Neurological Insult Research Articles

An Objective Assessment of Neuromotor Control Using a Smartphone App After Repeated Subconcussive Blast Exposure.

Subconcussive blast exposure has been shown to alter neurological functioning. However, the extent to which neurological dysfunction persists after blast exposure is unknown. This longitudinal study examined the potential short- and long-term effects of repeated subconcussive blast exposure on neuromotor performance from heavy weapons training in military personnel. A total of 214 participants were assessed; 137 were exposed to repeated subconcussive blasts and 77 were not exposed to blasts (controls). Participants completed a short stepping-in-place task while an Android smartphone app placed on their thigh recorded movement kinematics. We showed acute suppression of neuromotor variability 6 h after subconcussive blast exposure, followed by a rebound to levels not different from baseline at the 72 h, 2-week, and 3-month post-tests. It is postulated that this suppression of neuromotor variability results from a reduction in the functional degrees of freedom from the subconcussive neurological insult. It is important to note that this change in behavior is short-lived, with a return to pre-blast exposure movement kinematics within 72 h.

TBC1D15-regulated mitochondria–lysosome membrane contact exerts neuroprotective effects by alleviating mitochondrial calcium overload in seizure

Mitochondrial calcium overload plays an important role in the neurological insults in seizure. The Rab7 GTPase-activating protein, Tre-2/Bub2/Cdc16 domain family member 15 (TBC1D15), is involved in the regulation of mitochondrial calcium dynamics by mediating mitochondria–lysosome membrane contact. However, whether TBC1D15-regulated mitochondria–lysosome membrane contact and mitochondrial calcium participate in neuronal injury in seizure is unclear. We aimed to investigate the effect of TBC1D15-regulated mitochondria–lysosome membrane contact on epileptiform discharge-induced neuronal damage and further explore the underlying mechanism. Lentiviral vectors (Lv) infection and stereotaxic adeno-associated virus (AAV) injection were used to regulate TBC1D15 expression before establishing in vitro epileptiform discharge and in vivo status epilepticus (SE) models. TBC1D15’s effect on inter-organellar interactions, mitochondrial calcium levels and neuronal injury in seizure was evaluated. The results showed that abnormalities in mitochondria–lysosome membrane contact, mitochondrial calcium overload, mitochondrial dysfunction, increased levels of reactive oxygen species, and prominent neuronal damage were partly relieved by TBC1D15 overexpression, whereas TBC1D15 knockdown markedly deteriorated these phenomena. Further examination revealed that epileptiform discharge-induced mitochondrial calcium overload in primary hippocampal neurons was closely associated with abnormal mitochondria–lysosome membrane contact. This study highlights the crucial role played by TBC1D15-regulated mitochondria–lysosome membrane contact in epileptiform discharge-induced neuronal injury by alleviating mitochondrial calcium overload.

Altered Mental Status in the Solid-Organ Transplant Recipient.

Patients undergoing solid-organ transplantation (SOT) face a tumultuous journey. Prior to transplant, their medical course is characterized by organ dysfunction, diminished quality of life, and reliance on organ support, all of which are endured in hopes of reaching the haven of organ transplantation. Peritransplant altered mental status may indicate neurologic insults acquired during transplant and may have long-lasting consequences. Even years after transplant, these patients are at heightened risk for neurologic dysfunction from a myriad of metabolic, toxic, and infectious causes. This review provides a comprehensive examination of causes, diagnostic approaches, neuroimaging findings, and management strategies for altered mental status in SOT recipients. Given their complexity and the numerous etiologies for neurologic dysfunction, liver transplant patients are a chief focus in this review; however, we also review lesser-known contributors to neurological injury across various transplant types. From hepatic encephalopathy to cerebral edema, seizures, and infections, this review highlights the importance of recognizing and managing pre- and posttransplant neurological complications to optimize patient outcomes.

