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 Table of Contents  
ORIGINAL ARTICLE
Year : 2017  |  Volume : 12  |  Issue : 4  |  Page : 229-233

Study of motor nerve conduction velocity in patients of thyroid dysfunction in central India


1 Department of Physiology, Jawaharlal Nehru Medical College, Wardha, Maharashtra, India
2 Department of Physiology, Shri Shankaracharya Institute of Medical Sciences, Bhilai, Chhattisgarh, India

Date of Web Publication17-May-2018

Correspondence Address:
Dr. Avinash Baliramji Taksande
Department of Physiology, Jawaharlal Nehru Medical College, Sawangi (M), Wardha, Maharashtra - 442 004
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jdmimsu.jdmimsu_100_17

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  Abstract 


Background: Hypothyroidism is a clinical disorder due to the deficiency of thyroid hormone. This hormone is a key regulator of cellular metabolism in our body. Hypothyroid state is usually asymptomatic, symptoms in the early phase while associated with a number of symptoms later affecting skin, heart, endocrine, brain, and nerves. Hyperthyroidism is less commonly associated with neuromuscular disorders and polyneuropathy. Objective: The objective of the study was to assess motor nerve functions in thyroid dysfunction patients. Study Design: This study design was a comparative study. Population: The study population was clinically diagnosed thyroid dysfunction patients and healthy individuals. Sample Size: The sample size was 82 (41 each in cases and control group). Materials and Methods: Neuro Perfect 2 – Channel EMG NCV EP, Medicaid, instrument was used. Parameters such as distal motor latency (DML), compound motor action potential CMAP amplitude, conduction velocity (CV) for motor nerve, and F-wave minimum latency of motor nerve were recorded and analyzed. Results: The median motor nerve CV (MNCV) and F-minimum latency were significantly reduced in cases as compared to controls on the right side (P < 0.05). The MNCV, DML, and F-minimum latency were significantly reduced in cases as compared to controls on the left side (P < 0.05). Conclusion: The findings suggest that polyneuropathy is associated with hypothyroidism. Further nerve conduction study might be useful to evaluate and to diagnose peripheral neuropathy in hypothyroid patients.

Keywords: Motor nerve function, sensory nerve function, thyroid dysfunction


How to cite this article:
Taksande AB, Jagzape AT, Deshpande V K. Study of motor nerve conduction velocity in patients of thyroid dysfunction in central India. J Datta Meghe Inst Med Sci Univ 2017;12:229-33

How to cite this URL:
Taksande AB, Jagzape AT, Deshpande V K. Study of motor nerve conduction velocity in patients of thyroid dysfunction in central India. J Datta Meghe Inst Med Sci Univ [serial online] 2017 [cited 2018 Aug 20];12:229-33. Available from: http://www.journaldmims.com/text.asp?2017/12/4/229/232572




  Introduction Top


Hypothyroidism is a clinical disorder due to the deficiency of thyroid hormone. This hormone is a key regulator of cellular metabolism in our body. This deficient state is estimated to affect 3.8%–4.6% of general population. Hypothyroid state is usually asymptomatic, symptoms in the early phase while associated with a number of symptoms later affecting skin, heart, endocrine, brain, and nerves. Peripheral polyneuropathy, a progressive nerve disorder to become chronic disability, may be due to the defect in axons, nerve cell body, or myelin sheath. It usually manifests as numbness, paresthesia, weakness, fatigue, loss of reflexes, and loss of vibration.[1]

Hyperthyroidism is less commonly associated with neuromuscular disorders and polyneuropathy is a relatively rare complication of hyperthyroidism.[2]

Electrophysiological assessment of sensory nerve action potential, CMAP amplitudes, distal motor latency (DML), sensory nerve conduction velocity (CV), and motor nerve CV (MNCV) helps to characterize and quantify the sensory and motor functions in the peripheral nerves.[3]

The purpose of the study is evaluating functional changes in the peripheral nervous system in thyroid dysfunction patients.

The study aims at assessing the electrophysiological functions of the motor nerves in cases of clinically manifested thyroid dysfunction.

The objective of the study is to assess motor nerve functions in thyroid dysfunction patients.


  Materials and Methods Top


Setting

This study was conducted at outpatient department (OPD) of a tertiary care hospital in Central India.

Study design

This study design was a comparative study.

Population

Clinically diagnosed thyroid dysfunction patients and healthy individuals selected conveniently.

Sample size

The sample size was 82 (41 each in study and control groups).

Inclusion criteria

Diagnosed cases of thyroid dysfunction of both gender and those who were in the age group of 18–60 years and attended OPD for treatment were included in the study.

Exclusion criteria

The individuals having following clinical conditions were excluded:

  • Known causes of neuropathy (diabetes mellitus, leprosy)
  • History of limb injuries/trauma
  • Ulcers
  • Cardiac pacemakers and cardiac pathology
  • Malignancy
  • Vascular pathology, bleeding, and clotting disorders
  • Neuromuscular transmission disorders and myopathy
  • Alcoholism.


