There is emerging evidence suggesting that a cortical stroke can cause delayed and remote hippocampal dysregulation, leading to cognitive impairment. In this study, we aimed to investigate motor and cognitive outcomes after experimental stroke, and their association with secondary neurodegenerative processes. Specifically, we used a photothrombotic stroke model targeting the motor and somatosensory cortices of mice. Motor function was assessed using the cylinder and grid walk tasks. Changes in cognition were assessed using a mouse touchscreen platform. Neuronal loss, gliosis and amyloid-β accumulation were investigated in the peri-infarct and ipsilateral hippocampal regions at 7, 28 and 84 days post-stroke. Our findings showed persistent impairment in cognitive function post-stroke, whilst there was a modest spontaneous motor recovery over the investigated period of 84 days. In the peri-infarct region, we detected a reduction in neuronal loss and decreased neuroinflammation over time post-stroke, which potentially explains the spontaneous motor recovery. Conversely, we observed persistent neuronal loss together with concomitant increased neuroinflammation and amyloid-β accumulation in the hippocampus, which likely accounts for the persistent cognitive dysfunction. Our findings indicate that cortical stroke induces secondary neurodegenerative processes in the hippocampus, a region remote from the primary infarct, potentially contributing to the progression of post-stroke cognitive impairment.
Matched MeSH terms: Motor Disorders/complications; Motor Disorders/physiopathology*
Parkinson's Disease (PD) is characterized as the commonest neurodegenerative illness that gradually degenerates the central nervous system. The goal of this review is to come out with a summary of the recent progress of numerous forms of sensors and systems that are related to diagnosis of PD in the past decades. The paper reviews the substantial researches on the application of technological tools (objective techniques) in the PD field applying different types of sensors proposed by previous researchers. In addition, this also includes the use of clinical tools (subjective techniques) for PD assessments, for instance, patient self-reports, patient diaries and the international gold standard reference scale, Unified Parkinson Disease Rating Scale (UPDRS). Comparative studies and critical descriptions of these approaches have been highlighted in this paper, giving an insight on the current state of the art. It is followed by explaining the merits of the multiple sensor fusion platform compared to single sensor platform for better monitoring progression of PD, and ends with thoughts about the future direction towards the need of multimodal sensor integration platform for the assessment of PD.
Matched MeSH terms: Motor Disorders/complications; Motor Disorders/diagnosis*; Motor Disorders/physiopathology*
Rett Syndrome (RTT) is a genetic disorder that is caused by mutations in the x-linked gene coding for methyl-CpG-biding-protein 2 (MECP2) and that mainly affects females. Male and female transgenic mouse models of RTT have been studied extensively, and we have learned a great deal regarding RTT neuropathology and how MeCP2 deficiency may be influencing brain function and maturation. In this manuscript we review what is known concerning structural and coinciding functional and behavioral deficits in RTT and in mouse models of MeCP2 deficiency. We also introduce our own corroborating data regarding behavioral phenotype and morphological alterations in volume of the cortex and striatum and the density of neurons, aberrations in experience-dependent plasticity within the barrel cortex and the impact of MeCP2 loss on glial structure. We conclude that regional structural changes in genetic models of RTT show great similarity to the alterations in brain structure of patients with RTT. These region-specific modifications often coincide with phenotype onset and contribute to larger issues of circuit connectivity, progression, and severity. Although the alterations seen in mouse models of RTT appear to be primarily due to cell-autonomous effects, there are also non-cell autonomous mechanisms including those caused by MeCP2-deficient glia that negatively impact healthy neuronal function. Collectively, this body of work has provided a solid foundation on which to continue to build our understanding of the role of MeCP2 on neuronal and glial structure and function, its greater impact on neural development, and potential new therapeutic avenues.
Matched MeSH terms: Motor Disorders/etiology; Motor Disorders/physiopathology
Cerebellar ataxia is a neurodegenerative disorder with no definitive treatment. Although several studies have demonstrated the neuroprotective effects of Hericium erinaceus (H.E.), its mechanisms in cerebellar ataxia remain largely unknown. Here, we investigated the neuroprotective effects of H.E. treatment in an animal model of 3-acetylpyridine (3-AP)-induced cerebellar ataxia. Animals administered 3-AP injection exhibited remarkable impairments in motor coordination and balance. There were no significant effects of 25 mg/kg H.E. on the 3-AP treatment group compared to the 3-AP saline group. Interestingly, there was also no significant difference in the 3-AP treatment group compared to the non-3-AP control, indicating a potential rescue of motor deficits. Our results revealed that 25 mg/kg H.E. normalised the neuroplasticity-related gene expression to the level of non-3-AP control. These findings were further supported by increased protein expressions of pERK1/2-pCREB-PSD95 as well as neuroprotective effects on cerebellar Purkinje cells in the 3-AP treatment group compared to the 3-AP saline group. In conclusion, our findings suggest that H.E. potentially rescued behavioural motor deficits through the neuroprotective mechanisms of ERK-CREB-PSD95 in an animal model of 3-AP-induced cerebellar ataxia.
Matched MeSH terms: Motor Disorders/genetics; Motor Disorders/metabolism; Motor Disorders/pathology; Motor Disorders/prevention & control*
[Purpose] Understanding the essential mechanisms in post-stroke recovery not only provides important basic insights into brain function and plasticity but can also guide the development of new therapeutic approaches for stroke patients. This review aims to give an overview of how various variables of Magnetic Resonance-Diffusion Tensor Imaging (MR-DTI) metrics of fractional anisotropy (FA) can be used as a reliable quantitative measurement and indicator of corticospinal tract (CST) changes, particularly in relation to functional motor outcome correlation with a Fugl-Meyer assessment in stroke rehabilitation. [Methods] PubMed electronic database was searched for the relevant literature, using key words of diffusion tensor imaging (dti), corticospinal tract, and stroke. [Results] We reviewed the role of FA in monitoring CST remodeling and its role of predicting motor recovery after stroke. We also discussed the mechanism of CST remodeling and its modulation from the value of FA and FMA-UE. [Conclusion] Heterogeneity of post-stroke brain disorganization and motor impairment is a recognized challenge in the development of accurate indicators of CST integrity. DTI-based FA measurements offer a reliable and evidence-based indicator for CST integrity that would aid in predicting motor recovery within the context of stroke rehabilitation.
Incidences of cerebral palsy (CP) in children are not quite common even though it is the most common motor disorder in children. Further quality of life in CP cases is not so good in young adult stages and has to face certain problems. However scalp haematoma formation in CP patient without injury to head is rarely been reported. The case is being reported for the first time from Malaysia. We report on a unique case of scalp haematoma in an 18-year-old girl of known CP patient with unknown cause. No history of trauma or fall with any of the focal neurological signs or symptoms was found. Clinical examination showed soft boggy swelling of 8 x 10 cm size, involving most of scalp and upper face. CT - scan showed scalp haematoma with right orbital extraconal lesion. She underwent incision and drainage of scalp lesion; consequently around 100 ml of clotted blood came out. At follow-up she was doing well.