Question: what are the differential diagnoses for this patient’s flaccid paralysis?

This patient presented an acute-onset symmetrical tetraparesis with hypotonia and normal deep tendon reflexes: an acute flaccid paralysis. Differential diagnoses include myopathies, neuromuscular transmission disorders, neuropathies and acute myelopathies.1

The most common global cause of acquired flaccid paralysis is Guillain-Barré syndrome, a polyradiculoneuropathy. Patients present acute, symmetrical paralysis, usually ascending and progressive. Frequently beginning in the lower limbs, symptoms progress over days to weeks, with decreased or absent deep tendon reflexes and cranial nerve involvement. A history of recent vaccination or infection is common. The diagnosis is typically clinical, supported by altered cerebrospinal fluid findings and electromyography.2 However, it does not typically recur.

Other causes of weakness include inflammatory myopathies that present progressive muscle weakness, mainly in proximal limbs, often with elevated muscle enzymes. Metabolic myopathies, rare genetic diseases, usually manifest with exercise intolerance or previous rhabdomyolysis episodes. Neuromuscular junction disorders, such as myasthenia gravis, are characterised by muscle fatiguability, typically involving the eye muscles. Acute myelopathies, such as transverse myelitis, can present with acute flaccid tetraparesis but this is usually associated with dysautonomia, pyramidal or sensory signs, particularly a sensory level. Again these conditions are not recurrent.

This patient’s recurrent weakness episodes raise the possibility of periodic paralysis. Periodic paralysis encompasses a rare group of skeletal muscle channelopathies, marked by recurrent muscle weakness. These episodes may correlate with varying serum potassium concentrations, presenting with hypokalaemia or hyperkalaemia.3 4 Two notable examples include familial periodic paralysis, an autosomal dominant disorder, and thyrotoxic periodic paralysis.

Question: what investigations would you perform?

The initial evaluation should include basic serum chemistries for metabolic abnormalities, such as electrolytes—especially serum potassium—blood glucose, arterial blood gases, lactate, muscle injury markers, liver enzymes, thyroid function and thyroid antibodies, depending on initial results. An electrocardiogram should aid in establishing the diagnosis.

The most relevant finding was a serum potassium of 2.89 mEq/L (normal 3.5–5.5). Transaminases, lactate and creatine kinase were normal. Arterial blood gas showed no acidosis, and neuroimaging was normal. He received intravenous potassium replacement, and 4 hours later his muscle strength had completely recovered.

Blood test results also showed low TSH (<0.01 mU/L; normal 0.4–4.3) and high free T4 (6.11 ng/dL; normal 0.78–2.9) and thyrotropin receptor antibody (TRAb) (4.7 UI/L; normal <1.75). Thyroid ultrasound scan showed heterogeneous echogenicity of the gland, with increased dimensions and hypervascular flow (thyroid imaging reporting and data system (TI-RADS)) 1. He was then treated with thiamazole for hyperthyroidism and a beta-blocker for control of adrenergic symptoms.

Question: what is the likely diagnosis and prognosis?

The resolution of acute-onset tetraparesis after potassium supplementation and hyperthyroidism treatment supports the diagnosis of thyrotoxic hypokalaemic periodic paralysis with Graves' disease as the underlying disorder; familial periodic paralysis is not associated with altered thyroid function.4 5 When identified and treated, thyrotoxic hypokalaemic periodic paralysis has an excellent prognosis and may be completely reversible in euthyroid status.

At outpatient follow-up 5 months later, his thyroid function was normal and there had been no new episodes of acute tetraparesis. His neurological examination was normal, with normal strength in all limbs.