Rapid ventricular pacing

Rapid ventricular pacing (RVP) is a procedure that temporarily lowers blood pressure by increasing heart rate and reducing ventricular filling time. RVP has been widely used to reduce blood vessel tension in many cardiovascular surgeries.

Rapid ventricular pacing (RVP) has recently been reintroduced into cerebrovascular surgery. It is more predictable than adenosine in response time and, thus, can be used during unanticipated complications, such as aneurysmal rupture. It also induces a shorter period of hypotension compared with adenosine. However, RVP is more invasive and more complex from an anesthesia standpoint. Vascular neurosurgeons should be familiar with these techniques and know their applications and limitations 1).


A 46-year-old man came to the Huashan Hospital Fudan University, Shanghai, China with intermittent right-side headache for 5 years, and left lower limb numbness for 3 months.

Magnetic resonance imaging (MRI) of the head and digital subtraction angiography confirmed the diagnosis of right middle cerebral artery (MCA) aneurysm.

Considering the large size of this MCA aneurysm, Rapid ventricular pacing (RVP) was used to reduce blood pressure during MCA aneurysm repair, and to lower the risk of intracranial hemorrhage during procedure.

Post procedure, there was no abnormality detected. Seven weeks after surgery, the patient’s muscle tone of right side extremities were grade V and left side extremities were grade IV. Computed tomography angiography confirmed no MCA aneurysm.

In cases of aneurysm rupture, RVP will induce a transient “very low pressure” condition, and give a valuable time frame to clip the ruptured aneurysm. Therefore RVP is a safe and effective method to provide transient reduction of cardiac output in intracranial aneurysm patients 2).1) Rangel-Castilla L, Russin JJ, Britz GW, Spetzler RF. Update on transient cardiac standstill in cerebrovascular surgery. Neurosurg Rev. 2015 Oct;38(4):595-602. doi: 10.1007/s10143-015-0637-z. Epub 2015 May 1. PubMed PMID: 25931209.2) Ping Y, Gu H. A case report on middle cerebral artery aneurysm treated by rapid ventricular pacing: A CARE compliant case report. Medicine (Baltimore). 2018 Nov;97(48):e13320. doi: 10.1097/MD.0000000000013320. PubMed PMID: 30508924.

Medically refractory trigeminal neuralgia treatment

see Trends in surgical treatment for trigeminal neuralgia

see Cost effectiveness in surgical treatment for trigeminal neuralgia.

Microvascular decompression

see Microvascular decompression for trigeminal neuralgia

Percutaneous procedures

see Percutaneous trigeminal rhizotomy.

Gamma Knife radiosurgery

see Gamma Knife radiosurgery for trigeminal neuralgia.


Microvascular decompression should be performed more prudently in elderly patients (>80 years old), and the indications for PR should be relatively relaxed. MVD + PR could improve the curative effect in patients with trigeminal neuralgia >80 years. Gamma knife treatment of trigeminal neuralgia had high safety, less complications, and positive curative effect, especially suitable for patients >80 years 1).


MVD results in superior rates of short- and long-term pain relief, facial numbness and dysesthesia control, and less recurrence amongst those in whom pain freedom was achieved, at the cost of greater postoperative complications when compared to SRS. Although no significant difference was found in terms of the need for retreatment surgery, there was a trend towards less procedures favoring MVD. First treatment by either technique represents the overall trends reported 2).

References

1) Yu R, Wang C, Qu C, Jiang J, Meng Q, Wang J, Wei S. Study on the Therapeutic Effects of Trigeminal Neuralgia With Microvascular Decompression and Stereotactic Gamma Knife Surgery in the Elderly. J Craniofac Surg. 2018 Nov 30. doi: 10.1097/SCS.0000000000004999. [Epub ahead of print] PubMed PMID: 30507874. 2) Lu VM, Duvall JB, Phan K, Jonker BP. First treatment and retreatment of medically refractive trigeminal neuralgia by stereotactic radiosurgery versus microvascular decompression: a systematic review and Meta-analysis. Br J Neurosurg. 2018 May 10:1-10. doi: 10.1080/02688697.2018.1472213. [Epub ahead of print] PubMed PMID: 29745268.

