Rechdi Ahdab

Analgesic effects of repetitive transcranial magnetic stimulation of the motor cortex in neuropathic pain: Influence of theta burst stimulation priming

‘Conventional’ protocols of high‐frequency repetitive transcranial magnetic stimulation (rTMS) delivered to M1 can produce analgesia. Theta burst stimulation (TBS), a novel rTMS paradigm, is thought to produce greater changes in M1 excitability than ‘conventional’ protocols. After a preliminary experiment showing no analgesic effect of continuous or intermittent TBS trains (cTBS or iTBS) delivered to M1 as single procedures, we used TBS to prime a subsequent session of ‘conventional’ 10 Hz‐rTMS.

Fatigue in Multiple Sclerosis: Neural Correlates and the Role of Non-Invasive Brain Stimulation

Multiple sclerosis (MS) is a chronic progressive inflammatory disease of the central nervous system (CNS) and the major cause of non-traumatic disability in young adults. Fatigue is a frequent symptom reported by the majority of MS patients during their disease course and drastically affects their quality of life. Despite its significant prevalence and impact, the underlying pathophysiological mechanisms are not well elucidated. MS fatigue is still considered the result of multifactorial and complex constellations, and is commonly classified into “primary” fatigue related to the pathological changes of the disease itself, and “secondary” fatigue attributed to mimicking symptoms, comorbid sleep and mood disorders, and medications side effects. Radiological, physiological, and endocrine data have raised hypotheses regarding the origin of this symptom, some of which have succeeded in identifying an association between MS fatigue and structural or functional abnormalities within various brain networks. Hence, the aim of this work is to reappraise the neural correlates of MS fatigue and to discuss the rationale for the emergent use of noninvasive brain stimulation (NIBS) techniques as potential treatments. This will include a presentation of the various NIBS modalities and a suggestion of their potential mechanisms of action in this context. Specific issues related to the value of transcranial direct current stimulation (tDCS) will be addressed.

Relapses in multiple sclerosis: effects of high-dose steroids on cortical excitability

High‐dose steroid administration is the usual treatment of multiple sclerosis (MS) relapse, but it remains to determine whether this treatment may act by changing the excitability of cortical circuitry.

Effects of left DLPFC versus right PPC tDCS on multiple sclerosis fatigue.

BACKGROUND AND OBJECTIVE Fatigue is a frequent and debilitating symptom in patients with multiple sclerosis (MS). Its classical treatments are still faced with limited benefits and numerous side effects. Hence, we aimed to evaluate the effects of transcranial direct current stimulation (tDCS), a noninvasive brain stimulation technique, on such a challenging symptom. Our secondary outcomes included the assessment of tDCS impact on mood and attentional performance. METHODS Ten fatigued MS patients were enrolled in a double-blind, sham-controlled, and cross-over study. Each patient randomly received three anodal tDCS blocks: active stimulation over the left dorsolateral prefrontal cortex (DLPFC), active stimulation over the right posterior parietal cortex (PPC), and sham stimulation over either cortical site. Both cortical targets are key components in the MS fatigue networks. The blocks consisted of five consecutive daily sessions and were held apart by a washout interval of three weeks. RESULTS Only active left DLPFC stimulation significantly ameliorated fatigue. Mood improvement was exclusively obtained following active right PPC stimulation. Neither intervention had effects on attention. CONCLUSION Our study supports the role of anodal tDCS over the left prefrontal in treating MS fatigue. The lack of tDCS effects on attention might be related to the heterogeneity of the studied cohort, the relatively small sample size, the protocol design and duration. Modifying these variables and coupling tDCS with neuroimaging might improve the clinical outcomes and enhance our understanding of the tDCS mechanism of actions.

Reappraisal of the Anatomical Landmarks of Motor and Premotor Cortical Regions for Image-Guided Brain Navigation in TMS Practice

Image‐guided navigation systems dedicated to transcranial magnetic stimulation (TMS) have been recently developed and offer the possibility to visualize directly the anatomical structure to be stimulated. Performing navigated TMS requires a perfect knowledge of cortical anatomy, which is very variable between subjects. This study aimed at providing a detailed description of sulcal and gyral anatomy of motor cortical regions with special interest to the inter‐individual variability of sulci. We attempted to identify the most stable structures, which can serve as anatomical landmarks for motor cortex mapping in navigated TMS practice. We analyzed the 3D reconstruction of 50 consecutive healthy adult brains (100 hemispheres). Different variants were identified regarding sulcal morphology, but several anatomical structures were found to be remarkably stable (four on dorsoventral axis and five on rostrocaudal axis). These landmarks were used to define a grid of 12 squares, which covered motor cortical regions. This grid was used to perform motor cortical mapping with navigated TMS in 12 healthy subjects from our cohort. The stereotactic coordinates (x‐y‐z) of the center of each of the 12 squares of the mapping grid were expressed into the standard Talairach space to determine the corresponding functional areas. We found that the regions whose stimulation produced almost constantly motor evoked potentials mainly correspond to the primary motor cortex, with rostral extension to premotor cortex and caudal extension to posterior parietal cortex. Our anatomy‐based approach should facilitate the expression and the comparison of the results obtained in motor mapping studies using navigated TMS. Hum Brain Mapp 35:2435–2447, 2014.

