CONSCIOUSNESS

An appreciation of the phenomenon of consciousness should precede a discussion of coma or “unconsciousness.” Many aspects of consciousness still remain a cardinal mystery of the human being. The essence of consciousness is an awareness of the environment and of the self. This awareness at least involves perception and memory, but the prerequisites for consciousness are alertness and attention. Primary consciousness is the state of having mental images of the present (the “remembered present”). Higher order consciousness is the ability to be aware of being conscious and is accompanied by memories of the past and the ability to plan for the future. It requires semantic ability, which is the ability to attach meaning to a symbol, and also the ability to manipulate those symbols. Higher order primates may have higher order consciousness to a limited degree.

Qualia are the high-order perceptions of qualities, such as the warmth of warm or the redness of red, that are experienced in the normal conscious state.¹ Free will, conscience, meta-memory (knowledge and beliefs about the functioning of one’s own memory systems), the analysis of one’s own thoughts, and imagination are all integral components of human higher order consciousness that remain mysterious. Much of the planning and execution that humans perform is unconscious or preconscious in the “zombie mode.” An example is sensory processing and gating. The automatisms of complex partial seizures are an extended pathological example of this. Penfield (1937) showed that electrical stimulation of the cortex could alter the content of consciousness and produce “experiential responses” that the patient usually realized were unreal. The “déjà vu” phenomenon is a natural example of this.

The neural correlates of consciousness are slowly yielding to the study of individual and group neuronal electrical activity, through the use of surface cortical electrodes and implanted microelectrodes, and to functional brain imaging. Although there is a modularity to brain function, it is the integration of all the modules that is necessary for consciousness. There also seems to be competition between different cortical areas and neurons to choose the best fit for a set of perceptual inputs. There are “essential nodes” for particular perceptions such as face recognition or color perception. Clearly, multiple nodes and regions of the brain, functioning in concert, are necessary for consciousness to exist.^2,3

Both the cerebral cortex and subcortical structures such as the thalamus are involved in consciousness. Dandy described temporary loss of consciousness after removal of both frontal lobes with sacrifice of the anterior cerebral arteries at the genu of the corpus callosum and speculated that the striatal damage was responsible for the coma.⁴ The reticular nucleus that surrounds the thalamus acts as a switch or “gate” to particular thalamic nuclei. It results in different patterns of activity of the thalamic nuclei and therefore in different weighting of sensory input. The intralaminar nucleus of the thalamus sets thresholds for the cortical response to the thalamic input. Thalamic gating is also influenced by feedback from the prefrontal cortex.⁵ The filtering of sensory information is done at a preconscious level so that attention is selectively directed, although it can also be altered at will.

Moruzzi and Magoun⁶ in 1949 produced electroencephalographic arousal by stimulating the brainstem reticular formation rostral to the mid-pons. They termed this system, including its rostral projection, the ascending reticular activating system (ARAS). This is an alerting or arousal system that also indirectly influences sensory processing in the cerebral cortex. It projects rostrally through the midline, intralaminar nucleus, and other nuclei of the thalamus, and via these structures to the cerebral cortex. Attention enables an awake and alert individual to select a task or a stimulus to process from a number of alternatives and to select a cognitive strategy to carry it out.⁵ The ARAS is thought to facilitate this process by enhancing the perception of differences between competing stimuli. The anterior cingulate gyrus is involved in a wide range of attentional and discriminatory activity and is involved in higher order motor control of many tasks. The parietal cortex is involved in attention in the visual field and the pulvinar of the thalamus is involved in selecting information for attention. The dorsolateral prefrontal cortex is also involved in attention, intention, and working memory; working memory is the term applied to the holding and manipulation of the current content of consciousness. The hippocampal system—including the fornices, the mammillary bodies and mammillothalamic tracts, the amygdala, the anterior thalamic nuclei, the medial dorsal thalamic nuclei, and the entorhinal cortex—are all involved with establishing new anterograde episodic memory. The amygdala, hippocampus, and associated limbic and nonlimbic structures are involved in the generation of internal feelings, emotions, and motivation.⁵

Various brainstem and basal nuclei form ascending and descending neural systems that influence large areas of the brain by releasing particular neurotransmitters. The cholinergic nuclei, such as the basal forebrain nuclei, the pedunculopontine nucleus, and the laterodorsal tegmental nuclei, play a role in alertness and arousal. Acetylcholine is probably an important neurotransmitter for memory function. The noradrenergic locus ceruleus and lateral tegmental nuclei of the pons assist in responding to sudden contrasting or adverse stimuli, and the locus ceruleus projection to the forebrain and visual cortex is involved in attention. The majority of the cell bodies of the dopaminergic system are in the ventral brainstem tegmentum and are involved in motor function and cognition. The dopaminergic nigrostriatal projection is also involved in motor function and attention. The serotonergic system of the midline raphe nuclei of the tegmentum, largely inhibitory in nature, has a stabilizing effect on information processing, is involved in sleep, and modulates the sleep-wake cycle.