Update: Intentional traumatic brain injury

Intentional traumatic brain injury

Epidemiology

Intentional injury has been associated with certain demographics and socioeconomic groups. Less is known about the relationship of intentional traumatic brain injury (TBI) to injury severity, mortality, and demographic and socioeconomic profile.


A planned secondary analysis of a prospective multicentre cohort study was conducted in 10 emergency departments EDs in Australia and New Zealand, including children aged <18 years with head injury (HI). Epidemiology codes were used to prospectively code the injuries. Demographic and clinical information including the rate of clinically important traumatic brain injury (ciTBI: HI leading to death, neurosurgery, intubation >1 day or admission ≥2 days with abnormal computed tomography [CT]) was descriptively analysed.

Intentional injuries were identified in 372 of 20 137 (1.8%) head-injured children. Injuries were caused by caregivers (103, 27.7%), by peers (97, 26.1%), by siblings (47, 12.6%), by strangers (35, 9.4%), by persons with unknown relation to the patient (21, 5.6%), other intentional injuries (8, 2.2%) or undetermined intent (61, 16.4%). About 75.7% of victims of assault by caregivers were <2 years, whereas in other categories, only 4.9% were <2 years. Overall, 66.9% of victims were male. Rates of CT performance and abnormal CT varied: assault by caregivers 68.9%/47.6%, by peers 18.6%/27.8%, by strangers 37.1%/5.7%. ciTBI rate was 22.3% in assault by caregivers, 3.1% when caused by peers and 0.0% with other perpetrators.

Intentional HI is infrequent in children. The most frequently identified perpetrators are caregivers and peers. Caregiver injuries are particularly severe 1).


A study identified 1,409 (8.0%) intentional TBIs and 16,211 (92.0%) unintentional TBIs. Of the intentional TBIs, 389 (27.6%) was self-inflicted TBI (Si-TBI) and 1,020 (72.4%) was other-inflicted TBI (Oi-TBI). The most common cause of Si-TBI was “jumping from high places” (32.1%), followed by “firearms” (30.6%). About half of Oi-TBI was because of “fight and brawl” (48.3%), followed by “struck by objects” (26.1%). Si-TBI was associated with younger age, female gender, and having more alcohol/drug abuse history. For Oi-TBI, younger age, male gender, having more alcohol/drug abuse history were independently associated.

This research provides the first comprehensive overview of intentional TBI based in Canada.

The comprehensive data set (CDS) of the Ontario trauma registry (OTR) provided the ability to identify who is at risk for intentional TBI. Prevention programs and more targeted rehabilitation services should be designed for this vulnerable population 2).

Outcome

Intentional injury is associated with significant morbidity and mortality.

Caregiver injuries are particularly severe in children 3).

Prospective data were obtained for 2,637 adults sustaining TBIs between January 1994 and September 1998. Descriptive, univariate, and multivariate analyses were conducted to determine the predictive value of intentional TBI on injury severity and mortality.

Gender, minority status, age, substance abuse, and residence in a zipcode with low average income were associated with intentional TBI. Multivariate analysis found minority status and substance abuse to be predictive of intentional injury after adjusting for other demographic variables studied. Intentional TBI was predictive of mortality and anatomic severity of injury to the head. Penetrating intentional TBI was predictive of injury severity with all injury severity markers studied.

Many demographic variables are risk factors for intentional TBI, and such injury is a risk factor for both injury severity and mortality. Future studies are needed to definitively link intentional TBI to disability and functional outcome 4).

