Parkinson’s disease (PD) is a progressive, degenerative disorder of the brain that is associated with a loss of dopaminergic neurons in the substantia nigr a; neurodegeneration in other areas of the central nervous system (CNS), such as the locus coeruleus and the cerebral cortex; and the presence of Lewy bodies. Loss of dopamine stimulation causes an imbalance between excitation and inhibition pathways of the basal ganglia (which coordinate motor activity), resulting in impairment in the voluntary control of movement.
Hallmarks of the disease include muscular (“cogwheel”) rigidity, resting (“pill-rolling”) tremor that decreases or disappears with movement, bradykinesia, and an unstable, flexed posture. Patients exhibit a narrow-based, shuffling gait and usually show progressive difficulties with activities of daily living (e.g., eating, dressing, writing). Micrographia may be present; in assessing disease progression, it is helpful to compare the patient’s previous handwriting samples to a recent sample.
Depression is the most common psychiatric complaint, and hallucinations may appear with more advanced disease, sometimes as an adverse side effect of medications used to treat the condition. Dementia occurs in about one-third of cases and presents with personality changes, psychomotor retardation, and memory problems. Anxiety, sleep problems, fatigue and autonomic dysfunction, including postural hypotension, are also common late in the course of disease.  
Age. About 1% of Americans over age 50 are affected, and prevalence increases with age. Typical age of onset is the late 50s, although 10% of cases present before age 40.
Environmental factors, such as pesticides and heavy metals, are being studied for possible roles in Parkinson’s disease, especially because specific toxins are known to target the substantia nigra.
Head trauma, CNS infections, low vitamin D levels, and the use of postsynaptic dopamine-receptor blockers (antiemetics, antipsychotics, and reserpine) are other risk factors that have been linked to PD.
Diagnosis of Parkinson’s disease is generally made using a thorough history and a complete physical examination, including a neurologic examination, showing at least 2 or more of the characteristic clinical findings of PD (bradykinesia, resting tremor, rigidity, postural instability). Presentation is often unilateral or asymmetric, especially at disease onset.
Although there are no commonly available laboratory tests or imaging modalities, clinical response to a dopamine agonist is strong supportive evidence for the diagnosis.
A head CT scan, brain MRI, and/or laboratory testing may be indicated in equivocal cases to rule out other diagnoses (e.g., Wilson’s disease, Huntington’s disease, cerebrovascular disease, normal pressure hydrocephalus, mass lesions). However, imaging is generally indicated only if the presentation is atypical or if focal symptoms are present.
Parkinson’s disease follows a progressive course. The disease advances in all cases, but the rate of progression varies, with younger patients often progressing more rapidly. While there is no cure, medical treatment can alleviate many of the symptoms and help improve quality of life. Medications should be used at their lowest effective dose.
Physical, occupational, and speech therapies are often beneficial, and social work consultation can help make daily living at home easier for the patient and prevent further disability. Exercise has been shown to be beneficial at all stages of the disease and can help both mood and mobility. Exercises should focus on conditioning, strengthening, and stretching (20 minutes at least 3 times weekly is a reasonable target). As balance worsens, appropriate precautions must be taken.
Medications that might cause Parkinsonian symptoms should be discontinued and alternative drugs used if necessary. Treatment is primarily aimed at increasing the availability of dopamine to the CNS and reducing symptoms. To date, there are no proven methods to slow or reverse disease progression.
The combination of levodopa (a dopamine metabolic precursor) plus carbidopa (which antagonizes the dopa decarboxylase enzyme that would otherwise convert levodopa to dopamine prior to reaching the brain) has proven to be the most effective therapy to improve symptoms, and is usually used as first-line therapy. Concern about potentially speeding Parkinson deterioration by early use of levodopa is probably unfounded. Common side effects include nausea, dizziness, and headaches; extended use of levodopa is correlated with development of symptoms of dopamine excess, such as dyskinesia and dystonia.
Dopamine agonists (bromocriptine, pramipexole, ropinirole, rotigotine, and apomorphine) improve symptoms and can delay the need for levodopa therapy. Apomorphine, an injectable, is used as a rescue therapy for patients with sudden akinesia. Side effects are similar to those seen with levodopa/carbidopa.
Monoamine oxidase inhibitors (type B) (Selegiline and Rasagiline) impede the breakdown of dopamine and may also prolong the action of levodopa.
