Dural arteriovenous fistula as a possible cause of Tolosa-Hunt syndrome: a case report

Itokawa, Kaori; Fukui, Miki; Yamamoto, Toshiyuki; Tamura, Naotoshi; Ishihara, Shouichiro; Araki, Nobuhito

doi:10.1007/s00415-010-5459-x

Cited by 8 publications

(3 citation statements)

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“…Third cranial nerve palsy without sparing of pupillary function and pain preceding the signs of neuropathy hint heavily at the diagnosis of THS but, while it is a difficult option for diabetic patients, a short experimental course of steroid therapy may be necessary for those whose diagnosis is uncertain. Beyond these, the differential diagnosis of THS includes other vascular diseases (such as cavernous sinus thrombosis and dural arteriovenous fistula (20)), neoplastic diseases (such as meningiomas (21), neurilemmoma, nasopharyngeal carcinoma, pituitary adenoma, lymphomas (22), and miscellaneous metastatic tumours (23,24)), infectious diseases (such as fungal infection, tuberculosis, syphilis, and actinomycosis), and specific granulomatous diseases (such as Wegener’s granulomatosis, sarcoidosis, giant cell arteritis and systemic lupus erythematosus). ‘Ophthalmoplegic migraine’ is a recurrent demyelinating or inflammatory cranial neuropathy, or a variant of THS with inflammation extending along the cranial nerve, and still controversial (12,25).…”

Section: Discussionmentioning

confidence: 99%

Validation of ICHD-3 beta diagnostic criteria for 13.7 Tolosa-Hunt syndrome: Analysis of 77 cases of painful ophthalmoplegia

et al. 2014

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Section: Discussionmentioning

confidence: 99%

Validation of ICHD-3 beta diagnostic criteria for 13.7 Tolosa-Hunt syndrome: Analysis of 77 cases of painful ophthalmoplegia

et al. 2014

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“…The more ominous abnormalities included ICA aneurysm and dissection. 29 30 31 32 Out of 54 cases of benign THS [Supplementary Tables 2 and 3 ], four showed vascular anomalies, 33 34 35 36 two of which were late-onset dural arteriovenous (AV) fistulas.…”

Section: R Esultsmentioning

confidence: 99%

Tolosa–Hunt Syndrome

Dutta

Anand

2021

Journal of Current Ophthalmology

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Purpose: To review the diagnostic criteria for Tolosa–Hunt syndrome (THS) and utility of recent modifications. Methods: We searched PubMed for keywords Tolosa Hunt and magnetic resonance imaging. We compared the three editions of International Classification of Headache Disorders and isolated case reports and case series with the assessment of cavernous internal carotid artery (ICA) caliber to find the prevalence of vascular anomalies. We also evaluated cases of THS with the involvement of extracavernous structures and the possible role of idiopathic hypertrophic pachymeningitis (HP). Cases diagnosed falsely as THS were also reviewed for the presence of atypical features and relevance of criterion D. We assessed nonconforming cases (those with normal neuroimaging benign THS) and idiopathic inflammatory orbital pseudotumor (IIPO). Results: Vascular abnormalities were found in 36.36% of THS cases. Benign THS may also show changes in ICA caliber. Evidence suggestive of idiopathic HP could be found in 57% of cases with the involvement of extracavernous structures, such as facial nerve and pituitary gland. Both THS and IIPO are steroid-responsive pathologies with similar clinical and radiological features. False-positive diagnosis of THS results from early labeling, based solely on clinical features and symptom resolution after steroid therapy. Conclusions: Benign THS may be a result of limitation of resolution of available neuroimaging technique or early testing. Early and late vascular changes can be seen in both THS and its benign variant; some of them are not innocuous. THS may be considered a type of focal idiopathic HP. IIPO may represent an anterior variant of THS. In the absence of histopathological diagnosis, steroid-induced resolution of symptoms should be confirmed radiologically and followed-up.

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“…16 Given that several pathologic processes in the formation and potential coexistence of intracranial aneurysms and cerebral arteriovenous malformations (AVM) overlap with MA and MMS-such as vascular stenosis, media thinning, internal elastic lamina damage, angiogenesis, aberrant microvascular hemodynamics, and vascular remodeling-signaling pathways and inflammatory and/or genetic biomarkers may also overlap. 40,60,72,105,161,167,168…”

Section: Dorschel and Wanebomentioning

confidence: 99%

Genetic and Proteomic Contributions to the Pathophysiology of Moyamoya Angiopathy and Related Vascular Diseases

Dorschel

Wanebo

2021

TACG

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This literature review describes the pathophysiological mechanisms of the current classes of proteins, cells, genes, and signaling pathways relevant to moyamoya angiopathy (MA), along with future research directions and implementation of current knowledge in clinical practice. Objective: This article is intended for physicians diagnosing, treating, and researching MA. Methods and Results: References were identified using a PubMed/Medline systematic computerized search of the medical literature from January 1, 1957, through August 4, 2020, conducted by the authors, using the key words and various combinations of the key words "moyamoya disease," "moyamoya syndrome," "biomarker," "proteome," "genetics," "stroke," "angiogenesis," "cerebral arteriopathy," "pathophysiology," and "etiology." Relevant articles and supplemental basic science articles published in English were included. Intimal hyperplasia, medial thinning, irregular elastic lamina, and creation of moyamoya vessels are the end pathologies of many distinct molecular and genetic processes. Currently, 8 primary classes of proteins are implicated in the pathophysiology of MA: gene-mutation products, enzymes, growth factors, transcription factors, adhesion molecules, inflammatory/ coagulation peptides, immune-related factors, and novel biomarker candidate proteins. We anticipate that this article will need to be updated in 5 years. Conclusion:It is increasingly apparent that MA encompasses a variety of distinct pathophysiologic conditions. Continued research into biomarkers, genetics, and signaling pathways associated with MA will improve and refine our understanding of moyamoya's complex pathophysiology. Future efforts will benefit from multicenter studies, familybased analyses, comparative trials, and close collaboration between the clinical setting and laboratory research.

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Dural arteriovenous fistula as a possible cause of Tolosa-Hunt syndrome: a case report

Cited by 8 publications

References 5 publications

Validation of ICHD-3 beta diagnostic criteria for 13.7 Tolosa-Hunt syndrome: Analysis of 77 cases of painful ophthalmoplegia

Validation of ICHD-3 beta diagnostic criteria for 13.7 Tolosa-Hunt syndrome: Analysis of 77 cases of painful ophthalmoplegia

Tolosa–Hunt Syndrome

Genetic and Proteomic Contributions to the Pathophysiology of Moyamoya Angiopathy and Related Vascular Diseases

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