The picture presented to us is that of a Horner syndrome (miosis with ptosis) so the possibilities are reduced to options 3 or 4, but they specify that the patient presents gait instability, which is not justified by a Horner due to carotid dissection affecting the superior cervical ganglion, which is what they want us to believe when they talk about pain in the neck and in the eye. If the patient really has ataxia, the only possible location would be the spinal cord.

A 25-year-old patient, during a tennis match, has intense pain in the neck and in the left eye. The next morning he wakes up with a feeling of gait instability and has palpebral ptosis of the left eye and anisocoria, with the left pupil being smaller than the right. The patient maintains good visual acuity. Where would you most likely locate the lesion?

[Bilateral internuclear ophthalmoplegia in association with basilar artery occlusive disease].

A 56 year-old man presented with vertigo and the right sided weakness. Neurological examination revealed a lethargic man with good orientation to three spheres. His neck was supple. He had anisocoria, the right pupil being larger than the left by 1.5 mm with sluggish light reaction bilaterally. He had exotropia of the right eye in primary gaze. The abduction of both eyes were full with terminal horizontal nystagmus. The adduction of both eyes were quite limited in each eye. He had a limited upward gaze with poor convergence. These were interpreted as the syndrome of the medial longitudinal fasciculus (MLF) bilaterally. He had a depressed gag reflex on the right side with tongue deviation to the right. He had a mild weakness of the right side limb and also had the right sided hemihyperesthesia including his face to pain and temperature. Twenty four hours after the onset, the left brachial angiography revealed a complete occlusion of the rostral portion of the basilar artery without visualization of the posterior cerebral and superior cerebellar arteries bilaterally. CT scans three days after the onset revealed a low density area in the mid pons with extension rostrally up to the mesencephalon. Four days later he became quadriplegic with bilateral horizontal gaze palsy. No more internuclear ophthalmoplegia is noted on both sides. The midline location of the MLF in the pons, and the separate blood supplies by different paramedian branches of the basilar artery, form the anatomical explanation for the frequent unilaterality of vascular and bilaterality of demyelinating lesions. Bilateral MLF syndrome has been considered almost pathognomonic of multiple sclerosis.(ABSTRACT TRUNCATED AT 250 WORDS)

[A 62-year-old man with an acute onset of consciousness disturbances].

We report a 62-year-old man who developed coma and died in a fulminant course. The patient was well until May 1, 1996 when he noted chillness, tenderness in his shoulders, and he went to bed without having his lunch and dinner. In the early morning of May 2, his families found him unresponsive and snoring; he was brought into the ER of our hospital. He had histories of hypertension, gout, and hyperlipidemia since 42 years of the age. On admission, his blood pressure was 120/70, heart rate 102 and regular, and body temperature 36.3 degrees C. His respiration was regular and he was not cyanotic. Low pitch rhonchi was heard in his right lower lung field. Otherwise general physical examination was unremarkable. Neurologic examination revealed that he was somnolent and he was only able to respond to simple questions such as opening eyes and grasping the examiner's hand, but he was unable to respond verbally. The optic discs were flat; the right pupil was slightly larger than the left, but both reacted to light. He showed ptosis on the left side, conjugate deviation of eyes to the left, and right facial paresis. The oculocephalic response and the corneal reflex were present. His right extremities were paralyzed and did not respond to pain Deep tendon reflexes were exaggerated on the right side and the plantar response was extensor on the right. No meningeal signs were present. Laboratory examination revealed the following abnormalities; WBC 18,400/ml, GOT 131 IU/l GPT 50 IU/l, CK616 IU/l, BUN 30 mg/dl, Cr 2.1 mg/ dl, glucose 339 mg/dl, and CRP 27.4 mg/dl. ECG showed sinus tachycardia and ST elevation in II, III and a VF leads and abnormal q waves in I, V5, and V6 leads. Chest X-ray revealed cardiac enlargement but the lung fields were clear. Cranial CT scan revealed low density areas in the left middle cerebral and left posterior cerebral artery territories. The patient was treated with intravenous glycerol infusion and other supportive measures. At 2: 10 AM on May 3, he developed sudden hypotension and cardiopulmonary arrest. He was pronounced dead at 3:45 AM. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that the patient had acute myocardial infarction involving the inferior and the true posterior walls and left internal carotid embolism from a mural thrombus. Post mortem examination revealed occlusion of the circumflex branch of the left coronary artery due to atherom plaque rupture and myocardial infarction involving the posterior and the lateral wall with a rupture in the postero-lateral wall. Marked atheromatous changes were seen in the left internal carotid, the middle cerebral and the basilar arteries; the left internal carotid and the middle cerebral arteries were almost occluded by thrombi and blood coagulate. The territories of the left middle cerebral and the occipital arteries were infarcted; but the left thalamic area was spared. The neuropathologist concluded that the infarction was thrombotic origin not an embolic one as the atherosclerotic changes were severe. Cardiac rupture appeared to be the cause of terminal sudden hypotension and cardiopulmonary arrest. It appears likely that a vegetation which had been attached to the aortic valve induced thromboembolic occlusion of the left internal carotid artery which had already been markedly sclerotic by atherosclerosis. It is also possible that the vegetations in the aortic valve came from mural thrombi at the site of acute myocardial infarction, as no bacteria were found in those vegetations.

[A 56-year-old man with fever, backache and tetraparesis].

