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Optic neuritis
CASE CONFERENCE neuritis, optic; optic neuritis; retrobulbar neuritis
Optic Neuritis [Javerbaum J, Mitchell JA, Dawson R: Optic neuritis. Ann Emerg Med November 1984;13:1061-1064.] INTRODUCTION John A Mitchell, MD: The case for discussion today is that of a 21-year-old previously healthy woman who came to our emergency department with an unusual, but not rare, presentation of an infrequent neuro-ophthalmologic disease. The case will be discussed by Jeffrey Iaverbaum, MD, of the Division of Neurology, Department of Medicine, and the Department of Emergency Medicine, Kern Medical Center.
CASE PRESENTATION Randy W Dawson, MD: The patient is a 21-year-old woman who arrived with the complaint of headache of two weeks' duration. The headache was characterized as a constant, nonpulsatile tightness, generalized at first but eventually located behind the right eye, with associated blurred vision in that eye. She denied nausea, aura, vomiting, unusual stress, or constitutional symptoms. Our patient had previously been in good health, with occasional headaches but none like the present one in either intensity or duration. She had a positive maternal history of migraine. On physical examination, the patient was alert and oriented; vital signs were normal; visual acuity was 20/20 OU; pupils were equal, round, and reactive to light and accommodation; extraocular muscle movements were normal; and cranial nerves II to XII were normal. The remaining general physical and neurological examinations were also normal. The patient was diagnosed as having atypical migraine; was treated with Demerol 50 mg IM, Phenergan 50 mg IM, and Aristacort, 40 mg IM; and was given a prescription for cafergot. She was instructed to return ff the headache did not improve. The patient did return the following day with blurred vision and persistent headache that were unresponsive to cafergot. Her visual acuity was 20/30 OU; otherwise, the physical examination remained unchanged. She was again diagnosed as having atypical migraine and was given Demerol and Phenergan. She was discharged with Tylenol with Codeine, and was instructed to rest and to return if the headache did not improve. The patient returned five days later complaining of loss of vision in her right eye. Her headache had subsided two days earlier, but upon arising that day she noted no vision in the right eye and "weak sight" in the left eye. She described vision in the left eye as grayish and somewhat clouded, which seemed to worsen while taking a hot shower. On physical examination the right pupil reacted consensually but not directly. Pupillary response in the left eye was normal. Visual acuity was light perception on the right and 20/20 on the left. There was a temporal hemianopsia on the left and the patient missed five plates on the color vision test. Funduscopic examination was normal bilaterally, with nonpainful extraocular muscle movements. The remaining cranial nerves were intact. There was no orbital, facial, or sinus tenderness, and the remaining neurological and physical examinations were normal. The laboratory values were all essentially normal, including CBC and dif-
13:11 November 1984
Annals of Emergency Medicine
Jeffrey Javerbaum, MD John A Mitchell, MD Randy Dawson, MD Bakersfield, California From the Emergency Medicine Residency Program, Kern Medical Center, Bakersfield, California. Address for reprints: Jeffrey Javerbaum, MD, Department of Emergency Medicine, Kern Medical Center, 1830 Flower Street, Bakersfield, California 93305.
1061/119
OPTIC NEURITIS Emergency Medicine Residency Program - Kern Medical Center
Fig. Conditions associated with optic neuritis/neuropathy.
ferential, ESR, electrolytes, BUN, glucose, thyroid studies, and a negative ANA and VDRL. On lumbar puncture, CSF was clear and acellular, with normal pressure and normal chemistries, including oligoclonal bands, myelin basic protein, and IgG. Skull radiography, sinus series, and CT scan were unremarkable.
