SECTION II. Central Nervous System
A Alzheimer’s Disease/Dementia
DEFINITION
Dementia is the clinical syndrome characterized by acquired persistent impairment of cognitive and emotional abilities severe enough to interfere with daily functioning and quality of life.
Alzheimer’s disease is a progressive and ultimately fatal disorder in which certain types of nerve cells in particular areas of the brain degenerate and die for unknown reasons. Vulnerable brain regions include the amygdala as well as the hippocampus and areas around the hippocampus, and affected cell populations include cortical pathways involved in catecholaminergic, seritonergic, and cholinergic transmission. Advancing pathology is believed to underlie the classic clinical presentation of memory deficits followed by gradual erosion of judgment, reasoning ability, verbal fluency, and other cognitive skills.
INCIDENCE AND PREVALENCE
Dementia occurs primarily late in life, the prevalence being about 1% at age 60 years, and it doubles every 5 years, reaching 30% to 50% by 85 years of age. Alzheimer’s disease is the most common of the progressive cortical dementias, accounting for about 70% of the dementias in persons older than 55 years of age.
ETIOLOGY
A specific cause or pathologic process is not identified for dementia. The two “hallmark” Alzheimer lesions observable at autopsy are amyloid plaques and neurofibrillary tangles. Plaques are extracellular deposits of abnormally processed amyloid precursor protein, and tangles are intracellular accumulations of the cytoskeletal protein tau.
Development of plaques and tangles may represent a fairly late stage in the disease process that may or may not reflect the fundamental biochemical disruptions at work in Alzheimer’s. Although the “amyloid hypothesis,” which assigns a central causative role to abnormal amyloid processing, remains the most widely embraced theory, other active areas of research include tau, inflammation, disruptions of cell-signaling pathways, and cardiovascular risk factors.
LABORATORY RESULTS
No specific laboratory test exists for the disease. Assess for alterations in values normally associated with the elderly population or those for specific coexisting disease states.
CLINICAL MANIFESTATIONS
Multiple diseases are representative of the disorder. Cortical dementias include Alzheimer’s disease, Pick’s disease, and frontal lobe degeneration. Subcortical dementias are associated with Parkinson’s disease, Huntington’s disease, and Creutzfeldt-Jakob disease. Dementia is associated with intellectual, language, memory, and judgment impairment.
Alzheimer’s disease is the most common cortical dementia and is characterized by progressive memory loss, predominantly loss of short-term memory. Language impairment manifests as difficulty in finding words for spontaneous speech. Performance of daily tasks such as meal preparation and personal hygiene becomes impaired. In addition, symptoms of mental depression and anxiety may be prominent.
Diagnosis is probable when associated with an insidious onset, progressive worsening of memory, and a normal level of consciousness. Computed tomography often displays ventricular dilation and marked cortical atrophy. A definitive diagnosis can be made only after examination of brain tissue demonstrating amyloid and fibrillar protein aggregates.
TREATMENT
No proven preventive therapies for dementia or Alzheimer’s disease are known. Drug therapy is consistently effective for prevention of progression of the disease. Symptomatic therapy is helpful during the early stages, especially if mental depression is prominent.
Key elements of disease management include timely diagnosis and effective use of available therapies to manage cognitive and behavioral symptoms. Other important considerations include identifying comorbid conditions and monitoring individuals for adequate nutrition, hydration, and pain management as well as signs of abuse.
Drugs currently approved specifically to treat Alzheimer symptoms all act chiefly by inhibiting acetylcholinesterase, the main enzyme that breaks down acetylcholine. Drugs with anticholinergic effects are avoided when treating mental depression. Anticholinesterase drugs such as tacrine or donepezil appear to have beneficial effects for some patients early in the disease.
ANESTHETIC CONSIDERATIONS
Management of this disease state is influenced by the pathophysiology of Alzheimer’s disease. Preoperative challenges are related to dealing with patients who are unable to comprehend their environment. Sedatives should rarely be administered, because mental confusion could result. Centrally acting anticholinergic drugs are also not recommended for inclusion in preoperative medication. Maintenance of anesthesia can be acceptably achieved with standard inhalation and intravenous agents.
PROGNOSIS
The course of the disease is one of progressive decline, and the median survival after the onset of dementia is 3.3 years.
B Autonomic Hyperreflexia/Dysautonomia
DEFINITION
Autonomic dysreflexia (or autonomic hyperreflexia) is a disorder that appears after resolution of spinal shock.
INCIDENCE AND PREVALENCE
The incidence and prevalence depend on the level of spinal cord transection. About 85% of patients with spinal cord transection above T5 may exhibit this syndrome. Autonomic dysreflexia is unlikely to be associated with spinal cord transection below T10. The stimulation of a surgical procedure, however, is a potent trigger of autonomic dysreflexia, even in patients with no previous history of this response.
