Spasticity occurs when a muscle involuntarily contracts when you move. It sometimes happens in your limbs after a stroke. It can be painful (like a charley horse), and it can create stiffness. When a muscle can’t complete its full range of motion, the surrounding tendons and soft tissue can become tight. This makes stretching the muscle much more difficult. If left untreated, the muscle can freeze permanently into an often-painful position.
Spasticity in the arm can cause a tight fist, bent elbow and arm pressed against the chest. This can seriously interfere with the ability to perform daily activities.
Spasticity in the leg may cause a stiff knee, pointed foot and curling toes.
How is it treated?
Health care providers consider the severity of spasticity, a person’s overall health and other factors when considering treatment, which may include:
Physical exercise and stretching: Stretching helps maintain full range of motion and prevents permanent muscle shortening.
Braces: can hold a muscle in a normal position to keep it from contracting.
Intrathecal baclofen therapy (ITB): delivers medication where it’s most effective and minimizes side effects that often accompany oral medications. A small pump is surgically implanted to supply baclofen to the spinal cord.
Oral medications: Several oral medications can help relax the nerves so that they don’t send a continuous message to the muscles to contract. Side effects may occur, such as weakness, drowsiness or nausea.
Injections: Some medications can be injected to block nerves and help relieve spasticity in a particular muscle group. This treatment weakens or paralyzes the overactive muscle. Side effects are minimized, but there may be soreness where injected. Which treatment is best for me?
Talk to your doctor about the most effective treatments for you. Every person responds differently to the various treatments.
Lack of tissue oxygenation associated with episodes of upper airway obstruction in patients with obstructive sleep apnea syndrome (OSAS) may increase the levels of alpha-synuclein in the blood and may contribute to the development of Parkinson’s disease, a study says.
Parkinson’s disease mainly results from the gradual loss of dopaminergic neurons in the substantia nigra, a region of the brain responsible for controlling movement.
The disease also seems to be associated with overproduction of the protein alpha-synuclein in nerve cells of the brain. When this protein clumps together, it gives rise to small toxic deposits inside brain cells, called Lewy bodies, inflicting damage and eventually killing them.
Of note, alpha-synuclein phosphorylation — a chemical modification in which a phosphate group is added to the protein — is known to occur in Parkinson’s disease, and is thought to be a critical step in disease progression as it enhances alpha-synuclein’s toxicity, possibly by increasing the formation of alpha synuclein aggregates.
“Recent studies found that [obstructive sleep apnea] was a risk factor for PD [Parkinson’s disease] onset, and hypoxia [lack of oxygen] may have contributed to it. [In addition,] previous studies both in vitro and in vivo revealed that hypoxia is able to induce overexpression of alpha‐synuclein (…). However, the detail mechanism remains to be further investigated,” the researchers wrote.
In this study, a group of Chinese scientists investigated the relationship between lack of tissue oxygenation caused by episodes of upper airway obstruction during sleep, and the levels of alpha-synuclein in patients with OSAS.
OSAS occurs when the throat muscles intermittently relax and block upper airways during sleep.
The study enrolled 42 patients who had been diagnosed with OSAS (eight with mild, 16 with moderate and 18 with severe OSAS) and 46 age- and sex-matched individuals with simple snoring (controls). The levels of total and phosphorylated alpha-synuclein in the patients’ blood plasma were measured by Enzyme-Linked Immunosorbent Assay (ELISA), a technique that allows researchers to measure the amount of a specific protein of interest using an enzymatic reaction).
Results showed that patients with OSAS had significantly higher levels of both total (37.68 ng/ml vs 21.08 ng/ml) and phosphorylated (26.87 ng/ml vs 14.61 ng/ml) alpha-synuclein in the plasma compared to controls.
Moreover, correlation analyses revealed the levels of both total and phosphorylated alpha-synuclein were positively correlated with the apnea–hypopnea index (an index that measures the severity of sleep apnea) and the oxygen desaturation index (an index that measures the number of times oxygen levels dip below a given threshold during sleep).
