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.
The definition of brain death
The definition of brain death is total irreversible cessation of the entire brain function, including the brainstem. It does not require every single brain neuron to lose function; instead it requires clinical cessation of the chemical functions of the brain.
Typical brain death sequence
There is a typical sequence of events that occur with brain death. An injury occurs which results in focal and then global edema causing an increase in intracranial pressure. Once the pressure reaches a certain level, blood flow will no longer reach the parenchyma and cell death begins to occur.
Summary of Brain Death Determination:
Summary of Brain Death Determination:
1) Coma or unresponsiveness
2) Absence of brainstem reflexes
3) Apnea (apnea testing)
Following transsphenoidal resection of a pituitary tumor, a patient develops seizures with a serum sodium of 155 mEq/L and serum osmolarity of 320 mOsm/kg. The patient has had 2400 mL of urine output over the past 24 hours. Which of the following is the MOST appropriate initial treatment
Central diabetes insipidus occurs due to failure of the pituitary to secrete antidiuretic hormone resulting in a high output of poorly concentrated urine, hypernatremia and polydipsia. It can become so severe that it is life-threatening thus treatment should be instituted quickly with (1) free water replacement and (2) possibly DDAVP. Central diabetes insipidus can be differentiated from nephrogenic diabetes insipidus based on responsiveness to DDAVP.
Cerebral blood volume and cerebral blood flow when changing PaCO2 from 55 to 25 mmHg
As a general rule, CBV changes in the same direction as CBF but the changes in CBV are smaller in magnitude.
CBF decreases__mL/100 g/min for each 1 mmHg decrease in PaCO2.
CBF decreases 1 to 2 mL/100 g/min for each 1 mmHg decrease in PaCO2.
subarachnoid hemorrhage grading system
Fisher Grades:
1: no blood detected
2: diffuse thin layer of subarachnoid blood (< 1 mm thick)
3: localized clot or thick layer of subarachnoid blood (> 1 mm thick)
4: intracerebral or intraventricular blood with diffuse or no subarachnoid blood
relevance of Fisher grading system
The relevance of the Fisher grading system for CT findings in subarachnoid hemorrhage is that the incidence and severity of vasospasm is related to the amount of subarachnoid blood present.
Modified Hunt and Hess Clinical Grades:
Modified Hunt and Hess Clinical Grades:
0: unruptured aneurysm on imaging
I: asymptomatic or minimal headache and slight nuchal rigidity
II: moderate to severe headache, nuchal rigidity, but no neurologic deficit other than cranial nerve palsy
III: drowsiness, confusion or mild focal deficit
IV: stupor, mild or severe hemiparesis, possible early decerebrate rigidity, vegetative disturbance
V: deep coma, decerebrate rigidity, moribund appearance
anterior cerebral artery infarct deficit
Anterior Cerebral Artery contralateral leg numbness and weakness
Posterior Cerebral Artery lesion deficit
Posterior Cerebral Artery contralteral homonymous hemianopsia
Middle Cerebral Artery deficit
Middle Cerebral Artery
If left sided lesion then
- Right face/arm numbness and weakness
- Broca/Wernicke aphasia
If right sided lesion then
- Left face/arm numbness and weakness
- Left hemispatial neglect
Nitrous oxide effect on CMRO2 and CBF
Nitrous oxide does not cause decoupling. Nitrous oxide both increases CMRO2 and CBF, thus is not a preferred agent in certain neurosurgical procedures. Additionally, an increase in CBF will lead to an increase in intracranial pressure (ICP). Thus, agents that increase CBF (e.g. nitrous oxide, volatile anesthetics, ketamine) will also increase ICP.
The order of non-depolarizing muscle relaxant potentiation is
The order of non-depolarizing muscle relaxant potentiation is desflurane > sevoflurane > isoflurane > halothane > TIVA (e.g. propofol).
Volatile anesthetics effect on (and at what concentration)
CMRO2
CBF
Volatile anesthetics decrease CMRO2, even at low concentrations. At high concentrations (1.5-2 MAC) they can increase CBF.
