CHF, congestive heart failure; DIC, disseminated intravascular coagulation; DKA, diabetic ketoacidosis; ETOH, ethanol; GI, gastrointestinal; GU, genitourinary; ICP, intracranial pressure; MI, myocardial infarction; RMSF, Rocky Mountain spotted fever; SAH, subarachnoid hemorrhage; SBE, subacute bacterial endocarditis; SLE, systemic lupus erythematosus; TTP, thrombotic thrombocytopenic purpura.

Abnormalities of respiration are important in the evaluation of patients with depressed consciousness. Abnormal respiratory patterns due to neurologic disease include Cheyne-Stokes respirations (CSR), central neurogenic hyperventilation, ataxic breathing, and apneustic breathing. In CSR, periods of hyperpnea alternate with periods of hypopnea. Respirations increase in depth and volume up to a peak, and then decline until there is a period of apnea, after which the cycle repeats. In posthyperventilation apnea, a brief period of hyperventilation is followed by apnea lasting 15 to 30 seconds or longer. Demonstration of posthyperventilation apnea requires the active cooperation of the patient. The mechanisms underlying CSR and posthyperventilation apnea are likely similar. CSR may be due to bilateral hemisphere lesions or bilateral thalamic lesions, as well as to increased intracranial pressure and cardiopulmonary dysfunction. CSR commonly induce a rhythmic pupillary dilatation during hyperpnea and constriction during apnea. The patient’s eyelids may open, and she may become more rousable during hyperpnea. In respiratory ataxia, the pattern of breathing is irregular, with erratic shallow and deep respiratory movements. Ataxic breathing occurs with dysfunction of the medullary respiratory centers and may signify impending agonal respirations and apnea. Central neurogenic hyperventilation refers to sustained, rapid, and regular hyperpnea. It is primarily associated with disease affecting the paramedian reticular formation in the low midbrain and upper pons, but it may also occur with lesions in other brainstem locations, either intra-axial or extraaxial. Apneustic breathing, which is rare, causes a prolonged inspiratory phase, and occurs in pontine lesions just rostral to the trigeminal motor nuclei, or cervicomedullary compression. Abnormal respiratory patterns may occur because of systemic disease, such as diabetic ketoacidosis (Table 51.1). Slow, regular respirations are noted with a variety of substance or drug intoxications and in severe myxedema.

Note the patient’s appearance and behavior, apparent age, grooming, and signs of acute or chronic illnesses such as fever, cyanosis, jaundice, pallor, and signs of dehydration and loss of weight. Assess responses to noises, verbal commands, visual stimuli, threats, and tactile and painful stimulation, and whether there has been incontinence. Note whether the patient, even in coma, appears to be comfortable and natural or assumes unnatural positions. Carefully observe spontaneous movements, and the reaction to various stimuli. Note general activity (immobile, underactive, restless, or hyperkinetic), tone (limp, relaxed, rigid, or tense), and the presence of abnormal movements (tremors, twitches, tics, grimaces, and spasms). Carphology (floccillation) is an involuntary tugging at the sheets and picking of imaginary objects from the bedclothes, and jactitation is a tossing to and fro on the bed; these may be seen in acute disease, high fevers, and exhaustion. Motor unrest and excessive activity are seen in both organic and psychogenic states. If there is seizure activity, note the distribution and pattern of spread of the convulsive movements and any associated manifestations such as the degree of impairment of consciousness, frothing at the mouth, tongue biting, and incontinence.

The behavior of the patient should be observed closely and as often as necessary until the diagnosis is established. Note the patient’s reactions to physicians, nurses, and relatives. Do the eyes follow people? Is there some awareness of what is happening in the immediate environment? The conduct may be constant or may vary from time to time. For instance, the patient may appear to be completely unconscious and fail to respond to any type of stimulation while the observer is in the room, yet when not aware of being watched, may open the eyes, make furtive glances, and move around.

After the general physical exam, a focused neurologic exam may help characterize the pathologic process. Specific attention should be paid to the level of responsiveness, pupils, eye movements, and motor responses.

Neurologic Examination

The details of the neurologic examination in the various states of disordered consciousness necessarily vary with the degree of impairment and depth of coma. As a minimum, the following must be assessed: level of consciousness, pupils, eye movements (including reflex movements), fundoscopic, motor status, reflexes, and meningeal signs. Other portions of the examination then follow as necessary. Coma is most often due to a metabolic process. With rare exception, metabolic encephalopathies are characterized by reactive pupils and a symmetric neurologic examination. Any asymmetry in motor or sensory responses and any pupillary or eye movement abnormality should prompt an immediate, vigorous search for structural disease.

