APEX Unit 7: Neuro Flash Cards

Discuss the Monroe-Kellie hypothesis.

-3 Components: brain, blood, and CSF -If there is an increase or decrease in any of these components, the others must inversely adjust to maintain a baseline.

How is dantrolene formulated? -How is it prepared?

-Each vial contains 20 mg dantrolene + 3 g of mannitol → the vial must be reconstituted with preservative free water -Warming the diluent can make the process much faster

Discuss the presentation and patho of autonomic hyperreflexia

- the classic presentation of autonomic hyperreflexia is HTN and bradycardia - stimulation below the level of SCI triggers a sympathetic reflex arc that creates a profound degree of vasoconstriction below the level of injury. This activates the baroreceotors reflex in the carotid sinus, which slows the heart rate. The body attempts to reduce afterload with vasodilation above the level of injury. other s/s: - reflex vasodilation above the level of spinal cord injury= nasal stuffiness HTN = headache and blurred vision -Malignant HTN= stroke, seizure, left ventricular failure, dysrhythmias, Pulm edema, and/or myocardial infarction

Describe the pathophy of myasthenia gravis

- myasthenia gravis is an autoimmune disease. IgG antibodies destroy Post-junctional, nicotinic, acetylcholine receptor 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.

how do you tx the patient with ICH who is on clopidogrel?

- plavix, aspirin, or both can be reversed with platelet transfusion. - no evidence of reversal with recombinant factor VIIa

List 6 situations that can precipitate autonomic hyperreflexia.

- stimulation of the hollow organs ( bladder, bowel, or uterus) - bladder cath -surgery- especially cystoscopy or colonoscopy -bowel movement -cutaneous stimulation -childbirth

what does the BBB do? what region of the brain are NOT protected by the blood-brain barrier?

- the blood-brain barrier separates the csf from the plasma. it has thight junctions that restrict passage 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

Discuss the presentation of gullain-barre

A flu-like illness usually prescedes paralysis by 1-3 weeks s/s: -flaccid paralysis begins in the distal extremities and ascends bilaterally towards the proximal extremities, trunk, and face -intercoastal muscle weakness impairs ventilation -facial and pharyngeal weakness causes difficult swallowing - sensory deficits include: paraesthesias, numbness, and/or pain -autonomic dysfunction is common: tachycardia or bradycardia, HTN or hypotension, diaphorsis or anhidrosis, and orthostatic hypotension

What bedside exam can assess the integrity of the corticospinal tract? -How do you interpret it?

- the corticospinal tract is the most important motor pathway. This pathway is often referred to as the pyramidal tract. All of the other motor pathways outside of the corticospinal ( pyramidal) tract are known collectively as the extrapyramidal tract. - the babinski test is a method to test the integrity of the corticospinal tract. a firm stimulus is applied to the underside of the foot yields the following responses normal response: downward motion of all the toes upper motor neuron injury: upward extension of the big toe with fanning of the other toes. Lower motor neuron injury: no response

Detail the anesthetic management of ALS.

- there is no evidence that supports a clear benefit of any technique -Sch can cause lethal hyperkalemia. lower motor neuron dysfunction is associated w/ proliferation of postjunctional nicotinic receptors -Increased sensitivity to nondepolarizing neuromuscular blockers -Bulbar muscle dysfunction increases the risk of pulmonary aspiration -Consider postoperative mechanical ventilation

how does nitroglycerine and nitroprusside affect ICP

- these agents are cerebral vasodilators. increasing CBF ( volume of blood in the brain), they increase ICP

**tx for cerebral vasospasm?

- triple H therapy ( hypervolemia, HTN, hemodilution to HCT 27-32) - liberal hydration supports blood pressure and CPP. also supports a state of hemodilution, which reduces blood viscosity, and cerebrovascular resistance. together improve cerebral blood flow. -nimodipine only CCB to reduce morbidity and mortality. does NOT relieve spasm but instead increase collateral blood flow.

what class of drugs is used to tx alzheimer's disease? how do they interact with succ?

- tx is palliative and aims to restore the concentration of ach. This is accomplished with cholinesterase, such as tacrine, donepexil, rivstgmine, and galantamine -cholinesterase inhibitors increase the duration of action of succ. although the clinical sig of this is debatable.

which cranial nerves resides in the central nervous system? what is the implication of this?

