We report on a case study of a Wistar rat that was investigated in detail because it exhibited no N3 sleep in electroencephalography (EEG) after lateral fluid-percussion injury (FPI)-induced traumatic brain injury (TBI). The rat (#112) belonged to a cohort of 28 adult Wistar rats exposed to lateral FPI. Rats were monitored by continuous video EEG for 30 days to follow-up on the evolution of sleep disturbances. The beam walking test was used to measure post-TBI functional recovery. Severity of the cortical lesion area, total brain volume, and cortical volume were measured from histological brain sections. Rat #112 had a normal body and skull appearance. Its baseline body weight did not differ from that of the rest of the cohort. At baseline, rat #112 crossed the beam in 6.3 sec (score range for the rest of the cohort, 4.7–44.3) and showed no evident slipping of the paws, scoring a 5.3 (score range for the rest of cohort, 4.3–6.0). On day 30 post-TBI, however, rat #112 was the only rat with a score of 0 on the beam. Histological analysis at 30 days post-TBI revealed a small 0.6-mm2post-TBI lesion in the somatosensory cortex (lesion size range for the rest of the cohort, 1.2–10.9). The brain volume of rat #112 was 2-fold larger than the mean volume of the rest of the cohort (1592 vs. 758 mm3), the ventricles were remarkably enlarged, and the layered cerebral cortex was very thin. Analysis of the sleep EEG revealed that rat #112 had rapid eye movement sleep and wakefulness, but no N3 sleep, during the 72-h EEG epoch analyzed. This case report demonstrates that brain abnormalities presumably unrelated to the impact-induced cortical lesion, such as presumed pre-existing hydrocephalus, may worsen TBI-induced behavioral and electrographical outcome measures and complicate the assessment of the cause of the abnormalities.