• Safety and Health at Work
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• v.3 no.4
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• pp.243-256
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• 2012

This article schematically reviews the clinical features, diagnostic approaches to, and toxicological implications of toxic encephalopathy. The review will focus on the most significant occupational causes of toxic encephalopathy. Chronic toxic encephalopathy, cerebellar syndrome, parkinsonism, and vascular encephalopathy are commonly encountered clinical syndromes of toxic encephalopathy. Few neurotoxins cause patients to present with pathognomonic neurological syndromes. The symptoms and signs of toxic encephalopathy may be mimicked by many psychiatric, metabolic, inflammatory, neoplastic, and degenerative diseases of the nervous system. Thus, the importance of good history-taking that considers exposure and a comprehensive neurological examination cannot be overemphasized in the diagnosis of toxic encephalopathy. Neuropsychological testing and neuroimaging typically play ancillary roles. The recognition of toxic encephalopathy is important because the correct diagnosis of occupational disease can prevent others (e.g., workers at the same worksite) from further harm by reducing their exposure to the toxin, and also often provides some indication of prognosis. Physicians must therefore be aware of the typical signs and symptoms of toxic encephalopathy, and close collaborations between neurologists and occupational physicians are needed to determine whether neurological disorders are related to occupational neurotoxin exposure.

• Journal of Korean Neurosurgical Society
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• v.52 no.3
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• pp.273-276
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• 2012

Metronidazole-induced encephalopathy is a very rare complication of the long standing use of metronidazole. The encephalopathy is bilateral and symmetric in nature. We report on the magnetic resonance imaging (MRI) and clinical course of metronidazole-induced encephalopathy in a 60-year-old female with a persistent anaerobic brain abscess after draining of the abscess. After 3 months of metronidazole administration, the patient complained of dysarthria, tingling sense of all extremities, and left hemiparesis. MRI revealed symmetric hyperintensity lesions in medulla, pons, dentate nuclei of cerebellum, and splenium of corpus callosum, all of which represent typical findings of metronidazole-induced encephalopathy. In addition, asymmetric lesions in midbrain, thalamus, putamen and cerebral subcortical white matter were noted. The patient recovered after discontinuation of metronidazole and the remaining abscess was successfully treated with meropenem and levofloxacine.

• Journal of Yeungnam Medical Science
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• v.21 no.1
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• pp.91-95
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• 2004

Wernicke's encephalopathy is an acute-onset illness characterized by mental confusion, ataxia and ophthalmoplegia due to a thiamine deficiency. Immediate administration of thiamine prevents progression of the disease and reverses brain lesions. We have experienced a case of Wernicke's encephalopathy associated with hyperemesis gravidarum. As Wernicke's encephalopathy is mostly associated with chronic alcoholism, the possibility of Wernicke's encephalopathy may be ignored in young women. We emphasize the need for thiamine supplementation in the patient requiring intravenous alimentation such as hyperemesis gravidarum.

• Childhood Kidney Diseases
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• v.8 no.1
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• pp.51-56
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• 2004

Hypertensive encephalopathy is an acute neurologic syndrome that occurs in association with abrupt and marked elevation of blood pressure and is characterized by headache, vomiting, seizure, visual disturbances and altered mental status. Hypertensive encephalopathy is most commonly associated with renal disease in children, including acute glomerulonephritis, reno-vascular hypertension, and end-stage renal disease. Hypertensive encephalopathy associated with nephrolithiasis has not been reported. We have experienced a 10-year-old boy with hypertensive encephalopathy associated with ureteral stone.

• Annals of Clinical Neurophysiology
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• v.16 no.1
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• pp.27-31
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• 2014

Thiamine deficiency can cause peripheral polyneuropathy and Wernicke's encephalopathy. Wernicke's encephalopathy is characterized by ataxia, ophthalmoplegia, nystagmus, and confusion, and typically presents acute and rapidly progressive course, whereas peripheral neuropathy associated with thiamine deficiency manifests chronic and slowly progressive one. However, acute and rapidly progressive axonal polyneuropathy combined with Wernicke's encephalopathy is quite rare and unusual. Here, we describe a patient with Wernicke's encephalopathy who presented with acute bilateral axonal neuropathy.

