Mental status
Kamal Shemisa PGY3
Internal Medicine
UHCMC
Objectives
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Definitions
Neurological Examination
Clinical Presentation
Diagnostic Evaluation
Encephalopathy vs. Structural Lesions
Case Vignette’s
Conclusions
Clinical Vignette
 65 yo male HF hospitalized overnight
for “volume overload” with plans to
diurese.
 You are called because he’s
unresponsive and difficult to arouse.
 You patiently ask the nurse to obtain
a set of vital signs and tell him that
you will be there to assess the
patient.
Clinical Vignette
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The read the note from last
night and its somewhat
helpful…
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Pmhx- Heart failure, HTN,
DM2, atrial fibrillation,
Hypothyroidism, OSA,
remote hx of prostate
cancer.
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The Hx obtained from the
family last evening was that
he was developing
progressive dyspnea,
abdominal distention,
decreased appetite and
lethargy the past few days.
He also was urinating
infrequently.
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Vital Signs:
 37.9
 HR-115 (atrial fib)
 BP 95/60
 RR-24 irregular
 Pulse ox on NRB was
94%
 UO 50 ml in the past 4
hours
Neuro: eyes are closed,
mumbling
incomprehensibly, he
doesn’t follow commands,
he grimaces when you
check his pupils (pinpoint
but reactive). He grimaces
/withdraws sluggishly to
stimulation.
Exam
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Neuro: unchanged; you verify the findings
HEENT: The face appears symmetric, the pupils are small
but reactive, mucous membranes are dry, conjunctivae are
pale, pharynx is unremarkable
Neck: obese, JVP is elevated, accessory muscle use is
noted, negative nuchal rigidity
Cardio: tachycardic and irregular, -mgr
Lungs: Tachypneic taking shallow breaths; BS are heard
bilaterally, crackles and rhonchi are heard over the right
anterior chest wall
Abdomen: is large; BS are present but diminished, the
abdomen and flanks are soft and non-tender, the liver is
large; there is presacral edema; there are no bruits or
pulsatile masses.
Extremities are tepid to touch; there +4 edema in the lower
extremities, with a tender erythematous region over the
dorsum of the foot.
What do you do next?
Answer the following questions
 Is the cause of the patients alteration in
mental status a reversible one i.e.
metabolic etiology?
 Or is there a structural etiology or primary
brain disorder, responsible for the patient’s
AMS
 i.e. stroke, meningitis, mass lesion, or
hydrocephalus?
Differential Diagnosis?
What laboratory should be obtained?
What Imaging is appropriate?
Acutely Altered States of
Consciousness
Clouding of consciousness
 Minimally reduced wakefulness or
awareness
 Hyper-excitability and irritability
(alternating with drowsiness).
 Drowsiness predominates the day and
agitation at night
Terminology
 Delerium: charac. Misperception of sensory stimul,
vivid hallucinations
 Obtundation: Mild to moderate reduction in alertness,
lesser interest in the environment.
 Stupor: (to be stunned), deep sleep unresponsiveness
requiring vigorous stimulation to arouse.
 Coma: deep sleep, a state of unresponsiveness and
cannot be aroused.
Disorders of Consciousness
 Acute
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Clouding
Delirium
Obtundation
Stupor
Coma
Locked in
 Chronic
 Dementia
 Hypersomnia
 Abulic
 Loss or impairment
of the ability to
make
decisions or act
independently.
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Akinetic mutism
Minimal Consciousness
Vegetative
Brain death
Answer
COMA!
Physiology behind the Arousal
 Ascending Arousal System
 Projections from the mesopontine tegmentum to
the forebrain
 Pedunculopontine and laterodorsal tegmental
to the paramedian midbrain reticular formation to
nuclei in the thalamus (later to the cortex)
Physiology
1) tonic variations are seen via EEG monitoring;
ex. in REM PP and LDT are firing fastest
2) Varied responses are due to cholinergic,
monoamine, and GABA receptors
Physiological State
 In physiological states the Central Nervous
System relies on sufficient
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Cerebral blood flow
Oxygenation
Glucose
Electrolyte and Osmotic homeostasis
Pharmacokinetics
Sterile environment
CSF hydrodynamics and pressure balances in a
closed container.
