Predicting the Need for Surgery in Patients with Lumbar Disc Herniation: A New Internally Validated Scoring System.

STUDY DESIGN: Prospective study. PURPOSE: To propose a scoring system for predicting the need for surgery in patients with lumbar disc herniation (LDH). OVERVIEW OF LITERATURE: The indications for surgery in patients with LDH are well established. However, the exact timing of surgery is not. According to surgeons, patients with failed conservative treatment who underwent delayed surgery, often after 6 months postsymptom initiation, have poor functional recovery and outcome. METHODS: The current study included patients with symptomatic LDH. Patients with an indication for emergent surgery such as profound or progressive motor deficit, cauda equina syndrome, and diagnoses other than single-level LDH were excluded from the analysis. All patients followed a conservative treatment regimen (a combination of physical therapy, pain medications, and/or spinal epidural steroid injections). Surgery was indicated for patients who continuously experienced pain despite maximal conservative therapy. RESULTS: In total, 134 patients met the inclusion and exclusion criteria. Among them, 108 (80.6%) responded to conservative management, and 26 (19.4%) underwent unilateral laminotomy and microdiscectomy. The symptom duration, disc degeneration grade on magnetic resonance imaging (Pfirrmann disc grade), herniated disc location and type, fragment size, and thecal sac diameter significantly differed between patients who responded to conservative treatment and those requiring surgery. The area under the receiver operating characteristic curve of the scoring system based on the anteroposterior size of the herniated disc fragment and herniated disc location and type was 0.81. CONCLUSIONS: A scoring system based on herniated disc/fragment size, location, and type can be applied to predict the need for surgery in patients with LDH. In the future, this tool can be used to prevent unnecessarily prolonged conservative management (>4-8 weeks).

CADASIL mutations sensitize the brain to ischemia via spreading depolarizations and abnormal extracellular potassium homeostasis.

Cerebral autosomal dominant arteriopathy, subcortical infarcts, and leukoencephalopathy (CADASIL) is the most common monogenic form of small vessel disease characterized by migraine with aura, leukoaraiosis, strokes, and dementia. CADASIL mutations cause cerebrovascular dysfunction in both animal models and humans. Here, we showed that 2 different human CADASIL mutations (Notch3 R90C or R169C) worsen ischemic stroke outcomes in transgenic mice; this was explained by the higher blood flow threshold to maintain tissue viability compared with that in wild type (WT) mice. Both mutants developed larger infarcts and worse neurological deficits compared with WT mice, regardless of age or sex after filament middle cerebral artery occlusion. However, full-field laser speckle flowmetry during distal middle cerebral artery occlusion showed comparable perfusion deficits in mutants and their respective WT controls. Circle of Willis anatomy and pial collateralization also did not differ among the genotypes. In contrast, mutants had a higher cerebral blood flow threshold, below which infarction ensued, suggesting increased sensitivity of brain tissue to ischemia. Electrophysiological recordings revealed a 1.5- to 2-fold higher frequency of peri-infarct spreading depolarizations in CADASIL mutants. Higher extracellular K+ elevations during spreading depolarizations in the mutants implicated a defect in extracellular K+ clearance. Altogether, these data reveal a mechanism of enhanced vulnerability to ischemic injury linked to abnormal extracellular ion homeostasis and susceptibility to ischemic depolarizations in CADASIL.

Intracranial pressure spikes trigger spreading depolarizations.

Spreading depolarizations are highly prevalent and spatiotemporally punctuated events worsening the outcome of brain injury. Trigger factors are poorly understood but may be linked to sudden worsening in supply-demand mismatch in compromised tissue. Sustained or transient elevations in intracranial pressure are also prevalent in the injured brain. Here, using a mouse model of large hemispheric ischaemic stroke, we show that mild and brief intracranial pressure elevations (20 or 30 mmHg for just 3 min) potently trigger spreading depolarizations in ischaemic penumbra (4-fold increase in spreading depolarization occurrence). We also show that 30 mmHg intracranial pressure spikes as brief as 30 s are equally effective. In contrast, sustained intracranial pressure elevations to the same level for 30 min do not significantly increase the spreading depolarization rate, suggesting that an abrupt disturbance in the steady state equilibrium is required to trigger a spreading depolarization. Laser speckle flowmetry consistently showed a reduction in tissue perfusion, and two-photon pO2 microscopy revealed a drop in venous pO2 during the intracranial pressure spikes suggesting increased oxygen extraction fraction, and therefore, worsening supply-demand mismatch. These haemodynamic changes during intracranial pressure spikes were associated with highly reproducible increases in extracellular potassium levels in penumbra. Consistent with the experimental data, a higher rate of intracranial pressure spikes was associated with spreading depolarization clusters in a retrospective series of patients with aneurysmal subarachnoid haemorrhage with strong temporal correspondence. Altogether, our data show that intracranial pressure spikes, even when mild and brief, are capable of triggering spreading depolarizations. Aggressive prevention of intracranial pressure spikes may help reduce spreading depolarization occurrence and improve outcomes after brain injury.