The γ-amino butyric acid (GABA) inhibitory neurons are widely dispersed throughout the central nervous system and are involved with the selection of sensory information. Barbiturates increase GABAergic activity in the ARAS. Glutamate and aspartate are the excitatory neurotransmitters that play a key role in cortical interplay.⁵ The N-methyl-D-aspartate (NMDA) receptor may be the main target for the action of general anesthetic agents that produce a pharmacological coma. The corollary, that the NMDA receptor is essential for consciousness, constitutes the Flohr hypothesis, about which there is considerable debate.⁷ Clearly, many other peptides and receptors are also involved in cortical function and consciousness.

Single neurons in the human entorhinal cortex have very specific responses (e.g., only to faces or only to different types of animal), and some temporal lobe neurons function at a different hierarchical level by responding to the extensively processed perception or imagining of an object and not to the raw retinal input.² Different components of consciousness therefore seem to exist from the level of individual neurons to that of different brain regions and, indeed, that of the whole brain.

Edelman (2004) proposed a theory called neural Darwinism, or neuronal group selection, to explain consciousness, as opposed to an instructive model in which the brain has computer-like properties with a set of programs and algorithms. The three tenets of neural Darwinism are that (1) developmental selection leads to a highly diverse group of circuits, (2) experiential selection leads to changes in the connection strength of synapses, and (3) reentrant mapping occurs, in which brain maps are coordinated in space and time through reentrant signaling across reciprocal connections. This coordination leads to widespread synchronization of widely dispersed neuronal groups, which integrates information such as the color and orientation of visual objects and which Edelman proposed is central to the understanding of consciousness. This is a possible solution to the binding problem, which is the seamless reintegration of separately processed aspects of a sensory percept at a preconscious level. According to neural Darwinism, the brain is a selectional system. Other examples of such systems in nature are evolution and the immune system. Another important characteristic of the brain is degeneracy, in which different elements of the brain can perform the same function and one element can carry out different functions in different neuronal networks at different times. This creates great diversity of brain function. There is no need in the theory of neural Darwinism for a homunculus in the head directing the brain and being the seat of consciousness.¹

The principal neural structures of consciousness according to Edelman’s (2004) theory are the cerebral cortex, the thalamus, and the reentrant loops between the two, which he called the dynamic thalamocortical core. He proposed that this neural activity generates the qualia of consciousness. The gamma, or 40-Hz, rhythm of the electroencephalogram (EEG) is believed to be produced by thalamocortical circuits during attention and sensory processing tasks. Attention is directed partly by the reticular nucleus of the thalamus and partly by the relationship of the basal ganglia to the frontal and parietal cortices. Higher order consciousness is based in part on episodic memory, which depends on the hippocampi, and in part on semantic and linguistic ability, which depend on the language cortices of Broca and Wernicke and associated areas (for further reading, see Edelman, 2004; Jasper et al, 1998; John, 2002; Metzinger, 2002; Young et al, 1998; Zeman, 2001).

COMA

The Anatomy and Pathophysiology of Coma

Diffuse lesions of both cerebral hemispheres (cortical and subcortical white matter) may cause coma. Bilateral diencephalic damage (especially to the paramedian dorsal thalamus) may also cause coma (Fig. 8-1). The extension of the thalamic lesions into the midbrain tegmentum has an even greater propensity for causing coma or severe neurological deficit, apathy, and impaired attention. Damage to the paramedian gray matter anywhere from the posterior hypothalamus to the tegmentum of the lower pons causes coma.^8,9 When the respiratory centers in the lower medulla are damaged, apnea ensues. The testing of brainstem reflexes and for apnea is the clinical means of confirming the destruction of theses critical areas. The irreversible destruction of critical brainstem areas usually follows catastrophic supratentorial events that cause brain herniation and subsequent compression and ischemia of the brainstem.

