Use of a microsnare to aid direct thrombolytic therapy of dural sinus thrombosis.
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Biomedical subjects
Publications and source records attributed to S Galetta.
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PURPOSE: Dural arteriovenous fistulas (DAVFs) are acquired arteriovenous shunts located within the dura. The highly variable natural history and symptomatology of DAVFs range from subjective bruit to intracranial hemorrhage and are related to the lesion's pattern of venous drainage and its effect on the drainage of adjacent brain. We examined the prevalence and features of DAVFs in patients with progressive dementia or encephalopathy. METHODS: The records and radiologic studies of 40 consecutive patients with DAVFs treated at our institution were reviewed. RESULTS: Five (12.5%) of 40 consecutive patients with DAVFs had encephalopathy or dementia. In each patient, high flow through the arteriovenous shunt combined with venous outflow obstruction caused impairment of cerebral venous drainage. Hemodynamically, the result was widespread venous hypertension causing diffuse ischemia and progressive dysfunction of brain parenchyma. Results of CT or MR imaging revealed abnormalities in each patient, reflecting the impaired parenchymal venous drainage. Pathologic findings in one patient confirmed the mechanism of cerebral dysfunction as venous hypertension. The hemodynamic mechanism and resulting abnormality appeared identical to that seen in progressive chronic myelopathy resulting from a spinal DAVF (Foix-Alajouanine syndrome). Remission of cognitive symptoms occurred in each patient after embolization. CONCLUSION: Venous hypertensive encephalopathy resulting from a DAVF should be considered a potentially reversible cause of vascular dementia in patients with progressive cognitive deficits.
Two patients with visual apperceptive agnosia were examined on tasks assessing the appreciation of visual material. Elementary visual functioning was relatively preserved, but they had profound difficulty recognizing and naming line drawings. More detailed evaluation revealed accurate recognition of regular geometric shapes and colors, but performance deteriorated when the shapes were made more complex visually, when multiple-choice arrays contained larger numbers of simple targets and foils, and when a mental manipulation such as a rotation was required. The recognition of letters and words was similarly compromised. Naming, recognition, and anomaly judgments of colored pictures and real objects were more accurate than similar decisions involving black-and-white line drawings. Visual imagery for shapes, letters, and objects appeared to be more accurate than visual perception of the same materials. We hypothesize that object recognition difficulty in visual apperceptive agnosia is due to two related factors: the impaired appreciation of the visual perceptual features that constitute objects, and a limitation in the cognitive resources that are available for processing demanding material within the visual modality.
Cyclosporine neurotoxicity has been described after liver, kidney, and bone marrow transplantation and has been associated with a number of risk factors, including hypomagnesemia and low serum cholesterol levels. Reports in heart transplant recipients are less common. We present a patient with cortical blindness secondary to cyclosporine after orthotopic heart transplantation. The patient had confusion, focal visual field defects, and bilateral occipital lobe lesions shown on magnetic resonance imaging. Although he had significant clinical improvement with decreasing cyclosporine levels, residual computerized visual field defects and magnetic resonance imaging abnormalities were documented several months later.
We report a case of unilateral transient and reversible facial paresis, which was superimposed on a congenital bifacial palsy in a young adult with Moebius syndrome. Our case illustrates the potential for two conditions, both affecting the facial nerve and both of unknown etiology, to be juxtaposed in a single individual. Worsening of facial palsy in the Moebius syndrome may not signify progressive disease.
Sarcoid optic neuropathy without fundus lesions is unusual. We present a case of optic neuropathy with spontaneous remission in one eye that paralleled the clinical course of demyelinative acute optic neuritis. The fellow eye had disc swelling with normal visual acuity but with a large blind spot and distended optic nerve sheaths seen on ultrasonography. The diagnosis of sarcoidosis was made by characteristic chest roentgenographic findings and confirmed by skin biopsy.
A 23-year-old obese woman presented with papilledema. Computed tomography showed no intracranial mass lesions and lumbar puncture revealed an increased opening pressure, confirming the diagnosis of pseudo-tumor cerebri. Standardized echography of the optic nerves was performed immediately before and after lumbar puncture. A marked reduction of cerebrospinal fluid pressure correlated with a decrease in the subarachnoid fluid of the optic nerve sheath.
Previous studies from our laboratories have reported the synthesis and pharmacological characteristics of a series of symmetrical opiate azines: naloxonazine, oxymorphonazine and naltrexonazine. We have now synthesized and characterized in binding assays and in vivo two asymmetrical azines: oxymorphone-naltrexonazine and oxymorphone-3-methoxynaltrexonazine. Oxymorphone-naltrexonazine, which theoretically could interact with the receptor as either an agonist or antagonist, displayed antagonist properties in vitro and in vivo. Oxymorphone-3-methoxynaltrexonazine, which theoretically could bind only as an agonist, possessed agonist properties in binding studies and was a potent analgesic in vivo.
