Coma and PVS Flashcards
coma
*severely depressed responsiveness
*defined by Glasgow Coma Scale
acute encephalopathy
*rapidly developing pathobiological process in brain
*within hours, days, less than 4 weeks
delirium
*clinical state characterized by combination of features (DSM-V)
*disturbance in awareness, attention, and cognition, short period, acute change, fluctuates, not explained by neurological disorder, direct consequence of medical condition
brain lesions that cause coma
*diffuse cortical damage; global anoxia
*diencephalon injury; tumor
*caudal diencephalon and upper midbrain paramedian basial stroke
*brainstem lesions involving ARAS
note - brainstem lesions may be very large without causing coma if they don’t involve the ARAS bilaterally
ascending arousal system
*cholinergic system - INPUT into the reticular nucleus, thalamus, and upper brainstem
*cortical activation (glutamate, norepinephrine, etc)
NREM sleep vs coma
*BOTH have EEG patterns (increased high voltage slow waves) and both have lack of activity of ascending arousal system
*sleep = intrinsically regulated inhibition of arousal system
*coma = impairment of the arousal system by damage, diffuse dysfunction of its diencephalon/forebrain targets
approach to patient with coma
- evaluate/treat circulation, airway, breathing, and cervical spine
- exclude/treat hypoglycemia or opioid/benzodiazepine overdose
- serum chemistries, arterial blood gas, urine toxicology screen
- emergent cranial CT (CT angio brain if appropriate) to determine if coma etiology is structural or vascular
“house” approach for etiology of coma
1) structural
2) vascular
3) electric
4) chemisty/metabolic
examples structural etiologies of coma
-subdural hygroma causing midline shift and falcine herniation
-left MCA ischemic stroke, causing malignant cerebral edema and uncal herniation
-right basal ganglia hemorrhage with intraventricular hemorrhage
-obstructive hydrocephalus causing bilateral midbrain compression
example vascular etiologies of coma
-brainstem infarcts caused by acute basilar artery thrombus
metabolic causes of coma/altered mental status
*hypoglycemia
*hypoxemia
*toxin accumulation
*neurotransmitter deficiency or surplus
diagnostic evaluation of altered mental status
*history
*physical exam
*labs
*imaging
important history for altered mental status
*onset
*recent symptoms
*injury
*known medical illness (ex a-fib)
*psych history
*access to drugs (therapeutic or recreational)
important physical exam for altered mental status
*ABC (airway, breathing, circulation)
*vitals - BP, HR, RR, respiratory patterns, O2 sats
*systemic exam (nuchal rigidity, trauma, ingestion/njection/illness)
*neuro exam:
-mental status: GCS, arousal, awareness
-brainstem reflexes (pupil eye mvmts, corneal, oculovestibular, oculocephalic, cough/gag)
-muscle (motor response, reflexes, tone)
-sensory/cerebellar !!
-fundoscopy
Cheynes-Stokes respiratory pattern in coma patient
*characterized by cyclical episodes of apnea and hyperventilation
*indicates INTACT brainstem respiratory reflexes
hyperventilation respiratory pattern in coma patient
indicative of:
-bihemispheric lesions
-midbrain
-pons
apneic respiratory pattern in coma patient
indicative of:
-bilateral pons
-severe metabolic derangement
pupil reflexes in acute uncal herniation
*3rd nerve palsy (dilated pupil, down and out)
3 P’s of acute lesions to PONS
*paralysis
*pinpoint pupils
*pyrexia (fever)
glasgow coma scale
*a numerical scale of 15 that determines a patient’s level of consciousness based on eye opening, verbal response, and motor response
*scored based on best response (not for each limb)
*GCS 8… intubate
GCS - eye opening scale
4 = spontaneously
3 = to speech
2 = to pain
1 = no response
GCS - verbal response scale
5 = oriented to time, person, and place
4 = confused
3 = inappropriate words
2 = incomprehensible
1 = no response
GCS - motor response scale
6 = obeys command
5 = moves to localized pain (actively shoving pain away)
4 = flex to withdraw from pain
3 = abnormal flexion (decorticate posturing)
2 = abnormal extension (decerebrate posturing)
1 = no response
brainstem deficits and limb weakness on same side indicates
cortical/subcortical damage
brainstem deficits and limb weakness on opposite sides of the body indicates
brainstem damage
falcine herniation - syndrome
contralateral leg weakness (if ACA gets compressed)
uncal herniation - syndrome
*sluggish then blown pupil
*parasympathetic fibers of CN3
*down and out eyeball with ipsilateral ptosis
*contralateral paralysis
*PCA infarction
**Kernohan’s notch on autopsy
transtentorial herniation - syndrome
diencephalic > mesencephalic > medullary stage
management of coma
*ABCs
*thiamine, glucose, narcan
*emergent neuroimaging
*evaluate for acute stroke
*evaluate for acute seizures
*early differential diagnosis drives early evaluation: structural/nonstructural/metabolic
coma: awareness and arousal states
*no arousal
*no awareness
vegetative state: awareness and arousal states
*full arousal
*no awareness
minimally conscious state: awareness and arousal states
*full arousal
*partial awareness
locked-in syndrome: awareness and arousal states
*full arousal
*full awareness
*NO VOLUNTARY MOVEMENT
persistent vegetative state
*unawareness unwakefulness syndrome
*a person is AWAKE but is showing NO SIGNS of awareness (opens eyes, wake up and fall asleep at regular intervals, have basic reflexes)
*no meaningful responses, such as following an object with their eyes or responding to voice
minimally conscious state
*person shows clear but minimal or inconsistent awareness
*periods where they can communicate or respond to commands
locked-in syndome
*person is both conscious and aware, but completely paralyzed and unable to speak
*able to move their eyes, sometimes able to communicate by blinking
*REVERSIBLE if caught in time
*causes: basilar stroke, central pontine myelinolysis, or pontine hemorrhage
akinetic mutism
*abulia (lack of will, drive, or initiative for action, speech, and thought)
*akinesia
*no cognitive function = no motivation
*intact sleep-wake cycle and NO MOTOR, SENSORY, or SPEECH DEFICITS
*bilateral basal medial frontal lobe
brain death
*NO evidence of BRAIN function
*NO evidence of BRAINSTEM function
*NO evidence of spontaneous breathing
*underlying irreversible brain injury
