Definition of spastic state: a movement disorder characterized by a velocity-dependent increase in the detrusor reflex (muscle tension) and overactive tendon reflexes, as a component of the upper motor neuron syndrome, which is caused by hyperexcitability of the detrusor reflex. The basic features of the spastic state are a persistent state of static muscle movement (tonicity) and frequent or intermittent muscle spasms of the trunk and extremities, which can be transmitted. Spasticity and tonicity interfere with the patient’s social activities, personal hygiene, skin breakdown and bed sores, and occasionally cause life-threatening systemic infections. Etiology of spastic states Spastic states are the result of central nervous system injury, which is divided into cerebral and spinal origin. The cerebral origin includes traumatic brain injury, stroke, cerebral palsy, hypoxic encephalopathy, and metabolic brain disease. Spinal cord origin is mainly spinal cord trauma, multiple sclerosis, spinal cord ischemia, degenerative myelopathy, cervical spondylosis, and transsphenoidal myelitis. The mechanism of spasticity is mainly the overgrowth of the traction reflex, which is the reflection of muscle contraction in the opposite direction caused by mechanical load traction on the muscle, and its receptors are the muscle shuttle and Golgi tendon organ. The latter is connected in series with the main muscle fibers (sometimes called extra-suspensory muscles). There are two types of afferent nerve fibers in the musculocutaneous plexus: one belongs to the fast-conducting, thicker (10µm-20µm) Iα afferent nerve fibers, which make excitatory synaptic connections with α motor neurons; the other afferent nerve fibers are the thinner (4-12µm) class II nerve fibers that originate from α motor neurons, large motor neurons in the anterior horn of the spinal cord. The dominant musculocutaneous motor nerve fibers are thinner (4-12 µm) and distributed at the ends of the musculocutaneous spinal cord, which originate from a small γ motor neuron in the anterior horn of the spinal cord. When the activity of the γ efferent nerve fibers is enhanced, the muscle fibers in the shuttle contract, thus increasing the sensitivity of the shuttle to sensory featurization. The increased afferent impulses cause excitation of the α motor neuron innervating the same muscle, causing the contraction of the extra-saccadic muscle, a reflex called the γ-loop. The movement of the γ efferent nerve fibers regulates the sensitivity of the intra-saccadic receptors, which in turn regulates the tensor reflex. When the extra-saccadic muscle contracts, the intra-saccadic muscle fibers will be relaxed, so their afferent impulses are reduced, the excitability of α-motor neurons is weakened, and the muscle contraction will not be sustained. The detrusor reflex is regulated by the central nervous system, and after central nervous system injury, the threshold of the detrusor reflex is reduced due to the loss of the cortical and other higher central retroflexes. gamma motor neurons become more sensitive, and the detrusor reflex of the spinal column causes limb spasm. The current clinical selective posterior spinal nerve rhizotomy is to cut the γ-loop. From the histochemical point of view, there are significant changes in neurotransmitters during the production of spasticity. First, there is a decrease in the release of inhibitory neurotransmitters (e.g., GABA), which increases Ca2+ influx, and sex leads to an increase in the release of excitatory neurotransmitters, such as glutamate, which exacerbates the spastic state. The spasticity is relieved by reducing the release of excitatory neurotransmitters with the GABA mimetic baclofen. Clinical manifestations of spasticity There are two basic features of spasticity: changes in muscle tone and changes in random motor control. In other words, a patient is subjected to upper motor neuron paralysis and spasticity. Patients exhibit tonicity of the trunk and limbs and uncontrollable muscle spasms, which can be carried out by one muscle or multiple muscle groups and can be transmitted to distant areas. Spasticity due to spinal cord injury can have different clinical manifestations depending on the site and segment of the injury. In addition to mild paralysis and paresis of the lower extremities, some patients have spasticity in only one limb, and the spastic limb is on the same side of the body (e.g., spinal cord hemisection syndrome), or have spasticity in only the upper extremities and retain some motor function (e.g., central spinal cord syndrome). Spastic states resulting from brain hemisphere injury, such as traumatic brain injury, stroke, cerebral palsy, and other brain dysfunctions, have more complex clinical features. Increased muscle tone is the primary clinical feature of upper motor neuron dysfunction, which is accompanied by dystonia, paresis, motor inability, ataxia, myoclonus, and other types of non-random movement disorders. Diagnosis and differential diagnosis of spasticity Based on the etiology of spasticity and other clinical features, it is not difficult to diagnose cerebral or spinal origin. However, the patient must have the basic features of spasticity, tonicity and spasticity of the trunk and limbs. Spasticity needs to be differentiated from dystonia, Parkinson’s disease, and myoclonus. Spasticity is associated with vertebral tract injuries, whereas dystonia, Parkinson’s disease, and myoclonus are extravertebral lesions. Although spasticity can be accompanied by myoclonus and altered muscle tone, dystonia, Parkinson’s disease, and myoclonus also have their typical clinical features, which are generally easy to distinguish. The drug treatment of spasticity 1, baclofen: It is designed to imitate the activity of gamma-aminobutyric acid (GABA), is one of the main neurological inhibitory neurotransmitters. 2, Diazepam: It is increased endogenous GABA release or excitatory synaptic response to glutamate, therefore, it is neither a GABA potent nor a GABA mimetic, it can get the effect of physiologically conveying GABA neurotransmitter. 3, Dantrolene: In clinical practice, it is effective when used alone or in combination with baclofen or diazepam. 4, intrathecal drug therapy: (1) intrathecal administration of morphine: intrathecal administration of morphine using an implanted pump and catheter system has been shown to be effective in the control of spasticity or tonicity of spinal origin. The antitussive effect of morphine is dependent on opioid-like -12 receptors and can be antagonized with naloxone. Experimental morphine injections are performed by lumbar puncture prior to pump implantation. (2) Intrathecal baclofen administration: Intrathecal pumping of baclofen has been shown to be particularly effective in the treatment of severe spasticity states. Continuous intrathecal baclofen administration is well tolerated by those administered through the pump system and is long-term and safe. In normal concentrations, baclofen engages GABA-B receptors at the spinal cord level, reducing calcium influx into presynaptic terminals and inhibiting excitatory neurotransmitter release. At high concentrations, baclofen reduces postsynaptic neuroexcitability (by antagonizing excitatory neurotransmitter activity at the synaptic “E”). The effect of treatment can be sustained by using an implanted drug pump and catheter system to release baclofen. This approach has been successful in treating spasticity of spinal origin. Intrathecal administration of baclofen differs from continuous infusion in that it allows for more precise control of spasticity and the ability to adjust the dose to the patient’s needs.