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REVIEW ARTICLE
Year : 2007  |  Volume : 51  |  Issue : 5  |  Page : 382 Table of Contents     

Parkinson's Disease and Anaesthesia


1 MD, FAMS, Hony.Consultant Anaesthetist, Apollo Gleneagles Hospital, Kolkata., India
2 MD, Specialist Registrar, Norfolk and Norwich University Hospital, Norwich, United Kingdom
3 MD, Assistant Professor of Anaesthesia, Medical College & Hospital, Kolkata, India
4 MD, Consultant Anaesthesiologist, Apollo Gleneagles Hospital, Kolkata, India
5 MD, MNAMS, Prof. & HOD of Anaesthesia, Midnapur Medical College, Midnapur, India
6 MD, Registrar of Anaesthesia, Apollo Gleneagles Hospital, Kolkata, India

Date of Acceptance15-Aug-2007
Date of Web Publication20-Mar-2010

Correspondence Address:
A Rudra
1, Shibnarayan Das Lane, Kolkata - 700006
India
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Source of Support: None, Conflict of Interest: None


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Parkinson's disease is a debilitating neurodegenerative disorder due to death of dopaminergic neurons of the substantia nigra that leads to resting tremor, muscle rigidity, and bradykinesia. Parkinson's disease is a common disease of elderly patients who present a particular anaesthetic challenge. Good number of patients are newly diagnosed at the time of preanaesthetic examinations. Variety of drugs may be used for symptomatic treatment. Controversies surrounding the use of the newer drugs and possible advances in neurosurgical interventions are discussed. Particular anaesthetic problems in Parkinson's disease include respiratory, cardiovascular, and neurological. Potential drug interactions are described and recommendations are made about suitable anaesthetic technique.

Keywords: Anaesthesia; Complications; Parkinson′s disease


How to cite this article:
Rudra A, Rudra P, Chatterjee S, Das T, Ray M, Kumar P. Parkinson's Disease and Anaesthesia. Indian J Anaesth 2007;51:382

How to cite this URL:
Rudra A, Rudra P, Chatterjee S, Das T, Ray M, Kumar P. Parkinson's Disease and Anaesthesia. Indian J Anaesth [serial online] 2007 [cited 2019 Sep 20];51:382. Available from: http://www.ijaweb.org/text.asp?2007/51/5/382/61167


   Introduction Top


Parkinson's disease is the most common example of a family of neurodegenerative disorders that may or may not be caused by virus. The disease is defined as a paucity and slowness of movement (bradykinesia), tremor at rest, rigidity, shuffling gait and flexed posture. Parkinson's disease is a relatively common disorder that occurs in all ethnic group with an approximate equal sex distribution [1] . Sporadic and idiopathic Parkinson's disease account for nearly 75% of all cases of  Parkinsonism More Details; the remaining 25% result from genetically defined aetiologies and other causes including other neurodegenerative disorders, cerebrovascular disease, and drugs [2] .

Parkinson's disease is an important cause of perioperative morbidity and, with an increasingly elderly population, it will be encountered with greater frequency in surgical patients. As many as 24% of subjects of Parkinson's disease were newly diagnosed at the time of preanaesthetic examinations. This highlights the diffi­culty of diagnosis and emphasizes that many elderly hos­pital patients may have undiagnosed Parkinson's disease [3] . Drugs used in anaesthesia may interact with anti-Par­kinsonian medication and there is controversy about the optimal anaesthetic management of patients with Parkinson's disease.

This review article explores the epidemiology, aeti­ology, pathogenesis, pathophysiology and the clinical fea­tures of Parkinson's disease. Potential drug interactions are described and recommendations are also made about suitable anaesthetic techniques.


   History Top


Parkinson's disease has been known since biblical times, but it was only in the nineteenth century that the syndrome was formally described by James Parkinson and termed 'the shaking palsy' [4] . In 1879, Charcot noted additional features including autonomic dysfunction [5] . The association between the substantia nigra and Parkinson's disease was discovered in 1893 but it was only in the latter half of the twentieth century that the neuropatho­logical and neurochemical characteristics of the disease were elucidated and logical strategies were devised [6],[7],[8],[9].


