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Research Article | Volume 15 Issue 3 (March, 2025) | Pages 827 - 831
Clinical, electrophysiological and aetiological profile of peripheral neuropathy in a tertiary care centre
 ,
 ,
1
Assistant Professor, Department of Neurology, Guntur Medical College, Guntur, Andhra Pradesh, INDIA
2
Associate Professor, Department of Neurology, Guntur Medical College, Guntur, Andhra Pradesh, INDIA
3
Post graduate, Department of Neurology, Guntur Medical College, Guntur, Andhra Pradesh, INDIA
Under a Creative Commons license
Open Access
Received
Feb. 16, 2025
Revised
Feb. 27, 2025
Accepted
March 10, 2025
Published
March 27, 2025
Abstract

Objectives: To study the clinical feature, aetiology, electrophysiological profile of peripheral neuropathy in a tertiary care hospital at Guntur. Materials and Methods: 85 cases of chronic peripheral neuropathy over a period of 12 months were studied in detail including presenting complaint, clinical examination, electro physiological studies and other relevant investigations.  Results: The affected age group was 18 yrs to 75 yr. There is male predominance with male to female ratio of 2.4:1. Out of 85 cases, both sensory and motor complaints in 51 (60%) cases, 31 cases (36.47%) are pure sensory and 3 (3.52%) cases are pure motor. urinary symptoms in 5 (5.88%) cases, cranial nerve involvement in 3(3.52%) cases, peripheral nerve thickening in 2 (2.35%) cases and Dysautonomia in one case. Clinically, Polyneuropathy in 56 (65.88%) cases, mononeuritis multiplex in 13(15.29%) cases, poly radiculo neuropathy in 12 (14.11%) cases and   mono neuropathy in 4 (4.70%) cases. Electro physiologically, 73 cases (85.8%) have involvement of both upper and lower limbs, only lower limbs involved in 12 (14.1%) cases. Electrodiagnostic studies showed axonal pattern in 59 (60%) cases, demyelination pattern in 26 (40%) cases. Etiologically, 29 cases (34.11%) have Diabetes, Impaired glucose tolerance seen in 5(5.88%) cases, immune mediated neuropathy in 21 (24.70%), CIDP in 12 (14.11%) cases, connective tissue diseases in 9 (10.58%) cases, 12 (14.11%)cases of infectious 6 cases (7.05%) were of hereditary, 6 cases (7.05%) were of alcohol related, 3 cases(3.52%) of paraneoplastic, drug induced in 2 (2.35%) cases, in  6 cases (7.05%)  we could not find cause. Out of 31 cases of pure sensory neuropathy, 9 patients (10.58%) were diabetic, leprosy in 5 (5.88%) cases, impaired glucose tolerance in 4 (4.7%) patients, 2 (2.35%) patients were alcohol related, 1 each (1.17%) for rheumatoid arthritis, HIV neuropathy, leflunomide induced neuropathy, celiac disease, metabolic cause and cryptogenic. Among 3 pure motor neuropathy one case (1.17%) was motor CIDP, 2 cases (2.35%) were of hereditary neuropathy. Conclusion: Peripheral neuropathy is more common among 30 to 70 years age, with male preponderance. Majority have distal symmetrical motor sensory poly neuropathy. Diabetes is the most common cause for chronic peripheral neuropathy, followed by immune mediated neuropathy. Hansens neuropathy more common infective neuropathy.

Keywords
INTRODUCTION

Peripheral nerve disorders are common neurological problems caused by dysfunction of peripheral motor, sensory, or autonomic nerves. The causes of neuropathies and their clinical Presentation is highly variable. The main causes of neuropathy are entrapments, systemic diseases, inflammatory, autoimmune disorders, inherited disorders, ischemic settings, paraneoplastic conditions, deficiency states, infections, and toxins1. The prevalence of peripheral neuropathy is 2.4% but in elderly above 55 years age group, it rises to 8%. Based on the duration of symptoms, the neuropathy can be categorized into acute (<4 weeks), subacute (4–12 weeks), or chronic (>12 weeks)2.

Mononeuropathy means focal involvement of a single nerve and implies a local process. Direct trauma, compression or entrapment, vascular lesions, and neoplastic infiltration are the most common causes. Multiple mononeuropathy or mononeuropathy multiplex signifies simultaneous or sequential damage to multiple non-contiguous nerves.

