Neuropathophysiology Flashcards
Describe the difference between the CNS & the PNS
The CNS are any neurons that are located in the brain and spinal cord (and do not exit) and the PNS are any neurons that are located in the periphery and outside of the CNS
Describe the organization of the Nervous system
The CNS is composed of the brain and spinal cord
The PNS is composed of the cranial nerves and spinal nerves it is further broken down into the somatic nervous system and the autonomic nervous system. The autonomic nervous system can further be broken down into the SNS, PSNS, and enteric systems
The SNS outflow leaves through the
thoracolumbar spinal cord region
PSNS outflow is via the
craniosacral region
Describe the reflex arc.
Sensory neurons in the periphery bring signal into spinal cord
interneurons provide a place for modulation from the brain
efferent neurons cause a response to the sensory neurons
Describe the meaning of cauda equina.
The spinal cord stops growing at ~T12-L1/L2 and this is known as the conus medullaris. The spinal cord axons however continue to grow and this is known as the cauda equina. This is where a spinal would be placed. An epidural could be placed anywhere
Describe the pathways of the autonomic nervous system.
PSNS: pre–> Ach onto nAChr–> post–> Ach onto muscarinic
SNS: pre–>Ach onto nAcher–> post–> norepi onto adrenergic
Adrenal medulla: pre–> Ach onto nAchr–>epi and norepi released into blood to act on adrenergic receptors
The composition of a nerve is important in understanding that
a lot of information can go in one nerve (receive sensory information and send out motor information)
Cranial nerves can innervate skeletal muscle and autonomic nervous system
The role of interneurons is to
provide an opportunity for modulation by the brain
Interneurons lie entirely within the CNS
Describe the generation of an action potential
The cell is at resting membrane potential
Action potential is generated and VGNa+ channels open and sodium comes into the cell
The second door of the VGNa+ channels close (putting them in an inactivated state) and the VGK+ channels open and K+ leaves the cell
As the cell begins to repolarize the VGNa+ channels move into the ready state
Describe the role of myelin.
Myelin allows for saltatory conduction and allows for quicker propagation of an action potential
Neuronal health and survival is dependent upon
blood delivering O2 and fuel and waste removal
Describe autoregulation in the brain.
Autoregulation in the brain is composed of the myogenic response (response to pressure) and the metabolic response (O2 lack theory)
Cerebral blood flow can be maintained over a wide range of MAP due to autoregulation in the brain
Osmotic pressure is
the pressure that opposes movement of water across the membrane
List the cellular processes activated by ischemia:
- Cellular acidosis
- Cellular swelling (cytotoxic edema)
- Neuroexcitotoxicity
- Enzymatic activation
- Nitric oxide production
- Inflammation
- Apoptosis
- Necrosis
Describe cellular acidosis.
Anaerobic metabolism leads to cell swelling because of lactic acid accumulation, increased intracellular H+, Na+/H+ exchanger protein moves H+ out of the cell in exchange for Na+ into the cell
Cell swells due to increased Na+
RMP becomes less negative, increasing AP probability
Describe cellular swelling (cytotoxic edema).
Reduced function of Na+/K+ ATP pump leads to swelling due to increased concentration of Na+ inside the cell
Describe neurotoxicity.
Brain glutamate levels rise because elevated intracellular Na+ brings neurons closer to threshold causing release of glutamate
Describe enzymatic activation.
Results from elevated brain glutamate levels because excessive glutamate causes Na+/Ca2+ influx into cell
causes neuron membrane damage and mitochondrial injury resulting in cell death
Describe the composition of the cranial vault.
Fixed space brain: 80% blood: 12% CSF: 8% Little reserve and no stretch
Cerebral perfusion pressure is equal to
MAP-ICP
Describe CSF in the cranial vault.
CSF is made in the choroid plexus. It circulates around the brain and drains via the arachnoid villi. If the arachnoid villi become blocked and CSF is unable to drain, there could be an increase in ICP which compromises CBF
Characteristics of cerebral blood flow
Brain receives 15% of cardiac output
little reserve of nutrients and O2; constant supply of blood is required
CBF remains constant due to autoregulation and other feedback mechanisms (not limitless though)
Cerebral blood flow averages
50 mL/100 g/min.
