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This Month in Archives of Neurology
September 2008

This Month in Archives of Neurology

Arch Neurol. 2008;65(9):1152-1153. doi:10.1001/archneur.65.9.1152

Return to Play After Athletic Concussion

The management of sport-related concussion, especially involving return-to-play decisions, is one of the most important challenges confronting sports medicine physicians and neurologists. Mayers (page 1158) points out that current guidelines for return to play are too lenient and that a postconcussion return-to-play interval of at least 4 weeks is imperative.

Monoclonal Therapies and Neurologic Disorders

Novak et al (page 1162) report that monoclonal antibody therapy for treating medical conditions has expanded greatly in the past 30 years, and monoclonal antibody treatments are currently being tested for conditions such as neuromuscular disorders and demyelinating diseases. The authors provide a well-focused and comprehensive review of this important clinical subject, highlighting the use of monoclonal antibodies in treating neurologic conditions and their neurologic adverse effects.

Bridging Anticoagulation After Cardioembolic Stroke

Hallevi and colleagues (page 1169) provide new data supporting the position that anticoagulation in patients with cardioembolic stroke can be safely started with warfarin shortly after stroke. However, they point out that heparin bridging (intravenous heparin in the acute phase followed by warfarin) and enoxaparin bridging (full-dose enoxaparin combined with warfarin) increase the risk of serious bleeding. Editorial perspective is provided by Robert J. Wityk, MD.

The timing of hemorrhagic transformation (HT). PH2 indicates parenchymal hematoma, grade 2.

The timing of hemorrhagic transformation (HT). PH2 indicates parenchymal hematoma, grade 2.

Aggressive Blood Pressure Lowering Before Intravenous Tissue Plasminogen Activator Treatment for Acute Stroke

Martin-Schild et al (page 1174) find that blood pressure reduction before intravenous tissue plasminogen activator (tPA) treatment may not be associated with a higher rate of hemorrhage or poor outcome. Their data indicate that patients with acute ischemic stroke who require aggressive blood pressure treatment should not be excluded from tPA therapy.

Diffusion Tensor Imaging and Functional Brain Injury

Fox and colleagues (page 1179) identified diffusion tensor imaging (DTI) evidence of pathological disruption of a small brainstem fiber pathway that is crucial for accurate horizontal eye movements. They noted important correlations between DTI changes and oculomotor dysfunction.

Transactivation Response DNA-Binding Protein 43 Mutations and Familial Amyotrophic Lateral Sclerosis

Mutations in transactivation response DNA-binding protein 43 (TDP-43) are a rare cause of familial non-SOD1 amyotrophic lateral sclerosis (ALS). Kühnlein and colleagues (page 1185), in providing an identification of TDP-43 mutations, provide strong evidence for a direct link between TDP-43 dysfunction and neurodegeneration in ALS.

Pain as a Nonmotor Symptom of Parkinson Disease

Defazio et al (page 1191) have found that the overall frequency of pain was significantly greater in patients with Parkinson disease than in control subjects. They establish that pain may be a nonmotor feature of Parkinson disease.

Cardiac Involvement With Limb-Girdle Type 2 and Becker Muscular Dystrophies

This study by Sveen et al (page 1196) demonstrates a high prevalence of cardiac involvement in patients with limb-girdle type 2 and Becker muscular dystrophies.

Prediction of Rate of Cognitive Decline by Cerebral Atrophy and White Matter Changes in Alzheimer Disease

Brickman et al (page 1202) show that the degree of cerebral atrophy and the severity of white matter hyperintensities (WMH) are associated with the rapidity of cognitive decline in Alzheimer disease (AD). They believe that atrophy and WMH may interact to have a synergistic effect on future decline. Patients with AD with both of these features have a particularly rapid degree of cognitive decline.

Inability of Alzheimer Disease Neuropathology to Explain Dementia in the Oldest-Old

Neuropathological features of dementia in oldest-old persons are not the same as those of cognitively impaired younger-old persons, as reported in this provocative and highly interesting report by Haroutunian and colleagues (page 1211).

Optical Coherence Tomography in Multiple Sclerosis

Cettomai et al (page 1218) demonstrate that mean retinal nerve fiber layer (RNFL) thickness can be reproducibly measured by experienced personnel using optical coherence tomography–3 (OCT-3). Measures of RNFL thickness from cohorts of age-matched controls and patients with multiple sclerosis from 3 research centers were highly similar. This shows that OCT-3 is a reliable means to follow up patients with ocular nerve lesions due to multiple sclerosis.

Gray Matter Atrophy and Benign Multiple Sclerosis

Mesaros et al (page 1223) report that cerebellar gray matter atrophy is a major determinant of irreversible locomotor disability in patients with multiple sclerosis. The absence of cognitive impairment and a longer disease duration and lower Expanded Disability Status Scale score may identify those patients with benign multiple sclerosis with the potential for a favorable disease evolution.

Cerebral Hypometabolism With Future Memory Decline

Caselli and colleagues (page 1231) find that patients with amnestic pre–mild cognitive impairment showed significantly greater correlations between cerebral hypometabolism and subsequent long-term memory decline than nondecliners in Alzheimer disease–affected brain regions.