Category Archives: Functional Neurosurgery

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).

References

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Hari A, Praharaj SS, Satish S, Ganesh V. Rare case of cerebello-pontine angle meningioma causing painful tic convulsif. Clin Neurol Neurosurg. 2014 Sep;124:135-7. doi: 10.1016/j.clineuro.2014.06.036. Epub 2014 Jul 8. PubMed PMID: 25048517.
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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)

Vega-Zelaya L, Pastor J, de Sola RG, Ortega GJ. Disrupted Ipsilateral Network Connectivity in Temporal Lobe Epilepsy. PLoS One. 2015 Oct 21;10(10):e0140859. doi: 10.1371/journal.pone.0140859. eCollection 2015. PubMed PMID: 26489091.
5)

Li H, Xue Z, Dulay MF Jr, Verma A, Karmonik C, Grossman RG, Wong ST. Fractional anisotropy asymmetry and the side of seizure origin for partial onset-temporal lobe epilepsy. Comput Med Imaging Graph. 2014 Jul 2. pii: S0895-6111(14)00102-5. doi: 10.1016/j.compmedimag.2014.06.009. [Epub ahead of print] PubMed PMID: 25037096.
6)

Stanišić M, Coello C, Ivanović J, Egge A, Danfors T, Hald J, Heminghyt E, Mikkelsen MM, Krossnes BK, Pripp AH, Larsson PG. Seizure outcomes in relation to the extent of resection of the perifocal fluorodeoxyglucose and flumazenil PET abnormalities in anteromedial temporal lobectomy. Acta Neurochir (Wien). 2015 Sep 8. [Epub ahead of print] PubMed PMID: 26350516.
7)

Mathon B, Bielle F, Samson S, Plaisant O, Dupont S, Bertrand A, Miles R, Nguyen-Michel VH, Lambrecq V, Calderon-Garcidueñas AL, Duyckaerts C, Carpentier A, Baulac M, Cornu P, Adam C, Clemenceau S, Navarro V. Predictive factors of long-term outcomes of surgery for mesial temporal lobe epilepsy associated with hippocampal sclerosis. Epilepsia. 2017 Jun 28. doi: 10.1111/epi.13831. [Epub ahead of print] PubMed PMID: 28656696.
8)

Tani N, Kishima H, Khoo HM, Yanagisawa T, Oshino S, Maruo T, Hosomi K, Hirata M, Kazui H, Nomura KT, Aly MM, Kato A, Yoshimine T. Electrical stimulation of the parahippocampal gyrus for prediction of posthippocampectomy verbal memory decline. J Neurosurg. 2016 Nov;125(5):1053-1060. PubMed PMID: 26771851.
9)

Wiebe S, Blume WT, Girvin JP, Eliasziw M; Effectiveness and Efficiency of Surgery for Temporal Lobe Epilepsy Study Group. A randomized, controlled trial of surgery for temporal-lobe epilepsy. N Engl J Med. 2001 Aug 2;345(5):311-8. PubMed PMID: 11484687.

Update: Microvascular decompression for trigeminal neuralgia

Microvascular decompression (MVD) via lateral suboccipital approach is the standard surgical intervention for trigeminal neuralgia (TN).

Outcome

It has proven to be the most successful and durable surgical approach for trigeminal neuralgia (TN).

However, not all patients with TN manifest unequivocal neurovascular compression (NVC). Furthermore, over time patients with an initially successful MVD manifest a relentless rate of TN recurrence.

It does not achieve 100 % cure rate. Re-exploration of the posterior fossa may carry increased risk over first-time MVD and is not always successful, so other treatments are needed.

Case series

2017

Clinical characteristics, intraoperative findings, and postoperative curative effects were analyzed in 72 patients with trigeminal neuralgia who were treated by microvascular decompression. The patients were divided into arterial and venous compression groups based on intraoperative findings. Surgical curative effects included immediate relief, delayed relief, obvious reduction, and invalid result. Among the 40 patients in the arterial compression group, 32 had immediate pain relief of pain (80.0%), 5 cases had delayed relief (12.5%), and 3 cases had an obvious reduction (7.5%). In the venous compression group, 12 patients had immediate relief of pain (37.5%), 13 cases had delayed relief (40.6%), and 7 cases had an obvious reduction (21.9%). During 2-year follow-up period, 6 patients in the arterial compression group experienced recurrence of trigeminal neuralgia, but there were no recurrences in the venous compression group. Simple artery compression was followed by early relief of trigeminal neuralgia more often than simple venous compression. However, the trigeminal neuralgia recurrence rate was higher in the artery compression group than in the venous compression group 1).

