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374
Abstracts
open label. (2) Three animal seizure models (maximal electric
shock-MES, pentylentetrazol seizure threshold-PST,
audiogenic seizure-AGS) were randomly divided into six
groups (n ¼ 10), i.p. NS10 ml/kg, CGZMT 10 g/kg,
CGZMT 20 g/kg, phenobarbital 50 mg/kg, clonazepam
(CZP) 0.1 mg/kg, CZP 1 mg/kg, respectively. Antiepileptic
effects were measured at CGZMT peak time and 7–14 days
afterwards. Three progresses (acquisition, consolidation and
retrieval) of learning-memory were measured by step down
test. The immunological functions effects of CGZMT were
studied by using the colorimetry, spectrophotometry (QHS),
quantitative hemolysis 3 H-TdR incorporation, and optical
microscope. Results: (1) Seizures-controlled rate was
64.6% in children with epilepsy. There were no relationships
with patient’s age, gender, duration of disease,
mono/polytherapy. (2) Seizures-free rate of CGZMT was
75% in MES, 80% in AGS and 100% (CGZMT 5 g/kg
was added CZP 0.1 mg/kg). CGZMT could prolong the
latency of PST. There was no statistical significance
compared with phenobarbital (PB). CGZMT had no adverse
effects and could accelerate learning speed and learningmemory
score. CGZMT could enhance the activity of
macrophage (MV), biological activity of interleukin-2
(IL-2), proliferation of T lymphocyte stimulated by concanavalin-A
(ConA), RBC-C 3 bRR and RBC-ICR, lower
proliferation of B lymphocyte stimulated by lipopolysaccharide
(LPS), level of antibody forming cell and hemolysin
antibody. Conclusion: CGZMT had antiepileptic efficacy
with accelerating cognitive function by increasing the activity
of MV, cell immune function and RBC adhesion function.
The improving of body immune state, i.e. ‘fu zheng gu
ben’.
SY-16-1
HIV-1/AIDS in children
SY-16
Infectious Diseases
A.L. Belman
School of Medicine, State University of New York, Stony
Brook, NY, USA
Since the initial descriptions of AIDS in children two
decades ago, much has been learned about the biology of
human immunodeficiency virus 1 (HIV-1) and the cells it
infects. Much has also been learned about maternal-infant
viral transmission and the natural history of HIV-1 infection.
Key studies led to strategies to interrupt maternal-infant
transmission resulting in a significant decline in neonatal
HIV-1 infection. More proficient diagnostic techniques
made possible early diagnosis of HIV-1 infected neonates
and infants during asymptomatic or mildly symptomatic
disease stages. Major treatment advances led to better control
of viral replication and thereby altered the course of disease
progression. HIV-1/AIDS associated neurological disorders
declined in parallel. A dramatic decline in the numbers of
infants born HIV-1 infected has been observed in countries
where currently recommended therapies are readily available.
Children with HIV-1/AIDS are living longer, many
already surviving into adolescence and young adulthood.
Unfortunately, worldwide, this is not the case; and it is worldwide
where the epidemic predominates and where the
complexity of medical care required and expensive drug
therapies are limited. Many issues remain. Just how HIV-1
affects the developing central nervous system (CNS) is still
not clearly understood and is the focus of continuing
research. The long-term effects of prenatal exposure to antiretroviral
agents are not yet known and continue to be
studied. Just exactly how HAART therapy may affect early
signs of pediatric HIV-1/AIDS associated CNS disease,
should it develop, is unclear. As new antiretroviral agents
are developed, and new combination drug regimens instituted,
the potential for neurological complications, toxicities,
and adverse drug interactions (for example with AEDS)
exists and will need to be identified and monitored.
SY-16-2
Viral encephalitis
Hj.M.I. Hussain
Penang, Malaysia
Traditionally discussions on viral encephalitis have
focused on Herpes viruses and Japanese Encephalitis.
However in recent years new viruses have been recognized
to cause outbreaks of viral encephalitis with a high case
fatality rate. Dengue hemorrhagic fever is often associated
with neurological manifestations especially headache,
altered sensorium and convulsions. These were thought
initially to arise from an encephalopathy secondary to circulatory
changes, cerebral hemorrhage or hepatic derangement.
Now the virus has been isolated from the cerebral
spinal fluid of patients with encephalopathy proving dengue
to be a neurotropic virus. In recent years outbreaks of Enterovirus
71 in Bulgaria, Malaysia and Taiwan have resulted in
many deaths among young children. Most of the children
died from fulminant pulmonary edema secondary to brainstem
encephalitis, similar to deaths from poliovirus in the
late fifties. Other affected children developed acute flaccid
paralysis. This raises concerns that Enterovirus 71 may
replace polio as a cause of acquired paralysis in children.
Most recently, a newly identified virus, the Nipah virus
caused an outbreak of encephalitis involving 265 adults in
Malaysia. There were 105 deaths with 12 relapses among
the survivors. As in Japanese encephalitis, swine are thought
to act as amplifying host for the Nipah virus. Spread to
humans is via direct contact with secretions and blood
products. Climatic and environmental changes are believed
to have precipitated the outbreak of Nipah encephalitis.
Continued global warming and deforestation may result in
similar outbreaks in future.