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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of intravenous flecainide (2 mg/kg) on cardiac output was evaluated by a dye dilution method in six healthy nonsmokers. The study was of a double-blind, crossover, placebo-controlled, randomized, and balanced design. Cardiac output, heart rate, and stroke volume were measured 0, 10, 30, 60, 90, 120, 150, 180, and 240 minutes after the beginning of the flecainide infusion. Flecainide reduced cardiac output and stroke volume during the first 90 minutes and heart rate increased during the first 30 minutes after flecainide. Visual analog scales for alertness and dry mouth were determined 0, 10, 60, and 240 minutes after dosing. Alertness was reduced 60 minutes after flecainide, but there was no increase in dryness of the mouth.
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PMID:Effect of flecainide on cardiac output. 397 50

Moxonidine is an imidazoline receptor modulator, specific for the I1-imidazoline receptor. The stimulation of imidazoline receptors represents a new mode of antihypertensive action to inhibit peripheral alpha-adrenergic tone by a central mechanism. Acute hemodynamic studies reveal moxonidine produces an acute fall of blood pressure and systemic vascular resistance. Heart rate, cardiac output, stroke volume, and pulmonary artery pressures are not affected. Left ventricular end-systolic and diastolic volumes are reduced. Ejection fraction is not significantly affected but 6-month studies showed a regression of left ventricular hypertrophy. After oral administration the maximum concentration of moxonidine is reached in about 1 hour, and elimination half-life is 2.5 hours, prolonged by renal insufficiency. The antihypertensive effect lasts longer than would be expected from the half-life. Open studies with moxonidine have revealed falls between 20 and 29 mmHg systolic, and between 10 and 19 mmHg diastolic blood pressure. In the largest study, over 12 months in 141 patients, most patients were controlled by 0.2 mg daily (58%) or 0.2 mg b.i.d. (38%). Moxonidine has been compared with representatives from each important class of antihypertensive drugs. In a crossover trial of clonidine in 20 patients, blood pressure control was similar, but the incidence of tiredness and dry mouth was less on moxonidine, as was the total number of patients experiencing side effects, 85% versus 30% (p < 0.01). In a larger parallel group study of moxonidine (n = 122) and clonidine (n = 30), blood pressure control was similar, but the overall incidence of side effects was less on moxonidine. In comparative studies of moxonidine with atenolol, ACE inhibitors, dihydropyridine calcium antagonists, hydrochlorothiazide, and alpha 1 blockade, the blood pressure control with representatives of these various classes of drugs was similar to moxonidine.
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PMID:Clinical experience with moxonidine. 806 79

Geriatric patients with major depression present clinical challenges not encountered in younger individuals, including a greater incidence of medical comorbidity, higher rates of multiple medication use, changes in drug metabolism due to age or physical illness, and increased sensitivity to antidepressant side effects. Nevertheless, successful treatment of depressive disorders in the elderly improves mental and physical functioning, decreases morbidity and perhaps mortality, and enhances quality of life. Recent research indicates that newer antidepressants are effective for late life depression and safer for older individuals. Among newer antidepressants, venlafaxine has a pharmacological profile that makes it an attractive choice for geriatric patients. It has limited potential to interact with other medications because it only weakly inhibits the cytochrome P450 system and binds to plasma proteins at a low level. Dosing may have to be adjusted for patients with renal failure, but typically not for those with liver disease or other medical conditions. Data from three double-blind and four open clinical trials support the safety and efficacy of venlafaxine for geriatric depression. Patients may experience transient, generally tolerable side effects such as insomnia, nausea, agitation, or dry mouth early in treatment, but more serious problems such as falls or cardiac rhythm disturbances seem to be rare. Treatment emergent hypertension occurs in a small percentage of older patients, generally at doses above 150 mg/day. Finally, emerging data suggest that venlafaxine may be effective for conditions such as stroke, anxiety, and neuropathic pain that frequently accompany depressive disorders in the elderly.
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PMID:Efficacy of venlafaxine in geriatric depression. 1109 16

