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Introduction:
The thyroid hormones maintain the various metabolic
functions by stimulating the O2 consumption in most of
the cells of our body and are also necessary for their normal
growth and maturation. The thyroid gland though is not
essential for life; its absence causes mental and physical
growth retardation. It may be also due to some intrinsic
disorders in thyroid or pituitary or hypothalamus.1- 3

The investigators studied nerve conduction parameters in
hypothyroid patients to observe the incidence of
neuropathy and functional status of peripheral nerves in
thyroid deficiency. 4-6 Most of them had shown that
deficiency of thyroid hormones cause motor neuropathy
by affecting different peripheral nerves but more
commonly the median nerve. The common nerve
conduction parameters done by the investigators include

Motor Neuropathy in Hypothyroidism: Clinical and Electrophysiological
Findings
Sabina Yeasmin1, Noorzahan Begum2, Shelina Begum3
1Associate Professor of Physiology, Dhaka Community Medical College, Dhaka. 2Professor and Chairman, Department of Physiology, Bangabandhu
Sheikh Mujib Medical University, 3Professor, Department of Physiology, Bangabandhu Sheikh Mujib Medical University, Shahbagh, Dhaka

Abstract:
Background: Hypothyroidism is a clinical condition associated with low levels of thyroid hormones with raised TSH.
Peripheral neuropathy may be associated with hypothyroidism which usually develops insidiously over a long period of
time due to irregular taking of drugs or lack of thyroid hormone replacement1. Objectives: The present study was done
to evaluate the clinical and electro-physiological findings in hypothyroid patients in order to evaluate the neuromuscular
dysfunction as well as motor neuropathy.  Method: In this study, 70 subjects with the age range from 20 to 50 years of
both sexes were included of whom 40 hypothyroids were taken in study group (B) with the duration of 6 months to 5
years and 30 healthy euthyroid subjects were taken as control (Group A). On the basis of their TSH level, group B was
further divided into group B1 with TSH level <60 MIU /L (less severe) and group B2 with TSH >60 MIU /L (severe
group). The d latency and NCV for motor nerve function were measured by NCV machine in median and ulnar nerve for
upper limb and in common peroneal nerve for lower limb. TT3, TT4 were measured by RIA and TSH by IRMA method.
All these parameters were measured on the day 1 (one) of their first visit. Data were analysed statistically by ANOVA
and Z test. Result: Both TT3, TT4 levels were significantly (P<0.01) lower in hypothyroids in comparison to those of
control.  Diminished or absence of most of the deep tendon reflexes were found in all the hypothyroids. Most of the
patients (67.5%) showed significantly higher (P <0.01) motor distal latencies (MDL) with lower (P> 0.001) conduction
velocities (MNCV) and all these changes were more marked in group B2. Conclusion: So, the study revealed that motor
neuropathy may be a consequence of hypothyroidism.

Key Words: Hypothyroidism, neuropathy, electrophysiology

[BSMMU J 2008; 1(1): 15-18]

Address of Correspondence: Dr. Sabina Yeasmin, Associate Professor
of  Physiology, Dhaka Community Medical College, Dhaka.

motor distal latencies (MDL), Motor conduction velocities
(MNCV) in different peripheral nerves. Motor conduction
impairment of the nerve revealed by the increased MDL
and decreased MNCV in that nerve. In thyroid deficiency,
the nerve conduction impairment is frequent in late stage
of neuropathy and the common complaints are usually
weakness of muscles of the limbs followed by the atrophy
of the affected muscles supplied partially or completely
by the nerves. 4-6

A good number of patients are suffering from thyroid
deficiency which varies from mild to its severe form in
our country.7 Due to lower socioeconomic status and
illiteracy, most of the patients were not aware about the
consequences as well as the complications of delayed or
irregular treatment. Again, occurrence of neuropathy may
have some relationship with the severity of thyroid
deficiency 2; so they need to be more conscious about



29

complications of the disease. A few published data are
available regarding the normal values of nerve conduction
parameters of healthy Bangladeshi population, 8 but no
published data has yet to be found on these aspects in
hypothyroid patients.

Therefore, the study has been done to find out the motor
nerve conduction status of some peripheral nerves as well
as to evaluate presence of motor neuropathy in hypothyroid
patients. Again, this study may also give a guideline to the
physicians for proper and better management of
hypothyroids and also to create awareness among this
group of patients so that they can take early and regular
treatment and thereby minimizes the occurrence of the
neuropathy in hypothyroidism.

