Managing Patient Dissatisfaction and Billing Reconsideration Requests in Outpatient Clinics.

Nurse leaders in many settings are responsible for clinic operations. Knowing the medical and financial stakes of each patient encounter, it is not surprising to encounter patients requesting reconsideration of bills after services are provided. This article provides recommendations on how to successfully navigate billing reconsideration requests in outpatient settings.

Disease-Based Prognostication: Myasthenia Gravis.

Myasthenia gravis (MG) is an acquired autoimmune neuromuscular junction transmission disorder that clinically presents as fluctuating or persistent weakness in various skeletal muscle groups. Neuroprognostication in MG begins with some basic observations on the natural history of the disease and known treatment outcomes. Our objective is to provide a framework that can assist a clinician who encounters the MG patient for the first time and attempts to prognosticate probable outcomes in individual patients. In this review article, we explore clinical type, age of onset, antibody status, severity of disease, thymus pathology, autoimmune, and other comorbidities as prognostic factors in MG.

Synaptotagmin 2 mutations cause an autosomal-dominant form of lambert-eaton myasthenic syndrome and nonprogressive motor neuropathy.

Synaptotagmin 2 is a synaptic vesicle protein that functions as a calcium sensor for neurotransmission but has not been previously associated with human disease. Via whole-exome sequencing, we identified heterozygous missense mutations in the C2B calcium-binding domain of the gene encoding Synaptotagmin 2 in two multigenerational families presenting with peripheral motor neuron syndromes. An essential calcium-binding aspartate residue, Asp307Ala, was disrupted by a c.920A>C change in one family that presented with an autosomal-dominant presynaptic neuromuscular junction disorder resembling Lambert-Eaton myasthenic syndrome. A c.923C>T variant affecting an adjacent residue (p.Pro308Leu) produced a presynaptic neuromuscular junction defect and a dominant hereditary motor neuropathy in a second family. Characterization of the mutation homologous to the human c.920A>C variant in Drosophila Synaptotagmin revealed a dominant disruption of synaptic vesicle exocytosis using this transgenic model. These findings indicate that Synaptotagmin 2 regulates neurotransmitter release at human peripheral motor nerve terminals. In addition, mutations in the Synaptotagmin 2 C2B domain represent an important cause of presynaptic congenital myasthenic syndromes and link them with hereditary motor axonopathies.

HIV neuropathy: an in vivo confocal microscopic study.

Several approaches exist for quantitative assessment of human immunodeficiency virus (HIV)-associated distal sensory polyneuropathy (DSP). While useful, each has some limitations. This study evaluated non-invasive, in vivo reflectance confocal microscopy (RCM) of Meissner corpuscles (MCs) as a measure of HIV-DSP. Forty-eight adults (29 HIV-infected, 19 controls) underwent RCM of MC density (MCs/mm(2)) at the arch, fingertip, and thenar eminence (TE); ankle skin biopsy to measure epidermal nerve fiber density (ENFD); electrophysiologic studies; and tactile, vibration, and thermal threshold testing. HIV+ subjects were clinically categorized as having DSP signs or no signs. MC densities were lower in HIV+ subjects with DSP signs than in controls (arch, p = 0.0003; fingertip, p < 0.0001; TE, p = 0.0002). Tactile thresholds in the TE and foot were worse in HIV-DSP than in controls, but in this mild DSP cohort, sural amplitudes, ENFD, and vibration and thermal thresholds did not differ significantly from controls. Fingertip MC densities and tactile thresholds at the foot were also lower in HIV+ subjects without DSP signs than in controls. Other sensory measures were not significantly different in HIV+ subjects without DSP signs than in controls. MC density correlated inversely with tactile thresholds at each imaging location. The results suggest that RCM of MC density complements existing sensory DSP measures and discriminates mild HIV-DSP from controls at a stage when sural amplitudes do not. Further studies are required to determine whether RCM of MC density can establish quantitative changes in DSP, in response to treatment or disease progression.

In vivo confocal microscopy of Meissner corpuscles as a novel sensory measure in CMT1A.

Reliable, valid, and responsive outcomes for different aspects of Charcot-Marie-Tooth (CMT) neuropathy have become increasingly important in an emerging era of therapy development. Measures of the sensory component of CMT in particular are limited. One novel approach with potential applicability to CMT is non-invasive in vivo reflectance confocal microscopy (RCM) of Meissner corpuscles (MCs). In this prospective study, we evaluated MC densities using RCM, and touch-pressure and vibration sensation thresholds in a cohort of Charcot-Marie-Tooth type 1A (CMT1A) subjects with comparison to healthy controls. MC density was lower in CMT1A subjects than in controls at the fingertip (digit V) (2.59 ± 2.73 MCs/mm(2) vs. 6.77 ± 3.68 MCs/mm(2) , p = 0.001), but not more proximally at the thenar eminence. Touch-pressure thresholds were higher in CMT1A than in controls at digit V (p = 0.002) and at the thenar eminence (p = 0.0001). Vibration thresholds in CMT1A at digit V were also higher than in controls (p = 0.0001). A lower MC density at digit V was associated with greater global CMT severity as reflected by the Charcot-Marie-Tooth neuropathy score (CMTNS) (r = -0.76, p = 0.004) and the Neuropathy impairment score (NIS) (r = -0.73, p = 0.007). Similarly, worse touch-pressure thresholds at the fingertip (digit V) were associated with more severe CMT1A on the CMTNS (r = 0.71, p = 0.009) and NIS (r = 0.70, p = 0.011). Vibration thresholds at digit V were not associated with either the CMTNS (r = 0.11, p = 0.74) or NIS (r = 0.21, p = 0.52). Non-invasive in vivo RCM of MC density at the hand and the evaluation of touch-pressure thresholds show promise as measures of sensory structure and function in CMT1A.

