Category Archives: Functional Neurosurgery

Update: L-Carnitine

L-Carnitine

Forty patients with severe traumatic brain injury were randomized into 2 groups. The l-carnitine (LCA-) group received standard treatment with placebo while the (LCA+) group received l-Carnitine 2g/day for one week. Neuron specific enolase (NSE) was measured on days 1, 3 and 7 after the initiation of the study. Neurocognitive and neurobehavioral disorders were recorded on the first and third months.

Neurocognitive function and NSE significantly improved within one week in both groups. Patient mortality was similar in LCA+ and LCA- groups (P value: 0.76). Brain edema was present in 7 patients in LCA+ group and 13 patients in LCA-group (P value: 0.044). While there was no difference in NSE levels between the two groups. Neurological function was preserved in the LCA+ group with an exception of attention deficit, which was frequent in the LCA+ group.

Mahmoodpoor et al. concluded that despite improvements in neurobehavioral function and the degree of cerebral edema, 7-days of treatment with l-Carnitine failed to reduce serum NSE levels or improve mortality rate at 90days in patients with TBI 1).


There is evidence in the literature for mitochondrial dysfunction in Parkinson’s disease as well as fatty acid beta-oxidation, involving l-carnitine.

Gill et al. investigated l-carnitine in the context of microglial activation, suggesting a potential new strategy of supplementation for PD patients. Preliminary results from this studies suggest that the treatment of activated microglia with the endogenous antioxidant l-carnitine can reverse the effects of detrimental neuroinflammation in vitro 2).

1)

Mahmoodpoor A, Shokouhi G, Hamishehkar H, Soleimanpour H, Sanaie S, Porhomayon J, Rasouli F, Nader ND. A pilot trial of l-carnitine in patients with traumatic brain injury: Effects on biomarkers of injury. J Crit Care. 2018 Feb 9;45:128-132. doi: 10.1016/j.jcrc.2018.01.029. [Epub ahead of print] PubMed PMID: 29454227.
2)

Gill EL, Raman S, Yost RA, Garrett TJ, Vedam-Mai V. l-Carnitine Inhibits Lipopolysaccharide-Induced Nitric Oxide Production of SIM-A9 Microglia Cells. ACS Chem Neurosci. 2018 Jan 31. doi: 10.1021/acschemneuro.7b00468. [Epub ahead of print] PubMed PMID: 29370524.

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).

1)

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
3) , 13)

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.
4) , 12)

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.
5)

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.
6)

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.
7)

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.
8)

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.
9)

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.
10)

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.
11)

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.
14)

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.
15)

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.

Update: Painful tic convulsif

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

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

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

Diagnosis

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

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


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

Treatment

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

Case series

2011

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

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

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

2009

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

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

2006

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

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

1984

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

Case reports

2017

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

2014

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

2013

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

2012

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


Painful tic convulsif caused by an arteriovenous malformation 15).

2011

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

2009

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

2007

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


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

2004

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

2002

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

2001

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

1995

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


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


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

1992

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

1991

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


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

1989

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

1984

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

1983

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

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Jiao W, Zhong J, Sun H, Zhu J, Zhou QM, Yang XS, Li ST. Microvascular decompression for the patient with painful tic convulsif after Bell palsy. J Craniofac Surg. 2013 May;24(3):e286-9. doi: 10.1097/SCS.0b013e31828f2b39. PubMed PMID: 23714994.
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Verghese J, Mahore A, Goel A. Arachnoid cyst associated with painful tic convulsif. J Clin Neurosci. 2012 May;19(5):763-4. doi: 10.1016/j.jocn.2011.07.039. Epub 2012 Feb 8. PubMed PMID: 22321360.
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Update: Mesial temporal lobe epilepsy

Temporal lobe epilepsy (TLE) is a chronic neurological condition characterized by recurrent seizures (epilepsy) which originate in the temporal lobe of the brain. The seizures involve sensory changes, for example smelling an unusual odour that is not there, and disturbance of memory.

Mesial temporal lobe epilepsy with hippocampal sclerosis (mTLE-HS) is the most common type of focal epilepsy.

