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Objective To identify grey matter alterations in patients suffering new daily persistent headache to enrich the pathophysiological concept of this rare headache disorder characterised by a distinct, clearly remembered onset and its instant chronification. Method Magnetic resonance-based voxel-based and surface-based morphometry was used to investigate 23 patients suffering from new daily persistent headache and 23 age- and gender-matched healthy controls with 1.5 Tesla MRI. Independent statistical analysis was performed at three sites using statistical parametric mapping, as well as FSL(FMRIB Software Library)-based approaches. Results No grey matter changes were detected using this sophisticated and cross-checked method. Conclusion The absence of structural brain changes in patients with new daily persistent headache contribute to the recent discussion regarding structural alterations in primary headache disorders in general and does not provide evidence for grey matter changes being associated with the pathophysiology of new daily persistent headache. Future research will have to determine the underlying pathophysiological mechanisms of this disorder.

Background Idarucizumab is a monoclonal antibody fragment with high affinity for dabigatran reversing its anticoagulant effects within minutes. Thereby, patients with acute ischemic stroke who are on dabigatran treatment may become eligible for thrombolysis with recombinant tissue-type plasminogen activator (rt-PA). In patients on dabigatran with intracerebral hemorrhage idarucizumab could prevent lesion growth. Aims To provide insights into the clinical use of idarucizumab in patients under effective dabigatran anticoagulation presenting with signs of acute ischemic stroke or intracranial hemorrhage. Methods Retrospective data collected from German neurological/neurosurgical departments administering idarucizumab following product launch from January 2016 to August 2018 were used. Results One-hundred and twenty stroke patients received idarucizumab in 61 stroke centers. Eighty patients treated with dabigatran presented with ischemic stroke and 40 patients suffered intracranial bleeding (intracerebral hemorrhage (ICH) in n = 27). In patients receiving intravenous thrombolysis with rt-PA following idarucizumab, 78% showed a median improvement of 7 points in National Institutes of Health Stroke Scale. No bleeding complications were reported. Hematoma growth was observed in 3 out of 27 patients with ICH. Outcome was favorable with a median National Institutes of Health Stroke Scale improvement of 4 points and modified Rankin score 0–3 in 61%. Six out of 40 individuals (15%) with intracranial bleeding died during hospital stay. Conclusion Administration of rt-PA after reversal of dabigatran activity with idarucizumab in case of acute ischemic stroke seems feasible, effective, and safe. In dabigatran-associated intracranial hemorrhage, idarucizumab appears to prevent hematoma growth and to improve outcome.

This chapter describes the sensory innervation of the face and head, focusing on anatomical substrates of clinical features that characterize cranial neuralgias. It draws attention to the key role of the caudal part of the trigeminal spinal nucleus and additional roles of the hypothalamus, descending modulation, and the parasympathetic system. The chapter provides an overview of neural excitability together with reasoning of how it can lead to various manifestations of cranial neuralgias. High-throughput ‘whole-genome sequencing’ studies demonstrate that rare mutations in genes involved in a wide range of neuronal functions underlie the risk for developing trigeminal neuralgia. Although still at an early stage, this research strongly suggests that most patients have inherited protein-changing mutations in several genes and that functionally different groups of genes are associated with different clinical subtypes distinguished by sex, age of onset, and presence of neurovascular compression.

Background Headache is a frequent symptom following COVID-19 immunization with a typical onset within days post-vaccination. Cases of cerebral venous thrombosis (CVT) have been reported in adenovirus vector-based COVID-19 vaccine recipients. Findings We reviewed all vaccine related CVT published cases by April 30, 2021. We assessed demographic, clinical variables and the interval between the vaccination and onset of headache. We assessed whether the presence of headache was associated with higher probability of death or intracranial hemorrhage. We identified 77 cases of CVT after COVID-19 vaccination. Patients’ age was below 60 years in 74/77 (95.8%) cases and 61/68 (89.7%) were women. Headache was described in 38/77 (49.4%) cases, and in 35/38 (92.1%) was associated with other symptoms. Multiple organ thrombosis was reported in 19/77 (24.7%) cases, intracranial hemorrhage in 33/77 (42.9%) cases and 19/77 (24.7%) patients died. The median time between vaccination and CVT-related headache onset was 8 (interquartile range 7.0–9.7) days. The presence of headache was associated with a higher odd of intracranial hemorrhage (OR 7.4; 95% CI: 2.7–20.8, p p = 0.213). Conclusion Delayed onset of headache following an adenovirus vector-based COVID-19 vaccine is associated with development of CVT. Patients with new-onset headache, 1 week after vaccination with an adenovirus vector-based vaccine, should receive a thorough clinical evaluation and CVT must be ruled out.

