Electroconvulsive therapy (ECT) has long been the criterion standard treatment modality for mood disorders refractory to psychopharmacologic management, with a well-established safety and efficacy profile. One observation of interest in the decades of research surrounding ECT has been the transient elevation in intracranial pressure (ICP) seen intraoperatively. Despite new research calling into question ECT's role in this physiologic effect, this collateral effect remains one of the few contraindications still in place today; however, they remain only relative.1 The pathologies that give providers pause in recommending ECT remain those that disturb homeostatic ICP; traditionally, these include central nervous system neoplasms, recent stroke, and idiopathic intracranial hypertension (IIH). Despite the significant incidence of co-occurring mood disorders in these disease processes, many patients go untreated despite otherwise being excellent candidates for ECT. A growing body of literature, however, has recognized ECT being safely delivered to patients experiencing ICP-altering pathologies, with good efficacy. A decision to treat thus should be based on a case-by-case basis specific to patient type and severity of psychiatric disease, counter balanced with patient goals of care and status of cranial pathophysiology.
Historically, safety data surrounding treatment of patients with comorbid IIH have lagged behind those of its counterparts (eg, neoplastic processes), with only 2 documented cases in the literature today.2,3 Recent studies have shown the prevalence of mood disorders in patients with IIH to be as high as 45%, and this cohort has demonstrated significant resistance to traditional therapies when compared with those without IIH experiencing mood disorders.4 In recognition of the substantial need to continue documenting safe treatment of those with IIH and mood disorders with ECT, we report our own case of a patient with IIH (with unique features relevant to new literature) and severe major depressive disorder who received several treatments of ECT. She possessed the empty sella sign on imaging, which holds unique relevance in the literature.4 Albeit at first resistant to treatment, over time, her affect has stabilized, and symptom severity has decreased, with no change from baseline ICP status. With appropriate multispecialty care, the benefit to functional status of ECT in our patient was substantial and quantifiable, while the risks remained negligible.
The patient is a 28-year-old woman who first presented to the outpatient psychiatric clinic in early 2021 at the request of her neurologist. Her neurologic symptoms were diffuse headaches that worsen with postural changes (ie, leaning forward), along with episodes of transient blurred vision, photosensitivity, and halos around lights. She also endorsed back pain and paresthesias. The patient was started on acetazolamide 500 mg and topiramate 75 mg daily. The brain Magnetic Resonance Venography displayed transverse sinus stenosis, and the magnetic resonance imaging of the brain showed partial empty sella syndrome along with optic nerve head flattening, orbital CSF distention, and optic nerve tortuosity. At follow-up examination, she noted resolution of blurry vision episodes but continuation of postural headaches that reach 10/10 on the pain scale. Lumbar puncture revealed an opening pressure of 24 mmH2O. The patient was referred for occipital nerve block and to neuro-ophthalmology for further evaluation. Baseline optic disk evaluations were negative for papilledema, but right-sided optic nerve elevation confirmed a history of elevated ICP.
Our patient first presented to the outpatient psychiatric clinic in early 2021 for medication management of major depressive disorder. She was first diagnosed in 2016 at an outside hospital with major depressive disorder and had failed trials of multiple medications, including aripiprazole, sertraline, quetiapine, escitalopram, fluoxetine, venlafaxine, mirtazapine, topiramate, and lurasidone. She reported one suicide attempt in 2020 before establishing in our system and one hospitalization for suicidal ideation. Her symptoms at the visit included anhedonia, 3 hours of sleep nightly, low energy, feelings of worthlessness, and low appetite to where she eats only 4 of 7 days weekly. Upon further questioning, our patient revealed that she was a victim of childhood trauma and over the past 2 months began to have nightmares, flashbacks, and avoidance of areas associated with the trauma. She also reported experiencing auditory and visual hallucinations of the perpetrators affiliated with her past trauma. She was diagnosed with severe, recurrent major depressive disorder with psychotic features and started on duloxetine 60 mg, with a future appointment to evaluate for ECT versus transcranial magnetic stimulation.
