Persistent lower abdominal pain induced by long peritoneal shunt catheter.

Persistent abdominal pain directly induced by a peritoneal catheter of a ventriculoperitoneal shunt, which is associated with no other complications such as bowel perforation, pseudocyst or infection, has not been previously reported. A 65-year-old woman with hydrocephalus developed persistent lower abdominal pain radiating to the perineal area after shunt insertion. Radiography suggested that the distal end of a peritoneal catheter was located in a cul-de-sac of the pelvis. Otherwise, all studies were negative for shunt infection, fluid collection, or other abdominal and pelvic events. The patient's pain resolved completely after surgery in which the peritoneal catheter was shortened. In the presence of unexplained, persistent lower abdominal pain after shunt placement, the need to shorten the peritoneal catheter should be considered.

Developmental venous anomaly, cavernous malformation, and capillary telangiectasia: spectrum of a single disease.

Developmental venous anomalies (DVAs), cavernous malformations, and capillary telangiectasias are related vascular malformations of the central nervous system. Mixed lesions of the central nervous system vasculature have been reported in a host of combinations, including many possible concomitant combinations of cavernous malformations, venous anomalies, capillary telangiectasias, and arteriovenous malformations (AVMs). We describe the natural history of disease in a female with developmental venous anomaly, cavernous malformation, and capillary telangiectasias appearing in sequence.

Retractorless surgery for intracranial aneurysms.

Microsurgical clipping of intracranial aneurysms often requires access to the subarachnoid space deep in the brain. In the past, fixed retractors have been used to maintain the surgical corridor. However, studies have shown that fixed retraction leads to brain injuries. Here we present strategies to replace conventional fixed retractor blades with dynamic retraction so that the brain is no longer under constant pressure. We show that dynamic retraction without fixed retractors, when combined with optimal patient position and neuroprotective anesthetics, can provide the surgeon with adequate visualization of aneurysms and excellent surgical outcomes.

Characterization of neuroprotection from excitotoxicity by moderate and profound hypothermia in cultured cortical neurons unmasks a temperature-insensitive component of glutamate neurotoxicity.

Although profound hypothermia has been used for decades to protect the human brain from hypoxic or ischemic insults, little is known about the underlying mechanism. We therefore report the first characterization of the effects of moderate (30 degrees C) and profound hypothermia (12 degrees to 20 degrees C) on excitotoxicity in cultured cortical neurons exposed to excitatory amino acids (EAA; glutamate, N-methyl-D-aspartate [NMDA], AMPA, or kainate) at different temperatures (12 degrees to 37 degrees C). Cooling neurons to 30 degrees C and 20 degrees C was neuroprotective, but cooling to 12 degrees C was toxic. The extent of protection depended on the temperature, the EAA receptor agonist employed, and the duration of the EAA challenge. Neurons challenged briefly (5 minutes) with all EAA were protected, as were neurons challenged for 60 minutes with NMDA, AMPA, or kainate. The protective effects of hypothermia (20 degrees and 30 degrees C) persisted after rewarming to 37 degrees C, but rewarming from 12 degrees C was deleterious. Surprisingly, however, prolonged (60 minutes) exposures to glutamate unmasked a temperature-insensitive component of glutamate neurotoxicity that was not seen with the other, synthetic EAA; this component was still mediated via NMDA receptors, not by ionotropic or metabotropic non-NMDA receptors. The temperature-insensitivity of glutamate toxicity was not explained by effects of hypothermia on EAA-evoked [Ca2+]i increases measured using high- and low-affinity Ca2+ indicators, nor by effects on mitochondrial production of reactive oxygen species. This first characterization of excitotoxicity at profoundly hypothermic temperatures reveals a previously unnoticed feature of glutamate neurotoxicity unseen with the other EAA, and also suggests that hypothermia protects the brain at the level of neurons by blocking, rather than slowing, excitotoxicity.

Linkage of the locus for cerebral cavernous hemangiomas to human chromosome 7q in four families of Mexican-American descent.

