Neuropsychiatric assessment of Gilles de la Tourette patients: Comparative study with other hyperkinetic and hypokinetic movement disorders
Identifieur interne : 002887 ( PascalFrancis/Corpus ); précédent : 002886; suivant : 002888Neuropsychiatric assessment of Gilles de la Tourette patients: Comparative study with other hyperkinetic and hypokinetic movement disorders
Auteurs : Jaime Kulisevsky ; Irene Litvan ; Marcelo L. Berthier ; Berta Pascual-Sedano ; Jane S. Paulsen ; Jeffrey L. CummingsSource :
- Movement disorders [ 0885-3185 ] ; 2001.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
The role of the basal ganglia in conditions with co-occurring movement disorders and neuropsychiatric symptoms is not well known. It has been hypothesized that hyperkinesia -disinhibited behaviors and hypokinesia-inhibited behaviors result from an imbalance between the direct and indirect striatal output pathways, and that differential involvement of these pathways could account for the concurrent abnormalities in movement and behavior observed in these disorders. This study aimed to evaluate whether the pattern and the extent of the neuropsychiatric manifestations of patients with GTS, a hyperkinetic movement disorder of basal ganglia origin, differs from that of patients with other basal ganglia hyperkinetic (e.g., HD) or hypokinetic (e.g., PSP) movement disorders, and to determine whether patients with GTS show a greater frequency of hyperactive behaviors (e.g., agitation, irritability, euphoria, or anxiety) than PSP patients, and are comparable to patients with HD. The Neuropsychiatric Inventory (NPI), a scale with established validity and reliability, was administered to 26 patients with GTS (mean age, 30.2 ± 2.2 years), and the results were compared with that of 29 patients with HD (mean ages 43.8 ± 2 years) and 34 with PSP (mean ± S.D. age, 66.6 ± 1.2 years). There was no difference between the groups in the total NPI scores. However, there was a double dissociation in behaviors: patients with hyperkinetic disorders (HD and GTS) exhibited significantly more agitation, irritability, anxiety, euphoria, and hyperkinesia, whereas hypokinetic patients (PSP) exhibited more apathy. Patients with GTS showed greater scores than HD patients in all those scores differentiating HD and GTS from PSP patients (e.g., agitation, irritability, anxiety and euphoria), and were differentiated in a logistic regression analysis from both HD and PSP patients in having significantly more anxiety. We found that patients with GTS manifested predominantly hyperactive behaviors similar but more pronounced than those presented by patients with HD, while those with PSP manifested hypoactive behaviors. Based on our findings and the proposed models of basal ganglia dysfunction in these disorders, we suggest that the hyperactive behaviors in GTS are comparable to those observed in HD, being both secondary to an excitatory subcortical output through the medial and orbitofrontal cortical circuits, while in PSP the hypoactive behaviors are secondary to hypostimulation of these circuits. Abnormalities of other brain structures (e.g., amygdala, brainstem nuclei) may account for the significantly higher anxiety scores differentiating GTS from HD patients.
