progressively expands to produce brain hernia-tion (see Chapter 14, “Brain Tumors”). As the her-niation progresses across the tentorium, the upper brainstem pushes downward, often rupturing
penetrating brainstem veins (Duret hemor-rhages), producing fatal brainstem hemorrhages and ischemia. Coma from infratentorial destruc-tion can be from ischemic brainstem stroke or a 166 FUNDAMENTALS OF NEUROLOGIC DISEASE
Table 16-1 Major Causes of Coma
Supratentorial Structural Infratentorial Structural Metabolic
(18% of Total) (14% of Total) (68% of Total)
Head Trauma Brainstem/cerebellar Drugs
Contusion with brain swelling* ischemic or Sedatives Subdural/epidural hematoma hemorrhagic stroke Opioids
Intracerebral hemorrhage Tranquilizers
Salicylates
Brain Tumor Brainstem/cerebellar Hypoxia
tumor Cardiac or respiratory arrest Severe anemia
Toxins (carbon monoxide)
Massive Stroke Blood-glucose abnormalities
Ischemic stroke Hypoglycemia coma from excess
insulin
Cerebral hemorrhage Hyperglycemic coma from
diabetes mellitus
Encephalitis Abnormal ionic central nervous system
environment
Hypo/hyper blood sodium, potas-sium, calcium, and magnesium
Brain abscess Organ diseases
Liver (hepatic coma) Kidney (uremic coma)
Lungs (CO2narcosis and respiratory failure)
Thyroid (myxedema coma) Brain cofactor deficiency
Thiamine (B1), cyanocobalamine (B12), and pyridoxine (B6) deficiency Poor cerebral perfusion
Hypertensive encephalopathy Obstructive hydrocephalus Bleeding with low blood volume Decreased cardiac output
(myocardial infarction and cardiac arrhythmia)
Toxins Ethanol
Methanol and ethylene glycol
* Bold type refers to the most-common causes within a category.
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mass (hemorrhage or tumor) involving the brain-stem or cerebellum, directly damaging or compress-ing the reticular formation. Metabolic-caused coma primarily affects reticular formation neurons.
Major Clinical and Laboratory Features There are three critical questions to be answered about a comatose patient: where is the lesion? what is the cause? and is the coma stable, improving, or worsening? Generally, the physician first deter-mines whether the etiologic category is supraten-torial, infratensupraten-torial, or metabolic. The next step is
to determine the cause within the category.
Obtaining a history, including drug use, from a friend or relative is extremely helpful in placing the patient into a category.
Table 16-2 gives the major clinical features found in each coma category (also refer to Figures 16-1 and 16-2). An elevated temperature and WBC count usually implies an infection (sepsis, pneu-monia, or CNS), while a low temperature usually implies the patient has been comatose in a cold environment for some period of time. Rapid regu-lar breathing often denotes a metabolic acidosis from a metabolic cause. During the physical
exam-CHAPTER 16—Coma and Cerebral Death 167
Table 16-2 Coma Characteristics Excluding Those Caused by Head Trauma
Supratentorial Infratentorial
Characteristic Structural Structural Metabolic
Early History Signs suggesting dysfunction Signs of cranial nerve Rapid onset (anoxia) or sub-of the hemisphere (hemi- dysfunction. Headaches and acute progression (drugs, paresis, hemisensory defect, stiff neck may be present. uremia, etc). Patient looks
aphasia, and visual defect). asleep. Headaches are
Headaches common. uncommon. Fever may be
present if sepsis or pneu-monia present.
Breathing Normal or Cheyne-Stokes Apneustic (deep inspiration, Normal or rapid due to sign (periodic cycles of long pause, and prolonged metabolic acidosis.
rapid breathing followed exhalation at a rate of ~ 5/s) by period of apnea). or ataxic (irregular, ineffective
breathing that is often shallow).