 

Electrophysiological studies provide a more precise localization of the lesion than may be possible by clinical examination and can separate axonal loss from focal segmental demyelination.

 

Objectives:

In patients of peripheral neuropathy,

  1. To study the clinical profile
  2. To study the electrophysiological profile
  3. To evaluate the etiological profile.
MATERIALS AND METHODS

Sample size and duration of study:

85 consecutive cases of chronic peripheral neuropathy attending the neurology department, Guntur during the period of January 2024 to December 2024 were enrolled in the study.

 

Study design:

It is a prospective observational study.

 

Inclusion criteria:

     1.All patients presenting with symptoms and signs suggesting of chronic peripheral neuropathy.

  1.   All the suspected cases of chronic peripheral neuropathy

 

Exclusion criteria:

  1. Acute and sub-acute cases of peripheral neuropathy
  2.   Myelopathy cases
  3.    Traumatic neuropathy cases.
  4. carpel tunnel syndrome cases.

 

Detailed history of the presenting complaints, past history, family history comorbid illnesses, past relevant medical history was taken. Detailed neurological examination was done. Complete blood hemogram, ESR, random blood glucose, renal function tests, liver function tests, serum thyroid profile, serum lipid profile, viral markers sent.  Specific tests like serum vitamin B12, HBA1C, serum electrophoresis, urine for Bence jones proteins, RA factor, ANA profile, vasculitis panel, Lymes serology, VDRL, MRI spine with contrast were done in selective cases. Electro diagnostic tests performed in all cases to know the pattern of involvement. Demyelinating neuropathy confirmed, if the distal latency exceeds 115% of the upper limit of the normal with the normal CMAP or more than 150% of the normal with reduced CMAP.  Axonal neuropathy is confirmed if amplitude was decreased with normal distal latency and conduction velocity3. Split Skin smear or nerve biopsy done, genetic testing done when necessary.

RESULTS

Table 1: Age & Sex distribution

Age (in years)

Male (57)

Female (28)

Total (85)

     18 - 30

6 (7.05%)

3 (10.71%)

9 (10.58%)

     31 - 50

20 (35.08%)

12 (42.85%)

32 (37.64%)

     51 - 70

23 (40.35%)

10 (35.71%)

33     (38.8%)

      > 71

8 (14.03%)

3 (10.71%)

11 (12.94%)

 

Table 2: Symptomatology

Symptom

N=85

Sensorimotor

51 (60%)

Pure sensory

31 (36.47%)

Pure motor

3 (3.52%)

Both upper & lower limbs involvement

79 (92.94%)

Only lower limbs

6 (7,05%)

Bladder involvement 

5 (5.88%)

Cranial nerve involvement     

3 (3.52%)

Skeletal deformities

3 (3.52%)

Peripheral nerve thickening

2 (2.35%)

Dysautonomia

1 (1.17%)

GIT symptoms    

1 (1.17%)

 

Table 3: Pattern of Neuropathy

Pattern

N=85

Demyelination (26)

Axonal

(59)

Poly neuropathy   

56 (65.88%)

12

44

Mono neuritis multiplex

    Hansens

    Sjogren

    Vasculitis

    Para neoplastic

    No cause found

13 (15.29%)

7

1

1

1

2

2

11

Poly radiculo neuropathy

   CIDP

   Rheumatoid arthritis, with GM1,GD1a ab

   Recurrent CIDP

   Childhood CIDP

   MADASM

   MMNCB

   Lymes

   Diabetes

12 (14.11%)

9

3

Mono neuropathy   

        Bilateral femoral

        Radial nerve

4 (4.70%)

3

1

 

3

1

 

Table 4: Aetiology

Aetiology

Number of cases (N=85)

Endocrine causes

       Diabetes

       Impaired glucose tolerance      

34 (40%)

29 (34.11%)

5 (5.88%)

Immune mediated

  CIDP

        Pure motor variant

        Sensory variant

        Recurrent CIDP  

         Childhood CIDP

        Pure motor variant

        MADSAM

      MMNCB 

      GM1,GD1a antibody

      Multiple myeloma

  Connective tissue diseases

     Rheumatoid arthritis

      Sjogren syndrome

      Systemic sclerosis

      Vasculitis

      Panel negative

21 (24.70%)