DISCUSSION Jeffrey Javerbaum, MD: Optic neuritis (ON) is a general term used to designate an inflammatory, degenerative, or demyelinating condition of the optic nerve1 which is usually acute and unilateral, and is accompanied by some loss of vision.2 The inflammation may be located anywhere from the optic disc to the optic chiasm3 Papillitis refers to inflammation involving that portion of the nerve that can be visualized ophthalmoscopically. It is characterized by swelling of the optic disc, and is generally indistinguishable from papilledema. Retrobulbar neuritis refers to inflammation situated more posteriorly and without acute fundusc0pic changes. The term ON is often used in a confusing and unrestricted sense to include many diverse forms of optic neuropathy. 3 It is useful to separate the more common demyelinating variety from rarer optic neuropathies arising secondary to systemic illness. In the latter instances (Figure}, the clinical presentation, course, and management will be affected by the associated disease. Among the many conditions underlying ON, multiple sclerosis {MS) is the most common.4 Perhaps for this reason the incidence of ON peaks in the twenties and declines with age.a, s Pathologically there is infiltration of the nerve with inflammatory cells followed by swelling and fragmentation of nerve tissue. Subsequently macrophages axe seen in the process of phagocytizing myelin breakdown productsA
Question: What are the symptoms of optic neuritis? Dr Javerbaum: Disturbance of vision in one eye is the most outstanding complaint. Visual acuity usually ranges from 20/200 to no light perception (NLP). The loss of vision is attributed to a scotoma in the central portion of the visual field.~ While visual loss is often rapid in onset, it may sometimes be progressive over weeks. 6 This problem may not be apparent until the unaffected eye is accidentally covered. The patient's vision may be described as blurred or dim - - as though looking through frosted glass. There may also be complaints of photophobia and diminution of vision in bright light.7 Another common disturbance is pain in or about the eye which is worsened by eye movement or palpation of the globe. As in our case, this pain may begin days to weeks before the onset of visual problems.2, s
Question: What physical signs are seen with optic neuritis? Dr Javerbaum: Visual acuity may be profoundly diminished on the involved side and may be worsened by bright illumination.7, 9 Complex visual field defects may be detected on careful screening. Most c o m m o n l y they are central scotomata involving the fixation point30 These scotomata may be more apparent with colored test objects than with white ones. 6 Hence, there may be an unsuspected loss of
120~062
Demyelination Primary (idiopathic) optic neuritis Multiple sclerosis Devic's disease Ischemia Atherosclerosis Temporal arteritis Periarteritis nodosa Systemic lupus erythematosis Inflammation Viral and postviral Encephalitis Meningitis Postvaccination (MMR, rabies) Tuberculosis, syphilis, mononucleosis Contiguous spread Intraocular inflammation Orbital inflammation Sinusitis Dental infections Metabolic disorders Diabetes mellitis Deficiency states (B1, B12) Toxins (methylalcohol, tobacco, arsenic, lead) Drugs (INH, ethambutol, quinine, penicillamine) Carcinoma
color vision detected by comparing colored objects viewed separately by each eye. Patients will report the colors appear "washed out" on the involved side. 2 This effect may be quantified using pseudoisochromatic plates. Loss of color vision occurs because of diminished input from the cones, which are most abundant at the macula. Close observation of the pupillary responses to light often shows a relative afferent pupillary defect (APD). This is due to loss of fibers in the afferent limb of the light reflex arc. While the pupils remain equal, there will be less constriction when light is shined into the involved eye than in the normal one. The involved pupil also may slowly redilate under sustained illumination.7 When each eye is illuminated in succession, there is a brisk constriction of the norreal pupil followed by a seemingly paradoxical dilation of the affected one in response to light.//This swinging flashlight test is reportedly abnormal in more than 90% of patients with ON. 12 Funduscopic abnormalities are seen in as many as 75% of patients with ON. 1 In acute papillitis, the disc may appear hyperemic and swollen, with blurred margins. The veins may be distended and without spontaneous pulsations. Scattered hemorrhages m a y be present about the disc. 2 While this picture may be identical to papilledema, a distinction can be made based on certain properties (Table). Following degeneration of a portion of the optic nerve fibers, optic atrophy may be a sequela of ON.6,13 Under these circumstances, the disc will appear pale, with margins that contrast sharply with the surrounding pink retina.
