Nonketotic hyperglycemia (NKH)–related seizures are not uncommon in clinical practice. Diabetic cases with focal brain insults, especially in the frontal motor centers, are more susceptible. With the aid of ictal and postictal single-photon emission computed tomography (SPECT) with technetium hexamethylpropylene amine oxime (HMPAO), we report a case of inadequately controlled diabetes without focal brain lesions first seen as NKH-related epilepsia partialis continua (EPC) with unilateral parietal origin.


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A 62-year-old man with diabetes mellitus used oral hypoglycemic agents for years for glucose control. However, poor compliance had been noted for several months. He started to have intermittent incoherent speech and self-talking episodes 1 month before admission. No special attention was paid until he had cluster bouts of paroxysmal alteration of consciousness with right-sided deviation of the eyeballs and the head, along with right facial twitching. Each episode lasted for 1–2 min. Postictal confusion followed. No previous history of epilepsy was known.

He was sent to our hospital, and the laboratory data showed blood glucose of 350 mg/dl; osmolarity, 290 mOsm/L; sodium, 134 mM, without ketone bodies. The HbA1C was 13%. Phenytoin (PHT) and insulin were prescribed. After the initial treatment, the blood glucose level was ∼250 mg/dl. However, the seizures persisted, although they decreased in frequency. Computed tomography and magnetic resonance imaging (MRI) studies of the brain revealed no abnormality. The electroencephalography (EEG) showed sharp waves at the left posterior head region involving the temporal and parietooccipital areas. The ictal SPECT showed hyperperfusion at the left posterior parietal area (Fig. 1).


Figure 1. Hyperperfusion at left posterior parietal area during ictal single-photon emission computed tomography (arrow).

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Under the impression of NKH-related EPC (complex partial status epilepticus), more rigorous glucose control with insulin was implemented, and PHT was discontinued. After 1 week, blood glucose was ∼150 mg/dl. The follow-up EEG was normal, and no more clinical seizures were observed. The postictal SPECT 20 days later demonstrated a normal perfusion pattern. However, 2 years later, recurrent EPC with frequent alteration of consciousness and incoherent speech episodes developed in the presence of NKH (blood glucose, 335 mg/dl; osmolarity, 298 mOsm/L; sodium, 134 mM; HbA1C, 13.8%). Aggressive glucose control was again implemented. No AED was prescribed. After blood glucose had been controlled (∼160 mg/dl), he was discharged without seizures. No further episodes of seizures occurred during the succeeding 24-month follow-up.


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In adult diabetic patients, hyperglycemia may precipitate seizures, especially those of focal origin (1–3). Extracellular glucose itself was suggested as a proconvulsant in a recent experimental study, even without a previous focal lesion (3). Among patients with NKH and EPC reported in medical literature, the reported ictal manifestations suggest a predilection to affect the frontal lobe motor centers, unilaterally or bilaterally (1).

One report of ictal manifestation with occipital origin was noted (2). However, many are not identified with a definite focal structural origin either by computed tomography or MRI studies (4). Our observations indicate that the seizure foci may originate in the parietal area. The seizures developing only in worsened hyperglycemia, and the recurrence of seizures in the setting of NKH helped establish the neuroendocrine syndrome. To our knowledge, this is the first report regarding NKH-related EPC with a parietal origin with a documented SPECT study.

Regional cerebral blood flow in the epileptic focus increases by ≤300% during a seizure (5). HMPAO tracers permit the study of ictal and delayed postictal change with more accuracy. With the aid of ictal SPECT, correct identification of the seizure focus is achieved in >70–90% of cases (6,7). Absence of a causative structural lesion on MRI might lead to an improper diagnosis, extensive monitoring, and unnecessary long-term treatment. We think that an ictal and a postictal SPECT would benefit in these situations.

In parietal lobe seizures, clinical semiology is more difficult to study (8). In contrast to occipital lobe seizures, parietal lobe seizures usually produce few reliable findings for localization. Rasmussen (9) reported that most patients had either unilateral motor or sensory phenomena. Extraparietal seizure spread to the occipital, mesial temporal, or frontal lobe regions was frequently reported. Ictal SPECT may show posterior parietal hyperperfusion when the seizures are of the psychoparetic type (8).

In experiments, diabetic hyperglycemic animals have been demonstrated to have more severe neuronal necrosis in the parietal cortex than do normoglycemic animals (10). Attention to parietal lobe semiology should not be overlooked when NKH-related seizures are encountered.

In conclusion, EPC that is related to NKH might have a unilateral parietal origin, which is best viewed from ictal and postictal SPECT studies.


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  • 1
    Brick JF, Gutrecht JA, Ringel RA. Reflex epilepsy and nonketotic hyperglycemia in the elderly: a specific neuroendocrine syndrome. Neurology 1989;39: 3949.
  • 2
    Harden CL, Rosenbaum DH, Daras M. Hyperglycemia presenting with occipital seizures. Epilepsia 1991;32: 21520.
  • 3
    Schwechter EM, Veliskova J, Velisek L. Correlation between extracellular glucose and seizure susceptibility in adult rats. Ann Neurol 2003;53: 91101.
  • 4
    Singh BM, Strobos RJ. Epilepsia partialis continua associated with nonketotic hyperglycemia: clinical and biochemical profile of 21 patients. Ann Neurol 1980;8: 15560.
  • 5
    Engel J Jr, Kuhl DE, Phelps ME, et al. Local cerebral metabolism during partial seizures. Neurology 1983;133: 40013.
  • 6
    Newton MR, Austin MC, Chan JG, et al. Ictal SPECT using technetium-99m-HMPAO: methods for rapid preparation and optimal deployment of tracer during spontaneous seizures. J Nucl Med 1993;34: 66670.
  • 7
    Hwang SI, Kim JH, Park SW, et al. Comparative analysis of MR imaging, positron emission tomography, and ictal single-photon emission CT in patients with neocortical epilepsy. AJNR Am J Neuroradiol 2001;22: 93746.
  • 8
    Ho SS, Berkovic SF, Newton MR, et al. Parietal lobe epilepsy: clinical features and seizure localization by ictal SPECT. Neurology 1994;44: 227784.
  • 9
    Salanova V, Andermann F, Rasmussen T, et al. Parietal lobe epilepsy: clinical manifestations and outcome in 82 patients treated surgically between 1929 and 1988. Brain 1995;118: 60727.
  • 10
    Li C, Li PA, He QP, et al. Effects of streptozotocin-induced hyperglycemia on brain damage following transient ischemia. Neurobiol Dis 1998;5: 11728.