Electroencephalography Quality and Application Times in a Pediatric Emergency Department Setting: A Feasibility Study.

BACKGROUND: Status epilepticus is the most common neurological emergency presenting to pediatric emergency departments. Nonconvulsive status epilepticus can be extremely challenging to diagnose, however, requiring electroencephalographic (EEG) confirmation for definitive diagnosis. We aimed to determine the feasibility of achieving a good-quality pediatric EEG recording within 20 minutes of presentation to the emergency department. METHODS: Single-center prospective feasibility study in Cork University Hospital, Ireland, between July 2021 and June 2022. Two-channel continuous EEG was recorded from children (1) aged <16 years and (2) with Glasgow Coma Scale <11 or a reduction in baseline Glasgow Coma Scale in the case of a child with a neurodisability. RESULTS: Twenty patients were included. The median age at presentation was 65.8 months (interquartile range, 23.2 to 119.0); 50% had a background diagnosis of epilepsy. The most common reason for EEG monitoring was status epilepticus (85%) followed by suspected nonconvulsive status (10%) and reduced consciousness of unknown etiology (5%). The mean length of recording was 93.1 minutes (S.D. 47.4). The mean time to application was 41.3 minutes (S.D. 11.7). The mean percent of artifact in all recordings was 19.3% (S.D. 15.9). Thirteen (65%) EEGs had <25% artifact. Artifact was higher in cases in which active airway management was ongoing. CONCLUSIONS: EEG monitoring can be achieved in a pediatric emergency department setting within one hour of presentation. Overall, artifact percentage was low outside of periods of airway manipulation. Future studies are required to determine its use in early seizure detection and its support role in clinical decision-making in these patients.

Case Report: Early Neonatal EEG in Two Infants with Pallister Killian Syndrome (PKS).

Pallister Killian Syndrome (PKS) is a rare genetic disorder caused by a mosaic tetrasomy of the short arm of chromosome 12. The syndrome is characterised by typical craniofacial dysmorphism, congenital anomalies and intellectual disability. Epilepsy is a known complication, with onset usually occurring in early childhood and characterised most commonly by spasms and myoclonic seizures. To the best of our knowledge, there have been no cases describing the early neonatal EEG in PKS and  electrographic seizures, to date. Here, we report two cases of PKS presenting in the neonatal period with distinctive EEG features and seizures.

Sex, pain, and the microbiome: The relationship between baseline gut microbiota composition, gender and somatic pain in healthy individuals.

BACKGROUND AND AIM: Relative to men, women present with pain conditions more commonly. Although consistent differences exist between men and women in terms of physiological pain sensitivity, the underlying mechanisms are incompletely understood and yet could inform the development of effective sex specific treatments for pain. The gut microbiota can modulate nervous system functioning, including pain signaling pathways. We hypothesized that the gut microbiota and critical components of the gut-brain axis might influence electrical pain thresholds. Further, we hypothesized that sex, menstrual cycle, and hormonal contraceptive use might account for inter-sex differences in pain perception. METHODS: Healthy, non-obese males (N = 15) and females (N = 16), (nine of whom were using hormonal contraceptives), were recruited. Male subjects were invited to undergo testing once, whereas females were invited three times across the menstrual cycle, based on self-reported early follicular (EF), late follicular (LF), or mid-luteal (ML) phase. On test days, electrical stimulation on the right ankle was performed; salivary cortisol levels were measured in the morning; levels of lipopolysaccharide-binding protein (LBP), soluble CD14 (sCD14), pro-inflammatory cytokines were assessed in plasma, and microbiota composition and short-chain fatty acids (SCFAs) levels were determined in fecal samples. RESULTS: We observed that the pain tolerance threshold/pain sensation threshold (PTT/PST) ratio was significantly lesser in women than men, but not PST or PTT alone. Further, hormonal contraceptive use was associated with increased LBP levels (LF & ML phase), whilst sCD14 levels or inflammatory cytokines were not affected. Interestingly, in women, hormonal contraceptive use was associated with an increase in the relative abundance of Erysipelatoclostridium, and the relative abundances of certain bacterial genera correlated positively with pain sensation thresholds (Prevotella and Megasphera) during the LF phase and cortisol awakening response (Anaerofustis) during the ML phase. In comparison with men, women displayed overall stronger associations between i) SCFAs data, ii) cortisol data, iii) inflammatory cytokines and PTT and PST. DISCUSSION AND CONCLUSION: Our findings support the hypothesis that the gut microbiota may be one of the factors determining the physiological inter-sex differences in pain perception. Further research is needed to investigate the molecular mechanisms by which specific sex hormones and gut microbes modulate pain signaling pathways, but this study highlights the possibilities for innovative individual targeted therapies for pain management.