- with the exception of the optic n ( CN2), all of the cranial nerves are part of the peripheral nervous system, this means the optic n is the only cranial nerve that is surrounded by the dura. - bc the optic nerve is part of the CNS, it is bathed by csf. If you inject LA into the optic nerve during regional anesthesia of the eye, you will have a big problem.

why are patients w/ myasthenia gravis prone to aspiration?

-Bulbar muscle weakness ( mouth and throat) manifests as difficulty handling oral secretions. This increases the risk of pulm aspirations

describe the production, circulation, and absorption of csf

-CSF production: ependymal cells of the chproid plexus at a rate of 30 ml/hr - circulation: remember Love My 3 Silly Lorn Magpies ( match to image) -Reabsorption: venous circulation via the arachnoid villi in the superior sagittal sinus

How do you treat MH?

-D/C triggering agent -Administer 100% O2 at > 10L/min -Administer dantrolene 2.5 mg/kg IV and repeat q5-10 minutes -Hyperventilate -Correct lactic acidosis with sodium bicarbonate -Treat hyperkalemia with Ca+2, dextrose/insulin -Protect against dysrhythmias -Maintain urine output -Cool the patient until the temperature drops below 38 degrees C -Monitoring coagulation ( watch fro DIC)

List 6 conditions that are NOT definitively linked to MH.

-Duchenne -becker -neuroleptic malignany syndrome -myotonia congenita -myotonia dystrophy -osteogensis imperfecta Duchenne muscular dystrophy is associated with MH-like condition characterized by rhabdomyolysis. it is possible halogentaed agents and succ can initiate this MH-like syndrome in these patients, so it is prudent to avoid these agents. Dantrolene does NOT treat this condition.

How does Head Position affect ICP

-Head elevation > 30 degrees facilities 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

-Name 4 areas where brain herniation can occur.

-Herniation of the cingulate gyrus under the falx -Herniation of the contents over the tentorium cerebelli -Herniation of the cerebellar tonsils through the foramen magnum -Herniation of contents through a site of surgery or trauma

describe the pathophysiology of ischemic optic neuropathy

-ION is a consequence of ischemia of the optic nerve. The most likely explanation is that venous congestion in the optic canal reduces perfusion pressure. increased intraabdominal and/or intrathoracic pressure can also increase intraocular pressure - ocular perfusion pressure= MAP- intraocular pressure - central retinal and posterior ciliary arteries are the highest risk because they are "watershed" areas- they lack anastomosis with other arteries. A rise in intraocular pressure can compress these vessels, which reduces oxygen to the retina.

discuss the pathophysiology of neurogenic shock

-Impairment of cardioaccelerator fibers (T1-T4) → unopposed cardiac vagal tone → bradycardia and reduced inotropy -Decreased SNS tone → vasodilation → venous pooling → decreased CO and BP -Impairment of sympathetic pathways from hypothalamus to blood vessels → inability to vasoconstrict or shiver → hypothermia *Hypothermia is the result of the inability of the cutaneous vasculature to vasoconstrictor, causing a redistribution of blood flow towards the periphery and allowing more heat to escape from the body

what surgical procedure presents the most sig risk of ION? what other procedures and patient risk factors?

- most common after spinal surgeries in prone position.

When does a patient with spinal cord injury become at risk for autonomic hyperreflexia? what factor (other than time) contributes to this risk?

- after the neurogenic shock phase ends ( 1-3 weeks), the body begins to mend itself in a pathological and disorganized way. There is a return of spinal sympathetic reflexes below the level of injury. However, without inhibitory influences that would normally come from above the level of injury, the sympathetic reflexes below the level of injury exist in an overactive state. This places the patient are risk for autonomic hypereflexia ( mass reflex) -while up to 85% of patients with injury above T6 will develop AH, it is very unlikely to occur in patients w/ an injury below T10. the higher the injury, the more intense the response

what is the definitive test for susceptibility to MH?

- anyone who has experienced MH or masseter spasm should referred for a halothane contracture test for Dx. Although this is the definitive test for Dx. It only has 80% specificity, so there is a risk of a false-negative result.

How do the patients w/ myasthenia gravis respond to NMB?

