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Transcranial magnetic stimulation (TMS) activates the underlying brain relays and networks without risk or pain. Rossini and Rossi review progress in TMS since 1985. TMS represents a formidable tool for exploring function (movement, language, memory, perception, plasticity) in the healthy and in damaged brain. TMS has potential for treatment of a number of disabling neurologic conditions including chronic pain, dystonias, epilepsy, migraine, and stroke.
see page 484
Benign MS at 20 years
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Sayao et al. evaluated the disease status in 169 patients with benign MS (EDSS 
3, at 10 years from onset) 20 years after onset, by which time almost half were no longer benign. No 10-year EDSS score appeared ideal in predicting benign status.
see page 496
The editorial by Sean J. Pittock suggests that if we could identify which patients will remain benign, disease-modifying treatments would not be indicated for them. Since most evidence supports a beneficial effect of disease-modifying agents (DMA) on relapse rate and MRI activity, patients with infrequent attacks and stable MRIs (whose clinical and radiologic profiles strongly differ from those generally enrolled in drug trials) would benefit less from DMAs than those with frequent attacks or evidence of substantial subclinical (MRI-based) disease activity. A watchful waiting approach with regular clinical and MRI monitoring before initiating treatment may be a preferable approach for some patients. However, the watchful waiting should not be misconstrued as a never treat approach. If the decision is made to delay treatment in a patient with a favorable disease profile, yearly clinical and radiologic surveillance is advised, with appropriate initiation of DMA should the clinical (relapses) or radiologic (new/enhancing lesions) status or patient wishes change.
see page 480
Beta-blocker treatment may be cerebroprotective during stroke
Laowattana and Oppenheimer found that activated sympathetic tone correlates with poorer prognosis after stroke. Prior beta-blocker therapy was associated with improved clinical presentation and lower coagulation and inflammatory indices as well as reduced sympathovagal balance after stroke. Beta-blocker treatment may be cerebroprotective in high-risk cerebrovascular disease patients.
see page 509
Cannabis in painful HIV-associated neuropathy
Abrams et al. studied the short-term effects of smoked cannabis in 50 patients with HIV-associated sensory neuropathy. In a randomized, placebo-controlled trial, cannabis decreased neuropathic pain and pain in an experimental model with an effect comparable to clinically proven oral drugs for chronic neuropathic pain.
see page 515
Psychiatric features in SGCE myoclonus-dystonia
Hess et al. evaluated psychiatric features in five families with SGCE mutation myoclonus-dystonia. They found that obsessive-compulsive disorder and alcohol dependence were increased in gene carriers with myoclonus-dystonia. They postulate that obsessive-compulsive disorder is associated with mutant SGCE, and alcohol dependence is reactive to palliative effects.
see page 522
Characteristics of HIV dementia in Thailand
Recent in vitro research suggests that HIV-1 subtype may impact neuropathogenesis. The study by Valcour et al. compared neuropsychological profiles among HIV-infected Thais (subtype CRF AE_01) with dementia, matched individuals without dementia, and seronegative controls, describing abnormalities similar to that seen in subtype B.
see page 525
Right-to-left shunt and lacunar stroke
Ueno et al. identified potential embolic sources in patients with lacunar stroke using transesophageal echocardiography. Patients with lacunar stroke having neither hypertension nor diabetes mellitus had a higher frequency of right-to-left shunt (82%) than patients with these risk factors or controls.
see page 528
Amyloid, hypometabolism, and cognition in AD
Edison et al. found that 90% of patients with AD show diffusely raised cortical amyloid with [11C]PIB-PET and reduced temporal glucose metabolism with FDG PET, which correlates with cognitive performance. High frontal amyloid and normal frontal glucose utilization in AD suggests amyloid plaque formation may not be directly responsible for the neuronal dysfunction.
see page 501
The editorial by Bateman and Eidelberg notes that as PIB PET is a molecular amyloid imaging technique, it has the potential of providing quantitative measures of amyloid in the brain, which previously could only be obtained postmortem. How PIB PET is applied will depend on the questions that are asked. The Edison et al. study gives further support for its applicability in identifying AD. It has an obvious role in research, and is potentially useful as a tool in clinical trials. Whether PET imaging with PIB or related radiotracers will be adopted as a diagnostic test for AD will require large controlled studies of AD compared to other dementias with follow-up pathologic confirmation.
see page 482
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