Methods:
This study was carried out in the Department of physiology,
BSMMU, Dhaka between January 2005 to December
2005. A total number of 70 subjects with the age range of
20 to 50 years of both sexes were included in this study,
of whom 30 euthyroids (TSH=0.3-5MIU/L) were included
in group A (control) and 40 hypothyroids were included
in group B (study group). They were further divided into
group B1 consisted of 15 hypothyroids with TSH < 60
MIU/L and group B2 consisted of 25 hypothyroid patients
with TSH> 60 MIU/L or severe group. Most of the
hypothyroid patients were under hormone replacement
therapy. The duration of the disease varied from 6 months
to 5 years. The objectives of the study were explained to
each of the subjects and their written consents were taken.
Detailed medical history was taken regarding drug intake
and their  clinical examinations were done. The common
features of motor nerve dysfunctions (weakness and
atrophy of the muscles of the limbs) were searched for in
all patients and all the informations were documented. The
hormones were measured by RIA14, 15 for TT3 and TT4
and IRMA16 for TSH. The nerve conduction studies were
done by electrophysiological method with a standard NCV
machine 5, 6.

The statistical analysis was done by one way ANOVA and
Z test. The study was performed at room temperature.

Results:
All the parametric variables were expressed as mean (±
SD). The comparison of the values were done among the
different groups. In this study, the mean TT3 and TT4 were
significantly lower in hypothyroids in comparison to those
of healthy group but the differences were not statistically
significant between two hypothyroid groups. (Table-I).

Table-I
The serum of TT3 and TT4 and TSH levels of the study

subjects (n=70)

Groups TT3 TT4
 (nmol/L) (nmol/L)

A (n=30) 2.18 ± 0.53 129 ± 28.51
(1.40-3.02) (71.19-172)

B1 (n=15) 1.31 ± 0.81 61.21 ± 29.81
 (1.3-2.7) (40-170)

B2 (n=25) 1.10 ± 0.85 54.4 ± 39.31
(0.45-1.25) (21-165)

          Statistical analysis

                                      P value

A vs B1 <0.01**  <0.001***
A vs B2  <0.001*** <0.001***
B1vs B2 0.75 

NS  0.889 NS

Results are expressed as Mean ± SD; One-way ANOVA (with
Post Hoc Test) was performed as the test of significance. Figures
in the parentheses indicate the ranges.

Group A=Euthyroids (control group), Group B1= Hypothyroids
with TSH level <60 MIU/L, Group B2= Hypothyroids with TSH
level >60 MIU/L,

 ***= P < 0.001, **= P <0.01.

n=Number of subjects, NS=Not significant.

Except diminished or absence of most of the deep tendon
reflexes, the typical clinical features of motor neuropathy
were absent in all patients.

Nerve study revealed, significantly higher (P < 0.01) distal
latency (MDL) and lower (P<0.001) conduction velocity
(MNCV) in both of the hypothyroid groups in comparison
to those of the control in median nerve  (Table II).

On the other hand, the differences of MDL were not
statistically significant between two hypothyroids and also
with that of control in ulnar nerve (Table-III).

Again, for common peroneal nerve, this value was higher
in both the hypothyroids but it was statistically significant
for severe group (Table 4). However, MNCV were
significantly, lower in both the hypothyroids for all nerves.
(TableII, III, IV).

All these parameters were statistically nonsignificant
between two hypothyroid groups.

Again, this study also revealed that, 27 (67.5%) of the
hypothyroid subjects showed the presence of neuropathy
by abnormal NCV, of whom 18 (66%) of the subjects were
in severe group and 9 (34%) were in less severe group.
(Table-V).

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Table-II
Nerve conduction parameters for motor function of

Median (M) nerve (n=70)

Groups d Latency (m sec) NCV (m/sec)
A (n=30) 2.92 ± 0.338 62.33 ± 5.274

(2.50-3.50) (66.00-74.00)
B1(n=15) 3.59 ±0.564 53.30 ± 5.046

(2.60-4.80) (43.00-61.00)
B2 (n=25) 3.90 ±0.0887  53.68 ± 6.053

(2.60-6.20) (44.00-66.00)

Statistical analysis
                                P value

A vs B1 <0.010**  <0.001***
A vs B2 <0.001***  < 0.001***
B1 vs B2 0.320 

NS 0.0991 NS

Results are expressed as Mean (± Standard deviation); One
way ANOVA (Post Hoc Test) was performed as the test of
significance, The figures in parenthesis indicate range.
Group A = Euthyroid control group,
Group B1 = Hypothyroids with TSH level < 60 m IU/L,
Group B2 = Hypothyroids with TSH level > 60 m IU/L,
d latency =  Distal Latency,
NCV = Nerve Conduction Velocity,
*** = P <0.001, ** = P<0.01, n = Number of subjects, NS
= Not Significant.

