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Primary central nervous system lymphomas are a rare lymphoid tumor. A small proportion of these lymphomas are low-grade B-cell lymphoma of the mucosa-associated lymphoid tissue (MALT) subgroup. A primary MALT-lymphoma of the dura is very rare, with only a few reports. These low-grade tumors respond favorably to a combination of surgery and post-operative regional external beam radiotherapy. Differentiating these lesions from primary lymphomas or other dural-based lesions is therefore critical to determine clinical management and future prognosis. We report a 29-year-old patient with visual loss and dural-based MALT lymphoma and discuss the pertinent findings as well as the clinical management of patients with this unusual lesion.

Objective: Minimally invasive surgical techniques have been described for the treatment of spinal pathology. Tethered cord syndrome is an under-diagnosed condition of abnormally rigid fixation of the spinal cord that results in spinal cord tension leading to ischemia. It can be the cause of incontinence, scoliosis, and chronic back and leg pain. In situations of spinal cord tether owing to fatty filum or tight filum terminale, the symptoms can be relieved by sectioning of the filum. We present a novel, minimally invasive technique for surgical untethering of the spinal cord by filum sectioning. The pathophysiology of tethered spinal cord and the advantages of minimally invasive surgical management of this entity are discussed., Methods: Three patients (ages 14, 35, and 46 yr) presented with long-standing leg and back pain and neuroradiological features of tethered cord syndrome and thickened, fatty filum terminale. Two patients presented with scoliosis and, upon further history, had subclinical incontinence; one of these patients had abnormal urodynamic studies., Results: All three patients underwent a minimally invasive approach to the L4/L5 level using the X-tube (Medtronic, Inc., Memphis, TN). A laminotomy was performed and the dura exposed. The dura was then opened and intradural microdissection delivered the fatty filum into the durotomy. Electrical stimulation was performed while the lower extremities and the anal sphincter were monitored for electromyographic activity. After acquisition of positive controls, the filum was identified by the lack of sphincter and lower extremity electromyographic responses and was then cauterized and cut. Dura was repaired with the use of endoscopic instrumentation. All patients had significant improvement of their leg and back pain, and one patient had resolution of the abnormal urodynamics., Conclusion: Tethered spinal cords can be safely and effectively untethered using minimally invasive surgery. This technique provides the advantage of reduced soft tissue injury, less postoperative pain, minimal blood loss, a smaller incision, and a shorter hospitalization. The minimal amount of tissue injury generated by this technique may also provide the added advantage of reduced scar formation and risk of retethering.

The transphenoidal procedure has become the preferred approach in the surgical management of sellar/parasellar tumors. Nevertheless, specific indications remain for the transcranial approach and the objective of this review is to evaluate the available data on outcomes following transcranial or transphenoidal approaches to sellar/parasellar tumors. We assess the indications used for each approach and parameters that favor one over the other. Factors such as tumor size, consistency and configuration are important variables in choosing the transcranial approach. Other important considerations include persistent visual loss after incomplete decompression via the transphenoidal route, ectatic midline carotid arteries, co-existent intracranial aneurysms and sphenoid sinusitis. We review the data on visual and endocrinological outcomes following the transcranial or transphenoidal approach and provide an argument that, while there appears to be a trend towards greater visual improvement after transcranial surgery for large-to-giant pituitary adenomas, this benefit is offset by a greater risk of postoperative pituitary dysfunction. There is no difference in the rate of recurrence between the two procedures in the published literature. Overall, craniotomies will continue to play a role in the management of patients with sellar/parasellar tumors, although patient selection and careful preoperative evaluation are key elements in choosing the most appropriate approach.

Although pituitary tumors may be present in up to 10% of the population, the pathophysiology of these lesions is not well characterized. Pituitary tumors are composed of monoclonal cell populations with disrupted control of replication pathways. The oncogenes and tumor suppressor genes that are common in other malignancies (i.e. jun, fos, myc, and p53) are rarely involved in the development of these tumors. However, oncogenes, such as gsp, can be present in up to 40% of hormonally active adenomas. The process of pituitary oncogenesis further appears to involve oncogenes such as cyclin E, cyclin D1, and the pituitary tumor transforming gene (PTTG). Finally, the cAMP signaling cascade plays a significant role in generation of both benign and malignant pituitary tumors. In this review, the biology of pituitary adenomas is explored with a special emphasis on potential targets for the development of targeted therapeutics.