   Epidemiology Top


In India, recently a change has been observed in demographic profile towards a growing aging popula­tion. The community based prevalence studies from In­dia have documented crude prevalence rates of Parkinson's disease from 7 to 328 per 100,000 in overall population above the age of 50 years [10],[11],[12],[13] . This differ­ence in prevalence rates is largely due to marked differ­ences in methodology and age structure of study popu­lation. Age and sex specific prevalence in India, showed progressive increase in rate along with aging in both gen­ders after fourth decade, but peak rate was observed in eighth decade among women and beyond eighth decade among men. Sex adjusted prevalence showed that the disorder was commoner among women [10] .

The EUROPARKINSON study found an overall prevalence of 1.6% for Parkinson's disease in a survey of 14,636 participants aged over 65 years in five Euro­pean countries [14] . The highest reported incidence is among whites.

Parkinson's disease affects more than 1 million in­dividuals in the United States (nearly 1% of those more than 55 years). Its peak age of onset is in the 60s (range is 35 to 85 years) and the course of illness ranges be­tween 10 and 25 years [2].


   Risk factors Top
[1],[2]

Include a positive family history, male gender, head injury, exposure to pesticides, consumption of well wa­ter, and rural living. Factors linked to a reduced inci­dence of Parkinson's disease include coffee drinking, smoking, use of nonsteroidal anti-inflammatory drugs, and oestrogen replacement in postmenopausal women.


   Pathogenesis Top


Parkinson's disease is characterized by the pro­gressive death of selected but heterogeneous popula­tions of neurons, including those dopaminergic neurons of the pars compacta of the substantia nigra. The pre­cise mechanisms responsible for cell death are largely unknown and may be due to mitochondrial dysfunction, oxidative stress, the actions of excitations with excess nitric oxide formation, deficient neurotrophic support, or immune mechanisms [15] . Although, still controversial, the final common pathway appears to be the induction of apoptosis in nigral dopaminergic neurons [16],[17] .


   Pathophysiology Top
[18],[19],[20]

The basal ganglia refers to the areas of basal fore­brain and midbrain known to be involved in the control of movement. They include the striatum, mainly comprising the caudate and putamen, the globus pallidus, the subthalamicnucleus and the main pigmented component of the substantia nigra known as the pars compacta. The clinically important motor circuit originates in the sen­sorimotor cortex and terminates in the supplementary motor areas. There is a one station direct pathway via the internal part of the pallidum and three station indirect pathway via the external globus pallidus, the subthalamic nucleus and the internal globus pallidus. Hence, the in­ternal globus pallidus is common to both pathways. The nigrostriatal pathway projects from the substantia nigra pars compacta to the striatum. Cholinergic internuncial neurons are excitatory to projection neurons and are in­hibited by dopamine. In Parkinson's disease, acetylcho­line is present in normal amounts in the striatum. How­ever, dopamine deficiency produces imbalance in the dopamine: acetylcholine ratio, thereby aggravating the symptoms of Parkinson's disease.

Parkinson's disease is characterized by a loss of dopaminergic neurons in the substantia nigra of the basal ganglia. This dopamine deficient state is associated with increased activity of inhibitory nuclei in the basal ganglia [using the neurotransmitter gamma-aminobutyric acid (GABA)], eventually leading to excessive inhibition, and effectively to a shutdown, of the thalamic and brainstem nuclei that receive the outflow from the basal ganglia. Excessive thalamic inhibition results in suppression of the cortical motor system with akinesia, rigidity, and tremor, while inhibition of brainstem locomotor areas may contribute to abnormalities of posture and gait.


