Mental status

1
Mental status

• Kamal Shemisa PGY3
• Internal Medicine
• UHCMC

2
Objectives

• Definitions
• Neurological Examination
• Clinical Presentation
• Diagnostic Evaluation
• Encephalopathy vs. Structural Lesions
• Case Vignettes
• Conclusions

3
Clinical Vignette

• 65 yo male HF hospitalized overnight for volume
  overload with plans to diurese.
• You are called because hes 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.

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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 doesnt follow commands, he
  grimaces when you check his pupils (pinpoint but
  reactive). He grimaces /withdraws sluggishly to
  stimulation.

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Exam

• 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.

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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 patients AMS
  
• i.e. stroke, meningitis, mass lesion, or
  hydrocephalus?

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Differential Diagnosis?
9

• What laboratory should be obtained?

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• What Imaging is appropriate?

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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

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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.

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Disorders of Consciousness

• Acute
• Clouding
• Delirium
• Obtundation
• Stupor
• Coma
• Locked in

• Chronic
• Dementia
• Hypersomnia
• Abulic
• Loss or impairment of the ability to make
  decisions or act independently.
• Akinetic mutism
• Minimal Consciousness
• Vegetative
• Brain death

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Answer

• COMA!

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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

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Physiological State

• In physiological states the Central Nervous
  System relies on sufficient
• Cerebral blood flow
• Oxygenation
• Glucose
• Electrolyte and Osmotic homeostasis
• Pharmacokinetics
• Sterile environment
• CSF hydrodynamics and pressure balances in a
  closed container.

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History

• From relatives, friends, attendants
• Onset
• Recent complaints of headache
• Recent injury
• Prior medical illness
• Psychiatric history
• Access to drugs

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General exam

• Vitals
• Evidence of trauma
• Acute or chronic systemic illness
• Drug ingestion?
• Nuchal rigidity

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General Exam

• Signs of head trauma otorrhea, hemotympanum,
  raccoon eyes, battle sign
• Nuchal rigidity or Brudzinskis
• Papilladema?
• Skin exam assess for rash, petechia, needle
  marks, jaundice, bullae
• Cardiac exam murmurs, bruits

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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, lt8
  severe.
• AVPU alert ?, voice?, pain?, UR?
• ACDU Alert?, confused?, drowsy?, UR?

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Exam

• Methods to elicit response
• Supra-orbital ridge
• Nail beds
• Sternum
• TM joints

Taken from Plum and Posner
24
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 examiners arm away is considered to be
  stuporous with localizing responses.

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Cerebral Circulation

• Is the brain receiving adequate blood flow
• CPPMAP-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

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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).

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Circulation

• The brain tightly controls circulation.
• The brain acts through the Autonomic nervous
  system to adjust systemic arterial pressure

• Non-neurologic causes
• vasodilators
• Hypovolumia
• pump failure
• Sepsis
• autonomic neuropathy

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Respirations

• Breathing is a sensorimotor act
• Respiratory Rhythm is an intrinsic property of
  the brainstem (ventro-lateral medulla).
• Vagus, GP nerves respond to stretch and
  chemoreceptors- (influence RR and TV)
• Forebrain can alter respiratons by emotional
  centers.

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Respirations

• Cheyne-stokes- alt. hyperpnea with apnea
• Hyperventilation (Kussmauls) sepsis, hepatic
  coma, metabolic acidosis, SAH, gliomas
  (localized acidosis)
• Apneustic end resp. pauses of 2-3 sec Pontine
  infarct, TT herniation
• Ataxic irregular gasping bilateral medullary
  lesions

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Cheyne-Stokes

• The Brain Stem is intact
• Hyperpnea phase lasts longer than apnea
• When Medullary sensors sense oxygen and increases
  in carbon dioxide tension? reduce the rate and TV
• Alveolar carbon dioxide reaches even higher
  levels? ramping up of respiration as the brain
  sees rising carbon dioxide
• By the time the brain begins to see a fall in CO2
  the levels in the alveoli are too low.
• Low level of carbon dioxide reaches the brain,
  respirations slow or even cease.

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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.

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Pupils

• Abnormalities of pupillary responses are of great
  localizing value.
• Single most important physical sign in
  differentiating metabolic from structural coma.

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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.

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Pupils

• Small Reactive Metabolic encephalopathy,
  Diencephalic Injuries
• Unilateral dilated and UR Pcom An, temporal lobe
  herniation.
• Unilateral Small Horners i.e sympathetic
  lesion?Cavernous sinus, ICA lesion, stellate
  ganglion.
• Midposition fixed Midbrain fixed mid or dilated
  (symp. Preserved).
• Pontine tegmental injury results in pinpoint
  pupils.
• Lateral Medullary tegmentum cause ipsilateral
  central Horners syndrome.

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Pupils

• Assess the level simultaneously with respirations

36
continued
Taken from Adult Neurology Jody Bloom
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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.

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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 examiners movement. i.e.
  Dolls Eyes.
• Nl responses in both horizontal and vertical
  suggest intact brainstem function.

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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.

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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.
  

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CWC

• Video
• http//www.youtube.com/watch?vH4iQkFUgG6k

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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

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Continued

• Roving eye movements (ping-pong gaze) metabolic
  encephalopathy.
• Nystagmus abnormal if irregular jerks present,
  convergence nystagmus.
• Typically seen dorsal midbrain lesions

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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.

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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
• Glabellar
• Palmomental
• Grasp (specific to bilateral frontal impairment)

Also seen elderly with severe cognitive
impairment.
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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

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Motor Responses
Taken from Adult Neurology Jody Bloom
48
Diagnostic testing

• Evaluate metabolic etiologies
• Glucose
• Electrolytes
• Hepatic function panel
• Toxin/drug screens
• Arterial blood gas
• urinalysis

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Metabolic Abnormalities

• 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 Wernickes

• Drug withdrawal
• Delerium Tremens
• ICU/post-operative delerium
• Infection acute or chronic meningitis,
  encephalitis, HIV encephalopathy
• Granulomatous disease
• SLE, Behcets , CADASIL
• Epilepsy
• Leukodystrophy and demyelinating conditions MS
• Marchiafava-Bignami
• CJD and prion disease
• Gliomatosis Cerebri

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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 doesnt follow commands, he
  grimaces when you check his pupils (pinpoint but
  reactive). He grimaces /withdraws sluggishly to
  stimulation.

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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

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Decision

• You Decide to intubate and transfer to MICU!

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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

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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).

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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

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Herniation Syndromes

1. Uncal
2. Central
3. Subfalcine/cingulate
4. Transcalvarial
5. Upward
6. Tonsillar

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Herniation

• Usually results from imbalances of pressure
  between different compartments leading to tissue
  herniation.

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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?

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Ring Enhancing Lesions

• Bacterial Abscess
• Metastatic Disease Adenocarcinoma
• Primary CNS lymphoma
• Primary CNS Neoplasm Glioma
• Post-radiation changes
• HIV associated lesions PML, CryptococcosToxoplasm
  osis, 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?

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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 babinskis
• Differential Diagnosis?

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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.

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Recap

• Definitions
• Neurological Examination
• Clinical Presentation
• Diagnostic Evaluation
• Encephalopathy vs. Structural Lesions
• Case Vignettes
• Conclusions