CLMD Stupor and Coma, Disorders of Equilibrium Flashcards
2 general causes of coma
Bilateral hemispheric dysfunction
Brainstem dysfunction (ARAS)
[could be both]
State of altered consciousness characterized by attention deficit, orientation disturbed, and stimuli misinterpreted
Confusion
State of altered consciousness characterized by disorientation, stimuli misinterpreted, visual hallucinations
Delirium
State of altered consciousness characterized by mental blunting, increased sleep, arouses to mild stimuli (voice)
Obtundation
State of altered consciousness characterized by arousal only to noxious stimuli and not environmental, only rudimentary awareness (e.g. purposful motor responses)
Stupor
State of altered consciousness characterized by unarousable, unresponsive, unaware state
Coma
Considerations for patient who presents with stupor/coma + HTN
Pheochromocytoma, drugs (amphetamine, cocaine, phencyclidine), increaced ICP, PRES
Considerations for patient who presents with stupor/coma + hypotension
Addison’s, sepsis, drugs (beta blockers, Ca channel blocker, TCAs, Li, sedatives, organophosphates, opioids, methanol), progression to brain death
Considerations for patient who presents with stupor/coma + hyperthermia
Infection, heat stroke, drugs (amphetamines, TCAs, cocaine, salicylates, neuroleptics), serotonin syndrome, central (pontine hemorrhage)
Considerations for patient who presents with stupor/coma + hypothermia
Hypothyroid
Hypoglycemia
Exposure
Drugs (opioids, sedatives, barbiturates, phenothiazine, EtOH)
Supratentorial causes of stupor and coma that affect unilateral hemisphere (mass effect)
Intracerebral hemorrhage Large MCA infarct Subdural hematoma Epidural hematoma Brain abscess Neoplasm
Supratentorial causes of stupor and coma that affect bilateral hemispheres
Subarachnoid hemorrhage Multiple infarcts Venous thrombosis Cerebral edema Acute hydrocephalus Multiple metastases
Subtentorial causes of stupor and coma
Pontine hemorrhage Basilar a. occlusion Central pontine myelinolysis Cerebellar hemorrhage/infarct Cerebellar/brainstem neoplasm Cerebellar abscess
Essential and nearly essential elements of neuro exam in stupor/coma pt
Essential: Pupillary responses Corneal reflex EOMs Cough/gag reflex Motor responses Respiratory pattern
Nearly essential:
Neck stiffness
Carotid auscultation
Funduscopic exam
Anisocoria — which is the abnormal pupil?
If its large pupil, it should fail to constrict to light
If its small pupil, it should fail to dilate in dark
3 P’s of pinpoint pupils
Pontine lesion
oPiates
Pilocarpine
Damage to frontal gaze centers vs. pontine gaze centers
Frontal gaze center lesion —> deviate eyes to opposite side
Pontine gaze center lesion —> deviate eyes to same side
Doll’s eyes maneuver tests which area of the brain?
Midpons — used to assess cranial nerves III, IV, and VI
Cold water irrigation with intact brainstem causes….
Eyes to deviate to irrigated side if unilateral irrigation
Eyes to deviate downward if bilateral irrigation
[low brainstem lesion responses are not there]
What does it mean for comatose pt to have decorticate, decerebrate or flaccid posturing?
Decorticate (arms flexed, legs extended) — hemispheric
Decerebrate (all extremities extended) - brainstem
Flaccid - pontomedullary or metabolic
Hyperpnea regularly alternating with apnea
Cheynes-Stokes respiratory pattern - indicates bilateral hemisphere or diencephalon involvement
Central neurogenic hyperventilation indicates damage where?
Midbrain
Long inspiration followed by apnea (mid/low pons)
Apneustic breathing
Ataxic, or completely irreglar breathing, indicates damage where?
Medullary respiratory center
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
Central transtentorial herniation
Early coma, small pupils, normal EOMs, posturing and later bilateral fixed pupils, respiratory arrest and death
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
Definition of brain death
Irreversible
Complete cessation of brain function (including respiration but not heartbeat)
Persistence
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
Importance of Romberg test
Tests proprioceptive ability (judges posture), not necessarily cerebellum
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
Typical direction of nystagmus in peripheral vs. CNS pathology
Peripheral: horizontal/diagonal
Central: can be vertical
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
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
Treatment for BPPV
Vestibular suppressants (meclizine, scopolamine, valium)
Antiemetics
Anxiolytics
Physical therapy and positional exercises often helpful
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
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
Drug-induced causes of equilibrium disorders
Alcohol Salicylates Antiepileptics (phenytoin, carbamazepine) Quinine compounds Abx (aminoglycosides) Diuretics Chemotherapeutics
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]
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
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]
What deficiency might present very similarly to vit b12 def?
Copper deficiency
What vitamin deficiency presents as spinocerebellar similar to friederich’s and is associated with peripheral neuropathy?
Vit E deficiency
