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Is the placement of shunts in patients with idiopathic normal-pressure hydrocephalus worth the risk? Results of a study based on continuous monitoring of intracranial pressure.

OBJECT: Data from many studies have demonstrated that shunt insertion in patients with idiopathic normal-pressure hydrocephalus (NPH) is associated with high morbidity and a lack of significant improvement; however, the use of strict diagnostic and treatment protocols can improve the results of surgery in these patients. The primary aim in this prospective study was to analyze the results of shunt placement in 43 patients with idiopathic NPH. A secondary aim was to determine the relationship between several clinical and neuroimaging factors, and patient outcome after surgery. METHODS: Thirty men and 13 women with a mean age of 71.1 +/- 6.9 years participated in this study. All patients underwent clinical, neuropsychological, and radiological assessment before and 6 months after surgery. In all patients continuous monitoring of intracranial pressure was performed using a fiberoptic extradural sensor. In 31 patients cerebrospinal fluid dynamics were also determined. Eighty-six percent of patients showed clinical improvement after shunt insertion, 11.6% showed no change, and 2.3% exhibited some worsening. Gait improved in 81.4% of the patients, sphincter control in 69.8%, and cognitive dysfunction in 39.5%. There was no treatment-related death. Early or late postsurgical complications occurred in six patients (14%), although all of these complications were minor or were satisfactorily resolved. The complete clinical triad, cortical sulci size, and periventricular lucencies were related to outcome, whereas patient age, symptom duration, ventricular dilation, and the degree of presurgical dementia were unrelated to outcome. CONCLUSIONS: Given the correct diagnosis, shunt insertion can produce marked improvement in patients with idiopathic NPH syndrome, causing few deaths and few clinically relevant complications.

Aged↗

Atresia of the right vertebral artery in a patient with acute aortic dissection.

A 49-year-old man had severe neurocognitive dysfunction after urgent operation for acute type A aortic dissection. Complete aortic arch replacement with single reimplantation of the arch branches was performed with the patient under deep hypothermic circulatory arrest. Retrospectively, my colleagues and I consider the atresia of the right vertebral artery to be responsible for this complication and discuss whether knowledge of the anomaly and adapting the operative strategy accordingly would have improved the neurologic outcome.

Aortic Dissection↗

Neuroprotection during cardiac surgery: a randomised trial of a platelet activating factor antagonist.

OBJECTIVE: To assess platelet activating factor (PAF) antagonists, potent neuroprotective agents in experimental cerebral dysfunction, in clinical practice. DESIGN: Double blind, minimised, placebo controlled trial of low and high dose PAF antagonist (lexipafant). SETTING: Cardiac surgery unit. PATIENTS: 150 patients undergoing coronary artery bypass graft (CABG) surgery using cardiopulmonary bypass. INTERVENTIONS: Randomisation to placebo, low dose (10 mg) or high dose (100 mg) lexipafant. MAIN OUTCOME MEASURES: Incidence of impairment on four established cognitive tests, undertaken before, five days, and three months after CABG, examined by three methods for defining impairment. RESULTS: The three groups were similar with respect to preoperative and intraoperative factors. Observed levels of cognitive impairment were less than had been predicted from previous studies. There was no difference in the groups in cognitive change scores at five days or three months. Group mean analysis showed significant time factors for all four tests but not for interactions or for the lexipafant group. A composite cognitive index, based on the aggregate of four normally distributed tests, showed a significant effect for timing of the test but not for the lexipafant group or interaction. Age, but not duration of bypass, was the most important determinant of postoperative cognitive impairment. CONCLUSIONS: The neuroprotective PAF antagonist lexipafant did not differentially reduce the level of cognitive impairment after CABG as determined by power estimates derived from published studies. The strongest predictors of cognitive impairment were age and timing of the test after operation.

Cognition Disorders↗

A prospective, randomized study of the effects of prostacyclin on neuropsychologic dysfunction after coronary artery operation.

