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Year : 2015  |  Volume : 10  |  Issue : 4  |  Page : 374-375

Occipital lobe seizures: Rare hyperglycemic sequelae of type 1 diabetes mellitus

1 Department of Family Medicine, Lakeshore Hospital and Research Centre, Ernakulam, Kerala, India
2 Lakeshore Hospital and Research Centre, Ernakulam, Kerala, India

Date of Web Publication20-Jan-2016

Correspondence Address:
Muhammed Jasim Abdul Jalal
Department of Family Medicine, Lakeshore Hospital and Research Centre, Nettoor P. O., Maradu, NH 47, Bye Pass, Ernakulam - 682 040, Kerala
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1817-1745.174449

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A 15-year-old boy presented with osmotic symptoms and photopsia. He had short-term memory impairment, visual hallucinations, and headache. His random blood sugar was 474 mg/dl, HbA1c −9.4%, and glutamic acid decarboxylase −65 >2000 IU/ml. Magnetic resonance imaging brain and cerebrospinal fluid study were normal. Digital electroencephalography was suggestive of bilateral hemispheric occipital lobe seizures. He responded well to insulin and antiepileptic medications.

Keywords: Hyperglycemia, occipital lobe seizures, type 1 diabetes mellitus

How to cite this article:
Jalal MJ, Menon MK, Kumar K A, Gomez R. Occipital lobe seizures: Rare hyperglycemic sequelae of type 1 diabetes mellitus. J Pediatr Neurosci 2015;10:374-5

How to cite this URL:
Jalal MJ, Menon MK, Kumar K A, Gomez R. Occipital lobe seizures: Rare hyperglycemic sequelae of type 1 diabetes mellitus. J Pediatr Neurosci [serial online] 2015 [cited 2022 Jan 16];10:374-5. Available from: https://www.pediatricneurosciences.com/text.asp?2015/10/4/374/174449

   Introduction Top

Hyperglycemia has a wide variety of neurological manifestations [1] including visual hallucinations,[1] seizures,[1] choreoathetosis,[2] hemiballismus,[3] dysphagia,[3] somatosensory symptoms or headache [4] associated with nausea and vomiting, and severe cases of coma.[2],[3] While seizures associated with hypoglycemia are mainly generalized, seizures associated with hyperglycemia are usually focal in nature.[3],[4] Previous reports have described occipital seizures associated with hyperglycemia, although the descriptions are rare, and few of them have showed electroencephalographic (EEG) findings.[5]

We report the clinical presentation of a 15-year-old child with hyperglycemia who presented with focal occipital seizures which was confirmed by EEG.

   Case Report Top

A 15-year-old boy with 2 weeks duration of osmotic symptoms (polyuria, polydipsia, and weight loss) was diagnosed to have diabetic ketoacidosis and was on insulin infusion. (Random blood sugar - 474 mg/dl, urine ketones positive, arterial blood gas – metabolic acidosis). He experienced flashes of lights (photopsia), well-formed visual hallucinations, fearfulness, and headache. There were no tonic-clonic movements. On examination, he appeared confused and anxious. He was hyper alert with ideas of persecution. He had recent and immediate memory impairment without any focal neurological deficits. His HbA1c was 9.4% and glutamic acid decarboxylase-65 (GAD-65) IgG serum enzyme immunoassay was >2000 IU/ml (normal value - <10 IU/ml). Magnetic resonance imaging brain and cerebrospinal fluid study were normal. His EEG showed spike and waves arising from the right occipital region suggestive of occipital lobe seizures [Figure 1]. He improved with hydration and insulin and responded very well to clobazam.
Figure 1: Electroencephalographic showing spike and waves arising from the right occipital region suggestive of occipital lobe seizures

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   Discussion Top

Seizure types described in patients with hyperglycemia are diverse.[1] This includes epilepsia partialis continua, which is the most frequent type and simple or complex partial seizures. The less common recognized types are apnea, somatosensory symptoms, aphasia, and visual disturbance.[2] Of the two distinct patterns of hyperglycemia (ketotic and nonketotic), the nonketotic hyperglycemia is more commonly associated with seizures.[3] A potential explanation is that ketoacidosis decreases neuronal excitability by increasing the levels of gamma-amino-butyric-acid (GABA) via activation of GAD, increased cellular concentration of glutamic acid, and decreased GABA shunt.[4]

Other than changes in GABA, ATP sensitive potassium channels (KATP) have been recently shown to be important in hyperglycemia-induced seizures. KATP channels are well-known for their action in pancreatic cells, where an increase in intracellular ATP/ADP ratio leads to closure of the channels preventing potassium efflux leading to cell membrane depolarization and insulin secretion.[5] Recent evidence indicates that neurons (e.g., hippocampal and neocortical) also have KATP channels, and these channels are responsible for increasing neuronal excitability in hyperglycemic environment.[6]

Our patient had a variety of transient neurological symptoms including occipital seizures in the form of a headache, well-formed visual hallucinations, and memory impairment. All these symptoms are consistent with a global brain dysfunction related to hyperglycemia.[4] Well-formed visual hallucinations in this patient could be an equivalent of Todd's phenomena following occipital seizures.[4] Previous reports are consistent with the semiology of our patient. Wang et al.[7] discussed a patient with flickering red objects in the right visual field associated with complex visual hallucinations. Raghavendra et al.[8] and Lavin [9] reported the presence of visual hallucinations in nonketotic hyperglycemic hyperosmolar state.

Occipital seizures are a unique presentation of hyperglycemia with EEG showing sequential spikes, slowing, and attenuation.[5] The focal character of the seizures described during hyperglycemia has been reported consistently over the years. Focal seizures are common in nonketotic hyperglycemia.[5] They have an excellent prognosis when glucose levels get controlled.[5]

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Conflicts of interest

There are no conflicts of interest.

   References Top

Maccario M. Neurological dysfunction associated with nonketotic hyperglycemia. Arch Neurol 1968;19:525-34.  Back to cited text no. 1
Chung SJ, Lee JH, Lee SA, No YJ, Im JH, Lee MC. Co-occurrence of seizure and chorea in a patient with nonketotic hyperglycemia. Eur Neurol 2005;54:230-2.  Back to cited text no. 2
Stahlman GC, Auerbach PS, Strickland WG. Neurologic manifestations of non-ketotic hyperglycemia. J Tenn Med Assoc 1988;81:77-80.  Back to cited text no. 3
Guisado R, Arieff AI. Neurologic manifestations of diabetic comas: Correlation with biochemical alterations in the brain. Metabolism 1975;24:665-79.  Back to cited text no. 4
Harden CL, Rosenbaum DH, Daras M. Hyperglycemia presenting with occipital seizures. Epilepsia 1991;32:215-20.  Back to cited text no. 5
Miki T, Seino S. Roles of KATP channels as metabolic sensors in acute metabolic changes. J Mol Cell Cardiol 2005;38:917-25.  Back to cited text no. 6
Wang CP, Hsieh PF, Chen CC, Lin WY, Hu WH, Yang DY, et al. Hyperglycemia with occipital seizures: Images and visual evoked potentials. Epilepsia 2005;46:1140-4.  Back to cited text no. 7
Raghavendra S, Ashalatha R, Thomas SV, Kesavadas C. Focal neuronal loss, reversible subcortical focal T2 hypointensity in seizures with a nonketotic hyperglycemic hyperosmolar state. Neuroradiology 2007;49:299-305.  Back to cited text no. 8
Lavin PJ. Hyperglycemic hemianopia: A reversible complication of non-ketotic hyperglycemia. Neurology 2005;65:616-9.  Back to cited text no. 9


  [Figure 1]


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