Category Archives: Operative Neurosurgery

Ophthalmic artery aneurysm surgery

Ophthalmic artery aneurysm surgery

The ophthalmic artery aneurysms can treated safe and effective through a frontolateral approach 1).

The most important risk associated with clipping ophthalmic artery aneurysms is a new visual deficit. Meticulous microsurgical technique is necessary during anterior clinoidectomy, aneurysm dissection, and clip application to optimize visual outcomes, and aggressive medical management postoperatively might potentially decrease the incidence of delayed visual deficits. As the results of endovascular therapy and specifically flow diverters become known, they warrant comparison with these surgical benchmarks to determine best practices 2).

For ophthalmic artery aneurysm treatment if necessary, the ophthalmic artery may be sacrificed without worsening of vision in the vast majority.

Surgery is technically demanding because these aneurysms are often large and may extend into the cavernous sinus 3) 4) 5) 6) 7) 8).

Care must be taken to avoid optic nerve injury caused by the retraction and/or the heat of the drill 9).

For unruptured intracranial aneurysm, drill off anterior clinoid process via an extradural approach before opening dura to approach aneurysm neck maybe safe. Not for ruptured.

Cutting the falciform ligament early decompresses the optic nerve, and helps minimize worsening of visual impairment from surgical manipulation.

In most cases, a side angled clip can be placed paralell to the parent artery along the neck of the aneurysm 10).

Contralateral approach

Case series

2018

Kamide et al. retrospectively reviewed results from microsurgical clipping of 208 OphA aneurysms in 198 patients.

Patient demographics, aneurysm morphology, clinical characteristics, and patient outcomes were recorded and analyzed.

Despite 20% of these aneurysms being large or giant in size, complete aneurysm occlusion was accomplished in 91% of 208 cases, with OphA patency preserved in 99.5%. The aneurysm recurrence rate was 3.1% and the retreatment rate was 0%.

Good outcomes (modified Rankin Scale score 0-2) were observed in 96.2% of patients overall and in all 156 patients with unruptured aneurysms. New visual field defects (hemianopsia or quadrantanopsia) were observed in 8 patients (3.8%), decreased visual acuity in 5 (2.4%), and monocular blindness in 9 (4.3%). Vision improved in 9 (52.9%) of the 17 patients with preoperative visual deficits.

The most important risk associated with clipping OphA aneurysms is a new visual deficit. Meticulous microsurgical technique is necessary during anterior clinoidectomy, aneurysm dissection, and clip application to optimize visual outcomes, and aggressive medical management postoperatively might potentially decrease the incidence of delayed visual deficits. As the results of endovascular therapy and specifically flow diverters become known, they warrant comparison with these surgical benchmarks to determine best practices 11).

2017

The clinical data of 95 patients with carotid ophthalmic artery aneurysms treated via frontolateral approach in the last 1.5 years in Beijing Tiantan Hospital and Beijing Anzhen Hospital were analyzed retrospectively.Before the operation, digital subtraction angiogram (DSA) was performed among all patients.The patients were divided into two groups by the lateral approach.According to preoperative classification, surgical characteristics and prognosis were summarized.

Ninety-five cases of ophthalmic aneurysms were divided into type Ⅰ of 44 cases (46.3%), type Ⅱ of 34 cases (35.7%) and type Ⅲ of 17cases (17.9%), according to the results of DSA.The diameter of aneurysm was <10 mm (35 cases), 10-25 mm (34 cases), and >25 mm (26 cases). In the 17 cases of subarachnoid hemorrhage (SAH), 8 cases were ruptured carotid-ophthalmic artery aneurysms.Among those 95 patients, 93 were clipped successfully, 2 was trapped.Multiple aneurysms in 5 cases were treated in one surgical session through the same approach.No aneurysm residual was found after postoperative CTA review.Ipsilateral vision of 3 cases were decline.Cerebral infarction was appeared in 9 cases.All the others had a good recovery.

The carotid-ophthalmic artery aneurysms could be well exposed. Microsurgery through frontolateral approach has the advantages such as minimal invasion, less effect on the patients’ look and simple procedure.The frontolateral approach is safe and effective in surgery for ophthalmic segment of the internal carotid artery aneurysms 12).

Case reports

Rustemi et al. illustrated the first case of indocyanine green videoangiography (ICG-VA) application in an optic penetrating ophthalmic artery aneurysm treatment. A 57-year-old woman presented with temporal hemianopsia, slight right visual acuity deficit, and new onset of headache. The cerebral angiography detected a right ophthalmic artery aneurysm medially and superiorly projecting. The A1 tract of the ipsilateral anterior cerebral artery was elevated and curved, being suspicious for an under optic aneurysm growth. Surgery was performed. Initially the aneurysm was not visible. ICG-VA permitted the transoptic aneurysm visualization. After optic canal opening, the aneurysm was clipped and transoptic ICG-VA confirmed the aneurysm occlusion. ICG-VA showed also the slight improvement of the optic nerve pial vascularization. Postoperatively, the visual acuity was 10/10 and the hemianopsia did not worsen.

The elevation and curve of the A1 tract in medially and superiorly projecting ophthalmic aneurysms may be an indirect sign of under optic growth, or optic splitting aneurysms. ICG-VA transoptic aneurysm detection and occlusion confirmation reduces the surgical maneuvers on the optic nerve, contributing to function preservation 13).

1) , 12)

Wang JT, Kan ZS, Wang S. [Surgical management of ophthalmic artery aneurysms via minimally invasive frontolateral approach]. Zhonghua Yi Xue Za Zhi. 2017 Apr 18;97(15):1179-1183. doi: 10.3760/cma.j.issn.0376-2491.2017.15.014. Chinese. PubMed PMID: 28427127.
2) , 11)

Kamide T, Tabani H, Safaee MM, Burkhardt JK, Lawton MT. Microsurgical clipping of ophthalmic artery aneurysms: surgical results and visual outcomes with 208 aneurysms. J Neurosurg. 2018 Jan 26:1-11. doi: 10.3171/2017.7.JNS17673. [Epub ahead of print] PubMed PMID: 29372879.
3)

Hosobuchi Y. Direct surgical treatment of giant intracranial aneurysms. J Neurosurg. 1979;51(6):743–756.
4)

Sundt T M Jr, Piepgras D G. Surgical approach to giant intracranial aneurysms. Operative experience with 80 cases. J Neurosurg. 1979;51(6):731–742.
5)

Almeida G M, Shibata M K, Bianco E. Carotid-ophthalmic aneurysms. Surg Neurol. 1976;5(1):41–45.
6)

Kattner K A, Bailes J, Fukushima T. Direct surgical management of large bulbous and giant aneurysms involving the paraclinoid segment of the internal carotid artery: report of 29 cases. Surg Neurol. 1998;49(5):471–480.
7)

Nutik S L. Ventral paraclinoid carotid aneurysms. J Neurosurg. 1988;69(3):340–344.
8)

Nutik S. Carotid paraclinoid aneurysms with intradural origin and intracavernous location. J Neurosurg. 1978;48(4):526–533
9)

Kumon Y, Sakaki S, Kohno K, Ohta S, Ohue S, Oka Y. Asymptomatic, unruptured carotid-ophthalmic artery aneurysms: angiographical differentiation of each type, operative results, and indications. Surg Neurol. 1997 Nov;48(5):465-72. PubMed PMID: 9352810.
10)

Day AL. Clinicoanatomic features of supraclinoid aneurysms. Clin Neurosurg. 1990;36:256-74. Review. PubMed PMID: 2403885.
13)

Rustemi O, Cester G, Causin F, Scienza R, Della Puppa A. Indocyanine Green Videoangiography Transoptic Visualization and Clipping Confirmation of an Optic Splitting Ophthalmic Artery Aneurysm. World Neurosurg. 2016 Jun;90:705.e5-705.e8. doi: 10.1016/j.wneu.2016.03.010. Epub 2016 Mar 12. PubMed PMID: 26979923.