This randomized, double-blind study was designed to evaluate the effect of prostacyclin (epoprostenol) on the incidence and severity of postoperative neuropsychologic dysfunction in patients undergoing coronary artery operation. Four days before operation and 1 week after operation, 100 patients having coronary artery bypass grafting underwent detailed neurologic and psychologic examinations and computed tomographic scans of the brain. The psychologic examination was repeated 2 months after operation. During cardiopulmonary bypass, all patients received 300 U/kg of heparin and then either buffer-diluent or prostacyclin (12.5 ng/kg/min from the time of heparinization until onset of cardiopulmonary bypass and 25 ng/kg/min during cardiopulmonary bypass). No deaths or major neurologic complications occurred in this series. Ninety-six patients completed the psychologic and neurologic evaluations 1 week after operation; 74 of these patients were evaluated psychologically 2 months after operation. Psychologic testing demonstrated similar declines in postoperative performance in both the prostacyclin-treated and the control groups; these changes were no longer present in either group 2 months after operation. Results of neurologic examinations and computed tomographic scans of the brain were unchanged. We conclude that the administration of prostacyclin during cardiopulmonary bypass in patients undergoing routine coronary artery operation has no effect on perioperative cognitive changes.

Adult↗

Confabulation, memory deficits, and frontal dysfunction.

This paper explores potential cognitive deficits underlying confabulation of patient, G.S., following an anterior communication artery aneurysm. G.S.'s performance on tasks assessing memory for temporal duration, temporal order, and speaker identification is examined as is his recollection of autobiographical events. We compare G.S. with three nonconfabulating patients matched with him for age, education, and neuropsychological measures of memory and frontal deficits and with three age- and education-matched control subjects. Like frontal control patients, G.S. underestimated temporal durations and showed poor source monitoring (speaker identification). In addition, G.S. showed an even more pronounced deficit in recall of autobiographical memories and relatively more detailed reports of laboratory-induced memories for imagined events. We suggest that this configuration of deficits rather than any single factor accounts for G.S.'s tendency to confabulate.

Amnesia↗

Late neuropsychological and behavioural outcome of children surgically treated for craniopharyngioma.

Late outcome in 12 children treated by radical surgery for craniopharyngioma is presented. None of the patients presented underwent fractionated traditional or stereotactic radiotherapy. The results show no neurological (except visual dysfunction in 6 subjects), cognitive or short-term memory deficits. Three children were found to have a minor attention deficit. In 5 cases "frontal lobe" malfunctioning was disclosed, and in 5 there were bursts of unpredictable anger. Three children showed worsening of functioning at school: a combination of various causes is suggested to explain the worsening of academic performances. The size of the sample calls for a careful evaluation of results, with due consideration for the influence of various factors on outcome. Multicentre studies are required to increase the sample size and achieve more general conclusions.

Adolescent↗

Risk factors for chronic insomnia following hospitalization.

AIM: This paper reports a study whose purpose was to determine whether there is an increase in the incidence of chronic insomnia following hospitalization and, if so, to identify patients at risk. BACKGROUND: The consequences of difficulty sleeping in hospital have received scant attention from clinicians or researchers. Implicit in this lack of interest is the assumption that difficulty in sleeping is a transient reaction to hospitalization that will resolve on discharge, an assumption not empirically supported. It has been argued that in susceptible people this type of temporary disruption to sleep can be the catalyst for the development of chronic insomnia. METHOD: Established sleep and depression rating instruments were used to monitor the sleep of 57 cardiac and 29 orthopaedic patients after elective surgery (n = 86), recruited through a hospital preadmission clinic. RESULTS: Preadmission chronic insomnia of 10% was consistent with general population prevalence estimates of 6-12%. Three months after discharge the incidence had almost doubled to 19%. Sixty-one per cent of this variance could be explained by hyperarousal, sleep hygiene issues, and dysfunctional cognitions about sleep. Depression was found to be a salient predictor but not an independent risk factor. Age, sex, and hospital-related data, such as score for difficulty sleeping in hospital, proved to be statistically insignificant. CONCLUSIONS: The results support the role of hyperarousal and dysfunctional sleep attitudes and behaviours as stronger predictors of chronic insomnia than patient demographics or environmental issues. Given that most of the patients were ambivalent about how they slept in hospital, with high satisfaction (71%) in the presence of significant disruption (63%), preadmission sleep education given to these patients prior to admission potentially contributed to the development of more realistic expectations of the quality of in-hospital sleep.

Adult↗

5,7-DHT-induced hippocampal 5-HT depletion attenuates behavioural deficits produced by 192 IgG-saporin lesions of septal cholinergic neurons in the rat.

