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INTRODUCTION: Parkinson's disease (PD) causes gait abnormalities that may be associated with an arm swing reduction. Medication and freezing of gait (FoG) may influence gait characteristics. However, these comparisons do not consider differences in gait speed and clinical characteristics in individuals with PD. OBJECTIVE: This study aims to analyze the effect of FoG and medication on the biomechanics of the trunk and upper limbs during gait in PD, controlling for gait speed and clinical differences between groups. METHODS: Twenty-two people with a clinical diagnosis of idiopathic PD in ON and OFF medication (11 FoG), and 35 healthy participants (control) were selected from two open data sets. All participants walked on the floor on a 10-m-long walkway. The joint and linear kinematic variables of gait were compared: (1) Freezers and nonfreezers in the ON condition and control; (2) Freezers and nonfreezers in the OFF condition and control; (3) Group (freezers and nonfreezers) and medication. RESULTS: The disease affects the upper limbs more strongly but not the trunk. The medication does not significantly influence the joint characteristics but rather the linear wrist displacement. The FoG does not affect trunk movement and partially influences the upper limbs. The interaction between medications and FoG suggests that the medication causes more substantial improvement in freezers than in nonfreezers. CONCLUSION: The study shows differences in the biomechanics of the upper limbs of people with PD, FoG, and the absence of medication. The future rehabilitation protocol should consider this aspect.

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BACKGROUND: Progressive Myoclonic Epilepsy (PME) is a group of rare diseases that are difficult to differentiate from one another based on phenotypical characteristics. CASE REPORT: We report a case of PME type 7 due to a pathogenic variant in KCNC1 with myoclonus improvement after epileptic seizures. DISCUSSION: Myoclonus improvement after seizures may be a clue to the diagnosis of Progressive Myoclonic Epilepsy type 7.

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Deep brain stimulation (DBS) is an interdisciplinary and reversible therapy that uses high-frequency electrical stimulation to correct aberrant neural pathways in motor and cognitive neurological disorders. However, the high frequency of the waves used in DBS can interfere with electrical recording devices (e.g., electrocardiogram, electroencephalogram, cardiac monitor), creating artifacts that hinder their interpretation. The compatibility of DBS with these devices varies and depends on factors such as the underlying disease and the configuration of the neurostimulator. In emergencies where obtaining an electrocardiogram is crucial, the need for more consensus on reducing electrical artifacts in patients with DBS becomes a significant challenge. Various strategies have been proposed to attenuate the artifact generated by DBS, such as changing the DBS configuration from monopolar to bipolar, temporarily deactivating DBS during electrocardiographic recording, applying frequency filters both lower and higher than those used by DBS, and using non-standard leads. However, the inexperience of medical personnel, variability in DBS models, or the lack of a controller at the time of approach limit the application of these strategies. Current evidence on their reproducibility and efficacy is limited. Due to the growing elderly population and the rising utilization of DBS, it is imperative to create electrocardiographic methods that are easily accessible and reproducible for general physicians and emergency services.

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BACKGROUND: Deficiencies in the thyroid hormone transporter monocarboxylate 8 (MCT8) due to pathogenic variants in the SLC16A2 gene (OMIM 300095) result in a complex phenotype with main endocrine and neurologic symptoms. This rare disorder, named Allan-Herndon-Dudley syndrome (AHDS) (OMIM 300523), is inherited in an X-linked trait. One of the prominent features of AHDS is the presence of movement disorders (MD), which are complex and carry a significant burden of the disease. CASES: Patient 1: male with hypotonia since birth, developmental delay, dystonic posturing at 4 months and at 15 months, and startle reaction developed with sensory stimuli. Patient 2: male, at 2 months, shows hypotonia and developmental delay, paroxysmal episodes triggered by a stimulus with sudden blush, tonic asymmetric posture, and no epileptiform activity. At 10 months, generalized dystonic posturing. Patient 3: typical neurodevelopmental milestones until 6 months; at 24 months, dystonia, startle reaction, and upper motoneuron signs. CONCLUSIONS: We aim to describe our patients diagnosed with AHDS, focusing on MD phenomenology and strengthening the phenotype-genotype correlations for this rare condition.