Invasive EEG monitoring is one of the best tools available for localization of epileptogenic foci in the brain. However, published data in mixed series of adult and pediatric patients show high incidence of epidural bacterial contamination, cerebrospinal fluid leakage, and skin infection after subdural electrode implantation. We sought to determine whether the complication rate from prolonged subdural electrode implantation would be lower in a purely pediatric series. Thirty-three subdural electrode implantation procedures were performed in 29 pediatric patients (age range 4-19) for an average of 7.2 days (range 3-14 days). Electrode number varied from 32 to >128 with a range of 4-11 electrode wires piercing the skin >1 cm from the primary incision. Of the 33 implantations and resections (66 craniotomies), 5 were for reimplantation. There were no permanent complications related to grid implantation. Transient complications included 1 case of prolonged prothrombin time and 1 patient with unexplained fever, both of which resolved upon removal of the grids. There were two culture-positive infections, one epidural and one superficial, both in patients undergoing reimplantation. There was no percutaneous cerebrospinal fluid leakage noted and no operation was aborted due to bleeding caused by grid placement. Our data suggest that subdural grid implantation in children is remarkably safe even for prolonged implantation, though infectious risk is significantly higher in reoperation (p = 0.019). This observation may contribute to lowering the threshold for two-stage invasive monitoring approaches in children with epilepsy., (Copyright 2006 S. Karger AG, Basel.)

Relationships between presynaptic function and short- and long-term plasticity were investigated at adult corticostriatal synapses. Wide variability was observed in the expression of short- and long-term synaptic plasticity. Intracellular records from 47 cells produced 17 examples of LTD (<90% of control), 10 examples of no long-term change (between 90-110% of control), and 20 examples of LTP (>110% of control). Similar variation existed in paired-pulse and posttetanic plasticities. The variability expressed in all three forms of plasticity appears to be related, based on correlations found between the paired-pulse ratio (PPR) and tetanus-induced short- (3 min posttetanus) and long-term plasticities (16-20 min posttetanus). These data suggest that tetanus-induced changes in synaptic strength are related to the intrinsic, preconditioned behavior of synapses. Every cell showing paired-pulse depression also expressed LTD in response to high-frequency activation of its afferents. Those synapses showing paired-pulse potentiation tended to express LTP, although exceptions did exist. Similar relationships were found in a parallel analysis of population spikes. PPR also changed in association with the expression of posttetanic and long-term depression. Greater paired-pulse potentiation was observed in medial intracellular recordings, but no medial to lateral differences were seen in posttetanic plasticities. Field recordings also showed a medial bias toward paired-pulse and posttetanic potentiation, but not in long-term plasticity. Block of postsynaptic L-type Ca(2+) channels with nifedipine eliminated LTD expression, but overall no differences were found between nifedipine and control cells., (Copyright 2000 Wiley-Liss, Inc.)

Global long-term potentiation (LTP) was induced in organotypic hippocampal slice cultures by a brief application of 10 mM glycine. Glycine-induced LTP was occluded by previous theta burst stimulation-induced potentiation, indicating that both phenomena share similar cellular processes. Glycine-induced LTP was associated with increased [3H]alpha-amino-3-hydroxyl-5-methyl-4-isoxazolepropionic acid (AMPA) binding in membrane fractions as well as increased amount of a selective spectrin breakdown product generated by calpain-mediated spectrin proteolysis. Antibodies against the C-terminal (C-Ab) and N-terminal (N-Ab) domains of GluR1 subunits were used to evaluate structural changes in AMPA receptor properties resulting from glycine-induced LTP. No quantitative or qualitative changes were observed in Western blots from membrane fractions prepared from glycine-treated slices with C-Ab. In contrast, Western blots stained with N-Ab revealed the formation of a 98-kDa species of GluR1 subunits as well as an increased amount of immunoreactivity after glycine-induced LTP. The amount of spectrin breakdown product was positively correlated with the amount of the 98-kDa species of GluR1 after glycine treatment. Functional modifications of AMPA receptors were evaluated by determining changes in the effect of pressure-applied AMPA on synaptic responses before and after glycine-induced LTP. Glycine treatment produced a significant increase in AMPA receptor function after potentiation that correlated with the degree of potentiation. The results indicate that LTP induction produces calpain activation, truncation of the C-Ab domain of GluR1 subunits of AMPA receptors, and increased AMPA receptor function. They also suggest that insertion of new receptors takes place after LTP induction.

