Neurology Lectures Dr.

Akram Al Mahdawi
Lec.8

COMA
Coma is defined as a state of
unresponsieness and unconsciousness .
It comes from the Greek word "koma,"
meaning deep sleep.
Coma can be a medical emergency that
requires intervention without always
knowing the cause .
Knowledge of CNS anatomy can give clues
to the cause

Wakefulness(arousal)-an independent autonomic-vegetative function maintained

by Reticular Activation System (from lower pons to thalamus ) ,thalamus
and projection to cerebral cortex.
Awareness is the content of consciousness and is the sum of cognitive and
affective mental functions such as learning ,memory,self awarness and
adaptive behavior.
Some related terms :

- Drowsiness-apparent sleep,can briefly aroused with oral command.

-Stupor-not respon to oral commands but respond to painful or noxious stimuli

- Confusion(delirium)-fluctuating state of impairment of both arousal and

awaress (attentional disorder)

Causes of Coma :
1. Sedative drugs and toxins 40%
2. Hypoxic-ischemic(cardiac arrest and anaesthetic accidents ) 25%
3. Structural lesion 20%
4. Metabolic,infection,organ failure 15%

Structural/ intrinsic causes could be :

 TRAUMA
 NEOPLASMS
 VASCULAR DISEASE
 FOCAL INFECTION
 HYDROCEPHALUS

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Neurology Lectures Dr. Akram Al Mahdawi
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Traumatic causes are :
 Concussion
 Cerebral contusion
 Epidural hematoma
 Subdural hematoma/effusion
 Intracerebral hematoma
 Diffuse axonal injury

Metabolic/Toxic causes are :

 Hypoxia-ischemia
Metabolic disorders-(hypoglycemia ,acidosis ,
hyperammonumemia ,uremia )
 Fluid and electrolyte imbalance
 Hypertensive encephalopathy
 Vitamin deficiency-thiamin, niacin, pyridoxine
 Mitochondrial disorders
 Toxins and poisons
 infections

Endocrine disorders
 Thyroid dysfunction
 Adrenal insufficiency
 Hypoparathyroidism
 Diabetic Ketoacidosis DKA

Hypoxic and ischemic causes :

 Shock
 Cardiac or pulmonary failure
 Near drowning
 Carbon monoxide poisoning
 Strangulation

Infectious Causes of Coma :

 Bacterial meningitis
 Brain abscess *
 Epidural, subdural empyema
 Fungal meningitis
 Protozoan infections-amebic, malarial, cysticercosis
 Viral encephalitis
 Postinfectious encephalomyelitis

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Neurology Lectures Dr. Akram Al Mahdawi
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* Note : brain abscess doesn’t cause coma directly but it
causes an increase in Intra cranial pressure that results in coma

Management
The most important thing to do is :
1-maintains AIRWAYS by :
- ensure airways are clean
- suck secretions ,salivations
- put stethoscope and check for breath sounds
-assess respiratory rate
- look for signs of cyanosis

2- CIRCULATORY support by :
- start IV cannula immediately
-check blood pressure ,check pulse
- check any signs of arrhythmia

3-Take 3 blood samples :

The 1st : to send it for routine laboratory investing e.g Hb , PCV , blood
glucose , serum electrolytes ….etc .
nd
The 2 : to send it for endocrinal investigations (hormonal) and for
toxins
rd
The 3 : keep it as spare for another investigations when needed …

4- Give Glusose as hypertonic saline ,meanwhile avoid any movement to the neck
to prevent further damage .

KEY TO DIAGNOSIS
 A good history
 A thorough physical exam
 Knowledge of CNS anatomy

History
- Family, friends, filed personal,patients wallets,pill bottles.
- Sudden-vascular(suggest cardiac causes or SAH ), seizure, trauma
- Prodromal,headache,vomiting,fever, (suggest raised ICP)
- Weakness
-Past History -Dm,HT, alcohol * ,drug abuse,epilepsy
-if its chronic progressive complients ,it mostly suggests TB or neoplasm

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Neurology Lectures Dr. Akram Al Mahdawi
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Note : on asking about alcohol , we should put in mind that it is always
underestimated ….