Classic centrally acting drugs such as clonidine and alpha-methyldopa induce peripheral sympatho-inhibition via the stimulation of alpha(2)-adrenoceptors in the brainstem. From a haemodynamic point of view this appears to be a useful mechanism to lower elevated blood pressure in hypertensives. Although not known in full detail, a complex relationship exists between the sympathetic nervous system and hypertensive disease; sympathetic inhibition therefore appears to be a logical target of antihypertensive drug treatment. Numerous attempts have been made to improve the unfavourable side-effect profile of the centrally actingalpha(2)-adrenoceptor stimulants. None of these attempts were successful, since both the central antihypertensive activity and the major side-effects (sedation, dry mouth) are mediated by alpha(2)-adrenoceptors. A new approach in this field has been offered by the introduction of centrally acting antihypertensives which interact with central imidazoline (I(1))-receptors and thus cause peripheral sympatho-inhibition. As such they offer haemodynamic benefits similar to those of the classic alpha(2)-adrenoceptor agonists. However, it is hoped that their side-effect profile will be more favourable because of their much weaker affinity for alpha(2)-adrenoceptors. Moxonidine and rilmenidine are the prototypes of centrally acting I(1)-receptor stimulants. The antihypertensive activity of these agents is caused by vasodilatation and a reduction of peripheral vascular resistance. Left ventricular end-diastolic and end-systolic volumes are reduced, whereas heart rate, stroke volume, cardiac output and pulmonary artery pressures are largely unchanged. Left ventricular hypertrophy (LVH) is reduced in the long term. Both drugs when applied in a once-daily dosage schedule appear to control hypertension in most patients. Both drugs have been compared with representative agents from the major classes of antihypertensives in controlled trials and have been found to be equally effective with respect to blood pressure control. The incidence and severity of side-effects is lower than for clonidine, in particular with respect to sedation. A rebound (withdrawal) phenomenon has so far not been reported for moxonidine and rilmenidine. In conclusion, I(1)-receptor stimulants appear to offer the potential to be developed as centrally acting agents with a better side-effect profile than the classic alpha(2)-adrenoceptor stimulants, but with similar haemodynamic properties.
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PMID:Renewed interest in centrally acting antihypertensive drugs. 1144 83

The aim of this study was to assess the specific influence of poststroke depression (PSD) on both basal functional status and rehabilitation results. We performed a case-control study in 290 stroke inpatients, matched for age (+/-1 year) and onset admission interval (+/-3 days) and divided in two groups according to the presence (PSD+) or absence (PSD-) of PSD. All PSD+ patients were treated with antidepressants (AD), mainly with fluoxetine. PSD+ patients, despite similar severity of stroke, showed greater disability in coping with activities of daily living (ADL) on admission and greater disability both in ADL and mobility at discharge than PSD- patients. Although both groups exhibited similar average functional improvement during rehabilitation, PSD- patients were nearly twice as likely to show excellent recovery both on ADL and mobility as PSD+ patients (OR = 1.95, 95% CI = 1.01-3.75 and OR = 2.23, 95% CI = 1.14-4.35, respectively). All AD drugs improved depressive symptoms. Few relevant side effects were observed: fluoxetine was discontinued in 2 patients because of insomnia and in 2 patients because of nausea; paroxetine was stopped in 1 patient because of nausea and dry mouth. Our results confirm the unfavorable influence of PSD on functional outcome, despite pharmacological treatment.
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PMID:Post-stroke depression, antidepressant treatment and rehabilitation results. A case-control study. 1164 94

Injections of botulinum toxin have revolutionised the treatment of focal spasticity. Before their advent, the medical treatment for focal spasticity involved oral anti-spasticity drugs, which had decidedly non-focal adverse effects, and phenol injections. Phenol injections could be difficult to perform, could cause sensory complications and had effects that were of uncertain duration and magnitude. Furthermore, few neurologists knew how to perform them as they were mostly the province of rehabilitation specialists. Botulinum toxin can produce focal, controllable muscle weakness of predictable duration, without sensory adverse effects. Randomised clinical trials (RCTs) involving patients with spasticity resulting from a variety of diseases (mainly stroke and multiple sclerosis) have clearly shown that botulinum toxin type A (Dysport and Botox) can temporarily (for approximately 3 months) reduce spastic hypertonia in the elbow, wrist and finger flexors of the upper limbs, and the hip adductors and ankle plantar flexors in the lower limbs. The clinical benefits from this reduction of neurological impairment are best shown in the upper limb, with less disability of passive function and reduced caregiver burden. In the lower limbs, there is improved perineal hygiene from hip adductor injections. The benefits of reducing ankle plantar flexor tone are less well established. Pain is also reduced, possibly by mechanisms other than muscle weakness. Improved active function has not yet been clearly demonstrated in RCTs, only in open-label trials. The safety of botulinum toxin-A is impressive, with minimal (mainly local) adverse effects. There are little data on the use of botulinum toxin type B (Myobloc or Neurobloc) in spasticity and the only RCT that has examined this did not show tone reduction; dry mouth appeared to be a very common adverse effect. There are also very little data to allow a benefit-risk comparison of phenol and botulinum toxin injections; each have their clinical and technical advantages and disadvantages, and phenol is much less costly than botulinum toxin.
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PMID:Botulinum toxin treatment of adult spasticity : a benefit-risk assessment. 1645 33

