Pooled retrospective analysis of 70 mg erenumab in episodic and chronic migraine: a two tertiary headache centers experience during clinical practice.

Erenumab is a monoclonal antibody, targeted against the calcitonin gene-related peptide (CGRP) receptor. Clinical studies have demonstrated prophylactic efficacy in both episodic (EM) and chronic migraine (CM). The aim of the present study is to evaluate the efficacy of treatment in tertiary headache centers under real-life conditions. In a retrospective analysis, the period of 3 months before and after initiation of erenumab therapy was compared. Relevant parameters (headache days, headache intensity, headache duration, acute medication, previous prophylaxis treatments) were collected from medical charts of all migraine patients (N = 82) who started treatment with erenumab between November 1st 2018 and May 1st 2019 at two tertiary headache centers in Germany. The sample included 68 female (82.9%) and 14 male patients aged between 22 and 78 years (mean 51.1 years, SD 10.5 years). Of these patients, 57.3% met the criteria for CM and 56.9% overused acute medication. Under therapy with erenumab, a significant reduction of headache days was observed from the first month on. The effect was most pronounced in the third month with a decrease in monthly headache days from 16.6 to 11.6 days (p < 0.001). There was also a significant reduction in reported headache intensity (p = 0.004) and average duration of headache attacks (p = 0.016). The 50% responder rate in patients with CM was lower in the first month compared to EM but then increased similarly to EM. Patients with medication overuse (MO) also responded to the therapy. There was a reduction in medication overuse from 57% at baseline to 29% after therapy (p = 0.011). Overall, a positive result of treatment with erenumab can be shown in a highly selected sample with severely affected migraine patients and a refractory course prior to treatment. This re-confirms the clinical trial data also for this highly selected group.

[Nummular headache : Subcutaneous peripheral nerve field stimulation as an individual therapeutic attempt]. / Münzkopfschmerz : Subkutane periphere Nervenfeldstimulation als individueller Therapieversuch.

BACKGROUND: Subcutaneous peripheral nerve field stimulation (sPNFS) is an established procedure for the treatment of chronic localized neuropathic pain of peripheral origin. The treatment of nummular headache primarily focuses on conservative methods with limited prospects of success. The role of sPNFS in the treatment of nummular headache has not been investigated as yet. QUESTION: Is the sPNFS an option in the management of nummular headache? MATERIALS AND METHODS: In addition to a summary of established methods in the treatment of nummular headache, sPNFS as a possible form of therapy is discussed. RESULTS: A positive effect of sPNFS in terms of the treatment of nummular headache is shown. DISCUSSION: sPNFS stimulates free subcutaneous nerves and transmits a pleasant form of paraesthesia in the area of pain. If regular conservative therapy has already been exhausted, then sPNFS might be an effective new option in the treatment of nummular headache. sPNFS is a minimally invasive and low-risk procedure. However, the high treatment cost and restrictions regarding fitness to undergo MRI are points of criticism. Further studies are needed to define its potential and role in the treatment of nummular headache.

A novel locus for autosomal dominant, non-syndromic hearing impairment (DFNA18) maps to chromosome 3q22 immediately adjacent to the DM2 locus.

Investigating a large German pedigree with non-syndromic hearing impairment of early onset and autosomal dominant mode of inheritance, linkage to known DFNA loci was excluded and in a subsequent genomic scan the phenotype was mapped to a 10-cM interval on chromosome 3q22; a maximum two-point lod score of 3.77 was obtained for the marker D3S1292. The new locus, DFNA18, is excluded from neighbouring deafness loci, DFNB15 and USH3, and it overlaps with the recently described DM2/PROMM locus. As hearing loss has been described as one feature of the PROMM phenotype, the DFNA18 gene might also be responsible for hearing loss in DM2/PROMM.

Motor cortex disinhibition in acute stroke.

OBJECTIVES: To test whether a disinhibition occurs in the human motor cortex after stroke. METHODS: Patients with a mild to moderate hemiparesis after an acute unilateral ischemic stroke were compared with age-matched healthy controls. We used paired transcranial magnetic stimuli (TMS) to investigate intracortical inhibition and facilitation. Single TMS were applied to obtain a cortical silent period. RESULTS: Intracortical inhibition was significantly reduced in the affected hemisphere at interstimulus intervals of 2, 3 and 4 ms. The cortical silent period was significantly prolonged when compared to the unaffected hemisphere of the patients and to the control group. Motor cortex disinhibition observed in stroke patients was associated either with minimal impairment at the onset of symptoms or with rapidly improving motor functions. CONCLUSIONS: Motor cortex disinhibition occurs in humans after stroke. We suggest that this disinhibition is indicative of compensatory mechanisms, which are involved in recovery-related reorganization.