ITE CA-2 Neuro Flashcards
What potentials are affected by volatiles and which one is least affected?
SSEPs (somatosensory evoked potentials), MEPs (motor evoked potentials), EEG, and VEPs (visual evoked potentials - most sensitive) are all affected in a dose-dependent manner by inhaled anesthetics. Auditory evoked potentials are minimally affected by volatile anesthetics.
In a patient who is normotensive, the most effective way to quickly reduce ICP is
In a patient who is normotensive, the most effective way to quickly reduce ICP is a propofol bolus.
SSEPs
Somatosensory evoked potentials (SSEPs) involve stimulation of the peripheral sensory nerve followed by measurement of that response somewhere along the sensory pathway, most commonly in the cerebral cortex. SSEPs measure the cortical, subcortical, spinal, and peripheral components. The most frequently stimulated peripheral nerves are the median, ulnar, or posterior tibial. SSEPs test primarily the dorsal column of the spinal cord (the posterior segments). SSEPs can be used for a variety of surgeries although most commonly they are used for intracranial, spinal, and vascular surgery. What constitutes a meaningful change in waveform is not standard and may be up to the physician monitoring them. Additionally, many of the studies that helped to identify meaningful changes in SSEP were performed in animals.
SSEP use during surgery does not guarantee nerve injury is not occurring because SSEPs monitor the posterior spinal columns only. If monitoring of the anterior columns is not concurrently being performed, profound deficits can occur without a change in SSEP signals. Proper planning and determining what types of evoked potential to monitor based on patient and surgical characteristics is vital.
Things that alter evoked potentials
Since nerves are reliant on oxygen for metabolism, anything that alters the delivery of oxygen to the tissue will result in ischemia and the potential to cause changes in the evoked potentials.
Depending on the site of monitoring and patient conditions, this can occur secondary to
hypotension,
decreased hemoglobin concentration causing a decline in oxygen-carrying capacity,
increased intracranial pressure prohibiting adequate perfusion, and
regional changes altering oxygen delivery.
Temperature changes may also alter evoked potentials.
The effects of hypothermia on SSEPs are complicated and depend on the degree of temperature change. Hypothermia may not be deleterious to the nervous system but may mimic changes in SSEPs including decreased amplitude and increased latency when temperatures reach 32 degrees Celsius. Hypocapnia to a level of 20-25 mmHg did not compromise SSEP monitoring, however, did result in a small degree of shortened latency which may be secondary to changes in pH. Hypercapnia to a level of 50 mmHg has no effect on SSEPs.
Pharmacologic agents can have a profound effect on evoked potentials. Volatile anesthetics have an inhibitory effect on neurotransmission, producing a dose-dependent increase in SSEP latency and decreased amplitude. There are marked changes when minimum alveolar concentrations exceed 0.5. The major intravenous anesthetic agents affect SSEPs in variable ways depending on the specific agent used. Most barbiturates, benzodiazepines, and propofol cause a dose-dependent increase in latency and decreased amplitude. Opioids tend to have less effect except when given in bolus doses. Etomidate and ketamine tend to increase amplitude; thus ketamine may be useful to improve neuromonitoring conditions acutely. Use of neuromuscular blocking drugs is not prohibited with SSEP monitoring. It is most important when performing SSEP monitoring to try and maintain a stable anesthetic concentration so if changes are noted they can be attributed to factors outside the anesthetic.
Motor evoked potentials
Motor evoked potentials (MEPs) are most often used during spinal and vascular surgery; however, they can also be useful in cortical surgery. MEPs have better correlation with postoperative outcome since they are inherently more sensitive to ischemic vascular insults. Electrical stimulation in the motor cortex via electrodes placed on the scalp starts the signal and the response is recorded in the extremities. MEPs monitor the anterior spinal cord pathways which is an earlier predictor of impeding damage to the spinal cord due to the more precarious blood supply (when compared with SSEPs). Electroencephalogram (EEG) monitors the cortex only, thus it cannot provide information about any other pathways. This is why SSEPs may be used during carotid endarterectomy to monitor for subcortical ischemia.