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Format Inist (serveur)
| NO : | PASCAL 02-0176680 INIST |
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| ET : | Neuropsychiatric assessment of Gilles de la Tourette patients: Comparative study with other hyperkinetic and hypokinetic movement disorders |
| AU : | KULISEVSKY (Jaime); LITVAN (Irene); BERTHIER (Marcelo L.); PASCUAL-SEDANO (Berta); PAULSEN (Jane S.); CUMMINGS (Jeffrey L.) |
| AF : | Movement Disorders Unit, Department of Neurology, Sant Pau Hospital, Autonomous University of Barcelona/Espagne (1 aut., 4 aut.); Cognitive Neuropharmacology Unit, Defense & Veteran Head Injury Program, Henry M. Jackson Foundation/Bethesda, Maryland/Etats-Unis (2 aut.); Neurology and Dermatology Department, University of Málaga/Espagne (3 aut.); Departments of Psychiatry and Neurology, University of Iowa/Iowa City, Iowa/Etats-Unis (5 aut.); Departments of Neurology and Psychiatry and Biobehavioral Science, University of California at Los Angeles School of Medicine/Los Angeles, California/Etats-Unis (6 aut.) |
| DT : | Publication en série; Niveau analytique |
| SO : | Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2001; Vol. 16; No. 6; Pp. 1098-1104; Bibl. 65 ref. |
| LA : | Anglais |
| EA : | The role of the basal ganglia in conditions with co-occurring movement disorders and neuropsychiatric symptoms is not well known. It has been hypothesized that hyperkinesia -disinhibited behaviors and hypokinesia-inhibited behaviors result from an imbalance between the direct and indirect striatal output pathways, and that differential involvement of these pathways could account for the concurrent abnormalities in movement and behavior observed in these disorders. This study aimed to evaluate whether the pattern and the extent of the neuropsychiatric manifestations of patients with GTS, a hyperkinetic movement disorder of basal ganglia origin, differs from that of patients with other basal ganglia hyperkinetic (e.g., HD) or hypokinetic (e.g., PSP) movement disorders, and to determine whether patients with GTS show a greater frequency of hyperactive behaviors (e.g., agitation, irritability, euphoria, or anxiety) than PSP patients, and are comparable to patients with HD. The Neuropsychiatric Inventory (NPI), a scale with established validity and reliability, was administered to 26 patients with GTS (mean age, 30.2 ± 2.2 years), and the results were compared with that of 29 patients with HD (mean ages 43.8 ± 2 years) and 34 with PSP (mean ± S.D. age, 66.6 ± 1.2 years). There was no difference between the groups in the total NPI scores. However, there was a double dissociation in behaviors: patients with hyperkinetic disorders (HD and GTS) exhibited significantly more agitation, irritability, anxiety, euphoria, and hyperkinesia, whereas hypokinetic patients (PSP) exhibited more apathy. Patients with GTS showed greater scores than HD patients in all those scores differentiating HD and GTS from PSP patients (e.g., agitation, irritability, anxiety and euphoria), and were differentiated in a logistic regression analysis from both HD and PSP patients in having significantly more anxiety. We found that patients with GTS manifested predominantly hyperactive behaviors similar but more pronounced than those presented by patients with HD, while those with PSP manifested hypoactive behaviors. Based on our findings and the proposed models of basal ganglia dysfunction in these disorders, we suggest that the hyperactive behaviors in GTS are comparable to those observed in HD, being both secondary to an excitatory subcortical output through the medial and orbitofrontal cortical circuits, while in PSP the hypoactive behaviors are secondary to hypostimulation of these circuits. Abnormalities of other brain structures (e.g., amygdala, brainstem nuclei) may account for the significantly higher anxiety scores differentiating GTS from HD patients. |
| CC : | 002B17G |
| FD : | Gilles de la Tourette syndrome; Trouble comportement; Psychopathologie; Chorée Huntington; Noyau gris central; Etude comparative; Physiopathologie; Homme |
| FG : | Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Maladie dégénérative; Extrapyramidal syndrome; Maladie héréditaire |
