Altered Consciousnss

Consciousness

“awareness of the environment and oneself”

“an awake and alert condition”

“one is capable of perceiving what’s happening in the surroundings”
“ability to respond in an appropriate manner to certain stimuli”

components of consciousness:

1. arousal and wakefulness

- functions of the ARAS and its projections

2. awareness or the content of consciousness

- function of the cerebral cortex representing
cognitive mental functions
Structures comprising the Consciousness System:

1. Reticular formation
2. Neurochemically-defined nuclear groups of
the brainstem
3. Thalamus and the thalamic nuclei
4. Thalamocortical pathway (tract)
5. Basal forebrain
6. Cerebral cortical areas
 Levels of Depressed Consciousness:
E. Benarroch, B. Westmoreland, et al: Medical Neurosciences, 3rd ed.

1. Alert

3. Confused - transient decline in cognitive functions in the presence of

normal arousal; decreased level of attention; impairment
of clear thinking

7. Somnolent - patient is easily arousable; appropriate verbal and motors

responses to sensory stimuli; when left alone patients drifts
to sleep state

4. Obtunded - alertness is mildly or moderately decreased; when left alone,

patient drifts back to sleep state; when aroused, shows slow
response to any stimuli

15. Stupor - moderate amount of spontaneous movements, and can

be aroused to respond purposefully to afferent stimuli; can
give brief responses to questions or simple commands

6. Coma - state of extended unconsciousness; unarousable, little or

no response to pain or noxious stimuli
 Levels of Depressed Consciousness:
M. Victor, A. Ropper: Adams and Victor’s Principles of Neurology, 7th ed.

1. Alert

3. Confused - “clouding of consciousness”; some degree of inattentiveness

and disorientation
mildly confused
moderately confused
severely confused

9. Drowsiness - inability to sustain a wakeful state without the application

of external stimuli; indistinguishable from light sleep

12. Stupor - can be roused only by vigorous and repeated stimuli, at which
time, patient opens his eyes, looks at the examiner, and does not
appear to be unconscious

5. Coma - incapable of being aroused by external stimuli

semi-coma
deep coma
 Levels of Depressed Consciousness:
B. Bates: Techniques of Physical Examination, 3rd ed.

2. Alert

2. Confused - mild diminution of consciousness with mental slowness,

inattentiveness, dulled perception, incoherent thought process,
patient is disoriented

3. Stupor - marked reduction in mental and physical activity, marked

slowness and reduction in response to commands or stimuli

4. Coma - complete loss of consciousness with unresponsiveness

to stimuli and voluntary movements
 Levels of Depressed Consciousness:
W. Demyer: Techniques of the Neurological Examination, 3rd ed.

1. Alert

3. Somnolence - patient can be aroused to a normal level of

awareness

6. Semicoma - patient can be aroused to some degree, but

cannot reach or sustain a normal level of
consciousness
lethargy
stupor

13. Coma - patient cannot be aroused

partial coma
deep coma
Glasgow Coma Scale

Eye Opening
Never 1
To pain 2
To verbal stimuli 3
Spontaneous 4

Best Verbal response

No response 1
Incomprehensible sounds 2
Inappropriate words 3
Disoriented 4
Oriented and converses 5

Best Motor Response

No response 1
Extension/Decerebrate 2
Flexion/Decorticate 3
Flexion withdrawal 4
Localizes Pain 5
Obeys command 6
 Clinical Approach to a Comatose Patient

1. Airway-Breathing-Circulation

Endotracheal intubation / oropharyngeal tube

Intravenous fluids
Do: a rapid neurological assessment while addressing
the vital functions
Do: initial ocular survey of the organ-systems of the body
while addressing A-B-C

2. General Physical Examination

signs of head injury
look for meningeal signs of irritation
 Clinical Approach to a Comatose Patient

1. Neurological Assessment

Always Inspect! Note for limb movement asymmetry

position of head and eyes; facial grimacing to a given stimulus
state of responsiveness / level of consciousness / GCS
involuntary movements of limbs
abnormal posturing