Early Eye Pupillary light reflexes are Pupil size often unequal and Normal size and reaction to Findings (see present but pupil size may may be unresponsive to light light, normal
Figure 16-2) be small or unilaterally (fixed). Eyes may not be vestibuloocular reflexes, dilated. Papilledema may parallel and vestibuloocular and no papilledema.
be seen. Vestibuloocular reflex is sluggish or absent.
reflexes may be present Papilledema is absent.
or impaired.
Motor (see Asymmetric spontaneous or Bilateral limb weakness or Symmetric spontaneous or Figure 16-3) pain-induced limb quadraparesis may be pain-induced limb
movements. Decorticate present. Decerebrate movements.
posturing (flexion of the posturing (unilateral or arm and extension of the bilateral extension of arms leg on the involved side) to and legs) to pain seen in pain may occur. mid-brain lesions.
Reflexes Often hyperactive with Often normal or hyperactive. Normal or depressed. No Babinski sign on Babinski signs may appear. Babinski signs.
contralateral side.
Neuroimaging Hemispheric mass (tumor, Mass in brainstem or Normal.
hemorrhage, abscess, and cerebellum and occasional stroke), shift of midline cerebellar tonsillar herniation structures, and brain through foramen magnum.
herniation. Occasional obstructive hydrocephalus.
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ination, attention should be paid to find signs of trauma (especially head or neck trauma), bleeding (external or internal), organ dysfunction (especially lungs, heart, kidney, and thyroid), and sepsis. Since mentation, fine sensation, and coordination cannot be tested in a comatose patient, the neurologic exam focuses on spontaneous or pain-induced limb movements, breathing patterns, ocular findings and cranial nerve function (Tables 16-2 and 16-3).
Important clues to a supratentorial location for the coma include an early history of progressive
unilateral hemispheric signs or a unilateral fixed dilated pupil. The late stages of a supratentorial coma are due to brainstem dysfunction and often appear similar to infratentorially caused coma.
Infratentorial structural coma usually has a rapid onset, involves multiple cranial nerves, and pro-duces brainstem findings before or accompanying coma. Table 16-3 lists the brainstem reflexes that can be evaluated in a comatose patient and the clues each give regarding brainstem localization.
Weakness may be unilateral if the brainstem lesion 168 FUNDAMENTALS OF NEUROLOGIC DISEASE
Normal Response Abnormal Response
Head to Left:
Eyes Hold Original Position
Head to Left:
Eyes Move With Head
Head Rotation or Doll's Eye Maneuver
Ice Water Caloric Test
A Normal Tonic Response A Negative Response
4∞ 4∞
Eyes Move Toward the Ear With Ice Water
Eyes Do Not Move
Figure 16-1 Assessment of vestibuloocular reflex in coma.
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is unilateral (brainstem stroke) or bilateral if the lesion involves both halves of the brainstem (brain-stem hemorrhage or tumor). Metabolic coma may have a rapid or subacute onset, usually produces mental changes before motor signs, has preserved pupillary reactions, rarely produces asymmetric motor, sensory, or reflex findings, and is often asso-ciated with systemic disease (abnormal blood find-ings and signs of other organ failure). Occasional patients have psychogenic coma characterized by normal muscle tone and reflexes, unpredictable vestibuloocular reflexes with the fast phase pre-served on ice water caloric testing, atypical irregu-lar breathing patterns, and nonphysiologic responses to cranial nerve testing.
Principles of Management and Prognosis In the emergency management of a comatose patient, the first step is control of the ABCs (air-way, breathing, and circulation) (Figure 16-3).
Steps include ensuring the airway is open, deliv-ering oxygen either nasally or via intubation if needed, and establishing intravenous access.
Commonly ordered tests include the following: a toxicology screen, a hemogram, electrolytes, liver-function studies, creatinine, glucose, cal-cium, and a “save-serum” specimen for possible future tests. Depending on the history and initial evaluation of the patient, the following drugs may be intravenously administered: thiamine, an
CHAPTER 16—Coma and Cerebral Death 169
Decorticate Posturing Decerebrate Posturing
Figure 16-2 Decorticate and decerebrate posturing reflexes. Supraorbital pressure induces posturing.
