Henry Woltman

Biographical Timeline

• Born on June 16, 1889, Westfield, Wisconsin, United States
• 1911 – Bachelor of Science, University of Minnesota
• 1913 – Doctor of Medicine, University of Minnesota. Internship at the University of Minnesota Hospital under neurologist Professor Arthur Hamilton
• 1917 – Doctor of Philosophy (PhD) in neurology, University of Minnesota defending thesis Brain changes associated with pernicious anemia. First assistant in neurology under Dr Walter D. Shelden at Mayo Clinic, Commissioned First Lieutenant in the Medical Corps of the United States Army
• 1918 – Instructor of neurology at the Mayo Graduate School of Medicine, University of Minnesota (Rochester)
• 1919 – Elected to staff at Mayo Clinic
• 1922 – Developed formalised scoring and notation system for neurological examinations
• 1928 – Co-described the Kernohan-Woltman Notch Phenomenon (KWNP)
• 1930-47 – Head of the Section of Neurology and Psychiatry at Mayo Clinic
• 1931 – Appointed professor of medicine at Mayo Clinic
• 1946 – President of the Staff of the Mayo Clinic
• 1947-1954 – Chairman of the combined Sections of Neurology and Psychiatry
• 1956 – Co-authored landmark paper on Stiff-Man Syndrome (Moersch-Woltman syndrome)
• Died on November 27, 1964 of cardiac arrest, while working at the Mayo Clinic on a history of the sections of neurology

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Medical Eponyms

Woltman’s Sign of Myxedema (1924)

Woltman’s sign (or the myxedema reflex) refers to the delayed relaxation phase of the deep tendon reflex, most commonly the Achilles reflex, in patients with hypothyroidism. Slowness of both the contraction and the relaxation of muscles in hypothyroid patients, best seen as the “hung-up” ankle jerk and occurring because of mechanical factors and slowness of contraction time, as in myotonia and pseudomyotonia. AKA the pseudomyotonic reflex

Although once considered nearly pathognomonic for hypothyroidism, delayed reflex relaxation can also be observed in elderly patients, those on beta-blockers, and in other conditions like anorexia nervosa. Nevertheless, it remains a useful diagnostic clue, particularly when correlated with symptoms of fatigue, cold intolerance, and thyroid function testing.

1924 – William Calvert Chaney (1889-1965) as a Mayo Clinic fellow under Woltman, publishes a detailed, objective study of the delayed relaxation phase of the Achilles tendon reflex in myxoedema using a mechanical apparatus and graphical tracings. While not naming Woltman, he credits the Mayo Clinic Section of Medicine for observing the finding “for a number of years”.

Chaney’s work demonstrated a consistent delay in muscle relaxation post-reflex in myxedema patients, correlated with reduced basal metabolic rate. While Woltman was not an author on the 1924 publication, he is believed to have mentored and guided Chaney’s investigations during his neurology fellowship.

1953 – Mayo Clinic physicians Millikan and Haines wrote that this finding was first observed by Woltman

Dr. Henry Woltman was, to our knowledge, the first to make this observation and following his suggestion Chaney in 1924 made graphic records which demonstrated the “delayed reaction” of the stretch reflexes in myxedema.

Millikan CH, Haines SF 1953

1956 – Woltman retired from the Mayo Clinic, the term “Woltman’s sign of myxedema” was formally coined, honouring his indirect but influential role in defining this clinical phenomenon.

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Kernohan-Woltman notch phenomenon (KWNP) (1928)

KWNP is a false localising sign that occurs in the context of transtentorial (uncal) herniation. The phenomenon results from compression of the contralateral cerebral peduncle (crus cerebri) against the tentorial edge, leading to motor weakness on the same side as the original lesion. This paradoxical presentation is contrary to typical neuroanatomical expectations.

1929 – Kernohan and Henry William Woltman (1889-1964) published “Incisura of the crus due to contralateral brain tumour” presenting a series of cases in which ipsilateral hemiparesis contradicted expected localising principles.

[There is] a discrepancy between the seat of the lesion and the side of the motor defect — which demands consideration in connection with a known mechanical distortion of midbrain structures.

Notching of the crus cerebri by the free margin of the tentorium could, we believe, explain the homolateral signs of the pyramidal tract noted in most of our cases

Kernohan & Woltman, 1929

The paper analysed autopsy-confirmed cases with supratentorial lesions, all showing a “notch” in the contralateral crus cerebri (cerebral peduncle). The authors attempted to rationalise clinical signs with pathological findings, correlating ipsilateral hemiparesis to contralateral peduncular damage, induced by transtentorial herniation.

The notch itself was interpreted as a result of the contralateral cerebral peduncle being compressed against the rigid tentorial edge by midline brain shift. Over time, this mechanical force led to demyelination and necrosis of descending corticospinal fibres, the structural basis of the paradoxical hemiparesis.

The phenomenon described is not merely of academic interest; it bears directly on problems of localisation, diagnosis, and surgical approach in cases of brain tumour.

