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126 Cards in this Set
- Front
- Back
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What is the most common type of headache?
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Tension
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Where do tension type headaches usually occur?
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Frontal, temporal, and occipital areas, and the neck. Usually unilateral but may be bilateral. Accompanied by a tight band.
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What usually precipitates a tension type headache?
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Physical or psychological stress. Physical may be postural, from cervical pathology, or from staring at glare, etc
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What baseline labwork/imaging should be done with tension type headache?
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Brain MRI, CBC, CMP, ESR/CRP
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List some of the differential diagnoses of tension-type headache
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Arnold-Chiari malformation, frontal sinusitis, CNS neoplasm, chronic subdural hematoma, temporal arteritis, other intracranial pathology
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What is the treatment of temporal arteritis? When do you start this? What tests should you get.
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High dose corticosteroids (prednisone 1 mg/kg/day), with a long taper. Start upon clinical suspicion even before imaging or biopsy (tender temporal areas, bruits, concurrent polymyalgia rheumatica, which occurs about 50% of the time). Temporal artery biopsy, though this may be negative, arterial ultrasound can show halo sign, ESR/CRP can be elevated, alk phos and platelets can be elevated.
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What is the preferred treatment of tension type headache?
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NSAIDs and non-narcotics. Education
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What are the drugs of choice for tension type prophylaxis?
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Antidepressants. Amitriptyline, starting at 25 mg po nightly, increased in 25 mg increments, Trazodone 75 to 300 mg po nightly, and fluoxetine 20 to 40 mg at lunch.
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What other treatments besides oral medications may help tension type headaches?
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Biofeedback, cervical epidural or facet injections performed on a daily or weekly basis.
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Migraine headaches almost always develop before what age?
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30
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What personality type often is associated with migraine headaches?
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Meticulous, complusive, rigid, neat nature
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Ingestion of what type of foods is often associated with migraine headaches?
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Citrus, chocolate, tyramine containing foods (aged cheese, smoked or cured meats), MSG, nitrates.
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What percentage of migraineurs experience an aura prior to the migraine? How may they present? What is thought to be the etiology of an aura?
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about 20%. May be visual, auditory, or olfactory. Thought to be caused by focal ischemia of the cerebral cortex.
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Are migraine headaches uni- or bilateral?
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Classically they are unilateral (Waldman says "always unilateral" though other sources say differently), though they can change sides. They can be bilateral, however, especially without aura.
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Where is the pain typically with a migraine headache?
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Usually peri- or retro-orbital
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What are two common triggers of migraine headaches specific to women?
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Menstruation and cycling on or off OCP
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What are some symptoms of migraines that are not found in tension type headaches?
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sonophobia, photophobia, changes in appetite, mood, and libido.
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Describe three manifestations of a visual aura associated with migraines
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1) Scotoma: small blind spots/lights
2) Fortification spectrum: zigzag disruption of the visual field. Aka scintillating scotoma. 3) Loss of an entire visual field. |
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What does "migraine with prolonged aura" mean?
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Neurological dysfunction associated with a migraine headache that lasts for longer than 24 hours.
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What is "migraine with complex aura" mean? What is its main risk?
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Migraine with severe neurological deficits, such as hemiplegia, aphasia. Sometimes these deficits can be permanent.
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Is the neurological exam with a migraine normal?
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Usually yes, though it may be skewed if there is an aura.
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What is the current theory as to the etiology of migraines?
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Currently unknown though thought to have something to do with pain control mechanisms of the trigeminal nucleus.
This is most likely the superior cerebellar artery. |
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List the baseline exams/tests done for migraine
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MRI with and without gadolinium, MRA of the neck and brain, ESR/CRP, CBC/CMP, neuro exam, opthalmological exam, ear exam, check sinus pain/sx.
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List differentials of migraine headaches
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similar to tension type headaches. Include intracranial pathology like neoplasm, hydrocephalus, pseudotumor cerebri, abscess, chronic subdural hematoma. Ocular pathology like glaucoma. Temporal arteritis, sinusitis, etc
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Give examples of abortive migraine therapy and when they should be used.
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Oral: Trial of indomethacin. Sympathomimetic amines (such as isometheptene), acetominophen. Other NSAIDs like naproxen. Ergot alkaloids, triptans. Sumatriptan 25 mg po x1, repeat if necessary at 2 hours for up to 100 mg/day.