Conversely, the levels of both total and phosphorylated alpha-synuclein in the plasma were negatively correlated with the lowest and mean oxyhemoglobin saturations — the fraction of hemoglobin (red blood cells) bound to oxygen relative to the total hemoglobin found in the blood.
“In summary, the present study found that increased alpha-synuclein levels in the plasma are correlated with the degree of hypoxia in OSAS, indicating that chronic hypoxia caused by OSAS may be involved in the pathogenesis [disease manifestations]” of Parkinson’s, the scientists concluded
A treatment for Parkinson’s Disease, called deep brain stimulation, implants electrical leads directly into brain tissue that deliver pulses of electricity.
Improvements from the procedure can include reduced tremors, stiffness and slowness of movement.
The cost for devices and surgery can range from $35,000 to $100,000, and is typically covered by private insurance and Medicare because of FDA approval.
It is most definitely brain surgery.
The skull is opened, and electrical leads are implanted directly into the tissue of the brain. These wires are connected to a small device that sends a small dose of electricity into the brain.
The treatment, called deep brain stimulation, means patients suffering from neurological disorders like Parkinson’s Disease can have the chance to live a normal life without constantly fighting their own bodies.
Tremors, or involuntary shaking while a limb is at rest, can be noticeably reduced or even eliminated. Patients regain mobility and are able to walk and even talk normally. YouTube is filled with hundreds of videos demonstrating the “life-changing” effects of a DBS device when active, as well as what patient functionality returns to when the device is turned off.
Popularly known as a “brain pacemaker,” deep brain stimulation works by blocking errant signals from damaged brain cells to “reset” the brain’s natural rhythm. During surgery a hole is inserted into the patient’s skull and electrical leads are implanted directly into the brain’s tissue. The leads are threaded out, and the skull is closed. These wires are threaded behind the ears, down the neck and to the front chest area, where they are connected to a watch-size device that emits a controlled amount of electricity. The entire unit, from wires to generator, are all buried just below the skin.
A growing medical technology niche
The generator, a self-contained unit with a battery, sends pulses of electricity through the leads to stimulate areas of the brain, reducing or in some cases even eliminating the most debilitating parts of the disease. A small, cellphone-size remote control can be used to adjust the “dosage” of electricity and can turn the device on and off.
Each DBS surgery can cost between $35,000 and $50,000, and upward of $70,000 to $100,000 for bilateral procedures (both sides of the brain), according to the National Parkinson Foundation. These estimates include the cost of the surgery, devices, anesthesia, hospital fees and physician fees. Device costs can run to tens of thousands of dollars:
In addition to the complications associated with surgery, DBS devices also require physical maintenance. Batteries in the devices are not rechargeable and need to be replaced, Wodziak said. The hardware can wear over time and may need maintenance. Medtronic says its devices are not susceptible to hacking, and include encrypted signal technology and proprietary algorithms to communicate with remote controllers.
Despite progress, experts and doctors are trying to determine exactly how electrical stimulation alleviates the symptoms of brain-related disabilities. Doctors are still debating if DBS directly affects the function of brain cells, if it simply introduces changes in the chemical composition and biology of the brain, or some combination of the two.
Advances in DBS technology
The treatment can be used to tackle additional neurological problems and other disorders including epilepsy, seizures and dystonia, which is the sustained, involuntary contraction of muscles and can lead to painful cramping of the feet or hands, curling toes, or turning and twisting of the neck. A version of the same technology can even be used on the spinal cord. This year the first DBS surgery for stroke recovery performed. It is also considered for depression and weight loss.
Although the treatment has been around since the 90’s, there have been some incremental advances to the technology, including leads capable of focusing electricity to increasingly specific parts of the brain and smaller generators capable of connecting to devices using Bluetooth.
Researchers also are exploring ways to create a non-invasive form of DBS. MIT scientists have developed a new method to stimulate cells inside the brain non-invasively, using multiple electric fields applied from outside the organ, according to a study conducted on mice that had its results published in the scientific journal Cell in June.