Dexmedetomidine directly binds to and inhibits Toll-like receptor 4

BackgroundWhile a number of anesthetics has been shown potentially associated with neurotoxicity in the developing brain, dexmedetomidine, a drug that was rather recently introduced into the perioperative setting, is considered beneficial from neurological wellbeing. However, the underlying mechanism of how dexmedetomidine affects brain health remains to be determined. Based on our recent study, we hypothesized that dexmedetomidine would directly bind to and inhibit Toll-like receptor 4 (TLR4), a critical receptor largely expressed in microglia and responsible for neurological insult. MethodsWe used TLR4 reporter assays to test if dexmedetomidine attenuates TLR4 activation. Furthermore, a direct binding of dexmedetomidine on TLR4 was tested using photoactivatable medetomidine. Lastly, the effect of dexmedetomidine on ketamine (anesthetic)-induced neurotoxicity was tested in rat pups (P7). ResultsWe showed that dexmedetomidine attenuated TLR4 activation using reporter assay (IC50 = 5.8 µg/mL). Photoactivatable dexmedetomidine delineated its direct binding sites on TLR4. We also showed that dexmedetomidine attenuated microglia activation both in vitro and in vivo. DiscussionWe proposed a novel mechanism of dexmedetomidine-mediated neuroprotection.

Inflammasome Proteins Are Reliable Biomarkers of the Inflammatory Response in Aneurysmal Subarachnoid Hemorrhage.

Aneurysmal subarachnoid hemorrhage (aSAH) is caused by abnormal blood vessel dilation and subsequent rupture, resulting in blood pooling in the subarachnoid space. This neurological insult results in the activation of the inflammasome, a multiprotein complex that processes pro-inflammatory interleukin (IL)-1 cytokines leading to morbidity and mortality. Moreover, increases in inflammasome proteins are associated with clinical deterioration in many neurological diseases. Limited studies have investigated inflammasome protein expression following aSAH. Reliable markers of the inflammatory response associated with aSAH may allow for earlier detection of patients at risk for complications and aid in the identification of novel pharmacologic targets. Here, we investigated whether inflammasome signaling proteins may serve as potential biomarkers of the inflammatory response in aSAH. Serum and cerebrospinal fluid (CSF) from fifteen aSAH subjects and healthy age-matched controls and hydrocephalus (CSF) no-aneurysm controls were evaluated for levels of inflammasome signaling proteins and downstream pro-inflammatory cytokines. Protein measurements were carried out using Simple Plex and Single-Molecule Array (Simoa) technology. The area under the curve (AUC) was calculated using receiver operating characteristics (ROCs) to obtain information on biomarker reliability, specificity, sensitivity, cut-off points, and likelihood ratio. In addition, a Spearman r correlation matrix was performed to determine the correlation between inflammasome protein levels and clinical outcome measures. aSAH subjects demonstrated elevated caspase-1, apoptosis-associated speck-like protein with a caspase recruiting domain (ASC), IL-18 and IL-1β levels in serum, and CSF when compared to controls. Each of these proteins was found to be a promising biomarker of inflammation in aSAH in the CSF. In addition, ASC, caspase-1, and IL-1β were found to be promising biomarkers of inflammation in aSAH in serum. Furthermore, we found that elevated levels of inflammasome proteins in serum are useful to predict worse functional outcomes following aSAH. Thus, the determination of inflammasome protein levels in CSF and serum in aSAH may be utilized as reliable biomarkers of inflammation in aSAH and used clinically to monitor patient outcomes.

Volume-based enteral feeding for ward patients with acute neurological conditions: a pilot prospective cohort study.

Patients requiring enteral nutrition (EN) after neurological insults experience feeding interruptions, contributing to inadequate nutrition delivery. This prospective cohort study investigated if volume-based enteral feeding (VBF) improved the delivery of prescribed EN volume in ward patients with acute neurological conditions. Over two sequential periods, the usual care group received standard continuous rate-based feeding, and the intervention group received VBF with bi-daily EN rate adjustments to achieve target daily volume. The primary outcome was percentage of prescribed daily EN formula volume delivered. Differences in energy and protein provision, weight, malnutrition and safety were explored. An evaluation survey captured nurse acceptability of the protocol. The intervention group (n = 32) achieved greater median interquartile range (IQR) EN adequacy of prescribed volume at 92% (88-97) compared to 67% (54-78) for usual care (n = 35) (p < 0.001). VBF compared to rate-based feeding resulted in patients receiving more kilojoules (131 [121-138] kJ/kg vs. 84 [64-99] kJ/kg; p < 0.001) and protein (1.3 [1.2-1.5] g/kg vs. 0.9 [0.6-1.1] g/kg; p < 0.001). There were no differences in gastrointestinal intolerance between groups. Compliance to the VBF protocol was 90%, and 78% of staff reported high confidence using the protocol. The intervention group had less median weight loss at discharge (-1.4 [0.1 to -4.3] kg) than usual care (-3.6 [-1.3 to 8.4] kg; p < 0.011), but no differences in malnutrition status were observed. A VBF protocol delivered greater EN volume, energy and protein following neurological injury. The VBF protocol was feasible with high acceptability from nursing staff.

