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Michael Swash - One of the best experts on this subject based on the ideXlab platform.
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fasciculation Cramp syndrome preceding anterior horn cell disease an intermediate syndrome
Journal of Neurology Neurosurgery and Psychiatry, 2011Co-Authors: Mamede De Carvalho, Michael SwashAbstract:Cramp-fasciculation syndrome (Cramp-FS) is an ill-defined condition with uncertain clinical limits. The authors studied a 55-year-old man with progressively more severe, widespread fasciculations and Cramps during a 6-year-period. Mild progressive lower motor neuron loss, shown by motor unit number and multi-motor unit potential (MUP) analysis, developed during the 4 years after onset, which stabilised during a further 2-year follow-up. Cramp-FS is generally a benign syndrome, probably with several causations. Our patient developed a limited form of anterior horn cell degeneration perhaps representing a syndrome transitional with amyotrophic lateral sclerosis. Cramp-FS merits more detailed study.
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Fasciculation-Cramp syndrome preceding anterior horn cell disease: an intermediate syndrome?
Journal of Neurology Neurosurgery and Psychiatry, 2010Co-Authors: Mamede De Carvalho, Michael SwashAbstract:Cramp-fasciculation syndrome (Cramp-FS) is an ill-defined condition with uncertain clinical limits. We studied a 55-year-old man with progressively more severe, widespread fasciculations and Cramps during a six-year period. Mild progressive lower motor neuron loss, shown by MUNE and multiMUP analysis, developed during the four years after onset, which stabilized during a further 2-year follow-up. Cramp-FS is generally a benign syndrome, probably with several causations. Our patient developed a limited form of anterior horn cell degeneration perhaps representing a syndrome transitional with amyotrophic lateral sclerosis. Cramp-FS merits more detailed study.
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Cramps, muscle pain, and fasciculations: Not always benign?
Neurology, 2004Co-Authors: Mamede De Carvalho, Michael SwashAbstract:Fasciculation and Cramps without weakness or muscle atrophy are recognized as a benign syndrome. The authors report a patient with Cramp and fasciculation, which persisted for 1 year without abnormal motor unit morphology on EMG before progressive weakness, muscle atrophy, and EMG abnormalities developed. This observation raises the possibility that lower motor neuron hyperexcitability may precede motor neuron death in motor neuron disease.
Takamitsu Yamamoto - One of the best experts on this subject based on the ideXlab platform.
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Thalamic deep brain stimulation for writer's Cramp
Journal of Neurosurgery, 2007Co-Authors: Chikashi Fukaya, Yoichi Katayama, Toshikazu Kano, Takafumi Nagaoka, Kazutaka Kobayashi, Hideki Oshima, Takamitsu YamamotoAbstract:Object Writer's Cramp is a type of idiopathic focal hand dystonia characterized by muscle Cramps that accompany execution of the writing task specifically. In this report, the authors describe the clinical outcome after thalamic deep brain stimulation (DBS) therapy in patients with writer's Cramp and present an illustrative case with which they compare the effects of pallidal and thalamic stimulation. In addition to these results for the clinical effectiveness, they also examine the best point and pattern for therapeutic stimulation of the motor thalamus, including the nucleus ventrooralis (VO) and the ventralis intermedius nucleus (VIM), for writer's Cramp. Methods The authors applied thalamic DBS in five patients with writer's Cramp. The inclusion criteria for the DBS trial in this disorder were a diagnosis of idiopathic writer's Cramp and the absence of a positive response to medication. The exclusion criteria included significant cognitive dysfunction, active psychiatric symptoms, and evidence of othe...
Kevin C Miller - One of the best experts on this subject based on the ideXlab platform.
