An Analysis of Retinal Nerve Fiber Layer Thickness before and after Pituitary Adenoma Surgery and its Correlation with Visual Acuity.

INTRODUCTION: Pituitary adenomas comprise approximately 10% of all intracranial tumors. Initially, subtle changes occur in the field of vision, which are difficult to assess clinically. It has been seen that following surgery of pituitary macroadenoma, total recovery of normal vision occurs in 35% of the patients, improvement of vision occurs in 60%, and in the rest there is no change in vision. Retinal nerve fiber layer thickness (RNFLT) undergoes retrograde degeneration following compression of optic apparatus by pituitary tumor. We planned a study to evaluate RNFLT before and after pituitary adenoma surgery and its correlation with visual acuity. MATERIAL AND METHODS: Twenty patients (40 eyes) with diagnosed pituitary adenoma were included in the study. Preoperative visual acuity, fundus and RNFL thickness were calculated using spectral-domain OCT Optovue, Heidelberg Engineering, Heidelberg, Germany (RT 100 version 5.1), and postoperative measurement was done after 1 and 3 months. Four-quadrant mean of RNFLT was calculated. Results were tabulated and analyzed. STATISTICAL ANALYSIS: Results of the study were analyzed using IBM SPSS Statistics version 19.0. RESULTS: There was no significant change in RNFLT after pituitary adenoma surgery, and it was found that patients with RNFLT within normal range preoperatively showed improvement in visual acuity after pituitary surgery. On the other hand, patients who had thinned-out RNFLT preoperatively showed no improvement in visual acuity. It was also found that once optic disc pallor sets due to chronic compression, then chances of its reversion to normal depend on its grading: only mild pallor disc has some chance to revert to normal, whereas moderate and severe pallor do not revert to normal. CONCLUSION: RNFLT and optic disc can be used as prognostic factors for evaluation of visual outcome in pituitary adenoma surgery.

Hypertrophic Olivary Degeneration and Holmes Tremor: Case Report and Review of the Literature.

BACKGROUND: Hypertrophic olivary degeneration (HOD) is very rare type of degeneration that causes hypertrophy rather than atrophy. The classical presentation of HOD is palatal myoclonus. However, HOD may rarely present with Holmes tremor (HT). HT is unusual symptomatic tremor characterized by combination of rest and intention tremor. It has been reported in small case series, so far. CASE DESCRIPTION: In this study, a man aged 62 years with HOD and HT spreading to the upper and lower extremities after pontine-midbrain hemorrhage due to cavernoma was presented. CONCLUSIONS: Although pontine-midbrain hemorrhage may cause HT in the late period, HOD can be revealed on magnetic resonance imaging. Tract anatomy, especially the Guillain-Mollaret triangle, should be considered to explain the relationship between HT and HOD.

Patterns of retrograde axonal degeneration in the visual system.

Conclusive evidence for existence of acquired retrograde axonal degeneration that is truly trans-synaptic (RTD) has not yet been provided for the human visual system. Convincing data rely on experimental data of lesions to the posterior visual pathways. This study aimed to overcome the limitations of previous human studies, namely pathology to the anterior visual pathways and neurodegenerative co-morbidity. In this prospective, longitudinal cohort retinal optical coherence tomography scans were acquired before and after elective partial temporal lobe resection in 25 patients for intractable epilepsy. Newly developed region of interest-specific, retinotopic areas substantially improved on conventional reported early treatment diabetic retinopathy study (ETDRS) grid-based optical coherence tomography data. Significant inner retinal layer atrophy separated patients with normal visual fields from those who developed a visual field defect. Acquired RTD affected the retinal nerve fibre layer, ganglion cell and inner plexiform layer and stopped at the level of the inner nuclear layer. There were significant correlations between the resected brain tissue volume and the ganglion cell layer region of interest (R = -0.78, P < 0.0001) and ganglion cell inner plexiform layer region of interest (R = -0.65, P = 0.0007). In one patient, damage to the anterior visual pathway resulted in occurrence of microcystic macular oedema as recognized from experimental data. In the remaining 24 patients with true RTD, atrophy rates in the first 3 months were strongly correlated with time from surgery for the ganglion cell layer region of interest (R = -0.74, P < 0.0001) and the ganglion cell inner plexiform layer region of interest (R = -0.51, P < 0.0001). The different time course of atrophy rates observed relate to brain tissue volume resection and suggest that three distinct patterns of retrograde axonal degeneration exist: (i) direct retrograde axonal degeneration; (ii) rapid and self-terminating RTD; and (iii) prolonged RTD representing a 'penumbra', which slowly succumbs to molecularly governed spatial cellular stoichiometric relationships. We speculate that the latter could be a promising target for neuroprotection.

