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Intracerebral 44 brain dysfunction 1 Hypertensive 36 A.

Main Photo

Diffuse intrinsic disorders of brain 38 2 Vascular anomaly 5 1. Epidural 4 2. Subarachnoid hemorrhage 13 c. Subdural 26 3. Concussion, nonconvulsive 9 d. Pituitary apoplexy 2 seizures, and postictal states 2. Infarction 9 4. Primary neuronal disorders 2 a. Arterial occlusions 7 B. Extrinsic and metabolic 1 Thrombotic 5 disorders 2 Embolic 2 1. Anoxia or ischemia 10 b. Venous occlusions 2 2. Hypoglycemia 16 3. Tumors 7 3. Nutritional 1 a.

Primary 2 4. Hepatic encephalopathy 17 b. Metastatic 5 5. Uremia and dialysis 8 4. Abscess 6 6. Pulmonary disease 3 a. Intracerebral 5 7. Endocrine disorders 12 b. Subdural 1 including diabetes 5. Closed head injury 1 8. Remote effects of cancer 0 II. Subtentorial lesions 65 9. Drug poisons A. Compressive lesions 12 Ionic and acid-base disorders 12 1. Cerebellar hemorrhage 5 Temperature regulation 9 2. Posterior fossa subdural or 1 Cerebellar infarct 2 IV. Cerebellar tumor 3 A. Conversion reactions 4 5. Cerebellar abscess 1 B. Depression 2 6. Basilar aneurysm 0 C. Pathophysiology of Signs and Symptoms of Coma 5.

Chapter 6 to behavioral stimuli. Chapter 7 to one class of stimuli. Chapter 9 reviews works is diffuse or very widespread, the level of some ethical problems encountered in treating consciousness is not reduced. For example, pa- unconscious individuals. Hence, a reduced level of consciousness is not Consciousness due to focal impairments of cognitive function, but rather to a global reduction in the level of Consciousness is the state of full awareness of behavioral responsiveness.

The normal activity of this sive to the examiner, for example, if the patient arousal system is linked behaviorally to the lacks sensory inputs, is paralyzed see locked- appearance of wakefulness. It should be appar- in syndrome, page 7 , or for psychologic reasons ent that cognition is not possible without a rea- decides not to respond. Thus, the determina- sonable degree of arousal. Pathologic alteration of the re- content and arousal. The content of conscious- lationships between the brain systems that are ness represents the sum of all functions medi- responsible for wakefulness and sleep can im- ated at a cerebral cortical level, including both pair consciousness.

The systems subserving nor- cognitive and affective responses. These func- mal sleep and wakefulness are reviewed later tions are subserved by unique networks of cor- in this chapter. Disturbance of con- result of brain injury rarely lasts more than 2 to sciousness i. A key dis- of the day. The beclou- women will revert to their maiden name. Pa- ded patient is usually incompletely oriented to tients are often fearful or irritable and may time and sometimes to place. Such patients are overreact or misinterpret normal activities of inattentive and perform poorly on repeating physicians and nurses.

Drowsiness is often pro- iner. Full-blown delirious states tend to come minent during the day, but agitation may pre- on rapidly and rarely last more than 4 to 7 days. However, fragments of misperceptions may The pathophysiology of brain function in such persist for several weeks, especially among al- patients has rarely been studied, but Posner and coholics and patients with cerebral involvement Plum3 found that cerebral oxygen consumption from collagen vascular diseases.

It the frontotemporal cortex and right basal gan- also occurs with systemic infectious processes glia of patients with subclinical hepatic ence- or as a component of encephalitis, during phalopathy. In a medical setting, such patients have gamma-aminobutyric acid GABA activity. Such patients have slower psychologic Chapter 5. Even when maximally aroused, the so that they may be treated appropriately by level of cognitive function may be impaired.

At the bedside, Such patients can be differentiated from those discussion should be with the patient, not, as with psychiatric impairment, such as catato- with an unconscious individual, about the pa- nia or severe depression, because they can be tient. Patients with large midpontine lesions of- aroused by vigorous stimulation to respond to ten are awake most of the time, with greatly simple stimuli. The patient may havioral responsiveness, and there may be some grimace in response to painful stimuli and limbs overlap among them.

Therefore, it is generally may demonstrate stereotyped withdrawal re- best to describe a patient by indicating what sponses, but the patient does not make local- stimuli do or do not result in responses and the izingresponsesordiscretedefensivemovements. Conventionally, the paralysis of all four limbs and the lower cranial term implies a diffuse or disseminated reduc- nerves. The development of multiple cogni- tions of this condition for the diagnosis of coma tive defects manifested by both: 1 Memory and for the specialized care such patients re- impairment impaired ability to learn new in- quire.

