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184 Cards in this Set
- Front
- Back
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Ach acts at what receptors before its hydrolysis by AchE?
|
nicotinic
muscarinic |
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|
how many receptors does Ach act on before hydrolysis?
|
1
|
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where is AchE located?
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in the synaptic junctionperipherally and in synaptic cleft centrally
on RBCs where function is unknown |
|
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pseudocholinesterase is found where?
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plasma
glial cells |
|
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what is the true substrate of pseudocholinesterase?
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butyrocholine
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all of the therapeutically useful cholinsterases inhibit what?
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AchE
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pseudocholinesterase is more sensitive to organophosphates or AchE?
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organophosphates
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organophosphate compounds are irreversible or reversible?
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irresversible
|
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in cases of organophosphate intoxication, what is the most effect enzyme?
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plasma pseudocholinesterase inhibit 100%
RBC AChE inhibit 50% |
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anionic site on Ache binds what?
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the choline moiety
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esteratic site (active site) of AchE binds:
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carbonyl carbon of Ach
|
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Ach breakdown by AchE takes how long?
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extremely rapid-microseconds
|
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drugs that compete with Ach for binding at the anionic or esteratic site cause:
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AchE inhibition
buildup of Ach at receptor site |
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can choline act as a AchE inhibitor?
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yes but a weak one
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some AchE inhibitors positively charged, act directly on nicotinic receptor site to produce:
|
positive agonist action
|
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Nicotinic receptors at motor endplate region appear more sensitive to agonist action of positively charged AChE inhibitors than nicotinic receptors on________
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ganglia or adrenal medulla
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Name the reversible AchE inhibitors
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Neostigmine
Edrophonium Pyridostigmine Physostigmine Tacrine Donepezil |
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Name the irreversible AchE inhibitors
|
Echothiophate
DFP diisopropyl flourophosphate |
|
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reversible Ache inhibitors compete with ACh binding to anionic and esteratic site by________ esteratic site
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carbamylating
form stronger bonds than Ach take longer the breakdown |
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what is not hydrolyzed by AchE but competes with ACh for binding to both esteratic and anionic sites -very short acting and rapidly excreted
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edrophonium
|
|
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what are the properties of irreversible Ache inhibitors?
|
1. phosphorylate esteratic site for 2 wks so new AChE must be synthesized to break Ach down
2. can alter structure of AchE so that it wont hydrolyzed ACh as well (aging of AChE) 3. extremely dangerous compounds should not be taken parenterally 4. kill by causing respiratory arrest- paralyze diaphragm and intercostal muscles by building up Ach at nictonic receptors to high enough levels that nicotinic receptors are desensitized |
|
|
SOME irreversible AchE inhibitors can cause:
|
neurotoxicity - involve ataxia, muscle paralysis, demyelination, appears 8-14 days after drug exposure
|
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reversible Ache inhibitors compete with ACh binding to anionic and esteratic site by________ esteratic site
|
carbamylating
form stronger bonds than Ach take longer the breakdown |
|
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what is not hydrolyzed by AchE but competes with ACh for binding to both esteratic and anionic sites -very short acting and rapidly excreted
|
edrophonium
|
|
|
what are the properties of irreversible Ache inhibitors?
|
1. phosphorylate esteratic site for 2 wks so new AChE must be synthesized to break Ach down
2. can alter structure of AchE so that it wont hydrolyzed ACh as well (aging of AChE) 3. extremely dangerous compounds should not be taken parenterally 4. kill by causing respiratory arrest- paralyze diaphragm and intercostal muscles by building up Ach at nictonic receptors to high enough levels that nicotinic receptors are desensitized |
|
|
SOME irreversible AchE inhibitors can cause:
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neurotoxicity - involve ataxia, muscle paralysis, demyelination, appears 8-14 days after drug exposure
|
|
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what are the therapeutic uses of AChE inhibitors?
