Weight change and clinical markers of cardiovascular disease risk during preventive treatment of migraine.

Migraine, particularly migraine with aura, and increased body weight are independent risk factors for cardiovascular disease (CVD). The association of weight change and clinical markers of CVD risk was evaluated in subjects participating in a randomized double-blind, parallel-group study of migraine-preventive treatment comparing 100 mg/day of topiramate and amitriptyline. Individuals from both treatment groups were pooled and stratified into three groups. The 'major weight gain' group gained > or = 5% of their baseline body weight at the conclusion of the study; the 'major weight loss' group lost > or = 5% of their baseline body weight. The third group had < 5% of weight change. The influence of weight change in headache outcomes, as well as in markers of CVD (blood pressure, cholesterol, C-reactive protein), was assessed using analysis of covariance. Of 331 subjects, 52 (16%) experienced major weight gain and 56 (17%) experienced major weight loss. Weight change was not associated with differential efficacy for the treatment of headache. However, contrasted with those with major weight loss, those who gained weight experienced elevations in mean diastolic blood pressure (+2.5 vs. -1.2 mmHg), heart rate (+7.6 vs. -1.3 beats per minute), glycosylated haemoglobin (+0.09% vs. -0.04%), total cholesterol (+6.4 vs. -6.3 mg/dl), low-density lipoprotein cholesterol (+7.0 vs. -4.4 mg/dl) and triglycerides (+15.3 vs. -10.4 mg/dl) and an increase in high-sensitivity C-reactive protein (+1.8 vs. -1.9 mg/l). Both groups experienced decreases in systolic blood pressure (-4.0 vs. -1.3 mmHg) and high-density lipoprotein cholesterol (-3.7 vs. -0.8 mg/dl). Increased weight during migraine treatment is not associated with poor headache treatment outcomes, but is associated with deterioration of CVD risk markers.

Utility of topiramate for the treatment of patients with chronic migraine in the presence or absence of acute medication overuse.

Chronic migraine has been linked to the excessive use of acute headache medications. Medication overuse (MO) is commonly considered the most significant risk factor for the progression of migraine from an episodic to a chronic condition. Managing MO is a challenge. Discontinuation of the acute medication can result in withdrawal headache, nausea, vomiting and sleep disturbances. This review summarizes the results from two similarly designed, randomized, placebo-controlled, multicentre studies of chronic migraine conducted in the USA and European Union. Both studies demonstrate the efficacy and safety of the migraine preventive medication, topiramate, for the treatment of chronic migraine in patient populations both with and without MO. These studies may have important implications for the future of chronic migraine management, suggesting that detoxification prior to initiating prophylactic therapy may not be required in all patients if MO is present.

Cerebral air embolism treated by pressure and hyperbaric oxygen.

We used pressure and hyperbaric oxygen to treat 2 patients with cerebral air embolism, occurring as the result of invasive medical procedures, and neither suffered any permanent damage detectable by clinical examination and MRI. This outcome contrasts with reports of infarct and disability among untreated victims of air embolism.

Relationship between volatile components of citrus fruit essential oils and antimicrobial action on Penicillium digitatum and penicillium italicum.

This study examined the effect of volatile components of citrus fruit essential oils on P. digitatum and P. italicum growth. The hydrodistilled essential oils of orange (Citrus sinensis cvv. "Washington navel", "Sanguinello", "Tarocco", "Moro", "Valencia late", and "Ovale"), bitter (sour) orange (C. aurantium), mandarin (C. deliciosa cv. "Avana"), grapefruit (C. paradisi cvv. "Marsh seedless" and "Red Blush"), citrange (C. sinensis x Poncirus trifoliata cvv. "Carrizo" and "Troyer"), and lemon (C. limon cv. "Femminello", collected in three periods), were characterized by a combination of GC and GC/MS analyses. The antifungal efficacy of the oils was then examined at progressively reduced rates. Findings showed a positive correlation between monoterpenes other than limonene and sesquiterpene content of the oils and the pathogen fungi inhibition. The best results were shown by the citrange oils, whose chemical composition is reported for the first time, and lemon. Furthermore P. digitatum was found to be more sensitive to the inhibitory action of the oils.

Geriatric headache. How to make the diagnosis and manage the pain.