Level of Responsiveness

Coma is a state of complete loss of consciousness from which the patient cannot be aroused by ordinary stimuli. There is complete unresponsiveness to self and the environment. The patient in coma has no awareness of herself, makes no voluntary movements, and has no sleep-wake cycles. Stupor is a state of partial or relative loss of response to the environment in which the patient’s consciousness may be impaired to varying degrees. The patient is difficult to arouse, and although brief stimulation may be possible, responses are slow and inadequate. The patient is otherwise oblivious to what is happening in the environment and promptly falls back into the stuporous state. The lethargic patient can usually be aroused or awakened and may then appear to be in complete possession of her senses, but promptly falls asleep when left alone. In confusional states, patients may appear alert, but are confused and disoriented. Terminologic description of the differences between various states of impaired altered consciousness is at best ambiguous. Because of imprecision and inconsistency in usage, such terms as semicoma and semistupor, all describing changes across a spectrum of altered awareness, are best avoided. It is preferable to describe the patient’s state of responsiveness or use an objective and well-defined scheme, such as the Glasgow coma scale (GCS), which has gained wide acceptance in the evaluation of patients with impaired consciousness, particularly in head injury. In the GCS, scores are obtained for ocular, verbal, and motor functions (Table 51.2). An alert person with normal eye and motor responses would score 15 points; a patient in profound coma would score three points. The FOUR (Full Outline of UnResponsiveness) score has four components (eye, motor, brainstem, and respiration); each component has a maximal score of four. It may address some shortcomings of the GCS, especially in ventilated patients. It can detect locked-in syndrome and is superior to the GCS due to the evaluation of brainstem reflexes, breathing patterns, and the ability to recognize different stages of herniation. Other coma scales are available, including the following: the Innsbruck, Glasgow-Liege, reaction level, coma recovery, ACDU (Alert, Confused, Drowsy, Unresponsive), and AVPU (Alert, responds to Voice, responds to Pain, Unresponsive). Although useful for grading the severity of coma, none of these scales are useful in differential diagnosis. Coma must be distinguished from the persistent vegetative state (PVS), locked-in syndrome, and mutism (see below).

The term AMS is often used to describe a variety of abnormalities of cerebral function. It is used haphazardly to describe patients who have impaired alertness, impaired cognition, or a deficit of higher cortical function. Strictly speaking, the term AMS should imply a change in the level of consciousness, somewhere on a continuum between confusion and coma. It should not be used to describe patients who have impaired cognition with a clear sensorium—those patients have dementia; patients who have focal deficits of higher cortical function, such as aphasia; or used to describe patients who have psychiatric disorders, such as psychosis or mania. Neurologically naive clinicians may lump all these conditions together under the rubric AMS. They are in fact distinctly different conditions, with different etiologies and treatments, and especially with different prognostic implications. In a study of 317 patients with AMS seen in an emergency department, 24% were unresponsive, 46% lethargic or difficult to arouse, 12% were agitated, and 18% displayed unusual behavior. Patients with Wernicke’s aphasia are often thought to have AMS or an acute confusional state.

It is necessary to make reasonable attempts to arouse the patient, and this usually includes assessing the response to a painful stimulus. Commonly used painful stimuli are supraorbital pressure, trapezius squeeze, sternal rub, and nail bed pressure. The stimulus must be adequate but remain humane and considerate. Avoid leaving bruises or other marks on the patient; the reason for these may be misinterpreted by family members and ancillary personnel. An effective and stealthy painful stimulus is to forcibly twist a key or the handle of a reflex hammer between two fingers or toes squeezed tightly together.

