No description available.

<p><strong>Objectives: </strong>To assess the reliability and validity of the Patient Specific Functional Scale when administered to people living with Parkinson’s Disease.<strong></strong></p> <p><strong>Methods and Materials: </strong>Twenty six people living with Parkinson’s Disease from Hamilton and Burlington were interviewed four times within a four month period. The participants answered the Movement Disorders Sponsored Unified Disease Rating Scale part II, the Parkinson’s Disease Questionnaire 39, and the Patient Specific Functional Scale. Reliability assessment addressed test-retest reliability and reliability of the change scores using Intraclass Correlation Coefficients. Validity assessment focused on convergent construct validity and longitudinal validity by correlating the Patient Specific Functional Scale with the other measures administered.</p> <p><strong>Results: </strong>The<strong> </strong>test retest reliability of the scores yielded by the PSFS was ICCpre= 0.72 (95%CI=0.47-0.86); ICCpost=0.83 (95%CI=0.66-0.92). The reliability of change scores was 0.50. In relation to the validity, no significant correlations were found between the Patient Specific Functional Scale and the other measures. <strong></strong></p> <p><strong>Conclusions: </strong>The PSFS yields reliable scores when it is administered to people living with PD. The Patient Specific Functional Scale does not target the same outcomes as the MDS-UPDRS part II and the PDQ-39. The PSFS does not detect change in functioning in people living with PD within a four month period.</p> / Master of Science (MSc)

No

In patients with Parkinson's disease (PD), the associated pathology follows a characteristic pattern involving inter alia the enteric nervous system (ENS), the dorsal motor nucleus of the vagus (DMV), the intermediolateral nucleus of the spinal cord and the substantia nigra, providing the basis for the neuropathological staging of the disease. Here we report that intragastrically administered rotenone, a commonly used pesticide that inhibits Complex I of the mitochondrial respiratory chain, is able to reproduce PD pathological staging as found in patients. Our results show that low doses of chronically and intragastrically administered rotenone induce alpha-synuclein accumulation in all the above-mentioned nervous system structures of wild-type mice. Moreover, we also observed inflammation and alpha-synuclein phosphorylation in the ENS and DMV. HPLC analysis showed no rotenone levels in the systemic blood or the central nervous system (detection limit [rotenone]<20 nM) and mitochondrial Complex I measurements showed no systemic Complex I inhibition after 1.5 months of treatment. These alterations are sequential, appearing only in synaptically connected nervous structures, treatment time-dependent and accompanied by inflammatory signs and motor dysfunctions. These results strongly suggest that the local effect of pesticides on the ENS might be sufficient to induce PD-like progression and to reproduce the neuroanatomical and neurochemical features of PD staging. It provides new insight into how environmental factors could trigger PD and suggests a transsynaptic mechanism by which PD might spread throughout the central nervous system.

<p>Cilj rada: Posmatrano je da li postoji povezanost kliničkih parametara, bihejvioralnih simptoma i postignuća na testovima kognitivnih funkcija sa karakteristikama hoda kod obolelih od Parkinsonove bolesti. Analizirana je i povezanost nalaza hiperehogenosti strukture substantia nigra dobijenog transkranijalnim parenhimskim ultrazvukom sa karakteristikama hoda.Materijal I metode: Istraživanjem je obuhvaćeno 60 obolelih od Parkinsonove bolesti (22 žene i 38 mu&scaron;karaca, sa trajanjem bolesti 5,06&plusmn;4,54 godina, ukupnim UPDRS 39,76&plusmn;36,65, UPDRS III 24,28&plusmn;15,18) koji su prema stadijumu bolesti po Hen i Jarovoj skali (H&amp;Y) podeljeni u tri podgrupe sa po 20 ispitanika: H&amp;Y 1, 2 i 3. Kontrolnu grupu činilo je 35 zdravih ispitanika (19 žena i 16 mu&scaron;karaca) koji se od grupe obolelih nisu razlikovali u pogledu godina starosti (oboleli 64,21&plusmn;6,92 godina, zdravi 63,45&plusmn;7,75, p=0,832) i godina obrazovanja (oboleli 12,63&plusmn;3,16 godina, zdravi 