OBJECTIVE: To determine with greater precision the map location of the locus associated with familial cavernous hemangiomas. BACKGROUND: Cavernous malformations of the brain are a significant cause of seizures, progressive or apoplectic neurologic deficit, and headache. Prevalence estimates from autopsy series vary from 0.39 to 0.9%. This disorder (OMIM #116860) can be inherited as an autosomal dominant trait with variable penetrance. Linkage to markers on the long arm of chromosome 7 was recently reported in separate reports in three apparently unrelated Hispanic kindreds as well as in two kindreds of non-Hispanic descent. DESIGN/METHODS: We examined clinically, by MRI scanning, and by pathologic examination of surgical specimens, members of four large Mexican-American families segregating cavernous hemangiomas of the brain. Linkage analysis was performed with use of blood specimens from morphologically proven cases. Two-point linkage analysis was performed with the MLINK program of the LINKAGE package. Multipoint analysis was performed between two markers and the disease locus with LINKMAP in the FASTLINKAGE package. Allele frequencies were set as described by the Genome Database (GDB). Maximum penetrance for the disease allele was set to 0.75. RESULTS: The highest lod score was observed for marker D7S652 with Zmax = 6.66 at theta(max) = 0.00. Multipoint LOD score analysis placed the disease locus in the 11 cM interval between markers D7S630 and D7S527 with Zmax = 9.19. Haplotype analysis is in agreement with the placement of the disease gene between D7S630 and D7S527 and further shows a minimal shared region within this interval, indicating a founder effect in the establishment of the mutation in these families. CONCLUSIONS: We confirmed the linkage of cavernous hemangioma to markers on the long arm of chromosome 7q, and the estimate of the map location has been refined to a region of shared haplotype between markers D7S630 and D7S527 in four Mexican-American families who may be descended from a common ancestor in Sonora County, Mexico.

Anterior communicating artery aneurysm paraparesis syndrome: clinical manifestations and pathologic correlates.

OBJECTIVE: Clinicopathologic evaluation of patients with lower extremity paraparesis/-plegia following rupture and repair of anterior communicating artery (ACoA) aneurysms. DESIGN: Institution-based retrospective review. SETTING: A tertiary neurologic referral center. PATIENTS, PARTICIPANTS: Seven of 101 patients with subarachnoid hemorrhage from ruptured ACoA aneurysms treated between January 1987 and December 1992. MAIN OUTCOME MEASURES: Neurologic status at latest follow-up examination. RESULTS: All patients presented with severe hemorrhage, poor clinical grade, and intracranial hypertension. Motor deficits developed within 7 days of aneurysm rupture and persisted for a mean duration of 39 days. Angiographic evidence of vasospasm in the anterior cerebral artery (ACA) distribution was documented in all cases, and paraparesis persisted beyond the angiographic resolution of vasospasm. All patients had evidence of frontal lobe dysfunction throughout their postoperative courses, and deep venous thrombosis and pulmonary emboli were common causes of morbidity and mortality. Autopsy data supported regional microvascular ischemia within the ACA distribution as the etiology of these motor deficits. CONCLUSIONS: The combination of vasospasm in the ACA distribution and lower extremity weakness associated with cognitive and affective impairment that resolves with time is common in patients with ACoA aneurysms. We propose that this constellation of clinical, radiographic, and pathologic findings be referred to as the "ACoA aneurysm paraparesis syndrome."

Ineffectiveness of DMSO in treating experimental brain ischemia.

A beneficial effect of dimethyl sulfoxide (DMSO) in the treatment of acute focal cerebral ischemia has not been proven. In the present study, two established experimental models of acute focal cerebral ischemia were treated with DMSO. Twenty adult cats lightly anesthetized with ketamine hydrochloride underwent right middle cerebral artery (MCA) occlusion for 6 hours. Ten cats were not treated and 10 cats received DMSO (2.5 g/kg i.v.) immediately after occlusion. No improvement of EEG findings, erythrocyte transit, regional cerebral blood flow (rCBF), blood-brain barrier permeability, or morphological findings were demonstrated in the DMSO-treated cats. In a second study, 15 conscious adult baboons underwent temporary left MCA occlusion (6 or 12 hours) using an implanted occluding device. Seven baboons were not treated and 8 baboons received continuous intravenous infusions of DMSO for 10 hours beginning 30 minutes after occlusion. Four of the baboons that were treated with DMSO also were treated with pentobarbital coma for 96 hours starting 4 hours after occlusion. Analysis of the neurological scores after 1 week survival indicated that treatment with DMSO alone and DMSO and pentobarbital coma did not improve the outcome. Morphological changes were similar in the 3 groups. The findings of our investigation indicate that DMSO is ineffective in treating acute focal cerebral ischemia.

