Duration of migraine is a predictor for response to botulinum toxin type A

OBJECTIVE: To identify the clinical characteristics and/or injection parameters that predict a favorable response to botulinum toxin type A in patients with episodic and chronic migraine. BACKGROUND: There is emerging scientific and clinical evidence to support the utility of botulinum toxin type A (BoNT-A) in the prophylaxis of episodic and chronic migraine headache. However, the patient characteristics and injection strategies that predict a favorable treatment response are unknown. METHODS: We conducted a prospective, open-label study on 74 patients from our clinic receiving BoNT-A for episodic or chronic migraine. For all patients, migraine-related disability (Migraine Disability Assesment [MIDAS]), headache frequency, and average headache intensity were obtained at baseline and at 3 months post-BoNT-A. Information regarding demographic characteristics and injection parameters was also collected. RESULTS: Sixty-one patients met the study criteria and were available for 3-month follow-up. At the 3-month follow-up visit, the mean MIDAS scores of the 61 qualified study patients had decreased from 102 at baseline to 49 (52% decrease, P<.001). The mean number of headache days was reduced from 60 to 39 (P<.001), and the mean headache intensity decreased from 7.6 at baseline to 5.9 (P<.001). Frequency of migraine attacks, presence of analgesic overuse, total BoNT-A dose, and presence of underlying muscle tenderness were not predictive of treatment response. Age and duration of migraine were the only clinical factors significantly predictive of treatment response. Age likely was a predictor only as a consequence of duration of illness as subjects with migraine duration greater than 30 years were significantly less likely to respond to treatment with BoNT-A. CONCLUSION: BoNT-A may be effective in decreasing headache frequency, headache intensity, and headache-related disability in episodic and chronic migraine patients. Duration of illness emerged as a predictor of treatment response. Randomized controlled studies should evaluate headache-related disability as a primary endpoint in patients with episodic and chronic headache.     

Mechanism of action of botulinum toxin type A in migraine prevention: a pilot study

OBJECTIVE: The main objective of this study is to determine whether change in migraine frequency is correlated with a denervation pattern of the corrugator muscle after local botulinum toxin type A injections. BACKGROUND: Recent studies suggest botulinum toxin type A is effective in preventing migraine. Relaxation of the corrugator muscle may be one of multiple targets of botulinum toxin type A in relieving migraine pain. METHODS: The pretreatment amplitude of the compound muscle action potential (CMAP) was obtained in 10 patients with a migraine frequency of two to six attacks per month following stimulation of the temporal branch of the facial nerve. Patients were subsequently injected with 20 units of botulinum toxin type A at predefined sites in the procerus and corrugator muscles. CMAP was obtained on days 7, 30, 60, and 90 after injection. Migraine frequency, as reported in headache diaries, was compared with the amplitudes obtained. RESULTS: A 50% decrease in CMAP was demonstrated in the total group by day 7. Maximal decline of CMAP was observed by day 30, and was sustained at day 60. Migraine frequency declined by 50% or more in 7 of 10 patients by day 60. Migraine response to botulinum toxin type A treatment did not correlate with the denervation pattern. CONCLUSION: Relaxation of the corrugator muscles is not solely responsible for the pain relief in migraine patients treated with botulinum toxin type A.     

Single-site botulinum toxin type a injection for elimination of migraine trigger points

BACKGROUND: Botulinum toxin may be effective in suppressing migraine. Most injection regimens utilized have involved multiple sites. PURPOSE: To evaluate prospectively the effect of botulinum toxin type A injections into the corrugator supercilii muscles alone on the frequency and severity of migraine. METHODS: Twenty-nine patients (24 women, 5 men) with migraine were enrolled in the study. Average age was 45 years (range, 24 to 63). The frequency (number of migraines per month) and intensity (recorded on an analog scale of 1 to 10, 10 being most severe) of headache were recorded before and after treatment. Twenty-five units of botulinum toxin type A was injected into each corrugator supercilii muscle, for a total of 50 units. RESULTS: At 2 months, 24 (83%) of 29 patients reported a positive response to the injection of botulinum toxin type A (P <.001). Sixteen patients (55%) reported complete elimination of headache (P <.001), 8 (28%) experienced significant improvement (at least 50% reduction in frequency or intensity) (P <.04), and 5 (17%) did not notice a change in headache. The duration of efficacy of the botulinum toxin type A injections ranged from 6 to 12 weeks, with an average of 8 weeks. In patients who had improvement in migraine but not complete elimination, the headache frequency decreased from 6.4 to 2.1 per month on average (P <.04), and the intensity decreased from 8.6 to 6.1 (P <.04). CONCLUSION: These results support the hypothesis that focal injection of botulinum toxin type A may be an effective therapy for migraine.     

