We studied the excitability of the visual and motor cortex in 36 patients with frequent migraine without aura (30 women, mean age 38.6 +/- 10.0 years) before and after treatment with topiramate (100 mg/day) using transcranial magnetic stimulation. Treatment with topiramate resulted in reduction of both headache frequency (12.0 +/- 1.3 to 5.8 +/- 3.2 migraine days per month; P = 0.004) and cortical excitability: motor cortex thresholds increased on the right side from 43.8 +/- 7.5% to 47.7 +/- 9.2% (P = 0.049) and on the left side from 43.4 +/- 7.0% to 47.2 +/- 9.6% (P = 0.047), and phosphene thresholds increased from 58.9 +/- 11.1% to 71.2 +/- 11.2% (P = 0.0001). Reduction of headache frequency correlated inversely with an increase of visual thresholds and did not correlate with motor thresholds. The effect of topiramate in migraine prevention is complex and can not be explained simply by inhibition of cortical excitability.
The review is devoted to the complex relationship between headache and sleep disorders. The shared neuroanatomical structures of the nervous system involved in pain perception and sleep are shown, and mechanisms of comorbidity between headaches and sleep disorders are considered. Various types of headaches in the continuum of the sleep–wake cycle are described. Both pharmacological and non-pharmacological approaches to treatment are examined in detail, with the biochemical basis of the drug action.
Objective In this narrative review, we summarize clinical and experimental data on the effect of light in migraine and discuss future prospects. Background Effective nonpharmacological treatment of hypersensitivity to light in migraine is an unmet clinical need. Current management strategies primarily consist of seeking a dark room and avoiding light exposure. Advances in the past 2 decades have improved our understanding of the underlying pathophysiology of how migraine is influenced by light. This may provide promising avenues for novel approaches in clinical management. Methods We searched MEDLINE for articles published from database inception up to September 1, 2021. We used the search term “migraine” with the search terms “light,” “photophobia,” “treatment,” “trigger,” “circadian rhythm,” “environment,” and/or “pathophysiology.” Results Light is commonly reported as a trigger factor of migraine attacks, however, early manifestation of photophobia and false attribution is likely the actual cause based on data deriving from retrospective, prospective, and experimental studies. The most common photophobia symptoms in migraine are exacerbation of headache by light and abnormal sensitivity to light with the underlying neural pathways likely being dependent on ongoing activity in the trigeminovascular system. Clinical studies and experimental models have identified mediators of photophobia and uncovered narrow wavebands of the light spectrum that may reduce pain intensity during a migraine attack. Consequently, novel devices have undergone exploratory clinical trials with promising results. Conclusion False attribution is likely the reason why light is commonly reported as a trigger factor of migraine attacks, and a prospective confirmation is required to prevent unnecessary avoidance. The observation that individuals with migraine are not equally photophobic to all wavebands of the light spectrum opens the potential for innovative pain management strategies. In this context, using human‐centric lighting (also called integrative lighting) to mimic the natural daylight cycle and avoid harmful wavebands through modern technology may prove beneficial. Future research should identify direct and indirect consequences of light and other environmental factors in migraine to fill out knowledge gaps and enable evidence‐based care strategies within institutions, work environments, and other settings.
These recommendations on the diagnosis and treatment of migraine were elaborated by Russian headache experts in accordance with the evidence-based practice. Together with the latest classification, diagnostic principles and criteria of different clinical sub-forms the consensus contains basic data on migraine epidemiology, pathophysiological mechanisms, differential diagnosis and most effective and evidence based approaches to pharmacological and non-pharmacological management of migraine patients.
Migraine is one of the most common types of headache, which can lead to a significant decrease in quality of life. Researchers identify migraine with aura, migraine without aura, and chronic migraine that substantially reduces the ability of patients to work and is frequently concurrent with mental disorders and drug-induced headache. The complications of migraine include status migrainosus, persistent aura without infarction, migrainous infarction (stroke), and a migraine aura-induced seizure. The diagnosis of migraine is based on complaints, past medical history, objective examination data, and the diagnostic criteria as laid down in the International Classification of Headache Disorders, 3 rd edition. Add-on trials are recommended only in the presence of red flags, such as the symptoms warning about the secondary nature of headache. Migraine treatment is aimed at reducing the frequency and intensity of attacks and the amount of analgesics taken. It includes three main approaches: behavioral therapy, seizure relief therapy, and preventive therapy. Behavioral therapy focuses on lifestyle modification. Nonsteroidal anti-inflammatory drugs, simple and combined analgesics, triptans, and antiemetic drugs for severe nausea or vomiting are recommended for seizure relief. Preventive therapy which includes antidepressants, anticonvulsants, beta-blockers, angiotensin II receptor antagonists, botulinum toxin type A-hemagglutinin complex and monoclonal antibodies to calcitonin gene-related peptide or its receptors, is indicated for frequent or severe migraine attacks and for chronic migraine. Pharmacotherapy is recommended to be combined with non-drug methods that involves cognitive behavioral therapy; progressive muscle relaxation; mindfulness; biofeedback; post-isometric relaxation; acupuncture; therapeutic exercises; greater occipital nerve block; non-invasive high-frequency repetitive transcranial magnetic stimulation; external stimulation of first trigeminal branch; and electrical stimulation of the occipital nerves (neurostimulation).
Контакты: Нина Владимировна Латышева ninalat@gmail.com В последние годы достигнуты значительные успехи мировой медицины в понимании причин и механизмов развития, а также в уточнении диагностических критериев и изучении терапевтических подходов при хронической мигрени (ХМ).
Cerebral infantile paralysis (CIP) is the main neurologic reason of children's disability all over the world. A competent choice of time and methods of rehabilitation allows social adaptation of children with this pathology and improves their motor and mental development prognosis. The article gives modern data on the neuronal plasticity, spare capacities of the developing brain, pathophysiological aspects of restoration and compensation of damaged structures of central nervous system. The emphasis is put on the consideration of neuroplasticity mechanisms from the point of view of their clinical relevance and role in the formation of pathological and compensatory patterns of movement and perception at CIP. Variants of restoration of motor and sensory functions in upper extremities of children with CIP based on the time and topics of brain damage are analyzed in detail. Approaches to pathogenetically grounded choice of methods and time of rehabilitation are discussed on the basis of the given data on spare capabilities of children's nervous system with the emphasis on restoration of upper extremities' function as one of the most complicated, although prospective, aspects of CIP treatment.
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