Max Wiznitzer
University Hospitals of Cleveland
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Publication
Featured researches published by Max Wiznitzer.
Vaccine | 2011
James J. Sejvar; Katrin S. Kohl; Jane Gidudu; Anthony A. Amato; Nandini Bakshi; Roger Baxter; Dale R. Burwen; David R. Cornblath; Jan Cleerbout; Kathryn M. Edwards; Ulrich Heininger; Richard Hughes; Najwa Khuri-Bulos; Rudolf Korinthenberg; Barbara J. Law; Ursula Munro; Helena C. Maltezou; Patricia Nell; James M. Oleske; Robert Sparks; Priscilla Velentgas; Patricia Vermeer; Max Wiznitzer
ames J. Sejvara,∗, Katrin S. Kohla, Jane Gidudua, Anthony Amatob, Nandini Bakshic, Roger Baxterc, ale R. Burwend, David R. Cornblathe, Jan Cleerbout f, Kathryn M. Edwardsg, Ulrich Heiningerh, ichard Hughes i, Najwa Khuri-Bulos j, Rudolf Korinthenbergk, Barbara J. Lawl, Ursula Munrom, elena C. Maltezoun, Patricia Nello,1, James Oleskep, Robert Sparksq, Priscilla Velentgasr, atricia Vermeers, Max Wiznitzer t, The Brighton Collaboration GBS Working Group2
Journal of Autism and Developmental Disorders | 1997
Robert L. Findling; Kathleen Maxwell; Lynette Scotese-Wojtila; Jie Huang; Toyoko S. Yamashita; Max Wiznitzer
Several reports have described salutary effects such as decreased physical aggression and improved social responsiveness being associated with the administration of high doses of pyridoxine and magnesium (HDPM) in open-labeled and controlled studies of patients with autism. Despite this fact, this intervention remains controversial. A 10-week double-blind, placebo-controlled trial was undertaken to examine both the efficacy and safety of HDPM in autism. Twelve patients were enrolled, and 10 patients (mean age 6 years 3 months) were able to complete the study. HDPM at an average dose of 638.9 mg of pyridoxine and 216.3 mg of magnesium oxide was ineffective in ameliorating autistic behaviors as assessed by the Childrens Psychiatric Rating Scale (CPRS), the Clinical Global Impression Scale, and the NIMH Global Obsessive Compulsive Scale. Furthermore, no clinically significant side effects were noted during HDPM administration. A trend for a transient change on the CPRS was found that was possibly due to a placebo response. This study raises doubts about the clinical effectiveness of HDPM in autistic disorder.
Neuropsychologia | 2004
Motomi Toichi; Robert L. Findling; Yasutaka Kubota; Joseph R. Calabrese; Max Wiznitzer; Nora K. McNamara; Kokichi Yamamoto
Both simple attention tasks (e.g. letter cancellation) and most tasks of higher cognitive processing (e.g. word generation) are known to activate the dorsolateral prefrontal cortex (PFC). While attention and higher cognitive processing differ phenomenologically, with attention tasks requiring great subjective effort despite their simplicity, possible physiological differences in the activation of the PFC between the two types of cognitive processing have remained uninvestigated. Hemodynamic changes in the PFC during activation due to tasks of attention and those of higher cognitive processing were examined using near-infrared spectroscopy in 10 Japanese and 10 American healthy adults. In tasks of higher cognitive processing, which included both verbal and non-verbal tasks, the concentration of oxygenated hemoglobin ([HbO2]) increased, and that of deoxygenated hemoglobin ([HbR]) decreased, with an increase in the tissue hemoglobin saturation (THS). In tasks of attention, which consisted of the letter cancellation and continuous performance test, both [HbO2] and [HbR] increased, with no significant changes in the THS observed. The distinctive patterns of hemodynamic changes were not affected by the factors of task difficulty or language. The change in [HbR] may be a physiological marker of the prefrontal lobe activation that discriminates between attention and higher cognitive processing. The increase in [HbR] suggests increased oxygen consumption of the PFC during tasks of attention, which might be related to the disproportionately great subjective effort associated with sustained attention. The physiological alteration in hemodynamic patterns according to changes in cognition needs to be examined in subjects with prefrontal lobe dysfunction, such as schizophrenia and mood disorder.
Journal of Child Neurology | 2004
Monisha Goyal; Mary Ann O'Riordan; Max Wiznitzer
Rett syndrome, a neurodevelopmental disorder, manifests in the first few years of life with developmental arrest, stereotyped behaviors, and respiratory abnormalities. Seizures occur in 70 to 80% of patients. Clinical drug trials have not demonstrated the superiority of any specific antiepilepsy drug. We report our experience with topiramate in eight patients with Rett syndrome. Topiramate was initiated as monotherapy in two patients and as adjunctive therapy in six patients. Seven patients had improved seizure control. Respiratory abnormalities improved by 50 to 75% in two patients and by 20 to 50% in two others. In our cohort, seven of eight patients showed improvement in seizure control and/or respiratory abnormalities on topiramate. Topiramate was well tolerated. The effect of topiramate, a broad-spectrum drug, could be due to its γ-aminobutyric acid (GABA)ergic and glutaminergic effects, both systems thought to be disordered in Rett syndrome. (J Child Neurol 2004;19:588-591).
