Developmental aspects of cerebrospinal fluid levels of beta-phenylethylamine and it's role in pediatric neurological disorders. (1/184)

To clarify the role of beta-phenylethylamine (PEA) in pediatric neurological disorders, we have measured the cerebrospinal fluid (CSF) levels of PEA in 12 children with aseptic meningitis--6 were in the acute phase and the other 6 were in the recovery phase--and 5 children with Rett Syndrome (RS). The findings were compared with those obtained from 13 age-matched children with leukemia as child controls and from 10 adults patients without any neurological symptoms and signs as control. In the control group, the CSF PEA level was negatively correlated with age until 200 months (17 years) old. The mean PEA levels in meningitis and RS were significantly lower than that of child controls (p < 0.03). The alteration in the CSF levels of PEA may be related to transient changes in the dopaminergic tone in aseptic meningitis and neurological impairment, especially in the dopaminergic neurons in RS.  (+info)

Aseptic meningitis in the newborn and young infant. (2/184)

When a toxic newborn or young infant presents with fever and lethargy or irritability, it is important to consider the diagnosis of meningitis even if the classic localizing signs and symptoms are absent. Cerebrospinal fluid should be obtained (unless lumbar puncture is clinically contraindicated) to enable initial therapy to be planned. Initial results of cerebrospinal fluid testing may not conclusively differentiate between aseptic and bacterial meningitis, and antimicrobial therapy for all likely organisms should be instituted until definitive culture results are available. Comprehensive therapy, including antibacterial and antiviral agents, should continue until a cause is identified and more specific therapy is initiated, an etiology is excluded or the patient improves considerably and the course of antimicrobial therapy is completed. Group B streptococcus is the most common bacterial etiologic agent in cases of meningitis that occur during the first month after birth. Etiologies of aseptic meningitis include viral infection, partially treated bacterial meningitis, congenital infections, drug reactions, postvaccination complications, systemic diseases and malignancy. Long-term sequelae of meningitis include neuromuscular impairments, learning disabilities and hearing loss. Prompt diagnosis and treatment are essential to improved outcome.  (+info)

Outbreak of aseptic meningitis due to ECHO-9 in northern Kyushu island in the summer of 1997. (3/184)

An outbreak of aseptic meningitis caused by echovirus type 9 (ECHO-9) occurred between June and August 1997 in the Chikugo area, Fukuoka, Japan. Clinical manifestations and laboratory data of 317 children with aseptic meningitis were analyzed. The age of the patients ranged from 1 month to 12 years with the highest incidence in 4 years old children. The male: female ratio was 2.0:1.0. Symptoms of the meningitis included fever (100%), headache (89.5%) and nausea and/or vomiting (85.6%). Skin rash was not frequent (2.2%) in contrast to previous reports of ECHO 9 infections. The number of white blood cells (WBC) in cerebrospinal fluid (CSF) ranged from 10 to 3,493 cells/microliter (median; 412 cells/microliter). The neutrophils were more than 50% of the WBC in CSF in one-fourth of the patients at diagnosis. Enteroviruses were identified from CSF utilizing virus culture and enterovirus-specific RT-PCR, and ECHO-9 infection was determined by antibody titer of paired sera. Finally 44 patients were diagnosed virologically or serologically as aseptic meningitis caused by ECHO-9. Sequence analysis revealed that two strains of ECHO-9 isolated from CSF in this epidemic were closely related to ECHO-9 virulent strain Barty.  (+info)

Neurologic complications in children with enterovirus 71 infection. (4/184)

