16. Stupor and Coma Flashcards
what are the 2 clinical dimensions of human consciousness? what brain neuronal systems do they correspond to?
- wakefulness: reticular system of rostral brainstem & its thalamic and forebrain ascending projections
- awareness of self/envt: diffuse network of thalamocortical and corticocortical circuits.
what is the relationship between wakefulness and awareness? can you have one without the other?
cannot be aware without being awake, but you can be awake without being aware.
consciousness: local or global brain function?
global
coma: def
eyes closed unresponsiveness from which subjects cannot respond to stimuli
stupor: def
Similar to coma, but subject can briefly respond with stimulation
sleep: def
normal, cyclical, active state with arousal to full responsiveness
are there degrees of the coma state?
yes: levels of depth depending on the degree of reflex response to stimulation
how does damage to the central tegmentum of pons/midbrain (reticular system) lead to coma?
damage to this network by tramua, ischemia, edema etc leads to coma because the ascending arousal mechanism is disturbed
awareness of self and environment requires wakefulness and the normal functioning of what?
the neuronal circuits between the thalamus and multiple regions of the cortex.
why are thalamic and cortical neurons more susceptible to damage than the reticular/arousal system?
they have higher metabolic demands
how is it possible that a brain insult can damage the cortical and thalamic neurons needed for awareness, yet spare the reticular system (arousal network)?
the reticular system is composed of phylogenetically older and less metabolically demanding neurons: selective damage can result in the vegetative state (wakefulness without awareness)
what two general things can cause coma?
structural damage (trauma, edema, inflammation, ischemia, mass lesions) or diffuse metabolic and toxic effects.
structural lesions that cause coma typically do so how?
increased ICP produces caudal displacement and ischemia of the midbrain and medial temporal lobe through the tentorial incisura. Induces dysfunction of cranial nerves, breathing, motor systems.
exactly how do metabolic encephalopathies disrupt the micro-environment?
alter the metabolic conditions required for normal neuronal excitability: 02, glucose, temp, electrolytes, pressure.
a mild metabolic encephalopathy can result in what?
slowness, lethargy
a severe metabolic encephalopathy can result in what?
coma
will a rapid onset of metabolic encephalopathy be more or less severe than a slow onset?
MORE severe
why do we ask patients to look up and down?
test for locked-in syndrome
ticking nasal hairs elicits what?
primitive reflex mechanisms that protect the airway
what are the levels of response to stimulus called?
- voluntary movement
- withdrawal
- reflex posturing
- none
which coma assessment scale is most useful? why?
FOUR scale > Glasgow because more accurately assesses brain stem function, quantifies awareness
WTF is nuchal rigidity?
stiff neck associated with meningitis
emergent lab testing for a coma pt includes what? (10)
- CBC
- electrolytes
- blood glucose
- renal and liver function
- coagulation tests
- thyroid function
- arterial blood gases
- blood alcohol
- urine drug screen
- EKG
neuro exam: 5 systems that can distinguish structural from metabolic causes of coma and determine functional brain level
- resp rate and pattern
- pupil size, shape, reactivity
- eye movements
- VOR
- motor responses to stimuli
Respiration: what are we watching for?
post-hyperventilation apnea (5 deep breaths, subsequent apnea)
Cheyne-Stokes resp (periods of apnea/hyperpnea)
rapid, deep breathing (Kussmaul) is compensating for a metabolic acidosis.
Pupillary size and reactivity: what are we looking for?
size and reactivity indicates function of optic & oculomotor nerves, midbrain, and sympathetic nerves
what can reactivity to light help us distinguish?
remain reactive through several depths of metabolic toxic coma; same reflex is lost earlier on in structural coma/herniation
what do pupils look like in metabolic encephalopathies
small, equal, reactive
what happens with a lesion to the oculomotor nerve OR midbrain?
- ipsilateral pupil becomes unreactive to light (due to damage to parasympathetic pupilloconstrictors)
- ipsalateral pupil dilates because of unopposed sympathetic pupillodilators
lesions to only pons and NOT midbrain can cause what of the pupils?
pinpoint pupils, with intact rxn to light (sympathetic dilator tract is damaged so parasympathetic constriction is unopposed)
with lesions rostral to the brain stem (ie to cortical gaze center), conjugate horizontal eye deviation points to side of lesions or away?
towards
with lesions of the brain stem, conjugate horizontal eye deviation points to side of lesions or away?
opposite side/away
tonic downward eye deviation suggests lesion where?
lesion of thalamus or dorsal midbrain
ocular bobbing with rapid downward and slow upward movement suggests lesion where?
pontine lesion
periodic alternating gaze (like ping pong gaze) suggests what?
portosystemic encephalopathy.
ocular skew deviation (one eye higher than the other) suggests lesion where?
brain stem lesion
how does the VOR assess brain stem and cerebral hemispheric function?
inducing eye movements
how is the VOR elicited?
ice water to ear canal
in patients with normal consciousness, what eye movements are seen with VOR?
horizontal nystagmus
with stupor at diencephalic level (like from metabolic encephalopathy) what eye movements are seen?
fast component of nystagmus is suppressed, response is full tonic conjugate eye movements toward injected ear
what are examples of stimulation that will elicit motor response?