12,57&plusmn;2,87, p=0,954). Iz analize su isključeni ispitanici čiji je skor MMSE bio manji od 24. Procena težine motornih znakova Parkinsonove bolesti vr&scaron;ena je Unifikovanom skalom za kvantifikovanje Parkinsonove bolesti, treći deo (UPDRS III). Za globalnu procenu kognicije je kori&scaron;ćena Revidirana Adenbrukova kogntivna skala (ACE- R), a za procenu egzekutivnih funkcija su kori&scaron;ćeni baterija za procenu frontalnih funkcija (FAB) i Egzekutivni intervju (EXIT-25). Za evaluaciju depresije kori&scaron;ćene su Hamiltonova skala za procenu depresije (HAM- D) i Bekova skala depresivnosti (BDI II), za procenu anksioznosti Hamiltonova skala za procenu anksioznosti (HAM- A), a za procenu apatije Skala apatije (AS).Određivanje vremenskih i prostornih parametara hoda vr&scaron;eno je pomoću GAITRite sistema, tokom &bdquo;on&rdquo; perioda. Analizirano je osam parametara hoda: vreme dvokoraka (CT), dužina dvokoraka (SL), vreme zamaha (ST) i vreme dvostrukog oslonca (DS), kao i njihovi koeficijenti varijacija (CV). Posmatran je i uticaj dvostrukog zadatka na parametre hoda. Kao dodatni zadatak tokom hoda primenjen je kognitivni zadatak (oduzima -7 tokom hoda), motorni zadatak (nosi ča&scaron;u punu vode) i kombinovani zadatak (oduzima i nosi ča&scaron;u istovremeno). Veličina hiperehogenosti substantia nigra merena je transkranijalnim parenhimskim ultrazvukom. Rezultati: U poređenju sa zdravim vr&scaron;njacima, oboleli od Parkinsonove bolesti imali su značajno izraženiji varijabilitet koraka pri hodu bez zadatka (skraćen SL, povećan CVSL i CVCT, varijabilitet koraka bio je jo&scaron; izraženiji, dok je pri motornom zadatku postojala i značajna razlika DS i CVDS (p&lt;0,05), tj. parametara kojima se izražava ravnoteža koraka. U uslovima kombinovanog zadatka ove razlike su se potencirale. Parametri hoda (SL, VCSL, CVCT I CVST) minimalno su se razlikovali kod obolelih u najranijim stadijumima bolesti (H&amp;Y 1) u odnosu na zdrave, dok su razlike postajale izraženije kako je bolest bila u odmaklijim stadijumima (H&amp;Y 2 I H&amp;Y 3). U grupi zdravih starost ispitanika korelirala je sa varijabilitetom koraka jedino u uslovima dvostrukog zadatka. Kod obolelih ova povezanost je uočena i pri hodu bez zadatka, a povezanost je bila jača u uslovima dvostrukog zadatka. Starost ispitanika i težina motornih znakova na UPDRS III korelirali su sa parametrima hoda kod obolelih od PB. Skorovi apatije i depresivnosti korelirali su sa promenama parametara hoda kod obolelih, s tim &scaron;to je apatija bila prisutna već u najranijim, a depresija tek u kasnijim stadijumima bolesti. Niža postignuća na testovima egzekutivnih funkcija povezana su sa pogor&scaron;anjem svih parametara hoda. Sa pogor&scaron;anjem parametara hoda tokom trajanja bolesti koreliraju i niža postignuća na testovima jezičkih i vidno- prostornih funkcija, kao i deficit pamćenja. Veličina hiperehogenosti korelira sa CV svih parametara hoda. Zaključak: Kod obolelih od Parkinsonove bolesti značajno se razlikuju vremenski i prostorni parametri hoda u poređenju sa zdravim, pre svega oni kojima se opisuje varijabilitet koraka. Ovi parametri su izraženiji kada se tokom hoda obavlja i dodatni kognitivni zadatak. Kada se tokom hoda obavlja motorni ili kombinovani motorni i kognitivni zadatak, pored varijabiliteta koraka javlja se i značajno produžen DS koji ukazuje na poremećaj ravnoteže. Na parametre hoda utiču starost ispitanika, težina i stadijum Parkinsonove bolesti. Apatija i depresija takođe značajno utiču na parametre hoda kod obolelih. Apatija se javlja u najranijim, a depresivnost tek u kasnijim stadijumima bolesti, &scaron;to govori u prilog stanovi&scaron;ta da je apatija zaseban simptom bolesti povezan sa dopaminergičkom disfunkcijom. Pogor&scaron;anja parametara hoda koreliraju sa o&scaron;tećenjem kognitivnih funkcija, pre svega egzekutivnih. U odmaklim stadijumima bolesti sa pogor&scaron;anjem hoda povezana su i lo&scaron;ija postignuća na testovima vidno-prostornih funkcija i pamćenja. Hiperehogenost substantia nigra na transkranijalnom parenhimskom ultrazvuku, koja se značajno če&scaron;će javlja i značajno je veće povr&scaron;ine kod obolelih u odnosu na zdrave, korelira sa varijabilitetom koraka.