grey matter averages more than white matter
Cerebral blood flow is equal to
CPP/R
Normal ICP is
<10 mmHg
Normal Cerebral perfusion pressure is
80-100 mmHg
The middle cerebral artery is important because
it carries 80% of the blood to the brain
Cerebral autoregulation is composed of the
metabolic: Co2 and metabolites (increased metabolic rate)
and the
myogenic: VSMC stretch (increased CPP
An increase in CPP will result in
vasoconstriction
A decrease in CPP will result in
vasodilation
CBF remains constant between MAPs of
60 to 160 mmHg
As the pressure increases, the amount of
vasoconstriction has to go up to keep blood flow constant
In chronic hypertension, the cerebral autoregulation curve is
shifted to the right
When the metabolic demand exceeds cerebral blood flow, we get
release of metabolites that cause vasodilation
When you have uncoupling of autoregulation,
you have an even narrower range where smooth muscle can adjust
Cerebral blood flow can be regulated via
Temperature- hyperthermia increases CBF & CMR
Blood viscosity- decreased hct decreases viscosity and can increase CBF
Anesthetics- increased CBF and decrease CMR
The average CMRO2 is
3 to 3.8 mL 02/ 100 grams/ minute
The movement of substances through the blood-brain barrier is governed by
Size
charge
lipid solubility
protein binding
What can get past the blood brain barrier?
O2, CO2, H2O, lipid soluble, anesthetics
What cannot get past the blood brain barrier?
H+, HCO3-, other small ions, proteins, mannitol
Mannitol can be used to
draw water out of the brain
The blood brain barrier can be disrupted by:
severe hypertension, cerebral ischemia, infection, marked hypercapnea, hypoxia, tumor, trauma, stroke, seizure activity
What is the adult production of CSF/day?
500 mL/day
the total volume of cranial and spinal CSF is 150 mL
The function of the CSF:
Protect CNS from trauma
CSF is found in:
ventricles of the brain
cisterns surrounding the brain
subarachnoid space of the brain and spinal cord
CSF is produced by:
predominantly choroid plexuses of the lateral ventricles
secreted by the ependymal cells of the choroid plexus
Central venous pressure is a
back pressure that hinders cerebral fluid drainage
Once compensation is exhausted within the cranial vault, the
ICP will increase dramatically
The brainstem is important because
within the brainstem we have the medulla (NTS, VMC, and DRG), pons, and the cerebellum
Discriminating touch pathway
crosses high
afferent to medulla
tracts travel via dorsal column
Pain, temperature pathway
cross low
afferent to spinal cord
travel via lateral column
Conduction velocity of pain is related to
the type of fiber and diameter of the neuron
type C fibers are the aching pain fibers
Persistent pain is composed of
nociceptive pain & neuropathic pain
Neuropathic pain results from
direct injury to the nerves
often have burning or electrical sensation
Nociceptive pain results from
the direct activation f nociceptors in the skin or soft tissue in response to tissue injury and arise from inflammation
With the pain pathways and CNS ascending tracts,
we don’t distinguish between the lateral spinothalamic (fast pain) and the anterior spinothalamic (slow pain)
we just want to block all of the pathways
Enkephalins are
part of the brain’s endogenous opioids and are released at the brain stem and spinal cord
Endorphins are
part of the brain’s endogenous opioids and are released at the hypothalamus and pituitary gland
Referred pain occurs when
we have two sensory inputs that synapse at the same interneuron and the brain is unable to distinguish the particular area
occurs more frequently in men>women
Describe the ischemia pathway in the brain.