2016

Indocyanine green videoangiography was performed in 17 TN patients undergoing microvascular decompression.

von Eckardstein et al., focused on whether ICG angiography is helpful in determining the site of conflict, particularly when not directly visible via the microscope, and whether fluorescence is strong enough to shine through the nerve obliterating the direct view of the compressing vessel.

In four patients, the site of conflict was immediately apparent after opening the cerebellopontine cistern, and ICG angiography did not provide the neurosurgeon with additional information. In another two patients, imaging quality and fluorescence were too poor. Of the remaining 11 patients with a hidden site of nerve-vessel conflict, ICG angiography was found to be helpful in anticipating the site of compression and the course of the artery in 7 patients, particularly in regard to the so-called shining-through effect through fiber bundles of the thinned nerve. Of all the patients, 88% reported at least improvement or cessation of their symptoms, including all of the patients with a shine-through effect.

ICG angiography could be a helpful adjunct in decompressing the trigeminal nerve and can guide the surgeon to the nerve-vessel conflict. Intensity of the fluorescence is powerful enough to shine through thinned and splayed trigeminal nerve fiber bundles 2).


A retrospective review of patient records from 1998 to 2015 identified a total of 942 patients with TN and 500 patients who underwent MVD. After excluding several cases, 306 patients underwent MVD as their first surgical intervention and 175 patients underwent subsequent MVD. Demographics and clinicopathological data and outcomes were obtained for analysis.

In patients who underwent subsequent MVD, surgical intervention was performed at an older age (55.22 vs 49.98 years old, p < 0.0001) and the duration of symptoms was greater (7.22 vs 4.45 years, p < 0.0001) than for patients in whom MVD was their first surgical intervention. Patients who underwent initial MVD had improved pain relief and no improvement in pain rates compared with those who had subsequent MVD (95.8% and 4.2% vs 90.3% and 9.7%, respectively, p = 0.0041). Patients who underwent initial MVD had significantly lower rates of facial numbness in the pre- and postoperative periods compared with patients who underwent subsequent MVD (p < 0.0001). The number of complications in both groups was similar (p = 0.4572).

The results demonstrate that patients who underwent other procedures prior to MVD had less pain relief and a higher incidence of facial numbness despite rates of complications similar to patients who underwent MVD as their first surgical intervention 3).

2015

A retrospective analysis of clinical data was performed in 99 patients who underwent MVD from May 2012 to June 2015. The outcome data from 27 MVD operations for 27 patients aged 70-80 years (mean 74.6 years) were compared with 72 MVD operations with 72 patients aged 25-69 years (mean 55.7 years). Preoperative comorbidities were recorded and postoperative worsening comorbidities and non-neurological complications were evaluated at discharge. Efficacy of the surgery and neurological complications were evaluated in July 2015.

No decrease in activity of daily living was found in any patient. Complete pain relief without medication was achieved in 77.8% and partial pain relief in 14.8% in the elderly group, and 83.3% and 9.7%, respectively, in the non-elderly group (p=0.750). Permanent neurological complication was not observed in the elderly group, whereas Vth nerve and VIIIth nerve complications were observed in the non-elderly group. Rates of preoperative multiple comorbidities and of cardiovascular comorbidity were significantly higher in the elderly group (p<0.01). Worsening comorbidity and new pathology at discharge were mainly hypertension in both groups, but glaucoma attack and asthma attack were observed in the elderly group. All pathologies were successfully managed.

MVD for elderly patients with TN can be achieved safely with careful perioperative management. Information of comorbidity should be shared with all staff involved in the treatment, who should work as a team to avoid worsening comorbidity. The possibility of unpredictable events in the elderly patients should always be considered 4).


