Un

(consciousness)
Dr Antony Thomas
Consultant Neurologist
UHCW
Alexandra Hospital
Redditch

Neural basis of
consciousness
Consciousness

cannot be
readily defined in terms of
anything else

state of awareness of self and

surrounding

 Mental

Status =
Arousal + Content

Anatomy of Mental Status

Ascending reticular activating system

(ARAS)

Activating systems of upper brainstem,

hypothalamus, thalamus

Determines the level of arousal

Cerebral hemispheres and interaction

between functional areas in cerebral
hemispheres

Determines the intellectual and emotional

functioning

Interaction between cerebral

hemispheres and activating systems

The content of consciousness

Sum of patients intellectual

(cognitive) functions and emotions
(affect)

Sensations, emotions, memories,

images, ideas (SEMII)
Depends upon the activities of the
cerebral cortex, the thalamus & their
interrelationship
Lesions
of these structures will diminish the
content of consciousness (without changing the
state of consciousness)

The state of consciousness (arousal)

The ascending RAS, from the lower

border of the pons to the ventromedial
thalamus
The cells of origin of this system
occupy a paramedian area in the
brainstem

Altered Mental Status

Abnormal change in level of arousal or altered
content of a patient's thought processes

Change in the level of arousal or

alertness

inattentiveness, lethargy, stupor, and coma.

Change in content

Relatively simple changes: e.g. speech,

calculations, spelling
More complex changes: emotions, behavior or
personality
Examples: confusion, disorientation, hallucinations,

Definitions of levels of arousal

(conciousness)

Alert (Conscious) - Appearance of wakefulness,

awareness of the self and environment
Lethargy - mild reduction in alertness

Obtundation - moderate reduction in alertness.

Increased response time to stimuli.

Stupor - Deep sleep, patient can be aroused only by

vigorous and repetitive stimulation. Returns to deep
sleep when not continually stimulated.

Coma (Unconscious) - Sleep like appearance and

behaviorally unresponsive to all external stimuli
(Unarousable unresponsiveness, eyes closed)

Psychogenic
unresponsiveness

The patient, although apparently

unconscious, usually shows some
response to external stimuli
An attempt to elicit the corneal reflex
may cause a vigorous contraction of
the orbicularis oculi
Marked resistance to passive
movement of the limbs may be
present, and signs of organic disease
are absent

Locked in syndrome

Patient is awake and alert, but unable

to move or speak.
Pontine lesions affect lateral eye
movement and motor control
Lesions often spare vertical eye
movements and blinking.

Vegetative

Locked-in

Confusional state

Major defect: lack of attention

Disorientation to time > place >

person

Patient thinks less clearly and more

slowly

Memory faulty (difficulty in repeating

numbers (digit span)

Misinterpretation of external stimuli

Drowsiness may alternate with hyper

Delirium

Markedly abnormal mental

state
Severe confusional state
PLUS Visual hallucinations &/or
delusions

(complex systematized dream like

state)

1.
2.
3.
4.
5.

Marked: disorientation, fear, irritability,

misperception of sensory stimuli
Pt. out of true contact with environment
and other people
Common causes:

Toxins
metabolic disorders
partial complex seizures
head trauma
acute febrile systemic illnesses

To cause coma, as defined as a

state of unconsciousness in which
the eyes are closed and sleep
wake cycles absent
Lesion of the cerebral
hemispheres extensive and
bilateral
Lesions of the brainstem: above
the lower 1/3 of the pons and
destroy both sides of the

The use of terms other than

coma and stupor to indicate the
degree of impairment of
consciousness is beset with
difficulties and more important
is the use of coma scales
(Glasgow Coma Scale)

Glasgow Coma Scale (GCS)

Best eye
response (E)

4 Eyes opening

Best verbal
response (V)

Best motor
response (M)

5 Oriented

6 Obeys commands

4 Confused

5 Localizes to pain

3 Inappropriate

4 Withdraws from

words

pain

2 Incomprehensible

3 Flexion in response

sounds

to pain

1 None

2 Extension to pain

spontaneously

3 Eye opening to
speech

2 Eye opening in
response to pain

1 No eye opening

1 No motor response

Individual elements as well as the sum

of the score are important.
Hence, the score is expressed in the
form "GCS 9 = E2 V4 M3 at 07:35

Generally, comas are classified as:

Severe, with GCS 8
Moderate, GCS 9 - 12
Minor, GCS 13.