We report a 56-year-old man who developed progressive paraparesis. He was apparently well, except for left Bell's palsy which developed on May 9 of 1994, for which he received stellate ganglion block on the left side more than ten times until July 2nd of 1994, when he noted pain in his left shoulder and in his lumbar region. On July 5th, he noted some difficulty in urination. On July 6th, he noted tingling sensation in his four extremities and difficulty in gait. He was admitted to another hospital where he was treated with intravenous infusion of glycerol. After this treatment, his gait and sensory disturbance showed some improvement, however, on July 7th, his shoulder and lumbar pain worsened, and he became unable to stand. His temperature went up to 39 degrees C on the next day. Lumbar CSF on that day contained 119 cells/microliters, 112 mg/dl of protein, and 53 mg/dl of sugar. He was transferred to our hospital on July 14th. His past medical history revealed that he had suffered from frequent bouts of osteomyelitis since the age of 13 years. He was operated on several times on osteomyelitis. He had been treated on his tooth ache until shortly before the onset of the present illness. He also received steroid hormone for his Bell's palsy. On admission, his consciousness varied from alert to stupor. His BP was 150/100 mmHg, HR 98/min and regular, BT 39.4 degrees C. The bulbar conjunctiva appeared somewhat icteric. Otherwise, general physical examination was unremarkable. On neurologic examination, there was no apparent dementia. Higher cerebral functions appeared intact. The optic discs were flat. Pupils were round and isocoric reacting to light and accommodation promptly. Ocular movements were full without nystagmus. Some exophthalmos was noted bilaterally. The sensation of the face and facial muscles were intact. The remaining cranial nerves also appeared intact. Nuchal rigidity was present. He was unable to stand or walk. Muscle strength was markedly diminished in all four limbs; manual muscle testing revealed 1 to 2/5 weakness in both upper and lower extremities bilaterally. Muscle stretch reflexes were decreased or lost in both upper and lower limbs, but the plantar response was extensor on the right. Sensation appeared to be diminished in legs, but detail was not clear because of disturbance of consciousness. Pertinent laboratory findings were as follows: WBC 12,800/microliter, GPT 58 IU/l, total bilirubin 2.65 mg/dl, and CRP 16.8 mg/dl. Cerebrospinal fluid contained 34 cells/microliter (approximately two thirds were neutrophils), RBC 1,110/microliter, 2,949 mg/dl of protein, and 119 mg/dl of glucose; stapylococcus aureus was cultured from the CSF. Myelogram showed a filling defect in the anterior epidural space between the low thoracic and the upper lumbar region. The patient was treated with cephotaxim, aminobenzyl penicillin, and chloramphenicol. On the second hospital day, his BT was still 39 degrees C and he was agitated His weakness was worse than the previous day. Spinal MRI was attempted; as he was agitated 5 mg of diazepam was given intravenously at 4 PM. His respiration was rapid and somewhat shallow. At 6 PM, gadolinium DTPA was injected intravenously; at that time, he was breathing and pupils were 3 mm on both sides. At 6:35 PM, an examiner noted that he stopped breathing; the left pupil was dilated to 5 mm. Cardiopulmonary resuscitation was initiated immediately, and intubation was performed. He was placed on a respirator. His blood pressure did not reach 100 mmHg; he was in deep coma. Cardiac arrest occurred at 8:53 AM on the next morning. The patient was discussed in a neurological CPC. Most of the participants thought that the patient had either spinal epidural empyema or spinal subdural abscess. The question was what might be the original focus of infection. Three possibilities were considered, i.e., stellate ganglion block, teeth infection, and osteomyelitis...

[A 76-year-old man with loss of vision and dementia].

We report a 76-year-old man who developed blurred vision and dementia. He was apparently well until April 4, 1990 (70-year-old at that time) when he had a sudden onset of bilateral loss of vision. Corrected vision was 0.1 (right) and 0.09 (left). He was admitted to the ophthalmology service of our hospital on April 9, 1990, and neurological consultation was asked on April 11. Neurologic examination revealed alert and oriented man without dementia. Higher cerebral functions were intact. He had bilateral large visual field defects with loss of vision; he was only able to count the digit number with his right eye and to recognize hand movement with his left eye. Otherwise neurologic examination was unremarkable. General physical examination was also unremarkable; he had no hypertension. Cranial CT scan was normal on April 11; lumber spinal fluid contained 1 cell/microliter, 63 mg/dl of sugar, and 97 mg/dl of protein; myelin basic protein was detected, however, oligoclonal bands were absent. He was treated with methylprednisolone pulse therapy and oral steroid, however, no improvement was noted in his vision. He started to show gaze paresis to left, ideomotor apraxia, agnosia of the body, and dementia. Cranial CT scan on June 11 revealed a low density area in the deep left parietal white matter facing the trigonal area of the lateral ventricle. He was discharged on July 2, 1990. Hasegawa dementia scale was 2/32.5 upon discharge. In the subsequent course, he showed improvement in his mental capacity and Hasegawa dementia scale was 22.5/32.5 in 1991, however, no improvement was noted in his vision. In 1994, he started to show mental decline in that he became disoriented, and showed delusional ideation of self persecution and depersonalization with occasional confusional state. He also showed unsteady gait. Cranial MRI on February 13, 1996 revealed a T2-high signal intensity lesion on each side of the parietal deep white matter more on the left and another T2-high signal intensity lesion in the left pons as well as in the right thalamus. He complained of right hypochondrial pain and was admitted to another hospital on April 22, 1996. He was markedly confused and demented. He continued to show bilateral loss of vision, but no motor palsy was noted. Cranial CT scan on April 23, 1996 revealed diffuse cortical atrophy and ventricular dilatation in addition to the low density areas in both parietal deep white matter. He developed jaundice in the middle of May. Abdominal CT scan revealed multiple low-to iso-density areas in the liver and marked iso-to high-density swelling of the right kidney. The patient expired on June 9th, 1996. The patient was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had had a carcinomatous limbic encephalitis with optic neuropathy and a choleduct carcinoma. Other opinions entertained included acute disseminated encephalomyelitis with optic neuritis, and granulomatous angiitis of the central nervous system. Some participants thought the primary site of the carcinoma was the right kidney with metastasis to the liver. Post mortem examination revealed a mixed type carcinoma in the right kidney with liver metastases. Neuropathologic examination revealed an incomplete softening in the optic chiasm and the left optic nerve, and in the left parieto-occipital areas. (The right hemisphere was frozen for future biochemical assay.) One of the adjacent cortical arteries had an organized thrombus. Other arteries and arterioles also showed sclerotic changes. Some of the leptomeningeal arteries were positive for Congored staining as well as for beta-amyloid immunostaining. Many senile plaques were seen diffusely in the cerebral cortex and neurofibrillary tangles were seen in the CA1 area and the parahippocampal gylus. No cellular infiltrations or demyelinated foci were seen. The neuropathologic features were consistent with circulatory disturbance based on the amyloid angiopa

[An adult case of congenital Horner's syndrome with heterochromia iridis--with special reference to alteration of Horner's sign associated with development].

It is well known that when the Horner's syndrome is congenital, a defect in pigmentation of the iris is usual; all or part of the iris remains light brown. We reported an adult case of congenital Horner's syndrome with remission and relapse of unilateral ptosis. A 25-year-old man was admitted to our hospital for ophthalmologic surgical treatment of right ptosis. According to the patient's mother, the patient was delivered with the aid of forceps at birth, and the right ptosis was observed during the first few days of his life. At 2 to 3 years of age, his parents noted lighter color of the right eye. The right ptosis was gradually improved as he grew older. However, he developed right ptosis again with left meralgia paresthesia since eighteen age. At age 25 years, he was noted to have right ptosis, right miosis (the left pupil measured 4.5 mm in diameter and the right 3.0 mm), right heterochromia iridis with pigmented iris nevi, and left meralgia paresthesia . Laboratory data of urine, blood and CSF as well as radiological studies of chest X-ray, skull X-ray, spine X-ray, brain MRI and spinal cord MRI showed unremarkable. Sweating test was intact, pharmacologic test to Horner's syndrome with 5% cocaine and 1.25% 1-epinephrine indicated that the damage was pointed to the post ganglionic sympathetic neuron. Ten patients with congenital Horner's syndrome reported in Japan since 1953 were reviewed including our case. Ten of eleven were male and Horner's sign was recorded on the left eye in 8 cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Neurology_Adams

Figure 12-2 illustrates the visual field defects caused by lesions of the retina, optic nerve and tract, lateral geniculate body, geniculocalcarine pathway, and striate cortex of the occipital lobe. In the alert, cooperative patient, the visual fields can be plotted fairly accurately at the bedside. With one of the patient’s eyes covered and the other fixed on the corresponding eye of the examiner (patient’s right with examiner’s left), a target—such as a moving finger, a cotton pledget, or a white disc mounted on a stick—is brought from the periphery toward the center of the visual field (confrontation testing). With the target at an equal distance between the eye of the examiner and that of the patient, the fields of the patient and examiner are then compared. Similarly, the patient’s blind spot can be aligned with the examiner’s, and its size determined by moving a small target outward from the blind spot until it is seen. For reasons not known, red-green test objects are more

An Interesting Case of Pupillary Changes During the Testing of Ocular Movements and its Influence on the Diagnosis?

