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Alteration of consciousness

Outline : Alteration of conscious

Definition Anatomy : reticular formation Pathophysiology Causes Diagnosis Management

Definition Consciousness
State of being fully response to stimuli and demonstating an awareness of self and environment

Consciousness can be divided into two constructs: Arousal Content Arousal without content defines the vegetative state ( big D2B )


Alteration of consciousness
Alert Delirious Normal Increased sleep, disorientation, fear, agitated, often visual hallucinations Moderate reduction in consciousness, decreased interest in environment Arousable only by vigorous and repeated stimulation Total absence of awareness of self and environment


Stupor Coma

Definitions : delirium
Plum and Posner: a floridly abnormal mental state characterized by disorien-tation, fear, irritability, misperception of sensory stimuli, and, often, visual hallucinations.

Definitions:acute confusional state

an acute organic mental syndrome featuring global cognitive impairment, attentional abnormalities, a reduced level of consciousness, increased or decreased psychomotor activity, and a disordered sleep-wake cycle
Lipowski ZJ 1990

Obtundation: the patient appears to sleep more hours than expected, but has some spontaneous awakening Stupor: only awakens when noxius stimulated Coma: does not awaken Vegetative state: after a period of coma, sleep-wake cycles return but there is no awareness

Consciousness depends on the interaction of the midbrain/thalamic reticular system (reticular activating system) and the cerebral cortex Thus, only a limited number of anatomic problems can cause unconsciousness:
Dysfunction of the midbrain/thalamic reticular system Dysfunction of both cerebral hemispheres A combination of the above two problems

Anatomy of consciousness
Brainstm Reticular formation Basal forebrain Neurochemically defined nuclear groups of the brainstem and basal forebrain Ascending projectional system Nonspecific thalamic nuclei Widespread areas of Cerebral cortex


Anatomy of consciousness

Cerebral cortex

Nonspecific thalamic nuclei

Basal forebrain Ascending projectional system

Reticular formation


Reticular formation
3 levels Mesencephalon Pontine Medulla

Basal Forebrain
includes the septal nuclei and the basal nucleus of Meynert.

Basal Forebrain

Stimulating the basal forebrain gives rise to EEG sychrony and sleep. located near the subarachnoid space

ventral to the lentiform nucleus

Neurochemically defined nuclear groups of the

brainstem and Basal forebrain
Ach : basal forebrain , dorsal tegmentum NE : Locus ceruleus 5-HT : Raphe nuclei Histamine : Hypothalamus

Nonspecific thalamic nuclei

Intralaminar thalamic nucleus Reticular thalamic nucleus Midline thalamic nucleus

mostly involved in arousal and alertness This makes a strongly inhibitory input to thalamic nuclei. important in sleep wake cycles

Ascending reticular activating system ARAS = reticular formation + ascending projection system + nonspecific thalamic nuclei

Reticular activating system (Ascending Arousal system)

Cerebral Cortex
Specific function : somatic , sensation , vision , auditory No single area

Pathophysiology of
Alteration of consciousness

Two types lesions 1. Diffuse lesion in cerebral hemisphere : hypoxia , hypoglycemia , hyperosmolar coma, acid-base imbalance, uremia, hepatic coma, etc 2. Focal destruction in reticular core of brainstem : herniation , direct lesions

Approach to alteration of consciosness

Diffuse encephalopathies

Supra-tentorial Infra-tentorial

Lesions ?
Spinomedullary junction ? Lower pons and medulla ? Upper pons (above TG nucleus)? Midbrain level ? Bilateral diencephalon ? Focal / unilateral cerebral hemisphere? Bilateral cerebral hemisphere?

Bilateral cerebral hemisphere?

Focal / unilateral cerebral hemisphere? Midbrain level ?

Bilateral diencephalon ? Lower pons and medulla ?

Upper pons (above TG nucleus)?

Spinomedullary junction ?