level for autonomica hyper reflexia
T6 or higher
myasthenia sx can be precipitated by
pregnancy, stress, hypokalemia
mutated voltage gated calcium channels
hypokalemic periodic paralysis
treatment for myasthenia
steroids and or immunotherapy
a-1 activation effect on bladder
contraction
alpha 1 activation effect on liver glycogenolysis
increased
myasthenia gravis
autoimmune disorder, igG antibodies, post-synaptic acetylcholine receptor dysfunction
which has normal reflexes?
myasthenia or lambert eaton
myasthenia
lambert eaton has absent or decreased reflexes
achondroplasia effect non-depolarizing NMBDs dose
no change
proximal muscle weakness
lambert eaton
lambert eaton
paraneoplastic syndrome, antibodies to pre-synaptic calcium channels
alpha 1 activation effect on uterus
contraction
beta 1 activation effect on cAMP production
increase
treatment of acute exacerbation parkinsons
atropine and diphenhydramine
neuro disorder ass’d with small cell lung cancer
lambert eaton
treatment for cholinergic crisis
atropine and pralidoxime
pralidoxime
treatment for organophosphate poisoning
reactivates cholinesterase
duration of sux in heterozygous variation of plasma cholinesterase?
20 min
what amine crosses BBB
physostigmine
ED95 of NMBDs
“The dose of a neuromuscular blocking drug required to produce an effect (e.g., 50%, 90%, or 95% depression of twitch height, commonly expressed as ED50, ED90, and ED95, respectively“. Thus, the ED95 is the amount of NMBD required to reduce twitch height by 95%.
termination effect of roc
diffusion away from receptors
Hypothermia effect on hyperkalemic and hypokalemic periodic paralysis.
Hypothermia is associated with paralytic attacks of both hyperkalemic and hypokalemic periodic paralysis. Hypothermia leads to further impairment of the dysfunctional ion channel.
Hyperkalemic periodic paralysis inheritance respiratory/cardiac effect manifestations potassium level during weakness treatment exercise?
autosomal dominant - complete penetrance
Hyperkalemic periodic paralysis is a unique channelopathy which causes periodic muscle weakness. Respiratory and cardiac muscle is not affected because they lack the mutated channel.
Attacks often begin in childhood and involve weakness to the point of near paralysis.
The weakness is accompanied by hyperkalemia often with potassium levels up to 6mEq.
To treat or prevent hyperkalemic periodic paralysis methods to suppress hyperkalemia can improve symptoms or abort an attack. Methods to prevent an attack of hyperkalemic periodic paralysis include: avoid potassium containing solutions, avoid hypothermia, administer glucose or insulin, and performing mild exercise. Hydrochlorothiazide is a potassium wasting diuretic and often given prophylactically.
Which NMBD has active metabolite nearly as potent and how is it cleared
Vecuronium has an active metabolite, 3-desacetyl-vecuronium, that has 80% of the potency of vecuronium. Accumulation of this renally-cleared metabolite can significantly prolong the duration of action of the drug, particularly when an infusion is used in a patient with renal failure.
NMBD with metabolite that can cause seizures and What’s the metabolite
Cisatracurium (and atracurium) is primarily metabolized (80%) to laudanosine. This renally-cleared excitatory amine can precipitate seizures, but does not have neuromuscular blocking activity. The clinical significance of laudanosine was more important with atracurium since it is much less potent than cisatracurium, and thus more of the metabolite is produced.
Stimulate muscarinic receptors
The muscarinic receptors are found at the peripheral target organs. Stimulation will cause bradycardia, bronchoconstriction, miosis, salivation, gastrointestinal hypermotility and increased gastric acid secretion.
What neurotransmitters in PNS vs SNS
For generalization, the terminals in the PNS postganglionic fibers release ACh, in the SNS, NE is the principle transmitter released (except for sweat glands which use ACh).
PNS arises from
The PNS arises from cranial nerves III, VII, IX, and X as well as the sacral segments.
Nicotinic vs muscarinic
Nicotinic receptors are ligand-gated channels typically found at the neuromuscular junction of skeletal muscle. Muscarinic receptors are G protein-coupled and found mostly in the peripheral visceral organs.
