Neurologic Dysfunction

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Chapter 37 Neurologic Dysfunction

Neurologic problems are among the most common, severe, and disabling complications that occur after cardiac surgery. The reported incidence varies from 0.4% to almost 80%, depending on how the deficit is defined.1 Roach found that perioperative adverse neurologic events occurred in 6.1% of adults after they had undergone coronary artery bypass graft (CABG) surgery. Half (3.1%) were classified as type 1 injury, including focal injury, stupor, and coma. The other half (3.0%), type 2 injury, had deterioration in intellectual function or memory or had seizures.2 Other investigators have found much higher rates of cognitive decline following cardiac surgery3 and, in a proportion of patients, this can be permanent. Stroke is the second most common cause of death following CABG surgery (after low cardiac output), and cardiac surgery is the most common cause of iatrogenic stroke. The direct economic cost of a stroke ranges from $90,000 to $280,000 over a patient’s life span.1. Various perioperative interventions may reduce the risk of brain injury; however, cardiac surgery is now being performed on people of increasing age and with multiple comorbidities, both of these factors increase the likelihood of neurologic complications.

There are three common presentations of acute neurologic dysfunction following cardiac surgery: (1) altered consciousness; (2) weakness; and (3) seizures. In the first section of this chapter, each of these presentations is reviewed. In the second section, a simplified neurologic examination, targeted to the likely pathologies, is described. In the final section, the common causes of neurologic injury are discussed in terms of risk factors, investigations, prevention, and treatment. Cognitive decline, the most common neurologic complication following cardiac surgery, is also discussed in the final section.


Altered Consciousness

The term “altered consciousness” encompasses a range of disorders that extend from an acute confusional state or delirium through coma and brain death. Consciousness can be viewed as a combination of wakefulness and awareness of self and of the environment. Wakefulness requires intact functioning of the ascending reticular activating system (ARAS) and the cerebral cortices. The ARAS extends from the midpons through midbrain and thalamus to the cerebral cortices. Awareness requires multiple functions, such as attention, sensation, perception, memory, motivation, and cognition.4 Multiple descriptive terms (e.g., obtunded, somnolent) are used to describe different levels of altered consciousness. They should be avoided because they are not used consistently, either in the literature or in practice. It is much better to describe consciousness in terms of an objective measure such as the Glasgow Coma Scale (GCS; Table 37-1).5

Table 37-1 Glasgow Coma Scale

Verbal Response Motor Response Eyes
5 = Appropriate 6 = Obeys commands 4 = Open spontaneously
4 = Disorientated 5 = Localizes to pain 3 = Open to command
3 = Unconnected words 4 = Withdraws to pain 2 = Open to pain
2 = Only sounds 3 = Abnormal flexion to pain 1 = No response
1 = Nothing (if extubated) 2 = Abnormal extension to pain  
  1 = No response  

Total = V + M + E = 3-15

From Teasdale G, Jennett B: Assessment of coma and impaired consciousness: a practical scale. Lancet 2: 81-84, 1974.

Depressed Consciousness and Coma

Consciousness is considered to be depressed when excessive sensory stimulation is required for arousal and wakefulness. However, when awake, patients may have normal movements and be able to open their eyes and talk. Depressed consciousness should be described in terms of the level of stimulation required to achieve arousal and whether thought processes appear to be preserved when awake. Comatose patients cannot be roused to consciousness; they are not awake or aware. They do not open their eyes, talk, or move, either spontaneously or on command. In response to painful stimuli, their eyes do not open, vocalization is limited or absent, and movements are reflexive. Coma is due to bilateral cortical dysfunction, lesions in the ARAS, or both. Lesions involving the brain-stem portion of the ARAS are commonly associated with oculomotor and breathing abnormalities.4

In the most common scenario after cardiac surgery, the patient fails to awaken (i.e., is comatose), either early after surgery when anesthesia is discontinued or (in longer term intensive care patients) when sedative and analgesic drugs are stopped.

Altered consciousness (including delirium, depressed consciousness, and coma) is common after cardiac surgery. The reported incidence varies from 8.4% to 32%, according to whether studies were prospective and whether structured interviews were used.7 Patients who do experience altered consciousness have significantly worse outcomes than do those who do not. The average length of stay in the hospital is almost double (14 days versus 8 days), and mortality rates triple.7 The most common causes of altered consciousness following cardiac surgery are stroke, microembolic injury, metabolic encephalopathy, and hypoxic ischemic encephalopathy; they are discussed subsequently.


