Thyroid Scan Uncovers Graves’ Disease Behind Treatment-Resistant Panic Attacks

For five weeks, doctors treated a 30-year-old woman for a psychiatric illness she did not have. She was waking at night screaming, gripped by panic attacks so severe and so resistant to medication that clinicians cycled her through a benzodiazepine and two different antidepressants — alprazolam, venlafaxine and trazodone — while her symptoms persisted unabated. The breakthrough came not from a psychiatric reassessment but from nuclear medicine: a scan that traced a radioactive tracer into her thyroid revealed the true culprit, Graves’ disease, an autoimmune disorder that was, in effect, flooding her nervous system with stress signals. The case, reported in the Wiley open-access journal Clinical Case Reports, is a vivid reminder that the border between psychiatry and endocrinology can be far blurrier than either specialty likes to admit — and that a single functional imaging study can end a diagnostic ordeal that repeated blood tests could not.

The woman’s symptom list read like a bewildering map of the autonomic nervous system. She experienced progressive shortness of breath, palpitations, muscle spasms and pins-and-needles sensations in her hands, feet and even her scalp, layered on top of chronic headaches, insomnia and severe nocturnal agitation. On examination, clinicians noted subtle but telling signs: mild bulging of both eyes — exophthalmos, a hallmark of Graves’ ophthalmopathy — fine tremors of the hands and persistent restlessness. Her pulse ran at roughly 110 beats per minute, her blood pressure remained normal, and she had shed about 2.5 kilograms over the preceding months without dieting. She reported no smoking or drug use and no family history of autoimmune thyroid disease. Because the neuropsychiatric features so thoroughly dominated the picture, she had already been evaluated and treated by multiple healthcare providers on the presumption of a primary panic or anxiety disorder before anyone examined her thyroid with real intent.

The initial workup cast its net wide, and every conventional test came back clean. Given the combination of chronic headaches, tremor and paresthesia at multiple sites, neurologists pursued possible central nervous system disease: a lumbar puncture was performed to exclude infection, inflammation or demyelinating disorders such as multiple sclerosis, and the cerebrospinal fluid — opening pressure, cell count, protein, glucose and cultures — proved entirely unremarkable. Comprehensive blood screening revealed only a mild iron deficiency anemia, with a hemoglobin of 12 grams per deciliter and a ferritin of just 10 nanograms per milliliter against a reference range of 13 to 150; iron and folic acid supplements were started, though the deficiency was far too slight to explain the severity of her autonomic and neuropsychiatric storm. Abdominal and pelvic CT imaging and a chest radiograph were equally unrevealing. Each negative result eliminated a suspect while leaving the most frightening symptoms — and their source — unexplained.

The first substantive clue came from the laboratory, and then it began to waver. Thyroid function tests repeated at three-day intervals drew a shifting picture. On day one the results showed overt hyperthyroidism: thyroid-stimulating hormone (TSH) suppressed to 0.22 microunits per milliliter against a reference range of 0.35 to 4.94, triiodothyronine (T3) elevated at 3.1 nanomoles per liter, and thyroxine (T4) high at 160 nanomoles per liter. By day four all three values had drifted back into the normal range; by day seven TSH sat at a comfortable 1.59 while T4 crept above range again at 154. This biochemical flickering between frank thyrotoxicosis and apparent euthyroidism created genuine uncertainty about what was happening inside the gland. Was this evolving Graves’ disease, in which immune-driven stimulation pushes the thyroid into hormone overproduction, or a transient thyroiditis, in which inflamed follicles rupture and leak preformed hormone into the circulation before settling? The distinction is far from academic: the two conditions call for opposite treatments, and mistaking one for the other can prolong illness or cause iatrogenic harm.

Graves’ disease is the most common cause of hyperthyroidism worldwide, and its core mechanism is well charted. The immune system manufactures stimulatory antibodies that bind the thyroid-stimulating hormone receptor, mimicking the pituitary hormone TSH and commanding the gland to grow and pour out thyroid hormone. The textbook presentation — racing heart, unexplained weight loss, heat intolerance and tremor — is widely taught, but the disease’s phenotypic range is notably varied, and it can announce itself as a purely neuropsychiatric illness. The report outlines why: excess thyroid hormones heighten the sensitivity of central and peripheral tissues to catecholamines by increasing the expression and activity of β-adrenergic receptors, generating palpitations, tremor, hyperarousal and anxiety states that closely mimic panic disorder. Thyroid hormone also acts directly on the brain, modulating serotonin, dopamine and norepinephrine systems that govern mood and emotional processing, while autonomic dysregulation — sympathetic overactivity paired with impaired parasympathetic modulation — has been implicated in the anxiety, disturbed sleep and nocturnal terror that hyperthyroid patients frequently describe.

