Migraine types-
1. Classic
2. Common
3. Complicated
4. Retinal
5. Opthalmoplegic
6. Benign mydriasis, episodic as a sign of migraine
7. Basilar (Bickerstaff) migraine
8. Hemiplegic
9. Vertiginous
10. Acephalgic
Non migraine headache
11. Tension
12. ebound
13. Cluster
14. Paroxysmal hemicrania (differentiate from cluster partly by female predominance, shorter duration and response to indomethacin)
15. Sunct syndrome-- unresponsive to indomethacin and SUNA syndrome
16.Ice pick headache
17. Ptussive headache (consider relation to Chiari malformation or rarely subdural hematoma)
18. Thunderclap headache
19. Greater occipital neuralgai
20. Hypnic headache
21. Carotid dissection
22. Temporal arteritis
23. Post-traumatic headache
24. Glossopharyngeal neuralgia
25. Intracranial hypertension (with or without pappilledema)
Headaches related to eye disease
26. Corneal erosion/disease
27. Intraocular disease-- include acute angle glaucoma, scleritis, iritis, uveitis.
28. Optic neuritis
29. Eye strain
Thursday, January 31, 2008
Tuesday, January 29, 2008
Differential diagnosis of ON
1. Anterior ischemic optic neuropathy (AION) often lacks the pain seen in ON
2. Painless visual loss without improvement over several weeks AION
3. Leber's hereditary optic neuropathy (LHON) occurs inyoung men with a mitochondrial disease; the presentation is unilateral unremitting progressive visual loss to bilateral visual loss over days to months with disc edema, peripappillary telangiectasias, and permanent visual loss.
4. Absent venous pulsations-- enlarged blind spot-- consider increased ICP
5. Orbital mass constricting the optic nerve may cause disc edema, proptosis, and EOM restriction unilaterally
6. Diabetic papillopathy in young diabetics often remits
7. Other inflammatory diseases: HIV, syphilis, TB, cryptococcus, toxoplasma, varicella, histoplasmosis, CMV, and h. zoster all can cause ON.
8. Macular star suggests toxoplasmosis.
9. Optic spinal "Asian" MS may be a form of NMO.
2. Painless visual loss without improvement over several weeks AION
3. Leber's hereditary optic neuropathy (LHON) occurs inyoung men with a mitochondrial disease; the presentation is unilateral unremitting progressive visual loss to bilateral visual loss over days to months with disc edema, peripappillary telangiectasias, and permanent visual loss.
4. Absent venous pulsations-- enlarged blind spot-- consider increased ICP
5. Orbital mass constricting the optic nerve may cause disc edema, proptosis, and EOM restriction unilaterally
6. Diabetic papillopathy in young diabetics often remits
7. Other inflammatory diseases: HIV, syphilis, TB, cryptococcus, toxoplasma, varicella, histoplasmosis, CMV, and h. zoster all can cause ON.
8. Macular star suggests toxoplasmosis.
9. Optic spinal "Asian" MS may be a form of NMO.
Optic neuritis, symptoms and signs
(review in the Neurologist 2000; 6:205-13) author Jane Chan MD
Symptoms
1. In acute ON more than 90 % have loss of central vision. Occasionally patients get loss of peripheral vision to one side or superiorly or inferiorly.
2. Mild orbital pain above or behind the eye, preceding or concurrently with the visual loss, aggravated by upwards movement of the eye, and last up to several weeks. This may be due to triggering of trigeminal stimulation of the optic nerve sheath.
3. Less conmon symptoms are photophobia, dullness or loss of colors, perceptions of phosphenes (flashing lights with noise or eye movements) or decreased depth perception.
Signs
1. Visual loss worsens over hours, days or minutes and peaks within days to a week. Maximal return occurs within 3-6 months and does not correlate to initial visual loss.
2. Patterns of visual field loss was varied as central scotoma resolves to a small dim central or a paracentral deficit. Patterns include an arcuate scotoma, altitudinal scotoma (superior or inferior),peripheral constriction, central or cecocentral scotoma, bitemporal or hemianopic deficit. Patterns can vary day to day or hour to hour.
3. Color and contrast visionare reduced. The color defect is usually more severe than the acuity loss. The Farnsworth-Munsell 100 hue test is highly sensitive and specific. The short version with caps 22-42 has similar sensitivity for monitoring after ON. More blue yellow defects occur acutely, more red green defects occur after 6 months. Patients also have a decreased sensation of brightness.
4. RAPD is almost always present in acute ON; absence suggests optic neuropathy or other etiology.
5. Half of the patients in the ONTT had abnormal fellow eyes (contrateral) and many of these thought their vision contralaterally was normal.
