Aphasic status epilepticus caused by nonketotic hyperglycemia without hyperosmolality

Key points.

• Nonketotic hyperglycemia (NKH) can cause focal seizures and aphasic status epilepticus (ASE) even without meeting hyperosmolar hyperglycemic state (HHS) criteria.

• Acute aphasia is not always stroke; early EEG is essential when MRI and vascular imaging do not explain the deficit.

• Prompt metabolic correction with insulin, with short‐term antiseizure medication when needed, can rapidly reverse both clinical symptoms and EEG abnormalities.

Nonketotic hyperglycemia (NKH) may provoke focal seizures in the absence of ketoacidosis or marked hyperosmolality. ¹ , ² , ³ , ⁴ We report a 52‐year‐old right‐handed man with untreated diabetes who presented with progressive aphasia and agitation, initially mimicking acute stroke. MRI revealed no structural lesion explaining aphasia (Figure 1A–C). ⁵ , ⁶ EEG showed recurrent 2–3 Hz rhythmic delta activity with spikes spreading from the left temporal region to the entire brain, consistent with aphasic status epilepticus (ASE) within the Salzburg criteria framework (Figure 2A–C). Serum glucose was markedly elevated (525 mg/dL), whereas serum osmolality remained below the threshold for hyperosmolar hyperglycemic state (295 mOsm/kg). Both the clinical symptoms and EEG abnormalities resolved promptly after correction of hyperglycemia with insulin and adjunctive antiseizure medication, which were subsequently discontinued. ⁷ NKH‐related ASE should be recognized as a reversible metabolic cause of nonconvulsive status epilepticus that can masquerade as cortical stroke. Early EEG assessment and prompt metabolic correction are essential to avoid diagnostic delay and ensure full recovery.

FIGURE 1.

Brain MRI on admission. Diffusion‐weighted imaging shows subtle restricted diffusion in the right corona radiata without corresponding FLAIR abnormalities. Bilateral middle cerebellar peduncles exhibit DWI hyperintensity with ADC isointensity. No lesion explains aphasia, and MR angiography demonstrates no vascular pathology.

FIGURE 2.

EEG findings. EEG demonstrates recurrent 2–3 Hz rhythmic delta activity with spikes over the left temporal region, compatible with aphasic status epilepticus. Bipolar montage shows partial phase reversal at T3. Interictal EEG after treatment reveals disappearance of rhythmic ictal activity.

CONFLICT OF INTEREST STATEMENT

None.

Test yourself.

1. Which of the following clinical features best supports the diagnosis of aphasic status epilepticus (ASE) rather than a post‐ictal state?

   1. History of prior epilepsy.
   2. Presence of motor weakness.
   3. Aphasia persisting unusually prolonged or fluctuating.
   4. Hyperosmolarity above 320 mOsm/kg.
   5. Ketone‐positive urine test.
2. Which EEG finding is most consistent with the diagnosis of aphasic status epilepticus localized to the left temporal lobe?

   1. Diffuse background slowing.
   2. Frontal alpha rhythm.
   3. 2–3 Hz rhythmic delta activity over the left temporal region.
   4. High‐voltage beta activity in the occipital region.
   5. Absence of any epileptiform activity.
3. What is the most appropriate initial treatment approach for aphasic status epilepticus caused by nonketotic hyperglycemia (NKH)?

   1. Thrombolytic therapy.
   2. Long‐term antipsychotic medication.
   3. Immediate initiation of antiepileptic drugs and insulin therapy.
   4. Oral hypoglycemic agents only.
   5. Surgical resection of epileptic focus.

Answers may be found in the supporting information .

Supporting information

Data S1.

Table S1.

Data S2.

DATA AVAILABILITY STATEMENT

The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.