Acute traumatic orbital cerebrospinal fluid cystocele mimicking orbital abscess.

Posttraumatic cranio-orbital cerebrospinal fluid (CSF) fistula is rare, occurring when there is a communication between orbit and subarachnoid space. This communication can be caused by orbital tumors with intracranial extension or can be a result of orbital surgery. Low suspicion for traumatic orbital CSF fistula can lead to delay in diagnosis, which increases the risk of meningitis. We report a cranio-orbital CSF cystocele and fistula that mimicked orbital cellulitis in a 3-year-old boy following an orbitocranial penetrating injury.

Follow up of patients with ocular scarring secondary to LOC syndrome treated by amniotic membrane transplantation.

AIMS: To document and discuss the long term outcome of a new ophthalmic treatment for laryngo-onycho-cutaneous (LOC) syndrome. METHODS: Two children were treated by excision of ocular granulation tissue and ocular surface rehabilitation with frozen amniotic membrane (AM). The clinical course of both patients was followed and documented at 2 years and 4 years following the surgery. RESULTS: Patient 1 demonstrated limited recurrence of granulation tissue at 10 months. After 36 months, re-growth of granulation and scar tissue required a further three subsequent operations to the right eye in an attempt to keep the optical axis clear. 4 years postoperatively, neither eye has a clear visual axis. In contrast similar surgery for the right eye of patient 2 has been highly successful, with only very limited non-progressive recurrence after 2 years of follow up. The operation to the left eye has been similarly effective although the follow up is only 6 months. CONCLUSIONS: Ocular surface rehabilitation with AM is the first partially effective treatment for the eye complications of LOC syndrome. The surprising benefit from AM may stem from the primary pathology of the condition. LOC syndrome is caused by a genetic defect resulting in an unusual N-terminal deletion of the alpha3a chain of the basement membrane protein laminin 5. One mechanism through which AM transplantation may act to reduce ocular scarring in this disease is to supplement the abnormal secreted laminin 5 with healthy transplanted laminin. Despite its initial efficacy one episode of AM treatment does not guarantee long term control of the scarring process and variations in AM graft efficacy may be related to other complicating factors such as limbal stem cell deficiency or severity of the initial scarring process.

Ocular surface reconstruction in LOGIC syndrome by amniotic membrane transplantation.

PURPOSE: To determine whether preserved amniotic membrane can be used to reconstruct the ocular surface after excision of the invading granulation material typical of LOGIC syndrome (laryngeal and ocular granulation tissue in children from the Indian subcontinent). METHODS: Granulation tissue was dissected and excised from both eyes of a 10-year-old boy with LOGIC syndrome. This procedure was followed by coverage of the corneal, scleral, and subtarsal regions of each eye with amniotic membrane, which had been stored for 6 months at -70 degrees C. RESULTS: Initial 2.5-month follow up demonstrated complete disappearance of granulation tissue. The fornices were patent, there was no recurrence of symblepharon, ocular inflammation was suppressed, and the patient reported markedly increased comfort. Both eyelids remained ptotic because of levator muscle atrophy secondary to many years of inability to open either eye. No residual scarring or evidence of granulation tissue was observed in that period. The 10-month follow up demonstrated limited recurrence, particularly where there was an intraoperative break in the amniotic membrane. CONCLUSIONS: After 24 operations to treat the ocular complications induced by LOGIC syndrome, amniotic membrane transplantation was the first effective treatment. In the early follow up period (2-3 months), there was complete cessation of the proliferation of granulation tissue and reepithelialization of the corneal surface. Longer follow up (10 months) demonstrated limited recurrence, which will require retreatment.

Expression of the inducible nitric oxide synthase in distinct cellular types after traumatic brain injury: an in situ hybridization and immunocytochemical study.

The Marmarou's acceleration traumatic brain injury (TBI) model, in situ hybridization and immunocytochemistry were utilized to study the temporal expression of the inducible form of nitric oxide synthase (iNOS) mRNA and protein in different cellular compartments of the rat brain. Four hours following TBI, expression of iNOS was observed in the endothelial cells of cerebral blood vessels, macrophages and many cortical and hippocampal neurons. In the cortex labeled neuronal and nonneuronal cells were primarily found in the superficial layers. In the hippocampus the strongest neuronal labeling was observed in the CAI and CA3 (lateral part) regions. By 24 h post TBI endothelial cells no longer expressed iNOS mRNA, and the macrophage and neuronal iNOS expression was reduced by 30-50%. The reduction was assessed by automated quantitation of the silver grains that occupy individual cellular profiles using an image analysis system. Immunocytochemistry revealed de novo iNOS synthesis in non-neuronal cells at the different time points, thus paralleling the changes in iNOS mRNA expression. In contrast, iNOS immunoreactivity in neurons was not observed before 24 h post TBI, suggesting failure of iNOS protein translation at 4 h after trauma. The results demonstrate complex spatial and temporal patterns of iNOS expression in discrete cellular populations, indicating different times of nitric oxide synthesis (and release) following TBI. Uncoupling of iNOS mRNA and protein synthesis in neurons suggests differential synthesis of nitric oxide in these cells as compared to non-neuronal cellular populations after trauma.

Management of diplopia on down-gaze following orbital trauma.

Diplopia in the inferior field due to orbital trauma is a notoriously difficult and disabling problem. Even if a blow-out fracture is repaired by current methods, patients may still have diplopia. There also exists another group in whom no demonstrable radiological fracture can be found, and yet there is a severe down gaze deficit. The possible mechanisms of this phenomenon are discussed and the results of horizontal muscle transposition surgery in a series of nine patients is reported. The authors conclude that this procedure is a valuable method of increasing the useful field of binocular single version in these patients.

Traumatic retinal angiopathy--associated with wearing of car seat belts.

Three patients who were involved in road traffic accidents and sustained seat belt related injuries developed a retinal angiopathy characterised by retinal haemorrhage, oedema and focal ischaemia. Significant unilateral visual loss (2/60 - 6/18) was reported 1-48 hours following injury and central or paracentral annular scotomata were present. Although there was good recovery of visual acuity all patients had permanent scotomata, colour vision defects and loss of contrast sensitivity. Residual retinal microvascular and haemodynamic changes were noted on fluorescein angiography and the visually evoked responses were uniformly depressed. The structural and functional alterations in the retina of patients who have sustained seat belt injuries have important medico-legal implications.