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Atlas of Endoscopic Neurosurgery of the Third Ventricle: Basic Principles for Ventricular Approaches and Essential Intraoperative Anatomy

Atlas of Endoscopic Neurosurgery of the Third Ventricle: Basic Principles for Ventricular Approaches and Essential Intraoperative Anatomy

Atlas of Endoscopic Neurosurgery of the Third Ventricle: Basic Principles for Ventricular Approaches and Essential Intraoperative Anatomy

By Roberto Alexandre Dezena

List Price: $199.00


This book describes in practical terms the endoscopic neurosurgery of the third ventricle and surrounding structures, emphasizing aspects of intraoperative endoscopic anatomy and ventricular approaches for main diseases, complemented by CT / MRI images. It is divided in two parts: Part I describes the evolution of the description of the ventricular system and traditional ventricular anatomy, besides the endoscopic neurosurgery evolution and current concepts, with images and schematic drawings, while Part II presents a collection of intraoperative images of endoscopic procedures, focusing in anatomy and main pathologies, complemented by schemes of the surgical approaches and CT / MRI images.

The Atlas of Endoscopic Neurosurgery of the Third Ventricle offers a revealing guide to the subject, addressing the needs of medical students, neuroscientists, neurologists and especially neurosurgeons.

Product Details

  • Original language: English
  • Number of items: 1
  • Dimensions: 11.41″ h x .88″ w x 8.51″ l,
  • Binding: Hardcover
  • 271 pages

About the Author

Roberto Alexandre Dezena: MD from the Federal University of Triângulo Mineiro, Uberaba, Brazil (2003), completed his residency training in Neurosurgery at Santa Casa de Misericórdia de Ribeirão Preto, Brazil (2009), achieved his PhD in Neurosurgery at Ribeirão Preto Medical School of University of São Paulo, Brazil (2011), and his Postdoctoral Fellowship at Federal University of Triângulo Mineiro, Uberaba, Brazil (2014). In Brazil, is Full Member of Brazilian Society of Neurosurgery (SBN) and Brazilian Academy of Neurosurgery (ABNc). Internationally, is Fellow of World Federation of Neurosurgical Societes (WFNS), Active Member of both International Society for Pediatric Neurosurgery (ISPN) and International Federation of Neuroendoscopy (IFNE), and Full Member of both Latin American Federation of Neurosurgery Societes (FLANC) and Latin American Group of Studies in Neuroendoscopy (GLEN). Fellow of University of Tübingen, Germany, and University of Hiroshima, Japan. Currently is Chief of Division of Neurosurgery at Clinics Hospital, Neurosurgery Residency Director, and Professor of Postgraduate Program in Health Sciences and Postgraduate Program in Applied Biosciences, all in Federal University of Triângulo Mineiro, Uberaba, Brazil. Main neurosurgical areas in vascular and neuro-oncology microneurosurgery, endoscopic neurosurgery, pediatric neurosurgery, spinal surgery and neurotrauma. Main research areas in endoscopic neurosurgery, pediatric neurosurgery, neurotrauma, experimental cerebral ischemia and basic neurosciences. Editorial Board Member of International Journal of Anesthesiology Research (Phaps), Journal of Neurology and Stroke (Medcrave), EC Neurology (EC), and International Journal of Pediatrics and Children Health (Savvy). Reviewer of several online international scientific journals, highlighting World Neurosurgery (WFNS), Neurological Research (Maney) and Journal of Neurosurgical Sciences (Minerva).


Update: Spine injury

Spine injury


At this moment there is persistent controversy within the spinal trauma community, which can be grouped under 6 headings:

First of all there is still no unanimity on the role and timing of medical and surgical interventions for patients with associated neurologic injury.

Type and timing of surgical intervention in multiply injured patients.

In some common injury types like odontoid fractures and thoracolumbar burst fracture, there is wide variation in practice between operative versus nonoperative management without clear reasons.

The role of different surgical approaches and techniques in certain injury types are not clarified yet.

Methods of nonoperative management and care of elderly patients with concurrent complex disorders are also areas where there is no consensus1).


Spinal cord injury

Whiplash-associated disorders

Pediatric spine injury

Cervical spine injury

Thoracolumbar spine fracture

Sacral fracture

Osteoporotic vertebral fracture

Spinal gunshot wound

Penetrating neck trauma

Traumatic spine injuries are often transferred to regional tertiary trauma centers from OSH and subsequently discharged from the trauma center’s emergency department (ED) suggesting secondary overtriage of such injuries.

A study to investigate interfacility transfers with spine injuries found high rate of secondary overtriage of neurologically intact patients with isolated spine injuries. Potential solutions include increasing spine coverage in community EDs, increasing direct communication between the OSH and spine specialist at the tertiary center, and utilization of teleradiology 2).


Hydrocephalus is a rare complication of traumatic spine injury. A literature review reflects the rare occurrence with cervical spine injury.

Dragojlovic et al present a case of traumatic injury to the lumbar spine from a gunshot wound, which caused communicating hydrocephalus. The patient sustained a gunshot wound to the lumbar spine and had an L4-5 laminectomy with exploration and removal of foreign bodies. At the time of surgery, the patient was found to have dense subarachnoid hemorrhage in the spinal column. He subsequently had intermittent headaches and altered mental status that resolved without intervention. The headaches worsened, so a computed tomography scan of the brain was obtained, which revealed hydrocephalus. A ventriculoperitoneal shunt was placed, and subsequent computed tomography scan of the brain showed reduced ventricle size. The patient returned to rehabilitation with complete resolution of hydrocephalus symptoms. Intrathecal hemorrhage with subsequent obstruction or decreased absorption of cerebrospinal fluid at the distal spinal cord was thought to lead to communicating hydrocephalus in this case of lumbar penetrating trauma. In patients with a history of hemorrhagic, traumatic spinal injury who subsequently experience headaches or altered mental status, hydrocephalus should be included in the differential diagnosis and adequately investigated 3).


ATLS® algorithm and spine trauma assessment. In Step „A“ cervical spine (C-Spine) protection is indispensable. Every unconscious patient is stabilized by stiff-neck. Patients with signs of chest injury in step „B” and abdominal injury in step „C“, especially retroperitoneal are highly suspicious for thoracic (T-) and/or (L-) lumbar spine injury. Normal motor exam and reflexes do not rule out significant spine injury in the comatose patient. Abnormal neurologic exam is a sign for substantial spinal column injury including spinal cord injury (SCI). Log roll in step „E” is important to assess the dorsum of the cervical to the sacral spine and to look out for any signs of bruising, open wounds, tender points and to palpate the paravertebral tissue and posterior processus in search for distraction injury. Spine precautions should only be discontinued when patients gain back consciousness and are alert to communicate sufficiently on spinal discomfort or neurologic sensations before the spine is cleared 4).

