To analyze the prognostic factors and therapeutic outcome of adult patients with isolated symptomatic stenosis of the middle cerebral artery (MCA). Forty-nine patients were retrospectively verified with isolated symptomatic stenosis of the MCA through both magnetic resonance angiogram and transcranial color-coded duplex sonography. Therapeutic outcome at 1 year or more was determined using a modified Barthel index (BI). For the purpose of analysis, the patients were divided into two groups: a good outcome group (BI > or = 12) and a poor outcome group (BI < 12 or recurrent stroke). The association between different therapeutic regimens and the percent free of recurrent stroke after the first event of cerebral infarction was assessed with Kaplan-Meier plots compared by a log-rank test. These patients accounted for 2.8% of all patients with the first event of cerebral infarction during the same period. At follow-up of 1 year or more, 63% had good outcomes whilst the other 37% had poor outcomes. Overall, 26.5% suffered from recurrent strokes during the follow-up period. According to the statistical analysis, the stepwise logistic regression revealed that only the National Institutes of Health Stroke Scale (NIHSS) at the time of admission was independently associated with a poor outcome. Furthermore, Kaplan-Meier analysis showed a significantly higher percentage of patients free of recurrent stroke events amongst those who were treated with warfarin. The NIHSS at the time of admission was a predictor of outcome amongst our patients, and stenosis of the MCA implies the danger of recurrent cerebral events. Our study also demonstrates the efficacy of oral anticoagulants in the secondary prevention in this specific group of patients. Therefore, we look forward to more prospective multicenter investigations in evaluating the efficiency of therapy in the future.

In this 16-year (1986-2001) retrospective study, 23 childhood patients were identified with Guillain-Barré syndrome. According to clinical and electrophysiologic findings, 18 patients manifested acute inflammatory demyelinating polyradiculoneuropathy, 2 had Miller Fisher syndrome, 1 had axonal forms, and 2 were unclassified. Seasonal preponderance was evident in 39% of patients with Guillain-Barré syndrome, developing the disease in the winter (November to January) with upper respiratory infection the most frequent preceding event. The most common manifestation was limb weakness, with various degrees of motor weakness in 22 patients. Bulbar involvement was the most common cranial palsy, and it was evident in 30% of the episodes. Only one of these progressed to mechanical ventilation during hospitalization. Altogether, approximately 61% of the episodes exhibited sensory symptoms. At a follow-up of 1 year or more, 20 patients recovered and 3 had residua. Furthermore, no fatality occurred in our study. Our study also demonstrates that the clinical course of childhood Guillain-Barré syndrome has a shorter recovery time as compared with an adult patient group. Therapeutic outcome is favorable for patients who receive prompt treatment.

BACKGROUND:To analyze the clinical features, causative pathogens and therapeutic outcomes of bacterial meningitis in hemodialyzed patients. PATIENTS AND METHODS:Two hundred and sixty-seven patients, > or = 16 yrs, were identified with culture-proven bacterial meningitis. In addition, the causative pathogens and therapeutic outcomes between uremic and non-uremic patients with adult bacterial meningitis were analyzed. RESULTS:Nine uremic patients with bacterial meningitis, accounting for 3% (9/267) of our adult patients with culture-proven bacterial meningitis had fever, disturbed consciousness and seizures. These were the three most common manifestations in our patients. The interval between the onset of symptoms and therapy start was 5-11 days (mean: 9 days). No patients were initially diagnosed with bacterial meningitis, two patients were initially suspected of having infection of unknown origin. In the non-uremic patient group, klebsiella pneumoniae, Staphylococcus aureus, and Streptococcus pneumoniae were the most frequently detected pathogens, while pseudomonas aeruginosa and coagulase-negative Staphylococcus were the most prevalent in the uremic patients group. The overall mortality rates for the non-uremic and uremic patient groups were 33 and 78% respectively. CONCLUSION:The mortality rate for bacterial meningitis in the uremic patients group remained high. Due to non-specific manifestations and slow evolution, bacterial meningitis was commonly misdiagnosed as uremic encephalopathy. Therefore, effective treatment was usually delayed. To avoid treatment failure, early diagnosis, careful monitoring of clinical condition and appropriate antibiotic choices are necessary.

