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