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Parkinson’s Disease

Parkinson's disease (PD), also known as paralysis agitans and Parkinsonism, is a progressive disorder of the CNS that typically affects older adults around the age of 60, prevalent in 1% of the population over the age of 55. The disease results in the widespread destruction of the areas of the basal ganglia that send dopamine secreting nerve fibers to the caudate nucleus and putamen. With the destruction of dopaminergic neurons the caudate nucleus and putamen become overly agitated, sending excitatory signals to the corticospinal motor system, leading to excitation and muscular rigidity. The high feedback gains without the inhibitory control of dopamine leads to tremor at a fixed rate of 3 to 6 cycles per second. In addition to the loss of dopaminergic neurons in the basal ganglia, other dopamine, monoamine and non-monoamine neurons may be destroyed in other parts of the brain. Diminished levels of norepinepherine, GABA (gamma amino butyric acid), GAD (glutamic acid decarboxylase, which acts on glutamic acid to produce GABA), serotonin, substance P, enkephalin, cholecystokinin and somatostatin have been observed in patients with PD. Reduced levels of homovanillic acid, a metabolite of dopamine, has been observed in the cerebrospinal fluid of PD patients, and is diagnostic marker. (Rubin 2001, 739-740; Berkow 1992, 1496-97)

PD is characterized by rigidity of the musculature, involuntary tremors and an inability to initiate movement (akinesia). Motor performance is impaired and the patient will have great difficulty in performing everyday activities such as shaving, brushing the teeth, eating with utensils, buttoning shirts and opening door handles. As the disease progresses, handwriting becomes illegible, walking difficult and speaking unintelligible. Rigidity of the facial muscles can give the face a mask-like appearance, characterized by a wide, unblinking stare, an open mouth and uncontrolled drooling. (Rubin 2001, 739-740; Berkow 1992, 1496-97)

The cause of PD is unknown, although many have speculated that it may be the result of environmental toxins. Epidemiological and experimental data suggests the potential involvement of specific agents that acts as neurotoxicants (e.g. pesticides) in the pathogenesis of nigrostriatal degeneration (Di Monte et al 2002). In one epidemiological study an increased risk for PD appeared to be associated with occupational exposure to Mn, Fe and Al, especially when the duration of exposure is longer than 30 years (Zayed et al 1990). These studies in support of PD as a post-industrial disease however is in contrast with a disease described in ancient Indian medical texts called kampavata, that very much resembles PD (Manyam 1990). There is increasing amount of evidence to suggest that the pathogenesis of PD relates to oxidative stress and a reduced ability to deal with it, primarily in the mitochondria of the dopaminergic neurons of the substansia nigra.

Secondary PD can be drug induced by antipsychotic drugs (e.g. haloperidol) that are dopamine antagonists. The chronic use of resperine, an alkaloid from Rauwolfia serpentina, leads to dopamine depletion and can precipitate secondary PD as well. Researchers have found an increased prevalence of PD in patients born during an influenza pandemic. Only 5% of patients with PD have a family history of the condition. (Rubin 2001, 739-740; Berkow 1992, 1496-97)

Medical management of PD

The focus of medical management of PD is to control the signs and symptoms for as long as possible while minimizing adverse effects. The various medications used in PD usually provide good symptomatic control for about four to six years, after which the condition usually progresses to postural instability and dementia. One focus in the medical management of PD is the development of neuroprotective drugs to prevent a loss of dopaminergic neurons. Of the drugs currently being investigated selegiline holds out the most promise, demonstrating neuroprotective effects in laboratory animals, but has provided conflicting data in clinical trials. Currently selegiline is employed as monotherapy in early PD to delay the usage of levodopa.

The symptomatic management of PD consists of levodopa (L-dopa), usually given with a peripheral decarboxylase inhibitor (PDI) such as carbidopa to inhibit dopamine formation outside of the brain, which can lead to heart and liver dysfunction. Unfortunately, L-dopa has a finite usage as its effectiveness declines over years of use, and thus it is reserved for the latter stages of the illness. Synthetic L-dopa also causes CNS side effects such as dyskinesia and psychosis; supplementing with L-tryptophan may reduce these side effects. There is also evidence that the L-dopa/carbidopa combination may accelerate disease progression or contribute to the development of motor fluctuations and dyskinesia. Specifically, levodopa administration increases dopamine turnover and may increase free radical production. As PD progresses fewer and fewer dopaminergic neurons are available to store and release the L-dopa-derived dopamine, resulting in clinical fluctuations.

In contrast to L-dopa the long-acting dopamine agonists such as bromocriptine and pergolide can provide relatively smooth and sustained receptor stimulation. Other drugs include the use of anticholinergics such as benzotropine mesylate to reduce ACh secretion, and MAOIs to inhibit dopamine metabolism. Surgical methods involve the destruction of portions of the basal ganglia, the thalamus and even the motor cortex to block basal ganglial feedback to the cortex, and are of varying success. The use of transplanted dopamine-rich fetal nerve tissue has been used as well, with some success, but this has raised some significant ethical issues. More recently, the use of an electrical oscillating unit that has been surgically implanted in the brain to inhibit ACh secretion has been used with success in a few patients, but is invasive and costly.