- b/c there is a reduction in number of nicotinic receptors ( type-m) at the meuromuscular junction, pts w/ myasthenia gravis have increased sensitivity to NDMB and resistance to succ. - remember that volatile anesthetics cause skeletal muscle relaxation by acting in the ventral horn of the spinal cord. In many cases, this eliminates the need for neuromuscular blockers

** what are the 5 determinates of cerebral blood flow? can you draw the chart?

- cerebral metabolic rate for oxygen ( CMRO2) - cerebral perfusion pressure -venous pressure -PaCO2 -PaO2

- Discuss the blood flow to the spinal cord?

- 1 anterior spinal artery ( anterior 2./3 of spinal cord) - 2 posterior spinal arteries ( posterior 1/3 of spinal cord) -6-8 radicular arteries

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.

List 8 consequences of too much Ca+2 inside of the skeletal myocyte.

- sustained muscle contraction - accelerated metabolic rate and rapid depletion of ATP -increased oxygen consumption -increased CO2 and heat production -mixed respiratory and lactic acidosis -sarcolemma breaks down

what is the most important radicular artery? which spinal segment does it typically enter the spinal cord?

- the artery of adamkiewicz is the most important radicular artery -along with the anterior spinal artery, the artery of adamiewickz supplies the anterior cord in the thoracolumbar region. It most commonly originates between T11-T12

what is the relationship between etomidate and seizures?

- etomidate can commonly cause myoclonus. this is not associated with icnreased EEG activity in pts that do not have epilepsy - in pts with seizure disorders, etomidate ( or methohexital or alfentanil) increases EEG activity and can be used to help determine the location of seizure foci during cortical mapping.

at what PaCO2 does maximal cebreal 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

list s/s of intracranial HTN (7)

- headache - N/V - papilledema ( swelling of the optic nerve) - decrease LOC - seizure - coma

what is the most common clinical finding in a patient with SAG? what are the other s/s?

- headache " worst one in my life" - consciousness is lost about 50% of the time, and other s/s include focal neurologic deficits, n/v, photophobia, and fever. - meningismus ( signs of meningitis) occur as blood spreads throughout and irritates the SA space. blood can block CSF flow, causing obstructive hydrocephalus and increasing ICP

describe the pathophy 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 synaptic cleft. - when the action potential depolarizes the nerve terminal, Ca+2 entry into the presynatic neuron is limited, thereby reducing the amount of Ach that is released into synaptic cleft. - The postsynaptic nicotinic receptor is present in normal quantity and functions normally.

what are 2 common ways of reducing ICP that should specifically be avoided in the patient with a traumatic brain injury?

- hyperventilation can worsen cerebral ischemia in patient with TBI. Hperventilation is only indicated as temporary measure to acutely reduce ICP - steroids worsen neurologic outcome

how does myasthenia gravis affect the pregnant mother and the fetus?

- 1/3 of women, pregnancy intensifies the symptoms of MG - Anti-AchR IgG antibodies cross the placenta and causes weakness in 15-20% of neonates. This can persist up to 2-4 weeks, which is consistent with the half-life of theAnti-AchE IgG antibodies in the neonate's circulation. These neonates may require airway management

List 4 conditions that reduce CPP as a function of increased venous pressure.

- A high venous pressure decrease cerebral venous drainage and icnreases cerebral volume. This cretes a backpressure to the brain that reduces the arterial/venous pressure gradient ( MAP- CVP) conditions that impair venous drainage: -jugular compression secondary to improper head positioning -increased intrathoracic pressure secondary to coughing or PEEP -vena cava thrombosis -vena cava syndrome

what is the normal value for CMRO2? what factors cause it to increase? to decrease?

- CMRO2 describes how much 02 the brain consumes per min. the reference value is 3.0-3.8 ml/o2/100g brain tissue/min - decreased by hypothermia ( 7% per 1 degree) halogenated aesthetics, propofol, etomidate, and barbiturates - increased by hyperthermia, seizures, ketamine, and nitrous oxide

How does hyperventilation affect CBF? what is the ideal PaCO2 to achieve this effect?

- CO2 dilates the cerebral vessels= decrease cerebral vascular resistance = increase CBF= increase ICP - hyperventilation ( Paco2 30-35 mmhg) constricts the cerebral vessels= increase cerebral vascular resistance= decrease CBF= decrease ICP - lowering PaCO2 ,30 mmhg increases the risk of cerebral ischemia due to vasoconstriction and shifting to the oxyhemoglobin dissociation curve to the left ( this reduces oxygen offloading)

what is the formula for cerebral perfusion pressure? what is normal?

