NEUROSCIENCE 5.

Disorders of Consciousness & Higher

Cortical Function
DR. DONABELLE M. CHU MD. May 6, 2024 LE 1
FPNA

● State of patient’s awareness of self-environment,

TABLE OF CONTENTS
responsiveness to external stimulation, and inner need.
I. WHAT IS CONSCIOUSNESS
● 2 components or dimensions:
a. Unconsciousness ● CONTENT/COGNITION
b. Arousal o Mental action or process of acquiring knowledge
II. STATES OF NORMAL AND IMPAIRED CONSCIOUSNESS through thought, experience and senses.
a. Normal Consciousness
b. Confusion
● AROUSAL
c. Drowsiness o To say one is conscious, they should have
d. Stupor cognition and should be arousable.
e. Coma
III. OTHER STATES OF IMPAIRED CONSCIOUSNESS
a. Delirium A. UNCONSCIOUSNESS
b. Obtundation
c. Vegetative State
● State of unawareness of self and environment.
d. Minimally Conscious State ● Suspension of mental activities + diminished responsiveness to
e. Locked-In Syndrome environmental stimuli.
IV. BRAIN DEATH PROTOCOL
a. PNA Brain Death Criteria ● If you’re unaware of yourself or your environment = suspension
b. Apnea Test of cognition or mental activities.
V. NEUROANATOMY OF CONSCIOUSNESS
a. Structures Involved for Consciousness
b. Ascending Reticular Activating System (RAS) B. AROUSAL
VI. IMPAIRED CONSCIOUSNESS PATHOLOGY ● Level of consciousness.
a. Pathologic Anatomy of Coma (Structural Causes)
VII. BRAIN HERNIATION SYNDROME ● Appearance of being awake (displayed by: facial muscles, eye
a. Central Herniation Syndrome opening, fixity of gaze and body posture).
b. Unical Syndrome ● May be elevated or depressed.
VIII. METABOLIC MECHANISMS THAT DISTURB CONSCIOUSNESS
a. Metabolic Mechanisms o Depressed sensorium/consciousness
IX. CLINICAL APPROACH TO PATIENT WITH DISTURBANCE IN o Elevated consciousness
CONSCIOUSNESS
a. Neurologic Examination of a Patient with Decreased Sensorium
X. MENTAL STATUS AND HIGHER CORTICAL FUNCTIONS
a. Mental Status Examination (MSE)
b. Higher Cortical Functions

LEGEND

IMPORTANT LECTURE BOOK PREVIOUS TRANS

⭐ 💬 📖 📋

REFERENCES

1. Disorders of Consciousness and Higher Cortical Function – Dr. Donabelle M. Chu

MD. FPNA (Asynchronous)
2. 2026 College of Medicine - Transcription
Figure 1. Spectrum of Arousal Lecture PPT]
LEARNING OBJECTIVES
▪ To discuss “consciousness” and enumerate disorders of II. 5 STATES OF NORMAL AND IMPAIRED
consciousness in terms of level of arousal.
CONSCIOUSNESS
▪ To enumerate neuroanatomic localization of consciousness.
▪ Discuss briefly the current brain death criteria. A. NORMAL CONSCIOUSNESS
▪ To discuss the approach to patients presenting with disorders of ● Normal person when awake or aware.
consciousness. o Px is fully awake/active
● Fully responsive to a thought or perception.
I. WHAT IS CONSCIOUSNESS? ● Indicates by his behavior and speech the same awareness of
● Not strictly a medical term (it is also literary, philosophic, and self and environment as that of the examiner.
psychological).

