Bipolar disorder: the high hidden inside depression

Clinical Rounds, the GPAtlas podcast. Mental Health (MH). 11 minutes. Published 2 October 2026. Free to listen.

Clinical source: our own Ocean article "Bipolar Disorder", last reviewed 23 April 2026. Prompted by this week's paper, "How to spot bipolar hidden in depression early".

Transcript

Sarah: Hello, and welcome to GPAtlas Clinical Rounds. I am Sarah, and today we are looking at bipolar disorder, specifically how easily it stays hidden inside what looks like garden variety depression. Diagnostic delay in bipolar illness can stretch past ten years, and a lot of that time is spent in our consulting rooms, being treated for unipolar depression that simply refuses to get better. This week there has been fresh attention on the clinical signals that help us suspect it earlier: an onset in the late teens or early twenties, a family history of serious mood disorder, and psychotic features during low or high spells. The evidence does not claim to solve the whole diagnostic problem overnight, but it does sharpen the question we ought to ask before we reach for the prescription pad.

Ben: Let me bring in a consultation that landed on my list on a Tuesday morning. A twenty- three-year-old woman, Chloe, booked in for a medication review. She had been diagnosed with depression at nineteen by another practice, tried sertraline up to 100 mg daily with very little benefit, and was switched six months ago to citalopram 20 mg daily, which she had taken faithfully. She sat down, looked exhausted, and said, doctor, the dark cloud is completely back. I cannot face my job in graphic design, I am sleeping twelve hours a day and still cannot get out of bed, and nothing brings me any joy. Then she looked straight at me and said, my previous doctor said if this one did not work, we should double the dose or add something stronger. So I looked at her notes. Four separate presentations over four years, all coded as recurrent depressive episodes, each managed with a dose escalation or a selective serotonin reuptake inhibitor switch. It read like standard treatment-resistant unipolar depression. But Chloe is twenty-three, her symptoms started in her late teens, and when I looked closer at the timeline, there was a six-week stretch about eighteen months ago where she had dropped out of follow-up altogether. I asked her about that time, and she smiled faintly and said she had not needed the surgery back then because she had never felt better in her life. She said she had stayed awake for five days straight, designing an entire online clothing collection, spending four thousand pounds on fabric on her credit card, and talking so fast her housemates complained they could not get a word in edgeways. At the time, she just thought the antidepressant had finally kicked in.

Sarah: That is the classic story, Ben, and it gives me a shiver every time I hear it. The patient experiences hypomania as recovery, not as pathology. Why would someone volunteer feeling creative, energetic, and confident as a symptom, especially when they have been dragging themselves through severe low mood for months? That is why the history in these presentations has to be proactive. In anyone sitting in front of us with recurrent depression, an early age of onset, or a poor response to first-line agents, we have to ask directly about periods of elevated or irritable mood lasting four days or more. Four days is the threshold for hypomania, whereas a full manic episode lasts at least seven days, or less if hospital admission is required. You have to ask specifically about sleep. Not just insomnia, but a reduced need for sleep while feeling totally energised. When people have true insomnia, they are exhausted and frustrated. In hypomania, they sleep three hours, jump out of bed at four in the morning, and start rearranging the furniture or launching a business. We must also ask about racing thoughts, pressured speech, grandiosity, and impulsive or high-risk behaviours, like spending sprees, reckless driving, or sexual indiscretions that are completely out of character. Then we look at modifiers. Family history is paramount. Is there bipolar disorder, psychosis, or severe recurrent depression in first-degree relatives? Has there ever been an episode triggered immediately by starting an antidepressant? Have there been postpartum mood swings or psychotic episodes? In terms of Chloe, you also need to screen thoroughly for psychotic symptoms during both her highs and her lows, looking for auditory hallucinations or persecutory and grandiose delusions, and evaluate current suicidal ideation and intent.

Ben: Absolutely, Sarah. And the examination side cannot be neglected, even though this is psychiatric. On mental state examination, I assessed Chloe's appearance, psychomotor retardation, speech rate and volume, thought content, and suicidal intent. Her mood was objectively low and flat, thought form was coherent, there were no delusions or hallucinations, and she denied active suicidal plans, though she felt utterly hopeless. But physical assessment matters just as much. Bipolar disorder carries a substantial cardiometabolic burden, partly from the illness itself and partly from the medications used to treat it. If this turns out to be bipolar disorder, secondary care will likely consider atypical antipsychotics or lithium. So I checked her pulse, her blood pressure, her weight and body mass index, and waist circumference right there in the room. Then I arranged baseline blood tests: a full blood count, urea and electrolytes, estimated glomerular filtration rate, liver function tests, serum calcium, thyroid function tests, fasting glucose or haemoglobin A-1-C, and a lipid profile. If she is destined for lithium, that baseline renal, calcium, and thyroid profile is non-negotiable, along with a baseline electrocardiogram, an E-C-G. The other crucial element of workup is substance use. Alcohol, excess caffeine, and illicit drugs like cocaine or amphetamines can mimic hypomanic states or severely destabilise an underlying mood disorder. Chloe reported she rarely drank and used no illicit substances, which made her timeline much clearer.