Materials

Instrument used was Neuro Perfect 2 – Channel EMG NCV EP, Medicaid [Figure 1].
Figure 1: Neuro Perfect 2– Channel EMG NCV EP, Medicaid

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This instrument was used to record parameters such as DML, CMAP amplitude, and CV for motor nerve, and F-wave minimum latency of motor nerve was recorded and analyzed.

Method of data collection

Nerve conduction study consisted of motor nerve conduction and F-wave study of motor nerves.

Motor nerve conduction study

Motor nerve conduction study involved stimulation of a motor nerve at two different sites, with maximum stimulus; the distance was measured and automatically divided by conduction time between the two points (difference between proximal and distal motor latencies) which gave the CV.

Ground electrode was placed between stimulating and recording electrodes. Surface disc electrode was placed on abductor pollicis brevis muscle for median, on abductor digiti minimi for ulnar nerve, on extensor digitorum brevis for peroneal, and on abductor hallucis for tibial nerve. Belly tendon montage was used with cathode and anode 3 cm apart. Nerve was stimulated at wrist and elbow for median, ulnar and at ankle, and at or below popliteal fossa for tibial and peroneal.

Setting for upper limb duration was set up at 100 μs, sweep speed was 5 ms/D, and filter was between 2 Hz to 5 KHz, and for lower limb duration was 200 μs, filter was between 2 Hz to 10 KHz, and sweep speed was kept the same as upper limb.

F-wave study

F-wave study involved supramaximal stimulation of motor nerves.

F wave recording electrode setting same as MNCS.

A large CMAP followed by a small irregular shaped CMAP was elicited. The latter was called F-wave.

Minimum 10 stimuli were passed to obtain the F waves on rastered scale and the minimum F-wave latencies were noted.

Setting for F-wave study was duration 100 μs, sweep speed was 10 ms/D, and filter was between 2 Hz to 10 KHz.


  Results Top


Statistical analysis was done using descriptive and inferential statistics using Chi-square test and student's t-test and software used in the analysis was SPSS17/0 version (SPSS Inc., Chicago, USA) and P < 0.05 was considered as level of significance.

Age-wise distribution of the study participants shows that there was no statistically significant difference between control and cases of hypothyroidism in age (P = 0.08). Gender-wise distribution of the study participants shows that there is a significant difference in the composition of groups (P = 0.0003) as there are more males (33/41) in the control group and the number of females in the study group is more (24/41) [Table 1].
Table 1: Distribution of subjects according to their demographic characteristics

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Nerve conduction abnormalities were found in patients of hypothyroidism as compared to controls.

The median MNCV and F-minimum latency were significantly reduced in cases as compared to controls on the right side.

There is statistically significant difference in the CV (P = 0.0001) and F-minimum (F-min) (P = 0.03) of the right median nerve. The statistically significant difference is also found for DML (P = 0.001), CV (P = 0.0001), and F-min (P = 0.001) of the left median nerve.

There is statistically significant difference in the CV (P = 0.0001) and F-min (P = 0.0001) of the right ulnar nerve. The statistically significant difference is also found for amplitude (amp) (P = 0.023), CV (P = 0.0001), and F-min (P = 0.0001) of the left ulnar nerve.

There is statistically significant difference in the DML (P = 0.0001) and CV (P = 0.0001) of the right tibial nerve. The statistically significant difference is also found for DML (P = 0.020), amp (P = 0.018), and CV (P = 0.0001) of the left tibial nerve.

There is statistically significant difference in the CV (P = 0.0001) and F-min (P = 0.019) and of the right peroneal nerve. The statistically significant difference is also found for DML (P = 0.006), amp (P = 0.0001), CV (P = 0.0001), and F-min (P = 0.025) of the left peroneal nerve [Table 2].
Table 2: Comparison of motor nerve conduction in two groups

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This indicates that the MNCV, DML, and F-minimum latency were significantly reduced in cases as compared to controls on left side.


  Discussion Top


The present study aimed at assessing the electrophysiological functions of the median, ulnar, tibial, and peroneal motor nerves in cases of clinically manifested thyroid dysfunction.

The findings reveal that there is subclinical peripheral nerve involvement in diagnosed cases of hypothyroidism. CV and F-minimum latency were significantly reduced in cases as compared to controls in bilateral median nerves and DML significantly reduced in cases as compared to controls in left median nerves (P< 0.05).

These findings for motor conduction parameters in hypothyroids are consistent with that reported by Kececi and Degirmenci, 2006,[4] El-Salem and Ammari, 2006,[5] and Yeasmin et al., 2008[6] The mechanisms involved in the development of neuropathy in hypothyroidism are not yet fully established.

Thyroid hormone is also known to influence the synthesis is of protein and the production of enzyme and of myelin sheath.[7],[8]

Myelin synthesis is an important factor in determining the speed of impulse transmission along the nerve length.[7],[9] Disturbed myelin synthesis during acute hypothyroidism may be the cause for demyelinating peripheral neuropathy in hypothyroid patients.

