Coincidence or Causality: Parathyroid Carcinoma in Chronic Kidney Disease-Case Report and Literature Review.

Parathyroid carcinoma (PC) associated with primary hyperparathyroidism (PHPT) has been well investigated in recent years. Data regarding PC evolution in secondary hyperparathyroidism (SHPT) due to chronic kidney disease (CKD) are, however, scarce. Most features that raise the suspicion of PC in PHPT are part of the usual SHPT evolution in CKD, mirroring the natural changes undergone by the parathyroid glands. Therefore, pre-surgically establishing the malignant or benign character of the lesions is cumbersome. We present two cases of PC in end-stage renal disease, one of which was bilateral, diagnosed after total parathyroidectomy in a high-volume parathyroid surgery center. A literature review of the data was also performed. A systematic search of the PubMed/MEDLINE database until January 2024 identified 42 cases of PC associated with SHPT. Understanding the PC features in CKD might improve associated bone and mineral disease management, and reduce the risk of metastasis, parathyromatosis, or recurrence. Irradiation, prolonged immunosuppression, long dialysis vintage, and genotype may predispose to the malignant transformation of chronically stimulated parathyroids. Despite postsurgical diagnosis, favorable outcomes occurred when distant metastases were absent, even without "en bloc" resection. Further research is warranted to delineate specific diagnostic and therapeutic approaches tailored to this particular patient subpopulation.

The sex-dependent impact of adipose tissue and inflammation on chronic pain - A cross-sectional study from the all of us research program.

Emerging evidence suggests an association between chronic pain and elevated body fat. We sought to determine if individuals with higher body fat, measured by hip circumference (HC) and waist circumference (WC), are at risk for chronic pain when they demonstrate higher expression of inflammatory markers. We investigated the incidence and severity of pain in patients with varying WC/HC and inflammatory markers (C-Reactive Protein, IL-6, leptin) using the NIH-sponsored All of Us Database. For each inflammatory marker and sex, participants were divided into four groups based on combinations of normal/high marker levels and small/large WC/HC. We used statistical analysis to compare WC/HC and pain severity (mean NRS pain score) between groups of the same sex. In females, but not males, combinations of elevated CRP with large WC/HC exerted additive effects on the incidence of chronic pain (p < 0.01) and severe pain (p < 0.001), as well as on the severity of pain evaluated by the mean NRS pain score (p < 0.01). This relationship held true for females with high IL-6 or leptin and large WC or HC (p < 0.001 for chronic pain and severe pain incidence, and p < 0.05 for pain severity). Neither IL-6 nor leptin showed any significant impact on pain in males. Obesity status and CRP exert additive prognostic effects for chronic pain in females, but not in males. The concomitant evaluation of other inflammatory factors, such as IL-6 or leptin in females, may further augment the prediction of chronic pain. PERSPECTIVE: This article investigates the relationship between chronic pain, obesity, and inflammatory markers. It could help elucidating sex difference in pain mechanisms, as well as the risk factors for chronic pain, potentially improving patient diagnosis, follow-up and treatment.

Thyroid, Gonadal and Adrenal Dysfunction in Kidney Transplant Recipients: A Review for the Clinician.

While chronic kidney disease-associated mineral and bone disorders (CKD-MBD) prevail in the endocrinological assessment of CKD patients, other endocrine abnormalities are usually overlooked. CKD is associated with significant thyroid, adrenal and gonadal dysfunction, while persistent and de novo endocrinological abnormalities are frequent among kidney transplant recipients (KTR). Low T3 levels prior to transplantation may help identify those at risk for delayed graft function and are often found in KTR. Thyroid surveillance after kidney transplantation should be considered due to structural anomalies that may occur. Despite the rapid recovery of gonadal hormonal secretion after renal transplantation, fertility is not completely restored. Testosterone may improve anemia and general symptoms in KTR with persistent hypogonadism. Female KTR may still experience abnormal uterine bleeding, for which estroprogestative administration may be beneficial. Glucocorticoid administration suppresses the hypothalamic-pituitary-adrenal axis in KTR, leading to metabolic syndrome. Patients should be informed about signs and symptoms of hypoadrenalism that may occur after glucocorticoid withdrawal, prompting adrenal function assessment. Clinicians should be more aware of the endocrine abnormalities experienced by their KTR patients, as these may significantly impact the quality of life. In clinical practice, awareness of the specific endocrine dysfunctions experienced by KTR patients ensures the correct management of these complications in a multidisciplinary team, while avoiding unnecessary treatment.

