Section

Disorders of consciousness

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.Consciousness

the state of the patients awareness of self and environment and his responsiveness to external stimulation and inner need.

Content of consciousnessOrientationpercepbilityattitudes emotions active

Structural basis1.ascending reticular activating system, ARAS reticular formation thalamus cerebral hemisphere alert state2.cortex

clinical manifestation1.according to level of consciousness2.according to content of consciousness

1.level of consciousness(1) Somnolent (2) Stupor (3) Coma lesser degree deep

Somnolent

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

comaThe 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 consciousnessConfusionDeliriumSpecial Type Decorticated Syndrome Akinetic mutism

confusionclouding of the sensoriumInability to think with customary speedMarked by some degree of inattentiveness and disorientation accompanied by illusions

Delirium stateHallucination, hyperactivityHigh fever, atropine overdose, alcohol

Decorticated syndromeNeocortical death ARAS is normal, arousal-nonarousal cycleOpen eyes, blink, swallow, eyes moveComa, Show no signs of awareness of the environment or inner needVegetative state, decerebrate rigidity 12 in 45 awakened in 2 weeks, >3 month:PVS

Akinetic mutismThe 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.

differential diagnosisAbuliaLocked-in syndrome

abuliaThe 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 syndromeLesion of the ventral pons (basis pons)Interrupts the corticobulbar and corticospinal pathwaysdepriving the patient of speech and the capacity to respond in any way except by vertical gaze and blinkingwakefulness

brain deathHarvard medical school committee 19681. Absence of cerebral function 2. Absence of brainstem function including spontaneous respiration3. Irreversibility

Brain death1. Absence of cerebral function: Deep coma, total lack of spontaneous movement, and of motor and vocal responses to all visual auditory and cutaneous stimulation2. No spontaneous respiration3. Absence of brain stem function: Dilated midposition fixed pupils, corneal reflex, oculocephalic and oculovestibular test, gag reflex(-), last for 12 hours4. EEG: flat or isoelectric (

Section Aphasia, apraxia, agnosia

aphasiaA loss or impairment of the production and/or the comprehension of the spoken or written language due to an acquired lesion of the brainNo higher order mental function disturbance i.e. Confusion, delirium, mental retardationNot dysarthriaNot aphonia

classification1.Parasylvian fissure aphasic syndrome Broca aphasia, Wernicke aphasia Conduction aphasia2.Transcortical aphasia Transcortical motor, sensory, mixed3.Global aphasia4.Anomic aphasia5.Subcortical aphasia syndrome thalamic aphasia, basal ganglion aphasia

Broca aphasiaPrimary deficit in speech productionDominant hemisphereInferior frontal gyrus, posterior portion

Wernicke aphasiaPrimary deficit in comprehensionParaphasia: literal: the grass is greel verbal: the grass is blueDisturbance in repetitionWernicke area: posterior portion of supratemporal gyrus

Transcortical aphasiaWatershed areaRepetition is remarkably preserved

Anomic aphasiaThe patient lose only the ability to name people and objectsMiddle temporal lobe

Global (Total) aphasiaLeft middle cerebral artery occlusionAll aspects of speech and language are affected Can say only a few words

Subcortical aphasiaThalamic aphasiaBasal ganglion aphasia: nonfluent, dysarthric, paraphasic

apraxiaThe 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.

apraxiaIdeomotor apraxiaIdeational apraxiaMelokinetic apraxiaConstructional apraxiaFacial-oral apraxiaDressing apraxia

agnosiaA highly-ordered perceptual disturbance, no elementary sensation disturbance, can not interpret sensations correctly.Due to disorders of the association areas in the parietal lobes.

agnosiaVisual agnosia: object, face, verbalAuditory agnosia: verbal Sensory agnosiaBody image disturbance non-dominant parietal lobeGerstmann syndrome finger agnosia, right-left confusion, dysgraphia, Dyscalculation Dominant hemisphere angular gyrus

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Section 3A.Disturbance of Vision

