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Biomedical subjects

S K Aurora

Publications and source records attributed to S K Aurora.

16 recordsLinked to original sources
PubMed2007

High prevalence of somatic symptoms and depression in women with disabling chronic headache.

OBJECTIVE: To better define, in women with headache, the relationship of depression and somatic symptoms to headache, characterized by diagnoses, frequency, and disability. METHODS: At six headache specialty clinics, women with headache were classified using ICHD-II criteria, and frequency was recorded. A questionnaire addressing demographics, age at onset of headache, headache-related disability, somatic symptom, and depression severity was completed. Logistic regression was performed to measure the associations of headache frequency and headache-related disability with somatic symptom and depression severity. RESULTS: A total of 1,032 women with headache completed the survey, 593 with episodic (96% with migraine) and 439 with chronic headache (87% with migraine). Low education and household income was more common in chronic headache sufferers and in persons with severe headache disability. Somatic symptom prevalence and severity was greater in persons with chronic headache and with severe headache-related disability. Significant correlation was observed between PHQ-9 and PHQ-15 scores (r = 0.62). Chronic headache, severe disability, and high somatic symptom severity were associated with major depressive disorder (OR = 25.1, 95% CI: 10.9 to 57.9), and this relationship was stronger in the subgroup with a diagnosis of migraine (OR = 31.8, 95% CI: 12.9 to 78.5). CONCLUSIONS: High somatic symptom severity is prevalent in women with chronic and severely disabling headaches. Synergistic relationship to major depression exists for high somatic symptom severity, chronic headache, and disabling headache, suggesting a psychobiological underpinning of these associations.

Activities of Daily Living↗
PubMed2003

Intranasal sumatriptan in cluster headache: randomized placebo-controlled double-blind study.

BACKGROUND: Current evidence-based acute treatments of cluster headache are limited to oxygen inhalation and subcutaneous sumatriptan. Intranasal sumatriptan is a new formulation with better tolerability than the subcutaneous route. Two open-label studies suggested efficacy of intranasal sumatriptan in cluster headache. METHODS: In a double-blind placebo-controlled randomized trial, patients with episodic or chronic cluster headache whose attacks lasted at least 45 minutes each treated one attack with 20 mg sumatriptan nasal spray and another one, at least 24 hours later, with matching placebo. They scored their headache on a five-point scale (very severe, severe, moderate, mild, or none) at 5, 10, 15, 20, and 30 minutes. The primary outcome measure was headache response (a decrease in pain from very severe, severe, or moderate to mild or none) at 30 minutes. Secondary outcome measures included pain-free rates, relief of associated symptoms, and rates of adverse events. Multilevel multivariate analysis was used for statistical analysis. RESULTS: Five study centers enrolled 118 patients in whom 154 attacks were treated: 77 with sumatriptan and 77 with placebo. The responder rates at 30 minutes were 57% for sumatriptan and 26% for placebo (p = 0.002). Pain-free rates at 30 minutes were 47% for sumatriptan and 18% for placebo (p = 0.003). Sumatriptan was also superior to placebo considering initial response, meaningful relief, and relief of associated symptoms. There were no serious adverse events. CONCLUSION: Sumatriptan nasal spray is effective and well tolerated in the acute treatment of cluster headache attacks of at least 45 minutes' duration.

Administration, Intranasal↗
PubMed2003

The threshold for phosphenes is lower in migraine.

We have reported a preliminary study confirming hyperexicitability of occipital cortex in migraine with aura (MwA) using transcranial magnetic stimulation (TMS). We have now completed a blinded study to investigate the occipital cortex in MwA and without aura (MwoA) compared with normal controls (NC) using TMS. TMS was performed using the Caldwell MES-10 stimulator. A circular coil 9.5 cm diameter was applied to the occipital scalp (7 cm above the inion). Stimulator intensity was increased in 10% increments until subjects reported visual phenomena or 100% intensity was reached. Stimulation intensity was then fine tuned to determine the threshold at which phosphenes were seen. Fisher's exact t-test and logrank test were used for statistical comparisons. Ten subjects with MwA and MwoA were compared to 10 NC. The difference in the proportion of subjects with phosphene generation was statistically significant (MwA 100%, MwoA 60% and NC 30%) [P = 0.003]. The difference in threshold levels for phosphenes was also significant for MwA 42.8%, and controls 57.3% [P = 0.0001]. There is a difference in threshold for excitability of occipital cortex in MwA and MwoA compared to NC. This is a direct neurophysiological correlate for clinical observations, which have inferred hyperexicitability of the occipital cortex in migraineurs.

Adult↗
PubMed2002

Functional MRI-BOLD of brainstem structures during visually triggered migraine.