Although not unconscious, locked-in pa- formation or to recall previously learned infor- tients are unable to respond to most stimuli. A mation ; 2 One or more of the following high level of clinical suspicion is required on cognitive disturbances: aphasia language dis- the part of the examiner to distinguish a locked- turbance , apraxia impaired ability to carry out in patient from one who is comatose.

The most motor activities despite intact motor function , common cause is a lesion of the base and teg- agnosia failure to recognize or identify objects mentum of the midpons that interrupts des- despite intact sensory function , disturbance in cending cortical control of motor functions. They an arbitrary restriction. Usually, the term de- may be taught to respond to the examiner by mentia is applied to the effects of primary dis- using eye blinks as a code. In some patients, however, it may be applies to chronic conditions carrying limited an essentially permanent condition.

For a de- hopes for improvement. Very few surviving pa- cally ill or develop comorbid brain disease.

Patients in the veg- ens when stimulated. Many patients with either etative state, like comatose patients, show no evi- acute or chronic alterations of consciousness dence of awareness of self or their environment. However, when awakened, Unlike brain death, in which the cerebral hemi- consciousness is clearly clouded. In the truly spheres and the brainstem both undergo over- hypersomniac patient, sleep appears normal whelming functional impairment, patients in and cognitive functions are normal when pa- vegetative states retain brainstem regulation of tients are awakened.

Hypersomnia results from cardiopulmonary function and visceral autono- hypothalamic dysfunction, as indicated later in mic regulation. Although the original term per- this chapter. The American does not initiate conversation or activity. Unlike hypersomnia, the Some patients recover from PVS see Chapter patient usually appears fully awake. Abulia is 9. Other terms in the literature designating the usually associated with bilateral frontal lobe dis- vegetative state include coma vigil and the apa- ease and, when severe, may evolve into akinetic llic state.

Although vig- altered consciousness in which sleep-wake cy- orous supportive care may keep the body pro- cles have returned, but externally obtainable cesses going for some time, particularly in an evidence for mental activity remains almost en- tirely absent and spontaneous motor activity is lacking. Such patients generally have lesions Table 1—2 Terms Used to Describe including the hypothalamus and adjacent basal Disorders of Consciousness forebrain. The minimally conscious state MCS is a con- Acute Subacute or Chronic cept that was recently developed by the Aspen Workgroup, a consortium of neurologists, neu- Clouding Dementia rosurgeons, neuropsychologists, and rehabilita- Delirium Hypersomnia tion specialists.

Pathophysiology of Signs and Symptoms of Coma 9. That the brain has been the brain. Structural processes that impair the dead for some time prior to the cessation of the function of the arousal system fall into two ca- heartbeat is attested to by the fact that the or- tegories: 1 supratentorial mass lesions, which gan in such cases is usually autolyzed respirator may compress deep diencephalic structures and brain when examined postmortem.

They are detailed in Chapter 8. Once the exam- Acute alterations of consciousness are dis- ination is completed, the examiner should be cussed in Chapters 2 through 5. Subacute and able to determine whether the source of the chronic alterations of consciousness are discus- impairment of consciousness is caused by a sed in Chapter 9. The clinician must determine rapidly is often scant or absent.

The neurologic exam- whether the cause of the impairment is struc- ination of a patient with impaired conscious- tural or metabolic, and what treatments must ness, fortunately, is brief, because the patient be instituted to save the life of the patient.

Since cannot detect sensory stimuli or provide vol- the last edition of this monograph in , untary motor responses. The key components there has been a revolution in brain imaging. In appropriate and reactivity of the pupils, 4 the eye move- clinical circumstances, if the initial examina- ments and oculovestibular responses, and 5 tion suggests structural brain damage, a scan the skeletal motor responses.

From this infor- may identify the cause of the alteration of con- mation, the examiner must be able to recon- sciousness and dictate the therapy. However, struct the type of the lesion and move swiftly when the scan does not give the cause, there is to lifesaving measures. Before reviewing the no simple solution; usually no single laboratory components of the coma examination in detail, test or screening procedure will sift out the however, it is necessary to understand the ba- critical initial diagnostic categories as effectively sic pathways in the brain that sustain wakeful, as a careful clinical evaluation.

Diagnosis of Stupor and Coma (Contemporary Neurology Series, No. 10).