The supinator approach to the lateral elbow: a technique description and literature review

We present the supinator approach for management of the lateral elbow which combines the principal features of the Kocher and Kaplan approaches. The Kaplan interval is connected to the Kocher interval by a transverse incision extending to the supinator crest. The supinator approach maintains a safe distance from the posterior interosseous nerve and is likely to avoid the insertional variations of the LUCL. In our experience, the supinator approach is reproducible, provides ample exposure of the radial head and lateral elbow and reduces the risk of instability and neurologic insult.

Palliative Care of Stroke Patients

Critical care clinicians frequently care for patients with acute brain injury, such as stroke. Regardless of the severity of the neurologic insult, these patients have life-altering deficits that threaten their personal identity and quality of life. The sudden nature of the injury often means that there has been little discussion between patients and their families about life-sustaining treatments, and most patients are unable to speak for themselves because of impaired cognition and communication. Thus, individuals experiencing stroke and their families present clinicians with unique and complex care needs in the acute care setting. Key professional organizations have endorsed the early integration of palliative care into the treatment of patients with stroke and devastating neurologic injury. Implementing interdisciplinary primary or specialty palliative care helps clinicians adopt a patient-centered approach to care and aids in decision-making.

Characteristics and Usefulness of Neurophysiological Monitoring in Corrective Procedures for Abnormally Curved Spine in Young Patients.

To identify and characterize events of deterioration in intraoperative neuromonitoring data during correction procedures for thoracic and lumbar abnormal spinal curvature in young patients. Records of 1,127 cases were retrospectively reviewed to identify events with deterioration of the neuromonitoring data. General etiological and demographic variables were summarized, and neuromonitoring events were studied and characterized. Adolescent idiopathic cases were associated with female dominance and older age. Nonadolescent idiopathic cases were associated with a higher rate of neuromonitoring events. The neuromonitoring events evolved during the different procedural stages, were primarily reflected in the motor-evoked potential data and affected a range of neural structures to varying degrees. Most of the events were resolved, partially or completely, following a corresponding intervention by the surgical team, before the end of the procedure. Significant immediate weakness of the lower extremities was demonstrated in patients with unresolved neuromonitoring events, most of them were nonadolescent idiopathic patients. Neurophysiological monitoring enables the intraoperative assessment of the integrity of neural pathways and allows the detection of surgery-related impending neural injuries. Neuromonitoring contributes to intraoperative decision making, either when data are uneventful and allow confident continuation or when data deteriorate and lead to corresponding intervention. Further awareness should be paid to the vulnerable characteristics of the patient, surgery course, and neuromonitoring data. Proper interpretation of the neuromonitoring data, together with corresponding intervention by the surgeon when necessary, has the potential to reduce postoperative neurological insults and improve clinical outcomes.

White matter connectivity and social functioning in survivors of pediatric brain tumor

ObjectiveSurvivors of pediatric brain tumors (SPBT) are at risk for social deficits, fewer friendships, and poor peer relations. SPBT also experience reduced brain connectivity via microstructural disruptions to white matter from neurological insults. Research with other populations implicates white matter connectivity as a key contributor to poor social functioning. This case-controlled diffusion-weighted imaging study evaluated structural connectivity in SPBT and typically developing controls (TDC) and associations between metrics of connectivity and social functioning.MethodsDiffusion weighted-imaging results from 19 SPBT and 19 TDC were analyzed using probabilistic white matter tractography. Survivors were at least 5 years post-diagnosis and 2 years off treatment. Graph theory statistics measured group differences across several connectivity metrics, including average strength, global efficiency, assortativity, clustering coefficient, modularity, and betweenness centrality. Analyses also evaluated the effects of neurological risk on connectivity among SPBT. Correlational analyses evaluated associations between connectivity and indices of social behavior.ResultsSPBT demonstrated reduced global connectivity compared to TDC. Several medical factors (e.g., chemotherapy, recurrence, multimodal therapy) were related to decreased connectivity across metrics of integration (e.g., average strength, global efficiency) in SPBT. Connectivity metrics were related to peer relationship quality and social challenges in the SPBT group and to social challenges in the total sample.ConclusionsMicrostructural white matter connectivity is diminished in SPBT and related to neurological risk and peer relationship quality. Additional neuroimaging research is needed to evaluate associations between brain connectivity metrics and social functioning in SPBT.