Phenotype of a second Irish variant causing hereditary amyloidogenic transthyretin amyloidosis.

INTRODUCTION: Hereditary amyloidogenic transthyretin (ATTR) amyloidosis is an autosomal dominant, multi-systemic and progressive disorder characterised by polyneuropathy, cardiomyopathy and dysautonomia to varying degrees. In Ireland, the p.Thr80Ala mutation has been well documented, but little has been reported about a second variant, the p.His110Asp mutation first discovered in a family native to county Cork. Here we elaborate on the phenotype of this recently identified mutation using an extended pedigree of the original kindred and include for the first time a second affected family. MATERIALS AND METHODS: Patients attending our centre with confirmed or suspected ATTR amyloidosis as a result of a p.His110Asp mutation were identified. Detailed chart reviews and patient interviews were completed. Data on symptoms, examination findings, neurophysiology, histology, biochemistry, and cardiac investigations were gathered. A large extended pedigree was plotted. RESULTS: A total of 17 members across four generations of one kindred, and 2 members of a previously unreported family were identified. A phenotype of progressive late-onset polyneuropathy with cardiac involvement was common to both families. An early manifestation was carpal tunnel syndrome, preceededing neuropathy by many years. Gastrointestinal and urinary symptoms were common. DISCUSSION: We describe a wider phenotype of the p.His110Asp mutation of transthyretin in two Irish families. Importantly, we describe cardiac involvement which was not previously emphasised. The discovery of a new unrelated family highlights the importance of clinical suspicion even in those without known family history. We suggest that this second important transthyretin mutation should be considered in patients of Irish origin.

Case Report: Electroencephalography in a neonate with isolated sulfite oxidase deficiency - a case report and literature review.

Isolated sulfite oxidase deficiency (ISOD) is a rare autosomal recessive neuro-metabolic disorder caused by a mutation in the sulfite oxidase (SUOX) gene situated on chromosome 12. Due to the deficiency of this mitochondrial enzyme (sulfite oxidase), the oxidative degradation of toxic sulfites is disrupted. The most common form of this disease has an early onset (classical ISOD) in the neonatal period, with hypotonia, poor feeding and intractable seizures, mimicking hypoxic-ischaemic encephalopathy. The evolution is rapidly progressive to severe developmental delay, microcephaly and early death. Unfortunately, there is no effective treatment and the prognosis is very poor. In this article, we described the evolution of early continuous electroencephalography (EEG) in a case of ISOD with neonatal onset, as severely encephalopathic background, with refractory seizures and distinct delta-beta complexes. The presence of the delta-beta complexes might be a diagnostic marker in ISOD. We also performed a literature review of published cases of neonatal ISOD that included EEG monitoring.

Pain after upper limb surgery under peripheral nerve block is associated with gut microbiome composition and diversity.

Gut microbiota play a role in certain pain states. Hence, these microbiota also influence somatic pain. We aimed to determine if there was an association between gut microbiota (composition and diversity) and postoperative pain. Patients (n = 20) undergoing surgical fixation of distal radius fracture under axillary brachial plexus block were studied. Gut microbiota diversity and abundance were analysed for association with: (i) a verbal pain rating scale of < 4/10 throughout the first 24 h after surgery (ii) a level of pain deemed "acceptable" by the patient during the first 24 h following surgery (iii) a maximum self-reported pain score during the first 24 h postoperatively and (iv) analgesic consumption during the first postoperative week. Analgesic consumption was inversely correlated with the Shannon index of alpha diversity. There were also significant differences, at the genus level (including Lachnospira), with respect to pain being "not acceptable" at 24 h postoperatively. Porphyromonas was more abundant in the group reporting an acceptable pain level at 24 h. An inverse correlation was noted between abundance of Collinsella and maximum self-reported pain score with movement. We have demonstrated for the first time that postoperative pain is associated with gut microbiota composition and diversity. Further work on the relationship between the gut microbiome and somatic pain may offer new therapeutic targets.

