ArticleJournal of neurotrauma2011
Craniotomy: true sham for traumatic brain injury, or a sham of a sham?
Article in Journal of neurotrauma, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 160 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
160 citing papers in PubMed, 1 synthesis or guideline pooled it, 310 citations in OpenAlex.
- Cyclooxygenase 2 Inhibitors for Headache After Elective Cranial Neurosurgery: Results from a Systematic Review of Efficacy of Cyclooxygenase 2 Inhibitors for Headache After Acute Brain Injury.Neurocritical care · 2025Pooled it
- Mechanical deformation explains distinct neuroimaging patterns and etiologies in brain trauma.NeuroImage · 2026Article
- Post-Craniotomy Headache: Current Concepts and Emerging Procedural Therapies.Current pain and headache reports · 2026Review
- Reversible Thermoactuation Unlocks Minimally Invasive Implantation and Retrieval of Soft Bioelectronics.Advanced materials (Deerfield Beach, Fla.) · 2026Article
- Thiol-Based Neuroprotective Copolymers Acutely Restore Redox Metabolism and Mediate Vasogenic Edema in a Mouse Model of Traumatic Brain Injury.Macromolecular bioscience · 2026Article
- Neurovascular and inflammatory effects of biperiden in the acute phase of moderate traumatic brain injury: evidence from a non-human primate model.Scientific reports · 2026Article
- Pre-Clinical Models of Traumatic Brain Injury-A Narrative Review Towards "Animal Neuro-ICUs".Biomedicines · 2026Review
- Transcriptomic analysis of the physiological responses to injuries induced accompanying intracortical microelectrode implantation.Biomaterials · 2026Article
- Immunosuppressive Formulations for Immunological Defense against Traumatic Brain Injury.Advanced healthcare materials · 2025Article
- L-Carnitine and Mildronate Demonstrate Divergent Protective Effects on Mitochondrial DNA Quality Control and Inflammation Following Traumatic Brain Injury.International journal of molecular sciences · 2025Article
- A Combination of Low Doses of Lithium and Valproate Improves Cognitive Outcomes after Mild Traumatic Brain Injury.Journal of neurotrauma · 2025Article
- Traumatic Brain Injury Promotes Neurogenesis and Oligodendrogenesis in Subcortical Brain Regions of Mice.Cells · 2025Article
- Article
- Repetitive Mild Closed-Head Injury Induced Synapse Loss and Increased Local BOLD-fMRI Signal Homogeneity.Journal of neurotrauma · 2024Article
- Article
- Comparative Brain Proteomic Analysis between Sham and Cerebral Ischemia Experimental Groups.International journal of molecular sciences · 2024Article
- Behavioral Interventions Can Improve Brain Injury-Induced Deficits in Behavioral Flexibility and Impulsivity Linked to Impaired Reward-Feedback Beta Oscillations.Journal of neurotrauma · 2024Article
- Exploratory assessment of the effect of systemic administration of soluble glycoprotein 130 on cognitive performance and chemokine levels in a mouse model of experimental traumatic brain injury.Journal of neuroinflammation · 2024Article
- Complement propagates visual system pathology following traumatic brain injury.Journal of neuroinflammation · 2024Article
- Bi-directional neuro-immune dysfunction after chronic experimental brain injury.Journal of neuroinflammation · 2024Article
100 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 1 institution in 1 country.
Funding
Abstract
Abstract Neurological dysfunction after traumatic brain injury (TBI) is caused by both the primary injury and a secondary cascade of biochemical and metabolic events. Since TBI can be caused by a variety of mechanisms, numerous models have been developed to facilitate its study. The most prevalent models are controlled cortical impact and fluid percussion injury. Both typically use "sham" (craniotomy alone) animals as controls. However, the sham operation is objectively damaging, and we hypothesized that the craniotomy itself may cause a unique brain injury distinct from the impact injury. To test this hypothesis, 38 adult female rats were assigned to one of three groups: control (anesthesia only); craniotomy performed by manual trephine; or craniotomy performed by electric dental drill. The rats were then subjected to behavioral testing, imaging analysis, and quantification of cortical concentrations of cytokines. Both craniotomy methods generate visible MRI lesions that persist for 14 days. The initial lesion generated by the drill technique is significantly larger than that generated by the trephine. Behavioral data mirrored lesion volume. For example, drill rats have significantly impaired sensory and motor responses compared to trephine or naïve rats. Finally, of the seven tested cytokines, KC-GRO and IFN-γ showed significant increases in both craniotomy models compared to naïve rats. We conclude that the traditional sham operation as a control confers profound proinflammatory, morphological, and behavioral damage, which confounds interpretation of conventional experimental brain injury models. Any experimental design incorporating "sham" procedures should distinguish among sham, experimentally injured, and healthy/naïve animals, to help reduce confounding factors.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.