Important Note!
If you have pain, consult with your physician and if possible eliminate the source of your pain!

This training can help you with the following situations: 

• if you undergo a painful examination or treatment at your doctor or dentist.
• if the source of your pain can not be found.
• if the pain despite adequate treatment does not subside.
• if the pain is a side-effect of another illness (and not to overload the body with pain medications).

Pain, Its Perception, and Pain Imaging

Anthony K.P. Jones, MB BS

Human Physiology and Pain Research Laboratory,
Manchester University Rheumatic Diseases Centre, Clinical Services Building, Hope Hospital, Salford, United Kingdom

The experience of pain can be defined only in terms of human consciousness. As with all sensory experience, there is no way of being certain that one person’s experience of pain is the same as another’s. There is therefore no absolute qualification of pain experience; it can only be estimated by verbal or magnitude scaling methods.

Pain should not be equated with nociception. Nociception is the response to excitation of nociceptors. Although nociception may give rise to the experience of pain, pain may arise in the absence of nociception. Conversely, nociception may also occur in the absence of pain. Hence the terms non-nociceptive pain (e.g., neurogenic and psychogenic pains) and nociceptive pain (e.g., inflammatory pain) must be clearly differentiated.

The spectrum of pain experience ranges from pain that may closely reflect physical events in tissue to pain that is generated without any peripheral physical input. The brain acts as a virtual reality system that may or may not be constrained by interactions with the body’s internal and external environment. 

The Brain-Pain Problem

Nociceptive second-order projections from the dorsal horn neurons to the brain are mainly (about 90%) via the opposite spinothalamic tract. Projections are mainly to the brain stem and the medial and lateral thalamic nuclei (Fig. 1; Bowsher 1957; Apkarian and Hodge 1989). However, there are also polysynaptic medial projections to the medial thalamic nuclei. The more medial projections and their corresponding thalamic nuclei are generally slower, with relatively poor spatial information. The lateral projections, in contrast, are somatotopic (projections are arranged in a body map) and subserved by relatively fast transmission. They project to primary and secondary somatosensory and insula cortices. The more medial structures are considered to subserve the so-called "medial pain system," as distinct from the projections of the lateral thalamic nuclei, which are thought to subserve the "lateral pain system" (see Jones and Derbyshire 1996 for more detailed discussion).

Vogt and colleagues considerably extended the concept of the medial pain system by demonstrating projections of the medial thalamic nuclei to area 24 of the anterior cingulate cortex (Sikes and Vogt 1992; Vogt et al. 1993). The anterior cingulate cortex is an extensive area of the limbic cortex overlying the corpus callosum and is involved in the integration of cognition, affect, and response selection (Dovinsky et al. 1995). There also are medial thalamic nociceptive projections to the prefrontal cortex (Tsubokawa et al. 1981). The descending connections of the anterior cingulate cortex to the medial thalamic nuclei and to the peri-aqueductal gray in the brain stem suggest that this system may also be involved in the modulation of reflex responses to noxious stimuli.

Partly because of the differences in latency of responses and their respective connections, researchers have suggested that the medial and lateral pain systems are mainly responsible for processing chronic and acute pain, respectively (Albe-Fessard et al. 1985). However, it is evident that these systems are interconnected and in parallel. Only at the level of the cortex do they become discrete. Stimulation or removal of somatosensory cortex in humans rarely causes or relieves pain (Devinsky et al. 1995). Indeed, damage to the spino-thalamo-cortical pathways is commonly associated with central deafferentation pain (Bowsher 1996). Deafferentation or removal of the anterior cingulate, however, does not abolish chronic pain but reduces the unpleasantness of it (Folz and White 1962). Further identification of cerebral structures involved in human pain processing and their physiological interactions has been facilitated by functional imaging techniques.

The intensity of sensation and pain perception is directly related to the energy level at the pain location. This explains why different people have different perceptions of pain. Is there a cause for pain, it is the built in response mechanism of a person if energy will increase or decrease in the location of the pain. This determines the intensity of the pain.

Utilize that mechanism and consciously learn to lower the energy level at the location of the pain and therefore lower the perceived intensity of the pain.

If you have pain in one of your hands, train as follows:

• In order to reduce pain perception with the PcE-Trainer, use the ULP-Hand Cable only by lowering the energy level in the hand(s).

If you have pain somewhere else, train as follows:

• In order to reduce pain perception with the PcE-Trainer, use the ULP-Hand Cable first by lowering the energy level in the hands.
• After that exercise with the ULP-Triple Cable by lowering the energy level at the location of the pain.