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1. tx of GI bladder atony
2. glaucoma- wide and narrow angle 3. myasthenia gravis - tx and diagnosis 4. terminate effect of an overdose of a curare like a competitive blocker 5. terminate attack of supraventricular tachycardia |
|
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neostigmine
|
due to positive charge will not cross BBB--> does not cause CNS effects
hydrolyzed to edrophonium by AChE duration of action: 2-4 hrs good drug for tx of paralytic ileus or bladder atony can be used for wide and narrow angle glaucoma was the drug of choice for tx of myasthenia gravis |
|
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autoimmune diseases in which body produces antibodies directly against nicotinic receptor at motor endplate of neuromuscular junction
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myasthenia gravis
80% of nicotinic receptors may be occupied with antibodies so Ach cant |
|
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what in myasthenia gravis correlates with severity of disease?
|
bungarotoxin
|
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do the antibodies (in MG) recognize nicotinic receptors on ganglia or adrenal medulla?
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NO
|
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what is the therapeutic approach to reversible AChE inhibitors?
|
buildup Ach at motor endplate and enable excess Ach to bind to receptors not occupied by antibodies
*Ach can then interact with more than one receptor more than on time to increase endplate potential |
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what is sometimes used if AChE inhibitors are not working?
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steroids
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what is sometimes done if thymic abnormalities exist and AchE inhibitors are not working?
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thymectomy
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a very rare disease that involves skeletal muscle weakness but has a different etiology
person produces antibodies directed against Ca2+ channel mediating Ach release from motor nerve terminal |
Myathenic syndrome = lambert eaton
|
|
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what is used to treat Lambert Eaton?
|
Guanidine
|
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how do you differentiate Lambert Eaton from MG?
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MG produces alpha-bungarotoxin
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what is considered the drug of choice for tx of myasthenia gravis?
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pyridostigmine
|
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what are the properties of pyridostigmine
|
positively charged and have longer duration of action than neostigmine
duration of action: 3-6 hrs absorbed better than neostigmine fewer side effects than neostigmine |
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what can be used to tx overdose of b-tubocurarine like drug
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edrophonium
|
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what can be used to treat supraventricular tachycardia? give a specific drug
|
edrophonium
|
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what drug has the following properties?
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competitively binds to both esteratic and anionic sites
very short acting - 5min not hydrolyzed by AchE rapidly cleared by kidneys |
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what is the drug of choice for diagnosis of myasthenia gravis?
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edrophonium
|
|
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what drug will cause immediate improvement in muscles strength upon IV injection?
|
endrophonium
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what drug is mainly used in eye in conjunction with pilocarpine for treatment of narrow angle glaucome until iridectomy can be done?
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physostigmine - not charged so will cross BBB and cause CNS effects
|
|
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what can be used as an antidote for atropine intoxication?
|
physostigmine
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what drug is approved for tx of Alzheimer's disease but only effective in about 20% of pts
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Tacrine (Cognex) - reversible AChE inhibitors that crosses the BBB and increases ACh levels centrally
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what is the 2nd drug to be approved for Alzheimer's
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Donepezil (Aricept)
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what drug has a high degree of selectivity for AChE in the CNS and little peripheral activity?
|
Donepezil (Aricept)
exhibits less hepatotoxicity than tacrine |
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what drug is positively charged, long acting, only used topically in eye for mainly wide angle glaucome-but other drugs are better
|
Echothiophate
|
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what organophosphate used as an insecticide
causes delayer neurotoxicity 8-14 days after drug exposure? |
Mipafox
|
|
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is there a drug antidote for delayed neuotoxicity?
|
NO
|
|
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what drug:
1. pulls organophosphate off esteratic site of AChE 2. must be given rapidly to prevent aging of AChE 3. work especially well at the NMJ |
Pralidoxime
|
|
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what blocks muscarinic effects of excess salivation, bronchoconstriction and bronchiole secretions caused by inhibition of AChE at muscarinic receptor sites
|
atropine
|
|
|
atropine is needed for tx for myasthenic gravis for how long?
|
2 weeks bc side effects of AChe inhibitors dissipate
|
|
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Is atrphine charged? cross BBB?
|
not charged
will cross BBB |
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Arrival of action potential at nerve terminal enhances what?
|
Ca2+ influx through channels
triggers ACh release from synaptic vesicles |
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action potential sweeps down motor nerve terminal and its propagation is dependent on what ion influx?
