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Biomedical subjects

P D Drummond

Publications and source records attributed to P D Drummond.

At least 19 recordsLinked to original sources
PubMed2006

Mechanisms of autonomic disturbance in the face during and between attacks of cluster headache.

Lacrimation and nasal secretion during attacks of cluster headache appear to be due to massive trigeminal-parasympathetic discharge. In addition, the presence of oculo-sympathetic deficit and loss of thermoregulatory sweating and flushing on the symptomatic side of the forehead indicate that the cervical sympathetic pathway to the face is injured in a subgroup of cluster headache patients. In this review, it is argued that a peripheral rather than a central lesion produces signs of cervical sympathetic deficit, probably resulting from compression of the sympathetic plexus around the internal carotid artery. Although trigeminal-parasympathetic discharge appears to be the main trigger for vasodilation during attacks, supersensitivity to neurotransmitters such as vasoactive intestinal polypeptide, together with release of sympathetic vasoconstrictor tone, may boost facial blood flow in patients with cervical sympathetic deficit. In addition, parasympathetic neural discharge may provoke aberrant facial sweating during attacks in patients with cervical sympathetic deficit. Although neither trigeminal-parasympathetic discharge nor cervical sympathetic deficit appears to be the primary trigger for attacks of cluster headache, these autonomic disturbances could contribute to the rapid escalation of pain once the attack begins. For example, a pericarotid inflammatory process that excites trigeminal nociceptors might initiate neurogenic inflammation and trigeminal-parasympathetic vasodilation. To complete the loop, neurogenic inflammation and trigeminal-parasympathetic vasodilation could provoke the release of mast cell products, which aggravate inflammation and intensify trigeminal discharge.

Animals↗
PubMed2006

Tryptophan depletion increases nausea, headache and photophobia in migraine sufferers.

Sensitivity to light was investigated 5 and 8 h after consumption of an amino acid drink which contained L-tryptophan (balanced amino acid condition: 19 controls and 22 migraine sufferers) or which produced a short-term reduction in brain serotonin synthesis by omitting L-tryptophan (tryptophan depletion condition: 16 controls and 16 migraine sufferers). Migraine sufferers reported more intense nausea, headache, glare- and light-induced pain than controls. In addition, glare- and light-induced pain were greater in the tryptophan depletion condition than in the balanced amino acid condition, in both migraine sufferers and controls. Eight hours after the amino acid drink, after participants had completed tests of pain sensitivity and motion sickness provocation, tryptophan depletion augmented headache in migraine sufferers and aggravated nausea in migraine sufferers and controls. These findings suggest that a reduction in brain synthesis of serotonin intensifies photophobia and other migrainous symptoms and thus might contribute to the pathogenesis of migraine.

Adolescent↗
PubMed2005

Einstein-Podolsky-Rosen correlations via dissociation of a molecular Bose-Einstein condensate.

Recent experimental measurements of atomic intensity correlations through atom shot noise suggest that atomic quadrature phase correlations may soon be measured with a similar precision. We propose a test of local realism with mesoscopic numbers of massive particles based on such measurements. Using dissociation of a Bose-Einstein condensate of diatomic molecules into bosonic atoms, we demonstrate that strongly entangled atomic beams may be produced which possess Einstein-Podolsky-Rosen (EPR) correlations in field quadratures in direct analogy to the position and momentum correlations originally considered by EPR.

Journal Article↗
PubMed2005

Radiofrequency heating of painful annular disruptions: one-year outcomes.

OBJECTIVE: Although several studies have reported on outcomes following heating of annular tears with a thermoresistive catheter (SpineCATH), no data are available on the efficacy of thermal treatment with a flexible radiofrequency electrode (discTRODE). A prospective case-control study was conducted to determine the efficacy of radiofrequency heating of painful annular tears in the lumbar spine. METHODS: After at least 6 months of conservative treatment, 46 patients were studied for the presence of single-level painful annular tears with magnetic resonance imaging and provocative discography. Thirty-one patients underwent heating of their annular tears with a flexible radiofrequency electrode placed across the posterior annulus. The remaining 15 patients, who mostly could not obtain funding for the procedure, continued with conservative management and acted as a control group. The Visual Analogue Scale (VAS), Oswestry Disability Index (ODI), and Medication Quantification Score (MQS) were obtained before and at 3-monthly intervals after treatment. RESULTS: The VAS decreased significantly after the radiofrequency treatment, and this decrease persisted at 12 months of follow-up. The VAS did not change over 12 months in untreated control subjects. The decrease in VAS was significantly greater in the treated patients than the control subjects. The ODI also decreased in treated patients but not in control subjects. The MQS did not change in either group over the 12-month follow-up period. CONCLUSIONS: Radiofrequency heating of annular tears can lead to an improvement in the pain of internal disc disruption. The improvement gained by this treatment method is significantly better than that obtained from conservative management.

