Cirrhosis of the liver represents the final common pathway of chronic liver injury, marked by irreversible fibrosis, regenerative nodules, and disruption of the normal hepatic architecture, which eventually culminates in portal hypertension and hepatic insufficiency¹. It remains a global health challenge, contributing significantly to morbidity and mortality worldwide. The principal etiological factors include chronic alcohol consumption, viral hepatitis (HBV, HCV), and non-alcoholic fatty liver disease (NAFLD^2. Although cirrhosis primarily involves hepatic parenchymal damage, its impact extends far beyond the liver. The condition exerts widespread systemic effects, involving the cardiovascular, renal, endocrine, and nervous systems. Among its neurological complications, the spectrum ranges from hepatic encephalopathy (HE) and cognitive dysfunction to myopathy and peripheral neuropathy (PN)^3,4. While hepatic encephalopathy has long been recognized and extensively studied, peripheral neuropathy remains one of the most underdiagnosed and underestimated neurological complications of liver disease, despite its potential reversibility and profound effect on patients’ daily function and quality of life^4,5.

Peripheral neuropathy in cirrhosis often develops silently and insidiously, progressing unnoticed for several years before presenting as distal paraesthesia, sensory loss, muscle weakness, diminished reflexes, or gait imbalance^6,7. The clinical picture typically resembles a length-dependent, symmetrical, sensorimotor polyneuropathy, with the distal lower limbs being most commonly affected.

Electrophysiological studies over the past decades have revealed that peripheral nerve dysfunction is extremely common in cirrhosis, affecting 40–80% of patients depending on disease severity and diagnostic technique^8,9. These electrophysiological changes typically manifest as slowing of nerve conduction velocity (NCV), prolonged distal latency, and reduction in compound muscle action potential (CMAP) amplitude—features suggestive of axonal neuropathy or a mixed axonal–demyelinating process^9,10.

What makes this condition particularly challenging is that clinical symptoms are often mild or entirely absent, and most cases remain subclinical, detectable only on nerve conduction studies (NCS)¹¹. As a result, PN in cirrhosis is often misinterpreted or attributed to other causes, such as diabetes, alcoholism, malnutrition, or vitamin deficiency, rather than being recognized as a direct neurological manifestation of liver disease^5,12.

Pathophysiological Mechanisms

The development of peripheral neuropathy in cirrhosis is multifactorial, resulting from a combination of metabolic, nutritional, vascular, and immune-mediated mechanisms.

Metabolic and Neurotoxic Mechanisms

Chronic liver dysfunction leads to the accumulation of neurotoxic metabolites such as ammonia, manganese, bilirubin, and false neurotransmitters, which interfere with axon–Schwann cell interactions, mitochondrial energy metabolism, and axonal transport^3,4,10.Ammonia, one of the most significant neurotoxins, disrupts astrocyte metabolism, leading to astrocytic swelling and glutamate-induced excitotoxicity, ultimately causing neuronal dysfunction and axonal degeneration^9,10.Manganese, normally excreted via bile, accumulates in both the central and peripheral nervous systems in chronic liver disease, disturbing dopaminergic transmission and myelin integrity^7,1.

Nutritional Deficiency

Malnutrition is common among cirrhotic patients due to anorexia, malabsorption, and alcohol-related gastrointestinal injury, leading to deficiencies of vitamins B₁ (thiamine), B₆ (pyridoxine), B₁₂, and folate^5,1. These vitamins are vital for neuronal repair, axonal conduction, and myelin synthesis. Their deficiency results in axonal degeneration and segmental demyelination, compounding hepatic neurotoxicity⁹.

 Oxidative Stress and Inflammatory Injury

Cirrhosis is characterized by chronic oxidative stress, resulting from an imbalance between free radicals and antioxidant defenses. This leads to lipid peroxidation of neuronal membranes, mitochondrial dysfunction, and subsequent axonal damage⁷.
In addition, pro-inflammatory cytokines such as TNF-α, IL-6, and interferon-γ increase vascular permeability and impair endoneurial microcirculation, further exacerbating nerve ischemia and demyelination^9,10.