Magnetic resonance imaging provides a method of visualizing multiple sclerosis plaques, but the age and activity of these plaques cannot be determined with routine magnetic resonance images. Gadolinium DTPA is a paramagnetic contrast agent that does not cross an intact blood-brain barrier. We studied 16 patients with multiple sclerosis, using magnetic resonance imaging, gadolinium-enhanced magnetic resonance imaging, and computed tomographic scans. Gadolinium enhancement of multiple sclerosis plaques correlated with the clinical activity of the disease and corresponded anatomically with the symptoms and signs. We conclude that gadolinium enhancement of magnetic resonance images is a promising tool in the investigation of multiple sclerosis lesions and that it may provide a method for objective follow-up in clinical trails.
Magnetic resonance (MR) images--both nonenhanced and enhanced with gadolinium DTPA/dimeglumine (Gd)--were compared with high-iodine (88.1 g I) computed tomographic (HICT) scans in demonstrating lesions in 15 patients known to have multiple sclerosis (MS). T1-weighted, mixed (T1, proton density, and T2), and T2-weighted MR pulse sequences were used. More than 20 lesions in each of 14 patients were demonstrated by pre-Gd mixed images and T2WI. Nine patients had clinical symptoms of active disease. Gd-enhanced T1WI showed at least one lesion that appeared to correspond with newly reported symptoms or signs. In addition, three clinically stable patients showed enhancement. Enhancement was best seen on 3-minute T1WI. HICT scans showed enhancement in four of the nine patients with active disease and in none of five clinically stable patients. Gd-enhanced MR imaging appears to be more sensitive than HICT in the detection of the transient abnormalities of the blood-brain barrier that occur in patients with active MS and appears capable of distinguishing active lesions that may correspond to the anatomic regions responsible for abnormal clinical findings.
Treating rat brain homogenates in vitro with oxymorphazone, the hydrazone derivative of oxymorphone, selectively inhibited in a long-acting manner the high-affinity (mu 1) binding of a number of 3H-opioids. This inhibition was not affected by extensive wash procedures which did effectively reverse classical opiates such as morphine and naloxone. A similar, persistent inhibition of binding was observed following in vivo administration of the drug. Both systemically and intracerebroventricularly, oxymorphazone produced a dose-dependent analgesia. Acutely, oxymorphazone (ED50, 0.6 mg/kg, sc) was approximately half as potent as oxymorphone (ED50, 0.3 mg/kg, sc) in the tail-flick assay. Administered at their ED50 doses, both compounds had the same durations of action. As the doses of drug were increased, however, the time course of oxymorphazone's analgesia became far more prolonged than that of oxymorphone. Following the administration of oxymorphazone (100 mg/kg), over 50% of the mice remained analgesic for greater than 24 hr, as opposed to none of the mice given oxymorphone (100 mg/kg). Oxymorphazone was far more potent intraventricularly (icv) than systemically. Fifty percent of the mice remained analgesic for greater than 20 hr following the injection of 40 micrograms/mouse (icv), whereas no mice remained analgesic after 20 hr following doses of oxymorphone as high as 50 micrograms/mouse (icv). These long-lasting analgesic actions of oxymorphazone could not be easily explained on pharmacokinetic grounds. Repeated administration of oxymorphazone daily for 3 days resulted in significant tolerance.
The 14-hydroxydihydromorphinone hydrazones have been quite useful in studying aspects of opiate receptor binding and function. The most extensively studied, naloxazone, effectively and selectively inhibits high affinity (mu1) sites in vitro and morphine analgesia in vivo. We now report on the actions of oxymorphazone on receptor binding in vitro and on analgesia in vivo. Oxymorphazone effectively lowers 3H-opioid binding despite extensive washes with the same selectively for high affinity, or mu1, binding sites as naloxazone. Acutely, oxymorphazone was less potent in vivo than oxymorphone (ED50's of 0.8 and 0.4 mg/kg, respectively). Both quantal dose response curves were parallel. At higher doses (100 mg/kg), 83% of animals given oxymorphazone over 20 hr previously were analgesic whereas none of the oxymorphone animals were (p less than 0.001). Oxymorphazone also produced prolonged analgesia after icv administration. These results, in addition to other studies, suggest that oxymorphazone's actions cannot be adequately explained by pharmacokinetic differences from oxymorphone and supports the hypothesis that the drug works via prolonged receptor binding.