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prophylactic stretching does not reduce Cramp susceptibility
Muscle & Nerve, 2018Co-Authors: Kevin C Miller, James D Harsen, Blaine C. LongAbstract:Introduction: Some clinicians advocate stretching to prevent muscle Cramps. It is unknown whether static or proprioceptive neuromuscular facilitation (PNF) stretching increases Cramp threshold frequency (TFc), a quantitative measure of Cramp susceptibility. Methods: Fifteen individuals completed this randomized, counterbalanced, cross-over study. We measured passive hallux range of motion (ROM) and then performed 3 minutes of either static stretching, PNF stretching (hold–relax—with agonist contraction), or no stretching. ROM was reassessed and TFc was measured. Results: PNF stretching increased hallux extension (pre-PNF 81 ± 11°, post-PNF 90 ± 10°; P 0.05). Static stretching increased hallux extension (pre-static 80 ± 11°, post-static 88 ± 9°; P 0.05). No ROM changes occurred with no stretching (P > 0.05). TFc was unaffected by stretching (no stretching 18 ± 7 Hz, PNF 16 ± 4 Hz, static 16 ± 5 Hz; P = 0.37). Conclusions: Static and PNF stretching increased hallux extension, but neither increased TFc. Acute stretching may not prevent muscle Cramping. Muscle Nerve, 2017
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Muscle Cramp susceptibility increases following a volitionally induced muscle Cramp.
Muscle & nerve, 2017Co-Authors: Kevin C Miller, Blaine C. Long, Jeffrey E. EdwardsAbstract:Introduction: Muscle Cramping may increase peripheral nervous system excitability. It is unknown if, and how long, Cramp susceptibility is affected by previous Cramping. We tested whether volitionally-induced muscle Cramps (VIMC) lowered Cramp threshold frequency (TFc) and how long TFc was affected post-VIMC. Methods: Fifteen Cramp-prone participants volitionally-induced a flexor hallucis brevis (FHB) Cramp on 4 separate days. FHB TFc was measured before VIMC (i.e., baseline) and 5, 30, and 60 minutes post-VIMC. VIMC electromyographic (EMG) amplitude, VIMC duration, and perceived VIMC intensity were measured to ensure consistency of VIMC between days. Results: VIMC EMG amplitude, duration, and perceived intensity were similar between days (P>0.05). VIMC lowered TFc; baseline TFc (18±6 Hz) was higher than 5-minute (14±6 Hz), 30-minute (14±5 Hz), and 60-minute TFc (14±5 Hz, P
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golgi tendon organ reflex inhibition following manually applied acute static stretching
Journal of Sports Sciences, 2014Co-Authors: Kevin C Miller, John A BurneAbstract:AbstractGolgi tendon organ disinhibition may contribute to exercise-associated muscle Cramp (henceforth referred to as “Cramps”) genesis. Static stretching pre-exercise is prescribed to prevent Cramps based on the assumption golgi tendon organ inhibition remains elevated post-stretching. We determined whether stretching increased gastrocnemius golgi tendon organ inhibition and, if so, the time course of this inhibition post-stretching. Twelve participants’ dominant limb medial gastrocnemius inhibition was measured before, and at 1, 5, 10, 15 and 30 min after investigators applied three, 1-min duration stretches. Participants maintained voluntary contraction intensities of 5% of their maximum while the Achilles tendon was stimulated transcutaneously 50 times. Five-hundred millisecond epochs of raw electromyographic activity were band-pass filtered, full-wave rectified and averaged. An algorithm identified inhibitory points and calculated the area, maximum and duration of inhibition. Area of inhibition (F1,...