This 16-year (1986-2001) retrospective study enrolled 80 infantile patients (aged, 30-365 days old) with culture-proven bacterial meningitis. The most prevalent pathogens were Salmonellaspecies, Streptococcus (S.) agalactiae, Escherichia (E.) coli, and Haemophilus (H.) influenzae, accounting for about 59% of the episodes. Meningitis caused by Salmonella species, E. coli and H. influenzae occurs more often in the older infants, while that caused by S. agalactiae occurs more often in young infants. Our study revealed a decrease in the proportion of Salmonella meningitis from 27% in the first 8 years to 9% in the second 8 years with E. coli replacing Salmonella species as the leading pathogen of this disease during the second period. Overall mortality rate for both periods of time was 11%. However, if we take those with undesirable poor outcomes into account, 43% of patients could be considered treatment failures. The study also reveals a high prevalence of neurological complications when this disease is caused by H. influenzae, S. pneumoniae, and Salmonella species. Stepwise logistic regression analysis revealed that only initial changing levels of consciousness (P = 0.006) were independently associated with treatment failure. The most frequent neurological complications associated with this disease included subdural empyema, hydrocephalus, cerebral infarctions, and seizures. Because therapeutic regimens may require attention to the eradication of bacterial pathogen but also the neurological complications, early diagnosis and choice of appropriate antibiotics are essential to increasing the possibility of survival.

This retrospective chart review describes the clinical features, pathogens, and outcomes of 46 patients with cerebrospinal fluid (CSF) shunt infections collected over 16 years. The overall CSF shunt infection rate was 2.1%, broken down into 1.7 and 9.3% in adult and pediatric groups, respectively. Fever and progressive consciousness disturbance were the most clinical features in the adult patient group, whereas disturbance of consciousness and abdominal symptoms and signs were the two most common clinical features in the pediatric patient group. The most frequently isolated microorganisms were of the Staphylococcus spp., including Staphylococcus aureus and coagulase negative Staphylococcus, which accounted for 47% of the episodes. Furthermore, increases in polymicrobial and Gram-negative bacilli infections were observed in our study. Due to the high proportion of oxacillin-resistant Staphylococcus spp. and polymicrobial infections, we recommend initial empirical antibiotics with both vancomycin and a third-generation cephalosporin for cases in which the causative bacteria has not been identified or for which the results of antimicrobial susceptibility tests are not available. For patients who develop smoldering fevers, progressive disturbed consciousness, seizures, or abdominal fullness after ventriculoperitoneal shunt procedures, CSF shunt infections should be suspected. Although some infections have been managed successfully with antimicrobial therapy alone, the timely use of appropriate antibiotics according to antimicrobial susceptibility testing and the removal of the shunt apparatus are essential for successful treatment.

In this study, 116 patients, at least 1 month of age but younger than 5 years, were identified with culture-proven bacterial meningitis. A comparison was made between the clinical data of the patients with and without seizures during hospitalization. Seizures during acute bacterial meningitis accounted for 47% (55/116) of the episodes. Time interval between the onset of bacterial meningitis and that of seizures was 1 to 20 days (mean, 4 days). Twelve of these 55 patients had one or more afebrile seizures after completing the treatment. At follow-up of at least 1 year after completing treatment, 26 patients had good outcomes, whereas the other 29 patients had poor outcomes. A strong correlation between the findings of abnormalities through neuroimaging and the occurrence of seizures during hospitalization was observed. The long-term outcomes of patients with infantile and childhood bacterial meningitis, who had seizures during the acute phase of bacterial meningitis, were worse than the outcomes of those who did not have such seizures. No child developed late seizures unless there were acute seizures. Factors associated with seizures during acute bacterial meningitis include disturbed consciousness on admission, abnormal neuroimaging findings, and low glucose and high concentration of total proteins in cerebrospinal fluid.

BACKGROUND Cerebral infarction is an important neurological complication of childhood bacterial meningitis, but little is known about its epidemiology and outcomes. AIM To determine the predictive factors, clinical features, causative pathogens, and outcomes of cerebral infarction secondary to perinatal and childhood bacterial meningitis. DESIGN Retrospective analysis METHODS Over the period 1986-2001, 166 perinatal and childhood patients were identified as having culture-proven bacterial meningitis, of whom 14 had cerebral infarction at admission. The clinical and CSF data of patients with and without cerebral infarctions on admission were compared. RESULTS Cerebral infarction patients accounted for 10% (14/166) of bacterial meningitis cases, mostly in the first year of life (11/14, 79%). Salmonella species (n = 4) and Streptococcus pneumoniae (n = 4) were the most frequent causative pathogens, accounting for 57% (8/14) of episodes. Single infarctions were found in four patients and multiple infarctions in 10. At 1 year follow-up, outcome was good in three, but poor in 11. Significant differences between the two patient groups at admission included age bands, presence of seizures, hydrocephalus, disturbed consciousness on admission, and CSF lactate concentration. DISCUSSION There was a high prevalence of cerebral infarctions when the disease was caused by S. pneumoniae and Salmonella species. Occurrence was highest in the first year of life, and the prognosis in this patient group is poor. Risk factors associated with cerebral infarction in our patients included age 28-365 days, seizures, hydrocephalus, disturbed consciousness on admission, and high CSF lactate concentrations.