Body composition, adipokines, FGF23-Klotho and bone in kidney transplantation: Is there a link?

BACKGROUND: Kidney transplantation-associated mineral and bone disorder (KT-MBD) still represents a black box on the long-term due to scarce available data. We aimed to investigate the impact of non-classical bone regulating factors (body composition, adipokines, inflammatory markers, fibroblast growth factor 23-FGF23 and α-Klotho) in long-standing kidney transplant (KT) recipients compared to the general population. METHODS: Our cross-sectional study, enrolling 59 KT patients and age, sex and body mass index-matched healthy general population volunteers, assessed the predictive role of the body composition, serum adipokines (leptin, adiponectin, resistin), inflammatory markers (erythrocyte sedimentation rate, C-reactive protein) and parathyroid hormone (PTH)-FGF23/α-Klotho axis upon bone mineral density (BMD) and osteocalcin, using correlation and linear multiple regression. RESULTS: The 59 KT recipients (mean transplantation span of 57.7 ± 7.2 months) had similar body composition but significantly lower BMD (p < 0.01) compared to the general population group. Total lean mass was independently associated with BMD in both groups. In KT patients, age, time spent on dialysis and PTH were the main negative independent predictors of BMD, after adjusting for possible confounders. Resistin and α-Klotho also negatively predicted lumbar bone density (p < 0.001), while adiponectin and α-Klotho positively predicted osteocalcin levels (p < 0.001) in KT recipients, independently of inflammatory markers. No significant associations were found between FGF23 and bone parameters in any of the groups. CONCLUSIONS: Age, PTH, time on dialysis and lean mass are among the main bone density predictors in long-standing KT patients. The bone impact of adipokine dysregulation and of α-Klotho merits further investigations in KT-MBD. Preserving lean mass for improved bone outcomes should be part of KT-MBD management on the long-term.

The impact of growth hormone replacement therapy on adipokines, but not upon Ghrelin.

BACKGROUND: Besides growth acceleration, growth hormone (GH) therapy of GH deficient (GHD) children improves body composition by decreasing body fat. This effect is due to GH interaction with lipid and carbohydrate metabolism, possibly also mediated by adipokines secreted by adipose tissue, and ghrelin. This study aimed to assess the impact of oneyear GH replacement therapy on the metabolic profile, adipokines, and acylated/ unacylated ghrelin of prepubertal children with GHD. METHODS: Prospective observational study of 42 non-obese, prepubertal children with GHD followed up for twelve months. Mean lipid, carbohydrate, adipokine profiles, acylated/unacylated ghrelin, and body composition data before therapy onset were compared with measurements obtained after 6 and 12 months of GH therapy. RESULTS: Total body fat content and body fat percentage decreased significantly, while the lipid profile improved over the study period in the 42 GHD children with a mean age of 9.2 ±2.6 years. The levels of leptin and unacylated ghrelin decreased significantly, whereas adiponectin and acylated ghrelin values increased after GH therapy. In regression analysis models, GH treatment (reflected by increased absolute values or standard deviations of IGF1) influences the variation of leptin and adiponectin, but not ghrelin, independently of body composition - lean or fat mass. CONCLUSIONS: GH replacement therapy improves body composition, lipid, and adipokine profile in GHD children. Also, GH replacement therapy directly impacts leptin and adiponectin concentrations, independently of body composition. Further research is needed to identify the molecular mechanisms and metabolic pathways by which the GH/IGF1 axis influences adipokines secretion.

Bone mineral density predictors in long-standing type 1 and type 2 diabetes mellitus.

BACKGROUND: Despite the increased fracture risk, bone mineral density (BMD) is variable in type 1 (T1D) and type 2 (T2D) diabetes mellitus. We aimed at comparing independent BMD predictors in T1D, T2D and control subjects, respectively. METHODS: Cross-sectional case-control study enrolling 30 T1D, 39 T2D and 69 age, sex and body mass index (BMI) - matched controls that underwent clinical examination, dual-energy X-ray absorptiometry (BMD at the lumbar spine and femoral neck) and serum determination of HbA1c and parameters of calcium and phosphate metabolism. RESULTS: T2D patients had similar BMD compared to T1D individuals (after adjusting for age, BMI and disease duration) and to matched controls, respectively. In multiple regression analysis, diabetes duration - but not HbA1c- negatively predicted femoral neck BMD in T1D (ß= -0.39, p = 0.014), while BMI was a positive predictor for lumbar spine (ß = 0.46, p = 0.006) and femoral neck BMD (ß = 0.44, p = 0.007) in T2D, besides gender influence. Age negatively predicted BMD in controls, but not in patients with diabetes. CONCLUSIONS: Long-standing diabetes and female gender particularly increase the risk for low bone mass in T1D. An increased body weight partially hinders BMD loss in T2D. The impact of age appears to be surpassed by that of other bone regulating factors in both T1D and T2D patients.