Interventional psychiatric evaluation deemed the patient an excellent candidate for ECT considering the presence of co-occurring psychotic features with depressive symptoms. Baseline Patient Health Questionnaire-9 was a 27/27. Because of the severe and refractory nature of her disease process and the deteriorating course, the benefit of treatment far surpassed the potential, relative risks as described for this procedure, particularly with multidisciplinary support from appropriate specialists (eg, neuro-ophthalmology, neurology, anesthesiology). The patient received an index series of 15 bitemporal treatments of ECT, continuing with a continuation phase afterward given good tolerance and improvement in depressive symptoms. The Patient Health Questionnaire-9 scores recorded before each treatment session are revealed remitted status by the end of the ECT series. Electroconvulsive therapy was delivered via a Thymatron System IV, with device settings of 45% energy and pulse widths of 0.5 ms. In addition, during the course of the patient's index series of ECT, she returned to her neuro-ophthalmologist for 3 serial intraocular pressure measurements, after treatments 3, 4, and 5, to ascertain whether she experienced an increase in intraocular pressure. While at first refractory, the patient has shown significant improvements in mood, energy, as well as cessation of auditory and visual hallucinations. This was confirmed by family members who have accompanied her to treatment. Her symptoms of PTSD are also in remission. Mild immediate postoperative complications of headache and infrequent amnesia are present. No intraoperative or long-term complications have developed. Follow-up retinal imaging revealed no changes in optic nerve elevation nor other signs of increased ICP from her baseline.
We deduce that ECT has been safe in our patient, who has received an index series of 15 bitemporal treatments as well as a continuation phase of 23 bitemporal treatments, with no change in neuro-ophthalmologic examination from baseline detected by serial intraocular pressure measurements in the midst of the patient's index series. Our foremost aim is that our case adds another key piece of evidence to the 2 case reports in the literature concerning safety of ECT in individuals with IIH, particularly those with demonstrated empty sella syndrome. Several key differences remain in our report that have currently unknown levels of significance. Adam et al2 and Moreno et al3 both reported patients who received 9 unilateral treatments, whereas our patient has completed 38 total bitemporal treatments with still no change in baseline ICP status.
Both Adam et al2 and Moreno et al3 described patients whose IIH symptoms paradoxically responded to ECT (whereas the contemporary thought would be an increase in ICP brought about by ECT treatment would worsen the symptoms). Another case report detailed remission of IIH with simple selective serotonin reuptake inhibitor therapy targeting the patient's mood symptoms.5 Although our patient's mood disorder symptoms have begun to remit, her IIH-related symptoms (ie, postural headaches) have not shown a response correlated to psychiatric treatment.
This case also demonstrates the only known documented case in the literature of a patient with an empty sella syndrome safely receiving and responding to ECT. The empty sella syndrome remains as of now the only significant difference possessed by patients with mood disorder compared with patients without mood disorder who went on to be diagnosed with IIH. The prevailing theory is that occult pituitary compression could lead to inherent disruption of the hypothalamic-pituitary-adrenal axis (HPA), perhaps through interference of cortisol pathways.4 This disturbance would lead to a prodromal mood disorder before classical IIH symptom onset. Similarly, multiple studies have demonstrated that ECT significantly activates the HPA axis with cortisol, adrenocorticotropic hormone, and vasopressin levels increased.4 It is unclear to how ECT's HPA axis activation may intersect with symptoms from pituitary compression. No follow-up brain imaging has been performed on our patient.
More case reports related to those who possess both IIH and mood disorders may help us understand more about the pathologies effect on mood and variation in efficacy of the therapies themselves. We encourage others to continue publishing their experiences and findings with this vulnerable and undertreated population. We conclude that with multidisciplinary care from psychiatry and neurology, combined with interval neuro-ophthalmology examinations, patients with IIH experiencing refractory mood disorders should readily be evaluated for ECT, because treatments can be safely delivered with appropriate preoperative planning and management with appropriate intraoperative and postoperative monitoring.
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2. Adam LA, Crowe RR. Use of ECT in idiopathic intracranial hypertension. J ECT
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3. Moreno MV, Cruz MR, CRM R, et al. Successful electroconvulsive therapy in a drug-refractory depressed patient with idiopathic intracranial hypertension. J ECT
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4. Puustinen T, Tervonen J, Avellan C, et al. Psychiatric disorders are a common prognostic marker for worse outcome in patients with idiopathic intracranial hypertension. Clin Neurol Neurosurg
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5. Ross DR, Coffey CE, Massey EW, et al. Depression and benign intracranial hypertension. Psychosomatics
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