I. These impulses are generated by stimuli that have

 

 

    
I.        
Introduction:

Nociception
is an essential sensory input as it ensures that individuals are aware of
harmful environments or pre-existing damage to their bodies and avoid worsening
or creating injuries due to unpleasant sensation of pain whenever nociceptive
impulses are generated. These impulses are generated by stimuli that have
potential to cause harm such as pressure, temperature or pH (Woolf, 2010; Stemkowski and Smith, 2012) and are then sensualised by the brain as pain in
order to avoid self-harm. The need to feel pain is shown clearly in individuals
born with Congenital Insensitivity to Pain (CIP). CIP children are at a high
risk of self-mutilation, permanent deformity (see Figure 1) and premature death
due to self-negligence (Cox et al.,
2006; Sasnur, Sasnur and Ghaus-Ul, 2011).

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While it
is important to note that pain is vital for self-management there are many
chronic pain conditions that arise without a nociceptive input such as
neuropathic pain (von Hehn, Baron and Woolf, 2012). Likewise, in conditions that are either terminal
or incurable (e.g. Trigeminal Neuralgia) pain has little to no benefit to the
individual’s physical health and detrimental effects on their mental health –
it can even lead to suicide (Zakrzewska and Linskey, 2014).

 

Contemporary
chronic pain management is extremely poor as balancing act must be played
between severity of side effects from chronic opioid (cognitive impairment, gastrointestinal
pathologies, tolerance, constipation, physical dependence, and respiratory
depression (Benyamin et al.,
2008)) or NSAID administration (gastrointestinal upset/ulceration
(Sostres et al.,
2010)) and
efficacy of pain relief. Side effects from pain management can reduce patient’s
quality of life (Dennison et al.,
2005) so much so that patients will discontinue
treatment due to adverse side effects (Sostres et al.,
2010; Baldini, Von Korff and Lin, 2012).

 

Not only
does chronic pain drastically reduce quality of life, but it also has a huge
financial burden both in terms of a reduced ability to work and in treatment (Phillips, 2009). In 1998 back pain alone cost the UK somewhere between
£6.7 – £12.3 trillion due to both direct and indirect causes (Maniadakis and Gray, 2000). Thus, it’s clear to see why pain management is so
important to understand and manage due to its detrimental effects on quality of
life and economies.

 

Chronic
pain causes changes in the expression and/or function of multiple different ion
channels in nociceptive neurones (von Hehn, Baron and Woolf, 2012). This includes an upregulation of many different
receptors such as voltage-gated calcium ion channels and NMDA receptors (Woolf, 2011). Calcium plays an important role in nociceptive
pathways where it can act as a neurotransmitter , a cofactor for
calcium-dependent enzymes or to modulate gene expression. With drugs
such as Pregabalin and Gabapentin that treat neuropathic pain via targeting
calcium ion channels  with mild side effects it has already been
demonstrated that there is potential in good pain management via modulation of
calcium ion channels while still maintaining appropriate acute pain responses and compliance from patients. Here I will review the role of
calcium ion channels in the nociceptive/pain pathways.

 

 

    
I.        
Introduction:

Nociception
is an essential sensory input as it ensures that individuals are aware of
harmful environments or pre-existing damage to their bodies and avoid worsening
or creating injuries due to unpleasant sensation of pain whenever nociceptive
impulses are generated. These impulses are generated by stimuli that have
potential to cause harm such as pressure, temperature or pH (Woolf, 2010; Stemkowski and Smith, 2012) and are then sensualised by the brain as pain in
order to avoid self-harm. The need to feel pain is shown clearly in individuals
born with Congenital Insensitivity to Pain (CIP). CIP children are at a high
risk of self-mutilation, permanent deformity (see Figure 1) and premature death
due to self-negligence (Cox et al.,
2006; Sasnur, Sasnur and Ghaus-Ul, 2011).

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For You For Only $13.90/page!


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While it
is important to note that pain is vital for self-management there are many
chronic pain conditions that arise without a nociceptive input such as
neuropathic pain (von Hehn, Baron and Woolf, 2012). Likewise, in conditions that are either terminal
or incurable (e.g. Trigeminal Neuralgia) pain has little to no benefit to the
individual’s physical health and detrimental effects on their mental health –
it can even lead to suicide (Zakrzewska and Linskey, 2014).

 

Contemporary
chronic pain management is extremely poor as balancing act must be played
between severity of side effects from chronic opioid (cognitive impairment, gastrointestinal
pathologies, tolerance, constipation, physical dependence, and respiratory
depression (Benyamin et al.,
2008)) or NSAID administration (gastrointestinal upset/ulceration
(Sostres et al.,
2010)) and
efficacy of pain relief. Side effects from pain management can reduce patient’s
quality of life (Dennison et al.,
2005) so much so that patients will discontinue
treatment due to adverse side effects (Sostres et al.,
2010; Baldini, Von Korff and Lin, 2012).

 

Not only
does chronic pain drastically reduce quality of life, but it also has a huge
financial burden both in terms of a reduced ability to work and in treatment (Phillips, 2009). In 1998 back pain alone cost the UK somewhere between
£6.7 – £12.3 trillion due to both direct and indirect causes (Maniadakis and Gray, 2000). Thus, it’s clear to see why pain management is so
important to understand and manage due to its detrimental effects on quality of
life and economies.

 

Chronic
pain causes changes in the expression and/or function of multiple different ion
channels in nociceptive neurones (von Hehn, Baron and Woolf, 2012). This includes an upregulation of many different
receptors such as voltage-gated calcium ion channels and NMDA receptors (Woolf, 2011). Calcium plays an important role in nociceptive
pathways where it can act as a neurotransmitter , a cofactor for
calcium-dependent enzymes or to modulate gene expression. With drugs
such as Pregabalin and Gabapentin that treat neuropathic pain via targeting
calcium ion channels  with mild side effects it has already been
demonstrated that there is potential in good pain management via modulation of
calcium ion channels while still maintaining appropriate acute pain responses and compliance from patients. Here I will review the role of
calcium ion channels in the nociceptive/pain pathways.

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