Table-III
Nerve conduction parameters for Motor function of

Ulnar (U) nerve (n=70)

Groups d Latency (m sec) NCV (m/sec)
A (n=30)  2.48 ± 0.207 60.13 ± 4.790)

 (2.00-2.70) (53.00-68.00)
B1 (n=15) 2.85 ±0.806 53.76 ± 5.309

(2.00-4.90) (45.00-60.00)
B2 (n=25) 2.87 ±0.688 53.26 ± 5.722

(2.10-4.20) (45.00-65.00)

Statistical analysis
                                                  P value
A vs B1 0.113

 NS  <0.01**
A vs B2  0.064 

NS < 0.001***
B1 vs B2 1.00 

NS 0.779 NS

Results are expressed as Mean (± Standard deviation); One way
ANOVA (Post Hoc Test) was performed as the test of
significance, The figures in parenthesis indicate range.
Group A = Euthyroid control group,
Group B1 = Hypothyroids with TSH level < 60 m IU/L,
Group B2 = Hypothyroids with TSH level > 60 m IU/L,
d latency = Distal Latency,
NCV = Nerve Conduction Velocity, *** = P <0.001, ** = P <0.01,
n = Number of subjects, NS = Not Significant.

Table-IV
Nerve conduction parameters for Motor function of

Common Peroneal (CP) nerve (n=70)

Groups d Latency (m sec) NCV (m/sec)
A (n=30) 3.60 ± 0.161 57.63 ± 4.230)

(3.30-3.90) (50.00-67.00)
B1 (n=15) 4.28 ±0.809 49.00 ± 3.273

(3.30-5.60) (43.00-57.00)
B2 (n=25) 2.87 ±0.688 53.26 ± 5.722

(3.40-9.50) (40.00-56.00)

Statistical analysis

                           P value
A vs B1 0.06

 NS <0.001***
A vs B2 <0.001*** <0.001***
B1 vs B2  0.435 

NS 0.786 NS

Results are expressed as Mean (± Standard deviation); One way
ANOVA (Post Hoc Test) was performed as the test of
significance, The figures in parenthesis indicate range.
Group A = Euthyroid control group,
Group B1 = Hypothyroids with TSH level < 60 m IU/L,
Group B2 = Hypothyroids with TSH level > 60 m IU/L,
d latency = Distal Latency,
NCV =Nerve Conduction Velocity,
*** = P <0.001,
n = Number of subjects, NS = Not Significant.

Table-V
Distribution of subjects by NCV (n=70)

Groups   n         Normal NCV          Abnormal NCV
 no  (%) no  (%)

A 30 27 90 3 10

 B 40 13 32.5 27 67.5 ***

B1 15 6 40 9 60

B2 25 7 28 18 72

Statistical analysis was done by ‘Z’ test as a test of
significance.
Z = 6.243
Group A=Euthyroid (control) group,
Group B= Hypothyroid group,
Group B1=Less severe hypothyroids,
Group B2 =Severe hypothyroids,
***=P<0.001
n=Number of subjects, NCV=Nerve conduction velocity.

Motor Neuropathy in Hypothyroidism: Clinical and Electrophysiological Findings Sabina Yeasmin et al

17



31

Discussion:
The hypothyroid patients showed no remarkable clinical
signs of motor neuropathy with the exception of a few
like diminished or absence of most of the deep tendon
reflexes but all the hypothyroids had significantly (P <0.01)
lower TT3 and TT4 levels compared to euthyroids.

Nerve conduction abnormalities were observed in a
significant number of hypothyroid patients by
electrophysiological studies. However, the nerve
conduction parameters in the control group were similar
or nearer to normal reference values .4, 9,11-13

Some other groups of investigators had also observed the
slowing of nerve conduction velocities in different
peripheral nerves but they did not mention about the
individual values of the parameters like motor distal
latency (MDL) and motor nerve conduction velocity
(MNCV). 5-6,14,16

Both the hypothyroid groups showed higher motor distal
latencies (MDL) with lower motor nerve conduction
velocities (MNCV) for median, ulnar and common
peroneal nerves. Again, the nerve conduction study
revealed the predominant impairment in the median nerve
among the three nerves as the differences of all the
parameters were statistically significant between
euthyroids and both the less severe and severe
hypothyroids in this nerve. The investigators of different
countries also mentioned about the similar involvement
of median nerve1, 5, 6,9,14,16.