The order of sensitivity for detection of venous/vascular air embolism (VAE), from lowest to greatest, for the following modalities is:
The order of sensitivity for detection of venous/vascular air embolism (VAE), from lowest to greatest, for the following modalities is: ECG, ETCO2, PAC, precordial Doppler, and TEE.
Local anesthetics which class more likely to cause allergy and why
In cases of true allergy, aminoester local anesthetics (procaine, chloroprocaine, etc) are more likely to elicit allergic reactions compared to aminoamides (lidocaine, bupivacaine, ropivacaine, etc) because the aminoesters are derivatives of paraaminobenzoic acid (PABA), a known allergen (hapten to be precise).
Allergic reaction to amide local anesthetics?
Although allergic reactions to aminoamides are very rare, patients may occasionally react to preservatives such as methylparaben contained in the aminoamide formulation. Multiple-dose vials of lidocaine typically contain 0.1% of methylparaben added as preservative, whereas single dose solutions are typically methylparaben free.
Methylparaben structurally similar to PABA
Myasthenia gravis
Criteria that may predict the need for postoperative mechanical ventilation include:
Criteria that may predict the need for postoperative mechanical ventilation include:
- Duration of disease 6+ years
- Presence of pulmonary disease(s) unrelated to MG (e.g., COPD)
- Vital capacity of < 2.9 L (or < 40 mL/kg)
- Negative inspiratory force (NIF) < 20 cm H2O (e.g. 10 cm H2O)
- Daily pyridostigmine dose > 750 mg
Exercise in Lambert-Eaton vs. Myasthenia Gravis
Lambert-Eaton = exercise improves strength MG = Fatigue with exercise
Myasthenic Syndrome
Lambert-Eaton
Co-existing disease Lambert-Eaton vs. MG
Lambert-Eaton Small Cell Lung Cancer
MG Thymoma
Response to relaxants Lambert-Eaton vs MG
Lambert-Eaton: sensitive to succ and NDNMBDs; poor response to anticholinesterases
MG: Resistant to succ; Sensitive to NDNMBDs; Good response to anticholinesterases
macronutrient cause hepatic steatosis in TPN
carbs
Phantom limb pain is what type of pain
Phantom limb pain is a type of neuropathic or central pain thought to be caused by misfiring spinal interneurons and maladaptive changes that occur within the sensory cortex after amputation.
Hyperkalemic periodic paralysis
triggers
Triggers for HKPP include potassium-rich meals or exogenous potassium administration, stress, rest after exercise, metabolic acidosis, and depolarizing muscle relaxants.
Hyperkalemic periodic paralysis pathophysiology
It is thought to occur due to a defect in the sodium channel.
Hypokalemic periodic paralysis pathophysiology
calcium channel defect
hypokalemic periodic paralysis triggers
high glucose meals, strenuous exercise, glucose-insulin infusions, stress, and hypothermia.
cerebral metabolism neuroprotective effects
Although anesthetic agents decrease cerebral metabolism, we do not know how this leads to its neuroprotective effects. This came from evidence showing that the degree of metabolic suppression does not correlate with the degree of protection.
protect the brain after an insult
There are multiple ways to protect the brain after an insult. This includes temperature management, euglycemia, decreasing the duration of the insult, certain medications, anesthetic agents, and prevention of reperfusion injury.
temp to protect brain during neurosurgery
Keeping patients between 35 to 36 degrees Celsius during neurosurgical procedures has been found to be the best management at this time, though most agree that avoidance of hyperthermia is key.
Average CBF ___
ischemia begins at ______
Irreversible brain damage at ______
Average CBF is 50 mL/ 100 g/min and ischemia begins at about 20 mL/100 g/min. At 6-12 mL/100 g/min, the energy supply is insufficient to support electrophysiologic activity (irreversible damage)
In a normal human brain, CBF remains constant between mean arterial pressures of
In a normal human brain, CBF remains constant between mean arterial pressures of about 60 and 160 mm Hg
Where do you inject for a spinal?
between arachnoid mater and pia mater
(pia mater adherent to spinal cord
inner surface of the dura mater abuts the arachnoid mater with potential space between the two)
Guillain-Barre Syndrome manifestations
Guillain-Barre Syndrome is characterized by
symmetrical ascending muscle weakness that may involve respiratory muscles and necessitate intubation.
