Midazolam is more likely to cause hypotension than etomidate in emergency department rapid sequence intubation. (49/342)

OBJECTIVE: To compare the haemodynamic effect of low dose midazolam and etomidate as induction agent in emergency department rapid sequence intubation. METHODS: A prospective observational study in two phases. In phase one, midazolam 2-4 mg was used as induction agent and in phase two, etomidate 0.2-0.3 mg/kg was used. The haemodynamic data were recorded before and after intubation for comparison. Changes in mean systolic blood pressure were analysed with SPSS software. RESULTS: A 10% decrease in mean systolic blood pressure was observed in the midazolam group (p = 0.001) while there was no significant change in the etomidate group. Some 19.5% of patients had hypotension after being given midazolam while only 3.6% with etomidate (p = 0.002). Patients older than 70 tended to have more hypotension episodes but the difference was not statistically significant. CONCLUSIONS: Midazolam, even in low dose, was more likely than etomidate to cause significant hypotension when used as an induction agent for rapid sequence intubation. Etomidate is a better alternative.  (+info)

Afferent input modulates neurotrophins and synaptic plasticity in the spinal cord. (50/342)

The effects of eliminating or decreasing neuromuscular activity on the expression of neurotrophins and associated molecules in the spinal cord and subsequent effects on spinal cord plasticity were determined. Spinal cord isolation (SI), which eliminates any supraspinal and peripheral monosynaptic input to the lumbar region but maintains the motoneuron-muscle connectivity, decreased the levels of brain-derived neurotrophic factor (BDNF) and neurotrophin 3 (NT-3) mRNA and protein in the isolated segments. Synapsin I, an important mediator for the effects of BDNF on synaptic plasticity, also was lower in the lumbar region of SI rats. In contrast, the levels of BDNF, synapsin, and growth-associated protein (GAP-43) were increased in the cervical spinal cord enlargement rostral to the isolated region, most likely reflecting an increased use of the forelimbs in the SI rats. GAP-43 levels were also increased in the lumbar spinal cord region, probably associated with compensatory mechanisms related to the deafferentation. In a separate set of experiments, the soleus muscle was paralyzed unilaterally via intramuscular botulinum toxin type A (BTX-A) injection to determine the effects of reducing the propioceptive input, of this normally highly active muscle on neurotrophin expression in the spinal cord. BDNF and synapsin I mRNAs were lower and NT-3 levels were higher in the lumbar hemicord ipsilateral to the BTX-A injection. Combined, these results indicate that the level of supraspinal and muscle afferent input plays an important role in modulating the levels of BDNF and NT-3 in the spinal cord.  (+info)

Botulinum toxin for cerebral palsy; where are we now? (51/342)

In this article, the evidence base for botulinum-A treatment acquired in recent years is outlined, and the practicalities involved in providing this service are described. Botulinum-A is relatively new, and possible improvements for the future are considered.  (+info)

Modulation of botulinum neurotoxin A catalytic domain stability by tyrosine phosphorylation. (52/342)

Botulinum neurotoxin A (BoNT A) is a substrate of the Src family of tyrosine kinases. Here, we report that the BoNT A light chain (LC) is phosphorylated in the tyrosine-71 located at N-terminus. Covalent modification of this residue notably increases the thermal stability of the endopeptidase activity, without affecting its catalytic efficacy. Similarly, mutation of this residue specifically affected the protein stability but not its endopeptidase function. Fusion of the Tat-translocating domain to the N-terminus of the enzyme produced a cell permeable, functional enzyme, as evidenced by immunocytochemistry and by the cleavage of cytosolic SNAP25 in intact PC12 cells. Noteworthy, truncation of cellular SNAP25 was reduced in cells when the Src kinase activity was inhibited with a specific antagonist, implying that tyrosine phosphorylation of BoNT A LC modulates the in vivo proteolytic activity of the neurotoxin. Taken together, these findings substantiate the tenet that tyrosine phosphorylation of BoNT A LC could be an important modulatory strategy of the neurotoxin stability and suggest that the phosphorylated neurotoxin may be a relevant molecule in vivo.  (+info)

