Biomedical subjects
D Milea
Publications and source records attributed to D Milea.
Upbeat nystagmus due to a small pontine lesion: evidence for the existence of a crossing ventral tegmental tract.
We report a patient with an isolated large upbeat nystagmus (UBN) in the primary position of gaze. Eye movements were filmed and recorded using electro-oculography. The upward vestibulo-ocular reflex gain, evaluated by pitching the head forward, was markedly reduced compared to when pitching the head back. The lesion was a probable lacunar infarction located in the paramedian and posterior part of the basis pontis, at the upper pons level. This UBN case, with one of the smallest brainstem lesions reported so far, supports the existence in humans of the crossing ventral tegmental tract, described in the cat and transmitting excitatory upward vestibular signals to the third nerve nucleus. It is also suggested that the decussation of this tract lies at the same upper pons level as in the cat but in a slightly more ventral location, i.e. in the posterior basis pontis.
Vertical nystagmus: clinical facts and hypotheses.
The pathophysiology of spontaneous upbeat (UBN) and downbeat (DBN) nystagmus is reviewed in the light of several instructive clinical findings and experimental data. UBN due to pontine lesions could result from damage to the ventral tegmental tract (VTT), originating in the superior vestibular nucleus (SVN), coursing through the ventral pons and transmitting excitatory upward vestibular signals to the third nerve nucleus. A VTT lesion probably leads to relative hypoactivity of the drive to the motoneurons of the elevator muscles with, consequently, an imbalance between the downward and upward systems, resulting in a downward slow phase. The results observed in internuclear ophthalmoplegia suggest that the medial longitudinal fasciculus (MLF) is involved in the transmission of both upward and downward vestibular signals. Since no clinical cases of DBN due to focal brainstem damage have been reported, it may be assumed that the transmission of downward vestibular signals depends only upon the MLF, whereas that of upward vestibular signals involves both the MLF and the VTT. The main focal lesions resulting in DBN affect the cerebellar flocculus and/or paraflocculus. Apparently, this structure tonically inhibits the SVN and its excitatory efferent tract (i.e. the VTT) but not the downward vestibular system. Therefore, a floccular lesion could result in a disinhibition of the SVN-VTT pathway with, consequently, relative hyperactivity of the drive to the motoneurons of the elevator muscles, resulting in an upward slow phase. UBN also results from lesions affecting the caudal medulla. An area in this region could form part of a feedback loop involved in upward gaze-holding, originating in a collateral branch of the VTT and comprising the caudal medulla, the flocculus and the SVN, successively. Therefore, it is suggested that the main types of spontaneous vertical nystagmus due to focal central lesions result from a primary dysfunction of the SVN-VTT pathway, which becomes hypoactive after pontine or caudal medullary lesions, thereby eliciting UBN, and hyperactive after floccular lesions, thereby eliciting DBN. Lastly, since gravity influences UBN and DBN and may facilitate the downward vestibular system and restrain the upward vestibular system, it is hypothesized that the excitatory SVN-VTT pathway, along with its specific floccular inhibition, has developed to counteract the gravity pull. This anatomical hyperdevelopment is apparently associated with a physiological upward velocity bias, since the gain of all upward slow eye movements is greater than that of downward slow eye movements in normal human subjects and in monkeys.
[Atypical ocular myasthenia gravis].
The diagnosis of ocular myasthenia gravis is rarely in doubt in patients with a proper history and typical clinical findings. However, myasthenia gravis can mimick any pupil-sparing eye movement disorder and several diseases may masquerade myasthenia gravis. We review the atypical presentations and differential diagnoses in ocular myasthenia gravis, describing four patients with some of these conditions (4th nerve palsy, near spasm reflex, one-and-a-half syndrome, orbital meningioma). The correct interpretation of the clinical findings associated with appropriate neuro-imaging studies allowed the appropriate diagnosis in these cases.
