Prof., Dr. :sherif wadie
Reticular activating system (RAS)

Good Consciousness
=
Alertness + Awareness

Diminished alertness =
Widespread abnormalities of cerebral
hemispheres or reduced activity of reticular
activating system (RAS)

Confusion :
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Impaired attention and concentration, manifest
disorientation in time, place and person, impersistent
thinking, speech and performance, reduced
comprehension and capacity to reason
Fluctuate in severity, typically worse at night
‘sundowning’
Perceptual disturbances and misinterpret voices,
common objects and actions of other persons
Confusion is also found in dementia (progressive
failure of language, memory, and other
intellectual functions)
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Delirium : confusion and associated agitation,
hallucination, convulsion and tremor
Amnesia : a loss of past memories and to an
ability to form new ones, despite alert and
normal attentiveness
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Alert : normal awake and responsive state
Drowsiness : state of apparent sleep, briefly
arousal with oral command
Lethargic : resembles sleepiness, but not
becoming fully alert, slow verbal response and
inattentive. Unable to adequately perform simple
concentration task (such as counting 20 to 1)
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Somnolent : easily aroused by voice or touch;
awakens and follows commands; required
stimulation to maintain arousal
Obtunded/Stuporous : arousable only with
repeated and painful stimulation; verbal output
is unintelligible or nil; some purposeful
movement to noxious stimulation
Comatose : no arousal despite vigorous
stimulation, no purposeful movement- only
posturing, brainstem reflexes often absent
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Dementia

Confusional state

Longstanding nature
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Acute

Varies little from time
to time
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Fluctuate
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Memory problem

Clouding of
consciousness
Medical or surgical disease
 Metabolic disorders
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Hepatic
Uremic
Hypo and hypernatremia
Hypercalcemia
Hypo and hyperglycemia
Hypoxia
Hypercapnia
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Infectious illness
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Pneumonia
Endocarditis
Urinary tract infection
Peritonitis
Congestive heart failure
Postoperative and posttraumatic states
Drug intoxication
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Opiates
Barbiturates
Other sedatives
Diseases of nervous system
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Cerebrovascular disease, tumor, abscess
Subdural hematoma
Meningitis
Encephalitis
Cerebral vasculitis
Hypertensive encephalopathy
causes of confusional state (5)
•Alcoholism.
•Depression.
•Diabetes.
•Drug overdose
•Head injuries
•Encephalitis
•Epilepsy
•Stroke
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History --- emphasizing the patient’s condition
before the onset of confusion
Clinical examination --- focus on

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signs of diminished attentiveness, disorientation,
and drowsiness and
the presence of localizing neurological signs
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-
Control underlying medical illness
Quiet the patient and protect him from injury
Discontinue drugs that could possibly be
responsible for the acute confusional state :
sedating, antianxiety, narcotic, anticholinergic,
antispasticity, corticosteroid, L-dopa,
metoclopramide, cimetidine, antidepressant,
antiarrhythmic, anticonvulsant, antibiotics.
-
-
Haloperidol, quetiapine, risperidone are
helpful in calming the agitated and
hallucinating patient, but should be used in the
lowest effective doses
In alcohol or sedative withdrawal—
chlordiazepoxide is the drug of choice. Chloral
hydrate, lorazepam, and diazepam are equally
effective
Eye opening:
Nil
To pain (applied to limbs)
To voice (including command)
Spontaneous (with blinking)
1
2
3
4
Motor response:
Nil
Arm extension to pain (nail bed pressure)
Arm flexion to pain (nail bed pressure)
Arm withdrawal from pain (nail bed pressure)
Hand localizes pain(supraorbital or chest pressure)
Obeys commands
1
2
3
4
5
6
Verbal response:
NIL
Groans (no re-cognizable words)
Inappropriate words (including expletives)
Confused speech
Orientated
1
2
3
4
5
Glasgow Coma Scale : Eye opening
(E)
Glasgow Coma Scale : Motor response
(M)
Glasgow Coma Scale : Verbal
response (V)
GLASGOW COMA SCORE
Notes
1.
2.
3.
4.
5.
scoring from the best response
verbal response will not correct in the condition
of aphasia, intubation and facial injury
sensory loss may interfere painful stimulation
eye opening may be interfered by orbital
swelling and 3rd CN palsy
arm movements may be impaired from local
trauma or cervical cord lesion
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History
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Circumstances and rapidity with which neurologic
symptoms developed
Immediately preceding medical and neurologic
symptoms
Use of medications, illicit drugs, or alcohol
Chronic liver, kidney, lung, heart, or other medical
disease
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Vital sign