Autonomic dysfunction is a commonly associated problem leading to
labile blood pressure,
arrhythmias,
orthostatic hypotension, and
possible circulatory collapse.
GCS score to indicate intubation
8
ABX that can prolong neuromuscular blockade
Lincomycin Clindamycin Polymyxins Aminoglycosides: gentamicin, amikacin, tobramycin, neomycin, and streptomycin Tetracyclines: -cycline
Tetanus mechanism
Tetanus toxin travels via retrograde axonal transport from peripheral to central neurons. Spastic paralysis occurs since the toxin prevents the release of inhibitory neurotransmitters (GABA) into the synaptic cleft between inhibitory interneurons and motor neurons. Tetanus toxin also enters brainstem and sympathetic nervous system neurons leading to autonomic dysfunction.
SNARE protein cleavage by tetanus toxin, therefore, prevents vesicle fusion and subsequent release of GABA and glycine into the synaptic cleft. Motor neurons subsequently lose their inhibitory control and contract repeatedly or for extended periods of time, causing muscle spasms and spastic paralysis.
drugs that don’t work well with BIS
Nitrous oxide and ketamine can induce anesthesia with a high BIS or entropy value. Dexmedetomidine can produce a low BIS or entropy value without inducing general anesthesia.
juvenile idiopathic arthritis (JIA)
JIA was formerly called juvenile rheumatoid arthritis, or JRA. Patients with JIA classically have multiple joint disease. In its most common form (oligoarticular arthritis), the knees, ankles, and wrists are usually involved. In polyarticular JIA, the hands are typically affected, and subcutaneous nodules may be present. There may also be anemia of chronic disease, lung nodules, and small stature. Systemic polyarthritis is the most extensive form of JIA and can affect the heart (pericarditis), lungs (pleuritis), the hematogenous system (leukocytosis), as well as multiple joints including those of the head and neck. Fever and splenomegaly may be present.
In all forms of JIA, the airway joints may be involved to varying degrees. Ankylosis of the temporomandibular joint leads to mandibular hypoplasia and microsomia, making mask ventilation and laryngoscopy difficult. Arthritis of the cricoarytenoid cartilage and joints may distort the glottic inlet anatomy and require down-sizing of endotracheal tube diameter. Arthritis of the atlantoaxial joint may be present, leading to torticollis and difficulty achieving ideal cervical motion for intubation. Flexion-extension cervical spine radiographs may be indicated to rule out dynamic neck instability (subluxation is exaggerated with neck extension and lessened in neck flexion). Chest radiography or even echocardiography may be necessary to rule out heart and lung involvement.
what monitoring is most resistant to volatiles
Brainstem auditory evoked potentials are the most resistant neuromonitoring modality to the effects of volatile anesthetics.
most sensitive monitoring to volatiles
VEPs are the most sensitive to the effects of volatile anesthetics.
Etomidate effect on cerebral metabolic rate (CMRO2), cerebral blood flow (CBF), intracranial pressure (ICP) cerebral perfusion pressure (CPP).
Etomidate leads to a decrease in cerebral metabolic rate (CMRO2), cerebral blood flow (CBF), and intracranial pressure (ICP) while being able to preserve cerebral perfusion pressure (CPP).
autonomic dysreflexia mechanism
Spinal cord reflexes from the stimuli trigger sympathetic activity (preganglionic sympathetic nerves) along the splanchnic outflow tract, but because of the SCI, inhibitory impulses from higher CNS centers (e.g. cerebral cortex, cerebellum, and brain stem) cannot reach below the level of SCI. Accordingly, intense generalized vasoconstriction occurs below the level of SCI while reflex cutaneous vasodilation occurs above the level of SCI (usually in proportion to the magnitude of the inciting stimulation).
Signs and symptoms of autonomic hyperreflexia
Signs and symptoms of AH reflect the imbalance above. The intense sympathetic response below the level of injury can cause acute hypertension (at least 20-40 mm Hg above baseline), reflex bradycardia, cardiac arrhythmias (e.g., premature ventricular contractions or atrial-ventricular conduction abnormalities), and myocardial infarction. The hypertension can further lead to headaches, blurred vision, retinal hemorrhage, intracranial hemorrhage, stroke, seizure, and/or cerebral edema. Additionally, the intense vasoconstriction leads to cool, dry, pale skin below the level of SCI. The reflex cutaneous vasodilation above the level of the SCI leads to nasal congestion; sweating; and warm, flushed skin on the upper extremities, shoulders, neck, and face.