References

1) , 3)

Babl FE, Pfeiffer H, Dalziel SR, Oakley E, Anderson V, Borland ML, Phillips N, Kochar A, Dalton S, Cheek JA, Gilhotra Y, Furyk J, Neutze J, Lyttle MD, Bressan S, Donath S, Hearps SJ, Crowe L; Paediatric Research in Emergency Departments International Collaborative (PREDICT). Paediatric intentional head injuries in the emergency department: A multicentre prospective cohort study. Emerg Med Australas. 2018 Nov 26. doi: 10.1111/1742-6723.13202. [Epub ahead of print] PubMed PMID: 30477046.
2)

Kim H, Colantonio A. Intentional traumatic brain injury in Ontario, Canada. J Trauma. 2008 Dec;65(6):1287-92. doi: 10.1097/TA.0b013e31817196f5. PubMed PMID: 19077615.
4)

Wagner AK, Sasser HC, Hammond FM, Wiercisiewski D, Alexander J. Intentional traumatic brain injury: epidemiology, risk factors, and associations with injury severity and mortality. J Trauma. 2000 Sep;49(3):404-10. Erratum in: J Trauma 2000 Nov;49(5):982. PubMed PMID: 11003315.

Update: Ochronosis

Ochronosis

Accumulation of homogentisic acid (HGA), and its metabolites in tissues causes ochronosis. The word ochronosis refers to the dark bluish-black discoloration of connective tissues including the sclera, cornea, auricular cartilage, heart valves, articular cartilage, tendons, and ligaments.

Alkaptonuria frequently occurs in association with lumbar disc disease. In patients with no other signs of alkaptonuria or ochronosis, early detection of the disease is important to treat involvement of other systems (e.g., cardiovascular and urinary) 1).

Neurogenic claudication resulting from focal ligamentum flavum hypertrophy in the lumbar spine due to ochronotic deposits has only been previously reported once in the literature. In a article, Yucetas and Ucler from Adiyaman present a 71-year-old male patient with alkaptonuria-associated degenerative L3-L4-L5 stenosis, diagnosed after lumbar decompressive laminectomy 2).


A rare case of ochronosis presenting with cervical compressive myelopathy 3).


A 45-year-old previously healthy female patient who was operated on for prolapsed lumbar disc herniation, and in whom the nucleus pulposus was discovered to be black intraoperatively. The alkaptonuria was diagnosed after histopathological examination of the black disc material. Elevated urinary concentration of homogentisic acid confirmed the diagnosis 4).


A 58-year-old woman with back pain. Radiographs and magnetic resonance imaging (MRI) revealed characteristic features of ochronotic spondyloarthropathy 5).


Kalevski et al. published a case of a 33-year old patient with alcaptonuria and lumbar disc herniation. After the surgical treatment the patient’s complaints were alleviated and almost no complaints were registered, during the next follow-up.

The most common symptoms seen in alkaptonuria are complaints of pain in large joints and back pain. They are usually associated with the main disease. This case demonstrates that even there is a small likelihood for a prolapsed lumbar disk, it should be sought in such patients as the surgical treatment is able to yields a positive results 6).


In 1994 Koh et al published a case of alkaptonuria with root canal stenosis 7).


Kaufmann et al. reported a patient with alkaptonuric ochronosis and multiple intracranial aneurysms presenting with subarachnoid hemorrhage. The ruptured aneurysm was surgically treated, with a satisfactory outcome. In view of the well-known association of other connective tissuedisorders with intracranial aneurysms, a potentially causal relationship is suggested between cerebral aneurysms and alkaptonuric ochronosis 8).

References

1)

Emel E, Karagöz F, Aydín IH, Hacísalihoğlu S, Seyithanoğlu MH. Alkaptonuria with lumbar disc herniation: a report of two cases. Spine (Phila Pa 1976). 2000 Aug 15;25(16):2141-4. PubMed PMID: 10954648.
2)

Yucetas SC, Ucler N. Black-Colored Ligamentum Flavum Due to Alkaptonuria. J Neurol Surg A Cent Eur Neurosurg. 2018 Nov 26. doi: 10.1055/s-0038-1675784. [Epub ahead of print] PubMed PMID: 30477028.
3)

Nelanuthala M, Kotta S, Talari S, Terapalli VK. A rare case of ochronosis presenting with cervical compressive myelopathy. Neurol India. 2018 Jul-Aug;66(4):1178-1181. doi: 10.4103/0028-3886.236956. PubMed PMID: 30038118.
4)