The best candidates for DBS
Have had PD symptoms for at least five years.
Have “on/off” fluctuations (when a person cycles between “on” time, when the medication is working to control symptoms, and “off” time, when medication has worn off and PD symptoms return), with or without dyskinesia. Dyskinesia is involuntary, irregular, writhing movement that can range from mild to violent and can sometimes be unpredictable.
Continue to have a good response to PD medications, especially carbidopa/levodopa (though the duration of response may be insufficient).
Have tried different combinations of carbidopa/levodopa and dopamineagonists under the supervision of a movement disorder neurologist or specialist.
Have tried other PD medications – such as entacapone, tolcapone, selegiline,apomorphine or amantadine – without beneficial results.
Have PD symptoms that interfere with daily activities.
(Source: National Parkinson Foundation)
It’s not a cure for Parkinson’s Disease.
Michael J. Fox, the actor who has become synonymous with the fight to find a cure for Parkinson’s and whose foundation offers guidancefor those considering the procedure, has spoken in the past about the potential benefits of DBS, but also its limitations. He was first diagnosed in 1991 and in the late 1990s, Fox had a type of brain surgery to relieve his tremors, a thalamotomy — which destroys a small portion of brain tissue — before DBS became an option.
For over a decade I have been part of a clinical trial at the vanguard of surgical innovation, the application of central thalamic deep brain stimulation (DBS) in severe traumatic brain injury. Our work resulted in a 2007 paper in Nature that indicated that DBS may promote functional recovery from severe traumatic brain injury years after injury .
This study was instructive in these ethical domains, as well as in scientific domains related to disorders of consciousness and mechanisms of recovery. More recently, however, the study has helped illustrate how society assesses the economics of surgical innovation in marginalized populations. In this paper I focus on this theme and consider the interplay of ethics and economics in innovative surgical research, paying particular attention to the interests of patients and their families .
Let me begin with a review of the case report. The subject was a 38-year-old who had remained in the minimally conscious state (MCS) for 6 years after having been assaulted. MCS is a disorder of consciousness functionally above the vegetative state . MCS patients have definite, albeit intermittent, evidence of consciousness. They may show intention, attention, and memory and have awareness of self, others, or the environment, but only episodically .
The subject had an initial Glasgow Coma Scale of 3. He progressed to MCS in 3 months. Upon study enrollment, he sometimes followed commands with eye movements. He could neither communicate nor take food by mouth and was dependent upon tube feedings [1, 10].
Over the course of the DBS study, the subject manifested improved levels of arousal, motor function, swallowing, and expressive speech, assessed by objective measures, including the JFK Coma Recovery Scale-Revised . Now he is more mobile, can eat food by mouth, and can communicate in short sentences. He also regained aspects of personal agency and is now able to express a preference when prompted .
Since publication of the research paper on this case, I am invariably asked about the costs of DBS and whether it was worth it. Although this is understandable, given the austerity of the times and the broader debate about distributive justice in health care, the question strikes me as problematic. Generally we do not bring cost into the equation when considering early clinical trials. The Food and Drug Administration does not weigh cost considerations when granting either an investigational new device (IDE) or new drug exemption (IND). At this stage of innovation, a premium is placed on discovery, recognizing that costs need not be assessed until after interventions are validated. Moreover, prices should come down as methods are refined.
So why the inevitable question? In my view, it is a proxy for deeply held, unexamined biases towards patients with severe brain injury and a belief that nothing can or should be done. These views date back to landmark legal cases like Quinlan, which asserted a right to die based on an irretrievable loss of a “cognitive or sapient life” in the permanent vegetative state [19, 7]. Although the Quinlan court’s establishment of patients’ or surrogates’ right to withhold life-sustaining treatment was an ethical good , generalizing hopelessness to all severe brain injury was not . By failing to distinguish between vegetative and minimally conscious states , we deprive patients in the latter of access to emerging modalities that might promote recovery .