Only from this perspective If the cause of coma is structural, it generally is it possible to understand how the compo- is due to a focal injury along the course of the nents of the coma examination test pathways neural pathways that generate and maintain a that are intertwined with those that maintain normal waking brain. Therefore, the clinical consciousness. Von Economo continued to write and lecture about this experience for the remainder of his life, until his premature death in from heart disease.

These observations became the basis for lesion studies done by Ranson in ,20 by Nauta in ,21 and by Swett and Hobson in ,22 in which they showed that the posterior lateral hypothalamic lesions in monkeys, rats, and cats could reproduce the prolonged sleepiness that von Economo had observed. Figure B1—1A. A photograph of Baron Constantin von Economo, and excerpts from the title page of his lecture on the localization of sleep and wake promoting systems in the brain.

From von Economo,19 with permission. Figure B1—1B. These indi- viduals would develop episodes of sleep attacks during which they had an over- whelming need to sleep. He noted that they also had attacks of cataplexy in which they lost all muscle tone, often when excited emotionally. Kinnier Wilson described a cohort of similar patients in London in However, several clinical ob- servations challenged this view. He encephalon. However, the most convincing found that after a transection between the me- body of evidence was assembled by Baron Con- dulla and the spinal cord, a preparation that he stantin von Economo,19 a Viennese neurologist called the encephale isole, or isolated brain, ani- who recorded his observations during an epide- mals showed a desynchronized low voltage, fast, mic of a unique disorder, encephalitis lethargica, i.

However, when he transected the War I. When awakened, they could interact in a showed a synchronized, or high-voltage, slow- relatively unimpaired fashion with the examiner, wave pattern indicative of deep sleep and the but soon fell asleep if not continuously stimu- animals were behaviorally unresponsive. Bremer lated. Many of these patients suffered from concluded that the forebrain fell asleep due to oculomotor abnormalities, and when they died, the lack of somatosensory and auditory sen- they were found to have lesions involving the sory inputs.

He did not address why the ani- paramedian reticular formation of the midbrain mals failed to respond to visual inputs either at the junction with the diencephalon. Other with EEG desynchronization or by making ver- patients during the same epidemic developed tical eye movements as do patients who are prolonged wakefulness, sleeping at most a few locked in. Conversely, when to test these deductions because naturally oc- they placed lesions in the paramedian reticu- curring lesions in patients, or experimental lar formation of the midbrain, the animals still lesions in animals that damaged the brainstem, showed cortical-evoked responses to somato- almost invariably destroyed important sensory sensory or auditory stimuli, but the background and motor pathways that complicated the inter- EEG was synchronized and the animals were pretation of the results.

As long as the only tool behaviorally unresponsive. Later studies showed for assessing activity of the cerebral hemispheres that electrical stimulation of the midbrain re- remained the clinical examination, this problem ticular core could excite forebrain desynchro- could not be resolved. The origin of the pathway was patients with various types of functional impair- not established in this early work. Although it was understood that the EEG voltages are due to the summated excitatory postsynaptic potentials in dendrites of cortical neurons, the reason for the synchronous waves of dendritic potentials remained elusive.

This potassium current then brings the cell back to a hyperpo- larized state, terminating the burst of action potentials. The more deeply the resting. A Waking B Slow-wave sleep. Single spikes Bursts Thalamic firing extracellular. This correlates with a desynchro- nized electroencephalogram. B During burst mode, the thalamic neurons are hyperpolarized by gamma-aminobutyric acid GABA -ergic afferents, deinactivating a low-threshold calcium current with a long plateau.

From Saper, C. Brain stem modulation of sensation, movement, and consciousness. Principles of Neural Science. McGraw-Hill, New York, , pp. By permission of McGraw-Hill. The bursting behavior of neurons in the thalamic relay nuclei, which are a major source of cortical inputs, is often thought to be a major source of cortical EEG.

The synchrony is credited to the thalamic reticular nucleus, which is a thin sheet of GABAergic neurons that covers the thalamus like a shroud. Thalamic axons on their way to the cerebral cortex, and cortical projections to the thalamus, give off collaterals to the reticular nucleus as they pass through it. Neurons in the re- ticular nucleus provide GABAergic inputs to the thalamic relay nuclei, which hy- perpolarizes them and sets them into bursting mode.

However, there is evidence that the synchrony of EEG rhythms across the ce- rebral cortex is due in large part to corticocortical connections, and that even isolated slabs of cortex can set up rhythmic slow-wave potentials. Periods of fore- and intralaminar nuclei which innervate the brain arousal returned after several days if the entire cortex more diffusely , and the reticu- animals were kept alive.

