Sonolência diurna excessiva pós-traumatismo de crânio: associação com movimentos periódicos de pernas e distúrbio de comportamento do sono REM: relato de caso Excessive daytime sleepiness after traumatic brain injury: association with periodic limb movements and REM behavior disorder: case report

Um homem de 52 anos, procurou o Hospital. Universitário de Brasília com queixa de sono agitado. Sua esposa relatava, desde há cerca de 10 anos, intensa movimentação de membros e agressividade em meio a sonhos violentos. Desde então apresentava sonolência diurna excessiva. Havia relato de traumatismo de crânio há 34 anos e coma de 2 meses de duração. A vídeo-polissonografia revelou comportamento agressivo e agitado durante o sono REM, e movimentos periódicos de pernas. Havia importante sonolência diurna no teste de latências de sono. Foi instituído tratamento com levodopa-benzerazida 100/25 mg à noite. Após 10 semanas de evolução, houve melhora da movimentação noturna global, e desaparecimento dos episódios ligados a sonhos de conteúdo violento. Este caso nos permite analisar a associação entre trauma craniano e alterações nas vias dopaminérgicas (movimentos periódicos das pernas e distúrbio de comportamento do sono REM) e revisar a importância dos distúrbios na produção de hipocretina hipotalâmica na fisiopatologia desse quadro clínico.<br>A 52 year-old male patient, had complaint of "restless sleep". His wife informed that for the past ten years the patient had presented intense and aggressive body movements, and sometimes, violent dreams. The patient also complained of excessive daytime sleepiness. His relevant previous medical history included a traumatic brain injury at the age of 28 which left him in coma for two months. A video-polysomnography showed periodic leg movements and, during REM sleep, aggressive and agitated behaviour. The multiple sleep latency test revealed extremely short latencies. Initially, he was treated with levodopa-benzerazide, 100/25 mg, 2 hours before bedtime. After 10 weeks his overnight behaviour pattern improved and leg movements diminished. This case supports the hypothesis of an association between cranial trauma and alterations in the dopaminergic pathways represented by periodic leg movements during sleep and a sleep behaviour disorder and proposes the possibility of hypothalamic hypocretin involvement in its pathophysiology

Too hard to control: compromised pain anticipation and modulation in mild traumatic brain injury

Mild traumatic brain injury (MTBI) is a vulnerability factor for the development of pain-related conditions above and beyond those related to comorbid traumatic and emotional symptoms. We acquired functional magnetic resonance imaging (fMRI) on a validated pain anticipation task and tested the hypotheses that individuals with a reported history of MTBI, compared with healthy comparison subjects, would show increased brain response to pain anticipation and ineffective pain modulation after controlling for psychiatric symptoms. Eighteen male subjects with a reported history of blast-related MTBI related to combat, and eighteen healthy male subjects with no reported history of MTBI (healthy controls) underwent fMRI during an event-related experimental pain paradigm with cued high or low intensity painful heat stimuli. No subjects in either group met diagnostic criteria for current mood or anxiety disorder. We found that relative to healthy comparison subjects, after controlling for traumatic and depressive symptoms, participants with a reported history of MTBI showed significantly stronger activations within midbrain periaqueductual grey (PAG), right dorsolateral prefrontal cortex and cuneus during pain anticipation. Furthermore, we found that brain injury was a significant moderator of the relationship between anticipatory PAG activation and reported subjective pain. Our results suggest that a potentially disrupted neurocognitive anticipatory network may result from damage to the endogenous pain modulatory system and underlie difficulties with regulatory pain processing following MTBI. In other words, our findings are consistent with a notion that brain injury makes it more difficult to control acute pain. Understanding these mechanisms of dysfunctional acute pain processing following MTBI may help shed light on the underlying causes of increased vulnerability for the development of pain-related conditions in this population