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No Need To Cover Your Legs Anymore...

The Vein Clinic is a group of consultant vascular surgeons who specialise in vein treatments.

Our specialists are accredited with The Ireland Medical Council and have a particular interest in venous disease. They offer you private treatment for varicose veins, thread veins and facial veins. Included in our ranks are leading experts on vein problems.

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No Need to Cover Your Legs - Expert Treatment of Varicose Veins and Thread Veins
Expert Management of Vein Problems...

The most modern methods of diagnosis and management of vein disorders are used in the Vein Clinic.

Our specialists are recognised by private medical insurance companies for the treatment of symptomatic vein problems. For those not insured we offer affordable packages for all our procedures. Cosmetic treatments are offered at competitive rates.

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Expert Management of Vein Problems - Expert Treatment of Varicose Veins and Thread Veins
Varicose Vein Treatments, Without Surgery...

Ultrasound Guided Foam Sclerotherapy and RF Ablation are modern treatments for for varicose veins which are performed as outpatient procedures.

These allow you to carry on life as normal; there is little or no discomfort and minimal bruising afterwards.

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Varicose Vein Treatments, Without Surgery - Expert Treatment of Varicose Veins and Thread Veins

Induced Spreading Depression in Rats is Associated with a Microarea of Selective Neuronal Necrosis

Two different theories of migraine aura exist: In the vascular theory of Wolff, intracerebral vasoconstriction causes migraine aura via energy deficiency, whereas in the neuronal theory of Lea˜o and Morison, spreading depression (SD) initiates the aura. Recently, it has been shown that the cerebrovascular constrictor endothelin-1 (ET-1) elicits SD when applied to the cortical surface, a finding that could provide a bridge between the vascular and the neuronal theories of migraine aura. Several arguments support the notion that ET-1–induced SD results from local vasoconstriction, but definite proof is missing. If ET-1 induces SD via vasoconstriction/ischemia, then neuronal damage is likely to occur, contrasting with the fact that SD in the otherwise normal cortex is not associated with any lesion. To test this hypothesis, we have performed a comprehensive histologic study of the effects of ET-1 when applied topically to the cerebral cortex of halothane-anesthetized rats. Our assessment included histologic stainings and immunohistochemistry for glial fibrillary acidic protein, heat shock protein 70, and transferase dUTP nick-end labeling assay. During ET-1 application, we recorded (i) subarachnoid direct current (DC) electroencephalogram, (ii) local cerebral blood flow by laser- Doppler flowmetry, and (iii) changes of oxyhemoglobin and deoxyhemoglobin by spectroscopy. At an ET-1 concentration of 1 lM, at which only 6 of 12 animals generated SD, a microarea with selective neuronal death was found only in those animals demonstrating SD. In another five selected animals, which had not shown SD in response to ET-1, SD was triggered at a second cranial window by KCl and propagated from there to the window exposed to ET-1. This treatment also resulted in a microarea of neuronal damage. In contrast, SD invading from outside did not induce neuronal damage in the absence of ET-1 (n = 4) or in the presence of ET-1 if ET-1 was coapplied with BQ-123, an ETA receptor antagonist (n = 4). In conclusion, SD in presence of ET- 1 induced a microarea of selective neuronal necrosis no matter where the SD originated. This effect of ET-1 appears to be mediated by the ETA receptor.

The Vein Clinic

Suites 509-510, Q house,
76 Furze Road, Sandyford, Dublin 18

Dublin 01-2937839

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