Cause Of Peripheral Neuropathy Research Articles

Using biothesiometer, Neuropathy Symptom Score, and Neuropathy Disability Score for the early detection of peripheral neuropathy: A cross-sectional study.

Patients with peripheral neuropathy could have damaged peripheral nerves, which leads to sensory and motor dysfunction. Diabetes, infections, and trauma are the major causes of peripheral neuropathy. Vibratory perception threshold (VPT) tools are commonly used to detect peripheral neuropathy. This study aims to determine the assessment of peripheral neuropathy through the different diagnostic tools in the community in Malaysia. A total number of 1283 participants were recruited from the seven retail pharmacies located in Selangor, Malaysia. The peripheral neuropathy test was conducted based on VPT tools on both feet using the digital biothesiometer. Following that, Neurological Symptom Score (NSS) and Neurological Disability Score (NDS) were taken from the participants to assess the neurological symptoms. Participants had an average age of 40.6 ± 12.9 years and were mostly of Chinese ethnicity (54.1%). The findings show that increasing age was associated with more severe peripheral neuropathy across the various assessment tools, but gender differences were found with the biothesiometer test and ethnicity has severity in the biothesiometer and disability scores. The sensitivity and specificity of the biothesiometer test were 0.63 and 0.84, respectively. The combined tool NSS and NDS had high specificity and a high positive predictive value, suggesting that it could be a reliable indicator of peripheral neuropathy when both scores are elevated. The findings show that the biothesiometer test, NSS, and NDS are considered screening VPT tools for diagnosing peripheral neuropathy. However, further evaluation and diagnostic testing are necessary in cases of a positive test result.

Peroneal Nerve Entrapment in Diabetes Mellitus.

This narrative mini-review discusses the association between peroneal nerve entrapment (PEN) and diabetes mellitus (DM). Generally, PEN is not a common cause of peripheral neuropathy in DM. Poor glycaemic control and DM duration are powerful risk factors for PEN. Underlying mechanisms involve neurodegeneration and entrapment of the peroneal nerve. Patients tend to present with chronic leg pain, gradual foot drop, steppage gait, or weakness of ankle dorsiflexion. Electrodiagnostic and imaging studies are very useful in diagnosis to determine the level at which entrapment occurs. Treatment varies based on the aetiology and severity of symptoms. It is initially conservative. Surgical nerve decompression management is required when entrapment is refractory to non-operative options.

Isoniazid-historical development, metabolism associated toxicity and a perspective on its pharmacological improvement.

Despite the extraordinary anti-tubercular activity of isoniazid (INH), the drug-induced hepatotoxicity and peripheral neuropathy pose a significant challenge to its wider clinical use. The primary cause of INH-induced hepatotoxicity is in vivo metabolism involving biotransformation on its terminal -NH2 group owing to its high nucleophilic nature. The human N-acetyltransferase-2 enzyme (NAT-2) exploits the reactivity of INH's terminal -NH2 functional group and inactivates it by transferring the acetyl group, which subsequently converts to toxic metabolites. This -NH2 group also tends to react with vital endogenous molecules such as pyridoxine, leading to their deficiency, a major cause of peripheral neuropathy. The elevation of liver functional markers is observed in 10%-20% of subjects on INH treatment. INH-induced risk of fatal hepatitis is about 0.05%-1%. The incidence of peripheral neuropathy is 2%-6.5%. In this review, we discuss the genesis and historical development of INH, and different reported mechanisms of action of INH. This is followed by a brief review of various clinical trials in chronological order, highlighting treatment-associated adverse events and their occurrence rates, including details such as geographical location, number of subjects, dosing concentration, and regimen used in these clinical studies. Further, we elaborated on various known metabolic transformations highlighting the involvement of the terminal -NH2 group of INH and corresponding host enzymes, the structure of different metabolites/conjugates, and their association with hepatotoxicity or neuritis. Post this deliberation, we propose a hydrolysable chemical derivatives-based approach as a way forward to restrict this metabolism.