IV: intravenous lidocaine with an anti-emetic Interventional: sphenopalatine ganglion block. These should be done immediately upon onset. |
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What medications are more likely to cause an analgesic rebound headache with migraines?
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caffeine-containing meds, barbituates, ergot-amines (e.g. the drug ergotamine, part of cafergot with caffeine), triptans, and narcotics.
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What conditions should the ergot amines and triptans not be used with?
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Those susceptible to exacerbation with stimulants. Such as hypertension, CHF/CAD, PVD, etc
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What is the mainstay of migraine prophylaxis oral meds? When should this not be used?
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beta blockers. Propranolol is the favored med. 80mg a day of extended release is a common preparation. Should not be used with reactive airway disease (asthma, etc)
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What are second line prophylactic treatments for migraine headaches?
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NSAIDs, alpha-2 agonists (clonidine), valproic acid, TCAs.
Depakote (divalproex sodium) can be started at 250 mg po daily |
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What is the male to female ratio of cluster headaches? How common are these type of headaches?
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5:1. Much less common than migraines or tension. About 1/200 (0.5% of the population).
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When do cluster headaches usually come on?
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Late 30s to early 40s.
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When do cluster headaches usually come on?
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About 90 minutes after the person falls asleep. Classically when a shift worker changes schedules and when there is a seasonal change in the length of the day, such as spring or fall.
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How long do cluster headaches usually last?
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Usually about an hour. Happens 2-3 times a day and last for 8-12 weeks, though can become more chronic.
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Describe the symptoms of a cluster headache.
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unilateral, associated with lacrimation and rhinorrhea, facial flushing, retro-orbital and temporal pain and burning. "Peau d'orange skin" or orange peel skin (looks almost like a port wine stain) over the malar region, telangiectasias, deeply furrowed glabellar folds.
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What are common precipitators of cluster headaches?
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Changes in altitude, vasoactive substances like nitrates, alcohol, and histamines.
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What testing should be done for cluster headache?
What other type of headache can look like a cluster headache and what's the easiest way to differentiate this? |
Same as with migraines and tension headaches. Migraine with and without gadolinium, MRA of the head and neck, ESR/CRP, CBC/CMP, neuro and ophthalmological exam.
Chronic paroxysmal hemicrania. Very similar to CH though this should "respond absolutely" to indomethacin and NSAIDs in general. |
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What is the preferred prophylactic treatment of cluster headache?
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1) Verapamil: first line
2) Steroids: less evidence. Oral prednisone of 80 mg daily in divided doses tapered by 10 mg daily. 3) Lithium, methysergide (no longer recommended), topimirate. Dosing of lithium: starting at 300mg po at bedtime and increased to BID after two days. If no side effects are noted, it can be increased to TID. Keep it at TID for ten days, then taper downward over the next week. 3) Rhizotomy, TENs, Microvascular decompression. |
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What is the preferred treatment for cluster headaches once they've come on? |
1) Oxygen 2) Triptans 3) Consider sphenopalatine ganglion blocks |
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What is the mechanism of methysergide? What is it used for? What is it's most important side effects and hence the reason it is now used less? What are three other reasons to use methysergide.
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it is an antagonist/partial agonist at several serotonin receptors. It is used in the treatment of migraine and cluster headaches. It rarely causes retroperitoneal and retropulmonary fibrosis. It may induce left sided heart failure. It may also be used with carcinoid syndrome, serotonin syndrome, and severe diarrhea.
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What is the most common demographic of pseudotumor cerebri and what is the most common presentation?
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Overweight females aged 20-45 with a headache that increases with valsalva maneuver and is associated with a variety of other nonspecific CNS findings.
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What part of the physical exam may give clue to pseudotumor cerebri?
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The ophthalmological exam, which may show slight papilledema on fundoscopy, and visual field deficits.
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List some comorbidities/associations with the etiology of pseudotumor cerebri.
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Broadly, it is thought to be a defect in absorption of CSF. Obesity and female sex are risk factors. Use of vitamin A, corticosteroids and tetracycline are risk factors. Blood dyscrasias, anemia, and respiratory insufficiency are risk factors.
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How is the diagnosis of pseudotumor cerebri made?
