disturbance of consciousness 孫苑庭.ppt
TRANSCRIPT
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Disturbance of Consciousness
Department of NeurologyR3 Yuan-Ting Sun
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Consciousness
Conscious level: wakefulness-alertness (GCS, drowsiness, stupor, coma)
Conscious content: awareness (confusion)
Maintained by a system of upper brainstem and thalamic neurons, the reticular activating system (RAS)
Integrated and organized several dimensions of higher cortical function, each of which resides to some extent in anatomically defined region
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Anatomic correlation of consciousness
Brainstem lesions that cause proximate damage to RAS
•Widespread damage in both hemispheres
•Global suppression of cerebral function
Conscious content
Conscious level—less severe
Conscious level--severe
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Conscious level--wakefulness
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Grading
Alert
Drowsiness Be aroused by touch or noise, can maintain alertness for some time
Stupor Be awakened by vigorous stimuli, have an effort to avoid uncomfortable stimulation
Coma Cannot be aroused by stimulation, no purposeful attempt is made to avoid painful stimuli
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Glasgow Coma Scale
Eye opening Verbal Motor response
1 None None None
2 To pain Sounds Decerebrate3 To speech Words Decorticate
4 Spontaneous Confused Withdraw to pain
5 Oriented Localizing to pain
6 Obey commands
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Conscious content--awareness
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Confusion Inattention and disorientation are the main earl
y signs Deterioration in memory, perception, comprehe
nsion, problem solving, language, praxis, visuspatial function and various aspects of emotional behavior
Single higher cortical function deficit is defined by dominant behavioral change (agnosia, apraxia, aphasia) rather than characterizing the state as confusion
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Acute confusion: delirium Hyper- agitated, positive symptoms Hypo- muted, negative symptoms
Chronic confusion: dementia (final) Beclouded dementia
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Pathophysiology of coma and confusion
Interruption of energy substrate delivery (hypoxia, ischemia, hypoglycemia)
Alteration of the neurophysiologic response of neuronal membranes (drug or alcohol intoxication, toxic endogenous metabolites, anesthesia, or epilepsy)
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Approach to the patient of conscious disturbance
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NE and PE (1)
Light reflex
Cornea reflex, Doll’s eye
Suction reflex
• Brainstem signs are a key to localization of the lesion in coma
• Coma associated with normal brainstem function indicates widespread and bilateral hemispheral decrease or dysfunction
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NE and PE (2) Pupil:
One enlarged, unreactive or poor reactive pupil midbrain lesion or herniation
Small reactive pupil (1-2.5mm) metabolic encephalopathy, hydrocephalus
Very small reactive pupil (<1mm)bilateral pontine damage, narcotic, barbiturate or BZD overdose
Body temperature: Hyperthermia (42-44): heat stroke, anticholinergic dr
ug overdose Hypothermia: hypoglycemia, circulatory failure, hypo
thyroidism, intoxication (BZD, barbiturate)
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NE and PE (3)
Respiratory pattern: Slow breathing: opiate or barbiturate intoxica
tion, hypothyroidism Deep, rapid breathing:
Kussmaul respiration: pneumonia, diabetic or uremic acidosis, pulmonary edema
Central hyperventilation midbrain, diencephalone
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NE and PE (4) Respiratory pattern:
Cheyne-stokes breathing: CHF, COPD Deep, bilateral hemispheral lesions
Apneustic breathing: a pause of 2-3s in full respiration, short cycle cheyne-stoke respiration low pontine lesion
Ataxic breathing: the rhythm is chaotic, irregularly interrupted and each breath varying in rate and depth dorsomedial medulla
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NE and PE (5) Blood pressure:
Hypertension (crisis): Herpertensive encephalopathy, ICH, hydrocephalus
Hypotension: MI, sepsis, adrenal insufficiency, internal hemorrhage, drug overdose (BZD, barbiturate)
Involuntary movement: Cerebellar fit: hypoxia Multifocal myoclonus: metabolic disorder or hypoxia Bilateral asterixis: metabolic encephalopathy or drug
effect
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Onset and course of conscious disturbance
24Hr 48Hr
Transient loss of consciousness
Sudden onset of loss of consciousness
Progressive change of consciousness
Rapid deterioration of consciousness
1.
2.
3.
4.
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Transient loss of consciousness
Without focal signs With focal signs
Seconds
Syncope Vertebral basilar insufficiency (VBI)
SeizureSAHMinutes
Basilar migraine
HoursEDH, SDH with lucid phaseBrain concussion
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Sudden/acute onset of loss of consciousness
With focal signs Without focal signs
Brainstem strokeHead trauma
HydrocephalusHypoglycemia
HypoxiaHypoperfusion
SAHVasculitis (ex. CNS
Lupus)
Metabolic derangement
Drug intoxication
Glucose,O2, CPR, detoxification
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Progressive change of consciousness
Metabolic derangement Electrolyte Sugar Liver and renal function
Sepsis Intracranial space taking lesion Hydrpcephalus
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Rapid deterioration of consciousness
Beclouded dementia due to systemic problem
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Coma-like syndromes
Vegetative state
awake coma, spontaneous eye open, yawning, random limb movement, preserved autonomic function
Global damage to cerebral cortex (preserved brainstem) ex: cardiac arrest
Akinetic mutism
Remains immobile and silent when unstimulate
Hydrocephalus, large bilateral lesions in the cingulate gyrus
Locked-in state
Awake but deefferented Ventral pons lesionGuillain-Barre syndrome
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Decorticate and decerebrate
Decorticate—severe bilateral damage in the hemispheres above midbrain
Decerebrate—damage to the corticospianl tract in the midbrain or caudal diencephalon