Catecholamines and Paroxysmal Sympathetic Hyperactivity after Traumatic Brain Injury

Abstract

Paroxysmal sympathetic hyperactivity (PSH) affects a significant minority of people in the intensive care unit after severe traumatic brain injury. Systematic research has yet to elucidate or quantify the extent of the role of the catecholamines or adrenocortical and thyroid axis hormonal influences in the condition. Data were prospectively collected on 80 consecutive patients, 18 of whom developed clinical signs of PSH (22.5%). Catecholamine and hormonal data were collected sequentially at 4-h intervals or during and between episodes of PSH. Evaluated variables showed 200-300% increases in catecholamines and, to a lesser extent, adrenocortical hormones during paroxysms. The majority of PSH episodes (72%) were noted to be in response to an observable triggering event. These changes were not observed in subjects without PSH. These data go some way to explain why PSH produces adverse consequences in survivors of TBI with the condition.

Identification and Management of Paroxysmal Sympathetic Hyperactivity After Traumatic Brain Injury

“…In the neurotransmitter system, paroxysm derives from uncontrollable adrenergic outflow resulting in increased circulating catecholamine (34,35). Research suggests that levels of adrenocorticotropic hormone (ACTH), epinephrine (E), norepinephrine (NE), and dopamine (D) significantly increase during paroxysm, while NE and D decrease, rather than ACTH and E, during the intermittent period (4,17,36). This is because NE and D arise from increased excitability of the sympathetic nervous system, whereas E is almost exclusively derived from the adrenal medulla (37).…”

“…This is because NE and D arise from increased excitability of the sympathetic nervous system, whereas E is almost exclusively derived from the adrenal medulla (37). In general, there is about a 2-or 3-fold increase in catecholamine and an ∼40% increase in adrenocortical hormones in serum (17,38). Changes in the neurotransmitter system, driven by stimuli, highlight the importance of considering the triggering event in pathogenetic research.…”

“…For example, the manifestations of tachypnea and hyperthermia in PSH patients may empirically lead to a misdiagnosis of pulmonary embolism, the hyperthermia may mislead to a diagnosis of septicemia, and the posturing may mislead to an epileptic seizure. In addition, early identification of this condition is further hindered by the absence of a clear understanding of the pathophysiology of PSH, though the current consensus is that autonomic hyperactivity only concerns the sympathetic nervous system (3,4,16,17). Currently, the Paroxysmal Sympathetic Hyperactivity-Assessment Measure (PSH-AM) scale consists of two separate constructs: (1) the clinical feature scale (CFS), to identify the intensity of cardinal features, and (2) the diagnosis likelihood tool (DLT), to evaluate the likelihood of the presence of PSH, and is by far the best diagnosis tool for PSH in TBI patients (1,3).…”

Diagnosis and Management of Patients with Paroxysmal Sympathetic Hyperactivity following Acute Brain Injuries Using a Consensus-Based Diagnostic Tool: A Single Institutional Case Series

“…As mentioned in the initial report (Baguley et al 2014), non-specific nature of PSH-AM in the differential diagnoses may be a limitation of this diagnostic tool in the ICU settings; the present patients 2 and 6 required a few weeks to be diagnosed as PSH after onset of the PSH features due to the concomitant diseases that mimicked PSH. Although early diagnostic biomarkers of PSH have yet to be developed, a very recent study has shown that plasma catecholamine concentrations markedly increased during PSH episodes (Fernandez-Ortega et al 2017), indicating additional usefulness of catecholamine levels for early diagnosis of this disorder. More recently, an observational cohort study of traumatic brain injury patients with impaired consciousness (GCS score ≤ 12) has shown that early fever might be an indication of autonomic dysfunction; among the clinical feature scale items of PSH-AM (Table 1), higher temperature scores within 3 days after ICU admission were associated with the development of PSH, indicating that early fever may be a herald of PSH following severe traumatic brain injury (Hinson et al 2017).…”

Paroxysmal Sympathetic Hyperactivity

“…2,7,23 Each episode has a rapid and often sudden onset. Most episodes are triggered by external stimulation, 24 but some may occur without an apparent trigger. Several signs of sympathetic excess must occur simultaneously to support the diagnosis of PSH, but not all manifestations of sympathetic hyperactivity need to be present with each episode.…”