Epilepsy and Alzheimer Disease
Palop and Mucke (SEE ARTICLE) review recent experimental data demonstrating that high levels of β-amyloid peptide (Aβ) in the brain can cause epileptiform activity and cognitive deficits in transgenic mouse models. They conclude that Aβ may contribute to cognitive decline in Alzheimer disease by eliciting similar aberrant neuronal activity in humans, and they discuss the potential clinical and therapeutic implications of this hypothesis.
Emerging Concepts in Epilepsy and Epileptogenesis
Dichter (SEE ARTICLE) asks 2 fundamental questions in his quest to understand the physiological mechanisms underlying seizure generation: how do seizures develop in the brain, and how does a normal brain become an epileptic brain after injury? These questions form the discussion of this most elegant and insightful review.
Sorting Out β-Amyloid Protein Production in Alzheimer Disease
Ma and colleagues (SEE ARTICLE) report the highly significant finding that sorLA/LR11, a transmembrane neuronal protein that reduces amyloid precursor protein trafficking to secretases, was significantly reduced in the cerebrospinal fluid of patients with Alzheimer disease. This finding may have great potential as a diagnostic biomarker for patients with LR11 deficits that promote β-amyloid peptide production or as an index of therapeutic responses in late-onset Alzheimer disease. Editorial perspective is provided by Richard Mayeux, MD, MSc, and Peter St. George-Hyslop, MD. (SEE ARTICLE)
NMDA Receptor Antibodies and New-Onset Epilepsy
Niehusmann et al (SEE ARTICLE) describe a new form of encephalitis associated with ovarian teratoma and with seizures and psychiatric symptoms. They have identified 19 female patients aged 15 to 45 years with unexplained new-onset epilepsy. Five of the 19 patients had antibodies against N-methyl-D-aspartate (NMDA) receptors. Only 1 patient had a neoplasm; thus the disorder is not always paraneoplastic.
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Clinical courses of the 5 patients positive for N-methyl-D-aspartate receptor (NMDAR) antibodies. CSF indicates cerebrospinal fluid; IVIG, intravenous immunoglobulin.
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Deep Brain Stimulation for Primary Dystonia
Isaias and colleagues (SEE ARTICLE) find that pallidal deep brain stimulation is a safe and effective treatment for primary generalized dystonia, with improvement sustained for up to 8 years in one patient.
Anti-CD25 Antibody Treatment for Multiple Sclerosis
Oh et al (SEE ARTICLE) show that reduction of regulatory T cells (Treg) did not negatively affect maintenance of central nervous system tolerance during anti-CD25 antibody treatment. Sustained reduction in the frequency of CD4+CD25+ Treg was observed during treatment.
Anti-CD25 Antibody Daclizumab Inhibits Inflammation and Stabilizes Multiple Sclerosis Disease Progression
Bielekova and colleagues (SEE ARTICLE) report that daclizumab monotherapy is an effective treatment in most patients with persistent disease activity during interferon beta therapy. Either a combination of daclizumab with interferon beta or higher doses of daclizumab may be necessary to achieve optimal therapeutic responses in all patients.
Neuropathies Occurring During TNF-
–Blocker Therapy
Lozeron et al (SEE ARTICLE) show that the influence of anti–TNF-
continuation on the long-term course of neuropathy is highly variable, suggesting that anti–TNF- withdrawal is not always necessary for neuropathic control.
Primary Sensorimotor Pathways in Writer's Cramp
Delmaire and colleagues (SEE ARTICLE) demonstrate the presence of diffusion abnormalities in fiber tracts connecting primary sensorimotor areas with subcortical structures in writer's cramp. These abnormalities support the role of the cortico-subcortical pathways in the pathophysiology of writer's cramp.
Sporadic Adult-Onset Upper Motor Neuron Syndromes
Brugman et al (SEE ARTICLE) provide evidence that in most patients with a sporadic adult-onset upper motor neuron syndrome, differentiation of sporadic presentations of hereditary spastic paraparesis from primary lateral sclerosis based on clinical characteristics is unreliable and therefore depends on genetic testing.
Amyotrophic Lateral Sclerosis in Sweden
Fang and colleagues (SEE ARTICLE) report that the incidence of amyotropic lateral sclerosis has been increasing during the last 1
decades in Sweden. The specific basis for this increase remains unknown.