Although these biases are expressed toward patients with severe brain injury, the lesson for surgical innovation is a generic one: when assessing new devices or techniques for marginalized populations (with chronic or out-of-fashion conditions), it is critical to consider costs and benefits free of unexamined biases. Anything less is discriminatory and unjust.
If we overcome these biases and actually apply objective standards to a hypothetical cost-benefits analysis of DBS in MCS, it is possible to imagine that up-front costs of patient assessment, DBS surgical implantation, and follow-up could result in a cost-effective intervention. As one colleague of mine, Dr. Frank Levy, put it in an October 2009 e-mail, those who purport to believe in cost-benefit analysis have a responsibility to apply those methods. They cannot just invoke their prejudices and stop there; they are obliged to collect and examine the data.
To this end and for the purposes of this analysis, let us postulate that DBS will be established as a viable therapy for MCS, with a significant number of subjects in clinical trials having had improvements comparable to those of the first subject. If we take this hypothetical—and I stress it remains hypothetical early in this work—as a predicate for a cost-benefit analysis, we can immediately see that DBS effects should decrease the fixed costs of institutional care.
The benefits seen in our first subject, if replicated, could have significant economic implications. His enhanced mobility reduces his need for prophylactic anticoagulation and its associated risks and costs. His nutritional status is improved with oral food intake, raising his albumin. This benefit, along with his enhanced mobility, decreases his risk of bedsores and accelerates healing when they do occur. His ability to swallow and manage his secretions—along with removal of the PEG and, again, his mobility—make it less likely he will develop an aspiration pneumonia. His cognitive improvements now allow him to respond to questions about pain, discomfort, and a whole range of symptoms. This should help his doctors diagnose brewing conditions more quickly and cost-effectively. Finally—and perhaps most critically—his enhanced cognitive abilities and growing ability to speak allow for more meaningful interactions with his family and loved ones.
Much of this can–and should be—cost out. If and when this intervention is validated, health economists will need to calculate the decreased incidence of the aforementioned complications of chronic care (e.g., the cost of a bedsore or hospitalization for aspiration pneumonia) in an appropriately sized cohort and weigh these fixed costs for this population against the putative decreased morbidity seen with DBS. Only then can an objective cost-benefit analysis be offered for this intervention.
Some might worry that the advent of DBS for MCS creates an application that will expand markets and expenditures, but severely brain-injured patients—and the cost associated with their chronic care—are already in the system. Their existence is a consequence of failed efforts in acute care to achieve better functional outcomes. In these circumstances, an effective therapy for MCS would not create a clinical need but rather respond to unmet ones brought about by acute care technologies that can save lives but not completely mend them.
The medical ethicist in me hopes that a validated therapeutic intervention for MCS would be sustained by humane intent alone. But I am not so naive as to think that good intentions alone will win the day. Too many patients in MCS are neglected and isolated in chronic care, receiving what is euphemistically called “custodial care,” minimally conscious but mistakenly diagnosed as being vegetative . One recent study estimated that error rate at an appalling 41 percent .
Against such odds, an eventual cost-benefit analysis of DBS for MCS could be instrumental, if this surgical innovation matures into a safe and effective therapy. When that occurs, a robust cost-benefit analysis would be helpful. Objective data might demonstrate, notwithstanding some recent critiques of medicine’s technological imperative , that medical innovation can sometimes be both humane and affordable. That is an important lesson for medicine and society.
Now that deep-brain stimulation (DBS) — a groundbreaking treatment for Parkinson’s disease — has been around for just over 30 years in the U.S., check out some stats and data about it. Plus, see how many members of the PatientsLikeMe community have had DBS and what they’ve said about it.
What is DBS and how does it work?
DBS is a procedure that uses a surgically implanted, battery-operated device called an implantable pulse generator (IPG) — similar to a heart pacemaker and about the size of a stopwatch. The IPG delivers electrical stimulation to specific areas in the brain that control movement, blocking the abnormal nerve signals that cause Parkinson’s disease (PD) symptoms.
