Meningeal rheumatoid nodules in a 55-year-old man presenting with chronic headaches and oculomotor nerve palsy: an uncommon extra-articular manifestation of rheumatoid arthritis

Rheumatoid arthritis (RA) is a multisystem inflammatory disease which can involve many organ systems including the central nervous system (CNS). Though not very common, the results can be severely debilitating. The spectrum of the CNS involvement includes meningitis, encephalitis and occasionally rheumatoid nodules. Its presentation is variable, though very rarely it can present as focal neurological deficits. Imaging can be suggestive, but diagnosis usually requires tissue biopsy. Treatment consists of high-dose steroids and immunosuppressants. We describe the case of a 55-year-old male patient with a history of RA presenting with a third nerve palsy and headache who was found to have rheumatoid nodules on biopsy. CNS involvement in RA should be considered in anyone with rheumatoid arthritis who presents with focal neurological deficits, though infections and space-occupying lesions should also be ruled out.

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Left suboccipital supracerebellar transtentorial approach for resection of tectal cavernous malformation

Neurosurgical Focus: Video ◽

10.3171/2019.10.focusvid.19394 ◽

2019 ◽

Vol 1 (2) ◽

pp. V19

Author(s):

Hussam Abou-Al-Shaar ◽

Timothy G. White ◽

Ivo Peto ◽

Amir R. Dehdashti

Keyword(s):

Nerve Palsy ◽

Oculomotor Nerve ◽

Oculomotor Nerve Palsy ◽

Entry Zone ◽

Third Nerve Palsy ◽

History Of ◽

Tectal Plate ◽

The Right ◽

Transtentorial Approach ◽

Third Nerve

A 64-year-old man with a midbrain cavernoma and prior bleeding presented with a 1-week history of diplopia, partial left oculomotor nerve palsy, and worsening dysmetria and right-sided weakness. MRI revealed a hemorrhagic left tectal plate and midbrain cavernoma. A left suboccipital supracerebellar transtentorial approach in the sitting position was performed for resection of his lesion utilizing the lateral mesencephalic sulcus safe entry zone. Postoperatively, he developed a partial right oculomotor nerve palsy; imaging depicted complete resection of the cavernoma. He recovered from the right third nerve palsy, weakness, and dysmetria, with significant improvement of his partial left third nerve palsy.The video can be found here: https://youtu.be/ofj8zFWNUGU.

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Pituitary Apoplexy Causing Compression of Third Cranial Nerve—Management

Indian Journal of Neurosurgery ◽

10.1055/s-0039-1694849 ◽

2019 ◽

Vol 08 (02) ◽

pp. 119-122

Author(s):

Václav Masopust

Keyword(s):

Cavernous Sinus ◽

Nerve Palsy ◽

Clinical Symptoms ◽

Rapid Development ◽

Sella Turcica ◽

Oculomotor Nerve ◽

Oculomotor Nerve Palsy ◽

Future Research ◽

Third Nerve Palsy ◽

Increased Pressure

AbstractLesions of the oculomotor nerve as the first sign of pituitary adenoma are rare. The cause of such lesions without other clinical symptoms is discussed in this study. A small cohort of 4 patients (3.1%) with oculomotor nerve palsy (third nerve palsy) as the only neurologic deficit, from 129 patients who got operated upon for pituitary adenomas, is presented. In this group (mean age: 55 years, range: 36–65 years), all patients (two women and two men) underwent surgery. In two cases, there was arrested pneumatization and thickened bone. In the remaining two cases, a macroscopically visible, very solid opaque diaphragm was present, after the removal of the tumor and thickened bone. Complete adjustment was observed in all patients within 1 week after the surgery. Two factors that seem to increase the high risk for the development of oculomotor nerve palsy are that the cavernous sinus may be the only weak structure surrounding the sella turcica when the diaphragm and bone are thickened; and the rapid development of increased pressure in this region. The increased pressure on the cavernous sinus during the anatomical variations is the primary cause for lesions on the oculomotor nerve. However, this conjecture cannot be statistically demonstrated because of the small number of cases. Future research should be conducted on larger samples to increase statistical inference and generalizability.

