Parkinson Disease
• Parkinson disease (PD) is a common movement disorder that typically affects individuals age 50 to 70 years. Clinical signs and symptoms: This neurodegenerative disease is characterized by bradykinesia, rigidity, postural instability, and resting (pill-rolling) tremor. Additional frequently occurring findings include facial masking, hypophonia, dysphagia, and gait disturbances. Early in the course of the disease, intellectual function is usually preserved, but declines in intellectual function can occur and may be severe over the course of the disease. Cause: Progressive loss of dopamine in the nigrostriatum. As the loss of dopamine occurs, the activity of the 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 dyskinesia, rigidity, postural instability, and tremor that are characteristic of the disease.
• Treatment: Directed at controlling the symptoms. A variety of drugs may be used for mild disease, including the anticholinergic agents trihexyphenidyl, benztropine, and ethopropazine; the irreversible monoamine oxidase (MAO) inhibitors selegiline and rasagiline; and the antiviral drug amantadine. Patients with moderate to severe disease are typically treated pharmacologically with dopaminergic agents, either levodopa (a precursor of dopamine) or a dopamine-receptor agonist. Levodopa 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. This includes catechol methyltransferase (COMT) inhibitors such as Stalevo and Tolcapone. Dopamine-receptor agonists include both ergot (bromocriptine, cabergoline, lisuride, and apomorphine) and nonergot derivatives (pramipexole and ropinirole). The surgical treatment of PD includes both ablative procedures (thalamotomy and pallidotomy) and electrical stimulation of the ventral intermediate nucleus of the thalamus, the globus pallidus internus, or the subthalamic nucleus.
• Anesthetic management: Medication for PD should be continued perioperatively, including the morning of surgery, because 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 exacerbation of symptoms. Diphenhydramine is particularly valuable 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. Cardiac irritability readily produces arrhythmias, so halothane, ketamine, and local anesthetic solutions containing epinephrine should be used cautiously. Although the response to NMBAs is generally normal, a rare occurrence of hyperkalemia after succinylcholine use has been reported. Adequacy of ventilation and airway reflexes should be carefully assessed before extubation of patients with moderate to severe disease.
• For patients undergoing surgical intervention (i.e., brain stimulator) for treatment of PD, general anesthesia can alter the threshold for stimulation, and correct placement of the electrodes can be affected. An awake craniotomy has been the norm for epilepsy surgery for some time, and, increasingly, it is being used for deep brain stimulation procedures as well. Two techniques are advocated—a true awake craniotomy with heavy sedation and an approach in which the patient receives a general anesthetic, usually total IV anesthesia (TIVA) with propofol and remifentanil, and a laryngeal mask airway for control of the airway. After appropriate surgical exposure, the IV infusions are discontinued, and the laryngeal mask airway is removed. The patient can be reanesthetized after the implantation of leads is complete.
Alzheimer Disease
Alzheimer disease (AD) is the most common neurodegenerative disease, representing 40% to 80% of all cases of dementia. It has a 20% prevalence in patients older than age 80 years.
• Characteristics: Slow decline in intellectual function (dementia); progressive memory impairment; decision-making impairments; emotional lability; extrapyramidal signs, including apraxia and aphasia
• Pathology: Neurofibrillary tangles that contain tau and neuritic protein plaques composed of the peptide β-amyloid
• Imaging: Marked cortical atrophy with ventricular enlargement
Anesthetic Management
• Often complicated by disorientation and uncooperativeness
• Postoperative cognitive impairment is a frequent observation, persisting for 1 to 3 days after surgery.
• Consent must be obtained from the next of kin or a legal guardian if the patient is legally incompetent.
• Because the use of centrally acting drugs must be minimized, premedication is usually not given.
• Centrally acting anticholinergics, such as atropine and scopolamine, could theoretically contribute to postoperative confusion. Glycopyrrolate, which does not cross the blood–brain barrier, may be the preferred agent when an anticholinergic is required.
Anesthetic agents are increasingly associated in laboratory studies with neuron injury and death. The implications of general anesthesia delivery both in the elderly as well as small children is currently subject of much investigation and debate. Consequently, anesthetic use may worsen dementia in the patients with AD; however, investigations are ongoing.
Multiple Sclerosis
Multiple sclerosis (MS) is characterized by reversible demyelination at random and multiple sites in the brain and spinal cord.
• Autoimmune disorder initiated by a viral infection. It primarily affects patients between 20 and 40 years of age with a 2:1 female predominance. With time, remissions become less complete, and the disease is progressive and incapacitating.
• Clinical manifestations frequently include sensory disturbances (paresthesias), visual problems (optic neuritis and diplopia), and motor weakness. Early diagnosis confirmed by analysis of cerebrospinal fluid (CSF) and magnetic resonance imaging. Treatment primarily symptomatic or slowing the disease process. Systemic effects of these therapies on coagulation, immunologic, and cardiac function should be reviewed preoperatively.
Anesthetic Management
• Avoid elective surgery during relapse. Preoperative consent should discuss counseling of the patient to the effect that the stress of surgery and anesthesia might worsen the symptoms. Avoid spinal anesthesia as reports allude to exacerbations of the disease. Peripheral nerve blocks are less of a concern because MS is a disease of the central nervous system. Epidural and other regional techniques appear to have no adverse effect.
• In the setting of paresis or paralysis, succinylcholine should be avoided because of hyperkalemia. Regardless of the anesthetic technique used, increases in body temperatures should be avoided. Demyelinated fibers are extremely sensitive to increases in temperature; an increase of as little as 0.5°C may completely block conduction.
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