However, it is clear lar nucleus. As noted in Box 1—2, the reticular that the slab of tissue from the rostral pons nucleus plays a critical role in regulating thala- through the caudal midbrain the mesopon- mocortical transmission by profoundly hyper- tine tegmentum contains neural structures polarizing thalamic relay neurons via GABAB that are critically important to forebrain receptors. Other neurons in At the time, little was known about the ori- the cholinergic pedunculopontine and later- gins of ascending projections from the meso- odorsal tegmental nuclei send axons into the pontine tegmentum to the forebrain, and the lateral hypothalamus, where they may contact arousal effect was attributed to neurons in the populations of neurons with diffuse cortical pro- reticular formation.

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However, more recent stud- jections see below. Pathophysiology of Signs and Symptoms of Coma Figure 1—1. Electroencephalogram EEG from a cat in which Frederic Bremer transected the cervicomedullary junction A , showing a normal, desynchronized waking activity. However, after a transection at the midcollicular level B , the EEG consisted of higher voltage slow waves, more typical of sleep or coma. In addition, at the mesopontine level the indicates that neurons in these monoaminergic brainstem contains at least three different mo- nuclei are most active during wakefulness, slow noamine groups whose axons project through down during slow-wave sleep, and stop almost the hypothalamus to the cerebral cortex.

Some of them Although the cholinergic and monoaminergic innervate the midline and intralaminar nuclei neurons in the mesopontine tegmentum have of the thalamus, and others pass through the traditionally been thought to play a major role lateral hypothalamus to the basal forebrain in regulating wake-sleep states, lesions of these and prefrontal cortex. Evidence from single- cell groups have relatively little effect on wake- unit recording studies in behaving animals sleep states or cortical EEG.

Hence, it was not surprising when the EEG appearance of sleep was found to resemble the high-voltage, slow waves that ap- pear during coma. However, in , Aserinsky and Kleitman37 reported the curi- ous observation that, when they recorded the EEG as well as the electromyogram EMG and the electro-oculogram EOG overnight, their subjects would period- ically enter a state of sleep in which their eyes would move and their EEG would appear to be similar to waking states, yet their eyes were closed and they were deeply unresponsive to external stimuli. More detailed study of the course of a night of sleep revealed that the REM and NREM periods tend to alternate in a rhythmic pattern through the night.

In quiet wakefulness, the EEG often begins to synchronize, with 8- to Hz alpha waves predominating, particularly posteriorly over the hemi- sphere. Muscle tone may diminish as well. The appearance of sleep spindles waxing and waning runs of alpha frequency waves and large waves in the 1- to 3-Hz delta range, called K complexes, denotes the onset of stage II NREM. The subject may then pass into the deeper stages of NREM, sometimes called slow-wave sleep, in which delta waves become a progressively more prominent stage III and then dominant stage IV feature.

During these periods, eye movements are few and muscle tone drops to very low levels. The subject abruptly transitions into a desynchronized, low-voltage EEG, with rapid and. Awake Sleep stage 1 2 3 4 REM. EEG 50 V 1s. Figure B1—3A. The main features of a polysomnogram showing the eye movements electro-oculogram [EOG] , muscle tone electromyogram [EMG] , and electroencephalogram EEG across the different stages of sleep and wakefulness. From Rechtschaffen, A, and Siegel, J. Sleep and dreaming.

As the night progresses, the subject typically will spend progressively less time in the deeper stages of NREM sleep, and more time in REM sleep, so that most of the REM sleep for the night comes in the last few bouts. Spontaneous awakenings during the night typically occur from the lighter stages of NREM sleep. Active dreams. Childhood Awake. Early adulthood Awake.

REM 1 Sleep stages. Old age Awake. Figure B1—3B. The stages of sleep through the night in a child, young adult, and older person. With aging, the amount of deep NREM sleep dimi- nishes, and sleep fragmentation with more frequent awakenings is seen. Box 1—3 Wake-Sleep States cont. This pattern, which is typical of young adults, changes dramatically across a life- time. Infants spend much more time asleep, and much more time in the deeper stages of NREM sleep, than adults. Thus, phenomena such as night terrors, bed wetting, and sleep walking tend to occur mainly during slow-wave sleep in children but disappear as the children become older and spend less time in those sleep stages.

Popula- for maintaining a wakeful state. Histamine H1 tions of neurons in the pre-locus coeruleus area blockers impair wakefulness in both animals and medial parabrachial nucleus have intense in- and humans,55 and transgenic mice lacking H1 puts to the basal forebrain. On concentrating hormone59,60 or GABA. Figure 1—2. A summary diagram of the ascending arousal system. The cholinergic system, shown in yellow, provides the main input to the relay and reticular nuclei of the thalamus from the upper brainstem.