Sixty patients with Guillain-Barré syndrome (GBS), aged 16-83 years, have been identified over a period of 7 years. Of 60 patients, 30 received the double filtration plasmapheresis (DFP), 4 received intravenous immunoglobulin, and the other 26 received supportive care only. Therapeutic outcomes at 1 year were determined using a modified Barthel index. At a follow-up of 1 year or longer, 31 patients (52%) had recovered, 24 (40%) had residua, and 5 (8%) had died. According to the statistical analysis, disability at the nadir and electrophysiological signs significantly influenced the long-term outcomes. Complications associated with DFP procedures included physiologic change, technique-related complications, and vascular access-related complications. None of our patients had fatal complications related to DFP treatment. Contrary to the established belief that the disease has a favorable outcome, several hospital-treated patients may still die or present residua even several months after the onset of symptoms. Because disability at the nadir influences the outcomes, early diagnosis and choice of appropriate treatment, which might include DFP, to prevent further neurological deficits, are essential to maximize the potential for survival.

To determine the epidemiologic trends, prognostic factors, and therapeutic results of neonatal bacterial meningitis, 60 neonatal patients with culture-proven neonatal bacterial meningitis were enrolled in this study. To compare changes over time, the appearance of disease among the patients was divided into two equal periods (1986-1993 and 1994-2001). Group B streptococci were the most common causative pathogens, accounting for approximately 32% of the episodes. Escherichia coli, the next most common pathogen, was more frequently observed in the second period. Seventy-seven percent of gram-negative bacilli isolates were resistant to ampicillin. Moreover, oxacillin-resistant Staphylococcus and ampicillin-resistant group B streptococci strains occurred in the second periods as late-onset neonatal bacterial meningitis. The overall mortality rates for the first and second study period were 17% and 8%, respectively. However, if individuals with poor outcomes were taken into account, 38% of patients were considered treatment failures. Significant prognostic factors included the presence of seizures, thrombocytopenia, and high cerebrospinal fluid protein and low cerebrospinal fluid glucose concentration. Although the mortality rate was significantly reduced in the second period, there has been increasing incidence of the emergence of resistant strains presenting a therapeutic challenge. The presentation in neonatal bacterial meningitis might be nonspecific, and blood culture results were negative in 45% of the episodes. Early diagnosis, choice of appropriate antibiotics, and correction of metabolic derangement are essential to improving outcomes. Chang C-J, Chang W-N, Huang L-T, Huang S-C, Chang Y-C, Hung P-L, Tasi C-Y, Lu C-H, Cheng B-C, Lee P-Y, Chang H-W. Neonatal bacterial meningitis in southern Taiwan.

To determine the clinical features, prognostic factors, and therapeutic results of Guillain–Barré syndrome (GBS) in order to improve the therapeutic strategy for this disease. We retrospectively reviewed the electrodiagnostic study and medical records of patients with GBS admitted to Chang Gung Memorial Hospital, Kaohsiung, between January 1986 and December 2000. Outcomes and prognosis were followed‐up after 1 year. Ninety‐six patients were enrolled in this study. According to the clinical and electrophysiological findings, 77 patients were acute inflammatory demyelinating polyradiculoneuropathy, seven were Miller Fisher syndrome, and six were axonal forms, and six were unclassified. At a follow‐up of 1 year, 61 patients (64%) recovered, 30 (31%) had residua and five (5%) died. Amongst these 30 had residua, including unassisted gait in 19, assisted gait in four, and wheel/bed bound in seven. According to the statistical analysis, disabilities at the nadir ( P < 0.0001) and at admission ( P = 0.014) were significant prognostic factors. Variables used for the stepwise logistic regression, and the results revealed that after analysis for all the above variables, only disability at the nadir ( P < 0.0001) was independently associated with the treatment failure rate. Our study revealed 27% of cases in need of respiratory support during hospitalization, and 5% of hospital‐treated patients die from the complications. Furthermore, 31% had residua at a follow‐up of 1 year or more. If prognostic factors are considered, disability at the nadir during hospitalization demonstrates consistently poor therapeutic outcomes. Therefore, early diagnosis, choice of appropriate treatment, and preventing complications during acute stages are essential to maximize the potential for survival.