PASSION Resident project

The PASSION Resident project is a European study that aims at establishing a new training syllabus for neurosurgical residents.

see Neurosurgical training in Europe.

The main goal is to shape young neurosurgeons in their resident years through the implementation of new training modules, including simulation courses that will improve their neurosurgical skills in an innovative way. Moreover this new methodology will allow standardised measurements with an objective perspective of their progress and achievements. Besides, we will assess all participants by means of some validated professional questionnaires.

This study will take place at the Besta NeuroSim Centre, within the IRCCS Carlo Besta Neurological Institute in Milan (Italy). It foresees the use of the most sophisticated and modern neurosurgical simulators available today. These simulators provide haptic feedback and a threedimensional virtual reality. Along with these technologically advanced systems (SimLab) the resident students participating will also have to perform microsurgical tasks at the WetLab station of the Center.

The PASSION Resident study project has been approved by our local Ethical Board (IRB). The study will start in March 2018.

WHO CAN PARTICIPATE?

All neurosurgery residents currently enrolled in any Center or Institute in Europe (currently enrolled in a residency program across Europe – PGY1, PGY2, PGY3, PGY4). All residents must have no neurosurgical simulation training or experience.

All participants must have completed these pre-requisites: three (3) EVD placement procedures and three (3) microscope-assisted dural sutures (at the end of an intra-cerebral lesion removal surgery).

HOW TO PARTICIPATE?

All applicants must send these following documents in the exact way in which they are described, to these email addresses: alessandro.perin@istituto-besta.it and nicole.riker@istituto-besta.it:

A. Pre and post-operative CT scan (or MRI) in DICOM format of three EVD operations done, specifying: a) number of attempts needed to reach the lateral ventricle; b) Role that the resident had (first/second operator; level of independence) during the procedure; please note that first-time positioned EVD will be eligible for the study, no EVD substitution will be considered; You can also upload the last EVDs you have positioned consecutively during the last period of your surgical activity (collection of this data does not necessarily need to be perspective).

B. Video Recordings (through the microscope) of the last three dural sutures done at the end of an intra-cerebral lesion removal surgery specifying: a) The microscopes magnification level and the caliber of the suturing stitch; b) the role that the resident had during the procedure (first/second operator; level of independence) and specify at what point of the registration the resident was actually operating at the microscope; c) Opening of any cisterns and/or of the cerebral ventricles; any post-operative complication referable to the dural suturing (CFS fistula, pseudomeningocele).

C. A document stating that the resident is officially enrolled in a residency program.

D. The attached form entirely and accurately filled out.

All data, namely DICOM images and microscope video recordings MUST be anonymous: they cannot and must not include any personal patient or surgeon information; the neurosurgeon’s Center must not be recognisable.

All data must be uploaded to Google Drive. Please share all of the requested information at passionstudy2017@gmail.com

The information sent will be examined by a commission of expert neurosurgeons, in an anonymous manner (blinded evaluation). The first 140 resident students to submit the required information will be selected as participants for this study.

NB: this study will not focus on patients but will only evaluate the neurosurgical actions done by residents; no personal data that belongs to patients will be shared, no personal information about patients/surgeons/Institutions will be posed at risk or published.

WHAT IS THE STRUCTURE OF THE STUDY?

At the end of the selection process the participants will be randomised into two groups: half of them will take part in the Wet Lab and the simulation sessions (SimLab), while the other half will take part in the Wet Lab only (Control group). The first group will be divided into smaller groups of six participants who will be at the Centre for five consecutive days; the second group (control) will be at the Center only on the first and last day. (Look at the scheme on the following page).

Every participant will undergo specific dexterity and spatial orientation tests along with a psychometric evaluation.

At the end of the candidates’ work at the Center, all residents must return to their medical activities and redo the exact pre-requisite tasks that were mandatory for the application process (3 EVD placements and 3 dural sutures) and send them back to the examining commission through the previously cited email addresses (POST-REQUISITES). This second data collection MUST be completed within 2 months after their return to their home Institutions.

FINANCIAL EXPENSES

The Best NeuroSim Center will cover all the expenses that regard the onsite study materials, namely brain tumour/dura models, mannequins, personnel and lunch tickets and accommodation for all participants. We ask participants to cover their travel expenses.

WHY SHOULD YOU PARTICIPATE?

First and foremost it would be a unique experience to work and collaborate within an international research group that for the first time ever aims at defining the potential beneficial impact that simulation might have on your learning process of both technical and non technical skills This would be achieved on a large scale by using top-notch, up-to-date simulators with haptic feedback that you will be entitled to use extensively. By participating in this innovative training you will have the chance to spend 5 days in one of the most renown and recognised neurosurgery Centres in the World, with a special focus on brain tumours and research and technology innovation. At the Besta Institute we operate on more than 3000 patients a year of whom 1000 are affected by CNS tumours; this is where the first European neurosurgical simulation Center was created. Here no matter whether part of the control group or the study groups you will be able to train some key neurosurgical tasks at the WetLab; moreover you will be using our simulators intensively (study group), or following all OR activities (control group).

Finally, as core members and contributors to this study you would all be named co-authors (in a study group publication entity) when the results of this study will be published.

ALL APPLICANTS MUST SEND THE REQUESTED ENROLMENT INFORMATION BY FEBRUARY 28th 2018.

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Update: Microvascular decompression for glossopharyngeal neuralgia

Microvascular decompression for glossopharyngeal neuralgia

For glossopharyngeal neuralgia treatment, should pharmacologic management be ineffective, surgical intervention is indicated. The first-choice treatment is typically microvascular decompression (MVD), as it has the highest initial and long-term success rates.

In 1932, Walter Edward Dandy 1) thought that the operative approach of GPN was the same with trigeminal neuralgia or Meniere’s disease.

Laha and Jannetta 2) proposed that GPN could be treated by surgically relieving the pressure that offending vascular structures imposed on the glossopharyngeal nerves.

Resnick et al. 3) reporteded excellent postoperative surgical results for 79%.

Patel et al. reported in 217 a immediate success rate of 90% 4).

There are three types of neurovascular compression (NVC): type I – NVC at the root entry zone (REZ) of the IX CN within the retro-olivary sulcus; type II – the vertebral artery causes NVC at the IX CN REZ by the shoulder of the artery, and the type III – a “sandwich-like” compression where the vertebral artery and the PICA perform a combination of NVC 5).

Technique

Once the anesthetic induction and intubation have been performed, the patient should be positioned in lateral decubitus fashion, fixing the head with a Mayfield head clamp, followed by the placement of an axillary roll. The neck should be narrowed with slight flexion and rotated approximately 10 degrees to the affected side. The vertex is tilted 15 degrees toward the floor. The shoulder is pulled out of the way and finally the patient is accommodated in such a way that the table can be rotated laterally or adjusted for a Trendelenburg position or reverse Trendelenburg position. For the incision, the mastoid eminence is initially demarcated, then a line is drawn from the external auditory canal to the inion to mark the transverse sinus. Then, a 3-4 cm arcuate or linear incision is performed, with the concave side toward the ear. Half of the incision should be above the mastoid notch or even more posteriorly in large, muscular or dolichocephalic patients. Subsequently, a retractor is placed and the bone is opened with a perforator, making sure to use bone wax in case of bleeding and filling the mastoid cells.