Catecholamine-O-methyl-transferase (COMT) inhibitors (entacapone, tolcapone) may slow the breakdown of dopamine by enhancing the effect and half-life of levodopa.
Amantadine (an antiviral medication) may be useful not only for its mild anti-Parkinson effects, but also as a mild psychostimulant and as treatment for severe dyskinesia.
Some evidence suggests that low-dose estrogen might be helpful in reducing motor symptoms in postmenopausal women taking anti-Parkinson medications. Further study is warranted.
Hallucinations may be treated with clozapine or quetiapine, tremor with benztropine or trihexyphenidyl, and depression with amitriptyline.
Surgical approaches (deep brain stimulation, or on rare occasions, thalamotomy or pallidotomy) may have a role in advanced disease, especially in patients with severe intractable dyskinesia, tremor, or rigidity.
Plant-based diets have been found to reduce the risk for developing Parkinson’s disease as well as being useful in its treatment. This may be due to protection against oxidative stress, which has emerged as a significant factor through the evidence on the roles of high fat diets, uric acid, and plant food components (e.g., flavonoids) on the risk for Parkinson’s disease.
Evidence of a fairly strong nature implicates dairy products and high fat diets as contributors to risk. Flavonoids, caffeine, alcohol, and adequate vitamin D status have emerged as protective factors, although evidence is stronger in men than in women. Established roles for diets that are low in protein or redistribute protein to evening meals have also been confirmed as useful for many patients. These factors are discussed below.
Low-fat diets. Previous evidence suggested that the prevalence of Parkinson’s disease correlates with intake of animal fat , and total and saturated fat. A more recent review and a meta-analysis concluded that the intake of polyunsaturated fat was significantly protective against PD. Another meta-analysis found an inverse association between the intake of alpha-linolenic acid and risk for PD.
Minimizing dairy products. A meta-analysis found an overall 40% higher risk for PD in individuals consuming the most dairy products compared with the lowest intake category. The effect was more pronounced among men than women.
One suggested mechanism for the associations between dairy intake and risk for PD is the presence of organochlorine pesticides in milk. Organochlorines may increase the susceptibility of dopaminergic neurons to cell death, and have been found to a greater extent in the substantia nigra of PD sufferers. The ability of higher dairy consumption to lower uric acid (a protective antioxidant) levels may also play a role in the association with PD. Uric acid is a known biomarker of PD severity and progression, and is found in lower levels in the substantia nigra of PD sufferers compared to normal individuals.
High intake of flavonoids. Widely distributed in plant-based foods and beverages, flavonoids have multiple functions. They interact with neuronal signaling pathways that are critical in controlling neuronal survival and differentiation, modulate the activity and expression of several antioxidant enzymes, and impact mitochondrial function and neuroinflammation. In the Health Professionals’ Follow-Up and Nurses Health’ Studies, men consuming the most flavonoids had a 40% lower risk for Parkinson’s disease when compared to those consuming the least.
Caffeinated beverages. A meta-analysis found a 25% lower risk for PD for individuals in the highest compared with lowest level of caffeine intake, an association that was more significant for men than for women.
Adequate vitamin D status. PD sufferers have lower circulating vitamin D levels than age-matched controls, along with lower bone mineral density and higher risk for both falls and fractures. The incidence of PD was also found to be three times greater in individuals with the lowest (compared to highest) vitamin D blood levels. A meta-analysis found that individuals with vitamin D blood levels in the deficient range had more than twice the risk for developing PD, compared with those in the normal range, while vitamin D supplementation was associated with a nearly 40% lower risk for this disease. A controlled clinical trial of daily 1200 IU of vitamin D supplements increased the blood level of vitamin D from a deficient to a normal range and significantly prevented the deterioration of the Hoehn and Yahr (HY) stage (a commonly used system for describing how the symptoms of PD progress) in patients with a vitamin D receptor phenotype (FokI TT) known to be associated with PD risk.
Alcohol. A meta-analysis found a roughly 20% lower risk in individuals who consumed the most compared to the lowest amount of alcohol overall; however, the effect was most pronounced in male beer drinkers.
Nutritional Factors in Treatment
The most immediate nutritional concerns in Parkinson’s disease treatment include changes in the absorption rate, blood levels, and CNS uptake of L-dopa. The protein content of meals, and particularly the distribution of protein intake throughout the day, has emerged as an important consideration in the effectiveness of L-dopa for many patients. Improvement in clinical response varies from 30% with protein redistribution to 82% with low-protein diets.
