central post stroke pain

1. Central Post Stroke Pain
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2. Contents
• Central Post Stroke Pain
• Introduction
• Epidemiology
• Pathophysiology
• Clinical Features
• Nociceptive Pain vs Neuropathic Pain
• Desensitization For CPSP
• Management
• Recent Evidences
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3. Post Stroke Pain
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Klit H et al. Lancet Neurol. (2009)
Figure 1: Common types of chronic pain that can occur after stroke
Diagram of the complexity of post-stroke pain. Individual patients can have
various combinations of one or several pain types (overlapping areas). The sizes
of the circles are approximate to relative frequency (spasticity 7%, headache
10%, CPSP 10%, shoulder pain 20%, musculoskeletal pain 40%). CPSP=central
post-stroke pain.

4. Introduction
Central Post Stroke Pain
• ‘‘CPSP is a neuropathic pain syndrome characterized by
constant or intermittent pain in a body part occurring after
stroke and associated with sensory abnormalities in the
painful body part.’’
• First described by Dejerine and Roussy(1906)
• Also known as Dejerine-Roussy syndrome or thalamic
syndrome
• Can arise from lesion in any of sensory tracts
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Andersen, Vestergaard, Ingeman-Nielsen, and Jensen (1996)

5. Epidemiology
• 10.5%(29) out of 275 stroke patients after 6
months of stroke
Hansen et al. (2012)
• 25%(16) out of 63 patients with Wallenberg lateral
medullary syndrome within 6 months
MacGowan et al. (1997)
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6. Pathophysiology
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The pain signals are transmitted to the lateral and
medial thalamus via the spinothalamic tract.
Lateral thalamus forms lateral
thalamocortical pain pathway, which
projects to the primary
somatosensory cortex (sensory
discrimination),secondary
somatosensory cortex (pain
intensity),and insula (thermal and
nociceptive information processing)
Medial thalamus forms medial
thalamocortical pathway, which
projects to the anterior cingulated
cortex(ACC) and involves affective
emotional aspects of pain

7. Pathophysiology
• Several hypotheses have been proposed to explain
central pain. The major ones are:
• Central imbalance
• Central sensitization
• Central disinhibition
• Alterations in spinothalamic tract
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(Hong et al., 2010; Klitet al., 2009; Kumar & Soni, 2009; Seifert et al., 2013).

8. Pathophysiology
• Central Imbalance:
• Dissociated sensory loss [abnormal temperature and
pain sensitivity but normal touch and vibration
perception] is an important phenomenon in central pain
suggesting the possibility of an imbalance
• It has been proposed that central pain and dysesthesia
could be induced by imbalance of integration between
spared dorsal column/medial lemniscus activity and
lesioned spinothalamic tract
• If this were the case, disturbance of thermal/pain
pathways and sparing of tactile-signaling pathways
might produce tactile allodynia
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(Greenspanet al., 2004; Kumar & Soni, 2009

9. Pathophysiology
• Central Imbalance:
• CPSP could be caused by an imbalance between the
lateral (sensory-discrimination)and the medial
(affective-emotion) pain systems
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10. Pathophysiology
• Central sensitization:
• A lesion in the CNS results in both anatomical,
neurochemical , excitotoxic, and inflammatory changes,
all of which might trigger an increase in neuronal
excitability.
• Combined with a loss of inhibition and increased
facilitation, this increased excitability can result in
central sensitisation, which in turn might lead to chronic
pain.
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(Vestergaard et al., 1995).

11. Pathophysiology
• Central disinhibition(Thermosensory disinhibition
hypothesis):
• Head and Holmes (1911) proposed that injury to the
lateral thalamus disinhibits medial thalamus activity and
causes pain by disrupting inhibitory pathways
(GABAergic pathways) between lateral and medial
pathways.
• Central pain is a thermoregulatory disorder that occurs
from the loss of the central inhibition of pain by cooling
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Skin temperatures below 25uC activate both the cold
thermoreceptors (Aδ fibre) and the nociceptors (C-fibre)

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Then these inputs pass to the thalamus via the lamina I layer: the Aδ fibre input goes
through the posterior part of the ventromedial nucleus (VMpo) in the lateral
thalamus to the dorsal posterior insula (dpIns), whereas the C fibre input passes via
the ventral caudal part of the medial dorsal nucleus of the thalamus to the anterior
cingulate cortex (ACC).
Usually, the Aδ fibres activate the dpIns to suppress the perception of pain at
the ACC but when the temperature decreases under 15uC, the C activity
predominates over the Aδ activity
Consequently, the ACC is no longer suppressed and hypothetically cold
temperatures are perceived as pain
(Craig & Bushnell, 1996; Kumar & Soni, 2009).

13. Pathophysiology
Alterations in spinothalamic tract
functions:
• CPSP develops from a lesion in
spinothalamic tract and evidence
indicates that patients with CPSP
almost invariably exhibit pain and
temperature sensitivity deficit
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A Comprehensive Review of Central Post-Stroke Pain 2015 7
Honget et al.2010

14. Site Of Lesion Which May Lead To
CPSP
• Thalamus:
• Ventrposterolateral (VPL) thalamic ischemic lesions, specifically
ventrocaudalis nucleus, may result in CPSP
• Lenticulocapsular hemorrhage(LCH)
• Brainstem:
• The most common site of brainstem stroke is the medulla
oblongata(medial and lateral medullary infarcts).
• Cortical lesions:
• All cortical lesions responsible for CP involve, exclusively or in
combination, the parietal lobe
• NOTE: It appears that site of lesion is more important than
the volume of lesion.
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15. Characteristics Of Central Pain
• Constant or intermittent pain associated often associated
with sensory abnormalities
• Allodynia and hyperalgesia
• Burning, aching, pricking, lacerating or throbbing
• Abnormal sensitivity to temperature
• Abnormal sensations(paresthesia and dysesthesia)
• Increased by emotional stress and physical activity, cold,
heat and fatigue
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A Comprehensive Review of Central Post-Stroke Pain 2015