| ED : | Gilles de la Tourette syndrome; Behavioral disorder; Psychopathology; Huntington disease; Basal ganglion; Comparative study; Pathophysiology; Human |
| EG : | Nervous system diseases; Central nervous system disease; Cerebral disorder; Degenerative disease; Extrapyramidal syndrome; Genetic disease |
| SD : | Gilles de la Tourette síndrome; Trastorno conducta; Psicopatología; Corea Huntington; Núcleo basal; Estudio comparativo; Fisiopatología; Hombre |
| LO : | INIST-20953.354000094252170120 |
| ID : | 02-0176680 |
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Paulsen</name><affiliation><inist:fA14 i1="04"><s1>Departments of Psychiatry and Neurology, University of Iowa</s1><s2>Iowa City, Iowa</s2><s3>USA</s3><sZ>5 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Cummings, Jeffrey L" sort="Cummings, Jeffrey L" uniqKey="Cummings J" first="Jeffrey L." last="Cummings">Jeffrey L. Cummings</name><affiliation><inist:fA14 i1="05"><s1>Departments of Neurology and Psychiatry and Biobehavioral Science, University of California at Los Angeles School of Medicine</s1><s2>Los Angeles, California</s2><s3>USA</s3><sZ>6 aut.</sZ></inist:fA14></affiliation></author></analytic><series><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno><imprint><date when="2001">2001</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Basal ganglion</term><term>Behavioral disorder</term><term>Comparative study</term><term>Gilles de la Tourette syndrome</term><term>Human</term><term>Huntington disease</term><term>Pathophysiology</term><term>Psychopathology</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Gilles de la Tourette syndrome</term><term>Trouble comportement</term><term>Psychopathologie</term><term>Chorée Huntington</term><term>Noyau gris central</term><term>Etude comparative</term><term>Physiopathologie</term><term>Homme</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The role of the basal ganglia in conditions with co-occurring movement disorders and neuropsychiatric symptoms is not well known. It has been hypothesized that hyperkinesia -disinhibited behaviors and hypokinesia-inhibited behaviors result from an imbalance between the direct and indirect striatal output pathways, and that differential involvement of these pathways could account for the concurrent abnormalities in movement and behavior observed in these disorders. This study aimed to evaluate whether the pattern and the extent of the neuropsychiatric manifestations of patients with GTS, a hyperkinetic movement disorder of basal ganglia origin, differs from that of patients with other basal ganglia hyperkinetic (e.g., HD) or hypokinetic (e.g., PSP) movement disorders, and to determine whether patients with GTS show a greater frequency of hyperactive behaviors (e.g., agitation, irritability, euphoria, or anxiety) than PSP patients, and are comparable to patients with HD. The Neuropsychiatric Inventory (NPI), a scale with established validity and reliability, was administered to 26 patients with GTS (mean age, 30.2 ± 2.2 years), and the results were compared with that of 29 patients with HD (mean ages 43.8 ± 2 years) and 34 with PSP (mean ± S.D. age, 66.6 ± 1.2 years). There was no difference between the groups in the total NPI scores. However, there was a double dissociation in behaviors: patients with hyperkinetic disorders (HD and GTS) exhibited significantly more agitation, irritability, anxiety, euphoria, and hyperkinesia, whereas hypokinetic patients (PSP) exhibited more apathy. Patients with GTS showed greater scores than HD patients in all those scores differentiating HD and GTS from PSP patients (e.g., agitation, irritability, anxiety and euphoria), and were differentiated in a logistic regression analysis from both HD and PSP patients in having significantly more anxiety. We found that patients with GTS manifested predominantly hyperactive behaviors similar but more pronounced than those presented by patients with HD, while those with PSP manifested hypoactive behaviors. Based on our findings and the proposed models of basal ganglia dysfunction in these disorders, we suggest that the hyperactive behaviors in GTS are comparable to those observed in HD, being both secondary to an excitatory subcortical output through the medial and orbitofrontal cortical circuits, while in PSP the hypoactive behaviors are secondary to hypostimulation of these circuits. Abnormalities of other brain structures (e.g., amygdala, brainstem nuclei) may account for the significantly higher anxiety scores differentiating GTS from HD patients.