To describe an unusual case presentation of a decompensating exotropia with an incidental pupil anomaly highlighting the importance of observing pupils during the assessment of ocular movements. A case whose signs included an exotropia and an enlarged tonic pupil which were initially mistaken for an atypical case of Oculomotor nerve palsy, triggering immediate imaging investigations. We discuss how understandable it would be for experienced clinicians to arrive at this case's misdiagnosis and how it could have been avoided thereby helping to preserve where possible costly resources of neuro imaging and inpatient stays. A 71 year old man who was seen as a tertiary referral case by the Queen Elizabeth Hospital Birmingham's (QEHB's) neuro-ophthalmology service, where a second opinion for the patient was sought from a neurology team from another hospital. He was seen by the orthoptist and neuro-ophthalmologist consultant. On presentation at QEHB visual acuity measured 6/9 Snellens in each eye with varifocals, improving to 6/6 with pinhole testing, the fundi and optic discs were normal. Anisocoria was noted with the left pupil being larger than the right pupil. Orthoptic assessment revealed a small angle left exotropia on cover test, increasing in size on alternate cover test with a blink type recovery to its original angle. An orthoptic diagnosis of a decompensating left microexotropia with identity was given. In the left eye there was a slight mechanical restriction in adduction, underacting superior rectus and a larger underacting inferior rectus with an "A" type alphabet pattern with symptoms of horizontal diplopia on all right gaze positions. There was no evidence of ptosis, convergence was intact and saccades were fast and appeared of a normal velocity. The anisocoria appeared more obvious when the patient looked to right gaze where his left pupil seemed to enlarge further. Assessment of the pupillary function led to the patient being diagnosed as having bilateral asymmetrical Adies (tonic) pupils. This case highlights the importance of not only carrying out a detailed pupil reaction assessment but also the necessity of observing the pupils during the assessment of ocular movements. This case highlights how anisocoria can mislead a clinician's attention to believing that only one particular pupil is abnormal where as it could be both. Also it highlights that the classic combination of symptoms and observations of diplopia, exotropia, longstanding incomitance and anisocoria in terms of a dilated pupil may not necessarily be an Oculomotor cranial nerve palsy and requiring the patient to undergo imaging investigations on an urgent basis may be avoided.

A cataract, 'a million cut' radial keratotomy, and Marfan syndrome February consultation #1.

A 56-year-old man with an ocular history of 20+ cut radial keratotomy (RK) in both eyes and Marfan syndrome presented with blurred vision in both eyes 2 years previously. He was intolerant of contact lenses and was correctable with spectacles for the past 10 years. His presenting photographs and corneal topographies are shown in Figures 1 and 2JOURNAL/jcrs/04.03/02158034-202102000-00022/figure1/v/2021-04-12T204757Z/r/image-tiffJOURNAL/jcrs/04.03/02158034-202102000-00022/figure2/v/2021-04-12T204757Z/r/image-tiff, respectively. His left eye had greater than 270 degrees of zonulopathy and a visually significant cataract. He underwent a planned pars plana lensectomy/vitrectomy and implantation of a scleral-fixated CZ70BD (Alcon Laboratories, Inc.) intraocular lens (IOL). He has enjoyed adequate vision in the left eye and now has a worsening cataract in his right eye. He is a practicing dentist and requested the fastest visual rehabilitation possible. His corrected distance visual acuity was 20/50 with a manifest refraction of +5.00-4.00 × 90 in the right eye and 20/25 with a manifest refraction of +1.75-2.50 × 180 in the left eye. Intraocular pressure (IOP) was measured at 16 mm Hg in both eyes, and extraocular motility, confrontational visual fields, and pupils were normal in both eyes. On slitlamp examination, he had mild ptosis in both eyes, the corneas had 20+ RK with multiple arcuate incisions at the 3- and 9-o'clock positions in both eyes, the anterior chamber (AC) was deep and quiet in both eyes, both irides had mild iridodonesis, the right lens had a 2 to 3+ nuclear sclerotic cataract with 6 clock hours of superotemporal zonulopathy that was only evident with dilation (Figure 3JOURNAL/jcrs/04.03/02158034-202102000-00022/figure3/v/2021-04-12T204757Z/r/image-tiff) and no phacodonesis. The left lens had a well-positioned CZ70BD IOL fixated at 6 and 12 o'clock without extrusion or exposure of the Gore-Tex suture. The posterior segment examination was unremarkable. What counseling would you provide for this patient in preparation for surgery? How would you plan the IOL calculations? What intraoperative techniques would you use to achieve the safest outcomes given his comorbidities?

[Superior oblique myokymia--a case report and pathogenetic consideration].

A 30-year-old male visited us with complaints of dizziness and diplopia of abrupt onset in September, 1988. Neurological studies demonstrated paroxysmal rotatory to-and-fro oscillations of the left eye. There has been the same clinical episode at 25 years of age, lasting approximately 6 months. The characteristics of his ocular involuntary movement with the mild IVth cranial nerve paresis were as follows: quick, nonrhythmic, initially counterclockwise-rolling, more prominent in moving the left eye to the lower medial side, persisting for 1-10 seconds and rapidly repeated oscillations. When oscillations were prominent, he complained of faintness in addition to double vision. Except for the ocular signs, other neurological and laboratory examinations including cerebrospinal fluid, brain MRI and brain stem auditory evoked response, failed to disclose the precise location and nature of the lesion. Abnormal ocular movement was fluctuating for 4 months and gradually disappeared without any medication. In conclusion, the faintness could be considered to result from a lesion of reticular activating system adjacent to the IVth cranial nerve nucleus and its rostral (excitatory or inhibitory) supranuclei, and it suggests that a responsible lesion of the abnormal ocular movement is located at a region of the dorsomedial midbrain.

Unilateral progressive epitheliopathy after LASIK.

