Electrophysiological changes in XXXX : from subclinical alterations to disabling abnormalities.

@entity1 @entity6 @entity16 @entity3949 @entity305 @entity51 @entity854
Clinical spectrum of @entity3949 is variable; it may be asymptomatic, but once established as @entity305 , it is irreversible and may finally be disabling. To estimate the prevalence of subclinical @entity3949 in the UAE, we undertook a pilot study by means of nerve conduction study (NCS) of peroneal motor and sural sensory studies in 60 @entity6 with no symptoms of @entity16 . Neurological examination revealed clinical abnormalities suggesting @entity305 in 26 @entity1 , 43% of the @entity1 . NCS revealed abnormal values in 63% of the whole @entity1 . Abnormal NCS was confirmed in 88% of the positive sign group. As to the negative sign group 44% had abnormalities in NCS. Prolonged F-wave latency was seen in 29% in no sign group and in 66% of the @entity1 with positive signs. We found close association between @entity51 score and abnormalities in NCS. Among various parameter of systemic nerve conduction study in subclinical @entity1 , prolonged F-wave latency seems the commonest abnormality suggesting morphological changes in subclinical @entity6 . Decrease in amplitude of compound sensory action potential of sural nerve is another @entity854 , which is, then, accompanied by a fall in motor amplitude of peroneal nerve in advanced @entity1 . Recently, our own group of Hirosaki has demonstrated that somatosensory central conduction time (CCT) between the spinal cord entry time and the arrival time to the sensory cortex is prolonged in @entity6 . This abnormality might be partly responsible for the irreversible sensory deficits of @entity3949 .