A Cross-Sectional Study on Clinical Profiles and Quality of Life of Patients with Neuropathic Pain

Background: Due to nerve damage in the central and peripheral nervous systems, people with neuropathic pain experience acute pain. This study evaluated the health effects of neuropathic pain and different types of pain according to various neuropathies. Objective: To evaluate the clinical characteristics and QOL of neuropathic pain patients. Study the most frequently given medications, evaluate patients with various types of neuropathic pain, determine the characteristics of neuropathic pain, analyse the effects of neuropathic pain on general health. Materials and Methods: A total of 102 patients were enrolled according to the inclusion and exclusion criteria. Patients were interviewed using Short-Form McGill Pain Questionnaire-2, RAND 36 Item Health Survey 1.0 Questionnaire. Percentage, mean, chi square and standard deviation was used mainly in Statistical analysis. Result: Out of 102 patients, 44.12% were female, and 55.88% were male. Mean age of male and female was 46.60 and 47.42 years respectively. Radiculopathy patients were in the majority (43.1%), followed by peripheral neuropathy (37.3%), myelopathy (16.7%), sciatic neuropathy (2%), and brachial plexopathy (1%). Diabetes was highest to cause peripheral neuropathy. The most commonly prescribed drug was pregabalin, and combination were gabapentin and nortriptyline. The total means of all subscales of SF-MPQ-2 questionnaire was 4.56(2.10). Mean of physical component and emotional component summary was 34.30(17.54), and 42.38(15.74). Conclusion: Diabetes, trauma, weightlifting can also cause neuropathic pain. Diabetes was among top cause for peripheral neuropathy. Burning, itching, numbness, tingling, cold freezing pain were prevalent. The emotional function of patients was better than physical function.

Pathogenic Mechanisms of Diabetic Neuropathy

Diabetes stands as the predominant cause of peripheral neuropathy, and diabetic neuropathy (DN) is an early-onset and most frequent complication of diabetes. Distal symmetric polyneuropathy is the major form of DN; however, various patterns of nerve injury can manifest. Growing evidence suggests that hyperglycemia-related metabolic disorders in neurons, Schwann cells, and vascular endothelial cells play a major role in the development and progression of DN; however, its pathogenesis and development of disease-modifying therapies warrant further investigation. Herein, recent studies regarding the possible pathogenic factors of DN (polyol and other collateral glycolysis pathways, glycation, oxidative stress, Rho/Rho kinase signaling pathways, etc.) and therapeutic strategies targeting these factors are introduced.

A pictorial guide for performing dynamic musculoskeletal ultrasound techniques of the Upper Limb

IntroductionDynamic techniques should be used to compliment static imaging in the field of Musculoskeletal ultrasound. Performing limb movements and imaging simultaneously, allows for diagnosing certain musculoskeletal conditions not otherwise confirmed by still images. This article aims to provide guidance on how to perform a selection of these dynamic musculoskeletal ultrasound techniques with a focus on the upper limb. MethodsThis pictorial guide features techniques gathered from literature review and experience gained in the field. ResultsApplication of dynamic ultrasound techniques has been evidenced in the literature to diagnose conditions such as trigger finger, dislocating tendons and causes of peripheral neuropathy. ConclusionMusculoskeletal conditions only elicited during limb movement can be difficult to diagnose. Appropriate use of dynamic techniques increases likelihood of correct diagnosis of the described conditions. Implications for practiceUltrasound provides a unique opportunity to visualise these conditions thus ultrasound users should aim to familiarise themselves with dynamic ultrasound techniques to improve patient outcomes.

Description of electroneuromiographic and laboratorial findings in leprosy neuropathy, according to its clinical forms: the confirmation of a spectral disease.

Leprosy is one of the most common infectious cause of peripheral neuropathy in the world and can lead to sequelae and physical disabilities. Electroneuromyography (ENMG) is the gold-standard test for evaluating neural impairment, detecting from subclinical abnormalities to advanced lesions. This study aims to describe the electroneuromyographic findings in patients with leprosy, according to their clinical forms. The study is a retrospective observational analysis of the medical records of patients with leprosy, of a National Reference Center of Sanitary Dermatology and Leprosy in Brazil between 2014 and 2022. 513 patients underwent ENMG at leprosy diagnosis and also underwent a clinical, serological and molecular evaluation of the disease. The electroneuromyographic findings showed 2,671 altered nerves, with an average of 6.9 (±5.1) altered nerves per patient. The most affected sensory nerves were the superficial peroneal (25.0%; 413/1649), sural (15.1%; 397/2627) and ulnar (13.8%; 363/2627), with average of 4.3 (±3.2) affected sensory nerves per patient. The most affected motor nerves were the ulnar (33.1%; 338/1022) and common peroneal (12.1%; 319/2627), with average of 2.6 (±2.5) motor nerves affected per patient. 126 patients presented normal ENMG and, among the 387 with abnormalities in the exam, 13.2% (51/387) had mononeuropathy and 86.8% (336/387) had multiple mononeuropathy. Axonal involvement was more frequent in primary neural leprosy, borderline-tuberculoid, borderline-lepromatous and lepromatous forms. Our findings support that leprosy is a spectral disease, characterized by a balance between host immunity and bacillary load. Therefore, the impairment and electroneuromyographic characteristics are distinct and may vary according to the clinical form.

