Recurrent Third Nerve Palsy Secondary to Instrinsic Schwannoma of the Third Cranial Nerve.

ABSTRACT: A 78 year-old woman has experienced multiple episodes of transient right third nerve palsy over the course of 15 years and has undergone multiple imaging studies as well as investigations for myasthenia gravis and giant cell arteritis in search for the diagnosis. When seen after the most recent episode, MRI with contrast and Fast-Imaging Employing Steady-State Acquisition protocol revealed a subtle enlargement and enhancement of the cisternal and proximal cavernous portions of the right third cranial nerve. An empiric diagnosis of schwannoma intrinsic to third cranial nerve was made. All patients with cyclical third nerve palsies should have appropriate neuroimaging to rule out subtle structural lesions before other investigations are undertaken.

Clinicopathological Correlates: Chronic Arsenic Toxicity Causing Bilateral Symmetric Progressive Optic Neuropathy.

A 70 year-old man presented with insidiously progressing central visual acuity loss in both eyes over several years. Objectively the only abnormality identified on the exam was questionable granularity in the fovea in each eye. Extensive work up which included neuro-imaging, screening blood work for toxic and nutritional causes of optic neuropathy as well as electroretinogram and fluorescein angiography to rule out subtle maculopathy was all unrevealing. When vision continued to deteriorate over the next several years investigations were repeated and again did not yield any positive results. Levels of heavy metals were then obtained after further progression of visual loss, revealing very high levels of arsenic. Subsequent investigations revealed that patient has been spending almost every weekend for the past 28 years alone at a remote country cottage where the sole supply of water was from the local well. He also recalled that 1.5 months after purchasing the cottage he developed hemorrhagic colitis requiring partial colectomy. The specimen from colectomy was located and total reflection x-ray fluorescence testing performed in a specialized lab revealed greatly increased level of arsenic particle in the colonic biopsy from 28 years ago. This case is a reminder that heavy metal toxicity should be considered in a differential diagnosis of patients with bilateral symmetric optic neuropathy.

Severe Intraoperative Orbital Venous Congestion during Resection of a Frontal Meningioma Presenting with Post-operative Vision Loss and Ophthalmoplegia: A Case Report.

We describe a unique case of a middle-aged man who noticed complete vision loss in the right eye after awaking from resection of a large right-sided frontal meningioma. Visual acuity was hand motions, and there were multiple signs of right orbital venous congestion. Magnetic resonance imaging and venography (MRI/V) of the brain and orbits demonstrated expected post-operative findings with no evidence of cavernous sinus thrombosis or fistula. Empiric treatment with intravenous antibiotics and intravenous methylprednisolone were ineffective. Immediate post-operative computerised tomography (CT) images were re-reviewed and revealed right restricted diffusion of the entire intraorbital right optic nerve. Discussion with the neurosurgical team revealed that during craniotomy, a prominent diploic venous plexus in the frontal bone adjacent to the meningioma was identified and coagulated with bone wax. Review of pre-operative imaging revealed large diploid flow voids in the right frontal bone, corresponding to the intraoperative findings. This prominent venous plexus appeared to drain from the meningioma posteriorly into the vein of Labbe. A second pathway drained anteriorly through the right angular vein into the orbit. We hypothesise that the posterior outflow pathway was coagulated intraoperatively, causing redirection of all venous outflow from the meningioma into the right orbit through the anterior pathway. This resulted in significant orbital hypertension with manifest signs and symptoms. Furthermore, sudden rise in intraorbital pressure led to infarction of the optic nerve, leaving the patient with hand motions vision. We suggest that pre-operative vascular imaging should be performed in patients with large meningiomas, as pre-operative embolisation of venous outflow channels may prevent severe post-operative complications.

When the Problem Became the Solution.

We present a unique case where a young man developed subtle cavernous sinus thrombosis (CST) due to underlying hypercoagulable state. He also had coexisting frontal lobe brain dural arteriovenous fistula (bdAVF). After CST developed, venous drainage from the optic nerve was redirected into the frontal lobe which was already under high venous pressure because of preexisting bdAVF. This caused backflow of venous blood into the optic nerve causing massive persistent optic nerve head swelling. Presumed acute venous hypertension event within bdAVF caused frontal mass effect presenting as seizure leading to thrombosis of bdAVF.

Comment faire d'un problème une solution. Nous voulons présenter ici le cas unique d'un jeune homme chez qui une thrombose du sinus caverneux s'est développée en raison d'une condition sous-jacente d'hypercoagulabilité. Ajoutons également que le lobe frontal de son cerveau donnait à voir des fistules artério-veineuses durales. Une fois développé ce type de thrombose, on a procédé à un drainage veineux à partir du nerf optique, drainage ensuite redirigé dans le lobe frontal, lequel faisait déjà face à des conditions de pression veineuse élevée à cause de ces fistules. Cela a entraîné le refoulement de sang veineux dans le nerf optique, ce qui a provoqué en retour une grave et persistante enflure de la tête du nerf optique. À cet égard, on peut présumer qu'une manifestation aigüe d'hypertension veineuse dans ces fistules a causé l'apparition de cet effet de masse du lobe frontal se manifestant par des crises convulsives, ce qui a fini par engendrer la thrombose des fistules artério-veineuses durales.