Transcript general introduction

Section Ⅰ
Disorders of consciousness
刘
海
若

伦敦火车出轨事故 凤凰卫视金
牌主持脑死亡
中国日报网站消息：据法新
社5月12日报道，在10日伦敦火
车出轨的事故中丧生的7人里，
包括两名台湾电视媒体工作人
员。曾经在台湾电视网TVBS工
作、现为香港凤凰卫视咨询台
主持人的刘海若头部受到重创，
已被诊断为脑死亡。
刘海若不是脑死亡 凌锋教授赴英会诊有结果
2002年05月20日17:04 北京晚报
前往英国为凤凰卫视记者刘海若会
诊的北京宣武医院凌锋教授昨天下
午1时3分返京。据凌教授介绍：刘
海若的伤情已有转机，目前有自主
呼吸，不是脑死亡。

宣武医院神经外科主任凌锋教
授与英国的医生一起检查了刘海若
的全身状况，并仔细讨论了病历及
CT片。 凌教授认为，刘海若已有
自主呼吸，另外对刺激有收缩反应，
并且有咳嗽，这些都证明她不是
“脑死亡”，生存下来是可能的。

刘海若苏醒创医学奇迹 八方援手力催凤凰重生
2002年08月16日每日新报
三个月前在英国因车祸陷入昏迷的凤凰卫视女
主播刘海若，不久前已在北京宣武医院恢复神
志。
 8月上旬，海若已经可以清晰地做出各种表情
反应了，当医生说出数字时，海若已经能用手
比划出动作了。主治医生凌锋表示，海若的病
情有了质的变化，虽然距离正常人反应的灵敏
程度还相差很远，但她已经不是植物人了，确
切地说———海若已经醒了。

Ⅰ.Consciousness
state of
the patient’s
awareness of self and environment
and
his responsiveness to external
stimulation and inner need.
 the
Content of consciousness

Orientation
 percepbility
 attitudes
 emotions
 active
Structural basis

1.ascending reticular activating system,
ARAS
reticular formation
thalamus
cerebral hemisphere alert state
 2.cortex
Ⅱ clinical manifestation
1.according to level of consciousness
2.according to content of consciousness
1.level of consciousness
(1) Somnolent
(2) Stupor
(3) Coma lesser degree
deep
Somnolent
stupor
Can be roused only by vigorous and
repeated stimuli, when left
unstimulated they quickly drift into a
sleeplike state.
coma

The patient who appears to be asleep and at
the same time incapable of being aroused by
external stimuli or inner need.
 lesser degree coma: reflex (+)
 Deep coma: no reaction of any kind is
obtainable, corneal, pupillary, pharyngeal,
tenden reflex (-)
2.content of consciousness
(1)
(2)
(3)
Confusion
Delirium
Special Type
Decorticated Syndrome
Akinetic mutism
confusion
 “clouding
of the sensorium”
 Inability to think with customary speed
 Marked by some degree of
inattentiveness and disorientation
accompanied by illusions
Delirium state

Hallucination, hyperactivity
 High fever, atropine overdose, alcohol
Decorticated syndrome

Neocortical death
 ARAS is normal, arousal-nonarousal cycle
 Open eyes, blink, swallow, eyes move
 Coma, Show no signs of awareness of the
environment or inner need
 Vegetative state, decerebrate rigidity
12 in 45 awakened in 2 weeks, >3 month:PVS
Akinetic mutism

The term akinetic mutism has been applied
to yet another group of patients who are
silent and inert as a result of bilateral
lesions of the anterior parts of the frontal
lobes, leaving the intact of the motor and
sensory pathways; the patient is profoundly
apathetic, lacking to an extreme degree the
psychic drive or impulse to action(abulia).
The abulic patient registers most of what is
happening about him and forms memories.
Ⅲ differential diagnosis
(1) Abulia
(2) Locked-in
syndrome
abulia

The patient are silent and inert as a result of
bilateral lesions of the anterior parts of the
frontal lobe, leaving intact the motor and
sensory pathways, the patient is lacking to
an extreme degree the psychic drive or
impulse to action.
Locked-in syndrome