Approaches to DD
Unresponsive
ABCs
Glucose, ABG, Lytes,
Mg, Ca, Tox,
ammonia
Y
IV D50, narcan,
flumazenil
Brainstem N
or other
Focal signs
Y

CT

Unconscious

Diffuse brain dysfunction

metabolic/ infectious
Focal lesions
Tumor, ICH/SAH/ infarction

Pseudo-Coma
Psychogenic,
Looked-in,
NM paralysis

LP CT

Approaches to DD
General examination:
On arrival to ER immediate attention to:
1. Airway
2. Circulation
3. establishing IV access
4. Blood should be withdrawn:
estimation of glucose # other
biochemical parameters # drug
screening

Attention is then directed

towards:
1. Assessment of the patient
2. Severity of the coma
3. Diagnostic evaluation

All possible information from:

1. Relatives
2. Paramedics
3. Ambulance personnel
4. Bystanders
particularly about the mode of onset

Previous medical history:

1.
2.

Clues obtained from the patient's

1.
2.

Epilepsy
DM, Drug history
Clothing or
Handbag

Careful examination for

1.

2.

Trauma requires complete exposure and

log roll to examine the back
Needle marks

If head trauma is suspected, the

examination must await adequate
stabilization of the neck.
Glasgow Coma Scale: the severity
of coma is essential for subsequent
management.
Following this, particular attention
should be paid to brainstem and
motor function.

Temperature
Hypothermia
Hypopituitarism, Hypothyroidism
Chlorpromazine
Exposure to low temperature
environments, cold-water
immersion
Risk of hypothermia in the
elderly with inadequately heated
rooms, exacerbated by

1.
2.

C/P: generalized rigidity and muscle

fasciculation but true shivering may
be absent. (a low-reading rectal
thermometer is required).
Hypoxia and hypercarbia are
common.
Treatment:
Gradual warming is necessary
May require peritoneal dialysis with
warm fluids.

Hyperthermia (febrile Coma)

Infective: encephalitis, meningitis

Vascular: pontine, subarachnoid hge
Metabolic: thyrotoxic, Addisonian
crisis
Toxic: belladonna, salicylate
poisoning
Sun stroke, heat stroke
Coma with 2ry infection: UTI,
pneumonia, bed sores.

Hyperthermia or heat stroke

Loss of thermoregulation dt. prolonged
exertion in a hot environment

Initial in body temperature with

profuse sweating followed by
hyperpyrexia, an abrupt cessation of
sweating, and then
rapid onset of coma, convulsions, and
death

This may be exacerbated by certain

drugs, Ecstasy abuseinvolving a loss
of the thirst reaction in individuals
engaged in prolonged dancing.
Other causes
Tetanus
Pontine hge
Lesions in the floor of the third ventricle
Neuroleptic malignant syndrome
Malignant hyperpyrexia with
anaesthetics.

Heat stroke neurological sequelae

Paraparesis.
Cerebellar ataxia.
Dementia (rare)

Pulse

Bradycardia: brain tumors, opiates,

myxedema.
Tachycardia: hyperthyroidism, uremia

Blood Pressure

High: hypertensive encephalopathy

Low: Addisonian crisis, alcohol,
barbiturate

Skin

Injuries, Bruises: traumatic causes

Dry Skin: DKA, Atropine
Moist skin: Hypoglycemic coma
Cherry-red: CO poisoning
Needle marks: drug addiction
Rashes: meningitis, endocarditis

Pupils

Size, inequality, reaction to a bright

light.
An important general rule: most
metabolic encephalopathies give
small pupils with preserved light
reflex.
Atropine, and cerebral anoxia tend to
dilate the pupils, and opiates will
constrict them.

Structural lesions are more commonly

associated with pupillary asymmetry
and with loss of light reflex.
Midbrain tectal lesions : round,
regular, medium-sized pupils, do not
react to light
Midbrain nuclear lesions: mediumsized pupils, fixed to all stimuli, often
irregular and unequal.
Cranial n III distal to the nucleus:
Ipsilateral fixed, dilated pupil.