Data on all patients with traumatic spine injuries admitted to the Alfred Hospital, Melbourne between May 1, 2009, and January 1, 2011, were collected:

There were 965 patients with traumatic spine injuries with 2,333 spine trauma levels. The general cohort showed a trimodal age distribution, male-to-female ratio of 2:2, motor vehicle accidents as the primary spine trauma mechanism, 47.7% patients with severe polytrauma as graded using the Injury Severity Score (ISS), 17.3% with traumatic brain injury (TBI), the majority of patients with one spine injury level, 7% neurological deficit rate, 12.8% spine trauma operative rate, and 5.2% mortality rate. Variables with statistical significance trending toward mortality were the elderly, motor vehicle occupants, severe ISS, TBI, C1-2 dissociations, and American Spinal Injury Association (ASIA) A, B, and C neurological grades. Variables with statistical significance trending toward the elderly were females; low falls; one spine injury level; type 2 odontoid fractures; subaxial cervical spine distraction injuries; ASIA A, B, and C neurological grades; and patients without neurological deficits. Of the general cohort, 50.3% of spine trauma survivors were discharged home, and 48.1% were discharged to rehabilitation facilities. This study provides baseline spine trauma epidemiological data. The trimodal age distribution of patients with traumatic spine injuries calls for further studies and intervention targeted toward the 46- to 55-year age group as this group represents the main providers of financial and social security. The study’s unique feature of delineating variables with statistical significance trending toward both mortality and the elderly also provides useful data to guide future research studies, benchmarking, public health policy, and efficient resource allocation for the management of spine trauma 5).


There is no universally accepted outcome instrument available that is specifically designed or validated for spinal trauma patients, contributing to controversies related to the optimal treatment and evaluation of many types of spinal injuries. Therefore, the AOSpine Knowledge Forum Trauma aims to develop such an instrument using the International Classification of Functioning Disability and Health (ICF) as its basis.

Experts from the 5 AOSpine International world regions were asked to give their opinion on the relevance of a compilation of 143 ICF categories for spinal trauma patients on a 3-point scale: “not relevant,” “probably relevant,” or “definitely relevant.” The responses were analyzed using frequency analysis. Possible differences in responses between the 5 world regions were analyzed with the Fisher exact test and descriptive statistics.

Of the 895 invited AOSpine International members, 150 (16.8%) participated in this study. A total of 13 (9.1%) ICF categories were identified as definitely relevant by more than 80% of the participants. Most of these categories were related to the ICF component “activities and participation” (n = 8), followed by “body functions” (n = 4), and “body structures” (n = 1). Only some minor regional differences were observed in the pattern of answers.

More than 80% of an international group of health care professionals experienced in the clinical care of adult spinal trauma patients indicated 13 of 143 ICF categories as definitely relevant to measure outcomes after spinal trauma. This study creates an evidence base to define a core set of ICF categories for outcome measurement in adult spinal trauma patients 6).

Early independent risk factors predictive of suboptimal physical health status identified in a level 1 trauma center in polytrauma patients with spine injuries were tachycardia, hyperglycemia, multiple chronic medical comorbidities, and thoracic spine injuries. Early spine trauma risk factors were shown not to predict suboptimal mental health status outcomes 7).



Oner C, Rajasekaran S, Chapman JR, Fehlings MG, Vaccaro AR, Schroeder GD, Sadiqi S, Harrop J. Spine Trauma-What Are the Current Controversies? J Orthop Trauma. 2017 Sep;31 Suppl 4:S1-S6. doi: 10.1097/BOT.0000000000000950. PubMed PMID: 28816869.

Bible JE, Kadakia RJ, Kay HF, Zhang CE, Casimir GE, Devin CJ. How often are interfacility transfers of spine injury patients truly necessary? Spine J. 2014 Apr 14. pii: S1529-9430(14)00379-9. doi: 10.1016/j.spinee.2014.01.065. [Epub ahead of print] PubMed PMID: 24743061.

Dragojlovic N, Stampas A, Kitagawa RS, Schmitt KM, Donovan W. Communicating Hydrocephalus Due to Traumatic Lumbar Spine Injury: Case Report and Literature Review. Am J Phys Med Rehabil. 2016 Jun 17. [Epub ahead of print] PubMed PMID: 27323322.

Tee JW, Chan CH, Fitzgerald MC, Liew SM, Rosenfeld JV. Epidemiological trends of spine trauma: an Australian level 1 trauma centre study. Global Spine J. 2013 Jun;3(2):75-84. doi: 10.1055/s-0033-1337124. Epub 2013 Mar 19. PubMed PMID: 24436855; PubMed Central PMCID: PMC3854579.

Oner FC, Sadiqi S, Lehr AM, Aarabi B, Dunn RN, Dvorak MF, Fehlings MG, Kandziora F, Post MW, Rajasekaran S, Vialle L, Vaccaro AR. Toward Developing a Specific Outcome Instrument for Spine Trauma: An Empirical Cross-sectional Multicenter ICF-Based Study by AOSpine Knowledge Forum Trauma. Spine (Phila Pa 1976). 2015 Sep 1;40(17):1371-1379. PubMed PMID: 26323025.

Tee JW, Chan CH, Gruen RL, Fitzgerald MC, Liew SM, Cameron PA, Rosenfeld JV.Early predictors of health-related quality of life outcomes in polytrauma patients with spine injuries: a level 1 trauma center study. Global Spine J. 2014 Feb;4(1):21-32. doi: 10.1055/s-0033-1358617. Epub 2013 Nov 6. PubMed PMID: 24494178.

Update: Spinal cord injury treatment

Spinal cord injury treatment

Substantial heterogeneity in the patient population, their presentation and underlying pathophysiology has sparked debates along the care spectrum from initial assessment to definitive treatment.

In seeking a cure, these patients often undergo treatments that lack scientific and methodological rigor.

Ahuja et al. reviews spinal cord injury (SCI) management followed by a discussion of the salient controversies in the field. Current care practices modeled on the American Association of Neurological Surgeons/Congress of Neurological Surgeons joint section guidelines are highlighted including key recommendations regarding immobilization, avoidance of hypotension, early International Standards for Neurological Classification of SCI examination and intensive care unit treatment. From a diagnostic perspective, the evolving roles of CT, MRI, and leading-edge microstructural MRI techniques are discussed with descriptions of the relevant clinical literature for each. Controversies in management relevant to clinicians including the timing of surgical decompression, methylprednisolone administration, blood pressure augmentation, intraoperative electrophysiological monitoring, and the role of surgery in central cord syndrome and pediatric SCI are also covered in detail. Finally, the article concludes with a reflection on clinical trial design tailored to the heterogeneous population of individuals with SCI 1).

Cell therapy


Increased spinal cord perfusion and blood pressure goals have been recommended for spinal cord injury (SCI).

Treatment consists of restoration of CSF flow, typically via arachnoidolysis and syrinx decompression Research into treatments for spinal cord injuries includes controlled hypothermia and stem cells, though many treatments have not been studied thoroughly and very little new research has been implemented in standard care.

Treatment of spinal cord injuries starts with restraining the spine and controlling inflammation to prevent further damage. The actual treatment can vary widely depending on the location and extent of the injury.

Acute spinal cord injury (SCI) is commonly treated by elevating the mean arterial pressure (MAP). Other potential interventions include cerebrospinal fluid drainage (CSFD).