BACKGROUND: Previously, hyperoxia and blood volume increase were reported in the red nucleus and substantia nigra during spontaneous migraine with aura. OBJECTIVE: To further understand the pathophysiologic role of these centers, activation of brainstem structures was investigated in patients with visually triggered migraine. METHODS: Twenty-six patients with migraine (23 with aura and 3 without aura), and 10 normal control subjects were studied with blood oxygen level-dependent (BOLD) fMRI during repeated checkerboard visual stimulation. Three axial image sections, which covered the occipital cortex and brainstem, were acquired 224 times with a temporal resolution of 3.5 seconds. RESULTS: Repetitive visual stimulation triggered symptoms in 12 patients; four who had migraine with aura developed both visual symptoms and headaches, and six who had migraine with aura and two who had migraine without aura had headaches only. Four patients who had migraine with aura experienced the onset of their usual aura or onset of their typical headache either during the experiment or immediately after. In the remaining 10 patients with migraine, and all control subjects, visual stimulation failed to trigger symptoms at any time. In 75% of the patients who developed symptoms during stimulation, baseline T2*-weighted MR signal intensities increased in the red nucleus and substantia nigra before occipital cortex signal elevation or the onset of visually triggered symptoms. CONCLUSION: Activation (hyperoxia and blood volume increase) of the red nucleus and substantia nigra in association with visually triggered symptoms of migraine suggest that these brainstem structures are a part of a neuronal network activated during an attack.

Adult↗
PubMed2001

Pathophysiology of migraine headache.

The underlying mechanism of migraine and pain has been unraveled recently with the advent of neuroimaging. In this article mechanism of migraine aura and the pain of migraine are discussed. In addition, interictal studies demonstrating hyperexcitability in migraine are reviewed.

Brain↗
PubMed2001

Self-reported photophobic symptoms in migraineurs and controls are reliable and predict diagnostic category accurately.

OBJECTIVES: To assess the reliability of self-reported photophobia across different patient populations and to examine how visual stress thresholds and photophobic symptoms may be predictive of diagnosis. BACKGROUND: Relatively little is known about interictal photophobia in migraine. In particular, the variability of photophobia across different patient groups has not previously been studied, and a pathophysiological hypothesis to account for the symptoms is not agreed upon. METHODS AND RESULTS: Study 1 compared 99 self-selected Dutch patients and 101 headache-free controls using survey methods. Patients both with and without aura were significantly more likely to report symptoms, such as the wearing of sunglasses in normal daylight, consistent with interictal photophobia. Study 2 replicated these findings in a series of consecutive referrals to a headache clinic in the United States. Study 3 used a specially designed laboratory test to examine the threshold for visual stress in those patients who had participated in study 2. Visual stress thresholds were significantly lower in patients than in controls. A discriminant function analysis of data from both studies 2 and 3 showed that diagnostic category (migraine; control) could be predicted from photophobic symptoms and visual stress thresholds at a level significantly better than chance. CONCLUSIONS: We suggest that interictal photophobia is common in migraine and similar across different patient populations. One pathophysiological hypothesis is that interictal photophobia is associated with cortical hypersensitivity to stimulation. The predictive validity of interictal photophobic symptoms suggests that clinical diagnosis may be aided by questioning the patient about light sensitivity in the period between attacks.

Humans↗
PubMed2000

Migraine: imaging the aura.

We currently conceive of a migraine attack as originating in the brain. Triggers of an attack initiate a depolarizing neuroelectric and metabolic event likened to the spreading depression of Leao. This event activates the headache and associated features of the attack by mechanisms that remain to be determined, but appear to involve either peripheral trigeminovascular or brainstem pathways, or both. The excitability of cell membranes, perhaps partly genetically determined, is the brain's susceptibility to attacks. Factors that increase or decrease neuronal excitability constitute the threshold for triggering attacks. Using a model of visual stress-induced migraine or by studying spontaneous attacks and applying advanced imaging and neurophysiological methods, results have been obtained that support spreading neuronal inhibition as the basis of aura. This neuroelectric event is accompanied by hyperoxia of the brain, possibly associated with vasodilation. Evidence has also been obtained that the spreading cortical event can activate the subcortical centers possibly involved in nociception and associated symptoms of the migraine attack. Susceptibility to migraine attacks appears to be related to brain hyperexcitability. These newer techniques of functional neuroimaging have confirmed the primary neural basis of the migraine attack with secondary vascular changes, reconciling previous theories into a neurovascular mechanism.

Brain↗
PubMed1999

The cortical silent period is shortened in migraine with aura.

