CURSO

SEMIOLOGÍA
Estado de consciencia y Esfera Mental
Dr. Alejandro Herrera Trujillo.
Médico Neurocirujano - Universidad del Valle
CPAEM Cirugía de Epilepsia - U Autónoma México
OBSERVAR

PENSAR PREGUNTAR

ESCUCHAR
ographs and Diagrams
FUNCIONES CORTICALES

CORTEZA ASOCIATIVA B
CORTEZA ASOCIATIVA
ANTERIOR:
POSTERIOR:
”ejecutiva”
“receptiva”
Atencion, planeacion,
Sensaciones, percepciones,
evaluacion, decision,
reconocimeintos,
ejecucion motora,
nominaciones y
control de distractores
conocimiento.
y desempeño social

D E
 FUNCIONES CORTICALES

HEMISFERIO DOMINANTE:
HEMISFERIO NO DOMINANTE:
Simbolico.
Visuoespacial y prosodia.
4 The Human Brain in Photographs and Diagrams Lenguaje y calculos

A B

C D E
and Diagrams
FUNCIONES CORTICALES
DONDE?

QUE?
 ATENCION

FRONTAL O DIFUSO
4 The Human Brain in Photographs and Diagrams

A B

DELETREAR UNA PALABRA AL REVES

C D E

REPETIR UNA SERIE DE NUMEROS

 8 The Human Brain in Photographs and Diagrams

Figure 1–5 A and B, The left and right cerebral hemispheres of the brain in
A Figures 1–1A, 1–3, 1–8, and 1–9, shown at about half actual size. Note in this
specimen how much farther posteriorly the lateral sulcus extends in the left

ORIENTACION
hemisphere (A), and how much larger the triangular and opercular parts of
the inferior frontal gyrus are on the left. A, Lateral view of the left hemisphere.
B, Lateral view of the right hemisphere.

12 The Human Brain in Photographs and Diagrams

Central Postcentral
8 The Human Brain in Photographs and Diagrams
Precentral
sulcus gyrus Supramarginal
gyrus
Frontal gyri: gyrus
superior Figure 1–5 A and B, The left and right cerebral h
middle A parietal
Superior Figures 1–1A, 1–3, 1–8, and 1–9, shown at about h
inferior lobule specimen how much farther posteriorly the latera
hemisphere (A), and how much larger the triang
Intraparietal the inferior frontal gyrus are on the left. A, Lateral v
A sulcus B, Lateral view of the right hemisphere.
3
Corpus callosum
2 Angular
Superior frontal Central
gyrus Septum
2
(body) sulcus
Cingulate sulcus gyrus
Cingulate
pellucidum1 (marginal branch)

gyrus Subparietal sulcus

Cingulate
sulcus B
Corpus callosum: Corpus callosum Occipital
rostrum (splenium)
genu Orbital gyri
gyri Parietooccipital
sulcus

Olfactory Calcarine
Preoccipital
sulcus
bulb Lateral
notch
sulcus Temporal gyri:
Thalamus
Postcentral
superior
Midbrain gyrus Central Precentral
Inferior frontal gyrus: middle
inferior Supramarginal sulcus gyrus
1. orbital part Frontal gyri:
Anterior cerebral artery 2. triangular partPons gyrus superior
Subcallosal gyrus 3. opercular part middle
Hypothalamic sulcus
Superior parietal inferior
Hypothalamus lobule Lateral
Cerebellum:
Uncus Medulla primary fissure
Central Postcentral sulcus
Rhinal sulcus Inferior vermis
Precentral
Occipitotemporal temporal
Intraparietal
hemisphere sulcus gyrus Supramarginal
gyrus gyrus gyrus
sulcus Frontal gyri: gyrus
Figure 1–7 A, Medial surface of the right half of a sagittally hemisected brain, shown actual size. The dashed line interconnecting the cingulate and subparietal superior
sulci is meant to indicate that in some brains these two sulci are continuous.
middle 2 Superior parietal
 174 The Human Brain in Photographs and Diagrams

Figure 8–33 A, Afferents to the amygdala.

The amygdala, one of the major constituents of the limbic
system, is a collection of nuclei underlying the uncus of the
medial temporal/limbic lobe. It is centrally involved in assess-
ing and remembering the emotional and drive-related signifi-
cance of stimuli—deciding, for example, whether to flee from
something or eat it. As such, it has widespread connections
with the cerebral cortex, thalamus, hypothalamus, a variety
of brainstem locations, and other sites.
bulb (through the lateral olfactory tract), and from a variety
of other subcortical sites (through the stria terminalis and
ventral “amygdalofugal” pathway). Cortical afferents arise in
limbic areas, especially orbital and anterior cingulate
cortex, and in association areas, especially sensory associa-
tion areas. Subcortical afferents arise in the hypothalamus
(and nearby sites, such as the septal nuclei), multiple tha-
lamic nuclei, and numerous brainstem sites, including the

MEMORIA
Afferents reach the amygdala from the cerebral cortex periaqueductal gray, parabrachial nuclei, and nucleus of
(through the white matter of the temporal lobe), the olfactory the solitary tract.

172 The Human Brain in Photographs and Diagrams

Figure 8–30 An overview of the limbic system.

The limbic system is a set of intricately inter- Cingu

connected structures that form a functional
bridge between large areas of cerebral cortex
and the input/output structures of the nervous
system. It forms the basis of autonomic, endo-
crine, and behavioral responses to homeostatic
challenges and events with implications for sur-
vival and reproduction, and it helps to ensure
that such events are remembered.
The principal structures of the limbic system
are the hippocampus and amygdala in the
medial temporal lobe, a collection of nuclei in
and near the hypothalamus, a ring of limbic
172 cortex that provides a link with the rest of the

REMEMORAR
The Human Brain in Photographs and Diagrams
cerebral cortex, and the interconnections of all
these areas. They are shown here in three-
dimensional reconstructions of the limbic
Figure 8–30 An overview of the limbic system.
system of the same brain shown in sagittal sec-
Amygdala
tions in Chapter 7. Limbic structures were out-
lined on serial sections by Jay B. Angevine Jr.; Hippocampus
The limbic system is a set of intricately inter- Cingulate gyrus Isthmus of the outlines were assembled into 3D reconstruc-
connected structures that form a functional cingulate gyrus tions by Cheryl Cotman.
bridge between large areas of cerebral cortex
and the input/output structures of the nervous
system. It forms the basis of autonomic, endo-
F
crine, and behavioral responses to homeostatic An Stria terminalis

challenges and events with implications for sur- F

vival and reproduction, and it helps to ensure S
Se
that such events are remembered. Habenula
The principal structures of the limbic system Hip
NA Habenulointerpedun
are the hippocampus and amygdala in the H Mammillothalamic t
medial temporal lobe, a collection of nuclei in Midbrain reticular fo
and near the hypothalamus, a ring of limbic AC
(shown here as one
limbic output to the
cortex that provides a link with the rest of the
cerebral cortex, and the interconnections of all
these areas. They are shown here in three- Hip

dimensional reconstructions of the limbic Am Stria termina

system of the same brain shown in sagittal sec-
Amygdala
tions in Chapter 7. Limbic structures were out-
lined on serial sections by Jay B. Angevine Jr.; Hippocampus Parahippocampal gyrus
outlines were assembled into 3D reconstruc-
tions by Cheryl Cotman. Stria medullaris
(of the thalamus)
Abbreviations:
AC, anterior commissure
Am, amygdala
An, anterior nucleus of the thalamus
F Stria terminalis F, fornix Habenula
An H, hypothalamus
F Hi, habenulointerpeduncular tract
Hip, hippocampus
M, mammillary body (of the hypothalamus)
S
Se MT, mammillothalamic tract Stria terminalis
NA, nucleus accumbens
Habenula
S, stria medullaris (of the thalamus)
Hip Habenulointerpeduncular tract Se, septal nuclei
NA
JUICIO Y AFECTO

C D

ABSTRACCIONES
PROVERBIOS
ABSTRACCIONES
 LENGUAJE Y DISCURSO

NOMINAR, REPETIR, SEGUIR COMANDOS

n Photographs and Diagrams

B
 PRAXIAS
n in Photographs and Diagrams

PEDIR TAREA DE SECUENCIAS

VER USAR UNA HERRAMIENTA COMUN
D E
 CALCULO
agrams

Repetición inmediata de
series.
100 menos Sietes.

