Thyroid Function in Psychiatric Illness
True thyroid dysfunction can present with symptoms as wide-ranging as depression, mania, psychosis, or poor cognition. Thus, we psychiatrists commonly order thyroid function tests for our psychiatric patients, as well as for medical patients with psychiatric symptoms. A recent review, however, notes that lab abnormalities suggesting thyroid dysfunction may not actually signify true thyroid disease. In fact, a wide spectrum of medical illnesses, psychiatric conditions, and medications can all affect thyroid function. Abnormal thyroid function in a depressed patient, for example, may simply reflect the impact of depressive illness upon thyroid function rather than vice versa (Dickerman AL and Barnhill JW, Am J Psychiatry 2012;169(2):127–133).
According to the literature review, the term “non-thyroidal illness” is used to describe abnormal thyroid function secondary to medical or psychiatric conditions. It’s quite common, occurring in 7% to 33% of patients hospitalized for psychiatric disorders. The specific thyroid lab findings among psychiatric patients can vary substantially. The most common finding is hyperthyroxinemia (elevated total and free T4) among patients with mood disorders, which may be due to redistribution of T4 out of tissues or due to hypersecretion of TSH by the hypothalamus during acute mood episodes. Other alterations can also be seen. Stimulants can increase TSH and total T4 levels while opioids can increase total T4 and T3 levels. Lithium can cause true hypothyroidism, while carbamazepine increases metabolism of thyroid hormones in the liver. Thus, patients on carbamazepine who take thyroid supplementation may require higher replacement doses.
The pathophysiology of non-thyroidal illness is not well understood, but it’s clear that abnormal thyroid function tests do very little to guide treatment decisions in psychiatric or acutely ill medical patients. In fact, thyroid function typically normalizes after treatment of the underlying condition. As a result, the authors suggest that psychiatric patients should only be screened for thyroid dysfunction if there’s a clinical reason to suggest it, such as signs or symptoms of actual thyroid disease (eg, goiter; hypothermia; unexplained tachycardia; muscle weakness) or relevant risk factors (eg, autoimmune disorder, lithium history, family history of thyroid disease).
TCPR’s Take: Routine testing of thyroid function among psychiatric and medical patients without signs or risk factors for thyroid disease often yields abnormal results in the absence of actual thyroid dysfunction, and treatment of the abnormal result is generally unnecessary. Sound clinical judgment should be used when ordering and interpreting thyroid function testing.
Deep Brain Stimulation: A New Somatic Therapy for Depression?
Deep brain stimulation (DBS) has suddenly begun popping up in both the medical journals and the mainstream media as a potential treatment for treatment resistant depression. DBS involves the placement of tiny electrodes in the brain that deliver pulses of current and modulate activity of certain neural pathways. For many years, neurologists have used DBS to treat Parkinson disease and other movement disorders, and it has been used experimentally in some cases of depression and OCD. Several groups have already shown that stimulation of the subcallosal cingulate gyrus—an area known to be overactive in depression—can have an antidepressant effect (Lozano AM et al, Biol Psych 2008;64(6):461–467). Most of the existing trials, however, were small, uncontrolled pilot studies. A recently published study offers additional evidence for a DBS effect in depression—including bipolar depression.
Investigators surgically implanted electrodes in the bilateral subcallosal cingulate of 17 adult patients with treatment-resistant unipolar or bipolar depression. All patients received open-label continuous stimulation for up to two years. Patients were permitted to continue antidepressant medication or therapy, but dose increases weren’t allowed during the first 24 weeks of the trial. There was a noticeable antidepressant effect of DBS in all patients, with gradual improvement in symptoms at 24 weeks, one year, and two years. In fact, after two full years of active stimulation, HAM-D scores had improved by an average of 70%. Nearly all (92%) patients showed a response (a decrease of >50% in HAM-D) and just over half (58%) entered remission (HAM-D score <8), with no spontaneous relapses of depression.
All patients had tried numerous antidepressants and had experienced at least a 12-month depressive episode prior to the trial, so these results are promising. However, there was no long-term control group, so it is unclear whether the long-term benefit was due to DBS or to medications, therapy, or the natural course of disease. All patients underwent a blind “sham” period immediately after the surgery; no current was delivered and no antidepressant effect was observed, but the sham phase was only four weeks in duration, making it difficult to draw a conclusion regarding a longer-term outcome.
There were few adverse events. Some, understandably, were from the surgery itself, while other minor complaints (nausea, headache, tingling in the hands) were most likely from the ongoing stimulation. The only side effect directly related to the device was infection in one patient. Two patients attempted suicide, but no one became manic or hypomanic, even those with bipolar depression. Interestingly, one patient accounted for 75% of the serious adverse events.
The investigators initially planned to include a discontinuation phase, during which patients would be observed for four weeks after the current was turned off. Three patients entered this phase, but all three reported increased suicidal ideation (and responded, but only gradually, when stimulation was restarted), so this phase was eliminated from the design for the rest of the patients (Holtzheimer PE et al, Arch Gen Psych 2012;69(2):150–158).
TCPR’s Take: Several reports have shown DBS to be a safe and effective therapy for treatment-resistant depression. However, it’s an invasive procedure with its own unique risks, and it’s still not clear how much of patients’ improvement can be attributed to DBS. Also, discontinuation seems to be associated with rapid relapse. Nevertheless, DBS may represent a helpful adjunct to other interventions and deserves further controlled study as a novel somatic therapy for depression.