scholarly journals Unilateral Oculomotor Nerve Palsy Associated with Leptomeningeal Carcinomatosis and Intracranial Hypertension

2021 ◽  
Vol 39 (4) ◽  
pp. 351-353
Author(s):  
Min-Sub Cho ◽  
Sung-Pa Park ◽  
Jong-Geun Seo
Keyword(s):  
Intracranial Hypertension ◽  
Cancer Cells ◽  
Cranial Nerve ◽  
Nerve Palsy ◽  
Visual Loss ◽  
Leptomeningeal Carcinomatosis ◽  
Meningeal Carcinomatosis ◽  
Oculomotor Nerve ◽  
Oculomotor Nerve Palsy ◽  
Cranial Nerve Palsies

Meningeal carcinomatosis is caused by cancer cells invading the meninges and can cause cranial nerve palsies or intracranial hypertension. Intracranial hypertension can present various symptoms such as headache, visual loss, diplopia and may rarely include unilateral cranial nerve palsy. We report a 57-year-old female with leptomeningeal carcinomatosis and intracranial hypertension who presented as unilateral oculomotor nerve palsy.

Sphenoid sinus mucocoele presenting with isolated oculomotor nerve palsy

1997 ◽  
Vol 111 (5) ◽  
pp. 471-473 ◽  
Author(s):  
Dharambir S. Sethi ◽  
David P. C. Lau ◽  
Chumpon Chan
Keyword(s):  
Cranial Nerve ◽  
Sphenoid Sinus ◽  
Nerve Palsy ◽  
Oculomotor Nerve ◽  
Oculomotor Nerve Palsy ◽  
Ocular Symptoms ◽  
Cranial Nerve Palsies ◽  
Close Relationship ◽  
Relationship Of ◽  
Specific Symptoms

AbstractWe describe two cases of sphenoid sinus mucocoele. Both presented with isolated oculomotor nerve palsy. Mucocoeles involving only the sphenoid sinus are uncommon. They are probably under-diagnosed as they may be asymptomatic or cause non-specific symptoms. Nasal symptoms occur infrequently but the close relationship of the sphenoid sinus to the orbital apex means that ocular symptoms including cranial nerve palsies are a common presenting feature. Involvement of the third cranial nerve in isolation is rare but has important neurosurgical implications which must be excluded before this symptom is attributed to the sphenoid sinus.

Pseudomyasthenia Resulting from a Posterior Carotid Artery Wall Aneurysm: A Novel Presentation: Case Report

Neurosurgery ◽  
2001 ◽  
Vol 49 (6) ◽  
pp. 1466-1469 ◽  
Author(s):  
Ramachandra P. Tummala ◽  
Andrew Harrison ◽  
Michael T. Madison ◽  
Eric S. Nussbaum
Keyword(s):  
Carotid Artery ◽  
Cranial Nerve ◽  
Cranial Nerve Palsy ◽  
Intracranial Aneurysms ◽  
Nerve Palsy ◽  
Oculomotor Nerve ◽  
Artery Wall ◽  
Carotid Artery Wall ◽  
Cranial Nerve Dysfunction ◽  
Cranial Nerve Palsies

ABSTRACT OBJECTIVE AND IMPORTANCE Painful oculomotor palsy can result from enlargement or rupture of intracranial aneurysms. The IIIrd cranial nerve dysfunction in this setting, whether partial or complete, is usually fixed or progressive and is sometimes reversible with surgery. We report an unusual oculomotor manifestation of a posterior carotid artery wall aneurysm, which mimicked ocular myasthenia gravis. CLINICAL PRESENTATION A 47-year-old woman developed painless, intermittent, partial IIIrd cranial nerve palsy. She presented with isolated episodic left-sided ptosis, which initially suggested a metabolic or neuromuscular disorder. However, digital subtraction angiography revealed a left posterior carotid artery wall aneurysm, just proximal to the origin of the posterior communicating artery. INTERVENTION The aneurysm was successfully clipped via a pterional craniotomy. During surgery, the aneurysm was observed to be compressing the oculomotor nerve. The patient's symptoms resolved after the operation. CONCLUSION The variability of incomplete IIIrd cranial nerve deficits can present a diagnostic challenge, and the approach for patients with isolated IIIrd cranial nerve palsies remains controversial. Although intracranial aneurysms compressing the oculomotor nerve classically produce fixed or progressive IIIrd cranial nerve palsies with pupillary involvement, anatomic variations may result in atypical presentations. With the exception of patients who present with pupil-sparing but otherwise complete IIIrd cranial nerve palsy, clinicians should always consider an intracranial aneurysm when confronted with even subtle dysfunction of the oculomotor nerve.

