This chapter examines the influence of spasticity and associated treatments on health care costs. Spasticity has the capacity to influence a number of health-related domains including mobility, self-care, caregiver burden, pain, and contracture. The chapter describes the rehabilitative interventions are critical to the management of spasticity both in isolation as well in combination with other treatment modalities. Several oral medications have potential utility as antispasticity agents. The medical literature has minimal discussion regarding the economic impact of oral spasticity agents. Perhaps no technique has affected the management of spasticity more than the introduction of focal neurolysis with botulinum neurotoxin (BoNT). Intrathecal baclofen (ITB) therapy is a highly potent and effective therapy for management of global spasticity. The chapter attempts to describe the economic impact of the hypertonic condition and the costs associated with the spasticity management techniques.
Your search for all content returned 31 results
Spasticity remains among the most vexing problems after severe traumatic brain injury (TBI). This chapter focuses on the issues most applicable to those with TBI throughout the continuum of care. In TBI there is both focal and diffuse brain damage that can disrupt supraspinal signals. There often are other observed changes to active and passive movement, resting postures, and muscle tone that can be mislabeled as spasticity during a TBI clinical evaluation. Some TBI patients will develop spasticity in the acute care setting. In general, nonpharmacological therapy is preferred in the acute TBI patient because it avoids potential central nervous system (CNS) side effects associated with many oral medications. Splinting and serial casting provide a period of prolonged stretching and are used in both acute and chronic TBI-related spasticity. Untreated pain can contribute to dysautonomia, agitation, and increased intracranial pressure in the acute TBI population.
This chapter focuses on the hereditary spastic paraplegias (HSP) and describes the spectrum of genes identified thus far. It summarizes the molecular genetic findings of each gene and discusses the major cell biological pathways involved in hereditary spastic paraplegia. Spastic paraparesis, increased stretch reflexes, and presence of pyramidal signs, often accompanied by neurogenic bladder disturbances and impairment of vibrations sense in the lower limbs, are the clinical hallmarks of all HSPs. Overexpression of exogenous spastin in cultured cells resulted in the localizing of spastin to microtubule asters. Drosophila models of spastin revealed irregularities in microtubules of neurons, severe reduction of the synaptic terminal area at the neuromuscular junction, and subsequent neurotransmission defects. Conversely, spastin overexpression resulted in more microtubule branching and shorter severed microtubule segments. Complicated HSP with pigmentary maculopathy, also known as Kjellin syndrome, is associated with mutations in spastizin.
The combination is the key feature of muscle spasticity, although it is important to recognize that spasticity is only one of a number of positive signs that materialize after an upper motor neuron (UMN) lesion. Spasticity as a phenomenon has a specific definition, but it is often used as a collective term for all positive signs of upper motor neuron syndrome (UMNS), many of which are not based on sensitivity of a muscle to stretch. In a spastic patient, however, once the threshold of the electromyographic (EMG) activity is triggered at a given degree of muscle stretch, the EMG activity persists until stretch is relinquished. The defining characteristic of clinical spasticity is excessive resistance of muscle to passive stretch, a resistance that intensifies as the examiner increases the rate of stretch in subsequent stretch maneuvers.
This chapter reviews the mechanism of action, techniques, proven benefits, and risks associated with phenol neurolysis along with a brief discussion of the use of alcohol. It provides a comparison between phenol and botulinum toxins (BoNT) and suggests situations in which the practitioner may preferentially select one intervention over another. Nerve blocks involve the application of substances to a nerve that will interfere with conduction along the nerve on a temporary or permanent basis; local anesthetics, phenol, and alcohol are most frequently used. Once the phenol is injected, there should be an almost immediate reduction/cessation of the muscle twitch, with a continued reduction in response to electrical stimulation over 1 to 2 minutes. Patient tolerance for the procedure varies considerably; patients may feel some discomfort from the electrical stimulation, from the needle search, and from some burning during the injection of phenol or alcohol.