 Vascular and Immune-Mediated Factors

Cirrhosis-related vascular changes, including altered hepatic and peripheral microcirculation, can lead to endoneurial hypoxia, contributing to ischemic axonopathy. Moreover, immune-mediated mechanisms, particularly in viral hepatitis (HBV, HCV)-related cirrhosis, may trigger autoimmune attacks against peripheral myelin and gangliosides, producing demyelinating neuropathies^7,9. Thus, the neuropathy observed in cirrhosis represents a multifactorial injury process in which metabolic, nutritional, vascular, and immune disturbances act synergistically to impair peripheral nerve function.

Electrophysiological Evidence and Indian Data

Electrophysiological evaluation has emerged as the most reliable and objective method to detect subclinical PN in liver cirrhosis. Numerous studies across populations have demonstrated that NCS abnormalities are much more common than clinical neuropathy, confirming that subclinical involvement precedes symptomatic disease^8,9,10.

In Indian studies, these findings have been corroborated: Kharbanda et al. (2003)¹² reported a 71% prevalence of PN in cirrhotic patients, predominantly sensory and axonal in pattern. Jain et al. (2014)⁷ found a 60% prevalence, identifying a mixed axonal–demyelinating pattern with clear sensory predominance. Hewedi et al. (2018)⁴ demonstrated that sensory nerve conduction velocity (NCV) declines were present even in compensated cirrhosis, emphasizing the early onset of neural involvement. Chaudhry et al. (1999)³ documented the coexistence of autonomic and sensorimotor neuropathies, suggesting that liver disease affects multiple components of the peripheral nervous system. Collectively, these studies establish that nerve conduction studies are indispensable for detecting early neuropathic involvement in cirrhosis long before irreversible disability occurs.

Despite this compelling evidence, routine neurological screening remains absent in the standard evaluation of cirrhotic patients. Symptoms are frequently overlooked or misattributed to nutritional deficiencies, alcohol toxicity, or hepatic encephalopathy^5,9,11. Consequently, the true prevalence of peripheral neuropathy in cirrhosis remains underestimated, and its clinical impact underappreciated.

Furthermore, commonly used scoring systems such as the Child–Turcotte–Pugh (CTP) and Model for End-Stage Liver Disease (MELD) focus exclusively on hepatic biochemical parameters, without addressing neurological involvement^10,11. This oversight delays diagnosis and precludes preventive interventions.

Early detection through nerve conduction studies (NCS) provides an opportunity for timely intervention including nutritional correction, antioxidant therapy, and neuroprotective support which may slow, halt, or even reverse the neuropathic process^9,12.

Hence, this study was undertaken to evaluate the pattern and extent of motor and sensory nerve involvement in patients with hepatic cirrhosis, to determine whether the neuropathy is primarily axonal or demyelinating, and to identify which nerves are most vulnerable. In doing so, it aims to bridge the gap between hepatic pathophysiology and peripheral neurophysiology, contributing to a more holistic understanding of the systemic impact of chronic liver disease.

This observational cross-sectional study was conducted in the Department of Physiology, Pt. B.D. Sharma PGIMS, Rohtak, between 2021 and 2024, after obtaining ethical clearance. Fifty male patients (aged 25–50 years) with clinically and biochemically confirmed cirrhosis were included. Exclusion criteria were diabetes mellitus, chronic renal failure, alcoholism-induced neuropathy, vitamin B12 deficiency, vitamin B6 deficiency, hypothyroidism, or use of neurotoxic drugs. Disease severity was graded using the Child-Pugh classification. Nerve Conduction Studies: Motor and sensory NCS were performed bilaterally using RMS EMG EP MK2 equipment under standard conditions. The following nerves were tested: median, ulnar, tibial for motor nerve component and median, ulnar, sural for sensory nerve component. Parameters recorded included Latency (ms), Amplitude (mV for motor; µV for sensory) and Conduction velocity (m/s) . Statistical analysis: Data were expressed as mean ± SD. Student’s unpaired t-test was used to compare patient data with age-matched controls. A p-value <0.05 was considered statistically significant.

