All of the following statements are correct, according to the presentation, EXCEPT:

1. Synaptogenesis describes a process of neuronal synapse formation; neuronal migration, maturation, and differentiation; and glial cell proliferation that occurs in the last trimester of pregnancy through the first 2 years of life.
2. Neurotransmitters such as GABA and glutamate promote the key elements of neuronal development, and the majority of current inhaled and intravenous anesthetics (except ketamine, nitrous oxide, and xenon) are GABA antagonists.
3. Early exposure (during synaptogenesis) to anesthesia in rats is detrimental to cognitive development.
4. Ketamine anesthesia during the first week of life causes long-lasting cognitive deficits in rhesus monkeys.

The correct answer is B.

Explanation: According to the presentation, most anesthetics have been shown to potentiate GABA (they are GABA agonists, not antagonists). Ketamine, PCP, nitrous oxide, and xenon are NMDA antagonists. The other statements regarding synaptogenesis and effects of early exposure to anesthesia in animals were described in the presentation.

Which of the following statements regarding animal exposure to general anesthesia is incorrect?

1. Dexmedetomidine has been shown in animals not to be toxic, and studies suggest it is neuroprotective when given with commonly used anesthetics.
2. In young animals, early exposure to general anesthesia is associated with long-term cognitive impairment.
3. In young animals, early exposure to general anesthesia is associated with mitochondrial degeneration and decrease in mitochondrial density in presynaptic terminals, suggesting that mitochondria are an important cellular target.
4. Pramipexole (PPX), which limits free oxygen radical production, does not seem to protect mitochondria or prevent anesthesia-induced cognitive impairment in rats.

The correct answer is D.

Explanation: Dr. Todorovic described a study in which rats exposed to GA+PPX and controls showed similar performances on cognitive testing; rats exposed to GA showed cognitive impairment. She also stated that dexmedetomidine has been shown in animals not to be toxic, and studies suggest it is neuroprotective when given with commonly used anesthetics.  Her presentation conclusions were as follows:

• Early exposure to general anesthesia causes developmental neuroapoptosis and long-term cognitive impairment.
• Mitochondria seem to be an important cellular target.
• Timely mitochondrial protection prevents anesthesia-induced cognitive impairment.

Which of the following statements regarding reversal is incorrect?

1. One method of pharmacological reversal is to increase acetylcholine level at the neuromuscular junction with acetylcholinesterase inhibitors such as neostigmine.
2. Nonpharmacologic reversal can be achieved by increasing clearance/degradation of neuromuscular blocking agents (NMBA) with plasma cholinesterase or cysteine adduction.
3. Nonpharmacologic reversal can be achieved by encapsulation with sugammadex or calabadion 1.
4. Pharmacologic reversal is the most effective because acetylcholinesterase inhibitors are not subject to a ceiling effect and their efficacy is not dependent upon the concentration of muscle relaxant.

The correct answer is D.

Explanation: Dr. Naguib states in his presentation that pharmacologic reversal is flawed because it has no effect on muscle relaxant concentration and acetylcholinesterase inhibitors have a ceiling effect, among other reasons. It is also stated that nonpharmacologic reversal is achieved with plasma cholinesterase or cysteine adduction, as well as encapusulation with suggamadex or calabadion 1.

Which of the following statements is not true, according to the presentation?

1. At high doses, L-cysteine is very neurotoxic.
2. Sugammadex is effective for reversing neuromuscular blockade induced by all studied compounds, including succinylcholine.
3. At appropriate doses, sugammadex has been shown to provide faster reversal after moderate and deep neuromuscular blockade when compared with neostigmine.
4. The efficacy of sugammadex is not influenced by general anesthetic regimen.

The correct answer is B.

Explanation: According to the presentation, sugammadex does not reverse NMB induced by succinylcholine or benzylisoquinolium compounds and its efficacy is not influenced by GA regimen. Dr. Naguib presented studies that showed sugammadex to provide faster reversal for moderate and deep blockade when compared with neostigmine. Lastly, it is stated in the presentation that L-cysteine is very neurotoxic at high doses.