Chronic ergot toxicity: A rare cause of lower extremity ischemia.
(41/1420)
Chronic ergot toxicity is a rare cause of lower extremity ischemia. The cornerstone of therapy in ergot toxicity is to discontinue the use of caffeine, cigarettes, and all ergot-containing medications. Although multiple different therapies have been recommended for acute toxicity, no specific treatment is uniformly recommended in chronic toxicity. We present a case of long-term ergot use for migraine headaches in a woman who had severe chronic lower extremity claudication. This case demonstrates the unique features associated with the diagnosis and management of chronic ergot toxicity. We recommend a conservative approach consisting of observation, antiplatelet agents, and the discontinuance of ergots. If symptoms progress to rest pain or gangrene, surgical treatment should be considered. (+info)
A question sheet to encourage written consultation questions.
(42/1420)
PROBLEM: Interviews with parents and children attending a hospital paediatric neurology clinic indicated they had difficulties in asking questions during consultations. AIM: To set up a process to enable parents and children to get the information they wanted. BACKGROUND AND SETTING: Two paediatric neurology clinics in separate hospitals in Greater Manchester, UK with a similar client group run by one consultant. DESIGN: Various styles of question sheets were evaluated. The one that was chosen asked patients to write down questions and hand these to the doctor at the beginning of the consultation. Question sheets were given to all patients attending one clinic over a 13 week period. STRATEGIES FOR CHANGE: Use of sheets: number of patients taking or refusing a sheet, with reasons for refusal, were recorded. Doctors noted those who handed questions sheets to them Satisfaction with sheets: patients completed a short feedback form after the consultation Effect on consultations: evaluated through interviews with the doctors. EFFECTS OF CHANGE: In total, 66 (41%) of the 162 patients offered the sheet declined: 14 had already prepared questions; eight being seen for the first time felt they did not know what to ask. Seventeen had used the sheet on a previous visit and did not need it again; 19 gave no reason; the rest said they had no questions. Seventy six (47%) patients produced a sheet in the consultation. Of those using the sheet, 64 (84%) liked it and 61 (80%) found it useful. Fifty two (68%) wished to use it at future consultations. The doctors reported that through questions articulated on the sheets many issues, fears, and misunderstandings emerged which otherwise would not have been identified. Concerns about increasing consultation time and clinical disruption did not materialize. In contrast, doctors reported patients to be taking more initiative and control, particularly on subsequent visits. None of these changes was noted in the comparison clinic. LESSONS LEARNT: An attractive, clear question sheet proved a simple but effective intervention in the consultation. Parents felt empowered to take control. The approach may have wider applicability, but implementation requires staff training and support to ensure its continuing use; this ensures medical staff adjust to a new consultation format, and that clinic nurses see the value of the sheets and continue to provide them. (+info)
Impact of genomics on drug discovery and clinical medicine.
(43/1420)
Genomics, particularly high-throughput sequencing and characterization of expressed human genes, has created new opportunities for drug discovery. Knowledge of all the human genes and their functions may allow effective preventive measures, and change drug research strategy and drug discovery development processes. Pharmacogenomics is the application of genomic technologies such as gene sequencing, statistical genetics, and gene expression analysis to drugs in clinical development and on the market. It applies the large-scale systematic approaches of genomics to speed the discovery of drug response markers, whether they act at the level of the drug target, drug metabolism, or disease pathways. The potential implication of genomics and pharmacogenomics in clinical research and clinical medicine is that disease could be treated according to genetic and specific individual markers, selecting medications and dosages that are optimized for individual patients. The possibility of defining patient populations genetically may improve outcomes by predicting individual responses to drugs, and could improve safety and efficacy in therapeutic areas such as neuropsychiatry, cardiovascular medicine, endocrinology (diabetes and obesity) and oncology. Ethical questions need to be addressed and guidelines established for the use of genomics in clinical research and clinical medicine. Significant achievements are possible with an interdisciplinary approach that includes genetic, technological and therapeutic measures. (+info)
The development of cutaneous allodynia during a migraine attack clinical evidence for the sequential recruitment of spinal and supraspinal nociceptive neurons in migraine.
(44/1420)
Recently, we showed that most migraine patients exhibit cutaneous allodynia inside and outside their pain-referred areas when examined during a fully developed migraine attack. In this report, we studied the way in which cutaneous allodynia develops by measuring the pain thresholds in the head and forearms bilaterally at several time points during a migraine attack in a 42-year-old male. Prior to the headache, he experienced visual, sensory, motor and speech aura. During the headache, he experienced photo-, phono- and odour-phobia, nausea and vomiting, worsening of the headache by coughing or moving his head, and cutaneous pain when shaving, combing his hair or touching his scalp. Comparisons between his pain thresholds in the absence of migraine and at 1, 2 and 4 h after the onset of migraine revealed the following. (i) After 1 h, mechanical and cold allodynia started to develop in the ipsilateral head but not in any other site. (ii) After 2 h, this allodynia increased on the ipsilateral head and spread to the contralateral head and ipsilateral forearm. (iii) After 4 h, heat allodynia was also detected while mechanical and cold allodynia continued to increase. These clinical observations suggest the following sequence of events along the trigeminovascular pain pathway of this patient. (i) A few minutes after the initial activation of his peripheral nociceptors, they became sensitized; this sensitization can mediate the symptoms of intracranial hypersensitivity. (ii) The barrage of impulses that came from the peripheral nociceptors activated second-order neurons and initiated their sensitization; this sensitization can mediate the development of cutaneous allodynia on the ipsilateral head. (iii) The barrage of impulses that came from the sensitized second-order neurons activated and eventually sensitized third-order neurons; this sensitization can mediate the development of cutaneous allodynia on the contralateral head and ipsilateral forearm at the 2-h point, over 1 h after the appearance of allodynia on the ipsilateral head. This interpretation calls for an early use of anti-migraine drugs that target peripheral nociceptors, before the development of central sensitization. If central sensitization develops, the therapeutic rationale is to suppress it. Because currently available drugs that aim to suppress central sensitization are ineffective, this study stresses the need to develop them for the treatment of migraine. (+info)
Naproxen sodium decreases migraine recurrence when administered with sumatriptan.