• The Journal of Pediatrics of Korean Medicine
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• v.18 no.2
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• pp.143-160
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• 2004

Objective: There were few reports on the treatment of Hypoxic ischemic encephalopathy. We treated a hypoxic ischemic encephalopathic patient after accident with Oriental medical approach, and get a significant result. this treatment shows the possibility of healing Hypoxic ischemic encephalopathy, So we are reporting that case. Method : The acupuncture, herb medication. rehabilitation therapy was applied for treting patient's chife symptom(involuntary movement, dystonia, aphasia, dysuria, constipation) Results : 1. Generally patients with Hypoxic ischemic encephalopathy show language impairment and cognition disorder for several weeks to months. After coma stage, first they recover consciousness but have various degree of confusional mentality, visual agnosia, extrapyramidal stiffness and motor disturbance. 2. Consciousness loss in acute stage of Hypoxic ischemic encephalopathy can be considered as Mental Confusion due to Phlegm(Dammisimgyu) in veiw point of Oriental medicine. 3. After oriental medical treatment, patient's chief symptoms were improved. Conclusion: We treated a hypoxic ischemic encephalopathic patient with Oriental medical approach and patient's chief symptoms were improved. this treatment shows the possibility of healing Hypoxic ischemic encephalopathy.

• Clinical and Experimental Pediatrics
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• v.64 no.12
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• pp.608-618
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• 2021

Hypoxic-ischemic encephalopathy (HIE) is the most common cause of neonatal encephalopathy with a global incidence of approximately 1 to 8 per 1,000 live births. Neonatal encephalopathy can cause neurodevelopmental and cognitive impairments in survivors of hypoxic-ischemic insults with and without functional motor deficits. Normal neurodevelopmental outcomes in early childhood do not preclude cognitive and behavioral difficulties in late childhood and adolescence because cognitive functions are not yet fully developed at this early age. Therapeutic hypothermia has been shown to significantly reduced death and severe disabilities in term newborns with HIE. However, children treated with hypothermia therapy remain at risk for cognitive impairments and follow-up is necessary throughout late childhood and adolescence. Novel adjunctive neuroprotective therapies combined with therapeutic hypothermia may enhance the survival and neurodevelopmental outcomes of infants with HIE. The extent and severity of brain injury on magnetic resonance imaging might predict neurodevelopmental outcomes and lead to targeted interven tions in children with a history of neonatal encephalopathy. We provide a summary of the long-term cognitive outcomes in late childhood and adolescence in children with a history of HIE and the association between pattern of brain injury and neurodevelopmental outcomes.

• Annals of Clinical Neurophysiology
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• v.16 no.1
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• pp.15-20
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• 2014

Background: Triphasic waves are one of the electroencephalographic patterns that can be usually seen in metabolic encephalopathy. The aim of this study is to compare the clinical and electrophysiologic profiles between patients with and without triphasic waves in metabolic encephalopathy, and reassess the significance of triphasic waves in metabolic encephalopathy. Methods: We recruited 127 patients with metabolic encephalopathy, who were admitted to our hospital. We divided these admitted patients into two groups; those with and without triphasic waves. We analyzed the difference of duration of hospitalization, mortality rate during admission, Glasgow Coma Scale, severity of electroencephalographic alteration, and presence of acute symptomatic seizures between these two groups. Results: Of the 127 patients with metabolic encephalopathy, we excluded 67 patients who did not have EEG, and 60 patients finally met the inclusion criteria for this study. Patients with triphasic waves had more severe electroencephalographic alterations, lower Glasgow Coma Scale, and more acute symptomatic seizures than those without triphasic waves. After adjusting the clinical variables, Glasgow Coma Scale and acute symptomatic seizures were only significantly different between patients with and without triphasic waves. Conclusions: We demonstrated that patients with triphasic waves in metabolic encephalopathy had more significant impairment of the brain function.

• Investigative Magnetic Resonance Imaging
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• v.21 no.2
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• pp.106-108
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• 2017

The perfusion change in acute symptomatic hypoglycemic encephalopathy (ASHE) is not well known. We present the perfusion-weighted imaging of a patient with ASHE. The area of diffusion-weighted imaging abnormalities and adjacent normal-appearing white matter showed increased cerebral blood volume and flow, and shortening of time-to-peak.

• Childhood Kidney Diseases
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• v.1 no.1
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• pp.73-78
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• 1997

The hypertensive encephalopathy is one of sudden convulsive cause in patients with acute post-streptococcal glomerulonephritis, but commonly, after the episode we can observe only mild to moderately hypertension in APSGN at ER. So these remains some question of what causes the convulsion in patients with APSGN. In this article, we report 3 cases of convulsion in APSGN with only moderate hypertension, the etiology of which proved to be due to hypertensive encephalopathy by the brain MRI. We believe that the brain MRI is a very useful test to diagnose the etiology of convulsion in APSGN and if brain edema in occipital lobe is detected by brain MRI, the convulsion would be due to hypertensive encephalopathy and the prognosis will be very good.