Up to 24% of PD patients may be classified with malnutrition, and these
patients have a 4-fold increase in risk for weight loss of 10 lbs or more, compared with age-matched controls. Reasons for this include impaired sensory perception (e.g., anosmia, dysgeusia), dysautonomia (e.g., constipation), dysphagia, dyskinesias, depression, and cognitive impairment. Conversely, excess weight gain may occur due to an increase in sedentary behavior. Individuals with chewing or swallowing difficulties should be referred to a speech therapist for appropriate changes in diet texture. A registered dietitian can help families plan meals that are also adequate in fluid and fiber (particularly insoluble fiber), an important concern to prevent constipation.
Timing of Protein Intake
Most patients do not note a major impact of food on their response to medication in terms of the onset of effect. Those who do may avoid problems by taking levodopa 30 minutes prior to eating, or at least 60 minutes after meals. However, some patients note that high-protein meals blunt the response to L-dopa, reflecting competition for neutral amino acid carriers across the blood-brain barrier. The beneficial effects (e.g., control of dyskinesias) on L-dopa bioavailability of a protein-reduced diet, or the redistribution of almost all protein to evening meals, have been demonstrated in patients who experience erratic responses to levodopa therapy. ,,, In these studies, reducing protein intake to amounts as low as 0.5g/kg body weight resulted in an improved therapeutic response in many individuals, as shown by improvements in neurologic scoring.
Similarly, redistributing all but 7 grams of protein intake to the evening meal resulted in improvement in the Northwest Disability and AIMS Dyskinesia Scale. In addition, the midday dosage of L-dopa was reduced in one-third of patients by an average of 9%. Caution may be required when redistributing most protein intake to the evening meal; this strategy can be so effective that an excess of L-dopa may enter the brain and trigger dyskinesia.
In addition, Parkinson’s disease patients who ate a plant-based diet experienced a significant reduction in the Unified Parkinson’s Disease Rating Scale (UDPRS), when compared with a similar group of patients eating an omnivorous diet.
A protein restriction-induced decrease in requirement for L-dopa may offer more than symptomatic benefit. It is well known that oxidative stress is central to the pathology of PD, and autoxidation of L-dopa increases oxidative stress in the substantia nigra. In addition, higher cumulative levodopa doses have been associated with the earlier occurrence of motor complications. Therefore, measures that reduce L-dopa dosages may prolong the period during which patients benefit from drug therapy.
In addition, high-protein meals raise blood levels of homocysteine (Hcys), a known risk factor for vascular disease. Hcys is known to be elevated in PD patients as a side effect of L-dopa and contributes to dopaminergic cell death. A meta-analysis found a significant relationship between plasma Hcys and cognitive dysfunction, thereby suggesting a possible need and benefit of testing for elevated Hcys levels and their treatment, respectively.
High dose parenteral thiamine. Free thiamine levels in the cerebrospinal fluid of patients with PD are lower than controls, and PD sufferers have lower levels of thiamine-dependent glucose metabolism in the brain than individuals without PD. Studies show that higher concentrations of thiamine may reduce alpha-synuclein concentrations, and clinical data in PD patients given 100-200 mg/d of I.M. thiamine have begun to support this notion, revealing significant improvement in typical PD symptoms. Further studies are needed to confirm these initial clinical trials.
Oxidative Stress and Parkinson’s Disease
Several factors have led to the theory that oxidative stress contributes to the risk for development of Parkinson’s disease, possibly by causing mitochondrial damage. This has resulted in trials of both medications (e.g., entacapone) that inhibit oxidation and supplements (e.g., coenzyme Q10) that scavenge free radicals (see below).
Coenzyme Q10. The neuroprotective effects of coenzyme Q10 (CoQ10) have been under investigation for a potential role in Parkinson’s disease treatment. A multicenter clinical trial in which patients were provided either 1,200 or 2,400 mg/d of CoQ10 in addition to 1,200 IU/day of vitamin E found no significant benefit. However, a controlled trial with the reduced form of CoQ10 that has shown greater neuroprotective effects found a significant improvement in the UDPRS when compared with placebo.
A nutrition consultation would be appropriate to assist the patient in restricting protein prior to the evening hours.
