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Revista CEFAC

On-line version ISSN 1982-0216

Rev. CEFAC vol.16 no.2 São Paulo Mar./Apr. 2014

http://dx.doi.org/10.1590/1982-02162014141-12 

REVISION ARTICLES

Interference of the early and late drug therapy in Parkinson disease in the management of dysphagia

Paula Pinheiro Gerszt 1  

Cintia Rodrigues Baltar 2  

Anderson Evangelista dos Santos 3  

Adriana Leico Oda 4  

1Phonoaudiologist; Administrative Technician in Education of the Federal University of the Espírito Santo;

Skilled in Dysphagia by CEFAC-RJ.

2Phonoaudiologist by Federal University of the Rio de Janeiro,

Phonoaudiologist in the Clementino Fraga Filho Universitary Hospital -

CFFUH and in the Getulio Vargas State Hospital;

Skilled in dysphagia by CEFAC - RJ.

3Phonoaudiologist; PhD Student in Sciences by Department of Anatomy of the Federal University of the Rio de Janeiro - FURJ.

4Phonoaudiologist of the ABRAMI (Brazilian Association of Myasthenia Gravis) and

ABRELA (Brazilian Association of Amyotrophic Lateral Sclerosis);

Teacher of the CEFAC;

Staff of the Skilling, Rehabilitation and Neurology Course of the Federal University of São Paulo - Paulista School of Medicine, PhD Student in Neurosciences by Federal University of São Paulo.

ABSTRACT

Parkinson’s disease shows a higher incidence in the elderly population generating progressive motor impairment, which affects several functions, among which stands out swallowing. The purpose of this study is to correlate the dysphagia in Parkinson’s disease with immediate and / or late effect of the drug treatment, which directly or indirectly, will interfere with speech therapy management. We carried out a literature review in electronic databases Lilacs, Scielo, Medline and Pubmed from 2001 to 2011, using the free terms “Parkinson Disease”; (Parkinson Disease), “swallowing”; (deglutition), “dysphagia”; (dysphagia), “pharmaceutical preparations”; (pharmaceutical preparations), “levodopa”;, “videofluoroscopy”; (videofluoroscopy), a government document (OPAS, 2002), relevant articles and copies of American and Brazilian literature about the theme. The literature appointments levodopa as the main pharmacological treatment of the Parkinson’s disease. However, the resolution of the motor symptoms must be balanced in function of important collateral effects, being immediate or later. Actually, there aren’t consistent answers in favour of the resolution of the dysphagia in consequence of pharmacological treatment, wich effects may interfere, direct or indirectly, on the dysphagic manifestations and of several ways. In this way, turns fundamental the record of the medications like part of the anamnese, considering that, such data may help orientation/reorientation of the phonoaudiologic management, specially interdisciplinary context. In despite of possibility of Parkinson’s patient to answer inconsistently to pharmacological therapy, is noteworthy that professional must pay attention to presence of collateral effects like modifiers factors of the dysphagia oropharyngea profile in the idiopatic Parkinson’s disease.

Key words: Parkinson’s Disease; Deglutition; Dysphagia; Levodopa

INTRODUCTION

The Parkinson disease is the second neurodegenerative infirmity more common after Alzheimer disease, affects mainly of the third age population1,2, with incidence,principally in the population up to 65 years old, and prevalence of 1 to 2% in the world and 3% in the Brazil3.

Of unknow etiology, is characterized by presence of multiple monoaminergic dysfunction, including the deficit of dopaminergic2, cholinergic, serotonergic and noradrenergic systems, that may to explain the symptoms called non-motors (disturbs of sleep, cognitive and depression dysfunctions), which can be associated with several brain regions injured4. Usually of easy diagnostic if of idiopathic-type, but with atypic components, the variety of differential diagnostics is great. Presents slow progression and clinical manifestations predominantly asymetrics3.

The cardinal signals are: rest tremor, bradykinesia, plastic muscular rigidity (presenting or not dentate wheel signal) and postural instability4,5. Other important clinical data include deambulation disturbs, masked facies, alterations of the voice, dysarthria, drooling, sexual dysfunction, cramps, pains, paresthesia, dysphagia, urinary incontinence, intestinal obstipation, micrograph, disturbs of the sleep, bradyphrenia, depression, dementia, cognitive alterations and sensory disturbs4,5. Logeman et al., 1973, suggest in study that the parkinsonian patients are affected for larynx stiffness, important postural disorders, associated involuntary movements and irregular and weak breathing4.

Considering to stiffness and bradykinesia, are regularly found in Parkinson disease alterations in the voice, in the articulation of words and in the oropharyngeal deglutition6. There are autors that refer, in initial and intermediary stages, are more evident alterations in the phonation and in the articulation of the speech, and in advanced stages arise reports about complaint in the deglutition. Other say that injuries of the deglutition can to appear as initial stages as advanced stages and that the predominant factor refer to apparent symptomatologic board3.