Obwohl die vestibulare Migrane eine haufige Ursache fur Schwindel ist und etwa 1 % der westlichen Weltbevolkerung betrifft, wird sie weithin nicht allgemein anerkannt und zu selten diagnostiziert. Diagnostische Kriterien fur die vestibulare Migrane wurden sowohl von der internationalen Kopfschmerzgesellschaft als auch der Barany-Gesellschaft konsentiert. Die verfugbaren Behandlungsoptionen fur die vestibulare Migrane orientieren sich im Allgemeinen an denen fur Migrane mit und ohne Aura.

A minority of headache patients have a secondary headache disorder. The medical literature presents and promotes red flags to increase the likelihood of identifying a secondary etiology. In this review, we aim to discuss the incidence and prevalence of secondary headaches as well as the data on sensitivity, specificity, and predictive value of red flags for secondary headaches. We review the following red flags: (1) systemic symptoms including fever; (2) neoplasm history; (3) neurologic deficit (including decreased consciousness); (4) sudden or abrupt onset; (5) older age (onset after 65 years); (6) pattern change or recent onset of new headache; (7) positional headache; (8) precipitated by sneezing, coughing, or exercise; (9) papilledema; (10) progressive headache and atypical presentations; (11) pregnancy or puerperium; (12) painful eye with autonomic features; (13) posttraumatic onset of headache; (14) pathology of the immune system such as HIV; (15) painkiller overuse or new drug at onset of headache. Using the systematic SNNOOP10 list to screen new headache patients will presumably increase the likelihood of detecting a secondary cause. The lack of prospective epidemiologic studies on red flags and the low incidence of many secondary headaches leave many questions unanswered and call for large prospective studies. A validated screening tool could reduce unneeded neuroimaging and costs.

Background Persistent postural-perceptual dizziness (PPPD) is the most common functional vestibular disorder. A multisensory mismatch altered by psychological influences is considered to be an important pathophysiological mechanism. Increased cortical and subcortical excitability may play a role in the pathophysiology of PPPD. We hypothesized that decreased motion perception thresholds reflect one mechanism of the abnormal vestibular responsiveness in this disorder. We investigated the vestibular perception thresholds and the vestibular ocular reflex with a rotatory chair experiment to gain insights in the processing and adaption to vestibular provocation. Methods In this cross-sectional study 26 female PPPD patients and 33 healthy female age matched controls (HC) were investigated sitting in a motorized rotary chair shielded regarding visual and acoustic stimuli. The chair was rotated for 20 minutes with slowly increasing velocity to a maximum of 72°/s. We functionally tested motion perception thresholds and vegetative responses to rotation as well as vestibular-ocular reflex thresholds. We additionally investigated several psychological comorbidities (i.e. depression, anxiety, somatosensory amplification) using validated scores. Conventional dizziness scores were obtained to quantify the experienced dizziness and impact on daily life. Results PPPD patients showed a significant reduced vestibulo-perceptual threshold (PPPD: 10.9°/s vs. HC: 29.5°/s; pp=0.043). No significant difference was measured regarding nystagmus parameters between both groups. Conclusion PPPD patients showed increased vegetative response as well as decreased vestibulo-perceptual thresholds which are related to disease duration. This is of interest as PPPD might be sustained by increased vestibular excitability leading to motion intolerance and induction of dizziness when exposed to movement.