Improved neurologic function after cerebrovascular accident with extracranial-intracranial arterial bypass.

This study, by use of direct measurement, sought to investigate the role of diminished cerebral blood flow on neurologic function after cerebrovascular accident (CVA). Twenty-seven patients had mean middle cerebral artery pressure (MCAP) measured intraoperatively prior to a superficial temporal artery to middle cerebral artery bypass. The ratio of MCAP to mean systemic blood pressure (BP) was less than 0.500 in 11 patients. Six of these 11 had preoperative neurologic deficit and four of these six had improved neurologic function after revascularization. In 16 patients the MCAP/BP was greater than 0.500, and none of the seven patients with neurologic deficit improved postoperatively. In general, the MCAP/BP correlated well with the angiographic severity of cerebrovascular disease. In 16 patients, unsuitable for conventional bypass, autogenous saphenous vein was used as a bypass from the subclavian or other extracranial artery to a cortical branch of the middle cerebral artery. One cerebral death and one CVA occurred postoperatively early in the series, but there have been no untoward events since deep barbituate anesthesia has been used. Diminished cerebral blood flow after CVA may leave a pool of viable but nonfunctional neurons. Extracranial-intracranial bypass may improve neurologic function in such patients.

Diffuse vasospasm after pretruncal nonaneurysmal subarachnoid hemorrhage.

Pretruncal (perimesencephalic) nonaneurysmal hemorrhage is a benign form of subarachnoid hemorrhage (SAH). Angiographic changes of vasospasm are uncommon in patients with this type of hemorrhage, and if vasospasm is present, it is mild and focal. We report two patients with pretruncal nonaneurysmal SAH who developed severe and diffuse vasospasm, expanding the clinical spectrum of this type of SAH. The first patient was a 40-year-old woman who suffered pretruncal nonaneurysmal SAH. Angiography performed on the seventh day post hemorrhage showed diffuse and severe vasospasm affecting both the anterior and the posterior circulation. The patient was treated with hypervolemia, and she remained asymptomatic. Follow-up angiography showed resolution of the vasospasm. The second patient was a 67-year-old woman who suffered pretruncal nonaneurysmal SAH. The results of the initial angiography were normal. Repeat angiography on the ninth day post hemorrhage showed severe vasospasm in the anterior circulation and moderate vasospasm in the posterior circulation. Nine hours later, the patient developed transient dysphasia, and she was treated with hypervolemia. Three days later, a transcranial Doppler examination showed normalization of blood velocities. The presence of diffuse and severe vasospasm does not exclude a diagnosis of pretruncal nonaneurysmal SAH.

Synovial cysts of the lumbosacral spine: diagnosis by MR imaging.

Intraspinal synovial or ganglion cysts are uncommon lesions associated with degenerative lumbosacral spine disease. CT usually reveals cystic lesions adjacent to a facet joint, and they may show calcification. MR imaging of four surgically confirmed cases of intraspinal synovial cysts revealed subtle signal changes compared with CSF. Short TR/TE images showed the lesions to be slightly hyperintense in three cases and isointense in one case. Long TR/TE sequences revealed a hyperintense appearance in two cases and a hypointense appearance in the others. A peripheral rim of decreased signal on long TR/TE images probably reflects fine calcification or hemorrhage in the margins of the cysts. The multiplanar and contrast characteristics of MR make this technique well suited to the diagnosis of herniated disk, degenerative facet disease, and synovial cyst.

Giant serpentine aneurysms: a review and presentation of five cases.

We present five cases of giant serpentine aneurysms (large, partially thrombosed aneurysms containing tortuous vascular channels with a separate entrance and outflow pathway) and review 28 cases reported in the literature. Giant serpentine aneurysms should be considered as a subgroup of giant aneurysms, distinct from saccular and fusiform varieties, given their unique clinical presentation and radiographic features.

Efficacy of endovascular treatment of meningiomas: evaluation with matched samples.

