Covid-19 and pituitary apoplexy

Covid-19 and pituitary apoplexy

Kamel et al. reported a case of pituitary apoplexy associated with COVID-19 infection. Based on a patient’s clinical findings, review of the other reported cases, as well as the available literature, they put forth a multitude of pathophysiological mechanisms induced by COVID-19 that can possibly lead to the development of pituitary apoplexy. In their opinion, the association between both conditions is not just a mere coincidence. Although the histopathological features of pituitary apoplexy associated with COVID-19 are similar to pituitary apoplexy induced by other etiologies, future research may disclose unique pathological fingerprints of COVID-19 virus that explains its capability of inducing pituitary apoplexy 1).


A 75-year-old man who presented with a headache and was later diagnosed with hypopituitarism secondary to pituitary apoplexy. This occurred 1 month following a mild-to-moderate COVID-19 infection with no other risk factors commonly associated with pituitary apoplexy. This case, therefore, supplements an emerging evidence base supporting a link between COVID-19 and pituitary apoplexy 2).


Martinez-Perez et al. identified 3 consecutive cases of PA and concomitant COVID-19 infection. The most common symptoms at presentation were headache and vision changes. The included patients were successfully treated with surgical decompression and medical management of the associated endocrinopathy, ultimately experiencing improvement in their visual symptoms at the latest follow-up examination. COVID-19 infection in the perioperative period was corroborated by polymerase chain reaction test results in all the patients.

With the addition of our series to the literature, 10 cases of PA in the setting of COVID-19 infection have been confirmed. The present series was limited in its ability to draw conclusions about the relationship between these 2 entities. However, COVID-19 infection might represent a risk factor for the development of PA. Further studies are required. 3).


A review underlines that there could be a specific involvement of the pituitary gland which fits into a progressively shaping endocrine phenotype of COVID-19. Moreover, the care for pituitary diseases need to continue despite the restrictions due to the emergency. Several pituitary diseases, such as hypopituitarism and Cushing disease, or due to frequent comorbidities such as diabetes may be a risk factor for severe COVID-19 in affected patients. There is the urgent need to collect in international multicentric efforts data on all these aspects of the pituitary involvement in the pandemic in order to issue evidence driven recommendations for the management of pituitary patients in the persistent COVID-19 emergency. 4).


Pituitary apoplexy attributed solely to COVID-19 in the absence of other identifiable causes. While much remains to be discovered and understood regarding COVID-19, they discuss the potential pathophysiology of COVID-19-associated pituitary apoplexy and raise awareness of this clinical complication 5)


A neuro-ophthalmic presentation of pituitary apoplexy under the setting of COVID-19 infection in a middle-aged man who presented to ophthalmic emergency with sudden bilateral loss of vision along with a history of fever past 10 days. There was sluggishly reacting pupils and RT-PCR for COVID was positive. Imaging pointed the diagnosis as pituitary macroadenoma with apopexy. In view of pandemic situation, patient was given symptomatic treatment as per the protocols and stabilized. Vision also showed improvement to some extent and the patient is awaiting neurosurgery 6).


A case of a previously healthy woman with severe acute respiratory syndrome coronavirus 2 infection associated with pituitary apoplexy. The plausible pathophysiological mechanisms of pituitary apoplexy in infectious coronavirus disease 2019 are discussed. 7).


A 27-year-old male patient case with progressive decrease in visual acuity, associated with respiratory symptoms and intense headache. Multilobar infiltrate with a reticulonodular pattern is evident on chest CT scan. Brain CT scan with pituitary macroadenoma apoplexy was shown. SARS-Cov2 was confirmed, and respiratory support initiated. However, the patient died shortly afterward, secondary to pulmonary complications.

The angiotensin-converting enzyme (ACE) II receptor is expressed in circumventricular organs and in cerebrovascular endothelial cells, which play a role in vascular autoregulation and cerebral blood flow. For this reason, is rational the hypothesize that brain ACE II could be involved in COVID-19 infection. Underlying mechanisms require further elucidation in the future 8).