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OBJECTIVE: To describe the recent trends in Parkinson's disease mortality in Mexico during 2000-2020. METHOD: The adjusted mortality rate per 100,000 inhabitants was calculated using the direct method and the world standard population. Trend analysis was performed with the Joinpoint software. RESULTS: The average mortality rate was 1.26/100,000 inhabitants (SD: 0.09), and males showed higher mortality than females (M/F ratio=1.60). Older individuals ≥70 years old showed higher mortality rates than the rest of the age groups. During the period of study, a significant increase in mortality was observed from 2000 to 2005, while from 2005 to 2020 no significant trend was observed in all the studied groups. CONCLUSIONS: In Mexico, males and older individuals showed the highest mortality rates. The socioeconomic regions with high levels of wellness showed the highest mortality rates levels. Parkinson's mortality rate has remained constant since 2005 in Mexico.

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Brain iron accumulation constitutes a pathognomonic indicator in several neurodegenerative disorders. Metal accumulation associated with dopaminergic neuronal death has been documented in Parkinson's disease. Through the use of in vivo and in vitro models, we demonstrated that lipid dysregulation manifests as a neuronal and glial response during iron overload. In this study, we show that cholesterol content and triacylglycerol (TAG) hydrolysis were strongly elevated in mice midbrain. Lipid cacostasis was concomitant with the loss of dopaminergic neurons, astrogliosis and elevated expression of α-synuclein. Exacerbated lipid peroxidation and markers of ferroptosis were evident in the midbrain from mice challenged with iron overload. An imbalance in the activity of lipolytic and acylation enzymes was identified, favoring neutral lipid hydrolysis, and consequently reducing TAG and cholesteryl ester levels. Notably, these observed alterations were accompanied by motor impairment in iron-treated mice. In addition, neuronal and glial cultures along with their secretomes were used to gain further insight into the mechanism underlying TAG hydrolysis and cholesterol accumulation as cellular responses to iron accumulation. We demonstrated that TAG hydrolysis in neurons is triggered by astrocyte secretomes. Moreover, we found that the ferroptosis inhibitor, ferrostatin-1, effectively prevents cholesterol accumulation both in neurons and astrocytes. Taken together, these results indicate that lipid disturbances occur in iron-overloaded mice as a consequence of iron-induced oxidative stress and depend on neuron-glia crosstalk. Our findings suggest that developing therapies aimed at restoring lipid homeostasis may lead to specific treatment for neurodegeneration associated with ferroptosis and brain iron accumulation.

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Stiff-person syndrome (SPS) is a rare neurological condition that frequently affects adults, with the neurologist diagnosing only one or two cases during his or her career. Reports of paediatric SPS are exceedingly rare, with less than 20 cases described in the literature.The patient presented was initially diagnosed with a functional movement disorder then a genetic dystonia, with a poor response to treatment trials and negative genetic testing. Consideration of Wilson's disease was refuted with non-supportive investigations and assessments.We aim to present the long road to diagnosing our first paediatric patient with SPS, who presented in middle childhood.

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BACKGROUND: Functional gait is a disorder of ambulation and balance internally inconsistent and incongruent with the phenotypic spectrum of neurological gait disorders. OBJECTIVES: This paper aims to clinically characterize patients with functional ataxia. METHODS: Patients with functional ataxia were analyzed out of 1350 patients in Ataxia Unit of the Federal University of São Paulo circa 2008 to 2022. RESULTS: Thirteen patients (1 %) presented with functional ataxia; all female, with a median age of 34.8 years. Six (46.2 %) had psychiatric comorbidities and 7 (53.8 %) endorsed a trigger. Diagnostic features included variable base and stride (100 %), "huffing and puffing" (30.7 %), knee-buckling (30.7 %), uneconomic posturing (38.5 %), tightrope walking (23 %), and trembling gait (15.4 %). Remarkably, no falls were reported in any case. 53.8 % recovered fully or partially, despite no treatment. CONCLUSIONS: Variability of base and stride are universal features of functional ataxia, yet falls are inconspicuous. Functional Ataxia is rare even in a specialized ataxia center.