Since 2004, there were a total of 51 patients with TIC and 12 with HS with available MRI scans. All patients underwent preoperative MRI to rule out non-surgical etiologies for facial pain and facial spasm, and confirm vascular compression. Follow-up after surgery was 13±22 months for the patients with TIC and 33±27 months for the patients with HS.

There were 45 responders to MVD in the TIC cohort (88%), with a Visual analog scale (VAS) of 1±3. All patients with HS responded to MVD between 25 and 100%, with a mean of 75±22%. Wound complications occurred in 10% of patients with MVD for TIC, and 1 patient reported hearing loss after MVD for HS, documented by audiogram. The congruence rate between the preoperative MRI and operative findings of vascular compression was 84% in TIC and 75% in HS.

MVD is an effective and safe modality of treatment for TIC and HS. In addition to ruling out structural lesions, MRI can offer additional information by highlighting vascular loops associated with compressions. On conventional scans as obtained here, the resolution of MRI was congruent with operative findings in 84% in TIC and 75% in HS. This review emphasizes that the decision to undertake MVD in TIC or HS should be based on clinical diagnosis and not visualization of a compressing vessel by MRI. Conversely, the presence of a compressing vessel by MRI demands perseverance by the surgeon until the nerve is decompressed 5).


The trigeminal nerve was sectioned into 5 zones. Zone 1, 2, 3, 4 was located at the rostral, caudal, ventral, and dorsal part of the nerve root entry zone (REZ) respectively, and zone 5 was located at the distal of the nerve root. This study contained 86 patients with trigeminal neuralgia underwent microvascular decompression. Every zone was exposed through preoperative imaging. During the operation, offending vessels were explored from zone 1 to zone 5, and different decompression techniques were used for different types of vessels.

Through zone exploration, the sensitivity of preoperative imaging was 96.5% and specificity was 100%. Location of the neurovascular conflict was in the zone 1 in 53.5% of the patients, zone 2 in 32.6%, zone 3 in 45.3%, zone 4 in 29.1%, and zone 5 in 34.9%. In total, 2 zones were both involved in 59.3%, and 3 zones were involved in 18.6%. All offending arteries were moved away and interposed with Teflon sponge. Offending veins of 11 patients were too small to interpose, and coagulated and cut was adopted. The other offending veins were interposed with wet gelatin and Teflon sponge, respectively 6).

2014

Lee et al. performed a retrospective review of cases of TN Type 1 (TN1) or Type 2 (TN2) involving patients 18 years or older who underwent evaluation (and surgery when indicated) at Oregon Health & Science University between July 2006 and February 2013. Surgical and imaging findings were correlated.

The review identified a total of 257 patients with TN (219 with TN1 and 38 with TN2) who underwent high-resolution MRI and MR angiography with 3D reconstruction of combined images using OsiriX. Imaging data revealed that the occurrence of TN1 and TN2 without NVC was 28.8% and 18.4%, respectively. A subgroup of 184 patients underwent surgical exploration. Imaging findings were highly correlated with surgical findings, with a sensitivity of 96% for TN1 and TN2 and a specificity of 90% for TN1 and 66% for TN2. Conclusions Magnetic resonance imaging detects NVC with a high degree of sensitivity. However, despite a diagnosis of TN1 or TN2, a significant number of patients have no NVC. Trigeminal neuralgia clearly occurs and recurs in the absence of NVC 7).

2002

A study comprises 42 cases of trigeminal neuralgia that underwent operation with endoscopic-assisted microvascular decompression between October 1992 and October 1998. This study was performed in the Ear, Nose, and Throat Department, Nord Hospital, in Marseille, France. The decompression was performed by means of a minimally invasive retrosigmoid approach without a cerebellar retractor. The cerebellopontine angle was then explored by a 30-degree endoscope that gives a panoramic view of this space, with clear visualization of the trigeminal nerve from the pons to Meckel’s cave, allowing for the identification of the precise location of the site of the conflict. Microvascular decompression was performed under the microscope by separating the offending vessel from the trigeminal nerve; separation was maintained by the insertion of a piece of Teflon.