Both MAP elevation alone and CSFD alone led to only short-term improvement of SCBF. The combination of MAP elevation and CSFD significantly and sustainably improved SCBF and spinal cord perfusion pressure. Although laser Doppler flowmetry can provide flow measurements to a tissue depth of only 1.5 mm, these results may represent pattern of blood flow changes in the entire spinal cord after injury 2).

Lumbar cerebrospinal fluid drainage after spinal cord injury, as used in the pig study by Martirosyan et al would reduce intrathecal pressure at the injury site only if the spinal cord is not compressed against the surrounding dura. Unfortunately, in most patients with severe spinal cord injury, the spinal cord is compressed against the surrounding dura; therefore, drainage of cerebrospinal fluid from the lumbar region will not reduce intrathecal pressure at the injury site 3).

Unfortunately, no data correlate the severity of spinal cord injury, the degree of spinal cord swelling, and persistent CSF flow across an injured segment in the human spinal cord. The physiological observations in animals and humans alike indicate that CSF drainage and induced hypertension warrant further investigation as a potential treatment for acute spinal cord injury 4).


In many cases, spinal cord injuries require substantial physical therapy and rehabilitation, especially if the patient’s injury interferes with activities of daily life.

Pharmacological Therapy

Despite a degree of theoretical progress, there is a lack of effective drugs that are able to improve the motor function of patients following spinal cord injury (SCI) 5) 6) 7) 8).

see Methylprednisolone for Spinal cord injury.

Dexamethasone acetate (DA) produces neuroprotective effects by inhibiting lipid peroxidation and inflammation by reducing cytokine release and expression. However, its clinical application is limited by its hydrophobicity, low biocompatibility and numerous side effects when using large dosage. Therefore, improving DA’s water solubility, biocompatibility and reducing its side effects are important goals that will improve its clinical utility. The objective of this study is to use a biodegradable polymer as the delivery vehicle for DA to achieve the synergism between inhibiting lipid peroxidation and inflammation effects of the hydrophobic-loaded drugs and the amphipathic delivery vehicle. Wang et al., successfully prepared DA-loaded polymeric micelles (DA/MPEG-PCL micelles) with monodispersed and approximately 25 nm in diameter, and released DA over an extended period in vitro. Additionally, in the hemisection spinal cord injury (SCI) model, DA micelles were more effective in promoting hindlimb functional recover, reducing glial scar and cyst formation in injured site, decreasing neuron lose and promoting axon regeneration. Therefore, data suggest that DA/MPEG-PCL micelles have the potential to be applied clinically in SCI therapy 9).


After traumatic spinal cord injury (TSCI), laminectomy does not improve intraspinal pressure (ISP), spinal cord perfusion pressure (SCPP) or the vascular pressure reactivity index (sPRx) at the injury site sufficiently because of dural compression.

21 patients with acute, severe TSCI had realignment of the fracture and surgical fixation; 11 had laminectomy (laminectomy group) and 10 had laminectomy and duroplasty (laminectomy + duroplasty group). Primary outcomes were MRI evidence of spinal cord decompression (increase in intradural space, cerebrospinal fluid around the injured cord) and spinal cord physiology (ISP, SCPP, sPRx). The laminectomy and laminectomy + duroplasty groups were well matched. Compared with the laminectomy group, the laminectomy + duroplasty group had greater increase in intradural space at the injury site and more effective decompression of the injured cord. In the laminectomy + duroplasty group, ISP was lower, SCPP higher and sPRx lower, i.e. improved vascular pressure reactivity, compared with the laminectomy group. Duroplasty caused cerebrospinal fluid leak that settled with lumbar drain in one patient and pseudomeningocele that resolved in five patients. We conclude that, after TSCI, laminectomy + duroplasty improves spinal cord radiological and physiological parameters more effectively than laminectomy 10).



Ahuja CS, Schroeder GD, Vaccaro AR, Fehlings MG. Spinal Cord Injury-What Are the Controversies? J Orthop Trauma. 2017 Sep;31 Suppl 4:S7-S13. doi: 10.1097/BOT.0000000000000943. PubMed PMID: 28816870.

Martirosyan NL, Kalani MY, Bichard WD, Baaj AA, Gonzalez LF, Preul MC, Theodore N. Cerebrospinal fluid drainage and induced hypertension improve spinal cord perfusion after acute spinal cord injury in pigs. Neurosurgery. 2015 Apr;76(4):461-9. doi: 10.1227/NEU.0000000000000638. PubMed PMID: 25621979.

Papadopoulos MC. Letter: Intrathecal Pressure After Spinal Cord Injury. Neurosurgery. 2015 Sep;77(3):E500. doi: 10.1227/NEU.0000000000000862. PubMed PMID: 26110999.

Martirosyan NL, Kalani MY, Theodore N. In Reply: Intrathecal Pressure After Spinal Cord Injury. Neurosurgery. 2015 Sep;77(3):E500-1. doi: 10.1227/NEU.0000000000000857. PubMed PMID: 26111000.

Hu R, Zhou J, Luo C, et al. Glial scar and neuroregeneration: Histological, functional, and magnetic resonance imaging analysis in chronic spinal cord injury. J Neurosurg Spine. 2010;13:169–180. doi: 10.3171/2010.3.SPINE09190.

Macias CA, Rosengart MR, Puyana JC, et al. The effects of trauma center care, admission volume, and surgical volume on paralysis after traumatic spinal cord injury. Ann Surg. 2009;249:10–17. doi: 10.1097/SLA.0b013e31818a1505.

Samantaray S, Sribnick EA, Das A, et al. Neuroprotective efficacy of estrogen in experimental spinal cord injury in rats. Ann NY Acad Sci. 2010;1199:90–94. doi: 10.1111/j.1749-6632.2009.05357.x.

Fu ES, Tummala RP. Neuroprotection in brain and spinal cord trauma. Curr Opin Anaesthesiol. 2005;18:181–187. doi: 10.1097/

Wang Y, Wu M, Gu L, Li X, He J, Zhou L, Tong A, Shi J, Zhu H, Xu J, Guo G. Effective improvement of the neuroprotective activity after spinal cord injury by synergistic effect of glucocorticoid with biodegradable amphipathic nanomicelles. Drug Deliv. 2017 Nov;24(1):391-401. doi: 10.1080/10717544.2016.1256003. PubMed PMID: 28165815.

Phang I, Werndle MC, Saadoun S, Varsos GV, Czosnyka M, Zoumprouli A, Papadopoulos MC. Expansion Duroplasty Improves Intraspinal Pressure, Spinal Cord Perfusion Pressure and Vascular Pressure Reactivity Index in Patients with Traumatic Spinal Cord Injury. J Neurotrauma. 2015 Feb 23. [Epub ahead of print] PubMed PMID: 25705999.

Update: AOSpine subaxial cervical spine injury classification system

AOSpine subaxial cervical spine injury classification system

See: aospine_subaxial_cervical_spine_injury_classification_system.pdf

This project describes a morphology-based subaxial cervical spine injury classification system. Using the same approach as the AOSpine Thoracolumbar Classification System, the goal was to develop a comprehensive yet simple classification system with high intra- and interobserver reliability to be used for clinical and research purposes.

