Section Ⅰ

Section ⅠSection Ⅰ

Disorders of consciousness

刘海若

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刘海若不是脑死亡凌锋教授赴英会诊有结果 20022002年年 0505月月 2020日日 17:04 17:04 北京晚报北京晚报

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刘海若苏醒创医学奇迹八方援手力催凤凰重生 22002002年年 0808月月 1616日日每日新报每日新报

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。

ⅠⅠ.Consciousness.Consciousness

the state of the patient’s awareness of self and environment and his responsiveness to external stimulation and inner need.

Content of consciousnessContent of consciousness

Orientationpercepbilityattitudes emotions active

1.ascending reticular activating system, ARAS

reticular formation thalamus cerebral hemisphere alert state

2.cortex

Structural basisStructural basis

Ⅱ Ⅱ clinical manifestationclinical manifestation

1.according to level of consciousness

2.according to content of consciousness

1.level of consciousness1.level of consciousness

(1) Somnolent

(2) Stupor

(3) Coma lesser degree

deep

SomnolentSomnolent

stuporstupor

Can be roused only by vigorous and repeated stimuli, when left unstimulated they quickly drift into a sleeplike state.

comacoma

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 obta

inable, corneal, pupillary, pharyngeal, tenden reflex (-)

2.content of consciousness2.content of consciousness

(1) Confusion

(2) Delirium

(3) Special Type

Decorticated Syndrome

Akinetic mutism

confusionconfusion

“clouding of the sensorium”Inability to think with customary speedMarked by some degree of

inattentiveness and disorientation accompanied by illusions

Delirium stateDelirium state

Hallucination, hyperactivityHigh fever, atropine overdose, alcohol

Decorticated syndromeDecorticated syndrome

Neocortical death ARAS is normal, arousal-nonarousal cycleOpen eyes, blink, swallow, eyes moveComa, Show no signs of awareness of the envir

onment or inner needVegetative state, decerebrate rigidity

12 in 45 awakened in 2 weeks, >3 month:PVS

Akinetic mutismAkinetic mutismThe term akinetic mutism has been applied t

o 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 Ⅲ differential diagnosisdifferential diagnosis

(1) Abulia

(2) Locked-in syndrome

abuliaabulia

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 syndromeLocked-in syndrome

Lesion of the ventral pons (basis pons)Interrupts the corticobulbar and corticos

pinal pathwaysdepriving the patient of speech and the ca

pacity to respond in any way except by vertical gaze and blinking

wakefulness

Ⅳ Ⅳ brain deathbrain deathHarvard medical school committeeHarvard medical school committee 19681968

1. Absence of cerebral function 2. Absence of brainstem function including spontaneous respiration3. Irreversibility

Brain deathBrain death 1. Absence of cerebral function: Deep coma, total lack of s

pontaneous 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 fix

ed 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 disturban

ce

Section ⅡSection Ⅱ

Aphasia, apraxia, agnosia

aphasiaaphasia

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 dysarthriaNot aphonia

classificationclassification 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 aphasiaBroca aphasia

Primary deficit in speech productionDominant hemisphereInferior frontal gyrus, posterior portion

Wernicke aphasiaWernicke aphasia

Primary deficit in comprehensionParaphasia: literal: the grass is greel

verbal: the grass is blueDisturbance in repetitionWernicke area: posterior portion of su

pratemporal gyrus

Transcortical aphasiaTranscortical aphasia

Watershed areaRepetition is remarkably preserved

Anomic aphasiaAnomic aphasia

The patient lose only the ability to name people and objects

Middle temporal lobe

Global (Total) aphasiaGlobal (Total) aphasia

Left middle cerebral artery occlusionAll aspects of speech and language are

affected Can say only a few words

Subcortical aphasiaSubcortical aphasia

Thalamic aphasiaBasal ganglion aphasia: nonfluent, dysarthri

c, paraphasic

apraxiaapraxia

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.

apraxiaapraxia

Ideomotor apraxiaIdeational apraxiaMelokinetic apraxiaConstructional apraxiaFacial-oral apraxiaDressing apraxia

agnosiaagnosia

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.

agnosiaagnosia 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刘海若不是脑死亡凌锋教授赴英会诊有结果 20022002年年 0505月月 2020日日 17:04 17:04 北京晚报北京晚报

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刘海若苏醒创医学奇迹八方援手力催凤凰重生 22002002年年 0808月月 1616日日每日新报每日新报

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刘海若住院实况首次播放恢复很快已能开口说话口说话 20022002年年 0909月月 0707日北京娱乐信报日北京娱乐信报

　　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亲刘凤翰兴奋地说。

　　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’，前几天过生日，她对我说，‘爸爸，生日快乐’。”

Section 3Section 3

A.Disturbance of Vision

B. Disturbance of Ocular Movement

A . Visual pathwayⅠA . Visual pathwayⅠRetina→optic nerve→ o

ptic chiasm→optic tract →lateral geniculate nucleus (LGN)→optic radiation→occipital lobe(calcarine sulcus)

