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Source: Clinical Neurophysiology
Condition: Reflex Sympathetic Dystrophy

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Total 20 results found since Jan 2013.

Deficits in startle-evoked arm movements increase with impairment following stroke
Conclusions: We conclude that the task-inappropriate flexor activity likely results from cortical or corticospinal damage leading to an unsuppressed or hypermetric classic startle reflex that interrupts startReact elbow extension.Significance: Given startReact’s functional role in compensation during environmental disturbances, our results may have important implications for our understanding deficits in stroke survivor’s response to unexpected environmental disturbances.
Source: Clinical Neurophysiology - January 10, 2014 Category: Neuroscience Authors: Claire Fletcher Honeycutt, Eric Jon Perreault Tags: Movement, Motor Control and Movement Disorders Source Type: research

Contributions of Motoneuron Hyperexcitability to Clinical Spasticity in Hemispheric Stroke Survivors
Spasticity, affecting up to 43% of chronic stroke survivors (Wissel et al., 2013), is diagnosed clinically as muscular hypertonia, coupled with other reflex disturbances. This hypertonia is defined as a velocity-dependent resistance to stretching due to exaggerated reflex responses (Lance, 1980). There are also concurrent mechanical changes of the muscular-tendon complex, which also contribute to increased muscle tone. Although spasticity can sometimes be beneficial for certain functional movements (e.g., making locomotion and body weight support possible), it is still a major neurological impairment that frequently limits...
Source: Clinical Neurophysiology - November 15, 2014 Category: Neuroscience Authors: Xiaogang Hu, Nina L. Suresh, Matthieu K. Chardon, William Z. Rymer Source Type: research

Ascending vestibular drive is asymmetrically distributed to the inferior oblique motoneuron pools in a subset of hemispheric stroke survivors
Spasticity is a frequent and often disabling sequel to hemispheric stroke (Watkins et al., 2002; Urban et al., 2010; Wissel et al., 2013). It is characterized by a velocity-dependent increase in the resistance of a limb to passive stretch, coupled with exaggerated tendon jerks resulting from hyperexcitability of the segmental reflex arc (Dietz and Sinkjaer, 2007; Lance, 1980). The etiology of spasticity is complex, and while emerging evidence implicates changes in motoneuron excitability (i.e., decreased reflex threshold; spontaneous motoneuron firing at sub-threshold levels) as central to the genesis of post-stroke spasti...
Source: Clinical Neurophysiology - February 5, 2016 Category: Neuroscience Authors: Derek M. Miller, James F. Baker, W. Zev Rymer Source Type: research

Somatosensory and auditory startle reflex in patients with stroke and spinal cord injury
Somatosensory startle reflex (SSSR) was recently studied in healthy subjects. Following corticospinal tract lesions caused by stroke or spinal cord injury (SCI), auditory startle reflex (ASR) has been reported to enhance due to reorganization of circuits rostral and caudal to the lesion. To further understand changes in SSSR and ASR, we investigated both responses in patients with spinal cord injury (SCI) and stroke.
Source: Clinical Neurophysiology - February 11, 2016 Category: Neuroscience Authors: M.E. Kiziltan, M. Sohtaoglu, A. Gunduz, M. Bozluolçay, N. Uzun Source Type: research

Flexion Synergy Overshadows Flexor Spasticity During Reaching in Chronic Moderate to Severe Hemiparetic Stroke
Clinicians will be required to quantitatively measure and directly target the contributing underlying motor impairments in individuals with hemiparetic stroke to realize advances beyond conventional care in restoring upper extremity function (Krakauer et al., 2012). In the context of reaching function, impairment in joint individuation is the best predictor of recovery outcome over other common impairments observed in chronic stroke such as weakness and spasticity (Zackowski et al., 2004). The term “spasticity” is defined traditionally as a velocity-dependent hyperactive stretch reflex (Lance, 1980; Thilmann et al., 19...
Source: Clinical Neurophysiology - May 12, 2017 Category: Neuroscience Authors: Michael D. Ellis, Ingrid Schut, Julius P.A. Dewald Source Type: research