12 (14.11%)

1

2

1

1

1

1

1

1

1

9 (10.58%)

2

1

2

2

2

Medical disorders

     Chronic kidney disease    

 

1

Hereditary neuropathy

      CMT 1

       CMT 2

             SPG11

     Not evaluated

6 (7.05%)

2

2

 

2

Infectious neuropathy

    leprosy

    Lymes

    Brucellosis

    HIV

Others (not evaluated)

12 (14.11%)

8

1

1

1

1

Alcohol related neuropathy

7 (8.23%)

Paraneoplastic

       NHL

       Ovarian carcinoma

       Anti Hu ab

3 (3.52%)

1

1

1

Drug induced

      Bortezomib (MM)

      Leflunomide  (RA)

2 (2.35%)

1

1

No cause found

6

              

Table 5: Pure Sensory Neuropathy

Cause

N=31

Demyelination

(7)

Axonal (24)

DM

   Entrapment

9

3

5

 

11

 

Sensory variant CIDP

1

-

2

Hansens

5

-

1

Leflunomide

1

-

1

Celiac disease

1

-

1

Impaired glucose intolerance

4

-

1

HIV neuropathy

1

-

-

Alcohol

2

-

1

Metabolic (CKD)

1

-

1

Rheumatoid arthritis

2

1

1

idiopathic

1

1

2

 

Table 6: Pure Motor Neuropathy

Cause

N=3

Axonal

Demyelination

Hereditary neuropathy

2

2

-

Motor CIDP

1

-

1

DISCUSSION

Peripheral neuropathy is a common neurological disorder, with variable presentation and numerous causes.

In our study age at presentation ranged from 18 year to 75 years, majority of cases are in the age range of 51 to 70 years, followed by 31 to 50 years age. There is male predominance i.e 67%, which is in accordance with study done by Sase and coworkers4, (62%) and Goel and coworkers, (61%)5.

The commonest cause of neuropathy includes diabetes and nutritional deficiencies6. Study done by Vishali et al7, found diabetes is the most common cause followed by entrapment neuropathy and idiopathic. In our study, prevalence of diabetic neuropathy was, which was in accordance with the study done by Bansal et al8.

Diabetes is the most common cause of insidious onset, gradually progressive neuropathy. It has variable presentations. Distal symmetrical poly neuropathy, with length dependent pattern is the most common finding. Entrapment neuropathy seen in 2 cases of diabetes, one had unilateral meralgia paresthetica, one person had asymmetrical progressive entrapment neuropathy of femoral nerve, with poor glycaemic control, for which plexopathy was ruled out by imaging. One middle aged diabetic with poor glycaemic control presented with progressive quadriparesis for which work up done including genetic panel, autoimmune, paraneoplastic panel were negative and nerve biopsy showed mixed. she was given rituximab, considering immune mediated neuropathy.

From the study done by Sase and coworkers4 GBS was the second most common cause. In study by Mygland and coworker’s9, alcoholic and toxic neuropathy was the next common cause. The second common cause in our study was immune mediated neuropathy. CIDP is reported as 6.2% in a study by Lubec and co- workers10, less compared to our study. Entrapment neuropathy was reported in 9% cases, in study by Sase and co wokers4, and it was 17% in study by Vishali et al7, followed by infective neuropathy.

Immune mediated neuropathy is the second most common aetiology in our study. Most of the CIDP cases were with diabetes, one case was nerve biopsy proven MADSAM. One case was DADS variant, one case was, bone marrow biopsy proven multiple myeloma, one was pure motor variant, 2 cases were sensory variant, 2 cases remitting and relapsing type, one case was childhood CIDP, one case GM1, GM2 antibody positive MMNCB, one case was GM1, GD1a antibody positive. Among connective tissue diseases, presented with mononeuritis multiplex pattern, 2 cases have been found to have Rheumatoid arthritis, 2 cases positive for SSA& SSB antibody.one pt had progressive quadriparesis with dysphagia, with oesophageal spasm and functional gut motility disorder with hearing deficit, work up done for systemic sclerosis and came positive. One case presented with insidious onset gradually progressive sensory ataxia with severe dysautonomia, autoimmune and paraneoplastic panel was negative, he responded with steroids than iv immunoglobulins. 2 cases clinically suspected as vasculitis with mononeuritis multiplex presentation, but panel was negative, but responded with steroids.