ischemia leads to low oxygen leading to low ATP leading to cell acidosis and ion pump failure
leads to chemical injury & neuroexcitotoxic injury
A neuroexcitotoxic injury causes
increased RMP and Action potentials–> increased glutamate–> increased calcium—> increased enzymes, ROS–> cell death
A chemical injury causes
damage to endothelial cells–> BBB disruption–> increase in ISF protein, increase in proinflammatory mediators–>inflammation–> cell death
eNOS is
an isoform of nitric oxide that is beneficial in ischemia because it causes arteriolar vasodilation, anti-inflammatory, and anti-thrombotic
iNOS and nNOS are formed from
ischemia and they combine with free radicals to damage cellular proteins, membranes, and DNA
Inflammation causes:
edema, clotting, and release of chemicals that are injurious or degradative
Cell derived chemical mediators such as
histamine, serotonin, and kinin cause disruption of the BBB because they increase the leakiness of the capillaries
Types of cerebral edema include:
cytotoxic, vasogenic, hydrostatic, osmotic, and interstitial
Cytotoxic edema result from
ischemia induced neuronal ion influx–> cell swelling
Vasogenic edema results from
ischemia–> damages endothelial cells–> BBB breakdown
Compare global ischemia to focal ischemia
global–> due to hypoperfusion
focal–> due to thrombus or embolus; discreet area
Types of stroke include
ischemic: thrombotic, embolic
hemorrhage: aneurysm rupture, AVM, intracerebral bleed, SAH
Global hypoperfusion results from
reduced CPP due to decreased MAP (shock) and/or increased ICP (CVA, trauma, infection, tumor)
Hemorrhagic intracerebral bleeds are associated with
hypertension, anticoagulation therapy or other coagulopathy, drug and alcohol abuse, neoplasia (tumors), amyloid angiopathy, infection
Aneurysm rupture can occur from
trauma, inflammation, atherosclerosis, or congenital
Aneurysm rupture typically occurs at
age 35-60
Aneurysms are typically (symptoms)
asymptomatic until rupture
Individuals are more susceptible to formation of aneurysm if they have
structural abnormalities, genetics, atherosclerosis, HTN, coarctation of aorta, or connective tissue disorder
The circle of willis (significance)
allows for collateral blood flow; if one area is blocked, blood can go all the way around and still perfuse other areas
With aneurysm rupture (pathophysiology of rupture)
there will be large increase in ICP decrease in CPP spread of blood--> inflammation cerebral vasoconstriction decrease in CBF (which may help stop further bleeding) loss of cerebrovascular autoregulation
Aneurysm rupture presents as
sudden onset of severe headache
nausea, vomiting, neck stiffness, photophobia
possible loss of consciousness
hypertensive and may have EKG abnormalities
Major sources of morbidity and mortality as it relates to aneurysm rupture include
Neurologic (ischemia from vasospasm and elevated ICP)
cardiopulmonary (arrhythmias, myocardial injury, pulmonary edema)
electrolyte abnormalities (hypomagnesemia, kalemia, natremia)
Many aneurysms occur at the
middle cerebral artery
devastating because it supplies a massive amount of brain tissue
An arteriovenous malformation is
vascular mass where blood flows directly from arteries to veins (no capillaries or neural innervation)
feeder vessels become dilated and shunt blood into malformation at the expense of surrounding tissue (steal)
An AVM manifests as
headache, cerebral hemorrhage, seizure, increased ICP or neurologic signs secondary to cerebral ischemia (steal effect)
An AVM is a result of
a congenital lesion
Anesthetic implications with AVM
can be very bloody surgery
deliberate hypotension may be used to decrease blood loss
avoid rise in CVP
An ischemic stroke is primarily the result of
thrombotic and embolic
The third leading cause of death in the United States is due to
ischemic stroke
An ischemic stroke is
an interrupted cerebral perfusion
creates vicious cycles of cell hypoxia, edema, and metabolic derangements
An embolic stroke is where
fragments from outside the brain break off and circulate and become lodged in intracranial vessels
can be thrombi, fat, air, tumor
There is a relationship between people who have cerebral artery disease and
CAD
A thrombotic stroke is the result of
thrombi formed in carotid or cerebral vessels
associated with atherosclerosis, hypercoagulation, sickle cell disease, and polycythemia vera
Conditions that favor a thrombus include
hypercoagulation and decreased perfusion
Risk factors for ischemic stroke include
increasing age, underlying atherosclerotic disease, history of prior transient ischemic attacks, associated with cardiovascular disease (a-fib, valve prosthesis, carotid disease, valve or carotid surgery, bacterial endocarditis)
For patients at risk of stroke, it is important to control
diabetes, HTN, and coagulation therapy
For patients who have already had a stroke, they may have
impaired cerebral autoregulation
Venous air embolism is the
entrainment of air or delivered gas into the venous or arterial vasculature
Takeaway for venous air embolism:
air into vein only occurs if PB> Pvenous (i.e. when the heart is lower then the brain and doing surgery above the heart), vein gets stuck open
The biggest concern with the venous air embolism is the
large volume of gas which can circulate to the lungs and lead to pulmonary embolism causing impaired gas exchange or for patients with a patent foramen ovale who could have a right to left shunt (causing MI & stroke)
