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Hemodynamic changes in simple partial epilepsy: A functional MRI study

To the Editor: We read with interest the article by Krings et al.1 describing functional MRI changes related to acute partial seizures. We report reversible focal MRI cortical enhancement associated with a similar clinical circumstance. A 77-year-old woman with no history of epilepsy had several episodes of loss of speech lasting 1 to 2 minutes each that occurred 2 hours before examination. She remained alert during these episodes, but had word-finding difficulty. She denied focal weakness, but complained of right facial twitching. She denied body jerking, incontinence, or alteration of consciousness. Two hours later, a neurologic examination performed during an acute event showed rhythmic right facial twitching with a nonfluent aphasia lasting a few minutes, consistent with a partial seizure. Afterwards, her speech was normal but she had a right facial droop and pronator drift, consistent with a postictal Todd’s paralysis. She was placed on phenytoin. MRI less than 30 minutes after the last seizure revealed an area of gyriform enhancement of the left dorsolateral frontal cortex and leptomeningeal/pial surface (figure). Noncontrast T1-weighted and T2-weighted images (T2WI) were normal (not shown). EEG the next day showed bifrontal intermittent rhythmic delta activity. No further seizures were noted and the neurologic examination was normal. Contrast-enhanced MRI 3 months later during clinical stability was normal (see the figure). Nineteen months after the last seizure, the EEG showed bilaterally independent temporal slowing. Transient neuroimaging lesions may occur in association with acute seizures, both during ictus and in the immediate postictal period.2-10 This is a case of transient focal cortical enhancement on MRI associated with acute seizures that extends the data of Krings et al. that epileptic activity leads to changes in cerebral hemodynamics. These transient events must be considered when interpreting MRI in patients with acute seizure. MRI may show hyperintensity on T2WI and parenchymal gadolinium enhancement in the seizure focus, sometimes extending to the surrounding brain.2,5,7 Lesions usually disappear with control of seizures.1,8,9 With an unclear clinical picture, such as unwitnessed seizures with postictal confusion or Todd’s paralysis, awareness of these phenomena of transient neuroimaging changes can help avoid potentially unnecessary diagnostic procedures in ruling out other causes such as stroke, tumor, or infection. Follow-up imaging may be helpful to exclude an underlying cause of the seizures or MRI lesion when clinically indicated.10 The pathophysiology of the MRI findings in our case is speculative. Krings et al.1 have shown sequential activation and deactivation during acute seizures that most likely relate to alterations in cerebral blood flow and metabolism in the epileptogenic and symptomatogenic zones. Functional nuclear imaging shows hyperperfusion during acute seizures followed by hypoperfusion.7 One hypothesis maintains that excitatory amino acids cause hypermetabolism/hyperperfusion on PET and SPECT scans and increased blood flow on MR and angiography.6 In the current case, the area of enhancement correlated well with the patient’s clinical seizure semiology, indicating that this was the site of the seizure. Thus, this transient cortical enhancement most likely reflects increased metabolic activity due to neuronal excitation with subsequent hyperemia and blood–brain barrier alterations at the seizure focus.