LEPROSY NEUROPATHY : CLINICAL PRESENTATION

Leprosy is a chronic infection caused by the bacteria M. leprae and causes damage to the skin and peripheral nervous system outside the brain and spinal cord, including the skin, mucous membranes of the nose, testicles, and eyes. This disease develops slowly over a long period, ranging from 6 months to 40 years, and can cause skin lesions and secondary defects. Leprosy is a common and treatable cause of peripheral neuropathy in many tropical and subtropical countries. Neuropathy is a condition that causes damage to the function and structure of the sensory, autonomic, and motor nerves in the peripheral nervous system. Complications of neuropathy can include loss of sensory abilities and muscle weakness. Impaired sensory nerve function is often the first symptom that appears in leprosy neuropathy. Therefore, early detection and treatment of neuropathy in leprosy is very important to prevent disability.

FM latency, FM ratio, F-wave latency versus F-wave index in the diagnosis of diabetic neuropathy

BackgroundDiabetes is one of the most common causes for peripheral neuropathy which warrants early diagnosis and treatment. The conventional nerve conduction studies appear to be normal if few of the nerve roots are escaping the lesion. In view of identifying a better clinical testing method, a late response index comprising most of the parameter of F wave was constructed and compared with the diagnosing ability of other parameters.MethodsThis hospital-based cross-sectional study was conducted among male diabetics aged 30 to 50 years in a tertiary care hospital. Maintaining an ambient temperature of 28 °C and following a supramaximal stimulation of the median nerve of both upper limbs, using a digitalized nerve conduction/electromyography/EP machine, the F-wave tracing was obtained.ResultsThe F-wave index detected a greater number of subjects with diabetic peripheral neuropathy when compared to F-wave mean latency, F M latency and F–M ratio.ConclusionF-wave index can be used as a surrogate electrophysiological study to detect peripheral neuropathy at an early stage and aids in better prognosis.

Peripheral neuropathy and neuropathic pain in the elderly

Neuropathic pain is a common symptom in the elderly and tends to increase according to the frequency of related underlying disease. In older patients, cognitive decline and accompanying medical conditions may make early diagnosis difficult. Therefore, a detailed history taking, neurological examination, and laboratory tests should be performed. Diabetic peripheral neuropathy, entrapment neuropathy, radiculopathy, postherpetic neuralgia, and chemotherapy-induced peripheral neuropathy are the major causes of peripheral neuropathy in the elderly. When treating elderly patients, the dose of drug should be adjusted in consideration of its side effects. An accurate diagnosis and treatment of neuropathic pain is essential to improve the quality of life of elderly patients.

Vitamin B12 Deficiency and Peripheral Neuropathy in patients with Type 2 Diabetes Mellitus Treated with Metformin. An integrative review

Background/Purpose: Type 2 diabetes mellitus (T2DM) is a worldwide pathology with several complications, and 50% of patients with T2DM develop peripheral neuropathy (PN) in the long term. The present study aimed to review the literature on the association between PN and vitamin B12 deficiency in patients with T2DM treated with metformin. Materials and methods: A literature review was carried out in the PubMed Central, Cochrane, Scielo, Scopus and Embase databases, from 2015 to 2021. We found 755 studies, of which 16 were included. Results: The serum level of vitamin B12 was lower in individuals with at least one neurological symptom. Treatment with metformin was associated with reduced serum vitamin B12 levels, and its use was defined as a probable cause of PN due to reduced vitamin B12. Studies that performed supplementation with methylcobalamin demonstrated significant improvement in neuropathic symptoms. Vitamin B12 supplementation therapy for diabetic patients undergoing metformin treatment has been suggested. Conclusion: Deficiency of vitamin B12 associated to metformin can be considered a risk factor for PN. Periodically evaluation of serum levels of vitamin B12 is recommended for patients on metformin treatment.

Whole exome/genome sequencing in cyclic vomiting syndrome reveals multiple candidate genes, suggesting a model of elevated intracellular cations and mitochondrial dysfunction.