General Physical Exam

Vital signs (imp.)
 Temperature -fever (may mean infection)
 Very high temperature and dry skin – consider heat stroke
 Hypothermia often seen in drug intoxication

 Hypothermia :could be due to sepsis , hypothyroidism , or

enviromental exposure

 Hyperthermia : could be due to CNS infection , sepsis , heat stroke ,

thyrotoxicosis , stroke , exposure to
certaintoxins(salicylates,anticholinergics,or
sympathomimmetics)

 Systolic BP of over 200 mmHg , with a diastolic BP over 130 mmHg ,

suggested ICH , thyrotoxicosis , or exposure to sympathomimmetic agents

 Bradycardia : ↑IICP , hypothyroidism , OD or toxins or ß-blockers

 Breathing smell : may suggest fetor hepaticus , uremia , acetone ,or
alcohol

Skin examination
 Cyanosis
 Cherry red - carbon monoxide .
 Cold,clammy-hypovolemia,cardiogenic.
 Worm-septic,anaphylactic.
 Razore scar,needle tracks
 AV shunting
 Bleeding tendency
 Café au lait spots - neurofibromatosis
 Shagreen patches - tuberous sclerosis
 Hyperpigmentation - Addison disease
 Petechiae and purpura - meningococcemia
 Signs of trauma – suspicious bruises

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Respiratory Patterns
 Chenyne stokes-compromised diencephalone,hepatic coma,hypoxia.
 Hyperventilation-compromised upper brain-stem,M acidosis.
 Apneustic-compromised pons,anoxia

NEUROLOGIC EXAM
1- Pupillary response :(very very very important)
 pupillary constriction is controlled by the parasympathetic
system in the third nerve
 Dilation mediated by the sympathetic system –hypothalamus to
spinal cord and then the superior cervical ganglia

Pupillary Roles
 Coma due to brain stem must haven impairment of pupillary
function,ocular motility or both.
 Light reflex resist to metabolic dysfunction,and help to differntiate
structural from metabolic.

Midbrain-Midpostion pupil,not react to light.

Pontine lesion-pinpoint pupils
:
- Mid-position , unreactive pupils means both parasympathetic and
sympathetic are affected - indicates mid brain lesions.
- Pinpoint pupils –parasympathetic innervation is intact but sympathetic nerve
is involved indicates pontine lesions
-Unilateral dilation –indicates uncal herniation from compression of
oculomotor nerve (see page 9)
-Bilat dilation -brain death,amphetamin intoxication, anticholinergic, cocaine

Pupillary reflex
 Metabolic causes of coma
 Can give a variety of changes but pupils usually remain
reactive
 Drugs:
 Narcotics-pinpoint but reactive
 Atropine-dilated and nonreactive

2- Corneal reflex
 Test the fifth nerve sensory and seventh nerve motor

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 Cotton on cornea and look for a blink or watch the lower eyelashes
move toward the midline
 Good test for mid and low pontine dysfunction

 EOM evaluates the cortex , and of the MLF(medial longitudinal

fascicle *) in the brain-stem
a)rove spontaneously and conjugate , the brain stem may be intact
b)persisting adduction : paresis of CN VI
c)persisting abduction : CN III dysfunction
d)dysconjugate gaze in the horizontal plane : various sedated states including
alcohol intoxication

3- Oculocephalic Reflex
 Tests-sensory from the eighth nerve , MLF * ,3rd, 4th 6th nerves
 Can only be done in patient with stable spine
 Turn the head quickly to the side and the eyes should move to
the opposite directions of the movement

 Intact brain stem-with cortical dysfunction-eye ball in opposite direction.

 Compressed brain stem-turn in same dirrection or in dysconjucated patterns
 Doll’s eye sign : (-) in normal people →to be supressed
(+) normal reflex in comatose patient

 Absent doll's sign the comatose patient indicates :

1. afferent limb dysfunction : from the labyrinth and the vestibular nerve or
from neck proprioceptors
2. efferent limb dysfunction : MLF , CN III & VI
3. connecting pathway between pons & medulla

(*)
what is MLF ???
MLF= medial longitudinal fascicle , a connection fibers that connect the
Abducent nerve of one side to the occulomotor nerve of the other side . (i.e :
connect the 6th cranial nerve one eye to the 3rd cranial nerve of the other eye )
It is important in conjugated eye movement .
It is surrounded in its course by RAS , so any affection to RAS will affect it .

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4- Oculovestiublar reflex
 Alternative to doll’s eye sign in the patient who had cervical spine injury .
Elevate the head 30 degrees ,place a catheter in the ear and inject ice
water (cool water)
- There are several possible results from the test:
1)normal : deviation of the eyes toward the stimulated ear, Nystagmus with
the fast component away from the stimulated ear.
Bil.Tonic deviation of the eyes toward the stimulated ear should last 30-120
seconds,and indicate an intact brain stem

2)absence : dysfunction of the pons , medulla or less commonly , CN

III,VI,VIII (COWS :summary of abnormal findings:
→→→”cows” Cool water – eyes move to Opposite side of stimulus
Warm water-eyes move to Same side of stimuls)

3)absence of the quick,corrective nystagmus indicates ,damage to the

cerebral hemispheres. A normal response in a comatose patient raises the
suspicious of psychogenic coma

4)both eyes deviate tonically toward the side of cold water infusion,the brain
stem is intact,but the source of coma may be from hemisphere
dysfunction,failing to correct eye position with rapid nystagmus