Ordónez-Rubiano et al. propose to target the opening of the bone depending on the CN affected. Three different approaches could be performed. The superior for the V CN (mini extreme-lateral or microasterional), the middle for VII and VIII CNs (usual for the cerebellopontine angle), and the inferior for the IX to XII CNs (mini far-lateral).

Once the dura is exposed, it is incised and stretched. The form in which the dura is opened includes the L or reverse L shape, 3-5 mm parallel to the sigmoid sinus and to the floor of the posterior fossa, after which they are secured with sutures for a wider exposure. A retractor is placed under the cerebellum and raised from its inferolateral margin, after which the microscope is introduced, and the retractor is advanced anteriorly until the spinal part of the XI CN is observed, the arachnoid is dissected, which allows to elevate the cerebellum and expose the remaining CNs within the jugular foramen. Once the rootlets of the IX CN are identified, they are separated from the rootlets of the X and XI CNs. The involved vessel is identified and dissected before the decompression and finally, the Teflon is placed between the two structures 6).

If there is no NVC, the glossopharyngeal nerve and the upper bundle of the X CN can be sectioned 7).

Case series

2018

Between 2006 and 2016, 228 idiopathic GPN patients underwent MVD in our department. Those cases were retrospectively reviewed with emphasis on intraoperative findings and long-term postoperative outcomes. The average period of follow-up was 54.3 ± 6.2 months.

Intraoperatively, the culprit was identified as the posterior inferior cerebellar artery (PICA) in 165 cases (72.3%), the vertebral artery (VA) in 14 (6.1%), vein in 10 (4.4%), and a combination of multiple arteries or venous offending vessels in 39 (17.2%). The immediately postoperative outcome was excellent in 204 cases (89.5%), good in 12 (5.3%), fair in 6 (2.6%) and poor in 6 (2.6%). More than 5-year follow-up was obtained in 107 cases (46.9%), which presented as excellent in 93 (86.9%), good in 6 (5.6%), fair in 3 (2.8%) and poor in 5 (4.7%). Thirty-seven (16.2%) of the patients experienced some postoperative neurological deficits immediately, such as dysphagia, hoarseness and facial paralysis, which has been improved at the last follow-up in most cases, except 2.

This investigation demonstrated that MVD is a safe and effective remedy for treatment of GPN 8).

2017

30 patients with intractable primary typical GPN who underwent MVD without rhizotomy and were followed for more than 2 years were included in the analysis. Each MVD was performed using one of four different surgical techniques: interposition of Teflon pieces, transposition of offending vessels using Teflon pieces, transposition of offending vessels using a fibrin-glue-coated Teflon sling, and removal of offending veins.

The posterior inferior cerebellar artery was responsible for neurovascular compression in 27 of 30 (90%) patients, either by itself or in combination with other vessels. The location of compression on the glossopharyngeal nerve varied; the root entry zone (REZ) only (63.3%) was most common, followed by both the REZ and distal portion (26.7%) and the distal portion alone (10.0%). In terms of detailed surgical techniques during MVD, the offending vessels were transposed in 24 (80%) patients, either using additional insulation, offered by Teflon pieces (15 patients), or using a fibrin glue-coated Teflon sling (9 patients). Simple insertion of Teflon pieces and removal of a small vein were also performed in five and one patient, respectively. During the 2 years following MVD, 29 of 30 (96.7%) patients were asymptomatic or experienced only occasional pain that did not require medication. Temporary hemodynamic instability occurred in two patients during MVD, and seven patients experienced transient postoperative complications. Neither persistent morbidity nor mortality was reported.

This study demonstrates that MVD without rhizotomy is a safe and effective treatment option for GPN 9).


From January 2004 to June 2006, 35 consecutive patients were diagnosed with GPN. All of them underwent MVD. Demographic data, clinical presentation, operative findings, clinical results, operative complications were reviewed.

A total of 33 patients (94.3%) experienced complete pain relief immediately after MVD. Long-term follow-up was available for 30 of these 35 patients, and 28 of these 30 patients continued to be pain-free. There was no long-term operative morbidity in all cases. One patient had a cerebrospinal fluid leak and 1 case presented with delayed facial palsy.

Classic GPN is usually caused by pulsatile neurovascular compression of the glossopharyngeal and vagus rootlets. MVD is a safe, effective, and durable operation for GPN 10).

2015

A retrospective review of the case notes of patients who had undergone surgery for GPN in the authors’ department between 2008 and 2013 was performed to investigate baseline characteristics and immediate outcomes during the hospitalization. For the long-term results, a telephone survey was performed, and information on pain recurrence and permanent complications was collected. Pain relief meant no pain or medication, any pain persisting after surgery was considered to be treatment failure, and any pain returning during the follow-up period was considered to be pain recurrence. For comparative study, the patients were divided into 2 cohorts, that is, patients treated with GPNR alone and those treated with GPNR+VNR.

One hundred three procedures, consisting of GPNR alone in 38 cases and GPNR+VNR in 65 cases, were performed in 103 consecutive patients with GPN. Seventy-nine of the 103 patients could be contacted for the follow-up study, with a mean follow-up duration of 2.73 years (range 1 month-5.75 years). While there were similar results (GPNR vs GPNR+VNR) in immediate pain relief rates (94.7% vs 93.8%), immediate complication rates (7.9% vs 4.6%), and long-term pain relief rates (92.3% vs 94.3%) between the 2 cohorts, a great difference was seen in long-term complications (3.8% vs 35.8%). The long-term complication rate for the combined GPNR+VNR cohort was 9.4 times higher than that in the GPNR cohort. There was no operative or perioperative mortality. Immediate complications occurred in 6 cases, consisting of poor wound healing in 3 cases, and CSF leakage, hoarseness, and dystaxia in 1 case each. Permanent complications occurred in 20 patients (25.3%) and included cough while drinking in 10 patients, pharyngeal discomfort in 8 patients, and hoarseness and dysphagia in 1 case each.

In general, this study indicates that GPNR alone or in combination with VNR is a safe, simple, and effective treatment option for GPN. It may be especially valuable for patients who are not suitable for the microvascular decompression (MVD) procedure and for surgeons who have little experience with MVD. Of note, this study renews the significance of GPNR alone, which, the authors believe, is at least valuable for a subgroup of GPN patients, with significantly fewer long-term complications than those for rhizotomy for both glossopharyngeal nerve and rootlets of the vagus nerve 11).

2002

Patel et al. present the experience with more than 200 patients and conducted a retrospective review of the database and identified patients who presented for treatment of presumed GPN. When possible, patients were contacted by telephone for collection of follow-up information regarding symptom relief, complications, functional outcomes, and patient satisfaction. Univariate and multivariate analyses were performed to identify predictors of good outcomes after MVD. Subgroup analyses were performed with quartiles of approximately 50 patients each, for assessment of the effects of improvements in techniques and anesthesia during this 20-year period.

They observed GPN to be more common among female (66.8%) than male (33.2%) patients, with an overall mean patient age of 50.2 years (standard deviation, 14.4 yr). The most common presenting symptoms were throat and ear pain and throat pain alone, and the mean duration of symptoms was 5.7 years (standard deviation, 5.8 yr; range, 1-32 yr). Symptoms appeared almost equally on the left side (54.8%) and the right side (45.2%). The overall immediate success rate exceeded 90%, and long-term patient outcomes and satisfaction were best for the typical GPN group (with pain restricted to the throat and palate). Complication rates decreased across quartiles for all categories evaluated.

