The authors conducted a retrospective study of 107 patients treated for syringomyelia associated with arachnoid scarring between 1976 and 1995 at the Departments of Neurosurgery at the Nordstadt Hospital in Hannover, Germany, and the University of California in Los Angeles, California. Twenty-nine patients have not been surgically treated to date because of their stable neurological status. Seventy-eight patients with progressive neurological deficits underwent a total of 121 surgical procedures and were followed for a mean period of 32 (+/- 37) months. All patients demonstrated arachnoid scarring at a level close to the syrinx. In 52 patients the arachnoid scarring was related to spinal trauma, whereas 55 had no history of trauma and developed arachnoid scarring was a result of an inflammatory reaction. Of these, 15 patients had undergone intradural surgery, eight had suffered from spinal meningitis, three had undergone peridural anesthesia, and one each presented with a history of osteomyelitis, spondylodiscitis, and subarachnoid hemorrhage. No obvious cause for the inflammatory reaction resulting in arachnoid scarring could be ascertained for the remaining 26 patients. The postoperative neurological outcome correlated with the severity of arachnoid pathology and the type of surgery performed. Shunting of the syrinx to the subarachnoid, pleural, or peritoneal cavity was associated with recurrence rates of 92% and 100% for focal and extensive scarring, respectively. Successful long-term management of the syrinx required microsurgical dissection of the arachnoid scar and decompression of the subarachnoid space with a fascia lata graft. This operation stabilized the preoperative progressive neurological course in 83% of patients with a focal arachnoid scar. For patients with extensive arachnoid scarring over multiple spinal levels or after previous surgery, clinical stabilization was achieved in only 17% with this technique.
A retrospective study was undertaken on 133 patients with a Chiari I malformation treated within the last 16 years at the Departments of Neurosurgery at the Nordstadt Hospital Hannover, Germany, and the University of California, Los Angeles, U.S.A. Ninety-seven patients presented with symptoms related to accompanying syringomyelia and 4 with associated syringobulbia. They underwent 149 surgical procedures and were followed for a mean of 39 +/- 52 months. A decompression at the foramen magnum was performed in 124 patients, while 22 of those with syringomyelia were treated by shunting (7 syringosubarachnoid shunts, 15 syringoperitoneal or -pleural shunts), and 3 by ventriculoperitoneal shunts for hydrocephalus. Except for ventriculoperitoneal shunting, at least a short-term decrease in size of an associated syrinx was observed for all procedures in the majority of cases. However, no long-term benefit was observed for syrinx shunting operations. The best clinical long-term results were obtained with decompression of the foramen magnum in patients with (86% free of a clinical recurrence) and without syringomyelia (77% free of a clinical recurrence). We advise against syrinx shunting, a large craniectomy, and obex plugging which are associated with higher recurrence rates. Instead, surgery should consist of a small craniectomy, opening of the dura, archnoid dissection to establish normal cerebrospinal fluid (CSF) outflow from the 4th ventricle, and a fascia lata dural graft.
Vasogenic brain edema was induced in cats by cold injury (six animals), brain tumors (five animals), and brain abscesses (six animals). Water and electrolyte content, specific gravity, blood volume, and the amount of extravasated serum proteins were determined in small tissue samples taken from gray and white matter at various distances from the lesion. Edema was strictly confined to the white matter of the affected hemisphere and declined from the lesion to the more peripheral regions. It was characterized by the extravasation of serum proteins and an increase of water and sodium content with little or unpredictable changes of potassium and blood volume. The calculated sodium content of edema fluid varied between 129 and 135 mueq/ml, and serum protein content between 8.1 and 11.9 mg/ml. In all three types of edema, specific gravity and water content correlated closely with the same slope and intercept of the calculated regression (y = 1.119-0.0011 x, r = -0.91). The results obtained indicate that the main denominator of specific gravity of edematous white matter is water content and that this relationship is not significantly altered by variations of blood volume or serum protein content.
SUMMARYThe effect of selective injury of hippocampal neurons on the consolidation of memory traces was studied in gerbils (meriones unguiculatus) after production of mild cerebral ischemia. The right carotid artery was permanently ligated, and animals without gross neurological deficits ("symptom-negative" gerbils) were selected. Eight days and eight weeks after vascular ligation, cell counts of hippocampal neurons were carried out and correlated with regional blood flow and the acquisition of operant behaviour. Eight days after carotid artery occlusion, learning behaviour was significantly impaired although the number of hippocampal neurons had not changed and blood flow had even increased above normal. After eight weeks, learning behaviour and blood flow were normal but now a significant loss of pyramidal neurons was present in the CA1 and CA2 sectors of the hippocampus. Our observations demonstrate that it is possible to detect subtle functional disturbances by appropriate behavioural investigation before manifestation of selective injury of the hippocampus. Recovery of integrative function, despite persistent cellular damage, provides further evidence for central nervous plasticity.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2025 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.