Journal Contents

Acta Ophthalmol Scand
Am Jour Ophthalmol
Arch Ophthalmol
Br J Ophthalmol
Can J Ophthalmol
J Cat Ref Surg
Cornea
Curr Eye Res
Eur J Ophthalmol
Eye
J Glaucoma
Graefes Ophthalmol
Indian J Ophthalmol
Int Ophthalmol Clin
Invest Ophth Vis Sci
Jpn J Ophthalmol
JPOS
Korean J Ophthal
J Neuroophthalmol
Ophthalmic Epidemiol
Ophthalmic Genet
Ophthal Plast Rec Surg
Ophthalmic Res
Ophthalmologica
Ophthalmology
Retina
Surv Ophthalmol
Ophthalmology Review Journal
J Neuroophthalmol[JOUR] Established 1995
1: J Neuroophthalmol. 2008 Dec;28(4):359. 

Delayed third cranial nerve palsy after aneurysm wrapping.

Almer ZE, Miller NR.

Publication Types:
    Letter

PMID: 19145142 [PubMed - in process]

2: J Neuroophthalmol. 2008 Dec;28(4):359-60. 

Anticholinergic esotropia.

Anderson JM, Brodsky MC.

Publication Types:
    Comment
    Letter

PMID: 19145141 [PubMed - in process]

3: J Neuroophthalmol. 2008 Dec;28(4):352-7. 

The 60th annual meeting of the American Academy of Neurology Chicago, Illinois,
April 12-19, 2008.

Wu-Chen WY, Moster ML.

Temple University School of Medicine, Philadelphia, Pennsylvania, USA.

PMID: 19145139 [PubMed - in process]

4: J Neuroophthalmol. 2008 Dec;28(4):348-51. 

Annual meeting of the Association for Research in Vision and Ophthalmology
(ARVO) Fort Lauderdale, April 27-May 1, 2008.

Pomeranz HD, Mudumbai R, Shindler KS.

North Shore Long Island Jewish Health System Great Neck, New York, USA.

PMID: 19145138 [PubMed - in process]

5: J Neuroophthalmol. 2008 Dec;28(4):337-47. 

The first Jacobson Lecture. Familial idiopathic intracranial hypertension.

Corbett JJ.

Department of Neurology, University of Mississippi Medical Center, Jackson,
Mississippi 39216, USA. jcorbett@neurology.umsmed.edu

BACKGROUND: Case reports of familial idiopathic intracranial hypertension (IIH)
have appeared sporadically and infrequently. METHODS: We reviewed the medical
records of all patients with IIH seen at our institution to identify the number
of familial cases. RESULTS: Out of a cohort of 237 patients with IIH, we
identified 27 members (25 women and 2 men) from 11 families, with IIH usually
self-reported or reported by the index case. In 7 of the 11 families, the
relationship was parent to child; in 4, it was sibling. Obesity was present in
85% of the family members. CONCLUSIONS: Familial IIH appears to be more common
than reported previously. A systematic evaluation of first-degree relatives may
help to identify more cases. A study of the patterns of inheritance and
associated co-morbidities may result in better understanding of the genetic
issues with this disorder.

PMID: 19145137 [PubMed - in process]

6: J Neuroophthalmol. 2008 Dec;28(4):329-36. 

Saccadic burst cell membrane dysfunction is responsible for saccadic
oscillations.

Shaikh AG, Ramat S, Optican LM, Miura K, Leigh RJ, Zee DS.

Department of Neurology, The Johns Hopkins University, Baltimore, Maryland
21287, USA. ashaikh@dizzy.med.jhu.edu

Saccadic oscillations threaten clear vision by causing image motion on the
retina. They are either purely horizontal (ocular flutter) or multidimensional
(opsoclonus). We propose that ion channel dysfunction in the burst cell membrane
is the underlying abnormality. We have tested this hypothesis by simulating a
neuromimetic computational model of the burst neurons. This biologically
realistic model mimics the physiologic properties and anatomic connections in
the brainstem saccade generator. A rebound firing after sustained inhibition,
called post-inhibitory rebound (PIR), and reciprocal inhibition between premotor
saccadic burst neurons are the key features of this conceptual scheme. PIR and
reciprocal inhibition make the circuits that generate the saccadic burst
inherently unstable and can lead to oscillations unless stabilized by external
inhibition. Our simulations suggest that alterations in membrane properties that
lead to an increase in PIR, a reduction in external glycinergic inhibition, or
both can cause saccadic oscillations.