Question: Are any special tests helpful in making the diagnosis of ON? Dr Javerbaum: The value of testing visual fields and color
Annals of Emergency Medicine
13:11 November 1984
TABLE. Features distinguishing papillitis from papilledema Papillitis Visual acuity Color vision Pupils VF
Papilledema
4, 4,
Normal Normal
APD Variable defects (esp. central scotomata) Unilateral
Normal 1" Blind spot Bilateral
vision has been mentioned. Routine CSF studies are rarely useful; protein and lymphocytes may be mildly elevated. 14 Abnormal oligoclonal bands or elevated CSI IgG or myelin basic protein may suggest a diagnosis of MS. s Approximately 70% of patients with MS have elevated CSF IgG, while 90% have abnormal oligoclonal bands, is Fluorescein angiography is not helpful in differentiating between papillitis and a moderate degree of papilledema. 9 Visual evoked potentials may be sensitive in demonstrating an optic nerve lesion, but provide no information concerning cause.iS, 16 There are reports of nerve enlargement and swelling on CT scan and ultrasound, lz-19 Question: What is the relation of optic neuritis to multiple sclerosis? Dr Javerbaum: In recent studies the risk of developing MS following ON ranges from 8.3% lo to 75%. 5 Standard criteria for the diagnosis of MS require more than one CNS lesion. 2o Whether the idiopathic variety of ON represents a self-limited, local variant of MS remains undetermined. Yet the strong association between ON and MS suggests that they may share a common etiology. A variety of infectious and autoimmune etiologies have been proposed, is Occasionally ON will be accompanied by transverse myelitis (Devic's disease). Hence, complete neurologic examination and a thorough probe for prior neurologic disturbance are essential in all patients with ON. For unknown reasons, elevated temperature can sometimes precipitate transient exacerbations of MS. This observation led to the formerly popular "hot bath test." By immersing the patient in warm water, clinicians were able to provoke otherwise subclinical neurologic dysfunction and confirm the diagnosis of MS. 21 Because bilateral ON appears more likely to progress to MS than does unilateral ON, 4 our patient's bilateral involvement and worsening of vision OS following a hot shower indicates an increased risk to develop MS. Finally, she has recently developed sensory disturbances in the left leg, now strongly suggesting that she has MS. Question: What is the natural history of optic neuritis?
Dr Javerbaum: Spontaneous recovery within one to four weeks is the role.2, 8 Vision usually returns to normal despite the development of optic atrophy in most patients. 6 Prognosis is further determined by the presence of underlying conditions, such as MS. 13:11 November 1984
Question: Is there any treatment for optic neuritis? Dr Javerbanm: Many clinicans will try systemic or retrobulbar corticosteroids in severe or refractory cases. Trials using steroids in this manner have shown a tendency to shorten duration of visual symptoms and to lessen ocular pain when treatment is begun early. No controlled study has shown any method of treatment to influence final visual outcome.8 Question: How should patients be managed in the emergency department? Dr Javerbaum: Before making the diagnosis of ON, be certain that the patient does not have another, more treatable illness or a more life-threatening situation. If the disc is swollen, one must rule out papilledema and the possibility of an intracranial mass or hemorrhage, or malignant hypertension. Pseudotumor cerebri presents with headache, visual disturbance and blurred discs, and requires prompt intervention. Retinal artery occlusion, retinal vein thrombosis, and temporal arteritis can all produce sudden visual loss, and should be managed urgently. ON secondary to INH therapy necessitates discontinuation of the drug. 22 While ON rarely is confused with meningitis, the latter possibility should always be given high priority in the emergency setring. Finally, complicated migraine is a diagnosis of exclusion, requiring that other explanations for headache with neurologic disturbance first be excluded. The initial misdiagnosis of atypical migraine in this case underscores that fact.