PURPOSE: To evaluate the clinical efficacy, cost-effectiveness, and safety of presurgical devascularization of meningiomas. METHODS: Matched samples of embolized and nonembolized groups of meningiomas were compared. The study variables for clinical efficacy were estimated blood loss, number of transfusions, surgical resection time, and length of hospitalization. The cost-effectiveness was evaluated by adjusting all hospital costs to 1991 dollar amounts, and adding additional embolization costs and fees to the hospital cost totals for the embolized group. A qualitative comparison of complications was made. RESULTS: All dependent variables evaluating the clinical efficacy of the procedure (estimate blood loss, 533 cc versus 836 cc; number of transfusions, 0.39 units versus 1.56 units; surgical resection time, 305.8 minutes versus 337.5 minutes; and length of hospitalization, 10.6 days versus 15.0 days) displayed trends of higher means in the nonembolized group; however, only the estimated blood loss and number of transfusions variables were significant. The cost-effectiveness of the procedure was not statistically significant. The mean cost was $29,605 for the embolized group and $38,449 for the nonembolized group. There were three major and nine minor complications in the nonembolized group and zero major and six minor complications in the embolized group. There were four additional minor complications caused by the embolization procedure. CONCLUSION: Endovascular devascularization of meningiomas is beneficial for large meningiomas because it diminishes the necessity of intraoperative transfusions and decreases blood loss. The additional day of hospitalization, emolization costs, and costs of complications do not conversely increase treatment costs. There were no major complications or adverse long-term effects caused by the embolization procedure.

Assessment of silent embolism from carotid endarterectomy by use of diffusion-weighted imaging: work in progress.

BACKGROUND AND PURPOSE: Transcranial Doppler studies have suggested that microemboli are released into the arterial circulation during the majority of carotid endarterectomy (CEA) procedures. This, together with the observation that neuropsychological performance may decline postoperatively, has led to concern that cerebral infarction may occur unrecognized during CEA. Our objective was to examine this risk with diffusion-weighted imaging, a technique that is highly sensitive to acute cerebral infarction. METHODS: Eighteen participants (median age, 68 years; age range, 56-87 years) were assessed with diffusion-weighted imaging and the National Institutes of Health Stroke Scale before and after CEA. Imaging was performed using single-shot echo-planar imaging with a maximum diffusion sensitivity of b = 1000 s/mm(2) applied to three orthogonal planes. Preoperative imaging was performed a median of 2.5 hours before surgery (range, 0.5-12.5 hours) and 15 hours after surgery (range, 1.5-58.5 hours). Two neuroradiologists independently interpreted the diffusion-weighted images, blinded to operative status and clinical findings. RESULTS: There was no diffusion-weighted imaging evidence of silent embolism in this series of 18 participants (95% confidence interval limits, 0 to 10%). Clinical complications were confined to one case of confusion occurring after CEA; the diffusion-weighted imaging results were normal in this case. CONCLUSION: There is no evidence from our series that silent cerebral infarction is a common occurrence during CEA. These data provide further support for the safety of CEA.

Extracranial-intracranial arterial bypass to a single branch of the middle cerebral artery in the management of a traumatic aneurysm.

This case required the clipping of a single branch of the middle cerebral artery for the treatment of a traumatic aneurysm. To ensure an adequate blood supply distal to the occlusion, we anastomosed the superficial temporal artery to that branch of the middle cerebral artery (MCA) distal to the aneurysm. Despite the low flow required to irrigate only one branch of the MCA, the anastomosis remained patient. This case demonstrates the feasibility of performing small vessel anastomoses in spite of low flow demand.

Endarterectomy of the intradural vertebral artery via the far lateral approach.

Transient ischemic attacks (TIAs) of the posterior circulation are associated with a significant risk of subsequent infarction, particularly when caused by stenotic lesions in the intracranial portion of the vertebral artery (VA). Eight patients who had persistent posterior circulation TIAs despite receiving maximal medical therapy (including anticoagulation) and who had angiographic evidence of severe stenosis of the proximal intracranial VA with poor collateral flow were treated by endarterectomy of the intradural VA. Their ages ranged from 52 to 65 years. Five of these operations were performed via the far lateral approach. In all patients, the contralateral VA was hypoplastic or occluded, or ended in the posterior inferior cerebellar artery. Postoperative angiograms showed that the arteries of five of the patients were widely patent, one was improved but still stenotic, and two were occluded. The latter two patients subsequently underwent thrombectomy, after which the artery was patent in one patient and remained occluded in the other. After surgery, the TIAs of seven patients were relieved completely, and the patients were neurologically intact. The patient with persistent occlusion ultimately had moderate disability. Complications included the two cases of thrombotic occlusion that required a second operation, three cases of communicating hydrocephalus that required lumboperitoneal shunts, and two cases of transient dysfunction of the 9th and 10th cranial nerves. Suitable patients with persistent posterior circulation TIAs refractory to medical therapy who have appropriate angiographic evidence of proximal VA stenosis and poor collateral flow may benefit from endarterectomy of the intradural VA.(ABSTRACT TRUNCATED AT 250 WORDS)

Spinal cord cavernous malformation in a patient with familial intracranial cavernous malformations.