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Post traumatic isolated ipsilateral oculomotor nerve palsy

Romanian Neurosurgery ◽

10.33962/roneuro-2019-035 ◽

2019 ◽

pp. 188-190

Author(s):

Praveen Kumar ◽

Sharad Pandey ◽

Kulwant Singh ◽

Mukesh Sharma ◽

Prarthana Saxena

Keyword(s):

Subdural Hematoma ◽

Nerve Palsy ◽

Chronic Subdural Hematoma ◽

Oculomotor Nerve Palsy ◽

Rare Presentation ◽

Third Nerve Palsy ◽

Common Causes ◽

History Of ◽

Post Traumatic ◽

Third Nerve

The common causes of isolated third nerve palsy are microvascular infarction, intracranial aneurysm, diabetes, hypertension and atherosclerosis. Here we are presenting a case of 26-year female presenting with a history of head injury two months back. She presented with ptosis on the left side. On computed tomography, a large left-sided chronic subdural hematoma with significant midline shift was found. Isolated ipsilateral third nerve palsy is a rare presentation with unilateral chronic subdural hematoma. Improvement in ptosis after surgery indicate a good neurological outcome.

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Delayed Pneumocephalus-Induced Cranial Neuropathy

Case Reports in Medicine ◽

10.1155/2013/105087 ◽

2013 ◽

Vol 2013 ◽

pp. 1-5 ◽

Cited By ~ 11

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.

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

Headache Medicine ◽

10.48208/headachemed.2011.18 ◽

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.

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Early Endovascular Management of Oculomotor Nerve Palsy Associated with Posterior Communicating Artery Aneurysms

Interventional Neuroradiology ◽

10.1177/159101991001600102 ◽

2010 ◽

Vol 16 (1) ◽

pp. 17-21 ◽

Cited By ~ 18

Author(s):

A. Santillan ◽

W.E. Zink ◽

J. Knopman ◽

H.A. Riina ◽

Y.P. Gobin

Keyword(s):

Nerve Palsy ◽

Clinical Presentation ◽

Endovascular Embolization ◽

Oculomotor Nerve ◽

Posterior Communicating Artery ◽

Oculomotor Nerve Palsy ◽

Endovascular Management ◽

Third Nerve Palsy ◽

The Third ◽

Third Nerve

Palsy of the third cranial nerve (oculomotor nerve, CNIII) is a well-known clinical presentation of posterior communicating artery (P-com) aneurysm. We report a series of 11 patients with partial or complete third nerve palsy secondary to P-com aneurysm. All were treated with endovascular embolization within seven days of symptom onset. Third nerve palsy symptoms resolved in 7/11 (64%), improved in 2/11 (18%) and did not change in 2/11 (18%) patients

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Aberrant regeneration in idiopathic oculomotor nerve palsy

Journal of Neurosurgery ◽

10.3171/jns.1980.52.6.0854 ◽

1980 ◽

Vol 52 (6) ◽

pp. 854-856 ◽

Cited By ~ 5

Author(s):

Jose F. Laguna ◽

Michael S. Smith

Keyword(s):

Nerve Palsy ◽

Oculomotor Nerve ◽

Oculomotor Nerve Palsy ◽

Content Type ◽

Third Nerve Palsy ◽

Aberrant Regeneration ◽

Oculomotor Function ◽

Third Nerve ◽

Fine Print

✓ Aberrant regeneration of the oculomotor nerve usually follows injury to the nerve by posterior communicating artery aneurysms or trauma. A case of idiopathic third nerve palsy with pupillary involvement occurred in an otherwise healthy 38-year-old man. Follow-up examination 32 months later showed evidence of oculomotor function with aberrant regeneration.

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An arm and a leg: A case of rheumatoid vasculitis and antiphospholipid antibody syndrome

SAGE Open Medical Case Reports ◽

10.1177/2050313x211015895 ◽

2021 ◽

Vol 9 ◽

pp. 2050313X2110158

Author(s):

Jay Ghadiali ◽

Aditya Talwar ◽

Colin Ligon

Keyword(s):