The treatment of Parkinson disease may to involve non-pharmacological measures, like phonoaudiologic therapy, actions that help the patients to compensate the limitations imposed by disease, besides fundamentals, inclusive, to delay the evolution itself. The pharmacological approach involve a group of drugs that possess symptomatic action and, in despite of improve significantly the life quality of the patients, involve a myriad of adverse effects5,7. The surgery treatment will not be discussed here.

Being the deglutition a complex motor activity indispensable to health and survive of the individuals, which commitment is present in the Parkinson disease, this study, in particular, compelling us to better knowledge about the theme. By the way elucidation of informations about Parkinson disease and its manifestations, powerfully succeded from drug treatment, we seek to understand positive and negative effects of the antiparkinsonian drugs about the dysphagic board, besides about general health state of the patient, in a manner to make up bases that support apropriately the phonoaudiologic work.

The purpose of this study self justify by necessity of help the phonoaudiologist to distinguish the classic and/or secondary manifestations to the use of dopaminomimetic drugs, a relevant subject to the clinical thinking in the phonoaudiologic evaluation and management, considering the risks of bronchoaspiration, dehydration and/or proteic-caloric desnutrition in the Parkinson disease. Such necessity constitutes one of the first steps for differentiated and more effective therapeutic approach.

Thereafter, the intention of the present study is to relate the dysphagia in the Parkinson disease to the early and/or late effects of drug therapy, that, direct or indirect manner, will interfer in the phonoaudiologic management.

METHOD

Retrospective study, with bibliographic revision beginned at June 2011 and conducted by search in the eletronic data bases Lilacs, Scielo, Medline and PubMed in the period between 2001 and 2011. Were used the free terms “Parkinson disease”;, “deglutition”;, “dysphagia”;, “pharmaceutical preparations”;, “levodopa”;, and “videofluoroscopy”;. The works were analyzed since adoption of metodology of systematic review. Were found 140 articles, of which, 29 were chosen for to be related with deglutition function, Parkinson disease and drug treatment in the Parkinson disease. Were considered the articles published in portuguese, spanish and english, in according to the limits “humans”;, “adults above than 19 years old”; and “male and female genre”;. Since the previous knowledge that such works proportionated help to basic explaining of the theme, were added to searched literature a governmental document (OPAS, 2002), articles (Korchonouv, 2010; Bedin and Ferraz, 2003), thesis (Carrara-de-Angelis E, 2000; Gasparim AZ, 2007) and issues of the american literature (Kandel, Schwartz and Jessell, 2000; Schapira and Olanov, 2005; Purves, 2004) that discuss about dopaminergic system and dopaminomimetics drugs, totalizing 42 publications in this study.

REVIEW OF LITERATURE

The neurochemistry organziation and the neuromuscular integration are in the base of the motor control, including several parallel pathways among cortical and subcortical areas, specially the basal ganglia. The functional diversity of the motor control is underlying to the complex organization of the mesolimbic, mesocortical and, principally, mesostriatal dopaminergic systems, whose functional network results from a extent integration between dopaminergic, glutamatergic and gabaergic neurons, such as from repertoire of the receptors correlates8-10. Two classic pathways known help in comprehension of the functioning of the basal ganglia. In the named direct pathway, the upper motor neurons are free from continous tonic inhibition exerced by inner globus pallidus and by substantia nigra pars reticulata on the thalamus; in the indirect pathway, this index of tonic inhibition increases consequently to the activity of subthalamus, thereby, injurying the action of the thalamocortical neurons on the upper motor neurons8-10. The substantia nigra pars compacta and the ventral tegmental area send dopamine to striate. The synapses among this substantia nigra pars compacta and the ventral tegmental area self contact in the base of the spine dendritic of the striate cells, near to the synapses between striatal cells and cortical projections, and, consequently, capable to modulate its glutamatergic effects8. Thereby, is easy to conclude that, with destruction of the cells of the substantia nigra pars compacta, the inhibitory discharge stays abnormally high, in consequence of the spontaneous activity of the globus pallidus, and the thalamic activation is less probable to occur. In despite of intrincate dopaminergic circuitry involved in the basal ganglia, the signaling initialized bydifferent receptors correlates, underlying to the direct and indirect pathways, reflect the modulatory complexity of the basal ganglia on the upper motor neurons.

Among dopaminergic receptors localized in the striatal cells, there are 5 identified human subtypes: type D1 dopaminergic receptors (D1 e D5) and type D2 dopaminergic receptors (D2, D3 e D4). This receptors are defined by capacity to stimulate (type D1) or to inhibit (type D2) the adenylciclase. This capacity reflects its different interactions with the G-protein, wich can to possess the sequences of different amino acids, tha justifies the specificity of each receptor11. A nigral axon can to influence both types of receptors in the group of striatal neurons responsible for muscular contraction agonist-antagonist, proportionating the dopaminergic effect on the agonist (acceleration of the contraction) and antagonist (reduction of the tonus) skeletal muscle during the moviment12.

