My publications focus on clinical topics, revealing the presence of distorted central processing of perception in patients with entrapment neuropathies and uncovering the therapeutic mechanisms of conservative treatment approaches for musculoskeletal conditions.
Carpal Tunnel Study
Oxford University Study
Do you have numbness, tingling or pain in your hand?
You may be eligible to participate in a study conducted by researchers of the University of Oxford looking at the mechanisms causing nerve related pain.
Annina Schmid Dissects Nerve Disorders
Article in The Scientist Jan 2018
A background in physiotherapy helps the Oxford-based researcher mix basic science with clinical work to better understand pain stemming from nerve compression.
Dr Annina "Nina" B Schmid
PhD, MManipTher, PT OMTsvomp
Nuffield Department of Clinial Neurosciences University of Oxford
See all publications here.
Dr Annina "Nina" B Schmid
My name is Annina Schmid, many people know me as Nina Schmid. I grew up in Switzerland, trained and worked as a Physiotherapist before I specialised as a musculoskeletal therapist by doing a Masters degree at Curtin University of Technology in Perth Australia. I then started my research in Switzerland before moving to Brisbane, Australia, where I completed a PhD in Neuroscience at The University of Queensland. Currently, I am an Associate Professor at the Nuffield Department of the Oxford University in the UK and maintain a small clinical workload in a private practice in Banbury (UK).
My research is driven by questions with arise during my clinical work and focusses on neuropathic pain especially in patients with entrapment neuropathies. My projects aim to advance our understanding of the pathomechanisms involved in entrapment neuropathies, neuropathic pain and nerve regeneration to ultimately improve management of these patients.
- FMRIB graduate programme
The University of Oxford 2014-2015
- PhD in Neuroscience 2011
The University of Queensland, Brisbane, Australia
The School of Health and Rehabilitation Sciences and the School of Biomedical Sciences
Research project: Implications of mild peripheral nerve compression beyond the lesion site: Mechanisms and Interventions.
Supervisors: Prof EM McLachlan, A/Prof MW Coppieters, Dr MJ Ruitenberg, Prof PW Hodges
- Master of Manipulative Therapy 2005
Curtin University of Technology, Perth, Australia
Rewarded Brian Edwards Prize for highest achievement in clinical practice
- Bachelor in Physiotherapy FH 2001
School of Physiotherapy, Aargau, Switzerland
- FMRIB graduate programme
Courses and Workshops
Below is a list of available workshops and courses in pain related areas of neuroscience.
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My research is driven by questions which arise during my clinical work. Patients with entrapment neuropathies frequently report symptoms outside the affected nerve territory. These symptoms cannot be attributed to a purely local pathomechanism at the level of the compressed nerve. It is also apparent that a subgroup of patients with entrapment neuropathies develops debilitating neuropathic pain that is resistant to treatment whereas others recover spontaneously. These observations prompted me to further study the pathomechanisms of entrapment neuropathies with the aim to improve management of these patients. I am currently focussing on two topics: the role of neuroinflammation in neuropathic pain and nerve fibre degeneration/regeneration.
To answer our research questions, my projects contain a unique mix of both clinical as well as basic science.
I and my co-authors refined an animal model that closely mimics human entrapment neuropathies.
This model is characterised by demyelination, sparing of nerve fibers and behavioural signs of hyperalgesia and therefore provides a solid tool to further study the pathomechanisms of compression neuropathies. Using this model, I recently demonstrated that mild nerve compression is sufficient to induce a local and remote inflammatory response inside the nervous system. The identified remote inflammatory response with recruitment of macrophages and T-lymphoctyes as well as proliferation of satellite glia cells around the nerve cells in the dorsal root ganglia close to the spinal cord may explain the spread of symptoms beyond the lesion site found in some patients with entrapment neuropathies.
Using this model, we also identified preferential small fibre degeneration. This contradicts previous beliefs that the large fibre population is mainly affected in nerve injuries.
Clinical Studies in patients with nerve entrapments
In my clinical work, I often use carpal tunnel syndrome as a model system, as it is the most common entrapment neuropathy and provides unique access to human tissues. I am however also studying other entrapment neuropathies, such as ‘sciatica’. My clinical research pursues two lines of studies.
A first line focusses on the understanding of pathomechanisms in entrapment neuropathies, translating our findings from the preclinical model to humans. In this line of research, we have demonstrated the presence of central pain mechanisms in patients with carpal tunnel syndrome using different methodologies such as quantitative sensory testing and a cortical task involving left/right judgement of body parts. We have also for the first time shown that small fibres degenerate in patients with entrapment neuropathies. Interestingly, we found a small fibre deficit even in patients in whom large fibre tests are still normal. This suggests that we may need to include tests for small fibre integrity in our clinical diagnosis of patients with entrapment neuropathies. I have also pioneered the development of MR neurography (a specialised magnetic resonance imaging method designed to visualise nerves) at ultra-high field strength and have contributed to the first ever genome wide association study identifying genetic susceptibility loci in over 12’000 patients with carpal tunnel syndrome.
In our current projects focussing on pathomechanisms, we are investigating the regeneration capacity of nerve fibres in carpal tunnel syndrome as a human model system of focal nerve injury. We are also further characterising the molecular and cellular components of neuroinflammation in patients with entrapment neuropathies.
In a second line of clinical research, I am investigating potential management strategies for patients with entrapment neurophathies. Our work aims to better understand the therapeutic mechanisms of physiotherapeutic interventions. In a systematic review, I highlighted that some of the therapeutic effects of passive cervical joint mobilisations can be attributed to a central nervous system component (see paradigm shift). I also demonstrated that a likely therapeutic effect of nerve and tendon gliding exercises is a reduction of intraneural swelling. Given my findings of local and remote intraneural inflammation in the animal model, such therapeutic mechanisms would be an important conservative treatment avenue for patients with entrapment syndromes. We have just recently completed a large randomised clinical trial investigating whether education, splinting and nerve and tendon gliding exercises can reduce the need for surgery in patients with carpal tunnel syndrome who are already on the surgical waitlist. This is a good example of how I have taken my research all the way from the preclinical model to influencing management in patients.
In summary, my research comprises a unique mix of preclinical and clinical studies focussed around entrapment neuropathies. I am using a wide range of methods including MR neurography, neurophysiology, quantitative sensory testing and histological and molecular tissue analyses.