Kahveci R, Ergüngör MF, Günaydin A, Temiz A. Alkaptonuric patient presenting with “black” disc: a case report. Acta Orthop Traumatol Turc. 2013;47(2):134-8. Review. PubMed PMID: 23619548.
5)

Al-Mahfoudh R, Clark S, Buxton N. Alkaptonuria presenting with ochronotic spondyloarthropathy. Br J Neurosurg. 2008 Dec;22(6):805-7. doi: 10.1080/02688690802226368. Review. PubMed PMID: 19085367.
6)

Kalevski SK, Haritonov DG, Peev NA. Alcaptonuria with lumbar disc prolapse: case study and review of the literature. Spine J. 2007 Jul-Aug;7(4):495-8. Epub 2006 Dec 29. Review. PubMed PMID: 17630148.
7)

Koh KB, Low EH, Ch’ng SL, Zakiah I. A case of alkaptonuria with root canal stenosis. Singapore Med J. 1994 Feb;35(1):106-7. PubMed PMID: 8009267.
8)

Kaufmann AM, Reddy KK, West M, Halliday WJ. Alkaptonuric ochronosis and multiple intracranial aneurysms. Surg Neurol. 1990 Mar;33(3):213-6. PubMed PMID: 2315833.

Update: Cerebral cavernous malformation pathogenesis

Cerebral cavernous malformation pathogenesis

Genes mutated in cerebral cavernous malformation (CCM) encode proteins that modulate junction formation between vascular endothelial cells.

Most cerebral cavernous malformations are linked to loss-of-function mutations in 1 of 3 genes, namely CCM1 (originally called KRIT1), CCM2(MGC4607), or CCM3 (PDCD10).

How disruption of the CCM complex results in disease remains controversial, with numerous signalling pathways (including Rho, SMAD and Wnt/β-catenin) and processes such as endothelial mesenchymal transition (EndMT) proposed to have causal roles. CCM2 binds to MEKK3 1).

Although a role for these three genes in the formation of these intracranial vascular lesions has been established since the 1990s, additional works have further elucidated the molecular mechanisms by which mutations in these genes and the resultant aberrant proteins interact, leading to the formation of CCMs.

Therefore, it is reasonable to assume that a molecular pathway exists that requires all three proteins to function together correctly for proper cellular function. Moreover, research is demonstrating how each component protein is capable of interacting with numerous other signaling and cytoskeletal molecules allowing for a diverse range of functions in molecular signaling pathways via unique protein–protein interactions.

Significant research findings from 2000 to 2015 have further enhanced our understanding of the pathogenesis of CCM formation. The use of advanced sequencing technologies to characterize genomic mutations and the identification of new signaling pathways and protein–protein interactions have led to great strides in understanding the molecular genetics involved in the development of CCMs. However, many unanswered questions remain, and future studies are clearly needed to improve our understanding of CCM pathogenesis. “Gene to protein to disease” mechanisms involved in the pathogenesis of CCMs should shed further light on potential therapeutic targets. 2).

The Phosphoinositide 3 kinase (PI3K)/Akt pathway is known to play a major role in angiogenesis. Studies have shown that the phosphatase and tensin homologue deleted on chromosome ten (PTEN), a tumor suppressor, is an antagonist regulator of the PI3K/Akt pathway and mediates angiogenesis by activating vascular endothelial growth factor (VEGF) expression.

Understanding the biology of these proteins with respect to their signaling counterpart will help to guide future research towards new therapeutic targets applicable for CCM treatment 3).


Studies identify gain of MEKK3 signalling and KLF2/4 function as causal mechanisms for CCM pathogenesis that may be targeted to develop new CCM therapeutics 4).

CCMs arise from the loss of an adaptor complex that negatively regulates MEKK3KLF2/4 signalling in brain endothelial cells, but upstream activators of this disease pathway have yet to be identified.