Background and purpose Vestibular migraine (VM) patients are ictally and interictally hypersensitive for self-motion and visual perception. Increased cortical excitability of the vestibular system represented by lowered motion perception thresholds might play an important role in the pathophysiology of VM. We aimed to compare motion perception thresholds and the vegetative response to rotatory motion, as well as the vestibulo-ocular reflex (VOR) during rotation in VM patients compared to healthy controls (HC). Methods In this cross-sectional study, 28 female VM patients in the interictal state and 33 age- and gender-matched HC were investigated sitting in a motorized rotary chair shielded regarding visual and acoustic stimuli for 20 min with slowly increasing velocity (maximum = 72°/s). The motion perception threshold was indicated by the participants by pushing a button. During and after rotation, participants rated the presence and extent of motion sickness using a sickness rating scale. Results We detected lower motion perception thresholds (7.54°/s vs. 23.49°/s; p < 0.001) in VM patients compared to HC but no difference at the basic VOR thresholds. Furthermore, the patients showed enhanced susceptibility to motion sickness during and after the rotation. Conclusions We provide evidence for decreased motion perception thresholds and pronounced susceptibility to motion sickness in VM patients in the interictal state, which could indicate alterations in higher levels of vestibular processing. Future studies should determine whether this could be the pathophysiological hallmark of VM either as a unique disease entity or in differentiation from other forms of migraine.

ZUSAMMENFASSUNGSekundäre Kopfschmerzen, die auf die Exposition, den Übergebrauch oder den Entzug einer Substanz zurückzuführen sind, sind in Kapitel 8 der 3. Auflage der Internationalen Klassifikation von Kopfschmerzerkrankungen (ICHD-3) aufgeführt. Es werden 3 Unterkapitel unterschieden: 8.1. Kopfschmerz zurückzuführen auf Substanzgebrauch oder Substanzexposition, 8.2. Kopfschmerz zurückzuführen auf einen Medikamentenübergebrauch und 8.3. Kopfschmerz zurückzuführen auf den Entzug einer Substanz. Ersterer – Kopfschmerz zurückzuführen auf Substanzgebrauch oder Substanzexposition – bezieht sich auf einen Kopfschmerz mit Beginn unmittelbar oder innerhalb von Stunden nach der Exposition. Hingegen ist der „Kopfschmerz zurückzuführen auf einen Medikamentenübergebrauch“ (MOH) definiert als ein Kopfschmerz, der an 15 oder mehr Tagen pro Monat bei Patienten mit einer vorbestehenden primären Kopfschmerzerkrankung auftritt und sich als Folge der regelmäßigen Einnahme akuter Kopfschmerzmedikamenten über einen Zeitraum von mehr als 3 aufeinanderfolgende Monate entwickelt hat. Bezüglich letzterem, ist der Entzug von Koffein, Östrogen und Opioiden am häufigsten mit der Entwicklung von Kopfschmerzen assoziiert.Der vorliegende Artikel soll einen Überblick über die neuesten Erkenntnisse zur Klassifikation, Pathophysiologie und zu Behandlungsstrategien dieser sekundären Kopfschmerzentitäten geben und legt den Schwerpunkt dabei auf die Unterkapitel 8.1 und 8.2. der ICHD-3-Klassifikation.