Figure 8-1 Computed tomographic scan showing the trajectory of small metal shrapnel fragments across both thalami and internal capsules of a young man who was a victim of a bomb blast. The entry point was just above and behind the right ear, and one fragment was lodged beneath the temporal bone on the left side. He remained deeply comatose after this injury, breathing spontaneously but with minimal response of his limbs to pain and with no eye opening.

The sequence of cardiovascular changes resulting from progressive mechanical compression and/or ischemia of the brainstem begins with vagal stimulation, which causes decreases in heart rate, mean arterial pressure, and cardiac output. As the pons becomes ischemic, sympathetic stimulation occurs, which results in hypertension with persistence of the bradycardia (Cushing’s reflex). As the medulla becomes ischemic, there is unopposed sympathetic stimulation with tachycardia, increased mean arterial pressure, and increased cardiac output. This sequence has been called an “autonomic storm” and has not been well recognized in intensive care unit patients, partly because it may have occurred by the time the patient is admitted to intensive care unit and may be affected by treatment or the presence of other injuries.¹⁰

Clinical Assessment of the Comatose Patient

A full neurological and general examination of the patient must be undertaken. Some of the pertinent components of the examination are described as follows.^5,9

Assessment of the Conscious State

The Glasgow Coma Scale (GCS) was devised to provide a simple, reliable, and reproducible method of assessment of conscious state so as to avoid misinterpretation and blurring of terms such as stupor, semicoma, and confusion.¹¹ It has become a universally accepted scale for neurological observation, prognostication, and grading severity and has been found to have good interrater reliability. It was originally a 14-point scale but has been extended to 15 points by splitting limb flexion into two tiers: flexion-withdrawal and flexion-abnormal. Abnormal flexion is defined as any two elements of stereotyped flexion posture, extreme wrist flexion, adduction of the upper arm, and fisting of the fingers over the thumb.^12,13 The 15-point scale is the preferred scale for research studies. The GCS is scored on the best response in each of the three categories: eye opening, vocalization, and limb movement (Table 8-2). Testing nail bed pressure with a pencil is the recommended method of applying a painful stimulus. Patients who do not open their eyes, do not speak, and are not obeying commands are said to be comatose. Many clinicians regard a maximum GCS score of 8 as the cutoff for coma. Some limitations to the usefulness of the GCS do exist, however. For example, periorbital swelling and endotracheal intubation, both common conditions in the trauma patient, prevent the accurate assessment of eye opening and verbal response, respectively. Some centers record a “T” next to the score when the patient is intubated and the verbal score cannot be assessed. The GCS is commonly used to monitor neurological progress, and a drop in the GCS of 2 points or more is a sensitive measure of neurological deterioration and necessitates action to halt the progression. Age and depth of coma are the principal predictors of poor outcome or death after traumatic brain injury. Repeated GCS assessments and the recognition of confounding factors are required for any confidence in prediction of outcome.

TABLE 8-2 Glasgow Coma Scale and Paediatric Glasgow Coma Scale

The conscious state is more difficult to assess in infants and young children, and special pediatric coma scales have been devised.¹⁴ The Paediatric Glasgow Coma Scale is a simple system based on the GCS with age-related norms for verbal and motor responses (see Table 8-2).¹⁵

A rapid and simple assessment of conscious state is the “AVPU” system, in which the examiner assesses the level of response on a four-tiered scale: A is alertness, V is any response to vocal stimuli (what response? opens eyes? moves? vocalizes? any of the above?), P is response only to painful stimuli, and U is unresponsiveness to all stimuli. This scale is used in the primary survey of trauma patients as taught on the Advanced Trauma Life Support Course of the American College of Surgeons. The GCS may also be used in the primary survey and is used in the secondary trauma survey, which includes a comprehensive general examination.

Respiratory Pattern

1. Normal pattern.

2. Cheyne-Stokes: periodic increase and decrease of rate and depth, followed by an expiratory pause and then a repeated pattern; seen with diencephalic pathology and bilateral hemisphere dysfunction (nonspecific).

3. Hyperventilation: raises suspicion of hypoxia or metabolic coma with acidosis, such as with ethylene glycol, methanol, salicylates, and lactic acidosis. Central neurogenic hyperventilation may occur with midbrain damage.

4. Cluster breathing: periods of rapid irregular breathing separated by periods of apnea; is similar to Cheyne-Stokes respiration but without the crescendo/decrescendo pattern or regularity of the latter. This is seen with high medullary or low pontine lesions.