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B. CONFUSION o Deep coma – non-responsive, reflexes not present, no

● Awake but disoriented/inattentive. brain function.
● Inability to sync with customary speed, clarity, and coherence.
● Marked by some degree of inattentiveness and disorientation. III. OTHER STATES OF IMPAIRED CONSCIOUSNESS
A. DELIRIUM
C. DROWSINESS ● Characterized by misperception of sensory stimuli and, often,
● Also termed lethargy or somnolence. vivid hallucinations.
● Inability to sustain a wakeful state without the application of ● Develops over a short period of time and tends to fluctuate during
external stimuli. course of the day.
● May be accompanied by agitation occasionally.
● Inattentiveness, mild confusion and/or drowsiness can be
improved with arousal.
B. OBTUNDATION
● Imagine a very sleepy person,
● Literally means mental blunting or torpidity.
o No one talking to them or no stimulus = they get sleepy
o It is the level between drowsy and stupor. When we say
or fall asleep. obtundation or the patient is obtunded, the patient is arousable
o Apply stimulus to arouse them by calling their attention by tactile stimulation.
or constantly talking to them = can maintain ● Mild to moderate reduction in alertness accompanied by a lesser
wakefulness. interest in the environment.
o When you stop interacting with the patient they will ● Slower psychologic responses to stimulation
return to a sleepy state. o If you call on the patient, if he doesn’t respond, then you tap
on him and he responds, that patient is obtunded.
D. STUPOR o But if you tap the patient and the response is that you still have
● Responsive to pain. to inflict pain on the patient before he would respond, then that
● State in which the patient can be aroused only by vigorous patient is stupor.
● May have increased number of hours of sleep and may be drowsy
and repeated stimuli (painful/noxious) at which time he opens
between sleep bouts.
his eyes, looks at the examiner, and does not appear to be
conscious. C. VEGETATIVE STATE
● Response to spoken commands: absent or slow and inadequate.
● Denotes recovery of crude cycling of arousal states heralded by
● Px looks like he’s asleep (decreased state) and will not be alert the appearance of “eyes-open” period in an unresponsive
when calling his name but applying painful stimuli (pinching or patient.
applying sternal rub) will wake them up or make them respond. ● No evidence of awareness of self or their environment
o Wakefulness after painful stimuli is sometimes ● Patient may blink in response to threat or to light and intermittently
unsustained – slightly open eyes and immediately close the eyes move from side to side, seemingly following objects or
again fixating momentarily.
▪ Consider the patient to be stuporous. o May seem awake but there is no awareness of self and the
● Drowsy vs Stuporous environment.
● Drowsy ● Exhibit sleep-wake cycle; appear awake; responds to pain but not
o Call patient = patient responds purposive.
● Persistent Vegetative State
o Constantly talking = sustains wakefulness
o Patients remaining in a vegetative state that lasts for more
o Stop talking = patient goes back to sleep than a month.
o VERBAL STIMULATION
● Stuporous D. MINIMALLY CONSCIOUS STATE
o Painful stimulus = patient responds ● Patient is capable of some rudimentary behavior such as
o Wakefulness = not sustained (immediately falls following a simple command, gesturing, or producing single
asleep or closes eyes) words or brief phrases, always in an inconsistent way from one
o PAINFUL STIMULATION examination to another.
○ It is sometimes the patient follows or the patient is conscious
E. COMA but sometimes, the patient is minimally conscious.
● Deep sleep or trance.
● State of unresponsiveness in which the patient lies with eyes E. LOCKED-IN SYNDROME
closed and cannot be aroused to respond appropriately to ● Patient is de-efferented, resulting in paralysis of all four limbs
stimuli, even with vigorous stimulation. and the lower cranial nerves.
o Even if you inflict very painful stimulation, patient will ● Conscious but unable to respond to most stimuli.
● Affection of the basis pontis, leaving the pontine tegmentum intact
not be aroused nor respond.
● Retain control of vertical eye movements and eyelid opening –
● Light coma and Deep coma
found in the midbrain.
o Light coma – unresponsive but there is still presence of
brainstem reflexes IV. BRAIN DEATH PROTOCOL
▪ Pupillary light response or reflex A. PNA Brain Death Criteria Revised 2017
▪ Corneal reflex ● Purpose: To define the state of brain death to determine
▪ Gag reflex eligibility for organ donation.
▪ Spontaneous breathing ● Brain death is the physical state wherein all the following criteria
are met:

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○ Irreversible coma is present:

