To identify the prevalence of head injuries and related symptoms among college athletes and examine knowledge of head injury consequences and behavioral tendencies of athletes in the presence of symptoms. Retrospective survey. A total of 461 male and female athletes beginning competitive play at the University of Akron (Akron, OH) during the years 1995 to 2001. Responses to survey questions were analyzed to determine the frequency of concussions and injury-related symptoms (eg, dizziness, headache, nausea or vomiting) in addition to behavioral responses in the presence of certain symptoms (eg, playing with headache, failure to report symptoms while playing). Written responses to queries regarding symptom knowledge were analyzed for thematic content and were used to identify deficiencies in signs and symptoms of concussion. Nearly 32% of all athletes had experienced a blow to the head causing dizziness, with over 1/4 confirming various somatic symptoms following a blow to the head (eg, seeing stars, nausea or vomiting, head pain). Continuing to play despite symptom presence was noted (eg, dizziness, 28.2%; headache, 30.4%), with 19.5% reporting a concussion diagnosis. Knowledge of head injury consequences was found to be deficient, with 56% indicating no knowledge of the possible consequences following a head injury. Of those providing responses, the majority reflected awareness of cognitive (eg, memory problems) and physical (eg, brain damage) consequences. A sizable number of athletes may enter collegiate play with a previous concussion diagnosis, and many more are likely to have experienced symptoms suggestive of a mild head injury. Of considerable concern is the tendency to play while symptomatic (eg, headache, dizziness) and the failure to report symptoms while playing—especially among football players (25.2%). The apparent deficiency in athlete knowledge of head injury consequences raises concern regarding athlete recognition of potentially problematic symptoms and represents an important area for educational intervention.
The role of the hippocampus and perirhinal-entorhinal cortex was examined in an olfactory discrimination paradigm. Small neurotoxic lesions of the hippocampus (21% tissue damage) yielded relatively unimpaired olfactory retention across brief (30 s), intermediate (approximately 5 min), and 24-hr delays, whereas impairments were noted at 5-day retention intervals. Larger hippocampal lesions (63% tissue damage) spared memory at intermediate delays, with no impact at 8-day retention intervals. Aspiration lesions directed at the perirhinal-entorhinal cortex produced a variable performance pattern, with impairments noted at intermediate, 24-hr, and 5-day delays. Results suggest the hippocampus is not specifically involved in retaining olfactory information, with additional consideration given to the relationship between lesion size and memory impairment.
Episodic memory is contextual memory linking temporal, spatial, emotional, and self-referential contexts. In this review, we placed particular emphasis on the emotional context because of its nexus with chronic pain effects. Psychological (e.g., depression, anxiety, stress, & loneliness) and medical (neurological, cardiovascular, chronic pain) conditions can adversely affect episodic memory. Furthermore, individual differences in emotional/affective experience as represented by trait personality variables (e.g., conscientiousness, openness to experience, introversion, extraversion, and neuroticism) can either facilitate or harm episodic memory performance. This paper aims to review episodic memory, its associated attention and executive function co-processes, the modulation of memory function as a result of affective experiences as represented by trait personality, and how coping mechanisms can serve as a buffer to maintain episodic memory function using Chiari malformation Type I (a chronic pain syndrome) as a model. Finally, allostatic load and pharmacological effects of pain medications on episodic memory are discussed.