The Diagnostic Yield of Electromyography at Detecting Abnormalities on Muscle Biopsy: A Single Center Experience.

Historically, electromyography (EMG) is utilized early in the diagnostic evaluation of neuromuscular disorders, but its importance may be diminishing with more sophisticated genetic, imaging and immunohistochemistry investigations now available. In the present study, the diagnostic yield of EMG at predicting pathological abnormalities confirmed by muscle biopsy was determined at our neuroscience center. A retrospective study of consecutive cases reviewed at neuromuscular multidisciplinary meetings between 2007 and 2016 identified patients who had EMG and muscle biopsy as part of their diagnostic evaluation. EMG and biopsy findings were categorized as myopathic, neurogenic or normal. The diagnostic accuracy was determined by calculating the concordance between EMG and pathological findings. Of the 175 cases included in the analysis, there was definite concordance between EMG and muscle biopsy findings in 134 cases (76.6%). Abnormal EMG produced sensitivity of 87% and specificity of 65% for abnormal muscle biopsy. Seventeen patients had a normal EMG and an abnormal muscle biopsy, of which 6 had histopathological findings consistent with mitochondrial myopathy, central core myopathy or glycogen storage disorder. Conflicting EMG and muscle biopsy findings were observed in 10 cases. Inclusion body myositis, chronic neuromuscular disorders and dual pathologies were associated with discordant findings. This study demonstrates that EMG has accurate predictive value in diagnosing neuromuscular disorders at our neuroscience center. EMG retains a vital role, particularly in initial diagnostic evaluations of neuromuscular disorders.

Ataxia pancytopenia syndrome due to SAMD9L mutation presenting as demyelinating neuropathy.

Ataxia pancytopenia (ATXPC) syndrome due to gain-of-function pathogenic variants in the SAMD9L gene has been described in 38 patients to date. It is characterized by variable neurological and hematological phenotypes including ataxia, pyramidal signs, cytopenias, and hematological malignancies. Peripheral neuropathy with slowing of conduction velocities has been reported in only two affected individuals. We describe a female with childhood onset neuropathy diagnosed as Charcot-Marie-Tooth disease type 1 with onset of cerebellar ataxia in her 50s. Cerebellar, pyramidal, and neuropathic features were found on examination. Additionally, she also had conjunctival telangiectasia. Nerve conduction studies confirmed a demyelinating neuropathy. MRI brain showed cerebellar atrophy with diffuse white matter hyperintensities. OCT demonstrated global thinning of the retinal nerve fiber layer (RNFL). Full blood count has always been normal. A previously described pathogenic variant in SAMD9L [c.2956C>T p.(Arg986Cys)] was identified on whole exome sequencing. This case extends the previously described phenotype to include conjunctival telangiectasia and RNFL thinning and suggests that ATXPC syndrome should be considered in the differential for inherited demyelinating neuropathies.

Acute severe sensory ganglionopathy in systemic lupus erythematous.

Sensory ganglionopathies (or neuronopathies) are a rare subgroup of neuropathies characterized by involvement of sensory neurons in the dorsal root ganglion. Although much less common than central nervous system involvement, patients with systemic lupus erythematous (SLE) can develop peripheral nervous system involvement (PNS) and most commonly a chronic length dependent symmetric sensorimotor axonal polyneuropathy as a late complication of the disease. Unlike in Sjogren's syndrome, SLE-associated sensory ganglionopathy is extremely rare and usually manifests in a chronic insidious fashion. We report a 24-year-old man with SLE-associated sensory ganglionopathy manifesting an unusually acute and severe disabling clinical course with a good response to immunosuppressive therapies. Timely recognition of this rare association and early targeted immunosuppression prevented severe neurological sequelae and preserved patient's ambulation. We demonstrate videos on the evolution of patient's neurological impairment and response to treatment, contributing to the current knowledge of the natural history of PNS involvement in SLE.

Impact of therapeutic hypothermia on infantile spasms: an observational cohort study.