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Na+
|
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what causes positively charged ions to enter open channels
|
Ach diffuses across synaptic junction and acts on nicotinic receptors
|
|
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increased influx of what ions will lead to muscle APs?
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Na+ and K+
|
|
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excitation in muscle tissue spreads via a:
|
transverse tubular system
|
|
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what filaments slide together with the help of Ca2+ released from sarcoplasmic reticulum to cause muscle contraction?
|
actin and myosin
|
|
|
drug that chelate Ca2+
|
aminoglycoside antibiotics
tetracycline |
|
|
drugs which chelate Ca2+ will reduce what?
|
prejunctional ACh release
potentially can interact with drugs which competitively block nicotinic receptor at motor endplate |
|
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chelating Ca2+ in muscles and prevent Ca2+ release from SR will:
|
reduce muscle contraction postjunctionally (dantrolene)
|
|
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nicotinic receptor antagonists are mainly used to produce:
|
muscle relaxation during general anesthesia so less anesthetic is required
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2 basic types of neuromuscular blocking agents
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competitive blockers-non-depolarizing
depolarizing neuromuscular blockers |
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competitive blockers-non-depolarizing
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compete with ACh at nicotinic receptor and act strictly as ACh antagonist when producing skeletal muscle relaxation
|
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examples of competitive blockers-non-depolarizing
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1. reversible Ache agent: neostigmine or edrophonium will override their blockade
2. prototype is tubocurarine |
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depolarizing neuromuscular blockers do what?
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agonists which initially cause persistent depolarization --> receptor desensitization
|
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depolarizing neuromuscular blockers initially produces
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muscle fasciculations prior to muscle relaxation
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depolarizing neuromuscular blockers elevate what?
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K+ plasma levels
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the prototype of depolarizing NM blockers is
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succinylcholine
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the prototype of competitive-blockers nondepolarizing
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d-tubocurarine
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d-tubocurarine lowers
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blood pressure by releasing histamine --> vasodilation
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d-tubocurarine causes some blockade of
|
ganglionic transmission through sympathetic division of ANS
removing sympathetic tone to arterioles and veins |
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pancuronium causes what cardiovascular effect?
|
increase in blood pressure
|
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vecuronium causes
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almost no histamine release
causes tachycardia |
|
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succinylcholine causes
|
releases vasodilator histamine
tends to slow heart rate reduces effectiveness of digitalis |
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succinylcholine should not be taken with what drugs?
why? |
digitalis-like drugs that compete with K+ to increase ventricular contraction or diuretics that lower plasma K+ levels
|
|
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how long is succinylcholine's duration of action?
|
about 5 minutes
|
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what drugs release histamine?
|
d-tubocurarine
succinylcholine cause bronchoconstriction dangerous to asthmatics |
|
|
nicotinic receptor antagonists can have adverse effects on respiration by
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causing respiratory paralysis by either antagonizing action of ACh at motor endplate region of diaphragm and intercostal muscles
or by causing receptor desensitization |
|
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succinylcholine elevates what ion?
it can also trigger an attack of: |
elevate plasma K+ levels
trigger attack of malignant hyperthermia Ca2+ levels greatly elevated |
|
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succinylcholine can do what in the eyes?