The parkinsonism is characterized by coexistence of brady- or hypokinesia with reduction of the acceleration of the agonist muscle contraction and increase of the tonus and rigidity. Type D1 receptors mediate the inhibition of the muscular tonus and the type D2 receptors promote or accelerate the contraction of synchronized manner during motion under action agonist-antagonist. In the Parkinson disease, with the nanomolar index of dopamine (type D1) low at striatal synaptic cleft, the tonus can not be sufficiently inhibited, inducing to hypertonicity state and apparent muscular rigidity. In addition, with the begin of the moviment, the micromolar index of dopamine necessary for activation of the normal motor act are not reached in the D2 system, culminating in reduction of the capacity of to produce moviment (bradykinesia). Without dopaminergic repair therapy, the progressive loss of the production and release of dopamine induces, each time more, a injuried stimulation of the type D1 and D2 receptors and worst of the rigidity and bradykinesia in the disease progression12.

In addition to modulation of the motor actions, injuries of the basal ganglia, also are associated to neuropsychiatry, cognitive and behavioural disorders, reflecting its role in several functions of the frontal lobe, not only associated to the moviment9. Parallel conections originated from upper regions of the cortex engage prefrontal and limbic regions, for example. Suggests that this modulation is seemed to classic motor pathway, in allusion to the function of to modulate origin and end of functions, such as, planning, working memory and attention, emotional regulation of the behavior and motivation. This may to explain the occurrence of cognitive deficits in the Parkinson disease.

The dopamine, noradrenaline and adrenaline belong to chatecolamine (biogenic amines) group, substances classified like little neurotransmitters. The synthesis occurs inside of the presynaptic terminals from the tyrosine amino acid, which is converted, by tyrosine hydroxylase enzime, to dihydroxyphenylalanine (levodopa), in a reaction that depends of oxygen like cosubstrate and the tetrahydrobiopterin like cofactor. The levodopa is, so, decarboxylated by aromatic amino acid, the DOPA decarboxylase, and yet are produced dopamine and carbonic gas. As supracited, after released, the dopamine links to specific dopaminergic receptors and the some β-adrenergic receptors. The dopamine is removed of the synaptic cleft by recaptation to inside of nervous terminals or inside of next glial cells by one Na-dependent transporter (the main involved in catabolism are monoamine oxydase and chatecol o-methyltransferase). Though dopamine do not cross easily the blood-brain barrier, it is possible to levodopa. The levodopa is absorbed in the small intestine, but is rapidly catabolized in the gastrointestinal tract and peripheral tissues.

The process of degeneration of nigrostriatal dopaminergic neurons induces reduction of the striatal dopamine modulation and, consequently, motor alterations. This model preconize that, increasing the dopaminergic stimulation or reducing the cholinergic or glutamatergic stimulation, the symptom resolve. The drug treatment would must, at least, to include the neuroprotection (reduction of the progression of the disease) and the symptomatic treatment (control of the symptoms). The neuroprotection is a objective yet not achieved, because the randomized and controlled clinical symptoms are insufficient to show that such drug has this property. Thereby, the symptomatic treatment is the choose for parkinsonian patients and with resultant incapacities7.

The selection of the accepted drug must to consider the stage of the disease, the symptomatology up to date, occurrence of side effects, age of patient, besides of the medications in practice and the cost of the ones. Thereby, there are, actually, several ways of symptomatic pharmacologic intervention. The figure 1 shows a resume of all described medications in the guideline of the OPAS (2002), associating benefits, pharmacokinetic and recommended diary dose:

The principal substances utilized in the treatment of the PD:

Among available drug therapies for Parkinson disease, the levodopa therapy, also called L-DOPA, have demonstrated better efficacy13,14 and low mortality, receiving large indication in the Parkinson disease treatment14 .

In despite of the therapeutic benefits achived with the use of the L-DOPA, its peripheral metabolization (outside of central nervous system) by decarboxylases-type enzimes prejudices the dopamine biodisponibility (product from the L-DOPA metabolization) and produces side effects, specially gastrointestinal ones. Thereby, the administration of L-DOPA associated with decarboxylase inhibitors (considering that such inhibitors don’t cross the blood-brain barrier) improve the dopamine biodisponibility in the central nervous system, demanding lower doses, besides of to reduce undesirable effects13-15. Noteworthy that the use of the L-DOPA associated with such inhibitors provides more stable and longer effects, and, consequently, the treatment can to extend to months or years14, retarding the appearing of motor complications that regularly follow itself to the prolonged use of the L-DOPA. Regularly, individuals with Parkinson disease under prolonged use of the L-DOPA present motor flutuations and dyskinesias16,17, presenting the known phenomenon like wearing off (shorter duration of medication effect), sudden/random on-off (gravely sudden of the symptoms of the Parkinson disease) and delayed ons or dose failures (initial later of the drug action)13,17. Thereby, with the progression of the disease, events of the freezing, postural instability, besides autonomic dysfunctions and dementia are presented and such patients don’t answering more to the treatment of the desirable manner7.

Like preventive action to the appearing of the motor complications secondary to the prolonged use of the L-DOPA, specially in stages more advanced of the disease, the method of choice have been the simultaneous use of this one with dopaminergic agonists5,7, of which can be exemplified anticholinergic, antiglutamatergics and monoamine oxydase (MAO) inhibitors7.