Tang et al. identify endothelial Toll-like receptor 4 (TLR4) and the gut microbiome as critical stimulants of cerebral cavernous malformationformation. Activation of TLR4 by Gram negative bacteria or lipopolysaccharide accelerates CCM formation, and genetic or pharmacologic blockade of TLR4 signalling prevents CCM formation in mice. Polymorphisms that increase expression of the TLR4 gene or the gene encoding its co-receptor CD14 are associated with higher CCM lesion burden in humans. Germ-free mice are protected from CCM formation, and a single course of antibiotics permanently alters CCM susceptibility in mice. These studies identify unexpected roles for the microbiome and innate immune signalling in the pathogenesis of a cerebrovascular disease, as well as strategies for its treatment 5).


In this scenario, the lack of effective pharmacologic options remains a critical barrier that poses an unfulfilled and urgent medical need 6).

References

1) , 4)

Zhou Z, Tang AT, Wong WY, Bamezai S, Goddard LM, Shenkar R, Zhou S, Yang J, Wright AC, Foley M, Arthur JS, Whitehead KJ, Awad IA, Li DY, Zheng X, Kahn ML. Cerebral cavernous malformations arise from endothelial gain of MEKK3-KLF2/4 signalling. Nature. 2016 Apr 7;532(7597):122-6. doi: 10.1038/nature17178. Epub 2016 Mar 30. Erratum in: Nature. 2016 May 25;536(7617):488. PubMed PMID: 27027284; PubMed Central PMCID: PMC4864035.
2)

Baranoski JF, Kalani MY, Przybylowski CJ, Zabramski JM. Cerebral Cavernous Malformations: Review of the Genetic and Protein-Protein Interactions Resulting in Disease Pathogenesis. Front Surg. 2016 Nov 14;3:60. Review. PubMed PMID: 27896269.
3)

Kar S, Samii A, Bertalanffy H. PTEN/PI3K/Akt/VEGF signaling and the cross talk to KRIT1, CCM2, and PDCD10 proteins in cerebral cavernous malformations. Neurosurg Rev. 2015 Apr;38(2):229-36; discussion 236-7. doi: 10.1007/s10143-014-0597-8. Epub 2014 Nov 19. PubMed PMID: 25403688.
5)

Tang AT, Choi JP, Kotzin JJ, Yang Y, Hong CC, Hobson N, Girard R, Zeineddine HA, Lightle R, Moore T, Cao Y, Shenkar R, Chen M, Mericko P, Yang J, Li L, Tanes C, Kobuley D, Võsa U, Whitehead KJ, Li DY, Franke L, Hart B, Schwaninger M, Henao-Mejia J, Morrison L, Kim H, Awad IA, Zheng X, Kahn ML. Endothelial TLR4 and the microbiome drive cerebral cavernous malformations. Nature. 2017 May 10. doi: 10.1038/nature22075. [Epub ahead of print] PubMed PMID: 28489816.
6)

Chohan MO, Marchiò S, Morrison LA, Sidman RL, Cavenee WK, Dejana E, Yonas H, Pasqualini R, Arap W. Emerging Pharmacologic Targets in Cerebral Cavernous Malformation and Potential Strategies to Alter the Natural History of a Difficult Disease: A Review. JAMA Neurol. 2018 Nov 26. doi: 10.1001/jamaneurol.2018.3634. [Epub ahead of print] PubMed PMID: 30476961.

EANS Basic Course in Cranial Surgery – Brno

EANS Basic Course in Cranial Surgery – Brno


Message from Course Chairmen Prof. Torstein R. Meling and Prof. Martin Smrcka:

It is our pleasure to welcome you to the second EANS Basic Course in Cranial Surgery in Brno. The event will be held from 20th to 23rd November 2018 and is organized in the Masaryk University Brno, Czech Republic. 

This dissection course is most suitable for neurosurgical residents in their first years of training as it will focus on the essential neurosurgical anatomy, the planning of surgical procedures, the handling of basic neurosurgical equipment, and the basic neurosurgical cranial approaches. The course capacity is limited to 20 participants.