■ The cause of coma is established and is sufficient to
account for the loss of brain function; B. APNEA TEST
■ The possibility of recovery of any brain function is
excluded;
■ Cessation of whole brain function persists for at least 4
hours of observation and therapy
○ Permanent cessation of whole brain function:
■ Coma unresponsive to all stimuli;
■ Absence of all brainstem function as evidenced by all the
following:
a. Fixed pupils
b. (-) corneal response
c. (-) oculovestibular response to ice water calorics
d. (-) gag reflex
e. (-) spontaneous respiration after apneic oxygenation

*NOTE: EEG is an optional test in patients in whom the above

cannot be tested

○ Exclusion to the above criteria include: drug and metabolic

intoxication, hypothermia, and shock
○ In children <5 years old and anencephalic infants, special
caution should be exercised.
○ The declaration of brain death shall be made by two different
physicians who are both not part of the transplant team; they
should preferably be a neurologist or neurosurgeon or internist
or anesthesiologist. The time the second declaration is made
shall be the time of death.

*NOTE: The apnea test is required and should be properly

performed as follows.

Figure 2. APNEA Test [Lecture PPT]

● 📋 Core temperature should be >36.5C, systolic BP should be

>90mmHG, and fluid balance is positive for the past 6 hours
● 📋 Preoxygenate the patient then get the ABG
● 📋 Disconnect the ventilator and put a catheter at carina to give
100% oxygen at 6L/min. Observe chest wall and abdominal wall
for movement.
● 📋 If still no respiratory movement for 8 minutes, get the ABG and
hook back the ventilator.
● 📋 if PCO2 is >60mmHg or PCO2 increases more than 20mmHg,
you can say that the patient has no spontaneous respiration, and
the APNEA test has been fulfilled.

V. NEUROANATOMY OF CONSCIOUSNESS
A. STRUCTURES INVOLVED FOR CONSCIOUSNESS

1. Rostral Pontine Tegmentum

2. Midbrain Tegmentum
3. Diencephalon
4. Caudate-Putamen (Striatum)
5. Medial Hemispheric Wall
6. One cerebral Hemisphere (esp. the cortex) and
corresponding deep white matter

● 💬 Lesion in any of these structures may cause disorders

wherein there is a decrease in consciousness.

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Medial Longitudinal Pathway (MLF)

● Controls CN III, IV, VI.
● Situated among the neurons of the reticulating activating system
(ARAS).
● Therefore, unresponsiveness due to brainstem damage, the
lesion affects ocular motility as well.

Figure 3. Structures involved in consciousness [Lecture PPT]

B. ASCENDING RETICULAR ACTIVATING SYSTEM (RAS)

● Composed of several neural circuits connecting the pons and

midbrain to the cerebral cortex.
o Via thalamus
o Via hypothalamus
● Complex polysynaptic fiber system that extends from the Figure 5. Medial Longitudinal Pathway and Bilateral Hemispheric
pons through the midbrain to the posterior portion of the Lesions [Lecture PPT]
hypothalamus and to the thalamic reticular formation.
Bilateral Cerebral Hemispheric Lesions
● Lesion may cause transient coma particularly when it involves
medial frontal lobes.

Posterior Hypothalamic Lesions

● Lesion in the diencephalon induce prolonged hypersomnia.
● Acute bilateral damage of the paraventricular thalamic nuclei is
attended by transient unresponsiveness.

V. IMPAIRED CONSCIOUSNESS: PATHOLOGY

Figure 4. Reticular Activating System [Lecture PPT]

● Not called the ARAS anymore, it is now called reticular

activating system (RAS) which consists of thalamus,
hypothalamus, and cerebral cortex.
● Ras lies in the paramedian tegmental region of the pons
and midbrain.
o Thalamus is the source of thalamocortical projections
that regulate and coordinate cortical activity.
● Neurotransmitters involved include dopamine,
norepinephrine, serotonin, histamine, acetylcholine, and Figure 6. Causes of Coma [Lecture PPT]
glutamate.
● Coma is produced by one or two broad groups of problems:
o STRUCTURAL, consisting either of
Thalamic Pathway
■ Discrete lesion in the upper brainstem and lower
● Consists primarily of cholinergic neurons in the pontine diencephalon.
tegmentum. ■ Widespread changes throughout the hemispheres.
o METABOLIC or SUBMICROSCOPIC, resulting in
suppression of neuronal activity.
Hypothalamic Pathway
● Composed of neurons that release monoamine neurotransmitters
(dopamine, norepinephrine, serotonin, histamine).

