Friedreich’s ataxia affects the cortical processing of tactile novelty detection
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1
Neurolygy depatrment, Hôpital Erasme, Université libre de Bruxelles (ULB), Belgium
Background : The mismatch negativity (MMN) is a novelty detection response evoked by deviant stimuli embedded in sequences of standard stimuli. In the somatosensory system, the MMN is generated at contralateral secondary somatosensory cortex (cS2). Previous studies have shown that the cerebellum is part of the somatosensory novelty detection network and that patients with unilateral cerebellar lesion have no or weaker somatosensory MMN (sMMN). Friedreich’s ataxia (FA) is a genetic disorder associated with a selective atrophy of the cerebellar dentate nucleus, which is a key node of the efferent dentatothalamic tract. So, FA may prove a good model to study the role of the cerebellum in tactile novelty detection.
Methods : 13 right-handed FA patients (9 females; 29 years (range 9-46), mean scale for the assessment and rating of ataxia (SARA): 23 (range 14-37.5), shorter allele (GAA1) mean expansion 688 (range 280-100) and 8 right-handed healthy adults (3 females, 29 years (range 23-45)) were measured with whole-scalp-covering magnetoencephalography (MEG, EleKta Oy) while they underwent an tactile oddball paradigm. Standard stimuli were pneumatic tactile stimulations of the right index fingertip and deviant stimuli corresponded to similar tactile stimulation simultaneously applied to the first two phalanxes of the index finger. Mismatch negativity responses associated with deviants were investigated at the sensor level. sMMN responses were assessed in the sensor space using non-parametric cluster statistics. sMMN neural sources were localized using conventional equivalent current dipole modeling. Post-hoc paired t-tests were applied on the corresponding sources intensity (standards or deviants) at the timing of maximum source amplitude within the time frame disclosed by sensor-level analyses.
Results: In healthy subjects, standard stimuli evoked responses at contralateral primary somatosensory cortex (cSI) with a mean latency of 23.75ms (range 15-33ms) and mean amplitude of 9 mA (range 6-16mA) and contralateral secondary somatosensory cortex (cSII) with a mean latency of 48.7ms (range 55-80 ms) and mean amplitude of 9.44 mA (range 7-19mA). Deviant stimuli led to a mean amplitude at cSI of 11.7 mA (range 9-19 mA) and mean amplitude at cSII of 23,7 mA (range 8,5-37 mA) leading to significant msMMN only at cSII. In FA patients, standards stimuli evoked at cSI in 12/13 patients with a mean latency of 65 ms (range: 50-80ms) for a mean amplitude of 7,4 mA (range 1,8-15,1mA) and cSII in 11/13 FA patients with a mean latency of 120ms (range 74-149 ms) and a mean amplitude of 6,2 mA (range 0,6-11 mA). Deviant stimuli led to a mean amplitude of 13,4 mA (range 4,4-34,4 mA) at cS1 and of 15,2 mA (7,2-31,4 mA) leading to a statistically significant mismatch both at cSI and cSII. Latency of cortical responses were significantly longer in FA patients. Still there was no correlation between SARA scores, GAA1 expansion, the latency or the amplitude of SEFs.
Conclusions: Somatosensory evoked fields are reliably found at cSI and CSII cortices with MEG in FA patients. Cerebellar dorsal nuclei atrophy in FA affects the cortical processing of tactile novelty detection with an increase is cSI and a decrease in cSII cortical responses.
Résumé en Français:
Lorsque le système tactile est stimulé, des ondes électriques peuvent être mesurées au niveau du cortex somato-sensoriel situé dans la partie haute et centrale de notre cerveau. L’arrivée de l’information tactile est détectée au niveau du cortex primaire tandis que des informations plus complexes génèrent une activité électrique dans le cortex secondaire. Dans cette étude, nous nous intéressons à la détection de nouveauté, c’est-à-dire la détection d’une stimulation tactile différente dans une suite de stimulations standards. Cette nouveauté induit une activité électrique dans le cortex secondaire qui peut être mesurée par magnétoencéphalographie. Des études précédentes ont suggéré que le cervelet pouvait jouer un rôle dans notre capacité à détecter la nouveauté. Afin de confirmer cette hypothèse, nous avons étudié ce phénomène chez les patients atteints d’ataxie de Friedriech car ils présentent une atrophie du cervelet et avons mis en évidence des modifications de la réponse électrique à la nouveauté chez ces patients.
Samenvatting in het Nederlands:
Wanneer het tastsysteem geprikkeld wordt, kunnen elektrische golven gemeten worden op de somatosensoriele hersenschors, centraal aan de bovenzijde van de hersenen. Deze tast-informatie is aanwijsbaar op het primaire niveau van de hersenschors, meer complexe informatie veroorzaakt een elektrische activiteit in de secundaire hersenschors. In deze studie richtten we ons op het ontdekken van nieuwe, anders dan gewone tastzinprikkels, binnen een reeks van standaardprikkels. Deze nieuwigheid leidt tot een elektrische activiteit in de secundaire cortex die kan gemeten worden door middel van magneto-encefalografie. Eerdere studies suggereerden dat de kleine hersenen een rol kunnen spelen in het ontdekken van nieuwigheden. Om deze hypothese te toetsen hebben we dit fenomeen bestudeerd bij patiënten die lijden aan de ataxie van Friedreich, gezien ze een atrofie van de kleine hersenen vertonen en we konden bewijzen dat er een wijziging is in de elektrische reactie op nieuwigheden bij deze patiënten.
Keywords:
Magnetoencephalography (MEG),
mismatch negativity (MMN),
somatosensory,
Friedreich Ataxia,
Cerebellum
Conference:
6th Belgian Brain Congress, MONS, Belgium, 8 Oct - 8 Oct, 2016.
Presentation Type:
Poster Presentation
Topic:
Brain and brain diseases: between heredity and environment
Citation:
Naeije
G,
Marty
B,
Wens
V,
Goldman
S,
Pandolfo
M and
De Tiège
X
(2016). Friedreich’s ataxia affects the cortical processing of tactile novelty detection.
Conference Abstract:
6th Belgian Brain Congress.
doi: 10.3389/conf.fnagi.2016.03.00073
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Received:
14 Jul 2016;
Published Online:
14 Jul 2016.
*
Correspondence:
Dr. Gilles Naeije, Neurolygy depatrment, Hôpital Erasme, Université libre de Bruxelles (ULB), brussels, Belgium, gilles.naeije@erasme.ulb.ac.be