The most common presentation of weakness early after cardiac surgery is hemiplegia due to stroke. Weakness may also be caused by spinal cord, nerve root, nerve plexus, or peripheral nerve lesions. Patients in intensive care units (ICUs), especially those who have multiple organ dysfunction syndrome (MODS), may also experience weakness caused by critical illness polyneuropathy or myopathy. Classically, weakness is divided into upper motor neuron (UMN) and lower motor neuron (LMN) patterns. UMN weakness results from disorders affecting the cerebral cortex, subcortical white matter, internal capsule, brain stem, or spinal cord. LMN weakness results from disorders affecting the cell bodies of the lower motor neurons in the brain stem nuclei or anterior horn of the spinal cord or the axons of the neurons as they pass to skeletal muscle. UMN lesions are associated with increased tone and reflexes, extensor plantar responses, clonus, and no muscle wasting or fasciculation. LMN lesions are associated with reduced tone, reduced or absent reflexes, flexor plantar responses, muscle wasting, and sometimes fasciculation. However, hypertonicity takes days to weeks to develop and acutely, UMN lesions commonly cause hypotonia. Wasting also takes weeks to develop and fasciculation is a feature mainly of anterior horn cell disease. If they occur, extensor plantar responses and increased deep tendon reflexes typically develop within a few hours and a few days, respectively, of a stroke, and therefore may be clinically useful in the acute setting.

The most important aspect of determining the site of the lesion causing weakness is to observe the pattern of weakness and look for associated localizing signs. Although many ICU patients are unable to cooperate with assessment of visual fields and sensation, this in itself is suggestive of a UMN lesion. Some useful features to remember are:


Seizures are the least common of the three clinical scenarios. Seizures are classified as generalized or partial (focal). Generalized seizures involve both cerebral hemispheres and motor manifestations are bilateral. They are usually associated with depressed consciousness. Most commonly they are tonic/clonic. The tonic component is sudden sustained muscular contraction that is followed by the clonic component, which is rhythmical muscular contraction. Seizures may also be only clonic or only tonic. Partial seizures are classified as simple or complex. Simple motor seizures usually arise from the frontal motor cortex and present as clonic movements of the face, trunk, or limbs without impaired consciousness. Simple sensory seizures may also occur but are less likely to be noticed in ICU patients. Complex partial seizures originate within the temporal lobe and are associated with impaired consciousness. They may involve motor (fumbling, chewing, semipurposeful movements), affective, memory, and visceral disturbances. Partial seizures may also evolve into tonic/clonic seizures (secondary generalization).

Seizures may also be classified as convulsive, in which there are external manifestations of the seizures, and nonconvulsive, in which there are no external manifestations. Nonconvulsive seizures, if frequent or continuous, can cause coma. Seizures may also be unrecognized if the patient has received neuromuscular blocking drugs. Unexplained tachycardia or bradycardia, hypertension, or pupillary dilatation may suggest nonconvulsive seizures or, in a paralyzed patient, convulsive seizures. An electroencephalogram (EEG) will confirm the diagnosis.

The most common types of seizures after cardiac surgery are generalized tonic/clonic seizures and simple motor seizures. Isolated seizures—that is, in the absence of signs of focal brain injury—are uncommon, occurring in only 0.4% of patients after cardiac surgery.2 Simple motor or sensory seizures strongly suggest a structural brain lesion, whereas generalized seizures may occur with or without a structural lesion.


A review of the patient’s history should establish whether there has been a previous neurologic problem and whether there are residual effects. Symptoms related to previous strokes and other neurologic problems commonly become worse after major surgery or critical illness.

There are two potential approaches to a neurologic examination in the ICU. First, there is the assessment of the conscious and cooperative patient, who usually has a focal deficit such as hemiplegia. This requires a standard complete neurologic examination, including full assessment of cranial nerves and motor and sensory systems. Second, there is assessment of the patient with altered consciousness who may or may not have localizing signs. This may be approached with an abbreviated and targeted neurologic examination.

The goal of the targeted neurologic examination is to determine the likely location of the lesion, and therefore the probable cause, in order to determine further investigations and treatment. A key aim is to differentiate patients who have a structural cause of coma (e.g., due to stroke) from those who have diffuse cortical dysfunction (e.g., due to metabolic encephalopathy). Lateralizing signs suggest a structural lesion, whereas involuntary movements (seizures, myoclonus, asterixis, or a “flapping tremor” on attempted sustained wrist extension), especially if generalized, suggest a diffuse process.4 The targeted examination has three principal components: (1) determination of the level of consciousness; (2) examination of the cranial nerves; and (3) limited assessment of the motor system.