Focal hyperhidrosis: diagnosis and management. (53/342)

Hyperhidrosis, a condition characterized by excessive sweating, can be generalized or focal. Generalized hyperhidrosis involves the entire body and is usually part of an underlying condition, most often an infectious, endocrine or neurologic disorder. Focal hyperhidrosis is idiopathic, occurring in otherwise healthy people. It affects 1 or more body areas, most often the palms, armpits, soles or face. Almost 3% of the general population, largely people aged between 25 and 64 years, experience hyperhidrosis. The condition carries a substantial psychological and social burden, since it interferes with daily activities. However, patients rarely seek a physician's help because many are unaware that they have a treatable medical disorder. Early detection and management of hyperhidrosis can significantly improve a patient's quality of life. There are various topical, systemic, surgical and nonsurgical treatments available with efficacy rates greater than 90%-95%.  (+info)

The use of apraclonidine eyedrops to treat ptosis after the administration of botulinum toxin to the upper face. (54/342)

A side effect of the injection of botulinum toxin into the upper third of the face is ptosis or lid droop. A therapy recommended to treat ptosis resulting from administration of botulinum toxins A and B is Iopidine (apraclonidine 0.5 %) eye drops. Apraclonidine is an alpha2-adrenergic agonist, which causes Muller muscles to contract quickly elevating the upper eyelid 1-3 mm. Little published data discusses the use of apraclonidine to treat such ptosis. This communication discusses the extant literature on this usage. Research needs to be done to establish the utility and dosing of apraclonidine for botulinum toxin-induced ptosis.  (+info)

Remote arteriolar dilations caused by methacholine: a role for CGRP sensory nerves? (55/342)

Remote vasodilation caused by arteriolar microapplication of acetylcholine cannot be completely attributed to passive cell-cell communication of a hyperpolarizing signal. The present study was undertaken to ascertain whether a neural component may be involved in the remote response. In the cheek pouch of anesthetized hamsters, methacholine (100 microM) was applied to the arteriole by micropipette for 5 s, and the arteriolar responses were measured at the site of application and at remote locations: 500 and 1,000 microm upstream from the application site. Superfusion with the local anesthetic bupivacaine attenuated a local dilatory response and abolished the conducted dilation response to methacholine. Localized micropipette application of bupivacaine 300 microm from the methacholine application site also attenuated the remote dilation but did not inhibit the local dilation. Blockade of neuromuscular transmission with botulinum neurotoxin A (1 U, 3 days), micropipette application of calcitonin gene-related peptide (CGRP) receptor inhibitor CGRP-(8-37) (10 microM) 300 microm upstream from the methacholine application site, and denervation of the CGRP sensory nerve by 2 days of capsaicin treatment reduced the conducted dilation response to methacholine but did not affect the local dilatory response. Together, these data support involvement of a TTX-insensitive nerve, specifically the CGRP containing nerve, in vascular communication. Understanding the effect of regulation of a novel neural network system on the vascular network may lead to a new insight into regulation of blood flow and intraorgan blood distribution.  (+info)

Botulinum toxin type A for the treatment of the upper limb spasticity after stroke: a meta-analysis. (56/342)

Muscle over-activity is one of the cardinal features of spasticity and it is a common disability of stroke patients. In this group, spasticity is responsible for several limitations that interfere in their daily activities and quality of life. To treat spasticity, neurologists usually prescribe drugs as baclofen, tizanidine or benzodiazepines or even use definitive treatment as phenol or surgery. Authors suggest the use of botulinum toxin type A (BTX-A) for spasticity in the upper limbs after stroke, but there are few papers with adequate methodology supporting this idea. In this article we summarize the data of previous double-blind, randomised clinical trials to asses, with a meta-analysis, if BTX-A is an adequate treatment for spasticity due to stroke. The results show a statistical superiority of BTX-A ov%r placebo on reducing muscle tone by the Modified Ashworth Scale (WMD= 0.95 [0.74 to 1.17]) in patients with post-stroke upper limb spasticity.  (+info)