Epilepsia | 2003
Monisha Goyal; Barbara Bangert; Max Wiznitzer
Summary: u2002Purpose: Although seizures are relatively common in acute childhood leukemias, evolution into epilepsy is rare.
Journal of Child Neurology | 2017
Max Wiznitzer
In 2015, Sartwelle and Johnson published a commentary (described as an original article) in this journal on the use of electronic fetal monitoring to prevent cerebral palsy caused by hypoxic-ischemic encephalopathy. This article, one of several on the same theme that have been published in medical and legal journals by one or both of these authors, claims that electronic fetal monitoring is ‘‘junk science’’ and should be excluded from the court room based on the Daubert legal principle. As stated in a federal judicial system publication, ‘‘the specific factors explicated by the Daubert Court are (1) whether the expert’s technique or theory can be or has been tested—that is, whether the expert’s theory can be challenged in some objective sense, or whether it is instead simply a subjective, conclusory approach that cannot reasonably be assessed for reliability; (2) whether the technique or theory has been subject to peer review and publication; (3) the known or potential rate of error of the technique or theory when applied; (4) the existence and maintenance of standards and controls; and (5) whether the technique or theory has been generally accepted in the scientific community.’’ Electronic fetal monitoring has been investigated with resultant publications and is widely used in the obstetrics community. Despite this acceptance, are Sartwelle and Johnson correct in their conclusion that electronic fetal monitoring is ‘‘junk science’’? The answer is no. In order to determine whether studies of the use of electronic fetal monitoring in lessening the cerebral palsy rate have reached valid conclusions, an understanding of the epidemiology of cerebral palsy is needed. In order for cerebral palsy to be a consequence of intrapartum asphyxia, the child should manifest a hypoxic-ischemic encephalopathy after birth. This is a form of neonatal encephalopathy. Recent estimates find that neonatal encephalopathy occurs in 3/1000 live births and hypoxic-ischemic encephalopathy occurs in 1.5/1000 live births. The birth prevalence of cerebral palsy is 1-2 per thousand live births, with 10% to 20% being caused by hypoxicischemic encephalopathy. Therefore, cerebral palsy due to hypoxic-ischemic encephalopathy has a prevalence of approximately 1-4 per 10 000 live births. In the 1960s-1970s, the time that electronic fetal monitoring studies were originally done, the belief that a higher percentage of cerebral palsy and intellectual disability was due to brain injury occurring in the intrapartum time period influenced study design. Animal and human studies showed a correlation between electronic fetal monitoring changes and fetal acidemia. Changes included depression of variability and accelerations and certain changes in fetal heart rate patterns. Sensitivity and positive predictive value were variable. Subsequently, studies were done involving hundreds or thousands of deliveries that usually found no major difference in neonatal mortality and morbidity when comparing the use of electronic fetal monitoring and intermittent auscultation. However, based on the knowledge that cerebral palsy due to hypoxic-ischemic encephalopathy is not common, it can be concluded that these trials were underpowered to detect differences in this major outcome. Furthermore, in most of these studies, hypoxicischemic encephalopathy or later cerebral palsy were not specific outcomes (ie, if one does not ask the right question, one cannot get the needed answer). Rather, outcomes such as neonatal intensive care unit admission, fetal death and neonatal mortality and morbidity, all of which can have different causes besides hypoxic-ischemic encephalopathy, were measured outcomes. The duration and type of fetal heart rate abnormalities were not common study variables, even though certain heart rate patterns, such as absent variability and recurrent late decelerations, recurrent variable decelerations, or bradycardia, have a stronger association with an adverse outcome and are classified as category III tracings. Therefore, it is not surprising that a consistent relationship between electronic fetal monitoring abnormalities and the occurrence of hypoxic-ischemic encephalopathy and later cerebral palsy was difficult to establish. There have been efforts to improve the reliability of electronic fetal monitoring interpretation and communication of electronic fetal monitoring abnormalities in a timely fashion to prevent their evolution into more ominous patterns. Recent studies have shown that neonatal outcomes improve when caregiver education programs are implemented and specific monitoring practices are utilized. In the United Kingdom, obstetrics
Vaccine | 2007
James J. Sejvar; Katrin S. Kohl; Roman Bilynsky; Dean A. Blumberg; Therese Cvetkovich; Jochem M. D. Galama; Jane Gidudu; Lakshmi Katikaneni; Najwa Khuri-Bulos; James M. Oleske; Terhi Tapiainen; Max Wiznitzer
The Lancet | 2003
Max Wiznitzer; Robert L. Findling
The Lancet | 2005
Max Wiznitzer
The Lancet | 2006
Monisha Goyal; Max Wiznitzer