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0885-3185</s0></fA01><fA03 i2="1"><s0>Mov. disord.</s0></fA03><fA05><s2>16</s2></fA05><fA06><s2>6</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Neuropsychiatric assessment of Gilles de la Tourette patients: Comparative study with other hyperkinetic and hypokinetic movement disorders</s1></fA08><fA11 i1="01" i2="1"><s1>KULISEVSKY (Jaime)</s1></fA11><fA11 i1="02" i2="1"><s1>LITVAN (Irene)</s1></fA11><fA11 i1="03" i2="1"><s1>BERTHIER (Marcelo L.)</s1></fA11><fA11 i1="04" i2="1"><s1>PASCUAL-SEDANO (Berta)</s1></fA11><fA11 i1="05" i2="1"><s1>PAULSEN (Jane S.)</s1></fA11><fA11 i1="06" i2="1"><s1>CUMMINGS (Jeffrey L.)</s1></fA11><fA14 i1="01"><s1>Movement Disorders Unit, Department of Neurology, Sant Pau Hospital, Autonomous University of Barcelona</s1><s3>ESP</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ></fA14><fA14 i1="02"><s1>Cognitive Neuropharmacology Unit, Defense & Veteran Head Injury Program, Henry M. Jackson Foundation</s1><s2>Bethesda, Maryland</s2><s3>USA</s3><sZ>2 aut.</sZ></fA14><fA14 i1="03"><s1>Neurology and Dermatology Department, University of Málaga</s1><s3>ESP</s3><sZ>3 aut.</sZ></fA14><fA14 i1="04"><s1>Departments of Psychiatry and Neurology, University of Iowa</s1><s2>Iowa City, Iowa</s2><s3>USA</s3><sZ>5 aut.</sZ></fA14><fA14 i1="05"><s1>Departments of Neurology and Psychiatry and Biobehavioral Science, University of California at Los Angeles School of Medicine</s1><s2>Los Angeles, California</s2><s3>USA</s3><sZ>6 aut.</sZ></fA14><fA20><s1>1098-1104</s1></fA20><fA21><s1>2001</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>20953</s2><s5>354000094252170120</s5></fA43><fA44><s0>0000</s0><s1>© 2002 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>65 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>02-0176680</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Movement disorders</s0></fA64><fA66 i1="01"><s0>USA</s0></fA66><fC01 i1="01" l="ENG"><s0>The role of the basal ganglia in conditions with co-occurring movement disorders and neuropsychiatric symptoms is not well known. It has been hypothesized that hyperkinesia -disinhibited behaviors and hypokinesia-inhibited behaviors result from an imbalance between the direct and indirect striatal output pathways, and that differential involvement of these pathways could account for the concurrent abnormalities in movement and behavior observed in these disorders. This study aimed to evaluate whether the pattern and the extent of the neuropsychiatric manifestations of patients with GTS, a hyperkinetic movement disorder of basal ganglia origin, differs from that of patients with other basal ganglia hyperkinetic (e.g., HD) or hypokinetic (e.g., PSP) movement disorders, and to determine whether patients with GTS show a greater frequency of hyperactive behaviors (e.g., agitation, irritability, euphoria, or anxiety) than PSP patients, and are comparable to patients with HD. The Neuropsychiatric Inventory (NPI), a scale with established validity and reliability, was administered to 26 patients with GTS (mean age, 30.2 ± 2.2 years), and the results were compared with that of 29 patients with HD (mean ages 43.8 ± 2 years) and 34 with PSP (mean ± S.D. age, 66.6 ± 1.2 years). There was no difference between the groups in the total NPI scores. However, there was a double dissociation in behaviors: patients with hyperkinetic disorders (HD and GTS) exhibited significantly more agitation, irritability, anxiety, euphoria, and hyperkinesia, whereas hypokinetic patients (PSP) exhibited more apathy. Patients with GTS showed greater scores than HD patients in all those scores differentiating HD and GTS from PSP patients (e.g., agitation, irritability, anxiety and euphoria), and were differentiated in a logistic regression analysis from both HD and PSP patients in having significantly more anxiety. We found that patients with GTS manifested predominantly hyperactive behaviors similar but more pronounced than those presented by patients with HD, while those with PSP manifested hypoactive behaviors. Based on our findings and the proposed models of basal ganglia dysfunction in these disorders, we suggest that the hyperactive behaviors in GTS are comparable to those observed in HD, being both secondary to an excitatory subcortical output through the medial and orbitofrontal cortical circuits, while in PSP the hypoactive behaviors are secondary to hypostimulation of these circuits. Abnormalities of other brain structures (e.g., amygdala, brainstem nuclei) may account for the significantly higher anxiety scores differentiating GTS from HD patients.