Repression of stimulated calcitonin gene-related peptide secretion by topiramate

OBJECTIVE: The goal of the proposed research was to determine the effect of topiramate on basal and stimulated release of calcitonin gene-related peptide (CGRP) from trigeminal ganglia neurons. BACKGROUND: CGRP is implicated in migraine headaches. Clinical evidence supports topiramate as an effective migraine prophylactic. In this study, the connection between topiramate and CGRP expression was investigated. METHODS: Primary cultures of rat trigeminal ganglia were utilized to determine the effects of topiramate on CGRP release stimulated by a depolarizing stimulus (KCl), nitric oxide, and/or protons. The amount of CGRP secreted into the culture media was determined using a CGRP-specific radioimmunoassay. RESULTS: Treatment of trigeminal cultures with KCl, nitric oxide donor S-nitroso-N-acetylpenicillamine, or protons (pH 5.5 media) caused a marked increase (3 to 5 fold) in the amount of CGRP release. Topiramate treatment repressed KCl-stimulated CGRP release in a time- and concentration-dependent manner. However, topiramate did not alter the amount of unstimulated or basal CGRP released from trigeminal neurons. In addition, topiramate inhibited nitric oxide and proton mediated CGRP secretion. CONCLUSIONS: Findings from these studies demonstrate that topiramate can directly repress the stimulated release of CGRP from sensory trigeminal neurons. We propose that topiramate's ability to prevent migraine attacks may involve inhibition of CGRP secretion from trigeminal neurons.     

Effect of carbon dioxide on calcitonin gene-related peptide secretion from trigeminal neurons

OBJECTIVE: The goal of this study was to determine whether the physiological effects of carbon dioxide (CO(2)) involve regulation of CGRP secretion from trigeminal sensory neurons. BACKGROUND: The neuropeptide calcitonin gene-related peptide (CGRP) is implicated in the pathophysiology of allergic rhinosinusitis and migraine. Recent clinical evidence supports the use of noninhaled intranasal delivery of 100% CO(2) for treatment of these diseases. Patients report 2 distinct physiological events: first, a short duration stinging or burning sensation within the nasal mucosa, and second, alleviation of primary symptoms. METHODS: Primary cultures of rat trigeminal ganglia were utilized to investigate the effects of CO(2) on CGRP release stimulated by a depolarizing stimulus (KCl), capsaicin, nitric oxide, and/or protons. The amount of CGRP secreted into the culture media was determined using a CGRP-specific radioimmunoassay. Intracellular pH and calcium levels were measured in cultured trigeminal neurons in response to CO(2) and stimulatory agents using fluorescent imaging techniques. RESULTS: Incubation of primary trigeminal ganglia cultures at pH 6.0 or 5.5 was shown to significantly stimulate CGRP release. Similarly, CO(2) treatment of cultures caused a time-dependent acidification of the media, achieving pH values of 5.5-6 that stimulated CGRP secretion. In addition, KCl, capsaicin, and a nitric oxide donor also caused a significant increase in CGRP release. Interestingly, CO(2) treatment of cultures under isohydric conditions, which prevents extracellular acidification while allowing changes in PCO(2) values, significantly repressed the stimulatory effects of KCl, capsaicin, and nitric oxide on CGRP secretion. We found that CO(2) treatment under isohydric conditions resulted in a decrease in intracellular pH and inhibition of the KCl- and capsaicin-mediated increases in intracellular calcium. CONCLUSIONS: Results from this study provide the first evidence of a unique regulatory mechanism by which CO(2) inhibits sensory nerve activation, and subsequent neuropeptide release. Furthermore, the observed inhibitory effect of CO(2) on CGRP secretion likely involves modulation of calcium channel activity and changes in intracellular pH.     