History
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From relatives, friends, attendants
Onset
Recent complaints of headache
Recent injury
Prior medical illness
Psychiatric history
Access to drugs
General exam
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Vitals
Evidence of trauma
Acute or chronic systemic illness
Drug ingestion?
Nuchal rigidity
General Exam
 Signs of head trauma; otorrhea,
hemotympanum, raccoon eyes, battle sign
 Nuchal rigidity or Brudzinski’s
 Papilladema?
 Skin exam: assess for rash, petechia,
needle marks, jaundice, bullae
 Cardiac exam: murmurs, bruits
The neurologic exam
Assess the level of consciousness
Hemodynamics
The pattern of breathing
The size and reactivity of the pupils
The eye movements and
oculovestibular responses
 The skeletal motor responses
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Coma Scales
 Glasgow coma scale: 13 mild, 9-12 moderate, <8 severe.
 AVPU: alert ?, voice?, pain?, UR?
 ACDU: Alert?, confused?, drowsy?, UR?
Exam
 Methods to elicit response
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Supra-orbital ridge
Nail beds
Sternum
TM joints
Taken from Plum and Posner
What does it mean?
 The level of response is important to the
initial consideration of the depth of
impairment of consciousness.
 Patients responding to voice or light
shaking are lethargic or obtunded
 Patient whose best response to deep pain is
to push the examiner’s arm away is
considered to be stuporous with
localizing responses.
Cerebral Circulation
 Is the brain receiving adequate blood flow
 CPP=MAP-ICP
 Cerebral autoregulation regulates perfusion to
the brain over a wide range of blood pressures.
 CPP is regulated by head position, MAP aug.,
CSF drainage, CO2 regulation
Circulation
 Neurogenic Shock: Damage to the descending
sympathetics pathway that support blood pressure
may result in a fall in blood pressure.
 Stokes-Adams attacks: periods of brief loss of
consciousness due to lack of adequate cerebral
perfusion. (baroreceptor dysfunction)
 Cushings reflex: Lesions that result in stimulation of
the sympatho-excitatory system may cause an
increase in blood pressure (ischemia, delerium
[amygdala-thalamus]).
Circulation
 The brain tightly
controls circulation.
 Non-neurologic causes:
 The brain acts
through the
Autonomic nervous
system to adjust
systemic arterial
pressure
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vasodilators
Hypovolumia
pump failure
Sepsis
autonomic neuropathy
Respirations
 Breathing is a sensorimotor act
 Respiratory Rhythm is an intrinsic
property of the brainstem (ventrolateral medulla).
 Vagus, GP nerves: respond to stretch
and chemoreceptors- (influence RR and
TV)
 Forebrain can alter respiratons by
emotional centers.
Respirations
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Cheyne-stokes- alt.
hyperpnea with apnea
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Hyperventilation
(Kussmaul’s): sepsis,
hepatic coma, metabolic
acidosis, [SAH, gliomas
(localized acidosis)]
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Apneustic: end resp.
pauses of 2-3 sec; Pontine
infarct, TT herniation
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Ataxic: irregular gasping
bilateral medullary lesions
Cheyne-Stokes
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The Brain Stem is intact
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Hyperpnea phase lasts longer than apnea
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When Medullary sensors sense oxygen and increases in
carbon dioxide tension reduce the rate and TV
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Alveolar carbon dioxide reaches even higher levels
ramping up of respiration as the brain sees rising carbon
dioxide
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By the time the brain begins to see a fall in CO2 the levels
in the alveoli are too low.
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Low level of carbon dioxide reaches the brain,
respirations slow or even cease.
continued
 Understand the feed back loop
between alveolar ventilation and
brain chemoreceptors are influenced
by:
 Circulatory delays (heart failure)
 Bilateral forebrain impairment: i.e.
diffuse metabolic process such as
uremia, hepatic failure, or bilateral
damage Diencephalic displacement.
Pupils
 Abnormalities of pupillary responses
are of great localizing value.
 Single most important physical sign in
differentiating metabolic from
structural coma.
Pupils
 Most pupillary responses are brisk but
some slow: illuminate the eye for 10
seconds.
 Consensual responses are normal
 Paradoxical dilation: (APD): lesion
of the optic nerve or retina.
Pupils
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Small Reactive: Metabolic encephalopathy, Diencephalic
Injuries
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Unilateral dilated and UR: Pcom An, temporal lobe herniation.