- CPP= MAP-ICP ( or CVP) whatever is higher -cerebral vasculature autoregulates its resistance ( vessel diameter) to provide a constant cerebral perfusion pressure of 50-150 mmhg - autoregulation is influenced by products of local metabolism, myogenic mechanisms, and autonomic innervation

which population of stroke patients should receive a thrombolytic agent

- NOT hemmorrhagic stroke - All strokes get emergent non-contrast CT - if tx can begin , 4.5 hrs after onset of s/s, the pt 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 drugs should be avoided in patients w/ each type of familiar periodic paralysis? how about temp?

- acetezolamide is the tx for both forms of this disease. it creates a non-anion gap acidosis, which protects against hypokalemia. It also facilitates renal potassium excretion, which gaurds against hyperkalemia * avoid hypothermia for both

What is the most signifiant source of morbidity and mortality in the patients with SAH

- cerebral vasospams is a delayed contraction of the cerebral arteries. it can lead to cerebral infarction and is the msopt sig source of morbidity and mortality in the patient w/ SAH - free hgb that is in contact with the outer surface of the cerebral arteries increase the risk of vasospasm. there is a positive correlation between the amount of blood on CT and vaspospasm.

what is the most common eye complication in the perioperative period? what is the most common cause of vision loss?

- corneal abrasion is the most common eye complication - ischemic optic neuropathy is the most common cause of vision loss

what is the function of CSF, and where is it located

- cushions the brain, provides buoyancy, and delivers optimal conditions for neurologic function - located: ventricles ( left, right, third and fourth), cisterns around the brain, and Subarachnpid spaces in the brain and spinal cord.

describe the pathophysiology of Alzheimer's disease

- development of diffuse beta amyloid-rich plaques and neurofibrillary tangles in the brain. consequences of plaque formation include: - dysfunctional synaptic transmission. This is most noticeable in nicotinic Ach neurons. - Apoptosis ( programmed cell death)

How can you tell the difference between cholinergic crisis and Myasthenic crisis?

-Pyridostigmine ( and anticholinesterase) is the first-line tx for myasthenia gravis. An OD can cause a cholingergic crisus, which can include skeletal muscle weakness. Since myasthenic crisis also presents w/ skeletal muscle weakness, it can be difficult to distinguish from cholinergic crisis the Dx is made by administering 1-2 mg IV edrophonium, otherwise known as the tensilon test - if muscle weakness is made worse, then the pt has cholinergic crisis (tx= anticholinergic) -If there is an improvement in muscle strength, then the patient had an exacerbation of myasthenic symptoms ( tx= anticholinesterase, immunosupression, plasmaphersis)

How do acidosis and alkalosis affect CBF?

-Respiratory acidoses increase CBF -Respiratory alkalosis decreases CBF -Metabolic disorders do not directly affect CBF, but can lead to respiratory derangements that can. - this is because H+ does not pass through the BBB. A compensatory change in min vent can, however affect CBF

Describe the pathophy of Gullain-Barre syndrome

-also known as Acute idiopathic polyneuritis, is 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 3 weeks and ends with full recovery in 4 weeks

During endovascular coil placement for a cerebral aneurysm, the aneurysm ruptures. What is the best treatment at this time?

-coiling requires heparin. - give protamine ( 1 mg per 100 U of heparin) Map should be lowered into the low/normal range -while it wasn't cited, adenosine can be given temporarily to arrest the heart, so the IR doc can control bleeding.

Name the 12 cranial nerves.

1. Olfactory 2. Optic 3. Oculomotor 4. Trochlear 5. Trigeminal 6. Abducens 7. Facial 8. Vestibulocochlear 9. Glossopharyngeal 10. Vagus 11. Accessory 12. Hypoglossal

Discuss the pathophysiology of amyotrophic lateral sclerosis

ALS causes progressive degeneration of motor neurons in the corticospinal tract. astrocytic gliosis replaces the affected motor neurons. Both the upper as well as the Lower motor neurons are affected. - the etiology is unknown

What is the relationship between CMRO2 and CBF?