nasal tickle, sternal rub, ice water irrigation.
what is decorticate posturing? what does it suggest?
arm flexed, ipsalateral leg extended. midbrain function
what is decerebrate posturing? what does it suggest?
both arm and ipsalateral leg are extended. pontine functional level
symmetric motor signs caused by what kind of encephalopathy?
metabolic-toxic
asymmetric motor signs caused by what kind of encephalopathy?
structural causes of coma
what happens when a pt has experienced hypoxic-ischemic neuronal damage during cardiopulmonary arrest?
myoclonic seizures, continuous or intermittent rhythmic clonic movements
what are the most impt things to stabilize with coma patients?
stabilize respiration, circulation, gain control of seizures, reduce ICP
for coma patients without focal findings or meningitis, what is given during assessment?
dextrose, thiamine, naloxone, flumazenil
if fever, nuchal rigidity, or leukocytosis, what should be done initially?
presumptive tx for meningitis with IV abx.
how do we emergently reduce ICP?
hyperventilation, IV mannitol (hyperosmolar), IV steroids if vasogenic edema from brain tumors, abscesses or meningitis
patients in coma from hypoxic-ischemic neuronal damage may benefit from what?
induced hypothermia
prognosis after traumatic brain injury predicted by what?
GCS
define the vegetative state
disorder of consciousness in which wakefulness is retained but awareness of self and envt is absent.
vegetative state: transient or permanent?
can be either
vegetative state: caused by what?
brain lesions that disconnect the cerebral cortices from the thalami, but but spare the brain stem and hypothalamus
vegetative state: where are the lesions located?
bilaterally in thalami, diffusely in cerebral cortex, or diffusely in white matter that connects cerebral cortex to thalami.
vegetative state: 2 main causes of lesions?
- cardiopulmonary arrest –> hypoxic/ischemic damage
- torque force –> axonal injury
patient in vegetative state: what will EEG show?
some have slow wave activity, some have no activity
what test shows a patient in a vegetative state doing ideational tasks?
fMRI
vegetative state: treatment?
nothing reverses the state. treatment should follow the patient’s stated wishes
vegetative state: prognosis?
non-traumatic causes: if don’t regain awareness within 3 months, less than 1%
traumatic cause: cannot estimate prognosis until after 1 year.
minimally conscious state: definition
altered consciousness, lack of responsiveness but partial/intermittent edicence of awareness.
how can you tell the difference between veg state and minimally conscious state?
MC: more likely to respond to sensory stimuli, stimulant meds, and to deep brain stimulation of thamamic nuclei.
what stimulant meds might you give to someone in the minimally conscious state?
levodopa, dopamine agonists (same as for Parkinson’s) stimulate thalamic dopaminergic neurons
locked in syndrome: definition
profound paralysis. may be mistaken for disorder of consciousness. paralysis with intact cognition.
locked in syndrome: what might produce it?
large infarction or hemorrhage in pontine tegmentum and base.
locked in syndrome: what are sx?
quadriplegia, pseudobulbar palsy, paralysis of horizontal eye movements, pinpoint pupils
locked in syndrome: what is state of awakeness, alertness, breathing, consciousness?
pts are awake and alert, breathe spontaneously, consciousness and have normal cognition
why do locked-in patients retain control of their vertical eye movements and eyelid movements?
controlled rostral to the pons
locked in syndrome: prognosis?
usually only a few months, but if otherwise healthy may last for several years
brain death: def?
irreversible cessation of all clinical brain functions. accepted determination of death.
brain death: cause?
trauma, hemorrhage, meningitis, hypoxic-ischemic neuronal damage from cardiac arrest of asphyxia.
brain death: how hypertension leads to ischemia?
edema can produce intracranial hypertension. when IC pressure exceeds MAP, intracranial blood flow ceases and ischemic death of brain neurons ceases.
brain death: diagnosis
deep coma, unresponsive to stimuli, absent pupillary light reflexes, vent-dependent
brain death: tx
none. organ donor
Reticular Activating System: definition
reticular formation. controls sleep/wake transitions
how would you determine if there is damage to the reticular formation?
- assess eye movements extraocular nuclei are close to reticular formation).
- caloric testing
- pupillary reactions
where is the reticular formation located?
posterior pons, middle of midbrain
Glascow Coma Scale considers what types of functions?
eye response, motor response, verbal response
the FOUR score includes what functions?
eye response, motor response, brainstem reflexes, respiratory fxn
what does the functional level refer to?
level at which the neuraxis is transected: anything below is ok, anything above is not working. distinguishes structural causes of coma from metabolic.
what’s the diencephalon?
thalamus/hypothalamus
post-hyperventilation apnea indicates what functional brain level?
upper diencephalon
Cheyne-Stokes breathing indicates what functional brain level?
lower diencephalon
central neurogenic hyperventilation indicates what functional brain level?
midbrain
apneustic breathing indicates what functional brain level?
midbrain-pons
ataxic breathing indicates what functional brain level?
pons-medulla
apnea indicates what functional brain level?
medulla
what direction will the functioning PONS move the eyes with ice water stimulation?
towards the ice water. tonic reflex.
what direction will the functioning cortex move the eyes with ice water stimulation?
away from the ice water (corrective reflex)
