F. Then Bergh

Stress regulation in multiple sclerosis-current issues and concepts

Since its first description by Charcot, psychological stress has been considered a triggering factor for exacerbations in multiple sclerosis, but until recently the clinical evidence for a causal relation was weak. Over the past years, a growing number of studies have started to elucidate this association and highlight potential mechanisms, including brain-immune communication. On 5 June 2005, a panel of international researchers discussed the current evidence. This article summarizes the observational, animal experimental, as well as human experimental findings on stress regulation in MS, as well as studies on the functioning of the major stress response systems, ie, the hypothalamo-pituitary-adrenal (HPA) axis and the autonomous nervous system (ANS) in MS. Consensus statements from the group to these aspects are given. Research objectives and strategies are delineated, as well as clinical implications. Multiple Sclerosis 2007; 13: 143–148. http://msj.sagepub.com

Subcortical Right Parietal AVM Rotational vertigo and caloric stimulation fMRI support a parietal representation of vestibular input.

Sirs: Cortical vestibular projection areas in humans have been identified by functional magnetic resonance imaging (fMRI) [5, 10, 13], SPECT [14] and PET [2]. Intracerebral electrical stimulation in epilepsy patients has confirmed many of these results [7]. The parietoinsular cortex appears to be the dominant region, with right-sided accentuation [3], with additional temporal and frontal regions [2, 5, 10, 13]. The most essential afferent vestibular pathway is thought to run via the nucleus ventralis posterior inferior thalami to a cortical parietal region around the intraparietal sulcus [12]. Clinically, supratentorial lesions as the cause of vestibular disorders with rotational vertigo have rarely been documented [1, 4, 8]. A 26-year-old man presented with rotational vertigo and a feeling of body traction and tilt to the right side (“as if making a right turn on a bicycle”), with no associated nausea or auditory disturbance. Symptoms lasted for several hours, waxing and waning. Similar symptoms had occurred and spontaneously remitted once before. He had suffered an intraventricular supratentorial hemorrhage six years earlier, when investigations including digital subtraction angiography (DSA) were normal. The neurological examination was entirely normal, including a comprehensive set of neuro-ophthalmological and neuro-otological bed-side tests. Caloric stimulation revealed regular excitability of the vestibular apparatus bilaterally without pathological nystagmus. There was no hypacusis. Routine EEG, performed on two separate occasions, was normal. Cranial MRI detected a hyperintense lesion of approximately 7 mm in the parietal white matter adjacent to the posterior horn of the right lateral ventricle (Fig. 1a) with punctate contrast enhancement and signal voids (Fig. 1b). There was no evidence for prior parenchymal hemorrhage on T2*weighted gradient echo images, and no abnormalities in the brainstem or cerebellum. An arteriovenous malformation (AVM) was suspected and confirmed by DSA (Fig. 1c). Functional MRI was performed with caloric stimulation (separate cold-water (4°C) irrigation of right and left external meatus [13]). Leftsided stimulation led to activation in the inferior parietal lobulus and the supramarginal gyrus bilaterally, predominantly on the right side (Fig. 2). This result is consisLETTER TO THE EDITORS

Morbus Wilson und Multiple Sklerose

Wilsons disease is a rare autosomal recessive disorder of hepatic copper transport leading to hepatic but also to highly variable neurological symptoms with basal ganglia and cerebellar manifestation. Symptoms, signs and results of investigations can overlap with those of other central nervous system disorders such as multiple sclerosis and sometimes delay diagnosis.We report on a 38-year-old male patient who was diagnosed with a hepatic form of Wilsons disease at age 12 and with multiple sclerosis at age 38. Intravenous radio copper test confirmed the diagnosis of Wilsons disease. Multiple sclerosis was diagnosed after occurrence of transient sensory disturbances in both legs, based on typical changes on MRI over the course of 2 years, in the cerebrospinal fluid and in multimodal evoked potentials.Although Wilsons disease and multiple sclerosis are known as distinct diseases with a completely different pathophysiology, symptoms and results of evoked potentials overlap, and they share a common historic background. Similarities and differences of both disorders are discussed.

Corticosteroid receptor expression and in vivo glucocorticoid sensitivity in multiple sclerosis

To estimate the efficiency of glucocorticoid signaling in multiple sclerosis in vivo, we measured mRNA expression of glucocorticoid receptor (GR), mineralocorticoid receptor (MR) and four genes regulated by GR and implicated in immune function, in whole blood. GR expression and MR expression were significantly lower in 52 patients than in 18 controls. In contrast, expression of GR regulated genes was increased (significantly for glucocorticoid induced leucine zipper, GILZ), especially in mildly impaired patients. Reduced GR expression appears to be compensated, either by hyperactive hypothalamo-pituitary-adrenal axis or by intracellular adaptations.