Ipsilateral transient amaurosis, mydriasis and light reflex absence after subconjunctival local anesthesia with mepivacaine in three patients with refractory glaucoma - a case report.

BACKGROUND: The subconjunctival anesthesia with local anesthetics is considered as a low-risk procedure allowing ocular surgery without serious complications typical for retro- or parabulbar anesthesia, especially in patients with preexisting Optic Nerve damage. We report development of ipsilateral transient amaurosis accompanied with mydriasis and both, direct and consensual light response absence. CASE PRESENTATION: Three patients with advanced refractory glaucoma undergoing laser cyclophotocoagulation (CPC) for intraocular pressure lowering experienced these adverse effects just few minutes after subconjunctival injection of mepivacaine 2% solution (Scandicaine® 2%, without vasoconstrictor supplementation). The vision was completely recovered to usual values in up to 20 h after mepivacaine application. Extensive ophthalmological examination, including cranial magnetic resonance imaging (MRI), revealed no further ocular abnormalities, especially no vascular constriction or thrombotic signs as well as no retinal detachment. The oculomotor function remained intact. The blockade of ipsilateral ciliary ganglion parasympathetic fibers by mepivacaine may be the responsible mechanism. Systemic pathways as drug-drug interactions seem to be unlikely involved. Importantly, all three patients tolerated the same procedure previously or at a later date without any complication. Overall, our thoroughly elaborated risk management could not determine the causative factor explaining the observed ocular complications just in the current occasion and not at other time points. CONCLUSIONS: Doctors should be aware and patients should be informed about such rare complications after subconjunctival local anesthetics administration. Adequate risk management should insure patients' safety.

Retinal Architecture and Melanopsin-Mediated Pupillary Response Characteristics: A Putative Pathophysiologic Signature for the Retino-Hypothalamic Tract in Multiple Sclerosis.

Importance: A neurophysiologic signature of the melanopsin-mediated persistent constriction phase of the pupillary light reflex may represent a surrogate biomarker for the integrity of the retinohypothalamic tract, with potential utility for investigating alterations in homeostatic mechanisms associated with brain disorders and implications for identifying new treatments. Objective: To characterize abnormalities of retinal architecture in patients with multiple sclerosis (MS) and corresponding alterations in the melanopsin-mediated sustained pupillary constriction response. Design, Setting, and Participants: The case-control study was an experimental assessment of various stimulus-induced pupillary response characteristics and was conducted at a university clinical center for MS from September 6, 2012, to February 2015. Twenty-four patients with MS (48 eyes) and 15 individuals serving as controls (30 eyes) participated. The melanopsin-mediated, sustained pupillary constriction phase response following cessation of a blue light stimulus was compared with the photoreceptor-mediated pupillary constriction phase response following cessation of a red light stimulus. Optical coherence tomography was used to characterize the association between pupillary response characteristics and alterations in retinal architecture, specifically, the thickness of the retinal ganglion cell layer and inner plexiform layer (GCL + IPL). Main Outcomes and Measures: Association of pupillary response characteristics with alterations in retinal architecture. Results: Of 24 patients with MS included in the analysis, 17 were women (71%); mean (SD) age was 47 (11) years. Compared with eyes from individuals with MS who had normal optical coherence tomography-derived measures of retinal GCL + IPL thickness, eyes of patients who had GCL + IPL thickness reductions to less than the first percentile exhibited a correspondingly significant attenuation of the melanopsin-mediated sustained pupillary response (mean [SD] pupillary diameter ratios at a point in time, 0.18 [0.1] vs 0.33 [0.09]; P < .001, generalized estimating equation models accounting for age and within-patient intereye correlations). Conclusions and Relevance: In this case-control study, attenuation of the melanopsin-mediated sustained pupillary constriction response was significantly associated with thinning of the GCL + IPL sector of the retina in the eyes of patients with MS, particularly those with a history of acute optic neuritis. Melanopsin-containing ganglion cells in the retina represent, at least in part, the composition of the retinohypothalamic tract. As such, our findings may signify the ability to elucidate a putative surrogate neurophysiologic signature that correlates with a constellation of homeostatic mechanisms in both health and illness.

Ophthalmologic correlates of disease severity in children and adolescents with Wolfram syndrome.