Pons (Tegmental lesions) : bilaterally

small pupils, {in pontine hge, may be
pinpoint, although reactive} assess the
light response using a magnifying glass
Lateral medullary lesion: ipsilateral
Horner's syndrome.
Occluded carotid artery causing
cerebral infarction: Pupil on that side is
often small

Diencephalons

Small, reactive

Midbrain

Medium-sized, fixed

Dilated, Fixed
Pons

Ipsilateral dilated, Fixed

small, pinpoint
In hge reactive
.

The oculocephalic (doll's head)

response
Caloric oculovestibular responses

Odour of breath

Acetone: DKA
Fetor Hepaticus: in hepatic coma
Urineferous odour: in uremic coma
Alcohol odour: in alcohol intoxication

Respiration

CheyneStokes respiration:
(hyperpnoea alternates with
apneas) is commonly found in
comatose patients, often with
cerebral disease, but is relatively
non-specific.
Rapid, regular respiration is also
common in comatose patients and is
often found with pneumonia or
acidosis.

Central neurogenic hyperventilation

Brainstem tegmentum (mostly tumors):
PO2, PCO2, and
Respiratory alkalosis in the absence of
any evidence of pulmonary disease

Sometimes complicates hepatic

encephalopathy

Apneustic breathing
Brainstem lesions Pons may also
give with a pause at full
inspiration
Ataxic:
Medullary lesions: irregular
respiration with random deep
and shallow breaths

Cheyne-Stocks

Central Neurogenic Hyperventilation

Apneustic

Cluster
Ataxic

Abnormal breathing patterns in

coma
Cheynes - Stokes
Central Neurogenic

Midbrain

Apneustic
Pons

Ataxic

Medulla
ARAS

Motor function

Particular attention should be directed

towards asymmetry of tone or
movement.
The plantar responses are usually
extensor, but asymmetry is again
important.
The tendon reflexes are less useful.
The motor response to painful stimuli
should be assessed carefully (part of

Painful stimuli: supraorbital nerve

pressure and nail-bed pressure.
Rubbing of the sternum should be
avoided (bruising and distress to the
relatives)
Patients may localize or exhibit a
variety of responses, asymmetry is
important

Flexion of the
upper limb with
extension of the
lower limb
(decorticate
response) and
extension of the
upper and lower
limb (decerebrate
response)
indicate a more
severe
disturbance and

Signs of lateralization

Unequal pupils
Deviation of the eyes to one side
Facial asymmetry
Turning of the head to one side
Unilateral hypo-hypertonia
Asymmetric deep reflexes
Unilateral extensor plantar response
(Babinski)

Head and neck

1.
2.

The head
Evidence of injury
Skull should be palpated for
depressed fractures.
The ears and nose: haemorrhage
and leakage of CSF
The fundi: papilloedema or
subhyaloid or retinal haemorrhages

1.
2.

Neck: In the presence of trauma to

the head, associated trauma to the
neck should be assumed until
proven otherwise.
Positive Kernig's sign : a meningitis
or SAH. If established as safe to do
so, the cervical spine should be
gently flexed
Neck stiffness may occur:
ICP
incipient tonsillar herniation

Causes of
COMA

CNS causes of coma

Cerebrovascular disease is a frequent
cause of coma.

Mechanism:
Impairment of perfusion of the RAS

With hypotension

Brainstem herniation ( parenchymal

hge, swelling from infarct, or more
rarely, extensive brainstem infarction)

Subarachnoid haemorrhage

Loss of consciousness is common

with SAH
only about 1/2 of patients
recover from the initial effects of
the haemorrhage.
Causes of coma:
1. Acute ICP and
2. Later, vasospasms,
hyponatraemia

Parenchymal haemorrhage

1.
2.

1.
2.

May cause a rapid decline in

consciousness, from
Rupture into the ventricles
or subsequent herniation and
brainstem compression.
Cerebellar haemorrhage or infarct with
Subsequent oedema
Direct brainstem compression, early
decompression can be lifesaving.