Temperature
 Fever
 Hypothermia -- <31°C causes coma
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Pulse
Respiratory rate and pattern
Blood pressure
Funduscopic examination
Cutaneous lesion

Observe
Movement : restless, twitching, multifocal
myoclonus, asterisks
 Decorticate rigidity
Suggest severe bilateral damage rostral to midbrain
 Decerebrate rigidity
Indicate damage to motor tracts in the midbrain or
caudal diencephalon
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Level of arousal and elicited movements
Brainstem reflexes

pupils
Ocular movements
 respiration
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DESCRIPTIONS
Small, reactive
INTERPRETATION
Metabolic causes
Diencephalic lesion
Midposition, fixed
Mid brain lesion
large, fixed
Pin point
Unilateral fixed dilated
Extensive brain stem lesion
Anoxia
Sedative overdose
Anticholinergic poisoning or
mydriatic eyedrops
Pontine lesion
Opiates
Third nerve palsy
Doll’s eye
maneuver
(Oculocephalic
reflex)
Cold caloric test
(Oculovestibular
reflex)
Condition
Awake
Cerebral dysfunction,
brainstem intact
Brain stem lesion
Doll’s eyes
Negative
Positive
Condition
Awake
Cerebral dysfunction,
brainstem intact
Brain stem lesion
Cold calorics
Nystagmus, N/V, pain
Negative
Slow deviation toward
water
Negative
Respiratory patterns
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Cheyne-Stokes respiration : bilateral cortical or
bilateral thalamic lesions, metabolic disturbances,
incipient transtentorial herniation
Hyperventilation : midbrain or pons lesions
Apneusis : lateral tegmentum of lower half of
pons
Cluster : lower pontine or high medullary lesions
Ataxic : dorsomedial medulla lesion
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Least useful sign because :
Acid-base derangements
 Hypoxia
 Cardiac influences

 Brain death
 Locked-in syndrome
 Vegetative state
 Frontal lobe disease
 Non-convulsive status epilepticus
 Psychiatric disorder (catatonia, depression)
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An awake but unresponsive state
Extensive damage in both cerebral hemisphere
Retained respiratory and autonomic functions
Cardiac arrest and head injury are the most
common causes.
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Awake patient has no means of
producing speech or volitional limb,
face and pharyngeal movements
Vertical eye movement and lid
elevation remain unimpaired
Infarction or hemorrhage of the
ventral pons
COMA
LOCALIZING SIGN
NO LOCALIZING SIGN
SUPRATENTORIAL INFRATENTORIAL
- CVD
- TUMOUR
- ABSCESS
STIFF NECK
NO STIFF NECK
STRUCTURAL DAMAGE
- HYPOXIA
- CARDIAC
ARREST
- ENCEPHALITIS
- SAH
- MENINGITIS
FUNCTIONAL NEURONAL
DEPRESSION
- HEPATIC
- URAEMIC
- POST ICTAL STATE
- FLUID ELECTROLYTE IMBALANCE
- DRUGS
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CBC
FBS
BUN, Creatinine
Electrolyte, calcium
LFT
Drug screen, toxicology screen
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EKG
CT or MRI brain
CSF exam
EEG
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Recovery from coma depends primarily on the
causes, rather than on the depth of coma
Intoxication and metabolic causes carry the best
prognosis
Coma from traumatic head injury far better than
those with coma from other structural causes
Coma from global hypoxic-ischemic carries least
favorable prognosis
At 3rd day, no papillary light reflex or GCS < 5 is
associated with poor prognosis

Central
transtentorial
herniation
Brain Herniation
 Uncal
transtentorial
herniation
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Intubation and hyperventilation (PCO2 25-30
mmHg)
Mannitol (0.5-1 gm/kg body weight or 20%
mannitol 200 cc. infusion 10-20 minutes
repeat every 4 hours if necessary
Furosemide 20-40 mg IV
Dexamethasone 4-10 mg IV q 6 hours
decrease perilesional vasogenic cerebral
edema. Active at 24-48 hours.
Consult surgery