Alterations in peripheral nerves are well documented in overt myxedema
but not in subclinical hypothyroidism. We performed electrophysiologi
c studies to investigate such abnormalities in patients with normal se
rum total T-4 and hyperresponsiveness of TSH to TRH, either with norma
l or high levels of basal circulating TSH. Subjects were divided in th
ree groups: (i) Hypothyroidism Stage I (group I) (n = 17, mean age = 3
9 +/- 4 years), T-4 = 9 +/- 0.7 mu g/dL, TSH = 4.3 +/- 0.4 mu U/mL, TS
H post-TRH (peak value) = 37.6 +/- 1.6 mu U/mL; (ii) Hypothyroidism St
age II (group II) (n = 10, mean age: 43 +/- 6 years), T-4 = 7.7 +/- 0.
8 mu g/dL, TSH = 20 +/- 5 mu U/mL, TSH post-TRH > 50 mu U/mL; (iii) Co
ntrol Group (n = 20, mean age 41 +/- 5 years), healthy subjects. All p
atients and controls were women. TRH test consisted in the iv injectio
n of 200 mu g TRH (normal peak value up to 25 mu U/mL, normal basal TS
H < 5.5 mu U/mL). None of the patients had carpal tunnel syndrome or a
ny other neurological or metabolic disturbances. We studied the distal
motor latencies, motor and sensory amplitudes, and nerve conduction v
elocities. The motor parameters were measured in the median and extern
al sciatic popliteal (ESP) nerves, and the sensory parameters in the m
edian and sural nerves. In most cases values were obtained from both r
ight and left nerves. Motor parameters: no differences were found betw
een all groups for conduction velocities (CV). The motor distal latenc
ies (MDL) in median nerves in groups I and II vs. controls were 3.6 +/
- 0.1 and 3.6 +/- 0.2 vs 3.0 +/- 0.1 msec (p < 0.05). The MDL in ESP n
erves vs controls were 4.5 +/- 0.1 and 4.9 +/- 0.2 vs 4.2 +/- 0.1 msec
(p < 0.05). Amplitudes in group I were only decreased in the ESP nerv
es when compared to controls: 4.8 +/- 0.8 vs 6.6 +/- 0.5 mV (p < 0.05)
. However, group II showed a significant shortening of the amplitude i
n both the median and ESP nerves when compared to controls: 6.9 +/- 0.
9 vs 8.6 +/- 0.2 mV (p < 0.05) and 3.4 +/- 0.7 vs 6.6 +/- 0.5 mV (p <
0.05), respectively. Sensory parameters: no differences were observed
for CV between the three groups. The amplitudes were significantly dec
reased in sural nerves in groups I and II when compared to the control
group: 26.8 +/- 2.4 and 21.3 +/- 2.0 vs 32.1 +/- 2.5 mu V (p < 0.05).
However, measurements in median nerve showed significant differences
only between group II and controls: 41.3 +/- 3.8 vs 52.5 +/- 4.1 mu V
(p < 0.05). As shown, MDL are increased in both stages of subclinical
hypothyroidism; amplitudes are low in stage n but are affected in the
leg nerves only in stage I. Nervous conduction speeds are normal in al
l groups. It is concluded that an incipient axonal alteration is prese
nt in subclinical hypothyroidism. The abnormality is more evident when
basal levels of TSH are increased. However, most of these alterations
are also present when hyperresponsiveness of TSH to TRH is the appare
nt unique abnormality of thyroid function.