A 36-year-old man was referred back to our clinic after an uneventful laser in situ keratomileusis (LASIK) surgery 6 months previously, with a chief complaint of declining vision in the left eye for the last several months. His pertinent ocular history prior to the LASIK surgery was significant for episodic left eye irritation and inflammation of the superior part of the left cornea secondary to contact lens-induced keratopathy, according to his optometrist.This was a femtosecond-assisted LASIK surgery using the WaveLight FS200 femtosecond laser (Alcon) with the Allegretto EX500 excimer laser (Alcon) for attempted correction of -4.50 diopter (D) of myopia in both eyes under an 8.8 mm flap with a thickness of 100 μm. The uncorrected distance visual acuity (UDVA) was 20/15 in both eyes for the first 2 weeks; at the 1-month follow-up visit, a well-demarcated, wavelike plaque of coarse, thickened corneal epithelium along the superior aspect of the cornea was noted. The UDVA had declined to 20/30 in the left eye. The right eye remained clear with a UDVA of 20/15. The patient was treated for presumed interface inflammation with 1% topical prednisolone acetate for 3 weeks on a tapering regimen and it was noted that there was some improvement in the vision subjectively although the epithelial ridge involving the superior one third of the LASIK flap was present without any change.Over the course of the next 2 months, a progressive decline in vision was noted in the left eye. At no point did his right eye experience symptoms or visual decline. Four months postoperatively the UDVA had declined to 20/60 in the left eye. A linear epithelial ridge extending from limbus at 11 to 2 o'clock position was noted superiorly; staining showed the ridge involved the superior aspect of the flap. The patient was again given corticosteroid treatment, which would improve the symptom of irritation without any change in the visual acuity. Over the course of the next few months, a new wave of abnormal epithelium involving the inferior aspect of the limbus and the flap, encompassing the 2 o'clock position of the flap from the 4 to 6 o'clock positions, was also noted ().(Figure is included in full-text article.)Conjunctival staining using lissamine green and fluorescein dye showed staining of the well-demarcated epithelial ridge superiorly and inferiorly involving the flap encroaching the visual axis. On examination, the patient's corrected distance visual acuity was now 20/80 in the left eye. , , and show the tomographic, topographic, and optical coherence tomography (OCT) results at the 6-month follow-up post-LASIK surgery.(Figure is included in full-text article.)(Figure is included in full-text article.)(Figure is included in full-text article.)Preoperatively the patient denied any ocular history but on further questioning at the 6-month follow-up visit, he provided information about the use of systemic isotretinoin (Accutane) for juvenile acne for 1 year at age 17 and potential exposure to chemicals during military service although he denied any specific ocular exposure. He is a barbeque enthusiast and brews his own alcohol but denies any thermal or direct injury to either eye. His mother had recently told him that he might have had battery acid exposure when he was very young, before age 10, but never required medical attention.What is the most likely diagnosis? What medical or surgical interventions would you recommend for this patient? What is the prognosis for this patient?

[An acute syndrome of opsoclonus and body tremulousness. A case report of benign encephalitis].

A 30-year-old woman was admitted to our hospital in May 1977, suffering from oscillation, body tremulousness and astasia-abasia. Two months prior to admission she had caught a common cold and felt paresthesia on the right arm. Three days before admission, she had photophobia, tremulousness of the trunk and head, and astasia-abasia. A neurological examination revealed difficulty in standing, and jerky movement of the body and right arm, her limbs were well coordinated. An ocular examination resulted in normal findings except for intermittent oscillation of the eyeballs. As the pupils and fundi were normal, so were the routine laboratory tests. The cerebrospinal fluid was clear and colorless under normal pressure, and showed no more than 6 mononuclear cells in any of the three examinations. CSF protein was registered 20 mg/dl, glucose 75 mg/dl, and no virus titers were elevated. Electroencephalogram was slightly abnormal due to a slowing of the Alpha wave in the background activity. Both computerized tomography and vertebral-angiography were normal. A slow and steady abatement of all symptoms started while she was taking steroid treatment in hospital. Electrooculogram showed irregular disconjugation of the eyes rotating or moving in horizontal and vertical direction. There movements conjugated or disconjugated in both eyes with 5-7 Hz of frequency and 10-20 degrees of amplitude. They decreased when the eyelids were closed or staying in a dark room. These ocular movements were regarded as opsoclonus. Then opsoclonus changed to flutter-like oscillation.(ABSTRACT TRUNCATED AT 250 WORDS)

Rapid, painless unilateral vision loss in a 37-year-old healthy woman.

A 37-year-old woman experienced painless, progressive vision loss to no light perception in the left eye over the course of 3 days. The right eye was unaffected. On examination, the only other abnormal finding was a +4 left afferent pupillary defect. She was initially diagnosed with retrobulbar optic neuritis and admitted for treatment with intravenous methylprednisolone. Neuro-imaging revealed a large right anterior cerebral artery aneurysm that crossed the midline to compress the left optic nerve. The aneurysm was treated with coil embolization, which was technically successful but which did not lead to significant improvement in vision.

Anatomy_Gray

Most of these changes are transient and are usually due to traction injuries during the surgical procedure. A 33-year-old fit and well woman came to the emergency department complaining of double vision and pain behind her right eye. She had no other symptoms. On examination of the right eye the pupil was dilated. There was a mild ptosis. Testing of eye movement revealed that the eye turned down and out and the pupillary reflex was not present. These findings revealed that the patient had an ipsilateral third nerve palsy (palsy of the oculomotor nerve [III]). The oculomotor nerve [III] is the main motor nerve to the ocular and extra-ocular muscles. It arises from the midbrain and pierces the dura mater to run in the lateral wall of the cavernous sinus. The oculomotor nerve [III] leaves the cranial cavity and enters the orbit through the superior orbital fissure. Within this fissure it divides into its superior and inferior divisions.

Anti-aquaporin-4 antibody-positive optic neuritis treated with double-filtration plasmapheresis.

The anti-aquaporin-4 (AQP4) antibody was recently reported to be associated with neuromyelitis optica (NMO). Optic nerve involvements in many NMO cases are bilateral and the prognosis is poor. However, it has been suggested that plasma exchange is effective for those patients when steroid pulse therapy is ineffective. Herein, we report successful treatment of a patient with NMO using double-filtration plasmapheresis (DFPP). A 22-year-old woman consulted a neurologist for neck pain in March 2008. High-intensity lesions were shown in the cervical spinal cord by T2-weighted magnetic resonance imaging. On July 15, the patient was referred to our department for a headache and pain and blurred vision in the left eye. The best-corrected visual acuity was 20/50 and 20/500 in the right and left eyes, respectively, with visual field defects observed in both. After 3 courses of steroid pulse therapy, anti-AQP4 antibodies were positive. In November, the patient again noticed visual acuity loss in the left eye and was treated by additional steroid pulse therapy, which was not effective. Next, she underwent plasma exchange therapy, though it was stopped due to hypotension and dyspnea. The next day, the patient underwent DFPP treatment and visual function gradually recovered. It is important to consider NMO when steroid pulse therapy is not effective. We successfully and safely treated NMO in a young adult patient using DFPP.

