This Month in Archives of Neurology

Eriksen and colleagues review current knowledge of the molecular cause of Parkinson disease, including the growing lines of evidence from both environmental risk factors and early-onset genetics that point to a convergence between energy metabolism and the disposal of damaged proteins. Impairments in mitochondrial and the ubiquitin-proteasome system functions significantly contribute to the pathogenesis of Parkinson disease. Their review summarizes recent insights gained from genetic and environmental studies.

Ergin and Ergin have conducted a meta-analysis of randomized controlled trials utilizing thrombolytic agents. Eleven placebo-controlled randomized trials of thrombolytic agents involving 3709 participants were included in the analysis. Their findings indicate that thrombolytic therapy does not significantly increase all-cause mortality.

Meeren and colleagues review and extend our understanding of the cortical focus theory of absence seizures. They conclude that a focus of seizure activity within the perioral region of the somatosensory cortex generalizes rapidly over the cortex. During the first cycles of the seizure the cortex drives the thalamus, while thereafter cortex and thalamus drive each other. In this way the cortical focus theory for generalized absence epilepsy bridges cortical and thalamic theories.

Hilker and colleagues measure the progression of dopaminergic impairment in Parkinson disease with the use of positron emission tomography. In this comprehensive and elegant study, the authors show that the neurodegenerative process in Parkinson disease follows a negative exponential course and slows down with increasing symptom duration, contradicting the long-latency hypothesis of Parkinson disease. Editorial perspective is provided by Joseph Jankovic, MD.

Ruland and colleagues find that among African American subjects with previous ischemic stroke, 76% were overweight or obese. Hypertension, dyslipidemia, and diabetes mellitus were all present in 43% of men and 29% of women with significant obesity. Thus, their data show the association of increasing risk factor profiles with increasing weight in African American stroke survivors.

Naidech and colleagues find that, despite an aggressive management strategy, rebleeding still occurred in 6.9% of patients and was associated with a dismal outcome. Poor Hunt-Hess grade and larger aneurysm size are related to rebleeding. Pharmacologic therapy to reduce the risk of rebleeding before aneurysm repair, particularly in patients with poor-grade neurologic status and large aneurysms, deserves renewed attention.

Weimar and colleagues studied 1964 consecutive patients admitted within 4 hours of the onset of acute cerebral ischemic symptoms and documented causes of neurologic worsening. Besides initial stroke severity and comorbid conditions, ultrasound and imaging can provide valuable information about the risk of worsening of stroke symptoms in the acute phase and thus can identify patients who could benefit most from intensive monitoring.

Sacco and colleagues conducted a post hoc analysis of data from the European Stroke Prevention Study 2 to assess the efficacy of aspirin plus extended-release dipyridamole compared with aspirin alone for the prevention of recurrent stroke among high-risk groups. Aspirin plus extended-release dipyridamole, they conclude, is more effective than aspirin alone.

Ikonomovic and colleagues document that choline acetyltransferase activity reduction in the primary visual cortex of patients with mild to moderate Alzheimer disease, but not patients with mild cognitive impairment, serves to distinguish between clinical and preclinical forms of the disease. It appears that this change relates to generalized cognitive abnormalities but not specifically to visuospatial function.

Doherty and colleagues describe midline splenium changes that are commonly seen on magnetic resonance imaging diffusion weighted imaging sequences. Multiple causes can result in splenium changes. Glucose and electrolyte abnormalities, seizure risk, ongoing infectious or parainfectious processes, and traumatic causes need to be emphasized in clinical evaluations.

Romi and colleagues show that some patients with myasthenia gravis have antibodies that bind in a cross-striational pattern to skeletal and heart muscle tissue sections. These antibodies react with epitopes on the muscle proteins titin and ryanodine, are found mainly in the serum of patients with thymoma and late-onset myasthenia gravis, and may correlate with myasthenia gravis severity.

Zhang and colleagues have studied the prevalences of Alzheimer disease and vascular dementia in 4 regions of China. In a comprehensive epidemiological survey, they find that the prevalence of dementia subtypes in China is comparable with that in Western countries.

Hoyt and colleagues show that while the apolipoprotein E ε4 allele is associated with an increased risk of developing Alzheimer disease, the presence of 2 apolipoprotein E ε4 alleles is associated with a slower clinical course of cognitive loss. These interesting and somewhat paradoxical findings are consistent with hypotheses that the biological processes contributing to the onset of Alzheimer disease are different from those involved in determining its clinical course.

Tan and colleagues show that an MDR1 (a multidrug transporter encoding a P-glycoprotein) haplotype containing single nucleotide polymorphisms e21/2677T and e26/3435T protects against Parkinson disease in ethnic Chinese, compatible with the observation of a recent positive selection of the T alleles of these 2 single nucleotide polymorphisms in this ethnic population.

Levy and colleagues find that axial (gait and postural) impairment in Parkinson disease may result from the combined effect of the disease and the aging process on nondopaminergic subcortical structures.