ITE Neuro Flashcards
Name that pathway!
Peripheral nerve ->
Ipsilateral dorsal root ganglia ->
Ipsilateral posterior and lateral SPINAL CORD ->
Decussation (crossover) of nerve fibers at cervicomedullary junction ->
Contralateral medial lemniscus (w/in BRAINSTEM) ->
Contralateral ventroposterolateral nucleus of THALAMUS->
Contralateral thalamocortical radiation ->
Contralateral sensorimotor cerebral cortex
Pathway for Sensory Evoked Potentials (SSEPs)
- ascending pathway
Name that pathway!
Lower limb cortex -> Internal capsule -> Brainstem (decussate at medulla) -> Corticospinal tract -> Peripheral n.
Pathway for Motor Evoked Potentials (SEPs)
Name that pathway!
Retina -> Optic n -> Optic chiasm -> Optic tract -> Superior Colliculus -> Visual cortex
Pathway for Visual Evoked Potentials (SEPs)
During multilevel spinal fusion, the ________ nerves are monitored so that the RIGHT side of the posterior spinal cord and LEFT brainstem and cortex can be assessed.
Right Median and Tibial nerves
*Neuronal cells along sensory pathway are at risk for surgical damage or ischemia
Ischemic changes in SSEPs are quantified by reduction in _____ of the signal strength and increase in its _______ (time to signal detection
amplitude
latency
________ is the most cost-effective, accurate, and reliable method of monitoring intracranial pressure.
Ventriculostomy catheter
- it also provides a way to drain CSF and samples for lab analysis
Noninvasive way to measure ICP
measuring optic nerve sheath diameter via ultrasound
- new, not standard
Autonomic hyperreflexia (or autonomic dysreflexia) is a syndrome that may occur in pts with spinal cord injuries above the level of \_\_\_. This is usually seen at \_\_\_\_\_ (time) after spinal cord injury.
T12
- particularly above T5!
2 weeks - 6 months
Why does Autonomic hyperreflexia (or autonomic dysreflexia) occur?
- ie: reflex bradycardia, severe HTN, arrythmias, MI, intense vasoconstriction (cool, dry, pale skin below SCI)
It occurs d/t cutaneous or visceral stimulation below the level of the SCI, and inhibitory impulses from higher CNS centers cannot reach and no longer help regulate.
- there is reflex cutaneous vasodilation above lvl of SCI (nasal congestion, sweating, warm, flushed skin in UE)
Prevention of Autonomic hyperreflexia (or autonomic dysreflexia) is best done with ____
spinal or epidural anesthesia w/ local anesthetic and/or deep GA
Treatment of Autonomic hyperreflexia (or autonomic dysreflexia)
Stop triggering event
Administer fast acting direct vasodilators (sodium nitroprusside, nitroglycerin, or nicardipine)
*BB can worsen reflexive bradycardia if given in setting of unopposed a-stimulation -> hypertensive crisis
What is the receptor theory of muscle relaxants? What is the responses/sensitivities thought to be d/t?
Upregulation of receptors is associated with :
HYPERsensitivity to agonists (succinylcholine) and
HYPOsensitivity to antagonists (rocuronium)
Thought to be d/t presence/absence of an isoform of AChR that develop after denervation or burn injuries
Mature postjunctional AChRs are composed of what subunits?
What do immature isoforms of AChR look like that only form after denervation or burn injuries?
5 subunits
- 2 a1
- B1
- delta
- epsilon
Isoform: (Immature upregulated receptors)
7 subunits
- 2a1B1dy
Why does succinylcholine admin in the presence of upregulated AChRs (ie. denervation or burn injuries) result in potentially lethal hyperkalemia?
The whole muscle membrane depolarizes ->
Massive efflux of potassium from cell
*Succinylcholine is a molecule closely resembling ACh
The parasympathetic component of the facial (VII), glossopharyngeal (IX), and vagus nerves (X) lie in the _______ (structure).
Medulla oblongata (of brainstem)
The parasympathetic component of the oculomotor nerve (III) lie in the _______ (structure).
midbrain (of brainstem)
Which cranial nerve has the most extensive distribution of the PNS?
Vagus nerve X
Full-flow CPB is maintained for ____ min after reaching goal temperature to ensure ____
20-30
adequate cerebral cooling prior to stopping circulation
Pts with ALS have high risk of having pulmonary complications d/t ______ involvement and respiratory muscle weakness.
- How does management change for succinylcholine vs roc?
bulbar muscle
Avoid sux
- ALS assoc. w/ LOSS of motor neurons, forming extrajunctional ACh receptors and can mount exaggerated response
- life threatening hyperK
Lower dose of Roc
- higher sensitivity, prolonged, exaggerated response
- upregulation of extrajunctional receptors on postsynaptic neurons
Normal ICP is ___ mmHg.
Elevated is ____ mmHg
5-15 mmHg
20 mmHg
MAC of nitrous oxide is ___
105%
How does nitrous oxide cause increase in ICP?
Increase in:
- cerebral metabolic rate
- cerebral blood flow
- can diffuse into air filled cavities
Intracranial space has 3 major components, and any changes to ICP can be made by altering them.
- Brain parenchyma
- Blood
- CSF
How do propofol, thiopental, and etomidate affect ICP?
All
- decrease ICP
- decrease Cerebral metabolic rate of O2 (CMRO2)
- decrease CBF
*opioids have little to no effect on CBF