MVD is a safe, effective form of therapy for GPN. It may be most beneficial for patients with typical GPN, especially when symptoms are restricted to deep throat pain only 12).

1995

Since 1971, 40 patients have undergone microvascular decompression of the glossopharyngeal and vagus nerves for treatment of typical glossopharyngeal neuralgia. This procedure provided excellent immediate results (complete or > 95% relief of pain) in 79%, with an additional 10% having a substantial (> 50%) reduction in pain. Long-term follow-up (mean, 48 mo; range, 6-170 mo) reveals excellent results (complete or > 95% reduction in pain without any medication) in 76% of the patients and substantial improvement in an additional 16%. There were two deaths at surgery (5%) both occurring early in the series as the result of hemodynamic lability causing intracranial hemorrhage. Three patients (8%) suffered permanent 9th nerve palsy 13).

1986

20 patients who had undergone microvascular decompression for the treatment of “idiopathic” trigeminal neuralgia (9 cases), hemifacial spasm (7 cases), glossopharyngeal neuralgia (3 cases) and paroxysmal vertigo and tinnitus (1 case) were followed up for 25 months on average. Permanent relief of symptoms was observed in 19 (95%), with sparing of cranial nerve function. Analysis of the clinical data shows that the patients described in the present series did not differ from those considered to suffer from “idiopathic” cranial nerve dysfunction syndromes. The importance of vascular cross compression as etiological factor in such conditions is stressed and the pathophysiology discussed. The term “cryptogenic” applied to trigeminal neuralgia or hemifacial spasm thus needs revising. Lastly, the indications of microvascular decompression in the treatment of “cryptogenic” cranial nerve dysfunction syndromes are defined 14).

1977

Microsurgical observations werw made of the cranial nerve root entry or exit zones 117 patients operated upon for the treatment of hyperactive-hypoactive dysfunction syndromes (trigeminal neuralgia, hemifacial spasm, acoustic nerve dysfunction, and glossopharyngeal neuralgia). Cross-compression or distortion of the appropriate nerve root at its entry or exit zone was noted in all patients. This compression or distortion was usually caused by normal or arteriosclerotic, elongated arterial loops, it was usually relieved by decompressive microsurgical techniques. A small percentage of patients were found to have compression of the nerve root at the entry-exit zone by a tumor, a vein, or some other structural abnormality; they were relieved by tumor excision or other measures as described. Relief was gradual postoperatively if the treated nerve was not stroked or manipulated at operation but it was immediate if the nerve was manipulated. Preoperative evidence of decreased nerve function improved postoperatively 15).

Case reports

A case of coexistent glossopharyngeal neuralgia and hemifacial spasm was treated by transposition of the vertebral artery. A 60-year-old man was referred to our hospital due to pain in the left posterior part of the tongue that was difficult to control with oral medication at a local hospital. The diagnosis was left glossopharyngeal neuralgia based on the symptoms, imaging findings, and lidocaine test results. Moreover, the patient had left hemifacial spasm. Microvascular decompression was performed, which confirmed that the vertebral artery was compressing the lower cranial nerve and the posterior inferior cerebellar artery was compressing the root exit zone of the facial nerve. The vertebral artery and posterior inferior cerebellar artery were transposed using TachoSil. After the surgery, both glossopharyngeal neuralgia and hemifacial spasm disappeared, and the patient was discharged 16).

1985

A case of combined trigeminal and glossopharyngeal neuralgia is described. The superior cerebellar artery and normal choroid plexus compressed and indented the root entry zones of the trigeminal and glossopharyngeal nerves, respectively. Complete relief was obtained after microvascular decompression and resection of the choroid plexus 17).


A case of glossopharyngeal neuralgia associated with episodic cardiac arrest and syncope is presented. Posterior fossa exploration showed that the left glossopharyngeal and vagus nerves were compressed by the posterior inferior cerebellar artery. Microvascular decompression resulted in complete relief of glossopharyngeal neuralgia, cardiac syncope, and seizure. The mechanism of glossopharyngeal neuralgia associated with cardiac syncope is discussed 18).


Murasawa A, Yamada K, Hayakawa T, Aragaki Y, Yoshimine T. Glossopharyngeal neuralgia treated by microvascular decompression–case report. Neurol Med Chir (Tokyo). 1985 Jul;25(7):551-3. PubMed PMID: 2415848 19).

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Dandy WE (1932) The treatment of trigeminal neuralgia by the cerebellar route. Ann Surg 96:787–795
2)

Laha RK, Jannetta PJ (1977) Glossopharyngeal neuralgia. J Neurosurg 47:316–320
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Resnick DK, Jannetta PJ, Bissonnette D, Jho HD, Lanzino G. Microvascular decompression for glossopharyngeal neuralgia. Neurosurgery. 1995 Jan;36(1):64-8; discussion 68-9. PubMed PMID: 7708170.
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Patel A, Kassam A, Horowitz M, Chang YF. Microvascular decompression in the management of glossopharyngeal neuralgia: analysis of 217 cases. Neurosurgery. 2002 Apr;50(4):705-10; discussion 710-1. PubMed PMID: 11904019.
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Tanrikulu L, Hastreiter P, Dörfler A, Buchfelder M, Naraghi R. Classification of neurovascular compression in glossopharyngeal neuralgia: Three-dimensional visualization of the glossopharyngeal nerve. Surg Neurol Int. 2015 Dec 24;6:189. doi: 10.4103/2152-7806.172534. eCollection 2015. PubMed PMID: 26759734; PubMed Central PMCID: PMC4697202.
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Ordónez-Rubiano EG, García-Chingaté CC, Rodríguez-Vargas S, Cifuentes-Lobelo HA, Perilla-Cepeda TA. Microvascular Decompression for a Patient with a Glossopharyngeal Neuralgia: A Technical Note. Cureus. 2017 Jul 20;9(7):e1494. doi: 10.7759/cureus.1494. PubMed PMID: 28948114; PubMed Central PMCID: PMC5606712.
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Rey-Dios R, Cohen-Gadol AA. Current neurosurgical management of glossopharyngeal neuralgia and technical nuances for microvascular decompression surgery. Neurosurg Focus. 2013 Mar;34(3):E8. doi: 10.3171/2012.12.FOCUS12391. Review. PubMed PMID: 23451790.
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Xia L, Li YS, Liu MX, Zhong J, Dou NN, Li B, Li ST. Microvascular decompression for glossopharyngeal neuralgia: a retrospective analysis of 228 cases. Acta Neurochir (Wien). 2018 Jan;160(1):117-123. doi: 10.1007/s00701-017-3347-1. Epub 2017 Nov 4. PubMed PMID: 29103137.
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Kim MK, Park JS, Ahn YH. Microvascular Decompression for Glossopharyngeal Neuralgia: Clinical Analyses of 30 Cases. J Korean Neurosurg Soc. 2017 Nov;60(6):738-748. doi: 10.3340/jkns.2017.0506.010. Epub 2017 Oct 25. PubMed PMID: 29142635; PubMed Central PMCID: PMC5678068.
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Zhao H, Zhang X, Zhu J, Tang YD, Li ST. Microvascular Decompression for Glossopharyngeal Neuralgia: Long-Term Follow-Up. World Neurosurg. 2017 Jun;102:151-156. doi: 10.1016/j.wneu.2017.02.106. Epub 2017 Mar 2. PubMed PMID: 28263933.
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Ma Y, Li YF, Wang QC, Wang B, Huang HT. Neurosurgical treatment of glossopharyngeal neuralgia: analysis of 103 cases. J Neurosurg. 2015 Sep 4:1-5. [Epub ahead of print] PubMed PMID: 26339847.
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Michelucci R, Tassinari CA, Samoggia G, Tognetti F, Calbucci F. Intracranial microvascular decompression for “cryptogenic” hemifacial spasm, trigeminal and glossopharyngeal neuralgia, paroxysmal vertigo and tinnitus: II. Clinical study and long-term follow up. Ital J Neurol Sci. 1986 Jun;7(3):367-74. PubMed PMID: 3733417.
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Jannetta PJ. Observations on the etiology of trigeminal neuralgia, hemifacial spasm, acoustic nerve dysfunction and glossopharyngeal neuralgia. Definitive microsurgical treatment and results in 117 patients. Neurochirurgia (Stuttg). 1977 Sep;20(5):145-54. PubMed PMID: 198692.
16)

