Disturbance of Consciousness

Department of NeurologyR3 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

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

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

Conscious content--awareness

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

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 dr

ug overdose Hypothermia: hypoglycemia, circulatory failure, hypo

thyroidism, intoxication (BZD, barbiturate)

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

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

24Hr 48Hr

Transient loss of consciousness

Sudden onset of loss of consciousness

Progressive change of consciousness

Rapid deterioration of consciousness

1.

2.

3.

4.

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

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

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

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

Decorticate and decerebrate

Decorticate—severe bilateral damage in the hemispheres above midbrain

Decerebrate—damage to the corticospianl tract in the midbrain or caudal diencephalon