Hypotension

1.
2.

The critical blood flow in humans

required to maintain effective
cerebral activity is about 20
ml/100 g/min and any fall below
this leads rapidly to cerebral
insufficiency.
The causes:
syncope in younger patients
cardiac disease in older patients.

Hypertensive encephalopathy

Now rare with better control of

blood pressure.
C/P: impaired consciousness,
grossly raised blood pressure,
papilloedema.
Neuropathologically: fibrinoid
necrosis, arteriolar thrombosis,
microinfarction, and cerebral
oedema (failure of autoregulation)

Raised intracranial pressure

Mass effects: tumours, abscesses,

haemorrhage, subdural,
extradural haematoma, brainstem
herniation distortion of the RAS.
C/P: depends on normal variation
in the tentorial aperture, site of
lesion, and the speed of
development.

Herniation and loss of consciousness

Lesions located deeply, laterally, or in
the temporal lobes > located at a
distance, such as the frontal and
occipital lobes.
Rate of growth: slowly growing
tumours may achieve a substantial
size and distortion of cerebral
structure without impairment of
consciousness, in contrast to small
rapidly expanding lesions

Central herniation involves

downward displacement of the
upper brainstem
Uncal herniation in which the
medial temporal lobe herniates
through the tentorium

Head injury

The leading cause of death below the

age of 45, head injury accounts for
1/2 of all trauma deaths
A major cause of patients presenting
with coma.
A history is usually available and, if
not, signs of injury such as bruising of
the scalp or skull fracture lead one to
the diagnosis

Other Neurological causes

Infections
Epileptic Seizures
Raised ICP ( Posterior Fossa tumours,
hydrocephalus)
Sleep disorders
Stroke
Basilar Artery Migraine

Others

Cardiac arrhythmia
HOCM
PE
AS

Metabolic causes of coma

Hepatic Coma
Renal Coma
DKA
HONK
Hypglycaemic Coma

Other endocrine causes of coma

Pituitary Failure
Pituitary Apoplexy
Myxedema Coma
Hyperthyroidism
Adrenocortical Failure

Ca, Mg metabolism
Hypo & Hyper Ca
Hypo & Hyper Mg

Seizures

Definition:-

A seizure is the clinical event that result from

abnormal excessive neuronal activity.

Etiology:-

-Alteration of consciousness, motor activity, behavior,

sensation or autonomic function.

-It may be viewed as a symptom of an underlying disease
process.

Classification:-

Acute non recurrent convulsions:One or more convulsive fits that occur during the same
acute illness & do not recur after recovery:

Febrile convulsions. hypertensive

encephalopathy.
CNs infections:- meningitis, encephalitis.
Intra cranial Hemorrhage: spontaneous, or
traumatic
Toxic:- e.g tetanus.
Intracranial tumors.
Anoxic:- sudden severe asphyxia.
Metabolic:- hypoglycemia, hypocalcaemia, hypo
or hypernateremia.

Chronic recurrent convulsions:-

Recurrent attacks of convulsions with symptoms

free intervals:*Epilepsy:
-- Idiopathic.
--Neurocutaneous synd. Such as Sturgeweber, neurofibromatosis, tuberous
scelosis.
Organic secondary to brain insult:- postinfection, post- traumatic, post- hypoxic,
post- toxic.
Benign neonatal convulsions.
*Degenerative brain disease.
*Congenital cerebral malformation.

Electrical rhythm in epilepsy

Epilepsy
Defined as Increased Neuronal
Excitability

Partial:- Epileptic focus start

localized and remain localized:
Classified according to level of consciousness:

No loss of consciousness:
Motor Sensory Autonomic.
Loss of Consciousness: Temporal lobe epilepsy.

Generalized:- Epileptic focus start

localized then become generalized.

Grandmal Febrile - Status epilepticus

Myoclonic
Clonic Atonic.-- Petite mal (typical and atypical)
Tonic.

