Cognitive dysfunction and migraine

Abstract Cognitive dysfunction has recently gained attention as a significant problem among migraine sufferers. All of the clinical studies show poor cognitive performance during migraine attacks, though, the interictal data are conflicting. Migraineurs show impaired cognitive function interictally in most of the clinic-based studies. Population-based studies did not reveal a difference in cognitive functions between migraineurs and controls. The specific cognitive domains involved are information processing speed, basic attention, executive functions, verbal and non-verbal memory and verbal skills. Neurophysiological, imaging and pharmacological studies support clinical symptoms of cognitive impairment in migraine. Longitudinal studies do not suggest progressive cognitive decline over time in migraine patients. Preventive medications and comorbid disorders such as depression and anxiety can impact cognitive function, but cannot fully explain the cognitive impairment in migraine. In contrast to migraine, tension type or cluster headache are not associated with cognitive impairment, at least during headache-free periods

Aura and Head pain:Relationship and gaps in the translational models

Migraine is a complex brain disorder and initiating events for acute attacks still remain unclear. It seems difficult to explain the development of migraine headache with one mechanism and/or a single anatomical location. Cortical spreading depression (CSD) is recognized as the biological substrate of migraine aura and experimental animal studies have provided mechanisms that possibly link CSD to the activation of trigeminal neurons mediating lateralized head pain. However, some CSD features do not match the clinical features of migraine headache and there are gaps in translating CSD to migraine with aura. Clinical features of migraine headache and results from research are critically evaluated; and consistent and inconsistent findings are discussed according to the known basic features of canonical CSD: typical SD limited to the cerebral cortex as it was originally defined. Alternatively, arguments related to the emergence of SD in other brain structures in addition to the cerebral cortex or CSD initiated dysfunction in the thalamocortical network are proposed. Accordingly, including thalamus, particularly reticular nucleus and higher order thalamic nuclei, which functions as a hub connecting the visual, somatosensory, language and motor cortical areas and subjects to modulation by brain stem projections into the CSD theory, would greatly improve our current understanding of migraine

Cognitive dysfunction and migraine

Cognitive dysfunction has recently gained attention as a significant problem among migraine sufferers. All of the clinical studies show poor cognitive performance during migraine attacks, though, the interictal data are conflicting. Migraineurs show impaired cognitive function interictally in most of the clinic-based studies. Population-based studies did not reveal a difference in cognitive functions between migraineurs and controls. The specific cognitive domains involved are information processing speed, basic attention, executive functions, verbal and non-verbal memory and verbal skills. Neurophysiological, imaging and pharmacological studies support clinical symptoms of cognitive impairment in migraine. Longitudinal studies do not suggest progressive cognitive decline over time in migraine patients. Preventive medications and comorbid disorders such as depression and anxiety can impact cognitive function, but cannot fully explain the cognitive impairment in migraine. In contrast to migraine, tension type or cluster headache are not associated with cognitive impairment, at least during headache-free periods

The effect of medial longitudinal arch height and medial longitudinal arch support insoles on postural balance in perimenopausal women

Background/aim: Changes in balance and postural control have been reported during the perimenopausal period. We investigated the effect of medial longitudinal arch height and medial arch support insoles on postural sway and balance in middle-aged perimenopausal women. Materials and methods: 29 women with normal arches and 29 women with low arches were included in the study. The foot arches of the participants were determined using the arch height index. The static balance index (SBI) measured by Kinesthetic Ability Trainer 3000 and functional reach test were used to evaluate postural balance. Measurements were obtained from all participants with and without medial arch support insoles. Results: The SBI-total scores without the insoles were found to be significantly higher in the lower arch group than in the normal arch group. SBI-total, SBI-anteroposterior, and SBI-mediolateral scores significantly improved in the low arch group in the presence of insoles, whereas the usage of insoles resulted in no difference in the normal arch group. In the presence of insoles, the reach distances to left and right sides increased in both groups, while the forward functional reach distances decreased. Conclusion: Medial longitudinal arch height and medial arch support insoles affect the balance parameters in perimenopausal women