Lesion of the ventral pons (basis pons)
 Interrupts the corticobulbar and
corticospinal pathways
 depriving the patient of speech and the
capacity to respond in any way except by
vertical gaze and blinking
 wakefulness
Ⅳ brain death
Harvard medical school committee 1968

1. Absence of cerebral function
 2. Absence of brainstem function

including spontaneous respiration
 3. Irreversibility
Brain death






1. Absence of cerebral function: Deep coma, total lack of
spontaneous movement, and of motor and vocal responses to
all visual auditory and cutaneous stimulation
2. No spontaneous respiration
3. Absence of brain stem function: Dilated midposition
fixed pupils, corneal reflex, oculocephalic and
oculovestibular test, gag reflex(-), last for 12 hours
4. EEG: flat or isoelectric (<2μV) during a 30-minutes
recording
5. Spinal reflex may persist
6. Exclude intoxication, hypothermia, metabolic
disturbance
Section Ⅱ
Aphasia, apraxia, agnosia
aphasia

A loss or impairment of the production
and/or the comprehension of the spoken or
written language due to an acquired lesion of
the brain
 No higher order mental function disturbance
i.e. Confusion, delirium, mental retardation
 Not dysarthria
 Not aphonia
classification





1.Parasylvian fissure aphasic syndrome
Broca aphasia, Wernicke aphasia
Conduction aphasia
2.Transcortical aphasia
Transcortical motor, sensory, mixed
3.Global aphasia
4.Anomic aphasia
5.Subcortical aphasia syndrome
thalamic aphasia, basal ganglion aphasia
Broca aphasia

Primary deficit in speech production
 Dominant hemisphere
 Inferior frontal gyrus, posterior portion
Wernicke aphasia

Primary deficit in comprehension
 Paraphasia: literal: the grass is greel
verbal: the grass is blue
 Disturbance in repetition
 Wernicke area: posterior portion of
supratemporal gyrus
Transcortical aphasia

Watershed area
 Repetition is remarkably preserved
Anomic aphasia

The patient lose only the ability to name
people and objects
 Middle temporal lobe
Global (Total) aphasia

Left middle cerebral artery occlusion
 All aspects of speech and language are
affected
 Can say only a few words
Subcortical aphasia

Thalamic aphasia
 Basal ganglion aphasia: nonfluent,
dysarthric, paraphasic
apraxia

The term apraxia is applied to a state in which a
clear-minded patient with no weakness, ataxia or
other extrapyramidal derangement and no defect of
the primary modes of sensation loses the ability to
execute highly complex and previously learned
skills and gestures.
apraxia

Ideomotor apraxia
 Ideational apraxia
 Melokinetic apraxia
 Constructional apraxia
 Facial-oral apraxia
 Dressing apraxia
agnosia

A highly-ordered perceptual disturbance, no
elementary sensation disturbance, can not
interpret sensations correctly.
 Due to disorders of the association areas in
the parietal lobes.
agnosia

Visual agnosia: object, face, verbal
 Auditory agnosia: verbal
 Sensory agnosia
 Body image disturbance
non-dominant parietal lobe
 Gerstmann syndrome
finger agnosia, right-left confusion, dysgraphia,
Dyscalculation
Dominant hemisphere angular gyrus

伦敦火车出轨事故 凤凰卫视金
牌主持脑死亡
中国日报网站消息：据法新
社5月12日报道，在10日伦敦火
车出轨的事故中丧生的7人里，
包括两名台湾电视媒体工作人
员。曾经在台湾电视网TVBS工
作、现为香港凤凰卫视咨询台
主持人的刘海若头部受到重创，
已被诊断为脑死亡。
刘海若不是脑死亡 凌锋教授赴英会诊有结果
2002年05月20日17:04 北京晚报
前往英国为凤凰卫视记者刘海若会
诊的北京宣武医院凌锋教授昨天下
午1时3分返京。据凌教授介绍：刘
海若的伤情已有转机，目前有自主
呼吸，不是脑死亡。

宣武医院神经外科主任凌锋教
授与英国的医生一起检查了刘海若
的全身状况，并仔细讨论了病历及
CT片。 凌教授认为，刘海若已有
自主呼吸，另外对刺激有收缩反应，
并且有咳嗽，这些都证明她不是
“脑死亡”，生存下来是可能的。