As a general rule - things that increase the amount of 02 the brain uses ( MRO2) tend to cause cerebral vasodilation ( increased CBF) Ex. hyperthermia or ketamine - Things that decrease the amount of 02 the brain uses (CMRO2) tend to cause cerebral vasoconstriction ( decreased CBF) ex. hypothermia, propofol, and thiopental halogenated anesthetics are an exception- they 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

** what is cushing Triad? what is the clinical relevance of this reflex?

Cushing triad indicates intracranial HTN. it includes: - HTN - Bradycardia - Irregular resp increased ICP reduces CPP, to preserve cerebral perfusion, blood pressure increases. HTN activates the baroreceptors reflex, leading to bradycardia. Compression of the medulla causes irregular respirations

How does dantrolene treat MH? -What are its most common side effects?

Dantrolene is classified as a muscle relaxant. it has two MOA: - it halts Ca+2 release from the RyR1 receptor -It prevents Ca=2 entry into the myocyte, which reduces the stimulus for calcium-induced release the most common side effects are muscle weakness and venous-irritation

compare the structure and function of the dorsal column w/ the spinothalamic tract

Dorsal column- medial lemniscal system - transmits mechanoreceptive sensation: fine touch, propioception, vibration, and pressure. -capable of two point discrimination- a high degree of localizing the stimulus -consists of large, myelinated, rapidly conducting fibers. -transmits sensory information faster than the anterolateral system -Think of this as a more evolved system Anterolateral system- spinothalamic tract - transmits: pain, temp, crude touch, tickle, itch, and sexual sensation -two point discrimination is not present -consists of smaller, myelinated, slower conducting fibers -think of this as more primitive system

When is ICP measurement indicated? what is the gold standard for measurement?

ICP measurement is indicated with a glasgow coma scale score equal or less than 7. - an intraventricular cath is the gold standard for ICP measurment. ICP can also be measured with a subdural bolt or a cath placed over the convexity of the cerebral cortex

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.

what is the most sensitive indicator of MH? what is the time course of the other s/s

The most sensitive indicator is an EtCO2 that rises out of proportion to MV. MH can occur as late as 6 hours after exposure to a triggering agent.

what is the incidence of cerebral vasospasm? when is it most likely to occur?

about 25% of patients following SAH, most likely 4-9 days following SAH

what is familial periodic paralysis and how can the two variants of this disease be distinguished from each other?

actu episodes of skeletal muscle weakness that is accompanied by hypo- or hyperkalemia - hypokalemic periodic paralysis: is daignosed if skeletal muscle weakness follows a glucose-insulin infusion. The patient becomes weak after the serum "k" is reduced -Hyperkalemic periodic paralysis : Id dx if skeletal muscle weakness follows oral potassium administration. the patient becomes weak after the serum K is increased.

What is tic douloureux? -What cranial nerve contributes to this problem?

also known as trigeminal neuralgia CN5, causes excruciating neuropathic pain in the face.

what is the function of the temporal lobe cortex?

auditory cortex and speech center

what is bell's palsy? what cranial nerve contributes to this problem?

bell's palsy results from injury to the facial n ( CN7) this causes ipsilatteral facial paralysis

what is the formula for cerebral blood flow? what are the normal values for global, cortical, and subcortical flow?

cerebral blood flow= cerebral perfusion pressure/ cerebral vascular resistance -Global: 45-55 ml/100g tissue/min or 15% of CO - cortical 75-80 ml/100g tissue/min -subcortical 20ml/100g tissue/min

whats the normal volume and specific gravity of csf?

csf volume: 150 ml specific gravity: 1.002-1.009

Describe the pathophysiology of Parkinson's disease.

depaminergic neurons in the basal ganglia are destroyed. too much ACH, little DA

what drugs increase the risk of extrapyramidal s/s in pts w/ parkinson's disease

drugs that antagonize dopamine should be avoided - metoclopramide -butyrophenones ( haloperidol and droperidol) -phenothiazinr (promethazine)

what is the relationship between hyperglycaemia 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 tx w/ insulin

Describe the organization of the 3 neuron

each pathway consists of 3 neurons - the first order neuron travels from the periphery to the spinal cord or brainstem -the second order neuron travels from the spinal cord or brainstem to subcortical structure -the third order neuron links the subcortical structure to the cerebral cortex

