The Comatose Patient

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Coma is the state in which the patient is unable to respond to any stimuli. The causes of coma include the following:

Meningeal infection

Increased intracranial pressure of any cause Subarachnoid hemorrhage Focal cerebral lesion

Brain-stem lesion affecting the reticular system Metabolic encephalopathy* Status post seizure activity

•Common causes include electrolyte abnormalities, endocrine disorders, liver or kidney failure, vitamin deficiencies, poisoning, intoxications, and marked changes in body temperature.


Parkinson's disease

Cerebellar ataxia



Parkinson's disease

Cerebellar ataxia


Sensory ataxia

Figure 21-59 Common types of gait abnormalities.

If the patient's friends or family members are available, speak with them. They can help in the evaluation of the patient by giving valuable information. Is there a history of hypertension, diabetes, epilepsy, substance abuse, or recent head trauma?

If there is any evidence of head trauma, radiographs of the cervical spine must be taken before the examiner moves the patient's neck.

The physical examination of the comatose patient should start with inspection. The clothing, age, and evidence of chronic illness provide valuable clues as to the cause of the coma. Does the patient have gingival enlargement consistent with antiepileptic medical therapy?* Is there a characteristic odor to the breath? The sweet smell of ketones may be present in diabetic ketoacidosis. An odor of alcohol may be present. Are there stigmata of chronic liver disease?

What is the posture of the patient? Patients with cerebral hemispheric dysfunction or a destructive lesion of the pyramidal tracts maintain a decorticate posture, whereas those patients with a midbrain or pons lesion maintain a decerebrate posture. In decorticate rigidity, the arms are adducted and the elbows, wrists, and fingers are flexed. The legs are internally rotated. In decerebrate rigidity, the arms are also adducted but they are rigidly extended at the elbows, and the forearms are pronated. The wrists and fingers are flexed. In both postures, the feet are plantarflexed. The positions of the arms and hands are shown in Figure 21-60.

The head should be evaluated for any areas of depression, as in a depressed skull fracture. Does the nose appear broken? Are there any broken teeth? Is there any clear, watery discharge from the nose or ear, suggestive of a leakage of cerebrospinal fluid?

The respiratory pattern should be evaluated. Central neurogenic hyperventilation is seen in lesions of the midbrain or pons. This type of respiration consists of rapid, deep, regular breathing. Cheyne-Stokes breathing is characterized by rhythmic changes in the breathing pattern. Periods of rapid breathing are separated by periods of apnea. Cheyne-Stokes breathing is associated with brain-stem compression or bilateral cerebral dysfunction.

*Commonly related to phenytoin (Dilantin) therapy.

Decerebrate posture

Decorticate posture

Figure 21-60 Postures of comatose patients.

Decorticate posture

The neurologic examination of the comatose patient is largely based on pupillary size and light reflexes. The pupils are small and reactive in bilateral cerebral dysfunction. They are dilated after an overdose of hallucinogenic agents or central nervous system stimulants. A unilateral fixed and dilated pupil is suggestive of pressure on the ipsilateral oculomotor nerve. Pupillary dilatation precedes paralysis of the extraocular muscles;this is because the pupillary nerve fibers are superficial to the fibers innervating the extraocular muscles and are more vulnerable to extrinsic stresses. This is an important sign of uncal herniation. In the presence of normally reactive pupils with absence of corneal reflexes and absence of extra-ocular movement, a metabolic abnormality may be the cause of the coma.

The fundus of the eye may provide a clue as to the cause of the coma.

If there is no evidence of a fracture of the cervical spine, oculocephalic reflexes should be tested. If a comatose patient's head is rapidly turned to one side while the eyelids are held open, the eyes should move conjugately to the other side. This is the doll's eyes reflex. In a patient with a lesion in the brain stem, the doll's eyes reflex is absent. The doll's eyes reflex can be elicited only in a comatose patient because alert individuals fixate on an object and override this reflex.

Caloric stimulation is used to enhance the doll's eyes reflex or to test movements in an individual with a fractured cervical spine. The patient should be placed with the head flexed at 30°. This orients the semicircular canal in a horizontal position. A large-bore syringe is filled with 20 to 30 mL of ice water, and the water is squeezed into one of the external auditory canals. The normal response is the development of nystagmus. Slowly the eyes move conjugately to the ipsilateral side and then move rapidly (nystagmus) back to the midline. The use of cold water causes nystagmus to the opposite side. If warm water is used, the eyes move rapidly toward the side being irrigated. This can easily be remembered by using the mnemonic COWS, which stands for ''cold opposite, warm same.''

An absence of the caloric response is seen in patients with a disruption of the connections between the vestibular nuclei and the sixth cranial nerve nucleus at the level of the brain stem.

As was indicated earlier in the chapter, headache is an important symptom of neurologic disease. Table 21-2 provides a differential diagnosis of headaches.

The correct assessment of a patient's motor activity can help localize the site of a lesion. The term extrapyramidal refers to those parts of the motor system that are not directly involved with the pyramidal tracts. The extrapyramidal system is composed of the basal ganglia, nuclei of the midbrain and reticular formation, and cerebellum. Table 21-3 lists the major areas and the specific motor problems associated with lesions of the lower motor neuron, the pyramidal tract, and the extrapyramidal tract. Table 21-4 summarizes the important signs and symptoms in five common chronic neurologic disorders.

