INTRODUCTION
Arachnoid cyst can be due to congenital, traumatic or inflammatory etiology. Usually it has a developmental origin. Arachnoid cyst develops when two layers of the arachnoid membrane do not unite in early fetal period, which is followed by accumulation of cerebrospinal fluid and cyst formation (1). Arachnoid cysts account for 1% of the intracranial space occupying lesions (2). The most common localization is middle cranial fossa (1). It is two times more frequent in right side of the brain (2-4). It is usually diagnosed during general medical evaluations (2,3). Main clinical findings include epilepsy, increased intracranial pressure, neurological deficit and macro cranium and developmental delay in children (5). Subdural hematomas are rare complications of arachnoid cysts (5). In the literature, knowledge on association between arachnoid cysts and psychiatric disorders is based on case reports (1,6,7).
Treatment of arachnoid cysts is controversial. Regarding complications of surgical treatments, conservative approaches are preferred in asymptomatic cases. Surgical interventions are advised in cysts which increase in size and cause neurological effects or become symptomatic via bleeding or hygroma (8).
In this case report, we presented a patient with left temporal, 33x17 mm, arachnoid cyst which does not compress neighboring tissues and does not lead to neurological signs who was treated successfully with ECT for major depressive disorder.
CASE
E.Y. was a patient who was 69 years old, illiterate, married with 6 children, and a housewife. She applied with demoralization, distress and abdominal pain complaints to our outpatient clinic. In her history, she stated sleep problems in the last two months, early waking, demoralization going on all day, significant loss of interest to all activities, abdominal pain, generalized body pain, lack of appetite and weight loss. Pessimism, guilt and suicidal thoughts were also present. She did not describe any psychosocial stress. The patient told that she had been using paroxetine 40mg/day for 2 months and that the treatment was not effective. Her psychiatric history revealed that, there were 3 past depressive episodes in the last 8 years and all episodes fully remitted after paroxetine treatment. She had cholecystectomy 40 years ago. There was no family history of psychiatric disorder.
In her psychiatric examination, she appeared older, her appearance was compatible with her socioeconomic status, and her self-care was decreased. Her mood was depressive and affect was anxious. Speech output was decreased. There were no perception problems and psychotic symptoms. Her thought content involved ideas of death and preoccupation with guilt. Her orientation was intact but she had problem in focusing and maintaining attention. Her sleep was decreased and psychomotor activity was slowed. Abstract thinking and calculation abilities were within normal range considering her age and education. Her insight and reasoning were intact.
Routine biochemistry, hemogram, sedimentation rate and thyroid function tests, vitamin B12 and folic acid levels, blood ammonia level and systemic physical examination were normal. Patient was diagnosed with major depression. Hamilton Depression Rating Scale (HAM-D) and Clinical Global Impression (CGI) scores were 31 and 7, respectively, during inpatient admission. Venlafaxine 75 mg/day and alprazolam 1.5 mg/day were initiated. Venlafaxine dosage was gradually increased to 150 mg/day in the second week of hospitalization. Venlafaxine dose was increased to 225mg for ongoing suicidal ideas and electroconvulsive therapy (ECT) was planned. Routine computerized brain tomography before ECT revealed left temporal, 33x17 mm cystic lesion in CSF density (arachnoid cyst). Neurological examination and consultation did not reveal any increased intracranial pressure signs. Cranial nerve examination was normal, deep tendon reflexes were normoactive and muscle power was 5/5 in upper and lower extremities. Brain surgery consultation did not suggest any surgical intervention. There was no papilledema. Radiology consultation revealed that the arachnoid cyst was not connected with ventricles and CSF. Since the patient did not respond to venlafaxine, paroxetine and alprazolam treatments and her suicidal ideas continued, it was decided to perform ECT. HAM-D was 28 and CGI was 6 before ECT. After informed consent was obtained from the patient and her relatives, bilateral ECT 3 times a week were initiated. Consciousness and orientation were assessed and neurological examination was done after each ECT session, no complication was detected. After second ECT session, suicidal thoughts disappeared and depressive symptoms began to improve. After seventh session of ECT, speech, energy and psychomotor activity of the patient were normal. Death ideas, somatic complaints and her preoccupations with guilt in her thought content improved completely. After thirty days of treatment, HAM-D was 3 and CGI was 1. Patient was discharged with venlafaxine 225 mg/day and alprazolam 0.75 mg/day treatment. CT imaging after her discharge did not reveal any changes in size or features of the arachnoid cyst.