26. A randomized controlled cross-over double blind study protocol on THC/CBD oromucosal spray as an add-on therapy for post-stroke spasticity
Understand if cannabinoids (THC:CBD) are useful in reducing post-stroke spasticity using a neurophysiological quantitative measure as primary endpoint.We will recruit 50 patients with spasticity following stroke to take THC:CBD in a double blind placebo-controlled crossover study. Spasticity will be assessed with a numeric rating scale for spasticity, the modified Ashworth scale and with the electromyographic recording of the stretch reflex. The cardiovascular risk will be assessed prior to inclusion.
Source: Clinical Neurophysiology - November 11, 2017 Category: Neuroscience Authors: L. Marinelli, M. Balestrino, L. Mori, L. Puce, G. Rosa, L. Giorello, A. Curr à, F. Fattapposta, C. Serrati, C. Gandolfo, G. Abbruzzese, C. Trompetto Source Type: research

Startling acoustic stimuli can evoke fast hand extension movements in stroke survivors
Movement deficits following stroke are particularly prevalent in the hand leading to significant reduction in independence and the ability to participate in daily functions (Latham, 1989). Therefore, new therapies that target the hand are extremely valuable. Startle-elicited movements have recently been implicated as a possible therapy target. The classic startle reflex that occurs during exposure to a startling stimulus, e.g. loud sound, results in the adoption of a protective stance (flexion of the upper joints).
Source: Clinical Neurophysiology - June 18, 2014 Category: Neuroscience Authors: Claire Fletcher Honeycutt, Ursina Andrea Tresch, Eric Jon Perreault Source Type: research

Asymmetries in vestibular evoked myogenic potentials in chronic stroke survivors with spastic hypertonia: Evidence for a vestibulospinal role
Spastic hypertonia or “spasticity” is a frequent and often disabling sequel to hemispheric stroke (Watkins et al., 2002; Urban et al., 2010). It is a motor disorder, manifesting as a sharply lateralized muscular hypertonia on the contralesional side with exaggerated phasic and tonic stretch reflex activity (Lance, 1980). Clinically, spasticity presents as an increase in the resistance of a passive limb to externally applied joint motion and is commonly associated with deficits in both motor and functional performance (Bohannon et al., 1987; O’Dwyer et al., 1996; Watkins et al., 2002; Sommerfeld et al., 2004).
Source: Clinical Neurophysiology - March 13, 2014 Category: Neuroscience Authors: Derek M. Miller, Cliff S. Klein, Nina L. Suresh, William Z. Rymer Source Type: research

Startling acoustic stimuli can evoke fast hand extension movements in stroke survivors
Movement deficits following stroke are particularly prevalent in the hand leading to significant reduction in independence and the ability to participate in daily functions (Latham, 1989). Therefore, new therapies that target the hand are extremely valuable. Startle-elicited movements have recently been implicated as a possible therapy target. The classic startle reflex that occurs during exposure to a startling stimulus, e.g. loud sound, results in the adoption of a protective stance (flexion of the upper joints).
Source: Clinical Neurophysiology - June 18, 2014 Category: Neuroscience Authors: Claire Fletcher Honeycutt, Ursina Andrea Tresch, Eric Jon Perreault Source Type: research

Asymmetries in vestibular evoked myogenic potentials in chronic stroke survivors with spastic hypertonia: Evidence for a vestibulospinal role
Spastic hypertonia or “spasticity” is a frequent and often disabling sequel to hemispheric stroke (Watkins et al., 2002; Urban et al., 2010). It is a motor disorder, manifesting as a sharply lateralized muscular hypertonia on the contralesional side with exaggerated phasic and tonic stretch reflex activity (Lance, 1980). Clinically, spasticity presents as an increase in the resistance of a passive limb to externally applied joint motion and is commonly associated with deficits in both motor and functional performance (Bohannon et al., 1987; O’Dwyer et al., 1996; Watkins et al., 2002; Sommerfeld et al., 2004).
Source: Clinical Neurophysiology - March 13, 2014 Category: Neuroscience Authors: Derek M. Miller, Cliff S. Klein, Nina L. Suresh, William Z. Rymer Source Type: research

