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This Month in Archives of Neurology
May 2002

This Month in The Archives of Neurology

Arch Neurol. 2002;59(5):681-683. doi:10.1001/archneur.59.5.681
Neurotherapeutics 2002

This issue of the ARCHIVES is a theme issue on "Neurotherapeutics 2002." It is our objective to emphasize new and emerging therapies for neurologic disease. Editorials that emphasize new developments in neurotherapeutics are included from Ira Shoulson, MD; David Pleasure, MD, and colleagues; Christopher G. Goetz, MD, and Vanessa K. Hinson, MD, PhD; Louis R. Caplan, MD; John J. Redington, MD, and Kenneth L. Tyler, MD; Hassan M. Fathallah-Shaykh, MD; Khurram Bashir, MD, MPH, and John N. Whitaker, MD; Paul C. Van Ness, MD; and J. Ned Pruitt II, MD, and Thomas R. Swift, MD.

Friedreich Ataxia: A Molecular Success Story

David R. Lynch and colleagues provide a splendid clinical and molecular review of recent exciting developments in the etiology of Friedreich ataxia. This is one of the major molecular genetic success stories of this decade.

Intravenous Immunotherapy for Diabetic Neuropathy

Sharma and colleagues describe their experience in treating diabetic demyelinating polyneuropathy with intravenous immunoglobulin therapy. The result is of one of significant clinical improvement in most patients in this study. It is an important article from a therapeutic and conceptual point of view.

Demyelinating Neuropathy in Diabetes Mellitus

Sharma et al describe their experience with patients with diabetes mellitus who seem to have a predisposition to develop chronic inflammatory demyelinating polyneuropathy. Their criteria for this spectrum of demyelinating disease are unique and offer new thoughts regarding the use of immunotherapy for diabetic demyelinating polyneuropathy.

Migrating Mononuclear Cells in Multiple Sclerosis

Gelati et al, using an in vitro model, have considered how intravenous methylprednisolone treatment in patients with multiple sclerosis (MS) could influence transmigration of mononuclear cells. They find that the absolute number of transmigrated mononuclear cells from methylprednisolone-treated patients with MS significantly decreased at 3 hours and increased again at 24 hours. Thus, their results indicate that methylprednisolone does affect transmigration of mononuclear cells across the blood-brain barrier and in so doing may affect activity and length of disease. These observations may play a pivotal role in appreciating more fully the pathogenesis of MS.

Bone Loss Due to Antiepileptic Drugs

Andress et al have considered the issue of bone loss in patients receiving long-term antiepileptic drug (AED) therapy. Femoral neck bone mineral density by dual energy x-ray absorptiometry (DEXA) was examined in patients receiving AEDs. Clearly, AED therapy does cause significant bone loss at the hip in the absence of vitamin D deficiency, and this loss can be measured using DEXA scanning. The syndrome is reversible with calcium and vitamin D replacement therapy. Clinicians need to know of this adverse effect of AEDs and of the means to easily monitor patients.

Homocysteine and Alzheimer Disease

Hogervorst and colleagues find that higher homocysteine levels are an independent risk factor for moderate to severe white matter changes in the cerebral hemispheres in patients with Alzheimer disease (AD). Logistic regression shows that leukoaraiosis was more prevalent in AD cases than in control subjects and that at an older age, higher levels of total homocysteine were independently associated with an increased risk of leukoaraiosis. Therapeutic lowering of elevated homocysteine levels with folic acid is achievable and should be rigorously studied as a means of affecting the level and extent of white matter changes associated with AD.

DNA Damage, Antioxidants, and Alzheimer Disease

Mecocci and colleagues measured lymphocyte DNA 8-hydroxy-2-deoxyguanosine (8-OHdG) content in patients with Alzheimer disease (AD) compared with age-matched controls. Lymphocyte DNA OhdG content was significantly higher and plasma levels of antioxidants were significantly lower in patients with AD compared with controls. Their findings support the view that lymphocyte 8 (OHdG) in patients with AD reflects a condition of increased oxidative stress related to low antioxidant status. Oxidative stress continues to emerge as a significant issue in the pathogenesis of AD and emphasizes the need for more effective antioxidant therapies.

Budipine in Treating Parkinson Disease

Przuntek et al have conducted a clinical trial of budipine as an additional form of therapy to a stable, optimally titrated level of the levodopa/dopadecarboxylase inhibitor, bromocriptine, and selegiline in patients with idiopathic Parkinson disease. Budipine provided further therapeutic benefit in these patients. This pharmacologic approach may be of value in selected patients requiring additional therapy.

Testosterone for Parkinson Disease

Okun and colleagues have found in their Parkinson disease (PD) registry that 35% of patients had plasma evidence of testosterone deficiency. Five patients with PD were treated with testosterone, with significant improvements in their refractory nonmotor symptoms. It is an area of evaluation that needs more emphasis to provide our patients with a fuller life.

Cognitive Impairment in Patients With Human Immunodeficiency Virus

De Ronchi and colleagues find that low education, low CD4+ cell count, and homosexual/bisexual and heterosexual risk behaviors are risk factors for cognitive impairment in persons with seropositive human immunodeficiency virus 1. Antiretroviral therapy exerts a beneficial effect in these patients and should be implemented early in the disease course.

Interleukin 4 Gene in Panencephalitis

Inoue and colleagues investigated the association of polymorphisms in cytokine, interferon, and interleukin (IL) genes in patients with subacute sclerosing panencephalitis (SSPE) in Japan. Their study found a distinct possibility that the IL-4 promoter gene –589T polymorphism with increased IL-4 synthesis in combination with interferon regulatory factor-1 allele does confer increased host genetic susceptibility to SSPE in this Japanese population. These markers may be of considerable value in identifying at-risk persons in susceptible populations.

Spectroscopic Imaging in Alzheimer Disease

Block and colleagues have used fast-proton spectroscopic imaging of the hippocampus and the laterotemporal and occipital lobes in patients with Alzheimer disease (AD) to detect regional metabolic changes that resemble the expected pattern of neuronal loss in AD. They find that N-acetylaspartate–total creatine (phosphocreatine and creatine) ratios were significantly reduced in the left and right hippocampus in patients with AD. Thus, neuronal function can be measured quantitatively using this metabolic mapping technique as a diagnostic means for AD, progression of disease, and potential response to new therapies.

Magnetic Resonance Imaging in Multiple System Atrophy and Parkinson Disease

Bhattacharya and colleagues have provided a comprehensive magnetic resonance imaging (MRI) assessment of patients with multiple system atrophy with predominant parkinsonism (MSA-P) and Parkinson disease (PD). The authors present detailed and clinically useful MRI criteria to differentiate the clinical forms of MSA and PD and provide a simple diagnostic algorithm for diagnosing this difficult spectrum of patients.

Crossed Cerebellar Atrophy

Teixeira and colleagues have thoroughly analyzed the frequency and pathogenetic factors of crossed cerebellar atrophy (CCA) in patients with epilepsy secondary to destructive brain insults of early development. Specific clinical phenotypes are presented and the results of varying levels of risk for CCA are given. This is a unique and valuable clinical and neuropathologic correlation study that offers clear insight into the basis of CCA.

Familial Parkinson Disease

Payami and colleagues show that Parkinson disease (PD) has a significant familial component. They find that compared with relatives of controls, age-specific risk of PD was increased by 7.76-fold in the relatives of patients with early-onset disease (P<.001) and by 2.95-fold in relatives of patients with late-onset disease (P = .02). Parkinson disease is both a genetic and environmentally induced disorder.

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