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Neuro 2 > Stupor & Coma > Flashcards

Stupor & Coma Flashcards

1
Q

Lethargy

A

sleepy but easily aroused

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2
Q

Hypersomnia

A

-excessively sleepy but normal cognition when awakened

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3
Q

Obtundation

A

mental blunting, dec. alertness

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4
Q

Stupor

A

eyes open only briefly after vigorous stimulation before returning to deep sleep
-cognition impaired

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5
Q

Coma

A

eyes remain closed after vigorous stimulation

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6
Q

Delirium

A
  • disoriented, misperception of sensory stimuli, hallucinations
  • vacillates b/w quite, sleepy periods & hyper-vigilance/agitation
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7
Q

Abulia

A
  • awake but apathetic, no spontaneity

- with vigorous stimulation, cognitive function may be normal (bilateral frontal lobe disease, lobotomized)

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8
Q

Akinetic Mutism

A
  • silent, alert-appearing immobility

- no mental activity with vigorous stimulation (disease of frontal lobes & hypothalamus)

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9
Q

Minimally Conscious State

A

-fragments of awareness

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10
Q

Vegetative State

A

-awake, no awareness or meaningful interaction with the environment

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11
Q

Consciousness

A
  1. Arousal: sleep-wake cycles
    - ascending arousal system of the rostral brainstem
    - disease causes stupor & coma
  2. Content: awareness of: oneself, environment
    - Corrtical circuits - cognition, purposeful interaction with world
    - Disease causes dementia
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12
Q

Cataplexy

A

-sudden involentary loss of muscle tone during emotional excitement

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13
Q

Primary Lesions that Cause Coma

A
  1. extensive, acute bihemispheric disease
  2. lesions of diencephalon (thalamus & hypothalamus)
  3. Lesions of midbrain peri-aqueductal grey
  4. Involvement of upper 1/3 of pontine tegmentum
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14
Q

Causes of Coma

A
  1. Structural Cause: supratentorial mass lesions, acute obstructive hydrocephalus, infratentorilal mass lesion
  2. Metabolic (non-structural): reversible injury (sedative overdose), irreversible injury (hypoxia in cardiac arrest)

**always rule out psychogenic coma

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15
Q

Oculomotor nerve is near the?

A

tentorium

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16
Q

Central Herniation

A
  • Rostral-Caudal deterioration
  • Diencephalon (thalamus & hypothalamus) to midbrain failure
    • reduced consciousness
    • small reactive pupils (1-3mm)
    • decorticate postruing
    • Cheyne-Stokes respirations
    • Midbrain failure follows (fixed mid-postiion pupils, decerebration)
17
Q

Infratentorial Lesions

A
  1. Intrinsic brainstem lesions:
    - top of basilar artery ischemic stroke
    - pontine hemorrhage
  2. Extrinsic lesions compress & distory the brainstem
    - cerebellar hemorrhage
    - cerebellar infarction
    - cerebellar brian tumor
18
Q

Primary Brainstem Lesions cause:

A
  • Segmental cranial nerve deficits
  • ascending (spinothalamic) tract dysfunction
  • descending (corticospinal, central sympathetic) tract dysfunction
  • early cerebellar signs
19
Q

Pontine Hemorrhage Clinical Syndrome

A
  • coma abrupt
  • pupils are pinpoint
  • decerebrate rigidity or flacid quadriplegia
  • horizontal gaze paresis
  • ocular bobbing
20
Q

Metabolic Encephalopathy (toxic-metabolic coma)

A
  • Non-cerebral disease may interfere w/metabolism of the cerebral cortex & rostral brainstem AAS
  • Endogenous toxins in uremia & hepatic failure
  • Exogenous toxins in drug overdose, poisons, & sepsis
  • Hypoxia, hypoglycemia, hypo & hyper-osmolality
  • Electrolyte & acid-base imbalances
  • Metabolic insult to brain is global, diffuse, symmetric
  • Neuro-exam is “non-focal”
  • Head CT is neg.
  • Pupils stay reactive even as other reflexes are lost
  • Asterixes, multifocal myoclonus & tremor
  • Stupor & coma are reversible with metabolic correction & ICU support
21
Q

Causes of Metabolic Encephalopathy

A
  • hypoxia, CO2 narosis, Hypoglycemia, Hyperglycemia, Hyperosmolar, Hyponatremia, Dehydration, Uremia, Liver failure, Hyperthermia, Hypotheria, Acidosis
  • Drug intox, toxins, sepsis, Wernicke’s, Post-ictal state, DIC, TTP, Sever anemia, Lupus
22
Q

Coma: Immediate Management

A
  • Stablilize vital signs (ABC’s first): secure ariway, cardiac monitor, IV access & blood drawing
  • Stabilize neck (trauma)
  • Determine the circumstances in which coma occurred
  • Rapidly examine patient
  • Empirical D50, thiamine, naloxone (opiate OD)
  • tasks performed simulaneously by ED team
23
Q

Respiratory Patterns in Coma

A

-Cheyne Stokes respirations can be an early sign of herniation, both central & transtentorial

24
Q

Noxious stimuli to arouse patients who do not respond to voice command?

A
  • supraorbital pressure
  • nailbed pinch
  • sternal rub
25
Q

Glasgow coma scale

A

-prognosis in head trauma
-highest 15
12 or better is excellent prognosis
-scores of 7 or below: nursing home care
-3 means death

26
Q

Flexor response to Pain

A

(decorticate posturing)

-due to loss of cortical control of brainstem

27
Q

Extensor response

A

(decerebrate posturing)

-arises with loss of red nucleus & rubrospinal tract in the midbrain

28
Q

Coma: Diagnostic Testing

A

-STAT Head CT (or MRI if available)
-CXR
-Tests: EEG (status epilepticus, brain death)
Spinal tap (CNS infection, subarachnoid hemorrhage)
Cervical Spine X-ray (trauma)
Stat toxicology: cocaine, opiates, phencyclidine, barbiturates, anticonvulsants, & sedatives, ethanol, methanol, ethylene glycol, acetaminophen, salixylates, tricyclics

29
Q

Treatment of Coma

A
  • Ensure Oxgenation
  • Maintain circulation
  • Control glucose
  • Lower Intracranial pressure
  • Stop Seizures
  • Treat Infection
  • Restore acid-base balance & electrolytes
  • Adjust body temperature
  • Give thiamine
  • Consider specific antidotes (naloxone, flumazenil)
  • Control agitation
30
Q

Coma Prognosis

A
  • Non-traumatic coma: absence of pupillary light & comeal reflex of 3 days carries poor prognosis
  • In hypoxic coma, absence of purposeful motor movements at 3 days also carries a poor prognosis

Neuro 2 (16 decks)

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