Aura and Head pain: relationship and gaps in the translational models

Migraine is a complex brain disorder and initiating events for acute attacks still remain unclear. It seems difficult to explain the development of migraine headache with one mechanism and/or a single anatomical location. Cortical spreading depression (CSD) is recognized as the biological substrate of migraine aura and experimental animal studies have provided mechanisms that possibly link CSD to the activation of trigeminal neurons mediating lateralized head pain. However, some CSD features do not match the clinical features of migraine headache and there are gaps in translating CSD to migraine with aura. Clinical features of migraine headache and results from research are critically evaluated; and consistent and inconsistent findings are discussed according to the known basic features of canonical CSD: typical SD limited to the cerebral cortex as it was originally defined. Alternatively, arguments related to the emergence of SD in other brain structures in addition to the cerebral cortex or CSD initiated dysfunction in the thalamocortical network are proposed. Accordingly, including thalamus, particularly reticular nucleus and higher order thalamic nuclei, which functions as a hub connecting the visual, somatosensory, language and motor cortical areas and subjects to modulation by brain stem projections into the CSD theory, would greatly improve our current understanding of migraine

Behavioral and cognitive animal models in headache research

Abstract Animal models have provided a growing body of information about the pathophysiology of headaches and novel therapeutic targets. In recent years, experiments in awake animals have gained attention as more relevant headache models. Pain can be assessed in animals using behavioral alterations, which includes sensory-discriminative, affective-emotional and cognitive aspects. Spontaneous behavioral alterations such as increased grooming, freezing, eye blinking, wet dog shake and head shake and decreased locomotion, rearing, food or water consumption observed during pain episodes are oftentimes easy to translate into clinical outcomes, but are giving little information about the localization and modality of the pain. Evoked pain response such as tactile and thermal hypersensitivity measures are less translatable but gives more insight into mechanisms of action. Mechanical allodynia is usually assessed with von Frey monofilaments and dynamic aesthesiometer, and thermal allodynia can be evaluated with acetone evaporation test and Hargreaves’ test in animal models. Anxiety and depression are the most frequent comorbid diseases in headache disorders. Anxiety-like behaviors are evaluated with the open-field, elevated plus-maze or light/dark box tests. Interpretation of the latter test is challenging in migraine models, as presence of photophobia or photosensitivity can also be measured in light/dark boxes. Depressive behavior is assessed with the forced-swim or tail suspension tests. The majority of headache patients complain of cognitive symptoms and migraine is associated with poor cognitive performance in clinic-based studies. Cluster headache and tension type headache patients also exhibit a reversible cognitive dysfunction during the headache attacks. However, only a limited number of animal studies have investigated cognitive aspects of headache disorders, which remains a relatively unexplored aspect of these pathologies. Thus, the headache field has an excellent and growing selection of model systems that are likely to yield exciting advances in the future

Behavioral and cognitive animal models in headache research

Animal models have provided a growing body of information about the pathophysiology of headaches and novel therapeutic targets. In recent years, experiments in awake animals have gained attention as more relevant headache models. Pain can be assessed in animals using behavioral alterations, which includes sensory-discriminative, affective-emotional and cognitive aspects. Spontaneous behavioral alterations such as increased grooming, freezing, eye blinking, wet dog shake and head shake and decreased locomotion, rearing, food or water consumption observed during pain episodes are oftentimes easy to translate into clinical outcomes, but are giving little information about the localization and modality of the pain. Evoked pain response such as tactile and thermal hypersensitivity measures are less translatable but gives more insight into mechanisms of action. Mechanical allodynia is usually assessed with von Frey monofilaments and dynamic aesthesiometer, and thermal allodynia can be evaluated with acetone evaporation test and Hargreaves' test in animal models. Anxiety and depression are the most frequent comorbid diseases in headache disorders. Anxiety-like behaviors are evaluated with the open-field, elevated plus-maze or light/dark box tests. Interpretation of the latter test is challenging in migraine models, as presence of photophobia or photosensitivity can also be measured in light/dark boxes. Depressive behavior is assessed with the forced-swim or tail suspension tests. The majority of headache patients complain of cognitive symptoms and migraine is associated with poor cognitive performance in clinic-based studies. Cluster headache and tension type headache patients also exhibit a reversible cognitive dysfunction during the headache attacks. However, only a limited number of animal studies have investigated cognitive aspects of headache disorders, which remains a relatively unexplored aspect of these pathologies. Thus, the headache field has an excellent and growing selection of model systems that are likely to yield exciting advances in the future

Metoclopramide inhibits trigeminovascular activation: evidence for effective acute attack treatment in migraine

