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Query: UMLS:C0026838 (spasticity)
 6,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Single nerve-fibre action potentials (APs) were recorded extracellularly from alpha and gamma-motoneurons and secondary muscle spindle afferents from a ventral S4 nerve root (some afferents are contained in lower sacral motor roots) in an individual with traumatic spinal cord lesion sub TH1. Simultaneous interspike intervals (IIs) of, and phases between, the APs of 5 nerve fibres were measured, and distributions were constructed. The II distributions were of a broad peak type. Phase distributions showed 1 to 3 peaks interpreted as phase relations between the firings of the nerve fibres. Under certain phase relations, the rhythmic firing of alpha and gamma-motoneurons is further interpreted as an interaction of oscillatory firing neuronal subnetworks driving alpha and gamma-motoneurons. Following repetitive touch and pin-prick stimulation in- and outside the anal reflex area, the II distributions of alpha and gamma-motoneurons and of secondary spindle afferents assimilated partly or fully, while preserving their phase relations. This coordinated firing is interpreted as the oscillatory firing of alpha neuronal networks building up an external loop to the periphery via the gamma-loop. Upon touch, pin-prick, and anal reflex stimulation, and anal and bladder catheter pulling, the values and the number of the phase relations changed. Mostly two phase relations per oscillation cycle were observed. Two phase relations probably represent the physiologic case for the somatic nervous system. Only one phase relation was found when full synchronization of all units occurred. Three phase relations were found when the parasympathetic nervous system division interacted with the somatic one. Based on data obtained from brain-dead individuals it is discussed that the increased synchronization and instability in the number and the values of phase relations suggested pathologic functioning of the caudal functionally disconnected spinal cord in patients with spinal cord lesions: Oscillatory firing neuronal networks, which lost their specific properties, interacted more easily and unspecifically with other oscillatory firing networks. Further, it is discussed that physiologic tremor is caused by chance synchronization of oscillatory firing neuronal networks and therefore originates in the central nervous system (CNS). Since spinal oscillators build up external loops to the periphery, it is suggested that in patients with incomplete spinal cord lesions it should be possible to re-preformate oscillatory firing neuronal networks by a rhythm training, to reduce spasticity and to re-train useful movements, especially locomotion.
Gen Physiol Biophys 1996 Aug
PMID:External loops of human premotor spinal oscillators identified by simultaneous measurements of interspike intervals and phase relations. 893 99

The key strategies on which the discovery of the functional organization of the central nervous system (CNS) under physiologic and pathophysiologic conditions have been based included (1) our measurements of phase and frequency coordination between the firings of alpha- and gamma-motoneurons and secondary muscle spindle afferents in the human spinal cord, (2) knowledge on CNS reorganization derived upon the improvement of the functions of the lesioned CNS in our patients in the short-term memory and the long-term memory (reorganization), and (3) the dynamic pattern approach for re-learning rhythmic coordinated behavior. The theory of self-organization and pattern formation in nonequilibrium systems is explicitly related to our measurements of the natural firing patterns of sets of identified single neurons in the human spinal premotor network and re-learned coordinated movements following spinal cord and brain lesions. Therapy induced cell proliferation, and maybe, neurogenesis seem to contribute to the host of structural changes during the process of re-learning of the lesioned CNS. So far, coordinated functions like movements could substantially be improved in every of the more than 100 patients with a CNS lesion by applying coordination dynamic therapy. As suggested by the data of our patients on re-learning, the human CNS seems to have a second integrative strategy for learning, re-learning, storing and recalling, which makes an essential contribution of the functional plasticity following a CNS lesion. A method has been developed by us for the simultaneous recording with wire electrodes of extracellular action potentials from single human afferent and efferent nerve fibres of undamaged sacral nerve roots. A classification scheme of the nerve fibres in the human peripheral nervous system (PNS) could be set up in which the individual classes of nerve fibres are characterized by group conduction velocities and group nerve fibre diameters. Natural impulse patterns of several identified single afferent and efferent nerve fibres (motoneuron axons) were extracted from multi-unit impulse patterns, and human CNS functions could be analyzed under physiologic and pathophysiologic conditions. With our discovery of premotor spinal oscillators it became possible to judge upon CNS neuronal network organization based on the firing patterns of these spinal oscillators and their driving afferents. Since motoneurons fire occasionally for low activation and oscillatory for high activation, the coherent organization of subnetworks to generate macroscopic function is very complex and for the time being, may be best described by the theory of coordination dynamics. Since oscillatory firing has also been observed by us in single motor unit firing patterns measured electromyographically, it seems possible to follow up therapeutic intervention in patients with spinal cord and brain lesions not only based on the activity levels and phases of motor programs during locomotion but also based on the physiologic and pathophysiologic firing patterns and recruitment of spinal oscillators. The improvement of the coordination dynamics of the CNS can be partly measured directly by rhythmicity upon the patient performing rhythmic movements coordinated up to milliseconds. Since rhythmic dynamic, coordinated, stereotyped movements are mainly located in the spinal cord and only little supraspinal drive is necessary to initiate, maintain, and terminate them, rhythmic, dynamic, coordinated movements were used in therapy to enforce reorganization of the lesioned CNS by improving the self-organization and relative coordination of spinal oscillators (and their interactions with occasionally firing motoneurons) which became pathologic in their firing following CNS lesion. Paraparetic, tetraparetic spinal cord and brain-lesioned patients re-learned running and other movements by an oscillator formation and coordination dynamic therapy. Our development in neurorehabilitation is in accordance with those of theoretical and computational neurosciences which deal with the self-organization of neuronal networks. In particular, jumping on a springboard 'in-phase' and in 'anti-phase' to re-learn phase relations of oscillator coupling can be understood in the framework of the Haken-Kelso-Bunz coordination dynamic model. By introducing broken symmetry, intention, learning and spasticity in the landscape of the potential function of the integrated CNS activity, the change in self-organization becomes understandable. Movement patterns re-learned by oscillator formation and coordination dynamic therapy evolve from reorganization and regeneration of the lesioned CNS by cooperative and competitive interplay between intrinsic coordination dynamics, extrinsic therapy related inputs with physiologic re-afferent input, including intention, motivation, supervised learning, interpersonal coordination, and genetic constraints including neurogenesis. (ABSTRACT TRUNCATED)
Gen Physiol Biophys 2000 Oct
PMID:Reorganization of the human central nervous system. 1125 67