D E
4 VISUOESPACIAL
The Human Brain in Photographs and Diagrams

A B
HIGHER CORTICAL FUNCTIONS: INTELLIGENCE AND MEMORY / 201

Figure 1 7 - 1 . The patient with normai vision and function shouid be abie to repro-
duce simpie drawings iil<e these in a reiativeiy short period.

become depressed and thus compound his faihng social and business abili-
ties.
Endogenous depression with normal intellectual ability may mimic de-
mentia. Euphoria and emotional lability may be part of intrinsic brain stem
disease as well as a drug response.
Early morning wakening, loss of interest, chronic fatigue, diminished ap-
petite, irritability, impotence, and frigidity are all common manifestations of
depression. Some patients eat to excess when depressed. Do not hesitate to
ask patients whether they are depressed, do they cry, do they feel like crying,
or does music or a sentimental story bring them to the verge of tears?
The cyclothymic, manic-depressive patient with organic disease presents a
challenge. In the down phase of his cycle he is negative about everything,
should know if the “feeling tone” or affect of the patient is normal or which
their left ear, close their eyes and stick out their tongue
lobe of the brain he or she has been “talking to”.
the patient know right from left (area 39, 40) of the
Intellectual function (LPC), cross the midline (area 39, 40 of the LPC), re
Some feel that an excellent measure of intellectual function is the sum total (right posterior parietal cortex), maintain their eyes cl
of information amassed by the patient. By asking a patient of normal intel-
ligence basic knowledge and to calculate, one gets a feeling for intellectual cortex; inability to do so is parietal impersistence) and th
function. This, of course, is affected greatly by educational status.
all tasks without getting stuck on an earlier task (impers
cortex). The ability to remember all four command
EVALUACIÓN RÁPIDA
Additions to the mental status

Visual praxis (Fig. 2.1)

memory.
Visual praxis tests the ability to copy a hand posture after seeing it for 2
seconds. The patient must see the hand (areas 7, 18, 19 of the occipital and

(a)

Fig. 2.1 Visual praxis.

The patient is asked to copy
the hand posture shown for
2 seconds. The hand is then
removed. This type of deficit
is seen in slightly demented
patients. (b) (a)
13
NEUROLOGIC EXAMINATION
ROBERT J. SCHWARTZMAN

Fig. 2.2
comman
respons
comman
the pati
ESFERA MENTAL (prueba diagnostica) C HAPTER 1: The Neurologic Examination 7

1. Orientation Name, address, current location (bldg), city, state, date (day),
month, year
2. Attention/ a. Digit span (present 1/second: record longest correct span)
Immediate recall 2-9-6-8-3, 5-7-1-9-4-6, 2-1-5-9-3-6-2
b. Four unrelated words
Learn: “apple, Mr. Johnson, charity, tunnel”
(# of trials needed to learn all four: ____)
3. Calculation 5 × 13, 65 - 7, 58 ÷ 2, 29 + 11
4. Abstraction Similarities
orange/banana, dog/horse, table/bookcase
5. Construction Draw clock face showing 11:20

Copy

6. Information President: first President

define an island; # weeks/year
7. Recall the four words
“apple, Mr. Johnson, charity, tunnel”
TOTAL SCORE
Subtract 1, 2, or 3 if there was more than 1 trial required to
learn the four words.

Fig. 1.3. Short test of mental status, or the “Kokmen.” (From Kokmen, E, Naessens, JM, and Offord,
KP: A short test of mental status: Description and preliminary results. Mayo Clin Proc 62:281-288,
1987. Used with permission of Mayo Foundation.)

postganglionic fibers in vascular headaches can
cause Horner syndrome.
Optic atrophy is characterized by decreased
visual acuity, abnormal color vision (dyschro-
matopsia), afferent pupillary defect, nerve fiber-
type visual field defect (eg, altitudinal visual
field defect), and swelling or atrophy of the optic
nerve (Fig. 1.8). Optic neuritis is the most
common cause of optic neuropathy in young
in middle-aged and older adults. An altitudinal
visual field defect (eg, the loss of vision in the
lower half of the visual field in one eye) often
occurs in anterior optic neuropathy, with swelling
of the optic disc from nonembolic occlusion of
a posterior ciliary artery. Further evaluation is
recommended for patients with any visual field
defect that suggests optic neuropathy.
Lack of time is often given as a reason for
 INTEGRACION CLINICA
• Compromiso cognitivo leve.
• Demencias (Alzheimer, cuerpos de Lewy, Demencia Parkinson,
Vascular, hidrocefalia presión normal, Frontotemporal)
• Delirium.
• Confusión.
• Intoxicaciones.
• Trastornos del sueño (narcolepsia).
• Depresión.
 CONCIENCIA
Men tought to know that from the brain, and from the brain
only, arise our pleasures, joys, laugh- ter and jests, as well as
our sorrows, pains, griefs and tears. Through it ... we think, see,
hear, and distinguish the ugly from the beautiful, the bad from
the good, the pleasant from the unpleasant ... sleeplessness,
inopportune mistakes, aimless anxieties, absent-mindedness,
and acts that are contrary to habit. These things that we suffer
all come from the brain.
Jones, 1923.
 CONTEXTUALIZACIÓN
1. Integración de eventos y experiencias, procesos neurales que
modulan la conducta, definen la inteligencia.
2. Separación conceptual e intelectual (no empírica) entre cerebro y
mente.
3. No es definible la conciencia por una teoría mecanistica (Leibniz,
1714).
4. Efecto inevitable de la cultura, la religión y el paradigma filosófico
en el concepto de conciencia.
“…generalmente incomprensible, lejos de ser una variable cientifica...privada,
invisible, proceso inmaterial, inaccesible a la observacion científica…” (Zeman,
2008)
Zeman, A. (2008). Consciousness: concepts, neurobiology, terminology of impairments, theoretical models and philosophical background. Handb Clin Neurol, 90, 3-31.
doi:10.1016/S0072-9752(07)01701-0
 DEFINICIONES
• ”consciousness”. • Self-consciousness:
Wakefulness ≈Arousal (SRA) yo y el otro.
Awareness. Aware that the awarenes of others is
“…allowing us to be aware of sensations, directed on him.
percepts, thoughts, memories, emotions, Self-perception: aware estimulos
desires, and intentions”. externos, propiocepcion, estados
Wakefulness without awareness: estado corporales (hambre, sed, calor) y estado
vegetativo. afectivo.
Awareness wothoud wakefulness: Self-monitoring: pasado y prediccion del
Sueño SMOR. futuro.
States of consciousness/ level of Self-recognition: reconocimiento del
consciousness. cuerpo propio.
• “conscience". Cum+scio. As awareness of awareness.
As self-knowledge.
often state-dependent, varying with conscious state
(Sutcliffe and de Lecea, 2002) (Fig. 1.4).
Evidence that REM sleep is dependent upon activity
in cholinergic nuclei, while noradrenergic and seroto-
nergic nuclei are least active in this phase of sleep,
has given rise to a ‘reciprocal interaction’ model of
sleep architecture (Pace-Schott and Hobson, 2002).
This proposes that the regular interaction of SWS and
REM sleep over the course of the night is regulated by
the waxing and waning of mutually inhibitory activity
is likely to demonstrate distinctive roles for the neuro-
transmitters of the ‘activating system’ in modulating
different aspects of arousal. ‘Wakefulness’, after all,
is shorthand for a set of associated neural, behavioral
and psychological functions that are, to some extent,
independently controlled, as evidenced by a number
of the disorders of consciousness discussed below.
In work exploring the idea that the neurotransmitters
linked with arousal make distinctive contributions,
Robbins and Everitt (1995) have found, using a con-

SISTEMA RETICULAR ACTIVANTE

in these nuclei. sistent set of behavioral tests, that selective damage

PFC
PFC
DS
Septal Habenula
n

DNAB Perirhinal Entorhinal

CX CX
VS A10
VS MFB VNAB A5 MFB
A7 A4 A9 A8
CTT A2
Amygdala OT
Hypothalamus A5 Piriform Amygdala
A1
A B CX

Cingulate
PFC Tectum
CX
Medial PFC
habenula Septal
DS n
Thalamus
DR
B7
dltn LC
MS B8
NBM tpp B6
VDBB B4
SN VS MFB B5
ICj HDBB B9
lP
Amygdala Amygdala B2
Hypothalamus
C D
B3 B1