6. PEARL-- RARELY an RAPD occurs in a retrochiasmal lesion due to pupillary fibers travelling together in optic tract
RED FLAGS or atypical features of optic neuritis
1. age greater than 50
2. Optic pallor at presentation
3. no pain
4. pain or vision loss that continues over weeks
5. poor visual recovery
6. associated systemic signs and symptoms
Symptoms
1. In acute ON more than 90 % have loss of central vision. Occasionally patients get loss of peripheral vision to one side or superiorly or inferiorly.
2. Mild orbital pain above or behind the eye, preceding or concurrently with the visual loss, aggravated by upwards movement of the eye, and last up to several weeks. This may be due to triggering of trigeminal stimulation of the optic nerve sheath.
3. Less conmon symptoms are photophobia, dullness or loss of colors, perceptions of phosphenes (flashing lights with noise or eye movements) or decreased depth perception.
Signs
1. Visual loss worsens over hours, days or minutes and peaks within days to a week. Maximal return occurs within 3-6 months and does not correlate to initial visual loss.
2. Patterns of visual field loss was varied as central scotoma resolves to a small dim central or a paracentral deficit. Patterns include an arcuate scotoma, altitudinal scotoma (superior or inferior),peripheral constriction, central or cecocentral scotoma, bitemporal or hemianopic deficit. Patterns can vary day to day or hour to hour.
3. Color and contrast visionare reduced. The color defect is usually more severe than the acuity loss. The Farnsworth-Munsell 100 hue test is highly sensitive and specific. The short version with caps 22-42 has similar sensitivity for monitoring after ON. More blue yellow defects occur acutely, more red green defects occur after 6 months. Patients also have a decreased sensation of brightness.
4. RAPD is almost always present in acute ON; absence suggests optic neuropathy or other etiology.
5. Half of the patients in the ONTT had abnormal fellow eyes (contrateral) and many of these thought their vision contralaterally was normal.
6. PEARL-- RARELY an RAPD occurs in a retrochiasmal lesion due to pupillary fibers travelling together in optic tract
RED FLAGS or atypical features of optic neuritis
1. age greater than 50
2. Optic pallor at presentation
3. no pain
4. pain or vision loss that continues over weeks
5. poor visual recovery
6. associated systemic signs and symptoms
Tests for myasthenia gravis: Pearls
1. Tensilon test should be unequivocal and not subjective. In one study all patients who had a positive test responded in the first 7 mg.
2. False positive tensilon tests occurred in LEMS< GBS, compressive cranial neuropathies and brain stem lesions (Seminars of Neurology 2003, author Pascuzzi).
3. Muscarinic effects (tearing, sweating,cramping, salivating and nausea) are common. Relative contraindications are cardiac arrythmias and asthma. Cardiac monitoring may not be universally required.
4. A neostigmine methylsulfate injection can be used in children with a longer onset and offset (latter is 30 minutes) but may be harder to interpret.
5. The ice pack test of placing the ice pack on for 2-5 minutes has reported high sensitivity and specificity but may be hard to tolerate for patients (Golnick AC et al. Opthalmology 1999 186:1282-6). The mean improvement with this test is 4.5 mm.
6. The rest test (close eyes for 3 minutes) results in a mean improvement of 2 mm of ptosis.
7. The sleep test (30 minutes) shows improvement in all Tensilon positive patients plus two others (out of 42 tested).
8. Lab tests of binding Ach receptors is positive in 50 % of OM patients (v. 90 % of MG patients overall); blocking antibodies add only another 1 percent sensitivity, and modulating antibodies actually do improve sensitivity slightly but also have more false positives. see Howard FJ et al. NY Acad Sci 1987; 505: 526-538).
9. False positive conditions with ACH receptor antibodies (again from Howard et al.) are: AI hepatitis, SLE, ALS, inflammatory neuropathies, LEMS, thyroid opthalmopathy, 1 degree relatives of MG patients, thymoma, RA, and patients taking penicillamine.
10. Striated muscle ab's as a marker for thymoma: they predict thymoma in patients with MG under 40 (80%) and thymoma in nonmyasthenics (positive in 25 % of those). False positives are seen in RA treated with penicillamine, LEMS, Bone marrow graft recipients, GVHD, and paraneoplastic disease (see Lennon, Neurol suppl 5, 1997 S23-27).
11. De Graefe's test 12. Mary Walker phenomenon-- inflation of cuff above normal systolic pressure causes fatigue. Deflation of the cuff causes exacerbation of MG in rest of the body
13. Fatigue-ability is the hallmark of MG. Test for with sustained upgaze test 30-60 sec (especially check medial rectus muscle> superior and lateral recti); sustained abduction of the arms (120 s); sustained elevation of the leg while lying supine (90 sec); repeated rising from a chair without using arms, up to 20 times, look for bfm's; counting aloud to 50.