Reversible Vertebral Artery Stenosis following Corticotherapy in Giant Cell Arteritis

Accessible online at: www.karger.com/ene Fig. 1. Initial cervical MRA revealing severe stenosis of both vertebral arteries (left). Following steroids, significant repermeabilization of the vertebral arteries (middle, right). The level of stenosis is identical in both arteries and corresponds to the junction between the intracranial and extracranial portions. Fig. 2. Sagittal T 2 -weighted MRI revealing widespread cerebellar stroke.

Analgesic effects of navigated motor cortex rTMS in patients with chronic neuropathic pain.

Repetitive transcranial magnetic stimulation (rTMS) can relieve neuropathic pain when applied at high frequency (HF: 5–20 Hz) over the primary motor cortex (M1), contralateral to pain side. In most studies, rTMS is delivered over the hand motor hot spot (hMHS), whatever pain location. Navigation systems have been developed to guide rTMS targeting, but their value to improve rTMS efficacy remains to be demonstrated.

Rapidly progressive amyotrophic lateral sclerosis initially masquerading as a demyelinating neuropathy.

Rare cases of demyelinating neuropathy have been described in association with amyotrophic lateral sclerosis (ALS). We report two patients with typical ALS whose initial electroneuromyographic (ENMG) presentation could suggest the existence of a process of motor nerve fiber demyelination. However, subsequent ENMG examinations and the fatal course of the disease in a few months rather supported severe ongoing axonal degeneration at the origin of motor nerve conduction abnormalities. Repeated examinations could be required to distinguish between ENMG features of concomitant demyelinating neuropathy and rapidly progressive motor neuron loss in ALS.

Congenital agenesis of internal carotid artery with ipsilateral Horner presenting as focal neurological symptoms

Internal carotid artery (ICA) agenesis is a rare developmental anomaly and is most frequently asymptomatic, but it may also present as cerebrovascular accidents. The association with Horner’s syndrome is exceptional. We present three cases of agenesis of ICA associated with Horner’s syndrome and hypochromia iridum presenting as focal neurological symptoms. A system of collaterals develops as a consequence of agenesis of the ICA, making the majority of cases asymptomatic. Three types of collateral circulations have been described. These collaterals increase the risk of aneurysm formation and the occurrence of life-threatening subarachnoid hemorrhages. The association of congenital Horner’s syndrome and hypochromia iridum without anhidrosis is highly suggestive of sympathetic pathway injury early in life. Such signs should prompt further diagnostic evaluation to demonstrate the presence of the agenesis of the carotid canal. Early diagnosis is essential to rule out potentially life-threatening associated vascular anomalies.

Neuropathy with anti-disialosyl IgM antibodies and multifocal persistent motor conduction blocks

In 1985, circulating IgM antibodies reacting with NeuAc(alpha2–8)NeuAc(alpha2–3)Gal-configured disialosyl gangliosides (including GD1b, GD3, GT1b, and GQ1b) were first described in a patient with chronic sensory neuropathy.1 The typical clinical picture of anti-disialosyl-associated neuropathy comprises marked sensory ataxia, areflexia, a relatively preserved motor function excepting ophtalmoplegia and a chronic or relapsing course.2 In half of the cases, IgM antibodies are also cold agglutinins, fulfilling all the conditions for the chronic ataxic neuropathy, ophthalmoplegia, monoclonal IgM protein, cold agglutinins and disialosyl antibodies (CANOMAD) syndrome. We report two patients with a chronic or relapsing sensory neuropathy and ophtalmoplegia associated with anti-disialosyl IgM antibodies who developed asymmetrical motor weakness related to multifocal persistent conduction blocks, an unusual feature in this context. A 39-year-old woman presented with gait ataxia and paraesthesias in the left foot. Paraesthesias spread up to both legs, and then to both hands within a year. Over the following year, ataxia worsened, and distal weakness appeared in the lower limbs, predominating on the left side. Clinical examination showed decreased sensation to all modalities in all four extremities, gait ataxia, dorsal and plantar flexion weakness, and absent tendon reflexes in the lower limbs. Six years after disease onset, she developed right hand and proximal lower limb weakness. Three years later, she presented with a right-sided ptosis …