To utilize whole exome or genome sequencing and the scientific literature for identifying candidate genes for cyclic vomiting syndrome (CVS), an idiopathic migraine variant with paroxysmal nausea and vomiting. A retrospective chart review of 80 unrelated participants, ascertained by a quaternary care CVS specialist, was conducted. Genes associated with paroxysmal symptoms were identified querying the literature for genes associated with dominant cases of intermittent vomiting or both discomfort and disability; among which the raw genetic sequence was reviewed. "Qualifying" variants were defined as coding, rare, and conserved. Additionally, "Key Qualifying" variants were Pathogenic/Likely Pathogenic, or "Clinical" based upon the presence of a corresponding diagnosis. Candidate association to CVS was based on a point system. Thirty-five paroxysmal genes were identified per the literature review. Among these, 12 genes were scored as "Highly likely" (SCN4A, CACNA1A, CACNA1S, RYR2, TRAP1, MEFV) or "Likely" (SCN9A, TNFRSF1A, POLG, SCN10A, POGZ, TRPA1) CVS related. Nine additional genes (OTC, ATP1A3, ATP1A2, GFAP, SLC2A1, TUBB3, PPM1D, CHAMP1, HMBS) had sufficient evidence in the literature but not from our study participants. Candidate status for mitochondrial DNA was confirmed by the literature and our study data. Among the above-listed 22 CVS candidate genes, a Key Qualifying variant was identified in 31/80 (34%), and any Qualifying variant was present in 61/80 (76%) of participants. These findings were highly statistically significant (p < 0.0001, p = 0.004, respectively) compared to an alternative hypothesis/control group regarding brain neurotransmitter receptor genes. Additional, post-analyses, less-intensive review of all genes (exome) outside our paroxysmal genes identified 13 additional genes as "Possibly" CVS related. All 22 CVS candidate genes are associated with either cation transport or energy metabolism (14 directly, 8 indirectly). Our findings suggest a cellular model in which aberrant ion gradients lead to mitochondrial dysfunction, or vice versa, in a pathogenic vicious cycle of cellular hyperexcitability. Among the non-paroxysmal genes identified, 5 are known causes of peripheral neuropathy. Our model is consistent with multiple current hypotheses of CVS.

ULNAR NERVE ABSCESS - A COMPRESSIVE SENSORY MOTOR NEUROPATHY

Introduction: Leprosy is characterized by a triad of hypoesthetic skin lesions, thickened peripheral nerves, and positive skin smear for Mycobacterium leprae. All peripheral nerve functions (sensory, motor, and autonomic) are disrupted in leprosy. The most severe and widespread impairment is in sensory functions. Varied kinds of leprosy show different patterns of nerve involvement. We would introduce a case report of ulnar nerve abscess Presentation of Case: in 21 years old gentlemen presented with swelling over distal third of right arm with tingling sensation over ulnar division right hand with inability to close right fist since last 1.5 years. In many developing nat Discussion: ions, like India, leprosy continues to be a widespread yet curable cause for peripheral neuropathy. Nerve abscess is an infrequent complication, usually associated with Type 1 reaction mostly in tuberculoid and borderline tuberculoid disease that can lead to irreversible nerve damage and deformities3. Leprosy-associated nerve abscess often requires surgical decompression and drainage of the abscess for possible restoration of nerve function2. We have Conclusion: encountered with a unique case of ulnar nerve abscess presenting as compressive neuropathy, due to external compression of swelling which presented as weakness of right hand. Leprosy is still a common and treatable causes of peripheral neuropathy; meticulous workup is a key factor to achieve prompt results

LEPROSY NEUROPATHY

Leprosy is a major cause of peripheral neuropathy in developing countries, affecting sensory, motor, and autonomic nerve function. Neuropathy complications can include sensory loss and muscle weakness. Impaired sensory nerve function is often the first symptom encountered in leprosy neuropathy. Early detection and treatment of neuropathy in leprosy are important to prevent disability.

A mechanistic understanding of the relationship between skin innervation and chemotherapy-induced neuropathic pain.

