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.

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.

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.

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.

Does distracting pain justify performing brain computed tomography in multiple traumas with mild head injury?

Traumatic brain injury (TBI) is a significant health concern classified as mild, moderate, and severe. Although the indications to perform brain computed tomography (CT) are clear in moderate and severe cases, there still exists controversy in mild TBI (mTBI). We designed the study to evaluate the significance of distracting pain in patients with mTBI. The study population included patients with mild traumatic brain injury (GCS ≥13). Moderate and high risk factors including age <18 months or ≥60 years, moderate to severe or progressive headache, ≥2 episodes of vomiting, loss of consciousness (LOC), post-traumatic amnesia, seizure or prior antiepileptic use, alcohol intoxication, previous neurosurgical procedures, uncontrolled hypertension, anticoagulant use, presence of focal neurologic deficits, deformities in craniofacial region, and penetrating injuries were excluded. The patients were then grouped based on presence (DP+) or absence (DP-) of another organ fracture with severe pain (based on VAS). The primary outcome was any abnormal findings on brain CT scans; 330 patients were enrolled (184 DP+ and 146 DP-). Overall, two DP+ and one DP- patients had mild cerebral edema in brain CT (p > 0.99). No patients had any neurologic symptoms or signs in follow-up. Our results show that in the absence of any other risk factors, distracting pain from other organs (limbs, pelvis, and non-cervical spine) cannot be regarded as a brain CT indication in patients with mild TBI, as it is never associated with significant intracranial lesions.

Factors predicting early deterioration in mild brain trauma: a prospective study.

PRIMARY OBJECTIVE: To evaluate risk factors for clinical deterioration in mild traumatic brain injury. RESEARCH DESIGN: Prospective cross-sectional. METHODS AND PROCEDURES: This study evaluated 203 patients with mild traumatic brain injury. A brain computed tomography scan was performed in all patients and they were observed for 6-48 hours. MAIN OUTCOMES AND RESULTS: Among these patients, 2.5% had cerebral contusions and the most common sites for contusions were frontal lobes; 94% of patients had no hematoma in the initial scan, while 3% had subgaleal haematoma, 1.5% had subdural haematoma, 1% showed subarachnoid haemorrhage, 0.5% intracerebral haemorrhage and 0.5% epidural haemorrhage. GCS was 15 in 96.6% and 13-14 in 3.4%. GCS deteriorated in three (1.5%). Presence of coagulopathy, anticoagulant drug use, GCS of 13-14 and increased age predicted further deterioration. Among CT findings, those with midline shift, cerebral contusion and diffuse cerebral oedema deteriorated more. Among different haematoma types, only SDH predicted a worse outcome. CONCLUSIONS: Although deterioration rarely occurs in patients with mild brain injury, those with coagulopathy, anticoagulant drug use, GCS of 13-14, increased age, midline shift, cerebral contusions, diffuse cerebral oedema and SDH were more prone to deterioration.

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).

The underlying factor structure of National Institutes of Health Stroke scale: an exploratory factor analysis.

The underlying structure of National Institutes of Health Stroke Scale (NIHSS) as the most widely used scale in clinical trials has been the focus of little attention. The aim of the current study was to elucidate the clustering pattern of NIHSS items in ischemic stroke patients. A series of 152 consecutive patients with first-ever ischemic strokes admitted to a university affiliated hospital were enrolled. NIHSS score was estimated on admission and correlation coefficients between its items were calculated. Further, exploratory factor analysis was used to study the clustering pattern of NIHSS items. Extinction neglect, visual field, and facial palsy were weakly associated with other NIHSS items. Factor analysis led to a four-factor structure. Factors 1 and 3 were determined by left brain function as items of right arm and leg motor, language and dysarthria loaded on both of them. By contrast, factor 2 reflected right brain involvement. Since visual field and ataxia loaded on factor 4, this factor was primarily associated with posterior strokes. Our study shows that a four-factor structure model is plausible for NIHSS. Further, for the first time, a single distinct factor is identified for posterior strokes.

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.

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.

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.

Mitochondrial mutation in Iranian patients with multiple sclerosis, correlation between haplogroups H, A and clinical manifestations.

As multiple sclerosis (MS) has long been known to be associated with Leber, hereditary optic neuropathy (LHON), a disease caused by mitochondrial (mtDNA) mutations, in this study we assessed possible involvement of mtDNA point mutation in MS patients. Fifty-two MS patients whose disease was confirmed with revised McDonald criteria and referred to Iranian Center of Neurological Research of Imam Khomeini hospital during 2006-2007 entered the study. Secondary mtDNA mutations, age, gender, clinical disability according to expanded disability status scale (EDSS), course of the disease, and presenting symptoms were the variables investigated in this study. DNA purification was performed by Diatom DNA Extraction Kit. Analysis of data was done by SPSS V11.5. The prevalent mutations with frequency of 19.2% were J, L, and T haplogroups. Haplotype A was more prevalent in patients with younger age of onset (P-value = 0.012) and high proportion of haplogroup H was associated with optic nerve involvement (P-value = 0.015). No motor symptoms were seen in haplogroup H patients. There is no significant relationship between duration of the disease and EDSS in different mutation of mtDNA.

Analysis of HLA DR2&DQ6 (DRB1*1501, DQA1*0102, DQB1*0602) haplotypes in Iranian patients with multiple sclerosis.

Multiple sclerosis (MS) is prototype of inflammatory demyelinating disease of the central nervous system .The etiology of MS remains unclear, but according to current data the disease develops in genetically susceptible individuals and may require additional environmental triggers. The human leukocyte antigen (HLA) class II alleles (DRB1*1501, DQA1*0102, DQB1*0602) may have the strongest genetic effect in MS. In this study, the role of these alleles were investigated in 183 Iranian patients with multiple sclerosis and compared with 100 healthy individuals. HLA typing for DRB1*1501, DQA1*0102, DQB1*0602 was performed by polymerase chain reaction (PCR) amplification with sequence-specific primers (PCR-SSP) method. The results show that, HLA DR B1*1501 was significantly more frequent among MS patients (46% vs. 20%, PV = 0.0006) but DQA1*0102 haplotype was negatively associated with MS (30% vs. 50%, PV = 0.0049) and no significant association was found with DQB1*0602 and MS patients in comparison with control group (24% and 30%, PV = 0.43). No significant correlation was observed among these alleles with sex, type of disease; initial symptoms, expanded disability status scale (EDSS), as well as age at onset and familial MS. This study therefore indicates that there is no association of above HLA haplotypes with clinical presentation, disease duration, and disability in Iranian patients with MS which is in line with other previous studies in different ethnic groups.

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.

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.

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.

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.

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.