Positive impact of the Therasuit method on gross motor function of children with autism spectrum disorder: Case series.

The Therasuit method is a valuable physiotherapeutic method to improve the gross motor function of children with neuromotor disorders. This series of case studies investigates the effect of the Therasuit method on the gross motor function of children with autism spectrum disorder (ASD). Therasuit method is a therapeutic intervention that involves the use of a therapeutic suit attached to a cage to stimulate gross motor skills, muscle strengthening, stretching, task training, and balance, which is a positive intervention for other neurodevelopmental disorders. The study was conducted with nine male children (42.1 + 4.1 months old) with ASD who received the Therasuit protocol for 4 weeks (20 sessions). The Gross Motor Function Measure (GMFM-88) was used to assess the children's gross motor function before and after the Therasuit method intervention. In dimension B, several skills showed improvement, including transfer to sitting, lean forward and return, trunk rotation without support, and transfer from sitting to all four stances. In dimension C, an increase was observed in skills such as being prone to all four stance transfers and reaching above the shoulders. In dimension D, maximum scores were achieved in skills such as pulling to stand on a large bench without assistance. The dimensions with the greatest impairment were D and E, corresponding to gross motor skills in orthostasis and dynamic skills in orthostasis, respectively. The findings suggest that the Therasuit method is a promising resource for treating motor impairments in children with ASD. However, further studies with a larger sample size, an adequate control condition, and random assignment of participants would be needed to provide stronger evidence of the method's effectiveness in this population.

Seguimento de pessoas acometidas por doenças cerebrovasculares em um hospital regional amazônico: uma metodologia WHO STEP Stroke / Follow-up of people affected by cerebrovascular disease in a regional amazonic hospital: a WHO STEPS Stroke methodology

O WHO STEP Stroke foi desenvolvida para monitorar casos de doenças cerebrovasculares e possibilitar comparações de incidências. Objetivo: Descrever o perfil sociodemográfico e funcionalidade de pacientes acometidos por AVC admitidos no Hospital Regional de Coari durante um ano, e acompanha-los ao longo de um mês após admissão. Método: Estudo descritivo observacional, prospectivo e de seguimento dos casos entre outubro de 2010 e outubro de 2011. Utilizou-se a primeira etapa (Step 1) do WHO STEP Stroke para avaliar as hospitalizações por AVC em Coari-AM. Foram acompanhados 23 pacientes através de questionário padrão em até dois dias na internação, 10 e 28 dias após a internação. Resultados: A população estudada tinha média de idade de 72,8 (DP= 12,4) anos, em sua maioria homens (65,7%), pardos (65,2%) e hipertensos (95,7%), com incidência hospitalar de 30 casos em 100.000 habitantes e taxa de letalidade em 10 dias de 30,4% e 28 dias de 34,8%. O comprometimento neurológico na internação teve mediana de 28 (IIQ= 15-38) pontos, sendo 73,9% classificados como grave. Houve comprometimento funcional entre os sobreviventes. Conclusão: Estudo revelou uma predominância de homens, com idade elevada, pardos, sem estudo formal, baixa renda e com histórico de hipertensão arterial e diabetes, como perfil de internação hospitalar por doenças cerebrovasculares no município. A incidência de casos hospitalares de AVC foi em 30 (por 100.000) em Coari-AM, com graves comprometimentos neurológicos na admissão, e altas taxas de letalidade e prejuízo funcional após 28 dias do evento, quando comparadas a outras localidades no Brasil e no mundo

The WHO STEP Stroke is a tool developed to monitor cases of cerebrovascular and allow comparison of its incidence throughout the world. Objective: To describe the sociodemographic profile and functionality of stroke inpatients admitted in Coari´s Regional Hospital and followed up one month after admittance. Method: This is a prospective, descriptive observational and follow-up study of cases between October 2010 and October 2011. In this study, we used the first step (Step 1) of the WHO STEP Stroke to assess stroke hospitalization in Coari-AM Twenty-three patients were monitored with a standard questionnaire up to two days after hospitalization, 10 days, and 28 after hospitalization. Results: The studied population had average age of 72.8 (SD= 12.4) years, mostly men (65.7%), brown (65.2%), and hypertensive (95.7%), with a hospital incidence of 30 cases for 100.000 people, and mortality in 10 days of 30.4% and 28 days of 34.8%. The neurological impairment at hospitalization had a median of 28 (IIQ= 15-38) points, with 73.9% classified as severe. There was an impairment in functionality among the survivors. Conclusion: This study showed the profile of hospital admittance for cerebrovascular disease in this city to be mainly composed by older men, brown, with no formal study, low income, and history of systemic arterial hypertension and diabetes. The hospital incidence for stroke was 30 (per 100.000) in Coari-AM, with severe neurological impairment at admission, with high mortality rates, and functional deficits 28 days after the event when compared to other regions in Brazil and in the world

Can an aversive, extinction-resistant memory trigger impairments in walking adaptability? An experimental study using adult rats.