Approach to alteration of consciosness

Diffuse encephalopathies

Supra-tentorial Infra-tentorial

Cause of
Alteration of consciousness

Isolated lesions to this portion of the ARAS produce coma, whereas lower lesions do not. Damage to the thalamus or hypothalamus can also alter consciousness, reflecting connections of these structures and the RAS; bilateral involvement is usually required

The cerebral cortex mediates content

If both cerebral hemispheres are dysfunctional, as in a severe metabolic encephalopathy, there is no detectable content Less severe diffuse disorders impair consciousness Focal hemispheral disorders do not by themselves affect consciousness
Herniation or elevated ICP may alter consciousness

Metabolic encephalopathy

Common metabolic causes of stupor and coma

1. Systemic metabolic diseases: eg, hepatic or renal failure, myxedema,hyperosmolar state
Altered mental state with normal brain stem function (especially normal pupils).

2. Stimulants: eg, cocaine, amphetamine, phencyclidine, tricyclic antidepressantdrugs

Fever in some; mydriasis (except miosis with phencyclidine); seizure

Common metabolic causes of stupor and coma

3. Sedatives: eg, alcohol, benzodiazepine, barbiturates, antiepileptic medications
Ataxia; impaired eye movements but normal pupils

4. Opiates

5. Seizure, postictal state: eg, drug overdose or withdrawal, and many othercauses
Fluctuating mental state; paradoxic improvement with benzodiazepine

6. Hypertensive encephalopathy
Headache, cortical blindness, seizure

Common metabolic causes of stupor and coma

7. Meningitis, encephalitis
Nuchal rigidity, seizure, cranial nerve abnormalities (especially sixth nerve)

8. Wernicke encephalopathy: eg, alcoholism and other causes of malnutrition

Abnormal eye movements, ataxia

Management of
Alteration of consciousness

Resuscitation in coma
Airway protection Blood pressure and pulse
Unexplained bradycardia: remember spinal cord injury Sedative drugs and positive pressure ventilation will reliably reduce preload

Evaluation of the comatose

Historical information
Rate of unconsciousness
Immediate vs. slowly progressive

Head injury Focal complaints before loss of consciousness Seizure activity Potential ingestions and exposures Potential for cervical spine injury

Evaluation of the comatose

Physical examination focused on
Pupillary responses Extraocular movements
Spontaneous roving eye movements Cervico-ocular reflexes (if cervical spine is intact!) Vestibulo-ocular reflexes Vertical eye movements

Urgent corrective measures

Hypotension Hypoxia Hypoglycemia Thiamine deficiency Narcotic overdose

Benzodiazepine overdose
Limited role for flumazenil, especially if mixed ingestion suspected

Coma evaluation: 5 steps

Pupils Eye movements Breathing Motor Symmetry

parasympathetic control of pupil size

sympathetic control of pupil size

Pupils:Key points
Size dependent on sympathetic and parasympathetic input Anatomically near the RAS Resistant to metabolic influences Small and reactive with metabolic causes Unilateral dilation indicates uncal herniation

Eye movements: Exam

Position at rest

Straight ahead Dysconjugate Conjugate deviation Oculocephalic reflex Positive Doll!s eyes Negative Doll!s eyes Oculovestibular reflex Cold calorics

Dolls eyes maneuver

Oculocephalic reflex
Eye response to head turning Proprioception from the neck triggers the pontine

conjugate eye center

Dolls + or -?

Dolls eyes maneuver

Positive Dolls eyes
= the eyes deviate relative to the head = stare at the ceiling

Negative Dolls eyes

= the eyes remain straight relative to the head

= turn to the wall

Condition Dolls eyes 1.Awake negative 2.Cerebral dysfunction, positive ( brain stem intact ) 3.Low brain stem lesion negative (pontine gaze center)

Eye movements: Key points

Symmetric responses seen with metabolic Asymmetric responses seen with structural causes

Respiratory pattern
Posthyperventilation apnea Cheyne-Stokes respiration Hyperventilation Central neurogenic hyperventilation Central reflex hyperpnea

Respiratory pattern
Apneustic respiration Cluster (Biot) breathing Ataxic respiration Apnea

Motor responses
Defensive or localizing Withdrawal Flexor (decorticate) posturing Extensor (decerebrate) posturing Leg flexion

Motor: Key points

Posturing is a reflex response to pain Symmetric responses seen with metabolic or structural causes

Asymmetric responses seen with structural causes