Retinal pathology in experimental optic neuritis is characterized by retrograde degeneration and gliosis.

The exact mechanisms and temporal sequence of neurodegeneration in multiple sclerosis are still unresolved. The visual pathway including its unmyelinated retinal axons, can serve as a prototypic model of neurodegeneration in experimental optic neuritis. We conducted a longitudinal study combining retinal imaging through optical coherence tomography (OCT) with immunohistochemical analyses of retinal and optic nerve tissue at various time points in experimental autoimmune encephalomyelitis (EAE).Inner retinal layer (IRL) thickness was measured in 30 EAE and 14 healthy control C57BL/6 J mice using OCT. Distribution of marker proteins was assessed by immunofluorescence staining and retinal mRNA levels were assayed using real-time PCR. Histological morphology was evaluated on light and electron microscopy images.Signs of inflammatory edema 11 days post immunisation coincided with IRL thickening, while neuro-axonal degeneration throughout the disease course contributed to IRL thinning observed after 20 days post immunisation. Retinal pathology, including axonal transport impairment, was observed early, prior to cellular infiltration (i.e. T-cells) in the optic nerve 11 days post immunisation. Yet, the effects of early retinal damage on OCT-derived readouts were outweighed by the initial inflammatory edema. Early microglial activation and astrocytosis was detected in the retina prior to retinal ganglion cell loss and persisted until 33 days post immunisation. Müller cell reactivity (i.e. aquaporin-4 and glutamine synthetase decrease) presented after 11 days post immunisation in the IRL. Severe neuro-axonal degeneration was observed in the optic nerve and retina until 33 days post immunisation.Initial signs of retinal pathology subsequent to early glial activity, suggests a need for prophylactic treatment of optic neuritis. Following early inflammation, Müller cells possibly respond to retinal pathology with compensatory mechanisms. Although the majority of the IRL damage observed is likely due to retrograde degeneration following optic neuritis, initial pathology, possibly due to gliosis, may contribute further to IRL thinning. These results add morphological substrate to our OCT findings. The extent and rapid onset of axonal and neuronal damage in this model appears relevant for testing interventions scaled to human optic neuritis.

Retinal Alteration Associated with an Arachnoid Cyst of the Pineal Region.

BACKGROUND: Retinal optical coherence tomography (OCT) is a noninvasive high-resolution imaging technique, which is considered a biomarker of neurodegeneration. Several intracranial lesions can induce retrograde neurodegeneration which can be assessed using OCT. The cysts of the pineal region are usually asymptomatic and most often are an incidental radiologic finding. CASE DESCRIPTION: We describe the case of a 50-year-old woman with an arachnoid cyst of the pineal region who complained of visual symptoms for 3 months. Bilateral macular thinning was demonstrated by OCT both on the preoperative and postoperative examinations, without any other clinical findings that could explain the results. CONCLUSIONS: We suggest that the retinal alteration is caused by retrograde neurodegeneration secondary to the pineal region mass.

Neurite orientation dispersion and density imaging of the nigrostriatal pathway in Parkinson's disease: Retrograde degeneration observed by tract-profile analysis.

INTRODUCTION: Parkinson's disease (PD) is marked by the degeneration of dopaminergic neurons in the nigrostriatal pathway (NSP). We aimed to identify the microstructural changes in the NSP of PD patients using neurite orientation dispersion and density imaging (NODDI). METHODS: NSPs of 29 PD patients, who were retrospectively selected from patients previously admitted to our institution, and 29 age- and gender-matched healthy controls were isolated via deterministic tractography. The NODDI indices, intracellular volume fraction (Vic), orientation dispersion index (OD), and isotropic volume fraction (Viso) were compared between the two groups. The significant results were assessed with a tract-profile analysis. The correlation between indices and disease duration or motor symptom severity was evaluated with the Pearson's correlation test. RESULTS: The contralateral distal Vic (p = 0.00028) of the nigrostriatal pathway was significantly lower in PD patients than in healthy controls. No correlations were detected between any of the indices and disease duration or motor symptom severity. CONCLUSIONS: NODDI can be used to identify retrograde degeneration of the NSP in PD patients and might be useful for monitoring the disease progression of PD.

Small bowel obstruction secondary to distal migration of the intestinal probe in a patient with an endoscopic gastrostomy for continuous carbidopa-levodopa infusion / Obstrucción de intestino delgado secundaria a migración distal de la sonda intestinal en una paciente con gastrostomía endoscópica para la infusión continua de carbidopa-levodopa

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[Structural retinal and optic nerve changes in patients with post-geniculate visual pathway damage]. / Strukturnye izmeneniia setchatki i zritel'nogo nerva pri porazhenii tsentral'nogo nevrona zritel'nogo puti.

