RT Journal Article
SR Electronic
T1 Multicore disease
JF Neurology
JO Neurology
FD Lippincott Williams & Wilkins
SP 1039
OP 1039
DO 10.1212/WNL.24.11.1039
VO 24
IS 11
A1 HARRIS BONNETTE
A1 ROBERT ROELOFS
A1 WILLIAM H. OLSON
YR 1974
UL http://n.neurology.org/content/24/11/1039.abstract
AB A 46-year-old white man had a 12-year history of progressive, symmetrical proximal weakness. Changes consistent with a myopathy were seen on electromyography, along with normal nerve conduction velocities. Serum creatine phosphokinase was slightly elevated. Muscle biopsies showed type I fiber predominance and focal areas of absent or increased oxidative enzyme activity, with other fibers containing focal areas of absent myofibril-lar ATPase activity. Serial sections showed little correlation between abnormalities demonstrated with oxidative enzymes and ATPase. Ultrastruc-tural changes included focal disruption of myofibrils and Z-band streaming. Similar morphologic changles have previously been described in a congenital, nonprogressive myopathy.