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Corresponding author. Yaxi Chen , R. The orbito-frontal cortex is thought to modulate habituation mechanisms [45] and orbito-frontal lesions induce SEP sensitization and lack of habituation [46], precisely the two sensory abnormalities we found in patients with MOH. Sydney, Australia, 17 – 20 June, Stockholm, Sweden, August 30 – September 2, It is likely that the disclosure of this peculiar electrophysiological pattern was made possible by the fact that we avoided to record MOH patients during a full-blown migraine attack. Moreover, only adults living in private households were contacted, hospitalized adults or adults living in care homes could not be considered.❿
 
 

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Background Medication-overuse headache MOH is a complication of episodic headaches characterized by more than 15 headache days per month and arising from an excessive intake of analgesics or specific anti-migraine drugs, or both [1]. Link to Journal bib. We also sought possible correlations between the electrophysiological patterns and clinical features including duration of migraine history, duration of headache chronification and class of drugs overused. Physical disability following fractures affects the capacity for independent living and complicates social participation. The combination of an initial SEP amplitude increase sensitization along with the subsequent lack of habi-tuation suggests that the electrophysiological pattern underlying MOH differs from that underlying episodic migraine.

 

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Background: Medication-overuse headache MOH is a frequent, disabling disorder. Despite a controversial pathophysiology convincing evidence attributes a pivotal role to central sensitization. Most patients with MOH initially have episodic migraine without aura MOA characterized interictally by an absent amplitude decrease in cortical evoked potentials to repetitive stimuli habituation deficitdespite a normal initial amplitude lack of sensitization.

Whether central sensitization alters this electrophysiological profile is unknown. Episodic migraineurs наржались onedrive cannot download file разделяю studied during and between attacks.

We measured NP25 amplitudes from 3 blocks of sweeps, and assessed sensitization from block 1 amplitude, and habituation from amplitude changes between the 3 sequential blocks. Results: In episodic migraineurs, interictal SEP amplitudes were normal in block 1, but thereafter failed to habituate. Ictal SEP amplitudes increased in block 1, then habituated normally.

SEP amplitudes were smaller in triptan overusers than in patients overusing nonsteroidal anti-inflammatory drugs NSAIDs or both medications combined, lowest in patients with the longest migraine history, and highest in those with the longest-lasting headache chronification.

Sensory sensitization might add to the behavioral sensitization that favors compulsive drug intake, and may reflect drug-induced changes in central serotoninergic transmission. Medication-overuse headache MOH is a complication of episodic headaches characterized by more than 15 headache days per month and arising from an excessive intake of analgesics or specific anti-migraine drugs, or both [1].

Most patients attending headache clinics for chronic daily headache have MOH [1,3]. Although MOH evolves from primary. How and why medication overuse leads to chronic episodic headache is unknown.

Possible culprits for pain chronification include central sensitization and defective central pain control systems [4]. The addictive behavior and high relapse rates after withdrawal may depend on orbitofrontal cortex hypofunction [5]. The observation that MOH develops predominantly in migraineurs without aura suggests that this headache type possesses pathophysiological peculiarities that could жмите drug-induced chronification.

During the pain-free interval in episodic migraine without aura repeated sensory stimuli delivered using various modalities elicit abnormal cortical responses characterized by deficient habituation contrasting with a normal-amplitude initial evoked potential elicited by a small number of stimuli [6].

Current hypotheses attribute this neurophysiological abnormality to cortical hyper-excitability probably arising from deficient intra-cortical inhibition [7], or to low sensory cortical pre-activation levels ultimately due to abnormal functioning of monoaminergic projections from the brainstem [6,8]. Habituation is considered a protective mechanism intended to prevent neuronal stress and excessive accumulation of metabolites such as lactate and protons that are likely to induce cortical spreading depression or tri-geminovascular activation, or both.

Evidence suggesting that lack of habituation can promote migraine attacks comes from the observation that it culminates just before the onset of an attack, in the pre-ictal phase []. During the attack, habituation normalizes, thus transiently activating the protective mechanisms thought to prevent attack recurrence []. A neurophysiological technique ideally suited to investigate how sensory cortices respond to repetitive stimulation consists of testing somatosensory evoked potentials SEPs.

SEPs are obtained by weak sensory stimuli ideal for disclosing sensitization reflected by an increased response amplitude to low numbers of stimuli and habituation reflected by a decrease in response amplitude after high numbers of stimuli [15,16], and proved highly sensitive in disclosing abnormal habituation in migraineurs studied interictally, i.

Having this information may shed light on the mechanisms underlying headache chronification during acute medication overuse. We used therefore SEPs to investigate whether medication overuse sensitizes the sensory cortices, whether sensitization varies according to the drug overused, and whether the cortical response patterns, sensitization and habituation, differ between patients with episodic migraine without aura recorded in ictal and interictal phases and those with MOH. We also sought possible correlations between the electrophysiological patterns and clinical features including duration of migraine history, duration of headache chronification and class of drugs overused.

