2017-2018 Columbia Neurology Residency Teach Block

Approach to “Altered Mental Status”

I. Definition:

-Consciousness: a state of full awareness of the self and one’s relationship to the environment. Consciousness consists of two components.

  • Content- impairment in specific cognitive domains can be caused by focal lesions (i.e. aphasia, neglect)
  • Level of arousal- can be caused by widespread cortical impairment or injury to the brainstem/specific dicencephalic pathways

**Note: The chief complaint of “altered mental status” most often refers to impairment in the level of arousal and/or attention, but a specific impairment such as aphasia that could be confounding the exam should be evaluated

II. Pathophysiology of Decreased Level of Arousal

  1. Structural Causes
  2. Supratentorial damage ormass lesions that may compress deep diencephalic structures and impair both hemispheric functions
  3. Diffuse bilateral hemispheric damage (i.e. hypoxic ischemic encephalopathy)
  4. Diencephalic injury (i.e. tumor destroying thebilateral thalami or hypothalamus)
  5. Infratentorial mass or destructive lesion, which damage the ascending arousal system at its origin in the high-brainstem
  6. High-pontine and lower midbrain paramedian tegmental injury (i.e. basilar artery occlusion)
  7. Pontine hemorrhage

**Note: Lesions below the level of the mid-pons do not impair consciousness but can lead to locked in syndrome

  1. Diffuse Metabolic Causes (i. e. sepsis, CHF exacerbation, hepatic encephalopathy, toxic ingestion, hyponatremia, etc)

III. Examination of the Comatose Patient

  1. Determine Level of Consciousness
  2. Address the patient verbally > If no response speak more loudly or shake the patient > If still no response give deep noxious stimuli
  3. Examples of noxious stimuli: nail bed pressure, supraorbital ridge pressure, sternal rub, and TMJ joints pressure
  1. Vitals Check
  2. Airway protection
  3. Pattern of breathing
  4. Intrinsic respiratory rhythm is generated in the ventrolateral medulla (integrates information from chemoreceptors, pulmonary stretch, emotional input from the cortex)
  5. Cheynes-Stokes breathing (indicates bilateral forebrain/diencephalic damage with intact brainstem reflexes)
  6. Hyperventilation (secondary to metabolic acidosis or high brainstem injury affecting the parabrachial nucleus causing central hyperventilation)
  7. Apneustic Breathing is a respiratory pause at each full inspiration (most commonly caused by pontine infarctions)
  8. Ataxic breathing (damage at the level of the respiratory rhythm generator at the upper medulla)
  9. Circulation (BP)
  10. Should ensure adequate blood pressure/mean arterial pressure for cerebral profusion
  11. CNS injury can cause decrease in sympathetic tone and also cause hypotension
  1. Size and Reactivity of the Pupils- pupillary pathway is highly resistant to metabolic insult and can differentiate between a metabolic coma from a structural coma
  2. Pupil dilation- pupillodilator muscles innerved by sympathetic ganglion cells in the superior cervical ganglion
  3. Pupil constriction- pupilloconstrictor muscles are innervated by the parasympathetic neurons in the ciliary ganglion (origin is the EW nucleus)
  4. Horner’s syndrome vs. Raeder’s Paratrigeminal Syndrome with only miosis and ptosis (localizes lesion along the sympathetic pathway)
  5. Midbrain pupils- Dilated (if unilateral with fixed dilation think either compressive aneurysm on CN III or uncal herniation)
  6. Pontine pupils- severely constricted
  1. Eye Movement and Oculovestibular Response- asymmetric oculomotor function identifies a patient with a structural rather than metabolic cause of coma
  2. Open eyelids
  3. Eyelids of a comatose patient will fall smoothly and gradually
  4. Forced eye closure may be seen in confused patients who are not comatose, or patients with eyelid apraxia (non-dominant parietal lesions)
  5. Test for corneal response which requires intact CN V1 and CN VII (if CN VII is weak, may only see a Bell’s phenomenon)
  6. Examine for spontaneous eye movements and resting position
  7. Slow roving eye movements typical of metabolic encephalopathy
  8. Gaze preference (towards the side of the frontal eyefield lesion)
  9. Nonconjugate (baseline strabismus, cranial nerve issue)
  10. Skew (medulla or lower pons lesion)
  11. Ocular bobbing (diffuse brainstem injury)
  12. Vestibulo-ocular responses- brisk head movements in lateral direction and hold head for a few seconds in the lateral position
  13. Awake patients can suppress the VOR
  14. Comatose patient with intact brainstem reflexes will have eyes move to midline
  15. If no response perform cold caloricsto confirm
  16. Cold water in unilateral ear- eyes move toward the irrigated side
  17. Cold water in both ears- eyes look down
  18. Warm water in both ears- eyes look up
  1. Skeletal motor responses
  2. Tone (spastic vs. rigidity vs. paratonia)
  3. Reflexes (including frontal release reflexes)
  4. Response
  5. Appropriate response is withdraw away from stimulus
  6. Triple Flexion (spinal cord or brainstem injury)
  7. Posturing
  8. Damage above the rostral midbrain: Flexor Posturing of the upper extremities and extension of the lower extremities
  9. Damage below the rostral midbrain: Extensor posturing of both upper and lower extremities (more ominous)

IV. Major Diagnostic Tests (combination depends on clinical picture, can give example cases here)

  1. Blood and urine testing
  2. NCHCT
  3. MRI
  4. LP
  5. EEG

Further Neuroanatomy that can be reviewed during the lecture:

Sympathetic pathway:

-First Order Neuron: Hypothalamus > Lateral brainstem > synapse at the nucleus of budge (C8-T2)

-Second Order Neuron: Sympathetic Chain > Superior Cervical Sympathetic Ganglion

-Third Order Neuron: Branch that controls sweating goes along the EC; branch that controls pupillary dilation and eyelid elevation goes along the IC > V1 > cavernous sinus > superior orbital fissure

CN III pathway:

-Emerges from between the cerebral peduncles > travels between the SCA and PCA > travels parallel to the Pcomm > cavernous sinus > superior orbital fissure

  • Superior Branch: Superior Rectus and LevatorPalpbrae
  • Inferior Branch: Medial Rectus, Inferior Rectus, Inferior oblique

CN IV pathway:

-Nerve cross before exiting on the dorsal side of the brainstem > wrap around the brainstem > cavernous sinus > superior orbital fissure

CN VI pathway (subject to compression with elevated ICP)

-Emerges on the ventral side of the pons > cavernous sinus > superior orbital fissure

Horizontal Gaze Pathway:

-Frontal eye field > contralateral PPRF > ipsilatal CN VI nucleus and via MLF to contralateral CN III

Reference:

Lecture is adapted from Chapters 1 and 2 of Plum and Posner’s Diagnosis of Stupor and Coma: Fourth Edition by Jerome B. Posner, Clifford b .Saper, Nicholas D. Schiff, Fred Plum. Copyright 2007.