Zeman,
Fig. 1.4. A.pharmacology
The (2008). Consciousness: concepts, neurobiology,
of the brainstem terminology
activating systems. (A) of impairments,
shows theoretical
the origin models andofphilosophical
and distribution the central background.
noradre- Handb Clin Neurol, 90, 3-31.
doi:10.1016/S0072-9752(07)01701-0
nergic pathways in the rat brain; (B) the dopaminergic pathways; (C) the cholinergic pathways; (D) the serotonergic pathways.
CTT ¼ central tegmental tract; dltn ¼ dorsolateral tegmental nucleus; DNAB ¼ dorsal noradrenergic ascending bundle; DR ¼
dorsal raphe; DS ¼ dorsal striatum; HDBB ¼ horizontal limb nucleus of the diagonal band of Broca; ICj ¼ islands of Calleja;
IP ¼ interpeduncular nucleus; LC ¼ locus ceruleus; MFB ¼ medial forebrain bundle; MS ¼ medial septum; NBM ¼ nucleus
basalis magnocellularis (Meynert in primates); OT ¼ olfactory tubercle; PFC ¼ prefrontal cortex; SN ¼ substantia nigra;
tpp ¼ tegmental pedunculopontine nucleus; VDBB ¼ vertical limb nucleus of the diagonal band of Broca; VNAB ¼ ventral
noradrenergic ascending bundle; VS ¼ ventral striatum. (With permission from Robbins and Everitt, 1995.)
 eyelid fluttering
bilateral or mild myoclonic
midline subcortical structures spasms.includingOn thesome
occasions, thalamus
mediodorsal simple behaviors
and uppersuch as repetitive
brainstem, whichtapping
could or
b counting
possibly leadare tounimpaired
disruption ofduring the seizures,
their activating but more-
function.
50
V complex
These changes taskswere
cannot continue. by marked
accompanied 7,10,24
No subjective
bilateralexperi-
hypometabolism
ences accompany in these
the frontal and frequent
relatively parietal association
seizures, as the
cortices
seizures (lateral
entailprefrontal,
a completeanterior ‘blackout’ cingulate,
of both orbital
the level of
c
frontal,
general and lateral
awareness parietal
and cortex).
consciousness By contrast,
contents.temporal
4

50
V
lobe Both
seizures humanin which consciousness
and animal was spared
studies suggest that (simple
absence sei-
partial seizures) were associated
zures are generated through abnormal cycles of synchro-with more-limited
b
changes,
nous neural mainlyfiring
confined that to the temporal
involve the twolobe, and were and
hemispheres
Figure 1 | EEG patterns for different seizure types. a | In generalized tonic–clonic not accompanied
nonspecific by such widespread impaired function

ALTERACION DE LA CONCIENCIA
the thalamic nuclei, which represent the target
seizures, diffuse high-frequency and high-amplitude spikes are apparent. ofof
the frontoparietal association cortices. Intracranial
the brainstem reticular activating projections. 4,36,42–47
b | Absence seizures are characterized by diffuse 3–4 Hz spike-and-wave REVIEWS
EEG recordings obtained from patients undergoing
These oscillations result in the classic EEG pattern of large-
complexes. c | In complex partial seizures, localized abnormal rhythmic activity temporal lobe seizures accompanied by impaired respon-
usually arises in the temporal lobe. amplitude, bilateral, 3–4 Hz spike-and-wave complexes,
siveness confirmed the pronounced slowing in bilateral
which usually last <10 s (Figure 1b).48,49
a frontal and parietal association cortices, which was par- Absence sei
a Studies
ticularly in animal
severe in themodels
late ictal have provided
phase sound evidence
and extended to are characteri
that spike–wave seizures, 87 which seem to be fairly
the early postictal period. Taken together, these neuro- 100general-

V behavior, with
ized onfindings
imaging EEG recordings,
provide solid might
support in fact intensely
for the hypothesis involve eyelid flutteri
occasions, sim
some corticothalamic networks, while other brain regions
Figure 4 | Patterns of brain activity associated with impaired consciousness during b that loss of consciousness during temporal lobe seizures counting are u
are relatively spared. 50–54
Human
could be caused by abnormal activity in the midline50sub- imaging studies have complex tasks
absence seizures. Activity is decreased (blue) in the medial prefrontal cortex,
V
anterior cingulate cortex, and precuneus–posterior cingulate cortex, and increased yielded
cortical controversial
structures (upper results, with some studiesacti-
brainstem–diencephalic showing ences accomp
(red) in the upper brainstem and midline, mediodorsal and intralaminar thalamic global increases in cerebral blood
vating systems) and associated widespread inhibition of flow 26,55–58
and others seizures entai
general aware
nuclei. The lateral frontoparietal association network shows a | both increased and c the showing variablecortex
frontoparietal patterns of increased
(Figure 5). or decreased brain
50
V Both human
decreased activity ictally and b | decreased activity postictally. Permission metabolism.59,60 This variability is likely to reflect both the zures are gene
obtained from Elsevier Ltd © Blumenfeld, H. Epilepsy and consciousness in Brain ‘default mode’
technical limitations ofand epilepsy
the methods used and the intrinsic nous neural fi
The Neurology of Consciousness (eds Laureys, S. & Tononi, G.) (2009).16 Figure 1 | EEG patterns for different seizure types. a | In generalized tonic–clonic
Meta-analysis
seizures, variability
diffuse inofEEG
high-frequencybrain
and functional
amplitude,
high-amplitude imaging
duration,
spikes are studies
and during
rhythmicity
apparent.
the nonspecifi
b of the brainst
the
ofmid
b | Absence to late
the absence
seizures 1990s
seizuresfirstbythemselves.
are characterized suggested
diffuse 3–4 Hzthat
4,61 cerebral blood
spike-and-wave
These oscillati
flowcOver
complexes. and metabolism
| In complex
the past fewmight
partial seizures, vary
years,localized between
abnormaldifferent
investigations cor-with
rhythmic activity
in patients amplitude, bil
usually arises in the temporal lobe.
tical regions during the passive resting
generalized spike–wave activity have achieved excellent state. 88,89
These which usually
a findings
standards provided a novel
of spatial and intellectual
temporal resolution framework by with
coupling Studies in an
which to identify the neural correlates
functional MRI (fMRI) with simultaneous EEG record- of consciousness that spike–wa
and altered conscious states, including epilepsy-induced ized on EEG r
ings. 39,62–67
Of note, preliminary EEG-fMRI findings con- some corticoth
loss of consciousness. A landmark study by Raichle and
firmed that generalized spike–wave seizures selectively are relatively
colleagues 90 used the oxygen extraction fraction to yielded contro
involve certain networks while sparing others. These
demonstrate effectively that, despite changes in cerebral global increas
studies have shown bilateral thalamic activation and cor-
blood flow and oxygen consumption, a metabolic equi- showing varia
tical signal decrease in the anterior and posterior midline metabolism.59
Figure 2 | Patterns of brain activity associated with impaired consciousness during librium is reached in terms of neuronal activity when
generalized tonic–clonic seizures. Activity is decreased (blue) in the medial regions
healthy and lateral
individuals arefrontal and parietal
in a resting state (that association
is, lying inareas technical limit
Figure 5 | Patterns of brain activity associated with impaired consciousness during variability in E
prefrontal cortex, anterior cingulate cortex, and precuneus–posterior cingulate b (Figure
the scanner, 3).awake,
Variable eyesfMRI
closed, signal
withincreases
cognitioninuncon- the lateral
complex partial seizures with medial temporal lobe focus. Activity is decreased of the absence
cortex, and increased (red) in the upper brainstem and the midline, mediodorsal
(blue) in the medial prefrontal cortex, anterior cingulate cortex, and precuneus– frontal and parietal cortical regions
strained by experimental stimulation or specific behav- have been reported Over the pa
and intralaminar thalamic nuclei. The lateral frontoparietal association network
posterior cingulate cortex, and increased (red) in the temporal lobe (seizure focus), ioral instructions from the investigator except to rest data
in addition to the decreases (Figure 4). After these generalized sp
shows a | increased activity ictally and b | decreased activity postictally.
upper brainstem and midline, mediodorsal and intralaminar thalamic nuclei, and Permission were combined with thethat results of the studies in animal standards of s
quietly). A neural network comprised the postero-
obtained from Elsevierassociation
Ltd © Blumenfeld, H. Epilepsy and consciousness in © functional MR
lateral frontoparietal cortex. Permission obtained from Elsevier Ltd models, some authors 4,15,16,36
formulated
medial parietal region (precuneus–posterior cingulate the hypothesis
The NeurologyH.
Blumenfeld, ofEpilepsy
Consciousness (eds Laureys,
and consciousness S. &Neurology
in The Tononi, G.)of (2009).
16
Consciousness ings.39,62–67 Of
that loss
cortex) along of consciousness
with lateral parietal, in absence ventro seizures
medial ispre- caused firmed that ge
(eds Laureys, S. & Tononi, G.) (2009).16
by a disruption
frontal, mid-dorsolateralof the normalprefrontal,information
and anterior processing
tem- in involve certa
studies that included patients with primary GTCS have poral specific
corticesbrain regions a(bilateral
exhibited remarkably association
high metaboliccortex and studies have sh
 CONSCIUSNESS
Atención selectiva
(Awareness) & Redirigida.