刘海若苏醒创医学奇迹 八方援手力催凤凰重生
2002年08月16日每日新报
三个月前在英国因车祸陷入昏迷的凤凰卫视女
主播刘海若，不久前已在北京宣武医院恢复神
志。
 8月上旬，海若已经可以清晰地做出各种表情
反应了，当医生说出数字时，海若已经能用手
比划出动作了。主治医生凌锋表示，海若的病
情有了质的变化，虽然距离正常人反应的灵敏
程度还相差很远，但她已经不是植物人了，确
切地说———海若已经醒了。

刘海若住院实况首次播放 恢复很快已能开
口说话2002年09月07日北京娱乐信报

信报讯(记者张迪) “真没想到海若的病情会恢复得
这么快，当我听见女儿对我说，‘爸爸，生日快乐’时，
心里真高兴啊。”昨天，凤凰卫视女主持人刘海若的父

昨天，宣武医院首次向媒体播放海若在医院里拍摄
的录像，但为了尊重海若及其家人，海若的面容被“隐
藏”起来。海若身穿浅蓝色条纹的住院服装，能很清晰
地讲话，她对前 来看望她的市卫生局的金局长说：
“谢谢金局长，谢谢大家对我的关心！”刘父说：“8
月18日那天，第一次听到了她叫‘爸爸’，前几天过生
Section 3
A.Disturbance of Vision
B. Disturbance of Ocular Movement
A Ⅰ. Visual pathway
Retina→optic nerve→
optic chiasm→optic tract
→lateral geniculate
nucleus (LGN)→optic
radiation→occipital
lobe(calcarine sulcus)
 Optic chiasm: fibers
from the nasal retinas
cross over

Ⅱ reduced vision
1. One eye
 Central retinal artery occlusion
 Amaurosis fugax
 Retro-bulbar optic neuritis
multiple sclerosis, neuromyelitis optica
 Foster-Kennedy syndrome
anosmia, optic atrophy on one side
Papilledema on the other side , seen in frontal lobe
tumor
Ⅱ reduced vision
2. Two eyes
 Cortical blindness :
dilated pupil, light reflex is preserved
 Toxic: methyl
 Deficiency: pernicious anaemia
Ⅲ visual field defect
1. Optic nerve:
uniocular blindness
Ⅲ visual field defect
2. Optic chiasm:
 bitemporal hemianopia
 seen in pituitary tumor,
craniopharyngioma
Ⅲ visual field defect
3. Optic tract:
homonymous hemianopia
Ⅲ visual field defect
4. 5. Optic radiation:
quadrant anopia
Ⅲ visual field defect
6. Visual cortex:
homonymous
hemianopia with
macular sparing
Ⅲ visual field defect