ID 452 – Sympathetic skin response in stroke patients
Sympathetic dysfunction could lead to life-threatening complications. The aim of this study was to investigate the relationship between the size, location, nature of the lesion, and the sympathetic skin response (SSR).Thirty patients with stroke and 30 healthy subjects were included in this study. All patients were investigated by using brain imaging and clinical scales. SSRs were elicited on four extremities in both groups. Latency and amplitude values of the responses were measured. In the patient group, SSR were analyzed both in the early (in the first month) and the late stages (one month later first recording) of the patients.
Source: Clinical Neurophysiology - February 11, 2016 Category: Neuroscience Authors: H. Erdem Tilki, G. Oztas Source Type: research

Stretch-reflex threshold modulation during active elbow movements in post-stroke survivors with spasticity
Spasticity is a common complication of stroke, occurring in ∼20-50% of patients in the first year (Wissel et al., 2013) and often associated with other sensory and motor impairments (e.g., muscle weakness, loss of dexterity). Spasticity is generally assessed by resistance or EMG responses to passive muscle stretches and has been attributed to exaggerated s pinal stretch reflexes (SRs) and alterations in intrinsic muscle properties (Dietz and Sinkjaer, 2007). For example, motor units of spastic muscles often have an impaired ability to relax (Lewek et al., 2007), prolonged spontaneous firing (Mottram et al., 2010) and low...
Source: Clinical Neurophysiology - August 3, 2017 Category: Neuroscience Authors: Nicolas A. Turpin, Anatol G. Feldman, Mindy F. Levin Source Type: research

PB3. Pharyngeal Electrical Stimulation in neurointensive care patients suffering from severe post-stroke dysphagia – Post stimulation increase of salivary substance P level may indicate treatment success
Dysphagia is one of the most important and prognostically relevant complications of acute stroke. Pharyngeal Electrical Stimulation (PES) is a treatment device that enhances cortical reorganization for the restoration of swallowing function after cerebral injury. Furthermore, it was shown that PES leads to a temporary increase of Substance P (SP) level in saliva but not serum in healthy adults. The neuropeptide SP likely acts as a neurotransmitter in the pharyngeal mucosa and enhances the swallow and cough reflex.
Source: Clinical Neurophysiology - July 10, 2018 Category: Neuroscience Authors: P. Muhle, S. Suntrup-Krueger, S. Bittner, T. Ruck, I. Claus, T. Marian, J.B. Schr öder, J. Minnerup, T. Warnecke, S.G. Meuth, R. Dziewas Source Type: research

Activation of elbow extensors during passive stretch of flexors in patients with post-stroke spasticity
Spasticity affects up to 40% of individuals after stroke (Wissel et al., 2013). The most widely accepted definition of spasticity describes it as one component of a complex motor system disorder characterized by a velocity-dependent increase in stretch reflex excitability associated with exaggerated tendon jerks (Lance, 1980).
Source: Clinical Neurophysiology - July 24, 2018 Category: Neuroscience Authors: Mindy F. Levin, John M. Solomon, Akash Shah, Andr éanne K. Blanchette, Anatol G. Feldman Source Type: research

Stimulation site and phase modulation of the withdrawal reflex during gait initiation
Muscular activity, neural mechanisms, and biomechanical forces are highly integrated in the gait initiation process (GIP) (Mann et al., 1979). In this complex process, forces generated by the legs serve to limit postural perturbations and provide forward propulsion. However, in patients with Parkinson’s disease (PD) or stroke, this process is sometimes disrupted (Hesse et al., 1997; Hass et al., 2005). In particular, people who suffered a stroke often have problems generating force in the starting leg and difficulties to load the limbs symmetrically during gait initiation (Brunt et al., 1995).
Source: Clinical Neurophysiology - February 14, 2015 Category: Neuroscience Authors: Miguel A. Richard, Erika G. Spaich, Mariano Serrao, Ole K. Andersen Source Type: research