Level of Consciousness

Various levels of consciousness may be distinguished.4 In patients with delirium, assessment of the presence of disordered thinking, memory, and attention may be performed by using a standardized score such as the Confusion Assessment Method for the ICU (CAM-ICU).8 Depressed consciousness should be described in terms of the patient’s spontaneous activity and responses to graded stimulation. The patient should be watched undisturbed for several minutes for body position, motor activity, eye opening, and verbalization (if not intubated). Purposeful movements (e.g., reaching for the endotracheal tube) and comfort positioning (e.g., crossing legs, shifting position) suggest that cortical integration is intact. Response to graded stimulation should be assessed by using the GCS (see Table 37-1). The GCS was initially designed for the assessment of patients with traumatic brain injury, but it has become widely used for evaluating consciousness level in almost all acutely ill patients. It has good interobserver reliability and is a powerful predictor of outcome in a wide range of disorders.9,10 The individual components as well as the total score should always be recorded (e.g., E1, V1, M3, total 5). The motor component is the most powerful predictor of outcome, and it is essential that this be performed and recorded correctly. The patient should be asked to follow commands (e.g., open your eyes, lift up your arm). If unable to respond, painful stimulation (e.g., sternal rub, supraorbital compression) is applied. If the patient makes any sort of flexion response, pain should be applied in the cranial nerve distribution (e.g., supraorbital pressure, squeezing ear lobes) to clearly distinguish flexor posturing, withdrawal, and localization. If asymmetry exists, the best response should be recorded. In ventilated patients, the GCS score should be revised to a maximum of 10, with the annotation that the patient is intubated.

Cranial Nerve Examination

It is usually possible to assess at least some components of the functioning of cranial nerves II through X.4 A full discussion of the significance of all of the possible abnormalities may be found in standard texts on coma.6,11 The core brain stem reflexes to assess are:

Eye examination is the most important in the comatose patient because of the proximity of the centers controlling the eyes to parts of the ARAS. Spontaneous roving eye movements (usually slow and conjugate) or periodic alternating eye movements suggest intact brain stem function. Normal pupillary light reflexes and eye movements indicate that the cause of coma is very likely above the midbrain. Unilateral pupillary dilatation is evidence of oculomotor nerve compression resulting from ipsilateral uncal herniation until demonstrated otherwise. Bilaterally dilated pupils that do not react to light are the result of central herniation, extensive midbrain injury, drug intoxication, or brain death. Conjugate lateral deviation of the eyes occurs with an ipsilateral hemispheric lesion or a contralateral hemispheric seizure focus. Cranial nerve abnormalities such as disconjugate eye movements suggest a brain stem lesion.

Motor Examination of the Limbs

The motor examination of the limbs is assessed partially at the time when the level of consciousness is assessed. Motor examination begins with the observation of spontaneous motor activity, including organized unprompted movements (e.g., yawning and leg crossing) and abnormal involuntary movements, such as seizures, myoclonus, and tremors. The presence of muscle wasting or fasciculations should also be noted. Response to painful stimuli is assessed as part the assessment of the GCS. Then, depending on the patient’s clinical state and level of consciousness, tone, power, and reflexes should be assessed in each limb. Examination of gait and coordination is rarely indicated (or possible) in the ICU. Tone is assessed by testing for resistance to passive flexion and extension. Increased tone is generally indicative of a chronic UMN lesion. Clonus is sustained rhythmical contraction of muscles when they are suddenly stretched. It may be tested for at the ankle by sudden dorsiflexion of the foot. If present, clonus is suggestive of a UMN lesion.

In an awake and cooperative patient, power should be assessed at all major limb joints and may be graded on a 6-point scale (Table 37-2). Although it may not determine the anatomic site of a lesion, assessment of power is helpful in evaluating the progression or deterioration in a patient’s condition. In the upper limb, deep tendon reflexes should be tested at the elbow (biceps and triceps) and wrist (supinator); in the lower limb, they should be tested at the knee and ankle. Reflexes may be recorded on a 5-point scale (see Table 37-2). Increased reflexes are suggestive of a UMN lesion. Reduced or even absent reflexes are consistent with an LMN lesion or a myopathy, but they are a relatively nonspecific finding in ICU patients. The plantar reflex is elicited by stroking the lateral undersurface of the foot; a normal response is flexion of the big toe. An extensor (Babinski) response is seen with UMN lesions, coma, and following generalized seizures. Asymmetries of motor response, tone, power, or reflexes suggest lateralization and make a structural cause of altered consciousness more likely.