Detail the anesthetic management of the patient w/ autonomic hyperreflexia

even though the patient does not have sensation below the level of SCI, stimulation to the affected areas can elicit autonomic hyperreflexia- prevention is paramount - general or spinal anesthesia are the best options - an epidural may be used for a laboring mother, however when compared to a spinal anesthetic, an epidural does not inhibit the sacral nerve roots to the same degree - HTN is best tx w/ removal or the stimulus, deepening the anesthetic, and a rapid acting vasodilator such as nitroprusside -bradycardia can be tx w/ atropine or glyco -administration of postive chronotrope w/ vasoconstrcitive preoperties will worsen HTN - adding lidocaine jelly to the cystoscope or foley cath does NOT prevent AH - succinylcholine should be avoided for at least 6 months following SCI

in the context of cerebral aneurysm, how is transmural pressure calculated

increase transmural pressure predisposes the aneurysm to rupture. as the vessel bursts, blood flows into the subarachnoid space. - transmural pressure= MAP- ICP - We like to think of MAP as the pressure pushing outwards against the aneuysmal 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 rupture is increased by HTN and/or an acute reduction in ICP ( opening of the dura)

What is the normal intracranial pressure? what values are considered abnormal?

intracranial pressure is the supratentorial CSF pressure - normal ICP= 5-15 mmhg - cerebral HTN occurs if ICP >20 mmhg

within the temporal lobe what does the broca area do?

motor control of speech

what is the function of the frontal lobe

motor cortex

How can you differentiate neurogenic shock from hypovolemic shock?

neurogeic shock= bradycardia, hypotension, hypothermia w/ pink, warm extremities ( cutaneous vasodilation) Hypovolemic shock: tachycardia, hypotension, and cool, clammy extremities

is nitrous oxide safe in the patient with a traumatic brain injury

no. can rapidly expand pneumothorazx or cause pneumocephalus.

Identify 3 conditions that are definitively linked to MH.

only 3 co-existing deseases: - king-denborough syndrome - central core disease - multiminicore disease * some text list evans myopathy as the third disease that is definitively linked to MH. However, it's not in the books or MHAUS website

How does mannitol reduce ICP? -What problems can arise when mannitol is used this way?

osmotic diuretic ( mannitol 0.25- 1.0 g/kg) increases serum osmolarity and "pulls" water across the BBB towards the bloodstream. - if the BBB is disrupted, mannitol enters the brain and promotes cerebral edema! -mannitol transiently increase blood volume, which increases blood volume, which can increase ICP and stress the failing heart

Discuss the use of succinylcholine in the patient with spinal cord injury.

should be avoided 24 hours after injury and should not be used for at least 6 months thereafter ( some books say a year)

what is the function of the parietal lobe cortex?

somatic senosry cortex

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 - the internal carotid arteries supply the anterior circulation. they enter the skull through the foramen lacerum - Aorta- carotid A.- internal carotid A. Circile of Willis - cerebral hemisphere Posterior - The vertebral arteries supply the posterior circulation. They enter the skull through the foramen magnum - aorta- subclavian a.- vertebral a. - basilar a- posterior fossa structure and cervical spinal cord.

enision the anatomy of the spinal cord and spinal nerve in cross-section

the spinal cord linkes the peripheral nerves to the brain. -sensory neurons enter from the periphery via dorsal nerve root - motor and autonomic neurons exit via the ventral nerve root

what surgical procedure can reduce symptoms in the patient with myasthenia gravis?

the thymus gland plays a key role in MG, and thymectomy brings symptom of relief to many patients - thymectomy reduces circulating Anti-AchE IgG in most patients. -Surgical approach may be via median sterontomy or by the transcervical approach

Contrast the presentation of upper vs lower motor neuron injury.

the upper motor neuron begin in the cerebral cortex and end in the ventral horn of the spinal cord. while the lower motor neurons begin in the ventral horn and end at the neuromuscular junction - upper motor neuron injury presents with hyperreflexia and spastic paralysis -lower motor neuron injury presents with impaired reflexes and flaccid paralysis

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

within the temporal lobe what does the wernicke's area do?

understand speech

what is the function of the occipital lobe cortex

vision cortex

how do you tx the pt with an ICH who is on warfarin

warfrin can be reversed with FFP, prothrombin complex concentrate, and.or recombinant factor VIIa. - vit K is NOT best option for acute warfarin reversal.