Sensory profiles in adults with and without ADHD.

BACKGROUND: Our previous work demonstrates that adults with ADHD produce more force at the fingertips compared to adults without ADHD. One possibility is that somatosensation is impaired in ADHD. However, ADHD is often comorbid with anxiety, and anxiety influences sensory responsivity. AIMS: The goal of the current work was to evaluate differences in the self-report of sensory experiences in adults with and without ADHD, while controlling for internalizing behaviors. METHODS AND PROCEDURES: Forty-five adults (23 with ADHD) completed a semi-structured interview for the diagnosis of ADHD, the Adolescent/Adult Sensory Profile (AASP), and the Achenbach Adult Self Report (ASR). OUTCOMES AND RESULTS: Adults with ADHD reported more hyper- and hypo- sensitivity compared to adults without ADHD, even when controlling for internalizing behaviors. Specifically, between group differences were found for low registration, sensation seeking, and sensory sensitivity scores, but not for sensation avoiding, and for movement, visual, touch, activity, audition, or taste/smell. CONCLUSIONS AND IMPLICATIONS: These findings demonstrate that sensory hyper- and hypo- sensitivity may be features of ADHD in adults. Further, they demonstrate that internalizing behaviors influence the perception of sensory experiences and thus should be accounted for in studies of sensory processing, integration, and modulation in adults with ADHD.

Retinal tissue oxygen tension in normoxic cats under enflurane anesthesia.

PURPOSE: General anesthesia reduces systemic blood pressure and, thus, ocular perfusion pressure (at constant intraocular pressure). Whether this reduction in ocular perfusion pressure produces retinal hypoxia is unknown. To answer this question, the authors measured inner retinal oxygen tension in cats under general enflurane anesthesia at three clinically relevant levels of anesthesia under normoxic conditions. METHODS: Polarographic oxygen microelectrodes were used to measure inner retinal oxygen tension in cats under enflurane anesthesia at 21% inspired oxygen tension. Measurements were made in the preretinal vitreous body within 100 to 200 microns of the internal limiting membrane of the retina. Three levels of enflurane anesthesia were used: 1.2%, 2.4%, and 3.6%, corresponding to 0.5, 1.0, and 1.5 minimal alveolar concentration. Intraocular pressure of the cats was maintained at a constant normal level throughout the experiments. RESULTS: Under normoxic conditions, inner retinal oxygen tension remained unchanged or increased slightly as ocular perfusion pressure decreased with deeper levels of enflurane anesthesia. CONCLUSION: Commonly used surgical levels of enflurane general anesthesia do not cause hypoxia of the inner retina in cats breathing 21% inspired oxygen. This may be the result of preservation of retinal vascular autoregulation under enflurane anesthesia, retinal vasodilatation secondary to a direct smooth muscle relaxing effect of enflurane, or decreased retinal oxygen use under enflurane anesthesia.

A new model of proliferative vitreoretinopathy.

PURPOSE: To design a new model of proliferative vitreoretinopathy (PVR) that would not rely on the addition of exogenous cells. The release of endogenous cells from surrounding attachments seems to be an early event in the pathogenesis of PVR. Because the proteolytic enzyme dispase dissociates tissues, the hypothesis was that an intraocular injection of dispase could trigger events that would cause PVR. The requirement for a surgical retinal break at the time of dispase injection was also examined. METHODS: One eye of Dutch Belted rabbits was injected with 0.003 U to 1.0 U dispase in the subretinal space or vitreous cavity. Control rabbits received a saline injection. An intentional retinal tear was created in animals in some groups. Observations were made for at least 10 weeks after surgery. RESULTS: Proliferative vitreoretinopathy developed in response to subretinal or intravitreal dispase, with or without creation of a controlled retinal break. Increased severity of PVR correlated with increasing doses of dispase. Evidence of PVR included preretinal membranes, distortion of myelin wings and retinal vessels, fixed retinal folds, and traction retinal detachment. Proliferative vitreoretinopathy did not develop in saline-treated control animals. CONCLUSIONS: Dispase initiated the development of PVR without the addition of exogenous cells, growth factors, or cytokines typically found in PVR membranes. A cascade of events was probably triggered by dispase, causing native cells and factors to produce PVR. The dispase model of PVR was technically easy to perform, permitted a clear view of the retina, and had a high success rate in development of PVR.

Peripheral retinal cryotherapy for postvitrectomy diabetic vitreous hemorrhage in phakic eyes.