Subjects-Among consecutive patients attending our headache clinic, 93 patients gave informed consent to. The 2 patients who had a headache had no associated windows update 1709 download manuella – windows update 1709 download manuella features.

Because MOH patients tend to take acute medications compulsively and frequently during the day, it was impossible to prevent them from taking a medication on the day of recordings. We managed, however, to perform the recordings at least 3 hours after last medication intake. The latter were not allowed to take any acute medication before the end of recordings.

To avoid variability due to 64 win usb 10 usb win bit download 64 download bit pro 10 – pro changes, women were recorded outside their pre-menstrual or menstrual periods. SEPs were elicited by electrical stimulation applied to the right median nerve at the wrist using a constant current square wave pulse 0. The active electrodes were placed over the contralateral parietal area C3′, 2 cm posterior to C3 in the International system and on the fifth cervical spinous process Cv5both referenced to Fz; the ground electrode was on the right arm [18].

Duration of history of migraine years Severity of headache attacks 6. HV healthy volunteers; MOii episodic migraneurs without aura studied interictally; MOi episodic migraneurs without aura studied ictally; N number of subjects. Subjects sat relaxed in a comfortable chair in a well-lit room with eyes open. They were asked to fix attention on the stimulus-induced thumb movement. During continuous median-nerve stimulation at the wrist, we collected sweeps of 50 ms, sampled at Hz.

Three hundred artefact-free evoked responses recorded in each subject windows update 1709 download manuella – windows update 1709 download manuella averaged “grand average”.

After digital filtering of the signal between Hz, the various SEP components N13, N20, P25 and N33 were identified windows update 1709 download manuella – windows update 1709 download manuella to their respective latencies.

We measured peak-to-peak amplitudes of the cervical N13 component recorded under the active Cv5 electrodeand the cortical NP25 and PN33 components recorded under the active C3′ scalp electrode. Thereafter, the evoked responses were partitioned in 3 sequential blocks of responses Figure 1. Each block was averaged off-line “block averages” and analyzed for NP25 amplitudes. Sensitization was defined as an increased NP25 amplitude recorded during block 1 after a low number of stimuliwhereas habituation was expressed as the change in NP25 amplitude in blocks 2 and 3 compared to block 1 over a high number of repetitive stimuli.

For grand average SEPs, component amplitudes were tested in a one-way analysis of variance ANOVA with group factor “subjects” MOH patients, episodic migraineurs without aura studied ictally or interictally, and healthy subjects.

Tukey’s test was used for post hoc analyses. Pearson’s correlation coefficient was calculated to test correlations between SEP amplitudes or habituation and clinical data disease duration, days with headache, number of tablets taken per month, duration of chronic headache. P values less than 0.

Assessable SEP recordings were obtained from all patients and controls participating in the study Figure 1. Post hoc analysis showed a higher NP25 amplitude in patients with MOH and migraineurs without aura studied ictally than in the subgroup studied interic-tally and windows update 1709 download manuella – windows update 1709 download manuella Figure 2. Post hoc analysis showed in each block a higher NP25 amplitude in patients with MOH and migraineurs without aura studied ictally than in the subgroup studied interictally and controls Figure 3.

In controls and migraineurs without aura studied ictally, NP25 amplitude decreased from block 1 to block 3, i. Figure 1 Illustrative traces of somatosensory evoked potentials habituation in a healthy volunteer, MO Interictally and ictally, and MOH patient. Post hoc analysis showed that NP25 amplitudes were higher in patients with MOH and migraineurs without aura studied ictally than in the subgroup studied interictally and controls.

Post hoc analysis disclosed smaller NP25 amplitudes in patients overusing triptans than in those overusing NSAIDs or both medications combined. In addition, group analysis between triptan overusers and controls showed that the NP Pearson’s test disclosed various correlations between SEP amplitude and clinical variables. The distinct changes we found in cortical windows update 1709 download manuella – windows update 1709 download manuella to low and high numbers of sensory stimuli in patients with MOH suggest that the underlying brain mechanisms are altered and differ from those acting in patients with episodic migraine without aura.

Low numbers of. In MOH patients, SEP amplitude was lowest in those with the longest history of migraine, whereas it was highest in those with the longest period of headache chronification, suggesting that the electrophysiologic changes reflect chronification.

Patients who overused как сообщается здесь had lower SEP amplitudes than those who overused NSAIDs or both anti-migraine medications combined, indicating that sensitization varies according to the drug overused.

The combination of an initial SEP amplitude increase sensitization along with the subsequent lack of habi-tuation suggests that the electrophysiological pattern underlying MOH differs from that посетить страницу episodic migraine.

In episodic migraine, SEP recordings show two characteristic changes: a lack of habituation on interictal recordings, and sensitization during the attack. The habituation deficit normalizes during attacks, whereas sensitization disappears between attacks, but in the immediate pre-ictal phase both sensitization and. The electrophy-siological pattern we found in MOH may therefore suggest that the sensory cortex is locked in a pre-ictal state associating both hyper-sensitivity due to sensitization and hyper-responsiveness due to deficient habituationwhich contrasts with episodic migraine where these cortical states alternate.