Summary Background Prednisone is commonly used for initial short-term therapy of episodic cluster headaches before preventive medication such as verapamil becomes effective, but this strategy has not been tested in large randomised trials. We aimed to access the safety and efficacy of this treatment approach. Methods This study was a multicentre, randomised, double-blind, placebo-controlled trial done in ten specialised headache centres in Germany. Patients with episodic cluster headaches who were aged between 18 and 65 years and within a current pain episode for not more than 30 days, received 100 mg oral prednisone for 5 days followed by tapering of 20 mg every 3 days, or matching placebo (17 days total exposure). All patients received oral verapamil for long-term prevention, starting with 40 mg three times daily and increasing to 120 mg three times daily by day 19; patients then continued with verapamil 120 mg throughout the study. Randomisation was computer-generated at a 1:1 ratio by use of an interactive web-response system, with stratification according to age, sex, and participating site. Participants, investigators, and those assessing outcomes were unaware of treatment allocation. The primary endpoint was the mean number of attacks within the first week of treatment with prednisone compared with placebo. An attack was defined as a unilateral headache with moderate-to-severe intensity of at least five on a numerical rating scale. All efficacy and safety analyses were done in the modified intention-to-treat (mITT) population, which consisted of all patients who had been randomly assigned to a trial group and received at least one dose of prednisone or placebo. The study was stopped early due to slow recruitment and expired funding. The study was registered with EudraCT (2011–006204–13) and with the German Clinical Trials Register (DRKS00004716). Findings Between April 5, 2013, and Jan 11, 2018, 118 patients were enrolled in the study. Two patients dropped out immediately and 116 patients were randomly assigned (57 patients to prednisone and 59 patients to placebo); 109 patients were included in the mITT analysis (53 patients assigned to prednisone and 56 patients assigned to placebo). Participants in the prednisone group had a mean of 7·1 (SD 6·5) attacks within the first week compared with 9·5 (6·0) attacks in the placebo group (difference −2·4 attacks, 95% CI −4·8 to −0·03; p=0·002). Two serious adverse events occurred, both in the placebo group (inguinal hernia and severe deterioration of cluster headache). A total of 270 adverse events were observed: in the prednisone group, 37 (71%) of 52 patients reported 135 adverse events (most common were headache, palpitations, dizziness, and nausea) and in the placebo group, 39 (71%) of 55 patients had 135 adverse events (most common were nausea, dizziness, and headache). Interpretation Oral prednisone was an effective short-term preventive therapy in our population of patients with episodic cluster headache. Our findings support the use of prednisone as a first-line treatment in parallel to the up-titration of verapamil, although the efficacy of prednisone alongside other long-term prevention requires additional investigation. Funding German Federal Ministry for Education and Research.

Background Secondary headaches attributed to exposure to or the overuse of a substance are classified under chapter eight in the International Classification of Headache Disorders 3rd edition. Three distinct sub-chapters consider: 1. Headache attributed to exposure to a substance, 2. Medication overuse headache, and 3. Headache attributed to substance withdrawal. Headache attributed to exposure to a substance refers to a headache with onset immediately or within hours after the exposure, while medication overuse headache is a headache occurring on 15 or more days per month that has developed as a consequence of regular usage of acute headache medication(s) for more than three consecutive months in a patient with a pre-existing primary headache disorder. The withdrawal of caffeine, oestrogen, and opioids is most often associated with the development of headache. Discussion Despite the current headache classification, there is no certainty of a causal relationship between the use of any substance and the development of headache. Some substances are likely to provoke headache in patients that suffer from a primary headache disorder like migraine, tension-type headache or cluster headache, while others were described to cause headache even in people that generally do not get headaches. Toxic agents, such as carbon monoxide (CO) are difficult to investigate systematically, while other substances such as nitric oxide (NO) were specifically used to induce headache experimentally. If a patient with an underlying primary headache disorder develops a headache, in temporal relation to exposure to a substance, which is significantly worse than the usual headache it is considered secondary. This is even more the case if the headache phenotype is different from the usually experienced headache characteristics. Medication overuse headache is a well-described, distinct disease entity with only marginally understood pathophysiology and associated psychological factors. Managing medication overuse headache patients includes education, detoxification, prophylactic treatments and treating comorbidities, which is reflected in available guidelines. Viewing medication overuse headache as a separate entity helps clinicians and researchers better recognise, treat and study the disorder. Conclusion Identification of substances that may cause or trigger secondary headache is important in order to educate patients and health care professionals about potential effects of these substances and prevent unnecessary suffering, as well as deterioration in quality of life. Treatment in case of medication overuse and other chronic headache should be decisive and effective.

OBJECTIVE The aim of this study was to collect and rate Green Flags, that is, symptoms or pieces of information indicating that a patient is more likely to suffer from a primary than from a secondary headache. BACKGROUND When assessing headaches, a central question to be answered is whether the pain is primary or secondary to another disorder. To maximize the likelihood of a correct diagnosis, relevant signs and symptoms must be sought, identified, and weighed against each other. METHODS The project was designed as a Delphi study. In the first round, an expert panel proposed green flags that were rated anonymously in two subsequent rounds. Proposals with an average rating of 4.0 and higher on a scale from 0 to 5 reached consensus. RESULTS Five Green Flags reached consensus: (i) "The current headache has already been present during childhood"; (ii) "The headache occurs in temporal relationship with the menstrual cycle"; (iii) "The patient has headache-free days"; (iv) "Close family members have the same headache phenotype"; and (v) "Headache occurred or stopped more than one week ago." CONCLUSIONS We propose five Green Flags for primary headache disorders. None being a pathognomonic sign, we recommend searching for both Green Flags and Red Flags. If both are present, a secondary headache should be suspected. Overall, the application of the Green Flag concept in clinical practice is likely to increase diagnostic accuracy and improve diagnostic resource allocation. Prospective studies in clinical populations should be conducted to validate these Green Flags.

