Michael B. Keough, Albert M. Isaacs, Geberth Urbaneja, Jarred Dronyk, Andrew P. Lapointe and Mark G. Hamilton
Acute low-pressure hydrocephalus (ALPH) is characterized by clinical manifestations of an apparent raised intracranial pressure (ICP) and ventriculomegaly despite measured ICP that is below the expected range (i.e., typically ≤ 5 cm H2O). ALPH is often refractory to standard hydrocephalus intervention protocols and the ICP paradox commonly leads to delayed diagnosis. The aim of this study was to characterize ALPH and develop an algorithm to facilitate diagnosis and management for patients with ALPH.
EMBASE, MEDLINE, and Google Scholar databases were searched for ALPH cases from its first description in 1994 until 2019. Cases that met inclusion criteria were pooled with cases managed at the authors’ institution. Patient characteristics, presenting signs/symptoms, precipitating factors, temporizing interventions, definitive treatment, and patient outcomes were recorded.
There were 195 patients identified, with 42 local and 153 from the literature review (53 pediatric patients and 142 adults). Decreased level of consciousness was the predominant clinical sign. The most common etiologies of hydrocephalus were neoplasm and hemorrhage. While the majority of ALPH occurred spontaneously, 39% of pediatric patients had previously undergone a lumbar puncture. Prior to ALPH diagnosis, 92% of pediatric and 39% of adult patients had a ventricular shunt in situ. The most common temporizing intervention was subatmospheric CSF drainage. The majority of patients underwent a shunt insertion/revision or endoscopic third ventriculostomy as definitive ALPH treatment. Although the mortality rate was 11%, 83% of pediatric and 49% of adult patients returned to their pre-ALPH neurological functional status after definitive treatment. Outcomes were related to both the severity of the underlying neurosurgical disease causing the hydrocephalus and the efficacy of ALPH treatment.
ALPH is an underrecognized variant phenotype of hydrocephalus that is associated with multiple etiologies and can be challenging to treat as it frequently does not initially respond to standard strategies of CSF shunting. With early recognition, ALPH can be effectively managed. A management algorithm is provided as a guide for this purpose.
Jacob R. Joseph, Jennylee S. Swallow, Kylene Willsey, Andrew P. Lapointe, Shokoufeh Khalatbari, Frederick K. Korley, Mark E. Oppenlander, Paul Park, Nicholas J. Szerlip and Steven P. Broglio
This prospective observational cohort study of high-school football athletes was performed to determine if high-acceleration head impacts (HHIs) that do not result in clinically diagnosed concussion still lead to increases in serum levels of biomarkers indicating traumatic brain injury (TBI) in asymptomatic athletes and to determine the longitudinal profile of these biomarkers over the course of the football season.
Sixteen varsity high-school football athletes underwent baseline neurocognitive testing and blood sampling for the biomarkers tau, ubiquitin C-terminal hydrolase L1 (UCH-L1), neurofilament light protein (NF-L), glial fibrillary acidic protein (GFAP), and spectrin breakdown products (SBDPs). All athletes wore helmet-based accelerometers to measure and record head impact data during all practices and games. At various time points during the season, 6 of these athletes met the criteria for HHI (linear acceleration > 95g and rotational acceleration > 3760 rad/sec); in these athletes a second blood sample was drawn at the end of the athletic event during which the HHI occurred. Five athletes who did not meet the criteria for HHI underwent repeat blood sampling following the final game of the season. In a separate analysis, all athletes who did not receive a diagnosis of concussion during the season (n = 12) underwent repeat neurocognitive testing and blood sampling after the end of the season.
Total tau levels increased 492.6% ± 109.8% from baseline to postsession values in athletes who received an HHI, compared with 164% ± 35% in athletes who did not receive an HHI (p = 0.03). Similarly, UCH-L1 levels increased 738.2% ± 163.3% in athletes following an HHI, compared with 237.7% ± 71.9% in athletes in whom there was no HHI (p = 0.03). At the end of the season, researchers found that tau levels had increased 0.6 ± 0.2 pg/ml (p = 0.003) and UCH-L1 levels had increased 144.3 ± 56 pg/ml (p = 0.002). No significant elevations in serum NF-L, GFAP, or SBDPs were seen between baseline and end-of–athletic event or end-of-season sampling (for all, p > 0.05).
In this pilot study on asymptomatic football athletes, an HHI was associated with increased markers of neuronal (UCH-L1) and axonal (tau) injury when compared with values in control athletes. These same markers were also increased in nonconcussed athletes following the football season.