Soleus H-Reflex Change in Poststroke Spasticity: Modulation due to Body Position

Purpose. This study is aimed at exploring how soleus H-reflex change in poststroke patients with spasticity influenced by body position. Materials and Methods. Twenty-four stroke patients with spastic hemiplegia and twelve age-matched healthy controls were investigated. Maximal Hoffmann-reflex (Hmax) and motor potential (Mmax) were elicited at the popliteal fossa in both prone and standing positions, respectively, and the Hmax/Mmax ratio at each body position was determined. Compare changes in reflex behavior in both spastic and contralateral muscles of stroke survivors in prone and standing positions, and match healthy subjects in the same position. Results. In healthy subjects, Hmax and Hmax/Mmax ratios were significantly decreased in the standing position compared to the prone position (Hmax: p = 0.000 , Hmax/Mmax: p = 0.016 ). However, Hmax/Mmax ratios were increased in standing position on both sides in poststroke patients with spasticity (unaffected side: p = 0.006 , affected side: p = 0.095 ). The Hmax and Hmax/Mmax ratios were significantly more increased on the affected side than unaffected side irrespective of the position. Conclusions. The motor neuron excitability of both sides was not suppressed but instead upregulated in the standing position in subjects with spasticity, which may suggest that there was abnormal regulation of the Ia pathway on both sides.

Acquisition of a simple motor skill: task-dependent adaptation and long-term changes in the human soleus stretch reflex

Changing the H reflex through operant conditioning leads to CNS multisite plasticity and can affect previously learned skills. To further understand the mechanisms of this plasticity, we operantly conditioned the initial component (M1) of the soleus stretch reflex. Unlike the H reflex, the stretch reflex is affected by fusimotor control, comprises several bursts of activity resulting from temporally dispersed afferent inputs, and may activate spinal motoneurons via several different spinal and supraspinal pathways. Neurologically normal participants completed 6 baseline sessions and 24 operant conditioning sessions in which they were encouraged to increase (M1up) or decrease (M1down) M1 size. Five of eight M1up participants significantly increased M1; the final M1 size of those five participants was 143 ± 15% (mean ± SE) of the baseline value. All eight M1down participants significantly decreased M1; their final M1 size was 62 ± 6% of baseline. Similar to the previous H-reflex conditioning studies, conditioned reflex change consisted of within-session task-dependent adaptation and across-session long-term change. Task-dependent adaptation was evident in conditioning session 1 with M1up and by session 4 with M1down. Long-term change was evident by session 10 with M1up and by session 16 with M1down. Task-dependent adaptation was greater with M1up than with the previous H-reflex upconditioning. This may reflect adaptive changes in muscle spindle sensitivity, which affects the stretch reflex but not the H reflex. Because the stretch reflex is related to motor function more directly than the H reflex, M1 conditioning may provide a valuable tool for exploring the functional impact of reflex conditioning and its potential therapeutic applications. NEW & NOTEWORTHY Since the activity of stretch reflex pathways contributes to locomotion, changing it through training may improve locomotor rehabilitation in people with CNS disorders. Here we show for the first time that people can change the size of the soleus spinal stretch reflex through operant conditioning. Conditioned stretch reflex change is the sum of task-dependent adaptation and long-term change, consistent with H-reflex conditioning yet different from it in the composition and amount of the two components.

Is reflex sympathetic dystrophy a valid concept?

Patients with reflex sympathetic dystrophy (RSD) affecting one limb show similar sympathetic traffic in nerves supplying the affected and unaffected limb, despite unilateral autonomic effector dysfunction. This argues against the notion that RSD is mediated by a reflex change in the pattern of sympathetic discharge and underlines the fact that autonomic effector disturbances give little information about underlying nerve traffic. [blumberg et al.]

THE MECHANISM OF THE PROTECTIVE ACTION OF CLAMPING THE RENAL PEDICLES OF DOGS WITH ALLOXAN DIABETES

Clamping of the renal vessels gives rise to a reflex change of circulation at the level of the vascular zone innervated by the splanchnic nerves. Bilateral cutting of the splanchnic nerves and of the inferior part of the sympathetic chain at the level of the thorax prevents the reflex, and annuls the protective action of clamping the vascular pedicles of the kidney. Renal lesions are not absolutely necessary for the production of alloxan diabetes, but may aggravate diabetes, probably by adding the toxic effects of retention of urine.