   Clinical features and diagnosis Top


The clinical effects of Parkinson's disease are caused by dopamine deficiency. Dopamine deficiency increases activity of gamma - aminobutyric acid (GABA). GABA inhibits thalamic and brainstem nuclei, which supress cortical motor activity, thereby causing tremor, akinesia, and gait and posture abnormalities. The most characteristic clinical features of Parkinson's disease are resting tremors. Tremors are characterized as rhythmic alternating flexion and extension of the thumbs and other digits at a rate of four to five movements per second ("Pill-rolling tremor"). The other clinical features include, cogwheel rigidity of the extremities, bradykine­sia, shuffling gait, stooped posture, and facial immobility. The earliest manifestations may be loss of associated arm swings when walking and absence of head rotation when turning the body. These features are all second­ary to diminished inhibition of the extra pyramidal motor system as a result of depletion of dopamine from the basal ganglia. Other features that occur in patients with Parkinson's disease are seborrhea, sialorrhea, orthos­tatic hypotension, bladder dysfunction, dementia, and mental depression.

There is no specific test to confirm Parkinson's disease; the diagnosis is made mainly on clinical grounds. Magnetic resonance imaging of the brain is usually nor­mal in Parkinson's disease but may be useful in demon­strating cerebrovascular disease or widespread brainstem atrophy in other neurodegenerative disorders [21] . Auto­nomic dysfunction is common in Parkinson's disorders. Sphincter electromyography, reflecting degeneration of Onuf's nucleus has been shown to be a useful test to distinguish Parkinson's disease from multiple system atrophy [22] .


   Treatment of Parkinson's disease Top


A. Drug therapy

Drug therapy is not required early in the course of Parkinsonism. Therapy is directed at (a) increasing the neuronal release of dopamine or the receptor's response to dopamine, (b) stimulating the receptor directly with bromocriptine and largotrile, (c) implanting dopaminergic tissue, or (d) decreasing cholinergic activity. The cru­cial factor is to educate the patient about the disease and how the drugs are likely to affect them. With guid­ance, patients can usually adapt a regimen to suit their particular lifestyle. The result may be that they take drugs at apparently peculiar times. A common scenario is that a patient's finely tuned drug regimen is thrown into dis­array on admission to hospital when the drug timings are forced into the available boxes on the drug card. It is very important to record the exact times when a patient's drugs are due, and to try to reproduce these as far as practicable in hospital [18] .

Levodopa is the single most effective therapy for patients with Parkinson's disease and early treatment with this drug prolongs life [23],[24] . When administered orally, how­ever, levodopa is converted to dopamine and causes side effects such as nausea, vomiting, myocardial irritability, decreased intravascular volume and orthostatic hypoten­sion due to suppression of the renin-angiotensin axis, con­fusion, psychiatric symptoms and depression, and the clas­sic "on-off" phenomenon seen with rapid shifts from mo­bility to immobility and involuntary movements. To avoid such side effects, levodopa is administered in combination with a carboxylase inhibitor (carbidopa). Sinemet, a com­mercially available preparation that contains carbidopa and levodopa in a fixed ratio (1:10 or 1:4) is generally used. Sinemet CR is a controlled - release formulation (con­taining 25 or 50 mg of carbidopa and 100 or 200 mg of levodopa). It should not be given to patients taking monoamine oxidase A inhibitors.

In an effort to delay the use of levodopa, other drugs such as selegiline (5 mg with breakfast and 5 mg with lunch) as adjunctive treatment in patients receiving levodopa, dopamine agonists [bromocriptine (1.25 mg twice daily) [25] and pergolide(0.05 mg daily) [26] ], Catechol-­O-methyl transferase (COMT) inhibitors, which inhibit the breakdown of dopamine in the periphery and in­creases its bioavailability [tolcapon (100to 200 mg twice daily) [27] , entacapon (200 mg with each dose of sinemet) [27] ], and apomorphine have been used as initial treatment [27] . Apomorphine is a short acting dopamine agonist that is administered subcutaneously, or sometimes sublingually or intranasally. Anticholinergic drugs [trihexyphenidryl (6-20 mg daily) [1] , benztropine mesylate (1-6 mg daily) [1] ] are effective. Amantadine (100 mg twice daily) [1] may be useful in patients with mild symptoms and no disabil­ity. Amantadine may exert a neuroprotective effect on neurons in the basal ganglia.