AIM: To establish the incidence of infantile spasms in children in the southern region of the Republic of Ireland and to compare the incidence of infantile spasms before and after the introduction of therapeutic hypothermia in infants with hypoxic-ischemic encephalopathy (HIE). METHOD: Children born between 2003 and 2015 and diagnosed with infantile spasms (epileptic spasms with or without hypsarrhythmia) in the first 2 years of life were identified through audits of electroencephalography reports and paediatric neurology patient lists. Data on live births were obtained from the regional hospital statistics databases. Medical charts of infantile spasm cases were reviewed for demographic information, diagnostic workup results, treatment response, disease course, and developmental outcome. RESULTS: Forty-two infants with infantile spasms were identified. The cumulative incidence of infantile spasms up to the age of 2 years was 4.01 per 10 000 live births. Difference due to sex was minimal (22 males, 20 females) and most infants were delivered at or near term with gestational ages ranging between 30.0 and 41.8 weeks (median [interquartile range] 39.6wks [38.1-40.0wks]). The aetiology for infantile spasms was identified in almost two-thirds of cases, with HIE being the single most common cause (n=7). Other causes included chromosomal and monogenetic abnormalities (n=8). Infantile spasms occurred in moderate and severe grades of HIE, with a significantly higher incidence in those with severe HIE (p=0.029). Infants with severe HIE who did not receive therapeutic hypothermia were six times more likely to develop infantile spasms compared to those who did, but the difference was not statistically significant (4 out of 16 vs 1 out of 24, p=0.138). INTERPRETATION: This study provides detailed information about infantile spasms before and after the introduction of therapeutic hypothermia. HIE severity is a risk factor for the development of infantile spasms. The introduction of therapeutic hypothermia may have had an impact, but the effect was hard to ascertain in this cohort due to the small number of infants. WHAT THIS PAPER ADDS: The incidence of infantile spasms and patient characteristics in the southern region of the Republic of Ireland is similar to internationally published data. None of the infants with a history of mild hypoxic-ischemic encephalopathy (HIE) developed infantile spasms. The risk of infantile spasms was higher in infants with severe HIE. Infantile spasms were more frequent in infants with severe HIE not treated with therapeutic hypothermia.

IMPACTO DE LA HIPOTERMIA COMO TRATAMIENTO EN LOS ESPASMOS INFANTILES: UN ESTUDIO DE COHORTE OBSERVACIONAL: OBJETIVO: Establecer la incidencia de los espasmos infantiles en niños de la República de Irlanda y comparar la incidencia de los espasmos infantiles antes y después de la introducción de la hipotermia terapéutica en niños con encefalopatía hipóxico-isquémica (EHI). MÉTODO: Niños nacidos entre 2003 y 2015 y diagnosticados con espasmos infantiles (espasmos epilépticos con o sin hipsarritmia) en los primeros 2 años de vida fueron identificados por medio de auditorías de reportes de electroencefalográficos y listas de pacientes de neurólogos infantiles. Datos sobre los nacidos vivos se obtuvieron de la base de datos estadística del hospital regional. Las historias clínicas de los casos de espasmos infantiles fueron revisadas para obtener datos demográficos, resultados diagnósticos, respuesta a tratamiento, curso de la enfermedad y resultados del desarrollo. RESULTADOS: Fueron identificados 42 niños con espasmos infantiles. La incidencia acumulada de los espasmos infantiles por encima de los 2 años fue de 4,01 por 10.000 nacidos vivos. La diferencia debida al sexo fue mínima (22 masculinos, 20 femeninos) y la mayoría nacieron en o cercano a término, con edad gestacional entre 30,0 y 41,8 semanas (media (rango Intercuartil) 39,6 semanas (38,1-40,0 semanas). La etiología de espasmos infantiles fue identificada en dos tercios de los casos, siendo EHI la causa más común (7 de 42). Otras causas incluyeron anormalidades cromosómicas y monogénicas (8 de 42). Los espasmos infantiles ocurrieron en los grados moderados y severos de EHI con incidencia significativamente mayor en aquellos casos severos de EHI (p=0,029). Los niños con EHI severo que no recibieron hipotermia terapéutica tuvieron una probabilidad seis veces mayor de desarrollar espasmos infantiles comparados con aquellos quienes la recibieron, pero la diferencia no era estadísticamente significativa (4 de 16 vs 1 de 14, p=0,138). INTERPRETACIÓN: Este estudio proporciona información detallada acerca de los espasmos infantiles antes y después de la introducción de la hipotermia terapéutica. La severidad de la EHI es un factor de riesgo para el desarrollo de los espasmos infantiles. La introducción de la hipotermia terapéutica puede haber tenido un impacto, pero el efecto fue difícil de determinar en esta cohorte debido al pequeño número de recién nacidos.