Intravascular Endothelin-1 does not trigger or increase susceptibility to Spreading Depolarizations.

OBJECTIVES: Spreading depolarizations (SD) likely manifest as aura in migraineurs. Triggers are unknown although vascular events have been implicated. Direct carotid puncture has been reported to trigger migraine with aura. The potent vasoconstrictor endothelin-1 (ET-1), which can be released from the endothelium under pathological conditions, may play a role. Here, we tested whether intracarotid ET-1 infusion triggers SD and whether systemic ET-1 infusion increases the susceptibility to SD. METHODS: Carotid infusions were performed in mice (C57BL/6, male) through a catheter placed at the carotid bifurcation via the external carotid artery. Intracarotid ET-1 (1.25 nmol/ml) was infused at various rates (2-16 µl/min) with or without heparin in the catheter and compared with vehicle infusion (PBS with 0.01% acetic acid) or sham-operated mice (n = 5). Systemic infusions ET-1 (1 nmol/kg, n = 7) or vehicle (n = 7) infusions were performed in rats (Sprague-Dawley, male) via the tail vein. Electrical SD threshold and KCl-induced SD frequency were measured after the infusion. RESULTS: Intracarotid infusion of saline (n = 19), vehicle (n = 7) or ET-1 (n = 12) all triggered SDs at various proportions (21%, 14% and 50%, respectively). These were often associated with severe hypoperfusion prior to SD onset. Heparinizing the infusion catheter completely prevented SD occurrence during the infusions (n = 8), implicating microembolization from carotid thrombi as the trigger. Sham-operated mice never developed SD. Systemic infusion of ET-1 did not affect the electrical SD threshold or KCl-induced SD frequency. CONCLUSION: Intravascular ET-1 does not trigger or increase susceptibility to SD. Microembolization was the likely trigger for migraine auras in patients during carotid puncture.

Neurovascular coupling during optogenetic functional activation: Local and remote stimulus-response characteristics, and uncoupling by spreading depression.

Neurovascular coupling is a fundamental response that links activity to perfusion. Traditional paradigms of neurovascular coupling utilize somatosensory stimulation to activate the primary sensory cortex through subcortical relays. Therefore, examination of neurovascular coupling in disease models can be confounded if the disease process affects these multisynaptic pathways. Optogenetic stimulation is an alternative to directly activate neurons, bypassing the subcortical relays. We employed minimally invasive optogenetic cortical activation through intact skull in Thy1-channelrhodopsin-2 transgenic mice, examined the blood flow changes using laser speckle imaging, and related these to evoked electrophysiological activity. Our data show that optogenetic activation of barrel cortex triggers intensity- and frequency-dependent hyperemia both locally within the barrel cortex (>50% CBF increase), and remotely within the ipsilateral motor cortex (>30% CBF increase). Intriguingly, activation of the barrel cortex causes a small (∼10%) but reproducible hypoperfusion within the contralateral barrel cortex, electrophysiologically linked to transhemispheric inhibition. Cortical spreading depression, known to cause neurovascular uncoupling, diminishes optogenetic hyperemia by more than 50% for up to an hour despite rapid recovery of evoked electrophysiological activity, recapitulating a unique feature of physiological neurovascular coupling. Altogether, these data establish a minimally invasive paradigm to investigate neurovascular coupling for longitudinal characterization of cerebrovascular pathologies.

Dysphagia of aberrant right subclavian artery treated by endoscopic dilation: An alternative to surgical treatment in select cases-A case report.

