What is uhthoffs phenomenon

Published May Panginikkod S, Rukmangadachar LA. Uhthoff Phenomenon. Updated February 28, Your Privacy Rights. To change or withdraw your consent choices for VerywellHealth. At any time, you can update your settings through the "EU Privacy" link at the bottom of any page. These choices will be signaled globally to our partners and will not affect browsing data.

We and our partners process data to: Actively scan device characteristics for identification. I Accept Show Purposes. Table of Contents View All. Table of Contents. Staying Active. Could It Be a Relapse? Keep in Mind No permanent neurological damage is done by Uhthoff's phenomenon. Was this page helpful? Thanks for your feedback! Sign Up. What are your concerns? Verywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles.

Read our editorial process to learn more about how we fact-check and keep our content accurate, reliable, and trustworthy. Related Articles. Knowledge of this phenomenon and its pathophysiology, therefore, is essential for recognition and appropriate treatment.

This activity reviews the pathophysiologic basis of Uhthoff phenomenon and describes how Uhthoff phenomenon can be distinguished from a relapse of multiple sclerosis. This activity highlights the role of interprofessional team members in collaborating to provide well-coordinated care and enhance outcomes for affected patients. Objectives: Outline the Uhthoff phenomenon. Describe how the Uhthoff phenomenon may, in select cases, suggest that further evaluation for multiple sclerosis is warranted.

Review how to evaluate a patient for multiple sclerosis. Explain the importance of improving coordination amongst the interprofessional team to enhance care for patients with multiple sclerosis.

Access free multiple choice questions on this topic. This phenomenon is named after Wilhelm Uhthoff, a German ophthalmologist who described it. In , Uhthoff first described exercise-induced amblyopia in multiple sclerosis patients. When Uhthoff studied this phenomenon, exercise was thought to be the etiology, and the significance of elevation in body temperature escaped his notice.

Six decades later in , the hot bath test was developed based on this phenomenon and was used as a diagnostic test for multiple sclerosis. The temporary worsening of neurological function in response to heat exposure affects the physical and cognitive function of multiple sclerosis patients and interfere with their activities of daily life and functional capacity.

An understanding of this phenomenon and its pathophysiology, therefore, is essential for recognition and appropriate treatment. Temperature-sensitive conduction blockade of partially demyelinated axons in the demyelinated plaques is the most widely accepted mechanism.

Studies have shown a decrease in conduction velocity in response to an increase in temperature in MS patients. Adduction velocity of eye movements in MS-related INO as measured by infrared eye movement recording techniques was reduced by a systematic increase in core body temperature and reversed to baseline with active cooling.

The normal myelinated nerve is a highly specialized structure, with clustering of sodium channels at the nodes of Ranvier. This facilitates saltatory conduction, whereas demyelination results in the widening of the nodal region leading to the transformation of faster saltatory conduction to slower membrane conduction.

Newly assembled sodium channels are subsequently inserted within the axonal membrane as an ion channel adaptation, but the newly incorporated sodium channels may exhibit altered physiological properties.

Demyelination reduces the safety factor of axons, defined as the ratio of the current available to initiate an action potential to the minimal current required. Hence, an increase in temperature even as little as 0. Almost all the precipitating factors of the Uthoff phenomenon cause elevated core body temperature. Events preceding the worsening of neurological symptoms should be analyzed during history taking. Factors including exercise, taking a hot bath or shower, exposure to the sun, menstrual cycle, psychological stress, hot meals, fever, and infection should be addressed as any of these can precipitate worsening of the symptoms in MS patients.

The transient worsening of the symptoms induced by such factors is termed 'pseudo exacerbation' or 'pseudo-relapse' as opposed to a true relapse or exacerbation in MS patients. Relapse or exacerbation is the hallmark of relapsing MS and is characterized by new focal neurological deficits lasting for at least 24 hours in the absence of fever or infection. Often, a detailed history is able to differentiate a true relapse from a pseudo-relapse. Examination reveals various neurological deficits pertaining to the location of demyelination including amblyopia, nystagmus, INO, muscular weakness, and abnormal reflexes.

Episodes of Uhthoff's phenomenon is generally considered to be the result of established demyelinating plaques in the setting of thermal stress. The key to making a diagnosis is detailed history from the patient regarding the circumstances in which the symptoms appeared. In patients with pseudo-relapse, care should be taken to rule out common precipitating factors like urinary tract infection, [18] upper respiratory tract infection, or metabolic abnormalities through laboratory tests.

Thus, the workup should include a detailed history and physical examination in addition to laboratory investigations to rule out metabolic, toxic, and infectious derangements. An MRI brain MRI C-spine, MRI T-spine with and without contrast to assess for any new contrast-enhancing lesions that could reveal a new clinical attack for the demyelinating condition the patient suffers.

For new diagnosis, a lumbar puncture may be indicated to pinpoint the demyelinating or inflammatory condition including basic CSF studies, meningoencephalitis panel, oligoclonal bands, IgG Index, NMO Aquaporin-4 or MOG antibodies, flow cytometry, cytology, among others. A fundamental principle in the prevention and treatment of Uhthoff's phenomena is to be familiar with the antecedent factors that can result in elevation of core body temperature, and their corresponding impact on the patient's neurological functioning and safety.

Patients should be counseled about the stimulating effects of taking hot showers or baths regarding reducing appendicular and core muscle strength leading to profound weakness and thereby placing them in grave danger of drowning.

Also, they should be cautioned against sauna, exposure to the sun when the outside temperature is greater than 30 C, hydrotherapy with water at high temperatures, short-wave radiotherapy, and paraffin application. The temporary worsening of neurological function in response to heat exposure affects the physical and cognitive function of multiple sclerosis patients and interfere with their activities of daily life and functional capacity.

This worsening needs to be differentiated from a true relapse or exacerbation of MS. This is further exacerbated by the onset of yet another relapse or flare. In some respects, I have been fortunate. My relapses have been few and far between. However, when it happens, all normal activity ceases for the duration. The point of including this digression here is that I feel especially brain-fogged today, as I have done for several days now. I suspect that I am in another relapse.

Inexplicably, it took several days of this brain-fogged existence, before it occurred to me that perhaps it was MS causing this sense of disconnection.