The clinical features and preoperative and postoperative electrodiagnostic studies were reviewed in two professional pitchers with a suprascapular neuropathy. These studies demonstrate that denervation of the infraspinatus and/or supraspinatus muscle is not always due to entrapment of the nerve at the suprascapular or spinoglenoid notches, as is often proposed. Similar studies in healthy pitchers during spring training and again at midseason demonstrate that slowing of suprascapular nerve conduction is detectable in some cases as the season progresses. Sagittal sections of a cadaver with the arm fixed in the acceleration phase of the pitching motion demonstrate five possible sites of trauma to the suprascapular nerve. Mechanisms proposed to explain these progressive, but potentially reversible, changes include consideration of biomechanical factors as well as anatomical features. An alternative hypothesis to nerve trauma that explains this symptom complex is intimal damage to the axillary or suprascapular artery and subsequent production of microemboli which become trapped in the suprascapular nerve vasa nervorum.

In baseball pitchers, injuries to the throwing arm are common due to the extreme stresses placed on the elbow and shoulder joints. These result in peripheral nerve syndromes including ulnar neuropathy at the elbow and suprascapular neuropathy at the shoulder. Recurrent trauma to the axillary artery causing aneurysm and thrombus formation may lead to distal ischemia and stroke. Careful evaluation is required to identify musculoskeletal, neurologic, and vascular causes of upper extremity symptoms in the throwing athlete.

A family is described in which five males have late-onset facial weakness, dysarthria, dysphagia, and slowly progressive proximal weakness. Electrodiagnostic studies and muscle biopsy were compatible with spinal muscular atrophy. This family appears quite similar to several previously reported families with late-onset X-linked recessive spinal and bulbar muscular atrophy. Because of the relative homogeneity of this particular phenotype of spinal muscular atrophy, a single metabolic derangement was sought. Three obligate carriers were studied, and no abnormality was detected. A further family with this condition is briefly discussed.

Two patients with painless hypertrophy of one calf had clinical and myelographic features compatible with an S-1 radiculopathy. Electromyographic studies revealed intermittent spontaneous discharges (bizarre repetitive potentials) in the affected extremity. Several patients have previously been described with S-1 radiculopathy and calf hypertrophy with or without spontaneous electrical activity. The hypertrophy in the two present cases could have been caused by continuous stretching (both patients were very active), by the abnormal electrical activity, or by a combination of the two. A neurogenic lesion must be excluded in patients with isolated hypertrophy of a calf muscle, even in the absence of radicular pain.