Tetanus acts by
Tetanus acts by preventing neurotransmitter release (glycine and GABA) from inhibitory neurons in the spinal cord. The lack of inhibition causes increased muscle contractions to the point of tetanus. Botulism toxin has a similar mechanism of preventing neurotransmitter release (acetylcholine), but botulism affects the alpha motor neuron causing flaccid paralysis.
mechanism of the polio virus
destruction of the motor neurons in the CNS is the mechanism of the polio virus to cause polio paralysis. Polio is caused by an enterovirus. Polio is spread via fecal-oral route and infects the multiple cells of the body. However, replication and destruction of cells in the CNS, particularly the spinal cord, cause paralysis.
trismus
lockjaw
MOST likely cause of neurogenic pulmonary edema within a few hours following traumatic brain injury?
Following neurologic insult, a massive sympathetic discharge from traumatic brain injury (TBI) and intracranial hypertension can lead to neurogenic pulmonary edema (NPE).
TBI and DIC
Severe TBI can cause release of brain thromboplastin into the systemic circulation. This can lead to disseminated intravascular coagulation (DIC)
blood brain barrier
flow of water driven by what
is it hydro or lipophilic
The BBB protects the CNS from pathogens and rapid fluctuations in its electrolyte-fluid balance. Water moves freely across the blood-brain barrier (BBB) based on the tonicity of intravascular fluid. With the pathologic disruption of the BBB, hydrostatic pressure becomes more central to intracranial fluid movement.
The pores of this wall are lipophilic and small, thereby repelling hydrophilic molecules such as charged ions as well as large molecules
spinal cord
what percent of blood supply from anterior
The spinal cord receives its blood supply from one anterior spinal artery providing about 75% of the blood supply, which supplies the motor tracts. The two posterior spinal arteries supply the sensory tracts.
anesthetic agents that may induce seizures
etomidate, methohexital, lidocaine, ketamine, high concentrations of sevo
N2O in neuro cases
Nitrous oxide causes an increase in cerebral metabolic rate, cerebral blood flow, and ICP. Nitrous oxide can also diffuse into air-filled cavities causing expansion of these areas (e.g. pneumothorax, pneumocephalus).
Barbiturates in neuro
Barbiturate anesthetics cause a decrease in cerebral metabolic rate, decreased cerebral blood flow, and therefore a decreased ICP.
In patients with pseudotumor cerebri, lumbar punctures can reduce ICP and potentially improve associated neurologic symptoms. Risks of the procedure include
In patients with pseudotumor cerebri, lumbar punctures can reduce ICP and potentially improve associated neurologic symptoms. Risks of the procedure include PDPH, back pain, bleeding, infection, and nerve damage. The incidence of paraparesis (partial loss of voluntary motor function) following a lumbar puncture has been documented to be around 1.5%.
Why hyperventilation affects CBF but arterial pH doesn’t
Within the physiologic range of PaCO2, cerebral blood flow (CBF) varies directly with PaCO2 while being minimally affected by arterial hydrogen ion (H+) concentrations. The changes in CBF caused by PaCO2 are directly related to the pH alterations caused by changes in the concentration of CO2 in the cerebrospinal fluid (CSF). This change occurs because CO2 freely diffuses across the blood-brain barrier (BBB) while H+ is excluded. Thus, changes in arterial CO2 concentration are directly reflected in CSF CO2 concentration, which results in rapid changes in CBF. Within normal ranges of PaCO2, CBF will increase 1 to 2 mL/100 g/min for each 1 mmHg increase in PaCO2. Acute changes in arterial H+ concentrations, as occur during metabolic acid-base derangements, do not result in a similar response as these changes in arterial pH are not reflected in the CSF due to the impermeability of the BBB to H+ ions.