This inhibits the reticular nucleus and activates the thalamic relay nuclei, putting them into transmission mode for relaying sensory information to the cerebral cortex. The cortex is activated simultaneously by a series of direct inputs, shown in red. These include monoaminergic inputs from the upper brainstem and posterior hypothalamus, such as noradrenaline NA from the locus coeruleus LC , sero- tonin 5-HT from the dorsal and median raphe nuclei, dopamine DA from the ventral periaqueductal gray matter vPAG , and histamine His from the tuberomammillary nucleus TMN ; peptidergic inputs from the hypothalamus such as orexin ORX and melanin-concentrating hormone MCH both from the lateral hypothalamus LH ; and both cholinergic ACh and gamma-aminobutyric acid GABA -ergic inputs from the basal forebrain BF.

Activation of the brainstem yellow path- way in the absence of the red pathways occurs during rapid eye movement REM sleep, resulting in the cortex entering a dreaming state. Hypo- thalamic regulation of sleep and circadian rhythms. Nature —, By permission of Nature Publishing Group.

Many are most active dur- magnocellular basal forebrain nuclei. Whereas focusing attention on rewarding tasks, rather axons from individual monoaminergic neurons than in the general level of cortical activity. Wilson opined that the epidemic of new cases of narcolepsy in those years was due to the worldwide epidemic of encephalitis from about to However, the prevalence of narcolepsy has remained relatively high, with a current rate of one per 2, population, and it has its peak incidence during the second and third decades of life.

About half of patients reported sleep paralysis, a curious state of inability to move during the transition from sleep to wakefulness or from wakefulness to sleep. The patient can distinguish that the hallucination is not real. EEG and EMG recordings during sleep and wakefulness show that narcoleptic patients fall asleep more frequently during the day, but they also awaken more frequently at night, so that they get about the same amount of sleep as normal individuals. EEG and EMG recordings demonstrated that these attacks have the appearance of cataplexy sudden loss of muscle tone, EEG showing either an awake pattern or large amounts of theta activity typical of rodents during REM sleep.

The animals also had short-onset REM periods when asleep, another hallmark of narcolepsy. At the same time, Emmanuel Mignot had been working at Stanford for nearly a decade to determine the cause of genetically inherited canine narcolepsy. Figure B1—4A. Narcolepsy is caused by loss of the orexin neurons in the posterior and lateral hypo- thalamus of the human brain. The panels plot the location of orexin neurons in the posterior hypo- thalamus in two subjects with normal brains on the left and two patients with narcolepsy on the right.

Reduced number of hypocretin neurons in hu- man narcolepsy. Neuron 27, —, By permission of Elsevier B. Box 1—4 Orexin and Narcolepsy cont. Over the following year, it became clear that most humans with narcolepsy do not have a genetic defect either of the orexin gene or of its receptors, although a few cases with onset during infancy and particularly severe narcolepsy were found to be due to this cause. The presence of type 2 orexin receptors on histaminergic neurons, type 1 recep- tors in the locus coeruleus, and both types of orexin receptors on serotoninergic and other neurons in the pontine reticular formation75 suggests that one or more of these targets may be critical for regulating the transitions to REM sleep that are disrupted in patients with narcolepsy.

These stantial connections with other components of sharp boundaries between wakefulness and the system. Another important property of the sleep are a key feature of normal physiology, as system is that nearly all of these components it would be maladaptive for animals to walk receive inputs from the ventrolateral preoptic around half-asleep or to spend long portions of nucleus.

As indicated in Box 1—3, during REM such lesions undoubtedly accounted for the in- sleep, the forebrain shows low-voltage, fast EEG somniac patients described by von Economo19 activity similar to wakefulness, and the ascend- see Box 1—1.

The Diagnosis of Stupor and Coma (Contemporary Neurology Series) by -

The ventrolateral preoptic nucleus VLPO , shown in purple, inhibits the components of the ascending arousal system during sleep. VLPO neurons contain both gamma-aminobutyric acid GABA and an inhibitory peptide, galanin, and send axons to most of the cell groups that compose the ascending arousal system. This unique relationship allows the VLPO neurons effectively to turn off the arousal systems during sleep.

Loss of VLPO neurons results in profound insomnia. Hypothalamic regulation of sleep and circadian rhythms. Figure 1—4. During wakefulness a , the orexin neurons ORX are active, stimu- lating the monoamine nuclei, which both cause arousal and inhibit the VLPO to prevent sleep. This mutually inhibitory relationship ensures that transitions between wake and sleep are rapid and complete. Figure 1—5.

