New-onset depressive symptoms in a chronic case of obsessive-compulsive disorder in elderly – Case report

INTRODUCTION

Obsessive-compulsive disorder (OCD) characterized by obsessions and/or compulsions. Obsessions are recurrent intrusive thoughts, images, impulses and urges that cause anxiety/distress, and compulsions are repetitive actions to relieve this anxiety/distress. It may have a typical chronic waxing or weaning course without complete symptom resolution or an episodic pattern with inter episodic asymptomatic periods. Depression is the most common comorbidity with OCD, with a lifetime risk of about 40 to 67%.^1,2 Various hypotheses attribute this comorbidity to OCD’s disabling and chronic character like overlapping structural and functional abnormalities in the Anterior cingulate cortex (ACC), thalamus and caudate nucleus,³ and the shared genetic factors.⁴

Primary brain tumors often lead to neuropsychiatric symptoms, which may be challenging to differentiate from primary psychiatric disorders. OCD has been linked to diseases such as brain infections, Sydenham’s chorea, CVAs, brain tumors, and traumatic brain injuries, albeit the research is restricted to case reports and case series.⁵ Lesions in the frontal lobe and basal ganglia have been associated with OCD, especially if late-onset.⁵ Previously documented central nervous system (CNS) lesions in patients with OCD include gliomatosis cerebri involving left temporal lobe;⁶ dysgerminoma involving basal ganglia and its different structures;⁷ suprasellar germinoma affecting bilateral basal ganglia,⁸ left frontal glioma.⁹ However, the literature suggests findings of obsessive–compulsive symptoms (OCS) rather than full-blown OCD, and usually of sudden and late onset. Moreover, the association of glioblastoma with OCD is rare. We present a known case of chronic OCD in which the depression emerged in a later course, and neuroimaging revealed a neurological lesion, highlighting the role of neuroimaging when a new set of symptoms emerged without any significant neurological symptoms.

CASE REPORT

A 47-year-old married male from rural background presented with doubts about dirt/filth contamination; arranging and rearranging household items; repeated cleaning of household items or other inanimate objects; excessive bathing and hand washing; intrusive images of cadavers, for 25 years with worsening for last two years. He also complained of low mood intermittently (not lasting more than a few days) for the past 22 years, but it had become more severe and persistent with spontaneous crying spells, feelings of hopelessness and worthlessness, disturbed sleep, and appetite for past 2 years. There was also a 20-years history of diffuse abdominal pain (on and off) and urinary hesitancy with increased frequency for last 1-2 years. There was no history of any known psychiatric or other medical disorders in past or family. Mental status examination revealed depressed affect, low reactivity and preoccupation with the illness, impaired concentration, and partial insight. The general and systemic examination including a neurological examination revealed no abnormality. Routine blood tests were unremarkable. A diagnosis of OCD with mixed obsessional thoughts and acts with dysthymia was made. Urine examination and ultrasound pelvis were done for urinary symptoms and abdominal pain, revealing blood in urine and mild prostatomegaly. The patient was put on low-dose Selective serotonin reuptake inhibitors (SSRI) (tablet sertraline 25mg/day) and benzodiazepine (tablet clonazepam 0.25mg/day) with the plan for further titration of doses and plan for evaluation from urology for urinary symptoms.

However, a routine CT scan head revealed an Intracranial lesion (ICL) on the left side of the brain. Further evaluation by MRI brain revealed a hyperdense lesion in the left medial temporal lobe. In addition, Contrast-Enhanced MRI (CE-MRI) brain was suggestive of the contrast-enhancing lesion in the left lateral ventricle’s left atrium extending to the temporal lobe with minimal surrounding edema without any midline shift. Consequently, the SSRI and benzodiazepine were stopped, an antiepileptic (tablet valproate 1000mg/day) was started and he was referred to the urology and neurosurgery, but he did not follow-up.