Sarah: Now, let us get into what changes in clinical practice. The traditional instinct in primary care when an antidepressant fails is to escalate: push citalopram from 20 mg to 40 mg, or add mirtazapine, or switch to venlafaxine. If Chloe has bipolar disorder, prescribing an antidepressant alone, especially escalating it, risks triggering a rapid switch into mania, mixed states, or destabilising the illness into rapid cycling. What changed in your consulting room on Monday was that you hit the pause button on antidepressant monotherapy. Diagnosis of bipolar disorder and initiation of disease- modifying treatment are strictly secondary care responsibilities. A G-P does not make the formal diagnosis de novo, and we do not initiate mood stabilisers in primary care without specialist guidance. So the immediate action for Chloe was an urgent referral to the community mental health team, specifying the recurrent depressive episodes, the early onset, and this clear historical period of four or more days of sustained overactivity, decreased sleep, and impulsive spending. In terms of her citalopram 20 mg, you do not abruptly stop it, as that causes severe discontinuation symptoms, but you certainly do not increase it. You explain your suspicion gently to her, prepare her for specialist evaluation, and agree a safety netting plan. You explain that while we wait, protecting her sleep pattern is essential. Sleep deprivation is one of the most potent triggers for acute mood swings. Once secondary care confirms the diagnosis, their first-line approach for bipolar depression might involve specialist-initiated quetiapine, olanzapine, or lamotrigine, with slow titration to avoid severe cutaneous reactions. If an antidepressant is ever used in bipolar disorder, it must be paired with an antimanic cover agent, never given alone.

Ben: And once that specialist assessment happens, the long-term management lands right back with us in general practice. That is the critical point: the psychiatrist makes the diagnosis and starts the drug, but the G-P holds the long game. Relapse prevention is anchored by lithium first-line. And lithium is a drug that demands meticulous primary care vigilance. We must always prescribe it by brand name, such as Priadel or Camcolit, because preparations have different bioavailability and are not interchangeable. It has a very narrow therapeutic window: the standard maintenance target is 0.6 to 0.8, though a target of 0.8 to 1.0 may be used for at least six months if the patient has relapses or subthreshold symptoms. Plasma lithium levels must be measured exactly twelve hours post- dose. When someone starts or changes dose, we check levels one week later and weekly until stable, then three-monthly for the first year, and six-monthly thereafter. Alongside that, we must check urea and electrolytes, estimated glomerular filtration rate, serum calcium, and thyroid function tests every six months, because long-term lithium risks nephrogenic diabetes insipidus, chronic renal failure, hypothyroidism, goitre, and hyperparathyroidism. Then there is the annual physical health check: body mass index, blood pressure, lipids, and haemoglobin A-1-C. If Chloe is eventually stabilised on lithium, we also have to educate her on drug interactions. Prescribing an N-Said, an A-C-E inhibitor, an angiotensin receptor blocker, or a thiazide diuretic can precipitate acute lithium toxicity by reducing renal clearance. Dehydration from an intercurrent illness will do the same.

Sarah: Let us highlight the big pitfall here, Ben, because it happens in every practice across the country. The pitfall is assuming that a patient returning with chronic, unresponsive depression simply has difficult unipolar illness and escalating their antidepressant therapy without screening for past highs. It is so easy to fall into the trap of doing a quick nine-question depression score, seeing a high number, and thinking, well, sertraline 50 mg did not work, let us go to 100 mg, then 150 mg, then switch to a dual-action drug. If you do not ask, the patient will almost never tell you about their hypomanic periods. They remember those times as the brief windows when they were finally happy, productive, and outgoing. They do not see them as an illness. Unless you explicitly ask, have you ever had days where you felt unusually wired, needed very little sleep, your thoughts were racing, and you took risks with money or relationships, that history will stay buried. Another critical pitfall is missing early signs of lithium toxicity in established patients. A patient presenting with a coarse tremor, vomiting, diarrhoea, unsteady gait, slurred speech, or confusion must have an immediate lithium level checked and urgent specialist or emergency medical review. Never write off a new tremor in a lithium-treated patient as simple anxiety or an essential tremor.

Sarah: Here are three practical points to take into your clinic on Monday. First, in any patient presenting with recurrent depression, an onset under twenty-five, or a poor response to treatment, ask directly about past periods of elevated mood, reduced need for sleep, and overactivity lasting four days or more. Second, never escalate or switch antidepressant monotherapy if you suspect bipolarity; refer to secondary care, who lead diagnosis and initiation. Third, when managing shared care for patients on lithium, prescribe strictly by brand, check twelve-hour post-dose levels every three to six months, monitor renal, thyroid, and calcium function half-yearly, and beware of drugs that reduce lithium clearance, especially N-Saids and A-C-E inhibitors.

Ben: Thank you for listening to GPAtlas Clinical Rounds. Keep an eye out for those hidden highs in your depression reviews this week, look after yourselves, and join us again next time.

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