Adult Long-Evans male rats sustained injections of 5,7-dihydroxytryptamine into the fimbria-fornix (2.5 microg/side) and the cingular bundle (1.5 microg/side) and/or to intraseptal injections of 192 IgG-saporin (0.4 microg/side) in order to deprive the hippocampus of its serotonergic and cholinergic innervations, respectively. Sham-operated rats were used as controls. The rats were tested for locomotor activity (postoperative days 18, 42 and 65), spontaneous T-maze alternation (days 20-29), beam-walking sensorimotor (days 34-38), water maze (days 53-64) and radial maze (days 80-133) performances. The cholinergic lesions, which decreased the hippocampal concentration of ACh by about 65%, induced nocturnal hyperlocomotion, reduced T-maze alternation, impaired reference-memory in the water maze and working-memory in the radial maze, but had no effect on beam-walking scores and working-memory in the water maze. The serotonergic lesions, which decreased the serotonergic innervation of the hippocampus by about 55%, failed to induce any behavioural deficit. In the group of rats given combined lesions, all deficits produced by the cholinergic lesions were observed, but the nocturnal hyperlocomotion and the working-memory deficits in the radial maze were attenuated significantly. These results suggest that attenuation of the serotonergic tone in the hippocampus may compensate for some dysfunctions subsequent to the loss of cholinergic hippocampal inputs. This observation is in close concordance with data showing that a reduction of the serotonergic tone, by pharmacological activation of somatodendritic 5-HT(1A) receptors on raphe neurons, attenuates the cognitive disturbances produced by the intrahippocampal infusion of the antimuscarinic drug, scopolamine. This work has been presented previously [Serotonin Club/Brain Research Bulletin conference, Serotonin: From Molecule to the Clinic (satellite to the Society for Neuroscience Meeting, New Orleans, USA, November 2-3, 2000)].

5,7-Dihydroxytryptamine↗

Opening the cardiac chambers does not make any difference in p300 measurement.

OBJECTIVE: Cognitive brain dysfunction after open heart surgery is a serious complication caused by cardiopulmonary bypass (CPB). The presence of gaseous and/or particulate emboli in the CPB circuit and cerebral hypoperfusion may be the causes of neurologic problems after cardiac operations. METHODS: In this prospective study we examined 42 consecutive cardiac surgery patients (24 mitral valve replacement [MVR] and 18 coronary artery bypass grafting [CABG] patients). In addition to determination of clinical measurements, cognitive brain function was measured objectively by P300 auditory-evoked potentials before operation, at day 7, and at 4-month follow-up. Electroencephalographic evaluations were also performed. RESULTS: In preoperative measures there was no difference between the groups (peak latencies in the MVR group were 324 +/- 8 milliseconds; CABG group, 318 +/- 6 milliseconds; P > .05). At day 7, cognitive P300 auditory-evoked potentials were significantly impaired (prolonged) in both groups compared to preoperative values (MVR group, 347 +/- 7 milliseconds; CABG group, 342 +/- 7 milliseconds; P < .05). P300 measurements almost returned to normal at 4-month follow-up (MVR group, 331 +/- 6 milliseconds; CABG group, 319 +/- 8 milliseconds; P > .05 compared to preoperative values). One week and 4 months after surgery no difference between the 2 groups could be found (P > .05). CONCLUSION: Postoperative patients had prolonged P300 values according to the preoperative measurements and we have not found any difference between the groups whether cardiac chambers were opened or not.

Adult↗

Normothermic cardiopulmonary bypass is beneficial for cognitive brain function after coronary artery bypass grafting--a prospective randomized trial.