IMPACTO DA HIPOTERMIA TERAPÊUTICA NOS ESPASMOS INFANTIS: UM ESTUDO DE COORTE OBSERVACIONAL: OBJETIVO: Estabelecer a incidência de espasmos infantis em crianças da República da Irlanda e comparar a incidência de espasmos infantis antes e após a introdução da hipotermia terapêutica em lactentes com encefalopatia hipóxica-isquêmica (EHI). MÉTODO: Crianças nascidas entre 2003 e 2015 e diagnosticadas com espasmos infantis (espasmos epilépticos com ou sem hipsarritmia) nos primeiros 2 anos de vida foram identificadas por meio de checagem dos relatórios de eletroencefalografia e listas de pacientes de neurologia pediátrica. Dados sobre nascidos vivos foram obtidos nas bases de dados estatísticas dos hospitais regionais. Prontuários médicos sobre casos de espasmos infantis foram revisados quanto a dados demográficos, resultados diagnósticos, resposta ao tratamento, curso da doença, e resultado desenvolvimental. RESULTADOS: Quarenta e dois lactentes com espasmos infantis foram identificados. A incidência cumulativa de espasmos infantis até os dois anos de idade foi 4,01 por 10.000 nascidos vidos. Diferenças devida ao sexo foram mínimas (22 meninos, 20 meninas) e a maior parte dos lactentes nasceu próximo ao termo, com idades gestacionais variando de 30,0 41,8 semanas (mediana [intervalo interquartil] 39,6 sem [38,1-40,0sem]). A etiologia dos espasmos infantis foi identificada em dois terços dos casos, com a EHI sendo a causa mais comum (7 em cada 42). Outras causas incluíram anormalidades cromossômicas e monogenéticas (8 em 42). Os espasmos infantis aconteceram em graus moderados a severos de EHI, com incidência significantemente maior naqueles com EHI severa (p=0,029). Lactentes com EHI severa que não receberam hipotermia terapêutica tinham seis vezes mais probabilidade de desenvolver espasmos infantis comparados com os que receberam, mas a diferença não foi estatisticamente significativa. (4 em16 vs 1 em 24, p=0,138). INTERPRETAÇÃO: Este esudo fornece informação detalhada sobre espasmos infantis antes e após a introdução de hipotermia terapêutica. A severidade da EHI é um fator de risco para o desenvolvimento de espasmos infantis. A introdução de hiportermia terapêutica por ter tido um impacto, mas o efeito foi difícil de assegurar nesta coorte devido ao pequeno número de lactentes.

Long-term outcomes in a 25-year-old female affected with lipin-1 deficiency.

Lipin-1 is a phosphatidic acid phosphohydrolase (EC 3.1.3.4) that catalyzes the dephosphorylation of phosphatidic acid to diacylglycerol and inorganic phosphate. Deficiency of this enzyme causes potentially fatal severe, recurrent episodes of rhabdomyolysis triggered by infection. The defect has only recently been recognized so little is known about the long-term outcome in adult patients with this disorder. We report the course and outcome of a 25-year-old female patient with lipin-1 deficiency after a recent episode of rhabdomyolysis requiring intensive care admission with a peak creatine kinase of 500 000 IU/L. One-year post discharge from intensive care, the patient has residual drop foot bilaterally consistent with bilateral common peroneal neuropathies in addition to a background residual distal myopathy.

Familial Hemiplegic Migraine With Asymmetric Encephalopathy Secondary to ATP1A2 Mutation: A Case Series.

INTRODUCTION: Familial hemiplegic migraine (FHM) is a genetic disease with a variable clinical phenotype. The imaging and electroencephalogram (EEG) correlates of FHM are not well described. CASE SERIES: We describe a case series of five young women aged 12 to 32 years. Each case presented with headache, encephalopathy, and hemiparesis of varying severity. One patient developed seizures. All patients improved spontaneously. INVESTIGATIONS: Asymmetric slow-wave activity was seen on electroencephalogram in each case. One patient developed marked unilateral cortical edema on MR imaging. Cerebro-spinal fluid (CSF) studies were normal for all patients. Genetic testing in each case showed a mutation of the ATP1A2 gene. One of the mutations identified is a novel mutation. DISCUSSION: Genetic mutation of the ATP1A2 gene results in a channelopathy which is thought to predispose to spreading depolarization, the probable physiologic correlate of migraine aura. We hypothesize that widespread prolonged depolarization accounts for the characteristic electroencephalogram findings in these cases. Familial hemiplegic migraine should be considered in the differential diagnosis of an asymmetric encephalopathy, particularly when CSF and imaging studies are normal.