Dyskinesias, motor flutuations and psychiatric symptoms are common complications in Parkinson patients in more advanced stages and with prolonged use of the L-DOPA17. The clozapine, neuroleptic and antipsychotic drug and with inhibitory action on the dopaminergic receptors showed positive effects in the control of the symptoms ones, without, however, to interfer in the motor deficiency board16,18. The amantadine, like classically described, exertes pre- and postsynaptic dopaminergic action, mild antiparkinsonian activity and come being used like antidyskinetic agent19.

Noteworthy that, in despite of the advantages of the symptomatic treatment, all this substances bring themselves undesirable side effects. Such effects can be motors or non-motors17 and some of this ones achieved the point of to limit the use of the substance. The clozapine, for example, may to cause a myriad of effects that limit the use, like excessive sedation, drooling, dry mouth, vomit, weakness or muscle spasm, dyspnea, tremor, neutropenia, thrombocytopenia, urinary incontinency, epigastric pain and diarrhoea, sickness and grave intestinal constipation, diplopia, hallucination and agitation16,18. Among cholinergic adverse effects, include deficits of memory, hallucinations, sedation and ailment. Secondary dyskinesias, when occur, are focal, resulting in blepharospasm, oromandibular dystonia, torticollis and essential tremor. Other muscarinic effects include dry mouth, constipation, sickness, blear sight, urinary retention, disorders of transpiration and tachycardia. In according to antiglutamatergics, its side effects generally are mild and include insomnia, anxiety, dizziness, disorders of motor coordenation, nervousness, sickness and vomit. Vocal myoclonus and peripheric neuropathy occur scarcely20.

Motor aspects of the deglutition in the PD:

Several authors afirm that the incidence of dysphagia is variable in the Parkinson disease, characterized by no symptoms21 and rarely refered by patients, that limits the early knowledge for approach. Monte et col., 2005, expose that dysphagia in the Parkinson disease presents of silence manner or refered with asphyxia, multiple deglutitions and regurgitation, being related in up to 70% of the cases22.

Lim (2008), afirm that the literature not have agree about the relation between the severity of the Parkinson disease and presence/severity of the dysphagia. Some studies did not find any relation among this factors, while others studies found worsen of the dysphagia during increase of the severity of the disease23,24. Suggests that the patients can to experiment symptoms of dysphagia later at the course of the disease in comparison with the others parkinsonian disorders. In despite of this, because of the poor correlation between the related symptoms and the instrumental evaluations, presymptomatic dysphagia can be present anad not identified23. Azevedo and Cardoso (2009) refer that the parkinsonian individuals present complaints related to disorders in the deglutition at advanced stages and hypothesized that this occurs because reduction of the sensibility in the aero-digestory tract5.

The respiratory insufficient because dysphagia and aspiration is considered thte principal cause of death of the disease3,5,22,23,25, that can be related with the presence of the dysphagia, associated to the difficult that the patients possesses in to locomote23. They can be more susceptible to swallowing at insufficient times of the respiratory cycle, that is, during the inspiration or during the production of poor subglotic flux. Also, there is tendency to inspiring after deglutition, independent of to swallowing at inspiratory stage. If the larynx is considered like a organ with regulatory capacities associated to function of deglutition, the stimulation of subglotic mechanoreceptors by expiratory aereo flux before of the deglutition sends signals to a “pattern generator”;, localized in the brainstem. This answer in velocity and muscle strength of proportional manner to the subglotic pression exerted. Such thinking may explain partially why the antiparkinsonian drugs do not improve consistently the deglutition function or do not prevent the progression of the dysphagia26.

Considering the capacity of the protection of the air pathway, studies discuss that, in some patients, the hability in to produce effective voluntary cough is compromised because of the rigidity of the thoracic wall, culminating in reduction of the pulmonary capacity and perturbing the production of the subglotic air pressure necessary to deflagration of the cough27. Miller (2011) verified in your assay that some patients with Parkinson disease did not present cough during and after repeated deglutitions, speculating that the same patients did get reducing the index of ingest through shorter and frequent deglutitions, or simply stopping the ingest, waiting to avoid penetration and/or aspiration21. Vey times, like occur wih the dysphagia, the individuals are unconscious of the injuried pulmonary function, thereby, such problems are not perceived until that appear more several disorders26.

Dentary problems may occur because the lack of orofacial muscle control, reduced saliva and compromised manual control, having also relating to cognitive deficit29. Bloem et cols. (2009) related the case of a patient of 71 years old with increased salivation and drooling, conducting to perioral lesions29. Lamonica (2003) shows, in research about clinical manifestations in the Parkinson disease, dysphagia related by 50% of the patients and drooling in 70% of the interviewed patients30. The dependence to eat and take a oral care, eating by tube, several medical diagnostics, smoking and quality of teeth are important predictors25.