BACKGROUND: Hypothermic and normothermic cardiopulmonary bypass (CPB) have resulted in apparently contradictionary cardiac and neurologic outcome. Cerebrovascular risk and cognitive dysfunction associated with normothermic CPB still remain uncertain. MATERIALS AND METHODS: In a prospective randomized study, we measured the effects of mildly hypothermic (32 degrees C, n=72) vs. normothermic (37 degrees C, n=72) CPB on cognitive brain function. All patients received elective coronary artery bypass grafting (mean age 62.1+/-6.3 years, mean ejection fraction 60.4+/-13%). Cognitive brain function was objectively measured by cognitive P300 auditory-evoked potentials before surgery, 1 week and 4 months after surgery, respectively. Additionally, standard psychometric tests ('trailmaking test A', 'mini-mental state') were performed and clinical outcome was monitored. RESULTS: Patients, operated with mild hypothermia, showed a marked impairment of cognitive brain function. As compared with before surgery (370+/-45 ms), P300 evoked potentials were prolonged at 1 week (385+/-37 ms; P<0.001) and even at 4 months (378+/-34 ms, P<0.001) after surgery, respectively. In contrast, patients operated with normothermic CPB, did not show an impairment of P300 peak latencies (before surgery 369+/-36 ms, 1 week after surgery 376+/-38 ms, n.s.; 4 months after surgery 371+/-32 ms, n.s.). Group comparison revealed a trend towards prolonged P300 peak latencies in the patient group undergoing mildly hypothermic CPB (P=0.0634) 1 week after surgery. Four months postoperatively, no difference between the two groups could be shown (P=n.s.) Trailmaking test A and mini mental state test failed to discriminate any difference. Five patients died (mild hypothermia n=3, normothermia n=2) postoperatively (cardiac related n=3, sepsis n=2). None of the patients experienced major adverse cerebrovascular events. CONCLUSIONS: Objective cognitive P300 auditory evoked potential measurements indicate, that subclinical impairment of cognitive brain function is more pronounced in patients undergoing mildly hypothermic CPB as compared with normothermic CPB for CABG.

Brain↗

Cognitive function after anaesthesia in the elderly.

Despite advances in peri operative care, a significant percentage of elderly patients experience transient post operative delirium and/or long-term post-operative cognitive dysfunction (POCD). This chapter reviews the aetiology, clinical features, preventive strategies and treatment of these syndromes. Pre-operative, intra-operative, and post-operative risk factors for delirium and POCD following cardiac and non-cardiac surgery are discussed. It is most likely that the aetiology of delirium and POCD is multifactorial and may include factors such as age, decreased pre-operative cognitive function, general health status and, possibly, intra-operative events. Currently there is no single therapy that can be recommended for treating post-operative cognitive deterioration. Primary prevention of delirium and POCD is probably the most effective treatment strategy. Several large clinical trials show the effectiveness of multicomponent intervention protocols that are designed to target well-documented risk factors in order to reduce the incidence of post-operative delirium and, possibly, POCD in the elderly.

Aged↗

Cognitive dysfunction in cholesterol embolic disease.

A patient who developed neurological and renal complications following coronary angiogram and coronary artery bypass grafting is reported. Neurological involvement was in the form of fluctuating sensorium and a subcortical pattern of dementia. Renal failure was seen in the form of raised urea and creatinine levels. Renal biopsy revealed the cause of the renal failure to be due to cholesterol embolic disease. While the sensorium often improved following renal replacement therapy (dialysis), the dementia was poorly responsive to therapy. The patient succumbed due to progressive renal failure. Awareness of the protean manifestations and a high index of suspicion are essential for appropriate diagnosis in order to enable the clinician to accurately prognosticate in this often fatal disease.

Basal Ganglia↗

Impaired baseline regional cerebral perfusion in patients referred for coronary artery bypass.

BACKGROUND: Cognitive dysfunction and cerebral vascular accidents remain some of the most devastating problems related to cardiac surgery. Despite the major advances in perioperative care and operative technique in coronary artery bypass, this cohort of patients appears to have poor cerebral physiologic reserve. The aim of this study was to describe regional cerebral perfusion of patients with coronary artery disease referred for coronary artery bypass grafting. METHODS: Eighty-two consecutive patients with coronary artery disease referred for coronary artery bypass grafting were enrolled after providing informed consent in an institutional review board-approved study. Patients with prior cerebral vascular accident, transient ischemic attacks, head trauma, or other neurologic afflictions were excluded from the study. We prospectively measured preoperative regional cerebral perfusion using single photon emission computed tomography (SPECT) imaging of 12 regions. Patients were determined to have an abnormal SPECT if regional cerebral perfusion was less than 2 standard deviations below the mean of age-matched controls. RESULTS: The mean age was 67.5 (range, 34-89) years. The study group comprised 22% women and 78% men with known risk factors for atherosclerosis: current tobacco use (30%), hypertension (69%), and diabetes (27%). Seventy-five percent of the SPECT scans demonstrated abnormal regional cerebral perfusions, which were associated with older age (P < .008), current tobacco use (P < .005), and diabetes mellitus (P < .005). The incidence of postoperative cerebral vascular accident was 5% and only occurred in patients with abnormal regional cerebral perfusion. CONCLUSION: Seventy-five percent of patients undergoing coronary bypass grafting have a significant impairment in regional cerebral perfusion compared with published age-matched controls, which may contribute to their proclivity for cerebral complications.