OBJECTIVES: Central neuronal hyperexcitability may be the physiological disturbance that predisposes subjects to migraine attacks. To test this hypothesis, we studied the cortical stimulation silent period (CSSP) elicited by transcranial magnetic stimulation (TMS), which is in part a measure of central inhibition of motor pathways in migraine with aura (MwA) patients and normal controls. METHODS: In nine MwA patients (mean age 35.9 +/- 7) and 9 controls (mean age 37.6 +/- 7), we carried out transcranial stimulation using a 95 mm circular coil and Caldwell MES 10 stimulator to determine resting motor threshold (MT) for bilateral FDI muscles. All subjects performed isometric voluntary contraction of bilateral FDI maintained at 20% of maximal effort, during which we measured bilateral CSSP at (i) the stimulus intensity (SI) determined for the MT and (ii) an SI of 1.5 x MT. RESULTS: Although the mean MT was higher in MwA compared with controls (63.1 +/- 14.4 vs 58.1 +/- 8.9), the difference was not significant. At an SI of 1.5 x MT the mean CSSP did not differ between the groups (MwA 141.7 +/- 31.9 vs controls 162.4 +/- 36.6). At the SI of the MT, however, the CSSP was shorter in MwA patients than in controls (62.9 +/- 27.3 vs 106.3 +/- 19.6, p = 0.001). There was an inverse correlation between the duration of CSSP and an increased frequency of headache (p = 0.02). CONCLUSIONS: The shortened CSSP that we measured in MWA patients compared to normal with low intensity magnetic stimulation suggests reduced central inhibition resulting in increased excitability of cortical neurons in migraine subjects. The association of CSSP reduction with increased frequency of migraine is further suggestive that brain excitability is the basis of susceptibility to migraine attacks.

Adult↗
PubMed1998

Silent period abnormalities in carpal tunnel syndrome.

Cutaneous silent period (CSP) was measured on stimulating digits 2 and 5 in 19 patients with carpal tunnel syndrome (CTS) and compared with 20 healthy volunteers. In 2 patients with severe CTS, CSP was absent on digit 2 but present on digit 5. In mild/moderate CTS digit 2 CSP mean duration was 50.9+/-13.9 ms, significantly longer than control subjects (36.9+/-8.7 ms) (P = 0.005). CSP was found to be abnormal in CTS, being absent in severe and prolonged in mild/moderate cases.

Adult↗
PubMed1998

Brain excitability in migraine: evidence from transcranial magnetic stimulation studies.

Central neuronal hyperexcitability is proposed to be the putative basis for the physiologic disturbances in migraine. Because there are no structural disturbances in migraine, only physiologic studies can provide insight into the underlying mechanisms. Recently, transcranial magnetic stimulation has been developed as a valuable research tool and can be used to study brain function noninvasively. This article is a review of the studies done in migraine using transcranial magnetic stimulation.

Evoked Potentials, Motor↗
PubMed1998

Transcranial magnetic stimulation confirms hyperexcitability of occipital cortex in migraine.

OBJECTIVES: We hypothesized that the hyperexcitability of occipital cortex neurons may predispose migraine subjects to develop spreading depression, the putative basis of migraine with aura (MwA). To date there is no direct physiologic correlate confirming this in patients. Accordingly, we evaluated the differences in the threshold of occipital cortex excitation between MwA patients and normal controls (C) using transcranial magnetic stimulation (TMS). METHODS: TMS was performed using the Cadwell MES 10 stimulator. A circular coil 9.5 cm in diameter was applied to the occipital scalp (7 cm above the inion). Stimulator intensity was increased in 10% increments until subjects reported visual phenomena or 100% intensity was reached. Stimulation intensity was then fine-tuned to determine the threshold at which phosphenes were just visualized. RESULTS: Eleven MwA patients, mean age 37 +/- 7 years, were compared with 11 C, mean age 37.7 +/- 7 years. The difference in the proportion of subjects with phosphene generation between MwA patients and C was significant (MwA patients 100% versus C 27.3%, p = 0.001). The mean threshold level for MwA patients was 44.2 +/- 8.6 versus 68.7 +/- 3.1 for C (p = 0.0001). All threshold levels for MwA patients were lower than the lowest threshold for C; the MwA patient with the lowest threshold had an aura after stimulation. CONCLUSIONS: The threshold for excitability of occipital cortex is lower in MwA patients compared with C. This is a direct neurophysiologic correlate for clinical observations that have indicated hyperexcitability of the occipital cortex in migraineurs.

Adult↗
PubMed1997

Effects of aspirin on platelet aggregation in smokers and nonsmokers.