The case of a 30-year-old woman with a hemorrhage caused by a rare intramedullary cavernous malformation is presented. The patient underwent laminectomy with total removal of the lesion. A cranial magnetic resonance imaging scan demonstrated multiple cavernous malformations. The patient's asymptomatic sister also had multiple intracranial cavernous malformations, one of which was associated with a venous malformation.

Revascularization and aneurysm surgery: current status.

Unclippable intracranial aneurysms are most effectively treated by hunterian ligation; however, the attendant risk of cerebral ischemia is significant. Many techniques have been used in an attempt to predict the safety of proximal vessel occlusion. Unfortunately, there is none that is risk-free and highly successful. A combination of stump pressure and cerebral blood flow measurements has been shown to be the most accurate in the acute assessment. In addition, recent studies have demonstrated that the long term risk of carotid ligation is significant. Extracranial-intracranial bypass grafting (EC-IC) has been shown to improve the safety of parent vessel ligation and is a low risk procedure. Whenever hunterian ligation is planned for the treatment of an intracranial aneurysm, EC-IC should be strongly considered.

Extracranial-intracranial bypass surgery: a critical analysis in light of the International Cooperative Study.

The ability of extracranial-intracranial bypass surgery to alter favorably the natural history of ischemic cerebrovascular disease remains in question. A recently completed prospective randomized multicenter cooperative trial failed to confirm the hypothesis that the procedure prevents further cerebral ischemia in patients with atherosclerotic internal carotid artery or middle cerebral artery disease. We analyze findings of the study in detail, including possible effects on the natural history of the disease beyond the immediate perioperative period. Potential sources of bias that may have unpredictably affected the study are discussed. These include observational bias (patient and therapist not blinded), "randomization-to-treatment" bias (high morbidity after randomization but before operation), and "prerandomization" or allocation bias (patients in the study representing a selected sample of the population with cerebrovascular disease). The extensive analysis of secondary subgroups with small numbers of patients is discussed in light of the statistical methods used. Two particular classes of patients not addressed in the study who might benefit from the procedure are defined. They are patients failing the best available medical therapy and patients with clearly documented hemodynamic compromise. Possible indications for bypass surgery are suggested for the various lesions in light of the trial and of recent reports on the natural history and pathophysiology of ischemic cerebrovascular disease. Selected cases illustrating these indications are presented.

The prospective application of a grading system for arteriovenous malformations.

The decision-making process whereby treatment is offered to a patient with an arteriovenous malformation (AVM) must be supported by an understanding of the risks related to the natural history of the AVM and the risks related to the treatment of that particular AVM. The ability to estimate the treatment risk for an individual patient is hampered by the marked variability in the complexity of AVMs. In 1986, an AVM grading system was proposed to predict surgical morbidity and mortality. This system is based on the AVM size, the neurological eloquence of adjacent brain, and the pattern of venous drainage. Grade I malformations are small, superficial, and located in noneloquent cortex; Grade V lesions are large, deep, and situated in neurologically critical areas; and Grade VI lesions are considered inoperable AVMs. A retrospective application of this grading scheme demonstrated its correlation with the incidence of postoperative neurological complications. A prospective application of the AVM grading system has been performed in 120 consecutive patients who had a complete microsurgical excision of their AVM, with or without AVM embolization. The AVM grading system accurately correlated with both new-temporary (P < 0.0001) and new-permanent (P = 0.008) neurological deficits. The permanent major neurological morbidity rates for Grades I through III were 0%, increasing to 21.9% in patients with Grade IV and 16.7% in patients with Grade V AVMs (P < 0.0001). One patient with a Grade III AVM died from an esophageal hemorrhage 15 months after her AVM was treated.(ABSTRACT TRUNCATED AT 250 WORDS)

Therapeutics for focal cerebral ischemia.

A review of the therapeutic modalities available for the treatment of focal cerebral ischemia is presented. The theoretical aspects and present practical applications of each treatment are discussed. The possibilities for future research and for the implementation of new modalities are indicated.