Apex Unit 7 Flashcards Neuro
Name 4 types of glial cells and describe the function of each.
.
List the name and function of the 4 lobes of the cerebral cortex.
Frontal – contains the motor cortex
Parietal – contains somatic sensory cortex
Occipital – contains vision cortex
Temporal – contains auditory cortex and speech centers
Wernicke’s area = understanding speech
Broca’s area = motor control of speech
Name the 12 cranial nerves.
Mnemonic: On Occasion Our Trusty Truck Acts Funny Very Good Vehicle Any How
What cranial nerves provide motor control of the eyes? How does each nerve contribute to the eye’s movement?
What bedside tests are used to assess the cranial nerves?
CN 1- 6
What bedside tests are used to assess the cranial nerves? CN 7-12
Which cranial nerve resides in the central nervous system? What is the implication of this?
With the exception of the optic n. (CN II), all of the cranial nerves are part of the peripheral nervous system. This means that the optic n is the only cranial nerve that is surrounded by the dura.
Because the optic nerve is part of the CNS, it is bathed by CSF. If you inject local anesthetic into the optic nerve during regional anesthesia of the eye, you will have a big problem.
What is tic douloureux? What cranial nerve contributes to this problem?
Tic douloureux (trigeminal neuralgia CN V) causes excruciating neuropathic pain in the face.
What is Bell’s palsy?
What cranial nerve contributes to this problem?
Bell’s palsy results from injury to the facial n. (CN VII).
This causes ipsilateral facial paralysis
What is the function of CSF, and where is it located?
The cerebrospinal fluid cushions the brain, provides buoyancy, and delivers optimal conditions for neurologic function. It is located in the:
Ventricles (left lateral, right lateral, third, and fourth)
Cisterns around the brain
Subarachnoid space in brain and spinal cord
What regions of the brain are NOT protected by the blood-brain-barrier?
The blood brain barrier separates the CSF from the plasma. It has tight junctions that restrict pass of large molecules and ions.
The BBB is not present at the chemoreceptor trigger zone, posterior pituitary gland, pineal gland, choroid plexus, and parts of the hypothalamus.
What is the normal volume and specific gravity of CSF?
CSF volume = 150 mL
Specific gravity = 1.002 - 1.009
Describe the production, circulation, and absorption of CSF.
CSF production: Ependymal cells of the choroid plexus at a rate of 30 mL/hr
Circulation: Remember - Love My 3 Silly 4 Lorn Magpies (match to image)
Reabsorption: Venous circulation via the arachnoid villi in the superior sagittal sinus.
What is the formula for cerebral blood flow? What are the normal values for global, cortical, and subcortical flow?
What are the 5 determinants of cerebral blood flow?
- Cerebral metabolic rate for oxygen (CMRO2)
- Cerebral perfusion pressure
- Venous pressure
- PaCO2
- PaO2
What is the normal value for CMRO2? What factors cause it to increase? To decrease?
CMRO2 describes how much O2 the brain consumes per minute. The reference value is 3.0 – 3.8 mL/O2/100g brain tissue/min.
Decreased by hypothermia (7% per 1 degree decrease), halogenated anesthetics, propofol, etomidate, and barbiturates.
Increased by hyperthermia, seizures, ketamine, and nitrous oxide.
What is the formula for cerebral perfusion pressure? What is normal?
CPP = MAP - ICP (or CVP) whichever is higher
The cerebral vasculature autoregulates its resistance (vessel diameter) to provide a constant cerebral perfusion pressure of 50 – 150 mmHg.
This ensures a relatively stable blood flow and confers protection against swings in blood pressure.
Autoregulation is influenced by products of local metabolism, myogenic mechanisms, and autonomic innervation.
Notice that 50 – 150 is cerebral perfusion pressure and NOT mean arterial pressure. This is an important point. To ensure a CPP of 50 mmHg, MAP must be 60 – 65 mmHg if ICP is in the normal range of 10 – 15 mmHg. If ICP is elevated, cerebral perfusion requires a higher mean arterial pressure.
What are the consequences of a CPP that exceeds the limits of autoregulation (too high and too low)?
