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第二章第二章 Symptomatology of the Neurological Diseases 方燕南方燕南第一节Disorders of consciousness Consciousness is the state of being aware of self and the environment.Disorders of consciousness is state of impaired consciousness in which the patient is not roused by external stimuli.Inattention,confusion,stupor,and coma are terms describing progressive states of impaired consciousnessAsending reticular activating systemclinical classification Severity degree of disorders of consciousness,range sizecontentstem reflect of consciousness to be divided:1.The descent of level of consciousness 2.Alteration of content of consciousness 3.special type1.The descent of level of consciousness (1)somnolent The somnolent patient may be roused by various stimuli and will then make appropriate motor and verbal responses.When aroused,such a patient may be clear mentally but often is somewhat confused.Illusions,delusions,hallucinations or delirium is common in such patients.somnolent In somnolence,the patient generally drifts back to sleep when the stimulus ceases.Spontaneous movements and spontaneous speech or muttering are usual.+(2)sopor In stupor,the patient will often have considerable spontaneous movement.He will respond to pain,loud auditory stimuli or bright lights.Repeated and persistent stimuli will often rouse the patient to the point where he will respond briefly to questions.Spontaneous movement are common.Control of bowel and bladder is variable.+(3)coma The patient is unaware of self and the environment .Coma is the most degree of depressed of consciousness in which the patient is not roused by external stimuli.Deep coma patient makes no response to any stimulus.The muscle-stretch reflexes,Babinski sign,the corneal reflex and even the pupillary response tend to disappear.There are no spontaneous movements,and the musculature is flaccid,and incontinent of urine and feces.The pulse is usually rapid,the respirations are periodic,and the blood pressure may trend toward shock levels.Semicoma At this level organized withdrawal or other simple adaptive movements occur in response to painful stimuli.Persistent tactile stimulation or shaking may produce a similar response.Verbal responses are limited to groaning or muttering.As soon as the stimulus ceases,the patient resumes his previous status.semicoma Reflex responses are present,but the patient is usually incontinent.Spontaneous movements are uncommon.diagnosis of level of coma Coma level mini semi deep response to pain +severe,+none spontaneous motor +few none by unconsciousness tendon reflect +weak extinct pupillo-reflect +weak extinct BP,R normal abnormal severe2.Alteration of content of consciousness(1)confusion:The inability to think with usual speed and clarity.There may be sleepy,inattention,disorientation in time and place.hysteria.(2)Delirium a confusion state characterized by hyperactivity.agitated,excited,and anxious,and may hallucinate,drowsines.Autonomic disturbances(sweating,HP)Motor abnomalities(tremor,myoclonus)Acute high fever,atropin toxic Chronic-alcoholism3a vigil(special type)(1)decorticated or apallic syndrome:initally comatose following globe cerebral infarction or cardiac arrest survive but remain unaware of their surroundings.They typically regain spontaneous eye-opening,sleep-wake cycles,and brainstem and spinal cord reflexes.Decorticated syndrome When this condition is fully developed,the patient rove his eyes but fails to follow objects or lights.Similarly he fails to turn his eyes toward a noise.He remains mute.Decorticated syndrome In less marked instances,the patient may follow objects or people slowly with his eyes;he may turn slowly toward a sound and look as if he were about to speak but does not.The patient responds to external stimuli in a manner similar to that of the patient in stupor or semicoma.Decorticated syndrome Some patients in a decorticated syndrome may be seen in coma of “toxic origin or in globe lesions.If the lesion implicate the diencephalon,either in midbrain lesion has not recovered,the term will be described by decerebral rigidity.