18 research outputs found
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