List 4 conditions that reduce CPP as a function of increased venous pressure.
A high venous pressure decreases cerebral venous drainage and increases cerebral volume. This creates a backpressure to the brain that reduces the arterial/venous pressure gradient (MAP – CVP).
Conditions that impair venous drainage include:
Jugular compression secondary to improper head positioning
Increased intrathoracic pressure secondary to coughing or PEEP
Vena cava thrombosis
Vena cava syndrome
What is the relationship between PaCO2 and CBF? What physiologic mechanism is responsible for this?
There is a linear relationship between PaCO2 and CBF.
The pH of the CSF around the arterioles controls cerebral vascular resistance.
At a PaCO2 of 40 mmHg, CBF is 50 mL/100 g brain tissue/min.
At what PaCO2 does maximal cerebral vasodilation occur? How about maximal cerebral vasoconstriction?
For every 1 mmHg increase (or decrease) in PaCO2, CBF will increase (or decrease) by 1 – 2 mL/100g brain tissue/min.
Maximal vasodilation occurs at a PaCO2 of 80 – 100 mmHg.
Maximal vasoconstriction occurs at a PaCO2 of 25 mmHg.
What is the relationship between CMRO2 and CBF?
As a general rule:
Things that increase the amount of O2 the brain uses (CMRO2) tend to cause cerebral vasodilation (increased CBF). Examples include hyperthermia or ketamine.
Things that decrease the amount of O2 the brain uses (CMRO2) tend to cause cerebral vasoconstriction (decreased CBF). Examples include hypothermia, propofol, and thiopental.
Halogenated anesthetics are an exception - the decouple the relationship between CMRO2 and CBF. Said another way, they reduce CMRO2, but they cause cerebral vasodilation. This explains why a patient with intracranial hypertension is better served with TIVA.
How do acidosis and alkalosis affect CBF?
Respiratory acidosis increases CBF.
Respiratory alkalosis decreases CBF.
Metabolic acidosis or alkalosis do not directly affect cerebral blood flow. This is because H+ does not pass through the blood brain barrier. A compensatory change in minute ventilation can, however, affect CBF.
How does PaO2 affect CBF?
A PaO2 below 50 – 60 mmHg causes cerebral vasodilation and increases CBF.
When PaO2 is above 60 mmHg, it does not affect cerebral blood flow.
What is the normal intracranial pressure? What values are considered abnormal?
Intracranial pressure is the supratentorial CSF pressure.
Normal ICP is 5 - 15 mmHg.
Cerebral hypertension occurs if ICP > 20 mmHg.
When is ICP measurement indicated?
What is the gold standard for measurement?
ICP measurement is indicated with a Glasgow Coma Scale score < 7.
An intraventricular catheter is the gold standard for ICP measurement. ICP can also be measured with a subdural bolt or a catheter placed over the convexity of the cerebral cortex.
List the signs and symptoms of intracranial hypertension.
- Headache
- N/V
- Papilledema (swelling of the optic nerve)
- Focal neurologic deficit
- Decreased LOC
- Seizure
- Coma
Discuss the Monroe-Kellie hypothesis.
- The brain lives in a rigid, bony box. Within this box, there are 3 components: brain, blood, and CSF.
- The Monroe-Kellie hypothesis describes the pressure-volume equilibrium between the brain, blood, and CSF within the confines of the cranium. It says that an increase in one of the components must be countered with a decrease in one or both of the others. If not, then pressure inside the cranium will rise.
What is Cushing’s triad? What is the clinical relevance of this reflex?
Cushing’s triad indicates intracranial hypertension. It includes:
- Hypertension
- Bradycardia
- Irregular respirations
Increased ICP reduces CPP. In an effort to preserve cerebral perfusion, blood pressure increases. Hypertension activates the baroreceptor reflex, leading to bradycardia. Compression of the medulla causes irregular respirations.
Name 4 areas where brain herniation can occur.
Brain herniation can occur at any of these 4 locations:
- Herniation of the cingulate gyrus under the falx.
- Herniation of contents over the tentorium cerebelli (transtentorial herniation).