5. Apneustic breathing: deep inspiration followed by breath holding, then long slow expiration at a rate of 6 breaths per minute; implies pontine damage (e.g., basilar artery occlusion). It is a rare pattern.

6. Ataxic (Biot’s) breathing: irregular and disorganized breathing; occurs with medullary dysfunction and is usually preterminal.

Vital Signs

The blood pressure, pulse, capillary return, core temperature, and the state of hydration should all be ascertained.

Pupil Examination

Pupillary size, shape, and reaction are integral components of the assessment of conscious state. The light reflex is the most useful in distinguishing metabolic from structural causes of coma.

1. Equal-sized and reactive pupils in a comatose patient indicate a metabolic or toxic cause, with the exceptions of anoxia, anticholinergics, glutethimide, and botulinum toxin, which cause fixed, dilated pupils. Narcotics cause small pupils (miosis) that react sluggishly.

2. Unequal-sized pupils imply a structural lesion of the brain or cranial nerves. One caveat is that direct ocular trauma may produce a mydriasis. A pupil that dilates after a cerebral insult is indicative of changing intracranial pathology with increasing tension on the ipsilateral oculomotor nerve resulting from uncal herniation through the tentorial hiatus. Dilated nonreactive pupils from the time of an injury imply irreparable brain damage or bilateral optic nerve injury. The miosis of Horner’s syndrome implies disruption of the sympathetic nervous system input to the pupil and may follow carotid occlusion or dissection, among other causes.

3. Bilateral pinpoint pupils occur with pontine lesions that leave the parasympathetic nerves unopposed.

4. Bilaterally fixed and dilated pupils (7 to 10 mm) occurs with medullary injury, with post-tonsillar or central herniation, after anoxia, or with hypothermia (<32° C).

5. Bilateral nonreactive pupils at the midposition(4 to 6 mm) occurs with an extensive midbrain lesion.

Eye Motion: Extraocular Muscle Function (Fig. 8-2)

Deviation of the Ocular Axes

Bilateral conjugate deviation

Frontal lobe lesion (frontal center for contralateral gaze): the eyes look toward the side of the lesion.

Pontine lesion: the eyes look away from the side of the lesion.

Medial thalamic lesion: the eyes look away from the side of the lesion.

Downward deviation: thalamic or midbrain pretectal lesions, metabolic cause (especially barbiturates).

Figure 8-2 Eye motion: extraocular muscle dysfunction.

Unilateral outward deviation with dilated pupil (nerve III palsy)

Unilateral inward deviation (nerve VI palsy)

Skew deviation: nerve III or IV nuclear or nerve injury, or an infratentorial lesion, especially of the dorsal midbrain.

Spontaneous Eye Movement

Ocular bobbing with rapid downward movement of the eyes and a slow return occurs with pontine lesions. Random conjugate eye movements are nonspecific for lesion location. In the uncommon periodic alternating gaze (“ping-pong gaze”), the eyes deviate side to side with a frequency of three to five per second and a pause of 2 to 3 seconds in each direction. This may indicate bilateral cerebral dysfunction.

Internuclear Ophthalmoplegia

Internuclear ophthalmoplegia is caused by a lesion of the medial longitudinal fasciculus. The eye on the side of the lesion does not adduct on spontaneous or reflex-induced eye movement.

Reflex Eye Movement

Oculocephalic reflex (doll’s-eye reflex)

In the awake patient, the eyes follow the movement of the head or, if the movement is performed slowly, there is contraversive conjugate eye movement if the eyes fixate on a stationary target. In the comatose patient with intact brainstem and cranial nerves, the reflex is preserved and the eyes move in the opposite direction when the head is turned laterally or the neck flexed and extended; that is, the conjugate eye movement is contraversive. When the brainstem is damaged, the reflex is lost, and the eyes follow the head movement. Cervical spine injury should be ruled out before this test is performed.

Oculovestibular reflex (iced water calorics)

The head of the bed is elevated 30 degrees (to place the “horizontal” semicircular canals in the true vertical position), and one ear is irrigated with 50 to 100 mL of iced water. A comatose patient with an intact brainstem has tonic conjugate eye movement to the side of the cold stimulus which may be delayed up to one minute or more. There is no fast component (the nystagmus), which is present in the conscious subject. Absence of response results from brain death, neuromuscular blockade, metabolic causes, and massive infratentorial pathology. Nystagmus without tonic deviation occurs in psychogenic coma. Tympanic membrane rupture or external auditory canal obstruction by blood or debris should be ruled out before this test is performed.

