Atormac
Neurology India
menu-bar5 Open access journal indexed with Index Medicus
  Users online: 2388  
 Home | Login 
About Editorial board Articlesmenu-bullet NSI Publicationsmenu-bullet Search Instructions Online Submission Subscribe Videos Etcetera Contact
  Navigate Here 
 Search
 
  
 Resource Links
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
    Article in PDF (854 KB)
    Citation Manager
    Access Statistics
    Reader Comments
    Email Alert *
    Add to My List *
* Registration required (free)  

 
  In this Article
   References
   Article Figures

 Article Access Statistics
    Viewed1711    
    Printed20    
    Emailed0    
    PDF Downloaded39    
    Comments [Add]    

Recommend this journal

 


 
Table of Contents    
LETTER TO EDITOR
Year : 2016  |  Volume : 64  |  Issue : 3  |  Page : 552-554

Gamma knife ventral capsulotomy for posttraumatic brain injury obsessive-compulsive disorder


1 Department of Neurosurgery, Center of Neuromodulation, Wexner Medical Center, The Ohio State University, Columbus, Ohio 43210, USA
2 Department of Psychiatry, Wexner Medical Center, The Ohio State University, Columbus, Ohio 43210, USA
3 Department of Radiation Oncology, Wexner Medical Center, The Ohio State University, Columbus, Ohio 43210, USA

Date of Web Publication3-May-2016

Correspondence Address:
Milind Deogaonkar
Department of Neurosurgery, Center of Neuromodulation, Wexner Medical Center, The Ohio State University, Columbus, Ohio 43210
USA
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.181549

Rights and Permissions



How to cite this article:
Sharma M, Young J, Grecula J, McGregor J, Deogaonkar M. Gamma knife ventral capsulotomy for posttraumatic brain injury obsessive-compulsive disorder. Neurol India 2016;64:552-4

How to cite this URL:
Sharma M, Young J, Grecula J, McGregor J, Deogaonkar M. Gamma knife ventral capsulotomy for posttraumatic brain injury obsessive-compulsive disorder. Neurol India [serial online] 2016 [cited 2019 Aug 21];64:552-4. Available from: http://www.neurologyindia.com/text.asp?2016/64/3/552/181549


Sir,

The incidence of obsessive-compulsive disorder (OCD) following traumatic brain injury (TBI) ranges between 1% and 15% in the literature,[1] compared to approximately 2–3% of idiopathic OCD in the United States and worldwide.[2] OCD is characterized by persistent obsessions with intrusive thoughts causing severe generalized anxiety and compulsions in the form of an urge to perform repetitive tasks (Diagnostic and Statistical Manual, V th edition). Medical management (selective serotonin reuptake inhibitors) in combination with cognitive behavior therapy (CBT) are the mainstay therapies for these patients. However, even with optimal medical and behavioral management, a treatment failure rate of 10–25% has been documented in the literature.[3]

Although deep brain stimulation (DBS) is the preferred surgical option, ablative procedures (capsulotomy/cingulotomy) provide an alternative option in selected patients.[4],[5] Ablative capsulotomy had been shown to have a response rate in the range between 37.5% and 78% in patients with refractory OCD.[4] Here, we report the efficacy of gamma knife capsulotomy in a patient with post-TBI OCD. We also review the pertinent literature. Our case is unique in that neither DBS nor an ablative procedure has been described for post-TBI OCD in the literature.

