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The Differential Diagnosis of Weakness: 5 Cases

The Differential Diagnosis of Weakness: 5 Cases

Determining the cause of generalized weakness can be a daunting task, since the differential diagnosis is vast. An overall approach to the patient who complains of generalized weakness is presented in our article. Here we offer an Algorithm that summarizes the diagnostic approach, along with 5 illustrative cases. Each demonstrates how anatomic localization, a refined differential diagnosis, and ancillary laboratory tests can be combined to help pinpoint the cause of the problem.

Case 1

Progressive Weakness in a Woman With Systemic Lupus Erythematosus

A 35-year-old woman with systemic lupus erythematosus (diagnosed 2 years earlier following an evaluation for arthralgias, adenopathy, and Raynaud phenomenon) presented with a 4-month history of progressive weakness. Initially, the patient complained of inability to walk long distances. Subsequently, she noticed that she had difficulty in climbing stairs, as well as in getting out of chairs and in getting off the toilet. Her weakness slowly progressed to the point where she required a cane to walk. During the past 4 to 6 weeks, weakness developed in the patient's arms. In particular, she described difficulty in lifting her arms to brush her teeth, comb her hair, and replace dishes in overhead cabinets. All the symptoms were equal bilaterally. The patient's weakness did not fluctuate throughout the day and was not affected by exercise. The patient denied any numbness, tingling, or pain. The family history was unremarkable.

Neurological examination revealed normal mental status; the cranial nerve examination was also normal. Bilateral mild atrophy of the shoulder girdle muscles was noted, along with symmetric weakness in the legs and arms, greater proximally than distally. Reflexes were mildly reduced but easy to elicit, and plantar stimulation produced downgoing toes. Sensory and coordination examinations were normal. The patient was able to walk only with assistance.

Laboratory studies revealed an erythrocyte sedimentation rate of 50 mm/h, a creatine kinase level of 5000 U/L, and a normal level of thyroid-stimulating hormone. Electrodiagnostic studies indicated a myopathy with muscle membrane irritability, suggesting an inflammatory, dystrophic, or toxic/metabolic myopathy. A follow-up muscle biopsy confirmed the presence of polymyositis. The patient's condition improved with corticosteroid treatment.

Step 1. Anatomic localization (examination): The neurological examination established the anatomic location. The presence of symmetric weakness, greater proximally than distally, in combination with the normal sensory and reflex examinations suggested the presence of a muscle disorder. This generated the initial differential diagnosis.

Step 2. Refined differential diagnosis (history): The history helped further refine the initial differential diagnosis. The subacute/chronic progression was consistent with an endocrine, inflammatory, toxin- or drug-induced myopathy; sarcoidosis; infectious disorder; or a late decompensation of a congenital or hereditary muscle disorder. There was no drug or toxin history. The family history was unremarkable, and the early developmental history did not suggest a congenital disorder. The history of systemic lupus erythematosus indicated the possibility of an inflammatory myopathy.

Step 3. Ancillary laboratory studies: The subsequent electromyographic and laboratory evaluations were consistent with an inflammatory myopathy; the follow-up muscle biopsy (with muscle selection directed by the electromyographic study) confirmed the diagnosis of polymyositis.


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