So far, no coherent and convincing theory has been developed to fully explain the pathogenesis of migraine, although many researchers and experts emphasize its association with spreading cortical depression, oxidative stress, vascular changes, nervous excitement, neurotransmitter release, and electrolyte disturbances. The contribution of magnesium deficiency to the induction of cortical depression or abnormal glutamatergic neurotransmission is a likely mechanism of the magnesium–migraine relationship. Hence, there is interest in various methods of assessing magnesium ion deficiency and attempts to study the relationship of its intra- and extracellular levels with the induction of migraine attacks. At the same time, many clinicians believe that magnesium supplementation in the right dose and form can be a treatment to prevent migraine attacks, especially in those patients who have identified contraindications to standard medications or their different preferences. However, there are no reliable publications confirming the role of magnesium deficiency in the diet as a factor causing migraine attacks. It also seems interesting to deepen the research on the administration of high doses of magnesium intravenously during migraine attacks. The aim of the study was to discuss the probable mechanisms of correlation of magnesium deficiency with migraine, as well as to present the current clinical proposals for the use of various magnesium preparations in complementary or substitute pharmacotherapy of migraine. The summary of the results of research and clinical observations to date gives hope of finding a trigger for migraine attacks (especially migraine with aura), which may turn out to be easy to diagnose and eliminate with pharmacological and dietary supplementation.

Consumption of caffeine in the diet, both daily and occasional, has a significant biological effect on the nervous system. Caffeine, through various and not yet fully investigated mechanisms, affects headaches. This is especially noticeable in migraine. In other headaches such as hypnic headache, post-dural puncture headache and spontaneous intracranial hypotension, caffeine is an important therapeutic agent. In turn, abrupt discontinuation of chronically used caffeine can cause caffeine-withdrawal headache. Caffeine can both relieve and trigger headaches.

Migraine is a chronic disease of global concern, regardless of socio-economic and cultural background. It most often and intensely affects young adults, especially women. Numerous mechanisms of a migraine attack have been identified (disturbances in the reaction of vessels, functions of neurotransmitters, cortical neurons, ion channels, receptors, the process of neurogenic inflammation), and many of its symptoms can be explained by activation of the hypothalamus and disturbances in its communication with other brain regions (including the brainstem). Numerous neuropeptides and neurochemical systems also play a role in migraine. One of them is melatonin, a hormone that allows the body to adapt to cyclically changing environmental and food conditions. In this article, we present the pathophysiological basis of melatonin release from the pineal gland and other tissues (including the intestines) under the influence of various stimuli (including light and food), and its role in stimulating the brain structures responsible for triggering a migraine attack. We analyze publications concerning research on the role of melatonin in various headaches, in various stages of migraine, and in various phases of the menstrual cycle in women with migraine, and its impact on the occurrence and severity of migraine attacks. Melatonin as an internally secreted substance, but also present naturally in many foods. It is possible to supplement melatonin in the form of pharmaceutical preparations, and it seems, to be a good complementary therapy (due to the lack of significant side effects and pharmacological interactions) in the treatment of migraine, especially: in women of childbearing age, in people taking multiple medications for other diseases, as well as those sensitive to pharmacotherapy.

So far, there is no consistent and convincing theory explaining the pathogenesis of migraines. Vascular disorders, the effect of oxidative stress on neurons, and the contribution of magnesium-calcium deficiencies in triggering cortical depression and abnormal glutaminergic neurotransmission are taken into account. However, there are no reliable publications confirming the role of dietary deficits of magnesium and latent tetany as factors triggering migraine attacks. The aim of the study was to evaluate the influence of latent magnesium deficiency assessed with the electrophysiological tetany test on the course of migraine. The study included: a group of 35 patients (29 women and six men; in mean age 41 years) with migraine and a control group of 24 (17 women and seven men; in mean age 39 years) healthy volunteers. Migraine diagnosis was based on the International Headache Society criteria, 3rd edition. All patients and controls after full general and neurological examination were subjected to a standard electrophysiological ischemic tetany test. Moreover, the level of magnesium in blood serum was tested and was in the normal range in all patients. Then, the incidence of a positive tetany EMG test results in the migraine group and the results in the subgroups with and without aura were compared to the results in the control group. Moreover, the relationship between clinical markers of spasmophilia and the results of the tetany test was investigated in the migraine group. As well as the relationship between migraine frequency and tetany test results. There was no statistically significant difference in the occurrence of the electrophysiological exponent of spasmophilia between the migraine and control group. Neither correlation between the occurrence of clinical symptoms nor the frequency of migraine attacks and the results of the tetany test was stated (p > 0.05). However, there was an apparent statistical difference between the subgroup of migraine patients with aura in relation to the control group (p < 0.05). The result raises hope to find a trigger for migraine attacks of this clinical form, the more that this factor may turn out to be easy to supplement with dietary supplementation.

Alcohol is a widely consumed beverage worldwide, and headaches, including migraine, tension-type headache (TTH), and other primary headaches, are common in the general population. Although epidemiological studies have shown a correlation between alcohol consumption and headaches, the specific pathophysiological mechanism of this headache remains unknown. We reviewed articles deemed relevant to the issue of alcohol as a trigger for various headaches, those that discussed alcohol consumption in these patient groups, and those that addressed the pathophysiological and clinical aspects of alcohol and headache. The review concluded that alcohol affects both migraine and non-migraine headaches. Alcohol-induced headache, classified as a secondary headache, is a throbbing, bilateral headache that is exacerbated by physical activity and is precipitated by alcohol consumption. TTH can be precipitated by alcohol consumption, and patients with TTH have more alcohol-related problems than those with migraine. Cluster headaches (CH) are often triggered by alcohol, but surprisingly, many CH patients consume alcohol, even during attacks. The relationship between alcohol and migraine is complex. Numerous components of alcoholic beverages can influence pain triggering and are responsible for migraine attacks. Red wine is one of the most frequently cited triggers for migraine attacks, a finding not always confirmed by the few prospective studies. However, there is no safe dose of alcohol, and therefore avoidance should be recommended.

The neuroinvasive and neurotropic character of coronaviruses is a likely reason for neurological complications which may occur during acute COVID illness and sometimes persist or newly emerge in the post-acute phase. Terminology and temporal classification remain heterogeneous. A retrospective case series was conducted in a single center (Department of Neurology, Bielański Hospital, Warsaw, Poland). Medical records from March 2020 to December 2023 were screened. Inclusion criteria: (1) confirmed SARS-CoV-2 infection (polymerase chain reaction or antigen test and radiological findings), (2) new neurological syndrome within acute, post-acute, or post-COVID interval, and (3) diagnostic documentation. Exclusion criteria: alternative established etiology fully explaining the neurological condition. Six cases were selected for detailed analysis due to diagnostic completeness as well as etiological and temporal diversity. Cases included: (1) persistent neurocognitive and sensory symptoms (post-COVID), (2) acute ischemic stroke with internal carotid artery dissection during severe COVID-19, (3) cytotoxic lesion of the corpus callosum (CLOCC) during acute COVID-19, (4) Guillain–Barré syndrome (post-acute), (5) longitudinally extensive transverse myelitis (post-acute), and (6) delayed autoimmune cerebral vasculitis (post-COVID). Neurological presentations ranged from mild persistent symptoms to fatal outcome. Neurological complications span inflammatory, vascular, and autoimmune mechanisms across distinct temporal phases of SARS-CoV-2 infection. Precise temporal classification and systematic diagnostic protocols are essential. Prospective longitudinal studies integrating biomarkers and standardized neuroimaging are required.