Symptomatic migraine: A systematic review to establish a clinically important diagnostic entity.

OBJECTIVE: To determine if a clinical presentation indistinguishable from migraine can occur due to an underlying condition or pathology, that is, "symptomatic migraine." BACKGROUND: It is currently not clear whether migraine truly can be caused by an underlying condition or pathology. Characterization of the etiology and clinical features of possible symptomatic migraine is of significant clinical importance and further may help elucidate the pathophysiology of migraine. METHODS: We devised operational diagnostic criteria for "symptomatic migraine" and "possible symptomatic migraine" requiring strong evidence for a causal relation between underlying cause and migraine symptoms adhering strictly to diagnostic criteria. PubMed was searched for case reports of symptomatic migraine from inception to March 2020. Only articles published in English or German were included. No restrictions were placed on study design. Relevant references in the articles were also included. Papers were systematically reviewed by two independent reviewers for detailed clinical features of migraine as well as the proposed underlying conditions and the effects of treatment of these conditions. RESULTS: Our search retrieved 1726 items. After screening, 109 papers comprising 504 cases were reviewed in detail. Eleven patients with migraine with aura (MWA) fulfilled our working criteria for symptomatic migraine, and 39 patients fulfilled our criteria for possible symptomatic migraine. The most common etiologies of symptomatic migraine were arteriovenous malformations, carotid stenosis, dissection or aneurysm, brain infarctions, meningioma, and various intra-axial tumors. CONCLUSIONS: Symptomatic MWA, indistinguishable from idiopathic MWA, may occur due to cortical lesions or microembolization. We found no clear evidence supporting the existence of symptomatic migraine without aura although we did identify possible cases. Our findings are limited by the available literature, and we suggest that prospective studies are needed.

[Sneddon's syndrome in a young woman with antiphospholipid syndrome, ischaemic apoplexy and epileptic seizures].

In this case report, a 28-year-old woman known with slight aortic regurgitation presented with partial complex epileptic seizures. On examination, livedo reticularis was noted, and cerebral MRI scans showed signs of clinical silent old lacunar infarctions. She was persistently triple positive for antiphospholipid antibodies in high titres and fulfilled the antiphospholipid syndrome criteria. The patient was diagnosed with Sneddon's syndrome, which is a rare thrombotic vasculopathy characterised by the combination of cerebrovascular disease with livedo reticularis. Her seizures stopped, after anticoagulation therapy with warfarin was initiated.

Field-testing of the ICHD-3 beta diagnostic criteria for classical trigeminal neuralgia.

INTRODUCTION: We aimed to field-test the beta version of the third edition of the International Classification of Headache Disorders (ICHD-3 beta) diagnostic criteria for classical trigeminal neuralgia (TN). The proposed beta draft of the 11th version of the International Classification of Diseases (ICD-11 beta) is almost exclusively based on the ICHD-3 beta classification structure although slightly abbreviated. We compared sensitivity and specificity to ICHD-2 criteria, and evaluated the needs for revision. METHODS: Clinical characteristics were systematically and prospectively collected from 206 consecutive TN patients and from 37 consecutive patients with persistent idiopathic facial pain in a cross-sectional study design. RESULTS: The specificity of ICHD-3 beta was similar to ICHD-2 (97.3% vs. 89.2%, p = 0.248) and the sensitivity was unchanged (76.2% vs. 74.3%, p = 0.134). The majority of false-negative diagnoses in TN patients were due to sensory abnormalities at clinical examination. With a proposed modified version of ICHD-3 beta it was possible to increase sensitivity to 96.1% (p < 0.001 compared to ICHD-3 beta) while maintaining specificity at 83.8% (p = 0.074 compared to ICHD-3 beta). CONCLUSION: ICHD-3 beta was not significantly different from ICHD-2 and both lacked sensitivity. A modification of the criteria improved the sensitivity greatly and is proposed for inclusion in the forthcoming ICHD-3.