- Herniation of the cerebellar tonsils through the foramen magnum.
- Herniation of contents through a site of surgery or trauma.
How does hyperventilation affect CBF? What is the ideal PaCO2 to achieve this effect?
CO2 dilates the cerebral vessels → ↓ cerebral vascular resistance → ↑ CBF → ↑ ICP.
Hyperventilation (PaCO2 30-35 mmHg) constricts the cerebral vessels → ↑ cerebral vascular resistance → ↓ CBF → ↓ ICP.
Lowering PaCO2 < 30 mmHg increases the risk of cerebral ischemia due to vasoconstriction and shifting the oxyhemoglobin dissociation curve to the left (this reduces oxygen offloading).
How do nitroglycerine and nitroprusside affect ICP?
These agents are cerebral vasodilators. By increasing CBF (volume of blood in the brain), they increase ICP.
How does head position affect ICP?
Head elevation > 30 degrees facilitates venous drainage away from the brain.
Neck flexion or extension can compress the jugular veins, reduce venous outflow, increase CBV, and increase ICP.
Head down positions increase CBV and ICP.
How does mannitol reduce ICP?
What problems can arise when mannitol is used in this way?
Osmotic diuretics (mannitol 0.25 - 1.0 g/kg) increases serum osmolarity and “pulls” water across the blood brain barrier towards the bloodstream.
- If the blood brain barrier is disrupted, mannitol enters the brain and promotes cerebral edema!
- Mannitol transiently increases blood volume, which can increase ICP and stress the failing heart.
Describe the anterior and posterior circulation of the brain. Where do these pathways converge?
The cerebral circulation can be divided into 2 separate circulations: anterior and posterior. They converge at the circle of Willis.
Anterior Circulation
- The internal carotid arteries supply the anterior circulation. They enter the skull through the foramen lacerum.
- Aorta → Carotid a. → Internal carotid a. → Circle of Willis → Cerebral hemispheres
Posterior Circulation
- The vertebral arteries supply the posterior circulation. They enter the skull through the foraman magnum.
- Aorta → Subclavian a. → Vertebral a.→ Basilar a. → Posterior fossa structures and cervical spinal cord
Describe the anatomy of the circle of Willis.
The anterior and posterior circulations converge at the circle of Willis. The primary function of the circle of Willis is to provide redundancy of blood flow in the brain. If one side of the circle becomes occluded, then the other side should theoretically be able to perfuse the affected areas of the brain.
Which population of stroke patients should receive a thrombolytic agent?
The type of CVA must be determined prior to treatment, because a thrombolytic should NOT be given to a patient with hemorrhagic stroke. Since the etiology of CVA cannot be determined by clinical criteria alone, the patient should receive an emergent non-contrast CT.
- If treatment can begin < 3 hours after the onset of symptoms, the patient with an ischemic CVA should receive an intravenous thrombolytic such as recombinant tissue plasminogen activator (tPA).
- Aspirin is an acceptable alternative if tPA cannot be administered.
What is the relationship between hyperglycemia and cerebral hypoxia?
During cerebral hypoxia, glucose is converted to lactic acid. Cerebral acidosis destroys brain tissue and is associated with worse outcomes. Monitor serum glucose and treat hyperglycemia with insulin.
Think about this when administering IV fluids that contain dextrose.
In the context of cerebral aneurysm, how is transmural pressure calculated?
An increased transmural pressure predisposes the aneurysm to rupture. As the vessel bursts, blood flows into the subarachnoid space.
We like to think of MAP as the pressure pushing outwards against the aneurysmal sac and ICP as the counter pressure that pushes against it. In essence, ICP creates a tamponade effect. Using this model, it’s easy to see that the risk of rupture is increased by hypertension and/or an acute reduction in ICP (opening of the dura).
What is the most common clinical finding in a patient with subarachnoid hemorrhage? What are the other s/sx?
The most common in a patient with SAH is an intense headache that is often described as the “worst one in my life.”