The appropriate positioning for a patient with a PFO who has a VAE would be
on the left side
Clinical manifestations of VAE include
cardiovascular: chest pain, bradyarrhythmias, tachyarrhythmias, increased filling pressure, ST segment changes
pulmonary: dyspnea, tachypnea, gasp reflex, hypoxemia, hypercarbia
Neurological: decreased CO leading to cerebral hypo-perfusion
VAE is detected via
abrupt decline in end-tidal carbon dioxide
may also see unexplained hypotension
Subarachnoid hemorrhage risk factors include
hypertension, diabetes, CAD
When a bleed that is intra-axial enters the subarachnoid space
it is now considered extra-axial and becomes a SAH
The meningeal layers include
the Pia mater
the arachnoid
the dura mater
Subarachnoid hemorrhages can originate
inside or outside the brain (intra or extra axial)
SAH key points:
If the villi become blocked, ICP will increase resulting in signs and symptoms
- can see a catecholamine surge d/t increased ICP and bleeding- pressure and inflammation on the brain
- brain inflammation can move systemically and can lead to increased adrenal release of catecholamines/ norepi release
- Second stroke due to cerebral vasospasm due to RBC+iron–> quenches NO–> NO can’t act on VSMC
The catecholamine surge results in
hypertension, dysrhythmias, and cardiac damage
An anesthetized brain is less
vulnerable to ischemic injury because anesthesia increases CBF and decreases CMR
For those who have suffered an ischemic brain event, it is important to
avoid hypotension
can allow for modest increases in BP
avoid hypocapnia as this reduces blood flow to the ischemic brain
Factors that affect (can be influenced by the CRNA) cerebral blood flow include
PaO2- decreased PaO2 leads to cerebral vasodilation
PaCO2- increased PaCO2 leads to cerebral vasodilation
H+-increased metabolites leads to cerebral vasodilation
Cell activity: increased activity leads to cerebral vasodilation
Temp is proportional to CBF
Viscosity is inversely proportional to CBF
MAP- autoregulation
Recovering from a CVA can take
4-6 weeks before autoregulation and CO2 sensitivity is re-established because it is an inflammatory mess
Hyperglycemia is associated with
an exacerbation of ischemic cerebral injury because it decreases tissue pH and further compromises the ischemic injury
The spinal cord is supplied with blood via
Ventral spinal blood supply: 2 posterior & 1 anterior
Segmental spinal blood supply (horizontal): provides additional blood supply to some but not all spinal cord levels
The adamkiewicz artery is
a major segmental supply of blood to the spinal cord
clamping the spinal cord at T9 will reduced blood supply to the spinal cord because that is above the level of Adamkiewicz
The Artery of Adamkiewicz is also known as
a radicular artery
Concerns with aortic cross clamping:
surgical procedures involve the thoracoabdominal aorta–> high 30 day mortality at 8% to 35%
hemodynamic changes can cause myocardial ischemia or heart failure
Hemodynamic changes related to cross clamping includes
increased blood pressure due to increased preload: veins distal to clamp empty and see myogenic constriction–> decreased capacitance–> blood shifts to heart/arterial side, increases preload resulting in increased BP
Increased SVR: cross clamp causes increased SVR secondary to increased catecholamines and ANGII release (decreased blood supply to the kidneys activates the RAAS)
With aortic unclamping, we may see
decreased blood pressure (decreased preload) b/c the veins re-open increasing the vascular capacitance and blood volume shifts to venous side
decreased SVR because metabolites accumulate distal to the clamp and result in reactive hyperemia and cause massive vasodilation
Clamp needs to gradually be released
Carotid artery disease is
atherosclerosis in the carotid artery
plaque in the artery wall–> arterial narrowing–> increased resistance–> decreased blood flow
Carotid artery disease is a risk for
ischemic stroke
difficult to manage because if they’re being treated for coronary plaque then they’re a stroke risk and if they’re being treated for their carotid plaque then they’re an MI risk
The medical management of the patient with carotid artery disease includes:
control of hypertension, hypercholesterolemia, and diabetes, smoking cessation, increased physical activity, and anti-platelet therapy
For patients undergoing a carotid endarterectomy,
regional anesthesia is preferred
probably have had a stroke previously so want to recognize implications of this
Patients undergoing carotid endarterectomy for carotid artery disease have significantly increased risk of
MI because venous stasis on same side as clamp, stress on heart to provide collateral enough blood flow, and surgery is pro-inflammatory
With carotid endarterectomy, positioning during surgery is important because
part of the surgery is one of the carotids is clamped
extreme head rotation can compress the artery and decreases CBF
Encephalopathy signs and symptoms include
motor cortex–> cerebral palsy
occipital lobe–> blindness
cerebral cortex–> cognitive impairment
Encephalopathy is
when the function of the brain is affected by some agent or condition
Brain insult/injury can be a result of (pathophysiology of encephalopathy)
chromosomal abnormalities, infection, trauma, radiation, exposure to toxic substances
fetal injury- due to maternal toxemia, DM, malnutrition
Perinatal injury- due to anoxia, trauma, infection
