<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>4(1)</volume><submitter>Kyyriainen J</submitter><pubmed_abstract>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-mm&lt;sup>2&lt;/sup> post-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 mm&lt;sup>3&lt;/sup>), 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.</pubmed_abstract><journal>Neurotrauma reports</journal><pagination>384-395</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10282974</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Sleep Disturbance and Severe Hydrocephalus in a Normally Behaving Wistar Rat With Traumatic Brain Injury.</pubmed_title><pmcid>PMC10282974</pmcid><pubmed_authors>Kyyriainen J</pubmed_authors><pubmed_authors>Hamalainen E</pubmed_authors><pubmed_authors>Andrade P</pubmed_authors><pubmed_authors>Pitkanen A</pubmed_authors></additional><is_claimable>false</is_claimable><name>Sleep Disturbance and Severe Hydrocephalus in a Normally Behaving Wistar Rat With Traumatic Brain Injury.</name><description>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-mm&lt;sup>2&lt;/sup> post-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 mm&lt;sup>3&lt;/sup>), 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.</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023</publication><modification>2025-04-04T07:38:37.495Z</modification><creation>2025-04-04T07:38:37.495Z</creation></dates><accession>S-EPMC10282974</accession><cross_references><pubmed>37350791</pubmed><doi>10.1089/neur.2022.0090</doi></cross_references></HashMap>