Publication Types:
    Research Support, N.I.H., Extramural
    Research Support, N.I.H., Intramural
    Research Support, Non-U.S. Gov\'t
    Research Support, U.S. Gov\'t, Non-P.H.S.

PMID: 19145136 [PubMed - in process]

7: J Neuroophthalmol. 2008 Dec;28(4):327-8. 

Dilated superior ophthalmic veins and posterior ischemic optic neuropathy after
prolonged spine surgery.

Reddy A, Foroozan R, Edmond JC, Hinckley LK.

Department of Ophthalmology, Baylor College of Medicine Houston, Texas, USA.

A 55-year-old man developed bilateral posterior ischemic optic neuropathy after
prolonged prone position lumbar laminectomy. Brain MRI performed 19 hours after
the procedure revealed markedly dilated superior ophthalmic veins, a finding
that had disappeared on a comparable study performed 5 months later. This first
report of dilated superior ophthalmic veins present in the immediate
postoperative period but not later may be important in suggesting that an
increase in orbital venous pressure during surgery contributes to the
development of postoperative posterior ischemic optic neuropathy (PION).

PMID: 19145135 [PubMed - in process]

8: J Neuroophthalmol. 2008 Dec;28(4):325-6. 

Suprasellar hemangioblastoma.

Miyata S, Mikami T, Minamida Y, Akiyama Y, Houkin K.

Department of Neurosurgery, Sapporo Medical University, Sapporo, Japan.

A 59-year-old woman presented with disturbance of consciousness and decreased
visual acuity caused by a suprasellar mass identified on MRI. A bifrontal
interhemispheric approach allowed removal of the top and lateral sides of the
tumor from the wall of the third ventricle. The hypothalamus appeared to be the
origin of the mass, which proved to be hemangioblastoma, a rare tumor in this
location.

PMID: 19145134 [PubMed - in process]

9: J Neuroophthalmol. 2008 Dec;28(4):320-4. 

Anatomic characteristics of the ophthalmic and posterior ciliary arteries.

Erdogmus S, Govsa F.

Department of Anatomy, Faculty of Medicine, Ege University, Izmir, Turkey.

BACKGROUND: There is little documentation of the course and relations of the
ophthalmic artery (OA) and posterior ciliary arteries (PCAs). METHODS: The
anatomic characteristics of the OA and PCAs were determined from a dissection of
19 neoprene-injected cadaver heads. RESULTS: The intraorbital OA had three
segments, considering its relation to the optic nerve in the sagittal plane. The
first segment extended from the point where the OA entered the orbit to its
curving point. The second segment coursed superomedially from the inferolateral
part of the optic nerve, crossing the optic nerve either superiorly or
inferiorly. The third segment extended from the curving point of the
superomedial distal portion of the second segment to the vessel\'s termination.
The OA was deviated at the junction of its first and second segments, defined as
its "angle"; and at the junction of the second and third segments, defined as
its "bend." The PCAs arose from the first OA segment, the angle of the OA, the
second OA segment and the OA bend. The patterns of branching of the PCAs were
medial and lateral and medial, lateral, and superior. The superior PCA and the
lateral PCA arose mainly from the angle of the OA, whereas the medial PCA arose
from the curving point of the OA. The most frequently observed PCA pattern was a
medial PCA and a lateral PCA. The average diameters of the medial PCA, the
superior PCA, and the lateral PCA were 0.65, 0.48, and 0.68 mm, respectively. In
all cases, pial arteries branching from the PCA and supplying the optic sheath
were observed to form a vascular plexus on the optic sheath. The OA and PCAs
were surrounded by a network of sympathetic nerves. CONCLUSIONS: Because the
most common pattern of PCAs is a medial and lateral branch, a surgical approach
to the orbit from those directions carries a higher risk of damage to those
vessels than a superior or inferior approach.

PMID: 19145133 [PubMed - in process]

10: J Neuroophthalmol. 2008 Dec;28(4):308-19. 