Postnatal injury- infection, metabolic disturbance, trauma, toxins, vascular disease
infectious- access CNS via brain or intraneuronal route
The epidural space is the
space between the vertebral column and the dura mater (there is only a ‘potential’ epidural space in the head between the skull and the dura mater)
The subdural space is the
space between the dura mater and the arachnoid mater
The subarachnoid space is the space
between the arachnoid mater and the pia mater
Causes of traumatic brain injury include
head strikes an object or vice-versa
deceleration events
trauma causes neural and glial injury, vascular injury
Types of traumatic brain injury include
extradural hematoma- can lead to herniation
subdural hematoma- can lead to herniation
intracerebral bleed
The best predictor of TBI outcome is
the glascow coma scale
50% of patients who present with GCS of 8 or less will die
Signs and symptoms of TBI include
altered consciousness, coma, seizures, vomiting, irritability, acute temporary cognitive decline
TBIs and children
children are especially susceptible to TBI
children have lower BP reserve
BUT have greater intracranial compliance
Causes of TBI include
fall, car accident, explosion
higher incidence among males
When treating a TBI, fluid resuscitation
should not contain glucose because it facilitates anaerobic metabolism and inflammation
Treatment of adult/pediatric TBI is directed at
preventing secondary brain injury from systemic hypotension, hypoxia, hypocapnia, and hyperglycemia
Patients who have had a TBI are at higher risk for
seizure
excitotoxicity due to glutamate release can lead to eptileptogenic focus
Types of seizure disorders include
generalized seizures
partial (focal) seizures
status epilepticus
A seizure is
action potentials gone awry from neurons that are hyper-excitable leading to release of glutamate
A seizure causes an increase in
cerebral oxygen demand and ATP demand
A seizure stops when
neurons are refractory or acidosis–> hyperpolarization
The time period immediately following a seizure is known as
postictal state and involves disorientation, confusion, fatigue, and headache
A prodroma is
the early manifestations of a seizure: malaise, headache hours to days before onset of seizure
An aura is
a peculiar sensation preceding onset of generalized seizure
The epileptogenic focus is
a group of neurons–> sudden changes in normal membrane potential makes them extremely hyperexcitable
With a seizure, we may see an increase in
O2 demand and ATP demand
Cerebral blood flow increase due to autoregulatory metabolic effect
length seizures however can lead to hypoxia, decreased pH, lactic acid and brain tissue injury
Status epilepticus is
a prolonged partial or generalized seizure without recovery between attacks or one seizure of >5 min duration
may or may not include convulsions
Risk factors for seizure include
genetic-idiopathic genetic predisposition for disorder associated with seizures- hypoparathyroid or hypocalcemia tumor, trauma, infection, or fever SAH, stroke damage metabolic origin- fever, uremia, hypoxemia, hyperglycemia, hyponatremia drugs or alcohol overdose or withdrawal fatigue or stress excessive sensory stimuli
Additional risk factors for seizure include
hyperthermia (increased brain glutamate release)
hypoxia, hypoglycemia/hyperglycemia- brain metabolism altered leading to decreased GABA neurotransmission and increased glutamate neurotransmission
Hyponatremia- neuron swelling due to extracellular hypoosmolarity leading to cerebral edema
sleep disorders- OSA, insomnia, restless leg syndrome
precipitating anesthesia- some anesthetics lower the AP threshold
Status epilepticus is a medical emergency because:
increased O2, ATP, and glucose use
need to check for clear airway, administer O@
consider using antiepileptic drugs
Elevated ICP is defined as
intracranial pressure >20 mmHg
Raised ICP is directly associated with
poor outcomes (the higher the ICP, the poorer the outcome)
Increased ICP can occur due to
brain edema
increased cerebral blood volume (reduced venous outflow or increased CBF)
Increased intracranial CSF volume
Intra and extra-axial mass lesions
The types of brain edema include
cytotoxic, vasogenic, hydrostatic, osmotic, and interstitial
Cytotoxic edema is
ischemia induced neuronal ion influx–> cell swelling
Vasogenic edema is
ischemia–> damages endothelial cells–> BBB breakdown in 2-3 days–> BBB breach–> plasma protein moves into cerebral ISF–> edema
Hydrostatic edema occurs when
cerebral autoregulation is disrupted
Osmotic edema is
dilution of the blood
Interstitial edema is
transependymal movement of CSF
Increased CSF volume can result from
decreased CSF absorption at the arachnoid villi
Obstruction to CSF circulation
Increased production of CSF
Decreased CSF absorption at the arachnoid villi can result from
SAH & infection
Obstruction to CSF circulation can result from
obstructive hydrocephalus, neoplasm, traumatic and spontaneous hemorrhage, infection
Increased production of CSF can result from
meningitis or choroid plexus tumors
Cushing’s triad is
a bad sign of increased ICP and it includes hypertension, bradycardia, and irregular respirations
Symptoms of elevated ICP include
headache, nausea/vomiting, paresthesia, somnolence, visual disturbances, auditory disturbances, and mental changes
Signs of elevated ICP include
hypertension, bradycardia, periodic breathing, seizures, midline shift > 0.5 cm.