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A. PATHOLOGIC ANATOMY OF COMA

coma, and cessation of most
(STRUCTURAL CAUSES)
neuronal metabolic and
synaptic functions
1. Discernible mass lesions
2. Destructive lesions in the midbrain or thalamus Below 8 to 10 mL/min/100g Neurons cannot survive
3. Widespread bilateral damage to the cortex, cerebral white matter

VI. BRAIN HERNIATION SYNDROMES

HYPOXIA
A. CENTRAL HERNIATION SYNDROME
● Oxygen consumption: approximately 4 mg/min/100 g brain tissue
● Rostra-caudal deterioration of brainstem function. ● Oxygen consumption of 2 mg/min/100 g is incompatible with an
● Follows rostro-caudal sequence confusion, apathy, alert state
○ Low oxygenation = Hypoxia, causing a decrease in
drowsiness Cheyne-stokes respiration small pupils which sensorium

react sluggishly to light bilateral decerebration loss of caloric

ENDOGENOUS METABOLIC TOXINS
responses slow irregular breathing
● DKA
○ Acetone bodies (acetoacetic acid b-hydroxybutyric acid, and
B. UNICAL SYNDROME acetone)
● Herniation of the medial temporal lobe into the tentorial opening ● Uremia
● Preceded by a unilateral pupillary dilatation ○ Phenolic derivatives of the aromatic amino acids
● Hepatic coma
VII. METABOLIC MECHANISMS THAT DISTURB ○ Elevation of blood NH3
CONSCIOUSNESS ● Lactic acidosis
○ May affect the brain by lowering arterial blood pH to less than
● Reduction in blood flow 7.0
● Reduction in cerebral metabolism ● The impairment of consciousness in pulmonary insufficiency is
● Toxins related mainly to hypercapnia (an increase in CO2 or CO2
○ Endogenous toxins retention)
○ Hyponatremia ● Hyponatremia (NA <120 meq/L)
○ Direct effect on neuronal membranes in the cerebrum ○ Neuronal dysfunction is probably due to the intracellular
○ RAS movement of water, leading to neuronal swelling and loss
○ Neurotransmitters and their receptors and potassium chloride from the cells
● Sudden and excessive neuronal discharges (seizures)
● Concussion
DRUG INTOXICATION
METABOLIC MECHANISMS ● Drugs such as general anesthetics, alcohol, opiates, barbiturates,
● Hypoxia phenytoin, antidepressants, and benzodiazepines: act on
● Global Ischemia neuronal membranes in the cerebrum and reticular activating
● Hypoglycemia system or on neurotransmitters and their receptors
● Hyper - and Hypo – osmolar states
● Acidosis VIII. CLINICAL APPROACH TO PATIENT WITH
● Alkalosis DISTURBANCE IN CONSCIOUSNESS
● Hypokalemia
● Hyperammonemia
● Stabilize the patient
● Hypercalcemia
○ A –Airway
● Hypercarbia
○ B – Breathing
● Drug intoxication
○ C – Circulation
● Get a good history
GLOBAL ISCHEMIA ○ Ask comorbid illness i.e., DM
○ Review medications
CEREBRAL BLOOD FLOW (CBF) ○ Ask about trauma/ head injury
○ Ask about mental state, drug or alcohol use
● Make a thorough general physical examination
55 mL/min/100g Normal ○ Check the vital signs (BP, HR, RR, T)
○ Inspect the skin
○ Check the odor of the breath
25 mL/min/100g Slowing of EEG and syncope ● Do a thorough neurologic examination
or impaired consciousness ○ Level of consciousness, coma scale i.e., GCS, FOUR
○ Pupillary reaction
○ Movements of eyes and corneal responses
Below 12 to 15 mL/min/100g Electrocerebral silence, ○ Limb movements, posturing
○ Patterns of breathing