Decorticate
Posturing

Vs

Decebrate
posturing
 Clinical Approach to a Comatose Patient

4. Neurological Assessment

Inspect! abnormal breathing patterns

Sites of the lesions:

1. Cheyne-Stokes respiration
- cerebral hemisphere

2. CNH
- midbrain

3. Apneustic Breathing
- upper pontine level

4. Ataxic Breathing
- medulla oblongata
 Clinical Approach to a Comatose Patient

5. Neurological Assessment

- check pupil responses

pin point - pontine hemorrhage; opiate poisoning
bilaterally fixed mid position
- midbrain lesion
unilateral or bilateral fixed and dilated
- supratentorial mass with uncal
herniation
enlarged, slowly reactive pupils
- metabolic causes

- examine ocular movements

do: oculocephalic reflex
oculovestibular reflex

- examine the fundi (fundoscopic examination)

look: papilledema; subhyaloid hemorrhage
 Useful guide in the examination of the brainstem/cranial nerve functions in a comatose
patient

Cranial nerves
II and III Absent pupillary reflexes
III, IV, VI, and VIII Absent oculocephalic reflex (Doll’s eye maneuver)
the eye moves passively in the direction of the horizontal
or vertical eye movements, rather than maintaining their
positions of gaze while the head is being moved by the
examiner
V and VII Absent corneal reflexes
No facial grimacing to deeply painful facial pain
VIII, III, and VI Absent water caloric reflexes (oculovestibular responses)
an intact reflex consists of transient tonic deviation
of the eyes towards the stimulated side when stimulated
with cold water
IX and X Absent gag reflex
no cough or gag in response to pharyngeal or tracheal
stimulation and suctioning

Absence of any respiratory effort, even after fully oxygenating the patient and then allowing
the pCO2 to rise to 50-60 mmHg (apnea test)
 Altered Consciousness

“Transient”
loss or episodic alteration
Loss of of consciousness
consciousness

“Persistent”
comatose state

Transient loss of consciousness

• seizures
• syncope
• cerebral ischemia / vertebrobasilar ischemia
• carotid sinus disease
• drop attacks
• sleep disorders
• metabolic (hypoglycemia)
 Differential Diagnosis of Transient Loss of Consciousness

Seizures Syncope

•can occur in any •upright position usually

position and time of the • prodrome – light headed, nausea, ringing in the ears,
day
dimming of vision, pallor, sweating
• hypotension and thready pulses
• Preceding aura may
be present • relatively rapid recovery

• Sudden-onset
• Urinary or fecal Situational syncope: Cardiac causes of syncope:
incontinence may be
present Left or right ventricular outflow
Emotion or pain
• Tongue bitting obstruction
Micturition
• Post-ictal confusion, Arrhythmias
drowsiness, and Coughing
“pump” failure
headache Postural
 Differential Diagnosis of Transient Loss of Consciousness
Vertebrobasilar ischemia
Carotid sinus disease
Drop attacks
Hyperventilation
Sleep disorders
• narcolepsy
• cataplexy
Metabolic (hypoglycemia)
Clinical Features
Additional brainstem symptoms (eg vertigo, diplopia)
Cerebrovascular risk factors
Peripheral pulses involvement
Syncope on turning head or neck or on neck massage
Postural hypotension confirmed on tilt table testing
Elderly females
No alteration of consciousness state
Rapid recovery
Episodic
Normal examination and investigation
Anxiety or situational (eg. Crowded rooms)
Perioral and/or digital tingling sensation, carpopedal spasm, chest pain
High respiratory rate, low pCO2, metabolic alkalosis
Inappropriate desire to fall asleep
Falls with emotional situations, eg. Laughing
Family history
Diabetic on treatment or relative of such a patient
Hepatic failure
Hypopituitarism, Addison’s disease
Insulinemia; glycogen storage disease
Excess alcohol
 Intracranial Causes of Persistent Alteration of Consciousness