Table no. 1: Comparison of nerve conduction studies between normal and cirrhotics.

A total of 50 male patients with clinically, radiologically, and biochemically confirmed liver cirrhosis were included in this study. The mean age of participants was 43.88 ± 6.35 years, and the average duration of illness was 4.2 ± 2.1 years. The majority of patients 72% were classified as Child-Pugh Class B, while the remaining 28% belonged to Class C, indicating that most participants had moderate to advanced hepatic dysfunction. Notably, none of the patients in this cohort fell into Child-Pugh Class A, reflecting that the study population primarily consisted of individuals with clinically significant liver disease.

Motor Nerve Conduction Findings

The motor nerve conduction velocities (NCVs) were found to be significantly reduced in cirrhotic patients when compared with established normative values reported in the Indian population by Misra, Kalita⁵ (p < 0.001 for all tested nerves).

The median motor nerve exhibited a mean NCV of 44.43 ± 7.25 m/s, which was markedly lower than the normal mean of 58.52 ± 3.76 m/s (p < 0.001). Similarly, the ulnar motor nerve showed a decline from 58.7 ± 5.1 m/s in healthy controls to 47.01 ± 6.32 m/s among cirrhotic patients (p < 0.001). The tibial motor nerve displayed the most pronounced impairment, with a reduction from 48.3 ± 4.57 m/s to 38.6 ± 6.14 m/s (p < 0.001).

This consistent slowing across all motor nerves reflects a significant compromise in peripheral motor conduction, primarily indicating axonal dysfunction with mild superimposed demyelination. The reduction was most severe in the tibial and ulnar nerves, a finding characteristic of length-dependent neuropathies typically caused by metabolic or toxic insults^1,4,9.

Additionally, the motor amplitudes were uniformly decreased across all tested nerves, providing further evidence of axonal degeneration as the predominant mechanism. These results align closely with the findings of Kharbanda¹² and Jain⁷, who similarly documented axonal motor involvement in cirrhotic populations, reinforcing that chronic hepatic dysfunction compromises both sensory and motor nerve integrity, with axonal loss as the hallmark lesion.

Sensory Nerve Conduction Findings

The sensory components were even more profoundly affected than the motor components, underscoring the sensory-predominant nature of peripheral neuropathy in cirrhosis^2,4,7.

The median sensory nerve displayed a mean NCV of 33.02 ± 12.18 m/s, which was significantly lower than the control mean of 54.17 ± 6.10 m/s (p < 0.001). The ulnar sensory nerve also showed a marked decline, from 50.9 ± 5.4 m/s in controls to 30.64 ± 11.47 m/s in patients (p < 0.001). The sural nerve, known to be the most sensitive indicator of distal sensory neuropathy, demonstrated a significant reduction from 45.45 ± 9.40 m/s in healthy subjects to 37.28 ± 12.8 m/s in cirrhotic individuals (p < 0.05).

These findings clearly indicate that sensory fibers are more vulnerable to metabolic and nutritional disturbances associated with liver dysfunction. Similar trends were described by Hewedi⁴ and Chaudhry³, who reported that sural and median sensory nerves are typically the earliest to show electrophysiological changes in patients with cirrhosis.

In our cohort, prolonged distal latencies and reduced sensory amplitudes were observed in these nerves, reflecting axonal degeneration with partial demyelination. Such changes are likely the result of chronic metabolic stress, accumulation of neurotoxins (ammonia, manganese), and vitamin deficiencies that collectively compromise axonal transport and myelin maintenance^7,9,1. Overall, the sensory nerve abnormalities in this study not only confirmed the subclinical nature of PN but also emphasized that nerve conduction studies (NCS) are significantly more sensitive than clinical examination in identifying early neuropathic involvement.

Pattern of Neuropathy

When clinical and electrophysiological data were analyzed together, 76% of patients exhibited bilateral, symmetrical, mixed sensorimotor polyneuropathy, while 24% had purely sensory involvement. Among these, a clear axonal predominance was observed in 68% of patients, indicated by a greater reduction in amplitude compared to conduction velocity. The remaining 8% of cases showed features consistent with demyelinating or mixed neuropathy.