NIVEL CONTENIDO
Realidad
(Wakefulness)
Fisica

Alucinación Ilusión
 TAXONOMÍA DE LAS VARIACIONES Y
ALTERACIONES DE LOS ESTADOS DE CONCIENCIA.
• Sueño no MOR, despierto / ”alteraciones sutiles”
sueño MOR. • Delirium, confusional, síndrome
• Coma. cerebral orgánico.
• Anestesia. • Estupor.
• Encefalopatía • Catatonia.
• Parasomnias.
• Estado de mínima conciencia.
• Estado vegetativo.
• Enclaustramiento.
• Muerte cerebral.
Working Party of the Royal College of Physicians, 2003.
enters a minimally conscious state (MCS). This is often followed by a period of
transient post-traumatic amnesia where the patient remains confused and amnesic.
In most cases, the patient recovers within a few weeks, but in some cases, they may
remain in a state of no awareness or minimal consciousness for several months or
even years or decades. Another exceptional condition the locked-in syndrome
(LIS), where the patient awake from the coma fully conscious but is unable to
move or communicate, except by eye movements.

Fig. 2.1 Illustration of the two major components of consciousness: the level of consciousness
(arousal or wakefulness) and the content of consciousness (awareness) in normal physiological
Cvetkovic,
states, where the levelD.,
and&theCosic,
content I.
of (2011). States
consciousness areof consciousness
generally : experimental
positively correlated,insights into meditation,
and in
pathological states or pharmacological coma (adapted from Laureys 2005)
waking, sleep, and dreams. Heidelberg: Springer.
 ALTERACIONES DEL CONTENIDO DE LA
CONCIENCIA
• Acromatopsia. Self-Awareness:
• Akinetopsia. • Des realización.
• Prosopagnosia. • Despersonalización.
• Anosognosia.
• Amnesia global transitoria.
• Demencia.
• Trastorno del miedo (Sd Kluber
Busy).
• Trastornos psicóticos.
 34 G.B. YOUNG AND E.F.M. WIJDICKS
“Unresponsive”

Yes
Aphasic
No Locked-in (central-peripheral)
Comatose
Psychogenic unresponsiveness
Catatonic
Yes
Laboratory studies for
No metabolic-toxic-inflammatory-
infectious causes Specific
Structural cause likely
CSF therapy
EEG
Yes

No No
Intrinsic brain stem Intrinsic hemispheres Extra axial

Yes Yes Yes

Consider specific medical or surgical options

Yes
No
Improvement
Im Discuss level of care

Fig. 2.1. Assessment of the unresponsive patient.

Young, G. B., & Wijdicks, E. F. (2008). Consciousness: its neurological relevance. Handb Clin Neurol, 90, 33-36.
doi:10.1016/S0072-9752(07)01702-2

lar blocking agents. Proof of consciousness, especially space or personal body space, and constitute a
with Guillain–Barré syndrome, can be obtained restricted or focal type of diminished consciousness.
through an EEG recording, which should show normal Neglect syndromes can occur dissociated from any
awake rhythms, e.g., the alpha rhythm that blocks problems with sensory pathways or primary sensory
EVALUACIÓN
NIVEL DE CONCIENCIA

NERVIOS CRANEALES

RESPUESTA MOTORA

SISTEMAAUTONOMICO
 EVALUACIÓN NEUROLOGICA
1. Papiledema.
2. Reactividad, tamaño y simetría pupilar (NCII-NCIII)
3. Trastorno oculomotor
4. Movimientos oculares espontáneos
5. Rfl. Corneal (NCV-NCVII).
6. Rfl. Vestibuloocular (NCVIII-NCIII*) y oculocefalogiro.
7. Rfl. faringeo de nausea (NCX-NCIX).
8. Rfl. Carinal o tusigeno (NCX-NC ).
9. Rigidez decorticacion (NR – Tg mesencefalico)/ decerebracion (Prot-bulbo).
10. Piramidalismo.
11. Automatismo respiratorio.
12. Evaluación con atropina
 mobilized until cervical spine instability has
been excluded by imaging. Resistance to neck
flexion in the presence of easy lateral move-
ment suggests meningeal inflammation such as
meningitis or subarachnoid hemorrhage. Flex-
ion of the legs upon flexing the neck (Brud-
zinski’s sign) confirms meningismus. Examina-
tion of the skin is also useful. Needle marks
suggest drug ingestion. Petechiae may suggest
meningitis or intravascular coagulation. Pres-
sure sores or bullae indicate that the patient
has been unconscious and lying in a single
position for an extended period of time, and
are especially frequent in patients with barbitu-
rate overdosage.1
EVALUACIÓN
LEVEL OF CONSCIOUSNESS
After conducting the brief history and exami-
nation as outlined above and stabilizing the
patients’ vital functions, the examiner should
A B
NIVEL DE CONCIENCIA
NERVIOS CRANEALES Figure 2–1. Methods for attempting to elicit responses from unconscious patients. Noxious stimuli can be delivered with
minimal trauma to the supraorbital ridge (A), the nail beds or the fingers or toes (B), the sternum (C) or the temporo-
mandibular joints (D).
RESPUESTA MOTORA
SISTEMAAUTONOMICO
brain or spinal cord. If there is no response to
the stimulus, a more vigorous midline stimulus
may be given by the sternal rub. By vigorously
pressing the examiner’s knuckles into the pa-
tient’s sternum and rubbing up and down the
chest, it is possible to create a sufficiently pain-
ful stimulus to arouse any subject who is not
deeply comatose.
The response of the patient is noted and
graded. The types of motor responses seen are
considered in the section on motor responses
(page 73). However, the level of response is
important to the initial consideration of the
depth of impairment of consciousness. In des-
cending order of arousability, a sleepy patient
who responds to being addressed verbally or
light shaking, or one who responds verbally to
more intense mechanical stimulation, is said to
be lethargic or obtunded. A patient whose best
response to deep pain is to attempt to push the
examiner’s arm away is considered to be stu-
porous, with localizing responses. Patients who
C D
 58 Plum and Posner’s Diagnosis of Stupor and Coma

causes sweating of the contralateral face), then

Localizing Value of Abnormal
Pupillary Responses in Patients
in Coma
Characteristic pupillary responses are seen
with lesions at specific sites in the neuraxis
(Figure 2–7).
Diencephalic injuries typically result in small,
reactive pupils. Bilateral, small, reactive pupils
are typically seen when there is bilateral dience-
phalic injury or compression, but also are seen
the lesion is likely to be along the course of the
internal carotid artery or in the cavernous si-
nus, superior orbital fissure, or the orbit itself
(Raeder’s paratrigeminal syndrome, although
in some cases the Horner’s syndrome is merely
incomplete). If there is a sweating defect con-
fined to the face (peripheral Horner’s syn-
drome), the defect must be extracranial (from
the T1–2 spinal level to the carotid bifurca-
tion). However, if the loss of sweating involves
the entire side of the body (central Horner’s