Doll's Eyes -- Definition/Introduction

The oculocephalic reflex is performed by holding a patient’s eyelids open and moving their head from side to side. The examination should only be performed on patients with a stable cervical spine without c-spine precautions. With the patient's eyelids open, the examiner briskly rotates the patient's head from side to side while the examiner observes the patient’s eyes. The examiner observes a positive oculocephalic reflex when the patient moves their eyes opposite of the rotation of their head, such that their eyes stay looking forward (like a doll’s eyes). The examiner observes a negative oculocephalic reflex when the patient’s eyes stay midline and do not move while the examiner rotates the head. A similar examination is performable for vertical eye movements. [6] Note that the designation of "positive" (eyes moving in the opposite direction of head movement indicating an intact brainstem function) or "negative" (eyes moving towards the same direction of head movement indicating severe brainstem dysfunction) doll's eyes reflex is an oversimplification and that some eye movement with nystagmus can occur in pathologic states. [7] The reflex is suppressed in a conscious adult with normal neurologic function but is active in a comatose patient with gross brainstem function, absent if there is damage to the reflex arc. [6]

Neurology_Adams

Normally, movement of the head at a rate of one to two cycles per second does not cause blurring of vision because of the rapidity with which the VOR accomplishes compensatory eye movements. Dynamic visual acuity is a term applied to testing by having the patient read an eye chart while the head is rotated back-and-forth. A substantial drop in acuity occurring with head movements at this speed is indicative of failure of the VOR. Zee has described yet another means of testing the VOR in which the examiner observes the optic nerve head while the patient rotates the head back and forth. With a normal VOR, the optic disc does not appear to move since the eye’s position in space has remained unchanged. However, if the VOR is impaired, the optic nerve head appears to oscillate. Visual Fixation Reflex (Suppression of the Vestibuloocular Reflex)

Consultation section. Cataract surgical problem.

A 68-year-old diabetic Pakistani presented with a 3 year history of progressive bilateral painless loss of vision. Although he was previously untreated for glaucoma, his examination revealed the following: visual acuity, finger counting in the right eye and 20/60 in the left; intraocular pressure (IOP), 41 and 31 mm Hg, respectively. Physical findings included bilateral shallow anterior chambers, minimal nuclear and cortical cataract formation, and extensive glaucomatous optic nerve cupping and atrophy worse in the right eye than in the left. Gonioscopy revealed angles narrowed to grade 1 for 360 degrees in both eyes. Visual field analysis was commensurate with the marked degree of optic nerve damage and reduced visual acuity. Bilateral laser iridotomies and a combination of topical antiglaucoma agents reduced IOP to the mid-20s in both eyes. Subsequently, the right eye had an uneventful trabeculectomy with application of intraoperative mitomycin. Postoperatively, the patient developed posterior aqueous entrapment and was managed with topical cycloplegics, aqueous suppressants, and corticosteroids. After a few weeks, a shallow anterior chamber was present centrally, a filtration bleb was noted, and IOP was 9 mm Hg. Unexpectedly, the patient returned to his native country, discontinued medications, and was lost to follow-up for 1 year. Upon his return, he presented with these findings: visual acuity, hand motion in the right eye and 20/60 in the left eye; IOP, 10 and 30 mm Hg, respectively. Physical findings in the right eye (Figure 1) included a superiorly oriented, thin-walled filtration bleb, a formed anterior chamber with multiple broad peripheral and midperipheral synechias, and a bound pupil covering a dense nuclear sclerotic cataract. The left eye had progressive glaucomatous optic nerve changes. Given the patient's history, now would you manage the glaucoma in the left eye, and what surgical methods would you plan for the right eye, assuming cataract surgery is indicated?

[Subacute sensory neuropathy manifestated by tonic pupils associated with small cell carcinoma of the lung].

Only a few cases of carcinomatous neuropathy with tonic pupils have been reported. In the present paper we described a 53-year-old woman with subacute sensory neuropathy who had presented with bilateral tonic pupils. She noticed numbness over the medial aspect of the left thigh in March, 1988, and then developed dysesthesia over the left forearm and hand, mild weakness of left upper and lower extremities and urinary disturbance. Neurological symptoms were subacutely progressive and she was bed-ridden in May. She was admitted to our hospital in June, 1988. On examination, she had body-weight loss of 6 kg during the last six months and general status was otherwise unremarkable. She had anisocoria; the left pupil was larger in daylight than the right, while smaller in dim light. The left pupil scarcely reacted to light, but promptly constricted to near vision. The right pupil constricted normally to light and near vision. An instillation of 0.0625% pilocarpine solution showed supersensitive response of both pupils. An instillation of 1.25% epinephrine solution demonstrated mild dilation of both pupils. Thus, it was conceivable that she had postganglionic ciliary nerve damage characteristic of tonic pupil as well as the lesion of sympathetic nerve innervating pupillary dilator. She had severe sensory ataxia and pseudoathetosis of the hands. Weakness was mild to moderate in extremities. Almost all deep tendon reflexes were absent. All modalities of sensation, particularly on deep sense, were severely involved with sea-level-type distribution below Th7, and over C2 to C3 regions on the left side.(ABSTRACT TRUNCATED AT 250 WORDS)

Human ocular torsional position before and after unilateral vestibular neurectomy.

The static ocular torsional position of both eyes of 23 patients was measured by means of fundus photographs one day before and one week after unilateral vestibular neurectomy for the treatment of acoustic neuroma, Ménière's disease or paroxysmal vertigo. The results showed that in all patients the vestibular neurectomy caused both eyes to tort (i.e. to roll around the visual axis) toward the side of the neurectomy when measured one week after operation. The extent of this torsion was an average of 9.5 degrees one week after operation and there was no statistically significant difference in the average magnitude of the torsion in the two eyes. In 8 of these patients, additional measurements were made at intervals up to one year after operation and it was found that in these patients there is a significant reduction in torsion over time from an average of 10.2 degrees one week after operation to an average of 2.8 degrees by 16 weeks after operation. The change in torsional eye position following the neurectomy was accompanied by a change in the perceived visual orientation of a small (9.5 degrees visual angle) illuminated horizontal line at a straight ahead eye level position in an otherwise completely darkened room. One week after operation when asked to adjust the line to the perceived gravitational horizontal by rotating it in roll (i.e. around an X axis), patients who had had a right vestibular neurectomy consistently set the line so that the right side of the line (from the patient's point of view) was below the true gravitational horizontal. Similarly patients after a left neurectomy consistently set the line so that the left side of the line was below the true gravitational horizontal. There is a high correlation (r = 0.95) between the direction and magnitude of the change in torsional eye position and the direction and magnitude of the change in the perceived visual horizontal one week after operation.(ABSTRACT TRUNCATED AT 250 WORDS)

Anisocoria after scopolamine transdermal patch contamination: A case report.