(45/1420)
Forty to 78% of the patients using sumatriptan for the acute treatment of migraine may present recurrence at least occasionally. The concomitant use of a NSAID (nonsteroidal anti-inflammatory drug) has been recommended to decrease the recurrence rate. Sixty seven patients that treated successfully 8 migraine attacks with 100 mg of sumatritpan PO and presented recurrence in at least 5 attacks were studied prospectively. The patients received 100 mg of sumatriptan and 550 mg of naproxen sodium PO to treat 4 consecutive moderate or severe migraine attacks. The recurrence rate, once at least 62.5% (5 out of 8 attacks), decreased to 14.2% (38 out of 268 attacks) with the combination of compounds (p<0.0001). We then studied two groups of 13 patients made randomicaly from the 67 initially evaluated, that were given sumatriptan 100 mg plus naproxen sodium 550 mg or placebo, in a double-blind design, to treat 3 other consecutive migraine attacks. Each group of patients treated 39 attacks. The recurrence among the patients taking sumatriptan plus placebo was 59% (23 out of 39 attacks) and the recurrence presented by the group taking sumatriptan plus naproxen was 25.5% (10 out of 39 attacks) (p<0.0003). We concluded that the combination of sumatriptan plus naproxen sodium decreases significantly migraine recurrence presented by patients taking sumatriptan alone. (+info)
Migraine: pharmacotherapy in the emergency department.
(46/1420)
Migraine can be a disabling condition for the sufferer. For the small number of patients who fail home therapy and seek treatment in an emergency department, there are a number of therapeutic options. This paper reviews the evidence regarding the effectiveness and safety of the following therapies: the phenothiazines, lignocaine (lidocaine), ketorolac, the ergot alkaloids, metoclopramide, the "triptans", haloperidol, pethidine and magnesium. Based on available evidence, the most effective agents seem to be prochlorperazine, chlorpromazine and sumatriptan, each of which have achieved greater then 70% efficacy in a number of studies. (+info)
Familial adult onset myoclonic epilepsy associated with migraine.
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We report a new type of migraine associated epileptic syndrome in a family: adult onset myoclonic epilepsy with benign course and migraine. Affected members of the family had myoclonic and rare generalised tonic-clonic seizures. Most of the patients, but not all, had a history of migraine. Also, some cases of the family had only migraine. This family will be discussed because of two distinct features. Firstly, in this family a different type of epilepsy, adult onset myoclonic epilepsy was diagnosed that has not been classified in the ILAE 1989, classification(s), but was similar to that previously reported in Japanese families. Secondly, in most of the cases migraine was associated with the epilepsy. (+info)
Nitric oxide-induced headache in patients with chronic tension-type headache.
(48/1420)
An experimental model of headache offers unique possibilities to study the mechanisms responsible for head pain. Using the glyceryl trinitrate [GTN; nitric oxide (NO) donor] model of experimental headache, we studied the intensity, quality and time profile of headache after infusion of GTN in 16 patients with chronic tension-type headache and in 16 healthy controls. Subjects were randomized to receive intravenous infusion of GTN (0.5 microg/kg per minute for 20 min) or placebo on two headache-free days separated by at least 1 week. Headache intensity was measured on a 10-point verbal rating scale during 2 h of observation and for the next 10 h after discharge from hospital. The primary endpoints were the difference between the area under the curve (AUC-intensities x duration) for headache recorded on the day of GTN treatment and on the day of placebo treatment in patients, and in patients and controls on the days of GTN treatment. In patients, the AUC on a GTN day [2221 (1572-3704); median with quartiles in parentheses], was significantly greater than on a placebo day [730 (60-1678), P: = 0. 008]. On the GTN day, the AUC in patients [2221 (1572-3704)] was significantly higher than in controls [43 (0-972), P: = 0.0001]. In patients, peak pain intensity occurred 8 h after infusion of GTN, whereas in controls it occurred 20 min after the start of infusion. The present study demonstrates that an NO-induced biphasic response with an immediate and a delayed headache is common to chronic tension-type headache and migraine. Furthermore, the NO-induced delayed headache has the characteristics of the primary headache disorder. This suggests that NO contributes to the mechanisms of several types of primary headaches and that NO-related central sensitization may be an important common denominator in the pain mechanisms of primary headaches. (+info)