Neuropathic pain is a frequent complication of chemotherapy-induced peripheral neurotoxicity (CIPN). Chemotherapy-induced peripheral neuropathies may serve as a model to study mechanisms of neuropathic pain, since several other common causes of peripheral neuropathy like painful diabetic neuropathy may be due to both neuropathic and non-neuropathic pain mechanisms like ischemia and inflammation. Experimental studies are ideally suited to study changes in morphology, phenotype and electrophysiologic characteristics of primary afferent neurons that are affected by chemotherapy and to correlate these changes to behaviors reflective of evoked pain, mainly hyperalgesia and allodynia. However, hyperalgesia and allodynia may only represent one aspect of human pain, i.e., the sensory-discriminative component, while patients with CIPN often describe their pain using words like annoying, tiring and dreadful, which are affective-emotional descriptors that cannot be tested in experimental animals. To understand why some patients with CIPN develop neuropathic pain and others not, and which are the components of neuropathic pain that they are experiencing, experimental and clinical pain research should be combined. Emerging evidence suggests that changes in subsets of primary afferent nerve fibers may contribute to specific aspects of neuropathic pain in both preclinical models and in patients with CIPN. In addition, the role of cutaneous neuroimmune interactions is considered. Since obtaining dorsal root ganglia and peripheral nerves in patients is problematic, analyses performed on skin biopsies from preclinical models as well as patients provide an opportunity to study changes in primary afferent nerve fibers and to associate these changes to human pain. In addition, other biomarkers of small fiber damage in CIPN, like corneal confocal microscope and quantitative sensory testing, may be considered.

Longitudinal physiological remoulding of lower limb skin as a cause of diabetic foot ulcer: a histopathological examination.

Diabetic foot ulcer (DFU) is recognised as a severe complication in patients with type 2 diabetes. With the increasing incidence of diabetes, it represents a major medical challenge. Several models have been proposed to explain its aetiology; however, they have never been assessed by longitudinal histopathological examination, which this study aims to address. Multiplex-immunofluorescence analysis was carried out with lengthwise serial skin specimens obtained from the medial thigh, lower leg, ankle, dorsum of foot and acrotarsium close to the DFU region of a patient with type 2 diabetes receiving above the knee amputation. Proximal-to-distal gradual loss of peripheral nerve was demonstrated, accompanied by compromised capillaries in the superficial papillary plexus and distended CD31-positive capillaries in the dorsum of foot. Neural fibres and capillaries were also significantly compromised in the sweat gland acinus in the ankle and dorsum of foot. Injuries in the superficial papillary plexus, sweat gland acinus, and sweat gland-associated adipose tissues were accompanied by significant infiltration of macrophages. These results indicated that longitudinal impairment of local blood circulation could be the cause of peripheral neuropathy, which initiated ulcer formation. Resultant chronic inflammation, involving sweat gland-associated adipose tissue, gave rise to impairment of wound healing, and thus DFU formation. Longitudinal histopathological examination demonstrated that impairment of local microvascular circulation (rather than the systemic complication caused by type 2 diabetes) was considered the primary cause of peripheral neuropathy, which initiated ulceration. Together with chronic inflammation in the superficial papillary plexus and sweat gland-associated adipose tissue, it resulted in the development of a DFU. Although this is a study of just one individual's limb, our study provided a unique observation, contributing mechanistic insights into developing novel intervening strategies to prevent and treat DFUs.

Neuropathy in Human Immunodeficiency Virus: A Review of the Underlying Pathogenesis and Treatment.

This article explores the various causes of the human immunodeficiency virus (HIV), and its associated neuropathy, including the effects of HIV on the nervous system and the long-standing therapy that is often provided to patients with HIV. Several studies regarding the neurotoxic effects of combined antiretroviral therapy (cART) and HIV were reviewed and various hypotheses were discussed. Furthermore, we present the nature of HIV-sensory neuropathy (HIV-SN) among different demographic populations and their subsequent risk factors predisposing them to this condition. It was observed that the incidence of the disease increases in increased survival of the patients as well as in males. Finally, the current approach to HIV-SN and its overlapping features with other causes of peripheral neuropathy have been discussed which demonstrates that a clinical examination is the most important clue for a healthcare professional to suspect the disease. Our main aim was to study the current perspectives and guidelines for diagnosing and managing a patient with HIV-SN to reduce disease prevalence and bring about a more aware frame of mind when following up with an HIV patient.

Movement disorders and neuropathies: overlaps and mimics in clinical practice.