</p> / <p>Objectives: The aim of the study was to assess the contribution of clinical presentation, behavioral symptoms and cognitive functioning to gait characteristics in Parkinson&rsquo;s disease (PD). Hyperechogenicity of the substantia nigra on transcranial parenchimal ultrasound and its correlations with gait characteristics was also analyzed. Material and Methods: The experimental group consisted of 60 patients suffering from Parkinson&rsquo;s disease (22 women and 38 men, disease duration 5.06&plusmn;4.54, Unified Parkinson&#39;s Disease Rating Scale (UPDRS) total 39.76&plusmn;36.65, and UPDRS III 24.28&plusmn;15.18), who were classified into three subgroups according to the Hoehn and Yahr (H&amp;Y) stage of the disease: H&amp;Y 1, H&amp;Y 2 and H&amp;Y 3, with each subgroup containing 20 patients. The control group included 35 healthy subjects (19 women and 16 men) who were matched for years of age (64.21&plusmn;6.92 years PD vs 63.45&plusmn;7.75 healthy; p= .832) and formal education (12.63&plusmn;3.16 years PD vs 12.57&plusmn;2.87 healthy, p= .954). The subjects with MMSE&lt;24 were concerned demented and excluded from further analysis. The disease severity was assessed by the UPDRS, motor part (UPDRS III). Addenbrooke&rsquo;s Cognitive Examination-Revised (ACE-R) was used in assessment of global cognition, while executive functions were examined by Frontal Assessment Battery (FAB) and Executive Interview (EXIT-25) Hamilton&rsquo;s Depression Rating Scale (HAM-D) and Beck&rsquo;s Depression Inventory (BDI II) were used to screen for symptoms of depression, and the Apathy Scale (AS) and Hamilton&rsquo;s Anxiety Rating Scale (HAM- A) were used to assess apathy and anxiety. The measurements of spatial and temporal parameters of gait were performed using the GAITRite system, during the &ldquo;on&rdquo; state. The following eight parameters were analyzed: Cycle Time (CT), Stride Length (SL), Swing Time (ST) and Double Support Time (DS), as well as their coefficients of variation (CV). The impact of dual task on gait parameters was also observed. The subjects were asked to walk and simultaneously perform cognitive task (subtracting -7), then motor task (carrying a glass of water) and eventually combined task (subtracting and carrying a glass of water), while walking on the GAITRite electronic pathway. Transcranial parenchymal ultrasound was used to measure hyperechogenicity of substantia nigra. Results: Compared to healthy controls, PD patients had significantly higher gait variability during gait without additional tasks (decreased SL, increased CVSL and CVCT; p&lt; .05), whereas with a cognitive task the variability was even higher. During the motor task DS and CVDS were significantly increased as well, implying gait instability. A combined task had similar effects as the motor task, affecting all parameters. When the experimental group was divided into subgroups, variability of gait (SL, VCSL, CVCTandCVST) was minor in subgroup H&amp;Y 1, but more pronounced in later stages (H&amp;Y 2 and H&amp;Y 3). The age correlated with gait variability (CVCT and CVSL) only during the dual task in healthy subjects, whereas in PD patients the association was significant during normal gait and increased on the dual task. The age and severity of the disease on the UPDRS III also correlated with gait parameters. Apathy and depression were also associated with gait variability. Symptoms of apathy were significant in the earliest stages (H&amp;Y 1), whereas depression was notable in the later stages (H&amp;Y 3). Worse scores on tests of executive functions correlated with impairment of gait parameters. The impact of diminished language, visuo-spatial and memory functions on gait was also significant. Hyperechogenicity of the substantia nigra on transcranial parenchymal ultrasound occurred more frequently and was larger in PD patients and correlated well with gait variability. Conclusion: There is a significant impairment of temporal and spatial gait parameters in PD patients compared to healthy subjects, particularly the parameters of gait variability. These parameters become even more impaired during a simultaneous cognitive task. When a motor or combined task is performed, there is additional increase of DS, implying impairment of stability. Also, age and disease severity affect gait in PD patients. Apathy is significant in early stages (H&amp;Y 1) and depression in later stages (H&amp;Y 3), the finding which may be explained by the dopaminergic origin of apathy. Impairment of cognitive functions, most importantly executive dysfunction, are also associated with gait variability. Lower scores at visuo-spatial, language and memory tests are associated with worsened gait parameters of gait in later stages of PD. Finally, hyperechogenicity of the substantia nigra on transcranial parenchymal sonography, which occurs more frequently and is larger in PD patients, correlates with gait variability.</p>