Intracranial Causes Clinical Features

Epilepsy Convulsions that are clinically unequivocal

May have incontinece
Tongue biting and other injuries may be present
Head trauma
• extradural or epidural Evidence of head injury or presence of basal skull fracture

hemorrhage
Remote history of head injury (several weeks or even months)
• subdural hemorrhage
Elderly patients and alcoholics are at particular risk, eg prone to accidental
falls
Cerebrovascular diseases
•Subarachnoid hemorrhage History of sudden severe/explosive headache
Associated with an initial loss of consciousness (collapse)
Presence of fever (central in origin)
Neck rigidity; presence of meningeal irritation
Focal neurological deficits particularly if with intracerebral extension or
complications

Presence of focal neurological deficits that are maximal at the onset

• Intracerebral hemorrhage
May have headache, profound alteration of consciousness at the onset

• Hypertensive Presence of hypertension, retinopathy, seizures

Encephalopathy Sudden-onset diffuse (not focal) neurological deficits
 Intracranial Causes of Persistent Alteration of Consciousness

Intracranial Causes Clinical Features

Infection of the CNS

Headache prominent early in the course; fever; signs of meningeal irritation
• Meningitis
Seizures (early encephalitic signs are prominent); fever; presence of profound
• Encephalitis signs of altered consciousness

Subacute-onset; headache may be present

Focal neurological deficits are present
• Cerebral abscess
Obvious signs of infections in the contiguous structures
 Extracranial Causes of Persistent Alteration of Consciousness

Extracranial Causes Some Prominent Clinical Features

Circulatory collapse
Cardiac causes (arrhythmia, Hypotension, tachycardia, rhythm disturbances; cardiac failure
myocardial infarction) May be preceded by cardiac manifestations (eg. Chest pain; dyspnea)

Rigor, pyrexia, vomiting, peripheral vasodilation

Septicemic shock
Obvious source of infection from some other organ system

Hypovolemia (blood loss) Obvious clinical source of blood loss; tachycardia, pale appearance
Metabolic causes
Hypo-or hypernatremia Muscle twitches, dehydration

Cardiac muscle excitability, ileus, diabetes insipidus

Hypo- or hyperkalemia

Hypo- or hyperglycemia Hemiplegia (reversible), seizures

Dehydration, hyperventilation, ketotic breath

Bradycardia/ initially tachycardia, hypotension, hypoventilation, rigidity, cardiac

Hypo- or hyperthermia arrest

Uremia Sallow skin, pale mucosae, hypertension

 Extracranial Causes of Persistent Alteration of Consciousness

Extracranial Causes Some Prominent Clinical Features

Metabolic Causes

Jaundice, signs of portal hypertension, GI bleeding, sepsis

Hepatic failure

Hypoxia Following respiratory failure, cardiorespiratory arrest, irreversible brain

damage will occur after 4 minutes of anoxia
Hypercapnia
Pink puffer, bounding pulses, papilledema, asterixis

Endocrine
Hypotension, abdominal pain, buccal and flexor pigmentation
Adrenal Crisis
Pallor, hypogonadism, bitemporal hemianopsia
Hypopituitarism
 Extracranial Causes of Persistent Alteration of Consciousness

Extracranial Causes Some Prominent Clinical Features

Circulatory collapse
Cardiac causes (arrhythmia, Hypotension, tachycardia, rhythm disturbances; cardiac failure
myocardial infarction) May be preceded by cardiac manifestations (eg. Chest pain; dyspnea)

Rigor, pyrexia, vomiting, peripheral vasodilation

Septicemic shock
Obvious source of infection from some other organ system

Hypovolemia (blood loss) Obvious clinical source of blood loss; tachycardia, pale appearance
Metabolic causes
Hypo-or hypernatremia Muscle twitches, dehydration

Cardiac muscle excitability, ileus, diabetes insipidus

Hypo- or hyperkalemia

Hypo- or hyperglycemia Hemiplegia (reversible), seizures

Dehydration, hyperventilation, ketotic breath

Bradycardia/ initially tachycardia, hypotension, hypoventilation, rigidity, cardiac

Hypo- or hyperthermia arrest

Uremia Sallow skin, pale mucosae, hypertension

In all comatose patient, attempt to rule out the following conditions:

1. Locked-in syndrome

lesion in the ventral pons

affects: corticobulbar and corticospinal tracts
patient is awake but unable to respond
patient communicates via vertical eye movements
and blinking