INTRODUCTION: The aberrant right subclavian artery (ARSA) is a rare cause of dysphagia. Surgical intervention has remained the mainstem of therapy, accompanied with certain morbidities and mortalities. Although rarely reported in literature, endoscopic dilation may be considered a suitable treatment alternative in patients who are not a surgical candidate or do not consent for surgery. We report a case suffering from dysphagia and diagnosed with ARSA treated by endoscopic dilation. PRESENTATION OF CASE: A 52-year-old male presented to our clinic in 2015 with dysphagia. Chest Computed Tomography scan confirmed the diagnosis of ARSA. He first underwent esophagogastroduodenoscopy (EGD) with staged dilation of the stricture, making him free of his symptoms for an approximate 2.5 years. Upon recurrence of symptoms in 2018, he underwent repeat endoscopic dilation, which again completely resolved the symptom with an excellent peri-operative and post-operative course. CONCLUSION: Endoscopic dilation of the esophageal stricture in patients with ARSA is a safe alternative to surgery in patients who are unable or unwilling to undergo surgery. It provides relief for a relatively long time and can be safely repeated multiple times upon recurrence.

Hydatid Cyst in the Lumbar Paravertebral Muscle: A Case Report.

A hydatid cyst is a zoonotic disease caused by the worm Echinococcus granulosus. In endemic regions, it is a well-known differential diagnosis of cystic lesions, especially in the liver, lungs, brain, and vertebral column. Primary paravertebral muscle involvement, however, is rarely reported. In the current report, we present the case of an 11-year-old girl complaining of back pain with a well-defined single cystic lesion in her lumbar paravertebral multifidus muscle evident in imaging studies. The patient had no concomitant lesion in her systemic evaluation. The cyst was resected totally with its daughter cysts, and the pathology confirmed the diagnosis of a hydatid cyst. Although the paravertebral muscle is an extremely rare site of infection for a hydatid cyst, it should be kept in mind in mass lesions with a cystic nature.

Relief Following Chronic Stress Augments Spreading Depolarization Susceptibility in Familial Hemiplegic Migraine Mice.

Cortical spreading depolarization (CSD) is the electrophysiological substrate of migraine aura, and a putative trigger of trigeminovascular activation and migraine headache. Many migraineurs report stress or relief after a stress triggers an attack. We tested whether various stress conditions might modulate CSD susceptibility and whether this is dependent on genetic factors. Male and female wild type and familial hemiplegic migraine type1 (FHM1) knock-in mice heterozygous for the S218L missense mutation were subjected to acute or chronic stress, or chronic stress followed by relief (36 h). Acute stress was induced by restraint and exposure to bright light and white noise (3 h). Chronic stress was induced for 28 days by two cycles of repeated exposure of mice to a rat (7 days), physical restraint (3 days), and forced swimming (3 days). Electrical CSD threshold and KCl-induced (300 mM) CSD frequency were determined in occipital cortex in vivo at the end of each protocol. Relief after chronic stress reduced the electrical CSD threshold and increased the frequency of KCl-induced CSDs in FHM1 mutants only. Acute or chronic stress without relief did not affect CSD susceptibility in either strain. Stress status did not affect CSD propagation speed, duration or amplitude. In summary, relief after chronic stress, but not acute or chronic stress alone, augments CSD in genetically susceptible mice. Therefore, enhanced CSD susceptibility may explain why, in certain patients, migraine attacks typically occur during a period of stress relief such as weekends or holidays.

Determinants of Optogenetic Cortical Spreading Depolarizations.

Cortical spreading depolarization (SD) is the electrophysiological event underlying migraine aura, and a critical contributor to secondary damage after brain injury. Experimental models of SD have been used for decades in migraine and brain injury research; however, they are highly invasive and often cause primary tissue injury, diminishing their translational value. Here we present a non-invasive method to trigger SDs using light-induced depolarization in transgenic mice expressing channelrhodopsin-2 in neurons (Thy1-ChR2-YFP). Focal illumination (470 nm, 1-10 mW) through intact skull using an optical fiber evokes power-dependent steady extracellular potential shifts and local elevations of extracellular [K+] that culminate in an SD when power exceeds a threshold. Using the model, we show that homozygous mice are significantly more susceptible to SD (i.e., lower light thresholds) than heterozygous ChR2 mice. Moreover, we show SD susceptibility differs significantly among cortical divisions (motor, whisker barrel, sensory, visual, in decreasing order of susceptibility), which correlates with relative channelrhodopsin-2 expression. Furthermore, the NMDA receptor antagonist MK-801 blocks the transition to SD without diminishing extracellular potential shifts. Altogether, our data show that the optogenetic SD model is highly suitable for examining physiological or pharmacological modulation of SD in acute and longitudinal studies.