PURPOSE: To describe an ophthalmic phenotype in children at relatively early stages of Wolfram syndrome. METHODS: Quantitative ophthalmic testing of visual acuity, color vision, automated visual field sensitivity, optic nerve pallor and cupping, and retinal nerve fiber layer (RNFL) thickness assessed by optical coherence tomography (OCT) was performed in 18 subjects 5-25 years of age. Subjects were also examined for presence or absence of afferent pupillary defects, cataracts, nystagmus, and strabismus. RESULTS: Subnormal visual acuity was detected in 89% of subjects, color vision deficits in 94%, visual field defects in 100%, optic disk pallor in 94%, abnormally large optic nerve cup:disk ratio in 33%, thinned RNFL in 100%, afferent pupillary defects in 61%, cataracts in 22%, nystagmus in 39%, and strabismus in 39% of subjects. RNFL thinning (P < 0.001), afferent pupillary defects (P = 0.01), strabismus (P = 0.04), and nystagmus (P = 0.04) were associated with more severe disease using the Wolfram United Rating Scale. CONCLUSIONS: Children and adolescents with Wolfram syndrome have multiple ophthalmic markers that correlate with overall disease severity. RNFL thickness measured by OCT may be the most reliable early marker.

Purtscher-like retinopathy after retrobulbar injection.

Purtscher-like retinopathy occurred in a 46-year-old Chinese male who received 5 mL of 2% lignocaine, retrobulbar injection, and underwent pterygium excision with conjunctiva graft. The visual acuity improved spontaneously from 20/120 on the first postoperative day to 20/20 within 8 weeks. The disc swelling, veinous tortuosity, retinal whitening, and hemorrhage resolved with time. However, relative afferent papillary defect and an arcuate visual field deficit persisted. The mechanisms of this Purtscher-like retinopathy are postulated.

Vertical gaze paralysis and intermittent unresponsiveness in a patient with a thalamomesencephalic stroke.

A patient with paralysis of upward gaze and downward gaze, absent oculocephalic reflexes, and absent vertical saccades also demonstrated intermittent stupor over the first 9 days of presentation. Magnetic resonance imaging (MRI) demonstrated an infarct in the tegmentum of the mesencephalon including the right red nucleus and the periaqueductal area, superior to the oculomotor nucleus, and contiguous through the left thalamus. The infarct included the area around the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF), as well as the midbrain reticular formation. Mechanisms are proposed for the unusual concurrent sign of intermittent unresponsiveness in this case.

Neural mechanisms of pupillary abnormality following thalamic lesions: experimental lesion and stimulation studies in cats, and consideration of pupillary findings in thalamic vascular lesions.

Neural mechanisms of the pupillary abnormality in thalamic lesions were experimentally studied in cats. Moderate to considerable anisocoria appeared after kainic acid lesions involving the medial thalamus. The pupil on the side of the lesion was larger than its partner. Only subtle or no pupillary inequality was produced by lateral thalamic lesions. Electrical stimulation of the midline and medial thalamus evoked dilation bilaterally in sympathectomized pupils. Thus, pupillary dilation produced by stimulation of the thalamus was shown to be mediated in part by the oculomotor parasympathetic nerve (OPN). There was no threshold difference between ipsilateral (ipsi) and contralateral (contra) pupils. However, amplitude of dilation was significantly larger in the contra pupil than in the ipsi, when stimulus was given to the pupillo-dilatory medial thalamic nuclei. In these, the mediodorsal, parataenial, central dorsal, paracentral (Pc), and parafascicular nuclei and the medial division of the medial pulvinar nucleus were included. Pupillary dilation mediated by the ocular sympathetic nerve (OSN) was investigated by stimulating Pc and comparing the ipsi-contra difference in the amplitude of dilation between sympathectomized and non-sympathectomized pairs of pupils. In contrast to the results in sympathectomized pairs, there was no ipsi-contra difference in the amplitude of dilation or it was larger in the ipsi pupil in non-sympathectomized pairs. From these, it was inferred that stimulation of Pc activated OSN ipsilaterally or bilaterally with ipsi dominance. It was concluded that the medial and midline thalamus exerts pupillo-dilatory effects through a set of neural mechanisms; 1) ipsi-dominant bilateral OPN inhibition, and 2) ipsi or ipsi-dominant bilateral OSN activation. Neural mechanisms of the pupillary abnormality in thalamic vascular lesions were also considered.