Tonic-Clonic Activity at Subarachnoid Hemorrhage Onset: Impact on Complications and Outcome

Objective: Tonic-clonic activity (TCA) at onset complicates 3% to 21% of cases of subarachnoid hemorrhage (SAH). The impact of onset TCA on in-hospital complications, including seizures, remains unclear. One study associated onset TCA with poor clinical outcome at 6 weeks after SAH, but to our knowledge no other studies have confirmed this relationship. This study aims to assess the impact of onset TCA on in-hospital complications, poor functional outcome, mortality, and epilepsy at 3 months. Methods: Analysis of a prospective study cohort of 1479 SAH patients admitted to Columbia University Medical Center between 1996 and 2012. TCA within 6 hours of hemorrhage onset was identified based on accounts of emergency care providers or family witnesses. Results: TCA at onset was described in 170 patients (11%). Patients with onset TCA were younger (P = 0.002), presented more often with poor clinical grade (55% vs. 26%, P<0.001) and had larger amounts of cisternal, intraventricular, and intracerebral blood than those without onset TCA (all, P<0.001). After adjusting for known confounders, onset TCA was significantly associated with in-hospital seizures (OR 3.80, 95%-CI: 2.43–5.96, P<0.001), in-hospital pneumonia (OR 1.56, 95%-CI: 1.06–2.31, p = 0.02), and delayed cerebral ischemia (OR 1.77, 95%-CI: 1.21–2.58, P = 0.003). At 3 months, however, onset TCA was not associated with poor functional outcome, mortality, and epilepsy after adjusting for age, admission clinical grade, and cisternal blood volume. Conclusions: Onset TCA is not a rare event as it complicates 11% of cases of SAH. New and clinically relevant findings are the association of onset TCA with in-hospital seizures, pneumonia and delayed cerebral ischemia. Despite the increased risk of in-hospital complications, onset TCA is not associated with disability, mortality, and epilepsy at 3 months

Causal Structure of Brain Physiology after Brain Injury from Subarachnoid Hemorrhage

High frequency physiologic data are routinely generated for intensive care patients. While massive amounts of data make it difficult for clinicians to extract meaningful signals, these data could provide insight into the state of critically ill patients and guide interventions. We develop uniquely customized computational methods to uncover the causal structure within systemic and brain physiologic measures recorded in a neurological intensive care unit after subarachnoid hemorrhage. While the data have many missing values, poor signal-to-noise ratio, and are composed from a heterogeneous patient population, our advanced imputation and causal inference techniques enable physiologic models to be learned for individuals. Our analyses confirm that complex physiologic relationships including demand and supply of oxygen underlie brain oxygen measurements and that mechanisms for brain swelling early after injury may differ from those that develop in a delayed fashion. These inference methods will enable wider use of ICU data to understand patient physiology

Supplemental Material, Supp_Table_1_final - Prognostic Value of the Neurological Examination in Cardiac Arrest Patients After Therapeutic Hypothermia

<p>Supplemental Material, Supp_Table_1_final for Prognostic Value of the Neurological Examination in Cardiac Arrest Patients After Therapeutic Hypothermia by Elizabeth A. Matthews, Jessica Magid-Bernstein, Evie Sobczak, Angela Velazquez, Cristina Maria Falo, Soojin Park, Jan Claassen, and Sachin Agarwal in The Neurohospitalist</p

Baseline features of included SAH patients with multimodality monitoring compared to SAH patients without.

<p>Baseline features of included SAH patients with multimodality monitoring compared to SAH patients without.</p

Causal relationships between systemic physiologic parameters during the initial post injury phase (days 0 to 3).

<p>Cardiovascular (top row, left panel), pulse contour analysis (top row, middle panel), respiratory (top row, right panel), and cardio-respiratory (bottom row) relationships.</p

Causal relationships between systemic physiologic parameters during the second post injury phase (days 4 to 7).

<p>Cardiovascular (top row, left panel), pulse contour analysis (top row, middle panel), respiratory (top row, right panel), and cardio-respiratory (bottom row) relationships.</p

Directionality and effect size of causal inferences.

<p>Data is displayed for intracranial pressure (ICP), partial brain tissue oxygenation (pbtO2), and total brain water content (TW%; each dot signifies one patient; red dots indicated a decrease and a black dot an increase in the variable of interest).</p

Data characteristics of the collected physiologic measures at two different time periods following brain hemorrhage (grey bars 0 to 3 days, black bars 4 to 7 days after SAH).

<p>Standard deviation represented as percent of the mean (top panel), average percent of time that a specific variable was available from the overall monitoring time (middle), and KPSS test illustrating the percent of patients that have non-stationary data for a variable (bottom panel; calculated as the ratio of the number of patients that have p-val < = 0.01) divided by total number of patients that have the variable.</p

Brain physiology phase 2: Relationships within brain monitoring parameters (top row) and with systemic parameters (bottom row).

<p>Brain physiology phase 2: Relationships within brain monitoring parameters (top row) and with systemic parameters (bottom row).</p

Systemic and brain physiologic parameters.

<p>Systemic and brain physiologic parameters.</p