The clinical presentation, symptoms, and signs in 20 new patients with the painful legs and moving toes syndrome are presented. Painful legs and moving toes may develop in the setting of spinal cord and cauda equina trauma, lumbar root lesions, injuries to bony or soft tissues of the feet, and peripheral neuropathy. In 4 of the 20 cases in the present study, no definite cause was found. Pain preceded the onset of toe movements in 18 cases, but in 2 the reverse sequence occurred. The pain had many of the characteristics of causalgia, but none of the patients exhibited the full picture of reflex sympathetic dystrophy, and peripheral trauma was the trigger in only 5 cases. Several patients reported that the occurrence of toe movements was closely related to the pain, although abolition of pain with lumbar sympathetic blocks was not necessarily associated with disappearance of the movements. Several features suggest a central origin for the movements. Symptoms may begin on one side and become bilateral; movements may be momentarily suppressed by voluntary action or exacerbated by changing posture; and electromyography reveals complex patterns of rhythmic activity with normal recruitment of motor units involving several myotomes. Three other patients with similar moving toes but no pain are also described. The occurrence of similar movements in the absence of pain raises the possibility that these cases represent examples at one end of a spectrum of disorders, with pain alone (causalgia) at the other end and the syndrome of painful legs and moving toes in between.(ABSTRACT TRUNCATED AT 250 WORDS)
The characteristics of demyelination and remyelination in the central nervous system of the cat were examined using quantitative single-fiber analysis. Internodal length, fiber diameter, and nodal gap length were measured in single fibers teased from the spinal cord of normal animals and of animals with transient experimental cord compression. Demyelination was primarily paranodal, but longer extents of myelin loss occurred. New myelin sheaths were formed by oligodendrocytes and organized into segments bounded by nodes. The internodal length remained inappropriately short for fiber diameter 6 months after compression. The findings demonstrate that the spinal cord is capable of remyelinating after injury, but whether this contributes to functional recovery remains unknown. MethodSeventeen adult cats were used, including those in the electron microscopy study described in the precedingpaper [lo]. Fourteen were subjected to acute compressive lesions of the spinal cord, and 3 were studied as histological controls. Details of the method of compressing the spinal cord at the first lumbar vertebra appear elsewhere [ l o , 131. Material for histological examination was prepared in a similar way for all 17 animals, using the method of Harrison, McDonald, and Ochoa [ 141. The 14 cats with compressive lesions were killed at the following times: 2 after 2 1 hours; 1 each after 2,3,5, and 7 days; 1 after 2 weeks, 1 after 3 weeks, 2 after 4 weeks, 1 after 5 weeks, 1 after 6 weeks, 1 after 3 monrhs, and 1 after 6 months. The spinal cord was fixed in situ by retrograde aortic perfusion using 4 to 5% glutaraldehyde in 0.15 M phosphate buffer (pH 7.4) followed by 400 ml of chromebuffered osmium tetroxide [ 15, 161. Total perfusion time was approximately 1 hour. An extensive thoracolumbar laminectomy was carried out, and the fixed spinal cord from approximately the tenth thoracic to the fourth lumbar vertebra was removed in toto and cut transversely into three equal blocks approximately 1.5 cm long. The blocks were then prepared for single-fiber studies by Ohlrich's method [17, 181. Longitudinal frozen sections 60 pm in thickness were teased in 60% glycerin under a Zeiss dissecting microscope with fine mounted needles using a modification of the technique for teasing peripheral nerve fibers [ 19,201. Great care was taken to minimize stretching and damage to the fibers .Measurements and photographs were made on isolated fibers with a Leitz light microscope using a calibrated ocular graticule. Magnifications of x250 were used to measure internodal length and x400 to measure external fiber diameter and nodal gap. In determining fiber diameter, the procedure of Williams and Kashef [21] was adopted in which the mean of the diameters measured at five equidistant points in each internode was used. The measurements
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