Woltman’s Sign, the delay in the relaxation phase of the Achilles reflex, has long been recognised as the hallmark of overt hypothyroidism. It is most easily observed with the ankle jerk [1] but delayed relaxation can readily be demonstrated in all deep tendon reflexes including the biceps [2,3]. With hypothyroid patients the relaxation phase can take up to a full second. Numerous devices were devised for timing the ankle jerk [4], including the Burdick photomotogram [3,5,6], but the physical sign is so distinctive that such aids are not required in clinical practice.
The phenomenon was first described in 1884 [7] but was overlooked until distinguished Mayo Clinic neurologist Dr Henry Woltman promoted its use. In 1924 his protege Chaney [8] published the first objective description of the delayed relaxation phase of muscle stretch reflexes. He considered it as a valuable aid to the diagnosis of hypothyroidism, because at that time many cases were not recognised. This continued to be a problem for decades. In 1958 Houston reiterated that the diagnosis of myxedema was often missed. He pleaded for the routine use of the Woltman sign in every clinical examination, because of itself it could suggest the diagnosis, as well as confirming the suspicion of hypothyroidism in those patients with symptoms [9].
In 1960 a scoring system was introduced by Wayne as an aid to diagnosing hypothyroidism using a statistical weighting of common symptoms and signs [10]. In a lecture to the Royal College of Physicians he made the distinction between the terms myxedema (the skin manifestation of hypothyroidism) and hypothyroidism per se. The Wayne Score depended on 7 common symptoms and 6 common signs. But he did not include abnormal reflexes! Eight years later his colleagues revised the Wayne Index. They noted that in the interval the significance of the sluggish ankle jerk had been ‘rediscovered’ [11]. In the revised Index, slowing of the ankle jerk had the strongest weighting of all of the clinical features of hypothyroidism [12].
By 1997, the development of highly sensitive and precise methods for the measurement of total and free thyroid hormones, especially Thyroxine (T4) and Thyrotropin (TSH), simplified the diagnosis of thyroid dysfunction. But there was concern about atypical and divergent laboratory results, and the emerging entity of subclinical hypothyroidism. Zulewski and colleagues developed a new clinical scoring system to assess the severity of thyroid failure and to monitor its treatment [13]. They found that of all the symptom and signs, delay in ankle reflex times was the most common finding, with the highest sensitivity (77%) and specificity (94%).
Advances in thyroid hormone physiology indicate that T4 as the major circulating thyroid hormone is in fact an inert precursor, and that virtually all of the peripheral action of thyroid hormones is mediated by intracellular T3 [14]. Further, the delayed relaxation is attributed to muscle pathology, specifically decreased myosin ATPase activity and decreased accumulation of calcium in the sarcoplasmic reticulum [15]. Knowing this, it should be expected that patients with a genetic impairment of muscle deiodinase [16], or with any other cause of intra-cellular T3 deficiency, will show the clinical end-organ evidence of abnormal reflexes despite having normal T4 and TSH levels.
We have come full circle these days. The art of the clinical examination has been supplanted by extremely reliable laboratory tests. Guidelines [17,18] recommend that the measurement of TSH and T4 are mostly sufficient to make a confident diagnosis. Yet again we need to ‘rediscover’ the importance of checking reflexes.
The guidelines state that treatment with thyroxine is the standard of care. However it is universally recognised that 10-15% of thyroxine-treated patients remain symptomatic with an impaired quality of life [19]. Psychosocial factors including unrealistic patient expectations, the awareness of having a chronic disease, chronic fatigue syndrome, and unrecognised co-morbidities [20] do not provide a sufficient explanation for their symptoms. Many of the dissatisfied group, perhaps more than half, show a positive Woltman’s sign. This is my common clinical experience [21,22]. These patients require combination therapy, which is the careful addition of Triiodothyronine (T3) to their thyroxine replacement. They will have a dramatic and pleasing response.
Testing the reflexes gives an immediate and reliable indication of thyroid function. In the clinical setting, doctors suspecting that a patient has an underactive thyroid should test the reflexes as well as ordering TSH and T4 levels. If there is overt hypothyroidism, routine treatment with thyroxine will normalise the blood levels and the reflexes. If TSH and T4 levels are normal but Woltman’s sign is positive, the patient should be given combination therapy. Several techniques of testing the ankle jerks are taught [23]. The plantar tap method is very convenient [24] and has the highest agreement between observers [25]. Experienced clinicians can use any one of these procedures to identify delayed relaxation.
These patients require careful documentation of their symptoms and signs, which should be re-assessed after treatment. Importantly a positive Woltman’s sign despite optimal thyroxine replacement therapy provides a highly specific marker for the presence of intra-cellular T3 deficiency. These cases will improve dramatically and permanently with combination therapy.
There is no conflict of interest to declare.
Figshare data repository/Biological Sciences/Video: delayed plantar tap reflex. Video first published courtesy of Elsevier in 2022 (see Reference 22).
https://doi.org/10.6084/m9.figshare.24920010.v1
I thank my colleagues Dr Christopher Glatthaar and Professor Satvinder Dhaliwal for their encouragement and support.
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