Poster 76 an unusual presentation of bilateral femoral nerve diabetic amyotrophy: A case report. Edward Albert G. Balbas, MD (East Carolina Univ, Greenville, NC); Scott Morioka, MD; Raymundo Millan, MD, e-mail: [email protected]

Poster 76 an unusual presentation of bilateral femoral nerve diabetic amyotrophy: A case report. Edward Albert G. Balbas, MD (East Carolina Univ, Greenville, NC); Scott Morioka, MD; Raymundo Millan, MD, e-mail: [email protected]

E24 2004 Academy Annual Assembly Abstracts demonstrates delayed involvement of bilateral neuromuscular structures almost 20y after mantle field radi...

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E24

2004 Academy Annual Assembly Abstracts

demonstrates delayed involvement of bilateral neuromuscular structures almost 20y after mantle field radiation for Hodgkin’s disease. The complication of right-sided shoulder pain from a partial rotator cuff tear and tendinopathy as well as cervical radiculopathy is probably causally related. Conclusions: Involvement of neuromuscular structures is a known complication of radiation therapy and can progress for years. Radiation fibrosis should be considered in the evaluation of musculoskeletal disorders of cancer survivors. Key Words: Brachial plexopathy; Electromyography; Hodgkin disease; Rehabilitation. Poster 76 An Unusual Presentation of Bilateral Femoral Nerve Diabetic Amyotrophy: A Case Report. Edward Albert G. Balbas, MD (East Carolina Univ, Greenville, NC); Scott Morioka, MD; Raymundo Millan, MD, e-mail: [email protected]. Disclosure: E.G. Balbas, None; S. Morioka, None; R. Millan, None. Setting: Acute rehabilitation hospital. Patient: 78-yo woman with type 2 diabetes mellitus, hypertension, coronary artery disease, and new-onset atrial fibrillation. Case Description: The patient was initially admitted for treatment of new-onset rapid atrial fibrillation. During her acute hospital stay she fell on her way to the bathroom. She had complained of weakness in both knees and decreased sensation in the lower extremities. She was medically managed in the intermediate unit and then was transferred to the rehabilitation service for strengthening and endurance training. Physical examination was remarkable for proximal muscle weakness and decreased sensation in both lower extremities. Electromyography and nerve conduction study showed evidence of bilateral severe, axonal, and demyelinating sensory and motor diabetic peripheral neuropathy with associated bilateral femoral diabetic amyotrophy. The patient was prescribed bilateral knee locking braces for ambulation. She was unable to ambulate initially when admitted to the rehabilitation unit but was able to ambulate 150ft on discharge day 22. Assessment/Results: Diabetic patients may develop a proximal neuropathy primarily manifesting as weakness of the hip flexors and adductors and knee extensors. This disorder may present in 1 of 2 different ways. 1 group is described as an abrupt onset of proximal thigh weakness that is rarely bilateral, referred to as proximal asymmetric neuropathy. The other type consists of a more gradual onset of progressive weakness over the course of a few days to several weeks. Weakness is typically bilateral and referred to as proximal symmetric neuropathy. Discussion: Our patient presented with an acute onset of bilateral proximal muscle weakness. Patients with this type of diabetic amyotrophy usually present with a gradual onset of symptoms. Conclusions: There has been no reported case in the literature of an acute-onset symmetric type of diabetic amyotrophy with only femoral nerve involvement. Key Words: Diabetic amyotrophy; Rehabilitation. Poster 77 Electrodiagnostic Testing in Paramyotonia Congenita: A Case Report. Sandra B. Maguire, MD (Spaulding Rehabil Hosp, Boston, MA); Lisa S. Krivickas, MD, e-mail: sbmaguire@ partners.org. Disclosure: S.B. Maguire, None; L.S. Krivickas, None. Setting: Outpatient electrodiagnostic lab. Patient: A 59-yo man with paramyotonia congenita, diagnosed clinically and using sodium channel gene mutation detection. Case Description: A standard electrodiagnostic evaluation was performed. Additionally, short (10s) and long (2min) exercise, plus cooling tests with electromyography, were performed. The right ulnar nerve was stimulated at the wrist, recording compound motor action potentials (CMAPs) from the abductor digiti minimi (ADM) muscle. Recordings were made periodically after short exercise until the amplitude approached baseline. Long exercise was then performed with CMAPs recorded periodically for 150min. For the cooling test, the left ulnar CMAP from the ADM muscle and needle exam of the first dorsal interosseous (FDI) were performed at 33°C. The left forearm was immersed in ice water until surface temperature was below 20°C for 7min, with CMAPs recorded during cooling. Needle exam of the FDI was immediately performed. As the forearm rewarmed, periodic CMAPs were recorded. Assessment/Results: Amplitude transiently increased (with subjective muscle tightness) in response to short and long exercise and normalized by 11min after short exercise with concurrent resolution of muscle tightness. After long exercise, the amplitude dropped to 44.3% of initial value by 33min, with incomplete recovery at 150min. Cooling did not change the needle exam; fibrillation potentials and myotonia persisted. Discussion: The electrodiagnostic findings resemble those described in the literature for hyperkalemic periodic paralysis more closely than those for paramyotonia congenita. The sodium channel gene mutation in this patient affected a different area of the sodium channel than previously identified in cases of paramyotonia congenita or hyperkalemic periodic paralysis. Conclusions: This case contributes to the understanding of variability in clinical phenotype, electrophysiology, and sodium channel mutations within the sodium channelopathies. Key Words: Electromyography; Myotonic Disorders; Rehabilitation; Sodium channels.