Consciousness is lost about 50% of the time, and other s/sx include focal neurologic deficits, N/V, photophobia, and fever. Meningismus (signs of meningitis) occurs as blood spreads throughout and irritates the subarachnoid space. Furthermore, blood can block CSF flow, causing obstructive hydrocephalus and increasing ICP.
What is the most significant source of morbidity and mortality in the patient with SAH?
Cerebral vasospasm is a delayed contraction of the cerebral arteries. It can lead to cerebral infarction and is the most significant source of morbidity and mortality in the patient with SAH.
Free hemoglobin that is in contact with the outer surface of the cerebral arteries increases the risk of vasospasm. Indeed, there is a positive correlation between the amount of blood observed on CT and the incidence of vasospasm.
How do you treat the patient with an intracerebral bleed who is on warfarin?
Warfarin can be reversed with FFP, prothrombin complex concentrate, and/or recombinant factor VIIa.
Vitamin K is not the best option for acute warfarin reversal.
When is the incidence of cerebral vasospasm?
When is it most likely to occur?
It occurs in about 25% of patients following SAH
and is most likely 4 - 9 days following SAH.
What is the treatment for cerebral vasospasm?
Triple H therapy (hypervolemia, hypertension, and hemodilution to Hct 27 - 32%) is the standard of care for vasospasm following SAH. Liberal hydration supports blood pressure and CPP. It also creates a state of hemodilution, which reduces blood viscosity and cerebrovascular resistance. Together these improve cerebral blood flow.
Nimodipine is the only calcium channel blocker shown to reduce morbidity and mortality associated with vasospasm. Interestingly, it does not actually relieve the spasm, but instead it increases collateral blood flow.
During endovascular coil placement for a cerebral aneurysm, the aneurysm ruptures. What is the best treatment at this time?
Patients who undergo endovascular coiling require heparinzation during the procedure.
If the aneurysm ruptures during the procedure, you should give protamine (1 mg of protamine per 100 U of heparin administered). MAP should be lowered into the low/normal range.
While it wasn’t cited in our references, adenosine can be given to temporarily arrest the heart, so the interventional radiologist can control the bleeding.
Be able to calculate the Glasgow coma scale.
The GCS provides an objective assessment of neurologic status. A GCS < 8 is consistent with traumatic brain injury.
Compare and contrast the 5 types of seizures.
Compare and contrast the 5 types of seizures.
Describe the pathophysiology of Parkinson’s disease.
In the patient with Parkinson’s disease, the dopaminergic neurons in the basal ganglia are destroyed.
What surgical procedure presents the most significant risk of ION? What are other procedure and patient risk factors?
ION is most common after spinal surgery in the prone position.
Discuss the blood flow to the spinal cord.
The spinal cord is perfused by:
- 1 Anterior spinal artery (anterior 2/3 of spinal cord)
- 2 Posterior spinal arteries (posterior 1/3 of spinal cord)
- 6 – 8 Radicular arteries
Envision the anatomy of the spinal cord and spinal nerve in cross section.
The spinal cord links the peripheral nerves to the brain.
- Sensory neurons from the periphery via the dorsal nerve root.
- Motor and autonomic neurons exit via the ventral nerve root.
Discuss the presentation and pathophysiology of autonomic hyperreflexia.
The classic presentation of autonomic hyperreflexia is hypertension and bradycardia.
Stimulation below the level of SCI triggers sympathetic reflex arc that creates a profound degree of vasoconstriction below the level of injury. This activates the baroreceptor reflex in the carotid bodies, which slows the heart rate. The body attempts to reduce afterload with vasodilation above the level of injury.
Other signs and symptoms include:
- Reflex vasodilation above the level of spinal cord injury → nasal stuffiness
- Hypertension → headache and blurred vision
- Malignant hypertension → stroke, seizure, left ventricular failure, dysrhythmias, pulmonary edema, and/or myocardial infarction.
Describe the pathophysiology of myasthenia gravis.
Myasthenia gravis is an autoimmune disease. IgG antibodies destroy post-junctional, nicotinic, acetylcholine receptors at the neuromuscular junction. Although Ach is present in sufficient quantity, there aren’t enough receptors to translate the extracellular signal into an intracellular response. This manifests as skeletal muscle weakness.
