ABSTRACT
PURPOSE: Although ketogenic diet(KD) is an old method of treating epilepsies, its outstanding antiepileptic effect in some epileptic patients need re-evaluation. This study was performed to evaluate the anti-epiletogenic effect of KD. METHODS: In the preliminary experiment, to select a proper animal model of status epilepticus(SE), an evaluation of EEG and behavioral characteristics of pilocarpine-induced SE model was done in 12 Sprague-Dawley rats. As the aim of the first experiment was to evaluate neuronal death in the hippocampus of similarly convulsed rats, the 10-20 mg/kg of diazepam i.p. injection was given to cease SE in each stage of SE in KD and regular diet(RD) rats. Previous diet was maintained for two weeks until the evaluation of pathological changes with H-E and C-V stainings(64 rats, second experiments). In order to investigate whether the differences in the neuronal damage cause different mossy fiber sprouting or not, 40 rats were fed with KD and RD(20 rats each) 4 hours before pilocarpine-induced SE. After the treatment of SE with diazepam, half of previous KD rats maintained with KD and remaining 10 rats were fed with RD. Also previous RD rats were fed with RD and KD in the same way. Mossy fiber sprouting and synaptic reorganization was determined by Timm's staining 4 weeks after SE. RESULTS: Pilocarpine-induced SE showed reliable EEG and behavioral patterns in all rats. Also, KD did not have any influence on SE induced by pilocarpine in terms of SE induction time and severity. Neuronal damages in CA1, CA3, and dentate gyrus were less prominent in the KD rats in every SE stage. Rats with RD before their SE showed significant Timm's(+) bands, whereas rats with KD after the SE did not show any differences. CONCLUSION: KD consistently protect neuronal damage caused by seizures in the hippocampus. This neuroprotection causes less mossy fiber synaptic reorganization.
Subject(s)
Animals , Humans , Rats , Dentate Gyrus , Diazepam , Diet , Electroencephalography , Epilepsy , Hippocampus , Diet, Ketogenic , Models, Animal , Neurons , Pilocarpine , Rats, Sprague-Dawley , Seizures , Status EpilepticusABSTRACT
PURPOSE: Although ketogenic diet(KD) is an old method of treating epilepsies, its outstanding antiepileptic effect in some epileptic patients need re-evaluation. This study was performed to evaluate the anti-epiletogenic effect of KD. METHODS: In the preliminary experiment, to select a proper animal model of status epilepticus(SE), an evaluation of EEG and behavioral characteristics of pilocarpine-induced SE model was done in 12 Sprague-Dawley rats. As the aim of the first experiment was to evaluate neuronal death in the hippocampus of similarly convulsed rats, the 10-20 mg/kg of diazepam i.p. injection was given to cease SE in each stage of SE in KD and regular diet(RD) rats. Previous diet was maintained for two weeks until the evaluation of pathological changes with H-E and C-V stainings(64 rats, second experiments). In order to investigate whether the differences in the neuronal damage cause different mossy fiber sprouting or not, 40 rats were fed with KD and RD(20 rats each) 4 hours before pilocarpine-induced SE. After the treatment of SE with diazepam, half of previous KD rats maintained with KD and remaining 10 rats were fed with RD. Also previous RD rats were fed with RD and KD in the same way. Mossy fiber sprouting and synaptic reorganization was determined by Timm's staining 4 weeks after SE. RESULTS: Pilocarpine-induced SE showed reliable EEG and behavioral patterns in all rats. Also, KD did not have any influence on SE induced by pilocarpine in terms of SE induction time and severity. Neuronal damages in CA1, CA3, and dentate gyrus were less prominent in the KD rats in every SE stage. Rats with RD before their SE showed significant Timm's(+) bands, whereas rats with KD after the SE did not show any differences. CONCLUSION: KD consistently protect neuronal damage caused by seizures in the hippocampus. This neuroprotection causes less mossy fiber synaptic reorganization.
Subject(s)
Animals , Humans , Rats , Dentate Gyrus , Diazepam , Diet , Electroencephalography , Epilepsy , Hippocampus , Diet, Ketogenic , Models, Animal , Neurons , Pilocarpine , Rats, Sprague-Dawley , Seizures , Status EpilepticusABSTRACT
The esophageal hiatal hernia is a herniation of an abdominal organ, usually the stomach, through the esophageal hiatus into thoracic cavity. It is a rare disease, usually congenital and frequently associated with gastroesophageal reflux and other congenital malformations in children. It is classified according to their anatomic characteristics as type I (sliding hiatal hernia), type II (paraesophageal hiatal hernia), type III (combined hiatal hernia) and type IV (multiorgan hiatal hernia). We experienced a case of type III congenital esophageal hiatal hernia simulating chest mass on simple chest x-ray because of right intrathoracic stomach secondary to congenital esophageal hiatal hernia and organoaxial rotation in 10 months male. After the operation, he showed an improved general condition and was discharged at the 14th hospital day. We report the case with the brief review of the related literatures.
Subject(s)
Child , Humans , Male , Gastroesophageal Reflux , Hernia, Hiatal , Rare Diseases , Stomach , Thoracic Cavity , ThoraxABSTRACT
PURPOSE: Cerebral palsy is a group of conditions characterized by nonprogressive motor and posture dysfunction developing during perinatal period due to brain damage. Combined sensory and cognitive disorders can evolve the secondary mental retardation or speech disorder. Brain evoked potential can evaluate the visual, auditory, somatosensory neuropathway, and the response of frontal, temporal, occipital lobe. We studied the usefulness of brain pvoked votential as a tool in the early diagnosis and treatment of sensory disorders in cerebral palsy. METHODS: We retrospectively reviewed the records of 86 cerebral palsy patients who were practiced brain evoked potential study in Chungnam National University Hospital from July, 1995 to June, 1999. We analyzed the visual, auditory, somatosensory evoked potential result and the correlations between the electroencephalography, radiologic brain imaging study and the brain evoked potential. RESULTS: 1) Clinical types of cerebral palsy were spastic type(85.0%), athetoid type(3.5%), mixed type(3.5%) and the remaining cases did not manifest any one the types above. 2) Abnormal evoked potential fingings were 25 cases(29.4%) in visual evoked potential, 16 cases(18.8%) in auditory evoked potential, 28 cases(37.8%) in median nerve evoked potential, 39 cases(52.7%) in tibial nerve evoked potential. 3) Electroencephalography, radiologic brain imaging study manifested no statistically significant correlations with the brain evoked potential result(P>0.05). CONCLUSION: As a noninnvasive neurophysiologic study, Brain evoked potential is a useful method predicting neurologic developmental progress and helpful to early diagnosis of sensory disorder in cerebral palsy patients.
Subject(s)
Humans , Brain , Cerebral Palsy , Early Diagnosis , Electroencephalography , Evoked Potentials , Evoked Potentials, Auditory , Evoked Potentials, Somatosensory , Evoked Potentials, Visual , Intellectual Disability , Median Nerve , Muscle Spasticity , Neuroimaging , Occipital Lobe , Posture , Retrospective Studies , Sensation Disorders , Tibial NerveABSTRACT
Vincristine is a chemotherapeutic agent used in the treatment of various neoplastic diseases. Accidental intrathecal vincristine instillation is a fatal error. We report a case of a 6-year-old boy with acute lymphocytic leukemia who suffered an accidental intrathecal vincristine administration. He suffered a progressive ascending chemical meningoencephalitis followed by coma, and died at the 5th day after injection. Several previous reports of intrathecal vincristine instillation are reviewed.