Sporadic Neurodegeneration Symposium

Genes, Environment and Therapeutic Strategies

July 31 - August 01, 2008


The Fairmont Copley Plaza

138 St. James Avenue

Boston, Massachusetts, USA

 

 

 

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 Parkinsonís 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 Ė 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 Parkinsonís 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 Parkinsonís 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.


 

  1. 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 Parkinsonís disease (PD). They lead to pronounced gait and mobility impairment.

 

  1. 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.

 

  1. Disease Neurologic Model for Parkinsonís 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.

 

 

  1. 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.

 

 

  1. 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.

 

 

  1. Practice of Tuina Therapy

 

 

 

 

 

 

 

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.

 

 

 

8. Case L: Multiple Sclerosis

 

 

 

 

 

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 Ė 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

 

 

  1. Case L: Effects of Tuina Therapy for MS

 

 

 

 

 

 

 

 

  1. Case M: Parkinsonís 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

 

 

 

 

  1. Case M: Effect of Tuina for PD

 

Conditions before Treatment

 

 

 

 

 

 

Regiment of Treatment

 

 

 

 

Conditions after Treatment

 

 

 

 

 

 

 

  1. 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 Parkinsonís 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.

 

 

  1. Summary

 

  1. 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 Parkinsonís disease.

 

  1. 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.

 

  1. 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.

 

  1. 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. 

 

 

  1. Future Perspective

 

In consultation with neurologists and scientists in Boston and New England areas, we hope to continue:

 

 

 

 


 

  1.  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. Greenfieldís neuropathology. London:  Arnold, 1997:  285-290.

 

Lublin FD, Reingold SC. (1996). Defining clinical course of MS. Neurology 1996; 46:907-911.