REFERENCES 1. Walsh FB, Hoyt WF: Clinical Neuroophthalmology, ed 3. Baltimore, Williams and Wilkins, 1969, pp 607-641. 2. Bradley WG, Whitty CWM: Acute optic neuritis: Its clinical features and their relation to prognosis for recovery of vision. J Neurol Neurosurg Psychiat 1967;30:531-538. 3. 8cheie HG, Albert DM: Textbook of Ophthalmology. Philadelphia, WB Saunders, 1977, pp 494-496. 4. Hutchinson WM: Acute optic neuritis and the prognosis for multiple sclerosis. J Neurol Neurosurg Psychiatr 1976;39:283289. 5. Nikoskelainen E, Frey H, Aimo S: Prognosis of optic neuritis with special reference to cerebrospinal fluid immunoglobulins and measles virus antibodies. Ann Neurol 1981;9:545-550. 6. Hyllsted I{, Moller PM: Follow-up on patients with a history of optic neuritis. Acta Ophthal 1961:39:655-662. 7. Gunn M: Discussion on retro-ocular neuritis. Trans Ophthal Soc UK 1897;17:107-217. 8. Perkin GD, Rose FC: Optic Neuritis and Its Differential Diagnosis. Oxford, England, Oxford University Press, 1979, pp 34-36, 172-182, 194-197. 9. Bender MB, Rudolph SH, Stacy CB: The neurology of the visual and oculomotor systems, in Baker AB, Baker LH (eds): Clinical Neurology, revised edition. Philadelphia, Harper and Row, 1982, vol 1, chap 4, p 10. 10. Isayama Y, Takahashi T, Shimoyoma T, et ah Acute optic neuritis and multiple sclerosis. Neurology (NY) 1982;32:73-76. 11. Levatin P: Pupillary escape in disease of the retina or optic nerve. Arch Ophthalmol 1959;62:768-779. 12. Cox TA, Thompson 8H, Corbett JJ: Relative afferent pupillary defects on optic neuritis. Am J Ophthalmol 1981;92:685-690.
Annals of Emergency Medicine
1063/121
OPTIC NEURITIS Emergency Medicine Residency Program - Kern Medical Center
Soc UK 1959;79:701-716.
i8. Rush JA, Kennerdell IS, Martinez AJ: Primary idiopathic inflammation of the optic nerve. Am ! Ophthalmol 1982;93: 312-316.
14. Sandberg-Wollheim M: Optic neuritis: Studies on the cerebrospinal fluid in relation to clinical course in sixty-one patients.
19. Coleman JD, Lizzi FC, Jack RL: Ultrasonography of the Eye and Orbit. Philadelphia, Lea and Febiger, 1977, p 307.
Acta Neurol Scand 1975;52:167-178.
20. Poser CM, Paty DW, Scheinberg L, et al: New diagnostic criteria for multiple sclerosis: Guidelines for research protocols. Ann Neurol 1983;13:227-331. 21. Michael JA, Davis FA: Effects of induced hyperthermia in multiple sclerosis: Differences in visual acuity during heating and recovery phases. Acta Neurol Scand 1973;49:141-151. 22. Mandell GL, Sande MA: Antimicrobial agents - - Drugs used in the chemotherapy of tuberculosis and leprosy, in Gilman AG, Goodman LS, Gilman A (eds): The Pharmacologic Basis of Therapeutics, ed 6. New York, Macmillan 1980, pp 1202-1203.
13. Lynn BH: Retrobulbar neuritis. A survey of the present condition of cases occurring over the last fifty-six years. Trans OphthaI
15. McFarlin DE, McFarland HF: Multiple sclerosis. N Engl J Med 1982;307:1183-1188, 1246-1250. 16. Cohen SN, Syndulko K, Tourtellotte WW: Visual evoked potentials in the diagnosis of multiple sclerosis, in Poser CM (ed): Diagnosis of Multiple Sclerosis. New York, Thiame-Stratton (in press). 17. Howard CW, Osher RH, Tomsak RL: Computed tomographic features in optic neuritis. Am ! Ophthalmol 1980;89:699-702.
