Neuro

• CP is not a risk for hyperkalemia after succinylcholine because acetylcholine receptors are not upregulated due to contractures
• For pts with MS, spinal anesthesia has been linked weakly to flareups so use epidural. 
• Lithium potentiates sux and non-depolarizing relaxants
• Pacemakers and epilepsy not contraindications to ECT
• 
  

• Sux and ALS - hyperkalemia 2/2 lower motor neuron involvement
• Sux and Duchenne's - high likelihood of MH and hyperkalemia
• Sux and Guillain-Barre syndrome - hyperkalemia
• Sux and Myotonic dystrophy - contractures making it hard to mask/ventilate
• Sux and Myasthenia Gravis - resistance
• Sux and Lambert Eaton - increased sensitivity
• Sux and MS - contraindicated if pt paretic

• In myotonic dystrophy, 4 concerns.
• contractures so no succinylcholine, neostigmine, and shivering (hypothermia)
• sensitivity to anesthetics, especially respiratory depressants
• aspiration risk
• possible MH

• Hypokalemic periodic paralysis vs Hyperkalemic
• Hypokalemic: Treat with diamox or spironolactone, avoiding carbs (insulin release), hyperventilation, alkalosis
• Hyperkalemic: treat with furosemide, carbs, calcium

http://www.aana.com/newsandjournal/Documents/p297-302.pdf

Comparing etomidate vs propofol vs thiopental for neuroprotection

Summary:
All three decrease ICP indirectly by decreasing CBF, which is directly decreased by reduction in CMRO2.

However, only etomidate exhibits properties where CBF and CMRO2 are decoupled. That is, etomidate decreased CMRO2 after CBF already reached a minimum. This may be good and bad depending on the goal. For example, inducing coma for poststroke may be bad with etomidate because increased BF with decreased metabolism means more oxygen lying around to develop free oxygen radicals.

Propofol seems to have anti-oxidant effects as in test animals, infarct size was smaller initially and animals had possibly better motor skills at day 21.

Brian waves/burst suppression/isoelectric
At sedative doses or at doses associated with excitation or disinhibition ("stage 2" anesthesia), median EEG frequency increases because alpha waves (7-13 Hz) typical of the awake state change to beta waves (13-30 Hz). As the depth of hypnosis increases, there is a decrease in frequency and an increase in amplitude (power) of the EEG waves. Surgical anesthesia is associated with an EEG characterized by a predominance of delta waves (0.5-3.5 Hz). Increasing the dose of thiopental further leads to burst suppression (characterized by alternating periods of delta waves and electrical inactivity) and, finally, a completely isoelectric ("flat-line") EEG.