Focal Status Epilepticus 9 Years After Brain Abscess
Clinical History & Presentation
Mr B, age 17 years with medical history notable for a prior brain abscess presented with new-onset seizures. At age 9 years, he had developed headaches and was found to have a right parietal brain abscess (Figure 1), which was resected with no complications or residual neurologic deficits. Mr B subsequently developed typically and was a very athletic child, participating in competitive baseball.
At age 17, Mr B fell while skiing as a result of what he described as his legs getting caught and tripping. He reported no loss of consciousness or head injury during the fall, and he had continued skiing for the remainder of the day without issues. Later that evening, however, he developed numbness and tingling in his left upper and lower extremities. The paresthesia occurred intermittently but with increased intensity over the next 2 days, and he eventually experienced a brief generalized tonic clonic seizure.
Diagnostic Studies
Mr B presented to a local emergency department where he had a normal neurologic examination, including findings of symmetric full strength and sensation to touch and temperature. A head CT and MRI brain showed his prior abscess resection cavity without acute findings of hemorrhage or other lesions (Figure 2). He was discharged with treatment of levetiracetam 500 mg twice daily. Over the next 2 days, he continued experiencing intermittent paresthesia of his left face, arm, and leg and had 3 additional brief (under 30 seconds) generalized tonic clonic seizures. Mr B was admitted for further work-up and treatment.
In the hospital, Mr B’s dose of levetiracetam was increased to 1000 mg twice daily. VideoEEG showed focal electroclinical and subclinical seizures occurring 2 to 12 times per hour, all arising from the midline parietal region with early spread to the right parietal occipital region (Figure 3). Clinical seizures were characterized by left-sided paresthesia.
Diagnosis
He was diagnosed with localization-related focal epilepsy, as all seizures appeared to originate from the right parietal brain abscess resection site.
Treatment and Follow-Up
Mr B received lorazepam and levetiracetam loads, with no improvement in seizure frequency. He then received lacosamide and valproic acid loads and was started on standing valproic acid, also with very little change in seizure frequency. On day 2 of admission, he received a load of fosphenytoin resulting in decreased seizure frequency and was started on standing phenytoin 2.5 mg/kg twice daily. He was also treated with 1 gram of methylprednisolone for 3 days, in consideration of the drug-resistant nature of his seizures. Valproic acid was discontinued for lack of efficacy.
After initiation of fosphenytonin and methylprednisolone, electrographic seizures stopped, but Mr B continued having events of more mild “tingling” and “numbness” in the left face, arm, and leg, with an electrographic correlate of fast activity in the midparietal region. It was thought this represented more subtle seizures that were difficult to detect on scalp EEG. These events stopped over the next 2 days with no electrographic or clinical seizures occurring at the time of discharge.
Neurosurgery was consulted because Mr B’s seizures were drug resistant and focal, suggesting he might be a good surgical candidate. After improvement with phenytoin and methylprednisolone, surgical options were not pursued, however. Resection of his seizure focus would be considered in the future if his seizures became difficult to control on medications.
Mr B opted to continue phenytoin at time of discharge in addition to levetiracetam because of concern for return of seizures. He presented for follow-up 1 month after discharge with no further seizures and was successfully weaned off phenytoin. He remains seizure-free on levetiracetam monotherapy at the time of this report.
Background
We present a case of localization-related focal epilepsy in an adolescent with a history of brain abscess resection. Prior studies have reported the incidence of epilepsy after brain abscess as 18.5% to 35.2%. Most persons with brain abscesses have acute symptomatic seizures at time of diagnosis.1
In a retrospective study of 205 individuals followed after brain abscess for 22 years, 17% had acute symptomatic seizures, 6.4% had delayed seizures, and none developed seizure more than 3 years after bacterial brain abscess.2 The case presented here is atypical in that 9 years elapsed between brain abscess and the first seizure. Considering the prolonged time lapse, we hypothesized Mr B had an area of gliosis from his prior brain abscess that was somehow irritated after a fall. Alternatively, he may have had a first focal seizure with paresthesia causing the fall while skiing, and never suffered a head injury.
Diagnosis
Paresthesia is a very common semiology for seizures originating from the parietal lobe. In a large review of 46 people with lesional symptomatic parietal lobe epilepsy, 72.2% reported tingling or numbness of the extremities.3 Parietal lobe seizures should be included in the differential diagnosis of a person with recurrent, intermittent, and stereotyped tingling or numbness involving on side of the body. It is also important to recognize the limitations of scalp EEG. In this case many of the focal sensory seizures appeared only as fast activity, which may be not have been recognized as a seizure had we not also captured more definitive seizures originating from the same location.
Treatment
Initial treatment with first-line antiseizure medications (ASMs) was not effective, requiring escalation to less-frequently used ASMs. Multiple studies have found fosphenytoin to be as effective as levetiracetam and valproic acid in treating status epilepticus.4-6 In this case, after lack of response to lorazepam, levetiracetam, valproic acid, and lacosamide, fosphenytoin was used, with a subsequent decrease in seizures. Fosphenytoin, however, was started at the same time as the methylprednisolone, so it is difficult to say with certainty which agent was most effective.
Although not a first-line medication, corticosteroids have been evaluated as a possible treatment for many types of epilepsies.7 A methylprednisolone pulse dose was effective in decreasing seizure frequency and epileptic discharges in 11 children with epileptic encephalopathy, even after steroid course was complete.8 A monthly pulse dose of methylprednisolone for 3 months was also found to be effective in decreasing seizure frequency by more than 50% in 12 of 14 people with drug-resistant epilepsy in a small case series from Mexico.9 Other smaller case reports have described success using steroids as an abortive for refractory seizures or status epilepticus.10 There are many theories regarding mechanism of action of steroids in aborting seizures, including: 1) γ-aminobutyric acid (GABA) receptor-mediated anticonvulsant effects; 2) systemic effects via the hypothalamic-pituitary-adrenal axis suppressing corticotropin-releasing hormone to decrease neuronal excitability; 3) effects on enzyme function; 4) modification of electrolyte concentrations, reducing cerebral water content; and 5) immunomodulatory or anti-inflammatory effects.8-10 In Mr B’s case, we were suspicious for focal inflammation secondary to the skiing fall possibly triggering seizures, and thus, trialed methylprednisolone with good effect.
Summary
Seizures are a common sequela of brain abscess, and although most are acute and symptomatic, some progress to epilepsy. Typically, when epilepsy develops, it presents within the first 3 years after brain abscess. We present a unique case of late-onset, lesional epilepsy localizing to a prior brain abscess resection site. The seizures started in setting of a fall and were possibly triggered by inflammation secondary to mild head trauma. After no response to typical ASMs, seizure control was achieved with methylprednisolone and fosphenytoin.
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