Anterior temporal lobectomy complications

Anterior temporal lobectomy complications

Even though the mortality after Anterior temporal lobectomy (ATL) is minimal, the overall morbidity cannot be ignored. Psychiatric disturbances, visual field defects, and cognitive disorders are the most common postoperative complications, and should be considered during the preoperative planning and consultation 1).

Visual field defects

ATL is often complicated by quadrantanopia. In some cases this can be severe enough to prohibit driving, even if a patient is free of seizures. These deficits are caused by damage to Meyers loop of the optic radiation, which shows considerable heterogeneity in its anterior extent. This structure cannot be distinguished using clinical magnetic resonance imaging sequences.

Optic radiation tractography by DTI could be a useful method to assess an individual patient’s risk of postoperative visual deficit 2)3).

van Lanen et al., developed a score method for the assessment of postoperative visual field defects after temporal lobe epilepsy surgery and assessed its feasibility for clinical use. A significant correlation between VFD and resection size for right-sided ATL was confirmed 4).

Cranial nerve (CN) deficits following anterior temporal lobectomy (ATL) are an uncommon but well-recognized complication. The usual CNs implicated in post-ATL complications include the oculomotor nervetrochlear nerve, and facial nerves.

Injury to the trigeminal nerve leading to neuropathic pain are described in 2 cases following temporal lobe resections for pharmacoresistant epilepsy. The possible pathophysiological mechanisms are discussed and the microsurgical anatomy of surgically relevant structures is reviewed. 5).

Case reports

Dickerson et al., from the Department of Neurosurgery, University of Mississippi Medical Center, JacksonUSA report the third known case and first of diffuse vasospasm. A 48-year-old woman underwent a transcortical anterior left temporal lobectomy. Eleven days later, she had new-onset expressive aphasia with narrowing of the anterior, middle, and posterior cerebral arteries, and increased velocities via transcranial Doppler. She was treated with fluids, nimodipine, and permissive hypertension. At 6 months, her speech was near baseline. Cerebral vasospasm may represent a rare cause of morbidity after anterior temporal lobectomy; a literature review on the subject is presented 6).

References

1)

Brotis AG, Giannis T, Kapsalaki E, Dardiotis E, Fountas KN. Complications after Anterior Temporal Lobectomy for Medically Intractable Epilepsy: A Systematic Review and Meta-Analysis. Stereotact Funct Neurosurg. 2019 Jul 9:1-14. doi: 10.1159/000500136. [Epub ahead of print] Review. PubMed PMID: 31288240.
2)

Borius PY, Roux FE, Valton L, Sol JC, Lotterie JA, Berry I. Can DTI fiber tracking of the optic radiations predict visual deficit after surgery? Clin Neurol Neurosurg. 2014 Jul;122:87-91. doi: 10.1016/j.clineuro.2014.04.017. Epub 2014 May 5. PubMed PMID: 24908224.
3)

James JS, Radhakrishnan A, Thomas B, Madhusoodanan M, Kesavadas C, Abraham M, Menon R, Rathore C, Vilanilam G. Diffusion tensor imaging tractography of Meyer’s loop in planning resective surgery for drug-resistant temporal lobe epilepsy. Epilepsy Res. 2015 Feb;110:95-104. doi: 10.1016/j.eplepsyres.2014.11.020. Epub 2014 Nov 27. PubMed PMID: 25616461.
4)

van Lanen RHGJ, Hoeberigs MC, Bauer NJC, Haeren RHL, Hoogland G, Colon A, Piersma C, Dings JTA, Schijns OEMG. Visual field deficits after epilepsy surgery: a new quantitative scoring method. Acta Neurochir (Wien). 2018 Jul;160(7):1325-1336. doi: 10.1007/s00701-018-3525-9. Epub 2018 Apr 5. PubMed PMID: 29623432; PubMed Central PMCID: PMC5995984.
5)

Gill I, Parrent AG, Steven DA. Trigeminal neuropathic pain as a complication of anterior temporal lobectomy: report of 2 cases. J Neurosurg. 2016 Apr;124(4):962-5. doi: 10.3171/2015.5.JNS15123. Epub 2015 Oct 30. PubMed PMID: 26517768.
6)

Dickerson JC, Hidalgo JA, Smalley ZS, Shiflett JM. Diffuse vasospasm after transcortical temporal lobectomy for intractable epilepsy. Acta Neurochir (Wien). 2018 Jul 10. doi: 10.1007/s00701-018-3606-9. [Epub ahead of print] PubMed PMID: 29987392.

Intraoperative neurophysiological monitoring for anterior cervical discectomy and fusion

Intraoperative neurophysiological monitoring for anterior cervical discectomy and fusion

Although Intraoperative neurophysiological monitoring has been shown to decrease the risk of neurological injury in deformity surgery, its utility in anterior cervical spine surgery (ACSS) remains controversial 1) 2) 3) 4) 5) 6)7) 8).

