Recurrent Seizures Following Focal Motor Status Epilepticus in a Patient with Non-Ketotic Hyperglycemia and Acute Cerebral Infarction

Lee, Jung Ju; Jung, Jinwoong; Kang, Kyusik; Park, Jong‐Moo; HyeEun, Shin; Kwon, Ohyun; Kim, Byung-Kun

doi:10.14581/jer.14007

Cited by 4 publications

(2 citation statements)

References 16 publications

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“…[4][5][6]13 There are some reports of cases with combined factors, that is, epileptogenic lesions along with metabolic disturbances. 10,[13][14][15] Metabolic disturbances may act as acute triggering factors for status epilepticus, lowering the seizure threshold in the epileptogenic area. Most patients respond well to antiepileptic drugs, but some are intractable to antiepileptic drugs and need other treatment, such as resective surgery.…”

Section: Discussionmentioning

confidence: 99%

Three Cases of Aphasic Status Epilepticus: Clinical and Electrographic Characteristics

Lee

Park

Kang

et al. 2021

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Aphasic status epilepticus (ASE) is unusual and has clinical characteristics similar to those of other disorders. Herein, we report 3 cases of ASE. A left-handed man (patient 1) showed continuous aphasia after the administration of flumazenil. He had underlying alcoholic liver cirrhosis and traumatic brain lesions in the right hemisphere. Electroencephalography (EEG) revealed periodic epileptiform discharges in the right frontotemporal area, which were intervened by rhythmic activity with spatiotemporal evolutions. A right-handed woman (patient 2) showed recurrent aphasia. Blood tests revealed a high blood glucose level (546 mg/dL) and high serum osmolality (309 mMol/L). Her EEG showed rhythmic activity in the left frontotemporal area with spatiotemporal evolutions on a normal background rhythm. She became seizure-free after the administration of an antiepileptic drug and strict glucose regulation. A right-handed woman (patient 3) developed subacute aphasia a week before hospital admission. She had a gradual decline of cognition 1 year before. Her EEG showed intermittent quasi-rhythmic fast activity in the frontotemporal area bilaterally, with fluctuating frequency and amplitude. The patient became seizure-free after the administration of an antiepileptic drug. Brain single-photon emission tomography performed after seizure control showed decreased perfusion in the left frontotemporal area. After discharge, her cognitive function gradually declined to a severe state of dementia. ASE can be caused by diverse etiologies; it is usually caused by cerebral lesions and less frequently by non-lesional etiologies or degenerative disorders. Adequate treatment of underlying disorders and seizures is critical for curing the symptoms of ASE.

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Section: Discussionmentioning

confidence: 99%

Three Cases of Aphasic Status Epilepticus: Clinical and Electrographic Characteristics

Lee

Park

Kang

et al. 2021

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“…These higher levels of glucose in the CNS result in a glucose neurotoxicity that can lead to abnormal brain function and trauma (Tomlinson and Gardiner, 2008). It is known that both type I and II diabetes increase seizure susceptibility especially in non-ketogenic hyperglycemic diabetic patients due to metabolic disturbances such as mild hyperosmolality (Lee et al, 2014). Moreover, it is well documented that people with diabetes are at greater risk for stroke when compared to non-diabetics and elevated blood glucose concentrations during stroke are associated with poor outcome (Desilles et al, 2013).…”

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confidence: 99%

Hyperglycemia reduces functional expression of astrocytic Kir4.1 channels and glial glutamate uptake

et al. 2015

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Diabetics are at risk for a number of serious health complications including an increased incidence of epilepsy and poorer recovery after ischemic stroke. Astrocytes play a critical role in protecting neurons by maintaining extracellular homeostasis and preventing neurotoxicity through glutamate uptake and potassium buffering. These functions are aided by the presence of potassium channels, such as Kir4.1 inwardly rectifying potassium channels, in the membranes of astrocytic glial cells. The purpose of the present study was to determine if hyperglycemia alters Kir4.1 potassium channel expression and homeostatic functions of astrocytes. We used q-PCR, Western blot, patch-clamp electrophysiology studying voltage and potassium step responses and a colorimetric glutamate clearance assay to assess Kir4.1 channel levels and homeostatic functions of astrocytes grown in normal and high glucose conditions. We found that astrocytes grown in high glucose (25 mM) had an approximately 50% reduction in Kir4.1 mRNA and protein expression as compared with those grown in normal glucose (5 mM). These reductions occurred within 4 to 7 days of exposure to hyperglycemia, whereas reversal occurred between 7 to 14 days after return to normal glucose. The decrease in functional Kir channels in the astrocytic membrane was confirmed using barium to block Kir channels. In the presence of 100 μm barium, the currents recorded from astrocytes in response to voltage steps were reduced by 45%. Furthermore, inward currents induced by stepping extracellular [K+]o from 3 to 10 mM (reflecting potassium uptake) were 50% reduced in astrocytes grown in high glucose. In addition, glutamate clearance by astrocytes grown in high glucose was significantly impaired. Taken together, our results suggest that down-regulation of astrocytic Kir4.1 channels by elevated glucose may contribute to the underlying pathophysiology of diabetes-induced CNS disorders and contribute to the poor prognosis after stroke.

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Modulation of Glucose Availability and Effects of Hypo- and Hyperglycemia on Status Epilepticus: What We Do Not Know Yet?

et al. 2020

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Recurrent Seizures Following Focal Motor Status Epilepticus in a Patient with Non-Ketotic Hyperglycemia and Acute Cerebral Infarction

Cited by 4 publications

References 16 publications

Three Cases of Aphasic Status Epilepticus: Clinical and Electrographic Characteristics

Three Cases of Aphasic Status Epilepticus: Clinical and Electrographic Characteristics

Hyperglycemia reduces functional expression of astrocytic Kir4.1 channels and glial glutamate uptake

Modulation of Glucose Availability and Effects of Hypo- and Hyperglycemia on Status Epilepticus: What We Do Not Know Yet?

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