Real-time non-invasive in vivo visible light detection of cortical spreading depolarizations in mice.

BACKGROUND: Cortical spreading depolarization (CSD) is a phenomenon classically associated with migraine aura. CSDs have also been implicated in secondary injury following ischemic stroke, intracerebral hemorrhage, subarachnoid hemorrhage, and traumatic brain injury; however, most investigations involving these disease processes do not account for the occurrence of CSDs. A major barrier to detection of CSDs in experimental models is that currently validated methods are invasive and require specialized equipment and a high level of expertise to implement. NEW METHOD: We present a low-cost, easy-to-implement approach to the detection of CSDs in the mouse through full-thickness intact skull. Our method uses the optical intrinsic signal from white light illumination (OIS-WL) and allows for real-time in vivo detection of CSDs using readily available USB cameras. RESULTS: OIS-WL detected 100% of CSDs that were seen with simultaneous electrode recording (69 CSDs in 28 mice), laser Doppler flowmetry (82 CSDs in 10 mice), laser speckle flowmetry (68 CSDs in 25 mice), or combined electrode recording plus laser speckle flowmetry (29 CSDs in 20 mice). OIS-WL detected 1 additional CSD that was missed by laser Doppler flowmetry. COMPARISON WITH EXISTING METHODS: OIS-WL is less invasive than electrophysiological recordings and easier to implement than laser speckle flowmetry. Moreover, it provides excellent spatial and temporal resolution for dynamic imaging of CSDs in the setting of brain injury. CONCLUSIONS: Detection of CSDs with an inexpensive USB camera and white light source provides a reliable method for the in vivo and non-invasive detection of CSDs through unaltered mouse skull.

Spreading depolarizations trigger caveolin-1-dependent endothelial transcytosis.

OBJECTIVE: Cortical spreading depolarizations (CSDs) are intense and ubiquitous depolarization waves relevant for the pathophysiology of migraine and brain injury. CSDs disrupt the blood-brain barrier (BBB), but the mechanisms are unknown. METHODS: A total of six CSDs were evoked over 1 hour by topical application of 300 mM of KCl or optogenetically with 470 nm (blue) LED over the right hemisphere in anesthetized mice (C57BL/6 J wild type, Thy1-ChR2-YFP line 18, and cav-1-/- ). BBB disruption was assessed by Evans blue (2% EB, 3 ml/kg, intra-arterial) or dextran (200 mg/kg, fluorescein, 70,000 MW, intra-arterial) extravasation in parietotemporal cortex at 3 to 24 hours after CSD. Endothelial cell ultrastructure was examined using transmission electron microscopy 0 to 24 hours after the same CSD protocol in order to assess vesicular trafficking, endothelial tight junctions, and pericyte integrity. Mice were treated with vehicle, isoform nonselective rho-associated kinase (ROCK) inhibitor fasudil (10 mg/kg, intraperitoneally 30 minutes before CSD), or ROCK-2 selective inhibitor KD025 (200 mg/kg, per oral twice-daily for 5 doses before CSD). RESULTS: We show that CSD-induced BBB opening to water and large molecules is mediated by increased endothelial transcytosis starting between 3 and 6 hours and lasting approximately 24 hours. Endothelial tight junctions, pericytes, and basement membrane remain preserved after CSDs. Moreover, we show that CSD-induced BBB disruption is exclusively caveolin-1-dependent and requires rho-kinase 2 activity. Importantly, hyperoxia failed to prevent CSD-induced BBB breakdown, suggesting that the latter is independent of tissue hypoxia. INTERPRETATION: Our data elucidate the mechanisms by which CSDs lead to transient BBB disruption, with diagnostic and therapeutic implications for migraine and brain injury.

Rho-kinase inhibitors do not expand hematoma volume in acute experimental intracerebral hemorrhage.

Rho-associated kinase (ROCK) is an emerging target in acute ischemic stroke. Early pre-hospital treatment with ROCK inhibitors may improve their efficacy, but their antithrombotic effects raise safety concerns in hemorrhagic stroke, precluding use prior to neuroimaging. Therefore, we tested whether ROCK inhibition affects the bleeding times, and worsens hematoma volume in a model of intracerebral hemorrhage (ICH) induced by intrastriatal collagenase injection in mice. Tail bleeding time was measured 1 h after treatment with isoform-nonselective inhibitor fasudil, or ROCK2-selective inhibitor KD025, or their vehicles. In the ICH model, treatments were administered 1 h after collagenase injection. Although KD025 but not fasudil prolonged the tail bleeding times, neither drug expanded the volume of ICH or worsened neurological deficits at 48 h compared with vehicle. Although more testing is needed in aged animals and comorbid models such as diabetes, these results suggest ROCK inhibitors may be safe for pre-hospital administration in acute stroke.