[Optochiasmal cavernoma: a rare cause of unilateral visual loss].
INTRODUCTION: Optic pathways cavernomas are rare vascular hamartomas that can present either with an acute chiasmal syndrome or slowly progressive visual loss. OBSERVATION: A 29-year-old patient presented with mild unilateral visual loss of rapid onset and monocular left temporal hemianopia. MRI disclosed a heterogenous enhancing optochiasmal lesion. Work-up found no evidence for an inflammatory, infectious or tumoral disease and therefore a neurosurgical approach of the lesion allowed diagnosis of cavernoma, confirmed by pathological examination. Successful resection resulted in partial recovery of the visual field. CONCLUSION: Optochiasmal cavernomas are rare, removal can improve visual outcome.
[Optic neuritis associated with infliximab].
Infliximab is a chimeric human-murine monoclonal antibody of the IgG1 type with a high affinity and specificity for tumor necrosis factor alpha (TNFalpha). Infliximab was used in Crohn disease, rheumatoid arthritis, spondyloarthropathy, juvenile idiopathic arthritis, Behcet's disease, Wegener's granulomatosis, HLA-B27-associated uveitis and chronic severe refractory uveitis. Reported adverse effects of this treatment were infections, development of antinuclear antibodies and anti double-stranded DNA, lymphomas, and exacerbation of demyelinating disease. We report a case of infliximab-associated optic neuritis with favorable outcome after systemic steroid treatment.
[Optic neuropathy associated with primary antiphospholipid syndrome].
We describe a 45-year-old male patient with an atypical unilateral optic neuropathy who was diagnosed with primary antiphospholipid syndrome. The initially poor vision lasting several months completely recovered and long-term oral anticoagulation therapy prevented potential further systemic thrombotic complications.
The role of the human dorsolateral prefrontal cortex in ocular motor behavior.
The dorsolateral prefrontal cortex (DLPFC) is involved in the preparation of saccadic eye movements. Lesion studies and functional magnetic resonance imaging (fMRI) studies suggest that the human DLPFC is located in area 46 of Brodmann. The DLPFC has direct connections with the main cortical ocular motor areas, that is with the frontal eye field (FEF) and the supplementary eye field (SEF) in the frontal lobe; with several (associative, attentional, and motor) areas in the posterior parietal cortex (PPC), including the parietal eye field (PEF); with the cingulate eye field in the anterior cingulate cortex; and directly downstream with the superior colliculus in the brainstem. Lesion and fMRI studies using the antisaccade paradigm have shown that the DLPFC is involved in the inhibition of unwanted reflexive saccades (triggered toward the target by the PEF), whereas the triggering of correct intentional antisaccades (made in the direction opposite to the target) may depend mainly upon the FEF. The DLPFC also controls short-term spatial working memory involved in memory-guided saccades, as shown by lesion and transcranial magnetic stimulation (TMS) studies. By contrast, medium-term spatial memory (after 25 s) may be controlled by the medial temporal cortex (MTC). Recently, TMS studies have suggested that the transmission of memorized information from the integrative parietal areas (PPC) to the MTC is performed via both an indirect pathway comprising the DLPFC (i.e., transmission in series) and a direct pathway bypassing the DLPFC (i.e., transmission in parallel). Furthermore, the DLPFC is involved in the preparation of predictive saccades (i.e., saccades made before the appearance of an expected target) and saccade sequences, and, therefore, also controls some aspects of temporal working memory. Lastly, the involvement of the DLPFC has recently been reported in tasks comprising a target selection or a directional decision to make for the forthcoming saccade. These different functions suggest that the DLPFC plays a major role in the decisional processes governing ocular motor behavior.
Antisaccade deficit after anterior cingulate cortex resection.