ETIOLOGY
Autonomic dysreflexia can be initiated by cutaneous or visceral stimulation below the level of spinal cord transection. Distention of a hollow viscus (bladder or rectum) is a common stimulus. This stimulus initiates afferent impulses that enter the spinal cord below that level. These impulses elicit reflex sympathetic activity over the splanchnic outflow tract. This outflow is isolated from inhibitory impulses such that generalized vasoconstriction persists below the level of injury. Vasoconstriction results in increased blood pressure, which is then perceived by the carotid sinus. Subsequent activation of the carotid sinus results in decreased efferent outflow from the sympathetic nervous system. Activity from the central nervous system is manifested as a predominance of parasympathetic nervous system activity at the heart and peripheral vasculature. This predominance cannot be produced below the level of spinal cord transection (this part of the body remains neurologically isolated). Therefore, vasoconstriction persists below the level of spinal cord transection. If spinal cord transection is above the level of splanchnic outflow (T4 to T6), vasodilation in the neurologically intact portion of the body is insufficient to offset the effects of vasoconstriction (reflected by persistent hypertension).
LABORATORY RESULTS
No tests are available.
CLINICAL MANIFESTATIONS
The hallmark symptoms of autonomic dysreflexia are paroxysmal hypertension, bradycardia, and cardiac dysrhythmias in response to stimuli below the level of transection (such as bladder catheterization). Hypertension persists because vasodilation cannot occur below the level of injury. Hyperreflexia is not observed until the spinal shock phase has passed. It is therefore usually seen when patients return to surgery for such procedures as cystoscopies, which are performed later in their recovery phase. The condition is caused by stimulation below the level of the lesion. It is typically caused by distention of the bladder or rectum that can be caused by bladder distention, defecation, childbirth, and even cutaneous stimulation. Nasal stuffiness reflects vasodilation. Other symptoms may include headache, blurred vision (from hypertension), increased operative blood loss, loss of consciousness, seizures, cardiac arrhythmias, and pulmonary edema.
TREATMENT
Treatment includes ganglionic blockers (trimetaphan, pentolinium), α-adrenergic antagonists (phentolamine, phenoxybenzamine), and direct-acting vasodilators (nitroprusside). General or regional anesthesia can be used. Drugs that lower blood pressure by central action alone are not predictably effective.
ANESTHETIC CONSIDERATIONS
Prevention of autonomic hyperreflexia is key in the treatment of autonomic dysreflexia. It can occur intraoperatively with local, spinal, and nitrous oxide–opioid general anesthesia. If autonomic hyperreflexia occurs, it is treated by removal of the stimulus, deepening anesthesia, and administration of direct-acting vasodilators. If left untreated, the hypertension crisis may progress to seizures, intracranial hemorrhage, or myocardial infarction. No episodes have been reported with the use of potent inhalation anesthetics. Bradycardia is treated with atropine or glycopyrrolate. Have nitroprusside and other cardioactive agents readily available to treat precipitous hypertension.
C Cerebrovascular Disease
DEFINITION
Cerebral vascular disorders are characterized by sudden neurologic deficits resulting from ischemia or hemorrhagic events. Cerebrovascular disease is any of a group of disorders that affects the vasculature of the brain, the primary disorder being cerebrovascular accident (CVA or “stroke”) as a result of hemorrhage and ischemia.
INCIDENCE AND PREVALENCE
Cerebrovascular disease is the third leading cause of death and the leading cause of disability in the United States. Women have lower stroke rates than men.
ETIOLOGY
The major risk factors for the development of cerebrovascular disease are hypertension and diabetes. Other risk factors include atherosclerosis, inflammatory processes, dissecting aneurysm, disorders affecting the myocardium, congestive heart failure, polycythemia, cigarette smoking, use of oral contraceptives, and postpartum infection. The different manifestations of cerebrovascular disease can be classified as
• Transient ischemic attack (TIA): A temporary, focal episode of neurologic dysfunction that develops suddenly and lasts a few minutes to hours, but usually not more than 24 hours. Approximately 41% of these patients may eventually suffer a stroke.
• Reversible ischemic neurologic deficit (RIND): Neurologic symptoms that persist up to 6 to 8 weeks before resolving.
• Progressive stroke: A stroke in progress. Neurologic symptoms and deficits develop slowly and are not reversible.
• Complete stroke: Neurologic deficits are permanent.
• Amaurosis fugax: A sudden, temporary, or fleeting blindness caused by a decrease in cerebral perfusion to the retina.
DIAGNOSTIC AND LABORATORY FINDINGS
Computed tomography, magnetic resonance imaging, cerebral angiography, and clinical examination are useful.
CLINICAL MANIFESTATIONS
Clinical manifestations involve numerous neurologic deficits. See the classification of symptoms in the section on etiology.