Perimetry while moving the eyes: implications for the variability of visual
field defects.

Toepfer A, Kasten E, Guenther T, Sabel BA.

Institute of Medical Psychology, Otto von Guericke University Magdeburg,
Magdeburg, Germany.

BACKGROUND: In standard perimetry, subjects fixate so that saccades are reduced
and testing precision is increased. However, because vision in daily life
requires eye movements, it is appropriate to assess visual fields during eye
movement. METHODS: Perimetry was carried out in 8 healthy subjects and in 16
patients with visual field defects under conditions of a stable and moving
fixation spot. Eye movements were simultaneously recorded with an eye tracker.
Outcome measures included stimulus detection, variability of visual field
border, and saccade amplitudes. RESULTS: Perimetric performance during stable
fixation was comparable to that during eye movement. All subjects showed 92%-96%
correct detections of the fixation controls and a stable and comparable blind
spot position in the stable and moving fixation spot conditions. The eye tracker
revealed that 97% of the time the eyes were positioned within +/-1 from
fixation. CONCLUSIONS: Visual fields obtained by perimetry while moving the eyes
is comparable to standard perimetry in which a stable fixation spot minimizes
eye movements.

PMID: 19145132 [PubMed - in process]

11: J Neuroophthalmol. 2008 Dec;28(4):305-7. 

Impairment of vertical saccades from an acute pontine lesion in multiple
sclerosis.

Rufa A, Cerase A, De Santi L, Mandala M, Nuti D, Giorgio A, Annunziata P.

Department of Neurological and Behavioural Sciences, Neuroradiology Unit, S.
Maria alle Scotte Hospital, Siena, Italy.

A 62-year-old woman with relapsing-remitting multiple sclerosis suddenly
complained of diplopia associated with bilateral adduction impairment, nystagmus
of the abducting eye bilaterally, and sparing of abduction, convergence, and
vertical eye movements, consistent with bilateral internuclear ophthalmoplegia.
Within 1 week, she had developed a complete horizontal gaze paralysis even with
the oculocephalic maneuver. Vertical saccades were slow and convergence was
preserved. There was a right lower motor neuron seventh cranial nerve palsy.
Brain MRI showed a new enhancing lesion involving the pontine tegmentum.
Clinical and MRI follow-up showed recovery after 6 months. The slowing of
vertical saccades may have been due to spread of the demyelinating lesion to the
adjacent paramedian pontine reticular formation, which contains omnipause
neurons lying in the raphe interpositus nucleus thought to inhibit excitatory
burst neurons for horizontal and vertical saccades. Our patient verifies the
fact that vertical saccadic abnormalities may occur from a lesion apparently
confined to the pons.

PMID: 19145131 [PubMed - in process]

12: J Neuroophthalmol. 2008 Dec;28(4):302-4. 

Ocular misalignment in Graves disease may mimic that of superior oblique palsy.

Chen VM, Dagi LR.

Department of Ophthalmology, Children\'s Hospital Boston, Boston, Massachusetts,
USA. vchen@tuftsmedicalcenter.org

BACKGROUND: The Parks-Bielschowsky three-step test (TST) can incorrectly
indicate that a superior oblique muscle is paretic in patients with restrictive
strabismus. Although this pitfall in diagnosis has been widely reported, no
large studies have examined the incidence of a positive TST in patients with
Graves disease. METHODS: We performed a retrospective chart review of 31
consecutive patients with Graves orbitopathy examined at Children\'s Hospital of
Boston from 2003 to 2007. We analyzed ocular ductions, misalignment, and
torsion, and thyroid function studies. RESULTS: Six (20%) of the patients had a
positive TST, 3 (10%) of which showed excyclotorsion in at least one eye.
However, of the 6 patients, 5 had obvious ocular adnexal signs of Graves disease
and 2 had obvious supraduction deficits, leaving only 1 (3%) patient in whom the
clinician would have mistakenly diagnosed a superior oblique palsy. CONCLUSIONS:
Although a positive TST occurs frequently in Graves disease, other clinical
features should allow distinction from superior oblique palsy in most patients.

PMID: 19145130 [PubMed - in process]

13: J Neuroophthalmol. 2008 Dec;28(4):296-301. 

Binocular vertical rectus muscle recession for comitant vertical strabismus.