Role of copeptin in the diagnosis of traumatic neuroendocrine dysfunction.

Traumatic neuroendocrine dysfunction may present with diabetes insipidus (DI) or with the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Both these pathologies involve a disturbance in the antidiuretic hormone (ADH) secretion, causing dysnatremias. Diagnosis of posttraumatic ADH dysfunction is hampered by technical difficulties in ADH assessment, and relies mostly on non-specific serum sodium, serum and urine osmolality and diuresis, often leading to misdiagnosis in the acute care setting. Research now focuses on the diagnostic role of copeptin, a peptide secreted together with ADH in an equimolar fashion, and which can be accurately evaluated. Recent studies identified cut-off values of 2.6 pmol/L for baseline copeptin and of 4.9 and 3.8 pmol/L for hypertonic saline infusion and arginine infusion stimulated copeptin, respectively, for the diagnosis of DI in patients with polyuria-polydipsia syndrome. Although SIADH is more difficult to be explored due to its heterogeneity, a ratio of copeptin to urinary sodium below 30 pmol/mmol identifies euvolemic hyponatremia. Exploring the role of copeptin assessment in patients with traumatic brain injury (TBI) in the acute phase may improve their diagnosis accuracy, management and outcome.

New insights into the metabolic-bone crosstalk in active acromegaly.

INTRODUCTION: Body composition (BC) and adipokines share bone active properties and display an altered profile in acromegaly. The fibroblast growth factor 23 (FGF23)/α-Klotho system, also involved in bone metabolism, is upregulated in growth hormone (GH) excess states. Hence, we aimed to investigate their impact on bone in active acromegaly, compared to controls. MATERIAL AND METHODS: BC, bone mineral density (BMD) (via dual X-ray absorptiometry), serum adipokines (leptin, adiponectin, resistin), parathyroid hormone (PTH), FGF23, α-Klotho, and osteocalcin were assessed in a cross-sectional study enrolling 35 patients with active acromegaly (Acro), compared to 35 sex, age, and body mass index (BMI) one-to-one matched healthy controls (CTL). RESULTS: The Acro group had higher bone density scores (p < 0.05), lower visceral fat depots (p = 0.011), and lower serum leptin (p < 0.001) but elevated adiponectin (p < 0.001) and resistin (p = 0.001) concentrations when compared to the CTL group. α-Klotho was not related to the GH/IGF1 axis in the Acro group. Resistin was higher in both diabetic and non-diabetic Acro compared to CTL (p < 0.05). Age and BC were the main independent BMD predictors in regression analysis in both groups, while IGF1 was a positive predictor of osteocalcin levels in the Acro (ß = 0.48, p = 0.006). The correlations between adipokines, the FGF23/α-Klotho system, and bone parameters, respectively, were lost after adjusting for age and BC. CONCLUSIONS: Age and BC were the main independent BMD predictors in the acromegalic patients with active disease, while IGF1 was independently associated with serum osteocalcin concentrations. The role of α-Klotho in evaluating acromegaly and the associated osteopathy in the long-term appears to be limited. Our study is among the first to report significant serum resistin changes in patients with active acromegaly, opening new insights in the GH-mediated insulin resistance. The GH-resistin relationship merits further investigations.

Sublingual desmopressin is efficient and safe in the therapy of lithiasic renal colic.