The overall pattern observed symmetrical, distal, length-dependent neuropathy with axonal dominance is consistent with the well-established electrophysiological signature of hepatic neuropathy described in previous research^1,2,4,7.
This finding strengthens the hypothesis that metabolic and toxic factors, rather than localized immune-mediated processes, are primarily responsible for the nerve damage seen in liver cirrhosis^8,9,10. The symmetrical distribution also mirrors the “dying-back” phenomenon typical of axonopathies, wherein distal fibers are the first to degenerate due to their higher metabolic demands and greater exposure to circulating neurotoxins.

Correlation with Disease Severity (CTP Class)

When the electrophysiological findings were compared across the Child-Turcotte-Pugh (CTP) classes, a clear trend emerged: 50% of patients in CTP Class A (compensated disease) exhibited abnormal NCS findings. 71% in Class B (moderate dysfunction) demonstrated neuropathic changes. 86% in Class C (severe hepatic dysfunction) showed significant nerve conduction abnormalities.

Although this progression from Class A to C did not reach statistical significance (p > 0.05), the increasing prevalence and severity of neuropathy across CTP classes indicate a dose-response relationship between worsening hepatic dysfunction and peripheral nerve injury ¹².

Comparable results have been reported by Agarwal¹⁴ and Chari¹⁵  , who observed that electrophysiological abnormalities correlate with the severity of liver dysfunction, even in the absence of overt clinical symptoms. These studies, along with the present findings, support the concept that neuropathy in cirrhosis often begins in the early stages of disease and progresses silently, driven by systemic metabolic derangements, ammonia toxicity, oxidative stress, and nutritional deficiencies, rather than being solely a consequence of reduced hepatic synthetic function^7,9,10.

This observation highlights a critical clinical insight: by the time cirrhotic neuropathy becomes symptomatic, substantial axonal loss may have already occurred, underscoring the need for early electrophysiological screening in all patients with chronic liver disease, regardless of the presence of neurological symptoms.

In summary, this study revealed that motor conduction velocities were significantly reduced across all nerves, particularly the tibial and ulnar, confirming axonal motor neuropathy. Sensory nerves, especially the sural and median nerves, were affected earlier and more severely, showing marked reductions in velocity and amplitude, confirming sensory predominance. 76% of patients had mixed sensorimotor neuropathy, with 68% showing axonal and 8% showing demyelinating features. Neuropathy prevalence increased from CTP A → B → C, suggesting disease progression impacts nerve physiology even before clinical manifestations appear. Together, these findings reaffirm that peripheral neuropathy is a highly prevalent, predominantly subclinical, and progressive complication of liver cirrhosis, arising from metabolic toxic mechanisms and nutritional deficiencies, and not merely from hepatic insufficiency.

.

The overall pattern of findings in this study, predominant sensory axonal involvement, bilateral symmetry, and its progressive association with disease severity, strongly reinforces the concept that peripheral neuropathy (PN) is an intrinsic and underrecognized neurological complication of chronic liver disease^1,2,3,7. This study adds to the growing body of evidence that peripheral nerve injury in cirrhosis occurs not as a rare incidental finding, but as a frequent, pathophysiologically rooted

manifestation of hepatic dysfunction.

Our results emphasize that electrophysiological testing is far more sensitive than clinical examination alone for detecting neuropathic changes. While only about one-third of our patients reported sensory symptoms, nearly three-fourths demonstrated abnormal nerve conduction findings, underscoring the subclinical nature of PN in cirrhosis. Similar observations were reported by Kharbanda¹² , Jain⁷ and Hewedi et al.⁴, who found that nerve conduction studies (NCS) could reveal neuropathy even in patients without overt neurological complaints. Thus, routine electrophysiological evaluation can serve as a valuable adjunct in identifying neuropathy early and preventing irreversible nerve damage through timely intervention.