14. The rare patient that presents with isolated respiratory involvement may have orthopnea, ie SOB while lying down.
15. Enhanced ptosis of contralateral side may occur with manual elevation of one ptotic lid
16. Unilateral frontal hypercontraction is a sign of weak lids.
17. Specific muscles to assess in suspected MG include eom's, oropharyngeal, facial, respiratory, axial and limb
18 Pseudo INO occurs when adducting eye does not adduct and abducting eye has nystagmus
19. Cover - uncover test can reveal weakness if done repeatedly.
20. Beware of holding target to fixate too close, will reveal a convergence abnormality rather than a true EOM abnormality.
21. Look for snarl with attempt to smile, inability to pucker to kiss
22. Pattern of weak jaw closure and strong jaw opening is expected in MG. Test temporalis/pterygoid separately. Weak jaw opening with pterygoid weakness is rarely found in MG.
23. Fatigue of swallowing does occur in MG
24. Slurp test touted in May, 2010 Neurology podcast for children with MG that parents can do to test for weakness. fill 4 oz cup with water with a straw and have child slurp after finishing the drink. Time it, use patient as own control.
2. False positive tensilon tests occurred in LEMS< GBS, compressive cranial neuropathies and brain stem lesions (Seminars of Neurology 2003, author Pascuzzi).
3. Muscarinic effects (tearing, sweating,cramping, salivating and nausea) are common. Relative contraindications are cardiac arrythmias and asthma. Cardiac monitoring may not be universally required.
4. A neostigmine methylsulfate injection can be used in children with a longer onset and offset (latter is 30 minutes) but may be harder to interpret.
5. The ice pack test of placing the ice pack on for 2-5 minutes has reported high sensitivity and specificity but may be hard to tolerate for patients (Golnick AC et al. Opthalmology 1999 186:1282-6). The mean improvement with this test is 4.5 mm.
6. The rest test (close eyes for 3 minutes) results in a mean improvement of 2 mm of ptosis.
7. The sleep test (30 minutes) shows improvement in all Tensilon positive patients plus two others (out of 42 tested).
8. Lab tests of binding Ach receptors is positive in 50 % of OM patients (v. 90 % of MG patients overall); blocking antibodies add only another 1 percent sensitivity, and modulating antibodies actually do improve sensitivity slightly but also have more false positives. see Howard FJ et al. NY Acad Sci 1987; 505: 526-538).
9. False positive conditions with ACH receptor antibodies (again from Howard et al.) are: AI hepatitis, SLE, ALS, inflammatory neuropathies, LEMS, thyroid opthalmopathy, 1 degree relatives of MG patients, thymoma, RA, and patients taking penicillamine.
10. Striated muscle ab's as a marker for thymoma: they predict thymoma in patients with MG under 40 (80%) and thymoma in nonmyasthenics (positive in 25 % of those). False positives are seen in RA treated with penicillamine, LEMS, Bone marrow graft recipients, GVHD, and paraneoplastic disease (see Lennon, Neurol suppl 5, 1997 S23-27).
11. De Graefe's test 12. Mary Walker phenomenon-- inflation of cuff above normal systolic pressure causes fatigue. Deflation of the cuff causes exacerbation of MG in rest of the body
13. Fatigue-ability is the hallmark of MG. Test for with sustained upgaze test 30-60 sec (especially check medial rectus muscle> superior and lateral recti); sustained abduction of the arms (120 s); sustained elevation of the leg while lying supine (90 sec); repeated rising from a chair without using arms, up to 20 times, look for bfm's; counting aloud to 50.
14. The rare patient that presents with isolated respiratory involvement may have orthopnea, ie SOB while lying down.
15. Enhanced ptosis of contralateral side may occur with manual elevation of one ptotic lid
16. Unilateral frontal hypercontraction is a sign of weak lids.
17. Specific muscles to assess in suspected MG include eom's, oropharyngeal, facial, respiratory, axial and limb
18 Pseudo INO occurs when adducting eye does not adduct and abducting eye has nystagmus
19. Cover - uncover test can reveal weakness if done repeatedly.
20. Beware of holding target to fixate too close, will reveal a convergence abnormality rather than a true EOM abnormality.
21. Look for snarl with attempt to smile, inability to pucker to kiss
22. Pattern of weak jaw closure and strong jaw opening is expected in MG. Test temporalis/pterygoid separately. Weak jaw opening with pterygoid weakness is rarely found in MG.
23. Fatigue of swallowing does occur in MG
24. Slurp test touted in May, 2010 Neurology podcast for children with MG that parents can do to test for weakness. fill 4 oz cup with water with a straw and have child slurp after finishing the drink. Time it, use patient as own control.
Signs and symptoms of ocular myasthenia
1. Unilateral or bilateral ptosis, usually variable through the day, with diplopia
2. Chief complaint may be blurred vision if lid covers pupil and ptosis is not recognized.
3. Hyper-retraction of the less affected lid can cause a complaint of ocular irritation due to exposure.Hyperretraction is a compensatory mechanism with increased neuronal firing in less affected eye.