Etiology

The most common cause is mesial temporal sclerosis.

Water homeostasis has been shown crucial for regulation of neuronal excitability. The control of water movement is achieved through a family of small integral membrane channel proteins called aquaporins (AQPs). Despite the fact that changes in water homeostasis occur in sclerotic hippocampi of people with temporal lobe epilepsy (TLE) , the expression of AQPs in the epileptic brain is not fully characterised 1).

Soluble human epoxide hydrolase 2 is increased in both lateral and medial temporal tissues in temporal lobe epilepsy. Further studies should be conducted as inhibition of this enzyme has resulted in a significant decrease in or stopping of seizures and attenuated neuro-inflammation in experimental epilepsy models in the current literature 2).

Pathophysiology

In order to understand the pathophysiology of temporal lobe epilepsy (TLE), and thus to develop new pharmacological treatments, in vivo animal models that present features similar to those seen in TLE patients have been developed during the last four decades. Some of these models are based on the systemic administration of chemoconvulsants to induce an initial precipitating injury (status epilepticus) that is followed by the appearance of recurrent seizures originating from limbic structures.

Kainic acid and pilocarpine models, have been widely employed in basic epilepsy research. Their behavioral, electroencephalographic and neuropathologic features and response of these models to antiepileptic drugs and the impact they might have in developing new treatments are explained in the work of Lévesque et al. 3).


The transition to the ictal stage is accompanied by increasing global synchronization and a more ordered spectral content of the signals, indicated by lower spectral entropy. The interictal connectivity imbalance (lower ipsilateral connectivity) is sustained during the seizure, irrespective of any appreciable imbalance in the spectral entropy of the mesial recordings 4).

Diagnosis

Fractional anisotropy asymmetry (FAA) values can be potentially used to identify the seizures of origin of TLE and to help understand the relationship between fiber tracts with the side of seizure origin of TLE 5).

The area of predominant perifocal 18F positron emission tomography hypometabolism and reduced [11C]flumazenil (11C-FMZ) -binding on PETscans is currently considered to contain the epileptogenic zone and corresponds anatomically to the area localizing epileptogenicity in patients with temporal lobe epilepsy (TLE).

Complicactions

Drug resistant epilepsy is a major clinical challenge affecting about 30% of temporal lobe epilepsy (TLE) patients.

The reasons for failure of surgical treatment for mesial temporal lobe epilepsy (MTLE) associated with hippocampal sclerosis (HS) remain unclear.

Treatment

Surgery

see Temporal lobe epilepsy surgery.

Surgical resection is the gold standard treatment for drug-resistant focal epilepsy, including mesial temporal lobe epilepsy (MTLE) and other focal cortical lesions with correlated electrophysiological features.

Surgical approaches for medically refractory mesial temporal lobe epilepsy (MTLE) that previously have been reported include anterior temporal lobectomy (ATL), transcortical selective amygdalohippocampectomy, transsylvian amygdalohippocampectomy, and subtemporal amygdalohippocampectomy.

Each approach has its advantages and potential pitfalls.

Anterior temporal lobectomy

Outcome

The extent of pre-surgical perifocal PET abnormalities, the extent of their resection, and the extent of non-resected abnormalities were not useful predictors of individual freedom from seizures in patients with TLE 6).

Case series

2017

Seizure, cognitive, and psychiatric outcomes were reviewed after 389 surgeries performed between 1990 and 2015 on patients aged 15-67 years at a tertiary center. Three surgical approaches were used: anterior temporal lobectomy (ATL; n = 209), transcortical selective amygdalohippocampectomy (SAH; n = 144), and transsylvian SAH (n = 36).

With an average follow-up of 8.7 years (range = 1.0-25.2), seizure outcome was classified as Engel I in 83.7% and Engel Ia in 57.1% of patients. The histological classification of HS was type 1 for 75.3% of patients, type 2 for 18.7%, and type 3 for 1.2%. Two factors were significantly associated with seizure recurrence: past history of status epilepticus and preoperative intracranial electroencephalographic recording. In contrast, neither HS type, the presence of a dual pathology, nor surgical approach was associated with seizure outcome. Risk of cognitive impairment was 3.12 (95% confidence interval = 1.27-7.70), greater in patients after ATL than in patients after transcortical SAH. A presurgical psychiatric history and postoperative cognitive impairment were associated with poor psychiatric outcome.

