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The Journal of the Louisiana State... Aug 1998Vocal cord paralysis is a multifacted problem that affects patients of all ages and presents initially to a wide range of healthcare professionals. It can cause... (Review)
Review
Vocal cord paralysis is a multifacted problem that affects patients of all ages and presents initially to a wide range of healthcare professionals. It can cause laryngeal dysfunction ranging from slight hoarseness to life-threatening airway obstruction. When confronted with a patient with new onset vocal cord paralysis, the physician should determine the etiology of the paralysis. Only after an accurate diagnosis, can restoration of laryngeal function be addressed. Peripheral lesions injuring the vagus nerve or its branches are responsible for 90% of all vocal cord paralysis. Etiologies include neoplasms, surgical iatrogenic injury, and blunt and penetrating trauma in the head, neck, and thorax. Thyroid surgery has historically been accountable for almost a third of reported unilateral vocal cord paralyses. However, recent review has demonstrated a dramatic reduction in this incidence to less than 5%. Numerous treatment options exist for patients with vocal cord paralysis. These treatments can drastically reduce the social and economic disability incurred by these patients.
Topics: Humans; Vocal Cord Paralysis
PubMed: 9770942
DOI: No ID Found -
Advances in Nephrology From the Necker... 1994
Review
Topics: Animals; Electrophysiology; Humans; Hyperkalemia; Muscles; Mutation; Paralyses, Familial Periodic; Paralysis; Periodicity; Sodium Channels
PubMed: 8154352
DOI: No ID Found -
Journal of Internal Medicine Jul 2017The human nervous system is a vast network carrying not only sensory and movement information, but also information to and from our organs, intimately linking it to our... (Review)
Review
The human nervous system is a vast network carrying not only sensory and movement information, but also information to and from our organs, intimately linking it to our overall health. Scientists and engineers have been working for decades to tap into this network and 'crack the neural code' by decoding neural signals and learning how to 'speak' the language of the nervous system. Progress has been made in developing neural decoding methods to decipher brain activity and bioelectronic technologies to treat rheumatoid arthritis, paralysis, epilepsy and for diagnosing brain-related diseases such as Parkinson's and Alzheimer's disease. In a recent first-in-human study involving paralysis, a paralysed male study participant regained movement in his hand, years after his injury, through the use of a bioelectronic neural bypass. This work combined neural decoding and neurostimulation methods to translate and re-route signals around damaged neural pathways within the central nervous system. By extending these methods to decipher neural messages in the peripheral nervous system, status information from our bodily functions and specific organs could be gained. This, one day, could allow real-time diagnostics to be performed to give us a deeper insight into a patient's condition, or potentially even predict disease or allow early diagnosis. The future of bioelectronic medicine is extremely bright and is wide open as new diagnostic and treatment options are developed for patients around the world.
Topics: Biosensing Techniques; Biotechnology; Brain; Electric Stimulation Therapy; Electronics, Medical; Forecasting; Humans; Neurons; Paralysis; Synaptic Transmission
PubMed: 28419590
DOI: 10.1111/joim.12610 -
Nature Nov 2018Spinal cord injury leads to severe locomotor deficits or even complete leg paralysis. Here we introduce targeted spinal cord stimulation neurotechnologies that enabled...
Spinal cord injury leads to severe locomotor deficits or even complete leg paralysis. Here we introduce targeted spinal cord stimulation neurotechnologies that enabled voluntary control of walking in individuals who had sustained a spinal cord injury more than four years ago and presented with permanent motor deficits or complete paralysis despite extensive rehabilitation. Using an implanted pulse generator with real-time triggering capabilities, we delivered trains of spatially selective stimulation to the lumbosacral spinal cord with timing that coincided with the intended movement. Within one week, this spatiotemporal stimulation had re-established adaptive control of paralysed muscles during overground walking. Locomotor performance improved during rehabilitation. After a few months, participants regained voluntary control over previously paralysed muscles without stimulation and could walk or cycle in ecological settings during spatiotemporal stimulation. These results establish a technological framework for improving neurological recovery and supporting the activities of daily living after spinal cord injury.
