Genes, Environment and Therapeutic Strategies
Poster Presentation
Tuina Therapy as Novel Therapeutic Strategy
for Neurodegenerative Diseases
Miles Chen1,2, PhD; Kent Logan2,3, MD and Langfang Zhang4
1Chi Wellness Longwood Clinic, Boston, MA; 2Chi NeuroHealth Clinic, Manchester, NH
3Exeter Hospital, Exeter, NH; 4Langfang Development Area Hospital, China.
Abstract
OBJECTIVE: Several neurodegenerative diseases including multiple sclerosis (MS) and Parkinson’s disease (PD) exhibit enhanced tone of spasticity and rigidity, respectively. It is believed that spastic tone is secondary to disturbance of both peripheral and central pathways. The enhanced activity of gamma motor neurons in muscle spindle and altered CNS pathways through dorsal reticulospinal tract inhibition and medial reticulospinal tract and vestibulospinal tract stimulation* play critical roles. Both spasticity and rigidity have a lower excitation threshold of gamma motor neuron – muscle spindle activity. Moreover, electrophysiologic studies reveal more continuous motor activity in rigidity than in spasticity.
DESIGN: At Chi Wellness and Chi NeuroHealth, LLC clinics we have designed a procedure of applying Tuina therapy as a novel therapeutic strategy to treat MS spasticity and Parkinson’s disease rigidity.
METHOD: Tuina is a deep, intense, Chinese physical therapy that can target muscles and other soft tissues. It allows practitioners to detect neuromuscular tension, pain and inflammation with spatial precision, and sustainably relieve them throughout the body. Tuina is often accompanied with certain soreness (similar to strenuous exercise) during and 1-2 days after the treatment.
RESULTS: We report a case study of MS and Parkinson’s disease patients after receiving Tuina therapy. Those patients receiving Tuina appreciate marked and sustained mitigation of extremity spasticity and rigidity. Gait dexterity, speed, and agility are improved. Extremity pain and stiffness are reduced. Sense of wellness is enhanced. Moreover, empiric observations support a direct relationship between Tuina intensity (discomfort) and patient response. These two cases are unique among our neurodegenerative diseases cases because the MS patient (Case L) is also a neurologist and author of this report, and the PD patient (Case M, a MIT professor) did not use any medications.
CONCLUSION: We suggest that Tuina may induce sustainable relief of spasticity and rigidity through certain neural plasticity. Pain may be a necessary signal for the brain to reorganize and overcome a monophasic or progressive injury such as seen in neurodegenerative disorders. We postulate that the ascending pain pathways may be capable of inducing reparative change to the descending spastic, motor pathways and muscle spindle gamma motor neuron overactivity. We hope to collaborate with clinicians in further clinical study of this treatment strategy for sporadic Neurodegeneration.
Spasticity and rigidity in MS, PD, Stroke patients
Spasticity and rigidity are detrimental as they impair sense of wellness in Multiple Sclerosis (MS), stoke and Parkinson’s disease (PD). They lead to pronounced gait and mobility impairment.
Disease Neurologic Model for Multiple Sclerosis
MS is a heterogeneous, autoimmune, inflammatory and neurodegenerative disease of CNS. Its course is relapsing-remitting 85%, primary progressive 10% with majority of former transitioning to secondary Progressive disease after 15-20 years (Lublin & Reingold, 1996). Symptoms include optic neuritis with loss visual acuity, diploplia, dysarthria, and sensorimotor and bowel / bladder dysfunction. Paramount sequela is spastic gait ataxia.
Disease Neurologic Model for Parkinson’s disease
PD is an alpha synucleopathy and neurodegenerative disorder affecting pigmented, olfactory, and enteric nuclei, the cortex, and most markedly the substantia nigra pars compacta (Lowe et al, 1997).
Symptoms include bradykinesia, tremor, postural instability, and rigidity.
Pharmacenticals Offer Suboptimal Relief to Spasticity & Rigidity
Spasticity: baclophen (GABA agonist), Tizanidine (alpha 2 adrenergic agonist), and benzodiazepines. These drugs have multiple side effects including light headedness, xerostomia, ataxia, hypotension, and bradyphrenia.