Fujii T, Otani N, Otsuka Y, Matsumoto T, Tanoue S, Ueno H, Tomura S, Tomiyama A, Toyooka T, Wada K, Mori K. [A Case of Coexistent Glossopharyngeal Neuralgia and Hemifacial Spasm Successfully Treated with Transposition of the Vertebral Artery]. No Shinkei Geka. 2017 Jun;45(6):503-508. doi: 10.11477/mf.1436203540. Review. Japanese. PubMed PMID: 28634310.
17)

Yoshioka J, Ueta K, Ohmoto T, Fujiwara T, Tabuchi K. Combined trigeminal and glossopharyngeal neuralgia. Surg Neurol. 1985 Oct;24(4):416-20. PubMed PMID: 4035551.
18)

Tsuboi M, Suzuki K, Nagao S, Nishimoto A. Glossopharyngeal neuralgia with cardiac syncope. A case successfully treated by microvascular decompression. Surg Neurol. 1985 Sep;24(3):279-83. PubMed PMID: 4023909.
19)

Murasawa A, Yamada K, Hayakawa T, Aragaki Y, Yoshimine T. Glossopharyngeal neuralgia treated by microvascular decompression–case report. Neurol Med Chir (Tokyo). 1985 Jul;25(7):551-3. PubMed PMID: 2415848.

Update: Geniculate neuralgia treatment

Geniculate neuralgia treatment

The treatment for geniculate neuralgia has not been established, although it seems reasonable that the therapeutic approaches used in other more common craniofacial neuralgias, such as trigeminal neuralgia, should be effective.

Conservative medical treatment is always the first-line therapy.

Mild cases may respond to carbamazepine sometimes in combination with phenytoin.

May responde to valproic acid.

Topical antibiotics for secondary infections of herpetic lesions.

Local anesthetic to external auditory canal.

Surgery

Surgical treatment should be offered if medical treatment fails. The two commonest surgical options are transection of the nervus intermedius, and microvascular decompression of the nerve at the nerve root entry zone of the brainstem. However, extracranial intratemporal division of the cutaneous branches of the facial nerve may offer a safer and similarly effective treatment.

The response to medical treatment for this condition varies between individuals. The long-term outcomes of surgery remain unknown because of limited data 1).

Rupa et al., postulate that geniculate ganglionectomy may be ineffective as the sole treatment for certain cases of geniculate neuralgia, and that nervus intermedius section may also be required to achieve a more complete deafferentation 2).

Excision of the nervus intermedius and/or of the geniculate ganglion by the middle cranial fossa approach without the production of facial paralysis, sometimes in combination with selective section of the Vth cranial nerve, has been successful in relieving the pain of geniculate neuralgia.

Microvascular decompression

Microvascular decompression may be effective as a treatment. Along its cisternal course, the nerve may be difficult to distinguish from the facial nerve. Based on case reports and small series, long-term pain control can be seen after nerve sectioning or microvascular decompression, but no prospective studies exist. Such studies are now necessary to shed light on the efficacy of surgical treatment of nervus intermedius neuralgia 3).

Complications

High-frequency hearing loss occurred after MVD for TGN, GPN, or GN, and the greatest incidence occurred on the ipsilateral side. This hearing loss may be a result of drill-induced noise and/or transient loss of cerebrospinal fluid during the course of the procedure. Changes in intraoperative BAEP waveforms were not useful in predicting HFHL after MVD. Repeated postoperative audiological examinations may be useful in assessing the prognosis of HFHL 4).

Case series

2002

Surgically excision of the nervus intermedius and geniculate ganglion via the middle cranial fossa approach, Review the long-term outcomes in 64 patients who were treated in this manner. Findings indicate that excision of the nervus intermedius and geniculate ganglion can be routinely performed without causing facial paralysis and that it is an effective definitive treatment for intractable geniculate neuralgia 5).

1991

A total of 31 surgical procedures were performed. Seventeen patients had sequential rhizotomies and one patient had microvascular decompression alone. Based on the clinical diagnosis, the nerves sectioned were singly or in combination: the nervus intermedius (14 patients), geniculate ganglion (10 patients), ninth nerve (14 patients), 10th nerve (11 patients), tympanic nerve (four patients), and chorda tympani nerve (one patient). Microvascular decompression of the involved nerves was undertaken in nine patients, in whom vascular loops were discovered. Adhesions (six patients), thickened arachnoid (three patients), and benign osteoma (one patient) were other intraoperative abnormalities noted. The overall success of these procedures in providing pain relief was 72.2%, and the mean follow-up period was 3.3 years (range 1 month to 14.5 years). There was no surgical mortality. Expected side effects were: decreased lacrimation, salivation, and taste related to nervus intermedius nerve section, and transient hoarseness and diminished gag related to ninth and 10th nerve section. Four patients developed sequelae consisting of sensorineural hearing loss, vertigo, and transient facial nerve paresis. One patient had a cerebrospinal fluid leak and another developed aseptic meningitis as postoperative complications. Except when primary glossopharyngeal neuralgia is the working diagnosis, a combined posterior cranial fossa-middle cranial fossa approach is recommended for adequate exploration and/or section of the fifth, ninth, and 10th cranial nerves as well as the geniculate ganglion and nervus intermedius 6).

1976

Excision of the nervus intermedius and/or of the geniculate ganglion by the middle cranial fossa approach without the production of facial paralysis, in any of 15 cases with geniculate neuralgia is reported. Use of these new techniques, sometimes in combination with selective section of the Vth cranial nerve, has been successful in relieving the pain of geniculate neuralgia 7).

Case reports

A 39-year-old man presented with a history of left “deep” ear pain within his ear canal. He noted occasional pain on the left side of his face around the ear. He had been treated with neuropathic pain medications without relief. His wife described suicidal ideations discussed by her husband because of the intense pain.

The patient’s neurologic examination was normal, and otolaryngologic consultation revealed no underlying structural disorder. Anatomic imaging revealed a tortuous vertebral artery-posterior inferior cerebellar artery complex with the posterior inferior cerebellar artery loop impinging on the root entry zone of the nervus intermedius-vestibulocochlear nerve complex and just inferior to the root entry zone of the facial nerve and a small anterior inferior cerebellar artery loop interposed between the cranial nerve VII-VIII complex and the hypoglossal and glossopharyngeal nerves. A left-sided retromastoid craniotomy was performed, and the nervus intermedius was transected. An arterial loop in contact with the lower cranial nerves at the level of the brainstem was mobilized with a polytetrafluoroethylene implant.

The patient indicated complete relief of his preoperative pain after surgery. He has remained pain-free with intact hearing and balance 8).

