Mental status

Kamal Shemisa PGY3Internal Medicine UHCMC

Objectives

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.

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

hoursNeuro: 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.

Clinical Vignette

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.

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

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

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)

Physiology1) 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

Cerebral blood flow Oxygenation Glucose Electrolyte and Osmotic homeostasis Pharmacokinetics Sterile environment CSF hydrodynamics and pressure balances in a

closed container.

History

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

General exam

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

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 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.

The brain acts through the Autonomic nervous system to adjust systemic arterial pressure

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

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.

Respirations Cheyne-stokes- alt.

hyperpnea with apnea

Hyperventilation (Kussmaul’s): 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

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.

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 Small Reactive: Metabolic encephalopathy, Diencephalic

Injuries

Unilateral dilated and UR: Pcom An, temporal lobe herniation.

Unilateral Small: Horner’s i.e sympathetic lesionCavernous 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 Horner’s syndrome.

Pupils

Assess the level simultaneously with respirations…

continued

Taken from Adult Neurology: Jody Bloom

Oculomotor responseAssesses 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=H4iQkFUgG6k

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 catchParkinsons

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 Glabellar Palmomental Grasp (specific to bilateral frontal impairment)

Also seen elderly with severe cognitive 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 Glucose Electrolytes Hepatic function panel Toxin/drug screens Arterial blood gas urinalysis

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: Wernicke’s

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 MSMarchiafava-Bignami

CJD and prion disease Gliomatosis Cerebri

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.

Clinical Vignette

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. Uncal2. Central3. Subfalcine/cingulate

4. Transcalvarial5. Upward6. 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

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 5You 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

Definitions Neurological Examination Clinical Presentation Diagnostic Evaluation Encephalopathy vs. Structural Lesions Case Vignette’s Conclusions