At 1983 Logeman proposes the swallowing videofluoroscopy, with possibility of to evaluate the dynamic of the full process of the oropharingeal deglutition, being analyzed disorders of oral phase, like tremor of phonoarticulatories organs, difficulties in the initial production of the alimentary bolus, reduction of the salivar secretion index, increase of the deglutition time, limitation of the projection of the tongue and mandible during chewing and presence of the repeated anteroposterior moviments of the tongue for propulsion of the bolus (“festination of the tongue muscle”;); in the pharingeal phase observed start delayed, with stop of the bolus in the vallecula space and in the piriform sinus, with risk of larynx penetration and aspiration, alterations of pharynx motility and of the cricopharynx function; in the esophageal phase occurred peristalsis reduction, with shorter transit time3. All this disorders discussed reflect the desintegration of the automatic and voluntary moviments caused by akinesia, bradykinesia and rigidity, characters of the Parkinson disease. In study with sample of 15 parkinsonian patients, 15 cerebral vascular accident-suffered patients and 14 health control patients, followed in videofluoroscopy exam, the parkinsonian patients presented alterations in the dynamic of the deglutition oral phase, probable to culminate in penetration and/or aspiration. As parkinsonian patients ascerebral vascular accident-suffered patients showed reduced ejection power (demanding more time of oropharingeal transit) or so, the called “ejection in two times”;, which oral content is swallowed with penetration of little content in the pharynx followed by swallowed rest bolus in continous act31.

During videofluoroscopy evaluation of the deglutition of elder parkinsonian patients, Bigal et cols. (2007) observed seemed manifestations to the found for Logemann (1983), including the difficulties in the formation of the bolus, inadequate labial closing, multiple deglutitions, terciary contractions of the esophageous and gastroesophageal reflux32. When qualitatively analyzed, was observed compatibility of the complaint of sensation of food stopped in the throat, remaining in valleculae and piriform recess, as well as necessity of successive deglutitions. The results of the Sung et al. (2010) suggests that the existence of pharyngeal and esophageal dysfunction, same before clinical manifestations of the dysphagia, may to reflect involvement as of the brainstem as of the myoenteric plexus at early stages of the disease23. Gasparim (2007) analyzed the efficacy of the deglutition and the cough reflex in cases of laryngeal penetration and/or tracheal aspiration by food, in different stages of severity of the Parkinson disease and observed that deglutition was efficacious for the foods with liquid and solid consistency in parkinsonian patients at 1 to 2,5 stages of the staging scale of Hoehn & Yahr (1976); and the pasty consistency in parkinsonian patients at stages 1 to 4; the cough reflex was efficacious for the pasty food at stages 1 to 434.

There are still other reports about alterations in the oral, pharyngeal and esophageal phases of the deglutition24,25,31,35, such as: 1) the prejudice of the ejection power, producing increase of the oropharyngeal transit time or swallowing of the oral content in two steps (in the first step, the swallowing of little alimentary bolus in the pharynx is followed by rest mass in continous act)31; 2) more time in the oral transit attributed to the tongue festination phenomenon, described by Troche (2008), suggesting that such phenomenon may be asociated to the bradykinesia, rigidity and voluntary behaviour of the oral phase of the deglutition25; 3) abnormal increase of the rest pressure of the pharynxesophageous transition, which, in despite of do not be the main factor of the dysphagia, may be present in some patients preceding the others alterations of deglutition and, maybe, to result in stop of the bolus at piriform sinus, culminating in larynxtracheal aspiration35.

Bramble et al, cited by Fuh et col. (1997), that focalize in to study the esophageous, suggests that cholinergic mechanisms and not only dopaminergic ones, are important to deglutition control36. Scarce studies have demonstrated, objectively, the drug treatment effects in the functions of deglutition and speech, as is showed in figure 2 3,19,22,23,36-40.

Dysphagia and medicamentous treatment in the PD.

In despite of rare evidences about the effects of the levodopa during swallowing23, affirms that oropharyngeal dysphagia in the idiopathic Parkinson disease is inconsistently responsive to pharmacologic therapy26. Some researchers already examined the deglutition process in a group of patients in different periods (in whatever moment, under dopaminergic effect; in other moment, without use of dopaminergic drugs) and discovered that the abnormalities, generally persist after administration of drugs, in despite of the increase of dose26, or demonstrate only low improve in dysphagia in a group of participants, with decline of the function in other23. Other research only shows low improve in the dysphagia in a group of participants and worsen of the dysphagic board in other one23. There are studies that relate reduction of the full time of the deglutition and improve of the buccal lingual facial motricity in patients treated with apomorfine, however, other studies shows that dysphagia is predominantly refratary to dopaminergic drug action and there are cases that worsenes with levodopa administration. Absent of clear association between motor dysfunction and abnormality of the deglutition, added to lack of benefit of the levodopa in some cases, brings to think about the involvement of other neurotransmission system with the deglutition disorders found in the Parkinson disease.