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OBJECTIVE: The objective of this study was to analyze the trends in publications on intrathecal baclofen (ITB) therapy. METHODS: We searched Elsevier's Scopus database in February 2022 to find articles focused on ITB therapy. Data extracted included citation count, publication year, author's country and income category, journal and its 5-year impact factor, research type, disease requiring ITB, and target population. RESULTS: The analysis covered 615 articles from 1985 to 2022. The average citation count per article was 27.47 (95% confidence interval 23.75-31.18) and the mean impact factor was 4.54 (95% confidence interval 3.84-5.24). The majority (76.42%) were primary research, with 8.1% being interventional and 91.9% observational. Even so, one half of the top ten most cited were interventional. Secondary research and case reports made up 12.68% and 10.73% respectively, with narrative reviews making up most of the secondary research (79.48%). Only 1 study conducted a meta-analysis. The United States was the most prolific country. High-income countries published 96.42% of articles. CONCLUSIONS: The rising number of ITB articles and citations indicates growing interest and expanding knowledge in this field. However, there's a notable scarcity of research from low- and middle-income countries, particularly those with high prevalence of ITB-treatable diseases. The need for more evidence to overcome potential barriers to ITB implementation is emphasized. Despite an increasing number of publications, a large proportion presented low levels of evidence, such as case reports and narrative reviews, highlighting the need for more rigorous research methods to solidify the evidence base for ITB therapy.

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People with Parkinson's disease (pwPD) have reduced adaptability to postural control during prolonged standing compared to neurologically healthy individuals (control). Objective. The study aimed to characterize postural changes during prolonged standing and their effect on postural control in pwPD compared to control. We recorded the body sway of the second lumbar vertebra of 23 pwPD and 23 control while they performed prolonged standing (15 min). The number and amplitude of the body sway patterns (shifts, fidgets, and drifts), the root mean square, velocity, and frequency of the body sway were analyzed. The number of shifts in the anterior-posterior (AP) and medial-lateral (ML) directions was greater for the pwPD than the control. In addition, the amplitudes of shifts in the AP direction and fidgets in the AP and ML directions were greater for the pwPD than the control. Our results show that: (1) A larger number of shifts of body sway suggest references positions are frequently changing; (2) Fidgets is a pumping mechanism and can be sensory-demand action to restore mechanoreceptors activity on the foot sole; and (3) No drift changes may suggest there is no slow migration of reference position. We conclude that pwPD exhibits different behavior than healthy ones during prolonged standing, suggesting that prolonged standing could distinguish individuals with Parkinson's disease.

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Abstract Background Meige's syndrome is a type of facial dystonia characterized by the simultaneous occurrence of blepharospasm and oromandibular dystonia. Although botulinum toxin type A (OBTA) injections are the standard treatment, evidence of their effectiveness and safety in this scenario is still lacking. Objective Our research aimed to evaluate the improvement and occurrence of side effects following injections of onabotulinum toxin type A (OBTA) in patients with Meige's syndrome. Methods Patients with Meige's syndrome undergoing botulinum toxin injections were enrolled in this study. We assessed dystonia intensity before and 14 days after OBTA injection using the Burke-Fahn-Marsden Dystonia Rating Scale (BFMDRS) to measure the response of symptoms in the eyes (blepharospasm) and mouth (oromandibular dystonia). Other variables, such as dosage, side effects, and demographic data, were also recorded. Results The study included 41 participants, with a mean age of 67.7 years and a female-to-male ratio of 3.5:1. The mean BFMDRS score before the injections was 8.89, and after 14 days, it was 2.88. The most reported side effect was ptosis, with a 7.3% incidence. OBTA significantly reduced dystonia severity (p < 0.0001). The clinical response for the blepharospasm component was superior to the oromandibular dystonia component. Conclusion Our results support that OBTA seems to be an effective and safe therapeutic option for treating Meige's syndrome. The effect of OBTA was more pronounced in the treatment of blepharospasm than in oromandibular dystonia.