A 28-year-old G5P1 38w1d female presented with 4 days of blurry vision, left dilated pupil, and headache. She tested positive for SARS-CoV-2 on routine nasal swab testing but denied cough or fever. Endocrine testing demonstrated an elevated serum prolactin level, and central hypothyroidism. MRI showed a cystic-solid lesion with a fluid level in the pituitary fossa and expansion of the sella consistent with pituitary apoplexy. Her visual symptoms improved with corticosteroid administration and surgery was delayed to two weeks after her initial COVID-19 infection and to allow for safe delivery of the child. A vaginal delivery under epidural anesthetic occurred at 39 weeks. Two days later, transsphenoidal resection of the mass was performed under strict COVID-19 precautions including use of Powered Air Purifying Respirators (PAPRs) and limited OR personnel given high risk of infection during endonasal procedures. Pathology demonstrated a liquefied hemorrhagic mass suggestive of pituitary apoplexy. She made a full recovery and was discharged home two days after surgery.

They demonstrate the first known case of successful elective induction of vaginal delivery and transsphenoidal intervention in a near full term gravid patient presenting with pituitary apoplexy and acute SARS-CoV-2 infection. Further reports may help determine if there is a causal relationship or if these events are unrelated. Close adherence to guidelines for caregivers can greatly reduce risk of infection. 9).


A 25 year old male presented with dyspnoea, cough and high fevers for 4 days. He was commenced on broad-spectrum antimicrobials and oxygen therapy. His respiratory function deteriorated in spite of these measures and he required mechanical ventilation. CT showed left upper lobe consolidation as well as multifocal ground-glass opacification. Case 2: A 43 year-old male presented with headache and was found incidentally to have pneumonia. He was recently diagnosed with pituitary apoplexy secondary to an adenoma with resultant pituitary insufficiency but MRI brain was stable. His respiratory function deteriorated in spite of antibiotics and he required mechanical ventilation. CT showed likely atypical infection with resultant ARDS. Outcome Both underwent nasopharyngeal RT-PCR testing for SARS-CoV-2. Patient 2 was positive. Patient 1 was extubated and made a good recovery. Patient 2 was transferred to another centre for ECMO therapy. He died 27 days after transfer. Conclusion Given the atypical presentations in generally otherwise young and healthy individuals, the decision was made outside of national guidance to perform testing for SARS-CoV-2. This diagnosis had far-reaching implications for the SARS-CoV-2 pandemic within Ireland 10).


1)

Kamel WA, Najibullah M, Saleh MS, Azab WA. Coronavirus disease 2019 infection and pituitary apoplexy: A causal relation or just a coincidence? A case report and review of the literature. Surg Neurol Int. 2021 Jun 28;12:317. doi: 10.25259/SNI_401_2021. PMID: 34345458; PMCID: PMC8326077.
2)

Liew SY, Seese R, Shames A, Majumdar K. Apoplexy in a previously undiagnosed pituitary macroadenoma in the setting of recent COVID-19 infection. BMJ Case Rep. 2021 Jul 28;14(7):e243607. doi: 10.1136/bcr-2021-243607. PMID: 34321266; PMCID: PMC8319972.
3)

Martinez-Perez R, Kortz MW, Carroll BW, Duran D, Neill JS, Luzardo GD, Zachariah MA. Coronavirus Disease 2019 and Pituitary Apoplexy: A Single-Center Case Series and Review of the Literature. World Neurosurg. 2021 Aug;152:e678-e687. doi: 10.1016/j.wneu.2021.06.004. Epub 2021 Jun 12. PMID: 34129968; PMCID: PMC8196470.
4)

Frara S, Allora A, Castellino L, di Filippo L, Loli P, Giustina A. COVID-19 and the pituitary. Pituitary. 2021 Jun;24(3):465-481. doi: 10.1007/s11102-021-01148-1. Epub 2021 May 3. PMID: 33939057; PMCID: PMC8089131.
5)

Bordes SJ, Phang-Lyn S, Najera E, Borghei-Razavi H, Adada B. Pituitary Apoplexy Attributed to COVID-19 Infection in the Absence of an Underlying Macroadenoma or Other Identifiable Cause. Cureus. 2021 Feb 12;13(2):e13315. doi: 10.7759/cureus.13315. PMID: 33732566; PMCID: PMC7956048.
6)

Katti V, Ramamurthy LB, Kanakpur S, Shet SD, Dhoot M. Neuro-ophthalmic presentation of COVID-19 disease: A case report. Indian J Ophthalmol. 2021 Apr;69(4):992-994. doi: 10.4103/ijo.IJO_3321_20. PMID: 33727476; PMCID: PMC8012961.
7)

