Assessment and management of pain

1. Assessment and Management
of Pain in Neurology Patients
Dwi Kartika Rukmi
kartikarukmi@ymail.com

3. PAIN
 ‘An unpleasant sensory and emotional experience
associated with actual or potential tissue damage, or
described in terms of such damage’
 Pain often acts as a protective mechanism to alert
the individual to potential tissue damage and to
cause reflex withdrawal from a painful stimulus.
 It can also cause behavioural responses that will limit
further tissue damage and promote healing, e.g. an
individual will reduce mobility following an injury or
surgery.

4. SOMATIC AND VISCERAL
PAIN
 Specialised pain receptors (nociceptors) are
located within the somatic and visceral
tissues (skin, muscles, joints, visceral organs
and arterial walls).
 Two types of receptor channels (neuron’s
order):
a. Detect the noxious stimuli
b. Set the stimulus threshold required in order
to generate an action potential

5. SOMATIC AND VISCERAL PAIN

6. Somatic/visceral pain pathways
 Neuron  dorsal horn
synapse via
spinothalamic and
spinoreticular tracts 
thalamus and reticular
formation
 A-delta fibres enter
laminae I, V and X, while
C fibres enter laminae I–V
 No sensation is perceived
until the impulse reaches
the brain, and pain is no
exception

7.  Pain fibres in reticular formation  contribute
to the autonomic responses. e.g. sweating,
tachycardia, elevated blood pressure and
respiratory rate.
 Pain fibres in thalamus  project pain to the
hypothalamus which is also thought to
contribute to the autonomic response, and to
the limbic system which triggers the
emotional response to pain

8. Pain pathways within the head
 Nociceptors within the cranium lie within the dura and
large intracranial arteries  brain doesn’t feel pain
 Pain fibres pons via N.V descend and
transmitted the pain impulses to the spinal trigeminal
nucleus and to the dorsal horn of C1 segment
connect with cerebral cortex where pain is perceived
 Fibres from the facial, glossopharyngeal and vagus
nerves also converge on the spinal trigeminal
nucleus and C1 dorsal horn

9. Chemical triggers of headache
 Irritation affecting the dura e.g. due to
meningitis or sub-arachnoid
haemorrhage  neurogenic
inflammation
 The chemical stimuli released during
this inflammatory process (e.g.
substance-P or calcitonin-gene related
peptide (CGRP))

10. GATE CONTROL THEORY
 Melzack and Wall (1965)

11. NEUROPATHIC PAIN
 Neuropathic pain follows injury to or dysfunction of
the nervous system and continues beyond the normal
period of healing
 Neuropathic pain is commonly experienced by people
with peripheral neuropathies or cranial nerve
disorders, but it also occurs with many neurological
and other conditions.
 Neuropathic pain is now also thought to be a feature
of persistent pain syndromes that are resistant to
standard analgesics

14. ASSESSMENT OF PAIN
 Assessment of pain
requires the nurse
to consider three
elements: the
quality or
description of the
pain, the quantity or
severity, and the
site/distribution of
the pain
 Or using PQRST
approach

15. PAIN ASSESMENT TOOL
 Visual Analogue Scales (VAS)
 0-100mm line marked that read ‘no pain’ to worst pain
imaginable’
 Valid and reliable and can be used to assess the effectiveness
of analgesia

16. PAIN ASSESMENT TOOL
 Verbal Rating Scale
 Verbal rating scales attempt to rate severity of pain using
adjectives (e.g. mild, moderate, severe)
 Poor sensitivity

17. PAIN ASSESMENT TOOL
 Numerical rating scales/ pain ruler
 Using scale between 0-5 or 0-10 with 0 ‘no pain’ and 5 or 10
‘worst possible pain’
 Valid, reliable, and have good sensitivity

18.  McGill pain
questionnaire (MPQ)
 The MPQ
encompasses all
aspects of pain
assessment, i.e.
intensity, quality and
location.
 Valid, reliable, and
can be used for the
assessment of
neuropathic pain and
is often considered to
be comprehensive,
sensitive and
accurate

19. ASSESSING PAIN IN
UNCONSCIOUS PATIENT
 Critical Care Pain Observation Tool
(CPOT)
 Valid and reliable
 Moderate to high inter-rater reliability,
regardless of the level of consciousness

21. ASSESSING PAIN IN
UNCONSCIOUS PATIENT
 Behavioural Pain Scale (BPS)
 Reliable and valid in assessing pain in
those with altered states of conscious-
ness, including patients who are
sedated and ventilated.

23. ASSESSING PAIN IN COGNITIVELY
IMPAIRED PATIENTS
 Difficult to assess (unable to communicate
effectively and sometime ‘no one asks’)
 For simple assess by using yes or no
response to describe any pain, ache or
discomfort
 Tool assessment for used are Abbey Pain
Scale and The Pain Assessment in
Advanced Dementia (PAINAD) Scale

26. ASSESSING NEUROPATHIC
PAIN
 Neuropathic pain often results in unique sensations,
so using verbal descriptors can be useful
 The Neuropathic Pain Scale (valid and reliable)
 The Leeds Assessment of Neuropathic
Symptoms and Signs Pain Scale (LANSS) (valid
and reliable)
 Other tools include: the Neuropathic Pain Symptom
Inventory (NPSI), theDouleurNeuropathique 4 (DN4),
and the Neuropathic Pain Questionnaire (NPQ), but
these have not all been prospectively validated.