B. Surgical therapy

Stereotactic lesions in the globus pallid shave been tried to alleviate the tremors and rigidity. Awake func­tional neurosurgery in patients with severe Parkinson's disease involves implantation of bilateral subthalamic nucleus (STN) neuromodulation stimulators. Adrenal medullary grafts and more recently, stem cell transplant [28] have shown progress in animal models of Parkinson's disease [29],[30] .


   Anaesthetic considerations Top


Apart from a routine history, physical examination, and preoperative testing, patients with Parkinson's dis­ease require additional assessment [Table 1].


   Respiratory system Top


Respiratory complications particularly aspiration pneumonia is the most common cause of death in the patients of Parkinson's disease [31],[32] . An obstructive ven­tilatory pattern has been observed in up to one-third of patients with Parkinson's disease [33],[34] . Furthermore, up­per airway dysfunction is an important factor in the re­tained secretions, atelectasis, aspiration, and respiratory infection, which are frequently seen in patients with Parkinson's disease. Other potential complications in­clude postextubation laryngospasm and postoperative respiratory failure [35],[36].


   Autonomic nervous system Top


Changes in various systemic functions, such as gastrointestinal, are common in Parkinson's disease. Moreover, changes may be iatrogenic as a result of the side effects of Parkinson's disease medication. There may be difficulty with salivation, micturition and gas­trointestinal function. Defective control of cardiovascu­lar system and temperature regulation may be present in some of the patients with Parkinson's disease. Presence of seborrhea is also an autonomic manifestation of the disease [37] .


   Cardiovascular system Top


Patients with Parkinson's disease may have cardiac arrhythmias and dependent oedema, however, ortho­static hypotension is the most disabling symptom [38] . Direct acting dopamine agonists (bromocriptine and lisuride) and antidepressant (amitriptyline) may also cause ortho­static hypotension.


   Gastrointestinal function Top


Sialorrhoea (common late manifestation) is prob­ably due to reduced automatic swallowing as a result of poverty of motor movement rather than autonomic dys­function. Levodopa minimizes sialorrhoea. Administra­tion of antimuscarinic drugs increases the viscosity of saliva and further impairs swallowing. Pathogenesis of dysphagia and abnormalities of oesophageal function is unclear. Constipation is a common symptom in Parkinson's disease.


   Anaesthesia in the patient with Parkinson's disease Top


Interruption of anti-Parkinson's drug therapy should be as brief as possible. The half life of levodopa is short (1-3 h) and interruption of therapy can result in severe skeletal muscle rigidity that interferes with ventilation [39] . Patients may self-administer additional dose of levodopa, so it is important to find out exactly how much they are taking [40] . Therefore, therapeutic drugs should be contin­ued through the morning of surgery with sip of water. Intravenous levodopa has been used successfully in perioperative period [41] , but without co-administration of a decarboxylase inhibitor (not yet available in intrave­nous form), cardiovascular side effects such as hyper­tension, hypotension, and dysrrhythmias can be antici­pated [42] . Levodopa and carbidopa are absorbed in the small intestine and thus first traverse the stomach mak­ing administration of tablets through a gastric tube sub­optimal or ineffective because patients with Parkinson's disease often have delayed gastric emptying [43] . As such, a duodenal feeding tube may be necessary when a pro­longed period of normal feeding is expected [44],[45] . Medi­cation that could cause extra pyramidal symptoms, dopam­ine antagonists [e.g. phenothiazines, butyrophenones (droperidol)], and metoclopramide could be withheld [46] . Pulmonary aspiration is a common cause of death among patients with Parkinson's disease. Prokinetic agents such as cisapride or domperidone have no effect on dopamin­ergic balance and are reasonable alternative to metoclopramide.

Autonomic insufficiency can also be a problem. This condition affects the ability of Parkinson's patients to respond to the hypovolaemia and vasodilatation some­times associated with anaesthesia and surgery [47],[48] . Orthostatic hypotension or thermoregulatory or genitourinary dysfunction suggests preexisting autonomic insuf­ficiency and should heighten awareness of the potential for perioperative haemodynamic instability and altered responses to vasopressors such as noradrenaline [49] .