DISCUSSION
Caution has been suggested when applying ECT to patients with intracranial masses (9). ECT may lead to some side effects by increasing intracranial pressure in patients with arachnoid cyst. Since some arachnoid cysts are connected to CSF, increased intracranial pressure during ECT may lead to enlargement of these cysts (10). After rupture of the cyst, patient may become symptomatic with subdural effusion, subdural hematoma or intrinsic bleeding (5). On the other hand, previous studies have suggested that, ECT may be safely administered, particularly in patients with meningioma or other tumors which do not cause increased intracranial pressure (9).
In the literature, 8 patients with intracranial arachnoid cysts were treated successfully with ECT; of these patients three were diagnosed with major depression and others were diagnosed with major depression with psychotic features, bipolar disorder, schizoaffective disorder, psychosis and catatonia (10-12). In three of these patients, ECT was administered after brain imaging did not reveal any growth of the cyst. In our report, arachnoid cyst was detected during routine pre-ECT CT and there were no prior brain images. ECT treatment was decided for presence of suicidal ideation and lack of treatment response. After seven sessions of ECT, there were no complications in the patient. Regarding this, the present case is the first in our country. This case shows that, if arachnoid cyst does not lead to increased intracranial pressure, edema or neurological signs and the cyst is not connected to CSF or ventricles, ECT may be an effective and safe treatment option.
REFERENCES
1. Bakim B, Karamustafalioglu KO, Ozalp G, Tankaya O, Kahraman N, Yavuz BG, Sengul HS. Arachnoid cyst and bipolar disorder: a case report. Journal of Mood Disorders 2012; 2:70-73. (Turkish)
2. Gosalakkal JA. Intracranial arachnoid cysts in children: a review of pathogenesis, clinical features, and management. Pediatr Neurol 2002; 26:93-98.
3. Gelabert-Gonzalez M. Intracranial arachnoid cysts. Rev Neurol 2004; 39:1161-1166.
4. Wester K. Gender distribution and sidedness of middle fossa arachnoid cysts: a review of cases diagnosed with computed imaging. Neurosurgery 1992; 31:940-944.
5. Parsch CS, Krauss J, Hoffmann E, Meixensberger J, Roosen K. Arachnoid cysts associated with subdural hematomas and hygromas: analysis of 16 cases, longterm follow-up, and review of the literature. Neurosurgery 1997; 40:483-490.
6. Bahk WM, Pae CU, Chae JH, Jun TY, Kim KS. A case of brief psychosis associated with an arachnoid cyst. Psychiatry Clin Neurosci 2002; 56:203-205.
7. Ozdemir B, Gulsun M. Arachnoid cyst and psychotic disorder: a case report. Düşünen Adam The Journal of Psychiatry and Neurological Sciences 2006; 19:217-220. (Turkish)
8. Santamarta D, Aguas J, Ferrer E. The natural history of arachnoid cysts: endoscopic and cine-mode MRI evidence of a slit-valve mechanism. Minim Invasive Neurosurg 1995; 38:133-137.
9. Weiner RD. American Psychiatric Association Committee on ECT. Electroconvulsive Therapy: Recommendations for Treatment, Training, and Privileging. Second Ed. Washington, DC: American Psychiatric Press, 2001.
10. Escalona PR, Coffey CE, Maus-Feldman J. Electroconvulsive therapy in a depressed patient with an intracranial arachnoid cyst: a brain magnetic resonance imaging study. Convuls Ther 1991; 7:133-138.
11. Perry CL, Lindell EP, Rasmussen KG. ECT in patients with arachnoid cysts. J ECT 2007; 23:36-37.
12. Desseilles M, Thiry JC, Monville JF, Ansseau M, Makhinson M. Electroconvulsive therapy for depression in a patient with an intracranial arachnoid cyst. J ECT 2009; 25:64-66.