A subaxial cervical spine injury classification system was developed using a consensus process among clinical experts. All investigators were required to successfully grade 10 cases to demonstrate comprehension of the system before grading 30 additional cases on two occasions, 1 month apart. Kappa coefficients (κ) were calculated for intraobserver and interobserver reliability.

The classification system is based on three injury morphology types similar to the TL system: compression injuries (A), tension band injuries (B), and translational injuries (C), with additional descriptions for facet injuries, as well as patient-specific modifiers and neurologic status. Intraobserver and interobserver reliability was substantial for all injury subtypes (κ = 0.75 and 0.64, respectively).

The AOSpine subaxial cervical spine injury classification system demonstrated substantial reliability in this initial assessment, and could be a valuable tool for communication, patient care and for research purposes 1).

The AOSpine subaxial cervical spine injury classification system (using the four main injury types or at the sub-types level) allows a significantly better agreement than the Allen and Ferguson classification of subaxial cervical spine injury. The A&F scheme does not allow reliable communication between medical professionals 2).

see also Subaxial Injury Classification (SLIC).

Case series


Aarabi et al. analyzed the relevant clinical, imaging, management, and American Spinal Injury Association (ASIA) impairment scale (AIS) grade conversion of 92 AIS grades A-C patients with cervical spine injury. We correlated morphology class with age, injury severity score (ISS), follow-up ASIA motor score (AMS), intramedullary lesion length (IMLL), and AIS grade conversion at 6 months after injury.

The mean age of patients was 39.3 years, 83 were men, and 69 were injured during an automobile accident or after a fall. The AOSpine class was A4 in 8, B2 in 5, B2A4 in 16, B3 in 19, and C in 44 patients. The mean ISS was 29.7 and AMS was 17.1. AIS grade was A in 48, B in 25, and C in 19 patients. Mean IMLL on postoperative magnetic resonance imaging was 72 mm: A4 = 68.1; B2A4 = 86.5; B2 = 59.3; B3 = 46.8; and C = 79.9. At a mean follow-up of 6 months, the mean AMS was 39.6. Compared to patients with class B3 injuries, those with class C injuries were significantly younger (P < 0.0001), had longer IMLL (P < 0.002), and were less likely to have AIS grade conversion to a better grade (P < 0.02).

The AOSpine subaxial cervical spine injury classification system successfully predicted injury severity (longer IMLL) and chances of neurologic recovery (AIS grade conversion) across different class subtypes 3).


Silva et al., evaluated the new classification

Patients with subaxial cervical spine trauma (SCST) treated at the authors’ institution according to the Subaxial Cervical Spine Injury Classification system were included. Five different blinded researchers classified patients’ injuries according to the new AOSpine system using CT imaging at 2 different times (4-week interval between each assessment). Reliability was assessed using the kappa index (κ), while validity was inferred by comparing the classification obtained with the treatment performed.

Fifty-one patients were included: 31 underwent surgical treatment, and 20 were managed nonsurgically. Intraobserver agreement for subgroups ranged from 0.61 to 0.93, and interobserver agreement was 0.51 (first assessment) and 0.6 (second assessment). Intraobserver agreement for groups ranged from 0.66 to 0.95, and interobserver agreement was 0.52 (first assessment) and 0.63 (second assessment). The kappa index in all evaluations was 0.67 for Type A, 0.08 for Type B, and 0.68 for Type C injuries, and for the facet modifier it was 0.33 (F1), 0.4 (F2), 0.56 (F3), and 0.75 (F4). Complete agreement for all components was attained in 25 cases (49%) (19 Type A and 6 Type C), and for subgroups it was attained in 22 cases (43.1%) (16 Type A0 and 6 Type C). Type A0 injuries were treated conservatively or surgically according to their neurological status and ligamentous status. Type C injuries were treated surgically in almost all cases, except one.

While the general reliability of the newer AOSpine system for SCST was acceptable for group classification, significant limitations were identified for subgroups. Type B injuries were rarely diagnosed, and only mild (Type A0) and extreme severe (Type C) injuries had a high rate of interobserver agreement. Facet modifiers and intermediate injury patterns require better descriptions to improve their low agreement in cases of SCST 4).



Vaccaro AR, Koerner JD, Radcliff KE, Oner FC, Reinhold M, Schnake KJ, Kandziora F, Fehlings MG, Dvorak MF, Aarabi B, Rajasekaran S, Schroeder GD, Kepler CK, Vialle LR. AOSpine subaxial cervical spine injury classification system. Eur Spine J. 2016 Jul;25(7):2173-84. doi: 10.1007/s00586-015-3831-3. Epub 2015 Feb 26. PubMed PMID: 25716661.

Urrutia J, Zamora T, Campos M, Yurac R, Palma J, Mobarec S, Prada C. A comparative agreement evaluation of two subaxial cervical spine injury classification systems: the AOSpine and the Allen and Ferguson schemes. Eur Spine J. 2016 Jul;25(7):2185-92. doi: 10.1007/s00586-016-4498-0. Epub 2016 Mar 5. PubMed PMID: 26945747.

Aarabi B, Oner C, Vaccaro AR, Schroeder GD, Akhtar-Danesh N. Application of AOSpine Subaxial Cervical Spine Injury Classification in Simple and Complex Cases. J Orthop Trauma. 2017 Sep;31 Suppl 4:S24-S32. doi: 10.1097/BOT.0000000000000944. PubMed PMID: 28816872.

Silva OT, Sabba MF, Lira HI, Ghizoni E, Tedeschi H, Patel AA, Joaquim AF. Evaluation of the reliability and validity of the newer AOSpine subaxial cervical injury classification (C-3 to C-7). J Neurosurg Spine. 2016 Sep;25(3):303-8. doi: 10.3171/2016.2.SPINE151039. Epub 2016 Apr 22. PubMed PMID: 27104288.

Update: Thoracolumbar burst fracture

Thoracolumbar burst fracture


Thoracolumbar spine fractures account for 90% of spinal fractures, with the thoracolumbar burst fracture. subtype corresponding to 20% of this total, with the majority occurring at the junctional area where mechanical load is maximal

(AOSpine Thoracolumbar Classification System Subtype A3 or A4).


A thoracolumbar burst fracture is usually unstable and can cause neurological deficits and angular deformity.

Burst fractures entail the involvement of the middle column, and therefore, they are typically associated with bone fragment in the spinal canal, which may cause compression of the spinal cordconus medullariscauda equina, or a combination of these.

Fortunately, approximately half of the patients with thoracolumbar burst fractures are neurologically intact due to the wide canal diameter.


Recent evidences have revealed that functional outcomes in the long term may be equivalent between operative and nonoperative management for neurologically intact thoracolumbar burst fractures. Nevertheless, consensus has not been met regarding the optimal treatment strategy for those with neurological deficits.

A review article summarizes the contemporary evidences to discuss the role of nonoperative management in the presence of neurological deficits and the optimal timing of decompression surgery for neurological recovery. In summary, although operative management is generally recommended for thoracolumbar fracture with significant neurological deficits, the evidence is weak, and nonoperative management can also be an option for those with solitary radicular symptoms. With regards to timing of operative management, high-quality studies comparing early and delayed intervention are lacking. Extrapolating from the evidence in cervical spine injury leads to an assumption that early intervention would also be beneficial for neurological recovery, but further studies are warranted to answer these questions 1).

