1 s, and to correlate nerve fibre density with sensory abnormalities.

2 ural damage, external-sphincter weakness, or sensory abnormalities.

3 ects of movement disorders include intrinsic sensory abnormalities and the effects of external sensor

4                Many forms of dHMN have minor sensory abnormalities and/or a significant upper-motor-n

5 the phenomenology and physiological basis of sensory abnormalities, and about the role of the basal g

6                    The data do not support a sensory abnormality as the primary cause of microstrabis

7 dysfunction and behavioral disorders and how sensory abnormalities can contribute to the etiology of

8          No clinical or electrophysiological sensory abnormality existed; however, skin biopsy result

9 parent including hyperactivity, seizures and sensory abnormalities including a characteristic increas

10  and whether its activity levels may lead to sensory abnormalities is still unclear.

11                                   Widespread sensory abnormalities, not limited to the CRPS limb, hav

12 ot be readily distinguished from the similar sensory abnormalities produced by the ensuing diabetic n

13                                              Sensory abnormalities such as numbness and paresthesias

14 ynaptic reorganization may contribute to the sensory abnormalities that accompany peripheral neuropat

15 ermine whether microstrabismic subjects have sensory abnormalities that could give rise to a small an

16 ic factor (GDNF) both prevented and reversed sensory abnormalities that developed in neuropathic pain