Optic chiasm: fibers from the nasal retinas cross over

Ⅱ Ⅱ reduced visionreduced vision1. One eyeCentral retinal artery occlusion Amaurosis fugaxRetro-bulbar optic neuritis

multiple sclerosis, neuromyelitis opticaFoster-Kennedy syndrome

anosmia, optic atrophy on one side

Papilledema on the other side , seen in frontal lobe tumor

Ⅱ Ⅱ reduced visionreduced vision

2. Two eyesCortical blindness :

dilated pupil, light reflex is preservedToxic: methyl Deficiency: pernicious anaemia

Ⅲ Ⅲ visual field defectvisual field defect

1. Optic nerve: uniocular blindness


2. Optic chiasm:bitemporal hemianopiaseen in pituitary tumor,

craniopharyngioma


3. Optic tract:

homonymous hemianopia


4. 5. Optic radiation: quadrant anopia


6. Visual cortex: homonymous hemianopia with macular sparing


1. Optic nerve: uniocular blindness2. Optic chiasm: bitemporal hemianopia

seen in pituitary tumor, craniopharyngioma3. Optic tract: homonymous hemianopia4. Optic radiation: quadrant anopia5. Visual cortex: homonymous hemianopia with ma

cular sparing

B. Disorder of ocular movementB. Disorder of ocular movement anatomyⅠ anatomyⅠ

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 Ⅰ anatomyanatomy

2. Trochlear nerve:

上斜肌 superior oblique muscle

3. Abducens nerve:

外直肌 lateral rectus muscle

Ⅱ Ⅱ ocular paralysisocular paralysis1. Ocular motor nerve paralysisPtosis Lateral deviation of the eyeInability to rotate the eye up

ward, inward and downwardDiplopiaDilated non-reactive pupil, p

aralysis of accommodation

Ⅱ Ⅱ ocular paralysisocular paralysis

2. Trochlear nerveCan not rotate down and outwardThe patient complains of special difficulty i

n reading or going downstairs


3. Abducens nerveParalysis of outward movementEye deviates mediallyDiplopia


4. Nuclear ophthalmoplegiaBrain stem lesion: infarction, MSAccompanied by ipsilateral cranial nerve pa

ralysis, contralateral hemiplegia

Ⅱ Ⅱ ocular paralysisocular paralysis5. Internuclear ophthalmoplegia (INO)


Gaze:frontal lobe→ paramedian pontine reticular formation→ abducens

medial longitudinal fasciculus →ocular motor

5. Internuclear ophthalmoplegia (INO)


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 Ⅱ ocular paralysisocular paralysis5.2 One-and-a-half syndr

omePontine center for gaze

and ipsilateral MLFOne eye lies fixed in the

midline for all horizontal movements; the other eye can make only abducting movements.


6. Superanuclear ophthalmoplegiaMiddle frontal gyrusNo diplopiaTwo eyes are equally affectedReflex movements are spared

Ⅲ Ⅲ alterations of the pupilsalterations of the pupils

1. Pupillary light reflexOptic nerve→optic chiasm→optic tract→ P

retectal area→bilateral E-W nuclei→ Oculomotor nerve→pupillary sphincter

Ⅲ Ⅲ alterations of the pupilsalterations of the pupils2. Horner signMiosis PtosisRetraction of eye-ballLoss of sweating on the

same side of faceDue to interruption of t

he sympathetic fiber.

Section 4 vertigo and deafnessSection 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 Ⅰ VertigoVertigo

To maintain balance: visual system

proprioceptive system

vestibular systemVestibular system: labyrinth

vestibular nerve

central pathway to cerebellum,

MLF, autonomic center

Ⅰ Ⅰ VertigoVertigoPeripheral Central

Location Labyrinth, vestibular nerve

Brain stem, cerebellum, cortex

Etiology Labyrinthitis, meniere’s disease, vestibular neuronitis, otitis media

VBI, acoustic neuroma, temporal epilepsy

Vertigo Severe, short attack May be prolonged

Nystagmus horizontal May be vertical

Other sign Deafness, tinnitus Cranial nerve palsy, contralateral pyramidal sign

Ⅱ Ⅱ deafnessdeafness

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 Ⅱ deafnessdeafness

1. Conductive deafness Otitis media, rupture of the tympanic memb

rane, cholesteatoma2. Sensorineural deafness Meniere’s disease, drugs—aminoglycosides,

acoustic neuroma, infarction, multiple sclerosis

Exam: Auditory evoked potentials

Section 5 SyncopeSection 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.


Ⅱ. Causes:

1. Reflex syncope

vasodepressor syncope, orthostatic hypotention, carotid sinus hypersensitivity,

micturitional, vagoglosssopharyngeal, associated with glossopharyngeal neuralgia


2. Cardiac syncope

arrythmia, myocardial, obstruction

3. Brain

TIA, arteritis

4. Other causes

anemia, hypoglycemia, hypoxia

Section 5 SyncopeSection 5 Syncope Ⅲ clinical feature

1. Prodrome dizziness, vertigo, pallor, sweating, dim visi

on, tinnitus2. Episode loss of consciousness, fall to ground, Bp<60

mmHg, if more than 25 seconds may have convulsion

3. Post episode Regain consciousness, no sequela

Thank you for listening!Thank you for listening!

佡剑非 nǎo

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Section Ⅰ

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