COMA

RELATED DISORDERS OF
CONSCIOUSNESS
 COMA

= suspension of consciousness a state of continuous

awareness of one self and one environment
Consciousness depend by the integrity of reticular
activating system of the upper brainstem = paramedian
regions of the upper (rostral) pontine and midbrain
tegmentum + thalamic nuclei (PM, parafascicular,
medial portion of centromedian and intralaminar)

Receive collaterals of the direct spinothalamic pathways
whole cerebral cortex

modulates the incoming information via corticofugal
projections to the reticular formation
Coma-producing alterations in the brain are of two
main types

I one clearly morphologic

a) discrete paramedial lesions in the
upper brainstem and lower diencephalon
b) widespread bilateral damage to the
cortex and subcortical white matter
(traumatic damage, bilateral infarcts,
hemorrhages,encephalitis, hypoxia)
II submicroscopic suppression of neuronal
activity =metabolic, drugs , toxin
 Mass lesion cause coma
a) Direct extension of the lesion into the diencephalon and midbrain
b) Lateral displacement of deep central structures, often with temporal lobe
herniation compression, ischemia and secondary hemorrhages in the
midbrain and subthalamic region
central syndrome with downward displacement and bilateral
compression of the upper brainstem ! rostral-caudal deterioration of
brainstem function apathy, confusion, drowsiness , coma
Miotic pupils
uncal syndrome with unilateral displacement and uncal gyrus
herniation the Kernohan Woltman sign = compression of the opposite
cerebral peduncle Babinski sign and hemiparesis controlateral to the
original hemiparesis
! Differs mainly in that drowsiness in the early stages is accompanied or
preceded by unilateral pupillary dilatatation (most often on the side of the
mass)
3-5 mm drowsiness
5-8 mm stupor
8-9 mm coma
 Diagnosis

A. Positive diagnosis -1) Anamnesis antecedents, circumstances in which the person

was found, use of medications
2) Clinical exam - * general physical exam
* nuchal rigidity
* fundoscopy
**neurologic
3) Laboratory studies and imaging
B. Differential diagnosis
C. Causes of coma= Aethiological diagnose
! Coma is not a disease per se but is always a symptomatic expression of an underlying
disease.
When the comatose patient is first seen quickly make certain airway is clear
no bleeding
IV access
cervical
stabilisation
 Alterations in vital signs

A. TEMPERATURE - fever ! Intoxication with anticholinergic

hypothermia ! Alcohol,barbiturate, myxedema
B . RESPIRATION RATE slow breathing ! Barbiturate, opiate
rapid ! Diabetic and uremic acidosis
(Kussmaul respiration)
C. PULSE RATE slow ! Cushing fen.
D. BLOOD PRESSURE HTA - ! Increased intracranial pressure
- hTA !!!
E. INSPECTION OF THE SKIN
F. ODOR OF THE BREATH
 NEUROLOGIC EXAMINATION

A. Posture of the limbs and body

B. Presence or absence of spontaneous movements
- seizures
- multifocal myoclonus metabolic disorder (uremia,
anoxia, drug intoxication)
- decorticate rigidity lesions at a more rostral level
of the nervous system in the cerebral white matter or internal
capsule and thalamus
- decerebrate rigidity damage to motor tracts in
upper pons or midbrain = lesion below the level of the red nucleus

Reaction to noxious stimuli

 NEUROLOGIC EXAMINATION
the brainstem reflexes = pupillary response to light, eye
movements, corneal responses, respiratory pattern

D. Ocular movement resting position and spontaneous movements of the

globes
- deviation of one eye
- conjugate deviation ! The eyes look toward a
hemispheral lesion and away from a brainstem lesion
- ocular bobbing lesions in tegmentum of the
midbrain and pons
// ocular dipping intoxications and anoxia
- oculocephalic reflexes = dolleye movement
!Not present in a normal alert person // absence= damage
within the brainstem
- oculovestibular or caloric response // absence =
damage within the brainstem
absence of
nystagmus despite conjugate deviation = cerebral hemispheres damage
 NEUROLOGIC EXAMINATION