The traditional surgical approach, when indicated, involves spinal fixation and spinal arthrodesis. Newer studies have brought the need for fusion associated with internal fixation into question. Not performing arthrodesis could reduce surgical time and intraoperative bleeding without affecting clinical and radiological outcomes.

Diniz Jet al. aimed to assess the effect of fusion, adjuvant to internal fixation, on surgically treated thoracolumbar burst fractures.

A search of the Medline and Cochrane Central Register of Controlled Trials databases was performed to identify randomized trials that compared the use and nonuse of arthrodesis in association with internal fixation for the treatment of thoracolumbar burst fractures. The search encompassed all data in these databases up to February 28, 2016.

Five randomized/quasi-randomized trials, which involved a total of 220 patients and an average follow-up time of 69.1 months, were included in this review. No significant difference between groups in the final scores of the visual analog pain scale or Low Back Outcome Scale was detected. Surgical time and blood loss were significantly lower in the group of patients who did not undergo fusion (p < 0.05). Among the evaluated radiological outcomes, greater mobility in the affected segment was found in the group of those who did not undergo fusion. No significant difference between groups in the degree of kyphosis correction, loss of kyphosis correction, or final angle of kyphosis was observed.

The data reviewed in this study suggest that the use of arthrodesis did not improve clinical outcomes, but it was associated with increased surgical time and higher intraoperative bleeding and did not promote significant improvement in radiological parameters 2).

The expandable cage group showed better results in loss of kyphosis correction, operation time, and amount of intraoperative blood loss 3).


Bracing following operative stabilization of thoracolumbar fracture does not significantly improve stability, nor does it increase wound complications. Moreover, data suggests that post-operative bracing may not be a cost-effective measure 4).

In a systematic review in 2014 the evidence suggested that orthosis could not be necessary when TL burst fractures without neurologic deficit are treated conservatively. However, due to limitations related with number and size of the included studies, more RCTs with high quality are desirable for making recommendations with more certainty 5).



Kato S, Murray JC, Kwon BK, Schroeder GD, Vaccaro AR, Fehlings MG. Does Surgical Intervention or Timing of Surgery Have an Effect on Neurological Recovery in the Setting of a Thoracolumbar Burst Fracture? J Orthop Trauma. 2017 Sep;31 Suppl 4:S38-S43. doi: 10.1097/BOT.0000000000000946. PubMed PMID: 28816874.

Diniz JM, Botelho RV. Is fusion necessary for thoracolumbar burst fracture treated with spinal fixation? A systematic review and meta-analysis. J Neurosurg Spine. 2017 Aug 4:1-9. doi: 10.3171/2017.1.SPINE161014. [Epub ahead of print] PubMed PMID: 28777064.

Lee GJ, Lee JK, Hur H, Jang JW, Kim TS, Kim SH. Comparison of Clinical and Radiologic Results between Expandable Cages and Titanium Mesh Cages for Thoracolumbar Burst Fracture. J Korean Neurosurg Soc. 2014 Mar;55(3):142-7. doi: 10.3340/jkns.2014.55.3.142. Epub 2014 Mar 31. PubMed PMID: 24851149; PubMed Central PMCID: PMC4024813.

Piazza M, Sinha S, Agarwal P, Mallela A, Nayak N, Schuster J, Stein S. Post-operative bracing after pedicle screw fixation for thoracolumbar burst fractures: A cost-effectiveness study. J Clin Neurosci. 2017 Aug 8. pii: S0967-5868(17)30816-0. doi: 10.1016/j.jocn.2017.07.038. [Epub ahead of print] Review. PubMed PMID: 28800928.

Alcalá-Cerra G, Paternina-Caicedo AJ, Díaz-Becerra C, Moscote-Salazar LR, Fernandes-Joaquim A. Orthosis for thoracolumbar burst fractures without neurologic deficit: A systematic review of prospective randomized controlled trials. J Craniovertebr Junction Spine. 2014 Jan;5(1):25-32. doi: 10.4103/0974-8237.135213. PubMed PMID: 25013344; PubMed Central PMCID: PMC4085907.

Update: Trigeminal schwannoma radiosurgery

Stereotactic radiosurgery (SRS) is an effective and minimally invasive management option for patients with residual or newly diagnosed trigeminal schwannomas. The use resulted in good tumor control and functional improvement 1).

Predictors of a better treatment response included female sex, smaller tumor volume, root or ganglion tumor type, and the application of SRS as the primary treatment 2).

Cranial neuropathies are bothersome complications of radiosurgery, and tumor expansion in a cavernous sinus after radiosurgery appears to be the proximate cause of the complication. Loss of central enhancement could be used as a warning sign of cranial neuropathies, and for this vigilant patient monitoring is required 3).

Larger studies with open-ended follow-up review will be necessary to determine the long-term results and complications of GKS in the treatment of trigeminal schwannomas 4).

It is a promising alternative to conventional microsurgery in cases of neurinomas of the trigeminal nerve including neurotrophic keratopathy, to keep or restore vision 5).

Case series


The records of 52 patients who underwent stereotactic radiosurgery (SRS) for trigeminal schwannoma were reviewed using a retrospective study. The median patient age was 47.1 years (range, 18-77); 20 patients (38.5%) had undergone prior tumor resection and 32 (61.5%) underwent radiosurgery on the basis of imaging diagnosis only. The most frequent presenting symptoms were facial numbness (29 patients), jaw weakness (11 patients), facial pain (10 patients) and diplopia (4 patients). Fifty-two cases with solid tumors were mainly solid in 44 cases (84.6%), mostly cystic in 2 cases (3.8%), and cystic and solid mixed in 6 cases (11.5%). Two cases of mostly cystic tumor first underwent stereotactic cystic fluid aspiration and intracavitary irradiation, and then had MRI localization scan again for gamma knife treatment. The mean tumor volume was 7.2 ml (range, 0.5-38.2). The mean prescription radiation dose was 13.9 Gy (range, 11-17), and the mean prescription isodose configuration was 47.9%.

At a mean follow-up of 61 months (range, 12-156), neurological symptoms or signs improved in 35 patients (67.3%), 14 patients (26.9%) had a stable lesion, and worsening of the disease occurred in 2 patients (3.8%). On imaging, the schwannomas almost disappeared in 8 (15.4%), shrank in 32 (61.5%), remained stable in 5 (9.6%), and increased in size in 7 patients (13.5%). Tumor growth control was achieved in 45 (86.5%) of the 52 patients.

SRS is an effective and minimally invasive management option for patients with residual or newly diagnosed trigeminal schwannomas. The use of SRS to treat trigeminal schwannomas resulted in good tumor control and functional improvement 6).


The records of 33 consecutive patients with trigeminal schwannoma treated via Gamma Knife surgery were retrospectively reviewed. The median patient age was 49.5 years (range 15.1-82.5 years). Eleven patients had undergone prior tumor resection. Two patients had neurofibromatosis Type 2. Lesions were classified as root type (6 tumors), ganglion type (17 tumors), and dumbbell type (10 tumors) based on their location. The median radiosurgery target volume was 4.2 cm3 (range 0.5-18.0 cm3), and the median dose to the tumor margin was 15.0 Gy (range 12-20 Gy).

