Coursework: Biomedical & TCM Study of Parkinson’s disease

Biomedical & TCM Study of Parkinson’s disease

ATD III

AOMA Spring 2014

           

            In 1817 Dr. James Parkinson published the first detailed medical description of the disease in his work, An Essay on the Shaking Palsy (Lees, 2007). The disease was therefore named after him but it is also known as Idiopathic or Primary Parkinsonism, Hypo-kinetic Rigid Syndrome (HRS), or Paralysis Agitans. PD is a degenerative disorder effecting the central nervous system therefore it is mainly thought to be a movement disorder (Obeso, Rodriguez-Oroz, Benitez-Temino, Blesa, Guridi, Marin & Rodriguez, 2008). According to the Parkinson’s Disease Foundation of America, “Parkinson's disease (PD) is a chronic and progressive movement disorder, meaning that symptoms continue and worsen over time...The cause is unknown, and although there is presently no cure, there are treatment options such as medication and surgery to manage its symptoms” (pdf.org). Parkinson’s involves the malfunction and death of neurons in the substantia nigra of the brain called the basal ganglia. The basal ganglia are an organized network where different parts are activated under specific circumstances and for particular tasks. Those tasks involve movement control, as well as planning, emotion, associative learning and working memory. The basal ganglia control these systems by exerting a constant inhibitory influence, preventing them from becoming active at inappropriate times. When activation of a system is required to perform a particular task, inhibition is reduced by the basal ganglia using dopamine. In PD, due to neuronal death, dopamine function is low causing hypokinesia (Obeso, Rodriguez-Oroz, Benitez-Temino, Blesa, Guridi, Marin & Rodriguez, 2008). Loss of cells in other areas of the brain and body are also thought to contribute to Parkinson’s. For example, researchers have discovered that abnormal accumulation of the protein alpha-synuclein or Lewy Bodies are found in the regions of cell death in the mid-brain, brain stem and olfactory bulb. “While the pathophysiology of the neurodegenerative process can hardly be explained by Lewy bodies, the clinical symptoms do indicate a degenerative process located at the pre-synapse resulting in a neurotransmitter deficiency” (Schulz-Schaeffer, 2010).     

           Despite intensive research during the past several decades, the cause of Parkinson's disease remains unknown. Because there is no known cure PD remains the second most common neurodegenerative disorder affecting approximately one million people in the United States and seven million globally (Breteler & Lau, 2006). PD has a much higher prevalence in the elderly, risk levels rise from 1% at 60 to 4% at 80 years of age.  A comparative study done by the Department of Neurology at Burdwan Medical College in West Bengal, India found that,

            ...family history of Parkinson's disease and familial tremor

(p = 0.035), exposure to insecticides and pesticides (p = 0.049), well water use for drinking purposes (p = 0.03), Japanese B encephalitis (p = 0.04) and acute organophosphate poisoning (p = 0.046) were associated with the development of Parkinson's disease in this region of India

(Das et al., 2011).

This paper is a perfect example of the overall scientific communities’ findings. Familial gene mutations cause only a small proportion of all cases; it is shown that in most cases, non-genetic risk factors play a part. While many epidemiological studies were done to identify these non-genetic factors, most were either too small and methodologically limited. Only recently have larger cohort studies reached a stage at which they have enough “person-years of follow-up” to truly investigate non-genetic factors and their interactions (Lau & Breteler, 2006).  

            Currently, Parkinson’s is a “rule-out diagnosis” disease. Usually, a physician will diagnose PD based on medical history and a neurological examination. Resting tremor, rigidity, loss of postural reflexes and bradykinesia, are generally clinical criteria for a diagnosis of PD. Brain scans are sometimes used to assist in ruling out disorders that may have similar symptoms (Jankovic, 2007). The finding of Lewy bodies in an autopsy is also considered proof, though the procedure is expensive, invasive and uncommon. There are other clinical features which can lead to diagnosis including,

            ...secondary motor symptoms (eg, hypomimia, dysarthria, dysphagia, sialorrhoea, micrographia, shuffling gait, festination, freezing, dystonia, glabellar reflexes), non-motor symptoms (eg, autonomic dysfunction, cognitive/neurobehavioral abnormalities, sleep disorders and sensory abnormalities such as anosmia, paresthesias and pain)

(Jankovic, 2007).

A thorough knowledge of the broad clinical manifestations is the most essential tool in properly diagnosing PD. Because signs and symptoms are known to change over time it is recommend that the diagnosis be periodically reviewed (Jankovic, 2007).

            Western treatments are based on patient’s age, what the most troublesome symptoms are, the disease stage, and any risks. The drug L-dopa is considered the most effective at improving quality of life particularly in the early stages of PD, though long-term complications are an issue. Dopamine agonists and MAO-B inhibitors are also part of the main families of drugs useful for treating motor symptoms. Depending on what stage of the disease the patients is in, certain drugs are considered more useful than others. If the early stage PD patient has already developed some disability they are usually treated with L-dopa. L-dopa temporarily reduces motor symptoms, which are caused by a lack of dopamine, by converting into dopamine itself. Because L-dopa causes long-term complications, it’s use may be delayed by using the other medications mentioned such as the MAO-B inhibitors or dopamine agonists. This strategy is used to delay the onset of dyskinesias which occurs in the second stage as a complication of L-dopa usage.  For patients with advanced PD, dyskinesias refractory to conventional drugs and disabling motor symptoms, there are essentially three treatment options: deep-brain stimulation (DBS), intrajejunal L-dopa infusion, and apomorphine. DBS conveys electrical impulses, through implanted electrodes called a “brain pacemaker”, to specific parts of the brain (Gildenberg, 2005).

