Common Neuro-Ophthalmic Pitfalls: Case-Based Teaching

✍ Scribed by Dr Valerie A. Purvin, Dr Aki Kawasaki

• Publisher: Cambridge University Press
• Year: 2009
• Tongue: English
• Leaves: 235
• Series: Cambridge Medicine
• Edition: 1
• Category: Library

✦ Synopsis

Using real-life cases describing patients with neuro-ophthalmic disorders, this book is a case-based teaching tool that bridges the gap between textbook information and everyday clinical practice. Each case illustrates a particular area of frequent diagnostic confusion, and highlights the specific clinical features that should point to the correct diagnosis. Focusing on errors in this way serves as motivation to the clinician to master the material so that 'pitfalls' can be avoided. The level of the case discussions assumes that the reader has some familiarity with basic neuroanatomy, physiology and disease process but each case discussion furnishes a brief review of such information, always with an emphasis on those features that are clinically relevant. The case-histories are succinct and amply illustrated, including motility and fundus photographs, visual fields and radiographic studies. The narrative is moved along with questions to the reader, making it easy to follow the logic of the cases.

✦ Table of Contents

Cover......Page 1
Half-title......Page 3
Title......Page 5
Copyright......Page 6
Contents......Page 7
Foreword......Page 9
Preface......Page 11
Acknowledgements......Page 13
1 When ocular disease is mistaken for neurologic disease......Page 15
What maneuver might be helpful for confirming our suspicion that this patient’s double vision is ocular in nature?......Page 16
What test was done and what was the diagnosis?......Page 18
Having excluded compressive, inflammatory and infiltrative causes of optic neuropathy, what othermechanisms would you consider? How would you proceed?......Page 22
Painful mydriasis......Page 24
What clues suggest an alternative diagnosis?......Page 26
Invisible retinal disease......Page 27
What aspect of this patient’s positive visual phenomenon is highly atypical for migraine?......Page 28
What othermechanism of visual loss would you consider? Are there any historical features that are helpful here?......Page 31
Whymight a retinal stroke not have been apparent on examination?......Page 32
What specific aspect of this patient’s history suggests the correct localization of his visual problem?......Page 33
Swirling vision......Page 35
This patient’s work-up addressed the possibility of retinal vascular disease as the cause of his transientmonocular visual loss (TMVL). Is there something about his history, however, to suggest a different mechanism for his episodes?......Page 37
Twinkling scotoma......Page 38
Glaucoma......Page 39
Incidental elevation deficit......Page 41
What othermechanism could account for this patient’s abnormal ocularmotility besides a third nerve palsy?......Page 43
Diagnosis: Orbital floor fracture with muscle entrapment......Page 45
What clinical features help to localize the source of this patient’s ocularmotility disorder?......Page 46
What other forms of ptosismight share a similar history of worsening with sustained use?......Page 48
What is the anatomic significance of a superior division palsy?......Page 51
The investigation thus far has revealed no intracranial pathology. How would you proceed?......Page 52
What specific feature of her clinical course raises the possibility of orbital disease?......Page 54
Optic perineuritis......Page 57
Headaches and elevated discs......Page 59
Inferior altitudinal visual field defects......Page 64
Are there clues to the correct diagnosis in this case?......Page 65
Incidental abduction deficit......Page 67
Intermittent vertical diplopia......Page 68
How would you pursue a diagnosis of congenital fourth nerve palsy in this patient?......Page 69
Duane’s syndrome......Page 71
Congenital superior oblique palsy......Page 72
Is there a problem with the diagnosis of “chronic optic neuritis”?......Page 73
What additional radiographic evaluation should be obtained?......Page 75
Headache and papilledema......Page 77
Why is the current study incomplete?......Page 80
Diagnosis: Postganglionic Horner syndrome......Page 83
The above clinical findings are characteristic of a postganglionic Horner syndrome. Howmight this be related to her preceding trauma?......Page 84
What is the diagnosis? What confirmative study would you order?......Page 86
What aspect of this patient’s presentation provides the most compelling diagnostic clue?......Page 89
Bilateral idiopathic sixth nerve palsy......Page 90
What are the most common causes of bilateral sixth nerve palsy and what mechanism ismost likely in this case?......Page 91
Diagnosis: Clivus tumor......Page 93
What features of this case are atypical for a diagnosis of IIH? What alternative diagnosis should be considered?......Page 94
Vertical diplopia......Page 95
Diagnosis: Symmetric Graves’ disease......Page 96
Cerebral venous thrombosis......Page 97
Chronic sixth nerve palsy......Page 98
Empty sella......Page 99
Low cerebellar tonsils......Page 100
Sphenoid sinus mucocele......Page 101
Dolichoectatic basilar artery......Page 102
Dolichoectatic basilar artery......Page 104
Where is this patient’s lesion?......Page 105
Painful ophthalmoplegia and visual loss......Page 108
Based on the clinical findings, where is the lesion?......Page 109
What is thismotility pattern, and what does it tell you about the mechanism of the patient’s diplopia?......Page 110
What is the significance of this visual field pattern? Does it help to illuminate the findings on her MRI?......Page 112