Optokinetic nystagmus

Optokinetic nystagmus is a rhythmic involuntary conjugate ocular movement in response to the movement of full visual field images, either rotation of an image before the subject, such as a drum with vertical black stripes on a white background, or rocking of a mirror back and forth in front of the patient’s eyes. There is a biphasic response with an initial slow phase provoked by, and in the direction of, the stimulus. This is followed by a fast corrective phase. Optokinetic nystagmus may be elicited in patients feigning coma.

Herniation Syndromes (Coning)

Cerebral herniation is the displacement of cerebral tissue as a result of intracranial mass lesions. This displacement may disturb the conscious state by direct or indirect pressure on the diencephalon and brainstem. Indirect pressure means displacement of tissue at a distance from the mass. Coning is the name given to progressive cerebral herniation with secondary compression of the brainstem and resultant deepening coma. Computed tomography (CT) and magnetic resonance imaging have helped significantly to elucidate the anatomy of herniation. Plum and Posner (1982) in their classic treatise described progressive and predictable stages of herniation with cephalad-caudal progression. There are five types of supratentorial and infratentorial herniation (Fig. 8-3), described as follows.

Figure 8-3 Schematic diagram showing the various types of brain herniation. 1, Subfalcine or cingulate herniation, in this case caused by an adjacent tumor. Note the midline shift of the septum pellucidum resulting from the mass lesion in the adjacent portion of the brain. 2, Transtentorial uncal herniation with midbrain compression, in this case caused by an acute epidural hematoma. 3, Central herniation with vertical descent of the brainstem. 4, Cerebellar tonsillar herniation through the foramen magnum with compression of the medulla. 5, Upward cerebellar herniation with upper brainstem compression.

Supratentorial Herniation

Central (Transtentorial) Herniation

The classic description is of a sequential rostral-caudal failure from diencephalon to the midbrain, the pons, and finally the medulla. Central herniation is often caused by a tumor in the frontal, parietal, or occipital lobes that reaches the point of decompensation. The diencephalon may herniate through the tentorial incisura, damaging the pituitary stalk and causing diabetes insipidus. Vertical downward shift of the brainstem may be a critical factor in the development of the features of central herniation.¹⁶ The brainstem may become ischemic as a consequence of shearing of perforating arteries from the basilar artery. Resultant hemorrhages in brainstem are called Duret hemorrhages. CT may show a downward displacement of the pineal gland and effacement of the perimesencephalic (ambient) cisterns. The posterior cerebral arteries may be kinked at the tentorial edge as they pass onto the inferior surface of the occipital lobe, which results in occipital infarction and cortical blindness. This may further increase the intracranial pressure.

The clinical stages of central herniation are outlined in Table 8-3. It is difficult to discern these various stages (and those of the other types of coning) in many patients because of the speed of deterioration, the tendency of the stages to merge, and the mixed and complex pathology that may affect the supratentorial and infratentorial compartments, and because patients often receive early intervention with paralysis, endotracheal intubation, and ventilation that obscures or retards the clinical progression. Nevertheless, it is useful to think conceptually in these terms in contemplating the patient’s condition and the appropriate treatment.

TABLE 8-3 Stages of Central Herniation

Diencephalon Stage	May be caused by displacement or ischemia of the diencephalon
	This stage is reversible
Consciousness	Altered alertness is first sign
	Usually lethargy is present
	Some patients have agitation
	Later stupor, then coma
Respiration	Sighs, yawns, occasional pauses
Pupils	Small (1-3 mm), reacting
Oculomotor	Conjugate or slightly divergent roving eyes
	Doll’s-eye reflex present
	Parinaud’s syndrome with impaired upward gaze may be present
	Conjugate ipsilateral response to cold water calorics
Motor	Early: appropriate response to painful stimulus
	Contralateral hemiparesis may worsen
	Bilateral Babinski reflex; later, grasp reflexes
	Decorticate (contralateral to the lesion initially)
Midbrain–Upper Pons Stage	Prognosis is very poor when midbrain signs have developed; <5% having a good outcome if treatment is undertaken
Respiration	Cheyne-Stokes respiration → sustained tachypnea
Pupils	Moderately dilated: midposition (3-5 mm), fixed
Oculomotor	Doll’s-eye reflex impaired
	May be disconjugate
	May be internuclear ophthalmoplegia with medial moving eye moving less than the laterally moving eye)
	Response to calorics impaired
Motor	Decorticate → bilaterally decerebrate
Lower Pons–Medulla Stage
Respiration	Regular, shallow, and rapid (20-40/minute)
Pupils	Midposition (3-5 mm), fixed
Oculomotor	No doll’s-eye reflex
	Response to calorics absent
Motor	Flaccid, bilateral Babinski reflex
	May be lower limb flexion in response to pain
Medullary Stage (Terminal Stage)
Respiration	Slow, irregular; sighs, gasps, occasional hyperpnea alternating with apnea
Pupils	Widely dilated and fixed