Bergamin O, Wirth MG, Landau K.

Department of Ophthalmology, University Hospital of Zurich, Zurich, Switzerland.

BACKGROUND: Binocular vertical rectus muscle recession has not been formally
evaluated in the correction of comitant vertical strabismus. METHODS: Eight
patients with stable comitant vertical strabismus for at least 6 months were
included. All underwent recession of the superior rectus muscle of the
hypertropic eye combined with an equal or nearly equal recession of the inferior
rectus muscle in the hypotropic eye. On the day before surgery, on one of the
first three postoperative days, and at one year postoperatively, ocular
alignment in vertical and horizontal gaze directions were measured with
simultaneous and alternate cover test at a viewing distance of 5 meters, and
with the two dimensional Hess screen test. The field of single binocular vision
was determined with a Goldmann perimeter. The Lang stereopsis chart was
presented at the last follow-up visit. RESULTS: All patients were orthotropic at
the last postoperative follow-up visit. In primary gaze, the degree of vertical
and horizontal phoria diminished significantly. Normal alignment was achieved in
nearly all gaze directions and stereopsis was reestablished. The field of single
binocular vision enlarged after the surgery. CONCLUSIONS: Binocular vertical
rectus muscle recession is an effective surgical approach for patients with
comitant vertical ocular misalignment.

PMID: 19145129 [PubMed - in process]

14: J Neuroophthalmol. 2008 Dec;28(4):293-5. 

Ocular dipping in Creutzfeldt-Jakob disease.

Jeong SH, Kim SY, Park SH, Kim JS.

Department of Neurology, Seoul National University College of Medicine, Seoul,
Korea.

Ocular dipping refers to a slow downward deviation of both eyes followed by a
quick return to the midposition after a brief delay. Two patients with rapid
neurologic deterioration in Creutzfeldt-Jakob disease (CJD) displayed ocular
dipping, which quickly evolved into sustained downgaze deviation. Ocular dipping
may thus be a transitional sign in a vertical gaze disturbance.

PMID: 19145128 [PubMed - in process]

15: J Neuroophthalmol. 2008 Dec;28(4):289-92. 

Spontaneous intracranial hypotension presenting as a reversible dorsal midbrain
syndrome.

Fedi M, Cantello R, Shuey NH, Mitchell LA, Comi C, Monaco F, Versino M.

Department of Neurology, Austin Health, Heidelberg, Victoria, Australia.
marco.fedi@austin.org.au

A 47-year-old woman with postural headache, episodic stupor, and vertical gaze
palsy had brain imaging findings consistent with spontaneous intracranial
hypotension (SIH), including severe descent of the mesodiencephalic structures
and diffuse pachymeningeal enhancement. The source of the cerebrospinal fluid
leakage was a ruptured dorsal perineural cyst. Clinical symptoms improved after
a targeted epidural blood patch was performed. Dorsal midbrain syndrome has not
been reported previously as a manifestation of SIH. Perhaps distortion of
structures in this brain region can occur in SIH as it does in obstructive
hydrocephalus.

PMID: 19145127 [PubMed - in process]

16: J Neuroophthalmol. 2008 Dec;28(4):287-8. 

Periodic alternating nystagmus and periodic alternating skew deviation in
spinocerebellar ataxia type 6.

Colen CB, Ketko A, George E, Van Stavern GP.

Department of Neurological Surgery, Wayne State University, Detroit, Michigan,
USA.

The combination of periodic alternating nystagmus (PAN) and periodic alternating
skew deviation (PASD) is rare. We report a case of PAN and PASD in a patient
with spinocerebellar ataxia type 6 (SCA-6) and discuss the role of the
cerebellum as a plausible mechanism for this combined pathologic condition.

Publication Types:
    Research Support, Non-U.S. Gov\'t

PMID: 19145126 [PubMed - in process]

17: J Neuroophthalmol. 2008 Dec;28(4):283-6. 

Skew deviation as the initial manifestation of left paramedian thalamic
infarction.

Margolin E, Hanifan D, Berger MK, Ahmad OR, Trobe JD, Gebarski SS.

Department of Ophthalmology, University of Michigan Health System, Ann Arbor,
Michigan, USA.