E. Pupillary reactions - pupil diameter ! Enlarged pupil > 5mm

- the pupillary reactions ! With coma due to drug
intoxications and metabolic disorders, pupillary reactions are usually
spared
F. Eyelids and Corneal response loss= deepening loss of
consciousness
G. Respiratory pattern less localizing value
Kussmaul, Cheyne Stokes, apneustic
breathing, agonal gasp
 LEVELS OF CONSCIOUSNESS

CONSCIOUSNESS normal
CONFUSED disoriented,impaired thinking and responses
DELIRIOUS disoriented, restlessness, hallucinations, sometimes
delusions ! State I which hyperactivity is proeminent/ signs of the
overactivity of the autonomic nervous system
SOMNOLENT sleepy
DROWSINESS inablity
OBTUNDED decrease alertness, slowed psychomotor responses
STUPOROUS sleep like state (not unconscious) little/no
spontaneous activity
COMATOSE cannot be aroused; no response to stimuli
 Other neurologic conditions that simulate coma

VEGETATIVE STATE= awake but nonresponsive state

Yawning, coughing,swallowing and limb and head movements persist =
awake coma. Respiratory and autonomic functions are retained.
These people have emerged from coma after a period of days or weeks
AKINETIC MUTISM = partially or fully awake state in which patient is
immobile and mute
Lesions situated on the orbitofrontal surfaces
LOCKED IN STATE = an awake patient has no means of producing
speech or volitional movement, but retains vertical eye movements and lid
elevation MORSE CODE
Lesions that transect corticospinal and corticobulbar pathways infarcts
or hemorrhage of the ventral pons , pontine myelinolisis, Guillain- Barre
syndr., critical illness neuropathy
! PSYCHOGENIC COMA
 Classification of Coma and Differential
Diagnosis
I. Diseases that causes no focal or lateralizing neurologic signs, usually with
normal brainstem functions,CT scan and cellular content of the CSF are
normal.
A. Intoxication: alcohol, barbiturates and other sedative drugs, opiates, etc.
B. Metabolic disturbances: anoxia, diabetic acidosis, uremia, hepatic coma,
hypoglycemia, addisonian crisis, profound nutritional deficiency.
C. Severe systemic infections:pneumonia, typhoid fever, malaria, septicemia,
Waterhouse-Friderichsen syndrome.
D. Circulatory collapse from any cause.
E. Postseizure states.
F. Hypertensive encephalopathy and eclampsia.
G. Hyperthermia or hypothermia.
H. Concussion
I. Idiopathic recurring stupor and coma.
J. Acute hydrocephalus.
 II. Disease that cause meningeal irritation with or without fever , with an excess of
WBCs or RBCs in th CSF usually without focal or lateraliizng cerebral or brainstem
signs.
A. subarachnoid hemorrhage from rupture aneurism arteriovenous
malformation,occasionally trauma
B. acute bacterial meningitis
C. some forms of viral encephalitis
III Disease that cause focal brainstem or laterally cerebral signs, with or without
changes in the CSF. CT and MRI are usually abnormal
A. hemispheral hemorrhages or infarction
B. brainstem infarction due to thrombosis or embolism
C. brain abscess, subdural empyema.
D. epidural and subdural hemorrhage and brain contusion
E. brain tumor
F. miscellaneous : cortical vein thrombosis, some of forms viral encephalitis , focal
embolic encephalomalacia due to bacterial endocarditis, acute hemorrhage,
leukoencephalitis, disseminated postinfection, encephalomyelitis, and others
 TREATMENT

AIRWAY tracheal intubation

IV ACCESS naloxone
+ dextrose
+ thiamine (avoid
provoking Wernicke disease)
AETHIOLOGICAL TREATMENT
 BRAIN DEATH - CRITERIA

Coma of a known cause

Absence of motor responses
Absence of brainstem reflexes (pupillary, corneal, caloric, gag)
Absence of coughing in response to tracheal suction
Absence of respiratory drive at a PaCO2 60mmHg or 200mmHg
above baseline= APNEA TEST
Interval between exam usually 6h
Perform confirmatory tests cerebral angiography
EEG recording are obtained for at
least 30min with a 16-18 channel
TCD both MCA and AV
nuclear imaging with technetium