Cranial Nerves

Although cranial nerve (CN) examination cannot be carried out in any detail in a patient with altered consciousness, examination of the pupils and extraocular movements is critical in evaluation of the comatose patient. The pupils are critical in the evaluation of altered consciousness. The size, shape, position, equality, and reactivity are all important. Bilateral pinpoint pupils occur with opiate toxicity and other lesions of the pons, such as pontine hemorrhage or thrombosis of the basilar artery. The bilateral miosis seen in large pontine lesions is probably due to dysfunction of the descending sympathetic pathways bilaterally. The light reaction is preserved with lesions involving the descending sympathetic system, but may be very difficult to see without magnification when the pupils are extremely small. Focusing on a tiny pupil with the ophthalmoscope and turning the light off and then back on may reveal the residual light reactivity. Hypothermia can cause small, unreactive pupils. Bilateral large pupils in coma are usually an ominous sign, especially when unreactive to light. They occur as a terminal condition in many patients. Bilateral mydriasis may also occur in botulism or anticholinergic intoxication. Atropinic agents given during cardiopulmonary resuscitation may enlarge and fixate the pupils. Pilocarpine solution helps distinguish such pharmacologic blockade from mydriasis due to structural disease. Bilateral large, unreactive pupils that display hippos or dilate with neck scratching (ciliospinal reflex) suggest a tectal or pretectal lesion. Midposition (3 to 6 mm) unreactive pupils result from lesions affecting both sympathetic and parasympathetic pathways. They occur commonly as a feature of central transtentorial herniation. Abnormally shaped, for example, oval or elliptical, or misplaced (“ectopic”) pupils suggest midbrain disease (see Chapter 14).

Pupillary asymmetry usually indicates structural disease. A unilaterally dilated pupil, especially if unreactive to light, is most often a sign of third nerve palsy, and in the setting of coma usually indicates uncal herniation (Hutchinson pupil). Because of the peripheral location of the pupillary fibers in the third nerve, they are especially susceptible to pressure, and pupillary dilation often occurs prior to any eye movement abnormality. Rarely, paradoxical unilateral dilation of the pupil on the side opposite the lesion occurs as a false localizing sign, especially with subdural or intraparenchymal hemorrhage. Coma with a unilaterally dilated pupil could also result from subarachnoid hemorrhage due to a posterior communicating artery aneurysm. Lateral medullary syndrome may cause anisocoria due to Horner’s syndrome, along with evidence of brainstem dysfunction, but rarely causes coma. Horner’s syndrome may also occur with lesions involving the hypothalamus or thalamus (particularly hemorrhage). Ipsilateral Horner’s syndrome may occur because of carotid artery disease, especially occlusion, but is likely due to hypothalamic ischemia rather than dysfunction of the pericarotid sympathetic plexus. Rarely, seizures may cause transient anisocoria.

Pupillary reactivity is a key sign in distinguishing structural from metabolic coma. Normally reactive pupils in the setting of coma suggest metabolic encephalopathy, which typically affects consciousness and respiration earlier than pupillary function. Loss of pupillary reactivity is more consistent with structural disease or anoxia. Structural lesions of the brainstem usually cause abnormal pupillary responses, and in brain death pupillary responses are absent. Pupillary reactivity is usually preserved in drug-induced coma, except when extremely severe. Certain agents may cause earlier pupillary unreactivity. Glutethimide may cause asymmetric and poorly reactive pupils, but is rarely seen. Other agents that may fix the pupils include barbiturates, certain anticonvulsants, lidocaine, phenothiazines, and aminoglycosides. A notable exception to the rule that normally reactive pupils indicate metabolic encephalopathy is that posterior fossa mass effect exerted primarily on the mid and lower brainstem, such as cerebellar infarction or hemorrhage, may initially spare the pupils. Pupillary light reaction is a key prognostic sign. Loss of reactivity portends a poor outcome. Brain injury patients, even those with a GCS of 3, if the pupils remain reactive, may survive. Loss of pupillary reactivity for more than a few minutes after an anoxic insult carries a poor prognosis. In a series of patients undergoing craniotomy for traumatic hematomas, 25% of those with fixed pupils for less than 6 hours made a functional recovery. The ciliospinal reflex is another test of pupil reactivity, but it involves pathways caudal to the foramen magnum.