The site of conflict was detected at the root entry zone of the nerve in 35 patients (83.3%) and at Meckel’s cave in 7 patients (16.7%). In 32 cases (76.2%), the type of contact between the vessel and the nerve was of the simple type (1 vessel coming in contact with the nerve in a single point); in 6 cases (14.3%), it was a multiple type (2 vessels touching the nerve in the same point); and in 4 cases (9.5%), it was a nutcracker type (2 vessels compressing the nerve between them). After at least 1-year follow-up and a single operation (cases that required a second operation for revision were considered failures), a successful result was obtained in 31 cases (73.8%), and an improvement was obtained in 4 cases (9.5%). The operation was a failure or early recurrence occurred in 7 cases (16.7%). Postoperative complications were rare. A cerebrospinal fluid leak occurred in only 1 case (2.4%) and was subsequently treated with lumbar puncture and a compressive bandage.

The minimally invasive retrosigmoid endoscopic-assisted microvascular decompression is an acceptable treatment of primary trigeminal neuralgia. Endoscopy provides a unique way to explore the cerebellopontine angle and to identify the exact location of the neurovascular conflict 8).


1) Shi L, Gu X, Sun G, Guo J, Lin X, Zhang S, Qian C. After microvascular decompression to treat trigeminal neuralgia, both immediate pain relief and recurrence rates are higher in patients with arterial compression than with venous compression. Oncotarget. 2017 Jan 20. doi: 10.18632/oncotarget.14765. [Epub ahead of print] PubMed PMID: 28122347.
2) von Eckardstein KL, Mielke D, Akhavan-Sigari R, Rohde V. Enlightening the Cerebellopontine Angle: Intraoperative Indocyanine Green Angiography in Microvascular Decompression for Trigeminal Neuralgia. J Neurol Surg A Cent Eur Neurosurg. 2016 Sep 23. PubMed PMID: 27704490.
3) Theodros D, Rory Goodwin C, Bender MT, Zhou X, Garzon-Muvdi T, De la Garza-Ramos R, Abu-Bonsrah N, Mathios D, Blitz AM, Olivi A, Carson B, Bettegowda C, Lim M. Efficacy of primary microvascular decompression versus subsequent microvascular decompression for trigeminal neuralgia. J Neurosurg. 2016 Jul 15:1-7. [Epub ahead of print] PubMed PMID: 27419826.
4) Amagasaki K, Watanabe S, Naemura K, Shono N, Nakaguchi H. Safety of microvascular decompression for elderly patients with trigeminal neuralgia. Clin Neurol Neurosurg. 2015 Dec 31;141:77-81. doi: 10.1016/j.clineuro.2015.12.019. [Epub ahead of print] PubMed PMID: 26765772.
5) Hitchon PW, Zanaty M, Moritani T, Uc E, Pieper CL, He W, Noeller J. Microvascular decompression and MRI findings in trigeminal neuralgia and hemifacial spasm. A single center experience. Clin Neurol Neurosurg. 2015 Oct 22;139:216-220. doi: 10.1016/j.clineuro.2015.10.012. [Epub ahead of print] PubMed PMID: 26519891.
6) Feng BH, Zheng XS, Liu M, Wang XQ, Wang XH, Ying TT, Li ST. Microvascular Decompression for Trigeminal Neuralgia: Zone Exploration and Decompression Techniques. J Craniofac Surg. 2015 Oct 21. [Epub ahead of print] PubMed PMID: 26501973.
7) Lee A, McCartney S, Burbidge C, Raslan AM, Burchiel KJ. Trigeminal neuralgia occurs and recurs in the absence of neurovascular compression. J Neurosurg. 2014 May;120(5):1048-54. doi: 10.3171/2014.1.JNS131410. Epub 2014 Feb 7. PubMed PMID: 24506241.
8) El-Garem HF, Badr-El-Dine M, Talaat AM, Magnan J. Endoscopy as a tool in minimally invasive trigeminal neuralgia surgery. Otol Neurotol. 2002 Mar;23(2):132-5. PubMed PMID: 11875338.

Update: Stereoelectroencephalography complications

In a systematic review of stereoelectroencephalography complications, thirty-five major complications (including 4 fatalities) were reported among 4,000 patients (0.8%) implanted with 33,000 electrodes 1).

SEEG has low associated complications, particularly regarding hemorrhage and infection 2).


Serletis et al., published wound infection (0.08%), hemorrhagic complications (0.08%), and a transient neurological deficit (0.04%) in a total of 5 patients (2.5%). One patient (0.5%) ultimately died due to intracerebral hematoma directly ensuing from SEEG electrode placement 3).