By the other hand, other side effects can interfer of direct or indirect manner in the swallowing. Excessive sedation, diurnal sleepness, depression and psychotic disturbs, whether not limit the patients of to go the sessions, are sufficient to difficult ever therapeutic planning. The lack of adequate alert may to conduct the individual to do not feed adequately, compromising the nutritional board and, also, to get capsules by oral administration. Sickness and vomit maybe limit the access to phonoarticulatory organs during evaluation or therapy. Dizziness, postural hypotension and balance disorders certainly will induce the examiner/therapist worries in put the patient at confortable and apropriate postural, avoiding falls and proportionating him security. Weakness, muscle spasm, increase of tremors, coordenation disorders, ataxies, diskinesias, involving the appendicular or axial musculature, will can to have interference with major or minor punctuality. Mainly for the neurologic patients, the body postural maintenance is indispensable during the meals. In this context, is simple to understand that to assume different specific postures may to injury the swallowing. Motor alterations involving specific muscular groups of the deglutition may interfer directly in its performance. The drooling and sensation of dry mouth generally cause discomfort to patient, however, in the impossiblity of to change of the medication, we can help him to control major volume of the saliva or betake to measures that alleviate the sensation of dry mouth.

Is important to emphasize, also, that a diet rich in protein may to influence the distribution of the levodopa to blood stream and to central nervous system of negative form, because both compete in the gastrointestinal tract and in the blood-brain barrier. At advanced phases of the disease, this will culminate in a major time between drug ingestion and its action. Initially, because of the presence of residual neurons, this latency do not occurs. In such way, the diet of the patient would must be specially adjusted, with administration of levodopa one hour after of the meals, in times away from protein ingestion (and this , two hours after the levodopa ingestion or to the final of the day), with empty stomach, or, still, simultaneously to the diet rich in carbohydrates, which will facilitate the intestinal absorption5. Juri and Chaná (2006) suggests the levodopa administration, at least, thirty minutes before of the meals like a important measure to optimize the kinetic of the drug2. Thereby, in the desire to utilize, in a evaluation or therapy, a meal rich in protein, may be necessary to adjust the time of the intended attendance.

The profissional must to know the medication that is being administrated to the patient, to familiarize yourself with “on”; and “off”; periods, besides to pay attention to “wearing off”;, “sudden/random ‘on-off”; and “delayed ons”; phenomena. It is possible that the patients avoid to feed themselves at “off”; state. Still, the extending of this interval will may to reduce the total quantity of diary alimentary ingestion, culminating in desnutrition. This fact induces us to think that would have difference in the moment of to care of the patient, that is, at “on”; or “off”; periods, obtaining, during “on”; period, the better global motor rebound.

In general, at first contact with the patient, must be collected data, such as, disease duration, hour desired of the patient to realize your meals, medications in use and its posology and diary activity. Besides of the detailed investigation of the existence of symptoms and/or signals of dysphagia, must be asked whether the patient is under one or more effects of the administrated drugs. Such approach will stimulate the clinician to analyze the collected data with desire to distinguish the origin of the disorders. Besides, will can to define a corrective or attenuater therapeutic approach of the problem.

Besides of choice of the adequated exercises, maneuver and consistencies for each case, is needed to consider the possibility to readjust of the food options with a nutrition professional, with the finality of bypass the incompatibility between protein and levodopa in the gastrointestinal tract, as cited. Other important aspect is that the patient can to feel better performance when is at “on”; period of the medication and such fact to culminate in absences to the therapies when the same be with grave rigidity and difficulties of locomotion at combined hour to attendance. However, must give preference, specially in the first attendances, to the period that medication present itself active.

Considering the prevalent age group in the Parkinson disease, would be interesting to value the prevention of cognitive deficits, inclusive, by exposed in this review, about the relation between the basal ganglia and cortical and limbic areas. For example, since that perceives that the effects of the medication contribute for the limitation of the diary life activities, this must be related to the clinician (mainly because of the major frequency of contact between therapist and patient). Besides, other more specific approaches may be executed, obviously, as a therapy of group focalized to cognitive stimulation.

CONCLUSION

The discussions in the literature occur principally in turn of the levodopa, pointing it like a main pharmacologic treatment of the Parkinson disease. Several drugs are utilized in the treatment of this disorder. Until moment there are not consistent answers in favour of resolution of the dysphagia like result of pharmacologic treatment. The drugs alleviate the characteristic motor symptoms, however, at costs, of imediate or later, motor or non-motor side effects. Some of the non-motor effects present direct or indirect interferences about the dysphagic manifestations; motor effects may interfer in ever deglutition phase and to potentiate the existing difficulties; there are, yet, the risk of interferences about cognitive aspects, limiting ingestion by oral pathway, because of the voluntary and aware aspect of the some deglutition phases. Suggests the record of the medication utilized by the patient (and respective posology) and reflection about possibility of interferences of the pharmacologic therapeutic about the dysphagic board and general health state of the patient, intending bypassing it or removing it, since that possible, at interdisciplinary context.

Figure 1 – Medications utilized in the treatment of the Parkinson disease.  