Ghosh R, Roy D, Roy D, Mandal A, Dutta A, Naga D, Benito-León J. A Rare Case of SARS-CoV-2 Infection Associated With Pituitary Apoplexy Without Comorbidities. J Endocr Soc. 2021 Jan 2;5(3):bvaa203. doi: 10.1210/jendso/bvaa203. PMID: 33501401; PMCID: PMC7798947.
8)

Solorio-Pineda S, Almendárez-Sánchez CA, Tafur-Grandett AA, Ramos-Martínez GA, Huato-Reyes R, Ruiz-Flores MI, Sosa-Najera A. Pituitary macroadenoma apoplexy in a severe acute respiratory syndrome-coronavirus-2-positive testing: Causal or casual? Surg Neurol Int. 2020 Sep 25;11:304. doi: 10.25259/SNI_305_2020. PMID: 33093981; PMCID: PMC7568102.
9)

Chan JL, Gregory KD, Smithson SS, Naqvi M, Mamelak AN. Pituitary apoplexy associated with acute COVID-19 infection and pregnancy. Pituitary. 2020 Dec;23(6):716-720. doi: 10.1007/s11102-020-01080-w. Epub 2020 Sep 11. PMID: 32915365; PMCID: PMC7484495.
10)

Faller E, Lapthorne S, Barry R, Shamile F, Salleh F, Doyle D, O’Halloran D, Prentice M, Sadlier C. The Presentation and Diagnosis of the First Known Community-Transmitted Case of SARS-CoV-2 in the Republic of Ireland. Ir Med J. 2020 May 7;113(5):78. PMID: 32603572.

Cervical spondylotic myelopathy surgery outcome

Cervical spondylotic myelopathy surgery outcome

Indications and optimal timing for surgical treatment of degenerative cervical myelopathy (DCM) remain unclear, and data from daily clinical practice are warranted.

Gulati et al. investigated clinical outcomes following decompressive surgery for DCM.

Data were obtained from the Norwegian Registry for Spine Surgery. The primary outcome was change in the neck disability index (NDI) 1 yr after surgery. Secondary endpoints were the European myelopathy score (EMS), quality of life (EuroQoL 5D [EQ-5D]), numeric rating scales (NRS) for headache, neck pain, and arm pain, complications, and perceived benefit of surgery assessed by the Global Perceived Effect scale.

They included 905 patients operated between January 2012 and June 2018. There were significant improvements in all Patient-reported outcome measures (PROMs) including NDI (mean -10.0, 95% CI -11.5 to -8.4, P < .001), EMS (mean 1.0, 95% CI 0.8-1.1, P < .001), EQ-5D index score (mean 0.16, 95% CI 0.13-0.19, P < .001), EQ-5D visual analogue scale (mean 13.8, 95% CI 11.7-15.9, P < .001), headache NRS (mean -1.1, 95% CI -1.4 to -0.8, P < .001), neck pain NRS (mean -1.8, 95% CI -2.0 to -1.5, P < .001), and arm pain NRS (mean -1.7, 95% CI -1.9 to -1.4, P < .001). According to GPE scale assessments, 229/513 patients (44.6%) experienced “complete recovery” or felt “much better” at 1 yr. There were significant improvements in all PROMs for both mild and moderate-to-severe DCM. A total of 251 patients (27.7%) experienced adverse effects within 3 mo.

Surgery for DCM is associated with significant and clinically meaningful improvement across a wide range of PROMs 1).


Objective scoring of the post-operative neurological function did not correlate with patient-perceived outcomes in Degenerative cervical myelopathy outcome (DCM). Traditional testing of motor and sensory function as part of the neurological assessment may not be sensitive enough to assess the scope of neurological changes experienced by Degenerative cervical myelopathy patients 2).


Hamdan assessed the relation between MRI T2 Weighted images (T2WIhyperintense cord signal and clinical outcome after anterior cervical discectomy in patients with degenerative cervical disc herniation.