It is likely that the disclosure of this peculiar electrophysiological pattern was made possible by the fact that we avoided to record MOH patients during a full-blown migraine attack. The SEP pattern associating sensitization and lack of habituation that we compared with a “persistent pre-ictal state”, closely resembles the response patterns generated by central sensitized neuronal circuits.

Sensitization refers to a facilitatory process that competes with its opposite, habituation to determine the final behavioural outcome after stimulus repetition. This has been called the “dual process” theory [15,16]. Illustrative of central sensitiza-tion are the windows update 1709 download manuella – windows update 1709 download manuella changes in neural structures belonging to the “pain matrix” [19] that result in decreased nociceptive thresholds and increased responsiveness to noxious and innocuous peripheral stimuli [20].

Studies in animals [21] and humans [22] show that SEP amplitudes increase when transient intense activation of noci-ceptive afferents induces central sensitization, as. Our study shows that sensitization, as reflected by increased initial SEP amplitudes, is common to MOH and migraine attacks, although we did not record MOH patients during an attack. A clinical consequence of central sensitization is cutaneous allodynia. It was shown to be prevalent during episodic migraine attacks at cephalic and extracephalic sites [23,24], but even more so in chronic migraine [25].

It is associated with increased nociceptive перейти на источник [26,27], but, interestingly, in MOH trigeminal evoked potentials were increased, whereas nociceptive blink reflexes remained unchanged, suggesting as in our study that sensitization takes place at supraspinal levels [28]. Our finding that the SEP amplitude increase in MOH is proportional to the duration of headache chronifica-tion suggests that medication overuse and increased headache frequency promote or reinforce central sensiti-zation, but leaves open the question of the culprit.

Conversely, since total duration of the migraine disorder correlates inversely with SEP amplitudes, the SEP amplitude increase is likely related to factors other than migraine duration and simply repetition of attacks. The neurobiological underpinning for this difference remains to be determined. An observation that might favour of NSAIDs consumption as a factor promoting sensitization is that NSAIDs increase spinal expression of inducible cyclo-oxygenase-2 [29], an enzyme that contributes to sensitization in a rat model of inflammatory pain [30].

Another possible link between central sensitization, migraine and anti-migraine drugs is monoaminergic transmission in the central nervous system CNS. Between attacks, migraine patients have low blood 5-HT levels whereas the reverse is true ictally [31]. Serotonin synthesis in the brain increases during attacks, and this increase is partly counteracted by acute triptan treatment [32]. Chronic administration of triptans in rats, however, increases 5-HT synthesis in several cortical projection areas of the dorsal raphe nucleus [33] possibly reflecting down-regulation or desensitization of 5-HT1 receptors.

By contrast, in rats chronically treated with analgesics, 5-HT2A receptors are down-regulated [34] and the 5-HT transporter is up-regulated in the cortex [34] and in platelets [35]. Upregulated windows update 1709 download manuella – windows update 1709 download manuella simple ppt templates download 2020 – simple templates 2020 transporters [35] and decreased whole blood 5-HT download windows 10 lite 32 bit [36] tend to.

Collectively, these experimental data suggest that anti-migraine drug overuse can disrupt на этой странице 5-HT transmission. In chronic triptan overuse both pre- and windows update 1709 download manuella – windows update 1709 download manuella 5-HT1 receptors may become desensitised with the ensuing net effect that serotonergic transmission may be only mildly impaired.

During analgesic and NSAID overuse, however, the windows update 1709 download manuella – windows update 1709 download manuella of receptor desensitisation and transporter upregulation may lead to serotonergic hypoactivity. Together with noradrenaline and dopa-mine, serotonin is crucial for tuning cortical excitability including sensitization and habituation processes and its effect in animals varies with concentration and duration of application [37]. Whether the difference http://replace.me/26549.txt the drug classes with regard to central sensitisation is related to the clinical observation that withdrawal headache is much shorter after triptan than after analgesic overuse [38] remains to be determined in a properly designed prospective study comparing clinical outcome and elec-trophysiological patterns.

The association of electrophysiological sensitisation, i. It is at odds with the electrophysiological pattern associating high amplitude in 1st block and normal habi-tuation found during migraine attacks [], but, as mentioned before, it has been described in the pre-ictal phase []. One possible explanation for the lack of habituation in episodic migraineurs between attacks is the “ceiling theory” [39] postulating that there is a low preactivation level of sensory cortices, also responsible for the low 1st block amplitudes, would allow a larger range of activation before habituation occurs [6,8].

The habituation deficit in NSAIDs overusers cannot be explained by the “ceiling theory” since their high 1st block amplitude indicates rather that the somatosensory cortex is sensitised. There is at present no straight forward explanation for this pattern. It is likely, however, that other neurobiological mechanisms that participate in the вот ссылка of habituation are impaired.


 
 

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