|
increase intraocular pressure and should not be used in patients with narrow angle glaucoma
|
|
|
competitive neuromuscular blockers are
|
d-tubocurarine
pancuronium vecuronium |
|
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what drug:
rarely used because it causes cardiovascular difficulties and releases histamine causes skeletal muscle paralysis can override its blockade by AChE inhibitor broken down if given orally so must be given by IV duration of action 60-80 min only used as a surgical adjunct during general anesthesia |
d-tubocurarine
|
|
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fairly long acting competitive blocker
doesnt release much histamine better drug used in asmathics and cardiovascular probes doesnt cause much ganglionic blockade |
pancuronium
|
|
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duration of action intermediate
no ganglionic blockage or histamine release can cause tachycardia can be dangerous in hyperthyroid patient sensitized to catcholamines |
vecuronium
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|
|
the only depolarizing blocking drug used
agonist produces skeletal muscle relaxation very short duration of action due to breakdown by pseudocholinesterase mainly used in short term procedures releases histamine--> reduce BP causes bradycardia elevates K+ in plasma causes prolonged apnea in patients with atypical pseudocholinesterase no drug antidote for overdose more prone to cause malignant hyperthermia than other skeletal muscle relaxants |
succinylcholine
|
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when using d-tubocurarine like competitive neuromuscular blocker, why reduce anesthetics?
|
general anesthetics which stabilize postjunctional membrane (halothane isoflurane) and make depolarixation at nicotinic receptor more difficult
|
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what reduces prejunctional release of ACh by chelating Ca2+?
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aminoglycoside antibiotics (neomycin and kanamycin)
tetracycline less ACh arrives at nicotinic receptor for d-tubocurarine like drug to block therefore: reduce dose of competitive blocker if used as a surgical adjunct in pt taking one of these antibiotics |
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antidotes can be given to counteract what drugs?
|
d-tubocurarine
pancuronium vecuronium |
|
|
what inhibits AChE
builds up ACh in synaptic junction and overrides the competitive blockade? |
neostigmine
|
|
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there is no drug antidote for what drug?
|
succinylcholine
neostigmine will actually worsen effects |
|
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what exerts its effect by desensitizing nicotinic receptors to ACh?
|
succinylcholine
An AChE inhibitor will increase amount of ACh in the junction further desensitizing the receptors |
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name the contraindication of NM blockers
|
asthma-d-tubocurarine and succinylcholine
narrow angle glaucome and succinylcholine hyperthyroid condition and d-tubocurarine/vecuronium |
|
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what drug act on skeletal muscle to produce relaxation?
|
Dantrolene
Botulinum Cyclobenzaprine - acts centrally |
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what drug acts projunctionally to reduce ACh release
|
Botulinum
|
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how does dantrolene cause muscle relaxation?
|
reduce IC Ca2+ postjunctionally in skeletal muscle by reduce Ca2+ release from SR through binding and blocking ryanodine receptor channel
|
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general anesthetics + succinylcholine may causes what in surgery patients?
|
malignant hyperthermia
|
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how does dantrolene work to prevent explosive muscle contraction
|
chelates Ca2+ that is explosively released in exaggerated skeletal muscle contraction
body temp is elevated to dangerously high levels in malignant hyperthermia |
|
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how does botulinum toxon work?
|
reduces ACh release from motor nerve terminals
|
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botulinum is used in eyes to treat what
|
blepharospasm
|
|
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botulinum is used cosmetically to
|
reduce facial aging
|
|
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what is used to treat cerebral palsy spasms?
|
botulinum
|
|
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administer botulinum locally in the eye will cause
|
reduced spasmodic ocular movements
|
|
|
cyclobenzaprine is used for
|
muscle spasm
|
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why is cyclobenzaprine better than valium?
|
does not produce dependence
|
|
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cyclobenzaprine works by what mechanism?
|
unknown but blocks reuptake of NE
|
|
|
cyclobenzaprine should not be taken simultaneously with what?
