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Biomedical subjects

Holger Kaube

Publications and source records attributed to Holger Kaube.

14 recordsLinked to original sources
PubMed2006

Blink reflexes in patients with atypical odontalgia and matched healthy controls.

Atypical odontalgia (AO) is an orofacial pain condition which has been suggested to involve neuropathic pain mechanisms. The aim of this study was to use a brain stem reflex to investigate craniofacial nociceptive mechanisms in AO. In 38 AO patients and 27 matched healthy controls, the R2 component of the blink reflex (BR) was elicited using a "nociceptive-specific" electrode and recorded with surface electromyography electrodes on both orbicularis oculi muscles. The BR was tested by stimulation of both sides of the face of the participants before, during, and after an intraoral pain provocation test with capsaicin. The data were analyzed with three- and four-way mixed-model analyses of variance. The root mean square value of the ipsilateral R2 (R2i) was significantly reduced in patients compared with controls (P=0.046). No differences in R2 between stimulation sides were detected in either group (P>0.757). In all participants, R2 responses and the intensity of the pain evoked by the electrical stimulus were decreased during and after application of capsaicin compared with baseline (P<0.001). In patients, R2i onset latencies were significantly prolonged compared with controls (P=0.031). The present data show disturbances in the central processing of craniofacial information and that endogenous pain inhibitory systems in AO patients and healthy controls were activated to a similar degree by an acute intraoral nociceptive input. Additional clinical research with AO patients will be needed to determine to what extent neuropathic pain mechanisms are involved in this pain condition.

Adult↗
PubMed2006

Practical management of medication-overuse headache.

Epidemiological studies suggest that medication-overuse as defined by the International Headache Society is extremely common in patients with chronic daily headache. If all medication-overuse produces medication-overuse headache (MOH) in headache patients, it would be the third most frequent form of headache, after tension-type headache and migraine. Treatment of MOH is hindered by the absence of placebo-controlled, double-blind, randomised clinical trials. Nevertheless, several headache centers worldwide have developed expertise in the treatment of this syndrome, and have been quite successful. Here, we summarize available data on MOH, including clinical features, drugs used in withdrawal, as well as withdrawal strategies that have been described in the literature. We also include a detailed description of an in-patient and out-patient withdrawal procedure, reflecting personal experience and opinion of the authors.

Disease Management↗
PubMed2005

A positron emission tomographic study in spontaneous migraine.

BACKGROUND: Functional brain imaging in acute migraine has proved challenging because of the logistic problems associated with an episodic condition. Since the seminal observation of brainstem activation in migraine, there has been only a single case substantiating this finding. OBJECTIVE: To test the hypothesis that brainstem activation could be detected in migraine and to refine the anatomic localization with higher-resolution positron emission tomography than previously used. DESIGN: Using positron emission tomography with radioactive water (H(2)15O), we studied acute migraine attacks occurring spontaneously. Five patients underwent imaging in ictal and interictal states, and the differences were analyzed by means of statistical parametric mapping. SETTING: Tertiary referral center. PATIENTS: Six volunteers with episodic migraine were recruited from advertisements in migraine newsletters. One patient was excluded because of use of preventive medication. MAIN OUTCOME MEASURE: Brainstem activation during migraine state vs interictal state. RESULTS: Two patients had a typical migrainous aura before the onset of the headache. All of the attacks studied fulfilled standard diagnostic criteria for migraine. Comparing the migraine scans with interictal scans, there was significant activation in the dorsal pons, lateralized to the left (small volume correction, P = .003). Activation was also seen in the right anterior cingulate, posterior cingulate, cerebellum, thalamus, insula, prefrontal cortex, and temporal lobes. There was an area of deactivation in the migraine phase also located in the pons, lateralized to the right. CONCLUSIONS: Our findings provide clear evidence of dorsal pontine activation in migraine and reinforce the view that migraine is a subcortical disorder modulating afferent neural traffic.

Adult↗
PubMed2004

Empathy for pain involves the affective but not sensory components of pain.

Our ability to have an experience of another's pain is characteristic of empathy. Using functional imaging, we assessed brain activity while volunteers experienced a painful stimulus and compared it to that elicited when they observed a signal indicating that their loved one--present in the same room--was receiving a similar pain stimulus. Bilateral anterior insula (AI), rostral anterior cingulate cortex (ACC), brainstem, and cerebellum were activated when subjects received pain and also by a signal that a loved one experienced pain. AI and ACC activation correlated with individual empathy scores. Activity in the posterior insula/secondary somatosensory cortex, the sensorimotor cortex (SI/MI), and the caudal ACC was specific to receiving pain. Thus, a neural response in AI and rostral ACC, activated in common for "self" and "other" conditions, suggests that the neural substrate for empathic experience does not involve the entire "pain matrix." We conclude that only that part of the pain network associated with its affective qualities, but not its sensory qualities, mediates empathy.