This retrospective observational study was conducted on twenty-five patients with degenerative cervical disc prolapse associated with MRI T2WI hyperintense cord signal, at the Department of Neurosurgery, Qena University Hospital, South Valley University from August 2014 to December 2016. A complete clinical and radiological evaluation of the patients was done. Anterior cervical discectomy and fusion was done for all patients. Patients were clinically assessed preoperatively and postoperatively at 3, 6, and 12 months using Modified Japanese Orthopaedic Association scale (MJOA). Radiographic assessment was done by preoperative and postoperative T2WI MRI. The statistical analysis was done using Statistical Package for the Social Sciences (SPSS) software (version 22.0).

There were 25 patients included in the study; 16 (64%) females and 9 (36%) males. The mean age was 46.89 ± 7.52 standard deviation (SD) years with range from 26 to 64 years, 3 (12%) patients had worsened in the form of postoperative motor power deterioration, and 14 (56%) patients has no improvement and remain as preoperative condition. The remaining 8 (32%) patients had a reported postoperative improvement of symptoms and signs according to MJOA score. The mean follow-up period (in months) was 11 ± 2.34 (SD). Conclusion:

The presence of T2W hyperintense signal on preoperative MRI predicts a poor surgical outcome in patients with cervical disc prolapse. The regression of T2W ISI postoperatively correlates with better functional outcomes 3).


Whilst decompressive surgery can halt disease progression, existing spinal cord damage is often permanent, leaving patients with lifelong disability.

Early surgery improves the likelihood of recovery, yet the average time from onset of symptoms to correct diagnosis is over 2 years. The majority of delays occur initially, before and within primary care, mainly due to a lack of recognition. Symptom checkers are widely used by patients before medical consultation and can be useful for preliminary triage and diagnosis. Lack of recognition of Degenerative Cervical Myelopathy (DCM) by symptom checkers may contribute to the delay in diagnosis.

The impact of the changes in myelopathic signs following cervical decompression surgery and their relationship to functional outcome measures remains unclear.

Surgery is associated with a significant quality of life improvement. The intervention is cost effective and, from the perspective of the hospital payer, should be supported 4).

Surgical decompression for CSM is safe and results in improved functional status and quality of life in patients around the world, irrespective of differences in medical systems and socio-cultural determinants of health 5).

The successful management of CSM depends upon an early and accurate diagnosis, an objective assessment of impairment and disability, and an ability to predict outcome. In this field, quantitative measures are increasingly used by clinicians to grade functional and neurological status and to provide decision-making support 6).


In addition, objective assessment tools allow clinicians to quantify myelopathy severity, predict outcome, and evaluate surgical benefits by tracking improvements throughout follow-up 7) 8) 9).

Several outcome measures assess functional impairment and quality of life in patients with cervical myelopathy 10) 11) 12) 13) 14).

A validated “gold standard,” however, has not been established, preventing the development of quantitative guidelines for CSM management 15).

In this field, one of the most widely accepted tool for assessing functional status is the modified Japanese Orthopaedic Association scale (mJOA).

Some studies have found that resolution of T2 hyperintensity in subjects with CSM who undergo ventral decompressive surgery correlates with improved functional outcomes. Other studies have found little correlation with postoperative outcome 16) 17).

Machine learning for degenerative cervical myelopathy

see Machine learning for degenerative cervical myelopathy.