What to Tell the Family
To minimize deconditioning, patients should maintain an active lifestyle to the extent possible. Also, patients should be aware that Parkinson’s disease often causes weight loss. Family members can help reduce severe weight loss risk by providing breakfast, lunch, and between-meal snacks that are high in calories from whole grains (100% whole oats, oat bran, bulgur, barley, brown rice), fruits, 100% fruit juices, and vegetables. The family should ensure proper nutrient intake and be advised that protein deficiency is unlikely if adequate calories are consumed. Family members can improve the effectiveness of L-dopa therapy by reserving high-protein foods for evening meals. A qualified nutrition professional (e.g., registered dietitian) may be helpful in accomplishing these aims.
- Hornykiewicz O. The discovery of dopamine deficiency in the Parkinsonian brain . J Neural Transm Suppl. 2006;70:9-15.
- Gelb DJ, Oliver E, Gilman S. Diagnostic criteria for Parkinson disease. Arch Neurol. 1999;56(1):33-9. [PMID:9923759]
- Aarsland D, Larsen JP, Lim NG, et al. Range of neuropsychiatric disturbances in patients with Parkinson's disease. J Neurol Neurosurg Psychiatr. 1999;67(4):492-6. [PMID:10486397]
- Fénelon G, Mahieux F, Huon R, et al. Hallucinations in Parkinson's disease: prevalence, phenomenology and risk factors. Brain. 2000;123 ( Pt 4):733-45. [PMID:10734005]
- Oerlemans WG, de Weerd AW. The prevalence of sleep disorders in patients with Parkinson's disease. A self-reported, community-based survey. Sleep Med. 2002;3(2):147-9. [PMID:14592234]
- Friedman J, Friedman H. Fatigue in Parkinson's disease. Neurology. 1993;43(10):2016-8. [PMID:8413960]
- Asahina M, Vichayanrat E, Low DA, et al. Autonomic dysfunction in parkinsonian disorders: assessment and pathophysiology. J Neurol Neurosurg Psychiatr. 2013;84(6):674-80. [PMID:22942216]
- Noyce AJ, Bestwick JP, Silveira-Moriyama L, et al. Meta-analysis of early nonmotor features and risk factors for Parkinson disease. Ann Neurol. 2012;72(6):893-901. [PMID:23071076]
- Singleton AB, Farrer MJ, Bonifati V. The genetics of Parkinson's disease: progress and therapeutic implications. Mov Disord. 2013;28(1):14-23. [PMID:23389780]
- Pringsheim T, Jette N, Frolkis A, et al. The prevalence of Parkinson's disease: a systematic review and meta-analysis. Mov Disord. 2014;29(13):1583-90. [PMID:24976103]
- Ascherio A, Chen H, Weisskopf MG, et al. Pesticide exposure and risk for Parkinson's disease. Ann Neurol. 2006;60(2):197-203. [PMID:16802290]
- Willis AW, Evanoff BA, Lian M, et al. Metal emissions and urban incident Parkinson disease: a community health study of Medicare beneficiaries by using geographic information systems. Am J Epidemiol. 2010;172(12):1357-63. [PMID:20959505]
- Jafari S, Etminan M, Aminzadeh F, et al. Head injury and risk of Parkinson disease: a systematic review and meta-analysis. Mov Disord. 2013;28(9):1222-9. [PMID:23609436]
- Lv Z, Qi H, Wang L, et al. Vitamin D status and Parkinson's disease: a systematic review and meta-analysis. Neurol Sci. 2014;35(11):1723-30. [PMID:24847960]
- Hughes AJ, Daniel SE, Kilford L, et al. Accuracy of clinical diagnosis of idiopathic Parkinson's disease: a clinico-pathological study of 100 cases. J Neurol Neurosurg Psychiatr. 1992;55(3):181-4. [PMID:1564476]
- Shulman LM, Katzel LI, Ivey FM, et al. Randomized clinical trial of 3 types of physical exercise for patients with Parkinson disease. JAMA Neurol. 2013;70(2):183-90. [PMID:23128427]
- Connolly BS, Lang AE. Pharmacological treatment of Parkinson disease: a review. JAMA. 2014;311(16):1670-83. [PMID:24756517]