In the Cardinale et al., published series the major complication rate was 12 of 500 (2.4%), including 1 death for indirect morbidity. Median entry point localization error was 1.43 mm (interquartile range, 0.91-2.21 mm) with the traditional workflow and 0.78 mm (interquartile range, 0.49-1.08 mm) with the new one (P < 2.2 × 10). Median target point localization errors were 2.69 mm (interquartile range, 1.89-3.67 mm) and 1.77 mm (interquartile range, 1.25-2.51 mm; P < 2.2 × 10), respectively. 4).


Guénot et al had no general or neurologic complication occurred during the procedures. Two transient postprocedure side effects, consisting of paresthetic sensations in the mouth and mild apraxia of the hand, were observed 5).


In 10 patients that underwent this procedure, there were no derived complications 6).


The total complication rate was 4% in One hundred patients that underwent 101 robot-assisted SEEG procedures 7).


In the series of De Almeida et al., bilateral exploration of the temporal lobes has a morbidity rate of approximately 1%. A higher risk of hematomas occurs with the implantation of four or more electrodes in the frontal lobes 8).


1) Cardinale F, Casaceli G, Raneri F, Miller J, Lo Russo G. Implantation of Stereoelectroencephalography Electrodes: A Systematic Review. J Clin Neurophysiol. 2016 Dec;33(6):490-502. PubMed PMID: 27918344.
2) Yang M, Ma Y, Li W, Shi X, Hou Z, An N, Zhang C, Liu L, Yang H, Zhang D, Liu S. A Retrospective Analysis of Stereoelectroencephalography and Subdural Electroencephalography for Preoperative Evaluation of Intractable Epilepsy. Stereotact Funct Neurosurg. 2017 Jan 14;95(1):13-20. doi: 10.1159/000453275. [Epub ahead of print] PubMed PMID: 28088805.
3) Serletis D, Bulacio J, Bingaman W, Najm I, González-Martínez J. The stereotactic approach for mapping epileptic networks: a prospective study of 200 patients. J Neurosurg. 2014 Nov;121(5):1239-46. doi: 10.3171/2014.7.JNS132306. PubMed PMID: 25148007.
4) Cardinale F, Cossu M, Castana L, Casaceli G, Schiariti MP, Miserocchi A, Fuschillo D, Moscato A, Caborni C, Arnulfo G, Lo Russo G. Stereoelectroencephalography: surgical methodology, safety, and stereotactic application accuracy in 500 procedures. Neurosurgery. 2013 Mar;72(3):353-66; discussion 366. doi: 10.1227/NEU.0b013e31827d1161. PubMed PMID: 23168681.
5) Guénot M, Isnard J, Ryvlin P, Fischer C, Mauguière F, Sindou M. SEEG-guided RF thermocoagulation of epileptic foci: feasibility, safety, and preliminary results. Epilepsia. 2004 Nov;45(11):1368-74. PubMed PMID: 15509237.
6) Narváez-Martínez Y, García S, Roldán P, Torales J, Rumià J. [Stereoelectroencephalography by using O-Arm(®) and Vertek(®) passive articulated arm: Technical note and experience of an epilepsy referral centre]. Neurocirugia (Astur). 2016 Nov – Dec;27(6):277-284. doi: 10.1016/j.neucir.2016.05.002. Spanish. PubMed PMID: 27345416.
7) González-Martínez J, Bulacio J, Thompson S, Gale J, Smithason S, Najm I, Bingaman W. Technique, Results, and Complications Related to Robot-Assisted Stereoelectroencephalography. Neurosurgery. 2016 Feb;78(2):169-80. doi: 10.1227/NEU.0000000000001034. PubMed PMID: 26418870.
8) De Almeida AN, Olivier A, Quesney F, Dubeau F, Savard G, Andermann F. Efficacy of and morbidity associated with stereoelectroencephalography using computerized tomography–or magnetic resonance imaging-guided electrode implantation. J Neurosurg. 2006 Apr;104(4):483-7. PubMed PMID: 16619650.