(2)Akinetic mutism appears alert,but is silent and dose not move spontaneously or respond to external stimuli.This arise from bilateral frontal lobe damage,brain stem or the cortico-reticular pathways are interrupted but the motor and sensory pathways spared.diagnosis (1)abulia:Patients are awaken and have contacted with enviroment,but couldnt talk,no spontaneous activity.the sensory and motor pathway are complete and the memory still remain about their situation but had no response to stimulation,no desire,in a severe apathic state.in both frontal lesions.对生活要有追求和目的(2)Locked-in syndrome a lesion of the ventral pons interrupts,the corticobular and corticospinal pathways,with sparing of the reticular pathways.The patient is alert but unable to respond with speech or facial or limb movements.Locked-in syndrome The pathways for eye movement are spared,so the patient can respond with vertical eye movement and blinking.The patient is conscious but mute and paralysed.It is caused by a bilateral infarction in the upper brainstem.brain death 1.deep coma 2.respiratory arrest 3.Pons reflect are absent:pupillary,corneal,oropharyngeal responses,vestibulo-ocular and oculocephalic maneuvers 4.EEG flat,no somatosensory evoked potentials 5.tendon and abdomen reflect may be absent or nomal.6.no medicine toxic,lower temperature,and disorder of internal secretion.第二节一，Dysphasia Dysarthria is pure disorder of speech.Dysphasia is disorders of spoken and written language;it occurs with damage of the frontal,parietal,or temporal cortices.Brocas expressive and wernickes receptive dysphasias occur with damage of the dominant hemisphere .Languagepassclassification1.surround lateral fissure aphasia(1)Broca A.(2)Wernicke A.(3)conduction A.2.transcortical A.(broderzone A.syn.)(1)T.motor A.(2)T.sensory A.(3)mixed T.A.3.global A.4.anomic A.5,subcortical A.syn.(1)thalamic A.(2)basal ganglion A.clinical features(1)Brocas aphasia:Brocas area is the motor centre for the production of speech.This comprises nonfluent,hesitant speech with intact comprehension.The patient knows what he wants to say but has difficulty finding the correct words,often producing the wrong word.The ability to repeat words is better than spontaneous speech.(2)wernickes receptive dysphasia This arises from superior temporal lesions(Wernickes area ).This area is concerned with comprehension of written and spoken language.There is impaired comprehension of speech and written language without difficulty with expression.wernickes receptive dysphasia The speech is fluent but words are replaced with partly correct words and an incorrect words or newly created meaningless words(neologisms).Thus the speech does not make sense but the patient has poor insight into the problem.(3)Conduction dysphasia It occurs with damage to the arcuate fasciculus弓形纤维.The speech is fluent but jargon杂乱,with neologisms as in Wernickes dysphasia.Comprehension of language is intact,the patient is aware of the problem,and repetition is markedly impaired.(5)Nominal dysphasia It is an inability to name objects and arises from a lesion of the dominant parietal-temporal cortex.It may occur during recovery from the aforementioned dysphasia.(6)Global dysphasia It occurs with lesions of both Brocas and Wernickes areas.There is a combination of non-fluent speech and impaired comprehension of language.