Suppression of unwanted reflexive saccades is a crucial process allowing to sustain voluntary fixation, when required. This inhibition process, which is mainly controlled by the dorsolateral prefrontal cortex, may also involve other cortical and subcortical structures. We prospectively studied the effect of frontal cortical resections involving adjacent regions to the anterior cingulate cortex on the ability to inhibit reflexive saccades. This lesion study included six patients undergoing resection of frontal low grade gliomas, studied prior and after surgery with electro-oculography, using the antisaccade paradigm. Lesions were normalized and mapped in Talairach space allowing to detail the structures whose lesions were associated with antisaccade deficits. In three of the six patients significant early post-operative antisaccade errors were associated with resection of a common critical region, mainly involving the posterior part of the anterior cingulate cortex. This same region was spared in the three remaining patients with no antisaccade deficit, suggesting that the anterior cingulate cortex, known as the cingulate eye field, could play a role in suppression of unwanted saccades.
Concurrent excitatory and inhibitory effects of high frequency stimulation: an oculomotor study.
OBJECTIVE: To describe a reversible neurological condition resembling a crossed midbrain syndrome resulting from high frequency stimulation (HFS) in the midbrain. METHODS: Postoperative evaluation of quadripolar electrodes implanted in the area of the subthalamic nucleus of 25 patients with Parkinson's disease (PD) successfully treated by HFS. RESULTS: Four of the 25 patients experienced reversible acute diplopia, with dystonic posture and tremor in the contralateral upper limb when the white matter between the red nucleus and the substantia nigra was stimulated. The motor signs resembled those caused by lesions of the red nucleus. The ipsilateral resting eye position was "in and down" (three patients) or "in" (one patient). Enophthalmos was seen. Abduction was impaired and vertical eye movements were limited, but adduction was spared. The movements of the controlateral eye were normal. The ocular signs could be best explained by sustained hyperactivity of the extrinsic oculomotor nerve. Simultaneous tonic contraction of the superior rectus, the inferior rectus, and inferior oblique may cause the enophthalmos and partial limitation of upward and downward eye movements. Antagonist tonic contraction of the ipsilateral medial rectus severely impairs abduction. CONCLUSION: This crossed midbrain syndrome, possibly resulting from simultaneous activation of oculomotor nerve and lesion-like inhibition of the red nucleus suggests that high frequency stimulation has opposite effects on grey and white matter.
[Vision disorders of central origin].
Cortical blindness (or more generally, cerebral blindness) consists of bilateral visual loss with normal ocular examination and normal pupillary function, related to bilateral occipital lesions. Its most frequent cause in adults is hypoperfusion in the vertebral-basilar arteries, although other curable causes are described. Other syndromes, related to lesions of associative cortical areas or occipital-fugal connections may cause poorly defined visual complaints. Their recognition by the ophthalmologist is mandatory, as they may concern a potentially curable underlying disease.
Complete bilateral horizontal gaze paralysis disclosing multiple sclerosis.
Two women presented with bilateral internuclear ophthalmoplegia evolving in a few days to complete bilateral horizontal gaze paralysis. Convergence and vertical eye movements were normal. Cerebral MRI showed a few small white matter lesions in the lateral ventricle regions, and, at the brainstem level, a single, small, bilateral lesion affecting the posterior part of the medial pontine tegmentum and responsible for the clinical syndrome. The condition gradually improved in both patients, following a similar progression as at the onset: improvement first involved the adduction movements in both eyes, whereas bilateral abduction paresis still persisted for a few weeks, before complete recovery of eye movements. Bilateral damage to the medial longitudinal fasciculus and subsequent lateral extent of damage to the region of the two abducens emerging fibres may explain the clinical findings. In both cases, the cause was probably multiple sclerosis.
[Radiotherapy for age-related macular degeneration: risk factors of complications, prevention and treatment of side-effects].