We report a case of anisocoria that occurred after contamination with a scopolamine transdermal patch, and introduce a diagnostic approach for anisocoria patients. A 35-year-old woman with no past ophthalmologic history presented to the ophthalmology department complaining of a dilated pupil in the right eye. Corrected visual acuities was 20/20 in both eyes, and the intraocular pressures were 20 and 18 mm Hg in the right and left eye, respectively. The anterior chambers in both eyes were unremarkable on slit-lamp examination. The pupil size was 5.0 mm in the right eye and 2.0 mm in the left eye, and the extraocular muscles of both eyes were intact. The patient neither did present with facial anhidrosis nor did she present with ptosis. Furthermore, as we did not observe dilatation lag in the smaller pupil, we applied 1% apraclonidine in the left eye in order to rule out Horner syndrome and did not observe dilatation of the pupil. We then applied 0.125% and 1% pilocarpine to exclude oculomotor nerve palsy; however, it could not be ruled out as constriction of pupil to 3.1 mm in the right eye was observed after applying 1% pilocarpine. Moreover, upon further investigation, we discovered that the patient had a scopolamine transdermal patch applied for 2 days prior to the clinic visit. Artificial tears were administered and the patient was observed and monitored. The pupil size in the right eye gradually decreased to 4.5 mm on the second day of observation and to 3.6 mm on the fourth day of observation. A detailed history of the use of medications such as scopolamine patches in patients with unilateral dilated pupils without vision loss is of utmost importance. We report the exclusion of important diseases using pilocarpine and apraclonidine hydrochloride. It was confirmed that improvement naturally occurs over time.

[Saturday night retinopathy: A French case of post-compressive CRAO].

We report herein the first French case of Saturday Night Retinopathy. A 39-year-old man presented to the emergency room with unilateral vision loss in the left eye with redness but no pain. Visual acuity OS was "light perception" and OD 20/20. The left eye was hyperemic with a fixed, dilated pupil; fundus examination revealed a macular cherry-red spot within a pale, ischemic retina. The patient was admitted to a stroke centre. The neurological work-up and head CT were normal. He also underwent evaluation for possible carotid or cardiac etiologies, all of which were negative. Current smoking was the only cardiovascular risk factor found. The patient reportedly fell asleep face down at his kitchen table after consuming a large amount of alcohol, with his left eye pressed into his arm throughout the night. Six similar cases have been reported in the literature since 1973. The prognosis for vision is dismal. Only public awareness and prevention might avoid this serious functional disability.

Isolated Horner syndrome as a rare initial presentation of nasopharyngeal carcinoma: a case report.

Horner syndrome refers to a set of clinical presentations resulting from disruption of sympathetic innervation to the eye and adnexa. Classically, the clinical triad consists of ipsilateral blepharoptosis, pupillary miosis, and facial anhidrosis. Ocular sympathetic denervation may signify life-threatening causes. Timely investigation and accurate diagnosis are essential in patients with oculosympathetic denervation. A 33-year-old Asian man with a heavy smoking habit presented with a 3-week history of left ptosis and no other complaints. His visual acuity was 20/20 bilaterally. An ophthalmic examination was significant for mild ptosis of his left eyelid and anisocoria (smaller left pupil), which was greater in the dark. Both pupils reacted to light briskly without an afferent pupillary defect. Anhidrosis was found on the medial side of the left forehead. A 10% cocaine test was positive. At his first visit, neurologic examination was unremarkable. Comprehensive radiological investigations were scheduled for a left-sided isolated Horner syndrome. Two weeks after his first visit, he experienced a left-sided headache along with ipsilateral Horner syndrome. Neurologic examination revealed hypoesthesia in the left cranial nerve V<sub1-3</sub territories. Emergent computed tomography angiography was suspected for petrous part of the left internal carotid artery (ICA) dissection. Magnetic resonance imaging demonstrated an enhancing infiltrative lesion with its epicenter at the left sphenoid bone. The lesion encased the left ICA and invaded the left Meckel cave. Rhinoscopy with incisional biopsy revealed squamous cell nasopharyngeal carcinoma. This case involved an unusual initial presentation of nasopharyngeal carcinoma: isolated Horner syndrome with clinical progression to adjacent structures. Infiltration involving the Meckel cave and ICA at the foramen lacerum can present as postganglionic Horner syndrome associated with trigeminal pain and hypoesthesia. These clinical findings may mimic carotid artery dissection on computed tomography angiography. Detailed magnetic resonance imaging with careful attention to the skull base should be performed.

[Neurosyphilis presenting the left total ophthalmoplegia: a case report].

We report a 73-year-old woman with meningitis-type neurosyphilis presenting the main symptom of the left total ophthalmoplegia. Three months after the appearance of the deviation of the eyeball to the inside and ptosis of the left eyelid, the left eyelid was completely closed. On admission, about four months after the appearance of neurosyphilis, she showed paralysis of the left oculomotor nerve, trochlearis nerve and abducens nerve, and the right mydriasis and absent light reflex. She was diagnosed as meningovascular neurosyphilis because syphilitic antibodies reactions in both serum and cerebrospinal fluid were highly positive. We treated her with intravenous infusion drop of penicillin G (eighteen-million units/day) for ten days, and those symptoms mentioned above other than light reflex were completely recovered. Bilateral internal carotid arteries situated close each other at the supraclinoid portion. The internal carotid arteries were not enhanced on Gd-MRI and the stenosis of the arteries were not detected on MRA. However, we suppose that the inflammation of meninges at that portion spreads to the bilateral internal carotid arteries, and that the III, IV and VI nerves close to the left internal carotid artery were damaged. There have been no reports of meningovascular neurosyphilis with the manifestation of unilateral ophthalmoplegia. In the patients of meningovascular neurosyphilis, however, various cranial nerve palsies can be appeared. Therefore we suggest that neurosyphilis should always be taken into consideration as differential diagnosis of cranial nerve palsies.

A case of Brown-Sequard syndrome with associated Horner's syndrome after blunt injury to the cervical spine.

A 26 year old motorcyclist was received by the trauma team in our accident and emergency department after a head on collision with a motor vehicle. He had been correctly immobilised and his primary survey was essentially normal. He was alert and orientated with a Glasgow Coma score of 15 and had no symptoms or signs of spinal injury. His cervical spine radiography was also normal. Neurological examination however, revealed anisocoria, his left pupil being smaller than his right, and a Brown-Sequard syndrome, with a sensory level at C6. Immobilisation was maintained and he was transferred to the regional neurosurgical centre where magnetic resonance imaging revealed a contusion of the left half of the spinal cord adjacent to the 6th cervical vertebrae. Computed tomography revealed no bony injury but spinal column instability was demonstrated after flexion-extension spinal views and he underwent surgery to fuse his spine at the C5-C6 level. This report highlights the necessity to observe strict ATLS guidelines. This must include a thorough examination of the central and peripheral nervous system where spinal injury is suspected, even in the absence of radiographic abnormality and neck pain. This article also presents the unusual phenomena of Brown-Sequard syndrome and unilateral Horner's syndrome after blunt traumatic injury to the cervical spine.

