25 research outputs found
Spectrum of patients with EMG features of polyradiculopathy without neuropathy
We reviewed the medical records of 233 patients having electrodiagnostic evidence of polyradiculopathy. Patients with polyneuropathy or incomplete diagnostic evaluation were excluded. A clinical diagnosis was secured in 92 of the 118 remaining patients. Patients were separated into three groups based upon the anatomic location of root involvement: extradural (55), intradural-extraaxial (23), and intraaxial (14). Collectively, patients with intradural-extraaxial disorders had earlier disease onset, shorter symptom duration, and a higher disability score compared with the intraaxial or extradural groups. Pain was an initial complaint in 50 of 55 patients with extradural lesions, 20 of 23 with intradural-extraaxial disease, but only in 4 of 14 with intraaxial involvement. CSF abnormalities and reduced compound muscle action potential amplitudes were more common in the intradural-extraaxial group. We conclude that the anatomic localization of root involvement in patients with polyradiculopathy can be suggested by a combination of clinical, laboratory, and electrodiagnostic features.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/50147/1/880130112_ftp.pd
Zonisamide (CI-912) and Cognition: Results from Preliminary Study
Nine patients with refractory partial seizures were evaluated in a pilot study of a new anticonvulsant compound, zonisamide (l,2-benzisoxazole-3-methane-sulfonamide; CI-912). Cognitive functioning was evaluated prior to treatment with zonisamide and repeated after 12 and 24 weeks of treatment with zonisamide. At minimum steady-state plasma concentrations >30 jjug/ml, zonisamide appeared to affect specific cognitive functions such as acquisition and consolidation of new information. Previously learned material, such as vocabulary, and psychomotor performance were not affected. Verbal learning was affected, while visual-perceptual learning was unimpaired. These cognitive effects were observed in the absence of the usual clinical signs and symptoms of toxicity. A linear relationship was found between impairment of cognitive abilities and the minimum plasma concentration (r = -0.73; p < 0.05). Findings also suggest the development of tolerance to the adverse cognitive effects. RESUMEN En un estudio piloto realizado para valorar la eficacia de la zonisamida (1,2-Bencisoxazol-melanosulfonamida [CI-912]), un nuevo compuesto anticonvulsive se han evaluado unos 9 pa-cientes con ataques parciales refractarios al tratamiento. Se de-terminĂ la capacidad cognitiva anterior al tratamiento y se re-pitio 12 y 24 semanas despuĂs del tratamiento con zonisamida. Con concentraciones plasmĂticas mĂnimas estables per encima de 30 mcg/ml, la zonisamida afectĂ las funciones cognitives especĂficas tales como la adquisiciĂn y consolidaciĂn de nueva informaciĂn. El material aprendido previamente, tal como el vo-cabulario, y las funciones psicomotoras no se afectaron. El aprendizaje verbal se modificĂ mientras que el aprendizaje visuo-perfectivo no se modificĂ. Estos efectos cognitivos se ob-servaron en ausencia de los habituales signos y sĂntomas clĂnicos de toxicidad. Se encontrĂ una relaciĂn lineal entre la alteraciĂn de las posibilidades cognitivas y la concentraciĂn plasmĂtica mĂnima (r = -0.73, p < 0.05). Estos hallazgos tambiĂn sugieren el desarrollo de una tolerancia a los efectos cognitivos adversos. ZUSAMMENFASSUNG 9 Patienten mit rezidivierenden Partial-AnfĂllen wurden in einer Pilotstudie mit einer neuen antiepileptischen Substanz: Zonisamide untersucht. Die kognitiven Funktionen wurden vor der Behandlung mit Zonisamide geprtĂft und nach 12 und 24 Therapiewochen mit Zonisamide wiederholt. Bei einem Min-destplasmaspiegel von 30 mcg/ml schien Zonisamide spezifische kognitive FĂhigkeiten wie Aufnahme und Speicherung neuer In-formationen zu beeintrĂchtigen. Vorher gelernte Inhalte wie sprachliche und psychomotorische Fertigkeiten wurden nicht beeinfluĂt. Verbales Lernen war ebenfalls betroffen, wĂhrend visuell, perzeptives Lernen nicht verschlechtert war. Diese BeeintrĂchtigung kognitiver Funktionen wurde bei fehlenden klinischen Intoxikationszeichen beobachtet. Eine lineare Bezie-hung zwischen Verschlechterung kognitiver FĂhigkeiten und Mindest-Plasmaspiegel konnte hergestellt werden (r = -0,73; p < 0,05). Allerdings lassen die Ergebnisse auch auf eine GewĂhnung an diese unerwĂnschten Nebenwirkungen schlieĂen.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/65995/1/j.1528-1157.1987.tb03624.x.pd
Pilot Study of Zonisamide (1,2-Benzisoxazole-3-methanesulfonamide) in Patients with Refractory Partial Seizures
