Physiologic and Clinical Monitoring of Spastic Hypertonia

Hinderer, Steven R.; Dixon, K.

doi:10.1016/s1047-9651(18)30030-5

Cited by 29 publications

(8 citation statements)

References 34 publications

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“…The spasticity syndrome is generally considered by patients and clinicians to negatively interfere in DLA (Maynard et al, 1990;Skold et al, 1999) and gait (Gormley et al, 1997;Hinderer & Dixon, 2001;Jozefczyk, 2002). However approximately 40% of subjects have been reported to rate their spasticity symptoms as positive (Skold et al, 1999), facilitating movement transfers, standing and to further improve walking (Dietz, 2001;Gormley et al, 1997;Hinderer et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

“…However approximately 40% of subjects have been reported to rate their spasticity symptoms as positive (Skold et al, 1999), facilitating movement transfers, standing and to further improve walking (Dietz, 2001;Gormley et al, 1997;Hinderer et al, 2001). As such the assessment of the specific impact of different symptoms and signs of the spasticity syndrome on general daily activities is clinically relevant.…”

Section: Introductionmentioning

confidence: 99%

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Impact of specific symptoms of spasticity on voluntary lower limb muscle function, gait and daily activities during subacute and chronic spinal cord injury

Bravo-Esteban

Taylor

Abián-Vicén

et al. 2013

NRE

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BACKGROUND: Although the spasticity syndrome is an important sensorimotor disorder, the impact of grade of lower limb muscle hypertonia, spasm and clonus activity on voluntary muscle function, gait and daily activities has not been systematically analysed during subacute and chronic spinal cord injury (SCI). OBJECTIVE: To determine the prevalence of spasticity signs and symptoms during SCI, and to assess their impact on motor function and activities. METHODS: A descriptive transverse study of sixty-six subjects with SCI was performed by assessing injury characteristics, spasticity (modified Ashworth scale, Penn scale, SCATS scale) and motor function (lower limb manual muscle scores, WISCI II, spinal cord injury spasticity evaluation tool). RESULTS: Most subjects with the spasticity syndrome presented lower limb hypertonia and spasms during both subacute and chronic SCI, interfering with daily life activities. Subjects with incomplete SCI and hypertonia revealed a loss of voluntary flexor muscle activity, while extensors spasms contributed strongly to loss of gait function. The Penn spasms scale no correlated with muscle function or gait. CONCLUSIONS: Specific diagnosis of spasm activity during subacute SCI, and its impact on lower limb voluntary muscle activity, gait function and daily activities, is required to develop a more effective neurorehabilitation treatment strategy.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Impact of specific symptoms of spasticity on voluntary lower limb muscle function, gait and daily activities during subacute and chronic spinal cord injury

Bravo-Esteban

Taylor

Abián-Vicén

et al. 2013

NRE

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“…It also increases by 34% the number of neurons that extend axons [300,301] and speed of axon regeneration [302]. This influence is in part due to electrical stimulation promoting both Schwann cell migration and proliferation, and by acting directly on neurons to induce them to increase the distance axons are extended [303].…”

Section: Electrical Stimulationmentioning

confidence: 99%

Promoting Axon Regeneration and Neurological Recovery Following Traumatic Peripheral Nerve Injuries

Kuffler¹

2015

Int J Neurorehabilitation Eng

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Repairing Peripheral Nerves following Traumas Nerve crushWithin several days of crushing a peripheral nerve, the injured axons begin to regenerate through their distal pathway until they reach their original targets with which they restore neurological function. The larger the number of axons that regenerate through the distal nerve, the greater the extent of neurological recovery [1][2][3]. The number of axons that regenerate, and thus neurological recovery, is influenced by the physiological state of the distal denervated nerve pathway [4][5][6][7].Following a peripheral nerve crush, the injured axons begin to regenerate within 2 days of injury [8]. They may regenerate to their targets through their original pathway in association with and promoted by its Schwann cells, the neurotrophic factors they release, and the Schwann cell extracellular matrix [1,4,[9][10][11][12][13][14]. Thus, the distal nerve provides a simple means for promoting and directing the regenerating axons to their original targets [15][16][17][18]. However, when a nerve has a gap, the gap must be bridged with a material that is permissive to and promotes axon regeneration across the entire gap to reach the distal nerve stump, through which the axons must then be able to regenerate.The Schwann cells in the denervated distal nerve release neurotrophic factors that promote axon regeneration, but also release extracellular matrix components that promote and inhibit axon regeneration [19][20][21][22][23][24][25][26]. Thus, regeneration through the distal nerve is a balance of the influences of factors that both promote and inhibit regeneration. If the Schwann cells are present, such as after a simple nerve crush, virtually 100% of the axons regenerate and they innervate all the denervated synaptic sites. If the Schwann cells within the distal nerve pathway are killed, leaving only the extracellular matrix intact, the number of axons that regenerates to their targets decreases by 94%. This is because the factors required to trigger the regenerating axons to branch at extracellular matrix branch points are missing, axons do not branch, and therefore each axon reinnervates only a single denervated muscle fiber. Thus, Schwann cells along the distal nerve pathway and a AbstractFollowing a peripheral nerve crush, or when a peripheral the nerve is transected and the nerve stumps anastomosed, neurological recovery is generally excellent. This is because the axons merely have to regenerate through the distal portion of the nerve through the existing extracellular matrix of the denervated Schwann cells that direct and promote them to their distant denervated motor and sensory targets. However, when a length of a peripheral nerve is destroyed, and anastomosis is not possible, the standard surgical repair technique is to graft a length/s of autologous sensory nerve into the gap. Neurological recovery is generally good if the nerve gap is <2 cm in length, the repair is performed <4 months post trauma, and the patients are <25 years of age. Because the nerve ...

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“…TJ is also known as tendon reflex or T-reflex. The amplitude of TJ is evaluated by a 5-point clinical scale (Hinderer and Dixon, 2001) that quantifies the movement of a body segment in response to a tap to the skin overlying the tendon of the muscle operating across the joint or distal portion of the body segment. The TJ score aids in the differential diagnosis of many neurological conditions; however, the score is not always associated with the functional status of patients.…”

Section: Introductionmentioning

confidence: 99%