PURPOSE: To analyze the retinal and choroidal side-effects of radiotherapy given for age-related macular degeneration (ARMD) and to describe the risk factors of these complications and their treatment. MATERIAL: and methods: Two hundred and ninety five eyes in 270 patients with ARMD were treated using radiotherapy. Nineteen patients had diabetes. The doses were as follows: 15 Gy or less (4 eyes); 16 Gy/4 fractions (113 eyes); 18 Gy/5 fractions (35 eyes); 20 Gy/5 fractions (123 eyes); 24 Gy/6 fractions (2 eyes); 28.8 Gy/8 fractions (17 eyes); more than 28.8 Gy (1 eye). Patients had a regular follow-up visit with visual acuity, contrast sensitivity evaluation, biomicroscopic fundus examination, fluorescein and ICG angiographies every six months over a mean period of 15 months. RESULTS: Radiation retinopathy was noted in 15 eyes, a bilateral neovascular glaucoma in one patient, ischemic optic neuropathy in 5 eyes, choroidal telangiectasiae in 19 eyes, venous occlusion in 2 eyes, oedematous retinopathy with major exudation (ORME) in 31 eyes, and choroidal hematoma in 8 eyes. Radiation retinopathy, choroidal telangiectasiae and ORME were related to radiation dose. Radiation retinopathy was more severe and more frequent in patients with diabetes. Choroidal telangiectasiae were diagnosed with ICG angiography and were treated early with laser. CONCLUSION: Radiotherapy for ARMD should not be done in patients with diabetes. Hypofractionation is not recommended. ICG angiography should be considered essential in the follow-up of patients treated with radiotherapy.
Excimer laser photorefractive keratectomy in myopic eyes with corectopia.
Corectopia, the eccentric displacement of the pupil, may be associated with other abnormalities such as axial high myopia or ectopia lentis. We report the case of a patient presenting for surgery to correct bilateral myopia of 6.50 diopters (D) associated with corectopia. Excimer laser ablation was decentered and performed on the center of the abnormal pupils. After a 2 year follow-up, best corrected visual acuity was 20/20 with -1.00 D correction in each eye. To our knowledge, this is the first report of excimer laser photorefractive keratectomy for myopia associated with corectopia. The satisfactory results suggest that in abnormally eccentric pupils, excimer laser treatment of myopia may be successful when it is centered on the deviated pupil.
Neovascular glaucoma after bypass surgery in Takayasu's disease.
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Indocyanine green angiography in choroidal tuberculomas.
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Long term results of radiotherapy for subfoveal choroidal neovascularisation in age related macular degeneration.
BACKGROUND/AIMS: Radiotherapy has been proposed as an alternative treatment for patients with subfoveal choroidal neovascularisation (CNV) that is untreatable according to macular photocoagulation study guidelines. This prospective study was designed to evaluate whether radiotherapy may affect the functional and anatomical outcome in a large cohort of patients affected by subfoveal CNV, with a follow up period up to 24 months. METHODS: 212 patients (231 eyes) with newly diagnosed subfoveal CNV not amenable to laser therapy were included in this study. Two radiotherapy methods, the lateral beam technique (6 MV, 20 Gy in five fractions) and lateral arc therapy (25 MV, 16 to 20 Gy, in four or five fractions), were used. Comparisons of best corrected visual acuity (VA), fluorescein (FA) and indocyanine green (ICG) angiography, at inclusion and 6, 12, 18, and 24 months after radiotherapy were performed using univariate analysis. RESULTS: A VA improvement of two or more lines was observed in 34% at 12 months, 31% at 18 months, and 32% of the eyes at 24 months. Paired comparisons of CNV areas in FA and ICG showed no significant change between baseline and each visit. However, 12 and 18 months after treatment, 47% of the eyes showed a decrease of 10% or more in CNV size both in ICG and FA. Radiation side effects included radiation retinopathy (eight eyes), optic neuropathy (four eyes), choroidal vasculopathy (five eyes), and branch retinal vein occlusion (three eyes). CONCLUSION: Compared with the natural course of subfoveal CNV, the results of this prospective study suggest that radiotherapy could stabilise visual and anatomical outcome in selected cases.