Eye movements have been discussed in detail in Chapter 14, and the oculocephalic and oculovestibular reflexes in Chapter 17. Note the position of the eyes at rest, whether there is any nystagmus, and whether the range of ocular movement is full in both directions to passive head movement or oculovestibular stimulation. If there is any possibility of trauma, a cervical spine series should precede neck manipulation for eye movement examination. Roving eye movements indicate that brainstem function is intact. The roving eye movements or early coma cannot be mimicked, and their presence excludes psychogenic unresponsiveness. With deepening of coma, first to disappear is roving eye movement, then the oculocephalic response, and then the oculovestibular reflex. Conjugate eye deviation away from the paralyzed extremities is seen in destructive frontal lobe lesions; conjugate deviation in the direction of the paralyzed extremities indicates a brainstem lesion. Conjugate gaze deviation, sometimes with accompanying nystagmoid jerking, may also occur because of seizure activity in the frontal eye fields on the side the patient is looking away from. Thalamic hemorrhage can cause “wrong-way eyes,” with gaze deviation toward the hemiparesis. Vertical gaze deviations suggest brainstem disease; the most common is sustained downgaze with an upgaze deficit due to a lesion involving the upper midbrain or caudal thalamus. Hepatic encephalopathy can cause down-gaze deviation.

Reflex movements elicited by turning the head from side to side (doll’s eye movements, oculocephalic reflex) or by the injection of ice water into the external auditory canal (caloric test, oculovestibular reflex) may reveal isolated weakness of particular extraocular muscles, gaze paresis, or other eye movement abnormalities (Figure 51.1). Supratentorial lesions and metabolic processes usually do not affect the oculocephalic reflex. Wernicke’s encephalopathy is one metabolic encephalopathy that may affect eye movements; it is not limited to alcoholics. Caloric testing assesses the same brainstem reflexes as the doll’s eye maneuver and is used if the oculocephalic reflex is not intact. After ensuring the external auditory canal is clear, the head is flexed to a 30-degree angle above horizontal and 10 to 20 cc of ice water is instilled into the canal. If no response is obtained, larger volumes are used. After 15 to 60 seconds, eye deviation begins and may last several minutes. The expected response in coma is tonic deviation of the eyes toward the side of the irrigated ear. Warm water causes the opposite response. Testing of the other side may be done after about 5 minutes. Brainstem lesions affecting the pathways and nuclei subserving the reflex may cause an abnormal response. Dysconjugate movements may signal a lesion involving the medial longitudinal fasciculus or the CN III or VI pathways. In coma, absence of a response to cold calorics suggests sedative-hypnotic drug intoxication, a structural lesion of the brainstem, or brain death, unless there is evidence of a vestibular disorder, or exposure to vestibular-suppressant drugs. Some causes of metabolic coma may fix the eye movements while preserving pupillary reactivity. When the response is present, the eye movements may be dysconjugate. Some drugs, particularly sedative-hypnotic agents, tricyclics, and anticonvulsants, may affect eye movements in a comatose patient. Vertically dysconjugate gaze at rest may indicate skew deviation. The oculocephalic or bilateral oculovestibular testing can assess the vertical gaze pathways. Dysconjugacy usually indicates a brainstem lesion. Unusual spontaneous eye movements may occur in coma (e.g., ocular bobbing, ping-pong gaze, periodic alternating gaze deviation, repetitive divergence, nystagmoid jerking, ocular dipping), and the particular pattern often has localizing significance. If the patient is responsive enough, testing for optokinetic nystagmus may give important diagnostic information.

Note whether the eyes are open or closed and the width of the palpebral fissures on the two sides. When the eyelids are closed in a comatose patient, the lower pons is still functioning. Eyelids at half mast suggest it is not. In “eyes-open” coma, the eyelids are spastically retracted due to failure of levator inhibition with a lesion in the pons. Spontaneous blinking requires an intact pontine reticular formation. Asymmetry of the palpebral fissures may i ndicate either upper facial weakness on the side of the wider fissure or ptosis on the side of the narrower fissure. If the eyes are partially or completely closed, the examiner may try to open them by gently raising the upper lids, and then noting the speed with which the eyes close again. Unilateral orbicularis weakness may produce more leisurely closure on the affected side. In deep coma, the eyes may be open and a glassy stare evident. In profound illness, the patient often lies with the eyes only partially closed, even in sleep, so that a narrow portion of the cornea is visible between the upper and lower lids. In psychogenic unresponsiveness (hysterical coma), the patient may keep the eyes tightly closed and resist attempts to open them, yet open the eyes and glance around when unaware that someone is observing the action. Note whether there is any blinking, flickering, or tremor of the eyelids at rest or in response to a bright light or sudden noise. The corneal reflexes may be absent in coma; any asymmetry of the response may be significant.