Hormonal and metabolic changes associated with hypothyroidism are responsible for the electrophysiological changes in the form of abnormal peripheral nerve conduction study which occurs early in the disease course.

Thyroid hormone seems to increase ATPase activity and consequently, the activity of the ATP-dependent Na+/K + pump.

The increase in ATPase activity would be associated with an increase of ATP transport through the mitochondrial membranes.

In hypothyroidism, the ATP deficiency and the reduced activity of the ATPase enzyme induce a decrease in Na+/K + pump activity, with consequent alterations of pump dependent axonal transport.

This leads to axonal degeneration and peripheral neuropathy in hypothyroidism.[7]

The mucinous infiltrations found in the peripheral nerves could interfere mechanically with metabolic exchange of nutrients and catabolic products to and from the neuron, resulting in entrapment neuropathy in hypothyroidism.[2]

The deposition of mucopolysaccharide or the myxomatous tissue around the peripheral nerves may also lead to its compression and thereby results in swelling and degeneration of those nerves, leading to peripheral neuropathy in hypothyroidism.[10]

The median nerve entrapment at the wrist caused by the deposition of mucinous material in the tissues surrounding the nerve is one of the most frequent causes of peripheral nerve damage in hypothyroidism.[11],[12]

However, the neuropathy due to compression and that due to axonal degeneration is not fully distinguished.

There may be a combination of both of these which results in the development of peripheral neuropathy in hypothyroidism.

The motor neural dysfunction seen in the present study may be linked to the various functional and structural changes in peripheral nerves associated with deficiency of thyroid hormones.


  Conclusion Top


The present study findings suggest that the polyneuropathy is associated with hypothyroidism. It further suggests that nerve conduction study might be useful to evaluate and to diagnose peripheral neuropathy in hypothyroid patients.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Balaraman A, Natarajan G, Vishwanatha Rao B, Kabali B. A study of nerve conduction velocity in newly diagnosed hypothyroid females. World J Med Sci 2013;9:198-201.  Back to cited text no. 1
    
2.
Ajeena IM. Prevalence of neuromuscular abnormalities in newly diagnosed patients with thyroid dysfunction. Am J Res Commun 2013;1:79-88.  Back to cited text no. 2
    
3.
Mishra UK, Kalita J. Clinical neurophysiology. Elsiver pub. 2nd edition 2006.  Back to cited text no. 3
    
4.
Kececi H, Degirmenci Y. Hormone replacement therapy in hypothyroidism and nerve conduction study. Neurophysiol Clin 2006;36:79-83.  Back to cited text no. 4
[PUBMED]    
5.
El-Salem K, Ammari F. Neurophysiological changes in neurologically asymptomatic hypothyroid patients: A prospective cohort study. J Clin Neurophysiol 2006;23:568-72.  Back to cited text no. 5
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6.
Yeasmin S, Begum N, Begum S. Motor neuropathy in hypothyroidism: Clinical and electrophysiological findings. BSMMUJ 2008;1:15-8.  Back to cited text no. 6
    
7.
Bijen N, Murat Y, Mustafa G, Ilhan Y, Ali Ihsan B. Blink reflex in hypothyroidism. Endocrinologist 2007;17:144-7.  Back to cited text no. 7
    
8.
Ozkardes A, Ozata M, Beyhan Z, Corakci A, Vural O, Yardim M, et al. Acute hypothyroidism leads to reversible alterations in central nervous system as revealed by somatosensory evoked potentials. Electroencephalogr Clin Neurophysiol 1996;100:500-4.  Back to cited text no. 8
[PUBMED]    
9.
Ladenson PW, Stakes JW, Ridgway EC. Reversible alteration of the visual evoked potential in hypothyroidism. Am J Med 1984;77:1010-4.  Back to cited text no. 9
[PUBMED]    
10.
Shirabe T, Tawara S, Terao A, Araki S. Myxoedematous polyneuropathy: A light and electronmicroscopic study of the peripheral nerve and muscle. J Neurol Neurosurg Psychiatry 1975;38:241-7.  Back to cited text no. 10
[PUBMED]    
11.
Nemni R, Bottacchi E, Fazio R, Mamoli A, Corbo M, Camerlingo M, et al. Polyneuropathy in hypothyroidism: Clinical, electrophysiological and morphological findings in four cases. J Neurol Neurosurg Psychiatry 1987;50:1454-60.  Back to cited text no. 11
[PUBMED]    
12.
Yuksel G, Karlikaya G, Tanridag T, Önder U, Gülseren A. Nerve conduction studies, SEP and blink reflex studies in recently diagnosed, untreated thyroid disease patients. J Neurol Sci (Turkish) 2007;24:7-15.  Back to cited text no. 12
    


    Figures

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    Tables

  [Table 1], [Table 2]



 

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