OnabotulinumtoxinA (botulinum toxin type-A) in the prevention of migraine

Importance of the field: Migraine is a highly prevalent disorder with the potential to progress into a chronic disease. The disability and health effects associated with frequent episodes of migraine underscore the value of preventive pharmacotherapy.

Areas covered in this review: OnabotulinumtoxinA has been studied as a migraine preventive in numerous clinical trials and in a variety of subpopulations with migraine. Overall, results from the clinical trials are mixed. However, the largest and most recent parallel studies (n = 1330) conducted on subjects with chronic migraine achieved statistically significant efficacy on numerous endpoints including the primary endpoint of reduction of headache days.

What the reader will gain: This article reviews several clinical studies using onabotulinumtoxinA in migraine prevention and highlights some of the inherent difficulties defining study endpoints and outcomes that are relevant to clinician, patients, and regulatory agencies.

Take home message: Clinical trials utilizing onabotulinumtoxinA as a preventive therapy for migraine has revealed mixed results. In part this reflects the inherent difficulties in study design such as defining different subpopulations of migraine sufferers and trial end points that are meaningful to patient populations. Recent studies of subjects with chronic migraine appear to have positive results. If confirmed this would be the first preventive medication indicated specifically for chronic migraine.     

Inhibition of calcitonin gene-related peptide function: a promising strategy for treating migraine

The neuropeptide calcitonin gene-related peptide (CGRP) is implicated in the underlying pathology of migraine. Serum levels of CGRP, which are elevated during a migraine attack, have been reported to return to normal with alleviation of pain. In addition, CGRP administration has been shown to cause a migraine-like headache in susceptible individuals. Importantly, CGRP receptors are found on many cell types within the trigeminovascular system that are thought to play important roles in controlling inflammatory and nociceptive processes. Based on these findings, it was proposed that blockage of CGRP receptor function and, hence, the physiological effects of CGRP would be effective in aborting a migraine attack. This review will summarize key preclinical data that support the therapeutic potential of using CGRP receptor antagonists or molecules that bind CGRP within the context of current neurovascular theories on migraine pathology.     

Botox therapy for refractory chronic migraine

Chronic migraine is unfortunately both common and often resistant to treatment even with prophylactic medications known to be effective in populations with episodic migraine. We undertook an open-label study to evaluate the safety and utility of botulinum toxin type A injection therapy for patients with chronic migraine who previously had failed to respond to at least three prophylactic medications.     

Hourglass deformity after botulinum toxin type A injection

BACKGROUND: Complications, such as eyelid ptosis, have been attributed to botulinum toxin type A. An "hourglass" deformity, which is the consequence of temporalis muscle atrophy, has not been reported previously. OBJECTIVE: To report a transient muscle deformity of the temporalis muscle caused by botulinum toxin type A. METHODS: Patients who underwent injection of 25 units of botulinum toxin type A into the temporal muscle, in a fan-shaped fashion, during an ongoing study for treatment of migraine were noted to develop temporary depression of the temples. Preinjection and postinjection photographs were taken. Patients were also sent questionnaires to verify the observed information. RESULTS: Only 26 of 92 patients who underwent injection of botulinum toxin type A into the temporalis muscle subsequently reported depression of the muscle. When examined, all 92 patients exhibited this deformity ranging from minimal to significant. Patients who seemed to have less deformity were those who had excessive soft tissue overlying the muscle due to excess weight. CONCLUSION: A newly recognized deformity is reported subsequent to the injection of botulinum toxin type A into the temporalis muscle. Informing patients of this transient deformity may minimize concern following treatment.     