Chronic hepatitis C virus (HCV) infection is a highly prevalent systemic disease, which can cause a variety of neurological complications. The HCV-associated symptoms can be differentiated into central and peripheral nervous systems as well as the musculature. Important pathomechanisms are HCV-associated autoimmunity (e.g. mixed cryoglobulinemia with polyneuropathy) and direct neurotoxic effects of the virus (e.g. HCV-associated cognitive deficits). Distal symmetric polyneuropathies, small fiber neuropathies and cognitive deficits are the most prevalent neurological manifestations. Furthermore, HCV infection is a risk factor for ischemic and hemorrhagic stroke as well as Parkinson's disease. As HCV infection has become a permanently curable disease in90% of patients, early identification and antiviral treatment of HCV positive patients is of utmost importance.Die chronische Hepatitis-C-Virus(HCV)-Infektion ist eine hochprävalente Systemerkrankung, die verschiedene neurologische Komplikationen verursachen kann. Es lassen sich HCV-assoziierte Symptome im zentralen und peripheren Nervensystem sowie der Muskulatur unterscheiden. Wichtige Pathomechanismen sind die HCV-assoziierte Autoimmunität (z. B. gemischte Kryoglobulinämie mit Polyneuropathie) und direkte Neurotoxizität (z. B. bei HCV-assoziierten kognitiven Defiziten). Die häufigsten neurologischen Komplikationen sind distal-symmetrische Polyneuropathien, Small-fiber-Neuropathien und kognitive Defizite. Die HCV-Infektion stellt außerdem einen Risikofaktor für ischämische und hämorrhagische Schlaganfälle sowie den Morbus Parkinson dar. Die frühe Identifikation und antivirale Behandlung HCV-positiver Patienten steht im Zentrum der Behandlung. Durch neue antivirale Therapien können90 % der Patienten dauerhaft von der HCV-Infektion geheilt werden.

Chronic hepatitis C virus (HCV) infection is a highly prevalent systemic disease, which can cause a variety of neurological complications. The HCV-associated symptoms can be differentiated into central and peripheral nervous systems as well as the musculature. Important pathomechanisms are HCV-associated autoimmunity (e.g. mixed cryoglobulinemia with polyneuropathy) and direct neurotoxic effects of the virus (e.g. HCV-associated cognitive deficits). Distal symmetric polyneuropathies, small fiber neuropathies and cognitive deficits are the most prevalent neurological manifestations. Furthermore, HCV infection is a risk factor for ischemic and hemorrhagic stroke as well as Parkinson's disease. As HCV infection has become a permanently curable disease in >90% of patients, early identification and antiviral treatment of HCV positive patients is of utmost importance., Die chronische Hepatitis-C-Virus(HCV)-Infektion ist eine hochprävalente Systemerkrankung, die verschiedene neurologische Komplikationen verursachen kann. Es lassen sich HCV-assoziierte Symptome im zentralen und peripheren Nervensystem sowie der Muskulatur unterscheiden. Wichtige Pathomechanismen sind die HCV-assoziierte Autoimmunität (z. B. gemischte Kryoglobulinämie mit Polyneuropathie) und direkte Neurotoxizität (z. B. bei HCV-assoziierten kognitiven Defiziten). Die häufigsten neurologischen Komplikationen sind distal-symmetrische Polyneuropathien, Small-fiber-Neuropathien und kognitive Defizite. Die HCV-Infektion stellt außerdem einen Risikofaktor für ischämische und hämorrhagische Schlaganfälle sowie den Morbus Parkinson dar. Die frühe Identifikation und antivirale Behandlung HCV-positiver Patienten steht im Zentrum der Behandlung. Durch neue antivirale Therapien können >90 % der Patienten dauerhaft von der HCV-Infektion geheilt werden.