1)

Tang IP, Freeman SR, Kontorinis G, Tang MY, Rutherford SA, King AT, Lloyd SK. Geniculate neuralgia: a systematic review. J Laryngol Otol. 2014 May;128(5):394-9. doi: 10.1017/S0022215114000802. Review. PubMed PMID: 24819337.
2)

Rupa V, Weider DJ, Glasner S, Saunders RL. Geniculate ganglion: anatomic study with surgical implications. Am J Otol. 1992 Sep;13(5):470-3. PubMed PMID: 1443083.
3)

Tubbs RS, Steck DT, Mortazavi MM, Cohen-Gadol AA. The nervus intermedius: a review of its anatomy, function, pathology, and role in neurosurgery. World Neurosurg. 2013 May-Jun;79(5-6):763-7. doi: 10.1016/j.wneu.2012.03.023. Epub 2012 Apr 3. Review. PubMed PMID: 22484073.
4)

Thirumala P, Meigh K, Dasyam N, Shankar P, Sarma KR, Sarma DR, Habeych M, Crammond D, Balzer J. The incidence of high-frequency hearing loss after microvascular decompression for trigeminal neuralgia, glossopharyngeal neuralgia, or geniculate neuralgia. J Neurosurg. 2015 Dec;123(6):1500-6. doi: 10.3171/2014.10.JNS141101. Epub 2015 May 1. PubMed PMID: 25932612.
5)

Pulec JL. Geniculate neuralgia: long-term results of surgical treatment. Ear Nose Throat J. 2002 Jan;81(1):30-3. Review. PubMed PMID: 11816385.
6)

Rupa V, Saunders RL, Weider DJ. Geniculate neuralgia: the surgical management of primary otalgia. J Neurosurg. 1991 Oct;75(4):505-11. PubMed PMID: 1885967.
7)

Pulec JL. Geniculate neuralgia: diagnosis and surgical management. Laryngoscope. 1976 Jul;86(7):955-64. PubMed PMID: 933690.
8)

Tubbs RS, Mosier KM, Cohen-Gadol AA. Geniculate neuralgia: clinical, radiologic, and intraoperative correlates. World Neurosurg. 2013 Dec;80(6):e353-7. doi: 10.1016/j.wneu.2012.11.053. Epub 2012 Nov 23. PubMed PMID: 23178920.

Advances and Technical Standards in Neurosurgery: Volume 43

Advances and Technical Standards in Neurosurgery: Volume 43

List Price: $159.00
This volume reviews standard treatments for spinal dural arteriovenous fistulas, examining the anatomy of arteries and veins of the sylvian fissure, as well as microsurgical advances and the development of modern therapeutic strategies in intracranial meningiomas. The advances section presents a strategy for minimizing hearing loss after stereotactic radiosurgery for vestibular schwannomas, as well as a description of the mode of action and biology of ALA, including its interaction with tumor cells and the limits of this method. A dedicated chapter addresses the essential question of the limits (and merits) of various tractography techniques and of their importance for non-specialists, who may be tempted to use them uncritically. A further chapter examines molecular markers, which have become standard in neuropathological reports on intracranial tumors, reviewing the prognostic and predictive value of these modern molecular markers in gliomas. Additional chapters round out the coverage, offering a comprehensive overview of standard and advanced techniques.

Update: Chronic subdural hematoma recurrence

Chronic subdural hematoma recurrence

Epidemiology

Recurrence rates after chronic subdural hematoma (CSDH) evacuation with any of actual techniques twist drill craniostomy (TDC), burr hole craniostomy, craniotomy range from 5% to 30%. 1)

Risk factors

In the series of Han et al. independent risk factors for recurrence were as follows: age > 75 years (HR 1.72, 95% CI 1.03-2.88; p = 0.039), obesity (body mass index ≥ 25.0 kg/m2), and a bilateral operation 2).

Chon et al. shown that postoperative midline shifting (≥5 mm), diabetes mellitus, preoperative seizure, preoperative width of hematoma (≥20 mm), and anticoagulant therapy were independent predictors of the recurrence of chronic subdural hematoma.

According to internal architecture of hematoma, the rate of recurrence was significantly lower in the homogeneous and the trabecular type than the laminar and separated type 3).

see Chronic subdural hematoma and anticoagulant therapy.


The recurrence rate of chronic subdural hematoma cSDH seems to be related to the excessive neoangiogenesis in the parietal membrane, which is mediated via vascular endothelial growth factor (VEGF). This is found to be elevated in the hematoma fluid and is dependent on eicosanoid/prostaglandin and thromboxane synthesis via cyclooxygenase-2 (COX-2).


Antiplatelet therapy

Antiplatelet therapy significantly influences the recurrence of CSDH 4).

Pneumocephalus

Remaining pneumocephalus is seen as an approved factor of recurrence 5) 6).

Septation

Jack et al.found a 12% reoperation rate. CSDH septation (seen on computed tomogram scan) was found to be an independent risk factor for recurrence requiring reoperation (p=0.04). Larger post-operative subdural haematoma volume was also significantly associated with requiring a second drainage procedure (p<0.001). Independent risk factors of larger post-operative haematoma volume included septations within a CSDH (p<0.01), increased pre-operative haematoma volume (p<0.01), and a greater amount of parenchymal atrophy (p=0.04). A simple scoring system for quantifying recurrence risk was created and validated based on patient age (< or ≥80 years), haematoma volume (< or ≥160cc), and presence of septations within the subdural collection (yes or no).

Septations within CSDHs are associated with larger post-operative residual haematoma collections requiring repeat drainage. When septations are clearly visible within a CSDH, craniotomy might be more suitable as a primary procedure as it allows greater access to a septated subdural collection. The proposed scoring system combining haematoma volume, age, and presence of septations might be useful in identifying patients at higher risk for recurrence 7).

Membranectomy

Opening the internal hematoma membrane does not alter the rate of patients requiring revision surgery and the number of patients showing a marked residual hematoma six weeks after evacuation of a CSDH 8).

In the study of Lee et al, an extended surgical approach with partial membranectomy has no advantages regarding the rate of reoperation and the outcome. As initial treatment, burr-hole drainage with irrigation of the hematoma cavity and closed-system drainage is recommended. Extended craniotomy with membranectomy is now reserved for instances of acute rebleeding with solid hematoma 9).

Diabetes

Surgeons should consider informing patients with diabetes mellitus that this comorbidity is associated with an increased likelihood of recurrence

10) 11) 12).


Balser et al. report 11% recurrence, which included individuals who recurred as late as 3 years after initial diagnosis 13).

Close imaging follow-up is important for CSDH patients for recurrence prediction. Using quantitative CT volumetric analysis, strong evidence was provided that changes in the residual fluid volume during the ‘self-resolution’ period can be used as significantly radiological predictors of recurrence 14).

A structural equation model showed a significant association between increased antiinflammatory activity in hematoma fluid samples and a lower risk of recurrence, but this relationship was not statistically significant in venous blood samples. Moreover, these findings indicate that anti-inflammatory activities in the hematoma may play a role in the risk of a recurrence of CSDH 15).

Irrigation with artificial cerebrospinal fluid (ACF) decreased the rate of CSDH recurrence 16).

Treatment

There is no definite operative procedure for patients with intractable chronic subdural hematoma (CSDH).

Most recurrent hematomas are managed successfully with burr hole craniostomies with postoperative closed-system drainage. Refractory hematomas may be managed with a variety of techniques, including craniotomy or subdural-peritoneal shunt placement 17).

