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Introduction The incidence of electrographic seizures after non-traumatic intraparenchymal hemorrhage (IPH) ranges from 1.7% to 31%. It is unclear if the risk of seizures or hyperexcitable patterns (HEPs: any rhythmic delta activity except generalized, any periodic discharges, or any spike-wave pattern, using ACNS criteria) for deep IPH is similar to lobar, subarachnoid and subdural hemorrhages. We hypothesized that the incidence of seizures or hyperexcitable patterns (SZ or HEPs) in deep IPH is lower than reported, but thalamic involvement may confer higher risk due to its role in physiologic and pathologic rhythmic activity, such as sleep spindles and generalized spike wave discharges. Methods On retrospective review, 45 patients had deep IPH (defined as IPH not involving cortex/juxtacortical regions other than the insula (analyzed separately), with or without intraventricular hemorrhage IVH) and underwent continuous EEG (cEEG) between 1/2013 and 12/2016. Patients with involvement of cortex, subarachnoid or subdural areas were excluded. Age, sex, prior history of epilepsy, clinical seizure at ictus, anti-seizure drugs (ASDs), sedative infusions during EEG and surgical interventions such as ventriculostomy (EVD) or decompressive hemicraniectomy (DHC) were reviewed. The cEEG closest to admission was reviewed for seizures, HEPs, and generalized rhythmic delta activity (GRDA). The head CT in closest proximity to the index cEEG was reviewed for hematoma volume, thalamic involvement and insular involvement. Results Two of 45 patients had SZ, 7/45 had HEPs, 1/45 had both and a total of 8/45 had SZ or HEPs. Of the HEPs , LRDA was seen in 4/8, LPDs in 2/8, both LPDs and LRDA in 1/8. Of those with the lateralized HEPs, 4/7 were contralateral to IPH, 1/7 (14.2%) were bilateral and 2/7 were ipsilateral. Of the 5/7 with HEPs contralateral to the IPH, 2 had an EVD ipsilateral to the HEPs. Patients with SZ or HEPs had significantly higher hematoma volume compared to patients who did not have SZ or HEPs (32.7 ± 19.4 vs 15.4 ± 17.7, p = 0.02). Patients who underwent surgery (DHC/EVD or both) had higher incidence of HEPs or SZ compared to those who did not (7/23, 30.4% vs 1/22, 4.5%, p = 0.047). DHC was associated with significantly higher risk of SZ or HEPs (4/4, 100% vs 4/41, 9.8%, p Conclusion Risk of SZ or HEPs with deep IPH ± IVH was 17.7% and correlated with mean hematoma volume and DHC. The, risk in the absence of a surgical intervention was low (1/22, 4.5%, vs 7/23, 30.4% p = 0.047). Thalamic involvement did not correlate with SZ or HEPs in this small cohort of patients with deep IPH.

Introduction Refractory status epilepticus (RSE) is associated with a high mortality and morbidity. Due to ketamine’s desirable hemodynamic profile, its use in RSE has been noted to minimize the use of vasopressors. For other uses however, ketamine has been associated with hypotension, specifically in patients with depleted catecholamine stores evidenced by an elevated shock index. We report a case of myocardial depression with the use of ketamine for RSE. Methods A 64 year old, 65 kg man with a medical history significant for “weak heart” (presumed HFpEF given home medication list which only included carvedilol), chronic kidney disease, remote left middle cerebral artery stroke and resultant focal epilepsy, maintained on renally dosed levetiracetam was brought to the ER after three seizures. He received midazolam and levetiracetam 15 mg/kg, which transiently improved his mentation. He continued to have recurrent focal clonic seizures with impaired consciousness (8–11 seizures/hour lasting 2–3 min each). He was loaded with two doses of valproate 30 mg/kg followed by 40 mg/kg and levetiracetam 15 mg/kg. He also received carbamazepine 400 mg, clobazam 40 mg once and fosphenytoin 20 mg/kg phenytoin equivalent. He was subsequently intubated and midazolam infusion was initiated. Patient developed hypotension requiring norepinephrine infusion. Shock index prior to initiation of vasopressors ranged between 0.45–0.63 on a beta-blocker. Due to lack of sustained response to aforementioned anti-seizure drugs, ketamine was started (1.5 mg/kg bolus followed by an infusion uptitrated to 2 mg/kg/h), which resulted in resolution of status epilepticus but coincided with the need for escalating doses of norepinephrine and the addition of vasopressin. Midazolam infusion was discontinued. Echocardiogram (ECHO) on day 4 showed an ejection fraction (EF) of 38% with apical hypokinesis. Troponin T was elevated at 0.11 ng/ml with a BNP of 7050 pg/ml (up from 762 pg/ml a month prior). Results Ketamine was weaned off on hospital day 7 with improvement of his BP and discontinuation of vasopressors (within hours of ketamine discontinuation). Troponins normalized by day 7 (but in the setting of dialysis). Repeat ECHO on day 14 showed improved EF of 50–55% with persistent apical hypokinesis. Patient was discharged near his baseline to an acute rehabilitation facility on phenytoin and levetiracetam. Conclusion This case suggests that ketamine can be associated with cardiodepression as opposed to another cause (ie Takotsubo’s cardiomyopathy), given the temporal association of worsening and improving hemodynamics and cardiac function with the initiation and discontinuation of ketamine, respectively. Further studies are needed to understand the potential hemodynamic effect of ketamine in refractory status epilepticus, particularly in patients with underlying CHF who are often on beta blockers.