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Other modulatory systems, such as the extended ventrolateral preoptic nucleus Ex VLPO and the melanin-concentrating hormone MCH and orexin neurons in the hypothalamus, regulate REM sleep by their inputs to this switch. For example, injec- they are adjacent to the dorsal raphe nucleus. On the other hand, patients who cleus and pre-coeruleus region that contain take antidepressants that are either serotonin REM-active neurons.

This REM-on region con- or norepinephrine reuptake inhibitors or both tains two types of neurons. This effect may be mainly in the sublaterodorsal nucleus, project due to the excess monoamines activating the back to the REM-off area. In fact, both rodents to humans, consists of a sheet of neu- impaired states of consciousness and NREM rons divided into six layers.

Inputs from the tha- sleep are characterized by EEG patterns that lamic relay nuclei arrive mainly in layer IV, which include increased amounts of high-voltage slow consists of small granule cells. Inputs from other waves. Layers II and III consist of small- to medium- However, in sleep, the lack of activity is due to sized pyramidal cells, arrayed with their apical an intrinsically regulated inhibition of the arou- dendrites pointing toward the cortical surface. The apical den- the arousal system or to diffuse dysfunction of drites of the pyramidal cells in layers II, III, and its diencephalic or forebrain targets.

V receive afferents from thalamic and cortical Because sleep is a regulated state, it has axons that course through layer I parallel to the several characteristics that distinguish it from cortical surface. Layer VI comprises a varied coma. A key feature of sleep is that the subject collection of neurons of different shapes and can be aroused from it to wakefulness. Patients sizes the polymorph layer.

The deep part of not be arousable at all. In addition, sleeping layer V projects to the striatum. Layer VI pro- subjects undergo a variety of postural adjust- vides the reciprocal output from the cortex back ments, including yawning, stretching, and turn- to the thalamus. Sleeping subjects similar sensory or motor processes. Figure 1—6. A summary drawing of the laminar organization of the neurons and inputs to the cerebral cortex. The neuronal layers of the cerebral cortex are shown at the left, as seen in a Nissl stain, and in the middle of the drawing as seen in Golgi stains. Layer I has few if any neurons.

Layer IV contains very small granular cells, and layer VI, the polymorph layer, cells of multiple types. From Lorente de No R. Cerebral cortex: archi- tecture, intracortical connections, motor projections. In Fulton, JF. Physiology of the Nervous System. Oxford University Press, New York, , pp. By permission of Oxford University Press. However, the orga- The organization of the cortical column does nization of cortical information processing goes not vary much from mammals with the most through a series of critical stages during de- simple cortex, such as rodents, to primates with velopment, in which the maturing cortex gives much larger and more complex cortical devel- up a degree of plasticity but demonstrates im- opment.

What has changed cess may be irretrievably assigned to a region most across evolution has been the number of of cortex, and when that area is damaged, the columns. The hugely enlarged sheet of cortical individual not only loses the ability to perform columns in a human brain provides the mas- that operation, but also loses the very concept sively parallel processing power needed to per- that the information of that type exists.

Hence, form a sonata on the piano, solve a differential the individual with a large right parietal infarct equation, or send a rocket to another planet. We cerebral cortex specialize in certain types of have witnessed a patient with a large right pa- operations. Such a patient continues necessary to reassemble all aspects of our ex- to speak meaningless babble and is surprised perience into a single whole so that they can that others no longer understand his speech be monitored by an internal being, like a small because the very concept that language sym- person or homunculus watching a television bols are embedded in speech eludes him.

Although most people believe that they This concept of fractional loss of conscious- experience consciousness in this way, there is ness is critical because it explains confusional no a priori reason why such a self-experience states caused by focal cortical lesions. It is also a cannot be the neurophysiologic outcome of the common observation by clinicians that, if the massively parallel processing i. For example, to function as a whole, producing a state of people experience the visual world as an un- such severe cognitive impairment as to give the broken scene.

However, each of us has a pair of appearance of a global loss of consciousness. This blind spot can be dem- jection of a short-acting barbiturate into the onstrated by passing a small object along the carotid artery to anesthetize one hemisphere so visual horizon until it disappears. When the left hemisphere is single unbroken expanse, and this hole is pa- acutely anesthetized, the patient gives the ap- pered over with whatever visual material bor- pearance of confusion and is typically placid but ders it.