PURPOSE: To evaluate the effects of newer sublingual desmopressin administration in lithiasic renal colic, alone or combined with a nonsteroidal anti-inflammatory drug (NSAID). METHODS: Prospective single-blind study including an initial number of 249 patients with lithiasic renal colic was randomized as follows: group NSAID (71 patients) received ketorolac tromethamine (ketorolac) 30 mg im and sublingual placebo (vitamin C), groups D1 and D2 (57 and 62 patients) received sublingual desmopressin (Minirin Melt), 60 and 120 µg, respectively, whereas group C (59 patients) received a combination of 30 mg im ketorolac and 60 µg sublingual desmopressin. Pain intensity was assessed using the visual analogue scale before and thirty minutes after drug administration. Patients experiencing pain aggravation were rescued and excluded from the study. RESULTS: Dropout incidence was higher in the NSAID group than in the groups treated with desmopressin in monotherapy or combined with ketorolac (p < 0.05). Pain intensity was diminished at least as potently by the monotherapy with desmopressin and ketorolac. The higher dose of desmopressin and the combination therapy decreased pain intensity with 56 and 59%, respectively, significantly more than the 47% decrease obtained with ketorolac alone (p < 0.05 and p < 0.001). Mean pain decrease was higher in the combination group (C) than in the NSAID or D1 groups (p < 0.001 and p < 0.05, respectively), suggesting drug additivity. Patients did not experience severe side effects. CONCLUSIONS: Sublingual desmopressin is at least as potent as NSAID in the treatment of lithiasic renal colic. The combination of sublingual desmopressin and NSAID has additive analgesic effects.

Regional radiotherapy may improve outcomes in patients with early stage breast cancer undergoing breast conservation therapy.

BACKGROUND: Breast conservation therapy (BCT) is recommended as standard management of early breast cancer. The aim of this study was to retrospectively evaluate the results of BCT to identify prognostic factors predictive of treatment outcomes. PATIENTS AND METHODS: Four hundred and ninety-eight eligible women with unilateral stage I-II breast cancer who had undergone BCT were analyzed. RESULTS: The cumulative incidence of local recurrence (LR) was 1.9% and 3.7% at 3- and 5-years respectively. The 5-year disease-free, cancer-specific, and overall survival (DFS, CSS, OS) were 80.0%, 87.3% and 85.4% respectively. Significant independent predictors for LR included young age and absence of chemotherapy. Regional nodal radiotherapy was significantly associated with improved DFS and OS. CONCLUSION: Our results confirmed the efficacy of BCT in the treatment of early breast cancer and indicated that inclusion of regional nodal areas within the radiotherapy field might be beneficial in the BCT setting, particularly for patients with adverse risk features.

The vitamin D receptor gene FokI polymorphism: functional impact on the immune system.

1Alpha,25-dihydroxyvitamin D3 (1,25(OH)2D3) has important effects on the growth and function of multiple cell types. These pleiotropic effects of 1,25(OH)2D3 are mediated through binding to the vitamin D receptor (VDR). Several polymorphisms of the human VDR gene have been identified, with the FokI polymorphism resulting in VDR proteins with different structures, a long f-VDR or a shorter F-VDR. The aim of this study was to investigate the functional consequences of the FokI polymorphism in immune cells. In transfection experiments, the presence of the shorter F-VDR resulted in higher NF-kappaB- and NFAT-driven transcription as well as higher IL-12p40 promoter-driven transcription. Marginal differences were observed for AP-1-driven transcription, and no differential effects were observed for transactivation of a classical vitamin D-responsive element. Concordantly, in human monocytes and dendritic cells with a homozygous short FF VDR genotype, expression of IL-12 (mRNA and protein) was higher than in cells with a long ff VDR genotype. Additionally, lymphocytes with a short FF VDR genotype proliferated more strongly in response to phytohemagglutinin. Together, these data provide the first evidence that the VDR FokI polymorphism affects immune cell behavior, with a more active immune system for the short F-VDR, thus possibly playing a role in immune-mediated diseases.

Novel insights in the immune function of the vitamin D system: synergism with interferon-beta.

The 1,25(OH)(2)D(3) analog, TX527 (19-nor-14,20-bisepi-23-yne-1,25(OH)(2)D(3)), has an interesting dissociation profile between its potent immunomodulatory and its calcemic effects in vivo. The strong immunomodulatory potency of TX527 is reflected by its ability to attenuate experimental autoimmune encephalomyelitis (EAE), a murine model of multiple sclerosis (MS). At present most MS patients are being treated with systemic IFN-beta administration. The aim of this study was to investigate whether combining IFN-beta with TX527 could empower its EAE-protective effects. We evaluated also combinations with the standard immunosuppressant cyclosporin A (CsA). EAE was induced in SJL mice by PLP immunization, treatment was started 3 days before disease induction. The TX527+IFN-beta combination resulted in significant disease protection which was superior to the effect of both treatment separately. No disease amelioration, even aggravation, was obtained with the IFN-beta+CsA combination. By adding TX527 to the IFN-beta+CsA combination near complete protection from EAE was achieved (100% protection from paralysis, mean maximal score of 1.8+/-1.5, both p<0.05 versus controls and all individual treatments). From these data we conclude that adding TX527 to an IFN-beta and/or CsA treatment results in clear additional immunomodulatory effects in EAE prevention and is therefore a potentially interesting candidate to be considered in clinical intervention trials in MS.