Other treatments include the use of the amino acid glutamine and/or GABA to have a relaxing effect upon the rigidity and tremor in PD. Tryptophan supplementation has also been shown to be helpful, improving serotonin levels, and in reducing the side effects of L-dopa therapy. Vitamin B6 is an important cofactor in the synthesis of dopamine, as is iron and molecular oxygen, and thus these are important considerations (e.g. B6 and iron supplementation, hyperbaric oxygen).

Holistic management of PD

The focus of holistic management of PD is concentrated around keeping the patient off of medical treatment for as long as possible, and using a variety of therapies to limit free-radical damage and destruction to dopaminergic neurons. As PD is primarily a disease of aging, general measures are taken to promote good vascular health as well. One theory of the free-radical damage seen in PD is an underlying atherosclerotic condition, causing ‘mini’ strokes and progressive damage to the brain.

Botanicals

  • Cerebrovascular stimulants: Gingko (Gingko biloba), Perrywinkle (Vinca minor), Rosemary (Rosmarinus officinalis), Bilberry (Vaccinium spp), Cayenne (Capsicum spp), Ginger (Zingiber officinalis), Prickly Ash (Zanthoxylum spp.), Hawthorn (Crataegus spp.)
  • Nervine trophorestoratives, to protect neurons: Mandukaparni (Centella), Brahmi (Bacopa monniera), Sweet Flag (Acorus), Ashwagandha (Withania/Convovulus), Rosemary (Rosmarinus officinalis), Milky Oats (Avena sativa), St John’s Wort (Hypericum perforatum), Ling Zhi (Ganoderma spp), Siberian Ginseng (Eleutherococcus senticosus), Damiana (Turnera spp), Bala (Sida cordifolia), Amalaki (Phyllanthus emblica), Ginseng (Panax spp.), He Shou Wu (Polygonum multiflorum), Dang Gui (Angelica sinensis), Cordyceps, Grifolia, Coriolus
  • Antioxidant botanicals: Turmeric (Curcuma longa), Frankincense (Boswellia serrulata), Guggulu (Commiphora mukul), Hawthorn (Crataegus spp.), Amalaki (Phyllanthus emblica), Brahmi (Bacopa monniera), Guduchi (Tinospora cordifolia), Shilajitu, Gingko (Gingko biloba), Rosemary (Rosmarinus officinalis), Mandukaparni (Centella), Milk Thistle (Silybum marianum), Chai Hu (Buplerum spp.), Huang Qi (Astragalus membranaceus), Spirulina, Ling Zhi (Ganoderma spp.)
  • Antispasmodics, to relieve dyskinesia: Sweet Flag (Acorus spp.), Ashwagandha (Withania/Convovulus), Valerian (Valeriana spp.), Lobelia, Black Cohosh (Actaea/Cimicifuga racemosa)
  • Kapikacchu (Mucuna pruriens) (up to 7% natural source L-dopa), to supplement declining L-dopa levels; Huang Qi (Astragalus membranaceus) also contains natural L-dopa)
  • Anticholinergics, to relieve dyskinesia when other measures fail: Jimsonweed (Datura spp), Henbane (Hyocyamus niger), Belladonna (Atropa belladonna)

Supplements

  • vitamin A, 20,000 IU daily
  • vitamin B complex, 100 mg b.i.d.
  • vitamin C, to bowel tolerance
  • vitamin E, 800-1200 IU daily
  • EPA/DHA, 1000 mg each daily
  • iron, 20 mg b.i.d.
  • calcium/magnesium, 1:1, 800 mg each b.i.d.
  • chromium, 200 mcg t.i.d.
  • selenium, 200 mcg b.i.d.
  • zinc, 50 mg daily
  • CoQ10, 50 mg t.i.d.
  • grapeseed extract, 50 mg t.i.d.
  • superoxide dismutase, 100 mg b.i.d.
  • bioflavonoids, 3-5 g daily

Diet

  • Paleolithic diet, low carbohydrate diet to prevent CVD
  • emphasize antioxidant foods, e.g. garlic, onions, cruciferous vegetables; foods rich in anthocyanidins, e.g. blueberries, huckleberries, elderberries, red and black grapes
  • emphasize foods rich in tryptophan, e.g. oats, turkey, hard cheeses
  • consider including fava beans in diet, natural source of L-dopa
  • during L-dopa therapy limit protein to 1/7 of total caloric intake, as amino acids can interfere with L-dopa’s transport across the BBB

Topical

  • Balashvagandha taila abhyanga, shirodhara, shirovasti
  • acupuncture

Other

  • regular exercise
  • meditation, tai chi, hatha yoga
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