OBJECTIVE: To assess the relative antiaggregatory ability of aspirin on platelets of smoking and nonsmoking healthy volunteers. DESIGN: Prospective, randomized, crossover study. SETTING: Tertiary-care teaching institution. SUBJECTS: Eighteen healthy smoking and nonsmoking male volunteers. INTERVENTIONS: Each subject received aspirin 325 mg or ticlopidine 250 mg bid as an active control for 7 days in a crossover manner separated by a 1-month washout period. Whole blood platelet aggregation was measured on four occasions, twice at baseline and once after each drug treatment. OUTCOME MEASUREMENT: Whole blood ex vivo platelet aggregation in terms of impedance (omega) and adenosine triphosphate (ATP) release (nmol), as assessed using Lumi-aggregometry. RESULTS: Aspirin was associated with significantly less ATP release in both smokers (p = 0.01) and nonsmokers (p = 0.003). No significant differences in platelet aggregation were found between smokers and nonsmokers at baseline or with any treatment phases. Sixty-seven percent and 17% of volunteers receiving ticlopidine and aspirin, respectively, reported adverse effects. CONCLUSIONS: Twice-daily administration of aspirin for 7 days to healthy volunteers was well tolerated and also reduced platelet aggregation significantly regardless of smoking status.

Adenosine Triphosphate↗
PubMedDate not supplied

The occipital cortex is hyperexcitable in migraine: experimental evidence.

OBJECTIVES: Threshold for generation of magnetophosphenes has been reported to be lower in migraine. We compared the threshold for eliciting phosphenes by transcranial magnetic stimulation and the ability to visually trigger headache in a select group of individuals with migraine with and without aura to normal controls. METHODS: Transcranial magnetic stimulation was performed using the Cadwell MES-10 stimulator. A circular coil, 9.5 cm in diameter, was applied to the occipital scalp (7 cm above the inion). Stimulator intensity was increased in 10% increments until subjects reported visual phenomena or 100% intensity was reached. Stimulator intensity was then fine-tuned to determine the threshold at which phosphenes were seen. In the same subjects, visual stimulation was given in 3.0 T MRI and if a headache occurred the response was recorded. RESULTS: Fifteen subjects with migraine were compared to 8 controls. A significant proportion of the migraineurs (86.7%) developed phosphenes compared to the controls (25%) (P = .006). The probability of triggering a headache was also higher in the migraineurs (53%); no headache was triggered in the controls (P = .019). A significant correlation was found between the threshold for phosphenes on transcranial magnetic stimulation and visually triggered headache (P = .002). When only migraine was considered, there was again a significant trend (P = .084). CONCLUSIONS: There is a difference in threshold for excitability of occipital cortex in migraineurs and controls. The hyperexcitable visual cortex in migraine is predisposed to visually triggered headache.

Adult↗
PubMedDate not supplied

Periaqueductal gray matter dysfunction in migraine: cause or the burden of illness?

OBJECTIVE: The periaqueductal gray matter (PAG) is at the center of a powerful descending antinociceptive neuronal network. We studied iron homeostasis in the PAG as an indicator of function in patients with episodic migraine (EM) between attacks and patients with chronic daily headache (CDH) during headache. High-resolution magnetic resonance techniques were used to map the transverse relaxation rates R2, R2*, and R2' in the PAG, red nucleus (RN), and substantia nigra (SN). R2' is a measure of non-heme iron in tissues. METHODS: Seventeen patients diagnosed with EM with and without aura, 17 patients diagnosed with CDH and medication overuse, and 17 normal adults (N) were imaged with a 3.0-tesla magnetic resonance imaging system. For each subject, mean values of the relaxation rates, R2 (1/T2), R2* (1/T2*), and R2' (R2* - R2) were obtained for the PAG, RN, and SN. R2, R2*, and R2' values of the EM, CDH, and N groups were compared using analysis of variance, Student t test, and correlation analysis. RESULTS: In the PAG, there was a significant increase in mean R2' and R2* values in both the EM and CDH groups (P<.05) compared with the N group, but no significant difference in these values was demonstrated between the EM and CDH groups, or between those with migraine with or without aura in the EM group. Positive correlations were found for duration of illness with R2' in the EM and CDH groups. A decrease in mean R2' and R2* values also was observed in the RN and SN of the CDH group compared with the N and EM groups (P<.05), explained best by flow activation due to head pain. CONCLUSIONS: Iron homeostasis in the PAG was selectively, persistently, and progressively impaired in the EM and CDH groups, possibly caused by repeated migraine attacks. These results support and emphasize the role of the PAG as a possible "generator" of migraine attacks, potentially by dysfunctional control of the trigeminovascular nociceptive system.

Adult↗