Central Nervous System Diseases

Multiple sclerosis is characterized by multiple sites of demyelination in the brain and spinal cord, leading to visual disturbances, limb weakness, and paresthesias.
1. Therapy for multiple sclerosis is directed at modulating the immunologic and inflammatory responses that damage the central nervous system (CNS) (corticosteroids, interferon, glatiramer, mitoxantrone [maybe cardiotoxic]).
2. Management of Anesthesia. The effect of anesthesia and surgery on the course of multiple sclerosis is controversial.
  1. Regional and general anesthesia have been reported to exacerbate or have no effect on multiple sclerosis. Factors other than anesthesia, such as infection, emotional stress, and hyperpyrexia, may contribute to an increased risk of perioperative exacerbation.
  2. A neurologic examination before anesthesia and surgery is helpful to document coexisting neurologic deficits.
  3. Patients being treated with corticosteroids may require perioperative supplementation, and immunosuppressants may produce cardiotoxicity and subclinical cardiac dysfunction.
  4. Autonomic dysfunction caused by multiple sclerosis may produce exaggerated hypotensive effects in response to volatile anesthetics.
  5. Respiratory muscle weakness and dysfunction may increase the likelihood of the need for postoperative mechanical ventilation.
Epilepsy (Table 23-6: The Most Frequently Encountered Types of Seizures)
1. The sudden onset of seizures in a young to middle-aged adult should arouse the suspicion of focal brain disease (tumor); onset after 60 years of age is usually secondary to cerebrovascular disease.
2. The availability of new antiseizure drugs has increased the therapeutic options for patients with epilepsy (Table 23-7: Anticonvulsant Drugs). The newer antiseizure drugs target ion channels, γ-aminobutyric acid (GABA) receptors, amino acid receptors, and synaptic proteins.
3. Management of Anesthesia
  1. Antiseizure medications should be maintained throughout the perioperative period.
  2. An anesthetic technique that minimizes the risk of seizure activity should be used. Although most inhaled anesthetics, including nitrous oxide, have been reported to produce seizure activity, such activity during the administration of isoflurane and desflurane is extremely rare. (Sevoflurane may be epileptogenic, but the clinical significance is uncertain.) Ketamine may produce seizure activity in patients with known seizure disorders. Reported seizure activity after administration of opioids may reflect myoclonic activity.
Alzheimer disease is the major cause of dementia in the United States, and more than 5 million people in the United States have the disease. The incidence is 5% in persons older than age 65 years and 30% in those older than age 85 years.
1. Alzheimer disease is characterized by cognitive impairment, poor decision making, language deterioration, gait disturbances, seizures, agitation, and psychosis.
2. A positive diagnosis can, however, only be made at autopsy. Imaging studies show hippocampal atrophy (magnetic resonance imaging [MRI]) and glucose hypometabolism (positron emission tomography).
3. There is no specific therapy for Alzheimer disease, but the initial symptomatic therapy (nausea, bradycardia, syncope, fatigue) is with cholinesterase inhibitors and an N-methyl-D-aspartic acid (NMDA) receptor antagonist.
4. Animal studies have demonstrated that volatile, halogenated anesthetics produce neuronal changes that resemble the diseased neurons of patients with Alzheimer disease (thus, there is controversy about the use of halogenated anesthetics in neonates and elderly patients).
5. Postoperative cognitive dysfunction (POCD) is well known in elderly patients, but the causes remain elusive. Patients and their families should be advised that POCD can occur.
6. Sedative premedication should be used with caution, if at all, because mental confusion may worsen. If an anticholinergic is required, glycopyrrolate, which does not cross the blood–brain barrier, is preferable to atropine or scopolamine.
Parkinson disease is a degenerative disease of the CNS caused by the loss of dopaminergic fibers in the basal ganglia of the brain. It occurs in 1% of population older than age 60 years of age.
1. Typical clinical features are secondary to depletion of dopamine from the basal ganglia (Table 23-8: Clinical Features of Parkinson Disease).
2. Treatment protocols involve combinations of drugs designed to increase dopamine levels in the brain while blunting the peripheral effects of dopamine. The therapeutic regimen for patients with Parkinson's disease is complex and requires a skilled neurologist to individualize therapy.
  1. The combination of levodopa and carbidopa (which blocks peripheral conversion of levodopa to dopamine) is the most frequent treatment.
  2. Side effects of levodopa include depletion of myocardial norepinephrine stores, peripheral vasoconstriction, hypovolemia, and orthostatic hypotension.
  3. Use of surgical pallidotomy (local anesthesia) and implantation of deep brain stimulators may be a good option for selected patients.
3. Management of Anesthesia
  1. Drugs that may antagonize the effects of dopamine in the CNS (droperidol, metoclopramide, and possibly alfentanil) should be avoided.
  2. Levodopa has a brief half-life, and interruption of therapy for more than 6 to 12 hours may result in skeletal muscle rigidity that interferes with ventilation.
  3. Success with the use of selegiline for the treatment of parkinsonism increases the likelihood of having to anesthetize a patient who is receiving a monoamine oxidase-B inhibitor. (Meperidine should be avoided in these patients.)
  4. Autonomic dysfunction is common and manifests as esophageal dysfunction (risk of aspiration) and orthostatic hypotension (exaggerated decreases in blood pressure in response to volatile anesthetics).
  5. After surgery, these patients may develop mental confusion.

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