PURPOSE: To review the anatomic and visual outcomes of a consecutive series of phakic patients with postoperative diabetic vitreous hemorrhage (PDVH) who underwent revision vitrectomy with peripheral retinal cryotherapy. METHODS: We performed a retrospective chart review of consecutive phakic patients who underwent revision vitrectomy for PDVH who also received peripheral retinal cryotherapy. Final corrected visual acuities after revision vitrectomy with peripheral retinal cryotherapy were compared to corrected visual acuities before and at the time of PDVH. Anatomic outcomes such as retinal attachment, vitreous hemorrhage, iris neovascularization, lens opacity, and anterior hyaloidal neovascularization were considered. RESULTS: Nineteen (86%) of 22 eyes (21 patients) that underwent revision of vitrectomy and transscleral peripheral retinal cryotherapy for PDVH also received supplementary endolaser photocoagulation in the posterior pole. In 16 eyes (73%), no further vitreous hemorrhaging occurred after this procedure. In six eyes (27%), vitreous hemorrhage recurred after revision of vitrectomy and peripheral retinal cryotherapy but cleared spontaneously in three of these eyes. Of the three eyes with nonclearing recurrent vitreous hemorrhage after revision of vitrectomy and peripheral retinal cryotherapy, the cause for the vitreous hemorrhage was known for two: severe, progressive anterior hyaloidal neovascularization. With a mean follow-up +/- SD of 6.8 +/- 5.1 months (range, 0.5 to 19.5 months), final corrected visual acuity after revision of vitrectomy and peripheral retinal cryotherapy for PDVH improved over preoperative visual acuity (at which time vitreous hemorrhage was present) in 18 eyes (82%) because of removal of vitreous hemorrhage from the visual axis. However, final visual acuity reached or exceeded pre-PDVH visual acuity in only five of the 15 eyes for which pre-PDVH visual acuity was known. CONCLUSION: For phakic eyes with nonclearing PDVH, peripheral retinal cryotherapy (often augmented, when possible, by additional posterior pole endolaser photocoagulation) may be used to supplement previous retinal ablative therapy during revision of vitrectomy. This procedure leads to anatomic stabilization and visual improvement in the majority of eyes. Transscleral peripheral retinal cryotherapy is often feasible in situations (such as media opacity) that preclude use of peripheral retinal endolaser or indirect laser photocoagulation.

Optic nerve neovascularization in incontinentia pigmenti.

PURPOSE: To describe the presence of optic disk neovascularization in a child with incontinentia pigmenti. METHODS: A 6-month-old infant with incontinentia pigmenti developed optic disk neovascularization in addition to vascular abnormalities in the peripheral retina. Panretinal photocoagulation was performed. RESULT: The optic disk neovascularization regressed after panretinal photocoagulation. CONCLUSIONS: Optic disk neovascularization is another notable retinal manifestation of incontinentia pigmenti. When optic disk neovascularization is detected, retinal ablation should be considered as treatment.

Diabetic retinopathy.

Nonproliferative diabetic retinopathy may cause visual loss when associated with macular edema or macular ischemia (secondary to retinal capillary nonperfusion). Proliferative diabetic retinopathy may cause severe visual loss if complicated by vitreous hemorrhage or traction detachment of the macula. Patients with diabetes benefit from collaboration between the internist and ophthalmologist. Tighter control of blood glucose levels and lower blood pressure reduce the risk of progression of diabetic retinopathy. Regular dilated eye examinations and appropriate intervention with laser or vitrectomy surgery help to preserve vision in patients with established macular edema or proliferative diabetic retinopathy.

Scene control in prehospital care.

Skillful scene control, sensitive communication, and grace under pressure are all necessary for safe passage in and out of the volatile field environment. These skills must be nurtured and practiced. Ideas for their mastery are presented in this article. But everyone has a different style. To some, few of these ideas will be relevant. Others may embrace most. The skills most important to everyone are recognizing and controlling the forces acting on a scene and understanding the need for clear and calm leadership. Short of that, EMTs as well as patients fall prey to these forces, and personal safety and patient care are jeopardized.

Isovolemic hemodilution increases retinal tissue oxygen tension.

BACKGROUND: Therapeutic isovolemic hemodilution has been reported to improve blood flow and oxygen delivery. Few reliable measurements have been made, however, showing the effect of hemodilution on tissue oxygen tension. METHODS: We measured retinal oxygen tension during experimental isovolemic hemodilution in normal cats. Polarographic oxygen microelectrodes were placed in the vitreous humor within 100-200 microns of the retinal surface. RESULTS: Tissue oxygen tension increased initially during isovolemic hemodilution to a maximum approximately 50% above baseline at approximately two thirds of the original hematocrit level. Hemodilution beyond this point to lower hematocrits caused a steady decline in tissue oxygen tension. Cardiac output measured in one cat undergoing isovolemic hemodilution increased as hematocrit was lowered, but the cardiac erythrocyte flux actually decreased steadily. CONCLUSION: The observed increase in tissue oxygen tension with hemodilution appears to be explained by a lesser reduction in capillary than in systemic hematocrit, coupled with an increased capillary blood flow. The increase in tissue oxygen tension we observed could in part explain the clinically beneficial effects of hemodilution.