A 61-year-old Caucasian married male patient presented at our center with symptoms of OCD following TBI with consideration for DBS treatment. He sustained head injury after falling down a flight of stairs (12 steps) 11 years ago, which resulted in a right frontotemporoparietal subdural hematoma and bifrontal contusions. He underwent a right frontal craniotomy for evacuation of the hematoma. Since then, he had significant impairment in cognition and memory. He had obsessive symptoms such as keeping things meticulously clean prior to sustaining the TBI; however, he was able to perform daily routine activities and work appropriately. Following the TBI, his obsessive-compulsive symptoms had worsened substantially to the point that he was diagnosed to be having an OCD. His obsessions included fear that he would be punished if he is not careful enough, or if things were not “perfect.” In addition, he also described some fears concerning dirt and contamination. His compulsive behavior included themes of checking, counting, and symmetry. He had also spent excessive amount of time checking light switches in the house, the stove, and the locks on his wife's car. He was incapacitated by his OCD symptoms and had negligible symptom-free intervals. He was verbally, emotionally, and physically abused by his parents during childhood. He suffered from problems related to flashbacks and nightmares, and his family described him as being easily startled (hypervigilant) with a history of depression. His medical management included sertraline 100 mg 2 tablets daily, quetiapine 200 mg 2 tablets daily, and lamotrigine 100 mg 1 tablet 3 times daily. He was disheveled on appearance with distractible attention and was unable to concentrate. He was making a good eye contact and had a normal mood, an appropriate affect but with circumstantial and disorganized thought process, and decreased motor activity. His speech was slow and soft. His recent and remote memory was impaired and he also had a poor insight and judgment. His cognition was impaired with a poor impulse control. His Yale-Brown Obsessive Compulsive Scale (Y-BOCS) score was 31. In view of the severity of his cognitive deficits, it was not possible for him to participate in the cognitive behavioral therapy. Magnetic resonance imaging (MRI) of the brain revealed extensive bifrontal encephalomalacia with destructive changes involving subcortical structures [Figure 1]. In view of the extensive encephalomalacia, it was decided to go ahead with gamma knife capsulotomy instead of DBS.
Figure 1: (a-c) Preoperative magnetic resonance imaging of the brain (axial, sagittal, and coronal images) with contrast revealed extensive bifrontal encephalomalacia, left being greater than right (measuring 11 cm × 6.3 cm in dimension), milder bilateral anterior temporal pole encephalomalacia, and destructive changes involving the caudate nuclei, anterior corpus callosum, and anterior portions of the corticospinal tracts, specifically anterior limbs of the internal capsule and corona radiata; (d-f) magnetic resonance imaging of the brain with contrast (3 months postprocedure) revealed 6 mm contrast enhancing signal changes involving the caudate nuclei bilaterally; (g-i) magnetic resonance imaging of the brain with contrast (at a 6 month follow-up) showing the rim enhancement along bilateral anterior limbs of the internal capsule with extension to the caudate heads and anterior medial margins of the lentiform nuclei measuring 1.5 cm AP × 1.4 cm in the transverse plane on the right and 1.4 cm AP × 1.1 cm in the transverse plane on the left, with no mass effect

Click here to view


Following written informed and valid consent, the patient underwent a 3-Tesla MRI to identify the anterior limb of internal capsule (ALIC) under general anesthesia. Stereotactic MRI (1.5 Tesla) and radiotherapy planning utilizing a computed tomography (CT) scan was then obtained with a Leksell frame. These images were then coregistered and fused with the 3-Tesla MRI images at the gamma plan workstation. The x, y, and z coordinates for the right ALIC were obtained in reference to the coordinates of the anterior commissure (AC) [18 mm lateral, 8 mm anterior, and 3 mm superior]. The first shot was planned at this target and the second shot with a 4 mm collimator just inferior to the first shot. The process was repeated for the left ALIC. A dose of 90 Gy at the 50% isodose (180 Gy maximum) was prescribed for both the right and left ALIC. The dose plan utilized a total of four shots with the 4 mm collimator. The treatment was delivered using the Perfexion gamma knife system and the irradiation beam on time was 358.7 min. After the gamma knife radiosurgery, the patient's wife noticed changes in his obsessive-compulsive behavior. He was less engaged in a compulsive behavior such as walking in circles around the table and pulling at the threads of a fabric. There was a decrease in his overall anxiety and tapping behavior. There was also an improvement in his social interaction with his family and he developed a sense of humor. He was able to recall the procedure performed and able to tell the day, year and season but was not able to recollect the month. He was appropriately answering questions and was more engaged in the interview than on previous encounters. He was making a good eye contact and had a euthymic mood, congruent affect, appropriate thought process relevant to the topic (but was influenced by the cognitive deficits). His recent and remote memory had improved but he still had a poor insight and judgment. His cognition was impaired but he had an improved impulse control. His Y-BOCS score decreased to 24 at a 3-month follow-up. He showed continued improvement at the 6 month follow-up and went from persisting with constant symptoms to near constant symptoms with less distress and better control and with an increasing ability to resist his obsessive compulsive behaviour.

The establishment of the diagnosis of OCD following TBI is a complicated task as symptoms such as cognitive impairment/perseveration due to TBI (frontal/temporal lobe injury) may mimic obsessive-compulsive symptoms. Executive dysfunctions following a TBI may overlap the OCD symptomatology, thus masking the diagnosis.[6] The orbitofrontal cortex, limbic cortex, striatum, and thalamus have a role in the pathophysiology of post-TBI OCD. Recently, the prefrontal cortex has been shown to have a role in storing memories of behavioral sequences (structured event complexes [SECs]) and any deficit in this process of initiation-to-completion of SEC has been implicated in the pathogenesis of OCD.[7] Development of post-TBI OCD is influenced by factors such as the site of brain injury, the underlying preinjury subclinical predisposition, the presence of environmental stressors, and the postinjury rehabilitation. Our patient had subclinical obsessive symptoms prior to TBI. Another interesting feature of our report is that despite extensive bilateral frontal encephalomalacia following head injury, there was worsening of OCD symptoms. This might be attributed to the persisting deficits in behavioral memories.