Cognitive demands can influence the adaptation of walking, a crucial skill to maintain body stability and prevent falls. Whilst previous research has shown emotional load tunes goal-directed movements, little attention has been given to this finding. This study sought to assess the effects of suffering an extinction-resistant memory on skilled walking performance in adult rats, as an indicator of walking adaptability. Thus, 36 Wistar rats were divided in a two-part experiment. In the first part (n=16), the aversive, extinction-resistance memory paradigm was established using a fear-conditioning chamber. In the second, rats (n=20) were assessed in a neutral room using the ladder rung walking test before and tree days after inducing an extinction-resistance memory. In addition, the elevated plus-maze test was used to control the influence of the anxiety-like status on gait adaptability. Our results revealed the shock group exhibited worse walking adaptability (lower skilled walking score), when compared to the sham group. Moreover, the immobility time in the ladder rung walking test was similar to the controls, suggesting that gait adaptability performance was not a consequence of the fear generalization. No anxiety-like behavior was observed in the plus maze test. Finally, correlation coefficients also showed the skilled walking performance score was positively correlated with the number of gait cycles and trial time in the ladder rung walking test and the total crossings in the plus maze. Overall, these preliminary findings provide evidence to hypothesize an aversive, extinction-resistant experience might change the emotional load, affecting the ability to adapt walking.

Experimental Post-traumatic Stress Disorder Decreases Astrocyte Density and Changes Astrocytic Polarity in the CA1 Hippocampus of Male Rats.

Post-traumatic stress disorder (PTSD) is a psychiatric condition resulting from exposure to a traumatic event. It is characterized by several debilitating symptoms including re-experiencing the past trauma, avoidance behavior, increased fear, and hyperarousal. Key roles in the neuropathology of PTSD and its symptomatology have been attributed to the hippocampus and amygdala. These regions are involved in explicit memory processes and context encoding during fear conditioning. The aim of our study was to investigate whether PTSD is capable of altering the morphology, density and expression of glial fibrillary acidic protein (GFAP) in astrocytes from the CA1 region of the hippocampus and the medial amygdala and correlate the data obtained with the orientation index of the polarity of astrocytes. Thirty male rats were divided in two groups: control (n = 15) and PTSD (n = 15). The inescapable shock protocol, in which the animals are exposed to a single episode of footshock, was used to induce PTSD. Our results show that, in the hippocampus, PTSD is capable of decreasing the density of GFAP+ astrocytes as well as altering astrocytic morphology, as shown by the reductions observed in the total number of primary processes, in the number of primary processes in the lateral quadrants, and the degree of branching in the lateral quadrants. The analysis of the orientation index indicates that PTSD alters the polarity of hippocampal astrocytes. No alterations were observed in the amygdala astrocytes. Therefore, this study demonstrates notable changes in hippocampal astrocytes, supporting the concept that these cells play an important role in PTSD symptomatology.

Antidepressant Effects of Ketamine Are Not Related to ¹8F-FDG Metabolism or Tyrosine Hydroxylase Immunoreactivity in the Ventral Tegmental Area of Wistar Rats.

Major depressive disorder (MDD) is an important health problem that is often associated to stress. One of the main brain regions related to MDD is the ventral tegmental area (VTA), a dopaminergic center, part of the reward and motivation circuitry. Recent studies show that changes to VTA dopaminergic neurons are associated with depression and treatment. Ketamine has recently shown a fast, potent antidepressant effect in acute, sub-anesthetic doses. Thus, our aims were to elucidate if ketamine would be able to revert depression-like behaviors induced by a chronic unpredictable stress (CUS) protocol and if it could cause alterations to metabolism and tyrosine hydroxylase (TH)-immunoreactivity in VTA. For this, 48 Wistar rats were divided into four groups: control + saline (CTRL + SAL), control + ketamine (CTRL + KET), CUS + saline (CUS + SAL), CUS + ketamine (CUS + KET). The CUS groups underwent 28 days of CUS protocol. Saline or ketamine (10 mg/kg) was administered intraperitonially once on day 28. The behavior was assessed by the sucrose preference test, the open field test, and the forced swim test. Glucose brain metabolism was assessed and quantified with microPET. TH-immunoreactivity was assessed by estimating neuronal density and regional and cellular optical densities. A decrease in sucrose intake in the CUS groups and an increase in immobility was rapidly reverted by ketamine (p < 0.05). No difference was observed in the open field test. There was no alteration to VTA metabolism and TH-immunoreaction. These results suggest that the depressive-like behavior induced by CUS and the antidepressant effects of ketamine are unrelated to changes in neuronal metabolism or dopamine production in VTA.