Rheumatoid Arthritis ◽

High Dose ◽

Antiphospholipid Antibody ◽

Antiphospholipid Antibody Syndrome ◽

Rheumatoid Vasculitis ◽

Organ Systems ◽

Left Femoral Artery ◽

History Of ◽

High Degree ◽

Common Manifestation

Rheumatoid vasculitis is a rare extra-articular complication of rheumatoid arthritis. The most common manifestation is cutaneous; however, it can manifest in various organ systems and is associated with a high degree of morbidity and mortality. Diagnosis is challenging, and there are no validated diagnostic or classification criteria. Most cases should be confirmed with tissue biopsy when possible given the severity of disease and the extent of immunosuppression required to treat this condition. We report the case of a 54-year-old white woman with long-standing, uncontrolled, and seropositive rheumatoid arthritis with a history of elevated anticardiolipin IgG and IgM antibodies who presented with acute stenosis of her left femoral artery which ultimately required a left above-the-knee amputation. Histopathology revealed findings consistent with vasculitis and thrombosis, and subsequent imaging revealed multifocal arterial and venous thromboses. She was diagnosed with rheumatoid vasculitis and antiphospholipid antibody syndrome, and was treated with high-dose glucocorticoids, cyclophosphamide, and warfarin. Rheumatoid vasculitis is a rare but devastating complication of rheumatoid arthritis, and vigilance for this condition must be maintained, especially in patients with long-standing, seropositive disease.

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MRI Findings of Isolated Oculomotor Nerve Palsy after Mild Head Trauma in a Pediatric Patient: Case Report

Pediatric Neurosurgery ◽

10.1159/000512876 ◽

2021 ◽

pp. 1-5 ◽

Cited By ~ 1

Author(s):

Yunjin Im ◽

Jeong Rye Kim

Keyword(s):

Nerve Injury ◽

Head Trauma ◽

Nerve Palsy ◽

Brain Mri ◽

Skull Fracture ◽

Oculomotor Nerve ◽

Inversion Recovery ◽

Neurological Deficits ◽

Oculomotor Nerve Palsy ◽

Mri Findings

Introduction: Traumatic oculomotor nerve injury is usually caused by severe head trauma and is generally associated with other neurological deficits such as basilar skull fracture, orbital injury, or subarachnoid hemorrhage. Isolated traumatic oculomotor nerve injury after minor head trauma and its MRI findings are rarely reported. Case Presentation: We report a case of a 13-year-old girl with mydriasis, limited inferior and medial movement of the left eyeball, and left ptosis after a mild bump of the left forehead and eye into an electricity pole. The symptoms suggested left oculomotor nerve palsy, but initial facial computed tomography and brain MRI did not reveal any intracranial lesions or fractures in the skull and orbit. Cranial nerve MRI showed segmental hyperintensities and mild thickening of the left oculomotor nerve from the cavernous segment to the proximal orbital segment on T2 short tau inversion recovery and 3D fluid-attenuated inversion recovery volume isotropic turbo spin-echo acquisition sequences. The patient received treatment with oral pyridostigmine for 7 days and was fully recovered at 14 months after injury. Discussion: As traumatic oculomotor nerve palsy can occur without intracranial hematomas or skull base fractures, routine brain MRI may not always reveal abnormalities; thus, MRI dedicated to imaging of the oculomotor nerve using FS T2WI and high-resolution 3D sequences can be helpful for the diagnosis and management of patients suspected of isolated oculomotor nerve injury.

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Microprobe analysis of inclusion bodies related to two benzofuran derivatives

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100127785 ◽

1987 ◽

Vol 45 ◽

pp. 672-673

Author(s):

T. L. Benning ◽

P. Ingram ◽

J. D. Shelburne

Keyword(s):

Inclusion Bodies ◽

Uranyl Acetate ◽

Multiple Organ ◽

High Dose ◽

En Bloc ◽

Tissue Samples ◽

Transmission Electron ◽

Organ Systems ◽

Dense Inclusion ◽

Melanin Complex

Two benzofuran derivatives, chlorpromazine and amiodarone, are known to produce inclusion bodies in human tissues. Prolonged high dose chlorpromazine therapy causes hyperpigmentation of the skin with electron-dense inclusion bodies present in dermal histiocytes and endothelial cells ultrastructurally. The nature of the deposits is not known although a drug-melanin complex has been hypothesized. Amiodarone may also cause cutaneous hyperpigmentation and lamellar lysosomal inclusion bodies have been demonstrated within the cells of multiple organ systems. These lamellar bodies are believed to be the product of an amiodarone-induced phospholipid storage disorder. We performed transmission electron microscopy (TEM) and energy dispersive x-ray microanalysis (EDXA) on tissue samples from patients treated with these drugs, attempting to detect the sulfur atom of chlorpromazine and the iodine atom of amiodarone within their respective inclusion bodies.A skin biopsy from a patient with hyperpigmentation due to prolonged chlorpromazine therapy was fixed in 4% glutaraldehyde and processed without osmium tetroxide or en bloc uranyl acetate for Epon embedding.

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