Organophosphate poisoning leads to
Organophosphate poisoning leads to increased acetylcholine, which causes repeated receptor stimulation. Symptoms of this disorder follow muscarinic stimulation and are remembered with the mnemonic SLUDGE-Mi: salivation, lacrimation, urination, defecation, gastrointestinal upset, emesis, miosis.
The majority of patients with myelomeningocele also have…
The majority of patients with myelomeningocele also have Chiari II malformation, which involves herniation of the brainstem through the foramen magnum and frequently hydrocephalus secondary to blockage of the fourth ventricle.
anesthetic management for MS
Multiple sclerosis can lead to alterations in physiology that must be considered in the perioperative period. Specifically, it is important to minimize changes in body temperature, maintain fluid homeostasis, and maintain hemodynamics. Patients with multiple sclerosis may have autonomic instability that can lead to marked hypotension in response to anesthetic agents.
rate limiting step in formation of neurotransmitters
conversion of tyrosine to dopamine by tyrosine hydroxylase
neurotransmitters from preganglionic PNS preganglionic SNS postganglionic PNS postganglionic SNS 2 exceptions
preganglionic PNS - acetylcholine
preganglionic SNS - acetylcholine
postganglionic PNS - acetylcholine
postganglionic SNS - norepinephrine
postganglionic neurons of sweat glands release acetylcholine for the activation of muscarinic receptors
chromaffin cells of the adrenal medulla are analogous to post-ganglionic neurons—the adrenal medulla develops in tandem with the sympathetic nervous system and acts as a modified sympathetic ganglion. Within this endocrine gland, the pre-ganglionic neurons create synapses with chromaffin cells and stimulate the chromaffin cells to release norepinephrine and epinephrine directly into the blood.
evoked potential most sensitive to anesthetic medication
visual
SSEP monitor what pathway
ascending sensory pathway
CSF flows from third ventricle to 4th ventricle through…
aqueduct of sylvius
what agent increases amplitude of SSEP
etomidate
also increases latency
alteration in temperature will cause what percent change in cerebral blood flow
5-7% per 1 degree change in celsius
what percent change in cerebral blood flow occurs with 1mmHg change in PaCO2
2%
1-2 mL/100g/min
GCS
The GCS measures the following functions:
Eye Opening (E) 4 = spontaneous 3 = to sound 2 = to pressure/pain 1 = none NT = not testable
Verbal Response (V) 5 = orientated 4 = confused 3 = words, but not coherent 2 = sounds, but no words 1 = none NT = not testable
Motor Response (M) 6 = obeys command 5 = localizing to pain 4 = normal flexion/withdraws to pain 3 = abnormal flexion 2 = extension 1 = none NT = not testable
what cranial nerve bypasses the thalamus
olfactory
normal ICP
Intracranial pressure (ICP) is the pressure inside the skull and is normally between 5 and 15 mmHg. ICP is considered elevated when the pressure is greater than 20 mmHg.
formula for Cerebral perfusion pressure
MAP-ICP
Where is CSF produced
choroid plexus
Potentiation of neuromuscular blockade is seen with
Potentiation of neuromuscular blockade is seen with volatile anesthetics, local anesthetics, aminoglycosides, lithium, calcium channel blockers, acute phenytoin, and magnesium.
cisatracurium is synergistic with what
roc
Metoclopramide effects on NMBDs
Metoclopramide has inhibitory effects upon plasma cholinesterase, therefore it may prolong the duration of mivacurium and succinylcholine by means of reduced degradation. Cisatracurium metabolism includes Hofmann elimination and nonspecific ester hydrolysis and would not be affected by metoclopramide.
By how much does CBF change for every 1 mmHg change in PaCO2
Hyperventilation leads to decreased CBF by decreasing PaCO2. CBF changes 1-2 mL/100 g/min per every 1 mmHg change in PaCO2.