When the patient recovers, he or she there is no reason to think that it requires a typically is amnestic for the event, as much of physiologic reassembly of other stimuli for pre- memory is encoded verbally. Following a right sentation to a central homunculus. Rather, con- hemisphere injection, the patient also typically sciousness may be conceived as a property of appears to be confused and is unable to orient the integrated activity of the two cerebral hemi- to his or her surroundings, but can answer sim- spheres and not in need of a separate physical ple questions and perform simple commands.

If each of the independent anesthetized. A good example sphere. A very large space-occupying lesion may is seen in patients in whom the corpus callosum simultaneously damage both hemispheres or has been transected to prevent spread of epi- may compress the diencephalon, causing im- leptic seizures. Hence, loss of hand follow along right behind it unbuttoning. The brain requires a funnel to narrow down the choices from all of the possible modes of action to the single plan of motor behavior that will be pursued.

The physical substrate of this process is the basal ganglia. All cortical regions provide input to the striatum caudate, putamen, nucleus accumbens, and olfactory tubercle. The output from the striatum is predominantly to the globus pallidus, which it inhibits by using the neurotransmitter GABA. A classic optical illusion, illustrating the in- pallidum is activated, movement is disinhibited. From W. Used by permit too much striatal disinhibition of move- permission.

All rights reserved. Patients with movement disorders of- equally likely versions of an optical illusion si- ten can inhibit the unwanted movements for multaneously e. Rather, the self is aware of the two alter- carry out the action. Again, the conscious state native visual interpretations alternately. Simi- is best considered as an emergent property of larly, if it is necessary to pursue two different brain function, rather than directing it.

In formed with little conscious thought. Release of prefrontal cortex the ventral pallidum, which in turn inhibits the inhibition may even permit it to drive mental mediodorsal thalamic nucleus, the relay nu- imagery, producing hallucinations. Under such cleus for the prefrontal cortex.

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In fact, it may be more accurate to cortex. Figure 1—8. Brain lesions that cause coma. A Diffuse hemispheric damage, for example, due to hypoxic-ischemic encephalopathy see Patient 1—1. B Diencephalic injury, as in a patient with a tumor destroying the hypothalamus. C Damage to the paramedian portion of the upper midbrain and caudal diencephalon, as in a patient with a tip of the basilar embolus. D High pontine and lower midbrain paramedian tegmental injury e.

E Pontine hemorrhage, because it produces compression of the surrounding brainstem, can cause dysfunction that extends beyond the area of the tissue loss. This case shows the residual area of injury at autopsy 7 months after a pontine hemorrhage. Hence, the evaluation spheres or the ascending arousal system, includ- of the comatose patient becomes an exercise in ing the paramedian region of the upper brain- applying those principles to the evaluation of a stem or the diencephalon on both sides of the human with brain failure.

Figure 1—8 illustrates examples of such lesions that may cause coma. Conversely, uni- lateral hemispheric lesions, or lesions of the Structural Lesions That Cause brainstem at the level of the midpons or below, Altered Consciousness in Humans do not cause coma. Figure 1—9. Lesions of the brainstem may be very large without causing coma if they do not involve the ascending arousal system bilaterally. A Even an extensive infarction at the mesopontine level that does not include the dorsolateral pons on one side and leaves intact the paramedian midbrain can result in preservation of consciousness.

B Lesions at a low pontine and medullary level, even if they in- volve a hemorrhage, do not impair consciousness. Patient 1—2, p. Fortu- DAMAGE nately, most such cases included pathologic Bilateral and extensive damage to the cere- assessment, which is also all too infrequent in bral cortex occurs most often in the context of modern cases. A companion already receive the most glutamatergic input from had died, apparently the result of an attempted other cortical areas and in the CA1 region of double suicide.

On admission the man was unre- the hippocampus which receives exten- sponsive. Later, the neurons undergo pyknosis and Coarse rhonchi were heard throughout both lung apoptotic cell death Figure 1— On the second hospital day depopulated of pyramidal cells. On the fourth day he was Alternatively, in some patients with less ex- afebrile, his chest was clear, and he ambulated.

Throughout this after the anoxic event. Figure 1— Hypoxia typically causes more severe damage to large pyramidal cells in the cerebral cortex and hippo- campus compared to surrounding structures. The next day 13 days hippocampus, cerebellum, and occipital lobes ap- after the anoxia he became incontinent and peared generally well preserved, although a few unable to walk, swallow, or chew.