|
MAO inhibitor
|
|
|
side effects of cyclobenzaprine
|
similar to tricyclic antidepressants and scopolamine
include dry mouth, drowsiness, tachycardia, blurred vision |
|
|
little weakness of cranial muscle and major weakness of limbs (opposite pattern usually seen in myasthenia)
|
slow channel syndrome
|
|
|
what causes slow channel syndrome?
|
endplate potentials and spontaneous miniature end-plate potentials are prolonged even though normal amount of cholinesterase is present
opening of Ach receptor channel is abnormally prolonged may be due to mutation that has altered the receptor to spend more time in its open state |
|
|
some patients with lung cancer have neuromuscular disorder called
|
presynaptic facilitating neuromuscular block
|
|
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what is the physiological response of lambert eaton?
|
opposite of myasthenia
gradual increase in repetitive stimulation so that the final summated AP is 2-4x the amplitude of 1st potential presence of antibodies to voltage-gated calcium channels in presynaptic terminals |
|
|
animal models with lambert eaton have evidence of loss of:
|
presynaptic active zones
|
|
|
symptoms of lambert eaton is improved by what?
|
plasmapheresis or immunosuppressive drug therapy supporting the notion that circulating antibodies are responsible for disorder
|
|
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loss of calcium channels will impair release of ACH when nerve terminals are...
|
depolarized
|
|
|
guanidine promotes the release of what?
|
ACh
|
|
|
calcium gluconate can be used to treat
|
botulism
lambert eaton |
|
|
antibodies are made against what in MG?
|
nicotinic ACh receptor --> Interfere with synaptic transmission by reducing the number of functional receptors
|
|
|
since ACH is the transmitter at NMJ, what muscles are weakened? any clinical signs of denervation or muscle atrophy?
|
skeletal muscles
cranial muscles limb muscles no known clinical signs |
|
|
weakness of MG is reversed by intravenous injection of
|
inhibitors of AChE
|
|
|
what drugs increase the duration of action of ACh, therefore compensate for reduced ACh activity in myasthenia
|
pyridostigmine
neostigmine |
|
|
in Lambert eaton, there is very little ACh released therefore the ACh receptors are:
|
SUPERSENSITIZED
|
|
|
classical myasthenia is an immunological disorder
15% of have what? |
tumor of thymus
removal of thymus improves condition |
|
|
in MG fibers, the density of ACh receptors in human muscle fibers is:
|
reduced
|
|
|
density of functional ACh receptors is reduced as detected by autoradiography using what?
|
125 I-labeled alpha-bungarotoxin
|
|
|
what drugs can reverse the weakness of muscle (ptosis caused by MG)?
|
edrophonium
pyridostigmine physostigmine |
|
|
draining lymph of MG pt from thoracic lymph ducts
|
improve symptoms
|
|
|
return of lymph fluid to MG patient
|
recreate symptoms
but not when lymphocytes are replaced |
|
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the muscle AP in MG potential has a reduced ________ compared to normal muscle
|
safety margin
|
|
|
how is the geometry of the endplate disturbed in MG pts?
|
normal infolding is reduced
synaptic cleft is enlarged both reduce synaptic transmission likelihood transmission is blocked even though the process of ACh release i normal |
|
|
what do acetylcholinesterase inhibitors do?
|
increases the possibility of their interactions with ACh receptors
|
|
|
in animal models of MG, antibodies are directed against:
|
either 2 peptide sequence of EC domain of the native receptor (the main immunogenic region located on alpha-subunit and bungarotoxin-binding site)
|
|
|
in humans, the circulating MG antibodies are usually active against
|
the main immunogenic region
they do not occupy the receptor active (agonist) site |
|
|
activation of autoimmune T lymphocytes requires 3 molecules
|
1.immunogenic peptide in ACh receptor or mimic
2. a specific class II molecule of the MHC on the APC 3. antigen specific cell receptor |
|
|
what are some molecular tx for treatment of myasthenia gravis?
