穴位热痛刺激治疗无先兆偏头痛的近期镇痛疗效观察

目的 观察穴位热痛刺激治疗无先兆偏头痛患者的近期镇痛疗效。 方法 采用随机数字表法将120例无先兆偏头痛患者分为观察组及对照组，每组60例。对照组患者给予西比灵口服，每晚1次，每次5 mg，治疗4周为1个疗程。观察组患者在对照组干预基础上辅以穴位热痛刺激，取穴风池、率谷、阳陵泉、外关、太阳、印堂，选用Pathway疼痛及感觉评估系统配置的圆形刺激器，当刺激器加热至54.5 ℃时发放可调节脉冲热刺激，单个脉冲热刺激其脉宽为0.3 s，刺激间隔10 s，每个穴位连续刺激5次后换下一穴位，各穴位循环交替刺激，共治疗20 min，每日治疗1次，治疗4周为1个疗程。记录治疗前、后2组患者头痛发作频率、持续时间、疼痛视觉模拟评分(VAS)、头痛伴随症状评分、偏头痛特异生活质量问卷量表（MSQ）评分，并对比2组患者近期疗效差异。 结果 治疗后观察组患者头痛发作频率［（1.27±0.13）次/月］、头痛持续时间［（2.51±0.22）分钟/次］、疼痛VAS评分［（0.43±0.08）分］、头痛伴随症状评分［（0.21±0.20）分］、MSQ功能受限评分［（79.0±10.2）分］、功能障碍评分［（82.6±10.3）分］及情感评分［（85.2±10.5）分］均较治疗前及对照组明显改善（均P<0.05）；另外治疗后观察组患者总有效率（95.0%）亦显著优于对照组水平（80.0%），组间差异具有统计学意义（P<0.05）。所有患者在治疗期间其心率、血压均未出现不良反应，热痛刺激部位无感染、红肿等异常表现。 结论 穴位热痛刺激治疗无先兆偏头痛患者近期疗效显著，并且治疗过程安全可靠、副反应少，为偏头痛患者提供了一种新的治疗方法，值得临床推广、应用。     

A 40-year follow-up of school children with migraine

A prevalence study of 9000 Swedish school children conducted in 1955 showed that nearly 4% had migraine. The prevalence of migraine was 1.4% at 7 years of age and 5.3% at 15 years of age. From the age of 11 there was a gradual increase of migraine headache and a predominance among girls. A subgroup of 73 children with pronounced migraine and an average onset of 6 years was followed during a period of 40 years. The results showed that 23% of the children were migraine-free before the age of 25, boys significantly more often than girls. However, around the age of 50, more than half of the migraine group still had migraine attacks. A recall bias was found it that a number of the subjects in their middle-life (41%) could not remember that they had had aura symptoms previously. Of those who had become parents, 52% have in their present or previous families had one child or more who had developed recurrent headache, probably of the migraine-type.     

Higher variability of phosphene thresholds in migraineurs than in controls: a consecutive transcranial magnetic stimulation study

The aim of this study was to characterize the temporal course of phosphene thresholds (PT) using transcranial magnetic stimulation (TMS) in control subjects and in subjects with migraine and to observe whether changes in PT over time can predict a subsequent migraine attack. PTs were measured in 16 migraineurs [nine with aura (MA) and seven without aura (MoA)] and nine controls five times over an approximately 10-week period. Mean PTs were not significantly different between migraineurs and controls; however, there was a trend in MA showing lower thresholds. The minimum threshold values were also smaller in MA subjects than in MoA or control subjects. Generally, PTs had higher variance in migraineurs than in controls, revealing a significant increase in standard deviation of PTs in MA subjects. There was no significant difference of thresholds from the first to the last stimulation in controls and in MoA subjects, but the 3rd, 4th and 5th measurements of MA subjects were significantly lower than their first measurements. Four migraineurs experienced headache within 1 day after one of the measurements. They had either very low or very high PTs compared with the PT values which were not followed by a migraine attack. Our results imply that migraineurs show a higher variability among PT measurements over time than controls, revealing unstable excitability levels in these patients. Additionally, both particularly high and low PTs might predict a subsequent headache in some individuals.     

Olfactory auras in patients with temporal lobe epilepsy

PURPOSE: To investigate olfactory auras in patients with temporal lobe epilepsy (TLE). METHODS: We reviewed medical records of 217 Chinese patients who underwent temporal lobectomy for medically intractable TLE between 1987 and 1998 in Taiwan. Patients with olfactory auras asked for detailed characteristics of their auras. RESULTS: In all, 12 (5.5%) patients had olfactory auras, seven men and five women. All patients except one described and characterized the unpleasant olfactory auras. Olfactory auras were usually combined with other auras, most frequently sensations of epigastric rising, nausea, and fear. Association with gustatory hallucination was uncommon, in only one patient. On neuroimaging study, 11 patients had structural lesions involving the mesial temporal structures, two exclusively involving the amygdala. Histologic diagnosis included gliosis of the mesial temporal regions in seven (58.3%) patients, neoplasm in four (33.3%) patients, and arteriovenous malformation in one patient. Postoperatively, eight patients were seizure free. Three patients had rare seizures; however, none reported residual olfactory auras. CONCLUSIONS: Olfactory auras are infrequent in TLE. In this study, mesial temporal sclerosis is the most common etiology rather than tumors. Mesial temporal structures, especially the amygdala, may play important roles in the genesis of olfactory auras.     