Escalating signs and symptoms of elevated ICP include
headache, N/V, pupillary dilation, blurred vision, inability to adduct and abduct eye
focal neurological deficits, apathy, decreased consciousness, seizures, coma, Cushing’s triad, symptoms of brain herniation
The cushing reaction occurs when
increased ICP is equal to arterial pressure and blood supply to the brain is extremely diminished initiating the CNS ischemic response
When treating a patient with elevated ICP it is important to
delay mannitol administration until the cranium is open (AVM, Cerebral aneurysm or hemorrhage) hematoma can expand as brain tissue volume decreases
Anesthetic implications with elevated ICP include
head tilt 15 to 30 degrees, avoid coughing as this will increase CVP and PEEP
Hydrocephalus is
excess CSF fluid within the cranial vault
can be within the ventricles, subarachnoid space or both
Hydrocephalus has two types including
non-communicating (intraventricular) within ventricles and communicating (extraventricular) outside ventricles and into brain interstitium
Causes of hydrocephalus include
communicating- neoplasm, traumatic and spontaneous hemorrhage, infection
non-communicating- congenital deformity of aqueducts or ventricles
Acute hydrocephalus is
an emergent event because there is no time for stretch or compensation so a quick rise in pressure occurs
Signs and symptoms of hydrocephalus include
declining memory and cognitive function, unsteady gait, history of falling, inattentiveness, apathy, indifference
Anesthetic implications in regards to hydrocephalus include
preventing additional increase in ICP
avoid succinylcholine and ketamine as they increase ICP
hyperventilate patient if ICP symptoms arise
A ventriculoperitoneal shunt is
used to treat an excess of CSF
allows CSF to be reabsorbed through the lymph system
Signs and symptoms of Parkinson’s disease include
tremor, rigidity, bradykinesia, postural instability, dementia, depression, and ANS dysfunction
Parkinson’s disease is where neurons are
present but beginning to fail
The concern with bradykinesia in Parkinson’s patients is
increased aspiration risk because slow movement of all skeletal muscles
The takeaway for Parkinson’s disease includes
pathways are extremely complex and never assume giving NT will have local effects
series of excitatory and inhibitory proccesses
give dopamine for these patients
involves the loss of dopamine neurons–> too much GABA activity–> inhibits ability to create motion
Patients with Parkinson’s disease are prone to
opioid induced rigidity because opioid agonist inhibit dopamine
Anesthetic considerations for Parkinson’s patients include:
regional anesthesia is preferred because less anesthetics to the brain
PD patients are prone to hypotension b/c DA causes vasodilation
required continued L-dopa therapy so may have to give intraop
predisposed to rigidity with opioids
response to muscle relaxants is normal
Takeaways for Alzheimer’s disease include
- will need POA present but need to still speak to patient
- At risk for emergence delirium
- Ach disease (too little Ach) in the brain neurons so if giving anticholinergic make sure it does not cross BBB
Symptoms of Alzheimer’s disease include
memory loss, impaired learning, spatial disorientation, anomia, apraxia, paranoia, delusions and hallucinations
Risk factors for Alzheimer’s disease include
genetic (30% familial, functional defect in apolipoprotein E), chronic hypertension, head injury, female, chronic TIA
For patients with Alzheimer’s Disease, they may be taking
acetylcholinesterase inhibitors and thus we may choose to give glyco as this does not cross the BBB
Cerebral palsy is
a non-progressive syndrome where the neurons do not work from gestational brain damage
The initiating event of cerebral palsy is
cerebral hypoxia–> low ATP–> pump failure–> cell swelling–> inflammation–> damaged neurons
Hypoxia can occur in cerebral palsy due to
prenatal hypoxia, birth asphyxia, or low birth weight
Clinical manifestations of cerebral palsy include
basal ganglia and extrapyramidal tract damage–> dyskinetic cerebral palsy
poor fine motor coordination, jerky movements
cerebral cortical damage–> spastic cerebral palsy
increased muscle tone, exaggerated deep tendon reflexes, contractures, scoliosis
developmental delay, sensory abnormality, seizure risk
Anesthetic implications for patients with cerebral palsy include:
higher seizure risk, developmental delays may impair patient comprehension
often experience GERD–> aspiration risk
motor issues may lead to prolonged response to muscle relaxants