Background/aim: Metoclopramide is an effective and commonly used medication in acute migraine treatment but an experimental evidence base is lacking. We aimed to investigate the antimigraine effect of metoclopramide in a migraine model and whether the analgesic effect of metoclopramide was likely to be D-2 receptor-mediated. Materials and methods: Cortical spreading depression (CSD) was used to model migraine in adult male Wistar rats. Five CSDs were induced by pinprick. Metoclopramide (two different doses), raclopride, or 0.9\% saline were administered 30 min before CSD induction. Two hours after the experiments, brain tissues were examined for c-fos activation. Results: In metoclopramide groups brain stem c-fos expression was significantly lower than in the CSD side of the saline group (P = 0.002). In the raclopride group, ipsilateral brain stem c-fos expression was also lower than in the saline group (P = 0.002). No difference in c-fos expression in the ipsilateral trigeminal nucleus caudalis between the raclopride and metoclopramide groups was observed (P > 0.05). Conclusion: Metoclopramide is shown to suppress trigeminovascular activation for the first time, providing an experimental basis for its role in migraine. The analgesic effect of metoclopramide is likely to be mediated by D-2 receptors since raclopride, a selective D-2 receptor antagonist, suppresses trigeminovascular activation similarly

Somatosensory temporal discrimination remains intact in tension-type headache whereas it is disrupted in migraine attacks

Background and objective: Somatosensory temporal discrimination was recently reported as prolonged during migraine attacks, which is consistent with disrupted sensorial perception in migraine. However, knowledge about central sensory processing in tension-type headache is still lacking. This prospective, controlled study aimed to investigate somatosensory temporal discrimination thresholds in tension-type headache. Methods: The study included 10 tension-type headache patients, 10 migraine patients and 10 healthy volunteers without headache. Somatosensory temporal discrimination thresholds were evaluated during the headache attacks of tension-type headache and migraine patients. Results: Somatosensory temporal discrimination thresholds of tension-type headache patients (39.0 +/- 5.5ms for the right hand and 40.6 +/- 4.6ms for the left hand) were significantly lower than those of episodic migraine patients (137.1 +/- 35.8ms for the right hand and 118.4 +/- 34.3ms for the left hand, p < 0.0001 and p < 0.0001 respectively), and comparable to those of healthy volunteers (38.6 +/- 5.3ms for the right hand and 38.3 +/- 7.2ms for the left hand, p = 0.79 and p = 0.45 respectively). Conclusion: Central sensory processing, as tested by somatosensory temporal discrimination, was remarkably disrupted during the headache attacks in migraineurs, whereas it remained intact in the tension-type headache patients

Visual and Postural Motion-Evoked Dizziness Symptoms Are Predominant in Vestibular Migraine Patients

Background. Vestibular migraine (VM) is one of the most common underdiagnosed disorders. We aimed to study the clinical characteristics of VM patients who were referred to a neurology-headache unit by otolaryngology after exclusion of peripheral causes of vertigo. Methods. One hundred and one patients diagnosed with VM in the headache unit were included. Description of vestibular symptoms, demographic and clinical features, trigger factors, accompanying diseases, and response to vestibular-suppressant medications and prophylactic migraine treatment were evaluated. Results. Vestibular symptoms were triggered by daily head and body movements and mainly consisted of brief attacks lasting seconds (60.4\% of patients) although the total duration of the vestibular episode lasted hours or days. Other aggravating factors were moving visual stimuli, passive motion, and visually busy environments. Visually induced vestibular symptoms were defined by 71.3\% of the patients, and positional motion-induced vestibular symptoms were described by 82.2\% of the patients. Vestibular symptoms were mainly defined as feeling the ground slipping from under their feet (40.6\%), feeling like there is an earthquake or swaying (27.7\%), sensation of rocking on a boat (26.7\%), and sensation as if stepping on empty space (24.8\%). The majority of the patients (83.2\%) previously used vestibular-suppressant drugs, and these drugs were effective temporarily only in 12.9\%. Conclusions. Chronic recurrent dizziness symptoms, rather than internal or external vertigo, are predominant in our VM patients. Recurrent brief dizziness attacks induced upon routine visual and/or postural motion, longstanding symptoms with limited response to vestibular suppressants, and precipitation by typical migraine triggers are suggestive of VM