EVALUACIÓN
in almost all types of metabolic encephalopathy,
and therefore this finding is also of limited value
in identifying structural causes of coma.
A unilateral, small, reactive pupil accompa-
nied by ipsilateral ptosis is often of great di-
agnostic value. If there is no associated loss of
sweating in the face or the body (even after the
patient is placed under a heating lamp that
syndrome), it indicates a lesion involving the
pathway between the hypothalamus and the
spinal cord on the ipsilateral side. Although hy-
pothalamic unilateral injury can produce this
finding, lesions of the lateral brainstem tegmen-
tum are a more common cause.
Midbrain injuries may cause a wide range
of pupillary abnormalities, depending on the

NIVEL DE CONCIENCIA
Diffuse effects of
drugs, metabolic
encephalopathy, etc.:
small, reactive

Diencephalic: Pretectal:

NERVIOS CRANEALES small, reactive large, "fixed", hippus

RESPUESTA MOTORA
III nerve (uncall):
dilated, fixed

Midbrain: Pons:
SISTEMAAUTONOMICO midposition, fixed pinpoint

Figure 2–7. Summary of changes in pupils in patients with lesions at different levels of the brain that cause coma. (From
Saper, C. Brain stem modulation of sensation, movement, and consciousness. Chapter 45 in: Kandel, ER, Schwartz, JH, Jessel,
TM. Principles of Neural Science. 4th ed. McGraw-Hill, New York, 2000, pp. 871–909. By permission of McGraw-Hill.)
 EVALUACIÓN
NIVEL DE CONCIENCIA

Oculocephalic responses Caloric responses

Cool water Warm water
66

Turn right Turn left Tilt back Tilt forward Right side Left side Bilateral Bilateral
NERVIOS CRANEALES
A
Brainstem intact
(metabolic
encephalopathy)

RESPUESTA MOTORA
B
Right lateral
pontine lesion
(gaze paralysis)

SISTEMAAUTONOMICO
C
MLF lesion
(bilateral internuclear
ophthalmoplegia)

D
Right paramedian
pontine lesion
(1 1/2 syndrome)
 A Metabolic encephalopathy

EVALUACIÓN
NIVEL DE CONCIENCIA
B Upper midbrain damage

NERVIOS CRANEALES

C Upper pontine damage

RESPUESTA MOTORA

SISTEMAAUTONOMICO Figure 2–10. Motor responses to noxious stimulation in patients with acute cerebral dysfunction. Levels of associated
brain dysfunction are roughly indicated at left. Patients with forebrain or diencephalic lesions often have a hemiparesi
(note lack of motor response with left arm, externally rotated left foot, and left extensor plantar response), but can gen
erally make purposeful movements with the opposite side. Lesions involving the junction of the diencephalon and the mid
brain may show decorticate posturing, including flexion of the upper extremities and extension of the lower extremities. A
the lesion progresses into the midbrain, there is generally a shift to decerebrate posturing (C), in which there is extenso
posturing of both upper and lower extremities. (From Saper, C. Brain stem modulation of sensation, movement, and con
sciousness. Chapter 45 in: Kandel, ER, Schwartz, JH, Jessel, TM. Principles of Neural Science. 4th ed. McGraw-Hill, New
York, 2000, pp. 871–909. By permission of McGraw-Hill.)
 EVALUACIÓN
DOLL’S HEAD MANEUVER
NIVEL DE CONCIENCIA ICE WATER CALORICS
Downward with full lateral movements. Downward with full Downward with no
Early loss of upgaze and vergence lateral movements upward movement
then downgaze. (bilateral cold water)
NERVIOS CRANEALES

Bilateral
Babinski’s
RESPUESTA MOTORA

SISTEMAAUTONOMICO
Paratonic
resistance
Appropriate motor
response to noxious
orbital roof
pressure
 EVALUACIÓN
50 Plum and Posner’s Diagnosis of Stupor and Coma

A A

NIVEL DE CONCIENCIA

B
C
D
E

NERVIOS CRANEALES
B

RESPUESTA MOTORA
D

1 min

SISTEMAAUTONOMICO Figure 2–5. Different abnormal respiratory patterns are associated with pathologic lesions (shaded areas) at various levels
of the brain. Tracings by chest-abdomen pneumography, inspiration reads up. (A) Cheyne-Stokes respiration is seen with
metabolic encephalopathies and with lesions that impair forebrain or diencephalic function. (B) Central neurogenic
hyperventilation is most commonly seen in metabolic encephalopathies, but may rarely be seen in cases of high brainstem
tumors. (C) Apneusis, consisting of inspiratory pauses, may be seen in patients with bilateral pontine lesions. (D) Cluster
breathing and ataxic breathing are seen with lesions at the pontomedullary junction. (E) Apnea occurs when lesions en-
croach on the ventral respiratory group in the ventrolateral medulla bilaterally. (From Saper, C. Brain stem modulation of
sensation, movement, and consciousness. Chapter 45 in: Kandel, ER, Schwartz, JH, Jessel, TM. Principles of Neural Sci-
ence. 4th ed. McGraw-Hill, New York, 2000, pp. 871–909. By permission of McGraw-Hill.)

is reached. The hyperpneic phase usually lasts
longer than the apneic phase (Figure 2–5).
This rhythmic alternation in Cheyne-Stokes
respiration results from the interplay of normal
brainstem respiratory reflexes.42–45 When the
medullary chemosensory circuits sense ade-
quate oxygen and carbon dioxide tension, they
artery and the brain. By the time the brain be-
gins increasing the rate and depth of respira-
tion, the alveolar carbon dioxide has reached
even higher levels, and so there is a gradual
ramping up of respiration as the brain sees a
rising level of carbon dioxide, despite its ad-
ditional efforts. By the time the brain begins
 squeezed into the space between the tentorial edge and
the medial edge of the upper midbrain (Fig. 5.2).

5.4.1. Medial temporal grooving

To the abovementioned changes should be added the

pathological feature perhaps most specifically associated
with a mass and with raised intracranial pressure, namely
grooving of the medial temporal lobe by the tentorial
edge, particularly on the parahippocampal gyrus. Klint-
worth (1968) found such a visible groove on one or both
sides in 88% of normal brains. In 1% of normal brains Fig. 5.2. Extreme downward and medial uncal and parahip-

MECANISMOS
the impression was on the posterior portion of the para- pocampal herniation from a traumatic lesion. The groove
hippocampal gyrus. In pathological specimens this produced by the edge of the tentorium on the medial tem-
change may be grossly evident or detected only by a poral lobe is clearly seen and the temporal lobe tissue is
small degree of microscopic change in the brain tissue applied to, both displacing and distorting, the midbrain.
(With permission from Ropper, 1992.)
A.H. ROPPER
92 A.H. ROPPER
ns of these
present very along the line of the tentorium. There has been consider- lesion
are difficult
e only aper-
able ambiguity in the literature regarding the necessity the op
for actual herniation in the creation of this change. Since
pratentorial
ial opening.
this groove has also been used as a marker of raised pres- movem
sure during life, another problem that arises is the degree
ment of the
of grooving that should be considered pathological.
been m
re midbrain
d and found regardi
g (Fig. 5.1). 5.4.2. Secondary brainstem hemorrhages
ppocampus, anterio
ay be found A literature on the nature of secondary brainstem hemor-
al edge and
rhages emerged in parallel with the descriptions of tissue
cussed
5.2).
distortions and herniations. These hemorrhages represent tissue
the most severe degree of brainstem compression and
displacement and are typical of cases that were acutely occlusi
added the fatal, usually with coma from the onset (Fig. 5.3). Vary-
y associated
ing opinions have been offered regarding the origin of
was su
ure, namely
he tentorial these lesions but the bulk of evidence favors arterial rup- anothe
yrus. Klint- ture, as pointed out by Johnson and Yates (1956).
one or both Scheinker (1945) and Poppen et al. (1952) had pre- in the
rmal brains Fig. 5.2. Extreme downward and medial uncal and parahip- viously suggested venous congestion as the cause.
Fig. 5.1. Severe downward herniation of the upper brain-
of the para- pocampal herniation from a traumatic lesion. The groove Fig. 5.10.
stem through the tentorial aperture with ischemic changes An oftenCerebellar
cited paper by tonsillar herniation
Klintworth (1968) repeats thiswith impressions
imens this produced by the edge of the tentorium on the medial tem-
in tissue
the midbrain. made by the foramen magnum in a case
The source of the mass effect was traumatic view, with little substantiation, and posits venous of cerebral tumor.
conges-
d only by a
brain tissue
poral lobe is clearly seen and the temporal lobe
applied to, both displacing and distorting, thecontusion
is
midbrain. and swelling. tion from downward herniation, followed by restoration 5.7. S
(With permission from Ropper, 1992.)