The observed reduction in conduction velocity across both motor and sensory fibers likely reflects a combined process of axonal degeneration and segmental demyelination, arising from the cumulative neurotoxic and metabolic burden of hepatic dysfunction^7,9,10. In cirrhosis, chronic exposure to elevated levels of ammonia, manganese, bilirubin, and inflammatory cytokines induces oxidative stress and mitochondrial dysfunction in neurons. These biochemical insults disrupt axonal transport and energy metabolism, ultimately leading to axonal dropout and myelin instability ^9,10.

Ammonia, in particular, is known to alter astrocyte-neuron signaling and induce astrocytic swelling, which indirectly impairs neuronal excitability. Meanwhile, manganese, normally cleared by the liver via bile, accumulates in neural tissue and impairs dopaminergic neurotransmission, further aggravating peripheral and central nerve dysfunction^9,10.

The axonal pattern seen in most patients in this study, therefore, indicates chronic metabolic and oxidative injury rather than an acute demyelinating process. This pattern parallels that seen in diabetic and uremic neuropathies, where sustained metabolic derangement leads to distal axonal “dying-back” degeneration¹³.

Nutritional and Neurotrophic Factors

In addition to direct neurotoxicity, nutritional deficiencies appear to play a critical role in the pathogenesis of hepatic neuropathy. Deficiencies of thiamine (vitamin B₁), pyridoxine (vitamin B₆), folate, and vitamin B₁₂ are common in cirrhotic patients due to malabsorption, anorexia, and alcohol-related gastritis, compromising neuronal metabolism and myelin integrity, facilitating axonal degeneration¹¹.

Furthermore, cirrhosis is associated with reduced hepatic synthesis of neurotrophic factors such as nerve growth factor (NGF) and insulin-like growth factor-1 (IGF-1), which are crucial for axonal maintenance and regeneration. The deficiency of these growth factors may impair nerve repair mechanisms, predisposing to progressive neuropathic deterioration despite biochemical compensation¹¹.

Thus, hepatic neuropathy arises from a synergistic interplay between metabolic toxicity, nutritional deficiency, oxidative stress, and impaired neural repair, making it both a systemic and multifactorial disorder.

Electrophysiological Pattern and Nerve Vulnerability

The tibial and sural nerves were identified as the most frequently and severely affected nerves in this cohort. This finding can be attributed to their length and distal location, which make them more vulnerable to hypoxia, toxin exposure, and nutritional deficits. Such a pattern, characterized by symmetrical distal involvement, aligns with the “length-dependent axonopathy” or “dying-back neuropathy” pattern described in other metabolic conditions such as diabetes and renal failure¹³.

The predilection for distal sensory nerves supports the hypothesis that energy failure and oxidative injury preferentially damage long axons first due to their greater metabolic demand and longer transport distance. The resulting electrophysiological abnormalities, including low conduction velocity, reduced amplitudes, and prolonged latencies, mirror those reported in earlier studies by Hewedi⁴, Chaudhry³, and Kharbanda et al.¹², confirming that the sural and median sensory nerves are early markers of hepatic neuropathy.

Clinical Implications

The high prevalence of subclinical neuropathy found in this study has clear clinical and preventive implications. Since peripheral neuropathy is potentially reversible in its early stages, the incorporation of routine NCS screening into cirrhosis management protocols could allow for earlier detection and intervention.

Treatment strategies focusing on nutritional supplementation (vitamins B-complex, folate, antioxidants) and correction of metabolic derangements can help arrest or even reverse early nerve injury^9,11. Furthermore, rehabilitative interventions, including physiotherapy and balance training, may help improve functionality and reduce the risk of falls in symptomatic patients.

By integrating neurological assessment into hepatology care, clinicians can shift from reactive management of neuropathic complications to proactive prevention of nerve damage, thereby improving long-term quality of life for patients with chronic liver disease.

