Short Communications Suppression of Serum Prolactin Levels after Sports Concussion with Prompt Resolution Upon Independent Clinical Assessment To Permit Return-to-Play Michael F. La Fountaine, 1–3 Michita Toda, 4 Anthony Testa, 5 and William A. Bauman 3,6 Abstract A significant outflow of neurotransmitters and metabolites with associated enhanced cortical excitation occurs after concussive head trauma. Cellular changes in the acute post-injury period cannot be observed directly in humans, and as such, require indirect evidence from systems sufficiently sensitive to central neuronal cellular excitation. Dopamine is a neurotransmitter with numerous targets in the central and peripheral nervous system. Changes to central dopaminergic tone result in reciprocal responses to the level of serum prolactin (PRL). Thus, a concussion may lead to abnormal dopaminergic tone, resulting in dynamic perturbations in the serum PRL concentration. To determine the effect of concussion on serum PRL concentrations, venipuncture was performed in the morning in four male intercollegiate athletes (age, 20 – 1 years; height, 71 – 5 inches; weight, 174 – 21 pounds) within 48 h of concussion and again at 7 and 14 days post-injury. Serum PRL concentrations for each visit were categorized by quartile within the normal range. In all athletes, serum PRL concentrations increased from the lower quartiles in samples obtained closer to the time of injury to the higher quartiles at 14 days post-injury. These serum PRL changes accompanied the resolution of symptoms and the clinical decision to permit return-to-play. It may be postulated that transient augmentation of central dopaminergic tone resulted in inhibition of PRL secretion early after concussion and that disinhibition of PRL release occurred when central dopami- nergic tone subsequently returned to baseline levels. This novel observation provides evidence for dopaminergic dys- function after concussion that may be tracked by determination of serum PRL levels. Key words: adult brain injury; head trauma; hypopituitarism C oncussion is a complex pathophysiological process affecting the brain as a result of traumatic biomechanical forces. 1 Ac- cording to Walker’s explanation of the physiological basis of concussion, a concussive insult to the brain results in transient, widespread perturbations of cortical membranes that ultimately favor neuronal excitation. 2 This description has since been char- acterized as that of a marked outflow of neurometabolites and ex- citatory neurotransmitters whose concentrations do not resolve to pre-injury levels for several hours, if not days following the event. 3 These cellular changes in the acute post-injury period are unob- tainable by direct observation in humans and as such, require in- direct evidence from end-organs or systems that are sufficiently sensitive to these pathological central neuronal membrane changes. A meta-analysis determined a pooled prevalence of anterior pituitary deficiency of 27.5% following traumatic brain injury, 4 and a recent report in retired athletes demonstrated that a more signif- icant history (i.e., increased frequency) of concussive head trauma was associated with growth hormone (GH) failure in later life. 5 Overt manifestations and clinical syndromes of pituitary dysfunction have been demonstrated to occur in the post-concussive and chronic mild traumatic brain injury (mTBI) state; limited evidence for pi- tuitary dysfunction after single, multiple, or persistent concussion injury is highlighted by reports of reduced pituitary volume, 6 GH deficiency 7 and diabetes insipidus. 8 The premise to consider, then, is that if GH deficiency represents one of the more common patho- logical endpoints in the function of the hypothalamic-pituitary axis 1 School of Health and Medical Sciences, 2 Institute for Advanced Study of Rehabilitation and Sports Science, 5 Department of Athletics, Seton Hall University, South Orange, New Jersey. 3 VA Rehabilitation, Research, and Development National Center of Excellence for the Medical Consequences of Spinal Cord Injury, James J. Peters VA Medical Center, Bronx, New York. 4 Department of Athletics, University of Wisconsin-Madison, Madison, Wisconsin. 6 Departments of Medicine and Rehabilitation Medicine, Icahn School of Medicine at Mount Sinai, New York, New York. JOURNAL OF NEUROTRAUMA XX:1–3 (Month XX, 2015) ª Mary Ann Liebert, Inc. DOI: 10.1089/neu.2015.3968 1