122/1064
Annals of Emergency Medicine
13:11 November 1984
Optic Neuritis [Javerbaum J, Mitchell JA, Dawson R: Optic neuritis. Ann Emerg Med November 1984;13:1061-1064.] INTRODUCTION John A Mitchell, MD: The case for discussion today is that of a 21-year-old previously healthy woman who came to our emergency department with an unusual, but not rare, presentation of an infrequent neuro-ophthalmologic disease. The case will be discussed by Jeffrey Iaverbaum, MD, of the Division of Neurology, Department of Medicine, and the Department of Emergency Medicine, Kern Medical Center.
CASE PRESENTATION Randy W Dawson, MD: The patient is a 21-year-old woman who arrived with the complaint of headache of two weeks' duration. The headache was characterized as a constant, nonpulsatile tightness, generalized at first but eventually located behind the right eye, with associated blurred vision in that eye. She denied nausea, aura, vomiting, unusual stress, or constitutional symptoms. Our patient had previously been in good health, with occasional headaches but none like the present one in either intensity or duration. She had a positive maternal history of migraine. On physical examination, the patient was alert and oriented; vital signs were normal; visual acuity was 20/20 OU; pupils were equal, round, and reactive to light and accommodation; extraocular muscle movements were normal; and cranial nerves II to XII were normal. The remaining general physical and neurological examinations were also normal. The patient was diagnosed as having atypical migraine; was treated with Demerol 50 mg IM, Phenergan 50 mg IM, and Aristacort, 40 mg IM; and was given a prescription for cafergot. She was instructed to return ff the headache did not improve. The patient did return the following day with blurred vision and persistent headache that were unresponsive to cafergot. Her visual acuity was 20/30 OU; otherwise, the physical examination remained unchanged. She was again diagnosed as having atypical migraine and was given Demerol and Phenergan. She was discharged with Tylenol with Codeine, and was instructed to rest and to return if the headache did not improve. The patient returned five days later complaining of loss of vision in her right eye. Her headache had subsided two days earlier, but upon arising that day she noted no vision in the right eye and "weak sight" in the left eye. She described vision in the left eye as grayish and somewhat clouded, which seemed to worsen while taking a hot shower. On physical examination the right pupil reacted consensually but not directly. Pupillary response in the left eye was normal. Visual acuity was light perception on the right and 20/20 on the left. There was a temporal hemianopsia on the left and the patient missed five plates on the color vision test. Funduscopic examination was normal bilaterally, with nonpainful extraocular muscle movements. The remaining cranial nerves were intact. There was no orbital, facial, or sinus tenderness, and the remaining neurological and physical examinations were normal. The laboratory values were all essentially normal, including CBC and dif-
13:11 November 1984
Annals of Emergency Medicine
Jeffrey Javerbaum, MD John A Mitchell, MD Randy Dawson, MD Bakersfield, California From the Emergency Medicine Residency Program, Kern Medical Center, Bakersfield, California. Address for reprints: Jeffrey Javerbaum, MD, Department of Emergency Medicine, Kern Medical Center, 1830 Flower Street, Bakersfield, California 93305.
1061/119
OPTIC NEURITIS Emergency Medicine Residency Program - Kern Medical Center
Fig. Conditions associated with optic neuritis/neuropathy.
ferential, ESR, electrolytes, BUN, glucose, thyroid studies, and a negative ANA and VDRL. On lumbar puncture, CSF was clear and acellular, with normal pressure and normal chemistries, including oligoclonal bands, myelin basic protein, and IgG. Skull radiography, sinus series, and CT scan were unremarkable.