- Olanow CW. Levodopa: effect on cell death and the natural history of Parkinson's disease. Mov Disord. 2015;30(1):37-44. [PMID:25502620]
- Aquino CC, Fox SH. Clinical spectrum of levodopa-induced complications. Mov Disord. 2015;30(1):80-9. [PMID:25488260]
- Deleu D, Hanssens Y, Northway MG. Subcutaneous apomorphine : an evidence-based review of its use in Parkinson's disease. Drugs Aging. 2004;21(11):687-709. [PMID:15323576]
- Nutt JG. Catechol-O-methyltransferase inhibitors for treatment of Parkinson's disease. Lancet. 1998;351(9111):1221-2. [PMID:9643737]
- Schwab RS, Poskanzer DC, England AC, et al. Amantadine in Parkinson's disease. Review of more than two years' experience. JAMA. 1972;222(7):792-5. [PMID:4677928]
- Tsang KL, Ho SL, Lo SK. Estrogen improves motor disability in parkinsonian postmenopausal women with motor fluctuations. Neurology. 2000;54(12):2292-8. [PMID:10881255]
- Fasano A, Daniele A, Albanese A. Treatment of motor and non-motor features of Parkinson's disease with deep brain stimulation. Lancet Neurol. 2012;11(5):429-42. [PMID:22516078]
- Baroni L, Bonetto C, Tessan F, et al. Pilot dietary study with normoproteic protein-redistributed plant-food diet and motor performance in patients with Parkinson's disease. Nutr Neurosci. 2011;14(1):1-9. [PMID:21535916]
- Anderson C, Checkoway H, Franklin GM, et al. Dietary factors in Parkinson's disease: the role of food groups and specific foods. Mov Disord. 1999;14(1):21-7. [PMID:9918340]
- Logroscino G, Marder K, Cote L, et al. Dietary lipids and antioxidants in Parkinson's disease: a population-based, case-control study. Ann Neurol. 1996;39(1):89-94. [PMID:8572672]
- Johnson CC, Gorell JM, Rybicki BA, et al. Adult nutrient intake as a risk factor for Parkinson's disease. Int J Epidemiol. 1999;28(6):1102-9. [PMID:10661654]
- Agim ZS, Cannon JR. Dietary factors in the etiology of Parkinson's disease. Biomed Res Int. 2015;2015:672838. [PMID:25688361]
- Wang A, Lin Y, Wu Y, et al. Macronutrients intake and risk of Parkinson's disease: A meta-analysis. Geriatr Gerontol Int. 2015;15(5):606-16. [PMID:25163395]
- Kamel F, Goldman SM, Umbach DM, et al. Dietary fat intake, pesticide use, and Parkinson's disease. Parkinsonism Relat Disord. 2014;20(1):82-7. [PMID:24120951]
- Jiang W, Ju C, Jiang H, et al. Dairy foods intake and risk of Parkinson's disease: a dose-response meta-analysis of prospective cohort studies. Eur J Epidemiol. 2014;29(9):613-9. [PMID:24894826]
- Abbott RD, Ross GW, Petrovitch H, et al. Midlife milk consumption and substantia nigra neuron density at death. Neurology. 2016;86(6):512-9. [PMID:26658906]
- Chahine LM, Stern MB, Chen-Plotkin A. Blood-based biomarkers for Parkinson's disease. Parkinsonism Relat Disord. 2014;20 Suppl 1:S99-103. [PMID:24262199]
- Gao X, Cassidy A, Schwarzschild MA, et al. Habitual intake of dietary flavonoids and risk of Parkinson disease. Neurology. 2012;78(15):1138-45. [PMID:22491871]
- Costa J, Lunet N, Santos C, et al. Caffeine exposure and the risk of Parkinson's disease: a systematic review and meta-analysis of observational studies. J Alzheimers Dis. 2010;20 Suppl 1:S221-38. [PMID:20182023]
- Suzuki M, Yoshioka M, Hashimoto M, et al. Randomized, double-blind, placebo-controlled trial of vitamin D supplementation in Parkinson disease. Am J Clin Nutr. 2013;97(5):1004-13. [PMID:23485413]
- Knekt P, Kilkkinen A, Rissanen H, et al. Serum vitamin D and the risk of Parkinson disease. Arch Neurol. 2010;67(7):808-11. [PMID:20625085]