Methods to reduce sux myalgia
Calcium gluconate pretreatment -stabilizes cell membranes
Lidocaine - stabilizes cell membranes
Vitamin C - stabilize endothelial cells
Pretreatment with sux or NDNMBD does not reduce myalgias (but may reduce fasiculations)
Cerebral vasospasm is most likely to develop between how many days after a subarachnoid hemorrhage (SAH)
Cerebral vasospasm is most likely to develop between days 2-10 or 3-15 (depending on source) after a subarachnoid hemorrhage (SAH) and the exact reasons why this interval is the peak time period is not well understood.
Dibucaine number
- what is it proportional to?
- What numbers correlate with what?
proportional to the amount of normal pseudocholinesterase.
Dibucaine is a local anesthetic that was found to inhibit normal pseudocholinesterase activity by 80%, meaning a normal patient has a dibucaine number of 80. This number is proportional to the amount of normal pseudocholinesterase.
A dibucaine number of 20 indicates a homozygous patient, a dibucaine number of 40-70 indicates a heterozygous patient.
Phase 1 and phase 2 blockades of succ admin
- contraction with single twitch stimulus
- fasiculations
- repeated doses of succ
- resembles NDNMB
- minimal fade to TOF (TOF ratio is what?)
- enhancement of blockade by anticholinesterases
- infusion of succ
- can be partially reversed by anticholinesterases
Both phase 1 and phase 2 blockades of succinylcholine administration display decreased contraction with single twitch stimulus. Phase 1 blockade is associated with fasciculations, minimal fade to TOF (TOF ratio >70%), and enhancement of neuromuscular blockade (NMB) by anticholinesterases. Phase 2 blockade is associated with repeated doses or an infusion of succinylcholine, resembles NDNMB, and can be partially reversed with anticholinesterases.
OB and MS
The post-partum period is associated with an increase in MS symptoms and often exacerbations. Post-partum exacerbations occur in 20-40% of patients with MS.
Treatment for MS includes
Treatment for MS includes beta-interferon treatment, monoclonal antibody treatment (e.g. natalizumab), or immunosuppression. Steroids are not commonly used for chronic treatment but may be used to shorten an exacerbation.
Test for MH
The halothane-caffeine contracture test has highest sensitivity and is considered the current gold standard for diagnosis of malignant hyperthermia. While genetic testing for mutations of the ryanodine receptor has become increasingly common, not all genetic defects representing malignant hyperthermia have been identified.
MH
- inheritance
- pathophys
- inciting agents
- clinincal presentation
- continued progression leads to
Malignant hyperthermia is an autosomal genetic defect of calcium metabolism in skeletal muscle usually associated with a defective ryanodine receptor. The defective receptor allows excessive calcium intracellularly which can trigger skeletal muscle hypermetabolism. Inciting agents include volatile halogenated anesthetics and succinylcholine. Clinical presentation includes hyperthermia, rigidity, muscle breakdown, hypermetabolism with increased EtCO2, and hemodynamic instability. Continued progression leads to muscle breakdown, myoglobinuria, lactic acidosis, and ventricular arrhythmias.
What can transcranial doppler do
and what artery does it assess
Transcranial Doppler is used during the perioperative period for CEA procedures to measure blood flow velocities, detect embolization to the brain, identify shunt function or malfunction, and detect asymptomatic carotid artery occlusion and/or hyperperfusion syndrome.
The technique involves assessment of the middle cerebral artery.
Intraoperative embolization rate in CEA
90%+
Transcranial doppler. What flow rates correlate with what levels of ischemia
Ischemia is generally absent if TCD shows a mean flow velocity >40% of the preclamped value, is mild to moderate if 15-40% of the preclamped value, and is severe if < 15% of the preclamped value.
present with polyuria, hypernatremia, a high plasma osmolality, and a low urine osmolality Disorder pathophysiology etiology management
Diabetes insipidus (DI) is characterized by a deficiency of antidiuretic hormone and
can be caused by pituitary disease, trauma, infiltrative disease, brain tumors, and neurosurgical procedures.
Management includes administration of DDAVP and isotonic intravenous fluids to maintain euvolemia.
herniation and brain death
Brain death can occur without herniation and cerebellar herniation is not typical of brain death. However, herniation of any portion of the brain may occur as a result of the injury and edema that is associated with brain death.
