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In This Issue of JAMA Neurology |

In This Issue of JAMA Neurology FREE

JAMA Neurol. 2013;70(2):149-150. doi:10.1001/jamaneurol.2013.1605.
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Miocinovic and colleagues (page 163) provide a comprehensive review of deep brain stimulation focusing on movement disorders.

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Basal ganglia-thalamo-cortical circuit schematic in the normal and parkinsonian states. Thickness of the arrows indicates strength of the connections. Loss of substantia nigra neurons leads to increased thalamic inhibition. The diagram does not account for firing pattern and oscillatory activity, both of which are important factors in understanding the effects of deep brain stimulation on the network. D1 and D2 indicate postsynaptic dopamine receptor type; GPe, globus pallidus externus; GPi, globus pallidus internus; SNc, substantia nigra pars compacta; SNr, substantia nigra pars reticulata; STN, subthalamic nucleus; and Thal, thalamus.

Rudick et al (page 172) review the history of natalizumab therapy from target molecule discovery through regulatory approval, voluntary suspension, reapproval, and clinical use.

Shulman and coauthors (page 183) compare the efficacy of treadmill exercises and stretching and resistance exercises in improving gait speed, strength, and fitness for patients with Parkinson disease. Editorial perspective is provided by Liana S. Rosenthal, MD, and E. Ray Dorsey, MD, MBA (page 156).

Haley and colleagues (page 191) test the hypothesis that symptoms among Gulf War veterans, such as chronic diarrhea, dizziness, fatigue, and sexual dysfunction, are due to cholinergic autonomic dysfunction. They evaluated outcomes in representative samples meeting a validated case definition of Gulf War illness, with 3 variants and a control group. Editorial perspective is provided by Roy Freeman, MBChB (page 158).

Winer et al (page 201) determine whether the SOD1 protein in cerebral spinal fluid may be a pharmacodynamic marker for antisense oligonucleotide therapy and a disease marker for amyotrophic lateral sclerosis.

Zheng and coauthors (page 208) investigate the relationship between aspirin resistance and clinical and neuroimaging measures of stroke severity in acute stroke patients.

Scalfari and colleagues (page 214) study a cohort with multiple sclerosis and frequent early attacks to elucidate the relationship among early relapses, onset of progression, and severe disability.

Tsuang et al (page 223) conduct a genetic case-control study to test for an association between the apolipoprotein E (APOE) ϵ4 allele and dementias with synucleinopathy.

Klein and coauthors (page 229) determine, in patients seropositive for neuronal voltage-gated potassium channel (VGKC) complex autoantibodies, the spectrum of clinical presentations and frequency of leucine-rich glioma-inactivated protein 1 (LGI1) and contactin-associated protein-like 2 (CASPR2) as defined antigenic neuronal targets in the VGKC macromolecular complex.

Barros and colleagues (page 235) document and discuss the broad phenotypic variability in a Portuguese family with cerebellar ataxia, hemiplegic migraine, and related syndromes caused by missense mutation c.1748 (p.R583Q) in the CACNA1A gene.

Ziegler et al (page 241) test the hypothesis that the degeneration of the substantia nigra pars compacta (SNc) precedes that of the cholinergic basal forebrain (BF) in Parkinson disease (PD) by performing a matched case-control study among 29 patients with PD (Hoehn and Yahr stages 1-3) and 27 matched healthy control subjects. They used new multispectral structural magnetic resonance imaging tools to measure the volumes of the SNc and BF.

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Graphic Jump LocationImage not available.

Basal ganglia-thalamo-cortical circuit schematic in the normal and parkinsonian states. Thickness of the arrows indicates strength of the connections. Loss of substantia nigra neurons leads to increased thalamic inhibition. The diagram does not account for firing pattern and oscillatory activity, both of which are important factors in understanding the effects of deep brain stimulation on the network. D1 and D2 indicate postsynaptic dopamine receptor type; GPe, globus pallidus externus; GPi, globus pallidus internus; SNc, substantia nigra pars compacta; SNr, substantia nigra pars reticulata; STN, subthalamic nucleus; and Thal, thalamus.

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