|
1. use antibodies to MHC
2. administer peptides that compete with ACh receptors to block T Cells 3. use antibodies directed against T cells themselves |
|
|
it is not clear what initiates production of circulating antibodies to ACh receptor that cause myasthenia
there are 2 possibilities: |
1. persistent viral infection may alter the properties of the surface membrane making it immunogenic
2. bacterial and viral antigens may share epitopes with the ACh receptor antibodies produced against foreign organism may recognize and interfere with function of ACh receptor |
|
|
how are ACh receptors lost in MG?
|
crosslinking of ACh receptors by the antibody triggers and faciliatates th normal endocytosis and phagocytosis destruction of the receptor
causes 2-3x increase in receptor turnover rate |
|
|
are circulating antibodies found in all patients? does it correlate with severity of disease?
|
no
no |
|
|
in normal turnover of ACh receptors are randomly spaced and replaced every how many days?
|
5-7 days
|
|
|
crosslinking of antibodies facilitate normal endocytosis and phagocytotic destruction of receptors which leads to a what fold increases in receptor turnover?
|
2-3x
|
|
|
binding of the antireceptor antibody also activates a complement cascade that does what?
|
focal lysis of post synaptic membrane
primarily responsible for the alterations of postsynaptic membrane morphology observed in myasthenia |
|
|
autoimmune reaction depends on interaction of antigen (immunogenic peptide of ACh receptor):
|
an antigen-specific T cell receptor AND class II molecule of MHC expressed on APC
|
|
|
T cells become reactive against the ACh receptor and recognize the receptor in thymus
antigen-specific T cells have been detected in what organ? |
thymus
|
|
|
what are two standard therapies for MG?
|
thymectomy
anticholinesterase drugs |
|
|
what are the 2 distinct categories of MG?
|
1. acquired autoimmune form in older children and adults with ACh receptor antibodies
2. nonimmune heritable congenital form without ACh receptor antibodies |
|
|
in the heritable form of MG, what variations are there?
|
some patients have abnormalities in presynaptic terminals
others with apparent postsynaptic disorders congenital lack of cholinesterase, low numbers of ACh receptors, or alteration in ACh receptor capacity to react with ACh |
|
|
autoimmune reaction depends on interaction of antigen (immunogenic peptide of ACh receptor):
|
an antigen-specific T cell receptor AND class II molecule of MHC expressed on APC
|
|
|
T cells become reactive against the ACh receptor and recognize the receptor in thymus
antigen-specific T cells have been detected in what organ? |
thymus
|
|
|
what are two standard therapies for MG?
|
thymectomy
anticholinesterase drugs |
|
|
what are the 2 distinct categories of MG?
|
1. acquired autoimmune form in older children and adults with ACh receptor antibodies
2. nonimmune heritable congenital form without ACh receptor antibodies |
|
|
in the heritable form of MG, what variations are there?
|
some patients have abnormalities in presynaptic terminals
others with apparent postsynaptic disorders congenital lack of cholinesterase, low numbers of ACh receptors, or alteration in ACh receptor capacity to react with ACh |
|
|
what diseases shows a gradual increase in repetitive stimulation so that the final summated action potential is 2-4 times the amplitude of the first potential?
|
Lambert Eaton
|
|
|
what disease is probably due to presence of antibodies to voltage gated calcium channels in presynaptic terminal?
|
Lambert Eaton
|
|
|
loss of calcium channels in the presynaptic terminals will impair what?
|
the release of Ach when the nerve terminals are depolarized
|
|
|
how can we improve the symptoms of lambert eaton?
|
plasmpharesis
immunosuppressive drug |
|
|
what diseases impair endocytosis in presynaptic terminal?
|
myasthenic syndromes
|
|
|
what affects SNARE protein involved in vesicle fusion?
|
botulinum and tetanus
|
|
|
botulinum toxin is found to be associated with impaired what?
|
Ach release
|
|
|
you can treat botulism and LE syndrome with what agents to enhance release of ACh?