29. FACTORS INFLUENCING NURSING
ASSESSMENT OF PATIENTS’ PAIN

30. HEADACHE
 A headache can result from a specific
process (e.g. migraine) or be
symptomatic of lesions affecting cranial
structures (e.g. inflammation, bleeding
or raised ICP).
 The global prevalence of headache is
47% and it is one of the ten most
disabling conditions in the world.

31. Classification of headaches
 Primary headaches: migraine, tension-type
headaches (TTH), cluster headaches and
other trigeminal autonomic cephalalgias
 Secondary headaches: those caused by
other neurological conditions, such as
vascular, traumatic or infectious disorders
 Cranial neuralgias, central and primary facial
pain and other headaches

32. Migraine
 Prevalence estimated 10% of the
population
 Triggers of migraine

33. Pathophysiology of
Migraine
Charles, 2017

34. Sign and Symptom of
Migraine
 Onset: worst within an hour of
onset and can last between 4 – 72
hrs
 Migrain > 3 days  migrainosis
 Aura and non aura
 Migraine with aura (visual
disturbances)  10-20% patients
 Other symptom that may occurs:
paraesthesia (30%), motor
symptoms (e.g hemiplegic
migraine) (18%), delusion, déjà
vu, and hallucination.

35. Tension-type headache (TTH)
 The global prevalence of TTH is around 40% and
they may be described as chronic if they occur for 15
days per month or for 3 months or longer
 Female> male
 Episodic and chronic TTH

37. Pathophysiology of TTH
Fumal and
Schoenen,
2016

38. Sign and symptom of TTH Siu &
Ahmad, 2014

39. Cluster headache (CH)
 Prevalence: 0,2%
 Male> female
 Once it develops (usually during the
third or fourth decade), CH is thought to
be a lifelong condition.
 Cluster headaches can severely impact
on quality of life and can result in
anxiety and depression.

40. Aetiology of Cluster headache
 The aetiology of CH is unknown, but it is
now thought to be of neurovascular
origin and may have a similar trigeminal
aetiology to that of migraine
 Triggered in some by rhinitis (hay
fever), stress, extreme temperatures,
relaxation and afternoon naps, certain
foods, alcohol, smoking and sexual
activity.

41. Sign and symptom of CH` Siu &
Ahmad, 2014

42. Other causes of headache and
facial pain
 Post lumbar
puncture (LP)
headache 
 Medication overuse
headache (MOH)
 withdraw or
limiting the
medication use

43. ManagementofMigraine
(SIGN,2018)

44. ManagementofMigraine
(Peters,2018)

45. Other management of migraine
 Physical therapy/exercise: spinal manipulation, TENS
(transcutaneous electrical nerve stimulation)
 Lifestyle changes: Keeping regular habits such as
sleep, exercise, meals and work/relaxation, may help
to reduce headache frequency
 Avoid trigger
 Acupunture

46. TENS

47. Management of Tension Type
Headache (TTH)
Non Emergency: simple analgesic as paracetamol and
NSAIDs will usually effective. If TTH become frequent,
overuse medication should be assess
Emergency Department (Peters, 2018)

48. Other management of TTH
 Physical therapy/exercise: spinal
manipulation, touch, TENS,
cranial electrotherapy
 Pharmacology prophylaxis: non-
steroidal anti-inflammatory drugs
(NSAIDs), tricyclic
antidepressants, relaxation
therapies, and muscle relaxants
 Acupunture
 CBT (Cognitive behavioural
therapy)

49. Management of Cluster
Headache

50. Other Management of Cluster
Headache
 Surgical intervention
 Deep brain stimulation
 Normobaric and hyperbaric oxygen
therapy
 Pharmacology prophylaxis:
corticosteroid

52. Normo/Hyperbaric Oxygen
Therapy

53. PHARMACOLOGICAL OF
VISCERAL PAIN
 1. Nonopioids: aspirin, paracetamol  mild
pain
 2. Mild opioids: codeine  moderate pain
 3. Strong opioids: morphine  intractable,
severe pain
 Nurses have a vital role in both direct
adminis- tration of analgesics, monitoring their
effectiveness, and in educating patients
regarding their drug regime

54. PHARMACOLOGICAL OF
NEUROPATHIC PAIN
 Anti-depressants and anti-convulsants
are the front line management for
neuropathic pain
 Opiate drugs: tramadol (nausea and
vomiting side effect)

55. Other management of visceral
and neuropathic pain
 Distraction
 Massage
 Acupunture
 TENS

56. References
 Charles, A. 2017. The pathophysiology of migraine: implications for
clinical management. DOI:https://doi.org/10.1016/S1474-
4422(17)30435-0
 Fumal,A & Schoenen, J. 2016. Tension-type headache: current
research and clinical management. Lancet Neurol 2008; 7: 70–83
 Peters,GL.2018. Pharmacotherapy for Primary Headache Disorders in
the Emergency Department in
https://www.uspharmacist.com/article/pharmacotherapy-for-primary-
headache-disorders-in-the-emergency-department
 SIGN. 2018. Pharmacological management of migraine in
https://www.guidelines.co.uk/pain/sign-migraine-
guideline/454046.article
 Woodward,S & Mestecky,AM. 2011. Neuroscience Nursing: Evidence-
Based Theory and Practice. Black Willey Publisher. E-book