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Four criteria:
1) signs and symptoms of increased intracranial pressure, including papilledema. 2) MRI of the brain showing no space occupying lesions, small to normal ventricles and empty sella sign secondary to compression of the pituitary. 3) Increased CSF pressure with lumbar puncture (greater than 25 cm H2O). 4) Normal CSF analysis with cytology, cultures, and chemistry. |
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List treatment options for pseudotumor cerebri
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1) Lumbar puncture
2) Diuretic therapy: acetazolamide (try first), furosemide, or chlorthalidone. |
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In a patient with a history of headaches who has been getting progressively more frequent headaches, what is the most likely diagnosis? What should be the workup and treatment?
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Analgesic rebound headache. Workup new symptoms with the same protocol as if this were a new pathology (MRI brain, etc). Treatment is with discontinuation of the medication. This may require inpatient hospitalization.
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What is the most common reason for trigeminal neuralgia? What are other potential pathologies?
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Torturous blood vessels compressing the trigeminal nerve root as it exits the brainstem. Acoustic neuromas, cholesteatomas, aneurysms, angiomas, and bony abnormalities may also cause it.
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What is a common comorbidity with trigeminal neuralgia? What is its percentage?
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multiple sclerosis. 2-3%
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What part of the trigeminal nerve is affected with trigeminal neuralgia?
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Typically the unilateral maxillary (V2) or mandibular (V3) branch. If it is bilateral, it is usually the same branches.
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How long does trigeminal pain usually last?
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It usually starts suddenly and lasts about two minutes.
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What testing should be done for trigeminal neuralgia
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1) MRI of the brain and sinuses with and without gadolinium to evaluate for sinus disease, demyelinating/sclerotic lesions, and compressive pathology.
2) MRA of the head and neck to evaluate for vascular compression of the trigeminal nerve 3) CBC, CMP, ESR/CRP 4) Neurological and ophthalmological exam with measurement of intraocular pressure. |
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Contrast trigeminal neuralgia pain with TMJ pain and atypical facial pain.
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Atypical facial pain, temporal arteritis, and TMJ are typical dull and aching and the patient will often rub the area. Trigeminal neuralgia pain is extremely sharp, lancinating, and sudden and the patient will do anything not to touch this area
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If a patient presents with trigeminal neuralgia before age 50, what differential disease should be strongly suspected?
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Multiple sclerosis
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What is the first line treatment for trigeminal neuralgia? What is the main danger of this treatment and what should be done to monitor it?
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Carbamazepine 100mg po bid, increased every 48 hours by 200 mg until pain relief or 1200 mg total daily. When pain relief is obtained, keep using med for at least six months. It may cause blood dyscrasias, including aplastic anemia, thus baseline and repeat CBCs must be performed to monitor this. Check frequently for rashes.
Need to check the HLA-B*1502 allele as people with this are at high risk for carbamazepine. |
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What is second line treatment for trigeminal neuralgia? What labwork should be tested with these medications?
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Gabapentin and baclofen. CMP (gabapentin is cleared renally) and both may cause hepatic toxicity.
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What are invasive therapies for trigeminal neuralgia, going from least to most invasive?
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1) Trigeminal nerve block with bupivacaine (amino amide anesthetic) and corticosteroid.
2) Destruction of the gasserian ganglion by retrogasserian injection of glycerol and balloon compression. 3) Radiofrequency destruction of the gasserian ganglion. 4) Microvascular decompression of the trigeminal root. This is the preferred option prior to gasserian destruction. Gasserian destruction should be reserved for cases where surgery is contraindicated. |
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What is another name for temporal arteritis and what is it's typical demographic.
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White female (3:1 over male) who is over sixty.
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What is the percentage of patients with temporal arteritis who have polymyalgia rheumatica?
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about 50%
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What is the pathophysiology of temporal arteritis?
What other arteries might this pathology affect? |
Autoimmune pathology wherein giant multinucleated cells invade arteries containing elastin, such as the temporal, external carotid, and ophthalmic. Large arteries too like the aorta.
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What symptom is common in temporal arteritis and what symptom is considered pathognomonic of temporal arteritis until proved otherwise?
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Tenderness that is continuous over the temporal artery is common. Jaw claudication in the elderly with chewing is considered pathognomonic and should be treated and worked up until ruled out.
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What does the ESR usually run around with temporal arteritis?
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greater than 50 mm/hr in 90% of patients
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For all headaches, besides CBC, CRP, ESR, CRP, what other lab should be drawn?
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Thyroid profile (I like the full thing: TSH, T4, T3, reverse T3, anti-TPO and TG)
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What is a type of headache that presents very similarly to cluster headache but has a prevalence of only 1-3% of that? What gender does it usually affect? What type of medication does it typically respond very well to?