Hen egg white lysozyme vaccination induces acute shock in NOD mice.

To investigate whether vaccination could induce lethal shock and which mechanisms are involved in this phenomenon, we tested a panel of autoantigens or diabetes-irrelevant peptides or proteins in nonobese diabetic (NOD), Balb/c, and C57Bl/6 mice. Of the antigens tested, only nondiabetogenic hen egg white lysozyme induced a severe form of shock exclusively in NOD mice. The mechanism involved is suggestive of a Th(2)-mediated anaphylactic reaction possibly connected to activation of PAF and triggering of DIC.

Progesterone in gestational diabetes mellitus: guilty or not guilty?

Insulin resistance is one of the metabolic changes in pregnancy, but only a fraction of women develop overt impaired glucose tolerance or frank diabetes. Most women are able to compensate this altered metabolic state by increasing the amount of insulin produced by the pancreatic beta cells. Progesterone might well be the key to the development of gestational diabetes. Previously high progesterone levels have already been shown to be correlated with the development of glucose abnormalities in pregnancy and now, in a new paper, progesterone receptor-knockout mice are found to have improved glucose tolerance. These mice showed increased insulin secretion, which is probably linked to the presence of increased numbers of beta cells in their pancreas. Is progesterone therefore the 'ultimate bad guy', prohibiting normal adaptation of the pancreatic beta-cell reserve during pregnancy?

Acute shock induced by antigen vaccination in NOD mice.

Type 1 diabetes in NOD mice can be prevented through autoantigen vaccination by shifting lymphocyte differentiation toward a T-helper 2 (Th(2)) response. However, in other models of autoimmunity, this approach may be accompanied by unexpected triggering of Th(2)-dependent anaphylactic shock. To test the safety of vaccination therapy in the NOD mouse model, we evaluated the effects of immunization with a wide battery of antigens in NOD, BALB/c, and C57BL/6 mice. Surprisingly, a nondiabetogenic antigen, hen egg white lysozyme, induced severe shock exclusively in NOD mice (shock in 11 of 11 mice, lethal in 3 mice). Shock severity was further increased by a more pronounced Th(2) setting generated by 1alpha,25(OH)(2)D(3) administration (17 of 17 mice, lethal in 14 mice, P < 0.0001). Pretreatment with dexamethasone resulted in full rescue, indicating an immune-mediated mechanism. Serum IgE levels and Th(1)/Th(2) cytokine profile analysis showed that the shock phenomenon was paralleled by a Th(2) response. mRNA expression of platelet-activating factor receptor (PAF-R) was significantly higher in NOD mice (P < 0.01) and was further increased by 1alpha,25(OH)(2)D(3). Pretreatment with WEB2086 (PAF-R antagonist) again protected all mice from lethal shock, indicating PAF as an anaphylaxis effector. In conclusion, in NOD mice, vaccination leading to a Th(2) immune shift can result in a lethal anaphylactic reaction.

Digit distribution of proper digital nerve action potential.

Antidromic sensory nerve action potential testing is well characterized and commonly used to assess the sensory component of the upper limb median and ulnar nerves. The final terminal segments of these nerves are the proper digital nerves. Ring recording electrodes are commonly used to detect the proper digital nerves' antidromic responses. Attempts to record the separate contributions of individual digital nerves along the lateral aspects of each finger, using small surface electrodes, is shown to be unreliable for determining the integrity of a single terminal digital branch. We found between 50% to 77% of the stimulated terminal branch's response amplitude when recorded at electrodes positioned over the nonstimulated branch located 180 degrees from the activated terminal branch. Detecting a single terminal nerve response was achieved by using the fourth digit and the second digit with one of the second digit's branches neurophysiologically blocked by local anesthetic. The volume-conducted response from the opposite side of the finger resulted in this relatively large recorded response, which remains within the range of reference values precluding the simple use of antidromic techniques to assess injury to a single proper digital nerve. Techniques are proposed to avoid such pitfalls and to assess most accurately the desired response.

Carpal tunnel syndrome and the Riche-Cannieu anastomosis: electrophysiologic findings.