Neurologic Injury After Sacral Neuromodulation.

OBJECTIVE: Neurologic injury after sacral nerve stimulation (SNS) is rare, but the incidence is unknown. Infection is a potential mechanism for neurologic damage. This report illustrates the presentation, pathophysiology, diagnostic considerations, and treatment of epidural infection causing neurologic deficits after SNS. CASE REPORT: We present a case of a woman with severe fecal incontinence due to Crohn's disease who underwent SNS implantation and subsequently developed a wound infection requiring complete device explantation. A few days later, she presented with leg pain and weakness. Urgent evaluation and treatment of epidural infection were performed. She had persistent neurologic deficits 6 months later. CONCLUSIONS: Neurologic sequelae from an infection after SNS are a rare event and should be considered in patients with fevers, leg pain, and neurologic deficits.

Electrophysiologic features of SYT2 mutations causing a treatable neuromuscular syndrome.

OBJECTIVES: To describe the clinical and electrophysiologic features of synaptotagmin II (SYT2) mutations, a novel neuromuscular syndrome characterized by foot deformities and fatigable ocular and lower limb weakness, and the response to modulators of acetylcholine release. METHODS: We performed detailed clinical and neurophysiologic assessment in 2 multigenerational families with dominant SYT2 mutations (c.920T>G [p.Asp307Ala] and c.923G>A [p.Pro308Leu]). Serial clinical and electrophysiologic assessments were performed in members of one family treated first with pyridostigmine and then with 3,4-diaminopyridine. RESULTS: Electrophysiologic testing revealed features indicative of a presynaptic deficit in neurotransmitter release with posttetanic potentiation lasting up to 60 minutes. Treatment with 3,4-diaminopyridine produced both a clinical benefit and an improvement in neuromuscular transmission. CONCLUSION: SYT2 mutations cause a novel and potentially treatable complex presynaptic congenital myasthenic syndrome characterized by motor neuropathy causing lower limb wasting and foot deformities, with reflex potentiation following exercise and a uniquely prolonged period of posttetanic potentiation.

Acute bilateral painless radiculitis with abnormal Borrelia burgdorferi immunoblot.

A 57-year-old woman with a history of hypertension and hypothyroidism presented with painless left arm weakness and numbness 2 weeks before evaluation. Nerve conduction studies of the left arm revealed normal motor and sensory responses. Needle examination revealed acute denervation changes in all myotomes of the affected extremity, including cervical paraspinals on the left, and several myotomes on the contralateral side. The laboratory evaluation revealed normal anti-GM1 antibodies and 3 IgM/5 IgG bands on Lyme Western Blot. The patient began treatment with 28 days of intravenous ceftriaxone. On follow-up, patient had regained full strength of her extremities with no sensory deficits. Inflammatory borrelia radiculitis usually presents with pain in the distribution of the affected nerves and nerve roots. The novelty of this case report rests on (1) the absence of primary borreliosis symptomatology preceding the radiculitis and (2) the painless and bilateral clinical presentation in a patient with suspected Lyme radiculitis.

Expansion of mesenchymal stem cells on fibrinogen-rich protein surfaces derived from blood plasma.

Mesenchymal stem cells (MSCs) are present in low density in bone marrow and culture expansion is necessary to obtain sufficient numbers for many proposed therapies. Researchers have characterized MSC growth on tissue culture plastic (TCP), although few studies have explored proliferation on other growth substrates. Using adult equine MSCs, we evaluated proliferation on fibrinogen-rich precipitate (FRP) surfaces created from blood plasma. When seeded at 1 × 10(4) cells/cm(2) and passaged five times over 10 days, MSCs on FRP in medium containing fibroblast growth factor 2 (FGF2) resulted in a ∼2.5-fold increase in cell yield relative to TCP. In FGF2-free medium, FRP stimulated a 10.4-fold increase in cell yield over TCP after 10 days, although control cultures maintained in FGF2 on TCP demonstrated that the stimulatory effect of FRP was not as lasting as that of FGF2. Chondrogenic cultures demonstrated that FRP did not affect differentiation. On TCP, MSCs seeded at 500 cells/cm(2) experienced a 4.6-fold increase in cell yield over cultures seeded at 1 × 10(4) cells/cm(2) following 10 days of expansion. In 500 cells/cm(2) cultures, FRP stimulating a two-fold increase in cell yield over TCP without affecting differentiation. Low-density FRP cultures showed a more even distribution of cells than TCP, suggesting that FRP may accelerate proliferation by reducing contact inhibition that slows proliferation. In addition, FRP appears capable of binding FGF2, as FRP surfaces pre-conditioned with FGF2 supported greater proliferation than FGF2-free cultures. Taken together, these factors indicate that substrates obtained from simple and inexpensive processing of blood enhance MSC proliferation and promote efficient coverage of expansion surfaces.