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Pain in Parkinson's Disease. a Look at a Poorly Known Aspect of This Disease

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Pain in Parkinson's Disease. a Look at a Poorly Known Aspect of This Disease REVIEW DOI: 10.20986/resed.2019.3733/2019 Pain in Parkinson's disease. A look at a poorly known aspect of this disease J. Rotondo1, M. Toro1, M. Bolívar1,2, M. E. Seijas1 y C. Carrillo1 1Anestesiólogo. Medicina Intervencionista del Dolor. 2Unidad de Medicina del Dolor (UMD) del Instituto Médico la Floresta. Caracas. Venezuela. Expresidente AVED. ABSTRACT RESUMEN Parkinson's disease (PD) is a neurodegenerative La enfermedad de Parkinson (EP) es una enfermedad disease, the second most prevalent, after Alzhei- neurodegenerativa, la segunda con mayor prevalencia mer's disease. It presents both motor and non-mo- después de la enfermedad de Alzheimer. Presenta tanto tor symptoms; These include autonomic dysfunction, síntomas motores como no motores; entre estos últimos unexplained pain, cognitive impairment, anxiety, se encuentran disfunción autonómica, dolor inexplicable, depression, among others. Some of these patients deterioro cognitivo, ansiedad, depresión, entre otros. experience pain as an early symptom of Parkinson's, Algunos de estos pacientes experimentan el dolor como even before the expression of their disease. Among un síntoma temprano de Parkinson, incluso antes de la people who have PD and who experience pain, they expresión de su enfermedad. Entre las personas que describe it as a worrisome symptom, being a cause of tienen EP y que experimentan dolor, lo describen como suffering and disability. However, despite this, pain in un síntoma preocupante, siendo una causa de sufrimien- PD often remains undiagnosed and untreated. There- to y de incapacidad. Sin embargo, a pesar de ello, el fore, it is important to understand that pain can be dolor en la EP a menudo permanece sin diagnóstico y part of the Parkinson's experience and learn ways to sin tratamiento. Por tanto, es importante entender que manage it. el dolor puede ser parte de la experiencia del Parkinson This paper reviews current data on possible mech- y aprender las formas de manejarlo. anisms, classifi cations, evolution, potential risk factors Este trabajo revisa datos actuales sobre posibles and pain control in PD. The mechanism of pain in this mecanismos, clasifi caciones, evolución, factores de ries- situation is complex, and is infl uenced by different fac- go potenciales y control del dolor en la EP. El mecanismo tors, which may be linked to pathological changes in del dolor en esta situación es complejo, y está infl uenciado the anatomical structures involved in nociceptive mech- por distintos factores, pudiendo estar vinculado a cambios anisms. patológicos en las estructuras anatómicas involucradas en mecanismos nociceptivos. Key words: Pain, Parkinson's disease, dystonia, akathi- Palabras clave: Dolor, enfermedad de Parkinson, distonía, sia, dopamine. acatisia, dopamina. INTRODUCTION of 350 per 100,000 inhabitants is estimated; it is approximately twice more frequent in males than in Parkinson’s disease (PD) is presented as a chronic, females (1,2). long-term, irreversible pathology with symptoms that The PD was fi rst described in 1817 by the British worsen over time. PD is the second most frequent neurologist James Parkinson, who initially called it neurodegenerative disease after Alzheimer’s disease. “alteration of the motor system” (3). Currently, PD In countries such as the United States, a prevalence is defi ned as a progressive neurodegenerative con- Received: 21-08-2018 Accepted: 05-04-2019 Rotondo J, Toro M, Bolívar M, Seijas ME y Carrillo C. Dolor en la en- fermedad de Parkinson. Pain in parkinson's disease. A look at a poorly Correspondence: Julio Rotondo known aspect of this disease. Rev Soc Esp Dolor 2019;26(3):184-198. [email protected] 184 PAIN IN PARKINSON'S DISEASE. A LOOK AT A POORLY KNOWN ASPECT OF THIS DISEASE 185 dition that arises as a consequence of an alteration This neurodegenerative disease is characterized by in the production of dopamine by the dopaminergic the presence of tremor at rest, bradykinesia or hypoki- neurons of the substantia nigra (SN), which causes nesia, unstable gait and muscle rigidity, together with an imbalance in the extrapyramidal control of the other manifestations such as the alteration of postu- motor system; it is included within the movement ral reflexes, flexion posture and the phenomenon of disorders (4,5). freezing. To diagnose the disease, a patient should pre- Symptoms usually appear after the age of 60 and sent at least two of the symptoms above mentioned, it is very rare before the age of 30, although there being essential the presence of tremor or bradykinesia. is a minority of patients with early or juvenile onset Other frequent findings are unexplained pain, consti- (6,7). The prevalence ranges from 1% in the popu- pation, urinary retention, sexual dysfunction, demen- lation around 65 years of age, to 5% at 85 years of tia, depression, altered sleep patterns or weight loss age (8). After 90 years old, the onset of the disease is (9,12,13). They can be detected some years before uncommon (2,9). the