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By contrast, using grand-average responses indirect evidence for sensitization has been found in chronic TTH with increased nociceptive specific reflexes and evoked potentials.
Gray matter volume increase in the thalamus has also been found in chronic pain conditions such as back pain [30] and chronic post-traumatic headache [31].
Previously, central sensitization has been found in chronic, primary headaches but pain perception in MOH patients has only scarcely been studied and never in long-tem follow-up studies.
Increased blood levels of the TLR4 ligand lipopolysaccharide (LPS) have been found in chronic HIV infection and these levels correlate directly with immune activation and inversely with CD4+ T cell restoration after antiviral therapies.
Negative findings have also been found in chronic schizophrenia patients.
Its highest incidence has been found in chronic myelomonocytic leukemia (CMML) patients (50%) [ 8].
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Increased proportions of anaerobes, Gram-negative rods and Gram-positive cocci were found in chronic wounds.
Normal amplitude, area, latency [125 128] and slower recovery cycle [127] of the blink reflex R2 component was found in chronic TTH.
It has been found by applying almost every modality of sensory stimulation for evoked potentials (visual - VEP, auditory - AEP, somatosensory - SEP), as well as in visual evoked magnetoencephalographic (MEG) responses[1], thus it is considered as a biomarker of the interictal status, which normalises during the migraine attacks and cannot be found in chronic migraine.
Further, SMI32 immunoreactivity is found in chronic lesions from patients with MS [51].
Similar results were found in chronic GVHD mice.
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