Table 21-2 Differential Diagnosis of Headache






Increased intracranial pressure


Temporal arteritis* Older adults


Family history Young adults Female

Adolescent male


Family history



Orbitofrontal Unilateral


Generalized or occipital Variable


Bilateral Often occipital


Over temporal artery

Signs and Symptoms

Nausea Vomiting

Possible neurologic deficits

Unilateral nasal congestion Lacrimation

Hypertensive retinopathy Possible papilledema




Nuchal rigidity Fever

Tender temporal artery Loss of vision in ipsilateral eye

•See Chapter 25, The Geriatric Patient.

A comparison of the effects of upper and lower motor neuron lesions is shown in Table 21-5.

Paraplegia and quadriplegia are upper motor neuron defects. They can also involve lower motor neurons. Injury of the spinal cord can produce partial or complete paralysis. In patients with cervical or thoracic lesions, spasticity is present below the level of the lesion, and flaccid-ity is present in all muscles supplied from reflex arcs at the level of the lesion. In the presence of sacral lesions, a flaccid paralysis results. Table 21-6 summarizes motor involvement in spinal cord lesions.

Often a patient may complain of a decreased ability to perform a task. Physical examination may reveal decreased motor strength. Table 21-7 summarizes the major actions of the more common muscles and their corresponding cord segments.

Table 21-3 Effects of Various Lesions

Feature Lower Motor Neuron Pyramidal Tract Extrapyramidal Tract

Major effect

Flaccid paralysis

Muscle appearance

Muscle tone Muscle strength Coordination

Atrophy Fasciculations


Decreased or absent Absent or poor

Spastic paralysis Hyperactive reflexes

No paralysis

Mild atrophy from disuse Rest tremor

Increased Increased

Decreased or absent Normal

Absent or poor Slowed

Table 21-4 Common Neurologic Conditions and Their Signs and Symptoms Age at Onset

Condition (Year) Sex Signs and Symptoms

Multiple sclerosis 30-35


Amyotrophic lateral 50-80 sclerosis

Parkinson's disease 60-80



Nystagmus Diplopia

Slurring of speech

Muscular weakness


Poor coordination

Bowel and bladder dysfunction

Irregular twitching of involved muscles Muscular weakness Muscle atrophy*

Absence of sensory or mental deficits Rigidity

Slowing of movements Involuntary tremor Difficulty swallowing Tremor in upper extremities Jerky, ''cogwheel'' motions Slow, shuffling gait with loss of arm swing Masklike facial expression Body in moderate flexion Excessive salivation

Myasthenia gravis 20-50 Female Generalized muscular fatigue

Bilateral ptosis* Diplopia

Difficulty swallowing Voice weakness

Huntington's disease 35-50

Both sexes

Choreiform movements


Rapid movements

Facial grimacing


Personality change

Table 21-5 Comparison of Effects of Upper and Lower Motor Neuron Lesions

Upper Motor Lower Motor

Effect Neuron Lesion Neuron Lesion

Voluntary control Muscle tone Reflex arcs Pathologic reflexes Muscle atrophy


Spastic, increased Present Present Little or none


Flaccid, decreased Absent Not present Significant

Table 21-6 Motor Involvement in Spinal Cord Lesions Affected Cord

Segment Motor Involvement


Paralysis of neck, diaphragm, intercostals, and all four extremities


Spastic paralysis of trunk, arms, and legs; partial shoulder control

C6, C7

Spastic paralysis of trunk and legs; upper arm control; partial lower arm control


Spastic paralysis of trunk and legs; hand weakness only


Spastic paralysis of trunk and legs


Spastic paralysis of legs


Flaccid paralysis of legs


Flaccid paralysis of lower legs; bowel, bladder, and sexual function

affected affected

Table 21-6 Motor Involvement in Spinal Cord Lesions Affected Cord

Segment Motor Involvement

Table 21-7 Motor Function According to Cord Segments

Area of Body Action Tested Cord Segment

Shoulder Arm

Flexion, extension, or rotation of neck





Adduction of arm



Abduction of arm



Flexion of forearm



Extension of forearm



Supination of forearm



Pronation of forearm



Extension of hand



Flexion of hand


-C8, T1

Abduction of thumb


-C8, T1

Adduction of thumb



Abduction of little finger



Opposition of thumb



Flexion of hip



Extension of leg



Flexion of leg


L5, S1-S2

Adduction of thigh



Abduction of thigh


L5, S1-S2

Medial rotation of thigh


L5, S1

Lateral rotation of thigh


L5, S1-S2

Flexion of thigh



Dorsiflexion of foot


L5, S1

Plantar flexion of foot



Extension of great toe


L5, S1

Flexion of great toe



Spreading of toes



Useful Vocabulary

Listed here are the specific roots that nology related to neurologic diseases.

are important for understanding the termi-


Pertaining to






Loss of feeling




Loss of the power to recognize sensory stimuli


spinal cord


Radiographic study of the spinal cord




Muscular weakness affecting half the body




Paralysis of the eye muscles


spinal nerve root


Disease of a spinal nerve root

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