            Due to the negative long-term impact of L-dopa, the most effective drug used to treat PD, alternative medicine, such as acupuncture is of great value. As expected in TCM, there are widely varied mechanisms, differentiations and treatments for the symptoms associated with Parkinson’s. The most common mechanism is also the most simple, KD deficiency due to emotional stress, overwork, improper diet and excessive sexual activity. When these pathogens last a long period of time they will all eventually give rise to KD deficiency. Of course old age is always associated with a decline in KD Qi and therefore is usually part of any underlying geriatric disease. Once the KD is deficient it is easy for the LV to join and after some time this yin and blood deficiency will lead to a stirring of inner wind.

            From a TCM perspective, the main manifestations and age of onset of Parkinson’s disease indicate that the disease relates primarily to liver and kidney disharmony and liver-wind

(Xue).

When there is a deficient root it is not uncommon to find an excess elsewhere such as phlegm retention and blood stasis. It is therefore useful to nourish KD and LV yin, extinguish wind and if the symptoms are present, invigorate blood and/or transform phlegm. Tonify KD and LV with KD3, BL18, LV3, SP6, Ren4. Subdue wind with GB20 and G31 and four gates which also invigorates blood and Qi. If there is phlegm present use SP9 and ST40 combination, while if blood stasis is present use BL17 and SP10. In cases of severe tremor use HT3 and SI3 (Xue).

            Another way of looking at Parkinson’s from a TCM perspective is using channel theory. In a paper written in the Journal of Oriental Medicine on the subject, author Dr.

Walton-Hadlock sites an energetic blockage in the ST and LI meridians as the underlying mechanism. She goes on to say that in, “...100% of patients with idiopathic PD there is an unhealed energetic blockage in the foot at ST42 on the side of the body which first developed symptoms.” She goes on to recognize that saying “100%” sounds highly suspect but that she stands by her findings. When the patient’s history was taken she noted that in decades prior to the onset of PD, many experienced a decrease in hardiness along the ST and LI meridians and that all experienced a old uncared for foot injury. This injury eventually causes enough of a blockage that Qi could not pass beyond ST42 and therefore found alternate routs. The blocked Qi found passage through the SP channel but also by retro-flowing along the ST channel. Over time this retrograde Qi will overflow into the GB channel on the head. The “asymmetric change in the GB channel creates an electrical signal, which triggers a drop in dopamine level.” The paper goes much deeper into the mechanism and differentiation but summarize it as Rebellious Qi in the Stomach Channel, being held in place by injury combined with fear and will power (Walton- Hadlock, 2001). Other treatments include scalp acupuncture such as, GB5, 6, 19, 20; Du16, 17, 21 and BL 9, 10. Cupping along the back Du and BL meridian can also be helpful in harmonizing yin, yang, Qi and blood.

  

   Breteler, M., & Lau, L. (2006). Epidemiology of parkinson's disease. The Lancet Neurology, 5(6), 525-535. doi: 10.1016/S1474-4422(06)70471-9

Das, K., Ghosh, M., Nag, C., Nandy, S., Banerjee, M., Datta, M., & ... Chaterjee, G. (2011). Role of familial, environmental and occupational factors in the development of Parkinson's disease. Neuro-Degenerative Diseases, 8(5), 345-351. doi:10.1159/000323797

Gildenberg, P. (2005). Evolution of neuromodulation .Stereotactic and Functional Neurosurgery, 83, 71-79. doi: 10.1159/000086865

Jankovic, J. (2007). Parkinson's disease: Clinical features and diagnosis. Journal of Neurol Neurosurg Psychiatry , 79(4), 368-376.

Lees, A. J. Unresolved Issues Relating To The Shaking Palsy On The Celebration Of James Parkinson's 250th Birthday. Movement Disorders, S327-S334.

Obeso, J., Rodriguez-Oroz, M., Benitez-Temino, B., Blesa, F., Guridi, J., Marin, C., & Rodriguez, M. (2008). Functional organization of the basal ganglia: Therapeutic implications for parkinson's disease.Movement Disorders, 23(S3), 548-559.

Schulz-Schaeffer, W. (2010). The synaptic pathology of α-synuclein aggregation in dementia with lewy bodies, parkinson’s disease and parkinson’s disease dementia. Acta Neuropathologica, 120(2), 131-143.

Walton- Hadlock, J. (2001). Parkinson's Disease from TCM/Channel Perspective: Theory and Case Study.California Journal Of Oriental Medicine (CJOM), 12(1), 8.

What is parkinson’s disease?. (n.d.). Retrieved from www.pdf.org

Xue, Y. The Treatment of Parkinson's Disease by Acupuncture and Herbal Medicine. The Journal of Chinese Medicine.