Using mice genetically deficient in the complement (C)-system component C5, this study explored a potential novel role of the C-system in Ca(2+)-mediated control of glutamate AMPA receptor functions. We found that Ca2+ preincubation of frozen brain tissue sections enhances AMPA binding capacity more dynamically in C5 deficient (C5-) than congenic C5 sufficient (C5+) mice. The Ca(2+)-mediated response was mostly localized to the CA3 and CA1 subdivisions of the pyramidal layers of the hippocampal formation. In C5- mice, kainic acid (KA) excitotoxicity that models hippocampal neurodegeneration abolished the Ca(2+)-mediated induction of hippocampal AMPA binding. The changes in AMPA binding preceded temporally and overlapped anatomically the appearance of apoptotic features in the same hippocampal neuron layers. C5- mice showed greater hippocampal neurodegeneration then C5+ mice. NMDA binding controlled for specificity of glutamate-mediated changes and found no C5 genotypic influences. The study gives further credence to the role of the C-system in modifying the intensity and outcome during response to conditions leading to hippocampal neurodegeneration.

The present study investigated whether temperature-related changes in NMDA receptor sensitivity to ethanol might play a role in mediating the effects of body temperature on behavioral sensitivity to ethanol or in determining genotypic differences in sensitivity to ethanol. We accomplished this by determining the effects of ethanol on three different mouse genotypes (C57, LS, and SS) on two types of NMDA receptor-mediated responses at 30 degrees and 35 degrees C: (i) extracellularly recorded synaptic potentials elicited in the CA1 region of the in vitro hippocampal slice preparation by stimulation of the Schaffer-commisural pathway in the presence of the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor blocker, 6,7-dinitroquinoxaline-2,3-dione, and low magnesium concentration; and (ii) increase in [3H]MK-801 binding elicited by glutamate in telencephalic membrane preparations. Ethanol significantly decreased NMDA receptor-mediated excitatory postsynaptic potential (EPSP) amplitude and area in the three genotypes. In C57, the effect of ethanol on NMDA receptor-mediated EPSP amplitude and area was more pronounced at 30 degrees C, compared with that at 35 degrees C. In most cases, there was a good correlation between the effects of ethanol on EPSP amplitude and area. The order of sensitivity between the three genotypes was C57 = LS > SS at 35 degrees C and C57 > LS = SS at 30 degrees C. Similarly, ethanol significantly decreased glutamate-stimulated [3H]MK-801 binding in membrane fractions. The effect of ethanol was temperature-dependent, because ethanol produced more inhibition at 30 degrees C than at 35 degrees C in all genotypes. The effect of ethanol on MK-801 binding was concentration-dependent, and the sensitivity to 100 mM ethanol of the genotypes at 35 degrees C was LS > SS = C57, whereas it was SS > LS = C57 at 30 degrees C. Collectively, the results demonstrate that temperature is an important variable that can influence NMDA receptor sensitivity to ethanol measured via electrophysiological and binding techniques, and that temperature can influence relative sensitivity of NMDA receptors to ethanol between mouse genotypes. Furthermore, the findings indicate that temperature-induced changes in sensitivity of NMDA receptors to ethanol may play a role in mediating the effects of body temperature on behavioral sensitivity to ethanol in LS, but not C57 and SS mice.

Nitric oxide (NO) has recently been proposed to act as a retrograde messenger to produce long-term potentiation (LTP) in hippocampal area CA1. This notion is based largely on the absence of LTP when hippocampal slices are incubated in the presence of inhibitors of NO synthase (NOS) or of NO scavengers. In the present study, we tested the effects of such compounds on both the induction and maintenance of LTP in field CA1 of hippocampal slices. Incubation of slices in the presence of N-methyl-L-arginine (MLA) or L-nitro-arginine (LNA), two inhibitors of NOS, or in the presence of hemoglobin (Hb), a NO scavenger, produced a large reduction in the magnitude of LTP induced by a theta burst stimulation (TBS) paradigm. These compounds had no effect on the degree of paired-pulse facilitation but produced a significant reduction of the facilitation of postsynaptic responses occurring during TBS. On the other hand, MLA did not prevent the potentiation induced by application of tetraethylammonium (TEA). These results suggest that the inhibition of LTP produced by these agents could be due to an effect on a physiological mechanism that triggers LTP and not necessarily on an event that follows the triggering step.