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Background/Objectives: Clonus is an involuntary rhythmic muscle contraction after sudden muscle stretch that occurs as a result of a lesion in the upper motor neurons. The real mechanism behind clonus remains obscure. The objective of this study was to investigate the effects of central-acting tizanidine treatment and peripheral extremity cooling on clonus. Participants: Thirty-eight patients with upper motor neuron involvement and sustained clonus. Methods: The 38 patients were divided into 3 groups: cold group (n ¼ 19), tizanidine group (n ¼ 13), and patient control group (n ¼ 6). A separate group of 21 able-bodied volunteers served as controls for the cold group. The physiologic effects of cold application were measured in the able-bodied group and compared with the effects in the patients in the cold group. All participants were evaluated by clinical and electrophysiologic measurements. Results: Changes in clinical and electrophysiologic measurements in the cold group were statistically significant compared with those of the tizanidine and patient control groups. Conclusions: Subsequent and long-term cold application induced prolonged inhibitory effects on clonus. Tizanidine had no significant effect on clonus. Suppression of clonus by cold highlights the importance of peripheral input in relation to central mechanisms.

In patients with stroke, OPS and NIHSS had significant contribution to the estimation of the functional status and OPS was more effective than NIHSS.