5.7.1. M
along the line of the tentorium. There has been consider-
able ambiguity in the literature regarding the necessity
flaccid quadriplegia, as occurred in one of our patients
for actual herniation in the creation of this change. Since
this groove has also been used as a marker of raised pres-
(Ropper and Kanis, 2000), and a hemiplegia ipsilateral Numer
sure during life, another problem that arises is the degree to a cerebellar mass that is the result of compression of and ra
of grooving that should be considered pathological.
the pyramid (Kanis et al., 1994). The latter configura- the po
5.4.2. Secondary brainstem hemorrhages
tion is somewhat comparable to the Kernohan–Wolt- that oc
A literature on the nature of secondary brainstem hemor-
rhages emerged in parallel with the descriptions of tissue man phenomenon insofar as there is a horizontal (Fig. 5
 136 Plum and Posner’s Diagnosis of Stupor and Coma

cerebral end arteries, trauma, rupture of an ar- ness and 20% are in a coma when admitted.99

CAUSAS
teriovenous malformation, rupture of a mycotic Seizures are a common occurrence and may be
aneurysm, amyloid angiopathy, or hemorrhage nonconvulsive (see page 281), so that electro-
into a tumor. Rupture of a saccular aneurysm encephalographic (EEG) evaluation is valuable
can also cause an intraparenchymal hematoma, if there is impairment of consciousness.
but the picture is generally dominated by the Deep hemorrhages in the supratentorial re-
presence of subarachnoid blood. In contrast, gion include those into the basal ganglia, inter-
despite their differing pathophysiology, the nal capsule, and thalamus. Hemorrhages into
signs and symptoms of primary intracerebral the pons and cerebellum are discussed in the
hemorrhages are due to the compressive ef- section on infratentorial hemorrhages. Chung
fects of the hematoma, andSTROKE
thus areANOXIC–ISCHEMIC
moreANOXIC–ISCHEMIC
alike and colleagues divided patients with striato-195 130 Plum and Posner’s Diagnosis of Stupor and Coma Specific Causes of S
ISCHEMIC STROKE
ISCHEMIC AND AND ENCEPHALOPATHY
ENCEPHALOPATHY 195
than different, depending more on location capsular hemorrhages into six groups with vary-
than on the underlying pathologic process. ing clinical findings and prognoses.100 These
Spontaneous supratentorial intracerebral hem- included posterolateral (33%), affecting pri-
orrhages are therefore usually classified as lo- marily the posterior portion of the putamen;
bar or deep, with the latter sometimes extend- massive (24%), involving the entire striatal
ing intraventricularly. capsular region but occasionally sparing the
Lobar hemorrhages can occur anywhere in caudate nucleus and the anterior rim of the
the cerebral hemispheres, and may involve one internal capsule; lateral (21%), located be-
or multiple lobes (Figure 4–6A). As compared tween the external capsule and insular cortex;
to deeper hemorrhages, patients with lobar anterior (11%), involving the caudate nucleus;
hemorrhages are older, less likely to be male, middle (7%), involving the globus pallidus in
and less likely to be hypertensive. Severe head- the middle portion of the medial putamen; and
ache is a characteristic of lobar hemorrhages. posterior medial (4%), localized to the anterior
Focal neurologic deficits occur in almost 90% half of the posterior rim of the internal cap-
of patients and vary somewhat depending on sule. Consciousness was only rarely impaired
the site of the hemorrhage. About half the pa- in anterior and posterior medial lesions, but
tients have a decreased level of conscious- was impaired in about one-third of patients
Fig. 10.1. Infarction in the dominant cerebral hemisphere of
Fig. 10.2. Bilateral thalamic infarctions on fluid-attenuated
less than 24 hours’ duration.
inversion recovery (FLAIR) imaging within several hours of
Fig. 10.1. Infarction in the dominant cerebral hemisphere of onset.
Fig. 10.2. Bilateral thalamic infarctions on fluid-attenuated
less than 24 hours’ duration. Figure 4–4. A 66-year-old man was brought to the Emergency Department after sudden onset of a severe global headache
Bilateral internal carotid artery occlusion, either due inversion recovery (FLAIR) imaging within several hours of with nausea and vomiting. His legs collapsed under him. CT scan (A) showed blood in the cisterns
Figure 4–9. A pairsurrounding the circle
of scans without of from two patients with pontine strokes. (A) A
contrast
to atherosclerosis or cardiogenic embolism, can cause onset. Willis at the base of the brain, with blood extending into the interhemispheric mography
fissure at the
scanmidline, and thea right
demonstrating small Sylvian
hemorrhage into the right pontine base and tegmentu
fissure (arrow). A CT angiogram (B) showed that the anterior cerebral arteries were fused from
hypertension, whothepresented
anterior with
communicating
left hemiparesis and dysarthria. He was treated by blood pr
sudden coma, initially resembling a metabolic encepha- artery up to a bifurcation point, at which a large saccular aneurysm was noted (arrow). ACA,
(B) anterior cerebral artery; LVA, resonance imaging (MRI) scan of a medial pon
Bilateral lopathy,
internalwith carotid artery occlusion, either due deficits, and cerebellar dysfunction. The ‘top of the markedly. A diffusion-weighted magnetic
preservation of brainstem reflexes (Kwon left vertebral artery; RMCA, right middle cerebral artery. man with hypertension, hyperlipidemia, and prior history of coronary artery disease. He pres
basilar’ syndrome that most commonly produces this dysarthria, and diplopia. On examination, there was right lateral gaze paresis and inability to
to atherosclerosis or cardiogenic
et al., 2002). embolism,
With subsequent can swelling
cerebral cause and
picture is usually embolic in nature. The sources of gaze (one-and-a-half syndrome). There was extensive irregularity of the vertebrobasilar vesse
sudden coma, transtentorial herniation, athemetabolic
initially resembling brainstemencepha-
reflexes are lost often lacking unless a jet of blood from the rup- CT scanstreated with anticoagulants and improved slowly, although with significant residual diplopia and
are highly sensitive to subarach-
emboli
deficits, andarecerebellar
either the dysfunction.
proximal vertebrobasilar
The ‘top systemof the
in a few days and death occurs.
lopathy, with preservation of brainstem reflexes (Kwon tured aneurysm has damaged the brain. noid blood, making the diagnosis in more than
or more
basilar’ syndromeproximal thatsites,
mostespecially
commonly the produces
heart or arch this
et al., 2002). With subsequent cerebral swelling and 95% of cases if done within 12 hours60 (Figure
10.1.4. Posterior circulation ischemia picture is usually embolic in nature. The sourcesin of
of the aorta. Parvisi and Damasio (2003) showed a 4–4). MRI fluid-attenuated inversion recovery
transtentorial herniation, the brainstem reflexes are lost careful magnetic resonance imaging (MRI) study that the characteristic
(FLAIR) sequences may be more pattern of sudden
sensitive, 61,62 onset of there is not even a his
emboli are either the proximal vertebrobasilar
coma occurred acutely with ischemic strokes that
system unconsciousness with subarachnoid
tiny but reactive pupils headache.180
in a few days and death
Ischemia occurs.
within the basilar arterial system can pro- Patient 4–2 but in a patient with a suspected
or more proximal
involved the rostralsites, especially
pontine tegmentum the bilaterally,
heart or with arch (although it may require
hemorrhage if the CT is negative, a lumbar a magnifying glass or
duce impaired alertness at least initially with bilat- of theoraorta. Parvisi and Damasio (2003) In showed intoa the plus 20 57,62,63
puncture is mandatory. lens of As
thelumbar
ophthalmoscope
punc- to vi-
10.1.4. Posterior circulation ischemia without involvement of the midbrain. addition An 18-year-old woman was brought to the emer- sualize the light response). Most patients have SUPRATENTORIAL
eral thalamic damage and especially with damage to careful magnetic resonance imaging ture itself may introduce blood into the CSF,
pontine reticular nuclei, the lesions (MRI)
involvedstudy that
the locus gency department by her sister because she had impairment of oculocephalic responses, and LESIONS CAUSING
the paramedian regions (Steinke et al., 1992). Follow- been confused and forgetful for 2 days. She did not the analysiseyesof blood in the CSF is of great
may show skew deviation, ocular bobbing,
ing medial thalamic damage (Fig. can 10.2),
comaceruleus,
occurred the acutely
dorsal raphe, withtheischemic
parabrachial strokes that
nuclei, and importance.orSigns that suggest that the mayblood
Ischemia within the basilar arterial system pro-akinetic white matter between these structures. The lesions inter- offer a history of headache, but upon being asked, one of its variants. Patients have decer- The most common sup
mutism, profound memory impairment, or altered involved the rostral pontine tegmentum bilaterally, with the patient did admit that she had one. On ex- was presentebrate
beforerigidity,
the taporinclude
they may thedemonstrate
persis- flac- lesions causing coma re
duce impaired alertness at least initially with bilat- rupted involvement
important rostrally directed cholinergic, adrener- tence of thecidsame number ofWe redhave
cellsseen
in tubes
behavior canandevolve (Castaigne etdamage
al., 1981; or without
Tatu of the midbrain. In addition to amination the neck was stiff, but the neurologic quadriplegia. one patient in or ischemia, although t
eral thalamic damage especially with
Figure 4–6. Computed tomography scans from two patients to gic, intracerebral
with and serotonin pathways(A)
hemorrhages. as shows
well aaslargethe hemor-
reticular examination showed only lethargy and inatten- 1 and 4, or the
whompresence of crenated
a hematoma red bloodalong the
that dissected due to trauma, infection
et rhage
al., 1996). Unilateral paramedianlobe thalamic infarctionpontine reticular nuclei, the lesions involved the locus cells and/or medial
xanthochromia if the hemorrhage
the paramedian regions
into the(Steinke et al., 1992).
right parieto-occipital Follow-
in a 77-year-old woman who was previously
formation itself. Sincehealthy
theirand presented
patients werewith difficultyfor
followed tion. A CT scan disclosed a subarachnoid hemor- longitudinal fasciculus, and caused ini- mune response. To cau
produces
walking and confusion,
a headache. disorientation,
Examination showed left-sidedceruleus,
and behavioral neglect. She
only
the dorsal
1took
week 325from
mgraphe,
aspirin the parabrachial
at home
the stroke, it onis the
nuclei,
advice
possible of herand
that the rhage, with blood collection around the circle of is at least several hoursand
tial vertical old.adduction
Spectrophotome-ophthalmoparesis, torial lesion must eithe
ing medial changes
thalamic damage
primary(Castaigne
care doctor et
(Fig.
because
10.2),
al., 1981; Tatuakinetic
she suspected eta stroke.
al., 1996).
Thewhite
hematoma try of CSF wasis available
followed in some
about institutions.
an hour
64
later by loss of con- tical or subcortical stru
matterruptured
impairmentbetween of
into the
theselateral
consciousness
ventricle. The
structures.
with
(B) shows
lesions
pontine
a right
inter-
tegmental Willis on the right side. Lumbar puncture yielded
mutism, profound memory
thalamocapsular
Ocular movement impairment,
hemorrhage
abnormalitiesin aare or altered
60-year-old
common, man with a history of hypertension who was not being treated at the time of
especially Another alternative
sciousnessis(see
to centrifuge
Patient 2–1).the CSF in most
However, diffusely or affect the
the hemorrhage.
ruptedstrokes
important
is notrostrally
permanent directed
if the cholinergic,
patient survives adrener-
for a bloody fluid, with 23,000 red blood cells and 500
patients, the onset of coma
and test the supernate with a urine dipstick is so sudden that Following recovery from
behavior can ‘wrongevolve eyes’He
way (Castaigne (a presented
gazeetpalsywith
al., headache,
to1981; Tatu
the opposite left-sided
side),weakness and sensory loss, and some left-sided inattention. white blood cells. Cultures were negative. A ce-
gic, and serotonin
sufficient duration.pathways as well as the reticular for blood. If the bleeding preceded the tap by
et al., 1996).skew
Unilateral
deviation,paramedian
and verticalthalamic
gaze palsy infarction
(Steinke et al., rebral angiogram demonstrated a saccular aneu-
at least 6 hours, it is likely that there will be
1992). Motordisorientation,
deficits do not occur
formation itself. Since their patients were followed for rysm at the junction of the internal carotid and
produces confusion, andunless there is exten-
behavioral blood breakdown products in the CSF, which
sion into more caudal structures. only 10.1.5.
1 weekMultiplefrom the stroke,ischemia
territory it is possible that the middle cerebral arteries on the right.
can be visualized on the dipstick.
changes (Castaigne et al., 1981; Tatu et al., 1996).
Bilateral rostral midbrain and pontine tegmental impairment of consciousness with pontine tegmental
Ocular movement abnormalities are common, especially
lesions are almost always associated with impaired strokes is not territory
Multiple permanent if the patient
infarctions are notsurvives
uncommonly for a
‘wrong way eyes’ (a gaze palsy to the opposite side),
alertness (Chase et al., 1968) but strokes rarely involve sufficient duration.by impairment in alertness (Gootjes
accompanied
skew deviation, and vertical gaze palsy (Steinke
these regions selectively; thalamic damage is com- et al., et al., 2005). Elderly, postoperative patients are at risk
1992). Motormonly
deficits do not occur
associated. Damageunlessto there is exten-
the rostral brainstem for multiple embolic strokes or watershed ischemia (in
 lection for teenagers; this should be kept in mind when
advising these patients and their parents.
Fig. 12.1. Axial CT scan without contrast show
TRAUMATIC BRAIN INJURY 12.2.1.2. Contusion 219 sity area representing contusion (black arrow); h
presentation is infrequent and with only one-third pre- midlineCerebral
shift, orcontusions
effacementmostof the commonly
ventriclesoccur in areas
in asso- (white arrows) represent perilesional edema.
senting with the lucid interval (Munro and Maltby, ciation where sudden deceleration
with neurological deficit.ofThe
the head causesfrom
mortality the brain
1941; Woodhall et al., 1941; Jamieson and Yelland, an acuteto impact
subduralonhematoma
bony prominences
is quite –high,
namely, the tem-
ranging
of a meningeal artery. Other sources
1968; Kvarnes and Trumpy, 1978; Phonprasert et al., from 50% to 90%, and can be as high as 90–100% inup as
poral, frontal, and occipital poles. They show
include the meningeal veins or the cere
1980; Bricolo and Pasut, 1984). Other traumatic intra- patientshigh-density
who are onareas on CT scans(Kawamata
anticoagulants (Fig. 12.1).etOften
al., they
There is usually a concomitant skull fra
cranial lesions may occur concomitantly and may 1995). enlarge and coalesce into frank blood clot, and with
time usually develop perilesional edema. Cerebral 70% of epidural hematomas occur in the
expand after the epidural hematoma is evacuated. ietal region (Miller and Statham, 1995)
contusions may occasionally not be well visualized