BACKGROUND: Enterovirus 71 infection causes hand-foot-and-mouth disease in young children, which is characterized by several days of fever and vomiting, ulcerative lesions in the oral mucosa, and vesicles on the backs of the hands and feet. The initial illness resolves but is sometimes followed by aseptic meningitis, encephalomyelitis, or even acute flaccid paralysis similar to paralytic poliomyelitis. METHODS: We describe the neurologic complications associated with the enterovirus 71 epidemic that occurred in Taiwan in 1998. At three major hospitals we identified 41 children with culture-confirmed enterovirus 71 infection and acute neurologic manifestations. Magnetic resonance imaging (MRI) was performed in 4 patients with acute flaccid paralysis and 24 with rhombencephalitis. RESULTS: The mean age of the patients was 2.5 years (range, 3 months to 8.2 years). Twenty-eight patients had hand-foot-and-mouth disease (68 percent), and 6 had herpangina (15 percent). The other seven patients had no skin or mucosal lesions. Three neurologic syndromes were identified: aseptic meningitis (in 3 patients); brain-stem encephalitis, or rhombencephalitis (in 37); and acute flaccid paralysis (in 4), which followed rhombencephalitis in 3 patients. In 20 patients with rhombencephalitis, the syndrome was characterized by myoclonic jerks and tremor, ataxia, or both (grade I disease). Ten patients had myoclonus and cranial-nerve involvement (grade II disease). In seven patients the brain-stem infection produced transient myoclonus followed by the rapid onset of respiratory distress, cyanosis, poor peripheral perfusion, shock, coma, loss of the doll's eye reflex, and apnea (grade III disease); five of these patients died within 12 hours after admission. In 17 of the 24 patients with rhombencephalitis who underwent MRI, T2-weighted scans showed high-intensity lesions in the brain stem, most commonly in the pontine tegmentum. At follow-up, two of the patients with acute flaccid paralysis had residual limb weakness, and five of the patients with rhombencephalitis had persistent neurologic deficits, including myoclonus (in one child), cranial-nerve deficits (in two), and ventilator-dependent apnea (in two). CONCLUSIONS: In the 1998 enterovirus 71 epidemic in Taiwan, the chief neurologic complication was rhombencephalitis, which had a fatality rate of 14 percent. The most common initial symptoms were myoclonic jerks, and MRI usually showed evidence of brainstem involvement.  (+info)

Randomized trial of a slow-release versus a standard formulation of cytarabine for the intrathecal treatment of lymphomatous meningitis. (5/184)

PURPOSE: To evaluate the efficacy and safety of a slow-release formulation of cytarabine (DepoCyt; Chiron Corp, Emeryville, CA, and Skye Pharma, Inc, San Diego, CA) that maintains cytotoxic concentrations of cytarabine (ara-C) in the CSF of most patients for more than 14 days. PATIENTS AND METHODS: Twenty-eight patients with lymphoma and a positive CSF cytology were randomized to receive DepoCyt 50 mg once every 2 weeks or free ara-C 50 mg twice a week for 1 month. Patients whose CSF cytology converted to negative and who did not have neurologic progression received an additional 3 months of consolidation therapy and then 4 months of maintenance therapy. All patients received dexamethasone 4 mg orally bid on days 1 through 5 of each 2-week cycle. RESULTS: The response rate was 71% for DepoCyt and 15% for ara-C on an intent-to-treat basis (P =.006). All of the patients on the DepoCyt arm but only 53% of those on the ara-C arm were able to complete the planned 1-month induction therapy regimen. Time to neurologic progression and survival trend in favor of DepoCyt (median, 78.5 v 42 days and 99.5 v 63 days, respectively; P >.05). DepoCyt treatment was associated with an improved mean change in Karnofsky performance score at the end of induction (P =.041). The major adverse events on both arms were headache and arachnoiditis, which were often caused by the underlying disease. CONCLUSION: DepoCyt injected once every 2 weeks produced a high response rate and a better quality of life as measured by Karnofsky score relative to that produced by free ara-C injected twice a week.  (+info)

Molecular epidemiology and genetic diversity of echovirus type 30 (E30): genotypes correlate with temporal dynamics of E30 isolation. (6/184)

