superior rectus dysfunction, furthermore if the nuclear lesion is rostral, it may present with pupillary involvement and muscles may be spared. The patient went on to experience spontaneous complete resolution of symptoms with associated radiological shrinkage of the mass. Palsy refers to a complete weakness of a muscle while a paresis is a partial weakness. Surgical 3rd nerve: Painful with a dilated pupil and ptosis. This condition occurs when the facial nerve (seventh cranial nerve) is affected. In the patient with acute traumatic brain injury, this finding is highly indicative of brainstem compression.

A dorsal lesion with a slightly different configuration can produce the same type of ataxia plus a third nerve nuclear lesion and features of supranuclear eye movement dysfunction (Nothnagel syndrome). (7) A leading cause of nontraumatic third nerve paralysis is diabetes. He pointed out that an isolated third nerve palsy could be the first manifestation of diabetes and that almost all the cases improve completely. Any of the abducens nerve (cranial nerve 6), trochlear nerve (cranial nerve 4) or oculomotor (cranial nerve 3) may be responsible for double vision and poor eye movement. A complete blood count (CBC) and erythrocyte sedimentation rate (ESR) were normal and his blood sugar was adequately controlled. Remaining 14 MRI were normal. Glycosylated hemoglobin was 6.6%.

Pupillary involvement may be the only sign of CN III palsy. She denied any history of preceding trauma or any neurological symptoms in her upper or lower limb. Scanning of the brain was normal. On examination, the right eyelid was partially ptotic. Non-arteritic anterior ischaemic neuropathy is the most common subtype. Ophthalmoplegia in dural CCF may be caused by swelling of extraocular muscles due to venous congestion, ischemia of cranial nerves by vascular steal phenomenon, enlarged sinus causing compression, or a combination of one or more of the above mechanisms.[5] In our case, since DSA proved it to be posterior draining fistula which has minimal or no venous congestion, we believe that she suffered more ischemia than compression of third nerve, which might probably explain pupil sparing. Accommodation was impaired with delayed convergence of the right pupil.


We inserted the drains bilaterally into the cavity of the hematoma. Visual acuity, visual fields and funduscopy were normal. The remainder of the cranial nerve and neurological examination was normal. The costs of the various imaging technologies differ considerably. Some cranial nerve palsies resolve spontaneously, especially if they are due to microvascular causes such as DM and hypertension. His right eye presented total deficit of horizontal and vertical movements (with residual abduction). On thin-section (1 mm) T2-weighted imaging, the right oculomotor nerve was distorted as it coursed inferior to the P1 segment of the right PCA ().

MR angiography of the Circle of Willis (A) and lateral oblique view of the vertebrobasilar arterial system (B) demonstrating normal course of the left posterior cerebral artery. The nerve then enters and travels along the lateral wall of the cavernous sinus with cranial nerves IV, V, and VI as well as the carotid artery where the nerve divides into a superior and inferior branch. Cranial nerve palsies and central retinal artery occlusion, however, were common. Involvement of these structures can contribute to diplopia. Intraoperative photographs, preclipping view (left) showing that the infundibular dilatation (asterisk) had displaced the medially located oculomotor nerve (arrow), and post-clipping view (right). After a systematic review of the published literature, eight cases.2–8 of isolated ONP secondary to posterior intracranial circulation anatomical variants have been published. In 1973, Hopkins et al5 described an 81-year-old woman with ONP secondary to a tortuous fetal-type PCA.

Since then, three78 additional cases of ONP secondary to tortuous fetal-type PCA have been described. All four cases were conservatively managed and had spontaneous resolution of symptoms. A tortuous fetal-type PCA, due to its intimate relationship with the cisternal oculomotor nerve, can distort the traversing oculomotor nerve, especially when the PCA is directed in a ventrolateral direction. As the oculomotor nerve exits the midbrain and enters the interpeduncular cistern, it passes and comes into direct contact with the PCA superiorly and SCA inferiorly. The headache was also improved. In 2007, Suzuki et al6 reported the case of a 78-year-old whose oculomotor nerve was intraoperatively found to be compressed at the point between the arteriosclerotic PCA and SCA. Microvascular decompression was performed resulting in complete symptom resolution.

The classical description of a ‘pupil-sparing’ versus ‘pupil-involved’ ONP serves to aid the clinician in diagnosing a medical (eg, diabetes mellitus) versus surgical (eg, PCommA aneurysm) cause of ONP, respectively. This line of thought is fraught with potential for misdiagnosis. Many types of neuropathies will get better with time, without any treatment. However, Hashimoto et al3 reported a case of pupil-sparing ONP in a 74-year-old woman with superolateral displacement of the oculomotor nerve secondary to a tortuous basilar artery. The authors postulate that compression of the inferomedial segment of the cisternal oculomotor nerve resulted in ophthalmoplegia but not pupillary dysfunction due to sparing of the dorsomedial parasympathetic pupilloconstrictor fibres. With advances in MRI, the complete cisternal course of the oculomotor nerve can be visualised. As shown in the present case, MRI can allow visualisation of a distorted oculomotor nerve secondary to vascular compression.

Albrayam et al2 reported a 24-year-old woman with MRI evidence of a duplicated SCA and prominent PCA compressing the oculomotor nerve. For example, during the time period in which these three patients were seen, we examined 112 and 91 cases of vasculopathic 6th and 3rd nerve palsy, respectively in which stress was not an apparent factor. In conclusion, anatomical variations in the posterior intracranial circulation are rare causes of isolated ONP. MRI and MRA are sensitive modalities that should be utilised in the diagnosis of vascular compression causing ONP. Contributors: TT performed the literature search, wrote the article, identified the case and is the guarantor of the article. JWT came up with the idea of the article, wrote the article, identified the case and managed the case. YYW identified the case, wrote the article and managed the case.

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