Botulinum toxin type A as an effective prophylactic treatment in primary headache disorders

OBJECTIVE: To measure the effect of botulinum toxin type A (Botox, Allergan, Inc, Irvine, CA) treatment in 271 patients diagnosed with headache in accordance with International Headache Society (IHS) criteria. BACKGROUND: Botulinum toxin type A has shown promise for the treatment of headache in several clinical trials, but uncertainty remains as to how botulinum toxin type A optimally should be used for treating headache and which patients are best suited for this treatment. METHODS: This was a retrospective chart review of all patients who received botulinum toxin type A for the treatment of headache from January 1999 to February 2002. Patients were injected with an average dose of 63.2 U (SD, 14.5) of botulinum toxin type A on 2 or more visits, with treatments involving a "fixed-site" or a "follow-the-pain" (or a combination of both) approach. In the fixed-site approach, botulinum toxin type A was injected into the procerus, corrugator, frontalis, and temporalis muscles. In the follow-the-pain approach, botulinum toxin type A was injected into a combination of the procerus, corrugator, frontalis, temporalis, occipitalis, trapezius, and/or semispinalis capitis muscles. The primary outcomes for the trial were the reduction in headache days per month or headache intensity (0 to 3 scale) (or both) from baseline. Patients were diagnosed according to IHS criteria and subsequently classified into the following categories: chronic daily headache (more than 15 headache days per month), episodic tension-type headache, episodic migraine, and "mixed" HA (less than 15 headache days per month, combination of migraine and tension-type headache). RESULTS: Treatment period was an average of 8.6 months (SD, 6.4); patients received an average of 3.4 doses (SD, 1.6) 3 months apart. Of the 271 patients, 29 (10.7%) had episodic migraine, 17 (6.3%) had episodic tension-type headache, 71 (26.2%) had mixed headache, and 154 (56.8%) had chronic daily headache. Two-hundred fifty-six patients had data for the number of headache days per month, 117 had data for headache intensity, and all 271 had data for headache days or headache intensity. Botulinum toxin type A treatment significantly reduced the number of headache days per month from 18.9 (SD, 10.3) to 8.3 (SD, 8.9) (n=256, P<.001)--a 56% reduction. Headache intensity decreased from 2.4 points (SD, 0.6) to 1.8 points (SD, 0.8) (n=117, P<.001)--a 25% reduction. Of 263 patients surveyed, 225 (85.6%) reported improvement in headache frequency and intensity. There was no correlation of effect/lack of effect with reason for treatment, duration/number of treatments, injection technique, mean/total dose, age, gender, or comorbidity. Approximately 95% of patients did not experience medication side effects. CONCLUSION: These results suggest that botulinum toxin type A may be an effective and safe prophylactic treatment for a variety of moderate to severe chronic headache types.     

A型肉毒杆菌毒素治疗面肌痉挛235例临床研究

目的探讨A型肉毒杆菌毒素(BTXA)治疗面肌痉挛(HFS)的疗效及副作用.方法对235例HFS病人进行面肌多点注射BTXA,对治疗前后的病情分级进行比较,并随访12～36周.结果BTXA治疗的总有效率为98.3%(231/235),无全身反应,半年复发率为60%,药效作用时间平均16周;重复注射同样有效.结论局部注射BTXA是治疗HFS的一种有效手段.     

Botulinum toxin type A as migraine preventive treatment in patients previously failing oral prophylactic treatment due to compliance issues