B. Disturbance of Ocular Movement

A . Visual pathwayRetinaoptic nerve optic chiasmoptic tract lateral geniculate nucleus (LGN)optic radiationoccipital lobe(calcarine sulcus) Optic chiasm: fibers from the nasal retinas cross over

reduced 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

reduced vision2. Two eyesCortical blindness : dilated pupil, light reflex is preservedToxic: methyl Deficiency: pernicious anaemia

visual field defect1. Optic nerve: uniocular blindness

visual field defect2. Optic chiasm:bitemporal hemianopiaseen in pituitary tumor, craniopharyngioma

visual field defect3. Optic tract:homonymous hemianopia

visual field defect4. 5. Optic radiation: quadrant anopia

visual field defect6. Visual cortex: homonymous hemianopia with macular sparing

visual field defect1. 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 macular sparing

B. Disorder of ocular movement anatomy1. Oculomotor nerve: levator of lid superior rectus inferior rectus inferior oblique medial rectus pupillary sphincters ciliary muscle

anatomy2. Trochlear nerve: superior oblique muscle3. Abducens nerve: lateral rectus muscle

ocular paralysis1. Ocular motor nerve paralysisPtosis Lateral deviation of the eyeInability to rotate the eye upward, inward and downwardDiplopiaDilated non-reactive pupil, paralysis of accommodation

ocular paralysis2. Trochlear nerveCan not rotate down and outwardThe patient complains of special difficulty in reading or going downstairs

ocular paralysis3. Abducens nerveParalysis of outward movementEye deviates mediallyDiplopia

ocular paralysis4. Nuclear ophthalmoplegiaBrain stem lesion: infarction, MSAccompanied by ipsilateral cranial nerve paralysis, contralateral hemiplegia

ocular paralysis5. Internuclear ophthalmoplegia (INO)

ocular paralysisGaze:frontal lobe paramedian pontine reticular formation abducens medial longitudinal fasciculus ocular motor5. Internuclear ophthalmoplegia (INO)

ocular paralysis5.1 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.

ocular paralysis5.2 One-and-a-half syndromePontine center for gaze and ipsilateral MLFOne eye lies fixed in the midline for all horizontal movements; the other eye can make only abducting movements.

ocular paralysis6. Superanuclear ophthalmoplegiaMiddle frontal gyrusNo diplopiaTwo eyes are equally affectedReflex movements are spared

alterations of the pupils1. Pupillary light reflexOptic nerveoptic chiasmoptic tract Pretectal areabilateral E-W nuclei Oculomotor nervepupillary sphincter

alterations of the pupils2. Horner signMiosis PtosisRetraction of eye-ballLoss of sweating on the same side of faceDue to interruption of the sympathetic fiber.

Section 4 vertigo and deafness cranial nerve: vestibular nerve cochlear nerve. Vertigo All subjective and objective illusion of motion or position, usually rotational.

VertigoTo maintain balance: visual system proprioceptive system vestibular systemVestibular system: labyrinth vestibular nerve central pathway to cerebellum, MLF, autonomic center

Vertigo

Peripheral Central Location Labyrinth, vestibular nerveBrain stem, cerebellum, cortexEtiology Labyrinthitis, menieres disease, vestibular neuronitis, otitis mediaVBI, acoustic neuroma, temporal epilepsyVertigo Severe, short attack May be prolongedNystagmus horizontalMay be verticalOther sign Deafness, tinnitus Cranial nerve palsy, contralateral pyramidal sign

deafnessAuditory system:External auditory canaltympanic membrane stapesoval windoworgan of corti, hair cellcochlear nerve ponsbilateral lateral lemniscusinferior colliculusmedial geniculate bodytemporal lobe

deafness1. Conductive deafness Otitis media, rupture of the tympanic membrane, cholesteatoma2. Sensorineural deafness Menieres disease, drugsaminoglycosides, acoustic neuroma, infarction, multiple sclerosis Exam: Auditory evoked potentials

Section 5 Syncope. 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. Causes: 1. Reflex syncope vasodepressor syncope, orthostatic hypotention, carotid sinus hypersensitivity, micturitional, vagoglosssopharyngeal, associated with glossopharyngeal neuralgia

Section 5 Syncope2. Cardiac syncope arrythmia, myocardial, obstruction3. Brain TIA, arteritis4. Other causes anemia, hypoglycemia, hypoxia

Section 5 Syncope clinical feature1. Prodrome dizziness, vertigo, pallor, sweating, dim vision, tinnitus2. Episode loss of consciousness, fall to ground, Bp

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