Two cases of carpal tunnel syndrome with Riche-Cannieu anomalies are reported. Despite complete absence of a median nerve evoked compound muscle action potential from the thenar eminence, these patients had significant preservation of function and minimal muscle atrophy. Activation of the ulnar nerve at both the wrist and elbow generated easily obtainable compound muscle action potentials from the thenar eminence with initial negative onset. This observed preservation of function and electrophysiologic responses are best explained by the presence of a Riche-Cannieu anastomosis innervating the thenar eminence through branches from ulnar nerve. To our knowledge there has not been a report of similar cases in patients with profound carpal tunnel syndrome and a Riche-Cannieu anomaly. We review the clinical findings, the electrodiagnostic data, and the impact of a Riche-Cannieu anastomosis on advanced carpal tunnel syndrome.

Prevalence of denervation in paraspinal and foot intrinsic musculature.

OBJECTIVE: The primary purpose of this investigation was to determine the prevalence of abnormal spontaneous activity (positive sharp waves (PSWs) and fibrillation potentials (FPs)) in selected lumbosacral paraspinal and foot intrinsic muscles in an asymptomatic healthy population. DESIGN: This was a prospective assessment of 50 individuals without history or physical findings suggestive of peripheral neuromuscular disease whereby a monopolar needle electrode was located in the unilateral L4 and L5 paraspinal as well as abductor hallucis and extensor digitorum brevis muscles. These muscles were extensively evaluated for the presence of PSWs, FPs, and fasciculation potentials. RESULTS: Ten subjects per decade from 20-59 yr and ten subjects from 60-80 yr comprised the 50 participants (28 women), resulting in a mean age of 45+/-15.9 (range, 20-76) yr. A single individual (prevalence, 2%) demonstrated fibrillation potentials in the extensor digitorum brevis, and FPs and PSWs were detected in two subjects' (4% prevalence) L4/L5 paraspinal muscles. Ninety-four percent of the subjects had fasciculation potentials in the abductor hallucis, whereas 60% had these waveforms in the extensor digitorum brevis. Only 6% of subjects had fasciculation potentials in the L4 but not L5 paraspinal muscles. All subjects demonstrated both prototypical and "atypical" appearing endplate spikes in all of the muscles examined. CONCLUSIONS: We failed to confirm the previously reported prevalence of FPs and PSWs in both the paraspinal and foot intrinsic musculature. Atypical appearing endplate spikes, however, display configurations similar to FPs and PSWs and were present in all subjects. Failure to pay close attention to the discharge rate and rhythm of endplate spikes can lead to misinterpreting these waveforms as FPs and PSWs. It is likely that the previously reported high prevalence of spontaneous activity in healthy persons resulted from not fully appreciating the similarity between innervated and denervated spontaneous single muscle fiber discharge configurations.

Isolated sural neuropathy presenting as lateral ankle pain.

A case of job-related, unilateral traumatic sural neuropathy causing severe lateral ankle pain and impaired work performance for a 26-yr-old female grocery clerk is reported. This diagnosis is made both clinically and electrophysiologically. We review the pertinent electrophysiologic features, anatomy, and clinical findings in our patient with an isolated sural neuropathy. A review of the literature demonstrates that trauma is the most common cause of this unusual isolated neuropathy. Despite its rare occurrence, it should be considered in patients who present with lateral ankle pain and concomitant loss of sensation in the sural nerve distribution. The establishment of a neuropathic origin assists with management strategies that will differ from the more common musculoskeletal causes of lateral ankle pain. After an appropriate diagnosis and treatment, an excellent outcome resulted for our patient.

Physiologic basis of potentials recorded in electromyography.

The extracellularly recorded configuration of a single muscle fiber discharge is generally appreciated to be triphasic with an initially positive deflection. However, careful attention to waveform appearance during the electrodiagnostic medicine examination reveals that both innervated and denervated muscle waveforms may display a pantheon of configurations. Further, despite the fact that innervated and denervated single muscle fiber discharges arise from distinctly different intracellular action potential (IAP) configurations, their extracellularly recorded waveforms can appear quite similar, leading to potential misidentification and, hence, the possibility of an erroneous diagnostic conclusion. The least appreciated, but nevertheless critical, aspect of explanations for muscle waveform configurations is the relationship between the muscle fiber and recording electrode. Additionally, it is important to appreciate both the near-field and far-field aspects of single fiber and compound muscle action potentials. In this review, the leading/trailing dipole model is used to explain muscle waveform configurations in both innervated and denervated tissues.