Course dates:
 20 November (arrive in time for welcome dinner) – 23 November 2018


Venue:
 The course will take place at Masaryk University Brno, Faculty of Medicine, Anatomy Institute, Kamenice 3, 62500 Brno, Czech Republic


Target audience:
 All levels, but of the most benefit for neurosurgical residents in their first years of training.


Curriculum:
 Participants will learn the essential neurosurgical anatomy, the planning of surgical procedures, the handling of basic neurosurgical equipment, and the basic neurosurgical cranial approaches. Please click HERE for a more complete list.

Download the premliminary programme HERE.


2018 Faculty:

Course chairmen: T Meling (NO) / M Smrcka (CZ)

J Fiedler (CZ)
O Navratil (CZ)
V Priban (CZ)
S Rocka (LT)
M Sames (CZ)
E Simon (FR)
V Smolanka (UA)
N Velinov (BG)


Course Fee:

EANS Individual Member: €1150
Non-Member: €1250

The fee includes all tuition costs, subsistence during the course (lunches and coffee breaks) and the networking events listed below. Scrubs are provided. The fee does NOT include accommodation (please see accommodation suggestions below).


Networking opportunities:
 Welcome cocktail on Tuesday 20th November evening and Networking Dinner on Thursday 22nd November. Participants are free to make their own arrangements on Wednesday night.

Cancellation policy:
Cancellations received in writing before 20 days prior to the course start will be reimbursed.
Cancellations between 20 and 10 days prior to the course – minimum 50% refund.
Cancellations less than 10 days prior to the course – no refund (unless exceptional extenuating circumstances).


Accommodation suggestions:
 Campea Aparthotel, Studentská 1, Brno, 62500 – https://www.campea-aparthotel.cz

Travel: Brno has an international airport with particularly good connections to the UK (London Stansted and Luton) and Germany (Münich).

Participants can also arrive at either Vienna or Prague airports and take the train to Brno (slightly shorter transfer time from Vienna).

Please contact Petra Koubova for all inquiries.

 

First EANS Brno HandsOn Course

The inaugural EANS Brno HandsOn Course took place from 28 November to 1 December 2017, led by Course Chairmen, EANS Training Committee Chair Torstein Meling and Chief of Neurosurgery Department of University Hospital Brno Martin Smrcka.

The format was immediately successful and received excellent evaluations from the participations. Please see the testimonials below.

All the attendees were hard working and enthusistic. The atmosphere was serious while working but in free time we made friends and had fun:-)

I want to thank you for this course. It was great! Maybe it can be even better if we have a little bit more time for our approaches. Because, while we are residents, we really like do it precisely like it was discussed. And maybe we are not fast enough sometimes. Also I want to mention that we had some problems with brain tissue during our dissections. I understand that’s mostly because of the cadaveric status of the brain, but still if there is a way to improve it – it will even better than now. And I really want to thank all the faculty members. You were super friendly and useful during this course. I can’t wait to meet you once again. Thank you! Thank you so much for everything, enjoyed every second.

It was absolutely great! And I wish you all the best!

Good timing, everything was well balanced, maybe a bit more time for dissections.

It was amazing how the faculty was interested and enjoyed the time with us. And how they helped, gave advice…

UpToDate: Intraneural ganglion cyst

An intraneural ganglion cyst (INGC) is a non-neoplastic mucinous cyst within the epineurium of a nerve and commences from an adjoining joint 1) 2)3) 4) 5) 6) 7).

These cysts are filled with a mucinous material which is walled off by a fibrous layer 8) 9) 10)

An intraneural ganglion cyst is an uncommon occurrence of the peripheral nerves.

Types

The most common type is the peroneal intraneural ganglion cyst. Other reported sites of involvement are the radial, ulnar, median, sciatic, tibial, and posterior interosseus nerves. The first case of intraneural ganglion cyst of the tibial nerve was described in 1967.

Etiology

According to the most widely accepted theory (articular/synovial theory), the cysts are formed from a capsular defect of an adjacent joint, so that synovial fluid spreads along the epineurium of a nerve branch 11).