Adenosine is an endogenous modulator that has an inhibitory effect on neuronal activity. The aim of this work was to investigate the role of aminophylline, an adenosine receptor antagonist, on the long-term effects of status epilepticus (SE) in the developing brain. Four groups of rats at the postnatal age of 12 days were intraperitoneally administered with saline, aminophylline (50 mg/kg), lithium–pilocarpine (Li–PC) (3 mEq/kg–60 mg/kg), and Li–PC plus aminophylline, respectively. The four groups were tested for spatial memory using the Morris water maze task at P80 and motor performance by the Rotarod test at P100. The brains were then analyzed with cresyl violet stain for histological lesions and evaluated for mossy fiber sprouting with the Timm stain. At the acute stage, all rats subjected to Li–PC developed SE and no seizures were elicited in the saline-treated or aminophylline-treated rats. The seizure duration was longer in the Li–PC plus aminophylline group (346.9±32.7 min) as compared with that in the Li–PC group (265.2±9.8 min). The difference of mortality was not significant. Rats without seizures exhibited no motor imbalance, spatial deficits, or morphological changes. The rats with Li–PC-induced SE demonstrated spatial memory deficits without motor incoordination or morphological changes. However, the rats subjected to Li–PC plus aminophylline exhibited motor impairment and morphological changes, including neuronal cell loss in CA1 area and increased mossy fiber sprouting in CA3 area. In addition, the rats of Li–PC plus aminophylline had greater spatial memory deficits than that seen in rats with Li–PC. We concluded that an adenosine receptor antagonist, such as aminophylline, had synergistic effects on the SE-induced long-term deficit of cognition and motor performance in the developing brain. The present study may provide experimental evidence and lead to novel therapeutic interventions.

Here, we investigated whether aminophylline, an adenosine receptor antagonist used usually as a treatment for premature apnea, had synergistic effects on status epilepticus in the developing brain. On postnatal day 14 (P14), four groups of rats intraperitoneally received saline, aminophylline, lithium–pilocarpine (Li-PC), and Li-PC plus aminophylline, respectively. Subsequently, the Morris water maze task was performed at P80. The brains were then analyzed with cresyl violet stain for histological lesions and evaluated for mossy fiber sprouting with the Timm stain. No seizures were elicited in the saline-treated or aminophylline-treated rats. Both the Li-PC-treated and aminophylline plus Li-PC-treated rats exhibited seizures and there was no significant difference in mortality between the two groups. More interestingly, as in adulthood (P80), aminophylline aggravated the spatial deficits and histological damages seen in Li-PC-treated rats. In summary, this present study suggests that the use of adenosine receptor antagonists, such as aminophylline, exacerbates seizure-induced damage in the developing brain.

PURPOSE:Recurrent seizures in infants are associated with a high incidence of neurocognitive deficits. Animal models have suggested that the immature brain is less vulnerable to seizure-induced injury than is that in adult animals. We studied the effects of recurrent neonatal seizures on cognitive tasks performed when the animals were in adolescence and adulthood. METHODS:Seizures were induced by intraperitoneal injection of pentylenetetrazol (PTZ) for 5 consecutive days, starting from postnatal day 10 (P10). At P35 and P60, rats were tested for spatial memory by using the Morris water maze task. In adulthood, motor performance was examined by the Rotarod test, and activity level was assessed by the open field test. Seizure threshold was examined by inhalant flurothyl. To assess presence or absence of spontaneous seizures, rats were video recorded for 4 h/day for 10 consecutive days for the detection of spontaneous seizures. Finally, brains were examined for histologic evidence of injury with cresyl violet stain and Timm staining in the supragranular zone and CA3 pyramidal cell layers of the hippocampus. RESULTS:PTZ-treated rats showed significant spatial deficits in the Morris water maze at both P35 and P60. There were no differences in seizure threshold, motor balance, or activity level during the open field test. Spontaneous seizures were not recorded in any rat. The cresyl violet stain showed no cell loss in either the control or experimental rats. PTZ-treated rats exhibited more Timm staining in the CA3 subfield. However, the control and experimental rats showed similar Timm staining within the supragranular zone. CONCLUSIONS:Our findings indicate that recurrent PTZ-induced seizures result in long-term cognitive deficits and morphologic changes in the developing brain. Furthermore, these cognitive deficits could be detected during pubescence.

