CLMD Stupor and Coma, Disorders of Equilibrium Flashcards

1
Q

2 general causes of coma

A

Bilateral hemispheric dysfunction

Brainstem dysfunction (ARAS)

[could be both]

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2
Q

State of altered consciousness characterized by attention deficit, orientation disturbed, and stimuli misinterpreted

A

Confusion

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3
Q

State of altered consciousness characterized by disorientation, stimuli misinterpreted, visual hallucinations

A

Delirium

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4
Q

State of altered consciousness characterized by mental blunting, increased sleep, arouses to mild stimuli (voice)

A

Obtundation

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5
Q

State of altered consciousness characterized by arousal only to noxious stimuli and not environmental, only rudimentary awareness (e.g. purposful motor responses)

A

Stupor

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6
Q

State of altered consciousness characterized by unarousable, unresponsive, unaware state

A

Coma

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7
Q

Considerations for patient who presents with stupor/coma + HTN

A

Pheochromocytoma, drugs (amphetamine, cocaine, phencyclidine), increaced ICP, PRES

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8
Q

Considerations for patient who presents with stupor/coma + hypotension

A

Addison’s, sepsis, drugs (beta blockers, Ca channel blocker, TCAs, Li, sedatives, organophosphates, opioids, methanol), progression to brain death

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9
Q

Considerations for patient who presents with stupor/coma + hyperthermia

A

Infection, heat stroke, drugs (amphetamines, TCAs, cocaine, salicylates, neuroleptics), serotonin syndrome, central (pontine hemorrhage)

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10
Q

Considerations for patient who presents with stupor/coma + hypothermia

A

Hypothyroid
Hypoglycemia
Exposure
Drugs (opioids, sedatives, barbiturates, phenothiazine, EtOH)

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11
Q

Supratentorial causes of stupor and coma that affect unilateral hemisphere (mass effect)

A
Intracerebral hemorrhage
Large MCA infarct
Subdural hematoma
Epidural hematoma
Brain abscess
Neoplasm
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12
Q

Supratentorial causes of stupor and coma that affect bilateral hemispheres

A
Subarachnoid hemorrhage
Multiple infarcts
Venous thrombosis
Cerebral edema
Acute hydrocephalus
Multiple metastases
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13
Q

Subtentorial causes of stupor and coma

A
Pontine hemorrhage
Basilar a. occlusion
Central pontine myelinolysis
Cerebellar hemorrhage/infarct
Cerebellar/brainstem neoplasm
Cerebellar abscess
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14
Q

Essential and nearly essential elements of neuro exam in stupor/coma pt

A
Essential:
Pupillary responses
Corneal reflex
EOMs
Cough/gag reflex
Motor responses
Respiratory pattern

Nearly essential:
Neck stiffness
Carotid auscultation
Funduscopic exam

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15
Q

Anisocoria — which is the abnormal pupil?

A

If its large pupil, it should fail to constrict to light

If its small pupil, it should fail to dilate in dark

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16
Q

3 P’s of pinpoint pupils

A

Pontine lesion
oPiates
Pilocarpine

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17
Q

Damage to frontal gaze centers vs. pontine gaze centers

A

Frontal gaze center lesion —> deviate eyes to opposite side

Pontine gaze center lesion —> deviate eyes to same side

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18
Q

Doll’s eyes maneuver tests which area of the brain?

A

Midpons — used to assess cranial nerves III, IV, and VI

19
Q

Cold water irrigation with intact brainstem causes….

A

Eyes to deviate to irrigated side if unilateral irrigation

Eyes to deviate downward if bilateral irrigation

[low brainstem lesion responses are not there]

20
Q

What does it mean for comatose pt to have decorticate, decerebrate or flaccid posturing?

A

Decorticate (arms flexed, legs extended) — hemispheric

Decerebrate (all extremities extended) - brainstem

Flaccid - pontomedullary or metabolic

21
Q

Hyperpnea regularly alternating with apnea

A

Cheynes-Stokes respiratory pattern - indicates bilateral hemisphere or diencephalon involvement

22
Q

Central neurogenic hyperventilation indicates damage where?

23
Q

Long inspiration followed by apnea (mid/low pons)

A

Apneustic breathing

24
Q

Ataxic, or completely irreglar breathing, indicates damage where?