Demyelinating disorders include
multiple sclerosis, ALS, and Guillan Barre
Disorders of the neuromuscular junction include
LEMS & myasthenia gravis
Clinical features of multiple sclerosis include
fatigue, parasthesias, unsteady gait, muscle weakness, and atrophy, respiratory insufficiency, ANS dysfunction
Multiple sclerosis is the
chronic degeneration of all CNS neuron types
Multiple sclerosis predominantly occurs in
females and is an autoimmune disorder
Lesions in the spinal cord can cause
paresthesia, limb weakness, and bowel and bladder symptoms
Lesions in the brain stem can cause
autonomic dysfunction & abnormal ventilatory drive
Brain demyelination can cause
seizures, spasticity, emotional lability, visual loss, dysarthria, dysphagia, and cognitive dysfunction
For patients with MS it is important to avoid
succinylcholine due to risk for hyperkalemia since they have upregulation of nAchR
The MS neuron type summary:
Only CNS neurons involved
CNS neurons include: somatic motor, somatic sensory, autonomic, and higher brain neurons, PNS neurons are spared
If the patients disease involves ANS, then
cardiac arrhythmias and neurogenic bowel and bladder may occur
ALS is a
progressive, degenerative motor disease involving both upper and lower motor neurons
ALS is more common in
males> females
usually occurs after the 4th decade with peak occurrence at age 50
ALS can be caused by
heavy metal exposure
glutamate excitotoxicity
oxidant stress
hereditary component
ALS stands for
amyotrophic lateral sclerosis
Clinical manifestations of ALS include
muscle atrophy, fasiculations, difficulty swallowing, dysarthria (articulation), dysphonia (volume)
sensory, autonomic and cognitive functions preserved
Anesthetic implications of ALS include:
succinylcholine contraindicated due to hyperkalemia risk
non-depolarizing MR will have a prolonged response
aspiration risk and difficulty weaning mechanical vent
ALS neuron type summary:
only SOMATIC motor neurons are involved (not sensory)
cranial nerve somatic motor activity impaired but eye movement is spared
ANS, sensory, and non-motor CNS neurons are spared
Guillain-Barre syndrome is caused from
an inflammatory/immune disorder of the peripheral nerve immune cells/ Ab attack the Schwann cells resulting in destruction of the myelin sheath
Clinical features of Guillain-Barre include
muscle weakness that is progressive (more often legs than arms)
areflexia
cranial nerve and autonomic involvement
respiratory muscle failure
pulmonary aspiration
ANS involvement- sinus tachy bradyarrhythmia, excessive sweating
Guillain-Barre neuron type summary:
PNS neurons are impaired (both somatic and autonomic)
ANS function is impaired
Somatic motor is impaired
Somatic sensory is impaired
Cranial nerve function is impaired
CNS neurons are spared (cognition preserved)
Myasthenia gravis clinical features include
muscle weakness- increases with exercise- fatigability
eye, facial, bulbar, and limb muscle weakness
respiratory muscle weakness rare but possible postop complication
Myasthenia gravis is a
chronic autoimmune neuromuscular disease affecting nicotinic receptors at the endplate and decreasing chance of action potential
For patients with myasthenia gravis, _____ should be withheld on the day of surgery
acetylcholinesterase inhibitors because they can prolong the action of sux and increase the need for nondepolarizing neuromuscular blocking drugs
Muscular blocking drugs and myasthenia gravis:
relatively resistant to succinylcholine- may need increased dose
extremely sensitive to nondepolarizing neuromuscular blockers (faster onset and more prolonged block)
LEMS disease is known as
Lambert-Eaton Myasthenic syndrome
LEMS is an
autoimmune disease of the neuromuscular junction that acts on presynaptic VGCa2+ channels and prevents release of acetylcholine resulting in muscle weakness
Anesthetic implications of LEMS include:
paralytic reversal is often ineffective
autonomic disturbances may be present
increased sensitivity to succinylcholine
increased effectiveness of NDMR
Muscular dystrophy is
a defect of muscle fiber due to the absence of dystrophin protein which leads to weakness
Muscular dystrophy is found in
males because it is located on the X chromosome
The absence of dystrophin in muscular dystrophy
causes muscle weakness because it prevents contractile filaments from being connected to extracellular matrix and doing work
Anesthesia risks related to muscular dystrophy include
acute respiratory depression
rhabdomyolysis
hyperkalemic cardiac arrest
