Sacral neuromodulation for urinary retention caused by sexual abuse.

OBJECTIVE: This case report describes the use of sacral neuromodulation to treat urinary retention after sexual abuse. METHODS: Sacral neuromodulation was added to therapeutic regimen of a 38-year-old woman in whom chronic, complete urinary retention developed after psychological and sexual abuse during childhood. RESULTS: The combination of psychotherapy and neuromodulation restored the patient's ability to void, whereas psychotherapy alone had not. CONCLUSIONS: Although a multifactorial etiology of retention cannot be ruled out in this patient, neuromodulation might effectively treat urinary retention in cases of a conversion disorder after sexual abuse.

Treatment of syringomyelia associated with arachnoid scarring caused by arachnoiditis or trauma.

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.

The surgical treatment of Chiari I malformation.

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.

Stereotactic endoscopic treatment of colloid cysts of the third ventricle.

In order to avoid invasive procedures (transfrontal, transcallosal) in the surgical treatment of colloid cysts the stereotactic aspiration technique was introduced by Bosch, Rähn and Backlund in 1978. The viscosity of the intracystic colloid and the displacement of the cyst away from the aspiration needle are possible reasons for unsuccessful aspiration. GT-guided stereotactic endoscopic technique gives the opportunity to fenestrate the cyst wall under direct visual control. After CT-guided stereotactic puncture of the right lateral ventricle with the foramen of Monro as target a steerable endoscope is introduced and the foramen of Monro is passed. The wall of the cyst is fenestrated and coagulated by means of monopolar (or laser) coagulation. Using this technique we have treated four patients with colloid cysts. Immediately postoperatively all of them were relieved of their complaints and have been symptom-free for a mean follow up period of twelve months. Studies of cerebrospinal fluid flow patterns, performed prior to and every six months after the endoscopic intervention, confirmed a remarkable reduction of foraminal obstruction.

Somatosensory evoked potentials and intracranial pressure during chronic dilatation of an artificial extraparenchymal space-occupying lesion in cats.

Somatosensory evoked potentials (SEP) and intracranial pressure (ICP) were studied in cats, suffering from a chronic space-occupying lesion produced by enlargement of an epidural balloon over the left sensomotory cortex. Our study shows that latency alterations of SEP are not dependent on the degree of ICP. Additionally, the results obtained demonstrate that chronic space-occupying lesions cause continuous prolongation of SEP latencies, probably produced by atrophy of the compressed tissue. Regarding the clinical importance of SEP measurements, we concluded that they are not suitable for estimating the degree of ICP. However, they are useful to evaluate tissue damage caused by mass effects in the acute and chronic phase of various space-occupying processes.

[Delayed onset of postoperative deterioration in clivus chordoma and clivus meningioma]. / Die verzögert einsetzende, postoperative Verschlechterung bei Clivuschordomen und Clivusmeningeomen.

The starting-point of the presented retrospective, clinical study is the observation, that in some cases a delayed postoperative neurological deterioration develops after removal of great, extraparenchymal, infratentorial brain tumors. Therefore, we evaluated the postoperative clinical course of 50 clivuschordomas and clivusmeningiomas of the Neurosurgical University Clinic in Mainz (Germany). The results obtained show, that 1 of 3 patients develops a delayed, postoperative deterioration. Important factors, which cause that deterioration, are the age of patients and the size of tumors. Mostly, we found a perifocal edema concomitant to the delayed deterioration within the decompressed brain tissue. We call that phenomenon "decompression edema" as a "hypothesis a posteriori", which has to be proven experimentally.

Selective vulnerability of hippocampus and disturbances of memory storage after mild unilateral ischemia of gerbil brain.

The 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.

Regional morphology and biochemistry in experimental brain abscesses.

Brain abscesses were induced experimentally in six cats by stereotactic inoculation of Staphylococcus aureus A8 into the white matter of the left cerebral hemisphere. Seven days later, the brains were frozen in situ with liquid nitrogen and subsequently sawn into coronal sections of 5 mm thickness, while being cooled with liquid nitrogen. Thin slices were taken from those sections containing the largest expanse of abscess: slices of 5 micron thickness were stained histologically, and in adjacent 20 micron slices the regional distribution of ATP and glucose was mapped using substrate-specific bioluminescence methods. Furthermore, the NADH fluorescence from the surface of the tissue section was recorded. Six layers could be distinguished histologically in the abscess capsule, five of which showed different substrate patterns. Only in two layers a low metabolic activity could be observed, as shown by slight ATP bioluminescence. The pattern of the biochemical substrates in the white matter surrounding the abscess indicated a reduction in the cellular oxygen availability.

Relationship between specific gravity, water content, and serum protein extravasation in various types of vasogenic brain edema.

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.

Pathophysiological aspects of blood-brain barrier disturbances in experimental brain tumors and brain abscesses.

Experimental tumors and abscesses were produced by intrahemispheric inoculation of a blastomatous glial cell clone and of staphylococcus aureus, respectively. In both models severe vasogenic brain edema developed. The site of the barrier lesion was identified by systemic application of Evans blue or peroxidase, and the spread of edema by immunoautoradiographic localisation of extravasated serum proteins. In both experimental conditions, serum proteins accumulated diffusely in the white matter of the ipsilateral hemisphere, although the barrier lesion was strictly confined to the pathological focus. Water content of the edematous white matter in the vicinity of tumors and abscesses increased from 69.1 to 80.6 and 82.3 ml/100g w.w., respectively. This increase was associated with a volume-dependent decrease of flow, a parallel increase of sodium and an increase of extravasated serum proteins. The latter was determined by a newly developed immunochemical approach with appropriate corrections for the intravascular fraction of total serum protein content. The calculated concentration of sodium in edema fluid of tumors and abscesses amounted to 132 and 129 ueq/ml, respectively. The concentration of serum proteins was 8.7 and 6.4 mg/ml, respectively. Protein content of edema fluid, in consequence was less than 10% of blood serum. This suggests that fluid accumulation in vasogenic edema cannot be explained by the oncotic properties of extravasated proteins alone.