References


1) Gulati S, Vangen-Lønne V, Nygaard ØP, Gulati AM, Hammer TA, Johansen TO, Peul WC, Salvesen ØO, Solberg TK. Surgery for Degenerative Cervical Myelopathy: A Nationwide Registry-Based Observational Study With Patient-Reported Outcomes. Neurosurgery. 2021 Jul 29:nyab259. doi: 10.1093/neuros/nyab259. Epub ahead of print. PMID: 34325471.2) McGregor SM, Detombe S, Goncalves S, Doyle-Pettypiece P, Bartha R, Duggal N. Does the Neurological Exam Correlate with Patient Perceived Outcomes in Degenerative Cervical Myelopathy? World Neurosurg. 2019 Aug 2. pii: S1878-8750(19)32111-4. doi: 10.1016/j.wneu.2019.07.195. [Epub ahead of print] PubMed PMID: 31382071.3) Hamdan ARK. The Relation between Cord Signal and Clinical Outcome after Anterior Cervical Discectomy in Patients with Degenerative Cervical Disc Herniation. Asian J Neurosurg. 2019 Jan-Mar;14(1):106-110. doi: 10.4103/ajns.AJNS_262_17. PubMed PMID: 30937019; PubMed Central PMCID: PMC6417293.4) Witiw CD, Tetreault LA, Smieliauskas F, Kopjar B, Massicotte EM, Fehlings MG. Surgery for degenerative cervical myelopathy: a patient centered quality of life and health economic evaluation. Spine J. 2016 Oct 25. pii: S1529-9430(16)31022-1. doi: 10.1016/j.spinee.2016.10.015. [Epub ahead of print] PubMed PMID: 27793760.5) Fehlings MG, Ibrahim A, Tetreault L, Albanese V, Alvarado M, Arnold P, Barbagallo G, Bartels R, Bolger C, Defino H, Kale S, Massicotte E, Moraes O, Scerrati M, Tan G, Tanaka M, Toyone T, Yukawa Y, Zhou Q, Zileli M, Kopjar B. A Global Perspective on the Outcomes of Surgical Decompression in Patients with Cervical Spondylotic Myelopathy: Results from the Prospective Multicenter AOSpine International Study on 479 patients. Spine (Phila Pa 1976). 2015 May 27. [Epub ahead of print] PubMed PMID: 26020847.6) , 15) Singh A, Tetreault L, Casey A, et al. A summary of assessment tools for patients suffering from cervical spondylotic myelopathy: a systematic review on validity, reliability, and responsiveness [published online ahead of print September 5, 2013]. Eur Spine J. doi:10.1007/s00586-013-2935-x.7) Laing RJ. Measuring outcome in neurosurgery. Br J Neurosurg 2000;14:181–4.8) Holly LT, Matz PG, Anderson PA, et al. Clinical prognostic indicators of surgical outcome in cervical spondylotic myelopathy. J Neurosurg Spine 2009;11:112–8.9) Kalsi-Ryan S, Singh A, Massicotte EM, et al. Ancillary outcome measures for assessment of individuals with cervical spondylotic myelopathy. Spine (Phila Pa 1976) 2013;38:S111–22.10) Singh A, Crockard HA. Quantitative assessment of cervical spondylotic myelopathy by a simple walking test. Lancet 1999;354:370–3.11) Nurick S. The natural history and the results of surgical treatment of the spinal cord disorder associated with cervical spondylosis. Brain 1972;95:101–8.12) Olindo S, Signate A, Richech A, et al. Quantitative assessment of hand disability by the nine-hole-peg test (9-HPT) in cervical spondylotic myelopathy. J Neurol Neurosurg Psychiatry 2008;79:965–7.13) Hosono N, Sakaura H, Mukai Y, et al. A simple performance test for quantifying the severity of cervical myelopathy [erratum in: J Bone Joint Surg Br 2008;90:1534]. J Bone Joint Surg Br 2008;90:1210–3.14) Casey AT, Bland JM, Crockard HA. Development of a functional scoring system for rheumatoid arthritis patients with cervical myelopathy. Ann Rheum Dis 1996;55:901–6.16) Sarkar S, Turel MK, Jacob KS, Chacko AG. The evolution of T2-weighted intramedullary signal changes following ventral decompressive surgery for cervical spondylotic myelopathy. J Neurosurg Spine. 2014;21(4):538-546.17) Vedantam A, Rajshekhar V. Change in morphology of intramedullary T2- weighted increased signal intensity after anterior decompressive surgery for cervical spondylotic myelopathy. Spine (Phila Pa 1976). 2014;39(18):1458-1462.

Subthalamic deep brain stimulation for Parkinson’s disease outcome

The bilateral effects of deep brain stimulation (DBS) on motor and non-motor symptoms of Parkinson’s disease (PD) have been extensively studied and reviewed. However, the unilateral effects-in particular, the potential lateralized effects of left- versus right-sided DBS-have not been adequately recognized or studied.