Although many studies have reported risk factors or treatments in efforts to prevent recurrence, those have focused on single recurrence, and little cumulative data is available to analyze refractory CSDH.

Matsumoto et al. defined refractory CSDH as ≥2 recurrences, then analyzed and compared clinical factors between patients with single recurrence and those with refractory CSDH in a cohort study, to clarify whether patients with refractory CSDH experience different or more risk factors than patients with single recurrence, and whether burr-hole irrigation with closed-system drainage reduces refractory CSDH.

Seventy-five patients had at least one recurrence, with single recurrence in 62 patients and ≥2 recurrences in 13 patients. In comparing clinical characteristics, patients with refractory CSDH were significantly younger (P=0.04) and showed shorter interval to first recurrence (P<0.001). Organized CSDH was also significantly associated with refractory CSDH (P=0.02). Multivariate logistic regression analysis identified first recurrence interval <1 month (OR 6.66, P<0.001) and age <71 years (OR 4.16, P<0.001) as independent risk factors for refractory CSDH. On the other hand, burr-hole irrigation with closed-system drainage did not reduce refractory CSDH.

When patients with risk factors for refractory CSDH experience recurrence, alternative surgical procedures may be considered as the second surgery, because burr-hole irrigation with closed-system drainage did not reduce refractory CSDH 18).

Implantation of a reservoir 19) 20) 21).

Subdural-peritoneal shunt 22).

Middle meningeal artery embolization

Embolization of the MMA is effective for refractory CSDH or CSDH patients with a risk of recurrence, and is considered an effective therapeutic method to stop hematoma enlargement and promote resolution 23) 24) 25) 26) 27) 28).

A pilot study indicated that perioperative middle meningeal artery (MMA) embolization could be offered as the least invasive and most effectual means of treatment for resistant patients of CSDHs with 1 or more recurrences 29).

Chihara et al. have treated three cases of CSDH with MMA embolization to date, but there was a postoperative recurrence in one patient, which required a craniotomy for hematoma removal and capsulectomy. MMA embolization blocks the blood supply from the dura to the hematoma outer membrane in order to prevent recurrences of refractory CSDH. Histopathologic examination of the outer membrane of the hematoma excised during craniotomy showed foreign-body giant cells and neovascular proliferation associated with embolization. Because part of the hematoma was organized in this case, the CSDH did not resolve when the MMA was occluded, and the development of new collateral pathways in the hematoma outer membrane probably contributed to the recurrence. Therefore, in CSDH with some organized hematoma, MMA embolization may not be effective. Magnetic resonance imaging (MRI) should be performed in these patients before embolization 30).

Case series

2017

A retrospective analysis of 756 consecutive patients with CSDH who underwent bur hole surgery at the Hanyang University Medical Center (Seoul and Guri) between January 1, 2004, and December 31, 2014. During the 6-month follow-up, 104 patients (13.8%) with recurrence after surgery for CSDH were identified. Independent risk factors for recurrence were as follows: age > 75 years (HR 1.72, 95% CI 1.03-2.88; p = 0.039), obesity (body mass index ≥ 25.0 kg/m2), and a bilateral operation.

This study determined the risk factors for recurrence of CSDH and their effects on outcomes. Further studies are needed to account for these observations and to determine their underlying mechanisms 31).

2016

Chronic subdural hematomas (cSDHs) have shown an increasing incidence in an ageing population over the last 20 years, while unacceptable recurrence rates of up to 30 % persist. The chronic subdural hematoma recurrence rate seems to be related to the excessive neoangiogenesis in the parietal membrane, which is mediated via vascular endothelial growth factor (VEGF). This is found to be elevated in the haematoma fluid and is dependent on eicosanoid/prostaglandin and thromboxane synthesis via cyclooxygenase-2 (COX 2). With this investigator-initiated trial (IIT) it was thought to diminish the recurrence rate of operated-on cSDHs by administering a selective COX-2 inhibitor (Celecoxib) over 4 weeks’ time postoperatively in comparison to a control group.

The thesis of risk reduction of cSDH recurrence in COX-2-inhibited patients was to be determined in a prospective, randomised, two-armed, open phase-II/III study with inclusion of 180 patients over a 2-year time period in four German university hospitals. The treated- and untreated-patient data were to be analysed by Fisher’s exact test (significance level of alpha, 0.05 [two-sided]).

After screening of 246 patients from January 2009 to April 2010, the study had to be terminated prematurely as only 23 patients (9.3 %) could be enrolled because of on-going non-steroid anti-rheumatic (NSAR) drug treatment or contraindication to Celecoxib medication. In the study population, 13 patients were treated in the control group (six women, seven men; average age 66.8 years; one adverse event (AE)/serious adverse event (SAE) needing one re-operation because of progressive cSDH (7.7 %); ten patients were treated in the treatment group (one woman, nine men; average age 64.7 years; five AEs/SAEs needing two re-operations because of one progressive cSDH and one wound infection [20 %]). Significance levels are obsolete because of insufficient patient numbers.

The theoretical advantage of COX-2 inhibition in the recurrent cSDH could not be transferred into the treatment of German cSDH patients as 66.6 % of the patients showed strict contraindications for Celecoxib. Furthermore, 55 % of the patients were already treated with some kind of COX-2 inhibition and, nevertheless, developed cSDH. Thus, although conceptually appealing, an anti-angiogenic therapy with COX-2 inhibitors for cSDH could not be realised in this patient population due to the high prevalence of comorbidities excluding the administration of COX2 inhibitors 32).

2010

Recurrence rates after chronic subdural hematoma (CSDH) evacuation with any of actual techniques twist drill craniostomy (TDC), burr hole craniostomy, craniotomy range from 5% to 30%. Use of drain has improved recurrence rates when used with burr-hole craniostomy. Now, we analyze predictors of recurrence of TDC with drain.

Three hundred twelve consecutive patients with CSDH have been studied in a retrospective study. Operative technique in all patients consisted in TDC with drain. Data recorded included any associated comorbidity. Radiologic measures of the CSDH before and after the procedure were studied. Clinical evaluation included Modified Rankin Scale, Glasgow Coma Scale (GCS), and neurological deficits. Two groups were compared: recurrence group and nonrecurrence group. Follow-up was for at least 1 year.

Twelve percent experienced recurrence. Preoperative CSDH width, preoperative midline shift, postoperative midline width, postoperative CSDH width, and residual CSDH 1 month later were significantly associated with CSDH recurrence. The logistic regression model for the multivariate analysis revealed that postoperative midline shift and postoperative neurological deficit were significantly associated with CSDH recurrence. The duration of treatment with dexamethasone was found not to be related with recurrence. Mortality before hospital discharge was 1%. Hospital stay was 2.5 days.

TDC with drain has similar results in recurrence rates, morbidity, mortality, and outcome as other techniques as burr-hole craniostomy with drain. Preoperative and postoperative hematoma width and midline shift are independent predictors of recurrence. Brain re-expansion and time of drain maintenance are important factors related with recurrence of CSDH. Future CSDH reservoirs must avoid negative pressure and sudden pressure changes inside the whole closed drain system 33).

Case reports

2016

Mewada et al. report a case with right hemiparesis and aphasia 1 month after a fall from a bicycle. Computed tomography scan of the head showed left chronic subdural hematoma, which was evacuated by burr-hole drainage. The postoperative course was complicated by reaccumulation within short period of time. On superselective digital subtraction angiography of MMA, iatrogenic dAVF was found on left side. We embolized successfully it using n-butyl cyanoacrylate after a third irrigation. No reaccumulation found in the postoperative period or at last follow-up. They proposed a treatment protocol based on the own experience and literature review.

