PubMed · 15028834
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Giuseppe Brisinda, Federica Cadeddu, Giorgio Maria. 2004-03-18. Chronic constipation.. https://doi.org/10.1056/nejm200403183501219
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A consequence of spinal cord injury is a change in bladder reflex pathways resulting in the emergence of detrusor hyperreflexia and increased activity of the urethral sphincter. A basis for some of these alterations could be changes in the environment of bladder sensory nerve endings at the target organ. Recent evidence suggests that the urothelium (the lining of the urinary bladder) plays a prominent role in modulating bladder sensory nerve ending excitability. It is conceivable that factors and processes affecting the plasticity of bladder neurons after spinal cord injury may be partly due to changes occurring in the urothelium. Although the urothelium has classically been thought of as a passive barrier to ions/solutes, a number of novel properties have been recently attributed to these cells. Our work and that of others clearly demonstrates that the urothelium exhibits both "sensor" (expression of sensor molecules or response to thermal, mechanical and chemical stimuli) as well as "transducer" (release of factors/transmitters) properties. Taken together, these and other findings discussed in this chapter suggest a sensory function for the urothelium and that alterations in urothelial properties may contribute to afferent abnormalities following spinal cord injury.
OBJECTIVE: To evaluate the role of botulinum toxin type A in the prophylaxis of migraine headaches. DATA SOURCES: MEDLINE (1966-July 2005), Iowa Drug Information Service (1966-July 2005), and International Pharmaceutical Abstracts (1970-July 2005) searches were performed. Key search terms included botulinum and migraine. DATA SYNTHESIS: Patients who received botulinum toxin type A injections for treatment of hyperfunctional facial lines also experienced relief of migraine symptoms, leading to further investigation. Four clinical trials and 2 retrospective chart reviews evaluating the use of botulinum toxin type A injections for the prophylactic treatment of migraines are discussed. Limitations of these trials include problems with blinding, use of different injection sites, and inconsistent dosing. CONCLUSIONS: The results of 3 double-blind, placebo-controlled trials, 2 retrospective chart reviews, and an open-label study indicate that botulinum toxin type A may be a safe and efficacious prophylactic treatment for migraine headaches.
Botulinum toxin has been widely accepted as an effective therapy for controlling the symptoms of adductor spasmodic dysphonia (ADSD). Reported experience with botulinum treatment for abductor spasmodic dysphonia (ABSD) has been less impressive. Factors that may impair outcomes for ABSD include differences in the pathophysiology of ADSD and ABSD and limitation of maximal dose from airway restriction with posterior cricoarytenoid muscle (PCA) weakness. We report our experience with botulinum injection of the PCA with an asymmetric dose escalation protocol, based on clinical observations that in ABSD, abductor spasms are often stronger on one side, usually the left. The nondominant side was injected with 1.25 units. Dominant side dose began at 5 units, with step-wise increments of 5 units per week until one of three endpoints was reached: Elimination of breathy voice breaks, complete abductor paralysis of the dominant side, or airway compromise. Fourteen of 17 patients achieved good or fair voice, with dominant-side doses ranging from 10 to 25 units. Exercise intolerance limited PCA dose in two patients. One patient had persisting breathiness that improved with medialization thyroplasty. Asymmetric botulinum toxin injection into PCA muscles can suppress abductor spasm in patients with ABSD, but breathiness may persist, because of inadequate glottal closure.