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Chronic paroxysmal hemicrania. Usually affects females more, unlike cluster headaches. It typically responds very well to NSAIDs.
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What is the treatment for temporal arteritis?
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Immediate corticosteroids of about 80mg/day until symptoms resolve, with tapering by about 5 mg/wk as long as patient remains asymptomatic and ESR does not rise.
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What are six of the most common reasons for ocular pain?
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1) Styes/hordoeolum
2) Conjunctivitis 3) Corneal abrasions 4) Glaucoma 5) Uveitis 6) Optic neuritis |
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What is the most common bacteria of styes/hordeolum?
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Staphylococcus aureus
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For mild, topical styes, what treatment should be used? What happens if the stye progresses and what should be done?
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Non-neomycin containing antibiotic cream like polymyxin-B and bacitracin, with a warm compress. If this doesn't work and it gets worse, systemic antibiotics and rapid referral to an opthalmologist as this may progress to periorbital cellulitis.
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How do you diagnose and treat a corneal abrasion?
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Flourescein staining with a slit lamp reveals the abrasion without a foreign body. If suspected metallic fragment (carpentry accident, etc), consider plain films or CT.
Treat by everting the upper eyelid and rinse with copious amounts of sterile normal saline. Give non-neomycin topical antibiotic like polymyxin-B or bacitracin, use eye patch. |
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How do you treat conjunctivitis?
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Most of the time just with a warm compress. If bacterial conjunctivitis is suspected, non-neomycin topical antibiotics as well. If sexually-transmitted conjunctivitis, emergent ophthalmologist referral and culture.
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What is the underlying mechanism for glaucoma?
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Failure of adequate drainage of the aqueous humor inside the orbit.
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What type of glaucoma is called the "silent thief"? Why? What is seen on fundoscopic examination?
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Open angle glaucoma (the aqueous humor cannot adequately drain from the eye even though the angle between the iris and cornea is open). Causes insidiously increasing intraorbital pressure, slowly damaging the optic nerve. Disc cupping is seen on fundoscopy.
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What are symptoms of closed angle glaucoma?
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Acute severe eye pain, blurred vision, halo effect around lights, nausea, vomiting, red eye. Cornea looks steamy. The patient looks acutely ill. This is an emergency and the patient needs to see the ophthalmologist immediately.
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What should be done if uveitis is suspected?
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Ophthalmology referral. Commonly seen with autoimmune diseases, such as Behcet's, RA, Reiter's.
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What is the most common cause of optic neuritis? About what percentage of people with this disease have optic neuritis?
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Multiple sclerosis. 20%
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Besides the most common cause of optic neuritis, list eight other causes.
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1) HIV
2) TB 3) CMV 4) Temporal arteritis 5) Hepatitis B 6) Lyme disease 7) Radiation therapy 8) Sinusitis |
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What ethnicity is more susceptible to glaucoma? To optic neuritis?
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Blacks are more susceptible to glaucoma. Caucasians are more susceptible to optic neuritis.
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What are the three symptoms of optic neuritis?
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1) Eye pain
2) Vision loss 3) dyschromatopsia (loss of ability to distinguish colors) |
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How do you diagnose optic neuritis? What do you do to treat?
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Fundoscopic exam shows swollen, pale disc. Can be made with MRI too. Ophthalmology referral and treat with IV corticosteroids.
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What is the most common anatomical location to cause referred ear pain?
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The nasopharynx.
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What is Ramsay-Hunt Syndrome type II?
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zoster of the geniculate ganglion of the Facial nerve. Presents with facial paralysis, tongue issues, and pain over the ear. It also tends to have an erythematous rash over the face, such as zoster elsewhere.
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What are the most common malignancies of the nose?
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Basal and squamous cell carcinoma
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Give a most likely diagnosis of someone who previously had pharyngitis, now appears acutely ill and speaks in a "hot potato" voice. What should you do?
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Paraphyrangeal or retropharyngeal abscess. MRI, labs.
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What is "Eagle Syndrome"
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an elongated styloid process or calcification of the stylohyoid ligament, causing pain, oftentimes by interfering with the external carotid artery. Exacerbated with chewing and talking.
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With temporomandibular dysfunction, what is more common: intra-articular or extra-articular sources of pain?
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Extra-articular.
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What muscles may attach to the TMJ?
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temporalis, masseter, external pterygoid and internal pterygoid, sometimes the trapezius and sternocleidomastoid.
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Describe the two bones that make up the TMJ.