In our patient, due to extensive bilateral frontal encephalomalacia, it was not feasible to carry out the DBS procedure; therefore, gamma knife capsulotomy was considered. Ruck et al.,[8] targeted an area 19 to 21 mm anterior to the AC on the intercommissural line at the middle portion of the internal capsule at the level of the posterior part of the medial putaminal border (defined on stereotactic MRIs) using thermal radiofrequency or gamma knife. In this study, they reported a significant response (>35% reduction in Y-BOCS) in 48% of patients (n = 25) following unilateral or bilateral thermocapsulotomy or gamma capsulotomy at a mean follow-up of 10.9 years.[8] They also suggested that limiting the lateral and medial/posterior extension of the lesion increased the amelioration of OCD symptoms, and mitigation of side effects can be achieved. A response rate of 27% and 62% following a single and double shot of gamma knife capsulotomy bilaterally, respectively, for refractory OCD has been reported.[9] A randomized controlled study reported a response rate of 37.5% (3 out of 8 patients) following a double bilateral gamma knife capsulotomy at 12 months compared to a “no response rate” amongst the 8 sham patients.[10] At 54 months, two additional patients in the active group became responders in this study. In this study, the target coordinates were defined at the ventral portion of the ALIC, 7–10 mm rostral to the posterior border of the AC using 50% isodose with a maximum dose of 180 Gy.[10] Due to extensive bilateral frontal encephalomalacia, we targeted the region 8 mm anterior to the posterior border of AC. The adverse effects of gamma knife capsulotomy for OCD, such as cerebral edema and headache (20%), asymptomatic infarctions in the caudate nucleus (10%), and frontal lobe dysfunction (3%), have been reported in the literature.[9] Other adverse effects include weight gain, executive dysfunction, apathy, sexual disinhibition, and suicidal tendency.[8] The tendency of adverse effects increased with higher doses of radiation or multiple capsulotomies.[8]

OCD following TBI is a complex condition requiring a detailed examination to unveil the diagnosis. DBS remains the preferred surgical option in patients refractory to the medical management. Ablative procedure such as gamma knife capsulotomy can be a useful alternative to DBS in carefully selected patients.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Whelan-Goodinson R, Ponsford J, Johnston L, Grant F. Psychiatric disorders following traumatic brain injury: Their nature and frequency. J Head Trauma Rehabil 2009;24:324-32.  Back to cited text no. 1
    
2.
de Koning PP, Figee M, van den Munckhof P, Schuurman PR, Denys D. Current status of deep brain stimulation for obsessive-compulsive disorder: A clinical review of different targets. Curr Psychiatry Rep 2011;13:274-82.  Back to cited text no. 2
    
3.
Björgvinsson T, Hart J, Heffelfinger S. Obsessive-compulsive disorder: Update on assessment and treatment. J Psychiatr Pract 2007;13:362-72.  Back to cited text no. 3
    
4.
Sharma M, Saleh E, Deogaonkar M, Rezai A. DBS for obsessive-compulsive disorder. In: Sun B, Salles AD, editors. Neurosurgical Treatments for Psychiatric Disorders. Netherlands: Springer; 2015. p. 113-23.  Back to cited text no. 4
    
5.
Balasubramaniam V. Magnetic resonance image-guided stereotactic cingulotomy for intractable psychiatric disease. Neurosurgery 1997;40:107-8.  Back to cited text no. 5
[PUBMED]    
6.
Coetzer R, Stein DJ, Toit PL. Executive function in traumatic brain injury and obsessive-compulsive disorder: An overlap? Psychiatry Clin Neurosci 2001;55:83-7.  Back to cited text no. 6
    
7.
Huey ED, Zahn R, Krueger F, Moll J, Kapogiannis D, Wassermann EM, et al. A psychological and neuroanatomical model of obsessive-compulsive disorder. J Neuropsychiatry Clin Neurosci 2008;20:390-408.  Back to cited text no. 7
    
8.
Ruck C, Karlsson A, Steele JD, Edman G, Meyerson BA, Ericson K, et al. Capsulotomy for obsessive-compulsive disorder: Long-term follow-up of 25 patients. Arch Gen Psychiatry 2008;65:914-21.  Back to cited text no. 8
    
9.
Greenberg BD, Price LH, Rauch SL, Friehs G, Noren G, Malone D, et al. Neurosurgery for intractable obsessive-compulsive disorder and depression: Critical issues. Neurosurg Clin N Am 2003;14:199-212.  Back to cited text no. 9
    
10.
Lopes AC, Greenberg BD, Canteras MM, Batistuzzo MC, Hoexter MQ, Gentil AF, et al. Gamma ventral capsulotomy for obsessive-compulsive disorder: A randomized clinical trial. JAMA Psychiatry 2014;71:1066-76.  Back to cited text no. 10
    


    Figures

  [Figure 1]



 

Top
Print this article  Email this article
   
Online since 20th March '04
Published by Wolters Kluwer - Medknow