Resumo Antecedentes A síndrome de Meige (SM) é caracterizada pela ocorrência concomitante de blefarospasmo e distonia oromandibular. Embora a toxina onabotulínica do tipo A (TBA) seja o tratamento de escolha, há uma falta de evidências sobre sua eficácia e segurança nesse cenário. Objetivo O objetivo do nosso estudo foi avaliar os efeitos obtidos com a aplicação de TBA em pacientes com SM. Métodos Pacientes com SM que realizam aplicação de TBA foram convidados a participar desse estudo. Os participantes foram questionados sobre a intensidade da distonia antes e 14 dias após a injeção de TBA, utilizando a Escala de Distonia de Burke-Fahn-Marsden (EDBFM) para mensurar a resposta obtida em cada segmento. Outras variáveis, como dose, ocorrência de efeitos colaterais e dados demográficos, também foram registradas. Resultados O estudo contou com 41 participantes (idade média de 67,7; razão de 3,5 pacientes do sexo feminino para cada participante do sexo masculino). O escore médio na EDBFM antes das aplicações de TBA era 8,89, e, após 14 dias, 2,88. O efeito colateral mais reportado foi ptose (7.3%). A TBA foi capaz de reduzir a severidade da distonia (p < 0.0001), principalmente do blefarospasmo. Conclusão Nossos resultados corroboram que a TBA é uma terapêutica eficaz e segura no tratamento da SM. O efeito da TBA é superior no manejo do blefarospasmo em relação à distonia oromandibular.

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Abstract Spasmodic torticollis was an early designation used for cervical dystonia. The origin of this name is attributed to French physician and writer François Rabelais in the mid-sixteenth century. This early description of torticollis in the book Pantagruel was an inspiration for the understanding of cervical dystonia. The art expressed in Rabelais' literature - which was immortalized by the drawings of Gustave Doré - influenced poetry, art, and photography, and led to the adoption of the term torticollis in the neurological sciences.

Resumo Uma designação inicial usada para distonia cervical era torcicolo espasmódico. A origem desse termo é atribuída ao médico e escritor francês François Rabelais em meados do século XVI. Essa descrição inicial do torcicolo no livro Pantagruel foi uma inspiração para a compreensão da distonia cervical. A arte exibida na literatura de Rabelais - imortalizada pelos desenhos de Gustave Doré - influenciou a poesia, a arte e a fotografia, e levou à adoção do termo torcicolo nas ciências neurológicas.

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Abstract Background Wilson disease (WD) is an autosomal recessive disorder that leads to organ toxicity due to copper overload. Early diagnosis is complicated by the rarity and diversity of manifestations. Objective To describe the diagnostic features and response to treatment in our cohort of WD patients. Methods This was a retrospective analysis of 262 WD patients stratified by clinical presentation, complementary exams, ATP7B genotyping, and response to treatment. Results Symptoms occurred at an average age of 17.4 (7-49) years, and patients were followed up for an average of 9.6 (0-45) years. Patients presented mainly with hepatic (36.3%), neurologic (34.7%), and neuropsychiatric (8.3%) forms. Other presentations were hematologic, renal, or musculoskeletal, and 16.8% of the patients were asymptomatic. Kayser-Fleischer rings occurred in 78.3% of the patients, hypoceruloplasminemia in 98.3%, and elevated cupruria/24h in 73.0%, with an increase after D-penicillamine in 54.0%. Mutations of the ATP7B gene were detected in 84.4% of alleles. Brain magnetic resonance imaging showed abnormalities in the basal ganglia in 77.7% of patients. D-penicillamine was the first choice in 93.6% of the 245 patients, and 21.1% of these patients were switched due to adverse effects. The second-line therapies were zinc and trientine. The therapeutic response did not differ significantly between the drugs (p= 0.2). Nine patients underwent liver transplantation and 82 died. Conclusion Wilson disease is diagnosed at a late stage, and therapeutic options are limited. In people under 40 years of age with compatible manifestations, WD could be considered earlier in the differential diagnosis. There is a need to include ATP7B genotyping and therapeutic alternatives in clinical practice.

