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Disturbance of Consciousness 孫苑庭.ppt

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    Disturbance of Consciousness 孫苑庭.ppt Disturbance of Consciousness 孫苑庭.ppt Presentation Transcript

    • Disturbance of Consciousness Department of Neurology R3 Yuan-Ting Sun
    • 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
    • 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
    • Conscious level--wakefulness
    • Grading Cannot be aroused by stimulation, no purposeful attempt is made to avoid painful stimuli Coma Be awakened by vigorous stimuli, have an effort to avoid uncomfortable stimulation Stupor Be aroused by touch or noise, can maintain alertness for some time Drowsiness Alert
    • Glasgow Coma Scale Obey commands 6 Localizing to pain Oriented 5 Withdraw to pain Confused Spontaneous 4 Decorticate Words To speech 3 Decerebrate Sounds To pain 2 None None None 1 Motor response Verbal Eye opening
    • Conscious content--awareness
    • Confusion
      • Inattention and disorientation are the main early signs
      • Deterioration in memory, perception, comprehension, 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
      • Acute confusion: delirium
        • Hyper- agitated, positive symptoms
        • Hypo- muted, negative symptoms
      • Chronic confusion: dementia (final)
      • Beclouded dementia
    • 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)
    • Approach to the patient of conscious disturbance
    • 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
    • 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 drug overdose
        • Hypothermia: hypoglycemia, circulatory failure, hypothyroidism, intoxication (BZD, barbiturate)
    • NE and PE (3)
      • Respiratory pattern:
        • Slow breathing: opiate or barbiturate intoxication, hypothyroidism
        • Deep, rapid breathing:
          • Kussmaul respiration: pneumonia, diabetic or uremic acidosis, pulmonary edema
          • Central hyperventilation  midbrain, diencephalone
    • 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
    • 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
    • Onset and course of conscious disturbance Transient loss of consciousness Sudden onset of loss of consciousness Progressive change of consciousness Rapid deterioration of consciousness 1. 2. 3. 4. 24Hr 48Hr
    • Transient loss of consciousness Brain concussion Seizure SAH Syncope Without focal signs With focal signs EDH, SDH with lucid phase Hours Basilar migraine Minutes Vertebral basilar insufficiency (VBI) Seconds
    • Sudden/acute onset of loss of consciousness Metabolic derangement Drug intoxication Hydrocephalus Hypoglycemia Hypoxia Hypoperfusion SAH Vasculitis (ex. CNS Lupus) Brainstem stroke Head trauma With focal signs Without focal signs Glucose,O2, CPR, detoxification
    • Progressive change of consciousness
      • Metabolic derangement
        • Electrolyte
        • Sugar
        • Liver and renal function
      • Sepsis
      • Intracranial space taking lesion
      • Hydrpcephalus
    • Rapid deterioration of consciousness
      • Beclouded dementia due to systemic problem
    • Coma-like syndromes Ventral pons lesion Guillain-Barre syndrome Awake but deefferented Locked-in state Hydrocephalus, large bilateral lesions in the cingulate gyrus Remains immobile and silent when unstimulate Akinetic mutism Global damage to cerebral cortex (preserved brainstem) ex: cardiac arrest awake coma, spontaneous eye open, yawning, random limb movement, preserved autonomic function Vegetative state
    • Decorticate and decerebrate Decorticate—severe bilateral damage in the hemispheres above midbrain Decerebrate—damage to the corticospianl tract in the midbrain or caudal diencephalon 