Peripheral neuropathy emerges as a frequent yet underrecognized neurological complication in patients with liver cirrhosis, representing a significant but often silent contributor to morbidity. The findings of this study highlight that sensory nerve fibers are affected earlier and more severely than motor fibers, evidenced by marked reductions in amplitude and prolonged latencies on electrophysiological testing. The overall neuropathy pattern is predominantly axonal, with features that are symmetrical, distal, and length-dependent a characteristic hallmark of chronic metabolic or toxic injury rather than focal or immune-mediated disease. The subclinical nature of most cases, in which electrophysiological abnormalities precede overt symptoms, underscores the inadequacy of relying solely on clinical evaluation for detecting neuropathy in cirrhotic patients. Many individuals with compensated or moderately advanced liver disease already harbour early nerve dysfunction, which, if left unrecognised, may progress to irreversible axonal loss and physical disability. Given this high prevalence and early onset, routine electrophysiological screening should be integrated into the standard evaluation of patients with chronic liver disease. Early detection enables timely nutritional and metabolic interventions including vitamin B-complex supplementation, antioxidant therapy, and management of ammonia and manganese accumulation which can delay or reverse nerve damage before permanent deficits occur. Moreover, this study reinforces the need for a multidisciplinary approach in the management of cirrhosis. Collaboration between hepatologists, neurologists, physiologists, and rehabilitation specialists can help address the multisystem impact of hepatic dysfunction, improving both neurological outcomes and overall quality of life. In summary, peripheral neuropathy in cirrhosis is not merely a secondary consequence but an integral manifestation of systemic hepatic disease. Recognising and addressing it early can transform patient care from reactive symptom management to proactive prevention and neuroprotection. Integrating neurophysiological assessment into cirrhosis protocols represents a pivotal step toward reducing disability, enhancing recovery, and restoring the functional independence of affected individuals. Acknowledgments The authors acknowledge the support of the Departments of Medicine and Physiology, Pt. B.D. Sharma PGIMS, Rohtak, for their cooperation in data collection and patient recruitment. Funding This study did not receive any external funding. Conflicts of Interest The authors declare no conflict of interest.

1. Koike H, Sobue G. Alcoholic neuropathy. Curr Opin Neurol. 2006;19(5):481–486.
2. Butterworth RF. Pathophysiology of hepatic encephalopathy: a new look at ammonia. Metab Brain Dis. 2002;17(4):221–227.
3. Chaudhry V, Corse AM, O’Brian R, Cornblath DR, Klein AS, Thuluvath PJ. Autonomic and peripheral (sensorimotor) neuropathy in chronic liver disease: a clinical and electrophysiologic study. Hepatol .1999;29(6):1698–703.
4. Hewedi K, Dessouky Y, Emam HM, Essmat A, Elkader AA. Neurophysiological assessment of peripheral nerve functions in a sample of Egyptian patients with liver cirrhosis. Egyptian J Hospital Med. 2018;73(9):7512–6.
5. Misra UK, Kalita J. Clinical Neurophysiology. 2nd ed. Elsevier; 2006. Clinical neurophysiology: Nerve conduction study; 21–128.
6. Aller de la Fuente R. Nutrition and Chronic Liver Disease. Clinical Drug Investigation. 2022 Apr 29;42(S1):55–61.
7. Jain J, Singh R, Banait S, Verma N, Waghmare S. Magnitude of peripheral neuropathy in cirrhosis of liver patients from central rural India. Annals of Indian Academy of Neurology. 2014;17(4):409.
8. Schenck E, Dietz V. Alkoholische Polyneuropathie. Archiv for Psychiatrie und Nervenkrankheiten. 1975;220(2):159–70.
9. Krieger D, Krieger S, Theilmann L, Jansen O, Gass P, Lichtnecker H. Manganese and chronic hepatic encephalopathy. The Lancet. 1995 Jul;346(8970):270–4.
10. Rose CF, Butterworth RF, Zayed J, Normandin L, Todd KG, Michalak A, et al. Manganese deposition in basal ganglia structures results from both portal-systemic shunting and liver dysfunction. Gastroenterology. 1999 Sep 1;117(3):640–4.
11. Kalra N, Ramanathan S, Khandelwal N, Bhatia A, Dhiman R, Ajay K Duseja, et al. Correlation of HVPG level with ctp score, MELD Score, ascites, size of varices, and etiology in cirrhotic patients. Saudi Journal of Gastroenterology [Internet]. 2015 Sep 2 [cited 2025 Jun 7];22(2):109–9. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC4817293/.
12. Kharbanda PS, Prabhakar S, Chawla YK, et al. Peripheral neuropathy in liver cirrhosis. J Assoc Physicians India. 2003;51:341–344.
13. Mittal M, Singh PK, Kurian S. Study of prevalence and pattern of peripheral neuropathy in patients with liver cirrhosis. International Journal of Advances in Medicine. 2017 Jul 20;4(4):1041.
14. Bajaj BK, Agarwal MP, Ram BK. Autonomic neuropathy in patients with hepatic cirrhosis. Postgrad Med J. 2003;79(933):408–11.
15. Chari VR, B.C. Katiyar, Rastogi BL, Bhattacharya SK. Neuropathy in hepatic disorders. Journal of the neurological sciences. 1977 Jan 1;31(1):93–111.