As discussed elsewhere in this book, there are several pharmacological and surgical treatments available for trigeminal neuralgia from which the majority of patients may expect substantial benefit. Neuromodulation methods are therefore usually considered as third- or fourth-line treatment options and limited to refractory and atypical cases. In contrast, management of painful trigeminal neuropathy is notoriously difficult and, importantly, unresponsive to surgical interventions known to be effective in trigeminal neuralgia. Neuromodulation offers an alternative worth considering for patients whose neuropathy pain is refractory to pharmacotherapy. In this chapter, we will discuss both central and peripheral neuromodulatory treatments that show promise, although the evidence base still remains narrow.

To compare a new method of noninvasive intracranial pressure (nICP) measurement with conventional lumbar puncture (LP) opening pressure.In a prospective multicenter study, patients undergoing LP for diagnostic purposes underwent intracranial pressure measurements with HeadSense, a noninvasive transcranial acoustic device, and indirectly with LP. Noninvasive measurements were conducted with the head in a 30° tilt and in supine position before and after LP. The primary endpoint was the correlation between nICP measurement in supine position before LP and the LP opening pressure.There was no correlation between supine nICPs before LP and the LP opening pressures (r = -0.211, P = 0.358). The 30° head-tilt nICPs correlated with the supine nICPs before LP (r = 0.830, P0.01). There was no correlation between supine nICPs before and after LP (r = 0.056, P = 0.831) or between 30° head-tilt nICPs and LP opening pressures (r = -0.038, P = 0.861).There was no correlation between nICPs and LP opening pressures. Further development is warranted before transcranial acoustic HeadSense can become a clinical tool for investigating patients with neurologic conditions.

Functional neuroimaging was able to identify key structures for the pathophysiology of trigeminal autonomic cephalalgias (TACs) including cluster headache, paroxysmal hemicrania, and short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing or cranial autonomic features and hemicrania continua. The posterior hypothalamus was the structure most consistently depicted with functional imaging in different states of disease with and without pain. Network-oriented imaging techniques such as resting-state functional resonance imaging were able to show a broader involvement of human trigeminal pain processing in the underlying pathophysiological mechanisms of the different TACs, highlighting similarities between this distinct group of primary headache disorders, while also demonstrating the differences in brain activation across these disorders. The most important clinical assignment for neuroimaging research from the treating physician remains the objective and reliable distinction of each individual TAC syndrome from one another, to make the correct clinical diagnosis as the foundation for proper treatment. More research will be necessary to fulfill this unmet need.