Painful ophthalmoplegia......Page 114
Lateral geniculate body......Page 115
Painless central gray spot in a teenager......Page 117
What is the most likely cause of this patient’s neuroretinitis, and how would you test for it?......Page 118
This patient had an additional non-ocular symptom which she did not volunteer because she didn’t think it was relevant to her eye problem, yet this symptom was an important clue to the correct diagnosis. What question should be asked?......Page 121
What examination techniques can help in the detection of nystagmus when the oscillatory amplitude is particularly small?......Page 124
Farmer with an adduction deficit......Page 127
Dural-cavernous fistula......Page 128
Downbeat nystagmus......Page 129
Abnormal field and night blindness......Page 131
How would you describe this patient’s visual field defect? What diagnoses should be considered?......Page 132
Constricted fields after herniation......Page 134
What bedside test can help distinguish non-organic field loss from true constriction of the visual field?......Page 135
Sudden difficulty reading the paper......Page 136
What simple “bedside” test could be performed to further investigate this patient’s symptom?......Page 137
Post-cardiac bypass visual loss......Page 139
Diagnosis: Bilateral homonymous hemianopic scotomas secondary to bilateral occipital tip strokes......Page 141
Incidental field defect......Page 142
Diagnosis: Tilted disc syndrome......Page 144
Abnormal fields and temporal disc pallor......Page 146
Diagnosis: Dominant optic atrophy......Page 147
What aspect of this patient’s visual field defect is atypical for chiasmal compression and suggests instead an ocular disorder?......Page 148
Dominant optic atrophy......Page 149
Was there a “red flag” at the time of his initial presentation?......Page 151
Acute tonic pupil vs. pharmacologic mydriasis......Page 153
What examination finding can distinguish pharmacologic blockade from postganglionic denervation of the iris sphincter?......Page 154
Chronic tonic pupils vs. Argyll Robertson pupils......Page 156
Is there a physical finding that can differentiate chronic Adie’s pupils from Argyll Robertson pupils?......Page 157
What clinical findings would support a diagnosis of convergence spasm?......Page 158
Wernicke's encephalopathy vs. brainstem stroke......Page 160
What metabolic abnormality can produce this clinical picture?......Page 161
Chronic progressive external ophthalmoplegia vs. progressive supranuclear palsy......Page 163
This combination of horizontal and vertical gaze limitation with slowed saccades could be due to either supranuclear gaze palsy or ocular myopathy. How can we distinguish these two mechanisms?......Page 164
This patient’s right abduction deficit suggested a sixth nerve palsy. What othermechanism might be responsible and what clinical features suggest this alternative cause?......Page 166
Convergence spasm......Page 167
Sixth nerve palsy vs. orbital myositis......Page 168
10 Over-reliance on negative test results......Page 169
In the absence of any objective abnormalities, would you consider that thismight be non-organic visual loss, perhaps due to job-related stress?......Page 170
Visual loss due to nutritional deficiency was suspected based on hermacrocytosis, however her serum B12 level was within the normal range. What would you like to do next?......Page 171
Now we understand the basis of this patient’s visual field defect. But what is causing her persistent photopsias?......Page 172
Painless ptosis and diplopia......Page 174
Diagnosis: Ocularmyasthenia......Page 175
Which diagnostic possibilities should be addressed first?......Page 176
What additional test should be obtained?......Page 177
What is the most likely etiology in this patient and how would you proceed with the evaluation?......Page 179
Diagnosis: One-and-a-half syndromesecondary to a clinically isolated demyelinating event......Page 181
What disease processes would you consider here?......Page 182
Can you localize this patient’s problem?......Page 183
What other investigations might be helpful?......Page 186
What do youmake of this patient’s negative neuro-imaging in light of her clinical presentation?......Page 187
One-and-a-half syndrome......Page 191
Shunt failure with negative neuro-imaging......Page 192
Isolated unilateral mydriasis......Page 193
If an isolated, enlarged and poorly reactive pupil is not a sign of a pCOM aneurysm, what other causes should be considered?......Page 194
Acute unilateral visual loss with disc edema......Page 195
Can you diagnose the cause of this patient’s acute monocular visual loss based on the clinical findings? Are ancillary tests needed?......Page 197
What is the most likely diagnosis and what evaluation would be appropriate?......Page 198
Does this patient need neuro-imaging? An EEG? Other investigation?......Page 200
What feature in this case suggests nonorganic visual loss? Is additional ancillary testing needed?......Page 202
Vasculopathic cranial mononeuropathy......Page 203
Non-organic visual loss......Page 204
Management of idiopathic intracranial hypertension......Page 205
Evaluation and treatment of giant cell arteritis......Page 208
Overzealous treatment of blood pressure in NAION......Page 211
Prednisone for demyelinating optic neuritis......Page 213
Over-reliance on pyridostigmine bromide (Mestinon) in ocular myasthenias......Page 214
Failure to provide symptomatic treatment......Page 217
Non-arteritic anterior ischemic optic neuropathy......Page 219
Nystagmus......Page 220
Index......Page 221