CAUSAS
12.2.1.5. Diffuse axonal injury all epidural hematomas occur in the 20
12.2.1.4. Subdural hematoma on initial CT and appear more prominently on later
Diffuseimaging.
axonal injury is a of
Treatment common
cerebralcause of deranged
contusions is generally population (Jennett and Teasdale, 1981
This lesion is typically caused by high-speed injuries consciousness or coma
supportive in the neurological
with close absence of anobservation
intracranialbut, if the less adherent dura of the younger
and results when a bridging vein that traverses the sub- space-occupying
the contusionlesion. The mechanism
generates significantofdeleterious
this injury mass hematomas are classically lens-shaped o
dural space tears during a deceleration/acceleration- involveseffect, particularly a herniation syndrome, and
rotational acceleration and deceleration surgical and do not cross suture lines (Fig. 12.2).
type force. On a CT scan, acute subdural hematomas small hemorrhagic
decompression focimay
are seen in the corpus callosum,
be required. cuation is the mainstay of treatment.
are high-density lesions that are usually crescent- dorsolateral rostral brainstem, and gray/white matter The typical presentation of an epidur
shaped (Fig. 12.3). Subdural hematomas can become junctions within the hemispheres. There is microscopic head injury in a young person with a sh
more hypointense with time because of evolution of evidence12.2.1.3.
of injuryEpidural
to the hematoma
axons. Diffuse axonal injury unconsciousness. This is then followed by
blood products. Acute subdural hematomas should be A traumatic
is often accompanied epidural hematoma
by other primaryisbrain
a hemorrhage
injuries. into val, then depressed consciousness, contra
evacuated if they are causing a significant mass effect, epidural
Treatment space
of this andisismainly
injury commonly caused CT
supportive. by the
scansrupture paresis, and an ipsilateral dilated pupil.
218 S.S. LOLLIS ET AL. may demonstrate punctuate hemorrhagic foci. Magnetic
symptoms including headache, dizziness or light- resonance imaging (MRI) well demonstrates character-
headedness, visual disturbances, anosmia, balance diffi- istic abnormalities on T2-weighted images that are
culties, difficulty concentrating, impaired judgment, pathognomonic (Fig. 12.4).
emotional difficulties, personality changes, loss of
libido, disruption of sleep/wake cycles, photophobia,
and delirium. Treatment, again, is mainly supportive. 12.2.2. Secondary injury
Although rare, one must also be mindful of the con-
cept of a second impact syndrome where a person Much of the management of moderate to severe trau-
who suffers a second mild head injury while they are matic brain injury is aimed at preventing secondary
still symptomatic from their first one can develop injury. Secondary injury develops after the initial impact
malignant cerebral edema, which is refractory to all damage and can be caused by delayed expansion of intra-
treatments and carries a 50–100% mortality (Schneider, cranial hematoma, cerebral edema, hypoxia, hydrocepha-
1973; Saunders and Harbaugh, 1984). There is a predi- lus, and elevated ICP. The final pathway of secondary
lection for teenagers; this should be kept in mind when injury is generally ischemia – inadequate blood supply
advising these patients and their parents. and oxygenation to meet the metabolic demands of the
Fig.
Fig. 12.3. Axial CT scan shows hyperdense 12.1. Axial
crescentic CT scanbrain
lesion withouttissue.
contrastThe
Fig. 12.2. main
showing
Axial CTgoals
high-den- in preventing
scan (left) in the brainsecondary
windows show the high density lens-shaped epidural hematoma. B
12.2.1.2. Contusion
representing an acute subdural hematoma.sity area representing contusion
injury(black
are arrow);
to
(right) hypodense
provide
show areas
appropriate
associated oxygenation
fracture (arrow). and prevent
Cerebral contusions most commonly occur in areas (white arrows) represent perilesional edema.
where sudden deceleration of the head causes the brain
to impact on bony prominences – namely, the tem-
poral, frontal, and occipital poles. They show up as of a meningeal artery. Other sources of bleeding
high-density areas on CT scans (Fig. 12.1). Often they include the meningeal veins or the cerebral sinuses.
enlarge and coalesce into frank blood clot, and with There is usually a concomitant skull fracture. Some
time usually develop perilesional edema. Cerebral 70% of epidural hematomas occur in the temporopar-
contusions may occasionally not be well visualized ietal region (Miller and Statham, 1995) and 40% of
on initial CT and appear more prominently on later all epidural hematomas occur in the 20 and younger
imaging. Treatment of cerebral contusions is generally population (Jennett and Teasdale, 1981) because of
supportive with close neurological observation but, if the less adherent dura of the younger person. The
the contusion generates significant deleterious mass hematomas are classically lens-shaped or biconcave
effect, particularly a herniation syndrome, surgical and do not cross suture lines (Fig. 12.2). Surgical eva-
decompression may be required. cuation is the mainstay of treatment.
The typical presentation of an epidural follows a
 Much of the management of moderate to severe trau-
matic brain injury is aimed at preventing secondary
injury. Secondary injury develops after the initial impact
damage and can be caused by delayed expansion of intra-
cranial hematoma, cerebral edema, hypoxia, hydrocepha-
lus, and elevated ICP. The final pathway of secondary
injury is generally ischemia – inadequate blood supply
and oxygenation to meet the metabolic demands of the
CAUSAS
Fig. 12.3. Axial CT scan shows hyperdense crescentic lesion
representing an acute subdural hematoma.
brain tissue. The main goals in preventing secondary
injury are to provide appropriate oxygenation and prevent