- Shen L, Ji HF. Associations between Vitamin D Status, Supplementation, Outdoor Work and Risk of Parkinson's Disease: A Meta-Analysis Assessment. Nutrients. 2015;7(6):4817-27. [PMID:26083115]
- Virmani T, Tazan S, Mazzoni P, et al. Motor fluctuations due to interaction between dietary protein and levodopa in Parkinson's disease. J Clin Mov Disord. 2016;3:8. [PMID:27231577]
- Zhang D, Jiang H, Xie J. Alcohol intake and risk of Parkinson's disease: a meta-analysis of observational studies. Mov Disord. 2014;29(6):819-22. [PMID:24590499]
- Sheard JM, Ash S, Silburn PA, et al. Prevalence of malnutrition in Parkinson's disease: a systematic review. Nutr Rev. 2011;69(9):520-32. [PMID:21884132]
- Akbar U, He Y, Dai Y, et al. Weight loss and impact on quality of life in Parkinson's disease. PLoS ONE. 2015;10(5):e0124541. [PMID:25938478]
- Olanow CW, Watts RL, Koller WC. An algorithm (decision tree) for the management of Parkinson's disease (2001): treatment guidelines. Neurology. 2001;56(11 Suppl 5):S1-S88. [PMID:11402154]
- Berry EM, Growdon JH, Wurtman JJ, et al. A balanced carbohydrate: protein diet in the management of Parkinson's disease. Neurology. 1991;41(8):1295-7. [PMID:1866021]
- Magalingam KB, Radhakrishnan AK, Haleagrahara N. Protective Mechanisms of Flavonoids in Parkinson's Disease. Oxid Med Cell Longev. 2015;2015:314560. [PMID:26576219]
- Di Stefano A, Sozio P, Cocco A, et al. L-dopa- and dopamine-(R)-alpha-lipoic acid conjugates as multifunctional codrugs with antioxidant properties. J Med Chem. 2006;49(4):1486-93. [PMID:16480285]
- Hauser RA, McDermott MP, Messing S. Factors associated with the development of motor fluctuations and dyskinesias in Parkinson disease. Arch Neurol. 2006;63(12):1756-60. [PMID:17172616]
- Verhoef P, de Groot LC. Dietary determinants of plasma homocysteine concentrations. Semin Vasc Med. 2005;5(2):110-23. [PMID:16047264]
- Sharma M, Tiwari M, Tiwari RK. Hyperhomocysteinemia: Impact on Neurodegenerative Diseases. Basic Clin Pharmacol Toxicol. 2015;117(5):287-96. [PMID:26036286]
- Xie Y, Feng H, Peng S, et al. Association of plasma homocysteine, vitamin B12 and folate levels with cognitive function in Parkinson's disease: A meta-analysis. Neurosci Lett. 2017;636:190-195. [PMID:27840145]
- Costantini A, Fancellu R. An open-label pilot study with high-dose thiamine in Parkinson's disease. Neural Regen Res. 2016;11(3):406-7. [PMID:27127471]
- Luong KV, Nguyễn LT. The beneficial role of thiamine in Parkinson disease. CNS Neurosci Ther. 2013;19(7):461-8. [PMID:23462281]
- Hald A, Lotharius J. Oxidative stress and inflammation in Parkinson's disease: is there a causal link? Exp Neurol. 2005;193(2):279-90. [PMID:15869932]
- Liu J, Ames BN. Reducing mitochondrial decay with mitochondrial nutrients to delay and treat cognitive dysfunction, Alzheimer's disease, and Parkinson's disease. Nutr Neurosci. 2005;8(2):67-89. [PMID:16053240]
- Parkinson Study Group QE3 Investigators, Beal MF, Oakes D, et al. A randomized clinical trial of high-dosage coenzyme Q10 in early Parkinson disease: no evidence of benefit. JAMA Neurol. 2014;71(5):543-52. [PMID:24664227]
- Yoritaka A, Kawajiri S, Yamamoto Y, et al. Randomized, double-blind, placebo-controlled pilot trial of reduced coenzyme Q10 for Parkinson's disease. Parkinsonism Relat Disord. 2015;21(8):911-6. [PMID:26054881]
- Pincus JH, Barry K. Protein redistribution diet restores motor function in patients with dopa-resistant "off" periods. Neurology. 1988;38(3):481-3. [PMID:3126411]
- Mena I, Cotzias GC. Protein intake and treatment of Parkinson's disease with levodopa. N Engl J Med. 1975;292(4):181-4. [PMID:1109209]