At an average of 6 years (range 7.2-147.9 months), the rate of progression-free survival (PFS) at 1, 5, and 10 years after SRS was 97.0, 82.0, and 82.0%, respectively. Factors associated with improved PFS included female sex, smaller tumor volume, and a root or ganglion tumor type. Neurological symptoms or signs improved in 11 (33.3%) of 33 patients and were unchanged in 19 (57.6%). Three patients (9.1%) had symptomatic disease progression. Patients who had not undergone a prior tumor resection were significantly more likely to show improvement in neurological symptoms or signs.

Stereotactic radiosurgery is an effective and minimally invasive management option in patients with residual or newly diagnosed trigeminal schwannomas. Predictors of a better treatment response included female sex, smaller tumor volume, root or ganglion tumor type, and the application of SRS as the primary treatment 7).


Phi et al. reviewed the clinical records and radiological data in 22 consecutive patients who received GKS for a trigeminal schwannoma. The median tumor volume was 4.1 ml (0.2-12.0 ml), and the mean tumor margin dose was 13.3 +/- 1.3 Gy at an isodose line of 49.9 +/- 0.6% (mean +/- standard deviation). The median clinical follow-up period was 46 months (range 24-89 months), and the median length of imaging follow-up was 37 months (range 24-79 months).

Tumor growth control was achieved in 21 (95%) of the 22 patients. Facial pain responded best to radiosurgery, with two thirds of patients showing improvement. However, only one third of patients with facial hypesthesia improved. Six patients (27%) experienced new or worsening cranial neuropathies after GKS. Ten patients (46%) showed tumor expansion after radiosurgery, and nine of these also showed central enhancement loss. Loss of central enhancement, tumor expansion, and a tumor in a cavernous sinus were found to be significantly related to the emergence of cranial neuropathies.

The use of GKS to treat trigeminal schwannoma resulted in a high rate of tumor control and functional improvement. Cranial neuropathies are bothersome complications of radiosurgery, and tumor expansion in a cavernous sinus after radiosurgery appears to be the proximate cause of the complication. Loss of central enhancement could be used as a warning sign of cranial neuropathies, and for this vigilant patient monitoring is required 8).

Twenty-six patients with trigeminal schwannomas underwent GKS at the University of Virginia Lars Leksell Gamma Knife Center between 1989 and 2005. Five of these patients had neurofibromatosis and one patient was lost to follow up. The median tumor volume was 3.96 cm(3), and the mean follow-up period was 48.5 months. The median prescription radiation dose was 15 Gy, and the median prescription isodose configuration was 50%. There was clinical improvement in 18 patients (72%), a stable lesion in four patients (16%), and worsening of the disease in three patients (12%). On imaging, the schwannomas shrank in 12 patients (48%), remained stable in 10 patients (40%), and increased in size in three patients (12%). These results were comparable for primary and adjuvant GKSs. No tumor growth following GKS was observed in the patients with neurofibromatosis.

Gamma Knife surgery affords a favorable risk-to-benefit profile for patients harboring trigeminal schwannomas. Larger studies with open-ended follow-up review will be necessary to determine the long-term results and complications of GKS in the treatment of trigeminal schwannomas 9).


A patient developed severe corneal neovascularization within four weeks and the contact lens had to be removed. Three months later an MRI scan was performed, which showed an intracranial tumor originating from the first branch of the trigeminal nerve. Neurinoma of the trigeminal nerve was suspected, and this presumed diagnosis was confirmed by fine needle biopsy. The patient underwent radiosurgery seven weeks later. The epithelium closed, the cornea recovered and stayed stable until the last examination 18 months after radiosurgery.

Radiosurgery is a promising alternative to conventional microsurgery in cases of neurinomas of the trigeminal nerve including neurotrophic keratopathy, to keep or restore vision 10).


1) , 6)

Sun J, Zhang J, Yu X, Qi S, Du Y, Ni W, Hu Y, Tian Z. Stereotactic radiosurgery for trigeminal schwannoma: a clinical retrospective study in 52 cases. Stereotact Funct Neurosurg. 2013;91(4):236-42. doi: 10.1159/000345258. Epub 2013 Mar 26. PubMed PMID: 23548989.
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Kano H, Niranjan A, Kondziolka D, Flickinger JC, Dade Lunsford L. Stereotactic radiosurgery for trigeminal schwannoma: tumor control and functional preservation Clinical article. J Neurosurg. 2009 Mar;110(3):553-8. PubMed PMID: 19301456.
3) , 8)

Phi JH, Paek SH, Chung HT, Jeong SS, Park CK, Jung HW, Kim DG. Gamma Knife surgery and trigeminal schwannoma: is it possible to preserve cranial nerve function? J Neurosurg. 2007 Oct;107(4):727-32. PubMed PMID: 17937215.
4) , 9)

Sheehan J, Yen CP, Arkha Y, Schlesinger D, Steiner L. Gamma knife surgery for trigeminal schwannoma. J Neurosurg. 2007 May;106(5):839-45. PubMed PMID: 17542528.
5) , 10)

Ardjomand N, Can B, Schaffler G, Eustacchio S, Scarpatetti M, Pendl G. [Therapy of neurotrophic keratopathy in trigeminal schwannoma with radiosurgery]. Wien Klin Wochenschr. 2001 Aug 16;113(15-16):605-9. German. PubMed PMID: 11571839.

Update: Painful tic convulsif

Painful tic convulsif is a syndrome restricted to paroxysmal dysfunction of the fifth cranial nerve and seventh cranial nerves causing trigeminal neuralgia and hemifacial spasm together.

It occurs primarily in women over the age of 50 years and is usually associated with vertebrobasilar dolichoectasia and aneurysm 1).

Less frequently an arteriovenous malformation or cholesteatoma–which compresses the trigeminal and facial nerve roots in the posterior fossa. In rare instances this syndrome may be caused by disseminated sclerosis 2)


Magnetic resonance imaging (MRI), due to its inherent excellent contrast resolution, is an excellent modality for demonstrating the nerve compression by dilated and tortuous vessels seen in this condition. For this purpose, 3D MRI sequences are especially useful like constructive interference in steady state (CISS) and MR angiography. Both of these have been reported to be helpful in the diagnosis of this condition 3).

Mittal et al. report a case of PTC in which they were able to document facial and trigeminal nerve compression by VBD on MRI, using CISS and Time of flight magnetic resonance angiography 4).

Ten (6.8%) out of 146 patients with trigeminal neuralgia (TN) who underwent SPGR-MRI and 3D-TOF-MRA from August 1993 to October 1996, were found to have vascular compression caused by a tortuous vertebrobasilar system (TVBS). They were mostly males, demonstrated left-sided predominance, and had ipsilateral hemifacial spasm, compared with other 52 patients whose offending arteries were either superior cerebellar artery (SCA), anterior inferior cerebellar artery (AICA)or posterior inferior cerebellar artery (PICA). The patients who showed vascular compression by TVBS, presented an artery which compresses and dislocates the rootentry zone (REZ) of the trigeminal nerve, presses the brain stem at REZ and simultaneously compresses the REZ of the facial nerve. In addition, the diameters of the two branches of vertebrobasilar artery were not equal. These features indicate that the atherosclerotic change of the offending artery in TN caused by TVBS is more severe than that caused by SCA, AICA or PICA. This change causes an irregular running of artery which leads a strong compression of the trigeminal nerve REZ and of the brain stem. Consequently, the facial nerve REZ is severely affected leading to the presence of tic convulsif in TN caused by TVBS 5).