In some patients, it is possible to obtain facial movement by painful stimulation, such as supraorbital pressure, sternal rub, or pinprick stimulation of the face. The area of the upper nasolabial fold at the junction with the nose is particularly sensitive and a response to pinprick in this region can sometimes be obtained when there is no response over other parts of the face. It is important when examining facial sensation not to traumatize the face and leave pinprick marks, particularly in elderly patients with thin, fragile skin. Firm manual pressure over the supraorbital notch, at the point of emergence of the supraorbital nerve, will often produce facial grimacing. When facial movement does occur, compare the two sides for symmetry of the response. Elicitation of a blink response to loud noise provides a crude assessment of auditory function. The mouth may be either open or closed. In nonorganic unresponsiveness, the patient may resist attempts to passively open the mouth. A gag reflex may or may not be present. If present, the palate should rise in the midline.

No neurologic evaluation of coma, stupor, or disordered consciousness is complete without an ophthalmoscopic examination. The presence of papilledema is, of course, indicative of some process causing increased intracranial pressure. Papilledema takes a period of time to develop and may be absent in acute conditions. Normal spontaneous venous pulsations are a strong indicator of normal intracranial pressure, but absence of venous pulsations does not prove intracranial pressure is increased. Subarachnoid hemorrhage may produce subhyaloid hemorrhages in the retina. The ophthalmoscopic examination is also important in detecting systemic diseases responsible for altered consciousness (e.g., diabetes, hypertension, or endocarditis). It is not possible to test either visual acuity or the visual fields reliably if significant impairment of consciousness is present. If the patient is responsive enough, it may be possible to determine if the patient follows objects, or blinks to threat.

Examination of Motor Status

The motor examination in disorders of consciousness requires skilled observation. It may be difficult to recognize the presence of a hemiplegia in a comatose patient. If the hemiplegia has been of sudden onset, the paralyzed side of the body is usually flaccid. The width of the palpebral fissure is increased, the nasolabial fold is shallow, and the angle of the mouth droops on that side. There may be drooling of saliva and puffing out and retraction of the cheek on expiration and inspiration.

If both arms are lifted, or placed with the elbows resting on the bed and the forearms at right angles to the arms, then released by the examiner, the affected extremity falls more rapidly and in a flail-like manner, while the normal arm drops slowly or may even remain upright for a brief period before falling. If the lower extremities are lifted from the bed and then released, the affected extremity falls rapidly, while the normal limb drops more gradually to the bed. If the lower extremities are passively flexed with heels resting on the bed and then released, the paretic limb rapidly falls to an extended position with the hip in external rotation, while the unaffected limb maintains the posture for a few moments and then gradually returns to its original position. If the depression of consciousness is not too deep, there may be some response to painful stimulation. Pinching the skin on the normal side is followed by withdrawal of the part stimulated. In contrast, a painful stimulus on the paralyzed side causes no local movement, although grimacing or movements of the opposite side of the body may indicate that some sensation is retained. Other tests of motor function, such as evaluation of coordination and active movement, cannot be performed on unresponsive patients. It is important to appraise muscle tone, or resistance to passive movement, and to observe carefully for any abnormal movements. Generalized flaccidity may occur with critical illness polyneuropathy or myopathy. Flaccidity of both arms with normal tone in the legs may occur with border zone ischemia (man-in-the-barrel syndrome). Multifocal myoclonus, with widespread brief, random, asynchronous jerks, strongly suggests a metabolic or toxic etiology, especially hypoxic-ischemic encephalopathy. More subtle twitches, random or sustained, suggest nonconvulsive status epilepticus. Such twitches may be restricted to the facial muscles, fingers, or even the tongue.

Occasionally, spasticity instead of flaccidity develops after acute cerebral lesions. A previous spastic hemiplegia or extrapyramidal syndrome may have caused an alteration in tone that persists even in coma, and arthropathies and skeletal abnormalities may also interfere with joint movements. In catatonia, there may be a waxy resistance resembling that of extrapyramidal disease. Patients with AMS may have asterixis.

The motor responses to stimuli are probably the most important factor in gauging the depth of coma and prognosis. The highest level response is when the patient obeys simple commands (GCS 6). If there is no response to verbal commands, a painful stimulus is delivered. There are five possible outcomes. The patient may localize the painful stimulus and make appropriate movements to attempt to remove it (GCS 5). She may exhibit flexion withdrawal without localizing the stimulus (GCS 4). There may be abnormal flexor responses (decorticate rigidity, GCS 3), or, as the lowest level of response, an extensor response (decerebrate rigidity, GCS 2). The worst possible outcome is no response whatsoever (GCS 1).