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significant and serious dehydration does not affect skeletal muscle Cramp threshold frequency
British Journal of Sports Medicine, 2013Co-Authors: Kyle W Braulick, Kevin C Miller, Jay M Albrecht, Jared M Tucker, James E DealAbstract:Objective Many clinicians believe that exercise-associated muscle Cramps (EAMC) occur because of dehydration. Experimental research supporting this theory is lacking. Mild hypohydration (3% body mass loss) does not alter threshold frequency (TF), a measure of Cramp susceptibility, when fatigue and exercise intensity are controlled. No experimental research has examined TF following significant (3–5% body mass loss) or serious hypohydration (>5% body mass loss). Determine if significant or serious hypohydration, with moderate electrolyte losses, decreases TF. Design A prepost experimental design was used. Dominant limb flexor hallucis brevis Cramp TF, Cramp electromyography (EMG) amplitude and Cramp intensity were measured in 10 euhydrated, unacclimated men (age=24±4 years, height=184.2±4.8 cm, mass=84.8±11.4 kg). Subjects alternated exercising with their non-dominant limb or upper body on a cycle ergometer every 15 min at a moderate intensity until 5% body mass loss or volitional exhaustion (3.8±0.8 h; 39.1±1.5°C; humidity 18.4±3%). Cramp variables were reassessed posthypohydration. Results Subjects were well hydrated at the study9s onset (urine specific gravity=1.005±0.002). They lost 4.7±0.5% of their body mass (3.9±0.5 litres of fluid), 4.0±1.5 g of Na + and 0.6±0.1 g K + via exercise-induced sweating. Significant (n=5) or serious hypohydration (n=5) did not alter Cramp TF (euhydrated=15±5 Hz, hypohydrated=13±6 Hz; F 1,9 =3.0, p=0.12), Cramp intensity (euhydrated= 94.2±41%, hypohydrated=115.9±73%; F 1,9 =1.9, p=0.2) or Cramp EMG amplitude (euhydrated=0.18±0.06 µV, hypohydrated= 0.18±0.09 µV; F 1,9 =0.1, p=0.79). Conclusions Significant and serious hypohydration with moderate electrolyte losses does not alter Cramp susceptibility when fatigue and exercise intensity are controlled. Neuromuscular control may be more important in the onset of muscle Cramps than dehydration or electrolyte losses.
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Duration of electrically induced muscle Cramp increased by increasing stimulation frequency.
Journal of sport rehabilitation, 2011Co-Authors: Kevin C Miller, Kenneth L. Knight, Steven R. Wilding, Marcus B. StoneAbstract:Context: Electrically induced muscle Cramps (EIMC) do not last long enough to study many Cramp treatments. Increasing stimulation frequency lengthens Cramp duration; it is unknown which frequency elicits the longest EIMC. Objective: To determine which stimulation frequency elicits the longest EIMC and whether Cramp duration and stimulation frequency are correlated. Design: Randomized, crossover. Setting: Laboratory. Participants: 20 participants (12 male, 8 female; age 20.7 ± 0.6 y; height 174.9 ± 1.9 cm; mass 76.6 ± 2.2 kg) with a self-reported history of muscle Cramps in their lower extremities within the 6 mo before the study. Interventions: The dominant leg’s tibial nerve was percutaneously stimulated with 2-s-duration electrical stimuli trains starting at a frequency of 4 Hz. After 1 min of rest, stimulation frequency increased in 2-Hz increments until a Cramp occurred in the flexor hallucis brevis. The stimulation frequency at which a Cramp occurred was termed Cramp threshold frequency (TF). Cramp d...
Mamede De Carvalho - One of the best experts on this subject based on the ideXlab platform.
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fasciculation Cramp syndrome preceding anterior horn cell disease an intermediate syndrome
Journal of Neurology Neurosurgery and Psychiatry, 2011Co-Authors: Mamede De Carvalho, Michael SwashAbstract:Cramp-fasciculation syndrome (Cramp-FS) is an ill-defined condition with uncertain clinical limits. The authors studied a 55-year-old man with progressively more severe, widespread fasciculations and Cramps during a 6-year-period. Mild progressive lower motor neuron loss, shown by motor unit number and multi-motor unit potential (MUP) analysis, developed during the 4 years after onset, which stabilised during a further 2-year follow-up. Cramp-FS is generally a benign syndrome, probably with several causations. Our patient developed a limited form of anterior horn cell degeneration perhaps representing a syndrome transitional with amyotrophic lateral sclerosis. Cramp-FS merits more detailed study.