Figure 2 Comparison of 9 studies that relate drug actions to the deglutition disorders found in Parkinson Disease 

REFERÊNCIAS

. Chaná P, Fierro A, Reyes-Parada M, Sáez-Briones P. Comparación farmacocinética de Sinemet y Grifoparkin (levodopa/carbidopa 250/25 mg) en pacientes con enfermedad de Parkinson avanzada: un estudio con dosis única. Rev.Méd.Chile. 2003;131(6):623-31. [ Links ]

. Juri C, Chaná P. Levodopa en la enfermedad de Parkinson. ¿Qué hemos aprendido? Rev Méd Chile. 2006;134:893-901. [ Links ]

. Belo LR, Lins SC, Cunha DA, Lins O, Amorim CF. Eletromiografia de superfície da musculatura supra-hióidea durante a deglutição de idosos sem doenças neurológicas e idosos com parkinson. Rev. CEFAC. 2009;11(2):268-80. [ Links ]

. Palermo S, Basto ICC, Mendes MFX, Tavares EF, Santo DCL, Ribeiro AFC. Avaliação e intervenção fonoaudiológica na doença de Parkinson: análise clínica-epidemiológica de 32 pacientes. Rev Bras Neurol. 2009;45(4):17-24. [ Links ]

. Azevedo LL, Cardoso F. Ação da levodopa e sua influência na voz e na fala de indivíduos com doença de Parkinson. Rev Soc Bras Fonoaudiol. 2009;14(1):136-41. [ Links ]

. Felix VN, Corrêa SMA, Soares RJ. A therapeutic maneuver for oropharyngeal dysphagia in patients with Parkinson’s disease. Clinics. 2008;63(5):661-6. [ Links ]

. Protocolo Clínico e Diretrizes Terapêuticas. Doença de Parkinson - Levodopa/ Carbidopa, Levodopa/ Benserazida, Bromocriptina, Pergolida, Pramipexol, Cabergolina, Amantadina, Biperideno, Triexifenidil, Selegilina, Entacapona, Tolcapona. OPAS. Nov, 2002. Disponível em http://www.opas.org.br/medicamentos/docs/pcdt/do_d12_01.pdfLinks ]

. Purves D, Augustine GJ, Fitzpatrick D, Hall WC, LaMantia A-S, McNamara JO, Williams SM. Neuroscience. 3rd ed. Massachusetts: Sinauer Associated; 2004. [ Links ]

. Kandel ER, Schwartz JH, Jessell TM. Principals of Neural Science. 4th ed. New York: McGraw-Hill; 2000. [ Links ]

. Bedin S, Ferraz AC. Organização Funcional dos Circuitos dos Núcleos da Base Afetados na Doença de Parkinson e na Discinesia Induzida pela Levodopa. Saúde em Revista. 2003;5(9):77-88. [ Links ]

. Poewe W. Drug Therapy: Dopamine Agonists. In: Schapira e Olanow. Principles of treatment in Parkinson’s disease. Philadelphia: Elsevier; 2005. p. 25-47. [ Links ]

. Korchounov A, Meyer MF, Krasnianski M. Postsynaptic nigrostriatal dopamine receptors and their role in movement regulation. JNeural Transm. 2010;117(12): 1359-69. [ Links ]

. Niremberg MJ, Stanley F. The role of levodopa and cathecol-o-metyltransferase inhibitors. In: Schapira AH e Olanow CW. Principles of treatment in Parkinson’s disease. Philadelphia: Elsevier; 2005. p. 3-24. [ Links ]

. Venegas PF. Consideraciones sobre las complicaciones motoras y neurotoxicidad de la levodopa en la enfermedad de Parkinson. Rev Chil Neuro-Psiquiat. 2005;43(3):231-5. [ Links ]

. Scorza FA, Henriques LD, Albuquerque M. Doença de Parkinson – Tratamento medicamentoso e seu impacto na reabilitação de seus portadores. Mundo Saúde. 2001;25(4):365-70. [ Links ]

. Dicionário de Administração de Medicamentos na Enfermagem 2005/2006. Rio de Janeiro: EPUB; 2004. P. 504-5. [ Links ]

. Souza RG, Borges V, Sila SMCA, Ballalai, H. Quality of life scale in Parkinson’s disease PDQ-39 - (Brazilian Portuguese version) to assess patients with and without levodopa motor fluctuation. Arq Neuropsiquiatr. 2007;65(3-B):787-91. [ Links ]

. Gomide L, Kummer A, Cardoso F, Teixeira AL. Use of clozapine in Brazilian patients with Parkinson’s disease. Arq Neuropsiquiatr. 2008;66(3-B):611-4. [ Links ]

. Ziliani J, Rosa MN de. Enfermedad de Parkinson. Amantadina en discinesias por Levodopa. Rev Med Plata. 2003;37(3):19-22. [ Links ]

. Cersosimo MG, Koller WC. Other Drug Therapies for Parkinson’s disease. In: Schapira AH e Olanow CW. Principles of treatment in Parkinson’s disease. Philadelphia: Elsevier; 2005. p.49-66. [ Links ]