Abnormal flexor and extensor responses are referred to as posturing. Abnormal posturing may occur spontaneously, as well as in response to stimuli. It is not uncommon for posturing to be different on the two sides of the body. When there is difficulty distinguishing purposeful withdrawal from decorticate posturing, a painful stimulus to the inner arm is useful. Abduction of the arm away from the stimulus is a high-level avoidance response; adduction into the stimulus is a low-level reflex response. Posturing usually indicates structural disease of the nervous system and is particularly common after head injury. Posturing can also occur with severe metabolic encephalopathy, particularly sedative-hypnotic drug intoxication.

Decerebrate and decorticate rigidity are discussed in Chapter 28 and Chapter 41. In brief, decorticate posturing includes upper-extremity adduction and flexion and lower-extremity extension. In decerebrate posturing, there is extension of both upper and lower extremities. Decerebration is traditionally thought to indicate a lesion below the red nucleus but above the lateral vestibulospinal tracts. These neuroanatomic correlates do not seem to apply as well in humans as experimental animals. Decerebrate posturing occurs in patients with bilateral cerebral lesions, well above the red nucleus. The distinction is useful prognostically; patients with decorticate posturing in response to pain tend to have a better prognosis than those with decerebrate posturing.

Sensory Examination

Depending on the level of coma, the patient may not perceive even the most painful stimulus or may respond to painful stimuli by wincing and withdrawing the part of the body stimulated. Often, the examination must be limited to comparing responses to painful stimulation on the two sides of the body. Sensory stimuli may be delivered by pinching the skin, pricking with a sharp object, pressing over the supraorbital notch, and squeezing the muscle masses and tendons, particularly the Achilles tendon.

Reflexes

At a minimum, the principal tendon reflexes and the plantar responses should be tested. Frontal release signs (forced grasping, palmomental, and suck or snout responses) and paratonic rigidity may be present with AMS of either structural or metabolic origin. Asymmetry of responses may have some localizing value. Similarly, extensor plantar responses may occur with either structural or metabolic coma.

Meningeal Signs

The examiner should attempt to elicit signs of meningeal involvement by flexing the neck passively and rotating it from side to side in order to detect nuchal rigidity. The Kernig, Brudzinski, and related signs may be absent in some cases of deep coma despite the presence of meningeal irritation. In subarachnoid hemorrhage, it requires some hours for meningeal signs to develop, and they may be absent at the time of presentation.

DIFFERENTIAL DIAGNOSIS OF COMA

There are three possible etiologies for acute coma: (a) primary CNS disease, (b) depression of the CNS by a systemic metabolic process or drug intoxication, and (c) psychogenic unresponsiveness. Statistically, the most likely etiology is involvement of the CNS by a systemic metabolic process or drug intoxication. Patients with metabolic encephalopathy characteristically have a symmetrical examination, devoid of lateralizing or focal abnormalities, intact reflex eye movements, and reactive pupils.

Structural Lesions

There are three mechanisms whereby structural lesions may cause coma: (a) a lateralized hemispheric mass lesion causes increased intracranial pressure, herniation, and compression or hemorrhage into the upper midbrain with secondary impairment of the RAS; (b) a brainstem lesion, such as hemorrhage or infarction, damages the RAS directly; and (c) a disease process affects both cerebral hemispheres or both hemispheres and the RAS. The findings with a hemispheric mass lesion depend upon the stage of evolution of the process. In the early stages, there are usually lateralizing findings and asymmetries on examination consistent with a focal process. These include hemiparesis, focal seizures, aphasia, hemianopia, apraxia, and other signs of hemispheric dysfunction. As the lesion expands and intracranial pressure increases, the other hemisphere becomes involved, herniation develops, and the focal nature of the process becomes complicated by findings due to herniation. Asymmetric motor responses and abnormal eye movements usually persist until the terminal stages. Herniation syndromes are due to shifting of brain structures caused by increased intracranial pressure. They are evidence of severe disease and are life-threatening. A number of different herniation syndromes have been recognized. The more common and important are central transtentorial, lateral transtentorial (uncal), and tonsillar (foramen magnum) herniation (Figure 51.2, Table 51.3).

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