Lin et al. summarized the current evidence and controversies in the literature regarding the lateralized effects of DBS on motor and non-motor outcomes in PD patients. Publications in the English language before February 2021 were obtained from the PubMed database and included if they directly compared the effects of unilateral versus contralateral side DBS on the motor or non-motor outcomes in PD. The current literature is overall of low-quality and is biased by various confounders. Researchers have investigated mainly PD patients receiving subthalamic nucleus (STN) DBS while the potential lateralized effects of globus pallidus internus (GPi) DBS have not been adequately studied. Evidence suggests potential lateralized effects of STN DBS on axial motor symptoms and deleterious effects of left-sided DBS on language-related functions, in particular, the verbal fluency, in PD. The lateralized DBS effects on appendicular motor symptoms as well as other neurocognitive and neuropsychiatric domains remain inconclusive. Future studies should control for varying methodological approaches as well as clinical and DBS management heterogeneities, including symptom laterality, stimulation parameters, location of active contacts, and lead trajectories. This would contribute to improved treatment strategies such as personalized target selection, surgical planning, and postoperative management that ultimately benefit patients 1).


The surgical and clinical outcomes of asleep DBS for Parkinson’s disease are comparable to those of awake DBS 2).


Suboptimal targeting within the STN can give rise to intolerable sensorimotor side effects, such as dysarthria, contractions and paresthesias 3) 4) 5). eye movement perturbations, and psychiatric symptoms 6) 7) 8), limiting the management of motor symptoms. The small size of the STN motor territory and the consequences of spreading current to immediately adjacent structures obligate precise targeting. Neurosurgeons therefore rely on a combination of imaging, electrophysiology, kinesthetic responses, and stimulation testing to accurately place the DBS lead into the sensorimotor domain of STN 9) 10) 11).

Deep Brain Stimulation has been associated with post-operative neuropsychology changes, especially in verbal memory.

Deep brain stimulation (DBS) of subthalamic nucleus (STN) is widely accepted to treat advanced Parkinson disease (PD). However, published studies were mainly conducted in Western centers 12).

High frequency subthalamic nucleus (STN) deep brain stimulation (DBS) improves the cardinal motor signs of Parkinson’s disease (PD) and attenuates STN alpha/beta band neural synchrony in a voltage-dependent manner. While there is a growing interest in the behavioral effects of lower frequency (60 Hz) DBS, little is known about its effect on STN neural synchrony.

Low-frequency stimulation of the subthalamic nucleus via the optimal contacts is effective in improving overall motor function of patients with Parkinson Disease 13). In Parkinson’s disease significantly improved important aspects of QoL as measured by PDQ-39. The improvements were maintained at 2 years follow-up except for social support and communication. Sobstyl et al., demonstrated a positive correlation between changes in the off condition of motor UPDRS scores and Unified Dyskinesia Rating Scale in several PDQ-39 dimensions, whereas fluctuation UPDRS scores were negatively correlated with PDQ-39 mobility scores 14).

The degree of clinical improvement achieved by deep brain stimulation (DBS) is largely dependent on the accuracy of lead placement.

A study reports on the evaluation of intraoperative MRI (iMRI) for adjusting deviated electrodes to the accurate anatomical position during DBS surgery and acute intracranial changes 15).


Although dementia is a contraindication in deep brain stimulation for Parkinson’s disease, the concept is supported by little scientific evidence. Moreover, it is unclear whether PD with mild cognitive impairment (PD-MCI) or domain-specific cognitive impairments affect the outcome of DBS in non-demented PD patients.

Baseline cognitive levels of patients with PD who underwent DBS were classified into PD with dementia (PDD) (n = 15), PD-MCI (n = 210), and normal cognition (PD-NC) (n = 79). The impact of the cognitive level on key DBS outcome measures [mortality, nursing home admission, progression to Hoehn&Yahr (HY) stage 5 and progression to PDD] were analyzed using Cox regression models. Park et al. also investigated whether impairment of a specific cognitive domain could predict these outcomes in non-demented patients.

Results: Patients with PDD showed a substantially higher risk of nursing home admission and progression to HY stage 5 compared with patients with PD-MCI [hazard ratio (HR) 4.20, P = .002; HR = 5.29, P < .001] and PD-NC (HR 7.50, P < .001; HR = 7.93, P < .001). MCI did not alter the prognosis in patients without dementia, but those with visuospatial impairment showed poorer outcomes for nursing home admission (P = .015), progression to HY stage 5 (P = .027) and PDD (P = .006).

Conclusions: Cognitive profiles may stratify the pre-operative risk and predict long-term outcomes of DBS in PD 16).