Rigidity: carbidopa/ levodopa, ropinerole and pramipaxole (dopamine agonists), and the new monoamine oxidase inhibitors (type B). Side effects include nausea, vomiting, light headedness, dyskinesia, pathologic behavior with drug-to-drug and drug-to-food interactions.
History of Tuina Therapy in traditional Chinese Medicine
Tuina therapy is a Chinese physical and massage therapy. Its medical use was first recorded in an oracle bone dated 15,000 years old. The oldest survived medical treaty is 2,200 years old silk scrolls, called the Fifty Two Conditions and Treatments, discovered in an ancient tomb (Ma Huang Dui). It describes Tuina use for various branches of Chinese medicine.
Practice of Tuina Therapy
Tuina therapy consists of hundreds of physical manipulations.
In general, the manipulations of Tuina therapy are deeper and stronger than other types of physical therapy or massage.
During the treatment, patients will experience certain soreness and deep relaxation. After the treatment, soreness may last for 1-2 days and deep relaxation for up to two weeks.
At Chi Wellness Clinic, most patients with chronic pains or spasticity receive 1-2 hour Tuina therapy twice per week, but some patients once per week.
7. How Does Tuina Treat Spasticity & Rigidity?
· Through tactile sense, Tuina therapists find rigid and spastic muscles (including tendons).
· It is important to differentiate muscular tensions (stiffness) generated by muscular injury, inflammation, spasm or cramps from those by neurodegenerative processes. In the latter case, the level of muscle stiffness rises with pressure. This input-output curve of tensiological function could be developed for each patient.
· Tuina manipulations generate pressure and nociceptive sensations (mild soreness, burning etc) in the tense and spastic muscles through their exteroceptors or propioceptors.
The effective manipulations should process sustainable muscle relaxation, hence the I/O tensiological function should undergo steady gain changes.
8. Case L: Multiple Sclerosis
Case L is 40 years old gentleman who works as a board-certified neurologist.
He has a 22 year history of relapsing – remitting multiple sclerosis with sequela mild – moderate spastic gait ataxia.
Previous Treatment: Repetitive exacerbations with mounting lesion burden and neurologic sequela occurred despite use of two types of beta interferon, glutiramer, cyclophosphamide, and a monoclonal antibody.
9. Clinicotemporal Course of Case L
1986 summer Transient left pretibial numbness
1987 winter Transient vertigo
1988 fall Transient finger tip numbness
1989 spring Slight slowing of writing speed
1990 winter Transient vertigo
1990 summer OS optic neuritis
1990 fall Transient right arm weakness and clumsiness – MS diagnosis
1992 summer Last time being able to run
1993 winter Exacerbation requiring BWH admission for severe spastic Paraparesis, loss ability to read
1996 fall Transient dysphagia
2002 winter Marked worsening gait ataxia
1996-2008 1-2 exacerbations, mostly gait disturbance occurred per year
Case L: Effects of Tuina Therapy for MS
As a last resort, Case L sought alternative treatment at Chi Wellness Clinic, Boston in late summer 2006.
Case L received weekly, aggressive Tuina.
One to two days after therapy, once overt discomfort had ceased, gait stiffness had markedly lessened and mobility was enhanced.
Repeat weekly treatments further improved locomotion and agility.
After 4 months (once or twice weekly) one hour treatments with Tuina, decrease examiner-assessed muscle spasticity, complete cessation ankle clonus, and improved gait agility and stamina are noted.
Staying on feet all day as practicing neurologist was once a challenge yet is now easily achieved. The beneficial effects of Tuina last several months, hence strategic, repeat treatments are necessary.
Case M: Parkinson’s Disease
Case M is a sixty year old gentleman. He works as a full professor at MIT.
Clinicotemporal Course of Case M
1999 Case M started right hand tremor and unsteady gait. Both conditions got progressively worse.
2005 Left hand tremor started.
2007 His general conditions got much worse.
Previous Treatments
Case M consulted with a neurologist at MGH in 2003. He wished not to take dopamine medications worrying about their potential side-effects.
He sought acupuncture treatment elsewhere in 2006 for 1.5 years; but his conditions continued to worsen.