Adult↗
PubMed2005

Painful stimulation of the temple induces nausea, headache and extracranial vasodilation in migraine sufferers.

To determine whether painful stimulation of the temple would induce nausea, ice was applied to the temple for 30 s, three times at 4-min intervals in 23 migraine sufferers and 22 age- and sex-matched controls. On one occasion, the ice was applied in the presence of residual motion sickness induced by optokinetic stimulation. On another occasion, the ice application was not preceded by optokinetic stimulation (the baseline condition). In the baseline condition, nausea had developed in migraine sufferers but not controls by the third application of ice. In the presence of residual motion sickness, each painful stimulus intensified nausea and headache in migraine sufferers whereas symptoms were minimal in controls. Changes in frontotemporal pulse amplitude were monitored with photoelectric pulse transducers. The extracranial blood vessels dilated in migraine sufferers but not controls before the first application of ice in the baseline condition, presumably due to anticipatory anxiety. In contrast, the ice application did not provoke extracranial vasodilation in either group after optokinetic stimulation. The findings show that susceptibility to nausea and stress-induced extracranial vascular hyper-reactivity are associated with the migraine predisposition. They also suggest that head pain might intensify gastrointestinal disturbances during attacks of migraine.

Adult↗
PubMed2005

Painful stimulation of the temple during optokinetic stimulation triggers migraine-like attacks in migraine sufferers.

To determine whether motion sickness induced by optokinetic stimulation would trigger migraine-like attacks, 27 migraine sufferers and 23 controls attended the laboratory up to three times at intervals of at least 3 weeks. On one occasion subjects experienced up to 15 min of optokinetic stimulation, followed by three 30-s applications of ice to the temple at 4-min intervals. On another occasion, the ice applications preceded and accompanied optokinetic stimulation. On a third occasion, one hand was immersed in ice water for 30 s, three times at 4-min intervals before and during optokinetic stimulation. Subjects recorded headache activity in a diary over the course of the study. None of the controls experienced a migraine-like attack at any stage of the experiment. In migraine sufferers, the incidence of migraine-like attacks was greater than the expected daily incidence of 8% after sessions that involved painful stimulation of the temple during or after optokinetic stimulation (44% and 28% of the group, respectively) (P<0.001). In contrast, migraine-like attacks developed in only 13% of migraine sufferers after the session that involved immersing the hand in ice water during optokinetic stimulation (not significant). The development of nausea and headache during optokinetic stimulation increased the likelihood of migraine-like attacks afterwards. These findings indicate that motion sickness and head pain increase susceptibility to migrainous attacks in migraine sufferers, and suggest that the symptoms of migraine build upon each other in a vicious circle. Thus, targeting multiple symptoms should be more effective than targeting individual symptoms, both for preventing and treating attacks of migraine.

Adolescent↗
PubMed2004

Gaussian quantum Monte Carlo methods for fermions and bosons.

We introduce a new class of quantum Monte Carlo methods, based on a Gaussian quantum operator representation of fermionic states. The methods enable first-principles dynamical or equilibrium calculations in many-body Fermi systems, and, combined with the existing Gaussian representation for bosons, provide a unified method of simulating Bose-Fermi systems. As an application relevant to the Fermi sign problem, we calculate finite-temperature properties of the two dimensional Hubbard model and the dynamics in a simple model of coherent molecular dissociation.

Journal Article↗
PubMed2004

The effect of cutaneous mast cell degranulation on sensitivity to heat.

OBJECTIVE: To determine whether depletion of inflammatory mediators from cutaneous mast cells influences cutaneous sensitivity to heat or the thermal hyperalgesia provoked by capsaicin or noradrenaline. SUBJECTS: Ten healthy men. METHODS AND RESULTS: Compound 48/80 was introduced by iontophoresis into the forearm. Wheals at the site of compound 48/80 iontophoresis subsided over four pre-treatments, consistent with mast cell degranulation. Flares in the skin surrounding the compound 48/80 sites decreased after the first pre-treatment but persisted to some extent after wheals had disappeared, suggesting that a reagent produced during mast cell activation (e.g., a cytokine or lipoxygenase product released from degranulated mast cells) triggered a residual flare. Sensitivity to heat increased after the second administration of compound 48/80, possibly due to sensitization of thermal nociceptors by inflammatory mediators released from infiltrating leukocytes. However, the compound 48/80 pre-treatment inhibited the hyperalgesic effect of capsaicin. Pre-treatment with compound 48/80 did not prevent axon-reflex vasodilatation to noradrenaline or the hyperalgesic effect of noradrenaline in capsaicin-treated skin. CONCLUSIONS: Two mechanisms could account for the inhibitory effect of the compound 48/80 pre-treatment on the hyperalgesic effect of capsaicin. First, mast cell products could partly mediate the hyperalgesic effect of capsaicin. Second, partial desensitization of the vanilloid receptor subtype-1 by a reagent produced during mast cell activation (e.g., a lipoxygenase product) could mask the hyperalgesic effect of capsaicin. Mast cells do not appear to mediate the hyperalgesic effect of noradrenaline.