Echovirus type 30 (E30) (genus, Enterovirus; family, Picornaviridae) has caused large outbreaks of aseptic meningitis in many regions of the world in the last 40 years. U.S. enterovirus surveillance data for the period 1961 to 1998 indicated that the annual proportion of E30 isolations relative to total enterovirus isolations has fluctuated widely, from a low of 0% in 1966 to a high of 42% in 1998. Peaks of E30 isolations occurred in the years 1968 to 1969, 1981 to 1984, 1990 to 1993, and 1997 to 1998, coincident with large nationwide outbreaks of E30-associated aseptic meningitis. Analysis of the complete VP1 sequence (876 nucleotides) of 136 E30 strains isolated in geographically dispersed regions of the United States and nine other countries between 1956 and 1998 indicated that the currently circulating E30 strains are genetically distinct from those isolated 30 to 40 years ago. Phylogenetic reconstruction demonstrated the existence of at least four distinct genetic groups, three of which have not been isolated in North America since 1981. Two of the three groups disappeared during periods when E30 was isolated infrequently. All North American E30 strains isolated after 1988 were closely related to one another, and all post-1993 isolates were of the same lineage within this group. Surveillance data indicate that E30 causes large national outbreaks of 2- to 4-year durations, separated by periods of relative quiescence. Our results show that shifts in the overall genetic diversity of E30 and the predominant genetic type correlate temporally with the dynamics of E30 isolation. The sequence data also provide a basis for the application of molecular techniques for future epidemiologic investigations of E30 disease.  (+info)

Recurrent aseptic meningitis following non- steroidal anti-inflammatory drugs--a reminder. (7/184)

Non-steroidal anti-inflammatory drugs (NSAIDs) are rarely associated with side-effects affecting the central nervous system. A case of NSAID-induced recurrent aseptic meningitis is presented. Seven episodes of aseptic meningitis were documented in the patient's life-time (up to the age of 30). General practitioners' records available for the latest four episodes showed that a NSAID (naproxen, piroxicam or diclofenac) was prescribed in the month prior to admission on each occasion. The patient was symptom free for a 3-year period during which no NSAID was prescribed. Clinicians should always elicit a careful drug history (including over-the-counter medications) in patients with aseptic meningitis and be aware of this unusual side-effect of NSAIDs.  (+info)

Nested PCR for rapid detection of mumps virus in cerebrospinal fluid from patients with neurological diseases. (8/184)

In this study, we have developed a reverse transcription (RT)-nested polymerase chain reaction (n-PCR) for the detection of mumps virus RNA in cerebrospinal fluid (CSF) from patients with neurological infections. A specific 112-bp fragment was amplified by this method with primers from the nucleoprotein of the mumps virus genome. The mumps virus RT-n-PCR was capable of detecting 0.001 PFU/ml and 0.005 50% tissue culture infective dose/ml. This method was found to be specific, since no PCR product was detected in each of the CSF samples from patients with proven non-mumps virus-related meningitis or encephalitis. Mumps virus RNA was detected in all 18 CSF samples confirmed by culture to be infected with mumps virus. Positive PCR results were obtained for the CSF of 26 of 28 patients that were positive for signs of mumps virus infection (i.e., cultivable virus from urine or oropharyngeal samples or positivity for anti-mumps virus immunoglobulin M) but without cultivable virus in their CSF. Overall, mumps virus RNA was detected in CSF of 96% of the patients with a clinical diagnosis of viral central nervous system (CNS) disease and confirmed mumps virus infection, while mumps virus was isolated in CSF of only 39% of the patients. Furthermore, in a retrospective study, we were able to detect mumps virus RNA in 25 of 55 (46%) CSF samples from patients with a clinical diagnosis of viral CNS disease and negative laboratory evidence of viral infection including mumps virus infection. The 25 patients represent 12% of the 236 patients who had a clinical diagnosis of viral CNS infections and whose CSF was examined at our laboratory for a 2-year period. The findings confirm the importance of mumps virus as a causative agent of CNS infections in countries with low vaccine coverage rates. In summary, our study demonstrates the usefulness of the mumps virus RT-n-PCR for the diagnosis of mumps virus CNS disease and suggests that this assay may soon become the "gold standard" test for the diagnosis of mumps virus CNS infection.  (+info)