Adult↗
PubMed2004

Rare nocturnal headaches.

PURPOSE OF REVIEW: This review describes rare headaches that can occur at night or during sleep, with a focus on cluster headaches, paroxysmal hemicrania, short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing, hypnic headache and exploding head syndrome. RECENT FINDINGS: It is known that cluster headaches and hypnic headache are associated with rapid eye movement sleep, as illustrated by recent polysomnographic studies. Functional imaging studies have documented hypothalamic activation that is likely to be of relevance to circadian rhythms. These headache syndromes have been shown to respond to melatonin and lithium therapy, both of which have an indirect impact on the sleep-wake cycle. SUMMARY: There is growing evidence that cluster headache and hypnic headache are chronobiological disorders.

Animals↗
PubMed2003

Prophylactic Therapy for Migraine.

The term migraine is derived from the ancient Greek word hemicrania introduced by Galen in approximately 200 AD. However, descriptions of "sick headache" have been found dating back to as far as 3000 BC. Despite this, migraine is a condition that still remains underdiagnosed and undertreated. The development of effective abortive agents, such as the triptans, have had a significant impact on migraine management, but there still remains a substantial proportion of migraineurs in whom further medication is required in the form of preventatives. These have the potential to transform the lives of many migraine sufferers.

Journal Article↗
PubMed2003

Symptomatic migraine and sensitization of trigeminal nociception associated with contralateral pontine cavernoma.

A 38-year-old woman is described with symptomatic strictly right-sided migraine associated with a pontine cavernoma affecting the contralateral (left) nucleus raphe magnus. A persistent facilitation of the right-sided trigeminal nociception was detected interictally using the 'nociception specific' blink reflex, which was more pronounced during the acute attack. This case shows for the first time, an impairment of the anti-nociceptive brainstem nuclei and the facilitation of the trigeminal nociception in the same subject, thus providing further evidence for the key role of the brainstem raphe nuclei in the pathophysiology of migraine.

Adult↗
PubMed2002

The role of histamine in dural vessel dilation.

The pain of migraine is often throbbing suggesting an important role for the cranial blood vessels and their innervation by the trigeminal nerve. It is proposed that clinically effective anti-migraine compounds, such as 5-HT(1B/1D) agonists, have actions that include inhibiting calcitonin gene-related peptide (CGRP) release from trigeminal nerves. Human studies suggest that histamine can induce migraine possibly by activating nitric oxide (NO) synthase to promote endogenous NO production. The present studies investigated the effect of histamine and its antagonists on the cranial blood vessels using intravital microscopy to assess directly the diameter of dural arteries in sodium pentobarbitone anaesthetised rats. Electrical stimulation of a closed cranial window produces, by local depolarisation of nerves, dural vessel dilation that is monitored continuously on-line using video-microscopy and a video dimension analyser. Histamine infusion caused immediate and reproducible dilation of meningeal blood vessels (103.5+/-6%; n=40) that could be blocked by H(1)- (mepyramine) and H(2) (famotidine)-receptor antagonists (P<0.05), as well as a nitric oxide synthase inhibitor (N(G)-nitro-L-arginine methylester; P<0.05). Neurogenic dural vasodilation was not inhibited by H(2)-receptor antagonists, but was significantly inhibited by a H(1)-receptor antagonist at the high dose of 10 mg/kg. The present studies demonstrate that histamine is likely to activate NO synthase to promote NO production. There is also evidence that H(1)-receptors may be present on trigeminal neurones as the H(1)-receptor antagonist inhibited neurogenic vasodilation, albeit at a large dose.

Animals↗
PubMed2002

The effect of anti-migraine compounds on nitric oxide-induced dilation of dural meningeal vessels.

Migraine is characteristically accompanied by a throbbing quality of head pain thought to involve trigeminovascular afferents. Administration of nitric oxide (NO) donors provides the most reliable model of migraine induction in humans. The present studies used intravital microscopy to monitor the effect of local meningeal nerve stimulation and NO on dural blood vessels and any modulation of that effect by anti-migraine compounds. NO caused an immediate and reproducible dilation of meningeal blood vessels that was partially blocked by sumatriptan and indomethacin, while flunarizine and histamine H(1) and H(2) receptor antagonists were unable to block the dilation. Indomethacin also inhibited the neurogenic dilation while flunarizine did not. The present studies demonstrate that NO is unlikely to interact with histamine to produce its dilatory response. Sumatriptan and indomethacin inhibit the NO response by inhibiting trigeminal activation and calcitonin gene-related peptide (CGRP) release. Flunarizine does not modify either the neurogenic vasodilator response or the NO meningeal dilator response at least acutely.

