RESUMO
BACKGROUND: To date, it has been assumed that acute seizures which arise in the context of sudden, spontaneous, atraumatic, acute, arterial dissections (SAAADs) are downstream consequences of the dissections driven by syncope or focal brain lesions (FBLs). As this subject has not been formally investigated, likely due to its rarity, we reviewed published case reports (CRs) to examine the veracity of this assumption. METHODS: We included CR describing patients diagnosed with both acute seizures and arterial dissections in order to ascertain the temporal sequence between acute seizures and typical SAAAD symptoms. In addition, we quantified the frequency with which hypotension, bradycardia, and FBLs are associated with acute seizures in such cases. RESULTS: We found 45 published CRs, six (13.3%) of which involved traumatic arterial dissections and 39 (86.7%) which involved SAAADs. Of the latter, twenty-one (53.8%) described seizures that followed typical SAAAD symptoms (SAFO), and 18 (46.2%) that preceded all such symptoms (SATO). On average, blood pressure and heart rate for both groups exceeded the normal range. Of the CRs that included magnetic resonance imaging (MRI) scans, 8 (100%) SAFO but only 6 (54.5%) SATO patients demonstrated FBLs (p<0.03). A conspicuously large fraction of SATO patients had known epilepsy compared with SAFO patients, (33.3% vs 4.8%; p<0.02). In addition, SATO epilepsy patients' seizure semiologies frequently resembled their breakthrough seizures (BTS). The most common SAAAD associated with acute seizures was aortic dissection (AoD; 17/45; 37.8%). Nine CRs (20%) described patients who died soon after presentation, seven of which were associated with AoDs, including one epilepsy patient. Six of these seven AoDs occurred in patients who suffered from chronic hypertension (CHTN). All five deaths in the SATO group followed first ever seizures (FES) [four AoDs and one coronary artery dissection (CoAD)]. CONCLUSION: Acute seizures arising in the context of SAAADs are not necessarily associated with hypotension or FBLs, and frequently appear to precede the associated dissections. These results suggest that seizures could act as triggers for SAAADs. In addition, sudden unexpected atraumatic acute arterial dissection-related death after seizure (SUADAS) might be a distinct cause of sudden death in epilepsy patients.
RESUMO
We report a 60-year-old woman who presented to the emergency department after experiencing a witnessed unknown onset bilateral tonic clonic seizure (GTCS) that culminated in cardiac arrest. A neurology consultant uncovered a years-long history of frequent episodic staring followed by confusion and expressive aphasia, which strongly suggested that she suffered from epilepsy. Thus, her cardiac arrest and subsequent resuscitation met criteria for a near-sudden unexpected death in epilepsy (SUDEP) diagnosis. Serial bloodwork demonstrated transient troponin I elevations and leukocytoses, while a brain MRI revealed global cerebral anoxic injury and a small acute right cerebellar ischemic infarction. A review of her medical record uncovered a hospitalization sixteen months earlier for a likely GTCS whose workup showed similar troponin I elevations and leukocytoses, and surprisingly, a different small acute right cerebellar ischemic infarction in the same vascular territory. To our knowledge, this is the first report of subcortical ischemic infarctions occurring concurrently with GTCSs in a near-SUDEP patient. Aside from illustrating the key role of inpatient neurologists in the diagnosis of near-SUDEP, this manuscript discusses the potential significance of postictal ischemic infarctions, transient asymptomatic troponin elevations, and transient non-infectious leukocytoses in epilepsy patients with cardiovascular risk factors.