4. Dizziness, gait instability, blurring of "visual confusion" that improves with closing one eye
5. SPECIFIC SIGN OF MG: WHEN PTOTIC LID IS MANUALLY (passively) ELEVATED, THE CONTRALATERAL LID DROOPS
6. Cogan lid twitch sign: The patient looks down for 15 seconds, then rapidly up at the examiner's finger. The ptotic eyelid overshoots and is transiently higher than the contralateral lid then drops to its normal position. Its due to transient strengthening of the lid after resting the levator muscle.
7. Any pattern of EOM weakness
8. Dissociated gaze evoked nystagmus contralateral to the paretic eye.This is adaptive and due to increased pulses of innervation.
9. Orbicularis oculi weakness with ptosis is a strong suggestor of MG.
10. Peekaboo sign with gradual appearance of lagopthalmos after forceful lid closure of over a minute with fatigue and incomplete lid closure showing sclera, hence the name, is also seen in facial nerve disorders
11. Pupils are always normal, unlike botulism and IIIn palsy.
12. The "other" Babinski sign (aka "brow lift sign)-- "when orbicularis oculi contracts and the eye closes, the internal part of the frontalis contracts at the same time and the eyebrow raises during eye occlusion." This sign is helpfulin differentiating MG from blepharospasm.
2. Chief complaint may be blurred vision if lid covers pupil and ptosis is not recognized.
3. Hyper-retraction of the less affected lid can cause a complaint of ocular irritation due to exposure.Hyperretraction is a compensatory mechanism with increased neuronal firing in less affected eye.
4. Dizziness, gait instability, blurring of "visual confusion" that improves with closing one eye
5. SPECIFIC SIGN OF MG: WHEN PTOTIC LID IS MANUALLY (passively) ELEVATED, THE CONTRALATERAL LID DROOPS
6. Cogan lid twitch sign: The patient looks down for 15 seconds, then rapidly up at the examiner's finger. The ptotic eyelid overshoots and is transiently higher than the contralateral lid then drops to its normal position. Its due to transient strengthening of the lid after resting the levator muscle.
7. Any pattern of EOM weakness
8. Dissociated gaze evoked nystagmus contralateral to the paretic eye.This is adaptive and due to increased pulses of innervation.
9. Orbicularis oculi weakness with ptosis is a strong suggestor of MG.
10. Peekaboo sign with gradual appearance of lagopthalmos after forceful lid closure of over a minute with fatigue and incomplete lid closure showing sclera, hence the name, is also seen in facial nerve disorders
11. Pupils are always normal, unlike botulism and IIIn palsy.
12. The "other" Babinski sign (aka "brow lift sign)-- "when orbicularis oculi contracts and the eye closes, the internal part of the frontalis contracts at the same time and the eyebrow raises during eye occlusion." This sign is helpfulin differentiating MG from blepharospasm.
Differential diagnosis of ocular myasthenia
1.Any IV,VI, and partial IIInn palsies
2. Graves opthalmopathy (however, should not see ptosis, and may see lid retraction)
3. CPEO Chronic progressive external opthalmoplegia(get symmetric ptosis and EOM weakness, but unlike myasthenia, SACCADES ARE SLOW in CPEO
4. Oculopharyngeal dystrophy-- chronic, slowly progressive, family history present, bulbar mm are involved.
5. Glycogenosis type II -- ptosis is presenting feature often (Neurology 69 : 116 2007) with skeletal muscle weakness later. Muscle biopsy may be needed to show increased glycogen content and acid maltase deficiency,
6. Autoimmune encephalitis with diplopia: http://dementianotes.blogspot.com/2008/06/vgkc-autoantibodies-mimicking-cjd.html
2. Graves opthalmopathy (however, should not see ptosis, and may see lid retraction)
3. CPEO Chronic progressive external opthalmoplegia(get symmetric ptosis and EOM weakness, but unlike myasthenia, SACCADES ARE SLOW in CPEO
4. Oculopharyngeal dystrophy-- chronic, slowly progressive, family history present, bulbar mm are involved.
5. Glycogenosis type II -- ptosis is presenting feature often (Neurology 69 : 116 2007) with skeletal muscle weakness later. Muscle biopsy may be needed to show increased glycogen content and acid maltase deficiency,
6. Autoimmune encephalitis with diplopia: http://dementianotes.blogspot.com/2008/06/vgkc-autoantibodies-mimicking-cjd.html
Thursday, January 10, 2008
Seven agents approved for antimigraine prophylaxis
(list is in Lancet Neurology Dec 2007 editorial, suggests this applies to UK, in case some of the drugs sound unfamiliar). The seven are: methysergide, propanolol, timolol, pizotifen, flunarizine, valproate, and topiramate.
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