二，apraxia Apraxia is inability and is difficulty performing skilled movement in the absence of weakness,sensory loss,incoordination,or impaired comprehension.Apraxia arises from a lesion of the non-dominant parietal cortex and may be confined to the limbs,trunk,or face;apraxia 1.ideomotor apraxia:inability to carry out a task on request or by imitation,with normal comprehension and without disturbance of motor or sensory function.Left border superior-gyrus damage daily life normal2.ideational apraxia No precision ideation for complicated and fine motion daily life abnormal Left parietal cortex,border superior-gyrus,damage3.constructional apraxia There is difficulty in drawing simple objects(e.g.A house)and with construction(e.g.using building blocks).4.melokinetic apraxia The patient cannot use a pen or comb by upper limbs and walk by lower limbs and sit down or get up from a chair by his trunk.5.facial-oral apraxia The patient is asked to stick out his tongue or to whistle,but he cannot complete that motor.6.Dressing apraxia:There is difficulty with putting on clothes.三，agnosia Agnosia is the failure to appreciate the significance of a sensory stimulus without the aid of other senses in the presence of intact peripheral sensation(tactile,visual,and auditory).There are different types:clinical features 1.visual agnosia is the inability to recognize a familiar object by looking at it without touching it or hearing any sound from it,e.g.A telephone.It arises from a lesion of the(usually dominant)parietal-occipital lobe.It is the inability to recognize a sound such as a bell ringing without seeing or feeling the bell.It arises from a lesion of the dominant temporal lobe.2.Auditory agnosia3.Tactile agnosia It is the inability to recognize a familiar object placed in the hand with eyes closed e.g.Patients cannot recognize keys placed in the palm of their hand without looking at them or hearing them rattle.It arises from a lesion of the contralateral posterior parietal lobe.4.contralateral sensory inattention There is neglect of the opposite of the body;this may be motor,sensory,or visual,e.g.A hemiplegic patient may ignore the paralysed side or there may be denial of the hemiplegia.5.Gerstmann syndrome This consists of confusion of the right or left sides of the body,inability to distinguish the fingers of the hands(finger agnosia),and impairment of calculation(dyscalculia)and writing(dysgraphia).Difficulty with reading(dyslexia)may also occur.This is a lesion of the dominant parietal-angular gyrus.第四节二，第四节二，1,The auditory damage Deafness and tinnitus in the ear end-organ(cochlear)disease few neurological disorder.In the eighth crania nerve cochlear nerve damage vestibular nerve damageDifferential diagnosis of deafness(1).Conductive-impaired perception of low-pitched sounds.Rinnes test:bone conduction better.Weber test:to affected ear.ear lesion.(2).Sensorineural-impaired perception of high-pitched sounds.Rinnes test:nomal,Weber test:to normal eardeafness diagnosis Causes of sensorineural deafness 1.cochlea-meningtis,drugs,meniere disease.2.cochlea nerve-cerebello-pontine angle tumor.3.center-bilateral brainstem infarction,MS.Causes of conductive-disease of outer or middle ear (3).Mixture deafness:Conductive with Sensorineural deafness.Old-Age deafness.(4).Auditory hallucination-temporal lobe seizures.functional-hysteria2,Tinnitus Tinnitus is the sensation of ringing,buzzing,hissing,whistling in the ear.disease of the middle ear,inner ear,or cochlear component of the eighth nerve accompanied by some degree of deafness.Conductive deafness-with low-pitched tinnitus(except Menieres disease).Tinnitus diagnosis:blood flow in great vessels of the neckAVMcarotid artery stenosis(pulse).3.Hyperacusis Facial N.paralysis Stapes muscle paralysis第四节第四节 一一Differential diagnosisof Dizziness and VertigoVertigo divided two types:(1).-Vestibular peripheral vertigo,include:Labyrinthine failure,Menieres disease,Benign positional vertigo,Vestibular nerve lesions(2).