China
Africa
Explore chapters and articles related to this topic
Phantom Sensations (including Phantom Limb Pain)
Published in Alexander R. Toftness, Incredible Consequences of Brain Injury, 2023
Your ability to sense your body parts—where they are currently located, and what they are touching—is possible thanks to nerve cells that run like cables from your body parts all the way up into your brain. The cables then run back down again into each muscle, forming a loop of what is essentially electrical wiring. As examples, you have loops of nerve cell connections that keep track of your leg's placement in space, or whether your hand is bumping up against something dangerous like a hot stovetop. Many of these cells are in your body parts themselves and in your spine, but an important portion of these cells are in a part of your brain located near the very peak of your skull, called the sensorimotor cortex. This area is divided between two parts: unsurprisingly, the sensory and motor parts. The sensory cells are in charge of interpreting incoming sensations from each body part, such as touch. The motor cells are involved in sending out signals that cause each body part to move. It is because of these cells, left behind in the brain when a body part is removed, that phantom sensations are possible.
Neurological disorders
Published in Michael Horvat, Ronald V. Croce, Caterina Pesce, Ashley Fallaize, Developmental and Adapted Physical Education, 2019
Michael Horvat, Ronald V. Croce, Caterina Pesce, Ashley Fallaize
Locomotion: The development of locomotion or gait patterns is often affected in children with cerebral palsy. According to Bar-Or and Rowland (2004), children with cerebral palsy become deconditioned and lose their mobility. The primary focus in the generation and control of locomotion has been the role of higher brain centers, such as the sensorimotor cortex. The deficits in locomotion in children with cerebral palsy have been ascribed to damage to the basic circuitry serving pattern generation, to failed maturation of spinal reflexes and/or the descending systems that control them, and to changes in the mechanical properties of muscles (Leonard et al., 1991). Leonard et al. (1991) also found that normal features of adult gait did not develop in children with severe cerebral palsy. These problems were similar to those identified by Bar-Or (1983) and Unnithan et al. (1996). Bottos et al. (1995) also concluded that severe deformities, resulting from cerebral palsy, affected the choice of locomotion pattern and indicated that locomotion pattern, age at onset, and even manner of execution all influenced prognosis for walking.
The Life Enrichment Model
Published in Lisa D. Hinz, Beyond Self-Care for Helping Professionals, 2018
Information processing begins at the Kinesthetic/Sensory level of the ETC. This kind of brain activity corresponds to what some have called the reptilian brain (MacLean, 1985). Structures like the cerebellum, basal ganglia, primary motor cortex and sensorimotor cortex represent the evolutionarily oldest structures of the brain, those that do not require conscious thought in mediating behavior. Human beings do not have to think through the process of walking in order to put one foot in front of another. They do not have to engage in conscious thought in order to mediate sensory experiences and initiate automatic behaviors. If I place my hand on a hot stove, consciously thinking, “That stove is hot, I should move my hand” would take a few seconds. I would receive a third degree burn if I took that long to process the sensory stimulation. Instead, I react immediately based on what I experience: The sensation initiates action. It is adaptive and life-saving for all species to respond to noxious or dangerous stimuli without using slow and deliberate conscious thought, as well as to perform automatic behaviors like walking. The lack of conscious thought involved in the processing of movement and sensation information is what defines the reptilian brain.
Deficits underlying handgrip performance in mildly affected chronic stroke persons
Published in Topics in Stroke Rehabilitation, 2021
Esther Prados-Román, Irene Cabrera-Martos, Laura López-López, Janet Rodríguez-Torres, Irene Torres-Sánchez, Araceli Ortiz-Rubio, Marie Carmen Valenza
Jung et al.4 demonstrated that persons with weakness of the ipsilesional upper limb maximally recovered within 1-month poststroke but remained impaired in comparison with controls. Persistent impaired reaction time within the first year poststroke has been shown, indicating that ipsilesional upper limbs deficits might not be a temporary event.39,40 It has been shown that both the precision- and power-grip tasks activated the primary sensorimotor cortex contralateral to the grasping hand. The activations extended into the dorsal premotor cortex and the postcentral sulcus. Furthermore, the ventral premotor cortex showed bilateral activation with peaks of activity in the inferior part of the precentral gyrus.41 Among common assumptions motor deficits caused by disruption of ipsilesional projections of the corticospinal tract42 and changes in ipsilesional motor performance after nonaffected primary motor cortex disinhibition43 are included. However, little is known about the time course evolution of ipsilesional handgrip assessment, and even less about its implications for rehabilitation.40,44 Previous studies45,46 have reported difficulties in most clinical tests to detect fine changes in motor performance, specially the subtle ipsilesional motor deficits. Our study found significant differences on grip and pinch resistance to fatigue in the ipsilesional hand in comparison with controls. Moreover, significant differences were found on flexor digitorum superficialis muscle fatigue during a sustained handgrip contraction.
Obstetric Brachial Plexus Palsy: Can a Unilateral Birth Onset Peripheral Injury Significantly Affect Brain Development?
Published in Developmental Neurorehabilitation, 2020
Egmar Longo, Ryota Nishiyori, Theresa Cruz, Katharine Alter, Diane L. Damiano
One potential additional reason for why outcomes in some children with OBPP may be poorer than predicted from the extent of the peripheral injury may be secondary alterations to the cortical substrate resulting from diminished use of the limb starting at birth.7,8 It is known that following peripheral nerve injury, there is a loss of afferent signals to the sensorimotor cortex and a rapid change in the somatotopic organization in both the sensory and motor cortices may occur. This in turn may result in changes in white matter volume and interhemispheric connectivity. Abnormal activity has been found in many brain regions, including primary and supplementary motor cortices in individuals with OBPP; differences that may impact rehabilitation treatment effectiveness.9–10-11 Such alterations have been observed in children with cerebral palsy; however, in these children, the primary injury is in the brain.12–1314
Animal models of ischemic stroke and their impact on drug discovery
Published in Expert Opinion on Drug Discovery, 2019
Dirk M. Hermann, Aurel Popa-Wagner, Christoph Kleinschnitz, Thorsten R. Doeppner
Photothrombosis induces highly uniform brain lesions that can be placed with stereotactical precision in almost any brain structure, allowing brain plasticity and remodeling studies in the vicinity and remote of the brain lesion (Table 1). Photothrombosis has little and in case of the ring model a very artificial penumbra (Table 1). The model is therefore unsuited for studying neuroprotective drugs. Since microvascular clots are unusually rich in platelets, these clots can be resolved only to a limited extent by recombinant tissue-plasminogen activator (tPA) [32]. Brain infarcts may exhibit hemorrhages around the lesion core. Hence, the model is not suited for studying thrombolytic drugs (Table 1). Sensorimotor deficits of pure cortical strokes are usually mild and may show a large degree of spontaneous recovery depending on the precise localization and size of brain infarcts (Table 1). Spontaneous recovery is prominent after primary sensorimotor cortex injury. Spontaneous recovery then precludes behavioral analyses.