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Unilateral Small: Horner’s i.e sympathetic lesionCavernous
sinus, ICA lesion, stellate ganglion.
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Midposition fixed: Midbrain; fixed mid or dilated (symp.
Preserved).
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Pontine tegmental injury results in pinpoint pupils.
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Lateral Medullary tegmentum: cause ipsilateral central Horner’s
syndrome.
Pupils
 Assess the level simultaneously with
respirations…
continued
Taken from Adult Neurology: Jody Bloom
Oculomotor response
Assesses brainstem function:
 Blepharospasm- strong resistance to eyelid
opening is voluntary; not truly in coma.
(frontal lobes intact)
 Spontaneous blinking lost in coma. However
can be present in PVS
 Corneal reflex: elicited with cotton wisp or sterile
saline eye drops: closure of the eyelids and elevation
of the eyes suggest preservation of the brainstem
spinal V nucleus and facial nuclei.
Oculomotor Responses
 Eye movements are smooth and conjugate.
 Vestibulo-ocular responses: nl responses
generated is for eyes to rotate counter to
the direction of the examiner’s movement.
i.e. Doll’s Eyes.
 Nl responses in both horizontal and vertical
suggest intact brainstem function.
Vestibulo-ocular responses
 Unusual to have normal VOR in
structural causes of coma.
 Exaggerated responses to OC stim.
do occur particularly due to hepatic
failure.
Vestibulocular Reflex
 When do we do caloric testing???
 Patients who are deeply comatose may
respond sluggishly or not at all to OC
stim.
 50 ml syringe with plastic IV catheter is
gently advanced until it is near the TM.
Infuse at a rate 10 ml/minute until the
response is obtained.
CWC
 Video
 http://www.youtube.com/watch?v=H4iQ
kFUgG6k
VOR and CWC
 Metabolic encephalopathy- VOR is nl
 Right lateral pontine lesion-conjugate gaze
paralysis on right and nl. VOC on left.
 MLF lesion or bilateral INO- absent conjugate gaze
with single eye deviation on VOCR side elicited
 Paramedian pontine lesion- 11/2 syndrome
 Midbrain lesion-bilateral paralysis
Continued
 Roving eye movements (ping-pong
gaze): metabolic encephalopathy.
 Nystagmus: abnormal if irregular
jerks present, convergence
nystagmus.
 Typically seen dorsal midbrain lesions
Motor Responses
Assess tone:
 Spastic rigidity: spastic catchParkinsons
 Quick passive movement triggers rigidity
 Paratonic rigidity: metabolic
encephalopathy
 Increases with intensity of passive movement,
as if the patient willfully resists the examiner.
Motor responses
 Muscle stretch reflexes- may be increased who are
drowsy or confused.
 Cutaneous reflexes: cremasteric/abdominal reflexes
 Prefrontal cutaneous reflexes: “frontal release reflexes”
or primitive reflexes also emerge in drowsy patients
with.
 Rooting
 Snout
Also seen elderly with severe
 Glabellar
cognitive impairment.
 Palmomental
 Grasp (specific to bilateral frontal impairment)
Motor response
 Appropriate responses are ones that
attempt to escape the stimulus:
withdrawing.
 Likewise facial grimacing, increasing blood
pressure, pupillary dilation, movement of
the contralateral side.
 Inappropriate responses: posturing
Motor Responses
Taken from Adult Neurology: Jody Bloom
Diagnostic testing
 Evaluate metabolic etiologies
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Glucose
Electrolytes
Hepatic function panel
Toxin/drug screens
Arterial blood gas
urinalysis
Metabolic Abnormalities
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Hypo/hyper glycemia
Acid/base derangements
Hypo/hypercapnia
Hpoxia
Liver disease
(hyperammonia)
Renal Disease (uremia)
Pancreatic Encephalopathy
Endocrinopathy
Toxins: Sedatives,
opiates, ethanol
intoxication
Electrolyte
Hypo/hyperthermia
Nutritional: Wernicke’s
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Drug withdrawal
Delerium Tremens
ICU/post-operative
delerium
Infection: acute or chronic
meningitis, encephalitis,
HIV encephalopathy
Granulomatous disease
SLE, Behcet’s , CADASIL
Epilepsy
Leukodystrophy and
demyelinating conditions
MS
Marchiafava-Bignami
CJD and prion disease
Gliomatosis Cerebri
Clinical Vignette

The read the note from last
night and its somewhat
helpful…

Pmhx- Heart failure, HTN,
DM2, atrial fibrillation,
Hypothyroidism, OSA,
remote hx of prostate
cancer.