The standard modality of treatment is microvascular decompression, which has shown greater effectiveness and control of symptoms in the long-term. However medical treatment, which includes percutaneous infiltration of botulinum toxin, has produced similar results at medium-term in the control of each individual clinical manifestation, but it must be considered as an alternative in the choice of treatment 6).

Case series


Nine consecutive cases of coexistent HFS and TN caused by neurovascular confliction in the same side were studied. Except for one, the patients suffered from HFS followed by ipsilateral TN. All patients underwent MVD and were followed up for 3 to 30 months. Each surgery was analyzed retrospectively.

Intraoperatively, a looped vertebral artery (VA) shifted to the suffered side was found in 8 patients. The VA was regarded as the direct or indirect offending artery. After MVDs, the spasm ceased immediately in 6 patients; the other 3 patients had delayed relief within 3 months. The pain disappeared immediately in 7 of 9 patients. One patient felt relief after a week, and 1 had pain but improved slightly. No recurrence or complication was found.

A shifted VA loop may account for this tic convulsif syndrome. MVD is a reasonable and effective therapy with a high cure rate for the disease. The key to the surgery is to move the VA proximally. The dissection should be performed rostrally starting from the caudal cranial nerves 7).


Bilateral HFS and tic convulsif were encountered in 7 (0.4%) and 6 (0.37%) patients, respectively. Fifty-six (3.4%) patients were younger than 30 years old at the time of microvascular decompression.

HFS can result from tumor, vascular malformation, and dolichoectatic artery. Therefore, appropriate preoperative radiological investigations are crucial to achieve a correct diagnosis. The authors emphasize that distal compression or only venous compression can be responsible for persistent or recurrent symptoms postoperatively. In cases of bilateral HFS, a definite differential diagnosis is necessary for appropriate therapy. MVD is recommended as the treatment of choice in patients younger than 30 years old or patients with painful tic convulsif 8).


Boscá-Blasco et al. report the cases of four patients with combined TN and HFS out of a total of 247 patients with HFS who were treated with botulinum toxin. One patient had TN that was contralateral to the HFS, while the other three were ipsilateral, and one of these had bilateral HFS. In all four cases both the HFS and the TN improved with botulinum toxin treatment.

These four patients with TN and HFS suggest a common aetiology for the two disorders, due either to central neuronal hyperactivity or to vascular compression of several cranial nerves. The beneficial effect of botulinum toxin in both disorders supports the idea of this toxin having a central mechanism of action that acts by controlling neuronal hyperactivity in the brain stem, as well as its peripheral action 9).


Since Cushing’s 1920 description of this syndrome in three patients, 37 additional cases have been reported in the world literature. Of the 15 with adequate operative descriptions, 10 had vascular abnormalities and five had tumors. The authors report 11 cases of tic convulsif treated by microvascular decompression of both the fifth and seventh cranial nerves. At operation, 21 of 22 nerves were found to have root entry zone vascular compression. One trigeminal nerve was considered normal. One seventh nerve had a tumor displacing the anterior inferior cerebellar artery into its root entry zone. The average follow-up period in this series was 6 years 2 months (range 1 to 8 1/2 years). Eight patients (73%) were pain-free, two (18%) had frank recurrences, and one (9%) had mild discomfort. Eight patients (73%) were totally free of facial spasm, and two others (18%) had only a trace of residual spasm. These results are comparable to those achieved by treating the individual syndromes with microvascular decompression. Therefore, microvascular decompression of both the fifth and seventh cranial nerves is recommended as the treatment of choice in tic convulsif 10).

Case reports


Fenech et al. describe a unique presentation of bilateral PTC in a man with bilateral hemifacial spasm and trigeminal neuralgia secondary to neurovascular conflict of all four cranial nerves. Following failed medical and radiofrequency therapy, microvascular decompression of three of the four involved nerves was performed, where the offending vessels were mobilised and Teflon used to prevent conflict recurrence. He continues to respond to Botox for right hemifacial spasm. Since surgery, he remains pain free bilaterally and spasm free on the left 11).


Rare case of cerebello-pontine angle meningioma causing painful tic convulsif 12).


Jiao et al. report a case of a 77-year-old woman with coexistent trigeminal neuralgia and hemifacial spasm who had experienced Bell palsy half a year ago. The patient underwent microvascular decompression. Intraoperatively, the vertebrobasilar artery was found to deviate to the symptomatic side and a severe adhesion was observed in the cerebellopontine angle. Meanwhile, an ectatic anterior inferior cerebellar artery and 2 branches of the superior cerebellar artery were identified to compress the caudal root entry zone (REZ) of the VII nerve and the rostroventral cisternal portion of the V nerve, respectively. Postoperatively, the symptoms of spasm ceased immediately and the pain disappeared within 3 months. In this article, the pathogenesis of the patient’s illness was discussed and it was assumed that the adhesions developed from inflammatory reactions after Bell palsy and the anatomic features of the patient were the factors that generated the disorder. Microvascular decompression surgery is the suggested treatment of the disease, and the dissection should be started from the caudal cranial nerves while performing the operation 13).


Verghese et al. report an Posterior fossa arachnoid cyst that caused PTC in a 50-year-old woman. Her radiological evaluation revealed a median, well-circumscribed, cystic lesion of the posterior fossa suggestive of arachnoid cyst, pushing the cerebellum and brainstem anteriorly. Midline suboccipital craniotomy and marsupialization of cyst was performed with complete recovery of symptoms. This is the first report of a retrocerebellar arachnoid cyst causing PTC 14).

Painful tic convulsif caused by an arteriovenous malformation 15).


Giglia et al. present the case of a 50-year-old man suffering from “painful tic convulsif”, on the left side of the face, i.e., left trigeminal neuralgia associated with ipsilateral hemifacial spasm. An angio-MRI scan showed a neurovascular confliction of left superior cerebellar artery with the ipsilateral V cranial nerve and of the left inferior cerebellar artery with the ipsilateral VII cranial nerve. Neurophysiological evaluation through esteroceptive blink reflex showed the involvement of left facial nerve. An initial carbamazepine treatment (800 mg/daily) was completely ineffective, so the patient was shifted to lamotrigine 50 b.i.d. that was able to reduce attacks from 4 to 6 times per day to 1 to 2 per week. Considering the good response to the drug, the neurosurgeon decided to delay surgical treatment 16).


A 67-year-old woman who presented with a typical left hemifacial spasm of 8-month duration. After 2 months, she experienced lacinating and sharp shock-like pain in the left side of her face affecting the V1 and V2 territories and a discrete attenuation of nauseous reflex on the left side. CT angiography and MRI revealed significant compression of left cranial nerves V, VII, VIII, IX and X by a giant and tortuous vertebro-basilar arterial complex. This case illustrates the nonlinearity of the relationship between the presence of the stressor factor and the actual manifestation of the disease 17).