A key feature of myasthenia gravis is skeletal muscle weakness that becomes worse later in the day or that develops with exercise. Periods of rest allow for recovery of skeletal muscle function.
Describe the pathophysiology of Eaton-Lambert syndrome.
Eaton-Lambert syndrome is caused by IgG mediated destruction of the presynaptic voltage-gated calcium channel at the presynaptic nerve terminal.
When the action potential depolarizes the nerve terminal, Ca+2 entry into the presynaptic neuron is limited, thereby reducing the amount of Ach that is released into the synaptic cleft.
The postsynaptic nicotinic receptor is present in normal quantity and functions normally.
Compare and contrast myasthenia gravis to Eaton-Lambert syndrome in terms of pathophysiology, common co-morbidities, and response to neuromuscular blockers/reversals.
Describe the pathophysiology of Guillain-Barre syndrome.
Guillain-Barre Syndrome (acute idiopathic polyneuritis) is characterized by an immunologic assault on myelin in the peripheral nerves. The action potential can’t be conducted, so the motor endplate never receives the incoming signal.
It usually persists for ~ 2 weeks and ends with full recovery in ~ 4 weeks.
What drugs should be avoided in the patient with each type of familiar periodic paralysis? How about temperature?
Acetazolamide is the treatment for both forms of this disease. It creates a non-anion gap acidosis, which protects against hypokalemia. It also facilitates renal potassium excretion, which guards against hyperkalemia.
*Avoid hypothermia for both hypo- and hyperkalemic periodic paralysis!
Detail the functions of the following receptors in skeletal muscle: nicotinic, dihydropyridine, ryanodine, and SERCA2. Which is dysfunctional in the patient with malignant hyperthermia?
When the T-tubule is depolarized (Ach binds to nicotinic receptor at the NMJ), extracellular Ca+2 enters the myocyte via the dihydropyridine receptor at the T-tubule.
This activates the defective ryanodine receptor (RYR1), which instructs the sarcoplasmic reticulum to release way too much calcium into the cell. You can think of the RyR1 receptor as a Ca+2 faucet that can’t be turned off. Not only is there more Ca+2 to engage with the contractile elements, but the cell attempts to return the excess Ca+2 to the SR via the SERCA2 pump. Both processes consume a substantial amount of ATP, increase oxygen consumption, and increase CO2 production.
When the skeletal myocyte consumes all of its ATP, there is no ATP available to maintain the integrity of cell membranes. As a consequence, they break down and intracellular components (myoglobin and K+) are released into the systemic circulation.
What is the most sensitive indicator of MH?
What is the time course of the other s/sx?
The most sensitive indicator is an EtCO2 that rises out of proportion to minute ventilation. MH can occur as late as 6 hours after exposure to a triggering agent.
What is the Cobb angle, and what is its significance?
The Cobb Angle describes the magnitude of the spinal curvature.
Describe Cobb angle and its significance?
Contrast the early and late complications of scoliosis.
Scoliosis alters thoracic geometry, which compresses the lungs and creates a restrictive ventilatory defect. One side of the thorax becomes smaller than the other.
List 3 ways rheumatoid arthritis affects the airway.
What is the most common airway complication of rheumatoid arthritis? What is its clinical significance?
Atlantoaxial subluxation is the most common airway complication of RA.
This is due to weakening of the transverse axial ligament, which allows the odontoid to directly compress the spinal cord at the level of the foramen magnum. The patient is at risk for quadriparesis or paralysis.
As an aside, patients with Down syndrome are also at risk for AO subluxation.
Using a systems approach, list the complications of rheumatoid arthritis.
airway,pulm, cardiac, heme
Using a systems approach, list the complications of rheumatoid arthritis.
Using a systems based approach, list the complications of systemic lupus erythematosus.
SLE is a disease that targets young women (~1:1000). The most common problems of SLE are polyarthritis and dermatitis. Arthritis can affect any joint, but it generally does not involve the spine.
Only 33 – 50% of these patients develop the malar “butterfly” rash.