Poster 78 Acute Flaccid Paralysis in a Patient With West Nile Virus Infection: A Case Report. Mark Reznik, DO (Thomas Jefferson Univ, Philadelphia, PA); Ramadevi K. Swaminath, MD; David S. Dougherty, MD, e-mail: [email protected]. Disclosure: M. Reznik, None; R.K. Swaminath, None; D.S. Dougherty, None. Setting: Tertiary care medical center. Patient: A 56-yo man with West Nile virus (WNV) infection. Case Description: The patient developed progressive extremity and respiratory muscle weakness acutely after a viral prodrome. The initial electrodiagnostic studies revealed a predominantly axonal sensorimotor neuropathy with demyelinating features. Diagnosed with the acute motor sensory axonal neuropathy variant of Guillain-Barré syndrome (GBS), he achieved only partial success after treatment with both intravenous steroids and plasmapheresis. After 2mo in the inpatient rehabilitation unit, he regained functional strength in 3 of his extremities, but his left arm remained plegic. At discharge, the patient was able to ambulate household distances using a walker and required a moderate level of assistance for self-care. Assessment/Results: 14mo after his initial presentation, the patient’s left plegic arm continued to be his greatest motor deficit. He progressed to an independent level of functioning and was now able to ambulate community distances without

Arch Phys Med Rehabil Vol 85, September 2004

any assistive devices. Follow-up electrodiagnostic studies continued to show motoneuron loss as the principal feature of his paralysis. Discussion: Our findings suggest involvement of the anterior horn cells, similar to infections with the polio virus. Although many previous case studies have described the presentation of WNV infection as a poliomyelitis-like syndrome, our case and a few others suggest that demyelination as well as sensory involvement can be variants in the pathology of this disease. Conclusions: Areflexic weakness and acute flaccid paralysis, as prominent parts of the clinical presentation in many patients with WNV infection, may be caused by GBS or a poliomyelitis-like syndrome. It is possible to have features of both, making treatment decisions difficult. These patients continue to have varying degrees of functional and ambulatory deficits due to the permanent loss of motoneurons. Key Words: Paralysis; Rehabilitation; West Nile virus. Poster 79 Long-Term Electrodiagnostic and Clinical Improvement in Acute Flaccid Paraplegia Associated With West Nile Virus: A Case Report. Evan L. Rosenfeld, MD (Rehabil Inst Chicago, Chicago, IL); Christina Marciniak, MD, e-mail: [email protected]. Disclosure: E.L. Rosenfeld, None; C. Marciniak, None. Setting: Academic acute, free-standing inpatient rehabilitation hospital; and outpatient clinic at the same institution. Patient: 73-yo man with acute flaccid paralysis associated with West Nile virus (WNV) infection. Case Description: The patient presented for rehabilitation admission 16d after symptoms onset, with severe flaccid asymmetric weakness without sensory loss in the lower limbs. Cerebrospinal fluid and serum immunoglobulin M titers were positive for WNV. Electrodiagnostic studies demonstrated severe diffuse motor axonopathy consistent with an anterior myelitis. The patient participated in acute inpatient rehabilitation for 57d and continued with outpatient physical therapy during the entire follow-up period. He was evaluated both electrodiagnostically and clinically over the 18-mo follow-up. Assessment/Results: Electrodiagnostic testing at 6 and 18mo demonstrated continuing reinnervation, with the development of nascent voluntary motor unit action potentials (MUPs), first proximally and at 18mo distally in the left lower limb, including muscles in the distal left lower extremity, which did not demonstrate voluntary MUPs at initial and 6-mo studies. These findings corresponded with the patient’s ongoing clinical improvements; over time, he demonstrated increasing strength, with earlier return of strength to proximal