The Hx obtained from the
family last evening was that
he was developing
progressive dyspnea,
abdominal distention,
decreased appetite and
lethargy the past few days.
He also was urinating
infrequently.

Vital Signs:
 37.9
 HR-115 (atrial fib)
 BP 95/60
 RR-24 irregular
 Pulse ox on NRB was
94%
 UO 50 ml in the past 4
hours
Neuro: eyes are closed,
mumbling incomprehensibly,
he doesn’t follow commands,
he grimaces when you check
his pupils (pinpoint but
reactive). He grimaces
/withdraws sluggishly to
stimulation.
Work up
 7.47/36/65
 131/5.2/94/22/35/2.2
 Glucose-180
 Lactate-4.5
 Wbc-12.2
 Troponin-1.5
 ECG: shows Afib with
RVR with low voltages
diffusely without ST-T
wave changes, nl axis
and QRS interval.
 CXR- bilateral diffuse
parenchymal opacities
Decision
You Decide to intubate and transfer
to MICU!
Mechanisms of Structural coma
 Structural coma occurs with injury to
sarousal pathways through the brain.
 Supratentorial lesions: compress the
diencephalon.
 Infratentorial lesions: compress the
arousal structures
Neurological Imaging
CT- applied to anyone who does not a have an
immediately obvious source of coma.
 Obvious hemorrhages, fractures, remote
cerebral infarction and hydrocephalus can be
detected.
 Disadvantage is detecting acute infarction as
well as delaying care of a patient with impending
transtentorial herniation (blown pupil, gaze
palsy).
MRI
 MRI: time consuming, but is often necessary.
 DWI/ADC are the studies of choice for acute stroke
here.
 TI/T2/Flair in conjunction are suitable to detect acute
hemorrhage.
 MRA can reveal most stenoses, aneurysms or
occlusions.
 Use Gadolinium if you suspect metastatic disease or
abscess
Herniation Syndromes
1. Uncal
2. Central
3. Subfalcine/cingulate
4. Transcalvarial
5. Upward
6. Tonsillar
Herniation
 Usually results from imbalances of
pressure between different
compartments leading to tissue
herniation.
Case Vignette 2
 You are on Carpenter Team and are
assigned a 35 yo patient with HIV.
He has been complaining of
headache, nausea and vomitting, and
blurred vision. His CD4 count is 50.
What do you want to do next?
Ring Enhancing Lesions
Bacterial Abscess
Metastatic Disease: Adenocarcinoma
Primary CNS lymphoma
Primary CNS Neoplasm: Glioma
Post-radiation changes
HIV associated lesions: PML,
CryptococcosToxoplasmosis, Tuberculoma,
lymphoma
 Post-operative changes
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Case Vignette 3
 You are on Eckel team and your
patient overnight became acute
unresponsive. His eyes are closed,
pupils are pinpoint, downward gaze,
and his breathing is irregular. You
examine and you note decerebrate
posturing.
Where is the lesion?
Clinical Vignette 4
 You admit a patient on Weisman, she is a
58 yo female with recently diagnosed
breast cancer undergoing her final cycle of
high dose AC/herceptin chemo. She has
felt increasingly unsteady, complains of
blurred vision, lower extremity weakness.
On exam she has papilladema, 4/5 strength
in the legs, brisk patellar reflexes and
bilateral babinski’s
Differential Diagnosis?
Clinical vignette 5
You are the resident on Wearn team and
have admitted a 58 yo alcoholic male
patient presents to you from the ED
dehydrated in ARF after police find him in
alley way naked and disheveled.
You notice however that his face is “well kept”
on one side and the other half of his face is
unshaven.
When you ask him to stand up and walk he
falls to his left side.
Recap
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Definitions
Neurological Examination
Clinical Presentation
Diagnostic Evaluation
Encephalopathy vs. Structural Lesions
Case Vignette’s
Conclusions