-Vestibular central vertigo:Cerebellopontine angle lesions,Braistem lesionsVestibular peripheral vertigo It is true vertigo:the movement may be discribed as to-and-fro or up-and-down.Nystagmus:horizontalrotary Hearing damage:tinnitus,deafness unbalenced:gait unsteady a u t o n o m i c n e r v e s y m p t o m:vomiting,sweating,facial pale.Vestibular central vertigo Cerebellopontine angle lesions:nystagmus,gait,hearing as veatibular ataxia.Neurological signs-,nerve palsies ipsilateral cerebellar signs contrateralpyramidalweakness.Cause -acoustic neuroma,vascular lesion.Vestibular central vertigo Brainstem lesions Vertigo-severe and prolonged Nystagmus-vertical,multi-directional Hearing-unaffected brainstem signsVestibular central vertigo Cerebellar lesions Vertigo-involving connections of vestibular and flocculonodular node.Nystagmus-horizontal,to the side of the lesion.Gait-ataxia to the side of the lesion Hearing-unaffected cerebellar signsDizziness Dizziness-common ,to be describe by patients faintness,disorientation,drowsiness,visual disturbance,unsteadiness in the legs.Causes:Anxiety,Anaemia,Hypertension or Hypotension.第三节 eye The visual pathway extends from the retina to the occipital cortex.(look the picture)Optic nerve lesion blurred vision,pain,a central scotoma pupillary light reflex defect pale optic disc inflammatory of optic nerveVisual DisturbanceVisual Disturbance 1 1、One eye One eye (1(1suddenly blandness:Central suddenly blandness:Central retinal A.Obstruction-TIAretinal A.Obstruction-TIA(2(2prolong blandness:1)Optic prolong blandness:1)Optic papillitis or retrobulbar neuritispapillitis or retrobulbar neuritis 2)First defect of visual field-2)First defect of visual field-then blandness then blandness Foster-Kennedy syndrome:Frontal lobe tumors unilateral anosmia(嗅嗅 optic atrophy on the side of the tumor papilleddema on the opposite side.Visual Disturbance Visual Disturbance 2.Two eyes:(1)Temporary:see bilateral occipital lobe ischamia.Light reflect normal Pupillo-size normal A A intoxication or B12 deficientintoxication or B12 deficient (2 (2progressign progressign B)Primary optic N.atrophy.attenuation of the retinal vesselsattenuation of the retinal vessels optic disc pallor,border clearlyoptic disc pallor,border clearly a normal large physiological cupa normal large physiological cup impaired pupillary responses to impaired pupillary responses to light.light.such as optic N.or chiasm or optic such as optic N.or chiasm or optic tract or retina damage.MS.tract or retina damage.MS.C)papilloedemaswelling,bleeding of the optic disc early.Pale and no border of the optic later.bilateral.Causes:The optic nerve is covered with meninges and surrounded by subarachnoid fluid.venous drainage damage.papilloedemapapilloedema visual acuity normal blind spot enlarged optic disc swollen,elevated,with blurring of the disc margin engorgement and dilation of the retinal veins haemorrhages on the disc.Secondary optic N.atrophySecondary optic N.atrophy optic disc pale,slight optic disc pale,slight elevated,margins blurredelevated,margins blurred abnormal physiological cupabnormal physiological cup impaired afferent pupillary impaired afferent pupillary responses to light and optic sight.responses to light and optic sight.brain tumors.brain tumors.Identification 1)hypertension:small artery reflect 1)hypertension:small artery reflect light powerful light powerful，Artery-vein impressionArtery-vein impression。Malignant hypertension-retinal Malignant hypertension-retinal hemorrhage,normal sight,optic disc 3-hemorrhage,normal sight,optic disc 3-6 diopters 6 diopters。2)Pseudo-papilledema2)Pseudo-papilledema：Visual field normalVisual field normal optic disc projection2 diopters,optic disc projection2 diopters,Visual field defects 1.Optic chiasm lesion1.Optic chiasm lesion decussating fibres-bi-temporal decussating fibres-bi-temporal hemianopia hemianopia a lesion of nasal side retina of a lesion of nasal side retina of eyeseyes pituitary tumor pituitary tumor2.Homonymous hemianopia 1)Optic tract and Optic radiation lesion completely 2)Occipital cortex lesions(macular sparing)黄斑逃避 Macular fiber distribute to occipital cortex3.homonymous quadrantanopia 1)homonymous superior quadrantanopia Cusead by partial involvement of the optic radiation By a lesion in the left temporal lobe 2)homonymous inferior quadrantanopia Cusead by same one By left parietal lobeHomonymoushenianopiaEye boll movement disturbenceEye boll movement disturbence extraocular myoparalysis extraocular myoparalysis 1.Paralysis of the