Cold, clumpy accretion onto an active supermassive black hole.

Supermassive black holes in galaxy centres can grow by the accretion of gas, liberating energy that might regulate star formation on galaxy-wide scales. The nature of the gaseous fuel reservoirs that power black hole growth is nevertheless largely unconstrained by observations, and is instead routinely simplified as a smooth, spherical inflow of very hot gas. Recent theory and simulations instead predict that accretion can be dominated by a stochastic, clumpy distribution of very cold molecular clouds--a departure from the 'hot mode' accretion model--although unambiguous observational support for this prediction remains elusive. Here we report observations that reveal a cold, clumpy accretion flow towards a supermassive black hole fuel reservoir in the nucleus of the Abell 2597 Brightest Cluster Galaxy (BCG), a nearby (redshift z = 0.0821) giant elliptical galaxy surrounded by a dense halo of hot plasma. Under the right conditions, thermal instabilities produce a rain of cold clouds that fall towards the galaxy's centre, sustaining star formation amid a kiloparsec-scale molecular nebula that is found at its core. The observations show that these cold clouds also fuel black hole accretion, revealing 'shadows' cast by the molecular clouds as they move inward at about 300 kilometres per second towards the active supermassive black hole, which serves as a bright backlight. Corroborating evidence from prior observations of warmer atomic gas at extremely high spatial resolution, along with simple arguments based on geometry and probability, indicate that these clouds are within the innermost hundred parsecs of the black hole, and falling closer towards it.

DADS neuropathy associated with anti-TNF-α therapy.

A 52-year-old man with idiopathic Parkinson's disease and severe rheumatoid arthritis presented with a 1-year history of progressively worsening limb paraesthesia. Examination showed sensory loss in a glove and stocking distribution, absent reflexes and unsteady tandem gait. Nerve conduction studies suggested an acquired peripheral neuropathy with distal demyelination, which-together with the clinical phenotype-was consistent with a Distal Acquired Demyelinating Symmetric (DADS) neuropathy pattern. This was attributed to therapy with adalimumab, an antitumor necrosis factor (TNF)-α agent, which the patient had been taking for 2 years for rheumatoid arthritis. One month after discontinuing adalimumab, the limb paraesthesia had resolved completely and the patient had a normal tandem gait. Demyelinating disorders may rarely occur as complications of anti-TNF-α agents and therefore have implications for pretreatment counselling and ongoing monitoring. DADS neuropathy is a subtype of chronic inflammatory demyelinating polyradiculoneuropathy, which responds poorly to standard therapy and has not previously been described with anti-TNF-α therapy.

Acute encephalopathy in familial hemiplegic migraine with ATP1A2 mutation.

Familial hemiplegic migraine is a rare subtype of migraine with aura which includes motor weakness. A 32-year-old woman with known familial hemiplegic migraine (point mutation in Exon 22 of the ATP1A2 gene) presented with an acute confusional state, after an initially typical migraine. On examination, she had fever (38°C), agitated, with a right hemiparesis and dysphasia. Electroencephalography showed slowing of α rhythm and continuous rhythmical δ activity in the left hemisphere. She recovered 48 h after the onset of encephalopathic episode. Electroencephalography after recovery showed resolution of the abnormal slowing of the α waveforms.

Neuropathy in the hemodialysis population: a review of neurophysiology referrals in a tertiary center.

This was a retrospective observational study of neurophysiology referrals over 8 years from a tertiary referral center in Ireland. A total of 68 of the 73 referrals yielded one or more abnormalities. Thirty-nine (53%) patients had one or more mononeuropathies; iatrogenic mononeuropathies believed to be associated with arterio-venous fistula creation occurred in 15 patients. Polyneuropathy was identified in 43 patients (59%). Access to an experienced neurophysiology department offers valuable insight into dialysis-associated neuropathies, especially when associated with arterio-venous fistulae.