Approximately 10% of women and 5% of men at age 70 experience severe recurrent or constant headaches. Severe headache presenting for the first time in a patient over age 50 is unusual and requires a thorough medical and neurologic examination. Primary headache etiologies in older patients include migraine, tension-type, cluster, and the rare hypnic headache. For all of these, effective pain control includes pharmacologic and nonpharmacologic interventions. Secondary etiologies include temporal arteritis, medication-induced headache, cerebrovascular or cardiac ischemia, and intracranial hemorrhage or tumors. Head pain may also be cervicogenic or related to glaucoma or sleep apnea. In secondary cases, pain management is specific to treatment of the underlying structural or systemic disease.

Headaches and their relationship to sleep.

Despite the complex influences of normal sleep physiology and sleep disorders on the development or presentation of headache, it is important to recognize and understand these relationships. Successful outcomes depend on the provision of treatment interventions specifically directed toward each condition. Nocturnal or early morning headaches that are associated with OSA are often eradicated after the sleep disorder is successfully managed with CPAP, oral appliances, or surgery. Substantial improvement in headache can also result from the successful management of other sleep disorders that may incite headaches such as heavy snoring, PLMS, or the various forms of insomnia. To improve headache patterns associated with bruxism and TMD, it is often necessary to formulate a multidisciplinary treatment approach that combines oral appliance therapy, stress management, biofeedback, oromandibular physical therapy, and, at times, pharmacologic treatment (i.e., tricyclic antidepressant, intramuscular botulinum toxin injections). There are still many gaps in the understanding of the interrelationships of sleep physiology and headache pathophysiology. More well-designed clinical trials are needed so that enough data can be amassed for the formulation of evidence-based guidelines or consensus statements that can better delineate the identification, diagnostic evaluation, and treatment of sleep-related headache disorders and headaches that develop as a consequence of disordered sleep.

Cervicogenic headache: mechanisms, evaluation, and treatment strategies.

Cervicogenic headache is a chronic, hemicranial pain syndrome in which the sensation of pain originates in the cervical spine or soft tissues of the neck and is referred to the head. The trigeminocervical nucleus is a region of the upper cervical spinal cord where sensory nerve fibers in the descending tract of the trigeminal nerve converge with sensory fibers from the upper cervical roots. This convergence of nociceptive pathways allows for the referral of pain signals from the neck to the trigeminal sensory receptive fields of the face and head as well as activation of the trigeminovascular neuroinflammatory cascade, which is generally believed to be one of the important pathophysiologic mechanisms of migraine. Also relevant to this condition is the convergence of sensorimotor fibers of the spinal accessory nerve (CN XI) and upper cervical nerve roots, which ultimately converge with the descending tract of the trigeminal nerve. These connections may be the basis for the well-recognized patterns of referred pain from the trapezius and sternocleidomastoid muscles to the face and head. Diagnostic criteria have been established for cervicogenic headache, but presenting characteristics of this headache type may be difficult to distinguish from migraine, tension-type headache, or paroxysmal hemicrania. This article reviews the clinical presentation of cervicogenic headache, its proposed diagnostic criteria, pathophysiologic mechanisms, and methods of diagnostic evaluation. Guidelines for developing a successful multidisciplinary pain management program using medication, osteopathic manipulative treatment, other nonpharmacologic modes of treatment, and anesthetic interventions are presented.

Cervicogenic headache: diagnostic evaluation and treatment strategies.

Cervicogenic headache is a chronic, hemicranial pain syndrome in which the source of pain is located in the cervical spine or soft tissues of the neck but the sensation of pain is referred to the head. The trigeminocervical nucleus is a region of the upper cervical spinal cord where sensory nerve fibers in the descending tract of the trigeminal nerve converge with sensory fibers from the upper cervical roots. This convergence of upper cervical and trigeminal nociceptive pathways allows the referral of pain signals from the neck to the trigeminal sensory receptive fields of the face and head. The clinical presentation of cervicogenic headache suggests that there is an activation of the trigeminovascular neuroinflammatory cascade, which is thought to be one of the important pathophysiologic mechanisms of migraine. Another convergence of sensorimotor fibers has been described involving intercommunication between the spinal accessory nerve (CN XI), the upper cervical nerve roots, and ultimately the descending tract of the trigeminal nerve. This neural network may be the basis for the well- recognized patterns of referred pain from the trapezius and sternocleidomastoid muscles to the face and head. Diagnostic criteria have been established for cervicogenic headache but its presenting characteristics may be difficult to distinguish from migraine, tension-type headache, or hemicrania continua. A multidisciplinary treatment program integrating pharmacologic, nonpharmacologic, anesthetic, and rehabilitative interventions is recommended. This article reviews the clinical presentation of cervicogenic headache, its diagnostic evaluation, and treatment strategies.