Parkinsonian tremor is most likely due to oscillating neuronal activity within the CNS. Summarizing all the available evidence, peripheral factors only play a minor role in the generation, maintenance and modulation of PD tremor. Recent studies have shown that not a single but multiple oscillators are responsible. The most likely candidate producing these oscillations is the basal ganglia loop and its topographic organization might be responsible for the separation into different oscillators which, nevertheless, usually produce the same frequency. The neuronal mechanisms underlying these oscillations are not yet clear, but three hypotheses would be compatible with the presently available data from animal models and data recorded in patients. The first is a cortico-subthalamo-pallido-thalamic loop, the second is a pacemaker consisting of the external pallidum and the subthalamic nucleus, and the third is abnormal synchronization due to unknown mechanisms within the whole striato-pallido-thalamic pathway leading to a loss of segregation. Assuming the oscillator within the basal ganglia pathway, the mechanism of stereotactic surgery might be a desynchronization of the activity of the basal ganglia-thalamo-cortical or the cerebello-thalamo-cortical pathway.
Marchiafava-Bignami disease (MBD) is a rare complication of chronic alcoholism. Most reported cases have been diagnosed at autopsy. With CT and, especially, MRI it is possible to diagnose MBD in its early stages. Lesions of CNS structures other than the typical demyelination of the corpus callosum are described ante mortem in a patient with MBD. The more frequent use of CT and MRI in sudden onset encephalopathies of alcoholics could reveal the real incidence of MBD, and the consequent detection of other involved CNS systems might improve our knowledge about the aetiology, pathogenesis, prognosis and therapy of MBD.
4Cultech Limited, Christchurch Rd Port Talbot, Neath Port TalbotThere is a growing body of evidence indicating that the gut microbiota communicates with the CNS influencing mood and behaviour (1)(2)(3)(4)(5)(6)(7) and a role for the microbiota in the development of brain plasticity and the subsequent physiological response has been suggested (2) . Furthermore treatment with probiotics has been shown to alter functional task-related brain activity and changes in midbrain connectivity 9 . To date no study has demonstrated cognitive modification in response to probiotic treatment. The aims of the study were i) To examine the mood effects of probiotic supplementation at rest and in response to psychological stressors ii) To examine the effects of probiotic administration on cognitive functioning.In this pilot study, healthy participants (n = 50) were recruited to take part in a double blind, randomised, controlled trial. Participants were randomized to receive either a probiotic preparation comprising two strains of Lactobacillus acidophilus CUL60 (NCIMB 30157) and CUL21 (NCIMB 30156), Bifidobacterium lactis CUL34 (NCIMB 30172) and Bifidobacterium bifidum CUL20 (NCIMB 30153) at a total of 2.5 × 10 10 cfu/capsule or a placebo for 6 weeks. The sample population comprised 18 males and 32 females, mean age 23.22 years (range 19-38, SD 3.846), with a BMI <30. Participants underwent morphometric measurements (height, weight, % total body fat, hip and waist measurement) and completed mood, stress and depression questionnaires (Bond Lader Mood Scales, Stait Trait Anxiety Inventory and NASA Task Load Index). Participants also were required to perform a battery of computerised cognitive test (COMPASS) measuring attention, executive function, working memory and episodic memory.In terms of mood measures, a significant interaction showed that 'trait' anxiety levels decreased in the active probiotic condition whilst increasing in the placebo condition over the course of the 6 week intervention (p = 0.042). A significant interaction was also observed for tasks of attention; 'continuity of attention increased in response to the probiotic treatment and decreased with the placebo group (p = 0.035). No morphometric changes between the two treatment conditions were recorded during the intervention period. The findings of this pilot trial provide a justification for further studies to characterise the potential cognitive and mood enhancing benefits of probiotics in healthy populations.
Pain usually is the consequence of tissue damage that is signalled to the brain via the nociceptive system (nociceptive pain). Damage to the nociceptive system - in addition to causing sensory deficit - may paradoxically also induce a chronic pain state (neuropathic pain). Diagnostic workup of patients with neuropathic pain follows the usual procedure of Neurology, i. e. the aim is to identify the location of neural damage and the underlying disorder, so that a mechanism-oriented treatment may be initiated. Medical history - supported by specific questionnaires and a pain drawing by the patient - provides the basis for diagnosis. In the course of the physical examination, the sensory exam including careful documentation of the spatial extent of positive and negative signs is the most important part, since neuropathic pain is due to damage to the somatosensory system. Techniques for the objective documentation of sensory signs have been developed (e. g. by the DFNS), but their broad availability is still in teh process of being implemented. Thus, laboratory exams main serve the purpose of identifying the underlying etiology. Symptomatic treatment of neuropathic pain is relatively uniform, independent of etiologies (e. g. traumatic, metabolic, inflammatory), but differs from that of nociceptive pain. Typical analgesics have little efficacy in neuropathic pain - except for opioids. Major pharmacological treatment options include anticonvulsants (Ca-channel modulators, Na-channel blockers), antidepressants (noradrenaline reuptake inhibitors) and topicals (lidocaine, capsaicin). These medications exert specific molecular pharmacological effects against the pathophysiological mechanisms of neuropathic pain.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.