Proponents of intraoperative neurophysiological monitoring for ACSS claim that it improves patient safety and functional outcome whereas opponents refute this claim by citing increased cost and the lack of correlation between intraoperative neurophysiological monitoring abnormalities and postoperative neurological deficits especially with anterior cervical discectomy and fusions (ACDFs) 9) 10) 11) 12).


In a systematic review and meta-analysis from 2017, the risk of neurological injury after ACSS was low although procedures involving a corpectomy may carry a higher risk. For ACDFs, there is no difference in the risk of neurological injury with or without ION use. Unimodal ION has a higher specificity than multimodal ION and may minimize “subclinical” intraoperative alerts in ACSS 13)


A analysis of over 140,000 cases from the National Inpatient Sample data set, found that the use of intraoperative neurophysiological monitoringfor anterior cervical discectomy and fusion was not associated with a reduced rate of neurological complication14).

References

1)

Dawson EG, Sherman JE, Kanim LE, et al. Spinal cord monitoring. Results of the Scoliosis Research Society and the European Spinal Deformity Society survey. Spine. 1991;16:S361–4.
2)

Diab M, Smith AR, Kuklo TR. Neural complications in the surgical treatment of adolescent idiopathic scoliosis. Spine. 2007;32:2759–63.
3)

Eggspuehler A, Sutter MA, Grob D, et al. Multimodal intraoperative monitoring during surgery of spinal deformities in 217 patients. Eur Spine J. 2007;16:S188–96.
4)

Forbes HJ, Allen PW, Waller CS, et al. Spinal cord monitoring in scoliosis surgery. Experience with 1168 cases. J Bone Joint Surg Br. 1991;73:487–91.
5)

Kamerlink JR, Errico T, Xavier S, et al. Major intraoperative neurologic monitoring deficits in consecutive pediatric and adult spinal deformity patients at one institution. Spine. 2010;35:240–5.
6)

Nuwer MR, Emerson RG, Galloway G, et al. Evidence-based guideline update: intraoperative spinal monitoring with somato-sensory and transcranial electrical motor evoked potentials*. J Clin Neurophysiol. 2012;29:101–8.
7)

Resnick DK, Choudhri TF, Dailey AT, et al. Guidelines for the performance of fusion procedures for degenerative disease of the lumbar spine. Part 15: electrophysiological monitoring and lumbar fusion. J Neurosurg Spine. 2005;2:725–32.
8)

Zhuang Q, Wang S, Zhang J, et al. How to make the best use of intraoperative motor evoked potential monitoring? Experience in 1162 consecutive spinal deformity surgical procedures. Spine. 2014;39:E1425–32.
9)

Engler GL, Spielholz NJ, Bernhard WN, et al. Somatosensory evoked potentials during Harrington instrumentation for scoliosis. J Bone Joint Surg Am. 1978;60:528–32.
10)

Epstein NE, Danto J, Nardi D. Evaluation of intraoperative somatosensory-evoked potential monitoring during 100 cervical operations. Spine. 1993;18:737–47.
11)

Taunt CJ, Jr, Sidhu KS, Andrew SA. Somatosensory evoked potential monitoring during anterior cervical discectomy and fusion. Spine. 2005;30:1970–2.
12)

Traynelis VC, Abode-Iyamah KO, Leick KM, et al. Cervical decompression and reconstruction without intraoperative neurophysiological monitoring. J Neurosurg Spine. 2012;16:107–13.
13)

Ajiboye RM, Zoller SD, Sharma A, Mosich GM, Drysch A, Li J, Reza T, Pourtaheri S. Intraoperative Neuromonitoring for Anterior Cervical Spine Surgery: What Is the Evidence? Spine (Phila Pa 1976). 2017 Mar 15;42(6):385-393. doi: 10.1097/BRS.0000000000001767. Review. PubMed PMID: 27390917; PubMed Central PMCID: PMC5552368.
14)

Badhiwala JH, Nassiri F, Witiw CD, Mansouri A, Almenawer SA, da Costa L, Fehlings MG, Wilson JR. Investigating the utility of intraoperative neurophysiological monitoring for anterior cervical discectomy and fusion: analysis of over 140,000 cases from the National (Nationwide) Inpatient Sample data set. J Neurosurg Spine. 2019 Mar 29:1-11. doi: 10.3171/2019.1.SPINE181110. [Epub ahead of print] PubMed PMID: 30925481.

Anterior cingulate cortex functions

Anterior cingulate cortex functions

see also dorsal anterior cingulate cortex.

The anterior cingulate cortex, appears to play a role in a wide variety of autonomic functions, such as regulating blood pressure and heart rate.

It is also involved in rational cognitive functions, such as reward anticipation, decision-makingempathyimpulse control and emotion.