Adapted from Greenberg MS: Coma. In Greenberg MS, ed: Handbook of Neurosurgery, 5th ed. New York: Thieme, 2001, pp 118-127. Also see Plum and Posner (1982).

Uncal herniation

The uncus of the temporal lobe herniates over the free edge of the tentorium, compressing the midbrain and the oculomotor nerve. This is usually caused by a rapidly expanding middle cranial fossa epidural, subdural, or intratemporal lobe hematoma. The earliest sign of uncal herniation is the ipsilateral dilation of the pupil. A depressed state of consciousness is not a reliable early sign, but the patient may be confused or agitated. Once the brainstem is compromised, the conscious state may deteriorate rapidly to a deep coma. The mass lesion causing the uncal herniation usually causes a contralateral hemiparesis, but as the pressure increases, the opposite cerebral peduncle is compressed against the tentorium, which causes an ipsilateral hemiparesis (Kernohan’s sign). This is recognized at autopsy as Kernohan’s notch. As in central herniation, the posterior cerebral arteries may be compressed against the edge of the tentorium, which may cause occipital lobe infarcts. The early CT findings of uncal herniation are early unilateral encroachment on the suprasellar cistern and later brainstem displacement and flattening, flattening of the contralateral cerebral peduncle, and rotation of the midbrain. Contralateral hydrocephalus may occur. The clinical stages of uncal herniation are outlined in Table 8-4.

TABLE 8-4 The Stages of Uncal Herniation

Early Third Nerve Stage
Pupils	Unilateral dilating pupil, ipsilateral to lesion in 85% of patients; often sluggish
Oculomotor	Doll’s-eye reflex normal or disconjugate (failure of adduction of ipsilateral eye)
	Caloric reflex may be disconjugate
Respiration	Normal
Motor	Appropriate response to pain
	Contralateral Babinski reflex may be present
Late Third Nerve Stage
Consciousness	Stupor → coma
Pupil	Fully dilated (unilateral)
Oculomotor	Complete third nerve palsy with pupil dilatation (>6 mm) and ophthalmoplegia
Respiration	Hyperventilation sustained; in rare cases, Cheyne-Stokes respiration
Motor	Usually contralateral weakness
	If opposite cerebral peduncle is compressed against the tent, an ipsilateral hemiparesis (Kernohan’s sign) and then bilateral decerebrate posture develop
Midbrain–Upper Pons Stage
Pupils	Contralateral pupil dilates initially to midposition (5-6 mm)
Oculomotor	Palsy
Respirations	Sustained hyperpnea
Motor	Bilateral decerebrate rigidity

Adapted from Greenberg MS: Coma. In Greenberg MS, ed: Handbook of Neurosurgery, 5th ed. New York: Thieme, 2001, pp 118-127. Also see Plum and Posner (1982).

The distinction between uncal and central herniation is difficult when the compression has reached the midbrain and below. Prediction of the location of the pathology on the basis of the type of herniation syndrome is unreliable, inasmuch as central and uncal herniation may occur together. Decrease in consciousness occurs early in the sequence of central herniation but later in the sequence of uncal herniation. Cushing’s reflex, consisting of hypertension, bradycardia, and respiratory irregularity, which is a feature of medullary compression, is often absent with slowly progressive supratentorial mass lesions. The cause of the coma and the third nerve palsy in cases of presumed uncal herniation is not always uncal compression, because the degree of uncal herniation on imaging or at autopsy may not be correlated with clinical state. The anatomy varies among patients, and in some cases, there is no uncal herniation or it is the contralateral pupil that dilates first, so that the mechanism of the third nerve palsy is likely to be central (i.e., intrinsic to the midbrain) in these cases. Horizontal displacement of the central supratentorial structures may also contribute to or cause the depressed conscious state (see Investigation of Coma).¹⁷

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