Role of Bedside Multimodality Monitoring in the Detection of Cerebral Vasospasm Following Subarachnoid Hemorrhage.

BACKGROUND: Detection of delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (aSAH) in patients with a poor clinical exam is challenging. Brain tissue oxygen tension monitoring (PbtO2) and cerebral microdialysis (CMD) can detect ischemia and metabolic derangements. Our aim was to evaluate efficacy of these modalities in real-time detection of DCI. METHODS: All patients with aSAH who underwent with multimodality monitoring (MMM) with PbtO2 and/or CMD between the years of 2013 and 2015 at our institution were retrospectively studied. Mean PbTO2, lactate to pyruvate ratio (LPR), and glucose over the 24-h period prior to each angiogram for evaluation and treatment of vasospasm were correlated to the extent of vasospasm observed in the hemisphere with the monitors. The average measurements were also compared in the setting of presence and absence of angiographically significant vasospasm. RESULTS: A total of ten patients with aSAH who underwent MMM were identified. PbtO2 decline correlates with severity of proximal vasospasm (r = -0.66). PbtO2 was significantly lower in the setting of vasospasm (17.6 vs. 25.8, p = 0.003), but LPR (34.5 vs. 26.8, p = 0.1) and glucose (0.8 vs. 1.1, p = 0.6) were not significantly different. CONCLUSION: Proximal vasospasm after aSAH is associated with MMM indicator of tissue ischemia and/or metabolic derangement. PbtO2 and CMD help in real-time detection and management of DCI.

Early seizures and temporal lobe trauma predict post-traumatic epilepsy: A longitudinal study.

OBJECTIVE: Injury severity after traumatic brain injury (TBI) is a well-established risk factor for the development of post-traumatic epilepsy (PTE). However, whether lesion location influences the susceptibility of seizures and development of PTE longitudinally has yet to be defined. We hypothesized that lesion location, specifically in the temporal lobe, would be associated with an increased incidence of both early seizures and PTE. As secondary analysis measures, we assessed the degree of brain atrophy and functional recovery, and performed a between-group analysis, comparing patients who developed PTE with those who did not develop PTE. METHODS: We assessed early seizure incidence (n = 90) and longitudinal development of PTE (n = 46) in a prospective convenience sample of patients with moderate-severe TBI. Acutely, patients were monitored with prospective cEEG and a high-resolution Magnetic Resonance Imaging (MRI) scan for lesion location classification. Chronically, patients underwent a high-resolution MRI, clinical assessment, and were longitudinally monitored for development of epilepsy for a minimum of 2 years post-injury. RESULTS: Early seizures, occurring within the first week post-injury, occurred in 26.7% of the patients (n = 90). Within the cohort of subjects who had evidence of early seizures (n = 24), 75% had a hemorrhagic temporal lobe injury on admission. For longitudinal analyses (n = 46), 45.7% of patients developed PTE within a minimum of 2 years post-injury. Within the cohort of subjects who developed PTE (n = 21), 85.7% had a hemorrhagic temporal lobe injury on admission and 38.1% had early (convulsive or non-convulsive) seizures on cEEG monitoring during their acute ICU stay. In a between-group analysis, patients with PTE (n = 21) were more likely than patients who did not develop PTE (n = 25) to have a hemorrhagic temporal lobe injury (p < 0.001), worse functional recovery (p = 0.003), and greater temporal lobe atrophy (p = 0.029). CONCLUSION: Our results indicate that in a cohort of patients with a moderate-severe TBI, 1) lesion location specificity (e.g. the temporal lobe) is related to both a high incidence of early seizures and longitudinal development of PTE, 2) early seizures, whether convulsive or non-convulsive in nature, are associated with an increased risk for PTE development, and 3) patients who develop PTE have greater chronic temporal lobe atrophy and worse functional outcomes, compared to those who do not develop PTE, despite matched injury severity characteristics. This study provides the foundation for a future prospective study focused on elucidating the mechanisms and risk factors for epileptogenesis.

The epilepsy bioinformatics study for anti-epileptogenic therapy (EpiBioS4Rx) clinical biomarker: Study design and protocol.

The Epilepsy Bioinformatics Study for Anti-epileptogenic Therapy (EpiBioS4Rx) is a longitudinal prospective observational study funded by the National Institute of Health (NIH) to discover and validate observational biomarkers of epileptogenesis after traumatic brain injury (TBI). A multidisciplinary approach has been incorporated to investigate acute electrical, neuroanatomical, and blood biomarkers after TBI that may predict the development of post-traumatic epilepsy (PTE). We plan to enroll 300 moderate-severe TBI patients with a frontal and/or temporal lobe hemorrhagic contusion. Acute evaluation with blood, imaging and electroencephalographic monitoring will be performed and then patients will be tracked for 2 years to determine the incidence of PTE. Validation of selected biomarkers that are discovered in planned animal models will be a principal feature of this work. Specific hypotheses regarding the discovery of biomarkers have been set forth in this study. An international cohort of 13 centers spanning 2 continents will be developed to facilitate this study, and for future interventional studies.

Substance P signalling in primary motor cortex facilitates motor learning in rats.

Among the genes that are up-regulated in response to a reaching training in rats, Tachykinin 1 (Tac1)-a gene that encodes the neuropeptide Substance P (Sub P)-shows an especially strong expression. Using Real-Time RT-PCR, a detailed time-course of Tac1 expression could be defined: a significant peak occurs 7 hours after training ended at the first and second training session, whereas no up-regulation could be detected at a later time-point (sixth training session). To assess the physiological role of Sub P during movement acquisition, microinjections into the primary motor cortex (M1) contralateral to the trained paw were performed. When Sub P was injected before the first three sessions of a reaching training, effectiveness of motor learning became significantly increased. Injections at a time-point when rats already knew the task (i.e. training session ten and eleven) had no effect on reaching performance. Sub P injections did not influence the improvement of performance within a single training session, but retention of performance between sessions became strengthened at a very early stage (i.e. between baseline-training and first training session). Thus, Sub P facilitates motor learning in the very early phase of skill acquisition by supporting memory consolidation. In line with these findings, learning related expression of the precursor Tac1 occurs at early but not at later time-points during reaching training.

Holocord spinal epidural abscess.

Spinal epidural abscess is rare in infants and leads to major permanent neurological deficits if the condition is left untreated. Holocord epidural abscess is extremely rare. We report a patient with methicillin-resistant Staphylococcus aureus septicemia presenting with pneumonia, retroperitoneal abscess, and epidural abscess. A 7-month-old previously healthy girl presented with fever, irritability, tachypnea for 4 days and decreased movement of the right lower limb for 1 day. Magnetic resonance imaging of the spine demonstrated an extensive epidural abscess from second cervical to fifth lumbar vertebrae without osteomyelitis or discitis. The epidural abscess was treated with intravenous antibiotics for 6 weeks. At 3 months follow-up, no neurological deficits were present. Only a few case reports of holocord epidural abscess in children have been published. We present a case of conservatively treated holocord spinal abscess in an infant.