Electrophysiological deterioration over time in patients with huntington's disease
Identifieur interne : 001A10 ( PascalFrancis/Corpus ); précédent : 001A09; suivant : 001A11Electrophysiological deterioration over time in patients with huntington's disease
Auteurs : Jean-Pascal Lefaucheur ; Isabelle Menard-Lefaucheur ; Patrick Maison ; Sophie Baudic ; Pierre Cesaro ; Marc Peschanski ; Anne-Catherine Bachoud-LeviSource :
- Movement disorders [ 0885-3185 ] ; 2006.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
In recent studies aimed at assessing the effects of original therapeutic strategies applied to patients with Huntington's disease (HD), we observed informative changes in electrophysiological results that recovered normal values in coherence with clinical improvement. However, longitudinal studies were lacking for determining whether electrophysiological test results evolve in parallel with clinical markers of the natural course of the disease and could consequently provide objective quantifiable markers of disease progression. For this purpose, electrophysiological testing was performed annually in a cohort of 20 patients with HD over a 2-year period (three examinations). The study included the recording of sympathetic skin responses and blink reflexes (BRs) to supraorbital nerve stimulation, long latency reflexes (LLRs) and somatosensory evoked potentials (SEPs) to median nerve stimulation, and cortical silent periods (CSPs) to transcranial magnetic stimulation. Clinical evaluation was based on the Total Functional Capacity scale (TFC) and the Motor part of the Unified Huntington's Disease Rating Scale (UHDRS). A significant deterioration with time was found for BR latency, LLR presence, various SEP parameters (parietal N20 peak amplitude and frontal N30 presence) and CSP duration. Attenuation of the N20 peak and CSP shortening correlated with functional decline, as assessed by the TFC score, whereas delayed BR and LLR abolition correlated with UHDRS Motor score deterioration. This study shows that several electrophysiological parameters are closely associated with dysfunction of various neural circuits in HD and could be useful markers of disease progression.
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Pour connaître la documentation sur le format Inist Standard.
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Format Inist (serveur)
NO : | PASCAL 06-0518086 INIST |
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ET : | Electrophysiological deterioration over time in patients with huntington's disease |
AU : | LEFAUCHEUR (Jean-Pascal); MENARD-LEFAUCHEUR (Isabelle); MAISON (Patrick); BAUDIC (Sophie); CESARO (Pierre); PESCHANSKI (Marc); BACHOUD-LEVI (Anne-Catherine) |
AF : | Service de Physiologie - Explorations Fonctionnelles, Hôpital Henri Mondor, AP-HP/Créteil/France (1 aut., 2 aut.); INSERM U421, IM3, Faculté de Médecine/Créteil/France (1 aut., 3 aut., 4 aut., 5 aut., 6 aut., 7 aut.); Service de Pharmacologie Clinique, Hôpital Henri Mondor, AP-HP/Créteil/France (3 aut.); Service de Neurologie, Hôpital Henri Mondor, AP-HP/Créteil/France (5 aut., 7 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2006; Vol. 21; No. 9; Pp. 1350-1354; Bibl. 32 ref. |
LA : | Anglais |
EA : | In recent studies aimed at assessing the effects of original therapeutic strategies applied to patients with Huntington's disease (HD), we observed informative changes in electrophysiological results that recovered normal values in coherence with clinical improvement. However, longitudinal studies were lacking for determining whether electrophysiological test results evolve in parallel with clinical markers of the natural course of the disease and could consequently provide objective quantifiable markers of disease progression. For this purpose, electrophysiological testing was performed annually in a cohort of 20 patients with HD over a 2-year period (three examinations). The study included the recording of sympathetic skin responses and blink reflexes (BRs) to supraorbital nerve stimulation, long latency reflexes (LLRs) and somatosensory evoked potentials (SEPs) to median nerve stimulation, and cortical silent periods (CSPs) to transcranial magnetic stimulation. Clinical evaluation was based on the Total Functional Capacity scale (TFC) and the Motor part of the Unified Huntington's Disease Rating Scale (UHDRS). A significant deterioration with time was found for BR latency, LLR presence, various SEP parameters (parietal N20 peak amplitude and frontal N30 presence) and CSP duration. Attenuation of the N20 peak and CSP shortening correlated with functional decline, as assessed by the TFC score, whereas delayed BR and LLR abolition correlated with UHDRS Motor score deterioration. This study shows that several electrophysiological parameters are closely associated with dysfunction of various neural circuits in HD and could be useful markers of disease progression. |
CC : | 002B17; 002B17G; 002B17F |
FD : | Système nerveux pathologie; Chorée Huntington; Détérioration; Homme; Programme; Réflexe palpébral; Potentiel évoqué somatosensoriel; Période muette; Stimulation magnétique transcrânienne |
FG : | Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Maladie héréditaire; Système nerveux central pathologie; Electrophysiologie |
ED : | Nervous system diseases; Huntington disease; Deterioration; Human; Program; Palpebral reflex; Somatosensory evoked potential; Silent period; Transcranial magnetic stimulation |
EG : | Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Genetic disease; Central nervous system disease; Electrophysiology |
SD : | Sistema nervioso patología; Corea Huntington; Deterioración; Hombre; Programa; Reflejo palpebral; Potencial evocado somatosensorial |
LO : | INIST-20953.354000158780860080 |
ID : | 06-0518086 |
Links to Exploration step
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<front><div type="abstract" xml:lang="en">In recent studies aimed at assessing the effects of original therapeutic strategies applied to patients with Huntington's disease (HD), we observed informative changes in electrophysiological results that recovered normal values in coherence with clinical improvement. However, longitudinal studies were lacking for determining whether electrophysiological test results evolve in parallel with clinical markers of the natural course of the disease and could consequently provide objective quantifiable markers of disease progression. For this purpose, electrophysiological testing was performed annually in a cohort of 20 patients with HD over a 2-year period (three examinations). The study included the recording of sympathetic skin responses and blink reflexes (BRs) to supraorbital nerve stimulation, long latency reflexes (LLRs) and somatosensory evoked potentials (SEPs) to median nerve stimulation, and cortical silent periods (CSPs) to transcranial magnetic stimulation. Clinical evaluation was based on the Total Functional Capacity scale (TFC) and the Motor part of the Unified Huntington's Disease Rating Scale (UHDRS). A significant deterioration with time was found for BR latency, LLR presence, various SEP parameters (parietal N20 peak amplitude and frontal N30 presence) and CSP duration. Attenuation of the N20 peak and CSP shortening correlated with functional decline, as assessed by the TFC score, whereas delayed BR and LLR abolition correlated with UHDRS Motor score deterioration. This study shows that several electrophysiological parameters are closely associated with dysfunction of various neural circuits in HD and could be useful markers of disease progression.</div>
