Re: Diabetic Lumbosacral Radiculoplexus Neuropathy

Letters to the Editor Re: Diabetic Lumbosacral Radiculoplexus Neuropathy To the Editor, With keen interest we reviewed the article on diabetic lumbosacral radiculoplexus neuropathy by Greenberg et al in the August 2009 issue of PM&R [1]. These cases are challenging to manage and infrequently present to outpatient spine clinics with the assumption of spinal causality. Acute functional management involves fall prevention with the associated L2⫺4 more than L5 and S1 radicular nerve distribution weakness. The usual presentation includes profound quadriceps weakness, knee buckling, and falling. The authors recommend using an “orthoses (most often an AFO [anklefoot orthoses] for residual foot drop)” because foot drop is the most common long-term sequella of diabetic lumbosacral radiculoplexus neuropathy [2]. In our experience, acute management in patients with knee extensor weakness requires a knee-AFO with a locking mechanism to keep the knee in extension or offset knee joint to control the knee flexion moment at heel strike, yet allow swing phase. A knee immobilizer and a walker may be used until brace fabrication is completed. Conversely, a solid ankle AFO will increase the knee flexion moment at heel strike, increasing fall risk in patients without sufficient knee extensor strength [3]. The author’s choice to change the patients AFO to a knee AFO because of insufficient knee stabilization after 3 months of home therapy supports our recommendation. Thus treating practitioners should be keenly aware of proximal, ie, strength prior to orthotic prescription. Michael Jaffe, MD Physical Medicine & Rehabilitation Intermountain Healthcare Salt Lake City, UT

REFERENCES 1. Greenberg JS, Singh J, Falcon N. Evaluation and rehabilitation of a patient with diabetic lumbosacral radiculoplexus neuropathy. PM&R 2009;1(8):774-777. 2. Dyck PJB, WIndebank AJ. Diabetic and nondiabetic lumbosacral radiculoplexus neuropathies: New insights into pathophysiology and treatment. Muscle Nerve 2002;25:477-491. 3. Lehmann JF. The biomechanics of ankle foot orthoses: Prescription and design. Arch Phys Med Rehabil 1979;60:200-207.

Re: Post-Polio Syndrome To the Editor, I am writing in regards to the Point/Counterpoint on “Post-Polio Syndrome: A Perspective from Three Countries,” which appeared in the November 2009 issue of PM&R [1]. For the past 20 years, I have evaluated at least one post-polio patient weekly. In reviewing the case scenario, I believe that “pulmonary-thoracic compliance” should have been included in the discussion of fatigue. I note that the patient had polio at age 2, thus one could suspect some involvement of motor neurons to diaphragm or accessory ventilatory muscles so that 40 to 50 years later she could have had ventilatory insufficiency to explain her fatigue. Pulmonary-thoracic compliance is the work necessary to expand the lungs; most is related to pulmonary and less to thoracic, but both could play a role. This used to be measured by noting the volume of air inhaled with a given pressure on the tank ventilator and plotting at various inhalation pressures. It is amazing to note how the reduced pulmonary-thoracic compliance would not be identified by vital capacity or tidal volume alone and could explain the fatigue. There are, of course, other viable explanations for fatigue, but this is one that deserves mention. Ernest W. Johnson, MD Ohio State University Dodd Hall, Room 1036, Columbus, OH E.W.J. Disclosure: nothing to disclose

Richard Kendell, DO Physical Medicine & Rehabilitation University of Utah Salt Lake City, UT M.J. Disclosure: nothing to disclose R.K. Disclosure: nothing to disclose DOI: 10.1016/j.pmrj.2009.12.009

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DOI: 10.1016/j.pmrj.2010.01.008

REFERENCE 1. Grimby G, Li J, Vandenakker C, Sandel ME. Post-polio syndrome: A perspective from three countries. PM&R 2009;1:1035-1040.

© 2010 by the American Academy of Physical Medicine and Rehabilitation Vol. 2, 222, March 2010