heart failure/ arrhythmia
Muscle relaxants used in muscular dystrophy include
avoidance of succinylcholine and use of short-acting NDMR
Spinal cord injury is caused by
MVA, sports, and penetrating injuries
most injuries occur due to acceleration/deceleration, deformation forces
About half of the kids with a spinal cord injury have
an associated TBI
Spinal cord injury is most common in
males>females, age 16-30
Most spinal cord injuries occurs at
C1-C2, C4-C7, and T1-L2 as these are the most mobile portions of vertebral column
Describe a primary spinal cord injury
spinal cord stretching, tearing, compression of tissue, penetrating injury, vertebral stenosis, tumor, ischemia
Describe a secondary spinal cord injury
cytokine and amino acid release from injured cells leads to inflammation, free radical formation, cellular edema, and cellular apoptosis
Spinal cord stunning does not always
lead to neurogenic (spinal) shock
Management of an acute spinal cord injury includes:
immobilization of the injury, check for other injuries, support respiration, hypoxia and hypotension will exacerbate the SCI due to ischemia so need to treat
Spinal cord stunning does not always
lead to systemic shock
Spinal cord shock is the
temporary loss or depression of all or almost all neurological activity below the level of the spinal cord lesion
includes somatic sensory and motor neurons, neurons of the ANS and all spinal cord reflex activity
The distinguishing features of spinal cord stunning are
flaccid paralysis and absent spinal reflexes caudal to the level of the injury
Neurogenic shock is characterized by
profound hypotension and bradycardia due to lack of SNS tone
An injury above ____ leads to _____, whereas an injury below _____ leads to _____
T5 leads to neurogenic shock because loss of innervation of the sphlancnic bed causes hypotension
below T5 is spinal cord stunning
Concerns with patients with an abnormal vertebral column include
ability to be ventilated could be impaired and might be more difficult to intubate
Scoliosis is
a lateral rotational curvature of the spine due to a structural issue (rotation of the spine itself) or nonstructural issue (pain, posture)
Clinical manifestations of scoliosis include
spinal curvature, rounded shoulders, prominence of one hip, rib prominence
structural scoliosis compromises alveolar ventilation
Scoliosis is associated with
increased risk of mitral valve prolapse, increased pulmonary resistance, and pulmonary hypertension
Kyphosis is
a posterior rotation of the spine
Kyphoscoliosis is
both a posterior and lateral spine curvature
Ankylosing spondylitis is
chronic inflammatory joint disease that can affect vertebral joints and lead to joint remodeling
Ankylosing spondylitis is caused by
genetic predisposition
autoimmune disease attacks antigens on cartilage
Clinical manifestations of ankylosing spondylitis include
low back pain and stiffness, restricted motion of the spine, reflex muscle spasms, chest movement can be restricted
Spina bifida is
a congenital disorder characterized by a defect in the closure of the neural tube
not progressive but it will not get better
Clinical manifestations of spina bifida include
sphincter disturbance at the bowel and bladder
lower limb muscle weakness leads to gait changes and abnormal positioning of the feet
Anesthetic considerations of spina bifida include
patients are in a prone position and could have injury to eyes, brachial plexus, or impaired ventilation
Cauda equina syndrome can occur due to
compression of nerve roots below L1 caused by spine fracture or disk herniation
Other names for a spinal include
spinal, intrathecal, subdural, or subarachnoid
When placing a spinal,
we want to place below L3 to avoid injury the cell bodies because we are placing the spinal in the subarachnoid space
Clinical manifestations of cauda equina syndrome include
lower extremity motor deficits, variable sensorimotor dysfunction, variable reflex dysfunction, variable bowel, bladder, and sexual dysfunction
Cauda equina syndrome can be triggered by
spinal anesthesia that causes pooling of hyperbaric local anesthetics
to reduce risk avoid 5% lidocaine
Bleeding can occur in the
subdural space
intracerebral space
and subarachnoid space
The epidural is injected into the
space between the vertebral column and the dural layer
can be inserted at any level
If an epidural needle was incorrectly placed in the subarachnoid space, we may see
issues with the autonomic sensory such as tingling
dilation of vasculature leading to hypotension