Topics: Activities of Daily Living; Biomedical Technology; Computer Simulation; Electric Stimulation Therapy; Electromyography; Epidural Space; Humans; Leg; Locomotion; Male; Motor Neurons; Muscle, Skeletal; Paralysis; Spinal Cord; Spinal Cord Injuries; Walking
PubMed: 30382197
DOI: 10.1038/s41586-018-0649-2 -
JAMA Oct 1963
Topics: Humans; Muscular Dystrophies; Paralyses, Familial Periodic; Paralysis
PubMed: 14052009
DOI: No ID Found -
Canadian Medical Association Journal Dec 1949
Topics: Extremities; Humans; Paralyses, Familial Periodic; Paralysis
PubMed: 15393052
DOI: No ID Found -
Journal of Neurology, Neurosurgery, and... Aug 1953
Topics: Humans; Muscular Dystrophies; Paralyses, Familial Periodic; Paralysis
PubMed: 13085200
DOI: 10.1136/jnnp.16.3.178 -
Zentralblatt Fur Chirurgie Sep 2016Unilateral elevation of the diaphragm may be due to various causes and requires further elucidation when the aetiology is unknown. Elevation of the diaphragm is often... (Review)
Review
Unilateral elevation of the diaphragm may be due to various causes and requires further elucidation when the aetiology is unknown. Elevation of the diaphragm is often caused by diaphragmatic paralysis, either due to damage to the phrenic nerve or to the phrenic muscle. Patients typically complain of increased respiratory distress when lying down, bending or swimming. Basic diagnostic testing consists of a chest X-ray, as well as spirometry and computer tomography of the neck and chest. In many cases, no cause can be identified for the diaphragmatic paralysis. In symptomatic patients, diaphragm plication leads to fixation and thus to a reduction in the paradoxal respiratory movement of the paralysed diaphragm. In a large majority of studies, this results in significant and lasting improvement in vital capacity and respiratory distress. Spontaneous recovery of diaphragm paralysis is possible, even after several months, so a waiting period of at least 6 months should elapse before diaphragmatic plication is performed, if the clinical situation allows. The procedure can be performed minimally invasively, with low morbidity and mortality. When cutting the phrenic nerve, a nerve suture is recommended, if possible, or otherwise diaphragm plication during the procedure, especially in the case of pneumonectomy. This review provides an overview of the causes, pathophysiology, symptoms, diagnosis, therapy and results of diaphragmatic plication in acquired, unilateral diaphragmatic paralysis in adults, and suggests an algorithm for diagnostic testing and therapy.
Topics: Algorithms; Humans; Magnetic Resonance Imaging; Minimally Invasive Surgical Procedures; Postoperative Complications; Remission, Spontaneous; Respiratory Paralysis; Suture Techniques; Thoracic Surgical Procedures; Tomography, X-Ray Computed; Ultrasonography
PubMed: 27607888
DOI: 10.1055/s-0042-113192 -
Journal of Physiology, Paris 2002The neuromuscular junction is one of the most accessible mammalian synapses which offers a useful model to study long-term synaptic modifications occurring throughout... (Review)
Review
The neuromuscular junction is one of the most accessible mammalian synapses which offers a useful model to study long-term synaptic modifications occurring throughout life. It is also the natural target of botulinum neurotoxins (BoNTs) causing a selective blockade of the regulated exocytosis of acetylcholine thereby triggering a profound albeit transitory muscular paralysis. The scope of this review is to describe the principal steps implicated in botulinum toxin intoxication from the early events leading to a paralysis to the cellular response implementing an impressive synaptic remodelling culminating in the functional recovery of neuromuscular transmission. BoNT/A treatment promotes extensive sprouting emanating from intoxicated motor nerve terminals and the distal portion of motor axons. The current view is that sprouts have the ability to form functional synapses as they display a number of key proteins required for exocytosis: SNAP-25, VAMP/synaptobrevin, syntaxin-I, synaptotagmin-II, synaptophysin, and voltage-activated Na+, Ca2+ and Ca2+-activated K+ channels. Exo-endocytosis was demonstrated (using the styryl dye FM1-43) to occur only in the sprouts in vivo, at the time of functional recovery emphasising the direct role of nerve terminal outgrowth in implementing the restoration of functional neurotransmitter release (at a time when nerve stimulation again elicited muscle contraction). Interestingly, sprouts are only transitory since a second distinct phase of the rehabilitation process occurs with a return of synaptic activity to the original nerve terminals. This is accompanied by the elimination of the dispensable sprouts. The growth or elimination of these nerve processes appears to be strongly correlated with the level of synaptic activity at the parent terminal. The BoNT/A-induced extension and later removal of "functional" sprouts indicate their fundamental importance in the rehabilitation of paralysed endplates, a finding with ramifications for the vital process of nerve regeneration.
Topics: Acetylcholine; Animals; Botulinum Toxins; Humans; Neuromuscular Junction; Neuronal Plasticity; Paralysis; Recovery of Function; Synaptic Transmission
PubMed: 11755789
DOI: 10.1016/s0928-4257(01)00086-9 -
Medicina Clinica Nov 1987
Review
Topics: Humans; Hypokalemia; Paralyses, Familial Periodic; Paralysis; Periodicity
PubMed: 3323695
DOI: No ID Found