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<fC03 i1="02" i2="X" l="ENG"><s0>Huntington disease</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Corea Huntington</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Détérioration</s0>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Deterioration</s0>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Deterioración</s0>
<s5>09</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Homme</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Human</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Hombre</s0>
<s5>10</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Programme</s0>
<s5>11</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Program</s0>
<s5>11</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Programa</s0>
<s5>11</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Réflexe palpébral</s0>
<s5>12</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Palpebral reflex</s0>
<s5>12</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Reflejo palpebral</s0>
<s5>12</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Potentiel évoqué somatosensoriel</s0>
<s5>13</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Somatosensory evoked potential</s0>
<s5>13</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Potencial evocado somatosensorial</s0>
<s5>13</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Période muette</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Silent period</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Stimulation magnétique transcrânienne</s0>
<s4>CD</s4>
<s5>97</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Transcranial magnetic stimulation</s0>
<s4>CD</s4>
<s5>97</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Encéphale pathologie</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Maladie héréditaire</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Genetic disease</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Enfermedad hereditaria</s0>
<s5>40</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>41</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Electrophysiologie</s0>
<s5>42</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Electrophysiology</s0>
<s5>42</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Electrofisiología</s0>
<s5>42</s5>
</fC07>
<fN21><s1>338</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
<server><NO>PASCAL 06-0518086 INIST</NO>
<ET>Electrophysiological deterioration over time in patients with huntington's disease</ET>
<AU>LEFAUCHEUR (Jean-Pascal); MENARD-LEFAUCHEUR (Isabelle); MAISON (Patrick); BAUDIC (Sophie); CESARO (Pierre); PESCHANSKI (Marc); BACHOUD-LEVI (Anne-Catherine)</AU>
<AF>Service de Physiologie - Explorations Fonctionnelles, Hôpital Henri Mondor, AP-HP/Créteil/France (1 aut., 2 aut.); INSERM U421, IM3, Faculté de Médecine/Créteil/France (1 aut., 3 aut., 4 aut., 5 aut., 6 aut., 7 aut.); Service de Pharmacologie Clinique, Hôpital Henri Mondor, AP-HP/Créteil/France (3 aut.); Service de Neurologie, Hôpital Henri Mondor, AP-HP/Créteil/France (5 aut., 7 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2006; Vol. 21; No. 9; Pp. 1350-1354; Bibl. 32 ref.</SO>
<LA>Anglais</LA>
<EA>In recent studies aimed at assessing the effects of original therapeutic strategies applied to patients with Huntington's disease (HD), we observed informative changes in electrophysiological results that recovered normal values in coherence with clinical improvement. However, longitudinal studies were lacking for determining whether electrophysiological test results evolve in parallel with clinical markers of the natural course of the disease and could consequently provide objective quantifiable markers of disease progression. For this purpose, electrophysiological testing was performed annually in a cohort of 20 patients with HD over a 2-year period (three examinations). The study included the recording of sympathetic skin responses and blink reflexes (BRs) to supraorbital nerve stimulation, long latency reflexes (LLRs) and somatosensory evoked potentials (SEPs) to median nerve stimulation, and cortical silent periods (CSPs) to transcranial magnetic stimulation. Clinical evaluation was based on the Total Functional Capacity scale (TFC) and the Motor part of the Unified Huntington's Disease Rating Scale (UHDRS). A significant deterioration with time was found for BR latency, LLR presence, various SEP parameters (parietal N20 peak amplitude and frontal N30 presence) and CSP duration. Attenuation of the N20 peak and CSP shortening correlated with functional decline, as assessed by the TFC score, whereas delayed BR and LLR abolition correlated with UHDRS Motor score deterioration. This study shows that several electrophysiological parameters are closely associated with dysfunction of various neural circuits in HD and could be useful markers of disease progression.</EA>
<CC>002B17; 002B17G; 002B17F</CC>
<FD>Système nerveux pathologie; Chorée Huntington; Détérioration; Homme; Programme; Réflexe palpébral; Potentiel évoqué somatosensoriel; Période muette; Stimulation magnétique transcrânienne</FD>
<FG>Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Maladie héréditaire; Système nerveux central pathologie; Electrophysiologie</FG>
<ED>Nervous system diseases; Huntington disease; Deterioration; Human; Program; Palpebral reflex; Somatosensory evoked potential; Silent period; Transcranial magnetic stimulation</ED>
<EG>Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Genetic disease; Central nervous system disease; Electrophysiology</EG>
<SD>Sistema nervioso patología; Corea Huntington; Deterioración; Hombre; Programa; Reflejo palpebral; Potencial evocado somatosensorial</SD>
<LO>INIST-20953.354000158780860080</LO>
<ID>06-0518086</ID>
</server>
</inist>
</record>
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