From January to December 2016, eighteen participants with opiate drug addiction during physical detoxification who completed a Drug Rehabilitation Center of Anhui Province, and eighteen healthy controls recruited performed a cue-elicited craving task in a MRI scanner while signal data were collected. Two regions of interest were the right anterior cingulate and the left anterior cingulate, then the linear correlation between the whole brain and the anterior cingulates was calculated to find out the abnormal functional connectivity of the anterior cingulates.

Contrasted experimental group with the healthy controls, the functional connectivity of bilateral fusiform gyruscaudate nucleus, and the anterior cingulates was increased in the opiate drug addicts during physical detoxification group (P<0.05),and the functional connectivity between anterior cingulates and polus temporalis, hippocampi, Middle frontal gyrus of orbit, Supplementary motor area, dorsolateral superior frontal gyrus was decreased (P<0.05).

The anterior cingulates dysfunction of functional connectivity in a cue-elicited craving task may play a important role in the relapse of opiate drug addicts during physical detoxification 1).


Pica is most often reported in the presence of iron deficiency or gastrointestinal disturbance. The mechanism that underlies the behavior is poorly understood. Lesions to the anterior cingulate gyrus (ACG) can present in many ways, with signs and symptoms including motor and sensory changes, autonomic dysfunction, seizures, and behavioral alterations.

To date, no reports of pica, or eating disturbances, have been tied to anterior cingulate cortex lesions. In a article, Rangwala et al., describe the case of an 8-year-old boy presenting with pica consumption of paper who was shown to have a mass in the left ACG. After surgical resection of the lesion, all of the patient’s symptoms resolved and he returned to his normal life 2).


The somatosensory cortex encodes incoming sensory information from receptors all over the body. Affective touch is a type of sensory information that elicits an emotional reaction and is usually social in nature, such as a physical human touch. This type of information actually coded differently than other sensory information. Intensity of affective touch is still encoded in the primary somatosensory cortex, but the feeling of pleasantness associated with affective touch activates the anterior cingulate cortex more than the primary somatosensory cortex. Functional magnetic resonance imaging (fMRI) data shows that increased blood oxygen level contrast (BOLD) signal in the anterior cingulate cortex as well as the prefrontal cortex is highly correlated with pleasantness scores of an affective touch. Inhibitory transcranial magnetic stimulation (TMS) of the primary somatosensory cortex inhibits the perception of affective touch intensity, but not affective touch pleasantness. Therefore, the S1 is not directly involved in processing socially affective touch pleasantness, but still plays a role in discriminating touch location and intensity.


Qiao et al. reported a case of refractory epilepsy characterized by aura of extreme fear and hypermotor seizures, in which the left (dominant hemisphere) anterior cingulate gyrus (ACG) was determined to be the epileptogenic zone (EZ) through multiple modalities of presurgical evaluation including analysis of high frequency oscillation on intracranial EEG. Tailored resection of EZ was thus performed and pathological examination revealed focal cortical dysplasia (FCD) type IIb. The patient has been seizure free during an 18-month follow-up. The report has provided novel anatomical, electrophysiological and surgical evidences suggesting the critical role of ACG in ictal fear and possibility of surgical management of fear-manifesting refractory epilepsy 3).


Impaired wakefulness (IW) in normal pressure hydrocephalus (NPH) is associated with reduced relative regional cerebral blood flow (rrCBF) in the anterior cingulate cortex. Improved wakefulness following surgery corresponds to rrCBF increments in the frontal association cortex 4).

References

1)

Han Y, Sun T, Zheng XL, Jiang ZQ, Lou FY, Zhang SJ. [Task-related functional connectivity of anterior cingulate in opiate drug addicts during physical detoxification: a task fMRI study]. Zhonghua Yi Xue Za Zhi. 2019 Mar 5;99(9):700-703. doi: 10.3760/cma.j.issn.0376-2491.2019.09.013. Chinese. PubMed PMID: 30831621.
2)

Rangwala SD, Tobin MK, Birk DM, Butts JT, Nikas DC, Hahn YS. Pica in a Child with Anterior Cingulate Gyrus Oligodendroglioma: Case Report. Pediatr Neurosurg. 2017;52(4):279-283. doi: 10.1159/000477816. Epub 2017 Jul 14. PubMed PMID: 28704833.
3)

Qiao L, Yu T, Ni D, Wang X, Xu C, Liu C, Zhang G, Li Y. Correlation between extreme fear and focal cortical dysplasia in anterior cingulate gyrus: Evidence from a surgical case of refractory epilepsy. Clin Neurol Neurosurg. 2017 Oct 31;163:121-123. doi: 10.1016/j.clineuro.2017.10.025. [Epub ahead of print] PubMed PMID: 29101860.
4)

Tullberg M, Hellström P, Piechnik SK, Starmark JE, Wikkelsö C. Impaired wakefulness is associated with reduced anterior cingulate CBF in patients with normal pressure hydrocephalus. Acta Neurol Scand. 2004 Nov;110(5):322-30. PubMed PMID: 15476461.
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