Parkinson disease (PD) is a common movement disorder that typically afflicts individuals aged 50–70 years; it has a prevalence of 3% in the United States and Canada. This neurodegenera-tive disease is characterized by bradykinesia, rigid-ity, postural instability, and resting (pill-rolling) tremor. Additional frequently occurring findings include facial masking, hypophonia, dysphagia, and gait disturbances. Increasing problems with freezing, rigidity, and tremor eventually result in physical incapacitation. Early in the course of the disease, intellectual function is usually preserved, but declines in intellectual function may be severe as the disease progresses. PD is caused by a pro-gressive loss of dopamine in the nigrostriatum. The severity of loss of dopamine correlates with the severity of bradykinesia. Concurrent with the loss of dopamine, the activity of the gamma-aminobutyric acid (GABA) nuclei in the basal ganglia increases, leading to an inhibition of thalamic and brainstem nuclei. Thalamic inhibition, in turn, suppresses the motor system in the cortex, resulting in the charac-teristic signs and symptoms.
Medical treatment is directed at controlling the symptoms. A variety of drugs may be used for mild disease, including the anticholinergic agents trihexyphenidyl, benztropine, and ethopropa-zine; the irreversible monoamine oxidase (MAO) inhibitors selegiline and rasagiline; and the anti-viral drug, amantadine. Moderate to severe dis-ease is typically treated pharmacologically with dopaminergic agents, either levodopa (a precur-sor of dopamine) or a dopamine-receptor agonist. Levodopa, which is given with a decarboxylase inhibitor to retard the peripheral breakdown of the drug (thereby increasing its central delivery and decreasing the dose of levodopa that is required to control symptoms), is the most effective therapy and is used to treat moderate to severe symptoms. Catechol methyltransferase inhibitors are also used to prevent the decarboxylation of levodopa. Levodopa is available in either an immediate or sustained-release formulation, with durations of action of 2–4 hr and 3–6 hr, respectively. Side effects include nausea, vomiting, dyskinesias, sud-den sleepiness, cardiac irritability, and orthostatic hypotension. Dopamine receptor agonists include both ergot derivatives (bromocriptine, cabergoline, lisuride, and apomorphine) and nonergot deriva-tives (pramipexole and ropinirole). The nonergot derivatives have been shown to be beneficial when used as monotherapy in early PD; all dopamine receptor agonists are effective when given as com-bination therapy with levodopa in the treatment of moderate to severe PD. Side effects are similar to those found with the use of levodopa alone, and, in addition, include headache, confusion, and hallu-cinations. Pulmonary and retroperitoneal fibrosis, pleural effusion and thickening, Raynaud syn-drome, and erythromyalgia are more common side effects with the use of ergot derivatives than with nonergot derivatives.The surgical treatment of PD includes both ablative procedures (thalamotomy and pallidot-omy), as well as electrical stimulation of the ventral intermediate nucleus of the thalamus, the glo-bus pallidus internus, or the subthalamic nucleus. Pallidotomy is effective for treating the dyskinesia (70% to 90%), as well as the tremor, rigidity, brady-kinesia, and gait symptoms (30% to 50%) of the dis-order. Thalamotomy is most effective in treating the contralateral tremor, but not for the other symp-toms of the disease, and has been largely replaced by the use of thalamic stimulation. The efficacy of deep brain stimulation of the thalamus is related to the effect on tremor; it has little to no effect on the other symptoms of PD. Subthalamic stimula-tion improves all of the primary symptoms of PD and decreases the amount of medication necessary for symptom relief. Bilateral stimulation has greater efficacy than unilateral stimulation. Some decrease in cognitive function may occur with this treat-ment, and, therefore, it should be used with caution in patients with cognitive impairment. The effects of globus pallidus internus stimulation are simi-lar to those of pallidotomy with improvements in dyskinesia.
Medications for PD should be continued periopera-tively, including the morning of surgery. The half-life of levodopa is short. Abrupt withdrawal of levodopa can cause worsening of muscle rigidity and may interfere with ventilation. Phenothiazines, butyrophenones (droperidol), and metoclopramide can exacerbate symptoms as a consequence of their antidopaminergic activity and should be avoided. Anticholinergics (atropine) or antihistamines (diphenhydramine) may be used for acute exacerba-tion of symptoms. Diphenhydramine may be used for premedication and intraoperative sedation in patients with tremor. Induction of anesthesia in patients receiving long-term levodopa therapy may result in either marked hypotension or hypertension. Relative hypovolemia, catecholamine depletion, autonomic instability, and sensitization to catecholamines are probably contributory. Arterial blood pressure should be monitored carefully. Hypotension should be treated with small doses of a direct-acting vasopressor, such as phenylephrine, rather than ephedrine. The response to NMBs is generally normal, however, hyperkalemia may rarely follow succinylcholine. As mentioned previously, patients who fail medical treatment are candidates for surgical intervention—for example, an ablative therapy, such as a thalamotomy or pallidotomy or implantation of a deep brain stimulator of the sub-thalamic nucleus, the ventral intermediate nucleus, or the globus pallidus internus. Because general anesthesia alters the threshold for stimulation, correct placement of the electrodes can be affected. Awake craniotomy has been the norm for epilepsy surgery, and is being used increasingly for deep brain stimulation procedures. Two techniques are advocated—a true awake craniotomy with heavy sedation (dexmedetomidine is often used) and an approach in which the patient receives a general anesthetic, usually a total intravenous anesthetic with propofol and remifentanil and a laryngeal mask airway for control of the airway. Following appropri-ate surgical exposure, the intravenous infusions are discontinued, and the laryngeal mask airway is removed. The patient can be reanesthetized once the implantation of leads is complete.
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