1. Optic nerve: uniocular blindness
 2. Optic chiasm: bitemporal hemianopia
seen in pituitary tumor, craniopharyngioma
 3. Optic tract: homonymous hemianopia
 4. Optic radiation: quadrant anopia
 5. Visual cortex: homonymous hemianopia with
macular sparing
B. Disorder of ocular movement
Ⅰ anatomy
1. Oculomotor nerve:
 上睑提肌
levator of lid
 上直肌
superior rectus
 下直肌
inferior rectus
 下斜肌
inferior oblique
 内直肌
medial rectus
 瞳孔扩约肌 pupillary sphincters
 睫状肌
ciliary muscle
Ⅰ anatomy
2. Trochlear nerve:
上斜肌
superior oblique muscle
3. Abducens nerve:
外直肌
lateral rectus muscle
Ⅱ ocular paralysis
1. Ocular motor nerve paralysis
 Ptosis
 Lateral deviation of the eye
 Inability to rotate the eye
upward, inward and
downward
 Diplopia
 Dilated non-reactive pupil,
paralysis of accommodation
Ⅱ ocular paralysis
2. Trochlear nerve
 Can not rotate down and outward
 The patient complains of special difficulty
in reading or going downstairs
Ⅱ ocular paralysis
3. Abducens nerve
 Paralysis of outward movement
 Eye deviates medially
 Diplopia
Ⅱ ocular paralysis
4. Nuclear ophthalmoplegia
 Brain stem lesion: infarction, MS
 Accompanied by ipsilateral cranial nerve
paralysis, contralateral hemiplegia
Ⅱ ocular paralysis
5. Internuclear ophthalmoplegia (INO)
Ⅱ ocular paralysis
5. Internuclear ophthalmoplegia (INO)
Gaze:frontal lobe→
paramedian pontine
reticular formation→
abducens
medial longitudinal
fasciculus →ocular
motor
Ⅱ ocular paralysis
5.1 Anterior internuclear
ophthalmoplegia
With a lesion of the
left MLF, the left eye
fails to adduct when
the patient looks to the
right, this condition is
referred to as left
internuclear
ophthalmoplegia.
Ⅱ ocular paralysis
5.2 One-and-a-half
syndrome
 Pontine center for gaze
and ipsilateral MLF
 One eye lies fixed in the
midline for all
horizontal movements;
the other eye can make
only abducting
movements.
Ⅱ ocular paralysis
6. Superanuclear ophthalmoplegia
 Middle frontal gyrus
 No diplopia
 Two eyes are equally affected
 Reflex movements are spared
Ⅲ alterations of the pupils
1. Pupillary light reflex
 Optic nerve→optic chiasm→optic tract→
Pretectal area→bilateral E-W nuclei→
Oculomotor nerve→pupillary sphincter
Ⅲ alterations of the pupils
2. Horner sign
 Miosis
 Ptosis
 Retraction of eye-ball
 Loss of sweating on the
same side of face
 Due to interruption of
the sympathetic fiber.
Section 4 vertigo and deafness
Ⅷ cranial nerve: vestibular nerve
cochlear nerve
Ⅰ. Vertigo
All subjective and objective illusion of
motion or position, usually rotational.

Ⅰ Vertigo

To maintain balance: visual system
proprioceptive system
vestibular system
 Vestibular system: labyrinth
vestibular nerve
central pathway to cerebellum,
MLF, autonomic center
Ⅰ Vertigo
Peripheral
Central
Location
Labyrinth, vestibular
nerve
Brain stem,
cerebellum, cortex
Etiology
Vertigo
Labyrinthitis, meniere’s
disease, vestibular
neuronitis, otitis media
Severe, short attack
VBI, acoustic
neuroma, temporal
epilepsy
May be prolonged
Nystagmus
horizontal
May be vertical
Other sign
Deafness, tinnitus
Cranial nerve palsy,
contralateral
pyramidal sign
Ⅱ deafness
Auditory system:
 External auditory canal→tympanic membrane→
stapes→oval window→
 organ of corti, hair cell→cochlear nerve→
pons→bilateral lateral lemniscus→inferior
colliculus→medial geniculate body→temporal
lobe
Ⅱ deafness
1. Conductive deafness
Otitis media, rupture of the tympanic
membrane, cholesteatoma
2. Sensorineural deafness
Meniere’s disease, drugs—aminoglycosides,
acoustic neuroma, infarction, multiple
sclerosis
 Exam: Auditory evoked potentials
Section 5 Syncope
Ⅰ. Syncope
an episodic loss of consciousness and
postural tone and an inability to stand,
due to diminished flow of blood to the
brain.
Section 5 Syncope
Ⅱ. Causes:
1. Reflex syncope
vasodepressor syncope, orthostatic
hypotention, carotid sinus hypersensitivity,
micturitional, vagoglosssopharyngeal,
associated with glossopharyngeal neuralgia
Section 5 Syncope
2. Cardiac syncope
arrythmia, myocardial, obstruction
3. Brain
TIA, arteritis
4. Other causes
anemia, hypoglycemia, hypoxia
Section 5 Syncope
Ⅲ clinical feature
1. Prodrome
dizziness, vertigo, pallor, sweating, dim
vision, tinnitus
2. Episode
loss of consciousness, fall to ground,
Bp<60mmHg, if more than 25 seconds may
have convulsion
3. Post episode
Regain consciousness, no sequela
Thank you for listening!
佡剑非 nǎo
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