Movement disorders as well as peripheral neuropathies are extremely frequent in the general population; therefore, it is not uncommon to encounter patients with both these conditions. Often, the coexistence is coincidental, due to the high incidence of common causes of peripheral neuropathy, such as diabetes and other age-related disorders, as well as of Parkinson disease (PD), which has a typical late onset. Nonetheless, there is broad evidence that PD patients may commonly develop a sensory and/or autonomic polyneuropathy, triggered by intrinsic and/or extrinsic mechanisms. Similarly, some peripheral neuropathies may develop some movement disorders in the long run, such as tremor, and rarely dystonia and myoclonus, suggesting that central mechanisms may ensue in the pathogenesis of these diseases. Although rare, several acquired or hereditary causes may be responsible for the combination of movement and peripheral nerve disorders as a unique entity, some of which are potentially treatable, including paraneoplastic, autoimmune and nutritional aetiologies. Finally, genetic causes should be pursued in case of positive family history, young onset or multisystemic involvement, and examined for neuroacanthocytosis, spinocerebellar ataxias, mitochondrial disorders and less common causes of adult-onset cerebellar ataxias and spastic paraparesis. Deep phenotyping in terms of neurological and general examination, as well as laboratory tests, neuroimaging, neurophysiology, and next-generation genetic analysis, may guide the clinician toward the correct diagnosis and management.

21-LB: Transdermal Microneedle Device Delivery of Adipocyte-Specific AAVs to Overexpress Adipose Tissue Neurotrophic Factors in the Treatment of Diabetic Peripheral Neuropathy

Diabetes is the leading cause of peripheral neuropathy (PN) , which results in loss of nerve supply in tissues like skin, adipose and muscle. While there are currently few treatments for PN, early mitigation in the pre-diabetic state with tissue neurotrophic factors may improve nerve function in metabolically important tissues like adipose. We used an adipocyte-tropic adeno-associated virus (AAV; serotype Rec2) to deliver neurotrophic factors directly to scWAT using a transdermal microneedle device that we developed. This approach avoids potential off-target effects and aberrant axon outgrowth in skin that may increase pain. Using both the BTBRob/ob and C57BL/6J diet-induced neuropathy mouse models, we have demonstrated that AAVRec2-BDNF (brain derived neurotrophic factor, which we have implicated in controlling adipose innervation) delivery to scWAT with our device increased tissue innervation 14 days after treatment, marked by increased protein expression of pan-neuronal marker PGP9.5 and sympathetic nerve marker tyrosine hydroxylase (TH) . Longer periods of dietary obesity (25+ wks vs 16 wks) blunted the ability of AAVRec2-BDNF to increase innervation in scWAT, despite these mice showing an initial decrease in body weight compared to controls. This indicates there may be a critical window for therapy delivery during the progression to diabetic neuropathy during which interventions are more advantageous. Treatment with AAVRec2-NGF (nerve growth factor) also increased scWAT innervation in obese mice at 8 weeks post-treatment, as evidenced by increased protein expression of PGP9.5, TH and markers of axon outgrowth (Gap43, Vasp) . Thermal imaging above inguinal scWAT revealed an increase in temperature only in AAVRec2-NGF treated mice, supporting the idea that NGF-responsive nerves drive tissue browning and/or thermogenesis. Taken together, we have developed a novel treatment approach for delivering adipocyte-tropic AAVs to overexpress neurotrophic factors as a means to mitigate diabetes-associated PN. Disclosure M. Blaszkiewicz: None. K. L. Townsend: Other Relationship; Neuright, Inc.

Clinical profile of patients with pure neuritic leprosy: 20 years’ experience at a tertiary referral centre from North India

Introduction Pure neuritic leprosy (PNL) is characterized by enlargement of peripheral nerves, sensory loss without any cutaneous lesions, skin slit smear negativity and a variable lepromin test and histopathology. Methods This was a retrospective analysis of the clinical records of all the leprosy patients enrolled in the Leprosy Clinic, during the years 1999–2019. The patient records fulfilling the diagnostic criteria of PNL were considered for analysis. Results A total of 1225 patients registered leprosy cases, out of which 41 (3.3%) patients were diagnosed with PNL. Mean age was 31 years and 80% patients were male. Multiple nerves were affected in 25 (61%) patients and one nerve was found to be affected in only 16 (39%) patients. Grade 2 deformities were seen in 26 (63%) patients. All patients were treated with multi-drug therapy - 25 patients received the multibacillary regimen and 16 received the paucibacillary regimen; 27 (66%) patients completed the treatment as prescribed. Conclusion Leprosy is the most common treatable cause of peripheral neuropathy. Therefore, early detection of leprosy neuropathy is important for preventing deformities and disabilities. It may be advisable to treat all PNL cases with the multibacillary multidrug therapy in view of higher rate of deformities.