Adolescent↗
PubMed2004

Canonical Bose gas simulations with stochastic gauges.

A technique to simulate the grand canonical ensembles of interacting Bose gases is presented. Results are generated for many temperatures by averaging over energy-weighted stochastic paths, each corresponding to a solution of coupled Gross-Pitaevskii equations with phase noise. The stochastic gauge method used relies on an off-diagonal coherent-state expansion, thus taking into account all quantum correlations. As an example, the second-order spatial correlation function and momentum distribution for an interacting 1D Bose gas are calculated.

Journal Article↗
PubMed2004

Suppression of pain and the R2 component of the blink reflex during optokinetic stimulation.

The effect of exposure to a rotating optokinetic drum on the electrically evoked blink reflex was investigated in 20 healthy volunteers. Pain ratings and the area under the curve of the R2 component of the blink reflex to innocuous and nociceptive trigeminal stimulation decreased substantially during and after optokinetic stimulation. At low shock intensities, R2 decreased most during optokinetic stimulation in subjects who did not develop symptoms of motion sickness. In contrast, during the recovery period after optokinetic stimulation, suppression of R2 to moderate and intense stimuli was greatest in the most nauseated subjects. These findings suggest that a mechanism that suppresses symptoms of motion sickness during sensory conflict also inhibits activity in wide dynamic range neurones in the trigeminal nucleus caudalis. Nausea in the absence of sensory conflict may inhibit R2 to intense electrical stimulation by provoking diffuse noxious inhibitory controls.

Adaptation, Physiological↗
PubMed2004

Persistence of pain induced by startle and forehead cooling after sympathetic blockade in patients with complex regional pain syndrome.

BACKGROUND: Stimuli arousing sympathetic activity can increase ratings of clinical pain in patients with complex regional pain syndrome (CRPS). OBJECTIVE: To determine whether the increase in pain is mediated by peripheral sympathetic activity. METHODS: The effect of sympathetic ganglion blockade on pain evoked by a startle stimulus and cooling the forehead was investigated in 36 CRPS patients. RESULTS: Loss of vasoconstrictor reflexes and warming of the limb indicated that sympathetic blockade was effective in 26 cases. Before sympathetic blockade, pain increased in 12 of these 26 patients when they were startled. Pain increased in seven of the 12 patients and in another five cases when their forehead was cooled. As expected, pain that increased during sympathetic arousal generally subsided in patients with signs of sympathetic blockade. However, pain still increased in three of 12 of patients after the startle stimulus and in six of 12 of patients during forehead cooling, despite indisputable sympathetic blockade. CONCLUSIONS: These findings suggest that stimuli arousing sympathetic activity act by a central process to exacerbate pain in some patients, independent of the peripheral sympathetic nervous system. This may account for the lack of effect of peripheral sympathetic blockade on pain in some CRPS patients.

Adult↗
PubMed2003

Pair correlations in a finite-temperature 1D Bose gas.

We calculate the two-particle local correlation for an interacting 1D Bose gas at finite temperature and classify various physical regimes. We present the exact numerical solution by using the Yang-Yang equations and Hellmann-Feynman theorem and develop analytical approaches. Our results draw prospects for identifying the regimes of coherent output of an atom laser, and of finite-temperature "fermionization" through the measurement of the rates of two-body inelastic processes, such as photoassociation.

Journal Article↗
PubMed2003

Transcutaneous iontophoresis of methadone provokes local flushing and thermal hyperalgesia.

OBJECTIVE: To investigate whether the introduction of methadone into the skin of the human forearm produces wheals, cutaneous vasodilatation or thermal hyperalgesia and, if so, to determine whether these responses are mediated by opioid receptors. SUBJECTS: Healthy adults. METHODS AND RESULTS: In Experiment 1 (N = 11), the increase in local blood flow (monitored with a laser Doppler flowmeter) was greater after the iontophoresis of methadone than saline (mean increase +/- S.D. 12.6 +/- 8.8 versus 2.2 +/- 1.9 times greater than baseline, p < 0.01). Flushing did not spread into surrounding skin and wheals did not form. In Experiment 2, pre-treatment with naloxone (N = 12) prevented increases in blood flow to methadone whereas saline pre-treatment (N = 14) did not. The heat pain threshold was lower at the site of methadone administration than at an untreated site (42.8 +/- 2.3 degrees C versus 44.6 +/- 1.7 degrees C, p < 0.001), and this effect was inhibited by naloxone pre-treatment. However, naloxone pre-treatment also antagonized an inhibitory effect of methadone on the pain generated by a 7-second pulse of 45 degrees C heat. In Experiment 3 (N = 11), the iontophoresis of methadone was repeated after an interval of 1.5 h. Vasodilatation to methadone persisted after the second iontophoresis, and sensitivity to heat was greater at a site of methadone administration than at a site of saline administration or an untreated control site. CONCLUSIONS: Stimulation of mu-opioid receptors dilated cutaneous blood vessels, and evoked local thermal analgesia and hyperalgesia at different stimulus intensities. However, stimulation of mu-opioid receptors did not produce wheals or flares.