TITLE: Therapy of voice disorders AUTHOR: Michaela Horáková DEPARTMENT: Department of special education SUPERVISOR: Mgr. Miroslava Kotvová ABSTRACT: This diploma thesis deals with the voice disorders and their treatment options. The character of the thesis is mostly theoretical and the thesis is divided into four general parts. The first one elaborates the anatomy and physiology of the vocal tract as a basis for understanding mechanisms of voice pathology development, the second one is devoted to voice disorders and their categorization, and the third part deals with their therapy, as the czech literature reflects it. The last part of this thesis is dedicated to voice disorders therapy in the United States with a practical focus on therapeutical program Lee Silverman Voice Treatment (LSVT) widely used abroad during the treatment of voice disorders especially connected to Parkinson disease. The program is considered to be very effective and it is really popular outside of the Czech republic. LSVT is not well known in the Czech republic yet and there is actually only limited information devoted to this type of voice therapy. For this reason the thesis is based on analysis and comparison of the available foreign texts in order to inform the czech public about its theoretical basis, structure and system,...

Depuis sa première description par James Parkinson dans son essai sur la paralysie agitante, la maladie de Parkinson (PD) a été reconnue comme une maladie du système moteur identifié par une tétrade de symptômes, à savoir : akinésie, rigidité musculaire, tremblement au repos et instabilité posturale. Ces symptômes sont liés à la perte de la dopamine (DA) dans le striatum après la dégénérescence neuronale dans la substance noire (SN). Il est de plus en plus reconnu que les symptômes non moteurs et peut-être non dopaminergiques inévitablement émergent et s'aggravent au cours de la progression de la maladie. Les perturbations du sommeil sont parmi les principaux symptômes non moteurs et ont été reconnus comme marqueurs précliniques de la maladie. Les modèles de régulation du sommeil ont insisté sur deux processus distincts : un mécanisme de contrôle du sommeil, ou homéostat sommeil, et un oscillateur circadien. L'oscillateur circadien, basé dans le noyau suprachiasmatique (NSC) est responsable de la tendance à dormir pendant certaines phases du cycle de 24 heures et la consolidation du sommeil et de réveil en épisodes distincts. L'homéostat sommeil est chargé de surveiller et de réagir à la nécessité pour le sommeil, provoquant l'envie de dormir à dépendre sur les montants avant du sommeil ou de l'éveil. Alors que les perturbations dans les circuits et les processus homéostatiques impliqués dans la régulation du sommeil-éveil comportement sont documenté dans la maladie de Parkinson, l'implication potentielle des altérations du système circadien n'ont pas été étudiés en détail. Le but de ma thèse est d'étudier les modifications dans le système circadien en utilisant deux modèles animaux de PD : la souris et le primate non-humain / Since the first description by James Parkinson in his essay on the shaking palsy, Parkinson’s disease (PD) was recognized as a motor disease identified by a tetrad of symptoms, namely; akinesia, muscular rigidity, resting tremor and postural instability. These symptoms are known to be related to loss of dopamine (DA) in the striatum following neural degeneration in the substantia nigra (SN). It is increasingly recognized that non-motor and perhaps non-dopaminergic related symptoms inevitably emerge and worsen during disease progression. Sleep disruption is one of the major non-motor symptoms and has