1)

Lin Z, Zhang C, Li D, Sun B. Lateralized effects of deep brain stimulation in Parkinson’s disease: evidence and controversies. NPJ Parkinsons Dis. 2021 Jul 22;7(1):64. doi: 10.1038/s41531-021-00209-3. PMID: 34294724.
2)

Wang J, Ponce FA, Tao J, Yu HM, Liu JY, Wang YJ, Luan GM, Ou SW. Comparison of Awake and Asleep Deep Brain Stimulation for Parkinson’s Disease: A Detailed Analysis Through Literature Review. Neuromodulation. 2019 Dec 12. doi: 10.1111/ner.13061. [Epub ahead of print] Review. PubMed PMID: 31830772.
3) , 10)

Benabid AL, Chabardes S, Mitrofanis J, Pollak P: Deep brain stimulation of the subthalamic nucleus for the treatment of Parkinson’s disease. Lancet Neurol 8:67–81, 2009
4) , 11)

Groiss SJ, Wojtecki L, Südmeyer M, Schnitzler A: Deep brain stimulation in Parkinson’s disease. Ther Adv Neurol Disorder 2:20–28, 2009
5)

Zhang S, Zhou P, Jiang S, Wang W, Li P: Interleaving subthalamic nucleus deep brain stimulation to avoid side effects while achieving satisfactory motor benefits in Parkinson disease: a report of 12 cases. Medicine (Baltimore) 95:e5575, 2016
6)

Kulisevsky J, Berthier ML, Gironell A, Pascual-Sedano B, Molet J, Parés P: Mania following deep brain stimulation for Parkinson’s disease. Neurology 59:1421–1424, 2002
7)

Mallet L, Schüpbach M, N’Diaye K, Remy P, Bardinet E, Czernecki V, et al: Stimulation of subterritories of the subthalamic nucleus reveals its role in the integration of the emotional and motor aspects of behavior. Proc Natl Acad Sci U S A 104:10661–10666, 2007
8)

Raucher-Chéné D, Charrel CL, de Maindreville AD, Limosin F: Manic episode with psychotic symptoms in a patient with Parkinson’s disease treated by subthalamic nucleus stimulation: improvement on switching the target. J Neurol Sci 273:116–117, 2008
9)

Abosch A, Timmermann L, Bartley S, Rietkerk HG, Whiting D, Connolly PJ, et al: An international survey of deep brain stimulation procedural steps. Stereotact Funct Neurosurg 91:1–11, 2013
12)

Chiou SM, Lin YC, Huang HM. One-year Outcome of Bilateral Subthalamic Stimulation in Parkinson Disease: An Eastern Experience. World Neurosurg. 2015 Jun 10. pii: S1878-8750(15)00709-3. doi: 0.1016/j.wneu.2015.06.002. [Epub ahead of print] PubMed PMID: 26072454.
13)

Khoo HM, Kishima H, Hosomi K, Maruo T, Tani N, Oshino S, Shimokawa T, Yokoe M, Mochizuki H, Saitoh Y, Yoshimine T. Low-frequency subthalamic nucleus stimulation in Parkinson’s disease: A randomized clinical trial. Mov Disord. 2014 Jan 21. doi: 10.1002/mds.25810. [Epub ahead of print] PubMed PMID: 24449169.
14)

Sobstyl M, Ząbek M, Górecki W, Mossakowski Z. Quality of life in advanced Parkinson’s disease after bilateral subthalamic stimulation: 2 years follow-up study. Clin Neurol Neurosurg. 2014 Sep;124:161-5. doi: 10.1016/j.clineuro.2014.06.019. Epub 2014 Jun 23. PubMed PMID: 25051167.
15)

Cui Z, Pan L, Song H, Xu X, Xu B, Yu X, Ling Z. Intraoperative MRI for optimizing electrode placement for deep brain stimulation of the subthalamic nucleus in Parkinson disease. J Neurosurg. 2016 Jan;124(1):62-9. doi: 10.3171/2015.1.JNS141534. Epub 2015 Aug 14. PubMed PMID: 26274983.
16)

Park KW, Jo S, Kim MS, et al. Cognitive profile as a predictor of the long-term outcome after deep brain stimulation in Parkinson’s disease [published online ahead of print, 2020 Jul 28]. J Neurol Sci. 2020;417:117063. doi:10.1016/j.jns.2020.117063
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