Kernohan & Woltman, 1929

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Stiff-Man Syndrome (Moersch–Woltman Syndrome)

Stiff-Person Syndrome (SPS) is a rare, chronic neurological disorder characterised by progressive muscular rigidity, fluctuating painful spasms, and heightened sensitivity to external stimuli such as noise, touch, or emotional distress.

The condition primarily affects axial and proximal limb muscles, leading to hyperlordosis, impaired ambulation, and postural instability. Symptoms typically evolve over months to years and may wax and wane unpredictably. While the classic form is autoimmune, paraneoplastic and seronegative variants are increasingly recognised. Diagnosis is clinical, supported by EMG findings of continuous motor unit activity and serologic markers.

1956 – Frederick Paul Moersch (1889-1975) and Woltman of the Mayo Clinic published the first comprehensive clinical description of a rare neurological disorder they termed stiff-man syndrome. Based on 14 cases observed between 1924 and 1956, they identified a condition marked by progressive muscle rigidity, predominantly of the axial and proximal limb muscles, accompanied by painful spasms, exaggerated startle response, and a characteristic hyperlordotic posture.

The syndrome typically presented in midlife, affected both sexes, and often led to significant disability due to falls, contractures, and respiratory compromise. Moersch and Woltman hypothesized that the condition reflected a central disinhibition of motor pathways, though the underlying mechanism remained elusive at the time. The eponym Moersch–Woltman syndrome later emerged in recognition of their original clinical work.

1963 – Howard introduced diazepam as an effective treatment, leveraging its GABAergic activity

Modern research has since revealed that stiff-person syndrome (SPS) is frequently associated with autoimmune dysfunction, particularly anti-GAD (glutamic acid decarboxylase) antibodies, and may coexist with type 1 diabetes mellitus, thyroiditis, or paraneoplastic syndromes. GABAergic dysfunction is now understood as central to its pathophysiology.

1988 – Solimena et al. identified antibodies against glutamic acid decarboxylase (anti-GAD) in patients, implicating an autoimmune mechanism. This marked the transition of SPS from a purely clinical syndrome to a defined neuroimmunological disorder.

1990s–2000s – Further studies expanded the serologic profile, identifying antibodies to GABARAP, amphiphysin, and gephyrin, and differentiating classic SPS (typically anti-GAD-positive) from paraneoplastic variants (often anti-amphiphysin-positive and associated with malignancies, particularly breast cancer).

The spectrum of SPS now includes:

• Classic SPS (autoimmune, anti-GAD)
• Paraneoplastic SPS
• SPS variants: such as stiff-limb syndrome, progressive encephalomyelitis with rigidity and myoclonus (PERM), and stiff baby syndrome (which overlaps diagnostically with hyperekplexia but is likely distinct pathophysiologically).

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Major Publications

• Woltman HW. Brain changes associated with pernicious anemia. Thesis 1917
• Woltman HW. Brain changes associated with pernicious anaemia. American Journal of Physiology 1918; 45: 571–7
• Kernohan JW, Woltman HW. Incisura of the Crus Due to Contralateral Brain Tumor, Proceedings of the staff meetings of the Mayo Clinic 1928; 3(10): 69-70
• Kernohan JW, Woltman HW. Incisura of the crus due to contralateral brain tumour. Archives of Neurology and Psychiatry 1929; 21: 274–87. [Kernohan-Woltman notch phenomenon]
• Woltman HW, Wilder RM. Diabetes Mellitus: pathologic changes in the spinal cord peripheral nerves. Archives Internal Medicine 1929; 44: 576–603.
• Moersch FP, Woltman MD. Progressive fluctuating muscular rigidity and spasm (“stiff-man” syndrome); report of a case and some observations in 13 other cases. Proceedings of the Staff meetings of the Mayo Clinic. 1956 Jul 25;31(15):421-7.
• Chaney WE. Tendon reflexes in Myxoedema: valuable aid in diagnosis. Journal of the American Medical Association 1924; 82: 2013–2016

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References

Biography

• Corbin KB, Kernohan JW. Henry William Woltman, M.D. 1889–1964. Neurology. 1965; 15(4): 413.
• Moersch FP. Henry William Woltman MD. 1889 – 1964. Arch Neurol 1965; 13: 101–3.
• Eckman J. Henry W. Woltman, M. D., A Memorial. J Lancet. 1965 Feb;85:91-2.
• Henry W. Woltman. Minnesota Medicine 1965: 129
• Bibliography. Woltman, Henry W. WorldCat Identities

Eponymous terms

• Houston CS. The diagnostic importance of the myxoedema reflex (Woltman’s sign). Can Med Assoc J. 1958 Jan 15;78(2):108-12. 
• Todman D. Henry Woltman (1889-1964): Pioneering American Neurologist. J Med Biogr. 2008; 16(3): 162-6.
• Burkholder DB, Klaas JP, Kumar N, Boes CJ. The origin of Woltman’s sign of myxoedema. J Clin Neurosci. 2013; 20(9): 1204-6.