. Miller N, Allcock L, Hildreth AJ, Jones D, Noble E, Burn DJ. Swallowing problems in Parkinson Disease: frequency and clinical correlates. J Neurol Neurosurg Psychiatry. 2009;80(9):1047-9. [ Links ]

. Monte FS, Silva-Junior FP, Braga-Neto P. Swallowing abnormalities and dyscinesia in Parkinson’s Disease. Moviment Disorders. 2005;20(4):457-62. [ Links ]

. Lim A, Leow L, Huckabee ML, Frampton C, Anderson T. A pilot study of respiration and swallowing integration in Parkinson’s disease: “on”; and “off”; levodopa. Dysphagia. 2008;23(1):76-81. [ Links ]

. Potulska A, Friedman A, Królicki L, Spychala A. Swallowing disorders in Parkinson’s disease. Parkinsonism Relat Disord. 2003;9(6):349-53. [ Links ]

. Troche MS, Sapienza CM, Rosenbeck JC. Effects of bolus consistency on timing and safety of swallow in patients with Parkinson’s disease. Dysphagia. 2008;23 (1):26-32. [ Links ]

. Gross RD; Atwood CW Jr; Ross SB; Eichhorn KA; Olszewski JW; Doyle PJ. The coordination of breathing and swallowing in Parkinson’s disease. Dysphagia. 2008;23(2):136-45. [ Links ]

. Pitts T, Troche M, Mann G, Rosenbek J, Okun MS, Sapienza C. Using Voluntary cough to detect penetration and aspiration during oropharyngeal swallowing in patients with Parkinson Disease. Chest. 2010;138(6):1426-31. [ Links ]

. Bakke M, Larsen SL, Lautrup C, Karlsborg M. Orofacial Function and oral health in patients with Parkinson’s disease. Eur J Oral Sci. 2011;119(1):27-32. [ Links ]

. Bloem BR, Kalf JG, van de Kerkhof PC, Zwarts MJ. Debilitanting consequences of drooling. J Neurol. 2009;256(8):1382-3. [ Links ]

. Lamônica DAC, Saes SO, Paro PMM, Brasolotto AG, Barbosa AS. Doença de Parkinson: proposta para um protocolo de anamnese. Salusvita. 2003;22(3):363-71. [ Links ]

. Yamada EK, Siqueira KO, Xerez D, Koch HA, Costa MMB. A influência das fases oral e faríngea na dinâmica da deglutição. Arq Gastroenterol. 2004;41(1):18-23. [ Links ]

. Bigal A, Harumi D, Luz M, De Luccia G, Bilton T. Disfagia do idoso: estudo videofluoroscópico de idosos com e sem doença de Parkinson. Disturb Comun. 2007;19(2):213-23. [ Links ]

. Sung HY, Kim JS, Lee KS, Kim YI, Song IU, Chung SW, Yang DW, Cho YK, Park JM, Lee IS, Kim SW, Chung IS, Choi MG. The prevalence and patterns of pharyngoesophageal dysmotility in patients with early stage Parkinson’s disease. Mov Disord. 2010;25(14):2361-8. [ Links ]

. Gasparim AZ. Eficácia da deglutição e do reflexo de tosse na doença de Parkinson [dissertação]. Curitiba (Paraná): Universidade Tuiuti do Paraná; 2007. [ Links ]

. Higo R, Tayama N, Watanabe T, Niimi S. Abnormal elevation of resting pressure at the upper esophageal sphincter of Parkinson’s disease patients. Eur Arch Otorhinolaryngol. 2001; 258(10):552-6. [ Links ]

. Fuh JL, Lee R, Wang SJ, Lin CH, Wang P, Chiang J et al. Swallowing difficulty in Parkinson Desease. Clin Neurology and Neurosurgery. 1997;99(2):106-12. [ Links ]

. Hunter PC, Crfameri J, Austin S, Woodward MC, Hughes AJ. Response of Parkinsonian swallowing dysfunction to dopaminergic stimulation. J Neurol Neurosurg Psychiatry 1997;63:579-83. [ Links ]

. Carrara-de Angelis E. Deglutiçäo, configuraçäo laríngea, análise clínica e acústica computadorizada da voz de pacientes com doença de Parkinson [tese]. São Paulo (SP): UNIFESP; 2000. [ Links ]

. Coriolano MGWS, Lins OG, Belo LR, Menezes DC, Moraes SRA, Asano AG, et al. Monitorando a deglutição através da eletromiografia de superfície. Rev. CEFAC. 2010;12(3):434-40. [ Links ]

. Gasparim AZ, Jurkiewicz AL, Marques JM, Santos RS, Marcelino PCO, Herrero JF. Deglutição e tosse nos diferentes graus da doença de Parkinson. Arq. Int. otorrinolaringol. 2011;15(2):181-8. [ Links ]

Received: June 13, 2012; Accepted: January 07, 2013

Mailing Address: Paula Pinheiro Gerszt Departamento de Educação Integrada em Saúde Avenida Marechal Campos, n. 1468 - Maruípe Vitória - Espírito Santo CEP: 29040-090 E-mail: paulagerszt@hotmail.com

Conflict of interest: non-existent

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