5)only one eye movement ipsilateral to the stimulus→ internuclear

ophthamoplegia (INO)↔a brain stem structural lesion

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INO : here a cool water is injected in the right ear of the patient , there
is ipsilateral eye movement with no movement of the contra lateral
eye .(MLF lesion)

Glascow coma scale

 Eye opening Motor Response
Spontaneous 4 obeys commands 6
To command 3 localizes pain 5
To pain 2 withdraws to pain 4
None 1 abnormal flexion(decorticate) 3
 Verbal abnormal extension(decerebrate) 2
Oriented 5 none 1
Confused 4
Inappropriate words 3
Incomprehensible sounds 2
None 1
-----------------------------
TOTAL 3-15

 Light coma-spontanous swalling,yawning.

 Decorticate-damage above midbrain
 Decerbrate-damage to mid braine
 Psychogenic coma-leg crossing,arm cross

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Neurology Lectures Dr. Akram Al Mahdawi
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Herniation syndromes
Types :
1= subfalcine
2 = uncus
3 =caudal displacement
4 = cerebellar tonsils

 Tonsillar or Foramen Magnum Herniation

 Displacement of brainstem and cerebellar tonsils into the foramen
magnum
 Progressive LOC, hypertension, bradycardia and irregular
respirations (Cushing Triad)
 Transtentorial herniation
 Displacement of medial aspect of temporal lobe into tentorial hiatus
LOC, ipsilaterial pupillary dilatation, contralateral hemiparesise
(the uncus is medial part of temporal lobe , when there is raised ICP , the tissues
are pushed downwoard , the 1st structure that faces the uncual herniate is the
occulomotor 3rd nerve)
 Upward tentoral herniation
 Cerebellar vermis moves into incisura
 Produces brain stem compression

Work up for a patient with coma

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Neurology Lectures Dr. Akram Al Mahdawi
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Laboratory Work up
 CBC with diff PT,PTT, INR
 LFT’s
 Type and screen
 Toxic screen
 Blood, urine culture
 Chest x-ray
 Urine ketones, glucose
 Electrolytes Ca, Mg, BUN, creatinine

Other Lab work

 Blood ammonia
 Lead levels
 Serum cortisol
 Skeletal survey
 Amino acid profile
 Blood pyruvate and lactate
 Organic acid analysis
Other test to consider
 EEG
 MRI
 Echocardiogram
 CT scan

Treatment of elevated ICP

 Progression of treatment
 Mannitol, or 3% NaCl
 Sedation and pain medication
 Fever control
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 Intubation
 ICP monitor and drainage of CSF
 Paralysis
 Pentobarbital coma
 Surgery for decompression craniotomy
 INTUBATION
 Hyperventilate for a short period of time
 Keep head elevated
 Midline position to enhance venous drainage into the chest
 Check electrolytes
 Correct hyponatremia - produces brain swelling
 Restore low BP
 Cerebral perfusion pressure =MAP-ICP aim to keep
>50.

Medical Intervention of increased ICP

Decrease CSF
 Shunt fluid with external ventricultomy tube
 Diamox 25-100 mg/kg/day in 3 doses

Reduce the size of other compartment

 Mannitol or 3% NaCl
 Mannitol –0.25 to 1.0 gm/ kg
 Infuse over 10 to 15 minutes

MANNITOL
 Reduces ICP in two ways
 Reduces blood viscosity and blood vessel diameter so cerebral
blood volume and ICP decrease –rapid but transient
 Osmotic Effect
 Developes more slowly (15-30minutes)
 Water moves from parenchyma to blood
 Lasts for up to 6 hours.

3% Na- Cl

Give as 5ml/kg bolus over an hour

 Can be given in peripheral IV
 Sodium movement across the blood brain barrier is low.
 Therefore works similar to Mannitol

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 Possible side effects
Rebound increase of ICP when stopped
Central pontine myelinolysis
Subarachnoid hemorrhage

The Coma Cocktail

Intravenous glucose
→ prompt response of hypoglycemic coma
→ DM patient may experience symptoms of hypoglycemia at greater glucose
concentration then non-DM patient.
→1 ampule of 50% glucose water,

Thiamine
 a co-factor in the Kreb’s cycle & the pentose pathway.
Characteristics :
ataxia ,nystagmus , confusion ,hypotension , and ophthalmoplegia
not all are reversible
IV route is more safety then IM

Narcotic Antagonist
 ►Naloxone is a pure narcotic agent antagonist
→ 0.1 mg/kg in children , 2-4 mg IV in adult up to a totaldose of 4-6 mg
→ occational pulmonary edema or ventricular dysrhythmias had been seen
follow the naloxone administration , but most of the giving was safe

The End …

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A Nice Day !

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