Fig. 12.4. Axial FLAIR MRI scans show foci of hyperintense regions in brainstem, corpus callosum, and gray–white junctions
representing diffuse axonal injury.

zures usually demonstrate a slower and more irregular
EEG pattern (Penry et al., 1975; Holmes et al., 1987;
Camfield and Camfield, 2002).
13.3.2. Primary generalized tonic–clonic seizures
By definition, these seizures begin virtually simulta-
neously in both hemispheres, without warning and with
muscle artifact and identifiable spike-and-wave seizure
activity. Following the clonic phase there is a period of
postictal suppression of the EEG (Fig. 13.2).
13.3.3. Myoclonic seizures
Myoclonus is defined as a brief, shock-like jerk of a
muscle group. In generalized myoclonic seizures the
myoclonic jerks happen bilaterally and synchronously;

CAUSAS
abrupt coma; the motor manifestations are synchronous. however, in focal onset seizures myoclonic jerks of

Fig. 13.2. Generalized spike-and-wave activity with superimposed, repetitive, muscle artifact seen during the clonic phase of a
generalized tonic–clonic seizure. There is postictal EEG background suppression. From Brenner RP (2004). EEG in convulsive
and nonconvulsive status epilepticus. J Clin Neurophysiol 21: 319–331, with permission from Lippincott Williams & Wilkins.
sepsis are the predisposing conditions for patients with
systemic cancer, while skin-derived organisms such as
Staphylococcus aureus or Staphylococcus epidermidis
account for infections in patients with primary CNS
tumors. Use of corticosteroids renders patients immu-
nocompromised and makes them more prone to infec-
tions. Bone marrow transplantation and implantation of
CAUSAS
GliadelW chemotherapy wafers are recently becoming
more of an etiological factor in CNS infections and
treated bacterial meningitis, mycoplasmas, and fung
(Pruitt, 2003; Schiff and Wen, 2003). Among the vira
etiologies, herpes simplex encephalitis may be under-
estimated in cancer patients and is potentially fatal if
untreated (Schiff and Rosenblum, 1998).
Diagnosis of CNS infections in brain neoplasms can
be very challenging; high clinical suspicion leads to
diagnosis. Neuroimaging, lumbar puncture, and even
brain biopsy may be necessary to narrow the differentia
 CAUSAS 264 Plum and Posner’s Diagnosis of Stupor and Coma
158 Plum and Posner’s Diagnosis of Stupor and Coma

examinations. Another pit

assessing the CSF when
matic lumbar puncture o
spinal fluid white cell co
arachnoid bleeding, there
white cell to each 1,000 r
When there are more tha
cells beyond this ratio, th
treated as if there were m
otherwise by a repeat tap
Patients are occasional
velop the encephalopathy
white cells appear in the
The series of Carpenter
cludes several such cases
an example from our own

Patient 5–23
Figure 4–11. A pair of magnetic resonance images from the brain of a patient with herpes simplex 1 encephalitis. Note
the preferential involvement of the medial temporal lobe and orbitofrontal cortex (arrows in A) and insular cortex (arrow
in B). There is milder involvement of the contralateral side. A 28-year-old man compl
temperature elevation for s
mittent sore throat, chills, a
key differentiating point is that a much larger tive problems or impairment of consciousness, muscle or joint complaints
percentage of patients with ADEM present or if there are large plaques in the hemispheric felt tight. He saw his physic
with behavioral disturbances, whereas this is white matter. However, the proof of the di- be warm and appear acut
rare early in multiple sclerosis. Occasionally agnosis is established by the course of the ill-
patients with ADEM may become stuporous ness. Although ADEM can fluctuate, and new significant abnormalities o
 CAUSAS
Brain Death 337

Figure 8–1. Cerebral metabolism in brain death measured by 18F-fluorodeoxyglucose-positron emission tomography
demonstrating the unequivocal finding of an ‘‘empty skull.’’ (Sequence of images: sagittal [left]; transverse [middle]; and
coronal [right]). (From Laureys et al.,42 with permission.)

of faulty technique. A national cooperative

ELECTROENCEPHALOGRAPHY/
EVOKED POTENTIAL MEASUREMENTS
The EEG has little place in the determination of
brain death, except perhaps in those rare cases
where other clinical evidence is equivocal. An
group has published technical requirements
necessary to establish electrocerebral silence
(Table 8–5), and has produced an atlas illus-
trating potential problems of interpretation
of the EEG in coma.29 It should be noted that