We describe a 73-year-old man who developed diplopia as the initial
manifestation of a left thalamic infarction. By the time he reached the
emergency department, clouded consciousness precluded localization of the
lesion. Results of brain MRI were initially interpreted as negative.
Ophthalmologic examination several hours later disclosed a small vertical ocular
misalignment attributed to skew deviation. This finding led to careful scrutiny
of the upper brainstem on MRI. Comparison of the diffusion, apparent diffusion
coefficient, and exponential apparent diffusion coefficient MRI studies allowed
a diagnosis of subtle left thalamic infarction. The recognition of skew
deviation in this setting is important because it may be the most specific
indicator of a brainstem lesion.

PMID: 19145125 [PubMed - in process]

18: J Neuroophthalmol. 2008 Dec;28(4):278-82. 

Multifocal electroretinographic abnormalities in ethambutol-induced visual loss.

Liu Y, Dinkin MJ, Loewenstein JI, Rizzo JF 3rd, Cestari DM.

Neuro-Ophthalmology Service, Massachusetts Eye and Ear Infirmary, Harvard
Medical School, Boston, Massachusetts 02114, USA.

Two patients who developed decreased visual acuity after several months of
ethambutol treatment for Mycobacterium avium-intracellulare infection had
bitemporal visual field defects that suggested optic chiasm damage. Multifocal
electroretinography (mfERG) disclosed markedly low-amplitude responses at
fixation and in the regions corresponding to the visual field defects. These
results suggested that the visual dysfunction might be entirely attributable to
retinal rather than optic nerve toxicity. These are the first reported patients
to show mfERG abnormalities that correspond to bitemporal visual field defects
and add to the growing evidence that ethambutol damages the retina.

PMID: 19145124 [PubMed - in process]

19: J Neuroophthalmol. 2008 Dec;28(4):269-77. 

Incidence and clinical features of ethambutol-induced optic neuropathy in Korea.

Lee EJ, Kim SJ, Choung HK, Kim JH, Yu YS.

Department of Ophthalmology, Seoul National University College of Medicine,
Seoul, Korea.

BACKGROUND: The incidence, clinical manifestations, and contributory factors in
ethambutol-induced optic neuropathy (EON) have not been widely studied. METHODS:
A retrospective chart review of 857 patients who took ethambutol for treatment
of tuberculosis identified 89 patients who complained of decreased vision after
initiation of treatment and were therefore referred to the ophthalmology clinic
of Seoul National University Hospital, Korea, between January 2003 and December
2005. Information was extracted in regard to systemic illnesses, duration and
dose of ethambutol therapy, visual acuity, color vision, ophthalmoscopic
examination, visual fields, and visual evoked potentials (VEPs). RESULTS: EON
was diagnosed in 13 (1.5%) patients during a follow-up period of 12.54 +/- 9.97
months. The average dose of ethambutol was 17.85 +/- 2.21 mg/kg/day, and the
duration of therapy was 9.38 +/- 10.12 months. Ophthalmic findings included
decreased visual acuity (65.4%), abnormal visual fields (65.4%), abnormal color
vision (61.5%), optic disc pallor (38.5%), or increased latency on VEP tests
(65.4%). Slightly less than one third of patients showed improvement in visual
function after discontinuing ethambutol. The latency for recovery was 5.38 +/-
1.71 months. No patient with optic disc pallor at the time of diagnosis of EON
showed visual function improvement. Renal dysfunction and the daily dose of
ethambutol, but not the duration of treatment, contributed to EON. CONCLUSIONS:
Based on this study, the incidence of EON in Koreans is estimated to be <2%.
However, visual function after discontinuation of ethambutol is reversible in
only a minority of patients and does not occur if optic disc pallor is present.
Renal dysfunction and daily dose of ethambutol, but not duration of ethambutol
treatment, seem to be related to development of EON.

Publication Types:
    Research Support, Non-U.S. Gov\'t

PMID: 19145123 [PubMed - in process]

20: J Neuroophthalmol. 2008 Dec;28(4):265-8. 

Ethambutol optic neuropathy: how we can prevent 100,000 new cases of blindness
each year.

Sadun AA, Wang MY.

Publication Types:
    Comment
    Editorial

PMID: 19145122 [PubMed - in process]
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