He neither spoke sections showed minimal cytodegenerative chan- to nor recognized his family. He was admitted to a ges and reduction of neurons. Pathologic depression. Deterioration continued, and 28 days changes were not present in blood vessels, nor was after the initial anoxia he was readmitted to the there any interstitial edema. The striking alteration hospital. He did not re- cerebral white matter. Axons were also reduced in spond to pain, but would open his eyes momen- number but were better preserved than was the tarily to loud sounds.

Reactive astrocytes were consider- tive, and his plantar responses extensor. Laboratory ably increased. The condition of delayed post- were normal. He died 3 days later. The brain was grossly normal. There was no cerebral swelling. Coronal sections appeared normal with no evidence of pallidal ne- Another major class of patients with bilateral crosis. A series of drawings illustrating levels through the brain- stem at which lesions caused im- pairment of consciousness. For each case, the extent of the injury at each level was plotted, and the colors indicate the number of cases that involved injury to that area.

The overlay illustrates the importance of damage to the dorsolateral pon- tine tegmentum or the paramedian midbrain in causing coma. From Parvizi and Damasio, with permission. As a result, it is no exaggeration to can produce bilateral thalamic infarction. However, careful examination of the MRI scans illustrated by the historical vignettes on pages of such patients, or their brains postmortem, 30 and below. Walter Camp. Two years before we saw her, she ter 9 for many years after a hypoxic brain in- developed paralysis of the right vocal cord and jury.

Examination of her brain at the time of wasting of the right side of the tongue, followed by death disclosed unexpectedly widespread tha- insidiously progressing disability with an unsteady lamic neuronal loss. However, there was also gait and more weakness of the right limbs.

Four extensive damage to other brain areas, includ- days before coming to the hospital, she became ing the cerebral cortex, so that the thalamic much weaker on the right side, and 2 days later she damage alone may not have caused the clinical lost the ability to swallow. On the other hand, tha- When she entered the hospital she was alert and lamic injury is frequently found in patients with in full possession of her faculties.

She had upbeat nystagmus on upward Ischemic lesions of the hypothalamus are gaze and decreased appreciation of pinprick on the rare, because the hypothalamus is literally en- left side of the face. The right sides of the pharynx, circled by the main vessels of the circle of Willis palate, and tongue were paralyzed. The right arm and is fed by local penetrating vessels from all and leg were weak and atrophic, consistent with dis- the major arteries. However, the location of the use. An endotra- sigh, features that are usually lacking in patients cheal tube was placed and mechanical ventilation with coma due to brainstem lesions.

During that time she caudal diencephalon through the rostral pons. Several hypotensive crises were treated involving this territory bilaterally in which there promptly with infusions of pressor agents, but no was profound loss of consciousness see Figure pressor drugs were needed during the last 2 weeks 1— On the other hand, we have not seen loss of life. An anesthesiologist at- commanded to do so. There was no other voluntary tempted to inject the root with ethanol to elimi- movement. Four days before she died, she devel- nate the pain. During the ensuing 3 days, evidence of pressure was supported with pressors. She died of gastrointestinal On examination she had spontaneous eye move- hemorrhage 26 days after entering the hospital. A sory nerves, as well as all spinal motor function. CT scan showed hypodensity of the medulla border 2. On section, the and lower pons.

From this point, a way. She lived another 12 weeks in this setting, with- large hemorrhage extended forward to destroy the out regaining function, and rarely was observed to central medulla all the way to the pontine junction sleep. No postmortem examination was permitted. Figure 1—9B. Caudal to this, the hemorrhage the patient.

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J Physiol , — waking discharge of neurons in the posterior lateral , Brain Res , — Gelineau JBE. De la narcolepsie. Gaz Hop Paris , Activity of dorsal Orexins and raphe cells across the sleep-waking cycle and during orexin receptors: a family of hypothalamic neuropep- cataplexy in narcoleptic dogs.

J Physiol , —, tides and G protein-coupled receptors that regulate Cell 92, —, Kolta A, Reader TA. Modulatory effects of catechol- Can J Physiol Pharmacol 67, excitatory activity. Proc Natl Acad Sci 95, —, —, Effect of electrical stimu- To eat or to lation of locus coeruleus on the activity of neurons in sleep? Orexin in the regulation of feeding and wake- the cat visual cortex. Advances in the knowledge and understanding of stupor and coma, aided by the considerable impact of CT scanning on neurological diagnosis, are reflected in the new and substantially revised edition of a classic volume.

The authors have included new references and illustrations, yet this 3rd edition retains its unique approach to that art of diagnosis based on the understanding of pathophysiology and pathobiochemistry. Read more Read less. No customer reviews. Share your thoughts with other customers.

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