Association of fear auras with mood and anxiety disorders after temporal lobectomy

PURPOSE: Epilepsy has been associated with increased occurrence of behavioral disorders. Auras reflect abnormal stimulation of brain areas in close proximity to regions from which clinical seizures originate. The purpose of our study was to investigate whether fear auras are associated with a higher rate of mood and anxiety disorders before and 1 year after temporal lobectomy. METHODS: Twenty-two patients with fear auras were compared with matched groups with other auras and no auras. Neurologic and neuropsychological evaluations before, 1-2 months after, and 1 year after temporal lobectomy were reviewed for mood and anxiety disorders and psychotropic medication treatment. A logistic regression model examined effects of patient group and psychiatric status on postoperative psychiatric status. RESULTS: The majority of patients in the three groups experienced mood and anxiety disorders before surgery. Mood and anxiety disorders declined in the control, but not in the fear aura group after surgery. Presence of auras at 1 year after surgery was not related to psychiatric outcome. Postoperative mood and anxiety disorders were more common in patients with persistence of seizures and in those in the fear group who were seizure free. The minority of patients in all groups underwent psychotropic treatment before surgery, but the majority with fear auras underwent treatment after surgery. CONCLUSIONS: Postoperative mood and anxiety disorders were more common in fear aura patients after temporal lobectomy, in particular, if seizure free. Possible mechanisms include the role of the amygdala in fear conditioning, the concepts of forced normalization, and kindling.     

Migraine as a cerebrovascular risk factor

Introduction

Migraine has become an important vascular risk factor during the past few years, along with the presence of white matter and clinically silent ischaemic lesions. Whether these findings contribute to the migraine becoming chronic has been a source of debate. People with chronic migraine also have a less favourable metabolic profile.An exhaustive review of the literature has been made in order to try to clarify the relationship between migraine and vascular risk factors.

Development

Migraine, particularly with aura and in women < 45 years-old, is associated with an increased risk of cerebral infarction. This risk increases if the patient smokes or uses oral contraceptives. Migraine can also be a direct cause of a stroke, although it is an infrequent complication. Migraine with aura is associated with a risk factor of 12 of having subclinical infarctions in posterior fossa circulation.

Conclusions

Since migraine is an independent vascular risk factor, a better control of migraine attacks, as well as other possible concomitant vascular risk factors, should decrease the likelihood of a stroke. Overall, the real risk of infarction is low, with 3.8 new cases per 100,000 women and year.     

Genetics of migraine

Migraine is a complex brain disorder explained by the interaction of genetic and environmental factors. In monogenic migraines, including familial hemiplegic migraine and migraine with aura associated with hereditary small-vessel disorders, the identified genes encode proteins expressed in neurons, astrocytes or vessels, which all increase the susceptibility to cortical spreading depression. Study of monogenic migraines showed that the neurovascular unit plays a prominent role in migraine. Genome-wide association studies have identified multiple susceptibility variants that only cause a small increase of the global migraine risk. The variants belong to several complex networks of “pro-migraine” molecular abnormalities, which are mainly neuronal or vascular. Genetics has also underscored the importance of genetic factors shared between migraine and its major co-morbidities including depression and high blood pressure. Further studies are still needed to map all of the susceptibility loci for migraine and then to understand how these genomic variants lead to migraine cell phenotypes. Thanks to the advent of new technologies such as induced pluripotent stem cells, genetic data will hopefully finally be able to lead to therapeutic progress.     

Functional serotonin 5–HTTLPR polymorphism is a risk factor for migraine with aura

In the present work, we report that the functional serotonin transporter gene promoter (5–HTTLPR) polymorphism is involved in migraine pathogenesis. The distribution of 5–HTTLPR genotypes was significantly different in MA patients (S/S vs. S/L vs. L/L=32.7 vs. 42.3 vs. 25.0%), MO patients (18.5 vs. 39.1 vs. 42.4%) and CON (18.0 vs. 51.3 vs. 30.7%; chi–square test, p<0.05). In 5–HTTLPR S/S carriers, the odds ratio for MA risk was 2.60 (95% confidence interval [95%CI]=1.75–3.85) compared to CON, and it was 2.14 (95%CI=1.42–3.21) compared to MO. These data provide a further insight on the complex genotypephenotype relationship involved in MA pathogenesis, and might eventually result in new and individualised prognostic and therapeutic measures.     

Co-morbidity of migraine and epilepsy: a review of clinical features

Migraine and epilepsy are common neurological conditions that often co-exist. There are some common symptoms and in some patients there may be a diagnostic problem. The purpose of this study was to review the literature on the co-morbidity of migraine and epilepsy, and to differentiate their clinical characteristics. A search in Medline using the terms ‘migraine and epilepsy’ was conducted to identify articles published during the period 1963–1999. Articles describing co-morbidity of epilepsy and migraine have been reviewed. In the absence of convulsive episodes or a clearly migrainous profile (especially in children), confusion is most likely in patients affected by transient blindness, paroxysmal abdominal pain, unseen nocturnal events and “basilar” symptoms. Electroencephalographic abnormalities and response to an anticonvulsant may not clarify diagnosis. Although clinicians generally have little difficulty, rarely more investigations may be required for some patients. An isolated, single electroencephalogram may not provide definitive data unless an event is captured during the recording. Clinicians, therefore, have to rely mainly on the interpretation of the patient's history and clinical presentation. Received: 10 Juli 2000 / Accepted in revised form: 5 October 2000