Poststroke hemiparesis, together with abnormal muscle tone, is a major cause of morbidity and disability. Although most hemiparetic patients are able to reach different ambulatory levels with rehabilitation efforts, upper and lower limb spasticity can impede activities of daily living, personal hygiene, ambulation and, in some cases, functional improvement. The goals of spasticity management include increasing mobility and range of motion, attaining better hygiene, improving splint wear and other functional activities. Conservative measures, such as positioning, stretching and exercise are essential in spasticity management, but alone often are inadequate to effectively control it. Oral antispastic medications often provide limited effects with short duration and frequent unwanted systemic side effects, such as weakness, sedation and dry mouth. Therefore, neuromuscular blockade by local injections have become the first choice for the treatment of focal spasticity, particularly in stroke patients. Botulinum toxin (BTX), being one of the most potent biological toxins, acts by blocking neuromuscular transmission via inhibiting acetylcholine release. Currently, focal spasticity is being treated successfully with BTX via injecting in the spastic muscles. Two antigenically distinct serotypes of BTX are available on the market as type A and B. Clinical studies of BTX used for spastic hemiplegic patients are reviewed in this article in two major categories, upper and lower limb applications. This review addresses efficacy in terms of outcome measures, such as muscle tone reduction and functional outcome, as well as safety issues. Application modifications of dose, dilutions, site of injections and combination therapies with BTX injections are also discussed.
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PMID:Botulinum toxin in poststroke spasticity. 1760 49

The human sweating response is subject to the influence of diverse classes of drugs. Some act centrally at the hypothalamus or at spinal thermoregulatory centres, while others act at sympathetic ganglia or at the eccrine-neuroeffector junction. Pharmacological disturbances of sweating have broad clinical implications. Drugs that induce hyperhidrosis, or sweating in excess of that needed to maintain thermoregulation, can cause patient discomfort and embarrassment, and include cholinesterase inhibitors, selective serotonin reuptake inhibitors, opioids and tricyclic antidepressants. Drugs that induce hypohidrosis, or deficient sweating, can increase the risk of heat exhaustion or heat stroke and include antimuscarinic anticholinergic agents, carbonic anhydrase inhibitors and tricyclic antidepressants. As acetylcholine is the principal neuroeccrine mediator, anhidrosis is one of the clinical hallmarks by which acute anticholinergic toxicity may be recognized. The symptom of dry mouth often accompanies the less apparent symptom of hypohidrosis because the muscarinic M(3) acetylcholine receptor type predominates at both sweat and salivary glands. Management options include dose reduction, drug substitution or discontinuation. When compelling medical indications require continuation of a drug causing hyperhidrosis, the addition of a pharmacological agent to suppress sweating can help to reduce symptoms. When hypohidrotic drugs must be continued, deficient sweating can be managed by avoiding situations of heat stress and cooling the skin with externally applied water. The availability of clinical tests for the assessment of sudomotor dysfunction in neurological disease has enhanced recognition of the complex effects of drugs on sweating. Advances in the understanding of drug-induced anhidrosis have also enlarged the therapeutic repertoire of effective treatments for hyperhidrosis.
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PMID:Drug-induced hyperhidrosis and hypohidrosis: incidence, prevention and management. 1821 88

Aging per se has a small effect on oral tissues and functions, and most changes are secondary to extrinsic factors. The most common oral diseases in the elderly are increased tooth loss due to periodontal disease and dental caries, and oral precancer/cancer. There are many general, medical and socioeconomic factors related to dental disease (ie, disease, medications, cost, educational background, social class). Retaining less than 20 teeth is related to chewing difficulties. Tooth loss and the associated reduced masticatory performance lead to a diet poor in fibers, rich in saturated fat and cholesterols, related to cardiovascular disease, stroke, and gastrointestinal cancer. The presence of occlusal tooth contacts is also important for swallowing. Xerostomia is common in the elderly, causing pain and discomfort, and is usually related to disease and medication. Oral health parameters (ie, periodontal disease, tooth loss, poor oral hygiene) have also been related to cardiovascular disease, diabetes, bacterial pneumonia, and increased mortality, but the results are not yet conclusive, because of the many confounding factors. Oral health affects quality of life of the elderly, because of its impact on eating, comfort, appearance and socializing. On the other hand, impaired general condition deteriorates oral condition. It is therefore important for the medical practitioner to exchange information and cooperate with a dentist in order to improve patient care.
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PMID:The stomatognathic system in the elderly. Useful information for the medical practitioner. 1822 59

A woman with spastic hemiparesis from a stroke was injected with botulinum toxin type B (BoNTB) at a dose of 10,000 U. Although this had the desired effect of a reduction in her spasticity, she also developed severe dry mouth, which became refractory to local remedies such as moist towels, lip balms, and throat lozenges. She was then given pilocarpine (a muscarinic agonist) at a dose of 5 mg, three times a day, to which she responded well. This report describes another treatment option in rare cases of severe dry mouth after administration of BoNTB.
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PMID:Pilocarpine for the treatment of refractory dry mouth (xerostomia) associated with botulinum toxin type B. 1864 25


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