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The glenoid of the zygoma and the mandibular condyle.
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What trait is very common with temporomandibular dysfunction?
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bruxism
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Name two diagnostic tests for diagnosis of TMJ pain
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radiography including plain films (usually normal) and MRI. Injection of anesthetic into the joint.
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Describe the technique for injecting the TMJ
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patient lays supine, opens and closes mouth. Palpation reveals the joint just anteriorly and inferiorly to the external auditory meatus. Patient then holds mouth in neutral.Use 25 gauge one inch needle, insert just below the zygomatic arch, feel the pop as the needle enters the joint. Aspirate, inject about 0.5 mL of anesthetic and a little bit of corticosteroid.
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What diagnosis should be strongly considered with a patient with atypical face pain following trauma, with burning type pain and allodynia?
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Reflex sympathetic dystrophy of the face
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What is the most common cause of occipital neuralgia?
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blunt trauma to the greater or lesser occipital nerves. Often from repetitive microtrauma (head in extension with painting ceilings)
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Where do the greater and lesser occipital nerves arise?
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The greater from the dorsal primary rami second, and to a lesser extent, third cervical nerves. The greater pierces the fascial just below the superior nuchal ridge with the occipital artery.
The lesser occipital nerve arises from the ventral primary rami of the second and third cervical nerves. It passes along the posterior border of the sternocleidomastoid muscle. |
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Name some labwork that should be considered with cervical strain.
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Oftentimes nothing if it appears self limited. Consider ruling out an inflammatory arthropathy/myopathy if clinically suspected. CBC, CMP, ANA, RF, HLA-B27, ESR/CRP
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Where is cervicothoracic bursitis pain usually located? What is its purported cause?
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At the C7/T1 junction at midline. From repetitive hyperextension.
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What are two differential diagnoses of cervicothoracic bursitis.
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There are many. Waldman's lists fibromyalgia and ankylosing spondylitis (for which they recommend plain films of the sacrum).
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Describe the innervation of the cervical facet joint
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Each joint receives innervation from the level of that vertebra and the level above. C2/3 is innervated by the third occipital nerve and C3/4 is innervated by the medial branch of the dorsal ramus of C3.
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With intercostal neuralgia, if there is significant involvement of the motor portion of the subcostal nerve, besides pain, what may the patient complain of?
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Their abdomen bulging out.
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What is Tietze's Syndrome?
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costal pain secondary to enlargement of the costal cartilage. It was previously thought to be from a viral infection though this is no longer the case. It can be from repetitive strain, radiation therapy, or other causes.
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What is the Angle of Lois?
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the angle at which the manubrium articulates with the sternum
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Name some of the most common arthridites that can affect the manubriosternal joint.
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Osteoarthritis, rheumatoid arthritis, Reiter's syndrome, ankylosing spondylitis, psoriatic arthritis
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What is Bornholm disease?
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Pleurodynia caused by pleural infection with a Coxsackie B virus or other enteroviruses. Usually self-limiting
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List common labs for a vertebral compression fracture
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PT/INR, parathyroid hormone, SPEP, CBC, PSA, ESR/CRP, ANA
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List common labs for sacroiliac pain
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HLA-B27, CBC, CMP, ANA, CRP
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What are the three most common etiologies of coccydynia?
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Thought to be strain of the sacrococygeal ligament or coccyx fracture. Less commonly arthritis of the sacrococcygeal joint.
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What two muscles composes the pelvic diaphragm?
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The coccygeus and the levator ani
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What three muscles close the back part of the outlet of the pelvis?
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The levator ani, the coccygeus, and the piriformis
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Give three diagnostic criteria for reflex sympathetic dystrophy to the face.
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1) Prior history of trauma or pathology to the area (e.g. blunt trauma, neoplasm, arthritis, infection, CNS issue).
2) Constant sensation of burning with allodynia in a distribution not concordant with a cranial or peripheral nerve. 3) Trophic changes of the skin. |
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What does sudomotor mean?
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Something that stimulates the sweat glands.
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What are diagnostic procedures/tests that should be done to work up RSD of the face?
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MRIs of the brain and cervical spine. CBC, CMP, ANA, ESR/CRP. If all negative, then a stellate ganglion block should give significant relief.
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Differentiate trigeminal neuralgia and RSD of the face in regards to:
1) Intermittent/continuous 2) Dull/shocklike |
RSD is continuous and dull. Trigeminal neuralgia is intermittent and shocklike.