1. Koike H, Sobue G. Alcoholic neuropathy. Curr Opin Neurol. 2006;19(5):481–486.
2. Butterworth RF. Pathophysiology of hepatic encephalopathy: a new look at ammonia. Metab Brain Dis. 2002;17(4):221–227.
3. Chaudhry V, Corse AM, O’Brian R, Cornblath DR, Klein AS, Thuluvath PJ. Autonomic and peripheral (sensorimotor) neuropathy in chronic liver disease: a clinical and electrophysiologic study. Hepatol .1999;29(6):1698–703.
4. Hewedi K, Dessouky Y, Emam HM, Essmat A, Elkader AA. Neurophysiological assessment of peripheral nerve functions in a sample of Egyptian patients with liver cirrhosis. Egyptian J Hospital Med. 2018;73(9):7512–6.
5. Misra UK, Kalita J. Clinical Neurophysiology. 2nd ed. Elsevier; 2006. Clinical neurophysiology: Nerve conduction study; 21–128.
6. Aller de la Fuente R. Nutrition and Chronic Liver Disease. Clinical Drug Investigation. 2022 Apr 29;42(S1):55–61.
7. Jain J, Singh R, Banait S, Verma N, Waghmare S. Magnitude of peripheral neuropathy in cirrhosis of liver patients from central rural India. Annals of Indian Academy of Neurology. 2014;17(4):409.
8. Schenck E, Dietz V. Alkoholische Polyneuropathie. Archiv for Psychiatrie und Nervenkrankheiten. 1975;220(2):159–70.
9. Krieger D, Krieger S, Theilmann L, Jansen O, Gass P, Lichtnecker H. Manganese and chronic hepatic encephalopathy. The Lancet. 1995 Jul;346(8970):270–4.
10. Rose CF, Butterworth RF, Zayed J, Normandin L, Todd KG, Michalak A, et al. Manganese deposition in basal ganglia structures results from both portal-systemic shunting and liver dysfunction. Gastroenterology. 1999 Sep 1;117(3):640–4.
11. Kalra N, Ramanathan S, Khandelwal N, Bhatia A, Dhiman R, Ajay K Duseja, et al. Correlation of HVPG level with ctp score, MELD Score, ascites, size of varices, and etiology in cirrhotic patients. Saudi Journal of Gastroenterology [Internet]. 2015 Sep 2 [cited 2025 Jun 7];22(2):109–9. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC4817293/.
12. Kharbanda PS, Prabhakar S, Chawla YK, et al. Peripheral neuropathy in liver cirrhosis. J Assoc Physicians India. 2003;51:341–344.
13. Mittal M, Singh PK, Kurian S. Study of prevalence and pattern of peripheral neuropathy in patients with liver cirrhosis. International Journal of Advances in Medicine. 2017 Jul 20;4(4):1041.
14. Bajaj BK, Agarwal MP, Ram BK. Autonomic neuropathy in patients with hepatic cirrhosis. Postgrad Med J. 2003;79(933):408–11.
15. Chari VR, B.C. Katiyar, Rastogi BL, Bhattacharya SK. Neuropathy in hepatic disorders. Journal of the neurological sciences. 1977 Jan 1;31(1):93–111.