Refractory chronic subdural hematoma with reaccumulation within a short interval should be subjected to digital subtraction angiography of the MMA. Embolization of ipsilateral MMA is safe, effective, and a useful option for the treatment of iatrogenic dAVF and resolution of hematoma 34).


An 85-year-old male presented with left CSDH, which recurred five times. The hematoma was irrigated and drained through a left frontal burr hole during the first to third surgery and through a left parietal burr hole during the fourth and fifth surgery. The hematoma had no septation and was well-evacuated during each surgery. Antiplatelet therapy for preventing ischemic heart disease was stopped after the second surgery, the hematoma cavity was irrigated with artificial cerebrospinal fluid at the third surgery, and the direction of the drainage tube was changed to reduce the postoperative subdural air collection at the fourth surgery. However, none of these interventions was effective. He was successfully treated by fibrin glue injection into the hematoma cavity after the fifth surgery.

This procedure may be effective for refractory CSDH in elderly patients 35).


A 67-year-old man with dural arteriovenous fistula (AVF) presenting as a non-traumatic chronic subdural hematoma (CSDH). This previously healthy patient was hospitalized due to progressive headache with subacute onset. He underwent burr-hole surgery twice for evacuating the left CSDH that was thickest at the posterior temporal area. The operative procedure and finding was not extraordinary, but subdural hematoma slowly progressed for days following the revision surgery. After investigation by super-selective external carotid angiography, a dural AVF found near the transverse-sigmoid sinus was diagnosed. Dural AVF was completely occluded with trans-arterial injecting polyvinyl alchol particles into the petrosquamosal branch of the middle meningeal artery. The patient showed a good neurological outcome with no additional intervention. Brain surgeons have to consider the possibility of dural AVF and perform cerebral angiogram if necessary when they manage the cases that have a spontaneously occurred and repeatedly recurring CSDH 36).

2007

Spontaneous intracranial hypotension (SIH) is reported to cause chronic subdural hematoma (SDH), however diagnosis of SIH in patients with SDH is not always easy.

Takahashi et al. report a case of chronic SDH refractory to repeated drainage, which was attributed to SIH. A forty-five-year-old man who had been suffering from orthostatic headache for one month was admitted to our hospital presenting with unconsciousness and hemiparesis. CT on admission revealed a chronic subdural hematoma, which was successfully treated once with subdural drainage. However, the patient fell into unconscious again with recurrence of the hematoma within several days. After two more sessions of drainage, SIH due to cerebrospinal fluid leakage was diagnosed with spinal magnetic resonance imaging (MRI) and radionuclide cisternography. Spinal MRI demonstrated abnormal fluid accumulation in the thoracic epidural space, and the radionuclide cisternogram showed early excretion of tracer into urine as well as absence of intracranial tracer filling. After treatment with epidural blood patching, the hematoma rapidly disappeared and he was discharged without symptoms. In the treatment of chronic SDH, especially in young to middle aged patient without preceding trauma or hematological disorders, physicians should pay attention to underlying SIH to avoid multiple surgery. MRI of the spine as well as radionuclide cisternography is useful in evaluation of this condition 37).

1) , 33)

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Mori K, Maeda M (2001) Surgical treatment of chronic subdural hematoma in 500 consecutive cases: clinical characteristics, surgical outcome, complications, and recurrence rate. Neurol Med Chir (Tokyo) 41:371–381

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Stanišić M, Hald J, Rasmussen IA, Pripp AH, Ivanović J, Kolstad F, Sundseth J, Züchner M, Lindegaard KF (2013) Volume and densities of chronic subdural haematoma obtained from CT imaging as predictors of postoperative recurrence: a prospective study of 107 operated patients. Acta Neurochir 155:323–333

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Unterhofer C, Freyschlag CF, Thomé C, Ortler M. Opening the Internal Hematoma Membrane does not Alter the Recurrence Rate of Chronic Subdural Hematomas – A Prospective Randomized Trial. World Neurosurg. 2016 May 2. pii: S1878-8750(16)30210-8. doi: 10.1016/j.wneu.2016.04.081. [Epub ahead of print] PubMed PMID: 27150644.

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Lee JY, Ebel H, Ernestus RI, Klug N. Various surgical treatments of chronic subdural hematoma and outcome in 172 patients: is membranectomy necessary? Surg Neurol. 2004 Jun;61(6):523-7; discussion 527-8. PubMed PMID: 15165784.

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Pang CH, Lee SE, Kim CH, Kim JE, Kang HS, Park CK, Paek SH, Kim CH, Jahng TA, Kim JW, Kim YH, Kim DG, Chung CK, Jung HW, Yoo H. Acute intracranial bleeding and recurrence after bur hole craniostomy for chronic subdural hematoma. J Neurosurg. 2015 Jul;123(1):65-74. doi: 10.3171/2014.12.JNS141189. Epub 2015 Feb 13. PubMed PMID: 25679282.

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Balser D, Rodgers SD, Johnson B, Shi C, Tabak E, Samadani U. Evolving management of symptomatic chronic subdural hematoma: experience of a single institution and review of the literature. Neurol Res. 2013 Apr;35(3):233-42. doi: 10.1179/1743132813Y.0000000166. Review. PubMed PMID: 23485050.

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Xu FF, Chen JH, Leung GK, Hao SY, Xu L, Hou ZG, Mao X, Shi GZ, Li JS, Liu BY. Quantitative computer tomography analysis of post-operative subdural fluid volume predicts recurrence of chronic subdural haematoma. Brain Inj. 2014;28(8):1121-6. doi: 10.3109/02699052.2014.910702. Epub 2014 May 6. PubMed PMID: 24801643.

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Pripp AH, Stanišić M. The Correlation between Pro- and Anti-Inflammatory Cytokines in Chronic Subdural Hematoma Patients Assessed with Factor Analysis. PLoS One. 2014 Feb 27;9(2):e90149. doi: 10.1371/journal.pone.0090149. eCollection 2014. PubMed PMID: 24587250.

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Adachi A, Higuchi Y, Fujikawa A, Machida T, Sueyoshi S, Harigaya K, Ono J, Saeki N. Risk factors in chronic subdural hematoma: comparison of irrigation with artificial cerebrospinal fluid and normal saline in a cohort analysis. PLoS One. 2014 Aug 4;9(8):e103703. doi: 10.1371/journal.pone.0103703. eCollection 2014. PubMed PMID: 25089621; PubMed Central PMCID: PMC4121178.

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Desai VR, Scranton RA, Britz GW. Management of Recurrent Subdural Hematomas. Neurosurg Clin N Am. 2017 Apr;28(2):279-286. doi: 10.1016/j.nec.2016.11.010. Epub 2017 Jan 4. Review. PubMed PMID: 28325462.

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Matsumoto H, Hanayama H, Okada T, Sakurai Y, Minami H, Masuda A, Tominaga S, Miyaji K, Yamaura I, Yoshida Y, Yoshida K. Clinical investigation of refractory chronic subdural hematoma: a comparison of clinical factors between single and repeated recurrences. World Neurosurg. 2017 Aug 24. pii: S1878-8750(17)31402-X. doi: 10.1016/j.wneu.2017.08.101. [Epub ahead of print] PubMed PMID: 28844917.

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Sato M, Iwatsuki K, Akiyama C, Masana Y, Yoshimine T, Hayakawa T. [Use of Ommaya CSF reservoir for refractory chronic subdural hematoma]. No Shinkei Geka. 1999 Apr;27(4):323-8. Japanese. PubMed PMID: 10347846.

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