TREATMENT
Treatment includes risk-factor reduction (i.e., controlling hypertension, avoiding a high-fat diet, smoking cessation, and decreasing obesity).
ANESTHETIC CONSIDERATIONS
Preoperative evaluation should include a careful analysis of cardiovascular, neurologic, and pulmonary systems, as well as laboratory results and current medications. As expected, patients with cerebral vascular occlusive disease often have peripheral, renal, and cardiac occlusive disease as well. If the patient is scheduled for carotid endarterectomy, consider the benefits and risks associated with regional versus general anesthesia. Selection of anesthetic agents is based on the patient’s need and the surgeon’s desires. The goal is to ensure a smooth induction, maintenance, and emergence, with avoidance of wide swings in blood pressure. Moreover, an awake, extubated patient is the desired outcome so that immediate neurologic assessment can be performed. Cardioactive agents such as sodium nitroprusside, nitroglycerin, and phenylephrine (Neo-Synephrine) should be readily available.
D Hydrocephalus
DEFINITION
Hydrocephalus is an abnormal accumulation of cerebrospinal fluid (CSF) resulting either from an excessive production or from decreased absorption that leads to an increase in pressure in the ventricles of the brain. The rise in intraventricular pressure causes adjacent brain tissue compression and progressive enlargement of the cranium.
INCIDENCE AND PREVALENCE
Hydrocephalus in newborns occurs in 3 of every 1000 births and is usually secondary to meningomyelocele. Hydrocephalus is common after subarachnoid hemorrhage because of impaired CSF circulation through the basal cistern. It is often a complication of a ruptured brain aneurysm. Hydrocephalus may occur in neonates as a result of obstruction of CSF circulation within the brain’s ventricular system or at a site of reabsorption.
ETIOLOGY
Hydrocephalus can be divided into two main types: obstructive and nonobstructive. Obstructive hydrocephalus results from congenital malformation, scar tissue, fibrin deposits following intraventricular hemorrhage or infection, tumors, or cysts. There are three types of obstructive hydrocephalus: obstructive, communicating obstructive, and noncommunicating obstructive.
• Obstructive: This results from obstruction to CSF flow; depending on the site, it can be further divided into communicating or noncommunicating.
• Communicating obstructive (extraventricular hydrocephalus): This results from obstruction to CSF absorption by the arachnoid villi, usually from remote inflammatory disease or traumatic subarachnoid hemorrhage.
• Noncommunicating obstructive (extraventricular hydrocephalus): This is secondary to obstruction to CSF flow between the lateral and fourth ventricles (the ventricles dilate proximal but not distal to the obstruction).
Nonobstructive hydrocephalus results from excessive CSF production by the choroid plexus. Choroid plexus papillomas or benign tumors of the glomus of the lateral ventricles are common causes.
DIAGNOSTIC AND LABORATORY FINDINGS
Hydrocephalus can be diagnosed by computed tomography, by magnetic resonance imaging, and by signs of increased intracranial pressure.
CLINICAL MANIFESTATIONS
• Early signs and symptoms: Apnea, bradycardia, nausea and vomiting, increasing head circumference, headaches (most common), mentation changes, nystagmus, and decreased reflexes are noted.
• Late signs and symptoms: Bulging fontanelle, pupillary areflexia, nuchal rigidity, “setting sun” eyes, palsy of cranial nerve VI, limb spasticity, decreased level of consciousness leading to nonresponsiveness, widened pulse pressure, altered heart rate, visual changes, and hypertension are noted.
ANESTHETIC CONSIDERATIONS
With hydrocephalus, intracranial pressure is elevated. Hypoventilation, hypoxia, and hypertension are to be avoided. Baseline neurologic status must be established, and minimal to no premedication must be administered. Intravenous induction should be rapid and smooth with cricoid pressure. Once the airway is secure, hyperventilate the patient until ventricles are decompressed. The patient is maintained on nitrous oxide/oxygen and increments of thiopental if needed until intracranial pressure is reduced, and then an inhalation agent or opioid can be added. Sudden removal of large CSF volumes may lead to bradycardia and hypotension that can be prevented by rapid replacement with saline and/or gradual removal of CSF. Although heat is lost by surgical exposure, some degree of hypothermia may be appropriate in these patients. Narcotics are given in small amounts (or not given at all) to enable rapid neurologic assessment on awakening from anesthesia.
TREATMENT
A bypass shunt is inserted to allow CSF to flow from the lateral ventricles to the peritoneal cavity (ventriculoperitoneal shunt). This type of shunt is preferable because of the lower incidence of complications and need for revision with growth. Ventriculoatrial and ventriculopleural shunts are less popular because of the risk of infection, microemboli, and hydrothorax. The lumboperitoneal shunt (between the lumbar subarachnoid space and the peritoneal space) may be used.
E Intracranial Hypertension
DEFINITION AND ETIOLOGY
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