scholarly journals Delayed Pneumocephalus-Induced Cranial Neuropathy

2013 ◽  
Vol 2013 ◽  
pp. 1-5 ◽  
Author(s):  
Neena I. Marupudi ◽  
Monika Mittal ◽  
Sandeep Mittal
Keyword(s):  
Cranial Nerve ◽  
Nerve Palsy ◽  
Oculomotor Nerve ◽  
Nerve Compression ◽  
Neurological Deficits ◽  
Oculomotor Nerve Palsy ◽  
Cranial Neuropathy ◽  
Cranial Nerve Deficit ◽  
Moderate Amount ◽  
Interpeduncular Cistern

Pneumocephalus is a common occurrence after cranial surgery, with patients typically remaining asymptomatic from a moderate amount of intracranial air. Postsurgical pneumocephalus rarely causes focal neurological deficits; furthermore, cranial neuropathy from postsurgical pneumocephalus is exceedingly uncommon. Only 3 cases have been previously reported that describe direct cranial nerve compression from intracranial air resulting in an isolated single cranial nerve deficit. The authors present a patient who developed dysconjugate eye movements from bilateral oculomotor nerve palsy. Direct cranial nerve compression occurred as a result of postoperative pneumocephalus in the interpeduncular cistern. The isolated cranial neuropathy gradually recovered as the intracranial air was reabsorbed.

Bevacizumab-induced isolated oculomotor nerve palsy in glioblastoma multiforme

2021 ◽  
pp. 107815522110668
Author(s):  
Ezgi Değerli ◽  
Gülin Alkan ◽  
Nihan Şentürk Öztaş ◽  
Şahin Bedir ◽  
Sümeyra Derin ◽  
...  
Keyword(s):  
Side Effects ◽  
Glioblastoma Multiforme ◽  
Cranial Nerve ◽  
Nerve Palsy ◽  
Growth Factor Receptor ◽  
Recurrent Glioblastoma ◽  
Oculomotor Nerve ◽  
Oculomotor Nerve Palsy ◽  
Recurrent Glioblastoma Multiforme ◽  
Systemic Side Effects

Introduction: Bevacizumab, a monoclonal antibody against the vascular endothelial growth factor receptor, is the standard treatment of recurrent glioblastoma multiforme. In addition to common systemic side effects of bevacizumab, there are rare cases of cranial nerve palsy. Case report: We report a case of transient oculomotor nerve palsy after systemic administration of bevacizumab. Twenty-four hours after the systemic infusion of bevacizumab, transient oculomotor nerve palsy developed in a 49-year-old male patient. In the cranial MRI, there was no malignancy-related progression. Management and outcome: Bevacizumab treatment was discontinued. Methylprednisolone was started considering that bevacizumab increased the inflammatory response. Oculomotor nerve palsy resolved in 14 days. Discussion: There are many side effects of bevacizumab whose mechanisms of action have not been fully explained. Cranial nerve involvement is rarely reported. Our case is the first reported case of bevacizumab-induced oculomotor nerve palsy.

Functional anatomy of headache: circle of Willis aneurysms, third cranial nerve and pain

2011 ◽  
pp. 82-88
Author(s):  
Marcelo Moraes Valença ◽  
Luciana P. A. Andrade-Valença ◽  
Carolina Martins
Keyword(s):  
Cranial Nerve ◽  
Nerve Palsy ◽  
Functional Anatomy ◽  
Circle Of Willis ◽  
Oculomotor Nerve ◽  
Oculomotor Nerve Palsy ◽  
Microsurgical Anatomy ◽  
Third Nerve Palsy ◽  
The Right ◽  
Third Nerve

Patients with intracranial aneurysm located at the internal carotid artery-posterior communicating artery (ICA-PComA) often present pain on the orbit or fronto-temporal region ipsilateral to the aneurysm, as a warning sign a few days before rupture. Given the close proximity between ICA-PComA aneurysm and the oculomotor nerve, palsy of this cranial nerve may occurduring aneurysmal expansion (or rupture), resulting in progressive eyelid ptosis, dilatation of the pupil and double vision. In addition, aneurysm expansion may cause compression not only of the oculomotor nerve, but of other skull base pain-sensitive structures (e.g. dura-mater and vessels), and pain ipsilateral to the aneurysm formation is predictable. We reviewed the functional anatomy of circle of Willis, oculomotor nerve and its topographical relationships in order to better understand the pathophysiology linked to pain and third-nerve palsy caused by an expanding ICAPComA aneurysm. Silicone-injected, formalin fixed cadaveric heads were dissected to present the microsurgical anatomy of the oculomotor nerve and its topographical relationships. In addition, the relationship between the right ICA-PComA aneurysm and the right third-nerve is also shown using intraoperative images, obtained during surgical microdissection and clipping of an unruptured aneurysm. We also discuss about when and how to investigate patients with headache associated with an isolated third-nerve palsy.