Generalized tonic clonic

(grand-mal epilepsy)
The commonest form of childhood convulsions
60%:-An aura:- unusual behaviors recognized by the
mother.
-Tonic phase:- powerful sustained contraction(5
minutes): The patient falls to the ground stiff due to
powerful sustained contraction of all
muscles.
Arm flexed - Legs extended.
-Clonic phase:- Rhythmical contraction and
relaxation of muscles of limbs and face:- Biting

-Post epileptic phase:- The child falls in

deep sleep and afterwards he may be
confused or irritable.
Grand-mal epilepsy has good prognosis if
the first attack start after the age of
3years and the mental development is
normal.

Febrile convulsion
Definition:- Generalized tonic clonic
convulsions which occasionally occur at
the onset of acute extra-cranial infections.
Incidence:- 3-5% in all children.

Etiology:-

At the onset of acute extra-cranial infections

such as tonsillitis.
- Febrile seizures may signify a serious
underlying acute infections.
- In association with high environmental
temp.

Clinical picture:-

Criteria for diagnosis of simple febrile convulsions: Patient

free.

type:- Age: 6month to

6years. - Sex: male more than
female.
Family history: Strong positive.
- Neurologically & metabolically

Seizures stages: Pre-

Ictal:- Convulsions occur at the

onset of temperature 39o c or more.
Ictal:- Generalized tonic clonic.
Short duration:- 5-15 minutes.
Course:- Usually one convulsive fit
during the same illness.
Post-ictal:- Short postictal stupor.

Investigation
Laboratory:CSF analysis: Indicated if any doubt
exist regarding the possibility of
meningitis.
EEG:- Indicated in atypical febrile seizure

persists for more than 15 minutes or recurrent

more than
3 time/day, or focal seizures.

A child at risk for developing

epilepsy:-

Positive family history of epilepsy

Initial febrile seizures before the age of 6
months.
A febrile seizure.
Delayed developmental milestone.
Associated Respiratory manifestation
(cyanosis).

Prognosis:- Risk for developing epilepsy

is 1% in children without risk factors,9%
with risk factors.

Treatment:Immediate first aid measures.

Measures to lower the temperature:Cold fomentation / Antipyretics.
Treatment of the cause of fever e.g
Antibiotics for acute tonsillitis.
Short acting anticonvulsant:Diazepam (valium) 0.25mg/kg/dose.

Generalized absence = petit-mal

epilepsy

- The commonest age 5-9 years.

- Rare below 2years and never continue after
15 years.
- Short sudden loss of consciousness.
- The child suddenly stops talking and stares
for few seconds.
- Recovery is immediate and child resumes
talking.
- Not associated with limb movement.
- Recurrent up to more than 100 times/day.
- May affect school performance.

Myoclonic epilepsy
- Occurs at any age but is more seen in infants and
young children.
- Usually associated with mental retardation.
-The attack which is very frequent, present with
sudden symmetrical mass jerking involving all
limbs.

Juvenile myoclonic epilepsy

-Occurs during adolescence
A.D.
-Chromosome No. 6
The hallmark is morning myoclonus within 90
minutes after awakening.
-Resolved with Valporic acid therapy for life.

Atonic (a kinetic) epilepsy

- It is a type of myoclonic epilepsy.
- Transient loss of consciousness and falling on the
ground.
- Then immediately the child gets up and resumes
activity.
- The condition may be confused with petit mal.

Benign neonatal convulsions

-A.D.
- Chromosome No. 20
-Generalized clonic seizures
-Occurs toward the end of the 1st week of life.
-Called familial 5th day fits.
-Favorable prognosis.

Infantile spasm ( West syndrome)

Brief convulsion of the neck, trunk and arm muscles

followed by sustained muscle contraction lasting 2 to 10
seconds.
Occurs when the child awakening or going to sleep.
Each jerk is followed by a brief period of relaxation, many
clusters occurs each day.
EEG showed Hypsarrhythmia ( high- voltage slow waves,
spikes and polyspikes).
Peak age 3-8 months. - It could be mistaken for infantile
colic.
Treatment by ACTH,or oral steroids, or benzodiazepines,or
valproic acid and vigabatrinis also promising.

Status epilepticus
Definition:Continuous convulsion or repeated
convulsions without return of the level of
consciousness more than 20 min.
Causes:-Sudden withdrawal of anticonvulsant.
-Febrile convulsion in poorly controlled
epileptic patient.
-Metabolic or toxic.