This chapter reviews the most salient points related to the clinical presentation of upper motor neuron syndrome (UMNS) in the lower limb especially as it affects walking. Spasticity has classically meant increased excitability of skeletal muscle stretch reflexes, both phasic and tonic, that are typically present in most patients with a UMN lesion. There are many assessment techniques used in routine clinical examination of the patient with spasticity. Spasticity, muscle overactivity, contracture, or pain can all play a role in limited joint passive range of motion. OnabotulinumtoxinA injection is currently approved by the U.S. Food and Drug Administration (FDA) for the treatment of blepharospasm, facial spasm, strabismus, cervical dystonia, hyperhidrosis, and upper limb spasticity. Before using botulinum toxin (BoNT) for the clinical management of spasticity, the physician should be knowledgeable about the diagnosis and medical management of the condition producing the UMNS.
Spasticity in the patient with multiple sclerosis (MS) ultimately leads to a detrimental increase in disability resulting in increased energy requirement for daily activities and decreased quality of life. This chapter reviews the etiology, pathophysiology, diagnosis, and evaluation of spasticity in this patient population. In addition, treatment and management strategies of MS-associated spasticity are reviewed with emphasis on those items that are unique to this clinical population. In MS, spasticity can be due to lesions in the brain, spinal cord, or both, with lower limb spasticity almost twice as prevalent as upper limb spasticity. In addition, patients with MS are frequently treated with intravenous or oral steroids for exacerbations or maintenance therapy, which adds additional risk for bone mineral decline. People with MS and their caregivers should receive an education about the risk of developing spasticity and suggested methods to prevent the onset of spasticity.
The use of botulinum toxin (BoNT) to treat spasticity of the upper extremity has dramatically improved the care of patients with increased tone as part of the upper motor neuron syndrome (UMNS). The introduction of BoNT for the treatment of increased tone has greatly increased the ability of physicians to manage spasticity of the UMNS, focusing on symptoms that interfere with activities of daily living and the ability of the caregiver to care for the patient. Treatment of upper extremity spasticity with BoNT enables physicians to focus on specific activities and functions important to the patient and/or caregiver. In clinical practice, the dosing, technique, and benefits noted in the poststroke spasticity trials have been extrapolated to those with traumatic brain injury and cerebral palsy, but trials including adults with spasticity due to traumatic brain injury, adult cerebral palsy, and multiple sclerosis have been small.
Enhanced understanding will help researchers develop new means to treat impairments associated with upper motor neuron disorders. N-acetylaspartic acid (NAA) is located only in the neuronal tissue, with relative decreases in its concentration suggesting neuronal injury. Magnetic resonance spectroscopy (MRS) has detected reduced levels of NAA after traumatic brain injury (TBI) even in the presence of normal-appearing standard imaging, with evidence indicating it correlates with outcomes. The changes in cortical excitability induced by transcranial magnetic stimulation (TMS) have also been studied as a means to manage spasticity in several upper motor neuron conditions, including stroke, multiple sclerosis, cerebral palsy, and spinal cord injury. Transcranial direct current stimulation (TDCS) modulates the excitability of targeted brain regions by altering neuronal membrane potential based on the polarity of the low-voltage direct current that is transmitted through the skull via the electrodes.
The actual incidence of spasticity depends on the cause of the upper motor neuron (UMN) lesion. Reliable assessments are complicated by the fact that spasticity can vary throughout the day, change with different positions, and increase with any noxious stimulus, such as pressure sores, urinary tract infection, deep venous thrombosis, ingrown toenails, joint pain, or constipation. Arm and leg spasticity was measured using the Modified Ashworth Scale (MAS), and disability was measured with the modified Rankin Scale and the Barthel Index (BI). Although there was a weak correlation between spasticity and health-related quality of life (HRQL), the hemiparetic patients without spasticity had significantly better BI functioning scores and significantly better HRQL scales than patients with spasticity. Sports-related spinal cord injuries (SCIs) occur more commonly in children and teenagers, whereas work-related injuries are more common in adults.