DISCUSSION Jeffrey Javerbaum, MD: Optic neuritis (ON) is a general term used to designate an inflammatory, degenerative, or demyelinating condition of the optic nerve1 which is usually acute and unilateral, and is accompanied by some loss of vision.2 The inflammation may be located anywhere from the optic disc to the optic chiasm3 Papillitis refers to inflammation involving that portion of the nerve that can be visualized ophthalmoscopically. It is characterized by swelling of the optic disc, and is generally indistinguishable from papilledema. Retrobulbar neuritis refers to inflammation situated more posteriorly and without acute fundusc0pic changes. The term ON is often used in a confusing and unrestricted sense to include many diverse forms of optic neuropathy. 3 It is useful to separate the more common demyelinating variety from rarer optic neuropathies arising secondary to systemic illness. In the latter instances (Figure}, the clinical presentation, course, and management will be affected by the associated disease. Among the many conditions underlying ON, multiple sclerosis {MS) is the most common.4 Perhaps for this reason the incidence of ON peaks in the twenties and declines with age.a, s Pathologically there is infiltration of the nerve with inflammatory cells followed by swelling and fragmentation of nerve tissue. Subsequently macrophages axe seen in the process of phagocytizing myelin breakdown productsA
Question: What are the symptoms of optic neuritis? Dr Javerbaum: Disturbance of vision in one eye is the most outstanding complaint. Visual acuity usually ranges from 20/200 to no light perception (NLP). The loss of vision is attributed to a scotoma in the central portion of the visual field.~ While visual loss is often rapid in onset, it may sometimes be progressive over weeks. 6 This problem may not be apparent until the unaffected eye is accidentally covered. The patient's vision may be described as blurred or dim - - as though looking through frosted glass. There may also be complaints of photophobia and diminution of vision in bright light.7 Another common disturbance is pain in or about the eye which is worsened by eye movement or palpation of the globe. As in our case, this pain may begin days to weeks before the onset of visual problems.2, s
Question: What physical signs are seen with optic neuritis? Dr Javerbaum: Visual acuity may be profoundly diminished on the involved side and may be worsened by bright illumination.7, 9 Complex visual field defects may be detected on careful screening. Most c o m m o n l y they are central scotomata involving the fixation point30 These scotomata may be more apparent with colored test objects than with white ones. 6 Hence, there may be an unsuspected loss of
120~062
Demyelination Primary (idiopathic) optic neuritis Multiple sclerosis Devic's disease Ischemia Atherosclerosis Temporal arteritis Periarteritis nodosa Systemic lupus erythematosis Inflammation Viral and postviral Encephalitis Meningitis Postvaccination (MMR, rabies) Tuberculosis, syphilis, mononucleosis Contiguous spread Intraocular inflammation Orbital inflammation Sinusitis Dental infections Metabolic disorders Diabetes mellitis Deficiency states (B1, B12) Toxins (methylalcohol, tobacco, arsenic, lead) Drugs (INH, ethambutol, quinine, penicillamine) Carcinoma
color vision detected by comparing colored objects viewed separately by each eye. Patients will report the colors appear "washed out" on the involved side. 2 This effect may be quantified using pseudoisochromatic plates. Loss of color vision occurs because of diminished input from the cones, which are most abundant at the macula. Close observation of the pupillary responses to light often shows a relative afferent pupillary defect (APD). This is due to loss of fibers in the afferent limb of the light reflex arc. While the pupils remain equal, there will be less constriction when light is shined into the involved eye than in the normal one. The involved pupil also may slowly redilate under sustained illumination.7 When each eye is illuminated in succession, there is a brisk constriction of the norreal pupil followed by a seemingly paradoxical dilation of the affected one in response to light.//This swinging flashlight test is reportedly abnormal in more than 90% of patients with ON. 12 Funduscopic abnormalities are seen in as many as 75% of patients with ON. 1 In acute papillitis, the disc may appear hyperemic and swollen, with blurred margins. The veins may be distended and without spontaneous pulsations. Scattered hemorrhages m a y be present about the disc. 2 While this picture may be identical to papilledema, a distinction can be made based on certain properties (Table). Following degeneration of a portion of the optic nerve fibers, optic atrophy may be a sequela of ON.6,13 Under these circumstances, the disc will appear pale, with margins that contrast sharply with the surrounding pink retina.
