Be careful and always closely monitor your blood sugar,and its wise of you to also be on a low carb diet. The mission of the Epilepsy Foundation is to lead the fight to overcome the challenges of living with epilepsy and to accelerate therapies to stop seizures, find cures, and save lives. Skip to main content. Chat and Community Forums Closed Due to the popularity of social media, we have seen decreasing engagement on our forums and chat.
See all Posts in This Topic. Connect Get Social! Dilantin and high blood sugar. Medication Issues. I'm wondering if anyone else has had a similar experience with Dilantin or its generic The seizures pathogenesis caused by this disease is still controversial, as some people think that the main pathogenesis is the lack of insulin. Among the patients, insulin levels are sufficient to inhibit the free fatty acid metabolism and the subsequent ketoacidosis, but not enough to transport glucose into the cells [ 9 ].
High blood glucose levels increase the levels of urine glucose, causing osmotic diuresis effect and progressive dehydration, which would in turn increase the incidence of this disease.
Specific mechanisms also include: 1 osmotic changes. Hyperglycemia causes significant and rapid increase of intracellular osmotic pressure, leading to nerve cell dehydration, and changes in enzyme activity and brain cell energy metabolism. Membrane ion pump function is impaired, causing the loss of intracellular potassium and the subsequent sodium accumulation, which destroys the membrane potential and the stability of cell depolarization, ultimately resulting in seizures [ 4 ].
Citric acid cycle is inhibited in vivo in the patients with this disease, whereas GABA metabolism is increased, causing the increased brain energy consumption, and the reduced seizure threshold [ 10 ]. In contrast, seizures are less frequent in ketoacidosis patients, as ketosis acidosis increases intracellular activities of glutamate and tryptophan decarboxylase, leading to the increased content of brain inhibitory neurotransmitter GABA.
GABA is related to the rapid changes of synaptic sensitivities by binding to the neurons, which then increases the permeability of chloride ions. Under such conditions, the membrane potential is maintained at a stable resting potential level and the excitatory synaptic reactivities are weakened so that the epilepsy is prevented. Because of the diabetic hyperglycemia, plasma fibrinogen significantly increases, red blood cell and platelet aggregate, and blood is in a hypercoagulable state.
Such cells are sensitive to the metabolic disorders, high blood glucose condition especially is likely to cause seizures 4 immune abnormalities: the presence of glutamic acid decarboxylase autoantibodies in both type 1 diabetes and epilepsy.
Peltola, et al studied 51 cases of refractory epilepsy and found that these patients were autoantibody positive, with antibody titers similar to that in patients with type 1 diabetes, suggesting that intrinsic link might exist between them Their results supported the idea that immune dysfunction was involved in the hyperglycemia-related epilepsy [ 11 ] 5 studies suggest that NKH-related seizures might be linked to the brain barrier damage caused by long-term high blood glucose [ 12 ].
However, most of patients do not have seizures even if their blood glucose levels are high as the high levels of blood glucose are not the only factor for epilepsy. Other factors include individual health status and genetic factors [ 7 ]. In , Maccario et al. Tiamkao et al. When the seizure was under control, the average of blood sugar level was This paper reported eight cases with EEG showing spikes, slow waves, and scattered sharp slow waves.
In previously published reports, EEG results of patients with NKH-related epileptic seizures have shown normal waves or spikes, sharp slow or high amplitude slow waves [ 13 ]. Therefore, EEG is not very valuable in diagnosis of the disease. Imaging is not specific, either. This group mostly showed the normal imaging results, or age-related abnormalities such as old lacunar infarction, brain atrophy, and white matter demyelination, similar to most of the previous studies [ 5 , 6 ].
However, some studies [ 14 — 16 ] described a transient change in head MRI in a patient with NKH-induced seizures, that is, the reversible and Flair weighted hyperintense cortex, and low signal of white matter. He also displayed cytotoxic edema. Its mechanism was unclear. Possibly, the cortical ischemia seizures and angioedema, caused aggregation and deposition of iron radicals [ 14 — 16 ].
Some scholars believe that these changes result from the damages in blood-brain barrier caused by long-term high levels of blood sugar [ 12 ]. This article summarized the following clinical features of NKH-related epileptic seizures: 1 common in the elderly 2 with or without a previous history of diabetes and epilepsy 3. Seizures were always accompanied with a rapid rise in blood glucose. Plasma osmolality may be normal or slightly elevated, but not to the diagnostic criteria for diabetes hypertonic 4 urine ketone negative 5.
Seizures could not be effectively alleviated by antiepileptic drugs alone. Application of insulin to correct hyperglycemia and metabolic disorders ended the seizures 6 seizure-related lesions were not detected in the head imaging tests 7.
If blood glucose was under control, epilepsy did not occur any more. Analysis from the clinical effectiveness showed that the primary treatment for the NKH-related epileptic seizures included early, active, and rational rehydration and insulin hypoglycemic therapy, while closely monitoring blood glucose.
Such treatments are key to the success of salvage therapy among these patients. Phenytoin-induced insulin resistance can inhibit the release of insulin, and therefore increase the possibility of NKH-related seizures. Diazepam increase the opening frequency of GABA-mediated chloride ion channel.
Phenobarbital extended the start time of GABA-mediated chloride channel, by reducing the brain GABA levels among the patients with NKH-related seizures, Therefore, the stability and antiepileptic effects of phenobarbital and Diazepam decline [ 2 , 5 — 7 ] which explained why conventional antiepileptic drugs in those patients with epilepsy were not marketly effective. Antiepileptic drugs preferred include carbamazepine, clonazepam diazepam and other anti-epileptic drugs as they do not affect the levels of blood glucose.
Long-term use of anti-epileptic drugs is not necessary. If blood glucose and the seizures are well controlled, anti-epileptic drugs can be discontinued gradually.
Smooth phasing out the anti-epileptic drugs among the patients in the present study did not cause the recurrence. In short, NKH-related epileptic seizures has low occurrence rate in clinical practice. Epilepsy is often the first symptom. Compared with other diseases presenting clinical manifestations of epilepsy, they are not specific, and tend to be misdiagnosed.
Therefore, early recognition of this clinical syndrome and other seizure causes as well as early phase identification is critical, because the condition can be corrected by adjusting blood glucose level plus rapid rehydration. The disease pathogenesis is not entirely clear. In order to clarify the clinical features and pathogenesis of this disease, further research should be carried out in the imaging and electrophysiological aspects.
Nonketotic hyperglycemia-related epileptic seizures. Epilepsy Behav Case Rep. Focal seizures as a manifestation of hyperglycemia without ketoacidosis. A report of seven cases with review of thw literature.
Maccario M. Neurological dysfunction associated with nonketotic hyperglycemia. Arch Neurol. Nonketotic hyperglycemia and epilepsia partialis continua. Epileptic seizures in non-ketotic hyperglycemia. This was prescribed approximately six weeks earlier for right-sided focal seizures that were detected by electroencephalogram during a previous hospitalization for nonketotic hyperosmolar coma. No other medications were taken. The patient was treated with i. Her condition rapidly improved and insulin zinc suspension 35 units daily was prescribed on discharge.
0コメント