16. Diagnostic Criteria
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Klit H et al. Lancet Neurol. (2009)

17. Nociceptive vs Neuropathic pain
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Haanpaa M, Treede RD. Pain Clinical Updates (2010)

18. Nociceptive pain vs Neuropathic pain
• Nociceptive pain:
• Nociceptive pain arises as a result of mechanical,
thermal or chemical stimulation of the pain receptors
(nociceptors). The pain-conducting nerves are generally
not damaged.
• Neuropathic pain:
• Neuropathic pain is nerve pain that arises develops as a
direct consequence of injury or damage to various nerve
fibres.
• Neuropathic pain arises through damage to the central
and peripheral nervous systems, leading to impaired
pain processing.
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Haanpaa M, Treede RD. Pain Clinical Updates (2010)

19. Clinical Characteristic Neuropathic pain Nociceptive pain
Cause Injury to nervous system,
often accompanied by
maladaptive change in
nervous system
Potential damage to
tissues
Descriptors Lacinating, shooting,
electric-like, stabbing pain
Throbbing, aching,
pressure like pain
Sensory Deficits Common- e.g. numbness,
tingling, pricking
uncommon; if present they
have non-dermatomal
distribution
Motor defictis Neurological weakness
may be present if a motor
nerve is affected; dystonia
or spasticity may be
associated with CNS
lesions
May have pain induced
weakness
Hypersensitivity Often associated with non-
painful stimuli(allodynia)or
painful(exaggerated
response) stimuli
Uncommon except for
hypersensitivity in
immediate area of an
acute injury
Radiation Distal radiation common Proximal radiation more
common
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Scores ≥ 4/10 indicate neuropathic pain

21. Desensitization
• Treatment technique used to modify how sensitive
an area is to particular stimuli. This technique is
utilized to decrease, or normalize, the body's
response to particular sensations.
• Mechanism:
• Stimulus given to the affected area for short periods of
time, frequently throughout the day
• These small bursts of therapeutic activity shower the
brain with sensory input
• The brain responds to this demand by acclimating to the
sensation, thereby gradually decreasing the body’s pain
response to the particular stimuli.
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DESENSITISATION THERAPY IN POST STROKE PAIN SYNDROME: A CASE STUDY. Int J Physiother Res 2017

22. Desensitization
• Application
• Unpleasant stimuli to the hypersensitive area
• Stimuli are things that the body is routinely exposed to
• Do not elicit a painful response when presented to non-
affected areas of the body
• Stimuli may consist of different textures/fabrics, light or
deep pressure, vibration, heat or cold.
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DESENSITISATION THERAPY IN POST STROKE PAIN SYNDROME: A CASE STUDY. Int J Physiother Res 2017

23. Intervention
Desensitization Therapy:
The protocal followed 3 sessions a week for 2 months which
included:
• Tactile desensitization with cotton balls progressed to raw
materials for about 2 sessons in a week. Self administered
tactile desensitization for 10 sessions for 2 months
progressed from cotton balls to towel and hard surfaces
• Pressure desensitization given by rolling balls firmly on the
affected side for 3 min exposure to 2 min rest and again 3
min exposure, for about 10 sessions in 2months
.
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DESENSITISATION THERAPY IN POST STROKE PAIN SYNDROME: A CASE STUDY. Int J Physiother Res 2017

24. Intervention
• Stereognosis was treated with closure of eyes by
different object placed in hand and asked to
identify the object
• Proprioception desensitization given by positioning
the affected limb in a position and asked the
patient to explain in what position is arm with eye
closure
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DESENSITISATION THERAPY IN POST STROKE PAIN SYNDROME: A CASE STUDY. Int J Physiother Res 2017

25. CPSP Management
• Pharmacological Management:
• Anti Depressants: Adrenergically-active tricyclic anti-
depressents (TCAs) are currently the first line drugs. E.g.
amitriptyline(drug of choice)
• Anti-convulsive : gabapentin, pregabalin
• Anesthetics such as ketamine ,lidocaine ,propofol
• Opioids
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A Comprehensive Review of Central Post-Stroke Pain 2015

26. CPSP Management
• Neurostimulation Therapy:
• Used for treatment-resistant cases of CPSP.
• Invasive:
• Motor cortex stimulation
• Deep Brain Stimulation
• Non-Invasive:
• Repetitive transcranial magnetic stimulation (rTMS)
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A Comprehensive Review of Central Post-Stroke Pain 2015

27. Evidences
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Conclusion: 10HZ rTMS over the motor cortex for consecutive
1o days can produce satisfactory or partial analgesic effect on
patients with thalamic pain

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MCS significantly reduces the intensity of neurogenic pain. The
best long term results in the present study were achieved in
patients with thalamic syndrome.
Tanei et al. (2011) concluded that MCS provides
an effective treatment for CPSP, and suggested its
combination with DBS could provide additional therapeutic
efficacy in patients who do not experience satisfactory
pain relief from MCS alone.

29. References
• A Comprehensive Review of Central Post-Stroke
Pain 2015
• Central poststroke pain: An abstruse outcome
• DESENSITISATION THERAPY IN POST STROKE PAIN
SYNDROME: A CASE STUDY
• Central post-stroke pain: clinical characteristics,
pathophysiology and management 2009
• Central post-stroke pain: Current evidence 2008
• Gyanendra Kumar ⁎, Chetan Rasiklal Soni
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