Synthesis &

Pathophysiology of
Tension Type Headache

Khairul P. Surbakti

Department of Neurology
School of Medicine Sumatera Utara
University, Medan, Indonesia
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Tension Type Headache Prevalence >>
Pathophysiology issues <<
Before 1988 No precise definition of
TTH

Previous terms :

- muscle contraction headache

- tension headache
- psychomyogenic
- stress headache

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 ORIGIN OF PAIN

?
CENTRAL

><
MYOFASCIAL
TISSUE
MECHANISMS
IN
THE BRAIN

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 Myofascial Cutaneous Pain
Pain
Quality Dull,aching,cramping Sharp,pricking,stabbing,
burning

Localizatio Difficult to localize Localized with great

n accuracy

Referred Show referal to Very localized

Pain distant areas
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 Pain in TTH
Myofascial
Pain

Pain in TTH

Peripheral Central

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 Central pain modulation,
including psychological
factors

Brainstem nociceptors

Decreased pain threshold Abnormal muscle activity

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Psychological Agravating
Stress abnormal pain
processing

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 PERIPHERAL
MECHANISM

Myofascial tenderness = