A thorough investigation into the correlation between migraines and the gut microbiome: an in-depth analysis using Mendelian randomization studies.

Objective: A growing body of evidence underscores a significant association between neurological disorders, particularly migraines, and the gut microbiota. However, a research gap persists in understanding the cause-and-effect dynamics between these elements. Therefore, we employed robust methodologies aimed at thoroughly exploring the causal relationship between the gut microbiome and migraines. Methods: Employing bidirectional Two Sample Mendelian Randomization (TSMR) analysis, we investigated the causal association between the composition of the gut microbiota and migraines. Data summarizing the relationship between gut microbiota and migraines were extracted from one or more genome-wide association studies. The TSMR analysis employed five methods to assess the correlation between the gut microbiota and migraines, with the inverse variance-weighted method serving as the primary approach for analyzing causal links. Sensitivity analyses were applied to address horizontal pleiotropy and heterogeneity. Simultaneously, a meta-analysis was performed to strengthen the robustness of the findings. Additionally, a reverse TSMR was carried out to explore potential occurrences of reverse causal relationships. Results: The ongoing TSMR analysis identified a collection of 14 bacterial taxa connected to migraines. Among these, 8 taxa exhibited a protective effect, while 5 taxa had a detrimental impact, and 1 taxon maintained a neutral relationship. The reverse Mendelian randomization analysis highlighted stable outcomes for only one bacterial taxonomic group. Conclusion: The study confirms a causal relationship between the gut microbiota and migraines, offering a new perspective for migraine research. Strategically targeting specific bacterial taxa with dysregulation may be effective in both preventing and treating migraines, thus opening new avenues for therapeutic strategies.

Resolution of Sporadic Hemiplegic Migraine by Correcting a Cervical Spine Kyphosis Utilizing the Chiropractic BioPhysics® (CBP®) Technique: A Case Report With Long-Term Follow-Up.

A 19-year-old male suffered from sporadic hemiplegic migraine (SHM) for several years and experienced significant pain and disability with sensory and motor disturbances during the migraine headaches. Weakness, abnormal vision, abnormal sensation, one-sided disabling motor weakness, and other signs of SHM were diagnosed. The patient had received previous physical therapy, chiropractic and over-the-counter medications, as well as migraine-specific prescriptions without lasting improvements. Chiropractic BioPhysics® (CBP®) spinal structural rehabilitation protocols were used to increase cervical lordosis and improve cervical muscular strength, mobility, and posture. These protocols include spine-specific prescriptions for Mirror Image® postural exercises, traction, and spinal manipulative therapy. After 24 treatments over eight weeks, all subjective and objective outcomes improved dramatically with a near resolution of all initial symptoms of SHM. There were a significant increase in cervical lordosis and a reduction in forward head posture. The neck disability index improved from 26% to 6%, and all pain scores for all regions improved following treatment. A 10-month follow-up exam showed the outcomes were maintained. SHM is rare and debilitating, is part of the global burden of disease, and is a major cause of disability in the world. Reports of successful conservative and non-conservative long-term treatments for SHM are rare, and there are no clinical trials showing successful treatments for SHM. This successful case demonstrates preliminary evidence that CBP spinal structural rehabilitation may serve as a treatment option for SHM. Future studies are needed to replicate the findings from this case.

[The hereditary vessel disease CADASIL].

Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL) is a hereditary small vessel disease of the brain characterized by progressive white matter lesions, subcortical infarcts, and cognitive decline. This autosomal dominant disorder is caused by mutations in the NOTCH3 gene located on chromosome 19, resulting in the accumulation of granular osmiophilic material within the walls of small arteries and arterioles. Clinically, CADASIL typically manifests in mid-adulthood with recurrent ischemic events, migraine with aura, mood disturbances, and cognitive impairment. Neuroimaging plays a crucial role in the diagnosis of CADASIL, with characteristic findings including white matter hyperintensities particularly in the anterior temporal lobe and external capsule.

Migraine-like headache with aura induced by a small infarct in the parieto-occipital cortex: A case report.

A 56-year-old right-handed man was referred to our hospital for evaluation of sudden-onset transient quadrantanopia, which was followed by throbbing headache consistent with migraine with aura (MA). Magnetic resonance imaging (MRI) of the right parieto-occipital cortex on admission showed a hyperintense region on diffusion-weighted imaging, which disappeared 7 days later. A small cortical infarct in the parieto-occipital cortex can cause MA-like headache, and the present infarct lesion was only detectable on MRI during the acute phase. Performing MRI for patients with suspected acute MA might help identify the cause of MA-like headache and ensure appropriate management of patients.

The Dawn and Advancement of the Knowledge of the Genetics of Migraine.

Background: Migraine is a prevalent episodic brain disorder known for recurrent attacks of unilateral headaches, accompanied by complaints of photophobia, phonophobia, nausea, and vomiting. Two main categories of migraine are migraine with aura (MA) and migraine without aura (MO). Main body: Early twin and population studies have shown a genetic basis for these disorders, and efforts have been invested since to discern the genes involved. Many techniques, including candidate-gene association studies, loci linkage studies, genome-wide association, and transcription studies, have been used for this goal. As a result, several genes were pinned with concurrent and conflicting data among studies. It is important to understand the evolution of techniques and their findings. Conclusions: This review provides a chronological understanding of the different techniques used from the dawn of migraine genetic investigations and the genes linked with the migraine subtypes.

A Rare Case of Sporadic Hemiplegic Migraine Mimicking Stroke: A Diagnostic Challenge Solved by Comprehensive History Taking.

Migraine, a common affliction, manifests as debilitating headaches often accompanied by auras. However, hemiplegic migraine presents an unusual symptomatology, inducing unilateral paralysis during attacks. This condition, occurring in two forms, familial and sporadic, merits attention due to its rarity. To raise awareness of this ailment, we recount the case of a 33-year-old woman. This instance serves as a poignant reminder of the potential severity and complexity of hemiplegic migraines. By shedding light on this less-understood variant, we aim to enhance recognition and understanding within medical communities and among the general public. Additionally, emphasizing the importance of thorough history taking in identifying characteristic features, such as the presence of auras or unilateral paralysis preceding headaches, is paramount. Understanding these nuances aids in accurate diagnosis and formulation of tailored management strategies. It's imperative to recognize the distinct characteristics of hemiplegic migraines to ensure timely and appropriate management for affected individuals, offering them relief and improving their quality of life.

A Case of Multiple Cerebral Infarcts Due to Severe Anemia Preceded by Migraine-like Headache with Aura.

We herein report a 47-year-old woman who developed migraine-like headache with aura and subsequent multiple cerebral infarcts, likely due to severe iron deficiency anemia (IDA) from menorrhagia. The progression from IDA to ischemic stroke involves several pathophysiological mechanisms, including reduction of erythrocyte deformability, reactive thrombocytosis, and anemic hypoxia. We speculate that a microembolus first caused cortical spreading depression without infarcts and that a larger thromboembolus then caused multiple infarcts. This case highlights the transition from migraine-like headache to ischemic stroke. New-onset migraine-like headache is a warning of impending ischemic stroke, and IDA may be a potential underlying cause.

Migraine aura discrimination using machine learning: an fMRI study during ictal and interictal periods.

Functional magnetic resonance imaging (fMRI) studies on migraine with aura are challenging due to the rarity of patients with triggered cases. This study optimized methodologies to explore differences in ictal and interictal spatiotemporal activation patterns based on visual stimuli using fMRI in two patients with unique aura triggers. Both patients underwent separate fMRI sessions during the ictal and interictal periods. The Gaussian Process Classifier (GPC) was used to differentiate these periods by employing a machine learning temporal embedding approach and spatiotemporal activation patterns based on visual stimuli. When restricted to visual and occipital regions, GPC had an improved performance, with accuracy rates for patients A and B of roughly 86-90% and 77-81%, respectively (p < 0.01). The algorithm effectively differentiated visual stimulation and rest periods and identified times when aura symptoms manifested, as evident from the varying predicted probabilities in the GPC models. These findings contribute to our understanding of the role of visual processing and brain activity patterns in migraine with aura and the significance of temporal embedding techniques in examining aura phenomena. This finding has implications for diagnostic tools and therapeutic techniques, especially for patients suffering from aura symptoms.

Signatures of migraine aura in high-density-EEG.

OBJECTIVE: Cortical spreading depolarization is highly conserved among the species. It is easily detectable in direct cortical surface recordings and has been recorded in the cortex of humans with severe neurological disease. It is considered the pathophysiological correlate of human migraine aura, but direct electrophysiological evidence is still missing. As signatures of cortical spreading depolarization have been recognized in scalp EEG, we investigated typical spontaneous migraine aura, using full band high-density EEG (HD-EEG). METHODS: In this prospective study, patients with migraine with aura were investigated during spontaneous migraine aura and interictally. Time compressed HD-EEG were analyzed for the presence of cortical spreading depolarization characterized by (a) slow potential changes below 0.05 Hz, (b) suppression of faster activity from 0.5 Hz - 45 Hz (c) spreading of these changes to neighboring regions during the aura phase. Further, topographical changes in alpha-power spectral density (8-14 Hz) during aura were analyzed. RESULTS: In total, 26 HD-EEGs were recorded in patients with migraine with aura, thereof 10 HD-EEGs during aura. Eight HD-EEGs were recorded in the same subject. During aura, no slow potentials were recorded, but alpha-power was significantly decreased in parieto-occipito-temporal location on the hemisphere contralateral to visual aura, lasting into the headache phase. Interictal alpha-power in patients with migraine with aura did not differ significantly from age- and sex-matched healthy controls. CONCLUSIONS: Unequivocal signatures of spreading depolarization were not recorded with EEG on the intact scalp in migraine. The decrease in alpha-power contralateral to predominant visual symptoms is consistent with focal depression of spontaneous brain activity as a consequence of cortical spreading depolarization but is not specific thereof. SIGNIFICANCE: Cortical spreading depolarization is relevant in migraine, other paroxysmal neurological disorders and neurointensive care.

Causal association between systemic lupus erythematosus and the risk of migraine: A Mendelian randomization study.

BACKGROUND: Numerous studies have found that patients with systemic lupus erythematosus (SLE) often have comorbid headache, especially migraine. However, the causal relationship between genetically determined SLE and migraine risk remains unclear. Therefore, we conducted a Mendelian randomization (MR) study to explore this causal association. METHODS: Genome-wide association studies (GWAS) provided the instrumental variables. We selected summary data from GWAS of SLE as exposure (5201 SLE patients and 9066 controls). Both outcome GWAS data were from the Finnish Gene GWAS, including migraine with aura, migraine with aura and triptan purchases, and migraine without aura. The main MR approach was inverse-variance weighted. Pleiotropy and heterogeneity were detected using the MR pleiotropy residual sum and outlier, MR-Egger intercept test, leave-one-out analysis, and Cochran's Q test. RESULTS: There was a significant association between genetically predicted SLE susceptibility and increased risk of migraine with aura [odds ratio (OR) = 1.05, 95% confidence interval (CI) = 1.02-1.08, p = .001]. The result was consistent when the outcome was migraine with aura and triptan purchases [OR = 1.05, 95% CI = 1.02-1.08, p = .001]. However, we found no association between SLE and migraine without aura. Our MR study showed no pleiotropy or heterogeneity. CONCLUSIONS: Our study indicates that genetic susceptibility to SLE increases the incidence of migraine with aura but not migraine without aura. It is necessary for the routine evaluation and early recognition of migraine in patients with SLE in clinical settings.

Hemiplegic migraine.

Hemiplegic migraine (HM) is a rare subtype of migraine with aura in which the aura phase includes transient motor weakness. Diagnosis is based on the International Classification of Headache Disorders criteria (ICHD-3). The most important diagnostic tools remain a patient interview, neurological examination during attacks, and exclusion of other disorders, such as epilepsy, stroke, encephalitis and secondary headache syndromes. Hemiplegic migraine can occur either familial or sporadic. Three genes, CACNA1A, ATP1A2, and SCN1A have been identified. Taken together, mutations in these three genes predict increased neurotransmitter and potassium ion levels at the synaptic cleft, which facilitates cortical spreading depolarization, the phenomenon underlying the migraine aura. The presence of several symptoms, including extensive weakness and brainstem manifestations increase the likelihood of finding a monogenic cause. While the diagnosis can be confirmed by genetic testing, it cannot be excluded if one of the known (F)HM genes is not implicated. Most patients with hemiplegic migraine without a mutation in CACNA1A, ATP1A2, or SCN1A display a mild phenotype that is more akin to that of common (nonhemiplegic) migraine. Additional diagnostics such as brain imaging, cerebrospinal fluid analysis or an electroencephalography are mainly performed to exclude other causes of focal neurologic symptoms associated with hemiparesis and headache. Due to the rarity of the disorder, current treatment recommendations are based on small, unblinded studies and empirical data.

Migrainous infarction.

Migrainous infarction is defined as a migraine attack occurring as migraine with aura, typical of the patient's previous attacks, except that one or more aura symptoms persist for >60min, and neuroimaging demonstrates ischemic infarct in the relevant area. To better understand migrainous infarction, one must disentangle the complex interactions between migraine and stroke. In this chapter, we first discuss the migraine-stroke association in sections including "Increased Risks of Stroke and Subclinical Infarcts in Patients With Migraine," "Migrainous Headache Cooccurring or Triggered by Ischemic Stroke," "Stroke Progression in Patients With Migraine," and "Clinic Conditions Associated With Higher Risks of Both Migraine and Stroke." As an extreme example of migraine-stroke association, the annual incidence of migrainous infarction was reported to be 0.80/100,000/year, with the incidence in females nearly twofold that of male patients. Patients diagnosed with migrainous infarction are typically younger (average age 29-39 in case series), have fewer traditional vascular risk factors, and have more favorable prognosis compared to strokes from traditional risk factors. Thorough evaluation is recommended to rule out other etiologies of stroke. Patients diagnosed with migrainous infarction should receive antiplatelet therapy and migraine preventive therapy to avoid future events. Vasoactive medications, including triptans and ergots, should be avoided.

Clinical features of migraine with aura: a REFORM study.

BACKGROUND: About one-third of persons with migraine experience transient neurologic symptoms, referred to as aura. Despite its widespread prevalence, comprehensive clinical descriptions of migraine with aura remain sparse. Therefore, we aimed to provide an in-depth phenotypic analysis of aura symptoms and characteristics in a cross-sectional study of a large sample of adults diagnosed with migraine with aura. METHODS: Data were extracted from the baseline characteristics of participants in the Registry for Migraine (REFORM) study - a single-center, prospective, longitudinal cohort study. Participants were adults diagnosed with migraine aura, reporting ≥ 4 monthly migraine days in the preceding 3 months. Trained personnel conducted in-person semi-structured interviews, capturing details on the nature, duration, localization, and progression of individual aura symptoms. RESULTS: Of the 227 enrolled participants with migraine with aura, the mean age was 41.1 years, with a predominant female representation (n = 205 [90.3%]). Visual aura was present in 215 (94.7%) participants, somatosensory aura in 81 (35.7%), and speech and/or language aura in 31 (13.7%). A single type of aura was observed in 148 (65.2%) participants, whilst 79 (34.8%) reported multiple aura types. Most participants (n = 220 [96.9%]) described their aura symptoms as positive or gradually spreading. Headache in relation to aura was noted by 218 (96.0%) participants, with 177 (80.8%) stating that the onset of aura symptoms preceded the onset of headache. CONCLUSIONS: This study offers a detailed clinical depiction of persons with migraine with aura, who were predominantly enrolled from a tertiary care unit. The findings highlight potential gaps in the available literature on migraine with aura and should bolster clinicians' acumen in diagnosing migraine with aura in clinical settings.

Increased Cardio-ankle Vascular Index Values in Migraine Patients With Aura.

Patients with migraine with aura are at an increased risk of cardiovascular disease. There are limited data on arterial stiffness in migraine patients with aura. The present study evaluated arterial stiffness in these patients using the cardio-ankle vascular index (CAVI). This prospective study included 50 patients with migraine with aura (43 female, mean age 38.9 ± 9.9 years). The patient group was matched for age and gender with 50 healthy individuals with no history of migraine (43 female, mean age 39.3 ± 10.3 years). All patients and control subjects underwent a comprehensive clinical evaluation by an experienced neurologist and were interviewed about their headache histories. There was no significant difference in baseline demographic characteristics and echocardiographic parameters between migraine with aura patients and the control group. Both right and left CAVI values were significantly higher in the patients with migraine with aura (6.5 ± 1.2 vs 6.1 ± 0.7, P = .043 and 6.6 ± 1.2 vs 6.1 ± 0.7, P = .009, respectively). Arterial stiffness is an important mediator of cardiovascular diseases. We found that CAVI, a novel marker of the arterial stiffness, is increased in patients with migraine with aura.

Brain connectome-based imaging markers for identifiable signature of migraine with and without aura.

Background: Cortical spreading depression (CSD) has been considered the prominent theory for migraine with aura (MwA). However, it is also argued that CSD can exist in patients in a silent state, and not manifest as aura. Thus, the MwA classification based on aura may be questionable. This study aimed to capture whole-brain connectome-based imaging markers with identifiable signatures for MwA and migraine without aura (MwoA). Methods: A total of 88 migraine patients (32 MwA) and 49 healthy controls (HC) underwent a diffusion tensor imaging and resting-state functional magnetic resonance imaging scan. The whole-brain structural connectivity (SC) and functional connectivity (FC) analysis was employed to extract imaging features. The extracted features were subjected to an all-relevant feature selection process within cross-validation loops to pinpoint attributes demonstrating substantial efficacy for patient categorization. Based on the identified features, the predictive ability of the random forest classifiers constructed with the 88 migraine patients' sample was tested using an independent sample of 32 migraine patients (eight MwA). Results: Compared to MwoA and HC, MwA showed two reduced SC and six FC (five increased and one reduced) features [all P<0.01, after false discovery rate (FDR) correction], involving frontal areas, temporal areas, visual areas, amygdala, and thalamus. A total of four imaging features were significantly correlated with clinical rating scales in all patients (r=-0.38 to 0.47, P<0.01, after FDR correction). The predictive ability of the random forest classifiers achieved an accuracy of 78.1% in the external sample to identify MwA. Conclusions: The whole-brain connectivity features in our results may serve as connectome-based imaging markers for MwA identification. The alterations of SC and FC strength provide possible evidence in further understanding the heterogeneity and mechanism of MwA which may help for patient-specific decision-making.

No wearing-off effect of erenumab or fremanezumab for chronic migraine prevention: a single-center, real-world, observational study.

BACKGROUND: The present study investigates the wearing-off effect in adults with chronic migraine treated with erenumab or fremanezumab. METHODS: This real-world observational study was based on pre-collected headache diaries from chronic migraine patients in treatment with either monthly injections of 140 mg of erenumab or 225 mg of fremanezumab. Consistent wearing-off was defined as an increase of ≥2 weekly migraine days in the last week compared to the second week over two consecutive 4-week treatment periods. The primary endpoint was wearing-off in the total population. The secondary endpoints were difference in wearing-off in (i) a subgroup of patients treated with erenumab and fremanezumab and (ii) consistent wearing-off in patients with a ≥30% reduction in monthly migraine days, compared to baseline, in the two consecutive treatment months. RESULTS: In total, 100 patients (erenumab: n = 60, fremanezumab: n = 40) were included. Sixty-two out of 100 (62%) patients had consistent ≥30% treatment response on antibody therapy in both months (erenumab: n = 36, fremanezumab: n = 26). There was no consistent wearing-off over the two consecutive months from week 2 to week 4 (3.04%, p = 0.558). There was no wearing-off within the erenumab (p = 0.194) or the fremanezumab (p = 0.581) groups. Among the ≥30% treatment responders, there was no consistent wearing-off over the two consecutive months (2.6%, p = 0.573). CONCLUSIONS: There was no wearing-off in treatment responders, which is in alignment with premarketing data from placebo-controlled phase III studies. These data suggest that patients should be informed upfront that no wearing-off effect is expected because anxiety for attacks at the end of the month per se may generate migraine attacks.

Temporal Changes in Cerebral Blood Flow during Migraine with Aura of Alternating Left and Right Homonymous Hemianopsia.

A 16-year-old boy presented with sudden left homonymous hemianopsia followed by right ocular and occipital pain. Arterial spin labeling (ASL), a non-contrast magnetic resonance imaging technique used to evaluate perfusion, showed a decrease in cerebral blood flow in the right occipital lobe. Three hours after admission, the patient experienced right homonymous hemianopsia and ocular-to-occipital pain on the contralateral side. ASL revealed a decreased cerebral blood flow in the left occipital lobe. We ultimately diagnosed the patient with first-time migraine with aura, in which cortical spreading depression was visualized as decreased cerebral blood flow using ASL.

Increased presynaptic excitability in a migraine with aura mutation.

Migraine is a common and disabling neurological disorder. The headache and sensory amplifications of migraine are attributed to hyperexcitable sensory circuits, but a detailed understanding remains elusive. A mutation in casein kinase 1 delta (CK1δ) was identified in non-hemiplegic familial migraine with aura and advanced sleep phase syndrome. Mice carrying the CK1δT44A mutation were more susceptible to spreading depolarization (the phenomenon that underlies migraine aura), but mechanisms underlying this migraine-relevant phenotype were not known. We used a combination of whole-cell electrophysiology and multiphoton imaging, in vivo and in brain slices, to compare CK1δT44A mice (adult males) to their wild-type littermates. We found that despite comparable synaptic activity at rest, CK1δT44A neurons were more excitable upon repetitive stimulation than wild-type, with a reduction in presynaptic adaptation at excitatory but not inhibitory synapses. The mechanism of this adaptation deficit was a calcium-dependent enhancement of the size of the readily releasable pool of synaptic vesicles, and a resultant increase in glutamate release, in CK1δT44A compared to wild-type synapses. Consistent with this mechanism, CK1δT44A neurons showed an increase in the cumulative amplitude of excitatory post-synaptic currents, and a higher excitation-to-inhibition ratio during sustained activity compared to wild-type. At a local circuit level, action potential bursts elicited in CK1δT44A neurons triggered an increase in recurrent excitation compared to wild-type, and at a network level, CK1δT44A mice showed a longer duration of 'up state' activity, which is dependent on recurrent excitation. Finally, we demonstrated that the spreading depolarization susceptibility of CK1δT44A mice could be returned to wild-type levels with the same intervention (reduced extracellular calcium) that normalized presynaptic adaptation. Taken together, these findings show a stimulus-dependent presynaptic gain of function at glutamatergic synapses in a genetic model of migraine, that accounts for the increased spreading depolarization susceptibility and may also explain the sensory amplifications that are associated with the disease.

Migraine in an Adolescent with a Pineal Cyst Treated with Classical Individualized Homeopathy: A Case Report.