extraocular 1.Paralysis of the extraocular muscles-pupillae Sphincter muscles-pupillae Sphincter muscle is normalmuscle is normal Involving III,IV,IV nerveInvolving III,IV,IV nerveextraocular myoparalysisextraocular myoparalysis(1)paralysis of oculomotor nerve:(1)paralysis of oculomotor nerve:size of pupils and light reflex normal.size of pupils and light reflex normal.to be partially abducted to be partially abducted 外外 inability to adduct inability to adduct内内 eyelid droops(ptosis)eyelid droops(ptosis)diplopia.diplopia.extraocular myoparalysis extraocular myoparalysis 2)paralysis of trochlear nerve:2)paralysis of trochlear nerve:innervates the superior oblique innervates the superior oblique muscle.muscle.cannot move to down and to cannot move to down and to outward and has diplopia.outward and has diplopia.The patient dare not go down the The patient dare not go down the stairs.stairs.extraocular myoparalysisextraocular myoparalysis 3)paralysis of abducens nerve3)paralysis of abducens nerve impaired abduction of the affected impaired abduction of the affected eye.eye.2.Nuclear 2.Nuclear ophthalmoplegiaophthalmoplegia Pathology of one or Pathology of one or more of the III,IV.VI more of the III,IV.VI ocular motor nuclei.ocular motor nuclei.transient or permanent transient or permanent diplopia diplopia brainstem infarction brainstem infarction 1)Pre-Internuclear ophthalmoplegiaImpaired ascending pathway in brainstemeyes can adduct in same time3 Internuclear 3 Internuclear ophthalmoplegiaophthalmoplegiaDamage manifestationDamage manifestation patient patients eyeballs were moved to s eyeballs were moved to one lateralone lateral one eye abduction normal and one eye abduction normal and company with nystagmus company with nystagmus opposite eye inability to opposite eye inability to adduction at the same timeadduction at the same time convergence movement normal.convergence movement normal.(2)Post-internuclear ophthalegia one inferior-fiber of medial longitudinal-fasciculus damage.Eyeballs moved to one lateral,same lateral eye cannot abduct,and contralateral eye can adduct.(3)One-and-a-half syndrome impaired medial longitudinal fasciculus and the ipsilateral Paramedian Pontine Reticular Formation (PPRF,lateral gaze center).sometimes abducens nucleus(VI)One-and-a-half syndrome ipsilateral eye no abduction contralateral eye no adduction,with nystagmus causes-pontine infarct,MS,pons hemorrhage.4.Center ophthalmoplegia4.Center ophthalmoplegia Lesion in the cortex or brainstem with the level of the oculomotor nuclei impair conjugate movement of the eye,gaze palsy.Their features are not same.Gaze palsy call upon nucleus ophthalmoplegiaHemispheric lesions Destructed lesion(stroke)-both eyes toward the side of the lesion .Stimulated lesion-eyes deviating the discharging focus.Midbrain lesion Lesions of superior of midbrain-up gaze paralysis.pituitary tumor Parinauds syndrome(eyes not to upward and iso-directive movement)Oculomotor crisis-stimulated lesion in superior colliculus of midbrain eyes attackly to upwar Pakinson Syndrome after encephalitis Brainstem lesion unlike those from hemispheric lesions Destructed lesion(stroke)-both eyes toward the side of the normal hemiparesis.Stimulated lesion-eyes to the side of lesion.Disturbance of Adjustment of PupilDisturbance of Adjustment of Pupil1.pupil reaction to ight1.pupil reaction to ight2.Accommodation reflex2.Accommodation reflex affect accommodation without impairment of pupillary responses to light-midbrain lesions,PD.pupillary constriction damage-白喉diphtheria,infection of midbrain3.Argyll-Robertson pupilirregular in shape unequal in size light-near dissociation poorly reactive to light(frontal area of coping顶盖 damage)but normal response to accommodation.Neurosyphilis or MS is the cause.lesion in the midbrain.4.Adies pupil The tonic pupil is large Reacting sluggishly to changes in illumination.Pupil dilation after ceasing light e.g.normal woman ref
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