Case M: Effect of Tuina for PD
Conditions before Treatment
He demonstrated severe muscle tension, rigidity and pains through his body in addition to large-amplitude tremors.
The patient showed severe general anxiety, high pain sensitivity and emotional distress.
His urination was urgent and frequent with micturation occurring every 30-45 minutes.
He was severely sleep-derived as his tremors disrupted his sleep every 30-45 minutes at night.
His office hours at MIT were reduced to less than 4 hours per week.
Regiment of Treatment
Case M started his Tuina therapy and sometimes acupuncture in February 2008.
Initially, he received 2 hours of Tuina therapy twice per week. With two weeks, the patient showed some relief of rigidity and sleep-deprivation.
On the third week, the intensity of Tuina therapy was augmented to three hours per session, three times per week (Monday, Wednesday and Friday).
Conditions after Treatment
After three months of treatment, he experienced significant relief of rigidity and gait difficulties.
He was able to sleep for eight hours at night with one trip to bathroom.
His micturation frequency reduced from every 30 minutes to every three hours.
He became emotionally calm.
He continued to have tremors on both hands but the amplitudes of his tremors became small and less frequent. He was able to stop tremors by raising his arms over his head.
Hypothesis for the Effects of Tuina for Spasticity and Rigidity
Spasticity is believed to be secondary to disruption of balance between the dorsal reticulospinal tract which inhibits tone and medial reticulospinal tract and medial vestibulospinal tract which enhance tone (Brown, 1994).
Spasticity and rigidity may be similar as they both have lower excitatory threshold of gamma motor neuron firing and muscle spindle activity to cause hypertonia (Hallet, 1990). In case of spasticity, the dorsal reticulospinal tract activity is decreased and the medial reticulospinal tract and medial vestibulospinal tract actions are increased thus enhancing gamma motor neuron and tone of muscle spindle fiber.
According to our case observations, Tuina can reduce both rigidity and tremor in Parkinson’s disease and spasticity in MS. And Tuina can produce lasting relaxation many days after treatment. We hypothesize that
First, due to its deep, strong and targeted manipulations, Tuina may effect its therapeutic benefit of reducing spasticity and rigidity through pain pathways.
Second, stimulation of pain pathways enables Tuina to reduce spasticity and rigidity through neural plasticity and neuromodulation on descending motor pathways.
Third, Tuina manipulations may reduce spasticity and rigidity by acting locally on muscle and centrally through activating pain pathways.
Summary
We present our case studies of positive effects of Tuina therapy, a traditional Chinese physical therapy in reducing spasticity in Multiple Sclerosis, and rigidity and tremor in Parkinson’s disease.
As a hands-on therapy, Tuina uses tactile sense to detect and target the symptom (i.e. muscular tension or tone), and assess its efficacy of treatment.
Tuina therapy has potential to become an available, affordable and effective treatment for wide-range of health conditions including MS, PD, stroke and other neurodegenerative conditions.
Tuina therapy can provide a new therapeutic model for investigating how neuroplasticity can be utilized to recover loss of neural functions due to degenerative diseases.
Future Perspective
In consultation with neurologists and scientists in Boston and New England areas, we hope to continue:
To develop a rigorous treatment and clinical assessment protocol for using Tuina therapy in MS and PD patients;
To accumulate MS and PD cases to evaluate statistically its efficacy in relief of spasticity and rigidity;
To develop and test a therapeutic model for the effect of Tuina in spasticity and rigidity.
References
Brown P (1994). Pathophysiology of Spasticity. J Neurol Neurosurg Psychiatry 57:773.
Davidoff RA (1992). Skeletal muscle tone and misunderstood stretch reflex. Neurolgy 1992: 42-951.
Hallet M (1990). Clinical neurophysiology of akinesia. Rev Neurol 146:585-590.
Lance JW (1980). The control of muscle tone, reflexes, and movement: Robert Wartenburg Lecture. Neurology 30:1303.
Lowe J, et al. (1997). Disorder of movement and system degeneration. Greenfield’s neuropathology. London: Arnold, 1997: 285-290.
Lublin FD, Reingold SC. (1996). Defining clinical course of MS. Neurology 1996; 46:907-911.