A

Medullary respiratory center

25
Effects of uncal transtentorial herniation
Compression of CN III (ipsilateral dilated pupil, poor EOM, ptosis), then contralateral brainstem (ipsilateral hemiparesis, then respiratory abnormalities, fixed pupils, and death
26
Central transtentorial herniation
Early coma, small pupils, normal EOMs, posturing and later bilateral fixed pupils, respiratory arrest and death
27
Signs/symptoms of diffuse/metabolic coma
Confusion and stupor commonly precede motor signs Motor signs usually symmetrical Pupillary reactions usually preserved Asterixis, myoclonus, tremor, seizures common Acid-base imbalance with hyepr or hypoventilation frequently seen Level of consciousness may fluctuate
28
Definition of brain death
Irreversible Complete cessation of brain function (including respiration but not heartbeat) Persistence
29
Management of comatose pt
ABCs first H and P EKG to monitor for arrhythmias Give glucose and thiamine Give antidote if necessary (narcan) Adjust body temp Control agitation Stop seizures if present Labs: venous blood, arterial blood, urine, LP if neck stiffness Diagnostic tests: noncontrast CT, LP, possibly MRI and EEG
30
Importance of Romberg test
Tests proprioceptive ability (judges posture), not necessarily cerebellum
31
Which nonvertiginous altered static/dynamic balance condition is associated with a Romberg sign?
Sensory disequilibrium: proprioceptive deficit, visual impairment, compensated vestibular disorders, worse in the dark Motor and cerebellar disequilibrium do not show Romberg sign
32
Typical direction of nystagmus in peripheral vs. CNS pathology
Peripheral: horizontal/diagonal Central: can be vertical
33
Clinical syndrome characterized by brief recurrent episodes of vertigo triggered by changes in head position with respect to gravity; thought due to debris floating in endolymph of any of the semicircular canals (posterior most commoN)
BPPV
34
What in-office maneuver is typically used to diagnose BPPV?
Dix-Hallpike In posterior canal BPPV, nystagmus is provoked with affected ear down In anterior canal BPPV, nystagmus is provoked with affected ear up
35
Treatment for BPPV
Vestibular suppressants (meclizine, scopolamine, valium) Antiemetics Anxiolytics Physical therapy and positional exercises often helpful
36
Spontaneous attack of vertigo that does not involve hearing loss or tinnitus and resolves spontaneously; characterized by vertigo, nausea, and vomiting of acute onset, typically lasting up to 2 weeks and not characteristically positional
Vestibular neuronitis
37
Conditions characterized by recurrent episodes of spontaneous vertigo, low frequency hearing loss, tinnitus, and aural fullness possibly d/t increase in volume of labyrinthine endolymph because of poor absorption (endolymphatic hydrops) Onset between 20-50 y/o, M:F 1:3
Menieres disease
38
Drug-induced causes of equilibrium disorders
``` Alcohol Salicylates Antiepileptics (phenytoin, carbamazepine) Quinine compounds Abx (aminoglycosides) Diuretics Chemotherapeutics ```
39
Obligatory features of friedrich’s ataxia
Onset before age 20 Gait ataxia Progression of ataxia to involve all 4 limbs Dysarthria Impaired position/vibratory sense in legs Muscle weakness Absent tendon reflexes in legs [secondary features: extensor plantar responses, pes cavus, scoliosis, cardiomyopathy, +/- optic atrophy, nystagmus]
40
Progressive pancerebellar degeneration involving nystagmus, dysarthria, and gait, limb, and trunk ataxia which begins in infancy (<4 y/o) Characterized by progressive ataxia, oculocutaneous cutaneous findings, and immunologic deficiency
Ataxia-telangiectasia
41
Vitamin deficiency associated with insidious onset, vague fatigue, gait and balance problems, distal sensory loss, babinski signs, romberg sign, +/- Lhermitte sign
Vit B12 Deficiency [note that nitric oxide can deplete vit B12 and lead to these symptoms]
42
What deficiency might present very similarly to vit b12 def?
Copper deficiency
43
What vitamin deficiency presents as spinocerebellar similar to friederich’s and is associated with peripheral neuropathy?
Vit E deficiency