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● Decerebrate posturing
IX. NEUROLOGIC EXAMINATION OF A PATIENT WITH o Decerebrate posturing is worse than decorticate posturing.
DECREASED SENSORIUM Indicative of more severe brain damage at the rubrospinal
tract, red nucleus is involved indicating a lesion in lower
part
GLASCOW COMA SCALE (GCS)
o of the brainstem.
● Neurologists do not like to solely rely on the GCS. Disconnection of the cerebrum and the diencephalon from
● They are usually used for emergencies, especially if it’s a trauma the rest of the brainstem.
patient since it’s much faster to dictate the sensorium of the Lesion: below the midbrain.
patient in a scale. Seen in patient with pontine stroke.
● Eye opening o Manifestations:
○ 4 – spontaneous ▪ Extensions of upper extremities
○ 3 – to speech o Posture in Decerebrate Rigidity:
○ 2 – to pain ▪ Mouth – closed
○ 1 – no response ▪ Head – ext
● Verbal response ▪ Trunk – ext
○ 5 – oriented ▪ Arms – ext
○ 4 – confused ▪ Wrists – flex
○ 4 – inappropriate ▪ Fingers – flex
○ 2- incomprehensible ▪ Legs – ext
○ 1 – no response ▪ Feet – PF
● Motor response ▪ Toes–PF
○ 6 – obey/follows commands ▪ xProximal joints – ext
○ 5 – localizing pain ▪ Distal joints – flex
○ 4 – withdrawal from pain
▪ Forearms and legs – IR
○ 3 – flexion to pain
○ 2 – extension to pain
○ 1- no response

PUPILLARY REACTION
● Abnormalities of this reflex indicate structural lesions of the
midbrain or oculomotor nerve.

OCULOMOTOR RESPONSE
● Oculocephalic reflex (Doll’s eye reflex)
● Oculovestibular reflex (caloric reflex)
● Knowing these responses, you can be able to localize the
cause of disease in sensorium

EYE MOVEMENTS
● In comatose patients, absence of cortical control of eye
movements the comatose patient lacks voluntary saccades
including the quick phase of nystagmus and tracking eye
movements. Figure #. Posturing [Lecture PPT]
● If the brainstem is intact roving eye movements
● If the pontine reticular formation is intact (+) spontaneous
blinking PATTERNS OF BREATHING

● Apneustic breathing pattern is seen in patient with pontine

POSTURING lesion.
● Ataxic breathing pattern is associated with medullary lesion.
● Decorticate posturing ● Cheyne Stoke Breathing
o It is a severe brain damage. o Gradual increase then decrease, followed by apnea.
o Indicates may be a damage in areas including cerebral o Brain stem insult, increase ICP.
o hemisphere, internal capsule, thalamus, and in the
midbrain. o Lesion: above the red nucleus.
o Manifestations:
▪ Flexion of upper extremities and extension of lower
extremities.
▪ Arms are flex.
Figure #. Cheyne Stroke Breathing [Lecture PPT]

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X. MENTAL STATUS AND HIGHER CORTICAL

● Kussmaul’s Breathing FUNCTIONS
o Tachypnea and hyperpnea A. MENTAL STATUS EXAMINATION
o Metabolic acidosis and DKA
● Mental Status Examination
○ Relates to the mood and thoughts of a patient
■ Observe appearance and behaviour
● Are there signs of self-neglect? Does he appear
anxious? Depressed? Does his mood change rapidly
Figure #. Kussmaul’s Breathing [Lecture PPT] or is it appropriate?
■ Ask about the mood
● Abnormal breathing patterns may be due to: ■ Observe for the content of thought
o Compression at the level of the midbrain ■ Hallucinations and illusion
o Compression at the level of the midbrain-upper pons ○ Outline of Mental Status Examination (Refer to Appendix
o Compression at the level of the lower pons-upper medulla section)
■ For the content of thought it is important to differentiate
between illusions, hallucinations or delusions
Compression at the level of the Midbrain ● Illusions- misperception of real external stimulus, most
likely to occur when general level of sensory
● Eupneic breathing is called if there is a compression at the level stimulation is reduced.
of the midbrain. ● Hallucinations- False sensory perception experienced
without real external stimulus
● Delusions- Fixed false belief which cannot be
corrected by logic and are also not consistent with
culture and education of the patient.
Figure #. Eupneic [Lecture PPT] ● Sensorium
○ Consciousness
○ Attention span
Compression at the level of the Midbrain-Upper Pons ○ Orientation, for time, place, and person
○ Memory, recent and remote
○ Fund of information
○ Insight, judgement, and planning
○ Calculation