A new anticonvulsant compound, zonisamide (1,2 benzioxazole-methanesulfonamide), was studied in 10 adults with medically refractory partial seizures. Following a single oral dose of 400 mg, peak plasma levels occurred an average of 2.8 h after dosing, and the mean clearance from plasma was 2.34 L/h. Whole blood concentrations were high than plasma concentrations because of red blood cell binding. steady-state plasma concentrations were high than predicted from a linear kinetic model. In most patients, seizure frequency was reduced after zonisamide was substituted for a standard antiepileptic drug. Dose-related reversible side effects in the central nervous and gastrointestinal system were observed. Most patients tolerated doses between 5.2 and 12.5 mg/kg/day. RĂSUMĂ Un nouveau produit anticonvulsivant, le zonisamide (1,2 benziosoxazole-methylsulfonamide) a ĂtĂ administrĂĂ 10 adultes atteints de crises partielles non contrĂlĂes par le traitement mĂdical. AprĂs une dose unique orale de 400 mg, le pic du taux plasmatique survient en moyenne 2 h 1/2 aprĂs l'ingestion, et la clairance plasmatique moyenne est de 2,34 litres par heure. les concentrations sanguines totales sont plus ĂlevĂes que les concentrations plasmatiques, en raison de la liaison aux globules rouges, les concentrations plasmatiques Ă l'Ătat d'equilibre sont plus ĂlevĂes que celles que l'on peut dĂdurie d'un modĂle de cinĂtique linĂaire. Chez la plupart des patients, la frĂquence des crises a ĂtĂrĂduite par la substitution du zonisamide au traitement antiĂpileptique standard. Des effets secondaires doses-dĂpendants et rĂversibles ont ĂtĂ observĂs au niveau du systĂme nerveux central et du tube digestif. La plupart des patients ont tolĂrĂ des doses entre 5,2 et 12,5 mg/kg de poids par jour. RESUMEN En 10 adultos con ataques parciales refractarios a1 tratamiento mĂdico, se ha estudiado la acciĂn de un nuevo compuesto anticonvulsivo, la zonisamida (1,2 benzisoxazol-metanosulfonamida). Tras la ingestiĂn de una sola dosis oral de 400 mg., se alcanzaron los niveles pico en plasma en un promedio de 2.8 horas desputs de la dosis y el aclaramiento medio del plasma fuĂ de 2, 34 litros/hora. Las concentraciones en sangre fueron mĂs altas que las plasmĂticas debido a que la medicaciĂn se ligaba a los hematies. Las concentraciones plasmĂticas estables fueron mĂs altas que las previsibles de un modelo cinĂtico lineal. En la mayorĂa de los pacientes la frecuencia de los ataques se redujo despuĂs de cambiar la medicaciĂn antiepilĂptica standard por la zonisamida. TambiĂn se observaron los efectos colaterales sobre el tracto gastrointestinal y el sistema nervioso central que estaban relacionadas con la dosis y eran reversibles. La mayor parte de los pacientes tolerĂ dosis que oscilaban entre 5.2 y 12.5 mg/kg/dĂa. ZUSAMMENFASSUNG Ein neues Antikonvulsivum, Zonisamid (1,2 Benzisoxazol-Methansulfonamid) wurde bei 10 Envachsenen mit therapieresistenten PartialanfĂllen gesucht. Nach einer oralen Einzeldosis von 400 mg wurden Plasmaspitzenwerte im Durchschnitt nach 2, 8 Stunden erreicht. Die mittlere Clearance aus dem Plasma betrug 2, 34 L/Stunde. Ganzblutkonzentrationen waren hĂher als Plasmakonzentrationen aufgrund der Bindung an die roten BlutkĂrperchen. Die steady-state Plasmakonzentrationen waren hĂher als bei einem linearen kinetischen Modell zu envarten. Bei den meisten Patienten konnte die Anfallsfrequenz nach Substitution eines Standardantiepileptikums durch Zonisamid reduziert werden. Es bestanden dosisabhĂngige, reversible, zentral-nervĂse und gastrointestinale Nebenwirkungen. Die meisten Patienten tolerierten Dosen zwischen 5, 2 und 12, 5 mg/kg/Tag.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/65938/1/j.1528-1157.1985.tb05407.x.pd
Book Review: Amyotrophic Lateral Sclerosis (Progress in Clinical Neurologic Trials, Volume 1), edited by F. Clifford Rose. Published in 1990 by Demos Publications, New York, 238 pages, $59.95
Electrodiagnostic evolution of carcinomatous sensory neuronopathy
Sensory neuronopathy is a well-recognized remote effect of carcinoma. We report the clinical and electrodiagnostic evolution of a sensory neuronopathy in a patient with carcinoma of the lung. Serial electrophysiologic studies suggest transformation from normal peripheral nerve function through early posterior root involvement to absent sensory nerve function. Diffuse motor conduction abnormalities occurred late in the disease, perhaps reflecting motor axon changes associated with disuse.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/50144/1/880120612_ftp.pd
Acute arsenic intoxication presenting as guillainbarrĂa-like syndrome
Arsenic-induced polyneuropathy is traditionally classified as an axonal-loss type, electrodiagnostically resulting in low amplitude or absent sensory and motor responses, relatively preserved proximal and distal motor conduction rates, and distal denervation. We report four patients with a subacute onset progressive polyradiculoneuropathy following high-dose arsenic poisoning. In three patients, early electrodiagnostic testing demonstrated findings suggestive of an acquired segmental demyelinating polyradiculoneuropathy. Serial testing confirmed evolution into features of a distal dying-back neuropathy. We hypothesize that arsenic toxicity and the resultant biochemical derangement of the peripheral nerve cell leads to subtle changes in axonal function that produce, initially, segmental demyelination and eventually distal axonal degeneration. Acute arsenic toxicity must be suspected in patients with clinical and electrodiagnostic features supporting Guillain-BarrĂ syndrome.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/50138/1/880100203_ftp.pd