Along the way, the diagnostic team systematically eliminated rival explanations. Primary psychiatric disorders — panic disorder and generalized anxiety disorder — headed the list, but the persistence of autonomic symptoms, tremor and the eye findings despite psychiatric treatment argued against them. Pheochromocytoma, a catecholamine-secreting adrenal tumor capable of producing identical panic-like surges, was considered; so were hypoglycemia and electrolyte imbalances, both excluded by routine biochemistry. Silent and subacute thyroiditis remained live possibilities given the wavering hormone levels, while toxic multinodular goiter and solitary toxic adenoma were judged less likely on structural and imaging grounds. Factitious thyrotoxicosis — the surreptitious ingestion of thyroid hormone — was deemed improbable given the absence of exogenous hormone use, and iron deficiency-related neuropathy, raised because of the low ferritin, was considered insufficient to account for the breadth and severity of the manifestations. Each eliminated possibility narrowed the field toward the thyroid, yet the fluctuating laboratory values continued to obscure precisely which thyroid condition was at fault.

With serology wavering, ophthalmopathy present and the clinical severity outrunning the laboratory values, her physicians turned to functional imaging. A thyroid scintigraphy was performed using 5 millicuries of technetium-99m pertechnetate, a radiotracer that the thyroid concentrates through the same transport machinery it uses to harvest dietary iodine. The scan revealed a mildly to moderately enlarged gland with uniformly increased radiotracer uptake throughout both lobes — the diffuse, homogeneous glow that is the imaging signature of Graves’ disease. That single pattern effectively excluded the leading alternative: in destructive thyroiditis, inflamed and ruptured follicles cannot concentrate the tracer, so uptake is characteristically reduced even as blood hormone levels run high. A toxic adenoma or toxic multinodular goiter would have produced focal, patchy hot spots rather than uniform activity, and factitious thyrotoxicosis likewise yields suppressed uptake. Thyroid ultrasound had shown only mild diffuse enlargement with preserved texture and no nodules, while the mild bilateral exophthalmos — autoimmune infiltration of the tissue behind the eyes — had been present all along as a quiet clue pointing toward the correct diagnosis.

Once the scan settled the question, treatment advanced on two fronts. The patient began methimazole, an antithyroid drug that blocks hormone synthesis, at 5 milligrams three times daily, with the dose tapered stepwise over roughly eighteen months as serial thyroid function tests guided therapy; she now takes the medication only about twice a week. To blunt the adrenergic storm she received propranolol, a beta-blocker that muffles the exaggerated tissue response to catecholamines, starting at 10 milligrams twice daily, then reduced to an as-needed basis and ultimately discontinued altogether. The outcome was unambiguous. Across the eighteen-month follow-up, the panic attacks, night terrors, palpitations, paresthesia and tremor gradually faded until none remained. Thyroid function is now checked every three months and she stays under regular specialist supervision. The psychiatric symptoms that had resisted anxiolytics and antidepressants dissolved not through further psychotropic adjustment but by shutting down the hormonal engine that had been driving them — the strongest evidence that the panic disorder label was, from the start, an endocrine disease in disguise.

The case is not the first to document Graves’ disease wearing a psychiatric mask. The report cites a 2021 account in BioPsychoSocial Medicine in which Yasuda and colleagues described a 34-year-old woman with pre-existing diagnoses of panic disorder and bipolar illness whose evolving Graves’ disease was initially misread as panic attacks; by the time thyroid testing was finally obtained she was in thyroid storm, a life-threatening endocrine emergency, and required steroids, antithyroid drugs and radioactive iodine to recover. Another cited report, by Yamaguchi and colleagues, described a 38-year-old woman whose Graves’ disease surfaced as drooping eyelids, double vision, tremor and paresthesia and turned out to be complicated by ocular myasthenia — yet another illustration of the disorder’s talent for impersonating primary neurological conditions. In emergency departments and triage settings, the author warns, the overwhelming sense of impending doom that accompanies both panic disorder and thyrotoxicosis can steer clinicians prematurely toward psychotropic therapy, masking the endocrine disease underneath and postponing definitive treatment — sometimes with dangerous consequences.

The report is candid about its own limits: thyroid receptor antibody assays, the serological mainstay for confirming Graves’ disease, were never performed during the diagnostic evaluation. The treating physician, facing a prolonged symptomatic course, marked autonomic and neuropsychiatric manifestations and fluctuating thyroid function tests, prioritized rapid functional clarification, and selected scintigraphy as a readily available modality capable of distinguishing Graves’ disease from thyroiditis in a single examination. That decision, the author argues, illustrates a broader principle: when clinical findings and biochemical data tell conflicting stories, functional imaging can arbitrate. The case reinforces the necessity of keeping endocrine causes on the differential for any patient with treatment-resistant anxiety, panic attacks or nocturnal terror — particularly when autonomic signs such as tremor, tachycardia, weight loss or eye changes shadow the psychiatric picture. The lesson is an old one in medicine, but worth restating in an era of algorithmic triage: sometimes the organ that appears to be failing is not the one that is actually sick.