BACKGROUND: Migraine is one of the leading causes of morbidity and disability in the world. Its prevalence ranges from 5 to 40% in the pediatric population, with about 50% of these headaches continuing to adulthood. Incidental diagnosis of pineal cysts (PCs) is on the rise with the evolution of imaging techniques; the causal relationship of PC and individuals with headache however remains controversial, and complete resolution is uncommon. Conventional medicine stresses on the importance of tailored therapy in the management of pediatric migraine. CASE REPORT: An 11-year-old female, diagnosed with migraine with an aura and PC, was benefitted by individualized classical homeopathic therapy using the homeopathic preparation Phosphorous and Natrum muriaticum. The symptoms of migraine improved, and the incidentally diagnosed PC completely resolved during the course of treatment. CONCLUSION: Individualized classical homeopathy may have a role in effectively treating migraines and PCs in the pediatric population. There is a need for further scientific investigation with well-designed studies to prove the effectiveness of this therapeutic method, taking care to maintain the individualization principle of classical homeopathy.Migräne ist eine der führenden Ursachen für Krankheitslast und Behinderung weltweit. Ihre Prävalenz bei Kindern und Jugendlichen liegt im Bereich von 5­40%; hiervon sind etwa 50% bis ins Erwachsenenalter von den Kopfschmerzen betroffen. Zufallsdiagnosen von Pinealiszysten (PC) kommen im Zuge des Fortschritts bei den bildgebenden Verfahren immer häufiger vor, jedoch ist ein kausaler Zusammenhang der PC mit Kopfschmerzen umstritten, und ein vollständige Rückbildung kommt nicht häufig vor. Die Schulmedizin betont, wie wichtig eine maßgeschneiderte Therapie bei der Behandlung der Migräne im Kindesalter ist.Ein 11-jähriges Mädchen, bei dem eine Migräne mit Aura und eine Pinealiszyste diagnostiziert wurde, profitierte von einer individualisierten klassisch-homöopathischen Therapie mit den homöopathischen Präparaten Phosphorus und Natrum muriaticum. Die Migränesymptome besserten sich, und die zufällig diagnostizierte Pinealiszyste bildete sich im Laufe der Behandlung vollständig zurück.Die individualisierte klassische Homöopathie kann bei der wirksamen Behandlung von Migräne und Pinealiszysten bei Kindern und Jugendlichen eine Rolle spielen. Es bedarf weiterer wissenschaftlicher Untersuchungen mit gutem Studiendesign, um die Wirksamkeit dieser Behandlungsmethode nachzuweisen, wobei darauf zu achten ist, das Individualisierungsprinzip der klassischen Homöopathie aufrechtzuerhalten.

A Case of Migraine Aura Status in a Migraine Patient With Typical Aura Without Headache.

Migraine aura status (MAS) is a rare complication of migraine and is listed in the appendix of the International Classification of Headache, Third Edition. MAS occurs in migraine with aura (MwA) patients, with at least three auras occurring over a period of three days. We describe a case of MAS associated with a patient who had a migraine with a typical aura without headache (TAWH). She has experienced only visual auras, including periods of MAS complications, and has not experienced headaches or other auras, including sensory, speech, and motor. The patient is a 45-year-old woman. She had discomfort with visual aura without a headache every two to three months. The visual aura began to gradually darken a portion of the right side of the visual field binocularly, which gradually expanded around it and was surrounded by iridescent flashes running in a zig-zag pattern to the periphery. The area of the visual field abnormality gradually decreased and disappeared after approximately 15 minutes. One day, she had an aura once after dinner, and when she awoke without any trigger after going to bed, the aura appeared and repeated approximately three times. She experienced three to four auras the next day and the day after. In the six-month follow-up period, there was no further recurrence of MAS. Most previous reports of MAS have been associated with typical MwA, and there have been few other reports of MAS associated with TAWH as far as we could investigate.