Analgesics↗
PubMed2002

P/Q-type calcium-channel blockade in the periaqueductal gray facilitates trigeminal nociception: a functional genetic link for migraine?

The discovery of mis-sense mutations in the alpha1A subunit of the P/Q-type calcium channel in patients with familial hemiplegic migraine indicates the potential involvement of dysfunctional ion channels in migraine. The periaqueductal gray (PAG) region of the brainstem modulates craniovascular nociception and, through its role in the descending pain modulation system, may contribute to migraine pathophysiology. In this study we sought to investigate the possible link between the genetic mutations found in migraineurs and the PAG as a modulator of craniovascular nociception. We microinjected the P/Q-type calcium-channel blocker omega-agatoxin IVA into the rat ventrolateral PAG (vlPAG). We examined its effect on the nociceptive transmission of second-order neurons recorded in the trigeminal nucleus caudalis and activated by stimulation of the parietal dura mater. After injection of agatoxin into the vlPAG (n = 20) responses to dural stimulation were facilitated by 143% (p < 0.0001) for Adelta-fiber activity and 180% for C-fiber activity (p < 0.05). Similarly, spontaneous background activity increased by 163% (p < 0.0001). These results demonstrate that P/Q-type calcium channels in the PAG play a role in modulating trigeminal nociception and suggest a role for dysfunctional P/Q-type calcium channels in migraine pathophysiology.

Animals↗
PubMed2002

The electrophysiology of migraine.

Migraine is currently regarded as a neurovascular disorder of trigeminal sensory processing, generated centrally, probably at the level of the brainstem. In the past, electrophysiological techniques have drawn no definite conclusions on either interictal or ictal changes in migraineurs compared with controls, largely because of methodological differences. Recently, two findings have been shown consistently: an interictal increasing lack of habituation of evoked potentials with a normalization at the start of the attack and strong intensity dependence of auditory evoked potentials. These findings substantiate migraine sufferers as having an abnormal trait interictally, with the attack characterized by a change in the state of central processing. Exploitation of these differences may be a useful tool to study the mechanism of action of drugs used for the treatment of migraine.

Blinking↗
PubMed2001

Is the R3 component of the human blink reflex nociceptive in origin?

The R3 component of the blink reflex can reproducibly be evoked by noxious stimulation but can probably also be elicited by innocuous stimuli. This study was conducted to investigate the contribution of nociceptive A delta and C fibers to the generation of the electrically evoked R3 blink reflex. Electrical thresholds for detection, pain and all blink reflex components were determined and the modulatory effects of local anesthesia were investigated. The electrical R3 threshold of 4.6 +/- 0.5 mA (mean +/- SE) corresponded to 2.9 times the detection threshold and to 0.35 times the pain threshold. The R3 threshold was significantly below the pain threshold. Under local anesthesia of the supraorbital skin with a complete loss of warm and cold sensation, a loss of pinprick sensation, but a normal detection of tactile stimuli, the electrical pain threshold increased, all other thresholds remained unchanged. Under local anesthesia none of the reflex components were significantly reduced. Cutaneous A beta fibers and nociceptive A delta fibers, but not unmyelinated C fibers, contribute to the generation of the electrically evoked R3 component. According to the recruitment order in peripheral sensory nerves the electrical threshold of the R3 is mainly determined by activation of A beta fibers. Thus, it can not be assumed that the electrically evoked R3 is an adequate model to investigate nociceptive processing.

Adult↗
PubMedDate not supplied

A novel method of eliciting pain-related potentials by transcutaneous electrical stimulation.

BACKGROUND: Electrophysiological techniques such as laser and contact heat evoked pain-related potentials are very useful for studying trigeminal and somatic pain transmission in humans. These methods are, however, partly invasive, expensive, and therefore not available for broad clinical use. We recently proposed a novel technique of noninvasive transcutaneous electrical stimulation. OBJECTIVE: To elicit pain-related evoked potentials (PREP) by using a concentric planar electrode and demonstrate their nociceptive specificity. METHODS: We registered PREP following stimulation of the forehead and hand in 14 healthy volunteers. Latencies, peak-to-peak amplitudes, and conduction velocities of nociceptive fibers have been estimated. Effects of temporal and spatial summation and of cutaneous anesthesia were evaluated. RESULTS: Stimulation with the concentric planar electrode produced pinprick-like painful sensation. Cutaneous anesthesia led to abolishment of PREP responses. Estimated mean conduction velocity was 11.61 +/- 5.12 m/s, which corresponded well with conduction via A-delta fibers. Spatial as well as temporal summation resulted in a parallel increase of perceived pain intensity and PREP amplitudes. CONCLUSION: The technique is noninvasive, affordable, and easy to perform and allows quantitative assessment of human nociceptive pathways.

Adult↗