Incomplete Oculomotor Nerve Palsy Research Articles

Guillain-Barré Syndrome with Incomplete Oculomotor Nerve Palsy after Traumatic Brain Injury: Case Report and Literature Review

Guillain-Barré syndrome (GBS) is a severe peripheral neuroinflammatory demyelinating disease characterized by symmetrical progressive limb weakness, which can be accompanied by cranial nerve and sensory disturbances. There is usually a history of bacterial or viral infection prior to onset. GBS is rarely seen after traumatic brain injury (TBI). We report a case of a 66-year-old male patient who presented with dilated pupils, followed by respiratory failure and symmetrical quadriplegia during a conservative treatment for TBI. He was eventually diagnosed with GBS and was treated with intravenous immunoglobulin, followed by rehabilitation therapy with a good recovery. We summarize previous similar cases and analyze possible causes. It is suggested that the possibility of GBS should be considered when unexplained symptoms occurred in patients with TBI, such as respiratory failure, dilated pupils, and limb weakness.

Internal carotid artery aneurysm with incomplete isolated oculomotor nerve palsy: a case report

BackgroundOculomotor nerve palsy is a common and well-described disease with diverse etiologies. Clinicians should quickly and correctly diagnose and treat oculomotor nerve palsy according to its characteristics and the accompanying symptoms and signs. Intracranial aneurysm is an important and frequent cause of oculomotor nerve palsy. Considering the catastrophic consequences of rupture, the possibility of an urgent, life-threatening disease should always be considered.Case presentationA 63-year-old Chinese woman presented with intermittent left ptosis and diplopia and painless incomplete oculomotor nerve palsy without pupil involvement. She manifested no mydriasis or extraocular muscle weakness, and the light reflex was normal. Other cranial nerves and somatosensory and somatomotor examinations were normal. The neostigmine experiment and electromyography were normal, so the diagnosis of myasthenia gravis was excluded. Brain magnetic resonance angiography showed a 4-mm aneurysm located at the cavernous segment of the left internal carotid artery. Unfortunately, the patient refused digital subtraction angiography and was discharged home without further treatment.ConclusionNeuroimaging must be performed to exclude intracranial aneurysms in oculomotor nerve palsy regardless of whether the pupils are involved, as aneurysm rupture carries substantial morbidity and mortality.

Incomplete Oculomotor Nerve Palsy Caused by Internal Carotid Artery Giant Aneurysm with Fibromuscular Dysplasia

Incomplete Oculomotor Nerve Palsy Caused by Internal Carotid Artery Giant Aneurysm with Fibromuscular Dysplasia

Case of white‐eyed shunt carotid‐cavernous sinus fistula mimicking optic neuritis

AbstractBackgroundThe typical orbito‐ocular manifestations of carotid‐cavernous sinus fistulas are conjunctival hyperemia, chemosis and exophthalmos as a result of increased fistular flow directed anteriorly in the ophthalmic veins. These congestive features are absent if the flow is directed posteriorly, resulting in “white‐eyed shunts.” We describe a rare carotid‐cavernous sinus fistula case presenting with optic neuritis‐like manifestations.Case presentationA 71‐year‐old Japanese woman developed periorbital pain, impaired visual acuity with an upper horizontal visual field defect, diminished light reflexes and a relative afferent pupillary defect in her right eye. There were no congestive features in her eyes. Intraocular pressure was normal in both eyes, but fundoscopy revealed a pale optic disc in the right eye. Serum anti‐aquaporin‐4 antibodies were negative. Although optic neuritis was suspected, high‐dose corticosteroid administration did not result in improvement. When referred to Department of Neurology, Gunma University Hospital, she showed a subtle, incomplete oculomotor nerve palsy in the right eye. Magnetic resonance angiography suggested carotid‐cavernous sinus fistula (CCF), and cerebral angiography showed fistulous drainage into the cavernous sinus and inferior petrosal sinus, and a delayed opacification of the superior orbital and angular facial veins on the right side. A diagnosis of white‐eyed shunt CCF was made, and a coil embolization procedure was carried out. However, there was no symptom improvement.ConclusionsIt is difficult to diagnose white‐eyed shunt CCF based only on physical findings, especially when there is an absence of ocular congestive features. We discuss the possible mechanisms underlying the optic neuritis‐like symptoms of CCF.

Recovery of oculomotor nerve palsy after endovascular treatment of ruptured posterior communicating artery aneurysm.