Figure #. Sustained Regular Hyperventilation [Lecture PPT] B. HIGHER CORTICAL FUNCTIONS

● Higher Cortical Functions

○ Term usually used to refer to the Gnosias
○ Gnosia
■ The faculty of perceiving and recognizing
○ Tests for certain cerebral functions
■ Assignable to certain cortical regions, i.e., motor and
sensory activities
■ The product of complex, diffusely distributed activity
Figure #. (Rarely) Cheyne-Strokes [Lecture PPT]
● To test for higher cortical functions, you have to divide according
to different lobes and deteremine what higher cortical function is
Compression at the level of the Pons-Upper Medulla affected
● It is eupneic, although often more shallow and rapid than
normal.

Figure #. Eupneic [Lecture PPT]

● Ataxic: Slow and irregular in rate and amplitude.

Figure #. Ataxic [Lecture PPT]

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FRONTAL LOBE ■ Abulia: diminished motivation

○ Disinhibition of behavior – hypersexuality, poor social
interactions, gambling, drug use
○ Distinctive abnormality of gait – frontal ataxia
■ Bruns apraxia: inability to initiate the process of
walking despite of the power and coordination of the
legs are normal when tested in sitting or lying position
■ Patient have broad base, short steps and tendency to
fall backwards

● NEUROLOGIC EXAMINATION TECHNIQUES

○ Observation during history taking
○ Cognitive evaluation
■ MMSE
■ Montreal Cognitive Assessment (MOCA)
■ Frontal assesment battery
Figure 7. Regions of the Frontal Lobe [Lecture PPT] ■ Primitive reflexes- “Frontal release signs” normally
present in newborn and infants but abnormal in adults,
● Contains the primary motor complex, premotor/supplementary i.e., snout reflex, grasp reflex, palmomental reflex,
glabellar reflex, sucking and rooting reflex.
motor complex, frontal eye field, prefrontal cortex.

TEMPORAL LOBE

Figure 8. Subdivisions of Prefrontal Cortex [Lecture PPT]

● Subdivisions of the prefrontal cortex:

○ Dorsolateral prefrontal cortex: involve cognitive processes Figure 9. Regions of the Temporal Lobe [Lecture PPT
such as planning, cognitive flexibility, and working memory;
area responsible for problem solving, how to direct and ● Responsible for hearing, language and also memory
maintain attention to the task ● CLINICAL EFFECTS OF TEMPORAL LOBE LESIONS
■ Lesion in this area may cause difficulty in attention, ○ Visual disorders
working memory, planning, and cognitive flexibility ■ Field cuts
○ Orbitofrontal prefrontal cortex: involve in decision-making; ■ Since the visual pathway going through the temporal lobe
closely connected to the limbic system so it is associated with ○ Cortical deafness
the ability to make decisions based on emotional information. ○ Auditory agnosias
Also responsible for social attachment and emotional ■ Agnosia for sounds
regulation. ■ Amusia
■ Lesions in this area may cause social disinhibition ○ Word deafness (auditory verbal agnosia) – the essential
○ Ventromedial prefrontal cortex element in Wernicke’s aphasia
○ Auditory illusions
● CLINICAL EFFECTS OF FRONTAL LOBE LESIONS ○ Auditory hallucinations
○ Motor abnormalities – motor cortex ○ Vestibular disturbance
○ Speech and language disorders – related to the dominant ○ Disturbances on time perception
hemisphere, broca’s area ○ Disturbances of smell and taste
○ Incontinence of bowel and bladder ○ Disorders of memory, emotion, and behavior
○ Impairment of attention, concentration, capacity for sustained
mental activity, ability to shift from one line of thought or ● NEUROLOGIC EXAMINATION TECHNIQUES
action to another
○ Confrontation Test
○ Akinesia, apathy, and abulia – utilization behavior
■ Akinesia: loss of ability to move a muscle ○ Halstead-Reitan-Wepman Screening Test
○ Aphasia Square