How does hyperventilation stop working at decreasing CBF
After 6 to 8 hours, CBF returns to baseline levels due to a self-correcting CSF mechanism where bicarbonate is excreted from the CSF space.
Residual neuromuscular blockade is defined as
Residual neuromuscular blockade is defined as a train-of-four (TOF) ratio < 0.9 measured at the adductor pollicis muscle.
midline shift hernia
subfalcine
Subfalcine herniation results in a midline shift with mild initial symptoms including a diffuse headache. As the herniation progresses, contralateral leg weakness will tend to occur, though cranial nerves tend to not be affected by this specific herniation pattern.
Transtentorial (uncal) herniation
Transtentorial (uncal) herniation occurs when brain parenchyma is displaced caudally into the tentorial notch.
The classic progression of a transtentorial herniation includes an expanding supratentorial lesion, headache, ipsilateral or bilateral cranial nerve palsy, hemiparesis of either side or both sides of the body, somnolence, loss of consciousness, and eventually cerebellar herniation should the downward herniation not be corrected.
Cerebellar herniation
Cerebellar herniation, also called tonsillar herniation, is the caudal displacement of the cerebellar tonsils through the foramen magnum into the spinal canal.
Presenting symptoms of cerebellar herniation tend to be more generalized and include somnolence through inhibition of the reticular activating system, decerebrate positioning through impairment of the descending spinal tracts, and cardiopulmonary arrest through impairment of the brainstem cardiac and respiratory centers.
Progression of this herniation will result in damage to the cardiac and respiratory brainstem centers, ultimately resulting in brain death
Transcalvarial herniation
Transcalvarial herniation is an external herniation of the brain through a skull defect
volatiles and paralytics
mechanism
duration or intensity or both
All volatile agents augment neuromuscular blockade by directly causing skeletal muscle relaxation and acting synergistically with NMBDs. Desflurane causes the most block potentiation.
Although the combination of rocuronium and inhalation anesthetics augments the intensity of neuromuscular blockade, it does not significantly increase the duration of or slow the recovery from the blockade.
A decrease in amplitude or increase in latency on somatosensory evoked potential recordings may indicate
A decrease in amplitude or increase in latency on somatosensory evoked potential recordings may indicate sensory cortex ischemia.
Jugular bulb venous monitoring
Jugular bulb venous monitoring offers direct cerebral oxygenation monitoring and assessment of global cerebral oxygen metabolism. This information is obtained by measuring jugular venous oxygen saturation and arterial-jugular venous oxygen content differences. Jugular venous blood is obtained from a catheter inserted into jugular bulb ipsilateral to the surgical site.
Regional cerebral blood flow (rCBF) measurements
Regional cerebral blood flow (rCBF) measurements, in conjunction with EEG monitoring, allow detection of cerebral ischemia and critical rCBFs. Regional CBFs are measured by IV or ipsilateral carotid artery radioactive xenon injection, followed by analysis of decay via detectors placed over the ipsilateral cortex. Critical rCBFs for an anesthetic comprised of N2O and isoflurane or sevoflurane is 10 mL/100 g of brain tissue per minute.
Internal carotid artery stump pressures
Internal carotid artery stump pressures reflect the collateral flow back-pressure in the circle of Willis originating from the contralateral carotid artery. Stump pressures are inexpensive, dynamic, and are associated with detecting hypoperfusion at pressures < 50 mm Hg. They are not used to detect emboli.
Transcranial Doppler (TCD) ultrasonography during CEA
Transcranial Doppler (TCD) ultrasonography during CEA continually assesses mean blood flow velocity and detects microembolic events in the middle cerebral artery (MCA), thereby assisting in detection of intraoperative thromboembolic events. This modality is limited by the inability to detect global cerebral ischemia since it can only sense embolic events in the MCA.
Burst suppression proven in what cases
The induction of a pharmacologic burst suppression utilizing anesthetic agents has been shown to improve mortality in patients with status epilepticus that is refractory to all other abortive therapies.