Astrocyte morphology after ischemic and hemorrhagic experimental stroke has no influence on the different recovery patterns.

Stroke, broadly subdivided into ischemic and hemorrhagic subtypes, is a serious health-care problem worldwide. Previous studies have suggested ischemic and hemorrhagic stroke could present different functional recovery patterns. However, little attention has been given to this neurobiological finding. Coincidently, astrocyte morphology could be related to improved sensorimotor recovery after skilled reaching training and modulated by physical exercise and environmental enrichment. Therefore, it is possible that astrocyte morphology might be linked to differential recovery patterns between ischemic and hemorrhagic stroke. Thus, we decided to compare long-term GFAP-positive astrocyte morphology after ischemic (IS, n=5), hemorrhagic (HS, n=5) and sham (S, n=5) stroke groups (induced by endothelin-1, collagenase type IV-S and salina, respectively). Our results showed ischemic and hemorrhagic stroke subtypes induced similar long-term GFAP-positive astrocyte plasticity (P>0.05) for all evaluated measures (regional and cellular optical density; astrocytic primary processes ramification and length; density of GFAP positive astrocytes) in perilesional sensorimotor cortex and striatum. These interesting negative results discourage similar studies focused on long-term plasticity of GFAP-positive astrocyte morphology and recovery comparison of stroke subtypes.

Resveratrol prevents akinesia and restores neuronal tyrosine hydroxylase immunoreactivity in the substantia nigra pars compacta of diabetic rats.

This study evaluated the effects of resveratrol on locomotor behaviors, neuronal and glial densities, and tyrosine hydroxylase immunoreactivity in the substantia nigra pars compacta of rats with streptozotocin-induced diabetes. Animals were divided into four groups: non-diabetic rats treated with saline (SAL), non-diabetic rats treated with resveratrol (RSV), diabetic rats treated with saline (DM) and diabetic rats treated with resveratrol (DM+RSV). The animals received oral gavage with resveratrol (20 mg/kg) for 35 days. The open field test and the bar test were performed to evaluate bradykinesia and akinesia, respectively. The Nissl-stained neuronal and glial densities and the dopaminergic neuronal density were estimated using planar morphometry. Tyrosine hydroxylase immunoreactivity was evaluated using regional and cellular optical densitometry. In relation to the locomotor behaviors, it was observed that the DM group developed akinesia, which was attenuated by resveratrol in the DM+RSV group, while the DM and DM+RSV groups showed bradykinesia. Our main morpho-physiological results demonstrated: a decrease in the cellular tyrosine hydroxylase immunoreactivity in the DM group, which was attenuated by resveratrol in the DM+RSV group; a higher neuronal density in the RSV group, when compared to the DM and DM+RSV groups; an increase in the glial density in the DM group, which was also reversed by resveratrol in the DM+RSV group. Resveratrol treatment prevents akinesia development and restores neuronal tyrosine hydroxylase immunoreactivity and glial density in the substantia nigra pars compacta of diabetic rats, suggesting that this polyphenol could be a potential therapeutic option against diabetes-induced nigrostriatal dysfunctions.

Physical exercise increases GFAP expression and induces morphological changes in hippocampal astrocytes.

Physical exercise has an important influence on brain plasticity, which affects the neuron-glia interaction. Astrocytes are susceptible to plasticity, and induce and stabilize synapses, regulate the concentration of various molecules, and support neuronal energy metabolism. The aim of our study was to investigate whether physical exercise is capable of altering the morphology, density and expression of glial fibrillary acidic protein (GFAP) in astrocytes from the CA1 region of rat hippocampus. Thirteen male rats were divided in two groups: sedentary (n = 6) and exercise (n = 7). The animals in the exercise group were submitted to a protocol of daily physical exercise on a treadmill for four consecutive weeks. GFAP immunoreactivity was evaluated using optical densitometry and the morphological analyses were an adaptation of Sholl's concentric circles method. Our results show that physical exercise is capable of increasing the density of GFAP-positive astrocytes as well as the regional and cellular GFAP expression. In addition, physical exercise altered astrocytic morphology as shown by the increase observed in the degree of ramification in the lateral quadrants and in the length of the longest astrocytic processes in the central quadrants. Our data demonstrate important changes in astrocytes promoted by physical exercise, supporting the idea that these cells are involved in regulating neural activity and plasticity.