2. Persistent vegetative state

usually secondary to severe cerebral injury

patient recovers partially from a comatose state
no purposeful movements and no demonstrable
cognitive functions
In all comatose patient, attempt to rule out the following conditions:

3. Catatonia

silent, no volitional movements

no emotional response to external stimuli
patient resists an examiner’s attempt to move; patient
maintains limbs in fixed position
seen in schizophrenic catatonic state

4. Non-convulsive status epilepticus

suspect this condition in patients who don’t regain

consciousness after a convulsive status
epilepticus
End of segment
SEIZURE
 Seizures

•result from abnormal, sudden, excessive and asynchronous

electrical discharges from the cortical neurons

•the discharges are self-terminating and have a tendency to recur

Ictus - the seizure event itself

Aura - the subjective sensation or any phenomenon that
precedes and marks the onset of the
epileptic seizure
Prodrome - refers to premonitory changes in mood or
behaviour, may precede the attack by
some time
Epilepsy - recurrent seizure events with defin ite etiological
factor/s
Convulsion - seizure events with motor manifestations
Seizures
Seizures
Partial seizures

- deviation of the head

and eyes to one side
(aversive seizure)
points to an irritative
focus in the opposite
prefrontal region

- in simple partial seizures, consciousness is often preserved (see video)

- Jacksonian seizure starts as a clonic movement in one

portion of the body, usually the thumb, corner of the mouth,
or great toe, and spreads to adjacent muscular groups
over a few seconds or minutes

- the seizure event may persist on one part of the body or may
become generalized
Complex partial seizures

-differs from generalized motor seizures by:

1. frequent occurrence of an aura that arises from discharges

in the autonomic, visceral, olfactory portions of the
temporal lobe and limbic system

2. loss of awareness or contact with the environment, often

associated with behavioral or complex motor
movements for which the
patient is amnesic after the attacks
Complex partial seizures
Complex partial seizures

- subjective experiences of the aura:

hallucinations (olfactory, gustatory, visual, auditory)

illusions (space distortions, shrinkage, or angulations)
aberrations in cognition (déjà vu, sense of familiarity)
affective changes (anxiety, fear, rage)

- the seizure may terminate with only the subjective

component or may progress to the motor phase
evident by repetitive motor acts (chewing,
lip smacking, undressing, incoherence)
Tonic-clonic (grand mal) seizures

- abrupt-onset, w/o warning; usually begin with opening of the eyes

and mouth, flexion and abduction of the arms, and
extension of the legs

tonic phase
heralded by contraction of the respiratory
muscles resulting in vocalization; followed by
closure of the jaw, respiratory arrest with cyanosis,
and sphincter incontinence
persists for about 15-30 sec. followed immediately by
the clonic phase

clonic phase
violent, rhythmic muscular contractions affecting the whole
body and respiratory muscles
eye movements, facial grimacing, persistent apnea
lasts for about 1-2 min.
Tonic-clonic (grand mal) seizures
Absence seizures

- brief; loss of contact with the environment accompanied by

minimal motor manifestations

- abrupt in onset and described as a stare or cessation of an ongoing

behavior

- may be accompanied by fluttering of the eyelids or by few facial

twitches

- full recovery is evident after 5-10 sec.

Absence seizures
Etiology

• epilepsy is a symptom and sign of numerous neurological

disorders

• over 50% of patients have no apparent cause can be found

despite full and extensive investigation

• etiology will greatly vary depending on:

- the age of the patient

- surrounding circumstances in the history
Causes of seizures
The following are the most common differential diagnoses
In a patient presenting with seizures:

• syncopal attacks cardiac arrhythmias, carotid sinus

hypersensitivity, vasovagal attacks, postural
hypotension

present are: prodromal pallor, nausea, vomiting,

sweating, palpitations

• pseudoseizures hysterical, attention-seeking, feigned seizures

are common “especially in patients with known
seizures”

vital signs, pupils, pO2 and serum pH remain

unchanged, plantar responses are normal, the
EEG will reveal normal findings and no postictal
cortical activity slowing

