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Functional Connections of the Rostral Nucleus of the Solitary Tract in Viscerosensory Integration of Ingestion Reflexes
Published in I. Robin A. Barraco, Nucleus of the Solitary Tract, 2019
Gustatory and somatosensory nerves play a major role in the control of ingestion. This has been demonstrated by evaluating eating behavior after selective deafferentation. When trigeminal sensory nerves are cut in the rat, eating is profoundly impaired.11 Disrupted feeding results from dramatic reductions in the frequency of meal initiation, and disrupted somatosensory control of the consummatory responses of food grasping and chewing. The effects on chewing can be explained as a sensorimotor deficit resulting from the removal of the afferent limb of mouth-opening and tongue-extension reflexes. Trigeminal nerve branches that play the greatest role in mediating these ingestion reflexes are ones mediating sensation from the oral mucosa; specifically, the lingual and sphenopalatine nerves. These nerves supply general sensory innervation to the tongue and palate, respectively. If these nerves are sectioned bilaterally, rats exhibit persistent hypophagia and reduced responsiveness to food. Taste nerve resection also results in impairments of feeding, but the impairments are more subtle than with somatosensory nerve cuts.12 Bilateral transection of the chorda tympani impairs a rat’s ability to detect dilute salt solutions.13 Bilateral resection of the chorda tympani, together with the glossopharyngeal and vagus (pharyngeal branch) nerves, results in reduced responsiveness to food and water and elevated aversion thresholds to QHCL. Thus, compared with trigeminal denervation, taste denervation results in similar but quantitatively reduced effects on the initiation of eating and drinking.
Sensory contributions to control
Published in Andrea Utley, Motor Control, Learning and Development, 2018
The role of proprioception information for control of movement has been emphasized using a deafferentation model. Deafferentation refers to the elimination or interruption of sensory nerve impulses. Surgical deafferentation involves cutting or removing afferent neural pathways, which effectively stops information about the limb movement direction being sent to the central nervous system (CNS). Research has shown that when a single limb is deafferented in motorically mature monkeys, there is loss of effective purposive use of that extremity in a free situation (Taub and Berman 1963; Taub et al. 1977). The work showed that the limb was not paralyzed, but that the limb moved frequently albeit rather randomly. In addition, researchers reported that although the monkeys were found to have preserved gross motor control, they showed severe difficulties in using their limb proficiently (Bossom 1974; Knapp et al. 1963; Taub and Berman 1963). Just a little over 10 years later, Bizzi and coworkers showed that monkeys who were surgically deafferented could make accurate pointing movements even when proprioceptive feedback was no longer available, although it is important to note that the monkeys were trained prior to deafferentation to complete the same task (Bizzi and Polit 1979; Polit and Bizzi 1978).
Assessment and management of mild traumatic brain injury
Published in Mark J. Ashley, David A. Hovda, Traumatic Brain Injury, 2017
Mark J. Ashley, Matthew J. Ashley
Several factors such as severity of injury, genomic factors, neurophysiologic conditions at the time of injury, previous neurologic injury, substance abuse, delayed deafferentation, or other co-occurring conditions, such as pituitary dysfunction or sleep disorders, may contribute to symptom persistence. In some, delayed deafferentation may occur following the initial injury.30 Brain atrophy studied on a longitudinal basis was found to be progressive in a small group of MTBI patients, suggesting both a progression in a disease process as well as an association of degree of atrophy to severity of injury.31 More severe injuries, as distinguished by loss of consciousness, showed greater changes in brain parenchymal volume across time. These changes warrant longer follow-up for patients who may actually progressively develop symptoms.
Partial-Hand Prosthesis Users Show Improved Reach-to-Grasp Behaviour Compared to Transradial Prosthesis Users with Increased Task Complexity
Published in Journal of Motor Behavior, 2022
Bennett L. Alterman, Emily Keeton, Saif Ali, Katrina Binkley, William Hendrix, Perry J. Lee, Shuo Wang, James Kling, John T. Johnson, Lewis A. Wheaton
By 2050, there are projected to be nearly 4.8 million people living with upper-extremity amputation in the United States (Ziegler-Graham et al., 2008). The vast majority of these are distal to the wrist (“partial-hand”), comprising 92% of upper-extremity amputations (Dillingham et al., 2002). Transradial amputations are the most common major upper-extremity amputation (Dillingham et al., 2002). Amputation is a non-central nervous system injury that causes rapid neurobehavioural—and functionally neuroplastic—changes in the brain (Wheaton, 2017). Many patients exhibit a shift towards greater visual reliance for control of the affected limb (Blank et al., 2010; Metzger et al., 2010; Williams et al., 2016). This shift likely contributes to decreased motor function (Hughey & Wheaton, 2016), a finding mirrored in deafferentation literature (Sarlegna et al., 2006). Parr et al. (2018, 2019) suggest that the decrease in motor function is related to reductions in sensory feedback from the limb and resultant difficulties with spatiotemporal coupling between visual attention and action.
Virtual reality for tinnitus management: a randomized controlled trial
Published in International Journal of Audiology, 2022
Aniruddha K. Deshpande, Ishan Bhatt, Chanapong Rojanaworarit
The present study documented the effect of ST + VR intervention on tinnitus loudness and TFI scores. The underlying neurobiological mechanisms responsible for mediating the VR effect on tinnitus outcomes remain largely elusive. Tinnitus is associated with peripheral and central auditory structures (e.g. Henry et al. 2014). Auditory deafferentation caused due to ageing, noise, and ototoxic agents are known to induce hyperactivity in the central auditory structures (Vanneste and De Ridder 2016; Weisz et al. 2006). Tinnitus is associated with the tonotopic reorganisation of the auditory cortex – a consequence that may arise from the abnormal increase in the central gain and auditory deafferentation (e.g. Auerbach, Rodrigues, and Salvi 2014). Non-auditory structures, such as the anterior cingulate cortex, dorsal lateral prefrontal cortex, insula, orbitofrontal cortex, parahippocampus, and posterior cingulate cortex are also associated with tinnitus (Vanneste and De Ridder 2012). The complex interaction between cortical and subcortical networks (both auditory and non-auditory areas) might produce a clinical representation of tinnitus (e.g. Haider et al. 2018).
Considering hearing loss as a modifiable risk factor for dementia
Published in Expert Review of Neurotherapeutics, 2022
Katharine K. Brewster, Jennifer A. Deal, Frank R. Lin, Bret R. Rutherford
One may hypothesize that such behavioral and neural effects of HL may increase the risk for dementia through decreasing cognitive reserve, rather than directly effecting neuropathological biomarkers associated with dementia (Figure 1). For example, as social participation and engagement in leisure activities have been associated with increased cognitive reserve [68], it is possible that loneliness and depression secondary to HL may impair cognitive reserve and increase vulnerability to neuropathological contributors to dementia (e.g. emerging AD pathology or vascular disease). Likewise, deafferentation-induced frontotemporal atrophy and CCN dysregulation can deplete cortical resources that would otherwise be available to help mitigate and act as a ‘buffer’ against such neuropathological changes. According to such a model, HL imposes a constant load on an individual’s cognitive reserve, and clinical symptoms from existing brain pathology may manifest earlier as cognitive and functional impairment.