Oculomotor nerve palsy (ONP) may result from Posterior communicating artery (Pcom) aneurysms. Endovascular treatment of ruptured Pcom aneurysms generally is a safe procedure, but the effect of this therapy on ONP is incompletely elucidated. This retrospective study evaluates outcomes of ONP after endovascular treatment for ruptured Pcom aneurysm and with the intention to clarify predictors of recovery. From May 2010 to October 2015, 210 patients with Pcom aneurysms underwent endovascular treatment at our institution. Among them, 34 patients with ruptured aneurysms and either complete or incomplete ONP were identified. The outcomes and predictors of ONP recovery were analyzed. At the last available clinical follow-up, ONP resolution was complete in 21 (61.8%) patients and incomplete in 8 (23.5%) patients. The mean resolution time after embolization was 24.5days. Five patients showed no signs of ONP recovery. In no case was an initial incomplete ONP observed to worsen. There was a statistically insignificant trend toward complete recovery among patients with initial incomplete ONP (OR=4.17; 95% CI, 0.75-23.18; P=0.103). Endovascular treatment appears to be an effective treatment modality for ruptured Pcom aneurysm and related ONP. The initial incomplete ONP might encourage complete ONP recovery after endovascular treatment.

Effects of Endovascular Treatment on Cranial Nerve Palsy due to Unruptured Intracranial Aneurysms

This study aimed to assess the effects of endovascular treatment on cranial nerve palsy due to unruptured intracranial aneurysms. Endovascular coiling was performed in 203 patients with intracranial aneurysms between April 2002 and March 2012 in our hospital. Of these patients, 8(3.9%)presented with cranial nerve palsy due to unruptured intracranial aneurysms. Cranial nerve palsy involved the oculomotor nerve in 8 patients and the optic nerve in 2 patients. Two patients had both optic nerve and oculomotor nerve dysfunction. Patients with incomplete oculomotor nerve palsy at admission were more likely to have full recovery after coiling. Optic nerve dysfunction did not improve after coiling. Incomplete oculomotor nerve palsy, early treatment(≤15 days), and small aneurysms(≤10 mm)were likely to be associated with complete recovery after coiling. This study indicates that endovascular coiling may resolve cranial nerve palsy due to unruptured intracranial aneurysms in patients who have incomplete oculomotor nerve palsy due to small aneurysms and are treated as early as possible after symptom onset.

Recovery of oculomotor nerve palsy secondary to posterior communicating artery aneurysms

Background. Recent studies suggest more favourable recovery of oculomotor nerve palsy (ONP) caused by posterior communicating artery (PComA) aneurysms with microsurgical clipping compared to endovascular coiling. We describe a consecutive series of patients with ONP from PComA aneurysms treated by microsurgical clipping or endovascular coiling. Methods. We retrospectively reviewed medical records of all patients from 2005 to 2009 with complete or partial ONP from PComA aneurysms. Results. Twenty patients were identified, three with unruptured aneurysms. Two patients with ruptured aneurysms were unfit for treatment and therefore excluded. Of the 18 patients included (15 female), 9 underwent microsurgical clipping and 9 received endovascular coiling. Patients treated by surgical clipping were significantly younger compared to those treated by endovascular coiling (mean 52.3 vs. 67.9 years; p = 0.039). Five patients had incomplete ONP (3 clipped, 2 coiled) and thirteen had complete ONP. At 6 months, six of nine patients treated with clipping and five of nine patients treated with coiling had complete resolution of their ONP (p = 1.0); the remainder had partial improvement. There was no significant difference in duration of pre-treatment ONP, age, sex or status of aneurysm (ruptured or unruptured) between patients in the two groups or between those with full or partial recovery. However, all 5 patients with incomplete ONP at presentation recovered fully, compared with 6 of 13 patients who presented with complete ONP. Conclusions. We found no significant difference between clipping and coiling in the recovery of ONP due to PComA aneurysms. Patient who present with incomplete ONP are more likely to have a full recovery of ONP following either treatment modality than those who present with complete ONP.