The SAH and ATL approaches have similar beneficial effects on seizure control, whereas transcortical SAH tends to minimize cognitive deterioration after surgery. Variation in postsurgical outcome with the class of HS should be investigated further 7).

2016

A certain number of patients suffer significant decline in verbal memory after hippocampectomy. To prevent this disabling complication, a reliable test for predicting postoperative memory decline is greatly desired. Therefore, Tani et al., assessed the value of electrical stimulation of the parahippocampal gyrus (PHG) as a provocation test of verbal memory decline after hippocampectomy on the dominant side.

Eleven right-handed, Japanese-speaking patients with medically intractable left temporal lobe epilepsy (TLE) participated in the study. Before surgery, they underwent provocative testing via electrical stimulation of the left PHG during a verbal encoding task. Their pre- and posthippocampectomy memory function was evaluated according to the Wechsler Memory Scale-Revised (WMS-R) and/or Mini-Mental State Examination (MMSE) before and 6 months after surgery. The relationship between postsurgical memory decline and results of the provocative test was evaluated.

Left hippocampectomy was performed in 7 of the 11 patients. In 3 patients with a positive provocative recognition test, verbal memory function, as assessed by the WMS-R, decreased after hippocampectomy, whereas in 4 patients with a negative provocative recognition test, verbal memory function, as assessed by the WMS-R or MMSE, was preserved.

Results of the present study suggest that electrical stimulation of the PHG is a reliable provocative test to predict posthippocampectomy verbal memory decline 8).

2001

Eighty patients with temporal lobe epilepsy were randomly assigned to surgery (40 patients) or treatment with antiepileptic drugs for one year (40 patients). Optimal medical therapy and primary outcomes were assessed by epileptologists who were unaware of the patients’ treatment assignments. The primary outcome was freedom from seizures that impair awareness of self and surroundings. Secondary outcomes were the frequency and severity of seizures, the quality of life, disability, and death.

At one year, the cumulative proportion of patients who were free of seizures impairing awareness was 58 percent in the surgical group and 8 percent in the medical group (P<0.001). The patients in the surgical group had fewer seizures impairing awareness and a significantly better quality of life (P<0.001 for both comparisons) than the patients in the medical group. Four patients (10 percent) had adverse effects of surgery. One patient in the medical group died.

In temporal-lobe epilepsy, surgery is superior to prolonged medical therapy. Randomized trials of surgery for epilepsy are feasible and appear to yield precise estimates of treatment effects 9).

1)

Salman MM, Sheilabi MA, Bhattacharyya D, Kitchen P, Conner AC, Bill RM, Woodroofe MN, Conner MT, Princivalle AP. Transcriptome analysis suggests a role for the differential expression of cerebral aquaporins and the MAPK signalling pathway in human temporal lobe epilepsy. Eur J Neurosci. 2017 Jul 17. doi: 10.1111/ejn.13652. [Epub ahead of print] PubMed PMID: 28715131.
2)

Ahmedov ML, Kemerdere R, Baran O, Inal BB, Gumus A, Coskun C, Yeni SN, Eren B, Uzan M, Tanriverdi T. Tissue Expressions of Soluble Human Epoxide Hydrolase-2 Enzyme in Patients with Temporal Lobe Epilepsy. World Neurosurg. 2017 Jun 29. pii: S1878-8750(17)31032-X. doi: 10.1016/j.wneu.2017.06.137. [Epub ahead of print] PubMed PMID: 28669871.
3)

Lévesque M, Avoli M, Bernard C. Animal Models of temporal Lobe Epilepsy Following Systemic Chemoconvulsant Administration. J Neurosci Methods. 2015 Mar 10. pii: S0165-0270(15)00091-6. doi: 10.1016/j.jneumeth.2015.03.009. [Epub ahead of print] PubMed PMID: 25769270.
4)

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