muscles. By 18-mo follow-up, the patient also was ambulatory with modified independence for half a block. Discussion: Over 18mo, this patient with acute flaccid paralysis associated with WNV demonstrated slow but continuing recovery, both electrodiagnostically and clinically, suggesting that such persons can make gradual returns to functional and clinical baselines, which continue even at 1.5y postonset. Conclusions: Little is known about ultimate recovery in patients with WNV-associated anterior myelitis. Thus, it will be important to continue to document these ongoing improvements in a larger number of patients over an extensive follow-up period, in order to form more accurate assessments of prognosis and to optimize rehabilitation programs for such patients. Key Words: Electrodiagnosis; Myelitis; Rehabilitation; West Nile virus. Poster 80 Parsonage-Turner Syndrome due to West Nile Virus: A Case Report. John C. Keel, MD (Emory Univ, Atlanta, GA); Sushma Chandan, MD; Ruben Diaz, MD, e-mail: [email protected]. Disclosure: J.C. Keel, None; S. Chandan, None; R. Diaz, None. Setting: Veterans Administration medical center. Patient: A 68-yo man with fever, shoulder pain, and weakness. Case Description: The patient was admitted with a fever of 39.7°C. While hospitalized, he awoke 1 morning with new severe left shoulder pain. Within days he noticed weakness in the left shoulder. Pain subsided over the next days, but weakness persisted. On day 12 of hospitalization, serum tested positive for immunoglobulin M antibodies against West Nile virus (WNV). On day 14, we were consulted to evaluate the patient’s left shoulder pain and weakness. Assessment/Results: Exam revealed decreased mass in the left shoulder muscles. Passive range of motion (ROM) was normal and there were no signs of impingement. There was profound weakness of the left shoulder, but strength was normal in the right upper extremity and in both lower extremities. There were no upper motoneuron signs. Sensation was intact throughout the left upper extremity. Electrodiagnostic findings revealed acute axonal denervation in multiple distributions of the left brachial plexus. By day 15, the febrile illness had resolved, and the patient was discharged home. We recommended continued ROM exercise to prevent adhesive capsulitis and a sling to prevent subluxation of the humerus. Discussion: Parsonage-Turner syndrome, also known as neuralgic amyotrophy or brachial neuritis, is an uncommon disorder characterized by relatively sudden onset of pain in the shoulder followed by upper-extremity weakness. Etiology is unknown but may be due to antecedent infection or immunologic triggers. Patients may recover spontaneously over months to years. To our knowledge, this is the first description of Parsonage-Turner syndrome due to WNV. Conclusions: We describe a case of Parsonage-Turner syndrome in a patient infected with WNV. Key Words: Brachial plexus; Electrodiagnosis; Rehabilitation; West Nile virus. Poster 81: Refer to Abstract 38 in the EMG Poster Grand Rounds for the full abstract. e-mail: [email protected]. Poster 82 Comparison of Different Test Methods for the Vibration Perception Threshold Test and the Relationship to Nerve Conduction Studies. Hyun Jung Kim, MD, PhD (Eulji Gen Hosp, Eulji Univ, Seoul, Republic of Korea); Dong-Hwan Yun, MD; Young-Seok Park, MD; Kang-Sik Lee, MD, e-mail: [email protected]. Disclosure: H. Kim, None; D. Yun, None; Y. Park, None; K. Lee, None. Objective: To determine the most feasible method of using the vibration perception threshold (VPT) test to diagnose diabetic neuropathy. Design: Prospective cross-sectional. Setting: Electromyography laboratory of a university hospital. Participants: 57 subjects with diabetes. Interventions: Not applicable. Main Outcome Measures: Each subject underwent VPT testing using the limit-up and -down methods, and the 4-2-1 testing algorithm. The stimulus was applied to the distal pulp of the right index finger. Nerve conduction studies (NCSs) of both sensory and motor