onset of any of the cardinal motor signs (14). A Despite the research efforts, the causes that trigger landmark study showed that virtually all PD patients this disease are still unknown. In the pathogenesis of report at least one nonmotor symptom when these PD, several mechanisms are proposed as the cause of manifestations are actively investigated using specific the lesion of the group of neurons present in the SN, questionnaires, reaching an average of eight different without there being a directly related cause to date. symptoms per patient. In this study, the most frequent Among these mechanisms, a combination of genetic nonmotor symptoms were neuropsychiatric, gastroin- predisposition with environmental factors is proposed testinal and pain-related symptoms (15). Others report (4,5,9,10). The genetic factor, which initially was pro- that, in the early stages of the disease, the most com- posed as the only cause, is more associated with the mon nonmotor symptoms are hyposmia, pain and sleep atypical form of early onset of PD that represents a disorders (16). minority of cases (1,6), which supports the theory sta- Although pain has never been considered a primary ting that more than one factor (besides the genetic) symptom of PD, several researchers, including Charcot can be the cause of this disease (9,11). It has been (17), had already referred to painful aspects of the demonstrated with the identification of at least nine disease: Sometimes Parkinson’s is preceded by neu- loci and the cloning of genes involved in the familiar ralgic or rheumatoid pains, which are occasionally of form (11). great intensity, being located in the extremity (...) that The oxidation triggered by the presence of free will soon be affected (...) by the convulsive agitation. radicals (Table I), the action of exogenous toxins such as manganese and organophosphorus pestici- des are among the proposed environmental factors; NEUROANATOMIC AND NEUROPHYSIOLOGICAL other still unknown environmental factors have been CONSIDERATIONS OF PARKINSON’S DISEASE. considered (7,9); thus, acute exposure to 1-methyl- NEUROCHEMICAL SCHEME OF THE BASAL 4-phenyl-1,2,3,6 tetrahydropyridine, a toxic analogue GANGLIA CIRCUIT to meperidine that is commonly found as a contaminant in illicit psychostimulants, is a known cause of rapid Normally there is a balance between the contractile development of the PD and it has been used to obtain activity caused by acetylcholine and the inhibitory activi- experimental models for their study. ty mediated by dopamine, which allows adequate tone and muscle function. There are five types of dopamine receptors: D1, D2, D3, D4 and D5. The types D1 and D5 are excitatory, whereas the remaining receptors are inhibitory, which means that the net effect of dopamine is the inhibition of cell action. By binding to its receptor, TABLE I dopamine activates the G protein coupled to it. This cau- FINDINGS INDICATIVE OF OXIDATIVE STRESS ses the alpha subunits to separate from the rest of the IN PARKINSON'S DISEASE protein and activates the adenyl cyclase that manages to increase the levels of cyclic AMP. Finally, there is an Marcadores de estrés oxidativo inhibitory effect on the action of the cell which, in the – Decrease in reduced glutathione in the case of the muscle cell, would inhibit the contraction. In PD, the production of dopamine is impaired, and substantia nigra prevails the contractile effect of acetylcholine, whose – Increase in iron in the substantia nigra striatal concentration remains normal (18). – Decrease in the enzyme glutathione peroxidase In a healthy individual, the generation of coordinated – Increase in the activity of the enzyme superoxide motor movements by the brain lies in a balance bet- dismutase ween the activation of voluntary movements or direct – Increase in products derived from lipid pathway and the action of the inhibitory pathway or peroxidation (for example, malonyldialdehyde) indirect pathway. Neurotransmitter dopamine and its – Increase in polyunsaturated fatty acids in the receptors are involved in both pathways. Thus, under substantia nigra normal conditions, dopamine type 1 receptors (D1) are – Alteration of mitochondrial enzyme alpha involved, located in the internal globus pallidus (GPi) ketoglutarate dehydrogenase and in the reticular part of the SN, and dopaminer- gic neurons that project to the external globus pallidus 184 186 J. ROTONDO ET AL. Rev. Soc. Esp. del Dolor, Vol. 26, N.º 3, May-June 2019 (GPe), represented by D2 receptors, are also involved. D1 receptors and exert an inhibitory effect on GABAer- In patients with PD, due to the presence of a dopa- gic neurons with D2 receptors. The activity of these minergic degeneration, these pathways are affected, dopaminergic neurons is controlled by the GABAergic resulting in a hypoactivity in the direct pathway and a projections from the striatum and by the glutamatergic hyperactivation in the inhibitory pathway. projections of the STN. The main exit route of the basal The dorsal striatum (caudate-putamen) receives exci- ganglia takes place from GABAergic neurons of GPi, tatory stimuli, glutamatergic, from the cortical motor which project to the motor thalamus.
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