Association of bilaterally suppressed EEG amplitudes and outcomes in critically ill children.

Amplitude-integrated EEG (aEEG) is used to assess electrocortical activity in pediatric intensive care if (continuous) full channel EEG is unavailable but evidence regarding the meaning of suppressed aEEG amplitudes in children remains limited. This retrospective cohort study investigated the association of suppressed aEEG amplitudes in critically ill children with death or decline of neurological functioning at hospital discharge. Two hundred and thirty-five EEGs derived from individual patients <18 years in the pediatric intensive care unit at the University Hospital Essen (Germany) between 04/2014 and 07/2021, were converted into aEEGs and amplitudes analyzed with respect to age-specific percentiles. Crude and adjusted odds ratios (OR) for death, and functional decline at hospital discharge in patients with bilateral suppression of the upper or lower amplitude below the 10th percentile were calculated. Sensitivity, specificity, positive (PPV) and negative predictive values (NPV) were assessed. The median time from neurological insult to EEG recording was 2 days. PICU admission occurred due to neurological reasons in 43% and patients had high overall disease severity. Thirty-three (14%) patients died and 68 (29%) had a functional decline. Amplitude suppression was observed in 48% (upper amplitude) and 57% (lower amplitude), with unilateral suppression less frequent than bilateral suppression. Multivariable regression analyses yielded crude ORs between 4.61 and 14.29 and adjusted ORs between 2.55 and 8.87 for death and functional decline if upper or lower amplitudes were bilaterally suppressed. NPVs for bilaterally non-suppressed amplitudes were above 95% for death and above 83% for pediatric cerebral performance category Scale (PCPC) decline, whereas PPVs ranged between 22 and 32% for death and 49-52% for PCPC decline. This study found a high prevalence of suppressed aEEG amplitudes in critically ill children. Bilaterally normal amplitudes predicted good outcomes, whereas bilateral suppression was associated with increased odds for death and functional decline. aEEG assessment may serve as an element for risk stratification of PICU patients if conventional EEG is unavailable with excellent negative predictive abilities but requires additional information to identify patients at risk for poor outcomes.

Neurogenic Pulmonary Edema Associated with Hyponatremia, Primary Polydipsia, and Cannabis Use: A Case Report.

Neurogenic pulmonary edema is a rare and potentially life-threatening condition that can present as severe pulmonary edema after significant neurologic insults. This is the first documented instance that shows a plausible causal link between cannabis consumption, psychogenic polydipsia, and the subsequent development of neurogenic pulmonary edema associated with status epilepticus secondary to acute hyponatremia. We report a case of a 34-year-old female who presented to the emergency department altered and postictal after a witnessed new-onset seizure. She developed significant respiratory distress that required intubation. Her sodium was 121 millimoles per liter (mmol/L), from 137 mmol/L 36 hours prior on routine outpatient labs. Further history revealed excessive water ingestion after eating a cannabis edible prior to the seizure. This case highlights the importance of recognizing neurogenic pulmonary edema in connection with psychogenic polydipsia, severe hyponatremia, and status epilepticus subsequent to cannabis consumption.

P.037 Refractory status dystonicus and hypotension after cardiac arrest in a child with AADC deficiency post gene therapy: a case report

Background: Aromatic l-amino acid decarboxylase (AADC) deficiency is a metabolic disorder that causes deficient serotonin, dopamine, and catecholamine synthesis. How children respond to neurological insult post intracranial gene therapy remains underreported. We present a 10 year old girl with profound neurological injury after a brief in-hospital cardiac arrest, secondary to viral infection-induced respiratory failure, 4 years after gene therapy. Methods: Patient’s chart review included brain imaging, clinical notes, laboratory results, and treatment. Results: MRI showed symmetric abnormalities in the basal ganglia, thalami, cortex, and cerebellar hemispheres. CSF analysis showed homovanillic acid 27 nmol/L (reference range 167-563) and 5-hydroxyindoleacetic acid 7 nmol/L (reference range 67-189). She developed generalized dystonia and oculogyric crises which were not seen since before gene therapy. There was poor catecholamine production causing refractory hypotension. She required a one-month stay in ICU for hypotension and status dystonicus. Dystonia was controlled with high doses of 6 agents. Conclusions: We describe a patient with AADC deficiency post gene therapy who experienced disproportionately severe neurological injury and decreased AADC activity after hypoxic neurological insult. There may be unique considerations of dopaminergic neuron integrity, AADC gene promoter sensitivity, and cerebrovascular autoregulation in children with AADC deficiency post gene therapy.

