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This Month in Archives of Neurology
September 2001

This Month in Archives of Neurology

Arch Neurol. 2001;58(9):1343. doi:10.1001/archneur.58.9.1343

Concurrent Tick-borne Disease

Eskow and colleagues describe patients with concurrent central nervous system disease with Borrelia burgdorferi and Bartonella henselae infection in whom the disease process was prolonged and resistant to antibiotic therapy. Concurrent tick-borne infection needs to be considered in patients with presumed Lyme disease of a chronic and resistant nature. These points are put into critical perspective in an editorial by John J. Halperin, MD, and Gary P. Wormser, MD.

Bones, Minerals, and Antiepileptic Drugs

Valmadrid and colleagues point out that only a minority of pediatric and adult neurologists routinely evaluate patients treated with antiepileptic drugs (AEDs) for bone and mineral disease. Few neurologists prescribe prophylactic calcium or vitamin D for patients taking AEDs. Clearly, physician awareness of this problem is lacking, and greater attention to the skeletal health of patients taking AEDs is needed. Howard J. Heller, MD, and Khashayar Sakhaee, MD, provide editorial comment to reinforce these points.

Early Morning Off-Medication Movement Problems

Cubo and colleagues emphasize that dystonia is the most common form of off-medication dyskinesia seen in patients with advanced Parkinson disease. Choreic dyskinesias are rare in this group of patients. The authors emphasize that the presence and type of off-medication dyskinesia should be monitored in clinical and surgical studies of patients with Parkinson disease.

Apomorphine for Parkinsonian Off-State Events

Dewey et al document that apomorphine administered by intermittent subcutaneous injection is effective and safe for outpatient use to reverse off-state events that occur despite optimized oral antiparkinsonian medication. This is a well-documented and useful study with clear clinical therapeutic implications.

Neuron Loss in Preclinical Alzheimer Disease

In an elegant and well-controlled study, Price and colleagues show that there is little or no neuronal loss with aging or with preclinical Alzheimer disease (AD) but substantial loss with very mild AD. Their findings support the hypothesis that the neuropathologic burden of AD results in clinical deficits only when it produces significant neuronal loss. These clinical neuropathologic correlative findings are crucial to differentiate mild cognitive impairment from real AD.

Prefrontal Cortex in Aging and Alzheimer Disease

Salat and colleagues show that the orbital prefrontal cortex (PFC) is selectively preserved in healthy oldest old subjects. In contrast, degeneration within the PFC in Alzheimer disease is most prominent in the inferior PFC subregion. Thus, degeneration within the PFC has a sensitive and regionally distinct pattern, which differentiates healthy aging from Alzheimer disease.

Microembolism During Stenting and Angioplasty

Orlandi et al point out that cerebral microembolism is a common event, especially during guide-wire angioplasty alone as compared with stenting procedures. Stenting appears to be safer than angioplasty alone, and this important finding needs to be considered in stroke-prevention therapy.

Notch3 Gene Mutation With CADASIL

Oliveri et al emphasize the role of direct DNA sequence analysis for the diagnosis of CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy). They describe sequence analysis of the Notch3 gene and show a new missense mutation in codon 332 of exon 6, resulting in the replacement of an arginine residue with a cysteine.

Serotonin Transporter in Alzheimer Disease

Sukonick and colleagues have studied the serotonin transporter promoter region polymorphisms associated with behavior in patients with Alzheimer disease (AD). The *L/*L genotype was significantly associated with aggression in AD subjects. Similar results were obtained for the *L allele. Thus, increased expression of the transporter protein and increased speed of response to serotonin uptake inhibitor treatment may indicate the logical next step in managing aggressive behaviors in AD.

Neuroserpin Disease

Bradshaw and colleagues describe the cognitive and neurophysiological changes exhibited by individuals suffering from familial encephalopathy with neuroserpin inclusion bodies. Six of the 9 family members studied carried the disease mutation in the neuroserpin gene, which codes for a brain-specific serine protease inhibitor, neuroserpin. All subjects with the mutation had cognitive changes. This syndrome represents another form of frontal and frontal-subcortical degeneration.

Diphtheritic Polyneuropathy

Piradov and colleagues describe their experience with an epidemic of diphtheria that occurred between 1990 and 1995. The clinical features, the time of onset of neurological involvement after clinical infection, morbidity, and mortality are reviewed in 32 patients. On average, the symptoms of polyneuropathy manifested 30 days after the onset of diphtheria. Latency between onset of infection and polyneuropathy was shorter in patients with the most severe neurological disorders. Diphtheria and diphtheritic polyneuropathy are still with us in the 21st century on a worldwide basis, and these observations are of great value in reminding us of this serious infectious disease.

Uncoupling of the Eye and Mind in Aging

Mapstone and colleagues describe visual attention abilities in young and older normal subjects and patients with Alzheimer disease (AD). Of note, young subjects maintain central eye position regardless of peripheral distraction, whereas older subjects and patients with mild AD move their eyes to the periphery, presumably to widen the window of attention. These points are of interest in considering cognitive and memory functions with aging and AD.

Unfulfilled Therapy for Machado-Joseph Disease

Schulte and colleagues have carefully studied the efficacy of trimethoprim-sulfamethoxazole (TMS) in patients with spinal cerebellar ataxia type 3 or Machado-Joseph disease (MJD). Contrasting previous reports on smaller numbers of patients, TMS did not improve the neurological status of MJD patients in this study. It cannot be recommended as a form of therapy for MJD.