In general, spasticity is classified as a symptom of the upper motor neuron syndrome, characterized by an exaggeration of the stretch reflex secondary to hyperexcitability of spinal reflexes.2 Upper motor neurons originate in the brain and brain stem and project to lower motor neurons within the brain stem and spinal cord.11 The lower motor neurons are of two types, both of which originate in the ventral horn of the spinal cord: (1) alpha motor neurons project to extrafusal skeletal fibers and (2) gamma motor neurons project to intrafusal muscle fibers within the muscle spindle.11 With a lesion of the CNS comes interruption of the signals sent via the upper motor neurons to the lower motor neurons or related interneurons. Immediately following SCI, a period exists whereby the individual presents with flaccid muscle paralysis and loss of tendon reflexes below the level of the lesion.5 This period was first described in 1750, with the term 'spinal shock' introduced by Marshall Hall in 1850.30 Spinal shock has been reported to end from 1 to 3 days31 to a few weeks postinjury, with the gradual development of exaggerated tendon reflexes, increased muscle tone, and involuntary muscle spasms:5 the symptoms of spasticity. Recent animal research suggested that a recovery of relatively normal motor neuron excitability and plateau potential behavior (sustained depolarizations), in the absence of normal inhibitory control to turn off plateaus and associated sustained firing, may be implicated in the recovery of spinal shock following SCI.32
In general, spasticity is classified as a symptom of the upper motor neuron syndrome, characterized by an exaggeration of the stretch reflex secondary to hyperexcitability of spinal reflexes.2 Upper motor neurons originate in the brain and brain stem and project to lower motor neurons within the brain stem and spinal cord.11 The lower motor neurons are of two types, both of which originate in the ventral horn of the spinal cord: (1) alpha motor neurons project to extrafusal skeletal fibers and (2) gamma motor neurons project to intrafusal muscle fibers within the muscle spindle.11 With a lesion of the CNS comes interruption of the signals sent via the upper motor neurons to the lower motor neurons or related interneurons. Immediately following SCI, a period exists whereby the individual presents with flaccid muscle paralysis and loss of tendon reflexes below the level of the lesion.5 This period was first described in 1750, with the term 'spinal shock' introduced by Marshall Hall in 1850.30 Spinal shock has been reported to end from 1 to 3 days31 to a few weeks postinjury, with the gradual development of exaggerated tendon reflexes, increased muscle tone, and involuntary muscle spasms:5 the symptoms of spasticity. Recent animal research suggested that a recovery of relatively normal motor neuron excitability and plateau potential behavior (sustained depolarizations), in the absence of normal inhibitory control to turn off plateaus and associated sustained firing, may be implicated in the recovery of spinal shock following SCI.32
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