Behavior outcome after ischemic and hemorrhagic stroke, with similar brain damage, in rats.

Stroke causes disability and mortality worldwide and is divided into ischemic and hemorrhagic subtypes. Although clinical trials suggest distinct recovery profiles for ischemic and hemorrhagic events, this is not conclusive due to stroke heterogeneity. The aim of this study was to produce similar brain damage, using experimental models of ischemic (IS) and hemorrhagic (HS) stroke and evaluate the motor spontaneous recovery profile. We used 31 Wistar rats divided into the following groups: Sham (n=7), ischemic (IS) (n=12) or hemorrhagic (HS) (n=12). Brain ischemia or hemorrhage was induced by endotelin-1 (ET-1) and collagenase type IV-S (collagenase) microinjections, respectively. All groups were evaluated in the open field, cylinder and ladder walk behavioral tests at distinct time points as from baseline to 30 days post-surgery (30 PS). Histological and morphometric analyses were used to assess the volume of lost tissue and lesion length. Present results reveal that both forms of experimental stroke had a comparable long-term pattern of damage, since no differences were found in volume of tissue lost or lesion size 30 days after surgery. However, behavioral data showed that hemorrhagic rats were less impaired at skilled walking than ischemic ones at 15 and 30 days post-surgery. We suggest that experimentally comparable stroke design is useful because it reduces heterogeneity and facilitates the assessment of neurobiological differences related to stroke subtypes; and that spontaneous skilled walking recovery differs between experimental ischemic and hemorrhagic insults.

Physical exercise down-regulated locomotor side effects induced by haloperidol treatment in Wistar rats.

Extra-pyramidal symptoms (EPS) such as akinesia, dystonia, gait alteration and tremors are observed when dopamine D2-receptors are blocked by pharmacological agents such as haloperidol. These alterations produce a Parkinson disease-like state (PLS). Physical exercise has been proven to improve gait and locomotor symptoms in Parkinson's disease; we sought to elucidate the effects of physical exercise on PLS induced by chronic administration of haloperidol in rats. We used 48 rats distributed into four groups: Control, Exercise, Haloperidol, and Hal+Exe. All the animals received a daily injection of saline or haloperidol for 30 days, and the exercise groups underwent a daily 30-minute exercise protocol for 20 days. The animals were subjected to the ink-paw test, bar test and open-field test throughout the training period. The haloperidol-induced akinesia increased throughout the days of injections, but exercise was shown to alleviate it. The assessment showed shortened stride length and increased stance width with the use of haloperidol, which were significantly alleviated by exercise. These results indicate that exercise could be an interesting approach towards reducing unwanted EPS caused by haloperidol.

Effects of physical exercise on spatial memory and astroglial alterations in the hippocampus of diabetic rats.

Type 1 diabetes mellitus (T1DM) is associated with neurocognitive dysfunction and astrogliosis. Physical exercise prevents cognitive impairments and induces important brain modifications. The aim of our study was to investigate the effect of treadmill exercise on spatial memory and astrocytic function in the hippocampus of a T1DM model. Fifty-seven Wistar rats were divided into four groups: trained control (TC) (n = 15), non-trained control (NTC) (n = 13), trained diabetic (TD) (n = 14) and non-trained diabetic (NTD) (n = 15). One month after streptozotocin-induced diabetes, exercise groups were submitted to 5 weeks of physical training, and then, all groups were assessed in the novel object-placement recognition task. Locomotor activity was analyzed in the open field apparatus using Any-maze software. The expression of glial fibrillary acidic protein (GFAP) and S100B in hippocampus and cerebrospinal fluid were measured using ELISA assay, and hippocampal GFAP immunoreactivity was evaluated by means of immunohistochemistry and optical densitometry. The results showed that physical exercise prevents and/or reverts spatial memory impairments observed in NTD animals (P < 0.01). Decreased locomotor activity was observed in both the NTD and TD groups when compared with controls (P < 0.05). ELISA and immunohistochemistry analyzes showed there was a reduction in GFAP levels in the hippocampus of NTD animals, which was not found in TD group. ELISA also showed an increase in S100B levels in the cerebrospinal fluid from the NTD group (P < 0.01) and no such increase was found in the TD group. Our findings indicate that physical exercise prevents and/or reverts the cognitive deficits and astroglial alterations induced by T1DM.