AIM: To establish the possibility of retrograde trans-synaptic neural degeneration following acquired post-geniculate visual pathway damage. MATERIAL AND METHODS: Twenty-two patients with homonymous hemianopia caused by acquired post-geniculate visual pathway damage were examined. Peripapillary retinal nerve fiber layer (RNFL) thickness and ganglion cell complex (GCC) measurements were assessed with RTVue-100 Fourier-domain optical coherence tomography (OCT). RESULTS: In 12 out of 22 patients we detected binocular GCC thinning that was ipsilateral to post-geniculate involvement. Nine patients showed a decrease in the RNFL thickness. However, topographic correspondence between the post-geniculate lesion and RNFL thickness was established for 2 of them only. GCC thinning was more common in patients with hemianopsia acquired more than 6 months ago (p<0.0009). CONCLUSION: Having assessed the ganglion cell complex and retinal nerve fiber layer with OCT, we have proved possible that trans-synaptic retrograde degeneration develops in patients with post-geniculate visual pathway damage.

Trans-synaptic degeneration in the optic pathway. A study in clinically isolated syndrome and early relapsing-remitting multiple sclerosis with or without optic neuritis.

OBJECTIVE: Increasing evidence suggest that neuronal damage is an early and diffuse feature of Multiple Sclerosis (MS) pathology. Analysis of the optic pathway may help to clarify the mechanisms involved in grey matter damage in MS. Purpose of our study was to investigate the relationship between inflammation and neurodegeneration and to achieve evidence of trans-synaptic degeneration in the optic pathway in MS at clinical onset. METHODS: 50 clinically isolated syndromes/early relapse-onset MS (CIS/eRRMS) with mean disease duration of 4.0±3.5 months, 28 MRI healthy controls (HC) and 31 OCT-HC were studied. Ten patients had optic neuritis at presentation (MSON+), 40 presented with other symptoms (MSON-). MRI examination included 3D-T1, 3D-FLAIR and 3D-DIR sequences. Global cortical thickness (gCTh), pericalcarin CTh (pCTh) and white matter volume (WMV) were analysed by means of Freesurfer on 3D-T1 scans. Optic radiation morphology (OR) and volume (ORV) were reconstructed on the base of the Jülich's Atlas. White matter lesion volume (WMLV), OR-WMLV and percent WM damage (WMLV/WMV = WMLV% and OR-WMLV/ORV = ORWMLV%) were obtained by 3D-FLAIR image segmentation. 3D-DIR sequences were applied to identify inflammatory lesions of the optic nerve. Optic coherence tomography (OCT) protocol included the analysis of global peripapillary retinal nerve fiber layer (g-RNFL) and the 6 fundus oculi's sectors (temporal, T-RNFL; temporal superior, TS-RNFL; nasal superior, NS-RNFL; nasal, N-RNFL; nasal inferior, NI-RNFL, temporal inferior, TI-RNFL). The retina of both eyes was analyzed. The eyes of ON+ were further divided into affected (aON+) or not (naON+). RESULTS: No difference in CTh was found between CIS/eRRMS and HC, and between MSON+ and MSON-. Moreover, MSON+ and MSON- did not differ for any WM lesion load parameter. The most significant correlations between RNFL thickness and optic radiation WM pathology were found in MSON+. In these patients, the temporal RNFL inversely correlated to ipsilateral optic radiation WM lesion load (T-RNFL: r -0.7, p<0.05; TS-RNFL: r -0.7, p<0.05), while nasal RNFL inversely correlated to contralateral optic radiation WM lesion load (NI: r -0.8, p<0.01; NS-RNFL: r -0.8, p<0.01). CONCLUSIONS: Our findings suggest that in MSON+ the optic pathway is site of a diffuse pathological process that involves both directly and via trans-synaptic degeneration the RNFL.

Trans-synaptic Retrograde Degeneration in the Human Visual System: Slow, Silent, and Real.

Degeneration of neuron and axons following injury to cells with which they synapse is termed trans-synaptic degeneration. This phenomenon may be seen in postsynaptic neurons (anterograde) or in presynaptic neurons (retrograde). Retrograde trans-synaptic degeneration (RTSD) of the retinal ganglion cells and retinal nerve fiber layer following injury to the occipital lobe has been well documented histologically in animal studies, but its occurrence in the human retina was, for many years, felt to be limited to cases of neonatal injury during a critical period of neuronal development. Over the last decade, imaging techniques such as MRI and optical coherence tomography have allowed us to visualize and quantify RTSD and analyze its time course and relationship to degree of vision loss and age of cortical injury. A deeper understanding of RTSD in the human visual system may allow us to interfere with its occurrence, potentially allowing for greater recovery following visual cortex injury.