Safety and Tolerability of Immune Globulin Intravenous in Chronic S Inflammatory Demyelinating Polyradiculoneuropathy
Background: Chronic inflammatory demyelinating poly-radiculoneuropathy (CIDP) is a common inflammatory neuropathy that can be progressive, stepwise progressive, or relapsing and remitting. Objectives: To further evaluate the long-term safety and tolerability of immune globulin intravenous, 10% caprylate chromatography purified immune globulin intravenous in CIDP. Design: Randomized multicenter trial. Setting: Hospitals and outpatient clinics. Patients: Adults with CIDP (n = 113). Interventions: Immune globulin intravenous, 10% caprylate chromatography purified (2 g/kg of body weight) or placebo was infused as a baseline loading dose, followed by a maintenance dose (1 g/kg) every 3 weeks for up to 24 weeks. Patients who responded were rerandomized into a double-blind extension phase of immune globulin intravenous, 10% caprylate chromatography purified (1 g/kg) or placebo every 3 weeks for up to 24 weeks. Patients who relapsed during the extension phase were withdrawn from the study. Main Outcome Measures: Additional analyses of safety and tolerability. Results: Overall, 113 patients and 95 patients were exposed to immune globulin intravenous, 10% caprylate chromatography purified and placebo, respectively. Exposure to immune globulin intravenous, 10% caprylate chromatography purified was approximately twice that of placebo (1096 vs 575 infusions). Most maintenance dose courses were administered over 1 day in the immune globulin intravenous, 10% caprylate chromatography purified (89.1% of 783 dose courses) and placebo (91.1% of 359 dose courses) groups. The most common drug-related adverse events (AEs) with immune globulin intravenous, 10% caprylate chromatography purified were headache (4.0 per 100 infusions) and pyrexia (2.4 per 100 infusions). Five drug-related serious AEs (pulmonary embolism, pyrexia, vomiting, and 2 headache events) were reported in 3 patients (2.7%) exposed to immune globulin intravenous, 10% caprylate chromatography purified. The incidence of drug-elated serious AEs was higher after loading dose infusions than after maintenance dose infusions (4 AEs vs 1 AE). Age, weight, CIDP severity, and previous immune globulin intravenous exposure had no substantial effect on the percentage of patients with AEs, including serious AEs. Conclusion: Data support a favorable safety and tolerability profile for administration of immune globulin intravenous, 10% caprylate chromatography purified as CIDP maintenance therapy
How neurologists are paid: Part 3: Hospital support, Veterans Administration, and neurohospitalists
Part 1 of this series focused on factors influencing payment for patient care services and Part 2 described compensation plans for neurologists in private practice and in academic medicine. In Part 3, we review how hospital salary support and appointments to Veterans Administration hospitals contribute to the salary structure of neurologists. We also discuss neurohospitalist care and ways neurologists can potentially increase compensation from on-call pay, telemedicine, and the use of new transitional care and complex chronic care codes. We conclude with an emphasis on the important role of neurologists as team players in a health care system that will rely on efficient coordination of care among many health care workers
How neurologists are paid: Part 2: Private practice, research grants, academic and nonclinical activities
Part 1 of this series focused on factors influencing payment for patient care services. In Part 2, we review compensation models for nonpatient activity such as medical legal reviews, committee participation, and collaboration with the pharmaceutical industry. Compensation to neurologists in private practice is commonly in the form of guaranteed salary and bonuses. Salary for neurologists in academic medicine has changed considerably over the past 3 decades, from small departments with faculty supported by grants and volunteer faculty, to large departments with faculty split between those with research grant support and those focusing on patient care and teaching. Compensation models in academic medicine range from straight salary without bonus to straight salary with personal or shared bonus and salary based on relative value units
How neurologists are paid: Part 1: The Medicare payment system
Neurologists are facing yearly reductions in reimbursement for rendered services. These reductions arise from changes by Medicare, Medicaid, and third-party payers to achieve cost savings. In Part 1, we discuss reimbursement for office visits and procedures, the relative value scale, the conversion factor used by Medicare to transform work into payments, and the recently repealed sustainable growth rate. The establishment of new codes for transitional care and chronic care management may augment the salaries of neurologists who care for patients with chronic conditions. Medicare\u27s recent elimination of payment for consultations and the bundling of nerve conduction studies have dramatically affected reimbursement. Large discrepancies remain between compensation for procedures and office visits