Update in Pediatric Neurocritical Care: What a Neurologist Caring for Critically Ill Children Needs to Know.

Currently nearly one-quarter of admissions to pediatric intensive care units (PICUs) worldwide are for neurocritical care diagnoses that are associated with significant morbidity and mortality. Pediatric neurocritical care is a rapidly evolving field with unique challenges due to not only age-related responses to primary neurologic insults and their treatments but also the rarity of pediatric neurocritical care conditions at any given institution. The structure of pediatric neurocritical care services therefore is most commonly a collaborative model where critical care medicine physicians coordinate care and are supported by a multidisciplinary team of pediatric subspecialists, including neurologists. While pediatric neurocritical care lies at the intersection between critical care and the neurosciences, this narrative review focuses on the most common clinical scenarios encountered by pediatric neurologists as consultants in the PICU and synthesizes the recent evidence, best practices, and ongoing research in these cases. We provide an in-depth review of (1) the evaluation and management of abnormal movements (seizures/status epilepticus and status dystonicus); (2) acute weakness and paralysis (focusing on pediatric stroke and select pediatric neuroimmune conditions); (3) neuromonitoring modalities using a pathophysiology-driven approach; (4) neuroprotective strategies for which there is evidence (e.g., pediatric severe traumatic brain injury, post-cardiac arrest care, and ischemic stroke and hemorrhagic stroke); and (5) best practices for neuroprognostication in pediatric traumatic brain injury, cardiac arrest, and disorders of consciousness, with highlights of the 2023 updates on Brain Death/Death by Neurological Criteria. Our review of the current state of pediatric neurocritical care from the viewpoint of what a pediatric neurologist in the PICU needs to know is intended to improve knowledge for providers at the bedside with the goal of better patient care and outcomes.

Moyamoya Disease Masquerading as Hemiplegic Migraine in a Child: A Case Report From India

Moyamoya disease (MMD) is a chronic progressive steno-occlusive disease of the intracranial arterial vessels and their branches characterized by puff smoke appearance on angiography. Multifocal neurological insults and deficits are commonly observed in children with MMD. A 7-year-old boy presented with multiple episodes of transient hemiparesis preceded by headache, vomiting, and visual auras was initially labeled as sporadic hemiplegic migraine according to the International Headache Society criteria. However, the rare association of hemiplegic migraine with MMD compelled us to perform magnetic resonance imaging and digital subtraction angiography, which revealed MMD as the underlying cause for the alternating hemiplegia and headaches in the child.

Pharmacological inhibition of receptor-interacting protein kinase 2 (RIPK2) elicits neuroprotective effects following experimental ischemic stroke

Ischemic stroke induces a debilitating neurological insult, where inflammatory processes contribute greatly to the expansion and growth of the injury. Receptor-interacting protein kinase 2 (RIPK2) is most well-known for its role as the obligate kinase for NOD1/2 pattern recognition receptor signaling and is implicated in the pathology of various inflammatory conditions. Compared to a sham-operated control, ischemic stroke resulted in a dramatic increase in the active, phosphorylated form of RIPK2, indicating that RIPK2 may be implicated in the response to stroke injury. Here, we assessed the effects of pharmacological inhibition of RIPK2 to improve post-stroke outcomes in mice subjected to experimental ischemic stroke. We found that treatment at the onset of reperfusion with a RIPK2 inhibitor, which inhibits the phosphorylation and activation of RIPK2, resulted in marked improvements in post-stroke behavioral outcomes compared to the vehicle-administered group assessed 24 h after stroke. RIPK2 inhibitor-treated mice exhibited dramatic reductions in infarct volume, concurrent with reduced damage to the blood-brain barrier, as evidenced by reduced levels of active matrix metalloproteinase-9 (MMP-9) and leakage of blood-borne albumin in the ipsilateral cortex. To explore the protective mechanism of RIPK2 inhibition, we next pretreated mice with RIPK2 inhibitor or vehicle and examined transcriptomic alterations occurring in the ischemic brain 6 h after stroke. We observed a dramatic reduction in neuroinflammatory markers in the ipsilateral cortex of the inhibitor-treated group while also attaining a comprehensive view of the vast transcriptomic alterations occurring in the brain with inhibitor treatment through bulk RNA-sequencing of the injured cortex. Overall, we provide significant novel evidence that RIPK2 may represent a viable target for post-stroke pharmacotherapy and potentially other neuroinflammatory conditions.