One should be aware of the potential for increased catecholamine - induced tachyarrhythmias with levodopa and halothane. There are no reports of adverse responses to isoflurane, sevoflurane, or desflurane in patients with Parkinson's disease. Ketamine should be used cautiously, if at all, because of potential interactions between levodopa and its sympathomimetic properties. But, ketamine has been used without incident. The likelihood of coexisting heart disease in elderly patients with Parkinson's disease, however, makes the use of ketamine less attractive. However, in a single case report, ketamine temporarily stopped the motor symptoms of the disease [50] . Propofol produces both dyskinesias [51] and ablation of resting tremor [52] , suggesting that it may have both exci­tatory and inhibitory effects in this patient population. Alfentanil and fentanyl have a potential for an exacer­bation of muscle rigidity. Morphine was reported to de­crease dyskinesia in low doses but to increase dyskinesias at a high doses [53] . There have been reports of agitation, muscle rigidity, and hyperthermia in patients receiving pethidine and selegiline. However, clinical experience indicates that anaesthesia is usually uneventful in pa­tients receiving selegiline [39] . [Table 2]

There are no reported cases of non-depolarizing neuromuscular blocking drugs worsening the symptoms of Parkinson's disease. However, controversies exist regarding the use of suxamethonium. It has been re­ported by one investigator that, suxamethonium cause hyperkalaemia in Parkinson's disease [54] . However, an­other group of investigators claimed that suxamethonium does not induce hyperkalaemia [55] . If an anticholinergic agent is required, then glycopyrrolate bromide is the drug of choice in this group of patients, as it does not cross the blood brain barrier [56] . Adequacy of ventilation and airway reflexes should be carefully assessed prior to extubation of patients with moderate to severe disease. Ondansetron, a serotonin antagonist, appears to be a safe alternative to droperidol for prevention or treatment of emesis in these patients. Butyrophenones and phenothi­azines, which block dopamine receptors, exacerbate Parkinson's disease.

Regional anaesthesia has obvious advantages over general anaesthesia as it avoids the effects of general anaesthetics and neuromuscular blocking drugs, which may mask tremor. Moreover, patients can continue to take oral levodopa preoperatively, during surgery, if re­quired, and early in the postoperative period. Under re­gional anaesthesia, it is better, the patients should be awake and special attention should be given to verifica­tion of intact or at least baseline pharyngeal / laryngeal reflexes. If sedation is required, diphenhydramine has been described as useful due to its central anticholin­ergic activity. With regional anaesthesia, postoperative nausea and vomiting, which may prevent resumption of oral intake, is also avoided. However, with regional ana­esthesia positioning the patient may be difficult.

The patient's routine doses should be resumed as soon as possible in the postoperative period to avoid ex­acerbation of symptoms. In patient who are unable to take medications orally or by gastric tube, parenterally administered anticholinergic drugs such as trihexyphenidyl, benztropine, or diphenhydramine can be administered. Involuntary movements of the glottis and supraglottic structures cause intermittent airway obstruc­tion, laryngospasm, and respiratory arrest have been re­ported postoperatively in awake patients hours after sur­gery [18],[56] . Other postoperative care is centered on pul­monary toilet, prevention of thrombosis, early physical therapy and ambulation. These patients during their post­operative period are susceptible to develop mental con­fusion and even hallucinations. Therefore, the patient's caregivers should be advised of this possibility. Clozapine (abenzodiazepine) does not appear to worsen the move­ment disorders of Parkinson's disease and has been used postoperatively to stop levodopa induced hallucinations.

To conclude, there is no simple anaesthetic regi­men for patients with Parkinson's disease. The absence of randomized controlled trials evaluating various anaes­thetic techniques or drugs means that recommendation can only be based on data that have obvious limitations. Therefore, meticulous preoperative assessment, main­tenance of drug therapy up to the time of anaesthesia and afterwards, avoiding known precipitating agents are key factors in the reduction of postoperative morbidity and mortality.

 
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    Tables

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