Subtotal Resection of a Thalamic Glioblastoma Multiforme through Transsylvian Approach.

Glioblastoma multiforme (GBM) is a malignant brain tumor with an ominous prognosis. The standard treatment includes maximal safe resection plus adjuvant therapy. Thalamic GBMs, however, are unfavorable for microsurgical removal because of deep location and proximity to critical structures. We present a patient presenting with progressive hemiparesis and decreased consciousness with a large thalamic GBM who underwent subtotal resection through a transsylvian approach. His clinical and neurologic condition improved after surgery and he survived nine months after surgery. This may propose that in selected cases, more aggressive microsurgery for debulking of tumors might have some impact in the final outcome.​​​.

Brain Computed Tomography Angiography as an Ancillary Test in the Confirmation of Brain Death.

Introduction Brain death (BD) is the irreversible termination of the functioning of the brain. The diagnosis should be first made by clinical criteria and confirmed by using paraclinical confirmatory techniques (ancillary tests). While conventional brain angiography remains the standard method of choice, computed tomography angiography (CTA) has emerged as an alternative method. In this study, we tried to evaluate the accuracy of CTA for the diagnosis of BD. Methods In this study, we included nine patients with a clinical diagnosis of BD, confirmed by electroencephalography (EEG). CTA was then performed to compare the results. Results The most frequent cause for BD was multiple trauma (7/9) in our patients, followed by aneurysm rupture and brain infarct. CTA examination in all patients showed opacification of extracranial arteries and major branches of external carotid artery (ECA), including superficial temporal arteries (STAs), while no opacification was observed in the internal carotid arteries (ICA) including and beyond the cavernous segment, middle cerebral arteries (MCAs), anterior cerebral arteries (ACAs), distal vertebral arteries (VAs), and basilar artery (BA). Moreover, no opacification was observed in the internal cerebral veins (ICVs) or great cerebral vein (GCV). Conclusion The accuracy rate of CTA in the detection of intracranial circulatory arrest was 100%. CTA examinations confirmed BD diagnoses in all patients who had clinical and EEG BD diagnoses, and no confliction between CTA findings and clinical diagnoses was observed.

Traumatic Spinal Cord Injury: Long-Term Motor, Sensory, and Urinary Outcomes.

STUDY DESIGN: Retrospective study. PURPOSE: To evaluate how motor, sensory, and urinary outcomes of spinal cord injury (SCI) patients were influenced in the long term. OVERVIEW OF LITERATURE: SCI is a potentially disabling and devastating neurological outcome that can occur because of spinal column fractures. Most studies have not evaluated or have failed to show the influence of different surgical approaches and other parameters on neurological recovery. METHODS: A thorough history regarding sensory, motor, and urinary complaints was taken from 103 patients with SCI due to vertebral fracture; patients were followed by a thorough neurological examination. Subsequently, all medical records of patients, including neurological state after trauma, trauma mechanism, treatment protocol, surgical protocol, and imaging findings, were evaluated. RESULTS: Of the 103 patients, 73.8% were survivors of a major earthquake and 26.2% were victims of vehicle accidents; 92.2% patients were surgically treated, while 7.8% underwent conservative management. The mean follow-up duration was 10.3 years. In follow-up visits, 67.0%, 12.6%, 13.6%, and 6.8% patients showed no, partial, substantial, and complete motor improvement, respectively; 68.0%, 26.2%, and 5.8% showed no, mild, and substantial sensory improvement, respectively; and 73.8%, 17.5%, and 8.7% showed no, substantial, and complete urinary improvement, respectively. Logistic regression analysis showed that sex, age at injury time, follow-up duration, trauma mechanism, and stem cell therapy had no effect on motor, sensory, and urinary improvement. Higher initial scores on the American Spinal Injury Association (ASIA) classification, lumbar fracture level, and performance of laminectomy improved motor outcome; higher initial ASIA scores improved urinary and sensory outcomes. CONCLUSIONS: The initial ASIA score is the most important factor for prognosticating motor, sensory, and urinary improvement in SCI patients. Lumbar (L3-L5) and thoracic (T1-T10) fractures have the best and worst prognosis, respectively, in terms of motor recovery. Laminectomy during surgery improves motor function.