• transient ischemic attacks / cerebrovascular diseases

• metabolic causes, eg. hypoglycemia

End of segment
 Dementia

Dementia (WHO ICD-10)

a disorder characterized by both memory and

thinking deterioration sufficient to impair personal
activities of daily living; the memory impairment
affects the registration, storage and retrieval of new
information

• not a disease entity, rather a symptomatology with varied

etiology and clinical presentation

• impaired consciousness implies delirium rather than dementia

• the most common causes are Alzheimer and Vascular dementia,

both are seen in advanced age groups
 Common types of dementing diseases and their approximate
frequencies
Dementing Diseases %
Cerebra atrophy, mainly Alzheimer but including Lewy- 50
body, Parkinson, Pick
Multi-infarct dementia (Vascular type) 10
Alcoholic dementia 7
Intracranial tumors 5
Normal-pressure hydrocephalus 5
Huntington chorea 2
Chronic drug intoxications 3
Miscellaneous (hepatic failure, pernicious anemia, thyroid diseases, 6
ALS, Creutzfeldt_jacob disease, MS)

Head trauma 2
AIDS dementia 2
Pseudodementias (depression, hypomania, schizophrenia, 8
hysteria, undiagnosed)
M. Victor and A Ropper: Adams and Victor’s principles of Neurology 7th ed.
 Dementia

General clinical features:

The earliest feature of dementia, from most causes, is loss

of memory for recent events. Subsequent symptoms include abnormal
behavior, loss of intellect, mood changes, and difficulty coping with
ordinary routines.

Rate of progression:

• Alzheimer disease - slowly progressive over years

• Vascular dementia - progressive but often fluctuating or stepwise
with each stroke
• Encephalitis - over days to weeks
Some reversible forms of dementia:

Endocrinologic Hypothyroidism
Hypoparathyroidism

Metabolic Hepatic Encephalopathy

Vit. B12 deficiency

Hydrocephalic Post-infectious
NPH

Tumors Meningiomas

Pseudodementia Major Depression

Things to emphasize in the History and Examination of a demented
patient:

It is essential to get a history from a relative or friend, as well as

from the patient in order to gauge the following-

• rate of intellectual decline

• activities of daily living and social interaction
• nutritional status
• drug history
• general health and relevant disorders, eg. Stroke, head injury
• family history of dementia

Neurologic evaluation should focus more on the following-

 presence of focal neurologic deficits

 involuntary movements
 pseudobulbar signs
 presence of primitive reflexes, eg. Pout, grasp reflexes
 gait disorder
Things to emphasize in the History and Examination of a demented
patient:

Neurologic evaluation should focus more on the following-

 presence of focal neurologic deficits

 involuntary movements
 pseudobulbar signs
 presence of primitive reflexes, eg. Pout, grasp reflexes
 gait disorder
In all patients suspected with dementia, it is essential to utilize the
Mini-mental State Scale

Probable dementia = 24-27 score

 Primary degenerative dementia:

1. Alzheimer disease
2. Pick disease
3. Lewy-body dementia

Alzheimer disease

• accounts for more than ½ of patients with dementia

• at least ¼ of the population over 85 years have Alzheimer

Clinical symptomatology:
short term memory loss > long term memory
personality changes
depression
anxiety
other psychological features
Alzheimer disease

Clinical signs:

Early stages
- will reveal very little clues
- slight confusion on dates and location of the interview
- speech can be a little hesitant
- no focal neurological deficits

Later stages
- as the disease progresses, problems in language, praxis and
gnosis become increasingly apparent
- personal care deteriorates
- primitive reflexes emerge
- eventually, the patient becomes mute, bed-bound and incontinent
- condition generally lasts 7-15 years
Parting words on Alzheimer disease

 typically, a patient with Alzheimer disease does not

initiate the consultation

 there are seldom any focal neurological signs at the time

of the first assessment

 formal psychometry is usually essential to confirm the

diagnosis, rather than relying “only” on the screening test
such as the MMSE scale

 the main role of brain imaging in the assessment of Alzheimer

Is to exclude other “treatable” or “revesible” dementias
End of segment