The number of twitches correlate to the degree of nAChR blockade 0 1 2 3 4
The number of twitches correlate to the degree of nAChR blockade (0 = 100%, 1 = 90%, 2 = 80 %, 3 = 70-80%, 4 = ≤ 65-70%).
mitochondrial myopathies
things to avoid
safe anesthetics
anesthetics to use with caution
Patients with mitochondrial myopathies should have a thorough preoperative evaluation aimed at minimizing stress from anxiety, hypothermia, hypoglycemia, hypovolemia, and acidosis. Fasting can be a cause for stress and perioperative fasting should be managed with an intravenous infusion of maintenance fluids and dextrose to maintain perioperative glucose levels.
Anesthetic agents that are safe to use in these patients include midazolam, short-acting opioids, and alpha-2 agonists. Ketamine and low-dose nondepolarizing muscle relaxants are also likely safe. Volatile anesthetics, propofol, and depolarizing muscle relaxants should be used with caution. Lactated Ringer solution leads to lactate accumulation in these patients and should be used judiciously
Note:
- reduced metabolism of bupivacaine
- Propofol metabolism is impaired in these patients and while low bolus doses may be tolerated, propofol infusions in these patients may be associated with increased risk of propofol infusion syndrome.
- Nondepolarizing muscle relaxants should be used with reduced doses due to the sensitivity of muscle tissue in these patients and should be titrated to effect.
drug that can abolish microelectrode recordings during stereotactically guided brain surgery
Midazolam and all benzos has the potential to abolish MERs during stereotactically guided brain surgery, eliminating any functional confirmation of needle placement. Most other IV agents are acceptable for use for sedation in these cases including propofol, remifentanil, and dexmedetomidine.
EEG with prop infusion
The density spectral array will show high power in the slow-delta (0 to 4 Hz) and alpha (8 to 12 Hz) range and lower power in beta and gamma range with a propofol infusion at surgical levels of general anesthesia.
Thyrotoxic periodic paralysis
Thyrotoxic periodic paralysis is a rare skeletal muscle channelopathy that clinically mimics hypoPP in both presentation and treatment. It is caused by a mutation in inward rectifying potassium channels and is more common in Asian men. In addition to the avoidance of hypokalemia, this disorder also responds to the antithyroid medication methimazole.
skeletal muscle channelopathy and is characterized by a “warm-up effect” where muscle stiffness is normally worse after rest and improves with use
Myotonia congenita is a chloride channel skeletal muscle channelopathy and is characterized by a “warm-up effect” where muscle stiffness is normally worse after rest and improves with use
sleep stages and their EEG waves
The sleep stages, in order, are recalled with the mnemonic BATS Drink Blood: - Beta waves (awake) - Alpha waves (drowsy) - Theta waves (stage 1) - Spindles and K complexes (stage 2) - Delta waves (stage 3 and 4) - then back to Beta waves (awake) Note that the oscillation frequency starts high then progresses lower.
EEG frequency range
Name Frequency Range (Hertz, Cycles per Second) Slow < 1 Delta 1 to 4 Theta 5 to 8 Alpha 9 to 12 Beta 13 to 25 Gamma 26 to 80
EEG brain death,
EEG monitoring is a reliable and widely used method of confirming brain death, but can only be used as an ancillary test after standard criteria have been met. Although EEG confirmation is reliable and widely used, it is an ancillary test and not mandatory. Electrocerebral silence on EEG (< 2 uV/mm activity) is confirmatory, especially when combined with evoked responses, but a false positive may occur with high doses of anesthetics such as barbiturates.
Gray rami communicantes originate carry myelinated? which direction
Gray rami communicantes originate from adjacent paravertebral ganglia of the sympathetic trunk and contain postganglionic nerve fibers of the sympathetic nervous system. Gray rami are composed largely of unmyelinated neurons. White rami communicantes, on the other hand, are heavily myelinated neurons and give the rami their white appearance.
TrueLearn Insight : Helpful mnemonic: whIte on the way Into the sympathetic trunk, grEy Exiting the sympathetic trunk.
several risk factors exist that increase the potential for nerve injury during surgery…
several risk factors exist that increase the potential for nerve injury during surgery. Those include male sex, extremes of body habitus, prolonged hospitalization, and malnutrition.