Brain Death Criteria -- Clinical Significance -- I. Physical Examination

CN III, IV, VI: Loss of pupillary light reflex as mentioned above (CN III). For cranial nerves IV, VI, and VIII, the oculocephalic reflex can be tested by holding a patient's eyelids open and turning their head from side to side. A positive oculocephalic reflex is present when the eyes reflexively look in the position opposite to that of the direction the head is turning. When the oculocephalic reflex is absent, the eyes will turn in the same direction in which the head is turning (Doll's eyes). It is imperative to only perform this examination maneuver in patients with a stable cervical spine who are not in cervical spine precautions.

Management of hypotony-related maculopathy after combined phacoemulsification and trabeculectomy: January consultation #1.

A 59-year-old man with mild to moderate pigmentary glaucoma was referred for management of hypotony-related maculopathy 3 years after combined phacoemulsification and trabeculectomy in his right eye. His ocular history is significant for retinal detachment in the right eye that was surgically treated with a pars plana vitrectomy and scleral buckle 5 years prior to the current presentation and 1 year prior to his combined phacoemulsification-trabeculectomy procedure. After trabeculectomy, he reportedly had a wound leak with hypotony and choroidal effusion. The patient was referred to a second surgeon who performed a bleb revision with a pericardial patch graft, but the patient had a severe intraocular pressure (IOP) spike in the immediate postoperative period requiring suture removal. This resulted in recurrent hypotony with maculopathy. A second bleb revision with pericardial patch graft was performed but was not successful in raising the IOP out of the single digits or in resolving the maculopathy. Accordingly, the patient was referred for further assessment. At presentation, the patient's corrected distance visual acuity was 20/100 in the right eye and 20/20 in the left eye. Applanation tonometry IOP was 4 mm Hg and 16 mm Hg for the right and left eyes, respectively. Central corneal thickness was 609 μm in the right eye and 574 μm in the left eye. The right pupil was noted to be slightly irregular with a relative afferent pupillary defect. Slitlamp examination of the right eye was notable for a moderately elevated, Seidel test-negative bleb, and deep anterior chamber. The left eye had a Krukenberg spindle and mild nuclear sclerotic cataract but was otherwise unremarkable. Fundus examination of the right eye was notable for significant macular folds with edematous nerve fiber layer (NFL) and optic nerve. The left optic nerve and fundus examination were unremarkable. Gonioscopy revealed open angles with dense trabecular meshwork pigment in both eyes. There was a nicely patent superior sclerostomy in the right eye. There was no cyclodialysis cleft. Optical coherence tomography (OCT) of the macula showed chorioretinal folds and NFL edema in the right eye and was normal in the left eye (Figure 1JOURNAL/jcrs/04.03/02158034-202101000-00022/figure1/v/2021-01-04T143903Z/r/image-tiff). The OCT of the optic nerve in the right eye was distorted secondary to the chorioretinal folds, whereas the left eye was notable for mild superior thinning of the NFL (Figure 2JOURNAL/jcrs/04.03/02158034-202101000-00022/figure2/v/2021-01-04T143903Z/r/image-tiff). Humphrey visual field revealed a superior nasal step in the right eye (Figure 3JOURNAL/jcrs/04.03/02158034-202101000-00022/figure3/v/2021-01-04T143903Z/r/image-tiff). Axial lengths were 25.33 mm and 26.53 mm in the right and left eye, respectively; it is notable that the right eye had a shorter axial length despite the scleral buckle, which demonstrates the degree of axial shortening from hypotony (Figure 4JOURNAL/jcrs/04.03/02158034-202101000-00022/figure4/v/2021-01-04T143903Z/r/image-tiff). What would be your approach for managing this patient's hypotony? Does the fact that the referring surgeon had performed 2 failed bleb revision procedures prior to referral influence your approach? Given that a previous attempt at revision resulted in an extreme IOP spike would you also recommend a glaucoma procedure? If so, what procedure would you perform? Would you do it coincident with the revision or in a staged procedure later on an as-needed basis?

InternalMed_Harrison

The range of eye movements and whether they are equal in each eye should be observed. Peripheral eye movement disorders (e.g., cranial neuropathies, eye muscle weakness) are usually disconjugate (different in the two eyes). One should check pursuit (the ability to follow a smoothly moving target) and saccades (the ability to look back and forth accurately between two targets). Poor pursuit or inaccurate (dysmetric) saccades usually indicates central pathology, often involving the cerebellum. Finally, one should look for spon taneous nystagmus, an involuntary back-and-forth movement of the eyes. Nystagmus is most often of the jerk type, in which a slow drift (slow phase) in one direction alternates with a rapid saccadic movement (quick phase or fast phase) in the opposite direction that resets the position of the eyes in the orbits. Except in the case of acute vestibulopathy (e.g., vestibular neuritis), if primary position nystagmus is easily seen in the light, it is probably due to a

InternalMed_Harrison

FIguRE 39-2 Demonstration of a relative afferent pupil defect (Marcus Gunn pupil) in the left eye, done with the patient fixating on a distant target. A. With dim background lighting, the pupils are equal and relatively large. B. Shining a flashlight into the right eye evokes equal, strong constriction of both pupils. C. Swinging the flashlight over to the damaged left eye causes dilation of both pupils, although they remain smaller than in A. Swinging the flashlight back over to the healthy right eye would result in symmetric constriction back to the appearance shown in B. Note that the pupils always remain equal; the damage to the left retina/optic nerve is revealed by weaker bilateral pupil constriction to a flashlight in the left eye compared with the right eye. (From P Levatin: Arch Ophthalmol 62:768, 1959. Copyright © 1959 American Medical Association. All rights reserved.) damage to the ciliary ganglion in the orbit. Common mechanisms are infection (herpes zoster, influenza),

Acute iris toxicity following bilateral gel stent implantation with mitomycin-C and intracameral moxifloxacin January consultation #1.