been suggested as a preclinical marker of the disease. Models of sleep regulation have emphasized two distinct processes: a sleep-control mechanism, or sleep homeostat, and a circadian oscillator. The circadian oscillator, based in the suprachiasmatic nucleus (SCN), is responsible for the tendency to sleep during certain phases of the 24-hour cycle and the consolidation of sleep and wake into distinct episodes. The sleep homeostat is responsible for monitoring and reacting to the need for sleep, causing the urge to sleep to depend on prior amounts of sleep or wakefulness. While disruptions in the circuitry and the homeostatic processes involved in the regulation of sleep-wake behaviour is will documented in PD, the potential involvement of alterations of the circadian system have not been studied in detail. The aim of my thesis is to investigate alterations in the circadian timing system using two animal models of PD: the mouse and the non-human primate. Taken together, the studies show that disturbances of circadian functions occur after MPTP treatment in the non-human primate but not in the mouse model of PD. These results emphasize the limitations of the MPTP-treated mouse model of PD for the study of non-motor symptoms, and reinforce previous studies that question the adequacy of this model to replicate cardinal motor features of the disease. In contrast, results in the non-human primate model stress the importance of dopaminergic degeneration in the circadian organisation of behavioral sleep wake cycle in PD

O circuito neuronal relacionado à depressão na doença de Parkinson (DP), assim como os efeitos da terapia antidepressiva nestes pacientes, não é bem estabelecido. Os métodos de neuroimagem podem levar ao melhor conhecimento da patogênese e também dos mecanismos de ação relacionados a um tipo específico de tratamento. Para avaliar as diferenças da atividade neuronal, comparamos 21 pacientes com DP e diagnóstico de depressão e 16 sem depressão através de ressonância magnética funcional (RMf) em uma tarefa cognitiva que inclui percepção emocional e escolha forçada com duas opções. Estes 21 pacientes deprimidos foram aleatorizados em dois grupos de tratamento por 4 semanas: estimulação magnética transcraniana (EMT) ativa sobre o córtex pré-frontal dorsolateral esquerdo ( 5 Hz EMT - 120% do limiar motor) com pílula placebo e EMT placebo com 20 mg diária de fluoxetina. Os pacientes foram submetidos a um experimento de RMf cujo paradigma foi relacionado a eventos apresentação visual de faces de conteúdo emocional. Os pacientes sem depressão realizaram RMf duas vezes (teste reteste) e os deprimidos quatro vezes (duas vezes antes e duas depois do tratamento). As imagens dos pacientes com DP e depressão demonstraram menor atividade no córtex pré-frontal medial quando comparados aos pacientes com DP sem depressão. Ambos os subgrupos de pacientes com DP e depressão apresentaram melhora significativa e similar dos sintomas da depressão. Após o tratamento com EMT ativa observou-se menor atividade do giro fusiforme esquerdo, do cerebelo e do córtex pré-frontal dorsolateral direito e maior atividade do córtex pré-frontal dorsolateral esquerdo e do cíngulo anterior nas imagens de RMf quando comparados àquelas antes do tratamento. Por outro lado a fluoxetina determinou aumento da atividade do córtex pré-motor direito e do córtex pré-frontal medial direito em imagens de RMf realizadas após o tratamento. Observou-se efeito de interação entre os grupos (tempo (pré x pós) versus tipo de tratamento (fluoxetina x EMT)) no córtex préfrontal medial esquerdo sendo maior o aumento no grupo tratado com EMT. Nossos achados mostraram: 1) padrão diferente de atividade cerebral em pacientes com DP com e sem depressão; 2) efeitos antidepressivos da EMT e da fluoxetina foram semelhantes e significativos;e 3) em pacientes com DP e depressão os efeitos da EMT e fluoxetina são associados a diferentes mudanças da atividade cerebral, e em ambos as áreas encontradas são parte da rede neural relacionada à depressão. / The neural circuitry underlying depression in patients with Parkinson\'s disease (PD) is unknown, let alone the treatment effects of antidepressant therapy. Neuroimaging methods can give insights into the pathogenesis of depression and also