Nizar Souayah

Guillain–Barré syndrome after Gardasil vaccination: Data from Vaccine Adverse Event Reporting System 2006–2009

Using data from Vaccine Adverse Event Reporting System, we identified 69 reports of Guillain-Barré Syndrome (GBS) after Gardasil vaccination that occurred in the United States between 2006 and 2009. The onset of symptoms was within 6 weeks after vaccination in 70% of the patients in whom the date of vaccination was known. The estimated weekly reporting rate of post-Gardasil GBS within the first 6 weeks (6.6 per 10,000,000) was higher than that of the general population, and higher than post-Menactra and post-influenza vaccinations. Further prospective active surveillance for accurate ascertainment and identification of high-risk groups of GBS after Gardasil vaccination is warranted.

Guillain-Barré syndrome after vaccination in United States: data from the Centers for Disease Control and Prevention/Food and Drug Administration Vaccine Adverse Event Reporting System (1990-2005).

Background: There are isolated reports of Guillain-Barré syndrome (GBS) after receiving vaccination. Objective: To determine the rates and characteristics of GBS after administration of vaccination in United States Methods: We used data for 1990 to 2005 from the Vaccine Adverse Event Reporting System, which is a cooperative program of the Centers for Disease Control and Prevention and the US Food and Drug Administration. Results: There were 1000 cases (mean age, 47 years) of GBS reported after vaccination in the United States between 1990 and 2005. The onset of GBS was within 6 weeks in 774 cases, >6 weeks in 101, and unknown in 125. Death and disability after the event occurred in 32 (3.2%) and 167 (16.7%) subjects, respectively. The highest number (n = 632) of GBS cases was observed in subjects receiving influenza vaccine followed by hepatitis B vaccine (n = 94). Other vaccines or combinations of vaccines were associated with 274 cases of GBS. The incidence of GBS after influenza vaccination was marginally higher in subjects <65 years compared with those ≥65 years (P = 0.09); for hepatitis vaccine, the incidence was significantly higher (P < 0.0001) in the <65 group. Death was more frequent in subjects ≥65 years compared with those <65 years (P < 0.0001). Conclusions: Our results suggest that vaccines other than influenza vaccine can be associated with GBS. Vaccination-related GBS results in death or disability in one fifth of affected individuals, which is comparable to the reported rates in the general GBS population.

Effect of intravenous immunoglobulin on cerebellar ataxia and neuropathic pain associated with celiac disease

Background:  Cerebellar syndrome and small fiber neuropathy may complicate celiac disease (CD) and may be resistant to a strict gluten‐free diet.

Insights into neurologic localization by Rhazes, a medieval Islamic physician

Rhazes was born at Ray near modern Teheran in 864 AD. He wrote over 200 scientific treatises, many of which had a major impact on European medicine. His best known manuscript is Liber Continens, a medical encyclopedia. Herein are described Rhazes’s contributions to neurology, focusing on his description of cranial and spinal cord nerves and his clinical case reports, which illustrate his use of neuroanatomy to localize lesions. Relevant passages from facsimiles of the manuscripts Kitab al-Hawi (Liber Continens) and Al-Mansuri Fi At-Tibb (Liber Al Mansoori) were translated, reviewed, and used as references. In addition, Medline, Web, and manuscript searches on Rhazes and the history of medieval and Islamic medicine and neurology were conducted. Rhazes stated that nerves had motor or sensory functions, describing 7 cranial and 31 spinal cord nerves. He assigned a numerical order to the cranial nerves from the optic to the hypoglossal nerves. He classified the spinal nerves into 8 cervical, 12 thoracic, 5 lumbar, 3 sacral, and 3 coccygeal nerves. Rhazes showed an outstanding clinical ability to localize lesions, prognosticate, and describe therapeutic options and reported clinical observations, emphasizing the link between the anatomic location of a lesion and the clinical signs. Rhazes was a pioneer in applied neuroanatomy. He combined a knowledge of cranial and spinal cord nerve anatomy with an insightful use of clinical information to localize lesions in the nervous system.

Motor unit number estimate as a predictor of motor dysfunction in an animal model of type 1 diabetes

Peripheral neuropathy is a common complication of diabetes that leads to severe morbidity. In this study, we investigated the sensitivity of motor unit number estimate (MUNE) to detect early motor axon dysfunction in streptozotocin (STZ)-treated mice. We compared the findings with in vitro changes in the morphology and electrophysiology of the neuromuscular junction. Adult Thy1-YFP and Swiss Webster mice were made diabetic following three interdaily intraperitoneal STZ injections. Splay testing and rotarod performance assessed motor activity for 6 wk. Electromyography was carried out in the same time course, and compound muscle action potential (CMAP) amplitude, latency, and MUNE were estimated. Two-electrode voltage clamp was used to calculate quantal content (QC) of evoked transmitter release. We found that an early reduction in MUNE was evident before a detectable decline of motor activity. CMAP amplitude was not altered. MUNE decrease accompanied a drop of end-plate current amplitude and QC. We also observed small axonal loss, sprouting of nerve endings, and fragmentation of acetylcholine receptor clusters at the motor end plate. Our results suggest an early remodeling of motor units through the course of diabetic neuropathy, which can be readily detected by the MUNE technique. The early detection of MUNE anomalies is significant because it suggests that molecular changes associated with pathology and leading to neurodegeneration might already be occurring at this stage. Therefore, trials of interventions to prevent motor axon dysfunction in diabetic neuropathy should be administered at early stages of the disorder.

Trends in outcomes and hospitalization costs for traumatic brain injury in adult patients in the United States.

Several new therapeutic strategies have been introduced for the management of adult traumatic brain injury (TBI) over the last decade, such as the development of management pathways and specialized TBI units and improved treatment of cerebral perfusion. The purpose of this study is to compare TBI-related hospitalization outcomes in the United States between two time periods, 1993-1994 and 2006-2007. We determined the rates of occurrence, in-hospital outcomes, and mean hospital charges for patients hospitalized with adult TBI in 1993-1994 using the nationally representative all-payer Nationwide Inpatient Survey (NIS) database, and compared these outcomes with homologous data from 2006-2007. The incidence of TBI admissions was reduced by 35% in 2006-2007 compared with 1993-1994; (22/100,000 versus 34/100,000 population; p<0.0001). The mean length of hospitalization (mean±SD, in days) was significantly lower in 2006-2007 than in 1993-1994 (2.5±2.4 days versus 2.7±2.6 days; p<0.0001). In-hospital mortality increased significantly in 2006-2007 compared with 1993-1994 (0.8% versus 0.4%, p<0.0001). Average hospitalization charges were significantly higher in 2006-2007 compared with 19993-1994 (

Reductions in motor unit number estimates (MUNE) precede motor neuron loss in the plasma membrane calcium ATPase 2 (PMCA2)-heterozygous mice.

21,460±

Guillain-Barré syndrome triggered by influenza vaccination in a recipient of liver transplant on FK506.

21,212 versus

Necrotizing myopathies: an update.

5,142±

Hepatitis C: a review of its neurologic complications.

4,625; p<0.0001), even after adjusting for inflation. In both time periods, most hospitalized adult TBI patients were graded as mild (98.2% in 1993-1994 versus 98.0% in 2006-2007; p=0.20). There was a significant increase in average hospitalization charges and death rates in all TBI severity subgroups in 2006-2007 compared with 1993-1994. The decline in rate of hospitalization between the two time periods was predominantly related to the decline in the number of admissions of patients with mild TBI. Although the number of TBI admissions was reduced, a significant increase in average hospitalization charges and in-hospital mortality rate was observed in 2006-2007 compared with 1993-1994.