Table 37-2 Grading Power and Deep Tendon Reflexes

0 Complete paralysis
1 Flicker of contraction
2 Movement possible when gravity excluded
3 Movement possible against gravity but not if further resistance added
4 Movement possible against gravity and some resistance
5 Normal power
Deep Tendon Reflexes
0 Absent
+ Reduced
++ Normal
+++ Exaggerated
++++ Exaggerated with clonus

Sensory Examination

Accurate examination of sensation is difficult and time consuming and requires an awake and cooperative patient. It is most often performed in patients receiving epidural analgesia (see Chapter 12) but is also important if a spinal cord or peripheral nerve injury is suspected. If an awake patient has a motor deficit or complains of numbness and tingling, a careful sensory examination should be performed. Sensation is carried primarily in two spinal cord tracts: the spinothalamic pathway and the posterior columns. Pain and temperature fibers are carried in the spinothalamic tract. These fibers decussate (cross over) in the spinal cord a few segments above their nerve roots and ascend in the contralateral spinothalamic tract. Vibration and proprioception fibers are carried ipsilaterally in the posterior columns and decussate in the brain stem. Light touch fibers are carried in both pathways and, therefore, this sensory modality is the least discriminatory. Pain and temperature fibers can be tested by pin prick or ice; vibration sense can be tested by placing a 128 Hz tuning fork over a distal bony prominence and having the patient report the moment the tuning fork is deadened by the examiner; light touch may be tested by lightly dabbing (not stroking because this stimulates hairs) cotton wool over the skin.

Sensory deficits usually conform to one or more patterns: (1) dermatome distribution (see Fig. 12-3) due to a lesion involving a nerve root, nerve plexus, spinal cord, or regional nerve block (e.g., epidural); (2) peripheral nerve distribution; (3) glove or stocking distribution secondary to a distal symmetric peripheral neuropathy; (4) a hemisensory distribution due to a lesion involving the spinal cord, brain stem, thalamus, or sensory cortex.



Almost all (99%) strokes that occur after adult cardiac surgery are ischemic as opposed to hemorrhagic.12 The majority are due to macroemboli originating from the heart, aorta, or proximal arteries. In a review of 388 patients with stroke after isolated CABG surgery, 62% of cases were embolic; 10% were due to multiple causes; 9% were watershed (due to hypoperfusion, usually caused by a combination of extracranial arterial stenoses and systemic hypotension); 3% were lacunar (due to deep white matter ischemia in brain supplied by penetrating arteries); and 1% were thrombotic. The causes were unknown in 14%.12 When assessed prospectively, stroke is detected within the first 24 to 48 hours after surgery in at least two thirds of patients.7 Later-onset strokes are more common in patients with atrial fibrillation and in those undergoing valve surgery or placement of a ventricular assist device. The likelihood of death following cardiac surgery is three to six times higher in patients who have had strokes than those who have not. The length of stay in the ICU and the hospital is prolonged and more than half require in-patient rehabilitation.7

Clinical Presentation

Stroke can cause altered consciousness, focal neurologic signs, or both. Focal signs include weakness (typically a hemiplegia), visual field defects, and speech defects. Altered consciousness may occur when (1) there is a large hemispheric stroke; (2) there are multifocal infarctions; or (3) there is a posterior circulation stroke. Lesions in the prefrontal lobe, nondominant parietal lobe, or either occipital lobe may also cause altered consciousness and few or no localizing signs. Between 25% and 65% of strokes after cardiac surgery are multiple.13

Approximately one quarter of embolic strokes affect the posterior circulation. The posterior circulation supplies the brainstem, cerebellum, thalami, and occipital lobes. Emboli may affect any of the branches of the vertebrobasilar system. The most common site of obstruction is at the top of the basilar artery. Here an embolus can cause ischemia bilaterally to the thalami, midbrain, and occipital lobes. Clues to a posterior circulation stroke include altered consciousness, cranial nerve palsies, autonomic dysfunction, visual dysfunction, extensor posturing, and abnormal breathing.13

Strokes due to hypoperfusion result in a watershed pattern, in which infarction occurs in the border zones between either the anterior and middle cerebral arteries or the middle and posterior cerebral arteries. Patients with watershed infarction in the border zone between the anterior and middle cerebral arteries can present with the “man in a barrel”-type deficit, in which there is weakness of the proximal limbs and relative sparing of the hands and feet.

Risk Factors and Prevention

A number of investigators have developed preoperative predictive models to determine the risk for stroke. These models usually include the common risk factors for vascular disease, such as advanced age, previous stroke or transient ischemic attack, hypertension, diabetes, carotid artery stenosis, and peripheral vascular disease.1,7 In addition, they may include factors related to the cardiac procedure, such as the presence of unstable angina, valvular or combined cardiac operations, and aortic arch surgery.

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