Administration, Cutaneous↗
PubMed2003

The effect of trigeminal nociceptive stimulation on blink reflexes and pain evoked by stimulation of the supraorbital nerve.

The aim of this study was to investigate the effect of painful conditioning stimuli on pain and blink reflexes to supraorbital nerve stimulation. Electromyograph activity was recorded bilaterally from the orbicularis oculi muscles in 13 normal participants in response to low (2.3 mA) and high-intensity (18.6 mA) electrical stimulation of the left supraorbital nerve before, during and after the application of ice to the left or right temple or immersion of the left hand in ice-water for 60 s. The pain evoked by the high-intensity electrical stimulus was greater during painful conditioning stimulation of the ipsilateral temple than during the recovery period afterwards, and was greater than during painful conditioning stimulation of the contralateral temple. These findings imply that spatial summation of nociceptive signals across different divisions of the trigeminal nerve can heighten pain. However, painful conditioning stimulation, particularly to the right temple, strongly suppressed the R2 component of the blink reflex to the low-intensity stimulus, and also suppressed R2 to the high-intensity stimulus. Thus, an inhibitory influence (e.g. diffuse noxious inhibitory controls) appeared to mask ipsilateral segmental facilitation of R2 during ice-induced headache. This finding contrasts with recent electrophysiological evidence of trigeminal sensitization in migraine.

Adult↗
PubMed2002

Motion sickness and migraine: optokinetic stimulation increases scalp tenderness, pain sensitivity in the fingers and photophobia.

The aim of this study was to determine whether scalp tenderness and photophobia, two well-recognized symptoms of migraine, develop during the motion sickness induced by optokinetic stimulation. To investigate whether motion sickness has a general influence on pain perception, pain was also assessed in the fingertips. After optokinetic stimulation, nausea increased more and headache persisted longer in 21 migraine sufferers than in 15 non-headache controls. Scalp tenderness increased during optokinetic stimulation in nauseated subjects, and pain in the fingertips increased more and photophobia persisted longer in migraine sufferers than controls. These findings suggest that the disturbance responsible for nausea also sensitizes trigeminal nociceptive neurones or releases inhibitory controls on their discharge. A low nausea threshold and a propensity for sensitization to develop rapidly in nociceptive pathways may increase susceptibility to migraine.

Adult↗
PubMed2001

Pain increases during sympathetic arousal in patients with complex regional pain syndrome.

OBJECTIVE: To investigate the effect of sympathetic arousal on pain and vasomotor responses in healthy control subjects and patients with complex regional pain syndrome (CRPS), and to determine whether pain increases in patients with particular symptoms. METHODS: In experiments 1 and 2, capsaicin was applied to the forearm of 24 healthy subjects to induce thermal hyperalgesia. Vascular responses were monitored and subjects rated thermal hyperalgesia before and after being startled (experiment 1), and before, during, and after mental arithmetic, breath holding, forehead cooling, the Valsalva maneuver, and a cold pressor test in experiment 2. In a third experiment, sensitivity to heat, cold, and mechanical stimulation was investigated in 61 patients with CRPS. Pain ratings and vascular and electrodermal responses were recorded after patients were startled and during forehead cooling. RESULTS: In experiment 1, thermal hyperalgesia decreased in healthy control subjects after they were startled, and digital blood vessels constricted symmetrically. In experiment 2, thermal hyperalgesia decreased during and after other forms of sympathetic arousal. However, in experiment 3, ratings of clinical pain increased during forehead cooling or after being startled in over 70% of patients with CRPS. Pain increased most consistently during forehead cooling in patients with cold allodynia or punctate allodynia. Digital blood vessels constricted more intensely on the symptomatic than the nonsymptomatic side in patients with CRPS during sympathetic arousal. CONCLUSIONS: Normal inhibitory influences on pain during sympathetic arousal are compromised in the majority of patients with CRPS. The augmented vasoconstrictor response in the symptomatic limb during sympathetic arousal is consistent with adrenergic supersensitivity. An adrenergic sensitivity in nociceptive afferents might contribute to pain and hyperalgesia during sympathetic arousal in certain patients with CRPS.

Adolescent↗