Dieser Artikel gibt eine Ubersicht uber die neuesten relevanten Informationen zu Thema Kopf- und Gesichtsschmerzen. Epidemiologische Daten aus neuen Studien z. B. zum Zusammenhang von Migrane mit einem PFO, dem kardiovaskularen Risiko, dem Verhalten der Migranekopfschmerzen wahrend und nach der Menopause und der Entwicklung von „White Matter Lesions“ und der Migrane Genetik werden berichtet. Zur Pathophysiologie der Migrane gibt es Neuigkeiten zur Aktivitat des Hypothalamus wahrend der Prodromalphase und dem Zusammenspiel von Hypothalamus und Hirnstamm. Bezuglich der Attackentherapie konnten im letzten Jahr aus Studien und Metanalysen neue Informationen zum Triptaneinsatz, der Behandlung der menstruellen Migranen und den hemiplegischen Migranevarianten generiert werden. Des Weiteren besteht Hoffnung fur die bereits verloren geglaubte Substanzgruppe der CGRP (calcitoningene related peptide)-Antagonisten, da die bisherigen Studiendaten zu Ubrogepant keinen Hinweis auf Hepatotoxizitat geben und die Wirksamkeit der Substanz belegen. Die Neuigkeiten zur Migraneprophylaxe konzentrieren sich grostenteils auf den Stand der Untersuchungen zur Behandlung mit monoklonalen Antikorpern gegen CGRP und dessen Rezeptor, aber auch weiter Studiendaten zu bekannten Migraneprophlaktika und neuen interessanten Ansatzen werden kompakt diskutiert. Des Weiteren werden Neuigkeiten bezuglich des Kopfschmerz bei Medikamentenubergebrauch und dem Kopfschmerz von Spannungstyp, ebenso wie fur die trigeminoautonomen Kopfschmerzen, die Trigeminusneuralgie und den „Neu aufgetretenen taglichen Kopfschmerz“ ubersichtlich dargestellt. A review of the latest and most relevant information on different disorders of head and facial pain is presented. News from epidemiologic studies regarding the relationship between migraine and patent foramen ovale, the cardiovascular risk in migraine, and migraine behavior during menopause, and the development of white matter lesions or migraine genetics are presented. Regarding pathophysiology there are very recent insights regarding the role of the hypothalamus during prodromal phase and the interplay of brain-stem and hypothalamus during the attack. In the last year studies and metaanalysis generated new knowledge for the use of triptans in general as in menstrual related migraine and hemiplegic variants. Furthermore, new hope rises for the CGRP (calcitonin-gene related peptide)-antagonists, as the data for ubrogepant do not suggest hepatotoxicity but efficacy. In prophylactic migraine treatment the news are manly on how the new therapeutic approach with monoclonal antibodies against CGRP or its receptor is moving on. Additional newly generated data for already known prophylactic agents as for new approaches are compactly discussed. Although main developments in headache focus on migraine new data on trigemino-autonomic headache trigeminal neuralgia and new daily persistant headache became available.

The modern antiretroviral treatment of human immunodeficiency virus (HIV-1) infection has considerably lowered the incidence of opportunistic infections. With the exception of the most severe dementia manifestations, the incidence and prevalence of HIV-associated neurocognitive disorders (HAND) have not decreased, and HAND continues to be relevant in daily clinical practice. Now, HAND occurs in earlier stages of HIV infection, and the clinical course differs from that before the widespread use of combination antiretroviral treatment (cART). The predominant clinical feature is a subcortical dementia with deficits in the domains concentration, attention, and memory. Motor signs such as gait disturbance and impaired manual dexterity have become less prominent. Prior to the advent of cART, the cerebral dysfunction could at least partially be explained by the viral load and by virus-associated histopathological findings. In subjects where cART has led to undetectable or at least very low viral load, the pathogenic virus-brain interaction is less direct, and an array of poorly understood immunological and probably toxic phenomena are discussed. This paper gives an overview of the current concepts in the field of HAND and provides suggestions for the diagnostic and therapeutic management.

This case describes a middle-aged man with anti-dipeptidyl-peptidase-like protein 6 (DPPX) encephalitis who exhibited the triad of memory loss, diarrhea, and tremor. The progression of his disease resembled neurodegenerative disease, and his first presentation at our department was 2 years after the first onset of symptoms. Antibodies against DPPX were positive in both serum and cerebrospinal fluid. No related tumor was found. The patient was initially treated with corticosteroid therapy and plasmapheresis. Despite moderate response to this treatment, corticosteroids were ceased because of adverse effects such as Cushing syndrome, deep vein thrombosis, and osteoporosis. After five cycles of treatment with rituximab, the patient experienced no further progression of neurologic symptoms and no adverse effects. The case adds to the understanding of the diagnosis, treatment, and potential prognosis of anti-DPPX encephalitis.

Bei der zervikalen spondylotischen Myelopathie kommt es zu einer Affektion des zervikalen Ruckenmarks durch Kompression im Rahmen einer Spondylose mit der entsprechenden klinischen Symptomatik. Der Spontanverlauf der Erkrankung kann interindividuell sehr variabel sein, was zu Unsicherheiten hinsichtlich Behandlungsindikationen und etwaiger Operationsentscheidung fuhrt. Die konservative Therapie muss von engmaschigen Kontrollen begleitet werden, damit bei weiterer Progredienz die operative Dekompression des Ruckenmarks weitere Markschaden verhindern kann. Die Art der Operation und der Zugangsweg hangen vom pathophysiologischen Mechanismus ab, der zu der Spinalkanalstenose gefuhrt hat und vom Allgemeinzustand des Patienten.