Resumo Antecedentes A doença de Wilson (DW) é um distúrbio autossômico recessivo caracterizado por acúmulo de cobre lesivo aos órgãos. O diagnóstico precoce é dificultado pela raridade e diversidade de apresentações. Objetivo Descrever características ao diagnóstico e resposta ao tratamento em uma coorte de DW. Métodos Análise retrospectiva de 262 casos de DW quanto à apresentação clínica, exames complementares, genotipagem e resposta ao tratamento. Resultados Os sintomas surgiram em uma média aos 17,4 (7-49) anos, e os pacientes foram acompanhados por uma média de 9,6 (0-45) anos. Os pacientes apresentaram principalmente formas hepáticas (36,3%), neurológicas (34,7%) e neuropsiquiátricas (8,3%). Outras apresentações foram hematológicas, renais e musculoesqueléticas. Apenas 16,8% eram assintomáticos. Anéis de Kayser-Fleischer ocorreram em 78,3% dos pacientes, hipoceruloplasminemia em 98,3%, e cuprúria elevada/24h em 73,0%, com aumento após D-penicilamina em 54,0%. Mutações do gene ATP7B foram detectadas em 84,4% dos alelos pesquisados. A ressonância magnética cerebral mostrou alterações em gânglios da base em 77,7% dos pacientes. O tratamento com D-penicilamina foi a escolha inicial em 93,6% dos 245 casos e foi trocado em 21,1% devido a efeitos adversos. Terapias de segunda linha foram zinco e trientina. A resposta terapêutica não diferiu significativamente entre os medicamentos (p= 0,2). Nove pacientes receberam transplante hepático e 82 faleceram. Conclusão O diagnóstico da DW ainda ocorre em estágios tardios, e as opções terapêuticas são limitadas. A DW deve ser considerada precocemente no diagnóstico diferencial de pessoas com menos de 40 anos com manifestações compatíveis. É necessário incorporar na prática clínica a genotipagem do ATP7B e alternativas terapêuticas à penicilamina.

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Abstract Background Cerebellar ataxias comprise sporadic and genetic etiologies. Ataxia may also be a presenting feature in hereditary spastic paraplegias (HSPs). Objective To report a descriptive analysis of the frequency of different forms of cerebellar ataxia evaluated over 17 years in the Ataxia Unit of Universidade Federal de São Paulo, Brazil. Methods Charts of patients who were being followed from January 2007 to December 2023 were reviewed. We used descriptive statistics to present our results as frequencies and percentages of the overall analysis. Diagnosed patients were classified according to the following 9 groups: sporadic ataxia, spinocerebellar ataxias (SCAs), other autosomal dominant cerebellar ataxias, autosomal recessive cerebellar ataxias (ARCAs), mitochondrial ataxias, congenital ataxias, X-linked ataxias, HSPs, and others. Results There were 1,332 patients with ataxias or spastic paraplegias. Overall, 744 (55.85%) of all cases were successfully diagnosed: 101 sporadic ataxia, 326 SCAs, 20 of other autosomal dominant cerebellar ataxias, 186 ARCAs, 6 X-linked ataxias, 2 mitochondrial ataxias, 4 congenital ataxias, and 51 HSPs. Conclusion This study describes the frequency of cerebellar ataxias in a large group of patients followed for the past 17 years, of whom 55% obtained a definitive clinical or molecular diagnosis. Future demographic surveys in Brazil or Latin American remain necessary.

Resumo Antecedentes Ataxias cerebelares compreendem as etiologias esporádicas e genéticas. Ataxia também pode ser uma característica das paraplegias espásticas hereditárias (HSPs). Objetivo Relatar uma análise descritiva da frequência das diferentes formas de ataxias cerebelares avaliadas ao longo de 17 anos no Setor da Ataxias da Universidade Federal de São Paulo, Brasil. Métodos Prontuários de pacientes acompanhados de janeiro de 2007 a dezembro de 2023 foram revisados. Usamos análise descritiva para apresentar nossos resultados como frequências e percentuais. Os pacientes foram classificados de acordo com os 9 grupos seguintes: ataxias esporádicas, ataxias espinocerebelares (SCA), outras ataxias cerebelares autossômicas dominantes, ataxias cerebelares autossômicas recessivas (ARCA), ataxias mitocondriais, ataxias congênitas, ataxias ligadas ao X, PEH e outros. Resultados Foram avaliados 1.332 pacientes. Desse total, 744 tiveram um diagnóstico definitivo: 101 ataxias esporádicas, 326 SCA, 20 outras ataxias cerebelares autossômicas dominantes, 186 (ARCA), 6 ataxias ligadas ao X, 2 ataxias mitocondriais, 4 ataxias congênitas e 51 HSP. Conclusão Esse estudo descreve a frequência e a etiologia das ataxias em um grande grupo de pacientes acompanhados nos últimos 17 anos, dos quais 55% obtiveram diagnóstico clínico ou molecular definitivos. Estudos demográficos futuros do Brasil ou da América Latina continuam sendo necessários.