Take a look at some key dates, stats and facts related to DBS:
1987 – the year that French neurosurgeon Dr. Alim-Louis Benabid developed modern DBS
1997 – the year that the Food and Drug Administration (FDA) approved DBS in the U.S.
100,000+ – the number of people who’ve had DBS surgery
$35,000 to $50,000 – the cost of DBS surgery (bilateral procedures may cost upwards of $70,000 to $100,000) Please visit medgoassistance.com to get a free quote for much cheaper prices.
1,000 – the approximate number of hospitals and healthcare centers that perform DBS around the world
1,000 – the number of DBS surgeries some of the most experienced neurosurgeons have performed; PatientsLikeMe member tip: “If you decide to go through with [DBS], be sure and ask how many procedures the surgeon has done. The more they do it, the less risk for you.”
10 – the number of factors that neurologists may consider when deciding whether a person with PD may be a good candidate for DBS (for example, see these guidelines from the University of California, San Francisco [UCSF] and the University of Florida Health)
Talk with your neurologist about whether you’re a candidate for DBS, and consider seeking a second opinion. Primary considerations typically include:
Having a clear diagnosis of idiopathic PD (rather than atypical PD or more complex “Parkinson’s plus” syndromes)
Having good cognitive function
Showing clear improvement of motor symptoms with sinemet treatment (“In general [DBS] surgery makes the ‘off’ states more like the ‘on’ states but rarely does better than the best ‘on’ state,” according to UCSF)
Surgery is the only option to definitively manage scoliosis in children with cerebral palsy (CP), according to a recent review in the Journal of Spine Surgery. The study also detailed post-operative outcomes for the patients.
There is a strong link between having CP and developing scoliosis. The condition is estimated to occur in 21% to 64% of CP patients, according to “The Management Of Scoliosis In Children With Cerebral Palsy: A Review.” In children, scoliosis most often occurs between the ages of 10 and 18.
According to the authors, spasticity, muscle weakness, and poor muscle control contribute to spinal anomalies.
CP patients have two distinct types of scoliotic curves. Group-I involves double curves with a thoracic (middle back) and lumbar (lower back) component. These curves are most often seen in ambulatory patients with minimal pelvic obliquity (an abnormal pelvic tilt). Group-II involves single thoracic or lumbar curves that are more pronounced. They occur more frequently in quadriplegic patients, and almost all involve significant pelvic obliquity.
Hip contractures, leg-length discrepancy, or both may contribute to pelvic obliquity.
Children with CP and scoliosis can be treated by nonsurgical means, but studies suggest those measures only delay surgery.
“The aim of non-surgical management of scoliosis in CP is to improve sitting control and reduce or modify curve progression without the need for surgical intervention,” the researchers wrote. “There is a paucity of evidence for the use of modern bracing techniques. However, more recent studies suggest bracing improves sitting balance and trunk support, which provides better control of the head and neck as well as enhanced use of the upper limbs as they are not required to support the trunk in the sitting position.”
Intrathecal baclofen (ITB) pumps, which continuously deliver medication into the spinal fluid, have been shown to improve spasticity and pain, but it is not clear whether they can worsen scoliosis.
“Surgery remains the only option for the definitive management of scoliosis in CP,” the team wrote. “The aims of surgical correction include achieving a balanced spine, prevention of curve progression and improvement in functional quality of life.”
The authors noted that surgery should be carefully planned by a multi-disciplinary team and include a physical examination, and laboratory and imaging tests.
Post-operative complications involving the respiratory system frequently occur in children with CP, the team noted, as can implant complications and infections.
“The use of pre-operative non-invasive ventilation (NIV) training to strengthen respiratory muscles has shown promise in improving outcomes in patients with neuromuscular disease following spinal surgery,” the team wrote.
Studies have reported that parents and caregivers are typically satisfied with the results of surgery, with a majority willing to recommend it to others