Levetiracetam for hemifacial spasm

Levetiracetam proved its effectiveness and safety in the treatment of a case of HFS.Nevertheless, there is a need for further controlled studies with larger samples 1).


Kuroda et al., experienced two elderly hemifacial spasm (HFS) patients who exhibited a marked response to levetiracetam (LEV) without side effects. Although the exact underlying pharmacological mechanism remains unknown, we assume anti-kindling effect as one of the important pharmacological mechanism underlying the effect of LEV against HFS. Moreover, LEV is considered to be suitable for use in elderly patients because of its good tolerability. In addition, the lack of hepatic induction or inhibition makes it an easy and safe drug when used in addition to other anticonvulsants. Although the long-term benefit remains unknown, LEV may represent an alternative treatment for elderly HFS patients who are unable to undergo or decline surgical intervention and/or botulinum toxin injections or are intolerant to other anticonvulsants 2).


1) Biagio Carrieri P, Petracca M, Montella S. Efficacy of levetiracetam in hemifacial spasm: a case report. Clin Neuropharmacol. 2008 May-Jun;31(3):187-8. doi: 10.1097/WNF.0b013e3180ed44c8. PubMed PMID: 18520988.
2) Kuroda T, Saito Y, Fujita K, Yano S, Ishigaki S, Kato H, Murakami H, Ono K. Efficacy of levetiracetam in primary hemifacial spasm. J Clin Neurosci. 2016 Dec;34:213-215. doi: 10.1016/j.jocn.2016.05.025. PubMed PMID: 27460515.

Update: Foramen ovale

Oval opening in the greater wing of sphenoid bone transmitting the mandibular nerve as its major content. It serves as an important landmark for neurosurgeons in certain procedures as to gain access to trigeminal nerve. Therefore, its topographic position in relation to adjacent bony landmarks provides useful tool during these procedures.

Morphometric analysis was carried out on 104 foramina ovalia of 52 dry human skulls from South India. Following dimensions of foramen ovale were measured: antero-posterior length, transverse width, distance (d(1)) from tubercle of root of zygoma to the centre of the foramen (CF) and distance (d(2)) from the midline of the base of the skull to CF. Results: The mean antero-posterior length was 7.0±2.17mm on right side and 6.8±1.40mm on left side, mean transverse width was 5.0±0.42mm and 4.70±0.91mm on right and left side respectively. Mean d(1) was 32.58±1.72mm on right side and 32.75±1.76mm on left side. Mean d(2) was 25.83±1.26mm on right side and 25.08±1.31mm on left side. Conclusion: Regional variations in the morphometric measures may be useful in neurosurgical procedures like administration of anaesthesia involving the mandibular nerve 1).


Cannulation procedures, including those utilizing neuronavigational technology, are occasionally complicated by anatomical variation of the FO, sometimes resulting in miscannulation and subsequent adverse events. The FO, while commonly thought of as oval-shaped, has also been described as “almond,” “banana,” “D shape,” “pear,” and “triangular.” Because of the importance of the FO in neurosurgical procedures and the misunderstanding of FO shape, the aim of a study is to objectively describe the shape of the FO and its most likely shape variation. A total of 211 FO were evaluated by geometric morphometric analysis. A consensus shape is presented for the FO. No significant difference was found between the shapes of left- and right-sided FO. The most likely shape variation of the FO occurs as an inverse relationship between the anteromedial-posterolateral and anterolateral-posteromedial aspects of the foramen. The capacity to visualize the average FO shape and understand the most likely shape variance, as illustrated by Zdilla et al., will aid neurosurgeons in their approach to procedures requiring cannulation of the FO 2).


1) Patil J, Kumar N, K G MR, Ravindra S S, S N S, Nayak B S, Marpalli S, L S A. The foramen ovale morphometry of sphenoid bone in South Indian population. J Clin Diagn Res. 2013 Dec;7(12):2668-70. doi: 10.7860/JCDR/2013/7548.3727. Epub 2013 Dec 15. PubMed PMID: 24551606.
2) Zdilla MJ, Fijalkowski KM. The Shape of the Foramen Ovale: A Visualization Aid for Cannulation Procedures. J Craniofac Surg. 2016 Dec 23. doi: 10.1097/SCS.0000000000003325. [Epub ahead of print] PubMed PMID: 28027173.