The body is able to physiologically compensate for increases in intracranial volume through
The body is able to physiologically compensate for increases in intracranial volume through the redistribution of intracranial venous blood and CSF to extracranial veins and spinal CSF space respectively. This compensation occurs until blood is being maximally drained and CSF is maximally diverted at which point the intracranial space becomes an effectively closed system and small increases in intracranial volume (brain tissue, blood, or CSF) result in marked increases in intracranial pressure.
how is each type of potential affected by volatiles
Brainstem potentials are Barely affected, Sensory potentials are Somewhat affected, Motor potentials are Mostly affected, and Visual potentials are Very affected.
propofol EEG
Propofol sedation produces a pattern of large amplitude beta-gamma oscillations. A single bolus dose of propofol for induction generates a pattern of slow delta oscillations with loss of consciousness. A combination of slow-delta and alpha oscillations characterizes the maintenance of general anesthesia with a propofol infusion
ketamine EEG
The EEG signature of ketamine is beta and gamma oscillations, with slow range oscillations seen with larger doses.
dexmedetomidine EEG
The effects of dexmedetomidine on the EEG resemble those of non-rapid eye movement sleep, with slow delta oscillations and spindles in the high alpha to low beta bands, that DISAPPEAR at deeper levels of sedation.
inhaled anesthetics EEG
Theta oscillations are characteristic of inhaled anesthetics, at MAC concentrations and above, and they generate an even distribution of power from the slow to the alpha bands
can achieve burst suppression with what
Propofol, ketamine, and sevoflurane at sufficiently high concentrations can achieve burst suppression.
complications from sitting crani’s
Sitting craniotomies can have several complications due to positioning including venous air embolism, hypotension, midcervical quadriplegia, pneumocephalus, peripheral nerve injury, and facial swelling. Potential venous air embolism should be a consideration before starting any sitting craniotomy.
most cases of postop visual loss due to what
risk factors
most cases (~90%) of postoperative visual loss are secondary to ischemic optic neuropathy, which to date is still considered an idiopathic process. It is not thought to be the result of optic globe compression or faulty positioning. It is however associated with prone position, Mayfield pin use, anesthetic duration >6 hours, blood loss greater than 1000 mL, preexisting retinal disease, diabetes, hypertension, atherosclerosis, and anemia.
considerations for intracranial AVM embolizations
Tight hemodynamic control is paramount in AVM embolization procedures. Cerebral dysautoregulation can result in rapid and profound cerebral edema in the downstream vascular distributions. This edema may require rapid action on the part of the anesthesiologist consisting of therapeutic hypotension, hypocapnia, hypothermia, or administration of sedative-hypnotic agents such as barbiturates or propofol.
precurarization roc dose to prevent succ fasiculations
10% of ED95 dose, which would be 0.03 mg/kg
Precurarization should be given approximately 3-5 minutes prior to administration of succinylcholine.
The intubating dosage of succinylcholine when precurarization is used
The intubating dosage of succinylcholine should be increased from 1 mg/kg to 1.5 mg/kg when precurarization is used due to this antagonism from the nondepolarizing agent.
benefit of reducing fasiculations
less increase in intrabdominal pressure so less aspiration risk
why give mannitol slowly
Mannitol can indeed cause a vasodilatory effect causing engorgement of the brain and increased intracranial pressure, if given too quickly. This is why mannitol should be given over 10-15 minutes.
high dose steroids in TBI
The CRASH trial, a large multicenter randomized controlled trial found that large dose methylprednisolone increased 2-week mortality as well as 6-month negative outcomes in traumatic brain injury. Steroids do reduce brain edema and increased blood-brain barrier permeability associated with tumors, although they require at least 24 (preferably 48) hours to be efficacious.
propofol effect on
CMRO2
cerebral o2 consumption
intracranial pressure
Propofol decreases cerebral metabolic rate of oxygen consumption (CMRO2), cerebral oxygen consumption, and intracranial pressure.
steroid mypoathy symtpoms and labs
Chronic or high-dose use of steroids can lead to myopathy. It often presents with proximal muscle weakness and normal levels of creatine kinase.
Autoimmune destruction of pre-synaptic voltage-gated Calcium Channels
Lamber Eaton
DTR is LE vs MG
Deep tendon reflexes are reduced or absent with LEMS but typically normal in MG.
