Ian McDonald

Background: Alopecia areata (AA) is a common non‐scarring alopecia. Data continue to emerge on associations with autoimmune and other conditions. Janus kinase inhibitors (JAKi) are increasingly used to treat AA.Objectives: The aim was to assess variation in laboratory testing in patients with AA among hair experts internationally and to compare subspecialized clinical practice to current guidelines.Methods: Thirty hair experts from 14 countries and six continents contributed to develop a 24‐item survey collecting demographic information on respondents; methods of severity assessment; and laboratory testing practices in AA for mimics, contributory factors, associations, and workup for systemic therapy. The survey was distributed to a global network of expert hair specialists.Results: Of 214 respondents, 79.9% (171/214) had special interest/expertise in hair loss disorders, and 35.5% (n = 76) were based in Europe. Most cared for both adults and children (87.9%, n = 188). For clinical assessment, almost two‐thirds (63.6%, n = 136) used the Severity of Alopecia Tool and 38% (n = 84) used the Dermatology Life Quality Index. Only 24.3% (n = 52) typically tested for alternative infectious or inflammatory diagnoses, 39.7% (n = 85) typically tested for contributory conditions such as nutritional deficiencies, and 50.9% (n = 109) typically tested for co‐existent autoimmune illnesses. Thyroid function testing was routinely performed in 73.4% (n = 157) and complete blood count (CBC) was checked in 65.9% (n = 141). Compared to conventional systemic therapy, experts were more likely to check lipid levels, creatine kinase, coagulation profiles, thrombophilia screens, tuberculosis blood testing, hepatitis B and C serology before prescribing JAKi.Conclusions: Real world practice of laboratory testing for AA by hair experts, who may see more severe or complex alopecia, is variable. Most experts routinely perform thyroid function and CBC testing. We discuss evidence for indications for testing for AA mimics, contributory factors, associated autoimmune conditions, and before systemic therapy. Further research is required to characterise the role of laboratory testing in AA.

Physicians have long sought to explain neurological deficit and recovery on the basis of alterations in the agent of nervous action. The ancient Greeks knew that the brain influences muscles and they showed experimentally that the effects were mediated by nerves. Galen believed that the agent of action was the animal spirits. Ideas began to change with a new approach to knowledge and the revival of experimentation that followed the arrival in Venice of ancient Greek manuscripts after the fall of Constantinople in 1453. In the mid-18th century the notion of animal spirits was replaced by that of the vis nervosa and speculation began that the agent might be electrical. This was established by the mid-19th century. The nature of conduction in nerve was clearly different from that in a wire but how it took place remained uncertain until Hodgkin and Huxley proved the ionic hypothesis in the mid-20th century. In the following decades the membrane mechanisms of conduction failure and restoration were elucidated, with practical consequences in the form of improved diagnostic methods and the potential for more rational approaches to treatment. The demonstration that adaptive cortical plasticity contributes to recovery raises the possibility of new strategies for neurological rehabilitation.

Multiple sclerosis is an immune–mediated inflammatory demyelinating disease of the central nervous system clinically characterized by relapses and remissions of neurological disturbance. A typical relapse, exemplified by optic neuritis, increases in severity over a week or two and after approximately one month begins to remit. Resolution takes place over the course of two to three months. In the early stages, clinical recovery is virtually complete, though persistent abnormalities of conduction can usually be detected by evoked potential techniques and persistent structural abnormalities can be detected by magnetic resonance imaging (MRI). These techniques, together with cerebrospinal fluid examination for oligoclonal IgG, provide supporting evidence for the diagnosis which, in the absence of a specific test, nevertheless remains primarily clinical. The course of the disease is very variable, but after a number of years neurological deficit begins to accumulate after each relapse. In most patients, the relapsing and remitting phase of the disease is followed by a phase of continuous progression of disability. Cognitive disturbances can be detected in many patients even quite early in the course of the illness. Deficits in attention, memory and executive skills may be prominent and tend to become increasingly prominent as neurological deficit increases, although this is not always the case. There is some correlation between the extent of MRI abnormalities in the cerebral white matter and the severity of cognitive deficit. Depression and anxiety are commonly experienced but are poorly correlated to the lesion load seen on MRI. In contrast, the much rarer psychotic symptoms, euphoria and emotional lability are closely linked to the severity of white matter disease.