Question: Are any special tests helpful in making the diagnosis of ON? Dr Javerbaum: The value of testing visual fields and color
Annals of Emergency Medicine
13:11 November 1984
TABLE. Features distinguishing papillitis from papilledema Papillitis Visual acuity Color vision Pupils VF
Papilledema
4, 4,
Normal Normal
APD Variable defects (esp. central scotomata) Unilateral
Normal 1" Blind spot Bilateral
vision has been mentioned. Routine CSF studies are rarely useful; protein and lymphocytes may be mildly elevated. 14 Abnormal oligoclonal bands or elevated CSI IgG or myelin basic protein may suggest a diagnosis of MS. s Approximately 70% of patients with MS have elevated CSF IgG, while 90% have abnormal oligoclonal bands, is Fluorescein angiography is not helpful in differentiating between papillitis and a moderate degree of papilledema. 9 Visual evoked potentials may be sensitive in demonstrating an optic nerve lesion, but provide no information concerning cause.iS, 16 There are reports of nerve enlargement and swelling on CT scan and ultrasound, lz-19 Question: What is the relation of optic neuritis to multiple sclerosis? Dr Javerbaum: In recent studies the risk of developing MS following ON ranges from 8.3% lo to 75%. 5 Standard criteria for the diagnosis of MS require more than one CNS lesion. 2o Whether the idiopathic variety of ON represents a self-limited, local variant of MS remains undetermined. Yet the strong association between ON and MS suggests that they may share a common etiology. A variety of infectious and autoimmune etiologies have been proposed, is Occasionally ON will be accompanied by transverse myelitis (Devic's disease). Hence, complete neurologic examination and a thorough probe for prior neurologic disturbance are essential in all patients with ON. For unknown reasons, elevated temperature can sometimes precipitate transient exacerbations of MS. This observation led to the formerly popular "hot bath test." By immersing the patient in warm water, clinicians were able to provoke otherwise subclinical neurologic dysfunction and confirm the diagnosis of MS. 21 Because bilateral ON appears more likely to progress to MS than does unilateral ON, 4 our patient's bilateral involvement and worsening of vision OS following a hot shower indicates an increased risk to develop MS. Finally, she has recently developed sensory disturbances in the left leg, now strongly suggesting that she has MS. Question: What is the natural history of optic neuritis?
Dr Javerbaum: Spontaneous recovery within one to four weeks is the role.2, 8 Vision usually returns to normal despite the development of optic atrophy in most patients. 6 Prognosis is further determined by the presence of underlying conditions, such as MS. 13:11 November 1984
Question: Is there any treatment for optic neuritis? Dr Javerbanm: Many clinicans will try systemic or retrobulbar corticosteroids in severe or refractory cases. Trials using steroids in this manner have shown a tendency to shorten duration of visual symptoms and to lessen ocular pain when treatment is begun early. No controlled study has shown any method of treatment to influence final visual outcome.8 Question: How should patients be managed in the emergency department? Dr Javerbaum: Before making the diagnosis of ON, be certain that the patient does not have another, more treatable illness or a more life-threatening situation. If the disc is swollen, one must rule out papilledema and the possibility of an intracranial mass or hemorrhage, or malignant hypertension. Pseudotumor cerebri presents with headache, visual disturbance and blurred discs, and requires prompt intervention. Retinal artery occlusion, retinal vein thrombosis, and temporal arteritis can all produce sudden visual loss, and should be managed urgently. ON secondary to INH therapy necessitates discontinuation of the drug. 22 While ON rarely is confused with meningitis, the latter possibility should always be given high priority in the emergency setring. Finally, complicated migraine is a diagnosis of exclusion, requiring that other explanations for headache with neurologic disturbance first be excluded. The initial misdiagnosis of atypical migraine in this case underscores that fact.