Spinal cord infarction is uncommon and usually presents with sudden onset of paralysis and sensory disturbances. A variety of causes are described, but rarely with multiple factors involved. We report a case of a 63-year-old man with a history of diabetes mellitus, hypertension, and osteoarthritis who presented with acute onset of chest pain, numbness, and weakness associated with episodic hypotension. He had incomplete tetraplegia and was areflexic without spasticity. Pain and temperature sensations were impaired below the C7 dermatome and absent below the T4 dermatome bilaterally. Proprioception and vibration sensations were diminished on the right below the C6 dermatome. Magnetic resonance imaging showed spinal cord infarction affecting C6-T3 segments, and severe cervical and lumbar spine degenerative changes. This case illustrates an unusual presenting symptom of spinal infarction, the need to identify multiple risk factors for spinal cord infarction, and the importance of optimal preventive therapy in patients at risk.
J Gen Intern Med 2007 Jan
PMID:Spinal cord infarction with multiple etiologic factors. 1735 58

Stroke is the leading cause of disability and one of the most common causes of death worldwide. Outside the setting of acute management, secondary prevention and stroke rehabilitation, little has been written to address the ongoing symptomatic and palliative needs of these patients and their families. In this literature review, we look beyond secondary prevention with the aim of providing evidence-informed management guidelines for the myriad and often under-recognized symptomatic and palliative care needs of stroke survivors. Some of the most common and disabling post-stroke symptoms that are reviewed here include central post-stroke pain, hemiplegic shoulder pain, painful spasticity, fatigue, incontinence, post-stroke seizures, sexual dysfunction, sleep-disordered breathing, depression and emotionalism. We review the role of caregivers and explore ways to support them and, lastly, remind the reader to be perceptive to the patient's spiritual needs. The literature is most robust, including controlled trials, for central post-stroke pain and depression. Synthesis and discussion outside these areas are frequently limited to smaller studies, case reports and expert opinion. While some data exists to guide informed decision-making, there is an urgent need to document best practice and identify appropriate clinical standards for the full spectrum of symptoms experienced by stroke survivors. We present the current and established data to aid health care providers in symptomatic and palliative management of stroke survivors.
J Gen Intern Med 2012 Jul
PMID:Symptomatic and palliative care for stroke survivors. 2252 22

As more states legalize cannabis for medical use, people increasingly use cannabis to treat medical conditions. Well-documented harms of cannabis use include increased risk of fatal auto accidents, neurocognitive deficits, and increased risk of addiction. Observational data supports the use of cannabis for pain, nausea and vomiting related to chemotherapy, and multiple sclerosis spasticity symptoms. Given potential harms versus benefits of cannabis use, how should physicians counsel patients regarding their cannabis use? This paper briefly reviews the evidence supporting medical cannabis use for pain. We consider cannabis use as a harm reduction strategy for pain management. We encourage routine, longitudinal assessments of cannabis use among patients. We discuss the commercialization of cannabis for financial gain, contributing to potent and addictive cannabis. We highlight the concerning phenomena of cannabis dispensary workers as proxy clinicians. Finally, we present three strategies to reduce public harms associated with potent cannabis use including required testing and reporting of tetrahydrocannabinol/cannabidiol concentrations, rigorous study of high-potency cannabis available for purchase in dispensaries across the USA, and large-scale efforts to measure cannabis consumption in medical records so prospective, longitudinal studies can be conducted to correlate consumption measures with medical and psychiatric outcomes.
J Gen Intern Med 2020 Jun
PMID:The Void in Clinician Counseling of Cannabis Use. 3189 25