</s0></fC01><fC02 i1="01" i2="X"><s0>002B17G</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Gilles de la Tourette syndrome</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Gilles de la Tourette syndrome</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Gilles de la Tourette síndrome</s0><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Trouble comportement</s0><s5>04</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Behavioral disorder</s0><s5>04</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Trastorno conducta</s0><s5>04</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Psychopathologie</s0><s5>07</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Psychopathology</s0><s5>07</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Psicopatología</s0><s5>07</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Chorée Huntington</s0><s5>10</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Huntington disease</s0><s5>10</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Corea Huntington</s0><s5>10</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>Noyau gris central</s0><s5>13</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>Basal ganglion</s0><s5>13</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>Núcleo basal</s0><s5>13</s5></fC03><fC03 i1="06" i2="X" l="FRE"><s0>Etude comparative</s0><s5>16</s5></fC03><fC03 i1="06" i2="X" l="ENG"><s0>Comparative study</s0><s5>16</s5></fC03><fC03 i1="06" i2="X" l="SPA"><s0>Estudio comparativo</s0><s5>16</s5></fC03><fC03 i1="07" i2="X" l="FRE"><s0>Physiopathologie</s0><s5>17</s5></fC03><fC03 i1="07" i2="X" l="ENG"><s0>Pathophysiology</s0><s5>17</s5></fC03><fC03 i1="07" i2="X" l="SPA"><s0>Fisiopatología</s0><s5>17</s5></fC03><fC03 i1="08" i2="X" l="FRE"><s0>Homme</s0><s5>20</s5></fC03><fC03 i1="08" i2="X" l="ENG"><s0>Human</s0><s5>20</s5></fC03><fC03 i1="08" i2="X" l="SPA"><s0>Hombre</s0><s5>20</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Système nerveux pathologie</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Nervous system diseases</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Sistema nervioso patología</s0><s5>37</s5></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0><s5>38</s5></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Central nervous system disease</s0><s5>38</s5></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0><s5>38</s5></fC07><fC07 i1="03" i2="X" l="FRE"><s0>Encéphale pathologie</s0><s5>39</s5></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Cerebral disorder</s0><s5>39</s5></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Encéfalo patología</s0><s5>39</s5></fC07><fC07 i1="04" i2="X" l="FRE"><s0>Maladie dégénérative</s0><s5>40</s5></fC07><fC07 i1="04" i2="X" l="ENG"><s0>Degenerative disease</s0><s5>40</s5></fC07><fC07 i1="04" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0><s5>40</s5></fC07><fC07 i1="05" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0><s5>64</s5></fC07><fC07 i1="05" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0><s5>64</s5></fC07><fC07 i1="05" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0><s5>64</s5></fC07><fC07 i1="06" i2="X" l="FRE"><s0>Maladie héréditaire</s0><s5>66</s5></fC07><fC07 i1="06" i2="X" l="ENG"><s0>Genetic disease</s0><s5>66</s5></fC07><fC07 i1="06" i2="X" l="SPA"><s0>Enfermedad hereditaria</s0><s5>66</s5></fC07><fN21><s1>098</s1></fN21><fN82><s1>PSI</s1></fN82></pA></standard><server><NO>PASCAL 02-0176680 INIST</NO><ET>Neuropsychiatric assessment of Gilles de la Tourette patients: Comparative study with other hyperkinetic and hypokinetic movement disorders</ET><AU>KULISEVSKY (Jaime); LITVAN (Irene); BERTHIER (Marcelo L.); PASCUAL-SEDANO (Berta); PAULSEN (Jane S.); CUMMINGS (Jeffrey L.)