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Describe the treatment of RSD of the face
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1) Remove the nidus of offending tissue if possible
2) Frequent stellate ganglion blocks 3) Assist with sleep disturbances (e.g. gabapentin, TCAs) |
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What position is most comfortable with a dural puncture headache?
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The supine position.
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If a post dural puncture headache is suspected and there is a fever present, what should be the workup and treatment?
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MRI of the brain and possibly remainder of the neuraxis with and without gadolinium, lumbar puncture with cytology and stains, CBC, CMP, ESR. Start antibiotics to cover resistant staphylococcus.
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After the blood patch, what position should the patient be in? What should be done if the patient is refractory to the blood patch?
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Supine position for at least one day. If they are refractory, then repeat the blood patch the next day. Caffeine can be helpful. Some physicians think alcohol is helpful as it suppresses antidiuretic hormone.
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What is the frequency of glossopharyngeal neuralgia in comparison to trigeminal neuralgia?
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one hundred times less frequent.
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Where is the pain located with glossopharyngeal neuralgia?
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The tonsils, posterior tongue, and larynx region. It is unilateral the vast majority of the time. In the distribution of the ninth cranial nerve.
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Tumors located at what location often mimic glossopharyngeal neuralgia?
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at the cerebellopontine angle.
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What workup should be performed in a patient with suspected glossopharyngeal neuralgia?
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MRI of the brain and brainstem. CBC, CMP, CRP. Endoscopy of the hypopharynx with attention to the piriform sinuses to rule out malignancy.
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Tumors of what areas may mimic glossopharyngeal neuralgia? What class of autoimmune diseases?
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cerebellopontine angle, piriformis sinus, tumors of the tonsillar fossa. Demyelinating diseases and jaw claudication with temporal arteritis.
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What is first line pharmacological treatment for glossopharyngeal neuralgia, how should it be dosed, and what labs should be obtained?
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Carbamazepine 100mg po bid, increased every 48 hours by 200 mg until pain relief or 1200 mg total daily. When pain relief is obtained, keep using med for at least six months. It may cause blood dyscrasias, including aplastic anemia, thus baseline and repeat CBCs must be performed to monitor this. Check frequently for rashes.Need to check the HLA-B*1502 allele as people with this are at high risk for carbamazepine. |
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What is the maximum suggested total daily dose of baclofen?
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80 mg
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What are the interventional treatments of choice for glossopharyngeal neuralgia, going from what should be tried first to last?
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1) Glossopharyngeal nerve block, which may be done repeatedly with decreasing doses of corticosteroid.
2) Janetta's procedure: microvascular decompression of CN IX by the brainstem. 3) RF destruction of the glossopharyngeal nerve |
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Describe the two main classifications of torticollis and their subclassifications.
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1) By phase:
a) Tonic: continuous movement to one side b) Clonic: involuntary shaking of the head c) Tonic/clonic 2) By direction: a) Rotation b) Laterocollis: leaning of the head against the shoulder c) Retrocollis d) Anterocollis |
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With torticollis, what maneuver sometimes makes the dystonia momentarily cease?
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Touching the opposite side of the face.
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What lab/imaging workup should be done with torticollis?
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MRI of the brain, CBC, CMP, ESR. I think some imaging of the cervical spine as well, though Waldman's doesn't mention it.
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Describe the role of the geniculate ganglion of the facial nerve. |
The geniculate branch has the sensory bodies of the facial nerve and is equivalent to the dorsal root ganglia of the spine. The facial nerve starts in the brainstem at the pons, exits, goes around the posterior fossa to the internal auditory meatus into the petrous portion of the temporal bone. Within the petrous portion, the nerve courses through the "facial canal". In part of this canal (the labyrinthine segment) there is a bend (genu), where the geniculate ganglion is located. The motor and sensory aspects then split. As for the motor, after innervating the chorda tympani and stapedius, it continues, exiting at the stylomastoid foramen and splitting into five branches (temporal, zygomatic, buccal, mandibular, cervical). The sensory fibers go from the geniculate ganglion through the pterygoid canal to the pterygopalatine ganglion and also innervate the lacrimal gland. |
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Give a mnemonic for muscles innervated by V3 and what it stands for |
My tensors dig ants 4 MoM
Tensor veli palatini and tensor tympani Anterior digastric Four muscles of mastication: 1) Temporalis 2) Masseter 3) Medial pterygoid 4) Lateral pterygoid |
