Richard J. Barohn

Randomized double-blind study of botulinum toxin type B for sialorrhea in ALS patients

Twenty ALS patients with sialorrhea refractory to medical therapy were enrolled in this double‐blind, randomized study to receive either 2,500 U of botulinum toxin type B (BTxb) or placebo into the bilateral parotid and submandibular glands using electromyographic guidance. Patients who received BTxb reported a global impression of improvement of 82% at 2 weeks compared to 38% of those who received placebo (P < 0.05). This significant effect was sustained at 4 weeks. At 12 weeks, 50% of patients who received BTxb continued to report improvement compared to 14% of those who received placebo. There were no significant adverse events, including dysphagia, in the BTxb group, and there was no significant increase in the rate of decline of vital capacity. Muscle Nerve 39: 137–143, 2009

Correspondence Regarding: TDP-43 Proteinopathy and Motor Neuron Disease in Chronic Traumatic Encephalopathy. J Neuropathol Exp Neurol 2010:69;918-29

We read with interest the recent article “TDP-43 proteinopathy and motor neuron disease in chronic traumatic encephalopathy” by McKee et al (1). As neuromuscular specialists who care for large numbers of patients with amyotrophic lateral sclerosis (ALS), we have concerns about the conclusions drawn from 3 cases diagnosed as having ALS in life, while having histologic changes of both ALS and chronic traumatic encephalopathy (CTE) at autopsy. In their 12-paragraph discussion section and subsequent New York Times interview (2), the authors propose a cascade of events starting with head trauma, leading to TDP-43 proteinopathy, and ultimately to various clinical phenotypes including motor neuron disease. In support of this, they state, “… of all the putative environmental risk factors, trauma to the CNS emerges as one of the strongest and most consistent contenders for initiating the molecular cascades that result in ALS.” In actuality, the data linking trauma to ALS are significantly …