Objective.— To examine the efficacy and safety of and satisfaction with botulinum toxin type A (BoNTA; BOTOX^®: Allergan, Inc., Irvine, CA) for prophylactic treatment of migraine headache in patients previously failing prophylaxis because of issues pertaining to compliance. Background.— Numerous factors (eg, adverse effects, tolerability, cost, frequency of dosage, hesitancy to take daily medication, failure to complete treatment) negatively influence compliance with the preventive pharmacology for migraine prophylaxis. BoNTA may offer benefit in improving compliance because of its long duration of action, injectable route of administration, and its tolerability (adverse event [AE]) profile. Methods.— This was a randomized, double‐blind, single‐center, placebo‐controlled study (months 1 to 3) of BoNTA with a cross‐over to open‐label BoNTA treatment (months 4 to 6). Criteria for enrollment included patients with disabling headache (International Headache Society, International Classification of Headache Disorders [ICHD‐I] diagnosis 1.1, 1.2, 1.7, or 2.2, and Headache Impact Test [HIT]‐6 scores ≥56) previously failing prophylaxis because of compliance, tolerability, or adherence issues. After baseline evaluation, subjects were randomized 2 : 1 to a single set of BoNTA (139 units [U] total; 17 sites/6 muscle groups) or placebo injections. After month 3, only placebo‐treated subjects were eligible to receive BoNTA in the open‐label continuation study. Treatment outcomes were evaluated by headache episodes and days and maximum headache severity. Headache impact was assessed by the HIT‐6, Migraine Disability Assessment (MIDAS) score, and Quality of Life (QoL) questionnaires. Treatment satisfaction was assessed with the Migraine Impact Questionnaire (MIQ), which included MIDAS and QoL. Results.— Of the 73 subjects screened, 61 (40 BoNTA; 21 placebo) with migraine headache diagnosis 1.1 and 1.2 who met all study criteria were enrolled in the 3‐month, blinded study, with 54 completing the study; 19 of 21 placebo‐treated subjects participated in the open‐label period (months 4 to 6), with 18 completing the study. Between‐group comparisons, demonstrated through analysis of the subjects' headache diaries, did not reach statistical significance at months 1 to 3 for the number of headache episodes or days (primary endpoint). At month 2, a decrease from baseline in the number of headache episodes (?0.99 ± 2.38; P = .0147 vs 0.42 ± 3.23; P = not significant [NS]) and headache days (?1.52 ± 3.84; P = .0194 vs 0.23 ± 4.67; P = NS) was noted in the BoNTA‐treated subjects but not in the placebo‐treated subjects, respectively. During the open‐label study, BoNTA‐treated subjects had a decrease in the number of headache episodes at months 5 and 6 (?1.58 ± 2.88 and ?1.58 ± 2.85, respectively; P < .05 vs baseline for both) and headache days at months 5 and 6 (?2.84 ± 4.47 and ?2.73 ± 4.86, respectively; P < .05 vs baseline for both). BoNTA did not affect maximum headache severity compared with baseline or placebo during the first 3 months of the study. A decrease in HIT‐6 scores was significantly greater for BoNTA‐treated subjects than for placebo‐treated subjects at month 3 (?7.77 vs ?3.58, P = .0466). Within‐group decreases in HIT‐6 scores were significant in BoNTA‐treated subjects during each month of the blinded trial (?5.10 ± 8.85, ?6.63 ± 7.49, ?7.77 ± 8.78 for months 1 to 3, respectively; P < .0001 for all vs baseline) and throughout the open‐label portion of the study (?7.89 ± 6.48, ?10.39 ± 10.81, ?9.00 ± 11.12 for months 4 to 6, respectively; P < .01 for all vs baseline). The within‐group decrease in placebo‐treated subjects was significant at months 1 and 3 (?3.35 ± 6.07 and ?3.58 ± 5.40, respectively; P < .05 for both). At 3 months, BoNTA was significantly better than placebo (P = .001) in the reduction of MIDAS total score. The change from baseline in the MIDAS total scores was significant in BoNTA‐treated subjects (?21.62 ± 38.70; P < .0001) but not in placebo recipients (4.76 ± 18.85; P = NS). BoNTA‐treated subjects showed improvement in 11 of 13 and 7 of 13 assessments of treatment satisfaction in MIQ at months 3 and 6, respectively, while the placebo group showed no improvement at any measured time interval in the study. At month 3 (blinded period), there were no treatment‐related AEs reported in both groups. However, there were 18 possible/probable occurrences of treatment‐related AEs in the BoNTA group. At month 6 (open‐label period), 4 treatment‐related AEs were reported, along with 2 possible occurrences. The majority of treatment‐related AEs were transient and mild to moderate in severity, with no subjects discontinuing the study because of AEs. Conclusions.— BoNTA‐treated subjects showed improvements from baseline in measures of headache frequency, and improvements from baseline and in comparison with placebo treatment in headache impact and treatment satisfaction at multiple time points in this study. However, BoNTA‐treated subjects did not differ from placebo‐treated subjects in measures of headache frequency and severity. BoNTA may be a useful treatment option for headache patients demonstrating poor compliance, adherence, or AE profile with oral prophylactic regimens.     