Intracranial Neuromodulation for Neurologic Recovery

Neurologic insults (traumatic brain injuries, strokes, and spinal cord injuries) profoundly influence motor, cognitive, and psychological functions. Current medical and surgical therapies are often insufficient to address the functional deficits from these injuries. Intracranial neuromodulation, specifically deep brain stimulation (DBS) and motor cortex stimulation (MCS), has been studied to improve these deficits. Preclinical results demonstrate that DBS and MCS effectively potentiate the sequalae of neurologic insult. Clinical evidence is limited, but existing reports and clinical trials show the promising therapeutic potential of intracranial neuromodulation. Further study of intracranial neuromodulation treatment is warranted, with greater attention to confounding variables and methodology.

Developing thymocytes cue in unique subsets of neurons to support optimal thymic architecture

Abstract Peripheral nervous system innervation of various organs has been associated with the development and maintenance of the immune system. Interestingly, various neurological insults including brain tumors, intracranial metastases, and neurotropic infections have been shown to have profound impacts on peripheral immunity, including thymic size and cellularity. Therefore, we sought to determine whether the thymus was directly innervated. Using flow cytometry and confocal microscopy, we identified a population of cells within the thymus that contained both neuronal markers and morphology. Subsets expressed tyrosine hydroxylase, BIII tubulin and/or NeuN, distinguishing them from thymic epithelial cells. These cells do not express AIRE, further highlighting their neuronal identity. Interestingly, a subset of these neurons also express MCH-II, implying a potential role in T cell selection. Neuronal cell bodies and/or axonal processes were identified within the thymus. Using retrograde rabies virus-derived neurotracers, we confirmed axonal connections and the identity of thymic neurons. Finally, both neuronal and epithelial cells were absent in RAG-deficient mice, suggesting a shared differentiation or survival pathway. Both populations could be restored by introducing healthy bone marrow. To summarize, we describe a novel population of neuronal cells within the thymus that interact with developing thymocytes to establish optimal thymic architecture.

A rare case of extensive neurogenic heterotopic ossification: a case report

IntroductionNeurogenic Heterotopic ossification (NHO) is a potential sequalae and a detrimental complication following neurological insult. It is characterized by formation of localized gradually progressive, peri-articular lamellar bone formation in extra-skeletal tissues. We would like to report a rare case of heterotopic ossification involving all 4 limbs, in which we tried to restore joint mobility to improve his functional status so that he could perform his daily tasks.Case presentationWe present a case of a 33-year-old bed ridden male, diagnosed with NHO involving all 4 limbs (bilateral hip, right knee, right shoulder, left elbow). The patient had a crippled posture, significant pain and impaired range of motion hampering movement of all four limbs which prevented him from lying down supine, sitting, walking and performing activities of daily living. After three surgeries, the patient achieved wheelchair mobilization and upright posture with the assistance of calipers.ConclusionThe management of NHO requires a multidisciplinary approach involving orthopaedic surgeons, neurologists & rehabilitation specialists. Prognosis of NHO depends on factors such as extent of ossification, underlying neurological condition & patients overall health.

441 Glasgow Coma Scale Motor Score Predicts Need for Tracheostomy After Decompressive Craniectomy for Traumatic Brain Injury

INTRODUCTION: Traumatic brain injury (TBI) is a common problem worldwide. Severe TBI is sometimes treated with decompressive craniectomy. Many patients who survive require tracheostomy. The decision to proceed with tracheostomy and at what time is often ambiguous. Existing methods for predicting which patients with neurologic insult will require tracheostomy are aimed at stroke and spontaneous intracranial hemorrhage (ICH). METHODS: We performed a retrospective review of adult patients who underwent decompressive craniectomy for severe TBI at the University of Kansas Medical Center between 2007 and 2020. RESULTS: 100% of patients who have GCS motor score of 4 or less on POD 5 required tracheostomy. 80% of patients with GCS motor score of 5 on POD 5 required tracheostomy. Setting the threshold at GCS motor score of 5 on POD 5 for recommending proceeding with tracheostomy results in 86.7% sensitivity, 91.7% specificity, and 90.5% PPV with area under the receiver operator curve of 0.9101. CONCLUSIONS: GCS motor score of 5 or less on POD 5 from decompressive craniectomy for TBI is predictive of need for tracheostomy.