A case of right-sided HFS after which left TN developed, which is an unusual form of PTC. Both disorders were caused by bilateral vascular compression of the cranial nerves and successfully treated with botulinum toxin and carbamazepine. As PTC is benign in nature and can be treated with botulinum toxin, neuroradiological investigations should be performed for an accurate aetiological diagnosis, particularly in young patients with atypical disease manifestations 18).

Bilateral hemifacial spasm and trigeminal neuralgia: a unique form of painful tic convulsif 19).


A 80-year-old woman had a 10-year history of left trigeminal neuralgia and ipsilateral hemifacial spasm. She presented with intermittent left facial twitching and pain, especially upon swallowing. MRI revealed compression of the left trigeminal nerve by the left anterior inferior cerebellar artery and of the ipsilateral facial nerve by the posterior inferior cerebellar artery. Microvascular decompression of the lesions via left lateral suboccipital craniotomy resulted in immediate and complete symptom improvement. The case demonstrates that different arteries can affect the trigeminal and facial nerve at a stage that precedes compression by a tortuous vertebrobasilar artery. They suggest that the presence of PTC should be considered in patients with a tortuous vertebrobasilar artery, irrespective of the offending arteries 20).


A 70-year-old man with hemifacial spasm associated to trigeminal neuralgia secondary to an ectatic basilar artery. He was treated with botulinum toxin type A, 2.5 mouse units over five sites at the orbicularis oculi and one over the buccinator muscle. After botulinum toxin injections, relief was gained not only from twitching but also from pain. When the effects of the toxin vanished, spasms and pain recurred. Further infiltrations were given every 12 weeks following the same response pattern. This observation further validates the increasing role of botulinum toxin in pain management21).


A case is presented of painful tic convulsif caused by schwannoma in the cerebellopontine angle (CPA), with right trigeminal neuralgia and ipsilateral hemifacial spasm. Magnetic resonance images showed a 4 cm round mass displacing the 4th ventricle and distorting the brain stem in the right CPA. The schwannoma, which compressed the fifth and seventh cranial nerves directly, was subtotally removed by a suboccipital craniectomy. Postoperatively, the patient had a complete relief from the hemifacial spasm and marked improvement from trigeminal neuralgia. The painful tic convulsif in this case was probably produced by the tumor compressing and displacing the anterior cerebellar artery directly 22).


A case of painful tic convulsif (trigeminal neuralgia and ipsilateral hemifacial spasm) caused by cerebellopontine angle epidermoid tumor is presented. This tumor was compressed to the trigeminal nerve, and became attached to the facial and auditory nerves. The facial nerve exit-zone of brain stem was also compressed by the tumor along with a branch of the posterior inferior cerebellar artery. Total removal of the tumor was carried out and neuralgia and facial spasm disappeared. Painful tic convulsif caused by brain tumor is rare (eight cases in the literature plus our case), but epidermoid tumor is not rare as a cause of this complaint (seven in eight cases). In preoperative examination of this case, we could not detect this epidermoid in the cerebellopontine angle, because this tumor was the same intensity as CSF liquid on magnetic resonance imaging (T1 and T2 weighted image) and exerting hardly any mass effect on the brainstem. On encountering a case of painful tic convulsif of unknown origin despite the usual preoperative examinations, it may be useful that same kind of brain tumor, especially, epidermoid might be concealed in the cerebellopontine angle lesion 23).

A case is presented of painful tic convulsif caused by a posterior fossa meningioma, with right trigeminal neuralgia and ipsilateral hemifacial spasm. Magnetic resonance images showed an ectatic right vertebral artery as a signal-void area in the right cerebellopontine angle. At operation the tentorial meningioma, which did not compress either the fifth or the seventh cranial nerves directly, was totally removed via a suboccipital craniectomy. The patient had complete postoperative relief from the trigeminal neuralgia and her hemifacial spasm improved markedly with decreased frequency. From a pathophysiological standpoint, the painful tic convulsif in this case was probably produced by the tumor compressing and displacing the brainstem directly, with secondary neurovascular compression of the fifth and seventh nerves (the so-called “remote effect”) 24).

Painful tic convulsif caused by a brain tumor undiagnosed preoperatively 25).


Patient with painful tic convulsif caused by a brain tumor. The patient was admitted with right trigeminal neuralgia and ipsilateral facial spasm, i.e., painful tic convulsif. Preoperative computed tomography scans showed no apparent abnormalities; however, surgery revealed that these symptoms were associated with a pearly tumor located in the cerebellopontine angle. Subtotal resection for the decompression of the right trigeminal and facial nerves was performed and resulted in complete relief of the symptoms. Histological examination demonstrated the tumor to be an epidermoid cyst 26).


A 77-year-old woman had developed trigeminal neuralgia 12 years before admission and ipsilateral facial spasm 2 years before admission. Upon operation, the superior cerebellar artery was found to impinge upon the entry zone of the fifth nerve. In addition, the anterior inferior and posterior inferior cerebellar arteries were found to bend along the seventh nerve. Teflon sheets were placed between the nerves and offending arteries. She has been pain-free and spasm-free for the past 18 months. Pathomechanism of the association of the multiple compression syndromes and the treatment are discussed 27).

The case of trigeminal neuralgia and ipsilateral hemifacial spasm–painful tic convulsif–is presented. Microsurgical exploration revealed compression of the fifth and seventh cranial nerves by a tortuous contralateral vertebral artery. Neurovascular decompression of the roots entry/exit zone completely relieved preoperative facial pain and spasm 28).


A case of epidermoid tumor presenting with a painful tic convulsif was reported. A 35-year old male with trigeminal neuralgia and ipsilateral hemifacial spasm was diagnosed as having an epidermoid by CT and metrizamide CT cisternography and the symptoms were completely eliminated after the operation. In this case, metrizamide CT cisternography was very useful for preoperative diagnosis by demonstrating the characteristic findings of the epidermoid. It should be taken into consideration that there are some cases with trigeminal neuralgia and/or hemifacial spasm whose symptoms are due to brain tumors 29).


A patient had combined otalgia and intractable unilateral facial spasm, relieved by microsurgical vascular decompression of the seventh and eighth cranial nerve complex in the cerebellopontine angle without section of the intermediate nerve. A dolicho-ectatic anterior inferior cerebellar artery compressed the seventh and eighth cranial nerves complex, suggesting that vascular compression of the intermediate nerve or of the sensory portion of the facial nerve may cause geniculate neuralgia. “Tic convulsif” seems to be a combination of geniculate neuralgia and hemifacial spasm. This combination could be due to vascular compression of the sensory and motor components of the facial nerve at their junction with the brainstem 30).


A 49-year-old man with an epidermoid tumor had a hemifacial spasm on the left and ipsilateral trigeminal neuralgia–i.e., painful tic convulsif. Computed tomography scanning after metrizamide enhancement clearly demonstrated a cerebellopontine angle tumor. In the year since complete removal of the epidermoid tumor, the patient has been relieved of the facial pain and the hemifacial spasm is improved with decreased frequency of the spasm 31).



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