1. The major neurotransmitters found in the brain include the following:

2. The main energy substrate of the brain is glucose. Absence of oxygen (O₂) → anaerobic metabolism → insufficient adenosine triphosphate (ATP) production → shutdown of protein synthesis → neuron death.

Largest energy requirement in the brain is for pumping ions across cell membrane.

3. Twelve percent to 15% of cardiac output (CO) goes to the brain—a disproportionately large portion due to the high metabolic rate of the brain.

4. Increased PCO₂ → decreased pH → cerebral vasodilatation and increased cerebral blood flow (CBF). These changes are transient; blood flow returns to normal in 6 to 8 hours.

5. In steal, vessels supplying collateral flow to the area of a blocked artery are maximally dilated because of the metabolic demands of the ischemic tissue. High PCO₂ would cause blood flow to be shunted away to areas of less demand → “stealing” from areas that require extra O₂ and producing metabolites.

6. Mean arterial pressure (MAP) can vary from 50 to 150 mm Hg. Mild symptoms of cerebral ischemia occur at a MAP <40 mm Hg, although it may occur at higher blood pressures (BP) in patients with chronic, untreated hypertension.

Autoregulation can be abolished by trauma, hypoxia, certain anesthetics, and adjuvant anesthetic drugs.

7. The blood-brain barrier (BBB) can become disrupted by acute hypertension, osmotic shock, disease, tumor, trauma, irradiation, and ischemia.

CSF is secreted by the choroid plexus and absorbed by the arachnoid villi. The CSF volume in the brain is 100 to 150 mL and is completely replaced three to four times a day. Furosemide (Lasix) and acetazolamide (Diamox) reduce CSF formation.

8. Normal intracranial pressure (ICP) is <10 mm Hg. It is increased by the following:

9. Focal ischemia has the following three regions of tissue:

10. Seizures may be accompanied by systemic lactic acidosis, reduced arterial oxygenation, and increased CO₂, making it important to maintain ventilation, oxygenation, and BP.

1. The volatile anesthetics have direct vasodilatory effects that increase CBF (→ increased ICP), which will return to baseline levels after 3 hours of initial exposure to 1.3 minimal alveolar concentration (MAC) of anesthetic. The inhalation anesthetics also reduce the cerebral metabolic rate for O₂ ([CMRO₂]). Isoflurane (Forane) and sevoflurane (Ultane) reduce CMRO₂ the most. Enflurane (Ethrane) has been shown to induce seizure-type discharges potentiated by hypocapnia.

2. Nitrous oxide (N₂O) can increase CBF and ICP. Barbiturates and hypocapnia in combination may prevent these increases. A volatile anesthetic may add to the increases in CBF with N₂O.

3. Barbiturates:

Methohexital sodium (Brevital) is the exception; it can activate some seizure foci in patients with temporal lobe epilepsy. A major problem with barbiturates is that they can reduce MAP → possible reduced cerebral perfusion pressure (CPP).

4. Etomidate reduces CMRO₂ and CBF. It does not produce clinically significant cardiovascular depression, but suppresses the adrenocortical response to stress.

5. Propofol reduces CMRO₂ and CBF. Because it also reduces MAP, its effect on CPP must be closely monitored. Ketamine activates certain areas of the brain and can increase CBF and CMRO₂; as a result, it is not commonly used in neuroanesthesia.

6. Benzodiazepines have been shown to reduce CMRO2 and CBF, but in not as pronounced a manner as barbiturates. Opioids cause either a minor reduction or no effect on CBF and CMRO₂.

7. Hypothermia is the mainstay for reducing CMRO₂; the protection accrues primarily from reduction of glutamate and dopamine release. Four drugs that maintain ATP (by reduction of CMRO₂) are listed:

1. EEG waves recorded on the scalp are spontaneous electrical potentials generated by the pyramidal cells of the granular cortex. Quantification involves measuring the following:

Anesthesia affects the EEG by producing the following effects:

2. Parameters affecting the EEG include the following:

The EEG can be used to localize epileptic foci during surgery for intractable epilepsy. It is enhanced by hyperventilation, low-dose barbiturates, enflurane, and etomidate.

3. Sensory evoked potentials (SEPs) are used to monitor the integrity of specific sensorimotor pathways. SEPs—somatosensory (somatosensory evoked potential [SSEP]), auditory, and visual (visual evoked potential [VEP])—monitor ascending sensory pathways; motor evoked potential (MEP) tests the functional integrity of descending motor pathways. Injury is manifest as an increase in latency and a decrease in amplitude. Cortical EPs (VEP and SSEP) are more sensitive to anesthesia than brain stem EPs.

4. Anesthetic management for SEP monitoring:

Systemic hypotension below levels of cerebral autoregulation produces progressive decreases in amplitude of cortical SEPs until the waveform is lost, with no change in latency. Changes in PaO₂ and PaCO₂ also alter SEPs, probably reflecting changes in blood flow or O₂ delivery to neural tissues.

5. MEPs monitor signals through the dorsolateral and ventral spinal cord and can be recorded from the spinal cord, peripheral nerve, or muscle. Theoretically, continued stimulation can induce epileptic activity, neural damage, and cognitive or memory dysfunction. MEPs can be used during spinal cord surgery or during intracranial procedures that involve large or complicated vascular lesions with potential compromise to the motor cortex/tracts.

6. Whether ICP monitoring improves outcome is difficult to prove. Complications associated with placing an ICP monitor include infection, osteomyelitis, meningitis, leaks, catheter occlusion and drift, edema formation, and compromise of local blood flow. ICP monitoring is also costly.

7. Complications of angiography