Clinical features

As these cysts expand within the epineurium, they displace and compress the adjacent nerve fascicles leading to pain, paresthesia, tingling and muscle paralysis in the distribution of the involved nerve 12) 13).

Diagnosis

MRI is the method of choice for diagnosing intraneural ganglion cysts. However, ultrasound is also important 14).

Differential diagnosis

The differential considerations for cystic intraneural lesions include cystic nerve sheath tumors, atypical Baker’s cyst, and extraneural ganglion.

Cystic nerve sheath tumors such as schwannomas and extraneural ganglion can be differentiated from cystic intraneural lesions by MRI. A Baker’s cyst classically is more mass-like, with a characteristic location extending from the tibiofemoral joint to within the confines of the medial head of the gastrocnemius and the muscles of the joint capsule 15).

Treatment

Surgery is the only curative treatment with treatment success being dependent on ligature of the nerve endings supplying the articular branch 16).

Case series

Fricke et al. from Kiel, examined between 2011 and 2018 the patients using lower limb MRI. MRI scans were also performed for the follow-up examinations.

The patients had many symptoms. They were able to accurately detect the intraneural ganglion cysts on MRI and provide the treating surgeons with the basis for the operation to be performed.

The success of surgical therapy depends on the resection of the nerve endings supplying the joint as the only way to treat the origin of the disease and prevent recurrence. Based on there case studies, they can support the commonly favored articular/synovial theory. 17).

References

1) , 8)

Patel P, Schucany WG. A rare case of intraneural ganglion cyst involving the tibial nerve. Proc (Bayl Univ Med Cent) 2012;25:132–135.

2) , 9)

Uetani M, Hashmi R, Hayashi K, Nagatani Y, Narabayashi Y, Imamura K. Peripheral nerve intraneural ganglion cyst: MR findings in three cases. J Comput Assist Tomogr. 1998;22:629–632.

3) , 10)

Harbaugh KS, Tiel RL, Kline DG. Ganglion cyst involvement of peripheral nerves. J Neurosurg. 1997;87:403–408.

4)

Spinner RJ, Desy NM, Rock MG, Amrami KK. Peroneal intraneural ganglia. Part I. Techniques for successful diagnosis and treatment. Neurosurg Focus. 2007;22:E16.

5)

Jacobs RR, Maxwell JA, Kepes J. Ganglia of the nerve. Presentation of two unusual cases, a review of the literature, and a discussion of pathogenesis. Clin Orthop Relat Res. 1975:135–144.

6)

Adn M, Hamlat A, Morandi X, Guegan Y. Intraneural ganglion cyst of the tibial nerve. Acta Neurochir (Wien) 2006;148:885–889; discussion 889-890.

7)

Johnston JA, Lyne DE. Intraneural ganglion cyst of the peroneal nerve in a four-year-old girl: a case report. J Pediatr Orthop. 2007;27:944–946.

11) , 14) , 16) , 17)

Fricke T, Schmitt AD, Jansen O. Intraneural ganglion cysts of the lower limb. Rofo. 2018 Nov 19. doi: 10.1055/a-0777-2525. [Epub ahead of print] English, German. PubMed PMID: 30453381.

12)

Tehli O, Celikmez RC, Birgili B, Solmaz I, Celik E. Pure peroneal intraneural ganglion cyst ascending along the sciatic nerve. Turk Neurosurg. 2011;21:254–258.

13)

Liang T, Panu A, Crowther S, Low G, Lambert R. Ultrasound-guided aspiration and injection of an intraneural ganglion cyst of the common peroneal nerve. HSS J. 2013;9:270–274.

15)

Patel P, Schucany WG. A rare case of intraneural ganglion cyst involving the tibial nerve. Proc (Bayl Univ Med Cent). 2012 Apr;25(2):132-5. PubMed PMID: 22481843; PubMed Central PMCID: PMC3310510.
intraneural_ganglion_cyst.txt · Last modified: 2018/11/20 20:09 by administrador

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