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Abstract Background Hereditary or familial spastic paraplegias (SPG) comprise a group of genetically and phenotypically heterogeneous diseases characterized by progressive degeneration of the corticospinal tracts. The complicated forms evolve with other various neurological signs and symptoms, including movement disorders and ataxia. Objective To summarize the clinical descriptions of SPG that manifest with movement disorders or ataxias to assist the clinician in the task of diagnosing these diseases. Methods We conducted a narrative review of the literature, including case reports, case series, review articles and observational studies published in English until December 2022. Results Juvenile or early-onset parkinsonism with variable levodopa-responsiveness have been reported, mainly in SPG7 and SPG11. Dystonia can be observed in patients with SPG7, SPG11, SPG22, SPG26, SPG35, SPG48, SPG49, SPG58, SPG64 and SPG76. Tremor is not a frequent finding in patients with SPG, but it is described in different types of SPG, including SPG7, SPG9, SPG11, SPG15, and SPG76. Myoclonus is rarely described in SPG, affecting patients with SPG4, SPG7, SPG35, SPG48, and SPOAN (spastic paraplegia, optic atrophy, and neuropathy). SPG4, SPG6, SPG10, SPG27, SPG30 and SPG31 may rarely present with ataxia with cerebellar atrophy. And autosomal recessive SPG such as SPG7 and SPG11 can also present with ataxia. Conclusion Patients with SPG may present with different forms of movement disorders such as parkinsonism, dystonia, tremor, myoclonus and ataxia. The specific movement disorder in the clinical manifestation of a patient with SPG may be a clinical clue for the diagnosis.

Resumo Antecedentes As paraplegias espásticas hereditárias ou familiares (SPG) compreendem um grupo de doenças geneticamente e fenotipicamente heterogêneas caracterizadas por degeneração progressiva dos tratos corticospinais. As formas complicadas evoluem com vários outros sinais e sintomas neurológicos, incluindo distúrbios do movimento e ataxia. Objetivo Resumir as descrições clínicas de SPG que se manifestam com distúrbios do movimento ou ataxias para auxiliar o clínico na tarefa de diagnosticar essas doenças. Métodos Realizamos uma revisão da literatura, incluindo relatos de casos, séries de casos, artigos de revisão e estudos observacionais publicados em inglês até dezembro de 2022. Resultados O parkinsonismo juvenil ou de início precoce com resposta variável à levodopa foi relatado principalmente em SPG7 e SPG11. A distonia pode ser observada em pacientes com SPG7, SPG11, SPG22, SPG26, SPG35, SPG48, SPG49, SPG58, SPG64 e SPG76. O tremor não é um achado frequente em pacientes com SPG, mas é descrito em diferentes tipos de SPG, incluindo SPG7, SPG9, SPG11, SPG15 e SPG76. A mioclonia é raramente descrita em SPG, afetando pacientes com SPG4, SPG7, SPG35, SPG48 e SPOAN (paraplegia espástica, atrofia óptica e neuropatia). SPG4, SPG6, SPG10, SPG27, SPG30 e SPG31 podem raramente apresentar ataxia com atrofia cerebelar. E SPG autossômico recessivo, como SPG7 e SPG11, também pode apresentar ataxia. Conclusão Indivíduos com SPG podem apresentar diferentes formas de distúrbios do movimento, como parkinsonismo, distonia, tremor, mioclonia e ataxia. O distúrbio específico do movimento na manifestação clínica de um paciente com SPG pode ser uma pista clínica para o diagnóstico.

