Muscle cramps and contractures: causes and treatment.

Muscle cramps are painful, sudden, involuntary muscle contractions that are generally self-limiting. They are often part of the spectrum of normal human physiology and can be associated with a wide range of acquired and inherited causes. Cramps are only infrequently due to progressive systemic or neuromuscular diseases. Contractures can mimic cramps and are defined as shortenings of the muscle resulting in an inability of the muscle to relax normally, and are generally myogenic. General practitioners and neurologists frequently encounter patients with muscle cramps but more rarely those with contractures. The main questions for clinicians are: (1) Is this a muscle cramp, a contracture or a mimic? (2) Are the cramps exercise induced, idiopathic or symptomatic? (3) What is/are the presumed cause(s) of symptomatic muscle cramps or contractures? (4) What should be the diagnostic approach? and (5) How should we advise and treat patients with muscle cramps or contractures? We consider these questions and present a practical approach to muscle cramps and contractures, including their causes, pathophysiology and treatment options.

Weakness in the intensive care unit.

When asked to assess patients in an intensive care unit (ICU) who have respiratory muscle weakness, oropharyngeal weakness and a vulnerable airway, our immediate thought may be of Guillain-Barré syndrome or myasthenia gravis, but there are many other possible causes. For example, previously unrecognised chronic neurological conditions may decompensate and require ICU admission. Clinicians can use various clinical clues to help recognise them and need to understand how patterns of weakness reflect differing causes of reduced consciousness on ICU. Additionally, patients admitted to ICU for any reason may develop weakness during their stay, the most likely cause being ICU-acquired weakness. Assessing patients in ICU is challenging, hampered by physical barriers (machines, tubes), medication barriers (sedatives) and cognitive barriers (delirium, difficulty communicating). Nonetheless, we need to reach a clinical diagnosis, organise appropriate tests and communicate clearly with both patients and ICU colleagues.

IgG1 pan-neurofascin antibodies identify a severe yet treatable neuropathy with a high mortality.

OBJECTIVES: We aimed to define the clinical and serological characteristics of pan-neurofascin antibody-positive patients. METHODS: We tested serum from patients with suspected immune-mediated neuropathies for antibodies directed against nodal/paranodal protein antigens using a live cell-based assay and solid-phase platform. The clinical and serological characteristics of antibody-positive and seronegative patients were then compared. Sera positive for pan-neurofascin were also tested against live myelinated human stem cell-derived sensory neurons for antibody binding. RESULTS: Eight patients with IgG1-subclass antibodies directed against both isoforms of the nodal/paranodal cell adhesion molecule neurofascin were identified. All developed rapidly progressive tetraplegia. Cranial nerve deficits (100% vs 26%), autonomic dysfunction (75% vs 13%) and respiratory involvement (88% vs 14%) were more common than in seronegative patients. Four patients died despite treatment with one or more modalities of standard immunotherapy (intravenous immunoglobulin, steroids and/or plasmapheresis), whereas the four patients who later went on to receive the B cell-depleting therapy rituximab then began to show progressive functional improvements within weeks, became seronegative and ultimately became functionally independent. CONCLUSIONS: IgG1 pan-neurofascin antibodies define a very severe autoimmune neuropathy. We urgently recommend trials of targeted immunotherapy for this serologically classified patient group.

Muscle biopsy: what and why and when?

Skeletal muscle biopsy remains an important investigative tool in the diagnosis of a variety of muscle disorders. Traditionally, someone with a limb-girdle muscle weakness, myopathic changes on electrophysiology and raised serum creatine kinase (CK) would have a muscle biopsy. However, we are living through a genetics revolution, and so do all such patients still need a biopsy? When should we undertake a muscle biopsy in patients with a distal, scapuloperoneal or other patterns of muscle weakness? When should patients with myositis, rhabdomyolysis, myalgia, hyperCKaemia or a drug-related myopathy have a muscle biopsy? What does normal muscle histology look like and what changes occur in neurogenic and myopathic disorders? As with Kipling's six honest serving men, we hope that by addressing these issues we can all become more confident about when to request a muscle biopsy and develop clearer insights into muscle pathology.

Correction to: Smoking Policy Change Within Permanent Supportive Housing.

The original version of this article unfortunately contains mistakes. 1. On page 315, in the last sentence under the "Tobacco Use" subheading, the percentage should read "59.3%" rather than "55.6%". 2. On page 315, in the last sentence under the "Secondhand Smoke Exposure" subheading, the percentage "28.2%" should read "28.6%". 3. The presentation of "Post-policy" and "Pre-policy" terms in the Figs. 1 and 3 were incorrect. It should be read as: Figure 1: Pre-policy (n = 27); Post-policy (n = 16). Figure 3: Pre-policy (n = 55); Post-policy (n = 42). The corrected Figs. 1 and 3 are given below.

Smoking Policy Change Within Permanent Supportive Housing.

Smoke-free policies effectively reduce secondhand smoke (SHS) exposure among non-smokers, and reduce consumption, encourage quit attempts, and minimize relapse to smoking among smokers. Such policies are uncommon in permanent supportive housing (PSH) for formerly homeless individuals. In this study, we collaborated with a PSH provider in San Diego, California to assess a smoke-free policy that restricted indoor smoking. Between August and November 2015, residents completed a pre-policy questionnaire on attitudes toward smoke-free policies and exposure to secondhand smoke, and then 7-9 months after policy implementation residents were re-surveyed. At follow-up, there was a 59.7% reduction in indoor smoking. The proportion of residents who identified as current smokers reduced by 13% (95% CI: -38, 10.2). The proportion of residents who reported never smelling SHS indoors (apartment 24.2%, 95% CI: 4.2, 44.1; shared areas 17.2%, 95% CI: 1.7, 32.7); in outdoor areas next to the living unit (porches or patio 56.7%, 95% CI: 40.7, 72.8); and in other outdoor areas (parking lot 28.6%, 95% CI: 8.3, 48.9) was lower post-policy compared with pre-policy. Overall, resident support increased by 18.7%; however, the greatest increase in support occurred among current smokers (from 14.8 to 37.5%). Fewer current smokers reported that the policy would enable cessation at post-policy compared to pre-policy. Our findings demonstrate the feasibility of implementing smoke-free policies in PSH for formerly homeless adults. However, policy alone appears insufficient to trigger change in smoking behavior, highlighting the need for additional cessation resources to facilitate quitting.

Muscle hypertrophy and pseudohypertrophy.

The physical examination always begins with a thorough inspection and patients with potential neuromuscular weakness are no exception. One question neurologists routinely address during this early part of the assessment is whether or not there is muscle enlargement. This finding may reflect true muscle hypertrophy-myofibres enlarged from repetitive activity, for example, in myotonia congenita or neuromyotonia-or muscles enlarged by the infiltration of fat or other tissue termed pseudohypertrophy or false enlargement. Pseudohypertrophic muscles are frequently paradoxically weak. Recognising such a clinical clue at the bed side can facilitate a diagnosis or at least can narrow down the list of potential suspects. This paper outlines the conditions, both myopathic and neurogenic, that cause muscle enlargement.