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1.
J Glaucoma ; 15(1): 17-22, 2006 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-16378012

RESUMEN

BACKGROUND: Vascular dysregulation in open-angle glaucomas can be identified by measuring the blood circulation during exposure to cold water. Aim of this study was to find out whether the same cold stimulus would lead to functional changes in the visual evoked potentials (VEP) of the short-sensitive pathway in normals and glaucoma patients. PATIENTS AND METHODS: Blue-on-yellow pattern-visual evoked potentials were studied in 22 healthy control persons and 47 patients with primary open-angle glaucoma (25 high-pressure glaucomas, 22 normal pressure glaucomas with clinical signs of vasospastic hyperreactivity). A blue stripe pattern, presented in onset-offset mode on a yellow adaptation light served as the stimulus. Cold provocation was initiated by dipping one hand of the patient into cold water of 3 degrees C to 5 degrees C. The onset amplitudes and peak times were measured without cold exposition as well as two and four minutes after the cold exposition began. RESULTS: In the group of vasospastic glaucoma patients a significant reduction of visual evoked potential-amplitudes was observed during cold provocation (amplitude before ice exposition: 4.17 microV, amplitude following two minutes of ice exposition: 3.52 microV; paired test: P < 0.01). Other subject groups showed no significant amplitude reductions after cold provocation. Peak times of both open-angle glaucoma groups (132.3 +/- 18.7 milliseconds in high pressure, 132.7 +/- 14.5 milliseconds in normal pressure) were significantly increased in comparison to normals (117.4 +/- 8.0 milliseconds). However, no significant influence of the cold provocation on peak times could be found in all groups. CONCLUSION: Peak times of the blue-on-yellow visual evoked potentials are significantly prolonged in patients with primary open-angle glaucomas. Cold provocation causes a significant amplitude reduction of the blue-on-yellow visual evoked potential in the present normal-pressure glaucoma patients and reflects vascular dysregulation in patients with vasospastic hyperreactivity.


Asunto(s)
Frío , Potenciales Evocados Visuales/fisiología , Ojo/irrigación sanguínea , Glaucoma de Ángulo Abierto/fisiopatología , Vías Visuales/fisiopatología , Presión Sanguínea/fisiología , Temperatura Corporal , Femenino , Dedos/irrigación sanguínea , Humanos , Presión Intraocular/fisiología , Masculino , Persona de Mediana Edad , Pruebas del Campo Visual , Campos Visuales
2.
Klin Monbl Augenheilkd ; 220(6): 427-32, 2003 Jun.
Artículo en Alemán | MEDLINE | ID: mdl-12830399

RESUMEN

BACKGROUND: A variety of infectious and autoimmune diseases are described in association with pupillotonia. To our knowledge there is only one report on pupillotonia associated with hemiatrophia faciei. We describe another patient with this rare association. The aim is to investigate possible associations between both diseases. PATIENT: A twenty five-year-old male patient with hemiatrophia faciei, epilepsy and pupillotonia of the right eye since his twelfth birthday was presented for the first time at the age of fourteen at our institution. The patient underwent a complete neurological and paediatric as well as otolaryngological investigation; there was also an investigation by the internist. The patient also underwent a complete serological investigation for infectious and autoimmune disorders as well as an investigation of the local and systemic vascular reactivity by the "Ocular cold pressor test". The follow-up time is 11 years. RESULTS: The clinical picture of our patient was an association of hemiatrophia faciei, epilepsy and pupillotonia. There was no evidence of a local hyperactivity of the sympathetic nervous system. The serological investigation showed an elevated value of antinuclear antibodies. CONCLUSIONS: We assume that in our case the pupillotonia as well as the hemiatrophia faciei and the epilepsy is caused by a common autoimmune factor. All other aetiologies for these three diseases were excluded. Furthermore, the occurrence of pupillotonia, hemiatrophia faciei and epilepsy was simultaneous.


Asunto(s)
Enfermedades Autoinmunes/diagnóstico , Hemiatrofia Facial/diagnóstico , Pupila Tónica/diagnóstico , Adolescente , Adulto , Anticuerpos Antinucleares/sangre , Enfermedades Autoinmunes/inmunología , Niño , Diagnóstico Diferencial , Epilepsia Parcial Compleja/diagnóstico , Epilepsia Parcial Compleja/inmunología , Epilepsia del Lóbulo Temporal/diagnóstico , Epilepsia del Lóbulo Temporal/inmunología , Hemiatrofia Facial/inmunología , Estudios de Seguimiento , Humanos , Inmunoglobulina E/sangre , Masculino , Pupila Tónica/inmunología
3.
Klin Monbl Augenheilkd ; 220(1-2): 54-6, 2003.
Artículo en Alemán | MEDLINE | ID: mdl-12612849

RESUMEN

BACKGROUND: Myokymia of the obliquus superior muscle is a rare episodic microtremor caused by uncontrolled activities of the trochlearis nerve fibres. Epilepsy is also caused by spontaneous discharges of neurons. In our report we present an associated epilepsy which to the best of our knowledge is described for the first time. PATIENT: An 61-year old man with twitches of the right eye for 6 weeks and a subjective feeling of eye movement was investigated at our hospital. His history was void of any ophthalmologic diseases. However, he suffered from cryptogenetic epilepsy known since childhood. The morphological and orthoptical findings of his eyes were normal. During the slit-lamp investigation a unilateral rotating microtremor of the right eye induced by looking downward was seen. The neurologic investigation, magnetic resonance imaging and assessment of the thyreoid function did not show further pathological results. The patient underwent treatment with carbamazepine. Under this therapy he did not show any symptoms of myokymia during follow-up. SUMMARY: To the best of our knowledge this is the first case of myokymia of the obliquus superior muscle associated to epilepsy. To our opinion, any case of this syndrome should be investigated for epilepsy. A causal relation is unlikely since the most probable etiologies are either spontaneous discharges of trochlear nucleus neurons or a close contact between vessel and nerve analogously to trigeminal neuralgia.


Asunto(s)
Epilepsia Parcial Compleja/complicaciones , Enfermedades del Nervio Troclear/complicaciones , Anticonvulsivantes/uso terapéutico , Carbamazepina/uso terapéutico , Epilepsia Parcial Compleja/tratamiento farmacológico , Epilepsia Parcial Compleja/fisiopatología , Estudios de Seguimiento , Humanos , Masculino , Persona de Mediana Edad , Resultado del Tratamiento , Nervio Troclear/efectos de los fármacos , Nervio Troclear/fisiopatología , Enfermedades del Nervio Troclear/tratamiento farmacológico , Enfermedades del Nervio Troclear/fisiopatología
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