The mechanisms involved in the development of
neuropathy in hypothyroidism are not yet fully established
but different investigators suggested that the weight gain
in hypothyroids may be a contributory factor for
neuropathy. In addition, the deposition of
mucopolysaccharide or the myxedematous tissue may also
lead to compression over the peripheral nerves and thereby
results in swelling and degeneration of them4, 6.

 It has also been suggested that the thyroid hormones
stimulate the mitochondrial respiratory activity to produce
energy in the form of ATP during aerobiosis under normal
physiological condition. Hormones also increase the
ATPase activity and consequently Na+/K+ pump activity
in this group of patients. Therefore, deficiency of ATP
and reduced ATPase and decreased Na+/K+ pump activity
cause subsequent alteration of pump dependent axonal
transport and thereby may lead to peripheral neuropathy14.
Decrease glycogen degradation may also leads to energy
deficit in hypothyroidism 5,6,14,16. Though the neuropathy
due to compression and the peripheral neuropathy due to
axonal degeneration are not fully distinguished, most

likely, there may be a combination of both these two
factors, which results in the development of peripheral as
well as the motor neuropathy in hypothyroidism 4.

Therefore, this study revealed that motor neuropathy is
not an uncommon manifestation in patients suffering from
hypothyroidism even in our population.

References:
 1. Dyck PF, Lambert EH. Poly neuropathy associated with

hypothyroidism. J  Neuropathol Exp Neurol 1970; 29: 631-658.

2. Edwards CRW, Toft AD, Walker BR. Endocrine disease.  In:
Haslett C, Chilvers E R, Hunter J A A, Boon N A. (editors).
Davidson’s principles and practice of medicine. London: Harcourt
Brace and Company; 1999; pp 559-575.

3. Ganong WF. Review of medical Physiology. 21nd ed. Boston :
Mc Graw Hill;  2003. 320p.

4. Preston DC. Electromyography and Neuromuscular Disorders,
Clinical - Electrophysiological Correlations. 1st ed. USA:
Butterworth- Heinemann; 1998.  561p.

 5. Rao SN, Katiyar BC, Nair KRP, Misra S. Neuromuscular status
in hypothyroidism. Acta Neurol Scand 1980; 61:167-77.

6. Shirabbe T, Tawara S, Tetrao A, Araki S. Myxedematous
polyneuropathy: a light and electron microscopy study of
peripheral nerve and muscle. J Neurol Neurosurg Psychiatry 1975;
38:  241-47.

7. Record from the Thyroid Clinic, Nuclear medicine and Ultrasound
Centre, DMCH, Dhaka.

8. Sultana S. Some aspects of electrophysiological changes of
peripheral nerves in  diabetic patients of different duration [M
Phil thesis] [Dhaka]: Bangabandhu Sheikh Mujib Medical
University; 2003. 114 p.

9. Total Triiodothyronine (T3) Radioimmunoassay Kit (PR) IMK-
422   [Manual] 2005, Department Of Isotope. China Institute of
Atomic Energy, Beijing.

10. Total Thyroxine (T4) Radioimmunoassay Kit (PR) IMK-419
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11. TSH Immunoradiometric assay Kit IMK-432   [Manual], Beijing
Atom Hightech Co Ltd. , Beijing2005

12.   Kimura J.  Electrodiagnosis in diseases of nerve and muscle:
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103 p.

13. Misra UK, Kalita J. Late response Clinical Neurophysiology; nerve
conduction, electromyography and evoked potentials. 1st ed.  New
Delhi :  Churchill Livingstone Pvt Ltd. 1999.  20 p.

14. Nemni R, Bottacchi E, Fazio R, et al. Poly neuropathy in
hypothyroidism: Clinical, Electrophysiological  and morphological
findings in 4 cases. J Neurol Neurosurg Psychiatry 1987; 50: 1454-
1460.

15. Palumbo CF, Szabo RM, Olmsted SL. The effects of
hypothyroidism and thyroid replacement on the development of
carpal tunnel syndrome. J Hand Surg 2000; 734-739.

16. Torres CF, Moxley RT. Hypothyroid neuropathy and myopathy:
clinical and electrodiagnostic longitudinal findings. J Neurol 1990;
237:271-274.

17. Crevasse LE, Logue RB. Peripheral neuropathy in myxedema.
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