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opioids antagonist, and a bolus of 50% glucose solution.
If a supratentorial cause is suspected, the situa-tion becomes emergent and immediate cranial CT is indicated. If impending brain herniation is present, lowering of ICP is accomplished by intubation and hyperventilation (to cause cerebral vasoconstric-tion), administration of intravenous mannitol (to reduce cerebral fluid volume), and prompt surgical intervention (to remove a hemispheric mass or to remove CSF if obstructive hydrocephalus is present).
With infratentorial causes of coma, vital signs may rapidly worsen so intubation with mechanical ventilation and blood pressure drugs may be
needed. Neuroimaging can identify the cause, but surgical intervention is seldom indicated. If the cause of metabolic coma is due to insufficient cir-culation, oxygen, or glucose to the brain, rapid correction of the etiology may reverse the situa-tion. For many other causes, including organ dys-function and drug overdose, the patient should be stabilized, appropriate blood tests ordered to iden-tify the etiology, and treatment focused on correct-ing the underlycorrect-ing metabolic cause.
The outcome of a comatose patient varies with the etiology but in those with a structural brain lesion the mortality is high, with severe neurologic sequelae in survivors. The following generaliza-170 FUNDAMENTALS OF NEUROLOGIC DISEASE
Table 16-3 Bedside Examination of Cranial Nerves in a Comatose Patient
Cranial Brainstem
Nerves Location
Test Tested Testing Method Tested
Papillary II, III Normal: bright light shined into 1 eye causes both pupils promptly Mid-brain Light Reflex to reduce in size. Large pupil that is fixed to ipsilateral and
bilateral light implies damage to CN III.
Corneal V, VII Normal: touching cornea with cotton causes both eyelids to Pons Reflex promptly close or blink. Failure of both eyelids to blink when
stimulating 1 cornea implies dysfunction of ipsilateral CN V.
Failure of 1 eyelid to blink with direct and consensual corneal stimulation implies dysfunction of ipsilateral CN VII.
Symmetrical VII Normal: in light coma, ipsilateral or contralateral pain to face or Pons Face Movement body causes grimace of lower face. Unilateral grimace to
to Pain stimuli implies dysfunction of CN VII.
Vestibuloocular III, VI, VIII Normal: when rotating head laterally, the eyes remain fixed at Lower pons Reflex or original target. Abnormal test result occurs when eyes move to
mid-“Doll’s Eyes” with head on lateral rotation. brain
Maneuver
Ice-Water III, VI, VIII Normal: irrigation with 25–50 mL of cold or ice water in 1 ear Lower pons Caloric Test causes both eyes to move to side with water and stay fixed. to
mid-If 1 side is absent but the opposite side normal, damage to brain ipsilateral CN VIII is implied. If both sides are abnormal, this
implies brainstem lesion in pathways of vestibular nuclei to CN III and VI.
Gag Reflex IX, X Normal: suctioning of mouth or stimulation of posterior pharynx Medulla triggers gag reflex. Absent gag implies dysfunction to medullary gag center.
Cough Reflex IX, X Normal: spontaneous cough or cough upon stimulating trachea. Medulla Absent cough implies dysfunction to cough center.
Yawn or Sneeze V, IX, X Presence of these long loop reflexes implies brainstem function Medulla to
Reflexes reasonably intact. upper brain
Deep Tendon Spinal cord Normal: limb movement in response to percussion of joint tendon. Spinal cord Reflexes Presence implies lack of spinal shock and intact spinal cord level
level but does not imply brainstem or cortical function.
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tions help predict outcomes from coma in patients without head trauma. Head trauma has a better prognosis (see Chapter 18, “Traumatic Brain Injury and Subdural Hematoma”):
•
Coma seldom persists longer than 2 weeks.The patient dies, develops a persistent vegeta-tive state (a chronic condition in which he or she appears awake but has no evidence of cognition), or improves, opens the eyes, and regains consciousness.