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Neurology > Approach to Coma > Flashcards

Approach to Coma Flashcards

1
Q

Lethargy?

A

Sleepy but easily aroused

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2
Q

Hypersomnia?

A

Excessively sleepy but normal congition when awakened

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3
Q

Obtundation?

A

Mental blunting, decreased 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 between quiet, sleepy periods and hyper-vigilance/agitation

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7
Q

When do pts in comas develop eye opening and sleep wake cycles?

A

2-4 weeks

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8
Q

Abulia?

A

Awake but apathetic, no spontaneity. With vigourous stimulation, cognitive function may be normal. (bilateral frontal lobe disease, lobotomized)

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9
Q

Akinetic mutism?

A

Silent, alert-appearing immobility. No mental activity with vigorous stimulation (disease of frontal lobes and hypothalamus)

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10
Q

Minimally conscious state?

A

Fragments of awareness

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11
Q

Vegetative state?

A

Awake, no awareness or meaningful interaction with the enviroment

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12
Q

Patients in MCS may do what?

A

Reach for objects, grunt, or gesture in response to a command, Visually fixate and track

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13
Q

Components of consciousness?

A

Arousal, Content

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14
Q

How is arousal achieved?

A

Neural circuits that mediate sleep-wake cycles and involves a specific area of the upper brainstem referred to as the reticular activating system or ascending arousal system of the rostral brainstem

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15
Q

Disruption of the arousal system leads to?

A

Stupor and coma

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16
Q

What does the content system refer to?

A

Cerebral activity for self-awareness, cognition, and purposeful interactions with the environment

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17
Q

Are the content system behaviors premeditative or reflexive in nature?

A

Premeditative

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18
Q

Lesion in encephalitis lethargica?

A

Rostral periaqueductal grey matter and posterior 3rd ventricle

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19
Q

Cataplexy?

A

sudden involuntary loss of muscle tone during emotional excitement

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20
Q

Neuropathological patterns associated with coma?

A

A. Extensive, acute bihemispheric disease
B. Lesions of the diencephalon (thalamus and hypothalamus)
C. Lesions of midbrain peri-aqueductal grey matter
D-E. Involvement of upper one third of pontine tegmentum

21
Q

Reticular grey formation?

A

Mediates arousal

22
Q

Route of the reticular grey formation?

A

Upper third of the pons through the midbrain tegmentum, the floor of the third ventricle and into the thalami

23
Q

Injuries to what will cause coma?

A

Reticular grey formation

24
Q

Nuclei responsible for arousal are located where?

A

Ascending arousal system

25
Q

What makes up the ascending arousal system?

A

Two Cholinergic nuclei

Monoaminergic System nuclei

26
Q

What do the cholinergic nuclei of the AAS do?

A

Inhibit thalamic firing that increases wakefulness. This puts the thalamus in transmission mode for filtering and relaying sensory info to the cortex.

27
Q

What happens if you did not have the cholinergic projections to the thalamus?

A

Thalamus would continue their periodic electrical “bursting” and with their widespread connections to the cortex, induce sleep through synchronizing cortical electrical activity.

28
Q

Role of the monaminergic system in the AAS?

A

It has widespread connections to the cortex, both direct and indirect. Improves signal to noise ratio for messages from the thalamus and thereby prevents any misperception of incoming sensory stimuli

29
Q

What is the sleep promoting center?

A

The ventro-lateral preoptic nucleus (VLPO)

30
Q

What NT does VLPO use?

A

GABA

31
Q

Role of VLPO?

A

Inhibits the many nuclear centers that promote wakefulness and comprise the ascending arousal system.

32
Q

The AAS receives feedback from many sources including?

A

Thalamus, the Limbic System, the frontal and association cortex

33
Q

Causes of coma?

A

Structural, Metabolic, Psychogenic (rare)

34
Q

What do you always rule out first in a comatose patient?

A

Psychogenic coma

35
Q

Structural comas?

A

Supratentorial mass lesion
Acute obstructive hydrocephalus
Infratentorial mass lesion

36
Q

Metabolic comas?

A 
Reversible injury (sedative OD)
Irreversible injury (hypoxia in cardiac arrest)
37
Q

What does transtentorial (Uncal) herniation lead to?

A

Occulomotor entrapment as well as sometimes PCA entrapment.

38
Q

Common cause of transtentorial (Uncal) herniation?

A

Epidural hematoma from the laceration of middle meningeal artery

39
Q

What does a falcine herniation trap?

A

One of both ACAs

40
Q

How does a falcine herniation occur?

A

When mass effect pushes the brain under the falx cerebri

41
Q

How does central herniation present?

A

Rostral-Caudal deterioration

  • Diencephalon –> midbrain failure
  • Reduced conciousness
  • Small reactive pupils
  • Decorticate posturing
  • Cheyne - Stokes respirations
  • Midbrain failure follows (FIxed mid-position pupils, decerebration)
42
Q

Intrinsic brainstem lesions?

A

Top of the Basilar Artery ischemic stroke

Pontine hemorrhage

43
Q

Extrinsic brainstem lesions?

A

Compress and distort the brainstem

  • Cerebellar hemorrhage
  • Cerebellar infarction
  • Cerebellar brain tumor
44
Q

Primary brainstem lesions?

A

Segmental cranial nerve deficits
Ascending (spinothalamic) tract dysfunction
Descending (corticospinal, central sympathetic) tract dysfunction
Early cerebellar signs

45
Q

Pontine hemorrhage presentation?

A 
Abrupt coma
Pinpoint pupils
Decerebrate rigidity or flaccid quadriplegia
Horizontal gaze paresis
Ocular bobbing
46
Q

Metabolic insult to the brain is?

A

Global, diffuse, symmetric

47
Q

Neuro-exam shows in pts with metabolic insult?

A

Does not show any focal or lateralizing deficits

48
Q

What does head CT show in pts with metabolic insult?

A

Normal

49
Q

What is the state of the pupils in metabolic insult?

A

Reactive

Neurology (25 decks)

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