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November 10 Highlights

Severely painful feet are one of the most common problems seen by the peripheral neurologist. There are two articles in this issue on the use of skin punch biopsy for the study of unmyelinated sensory nerves as an approach to assessing this problem. The article by Herrmann et al. (p. 1634) shows that skin biopsy can define abnormalities not detected by sural nerve biopsy. A prospective study by Periquet et al. (p. 1641) shows that skin biopsy is the only way to identify diagnostic abnormalities in up to one-third of patients. The accompanying editorial by Kennedy and Said (p. 1614) considers the importance of the articles and suggests that skin biopsy should be used instead of sural nerve biopsy for diagnosis in some instances.

Fatigue

The patient who complains of fatigue seldom has a neuromuscular disease to account for the symptom. The article by Merkies et al. (p. 1648) studied 113 patients with neuropathies: Guillain-Barré syndrome, chronic inflammatory demyelinating peripheral neuropathy, and neuropathy with MGUS. Somewhat surprisingly, 80% of patients had fatigue, including the majority of those with normal strength, even years after recovering from the neuropathy.

MS: Effect of interferon beta on a surrogate marker and on T-cell responses

Whereas the frequency of MS attacks can be decreased by treatment, MS often progresses without clinically evident attacks. Biomarkers that detect this progression have been reported in several Neurology issues this year. In this issue, Rudick et al. (p. 1698) found progressive loss of brain parenchyma during a 2-year study of patients with relapsing-remitting MS. This loss of brain parenchyma (detected by MRI) was not evident by clinical findings. Patients taking interferon (IFN) ß-1a had a decrease in the rate of loss of brain parenchyma. Kozovska et al. (p. 1692) studied the effect of IFNß-1a on T-cells that react with myelin basic protein. IFNß both suppressed these T-cells and shifted the cytokine profile produced by T-cells. Both effects could contribute to the benefit of IFNß in MS.

MS: Pathogenesis

Two articles consider the pathogenesis of MS. Dowling et al. (p. 1676) investigated the cause of programed cell death (apoptosis). They show that a neurotrophin receptor is upregulated in MS. The accompanying Editorial by Rodriguez and Lucchinetti (p. 1615) considers the importance of oligodendrocyte death in terms of MS pathogenesis. De Keyser et al. (p. 1628) studied astrocytic ₂ adrenergic receptors in postmortem brain in MS patients and appropriate disease and normal controls. They found an absence of ₂ adrenergic receptors on MS microglia. This lack could result in heightened autoimmunity in MS, as ₂ adrenergic receptors can prevent the induction of major histocompatibility complex class 2 antigens.

Epilepsy

Duchowny et al. (p. 1724) studied 201 children (at 40 sites) with various partial epilepsies and found that adding lamotrigine significantly reduced seizure frequency. The drug was well-tolerated by most lamotrigine-treated patients but caused ataxia, tremor, and nausea in a small percentage of patients. Morris et al. (p. 1731) sought follow-up data on 454 patients who underwent implantation of a pulse generator for vagal nerve stimulation (VNS). The VNS patients had been studied in five clinical trials; 440 patients had data for study. Use of VNS declined each year but remained at 72% after 3 years. Seizure reduction persisted in this group. Hoarseness was a persistent complication. Although this follow-up study was uncontrolled, it suggests that the VNS benefits seen in acute trials continue during long-term use of the treatment.

Essential tremor

There is now substantial evidence that thalamic stimulation reduces the severity of essential tremor. Tröster et al. (p. 1774) evaluated the effects of the procedure on cognition, mood, and quality of life. They found improvement not only in tremor, but also on visuomotor coordination and on a number of cognitive measures. Quality of life also improved.

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