Adult↗

Neurocognitive correlates of stereotactic thalamotomy and thalamic stimulation in Parkinsonian patients.

In the present paper we have reviewed five different studies that relate to neuropsychological consequences of stereotactic thalamotomy and thalamic stimulation in patients with Parkinson's disease. The neuropsychological results are in a strict sense confined to thalamotomy and thalamic stimulation, although the more general message of the importance of investigating cognitive functions before and after surgery applies to other stereotactic techniques for surgical treatment of movement disorders as well. It is argued in the paper that stereotactic thalamotomy provides a unique model for basic research on the neuropsychology of the thalamus, while in return, neuropsychological tests for cognitive dysfunction after surgery may be the most important clinical follow-up. Three general conclusions seem warranted from the data. (1) Parkinsonian patients are impaired on a range of cognitive functions, including language processing, memory, and executive functions. (2) Stereotactic thalamotomy does not further impair the patient; instead, we observed improvement on some tests, particularly verbal memory. (3) In general, there does not seem to be a laterality effect, depending on which side the thalamotomy lesion is applied. An exception to this are dichotically presented simple speech sounds and autonomic responses. In both instances, left-sided brain stimulation produced enhanced performance, while lesioning the left thalamus impaired dichotic listening performance. Finally, we present a new hypothesis for a mechanism behind the thalamotomy effect, based in part on changes in arousal thresholds.

Aged↗

Absence of myocardial release of troponin T after coronary bypass surgery on a beating heart.

BACKGROUND: Coronary artery bypass grafting (CABG) operations in connection with cardiopulmonary bypass (CPB) appear to be associated with a number of side effects including trauma, cognitive dysfunction and myocardial damage. Accordingly, a current interest in performing CABG on a beating heart begins to emerge. This study examines the premise that conducting CABG on a beating heart limits the extent of myocardial injury and other complications. METHODS: Forty-five consecutive patients underwent CABG on a beating heart (group A, 12 patients) or in connection with CPB (group B, 33 patients). Inclusion criteria were poor left ventricular function and evolving myocardial ischemia or infarction. Results were assessed primarily on the basis of clinical outcome. In addition, measurement of plasma levels of troponin T (TnT), creatine kinase MB (CK-MB) and lactate dehydrogenase (LD) was conducted in 12 patients of group A preoperatively and 24 h after completion of surgery. These biological data were compared with those from control patients who underwent CABG in connection with CPB within the same time span. RESULTS: All patients in groups A and B survived the CABG procedure and those on a beating heart maintained an excellent perioperative hemodynamic measurements. The mean bypass time was 75 +/- 21 min and the mean cardiac standstill was 40 +/- 17 min. The intensive care unit stay was for group A: 18 +/- 4 h, group B: 48 +/- 12 h; and the total hospital stay was for group A: 6 +/- 1 days, group B: 8 +/- 3 days. Angiographic studies showed good anastomatic patency in both groups. Postoperative low output syndrome as indicated by the need of ionotropic drugs for more than 24 h was demonstrated in 4% and 6% of groups A and B, respectively. Limitation of myocardial injury in group A was demonstrated by the minimal increase in postoperative TnT levels (16.0 +/- 0.9 versus 30 +/- 8.0 pg/ml). A similar pattern of changes was observed with other infarction markers including CK-MB and LD. Contrastingly, the pre- and post-operative values of TnT in group B were 18 +/- 1.6 and 790 +/- 140 pg/ml, respectively. CONCLUSIONS: CABG on a beating heart shares many of the positive features of CPB with a distinct advantage of eliminating the intraoperative myocardial ischemia.

Adult↗

Is cardiopulmonary bypass still the cause of cognitive dysfunction after cardiac operations?

