Quantitative Sensory Testing (QST) - Does assessing ... - TI Pharma

1. General introduction
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drugs (NSAIDS) and paracetamol are considered not to be efficacious for this type of
pain (Dickenson 1995). Many patients require treatment with more than one drug or
classes of drugs, but the correct choice of drugs, and the optimal sequence for their use,
is still not defined. Therefore, management of pain should be tailored to the individual
patient on the basis of type of pain, the causative disease, and psychosocial aspects.
A treatment cascade was implemented recently, incorporating an evidence-based
symptomatic pharmacotherapy of neuropathic pain (Attal et al 2010; Dworkin et al
2007b).
During the last decades, basic pain research brought detailed understanding of concepts
and theories regarding pain mechanisms such as the gate control theory (Melzack
& Wall 1965) , the concept of neuroplasticity (Melzack et al 2001; Woolf & Salter
2000), and an understanding of the cellular and molecular mechanisms of peripheral
and central sensitisation (Basbaum et al 2009; Hunt & Mantyh 2001; Ji et al 2003).
These developments in the understanding of pain mechanisms have been translated
into clinical practice, resulting in a multimodal approach to pain relief. However, in
neuropathic pain patients a decrease of pain of more than 50% is only achieved in less
than one-third of the patients studied (Argoff et al 2006; Farrar et al 2001; McQuay et
al 1996; Sindrup & Jensen 1999; Ziegler 2008). The lack of efficacy could be based on
the limiting side-effect profile or due to addictive properties of the drug, which might
compromises the therapeutic dose window. On other hand, such a lack in treatment
efficacy might be based on the fact that neuropathic pain is still being classified based
on its underlying aetiology (Hansson 2003; Jensen et al 2001; Woolf & Mannion 1999).
There are, however, promising developments to address these short-comings.
Recently, a more neurological approach to categorise neuropathic pain was suggested.
In order to determine with a greater level of certainty whether a pain condition is
neuropathic, a grading system of definite, probable, possible and unlikely neuropathic
pain was proposed (Treede et al 2008). Briefly, the grade ‘unlikely’ excludes patients
lacking a history of a lesion or disease for a plausible neuroanatomical distribution
of their pains. The grade ‘possible’ is regarded as a working hypothesis, which does
not exclude, neither diagnoses neuropathic pain. Patients who fall into the category
‘possible’ neuropathic pain can be transferred into the grades ‘probable’ and ‘definite’
if neurologic examination and / or a test e.g. MRI, biopsy or laboratory parameter
confirm the diagnosis of the suspected lesion or disease, respectively. An advantage of
this grading system is the precise identification of a lesion or disease and the ability to
directly link these to somatosensory changes.
A few years ago, a new hypothetical concept was proposed, in which pain is classified
on the basis of underlying mechanisms (Dworkin et al 2003; Sindrup & Jensen 1999;
Woolf et al 1998). Supportive to this concept are clinical experimental studies (Attal
et al 2004; Baron et al 2009) indicating that a specific symptom might be generated by