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Extrapyramidal side effects (EPS) can be induced by neuroleptics that regulate the expression of transcription factor FosB and dopaminergic mediator DARPP-32 in the striatum. However, the long-term neurobiological changes in striatal projection neurons resulting from a cumulative dosage of typical and atypical antipsychotics are poorly understood. The present study aimed to determine the differential and long-lasting changes in FosB distribution and DARPP-32 phosphorylation in the striatum and nucleus accumbens (NAc) associated with chronic antipsychotic-induced EPS. Male C57Bl/6J mice received daily injections of Olanzapine (Olz, 15 mg/kg), Clozapine (Clz, 20 mg/kg), or Haloperidol (Hal, 1 mg/kg), for a period of 11 weeks with a 4-day withdrawal period before the last dosage. Catalepsy for detection of EPS, along with open-field and rotarod tests, were assessed as behavioral correlates of motor responses. Additionally, FosB and phosphorylated-DARPP-32 immunohistochemistry were examined in striatal regions after treatment. All antipsychotics produced catalepsy and reduced open-field exploration, such as impaired rota-rod performance after Olz and Hal. The washout period was critical for Clz-induced side effects reduction. Both Olz and Clz increased FosB in NAc Shell-region, and phosphoThr34-DARPP-32 in NAc. Only Clz reduced phosphoThr75-DARPP-32 in the dorsal striatum and showed FosB/phosphoThr34-Darpp-32-ir in the NAc Core region. This study provides evidence that atypical antipsychotics such as Olz and Clz also give rise to EPS effects frequently associated with a cumulative dosage of typical neuroleptics such as Hal. Nevertheless, FosB/phosphoThr34-Darpp-32-ir in the NAc Core region is associated with hypokinetic movements inhibition.

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The basal ganglia are a subcortical collection of interacting clusters of cell bodies, and are involved in reward, emotional, and motor circuits. Within all the brain processing necessary to carry out voluntary movement, the basal nuclei are fundamental, as they modulate the activity of the motor regions of the cortex. Despite being much studied, the motor circuit of the basal ganglia is still difficult to understand for many people at all, especially undergraduate and graduate students. This review article seeks to bring the functioning of this circuit with a simple and objective approach, exploring the functional anatomy, neurochemistry, neuronal pathways, related diseases, and interactions with other brain regions to coordinate voluntary movement.

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The neural correlates of locomotion impairments observed in people with Parkinson's disease (PD) are not fully understood. We investigated whether people with PD present distinct brain electrocortical activity during usual walking and the approach phase of obstacle avoidance when compared to healthy individuals. Fifteen people with PD and fourteen older adults walked overground in two conditions: usual walking and obstacle crossing. Scalp electroencephalography (EEG) was recorded using a mobile 64-channel EEG system. Independent components were clustered using a k-means clustering algorithm. Outcome measures included absolute power in several frequency bands and alpha/beta ratio. During the usual walk, people with PD presented a greater alpha/beta ratio in the left sensorimotor cortex than healthy individuals. While approaching obstacles, both groups reduced alpha and beta power in the premotor and right sensorimotor cortices (balance demand) and increased gamma power in the primary visual cortex (visual demand). Only people with PD reduced alpha power and alpha/beta ratio in the left sensorimotor cortex when approaching obstacles. These findings suggest that PD affects the cortical control of usual walking, leading to a greater proportion of low-frequency (alpha) neuronal firing in the sensorimotor cortex. Moreover, the planning for obstacle avoidance changes the electrocortical dynamics associated with increased balance and visual demands. People with PD rely on increased sensorimotor integration to modulate locomotion.

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BACKGROUND: Balance impairments in people with Parkinson's disease (PD) demonstrated mainly in challenging postural tasks, such as increased body oscillation may be attributed to the deficits in the brain structures functionality involved in postural control (e.g., motor cortex, midbrain, and brainstem). Although promising results, the effect of transcranial direct current stimulation (tDCS) on postural control in people with PD is unclear, especially in objective measures such as the center of pressure (CoP) parameters. Thus, we analyzed the effects of a single session of tDCS on the CoP parameters during the adapted tandem position in people with PD. METHODS: Nineteen people with PD participated in this crossover, randomized, and double-blind study. Anodal tDCS was applied over the primary motor cortex in two conditions of stimulation (2 mA/active and sham) on two different days for 20 min immediately before the postural control evaluation. Participants remained standing in an adapted tandem position for the postural control assessment for 30 s (three trials). CoP parameters were acquired by a force plate. RESULTS: No significant differences were demonstrated between stimulation conditions (p-value range = 0.15-0.89). CONCLUSIONS: Our results suggested that a single session of tDCS with 2 mA does not improve the postural control of people with PD during adapted tandem.

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