Factors Influencing Helmet Use, Head Injury, and Hospitalization Among Children Involved in Skateboarding and Snowboarding Accidents.

CONTEXT: Up to 75% of skateboarders and snowboarders admitted to the hospital sustain head injuries. It is unclear why not all children and teenagers wear helmets while snowboarding and skateboarding given the protection they afford. OBJECTIVES: To report on the prevalence of, and factors associated with, skateboarding and snowboarding in injured children and to explore factors that influence helmet use, head injury, and hospitalization in this sample. DESIGN: A cross-sectional study of skateboard- and snowboard-associated injuries from 2003 to 2012 among individuals younger than age 18 years using National Electronic Injury Surveillance System (NEISS) data from approximately 100 hospitals. MAIN OUTCOME MEASURES: Helmet use, head injury, and hospitalization. RESULTS: Of 1742 patients in the study, 852 (48.9%) and 890 (51.1%) were skateboarders and snowboarders, respectively. Overall, 907 (52.1%) did not use helmets, and 704 (40.4%) sustained head injuries. Multiple logistic regression analysis showed that age, race/ethnicity, location of boarding, and engaging in skateboarding influenced helmet use. Sex, race/ethnicity, helmet use, and skateboarding predicted head injury. Age, sex, skateboarding, and head injury predicted hospital admission. CONCLUSION: Statistically significant differences exist in helmet use, head injury, and hospitalization rates between skateboarders and snowboarders. Our findings suggest that injury prevention and outreach programs are needed to increase helmet use and reduce the risk of head injury and hospitalization in skateboarders and other at-risk groups. Further studies are needed to clarify the association between race/ethnicity and helmet use among skateboarders and snowboarders.

Pitting Oedema in a Patient with Lumbar Disc Herniation: Case report of an unusual association.

Oedema refers to the excessive accumulation of fluid within intercellular tissues as a result of disequilibrium between the capillary hydrostatic and oncotic pressure gradients. Lumbar disc herniation (LDH) commonly causes lower back pain and radicular leg pain. We report a 57-year-old female who presented to the neurosurgery clinic of the Bam University of Medical Sciences, Bam, Iran, in 2015 with pain and pitting oedema in the bilateral lower extremities. Magnetic resonance imaging confirmed a diagnosis of LDH of the L3-L4 and L4-L5 vertebrae. The patient subsequently underwent a bilateral laminotomy and foraminotomy of the involved vertebrae to relieve her pain. Following the surgery, there was a complete resolution of the LDH-related symptoms as well as the oedema. Although LDH has never before been associated with oedema, it may nevertheless cause lower limb oedema in exceptional and rare cases, as highlighted in this patient.

C2 Body Fracture: Report of Cases Managed Conservatively by Philadelphia Collar.

STUDY DESIGN: Case series. PURPOSE: To present results of conservative management in patients with pure C2 body fractures. OVERVIEW OF LITERATURE: Axis body fractures, a less common subgroup of C2 fractures, are commonly classified as vertical coronal, vertical sagittal, and transverse subtypes. While the treatment paradigm for other C2 fractures is clear, there is insufficient evidence to support treatment guidelines for C2 body fractures. METHODS: Eleven patients with pure C2 body fractures were managed with external immobilization and followed thereafter. RESULTS: All neurologic examinations were normal. In computed tomography (CT) scans, four, two, three, and two patients had a coronal, sagittal, horizontal, and burst fracture, respectively. Magnetic resonance imaging showed hematoma and partial rupture in the anterior longitudinal ligament in four patients, posterior ligamentous complex injury in one, and normal ligamentous structure in six. All fractures were managed conservatively using the Philadelphia collar, which was continued until complete disappearance of symptoms (within 1-3 months in all patients). The decision to discontinue the neck collar was made by a dynamic neck X-ray and CT scan that showed complete bony fusion. All patients were then followed for an additional 1.5 years (mean follow-up of 21 months for all patients). No patient showed any neurologic symptoms or deficits during the follow-up period. CONCLUSIONS: In patients with pure C2 body fracture, non-operative management with Philadelphia neck collar is a safe and efficacious option, even in the presence of some sort of ligamentous injury.