OBJECTIVE: The purpose of this study was to determine whether cognitive impairment is related to cardiopulmonary bypass. METHODS: Twenty-five patients undergoing coronary artery bypass grafting without cardiopulmonary bypass were matched with 50 patients undergoing coronary artery bypass grafting with cardiopulmonary bypass. All patients received the same anesthetic regimen, and one surgeon performed all the operations. A battery of 10 standard tests of neuropsychologic function were performed before, at discharge, and 3 months after the operation. A comprehensive multidimensional measure of subjective health status was used as the primary clinical measure of functional outcome. RESULTS: The groups were similar with respect to age, sex, and ventricular function and differed only in the need for a circumflex artery graft. Both groups showed significant improvement in the comprehensive multidimensional measure of subjective health status at 3 months. At discharge most neuropsychologic tests had deteriorated in both groups (the same 4 tests had deteriorated significantly in both groups, and an additional test had deteriorated significantly in the cardiopulmonary bypass group). At 3 months all but one test in the cardiopulmonary bypass group had returned to or exceeded baseline performance. The same 2 tests had improved significantly in both groups, and a further test had improved significantly in the group without cardiopulmonary bypass. At no specific time point was there a significant difference between the absolute or change scores between the groups on any of the tests. CONCLUSIONS: The similar pattern of early decline and late recovery of cognitive function in patients undergoing coronary artery bypass grafting with and without cardiopulmonary bypass suggests that cardiopulmonary bypass is not the major cause of postoperative cognitive impairment. This merits consideration in deciding optimal treatment strategies in coronary revascularization.

Cardiopulmonary Bypass↗

Cardiac surgical patients exposed to heparin-bonded circuits develop less postoperative cerebral dysfunction than patients exposed to non-heparin-bonded circuits.

A prospective randomized trial was used to study the incidence of cerebral dysfunction in patients undergoing cardiopulmonary bypass (CPB) with heparin-bonded vs non-heparin-bonded circuits. Although the etiology of postoperative cerebral dysfunction is controversial, activation of the systemic inflammatory response may play a role. After institutional approval and informed written consent, 39 elective coronary artery bypass (CABG) patients were studied. A battery of neuropsychometric tests (NPMTs) was performed preoperatively, and 5 days and 6 weeks postoperatively. Significant change in NPMT performance was defined as a 25% or greater decrease in postoperative performance, compared to baseline. The number of abnormal tests per patient was calculated. Analysis using the Mann-Whitney rank test was performed for the first follow-up. Patients randomized to heparin-bonded circuits had fewer abnormal NPMTs (>1 abnormal test) on postoperative day 5 (58 vs 70%, n=19 and 20) than patients randomized to non-heparin-bonded circuits. Patients exposed to heparin-bonded circuits had fewer abnormal tests (>1 abnormal test) at 6 weeks (36 vs 63%, n=14 and 16). Results suggested that the attenuation of systemic inflammation by heparin-bonded CPB circuits may lower the incidence of cerebral injury in cardiac surgical patients.

Cardiopulmonary Bypass↗

Corpus callosal changes associated with hydrocephalus: a report of two cases.

OBJECTIVE AND IMPORTANCE: Focal or diffuse corpus callosal changes can occur in patients with active hydrocephalus who undergo shunting procedures. The neural compression caused by active hydrocephalus and the conditions that follow ventricular shunting may contribute to the development of these changes. CLINICAL PRESENTATION: Two patients who underwent successful shunting for hydrocephalus subsequently developed thickening and diffuse signal changes in the corpus callosum, which were revealed by magnetic resonance imaging. The abnormal signal intensity extended laterally and linearly along the callosal fiber tracts and was not associated with mass effect. These changes persisted despite clinical improvement after the shunts were implanted. INTERVENTION: Detailed neuropsychological testing showed no evidence of residual cognitive impairment or any interruption of the interhemispheric transfer of information. It has been proposed that the impingement of the corpus callosum by the rigid falx may contribute to symptomatic hydrocephalus. Impingement may cause partial hemispheric disconnection, resulting from callosal axonal dysfunction. Our patients showed radiographic evidence of dramatic changes within the corpus callosum after ventricular shunting, consistent with a transcallosal demyelinating process. Patients demonstrated neither clinical nor neuropsychological evidence of callosal disconnection, even though the callosal changes persisted. In these two patients, it is reasonable to assume that the relative sparing of the splenium accounts for the lack of neuropsychological deficits. CONCLUSION: Based on our findings, conservative management, rather than a stereotactic biopsy or other forms of intervention, seems reasonable when these characteristic changes of the callosum are noted by magnetic resonance imaging after a shunt for hydrocephalus has been implanted in the patient.

Cerebrospinal Fluid Shunts↗