Arachnoid Cyst Causing Depression and Neuropsychiatric Symptoms: a Case Report

Abstract

Arachnoid cysts are benign space-occupying brain lesions that contain cerebrospinal fluid. Most cases are congenital in origin, caused by failed fusion of the arachnoid membrane early in fetal development. Cases are often incidentally detected on neuroimaging; however, rarely patients present with neuropsychiatric manifestations when cysts expand and cause a midline shift, compression of nearby brain tissue or cerebrospinal fluid compartments or both. We report a case of a 56-year-old woman with no past history or family history of psychiatric illness who developed acute-onset right-sided weakness, depressive symptoms, and other neuropsychiatric deficits. A diagnosis of organic mood disorder caused by an arachnoid cyst was made. Her symptoms and neuropsychiatric deficits remitted after cyst marsupialisation by open craniotomy. Therefore, it is important to investigate the organic aetiology in elderly patients who present with simultaneous mood disorder and cognitive dysfunction.

Introduction

Arachnoid cysts are benign space-occupying brain lesions that contain cerebrospinal fluid and account for 1% of all intracranial space-occupying lesions.¹ Most of these are primary cysts arising from congenital defects of cortical formation or as anomalies in the leptomeninges,² whereas secondary cysts arise from trauma, infection, or neoplasia. Enlargement of arachnoid cysts can be caused by fluid secretion from ependymal cells, fluid ingress secondary to an osmotic gradient, trapping of fluid by a ball/valve mechanism,³ and strenuous venous pulsation produced during Valsalva manoeuvres.⁴ Arachnoid cysts are more common in males than females with a prevalence ratio of 3:1.⁵

Tumours in the frontal lobe may result in apathy, disinhibition, euphoria, depression, dementia, lack of concern, poor judgement, disorientation, poor attention and concentration, personality changes, weakness of contralateral limbs, motor aphasia, and urinary incontinence.⁶ Damage to the ventromedial prefrontal cortex leads to impulsivity.⁷ Prefrontal lesions cause deficits in searching for spatio- temporal information.⁸ Lesions in the cerebral falx that involve bilateral medial aspects of the frontal lobe result in attention deficits in complex tasks.⁹ Vascular dementia in the frontal lobe results in dementia, lack of volition, emotional lability, small-stepped gait, dysarthria, and urinary incontinence.¹⁰ Left frontal astrocytoma can cause symptoms such as anxiety and obsessive behaviour,¹¹ as well as faecal incontinence and epileptic attacks.¹² Frontal lobe tumours on the right side may result in euphoria, poor attention and concentration, and poor judgement.¹³ Damage to structures functionally connected to the orbitofrontal cortex in the right hemisphere is associated with secondary mania.¹⁴ Pathology in the temporal lobe can cause pure amnesia,¹⁵ psychoses such as auditory hallucination, self- injurious behaviour,¹⁶ and schizophrenia.¹⁷ Damage to the parietal lobe may cause schizophrenia-like psychosis with severe paranoid delusions and delusions of reference, auditory hallucinations,18 and conversion.¹⁹ Occipital lobe tumours may cause visual hallucinations, auditory hallucinations, abnormalities in smell and taste, and increased intracranial pressure.²⁰

Case Presentation

In October 2014, a 56-year-old woman, who was illiterate and widowed, presented to the Department of Psychiatry at Yenepoya Medical College and Hospital, Mangalore, India. She had a 45-day history of weakness on her right-side body and face, slurring of speech, memory disturbances, low mood and loss of interest in work, frequent crying spells, social withdrawal, motor restlessness, poor self- care, reduced appetite, insomnia, irritability, disinhibited behaviour, and urinary incontinence.

On mental status examination, she had poor eye contact, dysphoric facial expression, and reduced speech rate and volume. Her thinking was retarded. She expressed feelings of worthlessness, hopelessness, and death wishes. Cognitive function tests were conducted (Table). The patients had perseveration in all frontal lobe tests and impairment in all parietal lobe tests. Temporal lobe tests showed that her immediate and recent memory was impaired, and she had a concrete level of thinking but poor insight. Both social and personal judgement was impaired.

Computed tomography and magnetic resonance imaging of her head showed a well-defined cystic lesion with a wall and septation within the left frontal lobe (Figure).

The patient was treated with sertraline with dose titrated to 100 mg in 3 weeks and she underwent cyst marsupialisation by open craniotomy. The cyst showed presence of pale white membranous tissue. Microscopically, the cyst wall contained fibrocollagenous tissue and was lined by a single layer of uniform flat cells, suggestive of arachnoid cyst. Fluid cytology showed few red blood cells, occasional degenerating inflammatory cells, and no malignant cells.

Postoperatively, the patient's recovery was uneventful, and her symptoms gradually resolved over 45 days of follow-up.

Discussion

In our patient, the arachnoid cyst was most likely congenital in origin because there was no history of head trauma. The recent cyst enlargement might have led to the manifestation of symptoms. Because there was no history of stressors, family history of mood disorders, and the age of onset was not typical of depression, a diagnosis of organic depressive disorder (International Classification of Diseases 10 code: F 06.32) caused by an arachnoid cyst was made. The patient's depressive symptoms began almost simultaneously with other neuropsychiatric symptoms. Thus, we ruled out stress secondary to the disability and knowing of the neurosurgical diagnosis.

Like other patients with frontal lobe lesions, our patient presented with mild weakness, cognitive deficits, disinhibited behaviour, urinary incontinence, and depression. This is consistent with a case report that described associations of right frontal lobe lesions with euphoria, and left frontal lobe lesions with depression and abulia.²¹ This laterality is based on the phenomenon of mood elevation when the left prefrontal cortex is activated. Thus, a left prefrontal lesion leads to depression. In addition, cognitive dysfunction occur more commonly with left frontal lobe lesions than right frontal lesions. Although our patient was treated with sertraline, significant improvement in neuropsychiatric symptoms occurred only after cyst decompression surgery, similar to previous reports in the literature.^22-24

Arachnoid cysts may lead to reversible impairments in cognition, executive function, and mood (depression or mania, depending on the laterality of the lesion). Surgical intervention to decompress the cyst can achieve significant improvement of the symptoms. It is important to investigate the organic aetiology in elderly patients who present with simultaneous mood disorder and cognitive dysfunction.

Declaration

The authors have no conflicts of interest to disclose.

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