in the mechanisms of action related to specific treatment choice. In order to evaluate differences between PD patients with and without concomitant depression we studied 21 patients with PD and depression and 16 PD patients without depression using fMRI. All patients were examined using an event-related fMRI paradigm based on visual presentation of faces with emotional content in a two options forced choice task. Furthermore the twenty-one PD depressed patients were randomized in two active treatment groups for 4 weeks: active rTMS over left dorsolateral prefrontal cortex (5 Hz rTMS - 120% motor threshold) with placebo pill and sham rTMS with fluoxetine 20 mg/day. Event-related fMRI with emotional stimuli was performed before and after treatment - in two sessions (test and re-test) at each time point. The same test-retest approach was adopted in the group of non-depressed PD patients. The analysis showed significant differences between depressed and non-depressed PD patients in the medial pre-frontal cortex, with reduced activation as detected by BOLD effect in the later group. The two groups of depressed PD patients showed a had a significant treatment effect, and with similar mood improvement. After rTMS treatment, there were brain activity decreases in left fusiform gyrus, cerebellum and right dorsolateral prefrontal cortex (DLPFC) and brain activity increases in left DLPFC and anterior cingulate gyrus as compared to baseline. In contrast, after fluoxetine treatment, there was brain activity increases in right premotor and right medial prefrontal cortex. There was a significant interaction effect between groups versus time in the left medial prefrontal cortex, suggesting that the activity in this area changed differently in the two treatment groups. Our findings show that medial prefrontal cortex is a critical area in the depression neural circuitry in PD. Antidepressant effects of rTMS and fluoxetine in PD are associated with changes in different areas of the depression-related neural network.

A Doença de Parkinson (DP) é causada pela degeneração progressiva de neurônios no sistema nervoso central, principalmente os neurônios dopaminérgicos nigroestriatais, levando a sintomas motores como a bradicinesia, rigidez e tremor. Os sintomas não motores (SNM), como a dor, estão presentes em muitos doentes e representam um impacto negativo na qualidade de vida. A estimulação encefálica profunda é um tratamento bem estabelecido para o tratamento dos sintomas motores da DP. Entretanto, o seu impacto sobre os sintomas não motores ainda é bastante desconhecido. O objetivo do presente estudo foi avaliar os efeitos da EEP sobre as diferentes características da dor e sensibilidade, e de outros SNM nos indivíduos com DP. Foram avaliados 41 indivíduos com diagnóstico de DP (14 do sexo feminino), idade de 60 ± 10,4 anos, com 15 ± 7,6 anos da duração da doença e estágio intermediário de evolução (Escala de Hoehn & Yahr = 2,80 ± 0,64). Os doentes foram submetidos a implante de sistema de estimulação bilateral do núcleo subtalâmico guiado por eletrofisiologia intraoperatória. Foram avaliados, prospectivamente, antes e um ano após, o procedimento de forma encoberta. O desfecho principal foi a mudança da prevalência da dor após a cirurgia. Os desfechos secundários incluíam mudanças nos sintomas motores (UPDRS parte III), na qualidade de vida (escala SF-36), na avaliação de humor (Escala Hospitalar de Ansiedade e Depressão [EHAD]), nos outros sintomas não motores (Escala dos sintomas não motores [ESNM]) e nas características da dor. Foram avaliadas as dimensões da dor (questionário de McGill), a intensidade e o impacto nas atividades de vida diária da dor (escala visual analógica da dor [EVA], inventário breve da dor [IBD]), a presença de dor neuropática (Douleur Neuropathique-4 Questionnaire [DN-4]) e o perfil dos sintomas neuropáticos (inventário de sintomas de dor neuropática (ISDN), o perfil de catastrofismo da dor (Escala catastrófica da dor [ECD]) e os limiares de sensitivos por meio da análise quantificada dos limiares de sensibilidade. Houve redução de prevalência da dor de 70% para 21% após a cirurgia (p < 0,05). Houve melhora na intensidade (EVA: antes = 80 ± 13,2; depois = 42,2 ± 17,8, p = 0,007) e nos diferentes aspectos da dor, além