A 72-year-old woman with moderate primary open-angle glaucoma was referred for management of her glaucoma and photophobia. Her ocular history is significant for routine cataract surgery in both eyes 6 years prior to presentation. She was diagnosed with glaucoma 7 months prior to presentation at which time the patient underwent sequential, ab externo, open conjunctival, Xen Gel Stent (Allergan, Inc.) placement with mitomycin-C (MMC) in each eye, approximately 2 weeks apart. The history obtained directly from the surgeon revealed that MMC dosing was 0.2 mL in a concentration of 0.2 mg/mL delivered through subconjunctival injection after placement of the gel stent. Intracameral moxifloxacin was injected at the time of surgery, and moxifloxacin and Maxitrol eyedrops were used in the postoperative period. The patient noted that, approximately 1 month after each surgery, she developed significant photophobia. An outside examination noted bilateral tonic pupils and concern for early bleb failure in the left eye. 2 months after the initial gel stent placement in the left eye, she underwent a bleb revision with a McCannel suture iris cerclage in the left eye. The intraocular pressure (IOP) in both eyes remained well controlled off pressure-lowering medications; however, the tonic pupils and photophobia persisted. The patient was subsequently referred for further assessment. At presentation, the patient's corrected distance visual acuity was 20/20 in each eye. Applanation tonometry IOP was 17 mm Hg and 14 mm Hg for the right and left eyes, respectively. Pupils were tonic and irregular. The lack of pupillary response prevented testing for relative afferent pupillary defects directly or by reverse testing. Slitlamp examination of the right eye was notable for a minimally elevated superior bleb and severe iris stromal atrophy with diffuse transillumination defects. The intraocular lens (IOL) appeared well positioned in the capsular bag without signs of pseudophacodonesis (Figure 1JOURNAL/jcrs/04.03/02158034-202201000-00021/figure1/v/2021-12-20T152346Z/r/image-tiff). The left eye was notable for a diffuse superior bleb and similar iris and IOL findings to the right eye, except for 2 McCannel iris sutures in the iris stroma (Figure 2JOURNAL/jcrs/04.03/02158034-202201000-00021/figure2/v/2021-12-20T152346Z/r/image-tiff). In both eyes, the anterior chambers were deep and quiet, and there were no corneal endothelial abnormalities. Fundus examinations of both the right and left eyes were notable for glaucomatous-appearing optic nerves and otherwise healthy macula, vessels, and periphery. Gonioscopy revealed open angles in each eye with fairly marked, densely layered pigment throughout the inferior angle and trabecular meshwork. The gel stents were positioned just anteriorly to the trabecular meshwork superiorly, well away from iris tissue. Optical coherence tomography (OCT) of the nerve fiber layer (NFL) showed moderate to severe thinning inferiorly and superiorly in the right eye, with mild to moderate thinning inferiorly in the left eye (Supplemental Figure 1, http://links.lww.com/JRS/A510). Ganglion cell analysis correlated with the NFL findings (Supplemental Figure 2, http://links.lww.com/JRS/A510). Humphrey visual field testing revealed a dense superior arcuate in the right eye and moderate inferior arcuate in the left eye (Supplemental Figures 3 and 4, http://links.lww.com/JRS/A510). OCT of the macula in both eyes was unremarkable. Finally, specular microscopy showed normal endothelial density and configuration of each eye (Supplemental Figure 5, http://links.lww.com/JRS/A510). What part of the patient's ocular history would you consider relevant to the development of tonic, atrophic pupils? What additional information would you want to know to help refine your differential diagnosis? What is your preferred surgical technique when implanting the Xen Gel Stent? Please include whether ab interno or ab externo and open or closed conjunctival approach to be used and mention antifibrosis dosing and method of administration. Finally, what would be your approach for managing this patient's severe photophobia, in the setting of her moderate open-angle glaucoma?

Recovery from bilateral vestibular failure: implications for visual and cervico-ocular function.

We report a patient who sustained severe bilateral labyrinthine lesions during Streptococcus suis meningitis but considerably recovered vestibular function over a 7 month period. This unique case allowed us to examine the cervico-ocular reflex (COR) and visual function at various levels of activity of his vestibular system. The slow phase COR, elicited by trunk oscillation (0.2 Hz) with the head earth-stationary, was negligible immediately after the acute vestibular loss but rose to a gain of 0.51 one month after. Seven months later, when vestibular function was improved, COR gain dropped to a gain of 0.15. Measurements of spatial visual function during whole body oscillation in the acute stage and after 6 months showed marked improvement which correlated entirely with VOR measurements in the dark and during optic fixation. This patient also showed the unique feature that, in the acute stage, eye movement gain and visual function were poorer during whole body motion than during identical visual target motion. These findings suggest that: i) the COR may be inhibited by the presence of vestibular signals, ii) spatial vision measurements provide accurate assessment of the patient's visual blur during head motion, and iii) the severe oscillopsia experienced by patients in the acute stage of vestibular loss may not only be due to the absence of the VOR; additional degradation in eye movements during head motion, perhaps arising from acutely distorted labyrinthine signals, may also play a part.

[Avulsion of the optic nerve: two case studies].

Avulsion of the optic nerve is a rare and serious injury. The authors report two cases of optic nerve avulsion. The first one concerns a 5-year-old boy who presented ocular trauma after falling on the handlebars of a bicycle. His visual acuity was light perception in the right eye, and his right pupil was unresponsive to light. The anterior segment was normal. The ophthalmoscopic examination showed a total separation of the optic nerve head from the sclera with peripapillary hemorrhage. The second case concerns a 30-year-old man who was hit in the right eye with a stick. On admission, he had no light perception in the right eye, a right afferent pupil defect, a small laceration of the right lower eye lid and no abnormalities on the anterior segment. The fundus examination showed a mild vitreous hemorrhage. Ocular ultrasonography showed vitreous hemorrhage coming directly from the optic nerve head in a mushroom pattern. A CT scan of the orbit revealed a thickened optic nerve. Color Doppler ultrasonography documented slowing of blood flow in the central retinal artery. The two patients received 1 mg/kg/day of prednisone for 2 weeks. No improvement was noted. Optic nerve avulsion is often caused by sudden and forceful rotation of the eye with tearing of the optic nerve as it exits the globe. The nerve can be partially or totally avulsed. The prognosis is usually poor.

Symptomatic trigeminal autonomic cephalalgia associated with allodynia in a patient with multiple sclerosis.

A patient with symptomatic trigeminal autonomic cephalalgia (TAC) provides a chance to understand the pathophysiology and anatomic correlates of TAC. A 28-year-old woman experienced intermittent sharp and excruciating pain over her right temporal, ear and neck regions for 3 days. The headaches lasted 10-20 minutes each, occurred 1-2 times a day, and were accompanied by prominent ipsilateral lacrimation and conjunctival injection. The patient had hiccups, 4-limb numbness and impaired visual acuity in both eyes. She had also had 3 episodes of left-side optic neuritis in the past half year. Neurologic examination showed brushing allodynia over the right face and scalp during the headache attacks. The visual acuity of her right eye was 6/60 and that of the left eye was 1/60. Brain magnetic resonance imaging showed non-enhancing lesions on the right lateral tegmentum of the lower pons where the spinal trigeminal nucleus is located and the floor of the 4th ventricle. The patient was diagnosed as having multiple sclerosis with symptomatic TAC. Her headaches, autonomic signs and allodynia subsided 3 days after pulse therapy and gabapentin treatment were given. We suggest that the spinal trigeminal nucleus lesion was responsible for the symptomatology of TAC and cutaneous allodynia in our patient.