Management:
1-Stop the convulsion by:- Diazepam 0.2 0.4mg / kg / dose I.V. or
0.5mg/kg/dose rectally.
- Chloral hydrate or paraldehyde:- 0.15 mg/kg
diluted in saline I.V or 0.5ml/kg/dose rectally
- If failed give general anesthesia (short acting
barbiturates).
2-Long-term anticonvulsant: Phenobarbitone 3-5mg/kg/day.
Diphenylhydantoin 5-8mg/kg/day.
3-Evaluation of the patient:
After the
attack Todd's paralysis may occur and then
resolve completely.

Partial (focal) seizures

Motor :

Jacksonian epilepsy
(simple partial motor seizures): Involve the motor area of the brain and the
patient is alert.
Consists of clonic movements in a localized
group of muscles. Commonly at the Corner
of mouth, Thumb, and Great toe.
Jacksonian march:- The neuronal discharge
may spread to other parts on the same side
or become generalized.
Rarely may continue for hours or day
(epilepsia partialis continue).
After the attack, there may be weakness of
the part involved (Todd's) paralysis.

Sensory seizures:- (simple partial

sensory seizures): Localized or spreading parasethesia:tingling, coldness, numbness electricity or

even pain.

Autonomic seizures- (simple partial

autonomic seizures):Autonomic manifestation:
-Sweating. - Tachycardia.
Diarrhea or Constipation.
Hypertension.
Abdominal pain (abdominal epilepsy).
Pupillary dilatation or constriction.

Temporal lobe (psychomotor)

Partial complex epilepsy

Sequence of events: Aura:- blinking of eyes, abnormal sound,
taste, smell or movement.
Absence:- loss of consciousness.
Automatism:- automatic movements e.g:
chewing, smacking of lips.
Amnesia:- recent amnesia for all events
during the attack.

Treatment of epilepsy

Duration of therapy: 3 or 4 years after the last convulsions in

grand-mal or petit mal epilepsy in an
otherwise normal child.
Longer period or even life long for those with
associated neurological problems.

Advice to parents & child:

1.
2.
3.

Give full information about the drug

therapy and stress on not to stop the
drug without medical advice.
Allow normal activities:- the child
should be attended by a responsible
adult while bathing or swimming.
Give clear instructions about the firstaid measures in case the seizures:
Ensure patent airway.
Avoid biting the tongue
Putting the child in the prone or side
position with head down.

Anticonvulsants:
Type of
seizures

Drug of
choice

Daily dose

Side effects

Neonatal

Phenobarbito
ne

3-5 mg/kg

Irritability,overacti
vity

Grand-mal

Na-Valproat,
Phentoin,

10-20mg/kg -Hepatic
dysfunction
4-Ataxia,gum
8mg/kg
hypertrophy.
-Rash, Leucopenia,
hepatic
10-20mg/kg dysfunction

Carpamazepi
ne

Focal motor

Carpamazepi
ne

4-8mg/kg

Rash, Leucopenia,
hepatic
dysfunction

Psychomotor

Carpamazepi
ne

4-8mg/kg

Rash, Leucopenia,
hepatic
dysfunction

Myoclonic,

Clonazepam

0.05-

Drowsiness,

New drugs used for treatment of

epilepsy:
-For generalized seizures:
Lamotrigine
Topiramate
Zonisamide
-For partial seizures:
*Gabapentine
-For Infatile spasm:
*Topiramate
*Vigabatrin

Poisoning, drug abuse, and

alcohol intoxication

1.
2.
3.

1.
2.
3.

The most commonly drugs in

suicide attempts are :
Benzodiazepines
Paracetamol
antidepressants.
Narcotic overdoses (heroin)
Pinpoint pupils
Shallow respirations , needle marks.
The coma is easily reversible with
naloxone

Alcohol intoxication
Apparent from the history, flushed
face, rapid pulse, and low blood
pressure. The smell of alcohol on the
breath.
Intoxicated are at increased risk of
hypothermia and of head injury can be
the cause of coma.
At low plasma concentrations of
alcohol, mental changes, at higher
levels, coma ensues, >350 mg/dl may
prove fatal.