de outros sintomas não motores (ESNM: antes = 114,80 ± 59,89; depois = 62,68 ± 22,76; p < 0,001), como a cognição, humor, atenção, alucinação e trato gastrointestinal. Houve melhora na detecção de estímulos térmicos e mecânicos após a cirurgia, além de redução da sensibilidade aos limiares de dor (p < 0,05). A melhora na intensidade da dor foi fortemente relacionada com a melhora na qualidade vida (r = 0,708; p < 0,005). Não houve correlação entre a melhora da dor e a resposta à dopamina pré-operatória ou a melhora motora após a cirurgia (r = 0,247; p = 0,197 e r = 0,249; p = 0,193, respectivamente). Concluise que a ECP do núcleo subtalâmico diminui a prevalência e diferentes aspectos da dor após a cirurgia, e essa melhora está diretamente associada à melhora da qualidade de vida. A melhora motora ou dos outros SNM não foi relacionada à melhora da dor, sugerindo que a ECP apresenta diferentes mecanismos de ação sobre os sintomas nos indivíduos com DP / Parkinson disease (PD) is caused by progressive degeneration of neurons throughout the nervous system, especially the dopamine neurons, leading to motor symptoms as bradykinesia, rigidity and tremor. Non-motor symptoms (NMS), such as pain, are present in a large proportion of Parkinson\'s disease patients and have a major negative impact on patients quality of life. Subthalamic deep brain stimulation has gained general use in the management of motor symptoms in these patients. However, its impact on non-motor symptoms remains largely unknown. The aim of this study was to evaluate the effect of subthalamic deep brain stimulation (STN-DBS) on the different characteristics of pain, sensibility and other NMS in patients with PD. Forty-one patients with PD were evaluated (14 female), mean age 60 ± 10,4 years. The mean duration of the disease was 15 ± 7.6 years, and the Hoehn & Yahr off-medication score was 2.80 ± 0.64. The patients underwent stereotactic implantation of bilateral subthalamic nucleus stimulation system guided by intraoperative electrophysiology. They were evaluated before and 01 year after surgery. The primary outcome was change in pain prevalence after surgery. Secondary outcome measures were changes in motor function (PDRS part III), quality of life (SF-36 scale), presence of NMS (Non-motor symptoms scale [NMSS] and Hospital Anxiety and Depression Scale [HADS]), and characteristics of pain. We evaluated pain dimensions (Short Form of McGill Pain Questionnaire [MPQ]), pain intensity and impact of pain in daily activities (Brief Pain Inventory [BPI] and Visual Analogic Scale [VAS]), presence of neuropathic pain (Douleur Neuropathique-4 Questionnaire [DN-4]) and its symptom profile (Neuropathic Pain Symptom Inventory [NPSI]), catastrophizing (Pain Catatrosphizing Scale [PCS]) and the sensory thresholds throught the quantitative sensory threshold test. The prevalence of pain changed from 70% to 21% after surgery (p < 0.001). There were also significant improvements in pain intensity (VAS: before = 80 ± 13.2; after = 42.2 ± 17.8, p = 0.007), in different aspects of pain and NMS (before = 114.80 ± 59.89; after = 62.68 ± 22.76; p < 0.001) as cognition, attention, mood and gastrointestinal function. There was improvement on cold and heat detection thresholds (p < 0.05). There was a strong correlation between the change in pain intensity and the improvement in quality of life (r = 0.708; p < 0.005). No correlation was found between pain improvement and preoperative response to levodopa or motor improvement during stimulation (r = 0.247; p = 0.197 and r = 0.249; p = 0.193, respectively) or with changes in other non-motor symptoms. In conclusion, STN-DBS decreased pain intensity. The pain relief was directly associated with improvement in quality of life. Motor and NMS improvements after STN-DBS did not correlate with pain relief, suggesting differents mechanisms of DBS action in PD patients

