Motor dysfunction develops in advanced cases of diabetic polyneuropathy [1,2]. In the clinic it is most frequently detected by inability to walk on heels which indicates a preponderance for the dorsal flexors of the ankle. Recently weakness of both the ankle dorsal and plantar flexors and of the knee extensors and flexors was found in long-term insulin-dependent diabetic (IDDM) patients with peripheral neuropathy at isokinetic dynamometry [3]. Furthermore, the weakness at the ankle and knee was closely related to the severity of neuropathy assessed clinically, electrophysiologically and at quantitative sensory examination.The present study was performed in order to clarify whether muscle weakness in diabetic patients with polyneuropathy is associated with muscular atrophy and secondly if present how the atrophy is topographically distributed. A non-invasive quantitative method for analysis of muscle volume was applied in the present study. Assessment of muscle morphology can be obtained with ultrasonomyography, X-ray computed tomography (CT), and magnetic resonance imaging (MRI) [4][5][6][7]. Ultrasonomyography is Diabetologia (1997) Summary Diabetic patients with polyneuropathy develop motor dysfunction. To establish whether motor dysfunction is associated with muscular atrophy the ankle dorsal and plantar flexors of the non-dominant leg were evaluated with magnetic resonance imaging in 8 patients with symptomatic neuropathy, in 8 nonneuropathic patients and in 16 individually matched control subjects. In the neuropathic patients the muscle strength of the ankle dorsal and plantar flexors was reduced by 41 % as compared to the non-neuropathic patients (p < 0.005). Volume of the ankle dorsal and plantar flexors was estimated with stereological techniques from consecutive cross-sectional images of the lower leg. The neuropathic patients had a 32 % reduction in volume as compared with the nonneuropathic patients (p < 0.005). To determine the regional distribution of atrophy cross-sectional magnetic resonance images were performed at predetermined levels of the lower leg in relation to bone landmarks. In the neuropathic patients there was an insignificant increase of 3 % of muscle area at the proximal lower leg level, whereas the atrophy was 43 % (p < 0.002) at the mid lower leg level and 65 % (p < 0.002) distally. Analysis of individual muscles confirmed that the atrophy predominated distally. We conclude that muscular atrophy underlies motor weakness at the ankle in diabetic patients with polyneuropathy and that the atrophy is most pronounced in distal muscles of the lower leg indicating that a length dependent neuropathic process explains the motor dysfunction. [Diabetologia (1997[Diabetologia ( ) 40: 1062[Diabetologia ( -1069

Valacyclovir treatment did not reduce the formation of active lesions in patients with relapsing-remitting MS who had two or more relapses during the previous 2-year period. In a subgroup of patients with high levels of disease activity who had more than one active MRI-evident lesion during 4 weeks, valacyclovir treatment was associated with a reduced number of new active MRI-evident lesions and with an increase in the number of scans free of new active lesions. The results of the exploratory subgroup analysis provide support for further studies of antiherpes therapy for patients with MS and high levels of MRI-evident disease activity.

The validity of the methods used for determination of muscle mass has not been evaluated previously. We determined muscle mass by estimating muscle volume with assumption-free stereological techniques applied to magnetic resonance imaging (MRI) in 18 healthy untrained subjects (6 women, 12 men) aged 41 yr (29-64 yr; median, range). Muscle mass was also estimated by measuring leg circumference and cross-sectional muscle areas (CSA) from MRIs at three predetermined levels. Power [peak torque (PT)] of the ankle dorsiflexors and plantar flexors was estimated by using isokinetic dynamometry. Dorsiflexor volume (r2 = 0.76, P < 5 x 10(-6)) and CSA (r2 = 0.73, P < 5 x 10(-5)) were related to PT, whereas circumference was not (r2 = 0.17, not significant). Correspondingly, a relationship to plantar PT was established for plantar flexor volume (r2 = 0.69, P < 5 x 10(-5)) and CSA (r2 = 0.46, P < 5 x 10(-3)) but not leg circumference (r2 = 0.15, not significant). SDs of the residuals were smaller for the relationship between dorsiflexor PT and volume than between PT and CSA (0.42 vs. 0.45) for plantar flexors (1.5 vs. 2.0). By using the Cavalieri method, six MRI sections and 15 min of point counting are sufficient to obtain a valid estimate of the volume of the muscles of the lower leg.

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