|
calcium gluconate and guanidine
|
|
|
trigeminal (motor)
|
Innervates muscles of mastication (masseter temporalis, lateral and medial pterygoids, and tensor veli palatine and tensor tympani, anterior belly of digastric and mylohyoid.
|
|
|
lesion of trigeminal (motor)
|
Interruption of motor fibers results in deviation of the jaw to the affected side. Upper motor neuron lesions usually have no signs.
|
|
|
facial (sensory)
|
general sensation to external ear -- spinal nucleus of V
taste for anterior 2/3 of tongue -- solitary nucleus (rostral part) motor to mimetic mm, platysma, stylohyoid, posterior belly of digastric, stapedius -- facial nucleus parasympathetic to lacrimal and salivery glands -- superior salivatory nucleus |
|
|
upper motor neuron lesion of facial
|
contralateral lower face
|
|
|
lower motor neuron lesion of facial
|
ispsilateral paralysis of face
hyperacusis (stapedius paralysis) ipsilateral corneal reflex absent |
|
|
glossopharyngeal IX sensory
|
spinal nucleus of V - general sensation to posterior 1/3 of tongue, middle ear, upper pharynx, eustachian tube
solitary nucleus: taste, posterior 1/3 of tongue, baro and chemoreceptors in carotid sinus and body |
|
|
glossopharyngeal IX motor
|
nucleus ambiguus - stylopharyngeus
inferior salivatory nucleus - parotid gland |
|
|
upper motor neuron lesion of IX
|
no symptoms bc bilateral innervation to nucleus ambiguus
|
|
|
LMN lesion of IX
|
ipsilateral loss of gag reflex (loss of sensation on upper pharynx)
|
|
|
vagus (sensory)
|
spinal nucleus of V: general sensation to lower pharynx, larynx, esophagus, auditory canal, tympanic membrane
nucleus ambiguus: pharyngeal muscles/cricothyroid, striated muscles of esophagus dorsal motor nucleus of X: parasympathetic to smooth and cardiac muscle and secretomotor to glands solitary nucleus - taste for epiglottis baro/chemoreceptors in aortic sinus and body, viscera of thorax and abdomen |
|
|
UMN vagus lesion
|
no symptoms
there is bilateral innervation to nucleus ambiguus and dorsal motor X |
|
|
LMN vagus lesion
|
ipsilateral paralysis of soft palate, pharynx, larynx, hoarsness, difficult in swallowing
|
|
|
spinal accessory (motor)
|
nucleus ambiguus - muscles of palate, intrinsic muscles of larynx (distributed with br of vagus)
anterior gray spinal cord C1-C6 (lateral part) --SCM and upper part of trapezius |
|
|
UMN lesions - accessory
|
paresis (weakness) of SCM and trapezius
|
|
|
LMN lesions - accessory
|
ipsilateral paralysis of muscles
|
|
|
hypoglossal nucleus
|
intrinsic and extrinsic muscles:
genioglossus, hyoglossus, styloglossus of the tongue |
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UMN lesion of XII
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spastic paralysis of contralateral tongue muscles
upon protrusion, tongue will deciate away from side of lesion |
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LMN lesion of XII
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flaccid paralysis of ipsilateral tongue
upon protrusion, tongue will deviate towards the side of lesion; atrophy |
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thrombosis of what artery causes locked in syndrome?
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basilar artery (ventral pons)
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Patients have intact cognitive function and are awake, with eye opening and normal sleep-wake cycles. They can hear and see. However, they cannot move their lower face, chew, swallow, speak, breathe, move their limbs, or move their eyes laterally. Vertical eye movement is possible; patients can open and close their eyes or blink a specific number of times to answer questions.
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locked in syndrome
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The midbrain is susceptible to damage during abrupt blows to the head such
as is automobile accidents and those experienced by boxers. This can result in |
decerebrate posturing/rigidity or damage to the substantia nigra
resulting in Parkinson’s disease |