Oculomotor nerve palsy by posterior communicating artery aneurysms: influence of surgical strategy on recovery

Resolution of oculomotor nerve palsy (ONP) after clipping of posterior communicating artery (PCoA) aneurysms has been well documented. However, whether additional decompression of the oculomotor nerve via aneurysm sac dissection or resection is superior to pure aneurysm clipping is the subject of much debate. Therefore, the objective in the present investigation was to analyze the influence of surgical strategy--specifically, clipping with or without aneurysm dissection--on ONP resolution. Between June 1999 and December 2010, 18 consecutive patients with ruptured and unruptured PCoA aneurysms causing ONP were treated at the authors' institution. Oculomotor nerve palsy was evaluated on admission and at follow-up. The electronic database MEDLINE was searched for additional data in published studies of PCoA aneurysms causing ONP. Two reviewers independently extracted data. Overall, 8 studies from the literature review and 6 patients in the current series (121 PCoA aneurysms) met the study inclusion criteria. Ninety-four aneurysms were treated with simple aneurysm neck clipping and 27 with clipping plus aneurysm sac decompression. The surgical strategy, simple aneurysm neck clipping versus clipping plus oculomotor nerve decompression, had no effect on full ONP resolution on univariate (p = 0.5) and multivariate analyses. On multivariate analysis, patients with incomplete ONP at admission were more likely to have full resolution of the palsy than were those with complete ONP at admission (p = 0.03, OR = 4.2, 95% CI 1.1-16). Data in the present study indicated that ONP caused by PCoA aneurysms improves after clipping without and with oculomotor nerve decompression. The resolution of ONP is inversely associated with the initial severity of ONP.

Persistent trigeminal artery presenting as intermittent isolated sixth nerve palsy

Persistent primitive carotid-basilar anastomoses are embryological vascular remnants and are uncommon.1 The most frequent embryonic communication between the carotid and vertebrobasilar systems is a persistent trigeminal artery (PTA). This has been observed in 0.1–0.2% of cerebral angiograms, usually as an incidental finding.2 Although the presence of PTAs is generally thought to be of uncertain significance, these arteries and their variants have been identified as a rare cause of cranial nerve dysfunction, including incomplete oculomotor nerve palsy, trigeminal neuralgia and hemifacial spasm,3,4 and there has been a reported case of a PTA variant with an aneurysm causing isolated sixth nerve palsy.

Incomplete Oculomotor Nerve Palsy Caused by an Unruptured Internal Carotid-Anterior Choroidal Artery Aneurysm-Case Report-

A 59-year-old woman visited our institute with the chief complaint of dizziness which persisted whenever she tried to focus on objects. She had not experienced apparent double vision and had no history of intracranial bleeding. Neurological examination revealed no abnormality except for exotropia at the mid-position and at upper gaze. Cerebral angiography revealed that the intracranial portion of the left internal carotid artery ran more horizontally and also identified an unruptured left internal carotid-anterior choroidal artery (IC-AChA) aneurysm of 3.0 mm diameter. The aneurysm at the origin of the AChA was confirmed during surgery. The proximal lateral wall of the aneurysm was in contact with the oculomotor nerve. This contact was released after complete obliteration of the aneurysm. The exotropia resolved 3 months later. Oculomotor nerve palsy usually indicates the presence of internal carotid-posterior communicating artery (IC-PcomA) aneurysm. Since sacrifice of the AChA will result in severe neurological deficits, accurate neuroimaging information is needed prior to the operation. Conventional angiography and/or three-dimensional computed tomography angiography should be performed to ascertain whether the aneurysm is an IC-PcomA or IC-AChA aneurysm, even if some neurosurgeons insist that conventional angiography is not always needed before surgery for an unruptured aneurysm.

Does the pupillary sparing oculomotor nerve palsy really spare the pupil?

We examined the pupillary cycle time (PCT) in eight elderly patients with isolated oculomotor nerve palsy (ONP) that was characterized by complete involvement of the extraocular muscles. In addition to advanced age, all patients had at least one other vasculopathic risk factor. Although in all cases the pupil was completely spared by clinical impression, the PCT was significantly prolonged compared with the other eye and well outside the normal range (mean 1590 +/- 212 msec on the involved side and 1076 +/- 110 on the uninvolved side). On re-examination, after an interval of 2-3 months, the PCT was either normal or markedly improved in all patients, paralleling the recovery of extraocular muscle function. These findings suggest that even in pure, noncompressive ONPs there is subclinical pupillary involvement. Repeated PCT examinations may provide an objective means to estimate recovery. Moreover, in the problematic subgroup of "pupil sparing" incomplete ONP, PCT monitoring during the first days may indicate possible progression of a compressive lesion.