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Fasciculation-Cramp syndrome preceding anterior horn cell disease: an intermediate syndrome?
Journal of Neurology Neurosurgery and Psychiatry, 2010Co-Authors: Mamede De Carvalho, Michael SwashAbstract:Cramp-fasciculation syndrome (Cramp-FS) is an ill-defined condition with uncertain clinical limits. We studied a 55-year-old man with progressively more severe, widespread fasciculations and Cramps during a six-year period. Mild progressive lower motor neuron loss, shown by MUNE and multiMUP analysis, developed during the four years after onset, which stabilized during a further 2-year follow-up. Cramp-FS is generally a benign syndrome, probably with several causations. Our patient developed a limited form of anterior horn cell degeneration perhaps representing a syndrome transitional with amyotrophic lateral sclerosis. Cramp-FS merits more detailed study.
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Cramps, muscle pain, and fasciculations: Not always benign?
Neurology, 2004Co-Authors: Mamede De Carvalho, Michael SwashAbstract:Fasciculation and Cramps without weakness or muscle atrophy are recognized as a benign syndrome. The authors report a patient with Cramp and fasciculation, which persisted for 1 year without abnormal motor unit morphology on EMG before progressive weakness, muscle atrophy, and EMG abnormalities developed. This observation raises the possibility that lower motor neuron hyperexcitability may precede motor neuron death in motor neuron disease.
Dirk Dressler - One of the best experts on this subject based on the ideXlab platform.
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Albert Schweitzer: A patient with writer’s Cramp
Parkinsonism & Related Disorders, 2011Co-Authors: Pawel Tacik, Christoph Schrader, E. Weber, Dirk DresslerAbstract:Abstract Albert Schweitzer (1875–1965) the world-famous philosopher, theologian, concert organist, musicologist, philanthropist and winner of the 1952 Nobel Peace Prize suffered throughout most of his life from severe and painful muscle Cramps in his right upper extremity which were triggered exclusively by handwriting. They led to tonic finger flexion and wrist extension and produced slow and clumsy handwriting of a reduced character size. Other motor functions including Schweitzer’s highly skilful and famous organ playing were not affected. Inheritance from his mother is likely. Schweitzer applied several coping strategies including a specific holding pattern for pens, usage of special pens, avoidance of handwriting and slowing of handwriting. With all these features Schweitzer presents as a classical case of action-specific dystonia in the form of a simple tonic writer’s Cramp. Interestingly, Schweitzer never received a medical diagnosis, although writer’s Cramp had already been identified and described as a medical condition. Impairment of his handwriting but not his organ playing may give insight into the multifactorial aetiology of writer’s Cramp.
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Albert Schweitzer: a patient with writer's Cramp.
Parkinsonism & related disorders, 2011Co-Authors: Pawel Tacik, Christoph Schrader, E. Weber, Dirk DresslerAbstract:Albert Schweitzer (1875-1965) the world-famous philosopher, theologian, concert organist, musicologist, philanthropist and winner of the 1952 Nobel Peace Prize suffered throughout most of his life from severe and painful muscle Cramps in his right upper extremity which were triggered exclusively by handwriting. They led to tonic finger flexion and wrist extension and produced slow and clumsy handwriting of a reduced character size. Other motor functions including Schweitzer's highly skilful and famous organ playing were not affected. Inheritance from his mother is likely. Schweitzer applied several coping strategies including a specific holding pattern for pens, usage of special pens, avoidance of handwriting and slowing of handwriting. With all these features Schweitzer presents as a classical case of action-specific dystonia in the form of a simple tonic writer's Cramp. Interestingly, Schweitzer never received a medical diagnosis, although writer's Cramp had already been identified and described as a medical condition. Impairment of his handwriting but not his organ playing may give insight into the multifactorial aetiology of writer's Cramp.