Recurrent neonatal seizures are associated with a high risk of neurological sequelae. The major concern is whether recurrent neonatal seizures induce adverse effects on long-term cognition and/or motor performance. Rats were treated with intraperitoneal (ip) bicuculline for 3 consecutive days, starting from Postnatal Day 5 (P5). Kainic acid (KA, 4 mg/kg ip) was injected at P53 to investigate the susceptibility to a second insult, and then cognitive function was tested using the Morris water maze, and motor performance using the Rotarod test, in adulthood (P60). Finally, histological assessments of brains were performed. The rats treated with bicuculline had no deficits in cognition function and pathology findings, but had worse motor performance and increased susceptibility to later KA challenge. Our findings indicate that recurrent bicuculline-induced seizures in the developing brain result in long-term motor deficits and increase the risk of subsequent cognitive damage in response to a second insult.

Purpose: Maternal deprivation is stressful for the neonate. The aim of this study was to investigate the short- and long-term effects of maternal separation on recurrent seizures in the developing brain.Methods: Rats were divided into four groups according to whether the rat pups were treated with maternal deprivation from postnatal day 2 (P2) to P9 or neonatal seizures induced by intraperitoneal (i.p.) injection of pentylenetetrazol (PTZ) from P10 to P14. Rats in the control group received saline i.p. injection from P10 to P14; rats in the isolation group underwent daily separation from their dams from P2 to P9; rats in the PTZ-treated group were subjected to PTZ-induced recurrent seizures from P 10 to P 14; rats in the isolation plus PTZ-treated group were subjected to maternal deprivation from P2 to P7 followed by serial seizures from P10 to P14. In addition, subsets of rats at P 15 were killed and the brains assessed for acute neuronal degeneration. Visual-spatial memory test using the Morris water maze task was performed at P80. After testing, the hippocampus was evaluated for histologic lesions and cyclic adenosine monophosphate (cAMP)-responsive element-binding protein phosphorylation at serine-133 (pCREB(Ser-133)), an important transcription factor underlying learning and memory.Results: All rats given PTZ developed recurrent seizures. After PTZ administration, rats with a history of maternal deprivation had more intense impairment than did rats with maternal deprivation and neonatal seizures than those without deprivation. Neuronal degeneration was most prominent in the rats exposed to maternal deprivation plus recurrent seizures. Rats receiving maternal deprivation or PTZ-induced recurrent seizures exhibited only spatial deficits, but no morphologic changes in the hippocampus. However, rats with maternal deprivation plus PTZ-induced recurrent seizures exhibited worse visual-spatial learning compared with rats with either isolation or PTZ-induced recurrent seizures alone. The levels of pCREB(Ser-133) may play a role in the decrease in the hippocampus from the rats subjected to maternal deprivation and/or PTZ-induced recurrent seizures, as compared with rats exposed to vehicle-control saline. These results indicate that repeated maternal deprivation can exacerbate long-term cognitive deficits resulting from neonatal seizures. In addition, impaired phosphorylation of CREBSer-133.Conclusions: Repeated maternal deprivation stress has synergistic effects with recurrent seizures in inducing neurologic damage in the developing brain.

Hepatic focal nodular hyperplasia is very rare in children. We present 3 cases aged from 8 to 17 years. All of them are girls, none of whom used oral contraceptives. Case 1 was a hepatitis B carrier and was incidentally found to have focal nodular hyperplasia (FNH). The other 2 cases presented with abdominal pain. Abdominal computed tomography revealed a solitary liver tumor in cases 2 and 3, but no abnormalities in case 1. A 7-cm tumor was located in the left lobe of the liver with compression of the stomach in the 2nd case. Abdominal magnetic resonance imaging (MRI) showed a mass with isointense density to liver parenchyma on T1WI and hyperdensity on T2WI in the 1st and the 3rd cases. The inferior vena cava was compressed and displaced anteriorly in the 1st case. Because of differences in the clinical presentation and imaging studies, the 1st and 2nd cases received resection while the 3rd case was treated conservatively. Pathologic findings confirmed the diagnosis of focal nodular hyperplasia in all 3 cases. We emphasize the importance of an MRI scan in the diagnosis of hepatic focal nodular hyperplasia, and different clinical manifestations and imaging studies may lead to different management.