Introdução: A disfunção da marcha é um dos maiores comprometimentos funcionais do paciente com a doença de Parkinson (DP). A estimulação cerebral profunda do núcleo subtalâmico tem mostrado melhora da marcha e equilíbrio. Esse efeito pode ser mantido e potencializado por programas de reabilitação motora específicos, como o treino em esteira sem e com suporte de peso corporal. No entanto, faltam estudos desses treinos em pacientes com a DP em uso desta estimulação. Objetivo: Comparar parâmetros cinemáticos lineares e angulares da marcha de pacientes com a DP em uso de estimulação cerebral profunda bilateral do núcleo subtalâmico, antes e após dois treinamentos: esteira sem e com suporte de peso corporal, associados à cinesioterapia convencional. Métodos: 12 pacientes (60,9 ± 10,6 anos; 20 ± 7 anos de doença e 20 ± 4 meses de tempo de cirurgia) completaram ambos os treinos em estudo cruzado fixo. Os pacientes passaram por 8 semanas de treino de marcha em esteira sem suporte de peso corporal e programa de cinesioterapia convencional, seguidas por 6 semanas de período sem intervenção. Posteriormente, realizaram 8 semanas de treino de marcha em esteira com suporte de peso corporal e o mesmo programa de cinesioterapia regular. As intervenções tiveram frequência de duas vezes por semana e duração de 90 minutos por sessão. A análise cinemática da marcha envolveu oito câmeras infravermelhas que detectaram 19 marcadores reflexivos nos membros inferiores dos pacientes. A análise estatística utilizou o teste Wilcoxon e foi adotado valor de p <= 0,05 como estatisticamente significante. Resultados: Ambos os treinos não mostraram diferenças significativas nos parâmetros lineares. Após o treino com suporte, observou-se aumento significativo dos seguintes parâmetros angulares: amplitude de movimento da pelve (inclinação, obliquidade e rotação); amplitude de movimento do quadril (abduçãoadução e rotação); % da fase de balanço que corresponde à flexão máxima do joelho e amplitude de movimento da progressão do pé. Conclusão: O treino em esteira com suporte de peso corporal mostrou capacidade de promover mudanças em parâmetros cinemáticos angulares da marcha. As implicações do treino em suspensão podem ter sido somadas aos efeitos neurofisiológicos da estimulação cerebral profunda e então desencadeado a melhora da mobilidade dos membros inferiores durante a marcha / Introduction: Gait disturbance is one of the hallmark features of Parkinson\'s disease (PD). Subthalamic nucleus deep brain stimulation (DBS) has shown improvements in gait and balance, and this effect can be maintained and enhanced by specific motor rehabilitation programs, such treadmill training without and with body weight support. However, at present there is a paucity of research on these combined interventions in PD with of this stimulation. Objective: To compare training-induced changes in gait linear and angular kinematic parameters among patients with PD who have used bilateral subthalamic nucleus DBS, and a combined intervention of conventional physical therapy with either treadmill training with body weight support or without support. Methods: 12 patients (age: 60.9 ± 10.6 years; disease duration: 20 ± 7 years; and time since DBS surgery: 20 ± 4 months) completed both training protocols in a fixed cross-over design. All patients received 8 weeks of treadmill training without body weight support in conjunction with conventional physical therapy, followed by a 6 weeks wash out period of no training. Thereafter, all patients received 8 weeks of body weight support treadmill training, in conjunction with the same conventional physical therapy. Both interventions had a frequency of two times per week, and duration of 90 minutes per session. Gait kinematic analysis involved eight infrared cameras that detected 19 reflective spherical markers attached to the limb lower of patients. Statistical analysis used the Wilcoxon and was adopted the value of p <= 0,05 as statistically significant. Results: Both the training no showed significant differences in linear parameters. After the body weight support training, observed there was a significant increase in following angular parameters: pelvis\' range of motion (tilt, obliquity, rotation); hip\'s range of motion (abduction-adduction and rotation); % Knee maximal flexion on Swing phase and foot progression\' range of motion. Conclusion: Treadmill training with body weight support showed an ability to promote changes in gait angular kinematic parameters. The implications of this training may have been added to the neurophysiological effects of DBS and then triggered the improved of mobility of lower limbs during gait