Case Presentation: A 75-year-old male presented to the Emergency Room for progressive altered mental status, speech difficulty, and generalized weakness over several days. He also reported a couple days of polyuria and polydipsia. Past medical history included Non-Insulin Dependent Diabetes Mellitus and Hypertension. Initial vital signs were within normal limits. General physical exam was unremarkable, but neurological exam revealed intermittent episodes of expressive aphasia. During episodes, the patient remained awake and alert but had severe expressive deficit with marked word-finding and naming difficulty. Cranial nerve exam was normal, and there were no motor or sensory abnormalities. Admission labs were remarkable for a glucose level of 676 mg/dL, a bicarbonate of 18 mmol/L with an anion gap of 17 mmol/L, and a sodium of 128 mmol/L. Due to aphasia, a code stroke was initially activated in the ED. CT head was negative for an acute hemorrhage. The neurology team had low suspicion for an acute ischemic stroke, attributing symptoms to metabolic derangements. Subsequently, the patient was admitted to the hospitalist service for further management of diabetic ketoacidosis (DKA). The patient received fluids and was started on an insulin regimen with improvement of metabolic abnormalities. The patient, however, continued to experience periodic episodes of aphasia. Further work-up included an MRI brain which showed no acute stroke. CT angiography of the head and neck showed no evidence of flow limiting stenosis. Neurology was re-consulted and recommended EEG and lumbar puncture to complete evaluation. Lumbar puncture was unremarkable, but EEG showed focal neuronal slowing in the left temporal lobe correlating with speech arrest. This was thought to represent a focal seizure originating from the left temporal lobe. Based on these findings, the patient was loaded with Keppra and started on a maintenance Keppra dose. Shortly after initiating Keppra, the patient began experiencing fewer and shorter episodes of aphasia. EEG showed resolution of the seizure focus. At two month follow-up, the patient had ran out of Keppra a week prior to the appointment but denied any recurrent episodes of aphasia since hospital discharge. It is hypothesized that DKA may have facilitated focal seizure activity, requiring prompt control of diabetes in addition to anti-epileptic medications.
Discussion: Episodic aphasia is characterized by temporary impairment of expression or comprehension of written or spoken language. The etiology of episodic aphasia is associated with transient injury or dysfunction within the language centers of the brain. This can be caused by a number of neurologic conditions including transient ischemic attacks, migraines with aura, infectious or metabolic conditions (1,2). In rare cases, periodic episodes of aphasia have also been reported as a manifestation of focal epileptic seizures (3-5). We have presented such a case that was seen on the medicine wards. The patient in our case was initially presumed to have aphasia associated with metabolic encephalopathy. However, his case demonstrates the importance of keeping a broad differential for aphasia that includes focal seizures.
Conclusions: Although a rare cause of isolated episodic aphasia, focal seizures should be considered in patients without other neurological, metabolic, or infectious etiology to explain aphasia. Early diagnosis and treatment of focal seizures can prevent further seizure progression and harmful long-term neurologic deficits.