REFERENCES 1. Walsh FB, Hoyt WF: Clinical Neuroophthalmology, ed 3. Baltimore, Williams and Wilkins, 1969, pp 607-641. 2. Bradley WG, Whitty CWM: Acute optic neuritis: Its clinical features and their relation to prognosis for recovery of vision. J Neurol Neurosurg Psychiat 1967;30:531-538. 3. 8cheie HG, Albert DM: Textbook of Ophthalmology. Philadelphia, WB Saunders, 1977, pp 494-496. 4. Hutchinson WM: Acute optic neuritis and the prognosis for multiple sclerosis. J Neurol Neurosurg Psychiatr 1976;39:283289. 5. Nikoskelainen E, Frey H, Aimo S: Prognosis of optic neuritis with special reference to cerebrospinal fluid immunoglobulins and measles virus antibodies. Ann Neurol 1981;9:545-550. 6. Hyllsted I{, Moller PM: Follow-up on patients with a history of optic neuritis. Acta Ophthal 1961:39:655-662. 7. Gunn M: Discussion on retro-ocular neuritis. Trans Ophthal Soc UK 1897;17:107-217. 8. Perkin GD, Rose FC: Optic Neuritis and Its Differential Diagnosis. Oxford, England, Oxford University Press, 1979, pp 34-36, 172-182, 194-197. 9. Bender MB, Rudolph SH, Stacy CB: The neurology of the visual and oculomotor systems, in Baker AB, Baker LH (eds): Clinical Neurology, revised edition. Philadelphia, Harper and Row, 1982, vol 1, chap 4, p 10. 10. Isayama Y, Takahashi T, Shimoyoma T, et ah Acute optic neuritis and multiple sclerosis. Neurology (NY) 1982;32:73-76. 11. Levatin P: Pupillary escape in disease of the retina or optic nerve. Arch Ophthalmol 1959;62:768-779. 12. Cox TA, Thompson 8H, Corbett JJ: Relative afferent pupillary defects on optic neuritis. Am J Ophthalmol 1981;92:685-690.
Annals of Emergency Medicine
1063/121
OPTIC NEURITIS Emergency Medicine Residency Program - Kern Medical Center
Soc UK 1959;79:701-716.
i8. Rush JA, Kennerdell IS, Martinez AJ: Primary idiopathic inflammation of the optic nerve. Am ! Ophthalmol 1982;93: 312-316.
14. Sandberg-Wollheim M: Optic neuritis: Studies on the cerebrospinal fluid in relation to clinical course in sixty-one patients.
19. Coleman JD, Lizzi FC, Jack RL: Ultrasonography of the Eye and Orbit. Philadelphia, Lea and Febiger, 1977, p 307.
Acta Neurol Scand 1975;52:167-178.
20. Poser CM, Paty DW, Scheinberg L, et al: New diagnostic criteria for multiple sclerosis: Guidelines for research protocols. Ann Neurol 1983;13:227-331. 21. Michael JA, Davis FA: Effects of induced hyperthermia in multiple sclerosis: Differences in visual acuity during heating and recovery phases. Acta Neurol Scand 1973;49:141-151. 22. Mandell GL, Sande MA: Antimicrobial agents - - Drugs used in the chemotherapy of tuberculosis and leprosy, in Gilman AG, Goodman LS, Gilman A (eds): The Pharmacologic Basis of Therapeutics, ed 6. New York, Macmillan 1980, pp 1202-1203.
13. Lynn BH: Retrobulbar neuritis. A survey of the present condition of cases occurring over the last fifty-six years. Trans OphthaI
15. McFarlin DE, McFarland HF: Multiple sclerosis. N Engl J Med 1982;307:1183-1188, 1246-1250. 16. Cohen SN, Syndulko K, Tourtellotte WW: Visual evoked potentials in the diagnosis of multiple sclerosis, in Poser CM (ed): Diagnosis of Multiple Sclerosis. New York, Thiame-Stratton (in press). 17. Howard CW, Osher RH, Tomsak RL: Computed tomographic features in optic neuritis. Am ! Ophthalmol 1980;89:699-702.
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Annals of Emergency Medicine
13:11 November 1984