Lasting reduction of postsurgical hyperalgesia after single injection of botulinum toxin type A in rat

A single injection of low doses of botulinum toxin type A (3.5 U/kg) completely abolished secondary mechanical hyperalgesia throughout its duration in a model of post surgical pain after gastrocnemius incision in rat.     

Botulinum toxin type a prophylactic treatment of episodic migraine: a randomized, double-blind, placebo-controlled exploratory study

OBJECTIVE: This exploratory trial evaluated the safety and efficacy of multiple treatments of botulinum toxin type A (BoNTA; BOTOX, Allergan, Inc., Irvine, CA, USA) as prophylactic treatment of episodic migraine headaches. DESIGN AND METHODS: This was an 11-month randomized, double-blind, placebo-controlled, exploratory study. Patients were screened during a 30-day baseline period, and eligible patients with 4 or more migraine episodes and < or =15 headache days entered a single-blind 30-day placebo run-in period. Patients were classified as placebo nonresponders (PNR) if they had at least 4 moderate-to-severe migraine episodes and did not experience at least a 50% decrease from baseline in the frequency of migraine episodes following their placebo treatment. All other subjects were classified as placebo responders (PR). Patients were randomized within each stratum (PNR, PR) to 3 treatments with BoNTA (110 to 260 U of BoNTA per treatment cycle) or placebo at 90-day intervals using a modified follow-the-pain treatment paradigm. The primary efficacy outcome measure was the mean change from baseline in the frequency of migraine episodes for the 30 days prior to day 180 in the PNR group. Secondary efficacy measures included the proportion of patients with a decrease from baseline of 50% or more migraine episodes per 30-day period. Patients were allowed to take concomitant acute and prophylactic headache medications. Adverse events were reported. RESULTS: A total of 809 patients were screened and 369 patients (89.2% female; mean age, 45 years; range, 20 to 65 years) entered the placebo run-in period and were subsequently randomized to BoNTA or placebo. The mean total dose of BoNTA was 190.5 units (U) (range, 110 U to 260 U). The predetermined primary efficacy endpoint was not met. Substantial mean improvements of 2.4 and 2.2 fewer migraine episodes per month at day 180 in the PNR stratum treated with BoNTA and placebo, respectively, were observed (P > .999). From day 180 through the end of the study (day 270) at least 50% of all patients in each treatment group had a decrease from baseline of 50% or more migraine episodes per 30-day period. However, in the group of patients with > or =12 headache days at baseline (and < or =15 headache days), BoNTA patients experienced a mean change from baseline of -4.0 headache episodes at day 180 compared with -1.9 headache episodes in the placebo group (P= .048). The majority of treatment-related adverse events were transient and mild to moderate in severity. Only 7 patients (1.9%) discontinued the study due to adverse events (6 BoNTA, 1 placebo). CONCLUSION: There were no statistically significant between-group differences in the mean change from baseline in the frequency of migraine episodes per 30-day period. There were substantial, sustained improvements during the course of the study in all groups. Multiple treatments with BoNTA were shown to be safe and well tolerated over an active treatment period lasting 9 months.     