Among infective causes, 8 cases were of Hansen’s neuropathy.  They presented as mononeuritis multiplex neuropathy. Out of them, 5 cases were on MDT treatment, 1 case completed the course, one case is defaulter and one case newly diagnosed with split skin smear .one case still had hypasthetic patch, one case had deformities, one case had peripheral nerve thickening. 2 cases had large fiber involvement. Electrodiagnostic studies showed motor involvement in 3 cases. It emphasises the need for considering any drug resistance of Hansen’s disease.

2 cases have insidious onset, gradually progressive quadriparesis with significant weight loss and wasting, with spine imaging showed root enhancement at conus, turned out to be positive for Lymes serology, improved with doxycycline. One case   had similar history with bladder involvement, turned out to be positive for brucella antibody.

Alcohol related neuropathy seen in 6 cases, most of them are painful. One case, presented with both small and large fiber neuropathy, dramatically improved with thiamine supplementation.

Among pure sensory neuropathy, one case had GIT symptoms, for the past 3 years. Due to constraints, antigliadin antibody could not be done. We could get duodenal biopsy showed lymphocytic infiltration but periodic acid Schiff base stain negative. But she responded with doxycycline.,

For chronic idiopathic neuropathy, Smith and his co-workers11 found only 31% to be idiopathic, remaining cases turned to be of impaired glucose intolerance. Another study by Hughes and co-workers12 did not find glucose intolerance, as the significant risk factor.

Among idiopathic cases, still we would like to consider immune mediated neuropathy where panel was negative, as research is going on for new antibodies.

CONCLUSION

Diabetes is the most common cause which emphasises the need for glycemic control apart with life style modification. Immune mediated neuropathy is in increasing trend, might be due to changes in environmental factors, life style and genetic and epigenetic factors. Infective causes also need to considered as a preventable cause. More studies in large sample are needed for better understanding the disease profile.

REFERENCES
  1. Bradley’s textbook of Neurology, 8th edition
  2. IAN textbook of neurology,2nd edition
  3. Shapiro textbook of electrophysiology, 4th edition
  4. Sase NS, Correia PWM. Clinical profile of peripheral neuropathy: A study of 100 patients. J Assoc Phys India 2009; 2: 1-6.
  5. Goel HC, Gupta OP, Bajaj S, Saxena RK. Clinical profile and electro diagnostic study of peripheral neuropathy. Association Physicians of India 1989;37(9):578-82.
  6. D England et al Distal symmetric polyneuropathy: a definition for clinical research: report of the American Academy of Neurology , the American Association of Electro diagnostic Medicine, and the American Academy and the American Academy, of Physical Medicine and Rehabilitation, Neurology; 2005 Jan 25; 64(2):199-207.
  7. Vishali et al , Profile of Peripheral Neuropathy in A Tertiary Care, Hospital in Punjab, India, Vol. 19 No. 4, October.-Dec 2017, JK SCIENCE.
  8. Dipika Bansal et al, Prevalence and risk factors of development of peripheral diabetic neuropathy in type 2 diabetes mellitus in a tertiary care setting, Diabetes Investigation 2014 Nov;5 (6): 714-2
  9. Mygland A, Monstad P. Chronic polyneuropathies in Vest- Agder, Norway. Eur J Neurol 2001 ;8(2):157-65
  10. Lubec D, Mullbacher W, Finisterer J, Mamoli B. Diagnostic work up in peripheral neuropathy: analysis of 171 cases. Postgraduate Medicine 1999; 75: 723-727
  11. Smith AG, Singleton JR. The Diagnostic Yield of a Standardized Approach to Idiopathic Sensory-Predominant Neuropathy. Archives of Internal Medicine 2004;164(9):1021-1025
  12. Hughes RAC, Umapathi T, Gray IA, et al. A controlled investigation of the cause of chronic idiopathic axonal polyneuropathy. Brain 2004;127(8): 1723-1730
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