Four months later, the patient presented this time to emergency with a three-day acute headache and vomiting without any history of loss of consciousness, seizures, altered sensorium, or limb weakness. A NCCT brain showed an increase in the size of the tumor with areas of central necrosis, the lesion was involving the body and the occipital horn of the left lateral ventricle, causing expansion of the occipital horn and compression of the body. The lesion also involved uncus and medial temporal lobe mass on the left side and had calcification foci, this time there was also midline shift of about 6 mm in mid- periventricular ooze. CE-MRI [Figures 1 and 2] brain revealed a well-defined lobulated heterogeneously enhancing mass lesion of size 4.6 x 4.3 x 4.3 cm in the occipital horn of the left lateral ventricle showing multiple foci of blooming and multiple T2 hyper/T1 hypointense cystic areas. There was dilatation of the left lateral ventricle with periventricular oozing, a mass effect with a midline shift to the right, compression over the midbrain and left cerebral peduncle. After left temporoparietal craniotomy with tumor excision, he was discharged on tablet valproate 1000mg/day, tablet haloperidol 5mg HS for 10 days, and tablet naproxen tablet 500mg (for headache) and was asked to follow-up for chemotherapy and radiotherapy. The histopathological report indicated glioblastoma grade 4.

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Figure 1:

Magnetic Resonance Imaging (MRI) T2-FLAIR axial section (a) showing a well-defined hyper-intensity, of approximately 4 x 4 x 4 cm in left trigonal region (red arrow). (b) The lesion has involved confluence of occipital horn of left lateral ventricle (orange arrow) in T1-Weighted axial sections taken at the level of Sylvia fissures. (c) The adjacent quadrigeminal cistern is seen open and mass is extending anteriorly and inferiorly (green arrows in a, c) along hippocampus (green arrow in a, c) and amygdala (red arrow). The medial temporal lobe is seen enlarged with loss of gyro pattern and mild crus compression. (d) The mass is showing hyper intensity even on diffusion restrictions (red arrow).

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Figure 2:

Magnetic Resonance Imaging (MRI) T1 contrast (a) coronal, (b) axial, and (c) sagittalsections shows heterogeneous enhancement pattern. The proximal part seems cystic with well-defined enhancement of wall (red arrows in a-c).

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DISCUSSION

Secondary depression in cases of OCD is common. In the above case, depression manifested itself several years after the onset of OCD. A previous study reported over 30% of people with intracranial tumors had depression, and around 14% of men and 25% of women had severe obsessions. Moreover, anterior tumors were associated with more severe depression and obsessions were more severe in patients with a right than left anterior brain tumor.¹⁰

Although, in the current case the lesion first appeared in the left medial temporal lobe. This is not surprising, considering prior case studies on OCD with ICL have indicated lesions in various regions. Kumar et al.⁶ also reported similar case, the lesion initially in the left temporal lobe and later involved multiple areas. The lesion in our case was glioblastoma, whereas previously, glioma, dysgerminoma, and gliomatosis cerebri have been reported.^6-9 Patients with primary brain tumors often have been found to have depression.¹⁰ The probable causes may be elevated interleukins, interferon, and Tumor necrosis factor (TNF) rather than just a psychological reaction.^11,12 Therefore, the appearance of depressive features, especially in the absence of any history of a mood episode, may also be due to the brain tumor. According to earlier research, neurological symptoms may be lacking in patients with brain lesions.¹⁰ The current case has a similar scenario where neurological features were minimal. While previous literature has described sudden or rapid onset of OCS or depressive symptoms associated with neurological lesions, this report highlights an unusual combination of long-standing OCD, new-onset depressive symptoms, and glioblastoma multiforme — not previously reported to our knowledge. Similar cases, if encountered clinically, should be documented to strengthen the literature, support larger studies, and facilitate earlier detection and intervention to improve prognosis.

CONCLUSION

The case demonstrated a typical chronic course with gradual worsening of symptoms. As is often observed in OCD cases, depressive symptoms appeared later in the course, accompanied by some atypical features. While such presentations are relatively common in OCD, neuroimaging in this case allowed for early diagnosis of the brain lesion, even in the absence of abnormal laboratory parameters or significant neurological signs. The appearance of new depressive or atypical symptoms in a known case of long-standing OCD associated with glioblastoma multiforme is rare. These findings are particularly important in elderly patients and warrant detailed evaluation, including neuroimaging. Therefore, brain imaging should be considered a routine component of assessment in such cases. Furthermore, close interdisciplinary collaboration among psychiatry, neurosurgery, and oncology is essential, and future studies should be planned through active coordination across these specialties.