A multicentre, double-blind, randomized, placebo-controlled, parallel group study of multiple treatments of botulinum toxin type A (BoNTA) for the prophylaxis of episodic migraine headaches

Our aim was to evaluate the safety and efficacy of botulinum toxin type A (BoNTA; BOTOX) for prophylaxis of episodic migraine. In this double-blind, placebo-controlled study, patients were randomized to 225, 150 or 75 U of BoNTA or placebo after a 30-day placebo run-in for three 90-day treatment cycles. The primary efficacy end-point was the mean reduction from baseline in the frequency of migraine episodes at day 180 in the placebo non-responder stratum. All groups (N = 495) improved, with no significant differences. At day 180, the frequency of migraine episodes was reduced from baseline means of 4.3, 4.7, 4.7 and 4.4 by 1.6, 1.7, 1.5 and 1.4 for BoNTA 225 U, 150 U and 75 U and placebo, respectively. The primary end-point was not met. Treatment-related adverse events were transient and mild to moderate. BoNTA treatment was safe and well tolerated but did not result in significantly greater improvement than placebo in this study. Several factors may have confounded the results.     

关节腔注射A型肉毒毒素治疗卒中后肩痛的疗效观察

目的:比较关节腔注射A型肉毒毒素(botulinum toxin type A,BTA)与类固醇治疗卒中后肩痛的疗效。方法:46例卒中后肩痛患者随机分为治疗组和对照组,超声引导下行关节腔注射,治疗组注射A型肉毒毒素和利多卡因,对照组注射曲安耐德和利多卡因。治疗前、治疗后即刻、1周后、4周后对患者进行评定。内容包括视觉模拟评分(VAS);Fugl-Meyer简式运动功能评定上肢部分;肩关节屈、外展、外旋被动关节活动度(ROM)。结果:治疗后即刻和1周后,两组VAS降低,与治疗前差异均有显著性意义(P0.05);4周后治疗组仍有差异(P0.05),对照组与治疗前无差异。两组的Fugl-Meyer简式运动功能评定在治疗后即刻和1周后均无改善,4周后两组评分均提高,与治疗前差异有显著性意义(P0.05)。治疗后即刻,两组外旋ROM改善,与治疗前差异均有显著性意义(P0.05),治疗组4周后仍有差异(P0.05),对照组1周后和治疗前差异无显著性意义。治疗1周后,对照组屈曲ROM改善,与治疗前差异有显著性意义(P0.05);4周后治疗组屈曲ROM改善,与治疗前差异有显著性意义(P0.05),对照组与治疗前无差异。两组外展ROM较治疗前无明显改善。结论:关节腔注射BTA能减轻卒中后肩痛的疼痛程度,并改善肩关节ROM,疗效可能优于曲安耐德。     

A型肉毒素在皮肤科疾病治疗中的进展

A型肉毒素是肉毒梭状芽孢杆菌在繁殖过程中分泌的A型毒性蛋白质,具有很强的神经毒性。其在皮肤美容方面的疗效显著而被熟知。除皮肤美容外,临床实践和前期研究均证实A型肉毒素在治疗皮肤病方面亦有明显疗效,且部分疾病经治疗预后明显优于传统治疗,如瘢痕与多汗症等。     

Botulinum toxin type A and divalproex sodium for prophylactic treatment of episodic or chronic migraine

OBJECTIVE: To compare the efficacy and safety of botulinum toxin type A (BoNTA; BOTOX: Allergan, Inc.) and divalproex sodium (DVPX; DEPAKOTE: Abbott Laboratories) as prophylaxis in reducing disability and impact associated with migraine. BACKGROUND: There is a need for effective, well-tolerated prophylactic treatment of migraine. DESIGN/METHODS: This was a randomized, double-blind, single-center prospective study. Fifty-nine patients received either BoNTA 100 U/placebo-DVPX bid or placebo-BoNTA/DVPX 250 mg bid. BoNTA/placebo injections were given at Day 0 and at Month 3. Patients were evaluated at Months 1, 3, 6, and 9. RESULTS: Both treatments showed significant improvements in migraine disability scores and reductions in headache days and headache index. A trend to decreased headache severity was observed with BoNTA. A greater percentage of DVPX patients reported adverse events possibly related to treatment (DVPX 75.8% vs BoNTA 50%, P = .04) and discontinued because of adverse events (DVPX 27.6% vs BoNTA 3.3%, P = .012). CONCLUSIONS: Both BoNTA and DVPX significantly reduced disability associated with migraine; BoNTA had a favorable tolerability profile compared with DVPX.