scholarly journals Pneumocephalus causing oculomotor nerve palsy: A case report

2020 ◽  
Vol 11 ◽  
pp. 302
Author(s):  
Mackenzie Eileen Goodrich ◽  
Adam M. Wolberg ◽  
Samir Kashyap ◽  
Stacey Podkovik ◽  
Jacob Bernstein ◽  
...  
Keyword(s):  
Cranial Nerve ◽  
Nerve Palsy ◽  
External Ventricular Drain ◽  
Cerebrospinal Fluid Leak ◽  
Common Finding ◽  
Oculomotor Nerve Palsy ◽  
The Third ◽  
Cranial Nerve Palsies ◽  
High Flow Oxygen ◽  
Fluid Leak

Background: Pneumocephalus, the presence of gas or air within the intracranial cavity, is a common finding after cranial procedures, though patients often remain asymptomatic. Rare cases of cranial nerve palsies in patients with pneumocephalus have been previously reported. However, only two prior reports document direct unilateral compression of the third cranial nerve secondary to pneumocephalus, resulting in an isolated deficit. Case Description: A 26-year-old male developed a unilateral oculomotor (III) nerve palsy after repair of a cerebrospinal fluid leak. The pneumocephalus was treated with a combination of an epidural drain, external ventricular drain (EVD), and high-flow oxygen. Following treatment, repeat computed tomography imaging of the head demonstrated that the pneumocephalus was progressively resorbed and the patient’s deficit resolved. Conclusion: In rare cases, isolated cranial nerve palsies, specifically of the third cranial nerve, can result from pneumocephalus following cranial procedures. Acute cranial nerve palsy secondary to pneumocephalus will often resolve without intervention as the air is resorbed, but direct decompression with an epidural drain and an EVD may expedite the resolution of deficits.

scholarly journals Episodic Oculomotor Nerve Palsy with Intracranial Hypertension and Carcinomatous Meningitis

2020 ◽  
Vol 44 (6) ◽  
pp. 399-402
Author(s):  
Turgut Sahin ◽  
Zerin Ozaydın Aksun ◽  
Canan Togay Isikay ◽  
Ozden Sener
Keyword(s):  
Intracranial Hypertension ◽  
Nerve Palsy ◽  
Oculomotor Nerve ◽  
Oculomotor Nerve Palsy ◽  
Carcinomatous Meningitis

scholarly journals Nasopharyngeal B-cell lymphoma with pan-hypopituitarism and oculomotor nerve palsy: a case report and review of the literature

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Maryam Zahedi ◽  
Reyhane Hizomi Arani ◽  
Maryam Tohidi ◽  
Shirin Haghighi ◽  
Masoud Mehrpour ◽  
...  
Keyword(s):  
B Cell ◽  
Cranial Nerve ◽  
Cranial Nerve Palsy ◽  
Nerve Palsy ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Oculomotor Nerve ◽  
Diabetic Woman ◽  
Oculomotor Nerve Palsy ◽  
Neoplastic Lesion

Abstract Background Primary nasopharyngeal lymphoma (NPL) is a very rare tumor of Waldeyer ring (WR) lymphoid tissue. It is challenging to differentiate lymphoma infiltration of pituitary from a pituitary adenoma, meningioma infiltration, and other sellar lesions to plan a suitable treatment strategy. We presented for the first time a unique case of NPL with an unusual presentation of oculomotor nerve palsy associated with pan-pituitary involvement in a diabetic patient. Case presentation A 64-year old diabetic woman with no previous history of malignancy presented with intermittent diplopia for about the last nine months. Severe headache, left eye ptosis and hypoglycemic episodes were added to her symptoms after a while. Further complaints include generalized weakness, loss of appetite, generalized musculoskeletal pain, and 6–7 kg weight loss within six months. Her family history was unremarkable. Physical examinations of eyes indicated left eye 3rd, 4th, and 6th nerve palsy. But, she was not anisocoric, and the pupillary reflexes were normal on both eyes. No lymphadenopathy, organomegaly and other abnormalities were found. Magnetic resonance imaging (MRI) showed a heterogeneous enhancement in the seller and suprasellar regions, enlargement of the stalk, parasellar dural enhancement and thickening of the sphenoid sinus without bone erosion. Also, both cavernous sinuses were infiltrated and both internal carotid arteries were encased by the neoplastic lesion. It suggested an infiltrative neoplastic lesion which compressed the cranial nerves. Pituitary hormone levels assessment indicated a pan-hypopituitarism. Following nasopharyngeal mucosal biopsy, the immunohistochemistry (IHC) findings revealed a low-grade non-Hodgkin’s B-cell lymphoma. Systemic workup, including cerebrospinal fluid (CSF) studies, bone marrow aspiration, chest and abdominopelvic high-resolution computed tomography (HRCT) indicated no other involvement by the lymphoma. After chemotherapy courses, central adrenal insufficiency, partial central diabetes incipidious (CDI) and central hypothyroidism have been resolved. To our best knowledge, we found 17 cases of NPL with cranial nerve palsy, 1 case of NPL with pan-hypopituitarism and no NPL case with both cranial nerve palsy and pituitary dysfunction. Conclusions The incidence of cranial neuropathy in patients with diabetes should not merely be attributed to diabetic neuropathy without further evaluation.

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