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■ To determine if it is at the frontal or temporal lobe

■ To determine what type of aphasia.
OCCIPITAL LOBE
PARIETAL LOBE

Figure 10. Parietal Lobe [Lecture PPT

Figure 11. Occipital Lobe [Lecture PPT]
● Responsible for sensory ● Mainly for vision
● CLINICAL EFFECTS OF PARIETAL LOBE LESIONS
● CLNICAL EFFECTS OF OCCIPITAL LOBE LESIONS
○ Cortical sensory syndromes
○ Visual field defects
■ Position sense
■ Astereognosis ○ Cortical blindness
■ Agraphesthesia (Agraphognosia) ○ Visual anosognosia
■ Two-point discrimination ○ Visual illusions and hallucinations
■ Detection of direction of movement of a tactile stimulus ○ Visual agnosias
■ Tactile inattention or extinction ■ Visual object agnosia
○ Asomatognosias ■ Simultanagnosia / simultagnosia
■ Anosognosia (hemispatial neglect) ■ Prosopagnosia
● Lack of awareness of any bodily deficits ■ Color agnosia
● Right parietal lesion
■ Gerstmann Syndrome- bilateral asomatognosia; consists ● NEUROLOGIC EXAMINATION TECHNIQUES
of finger agnosia, right-left confusion, dyscalculia, ○ Visual agnosia – differentiate from anomia
dysgraphia
○ Prosopagnosia – show familiar, popular faces
○ Ideomotor and Ideational Apraxia – Loss of the ability to
○ Simultanagnosia – bilateral visual stimuli
perform learned motor skills
■ Buccofacial Apraxia
■ Ideomotor- Inability to imitate hand gestures
■ Ideational apraxia - loss of ability to conceptualize, plan, REFERENCES
and execute complex sequence and actions

● NEUROLOGIC EXAMINATION TECHNIQUES

○ Tactile inattention or extinction
○ Hemineglect – line bisection test; clock-drawing test
○ Finger agnosia- You have to make the patient identify its
fingers
○ Right-left confusion
○ Dysgraphia
○ Dyscalculia
○ Test for apraxia – may be done by giving various commands
○ Dressing apraxia
○ Tests for constructional apraxia

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 NEUROSCIENCE 5.5

Disorders of Consciousness & Higher

Cortical Function
DR. DONABELLE M. CHU MD. May 6, 2024 LE 1
FPNA

APPENDIX

Outline of Mental Status Examination

I. General o Is the patient normal, hyperactive, agitated, quiet, immobile?

behavior and o Is the patient neat or slovenly?
appearance o Do the clothes match the patient’s age, peers, sex, and background?

II. Stream of talk o Does the patient converse normally?

o Is the speech rapid, incessant, under great pressure, or is it slow and lacking in spontaneity and prosody?
o Is the patient discursive, tangential, and unable to reach the conversational goal?

III. Mood and o Is the patient euphoric, agitated, giggling, silent, weeping, or angry?
affective o Is the mood appropriate?
responses o Is the patient emotionally labile?

IV. Content of o Does the patient have illusions, hallucinations or delusions, and misinterpretations?
thought o Does the patient suffer delusions of persecution and surveillance by malicious persons or forces?
o Is the patient preoccupied with bodily complaints, fears of cancer or heart disease, or other phobias?

V. Intellectual o Is the patient bright average, dull, or obviously demented or mentally retarded?
capacity

VI. Sensorium A. Consciousness

B. Attention span
C. Orientation for time, place, and person
D. Memory, recent and remote
E. Fund of information
F. Insight, judgement, and planning
G. Calculation

Appendix 1.

NEURO | DISORDERS OF CONSCIOUSNESS & HIGHER CORTICAL FUNCTION | Oconer, Pantoja, Trinchera, Villaseñor, Sapao (TH) 9 of 9
Villarico (TP)