</AU><AF>Movement Disorders Unit, Department of Neurology, Sant Pau Hospital, Autonomous University of Barcelona/Espagne (1 aut., 4 aut.); Cognitive Neuropharmacology Unit, Defense & Veteran Head Injury Program, Henry M. Jackson Foundation/Bethesda, Maryland/Etats-Unis (2 aut.); Neurology and Dermatology Department, University of Málaga/Espagne (3 aut.); Departments of Psychiatry and Neurology, University of Iowa/Iowa City, Iowa/Etats-Unis (5 aut.); Departments of Neurology and Psychiatry and Biobehavioral Science, University of California at Los Angeles School of Medicine/Los Angeles, California/Etats-Unis (6 aut.)</AF><DT>Publication en série; Niveau analytique</DT><SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2001; Vol. 16; No. 6; Pp. 1098-1104; Bibl. 65 ref.</SO><LA>Anglais</LA><EA>The role of the basal ganglia in conditions with co-occurring movement disorders and neuropsychiatric symptoms is not well known. It has been hypothesized that hyperkinesia -disinhibited behaviors and hypokinesia-inhibited behaviors result from an imbalance between the direct and indirect striatal output pathways, and that differential involvement of these pathways could account for the concurrent abnormalities in movement and behavior observed in these disorders. This study aimed to evaluate whether the pattern and the extent of the neuropsychiatric manifestations of patients with GTS, a hyperkinetic movement disorder of basal ganglia origin, differs from that of patients with other basal ganglia hyperkinetic (e.g., HD) or hypokinetic (e.g., PSP) movement disorders, and to determine whether patients with GTS show a greater frequency of hyperactive behaviors (e.g., agitation, irritability, euphoria, or anxiety) than PSP patients, and are comparable to patients with HD. The Neuropsychiatric Inventory (NPI), a scale with established validity and reliability, was administered to 26 patients with GTS (mean age, 30.2 ± 2.2 years), and the results were compared with that of 29 patients with HD (mean ages 43.8 ± 2 years) and 34 with PSP (mean ± S.D. age, 66.6 ± 1.2 years). There was no difference between the groups in the total NPI scores. However, there was a double dissociation in behaviors: patients with hyperkinetic disorders (HD and GTS) exhibited significantly more agitation, irritability, anxiety, euphoria, and hyperkinesia, whereas hypokinetic patients (PSP) exhibited more apathy. Patients with GTS showed greater scores than HD patients in all those scores differentiating HD and GTS from PSP patients (e.g., agitation, irritability, anxiety and euphoria), and were differentiated in a logistic regression analysis from both HD and PSP patients in having significantly more anxiety. We found that patients with GTS manifested predominantly hyperactive behaviors similar but more pronounced than those presented by patients with HD, while those with PSP manifested hypoactive behaviors. Based on our findings and the proposed models of basal ganglia dysfunction in these disorders, we suggest that the hyperactive behaviors in GTS are comparable to those observed in HD, being both secondary to an excitatory subcortical output through the medial and orbitofrontal cortical circuits, while in PSP the hypoactive behaviors are secondary to hypostimulation of these circuits. Abnormalities of other brain structures (e.g., amygdala, brainstem nuclei) may account for the significantly higher anxiety scores differentiating GTS from HD patients.</EA><CC>002B17G</CC><FD>Gilles de la Tourette syndrome; Trouble comportement; Psychopathologie; Chorée Huntington; Noyau gris central; Etude comparative; Physiopathologie; Homme</FD><FG>Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Maladie dégénérative; Extrapyramidal syndrome; Maladie héréditaire</FG><ED>Gilles de la Tourette syndrome; Behavioral disorder; Psychopathology; Huntington disease; Basal ganglion; Comparative study; Pathophysiology; Human</ED><EG>Nervous system diseases; Central nervous system disease; Cerebral disorder; Degenerative disease; Extrapyramidal syndrome; Genetic disease</EG><SD>Gilles de la Tourette síndrome; Trastorno conducta; Psicopatología; Corea Huntington; Núcleo basal; Estudio comparativo; Fisiopatología; Hombre</SD><LO>INIST-20953.354000094252170120</LO><ID>02-0176680</ID></server></inist></record>Pour manipuler ce document sous Unix (Dilib)
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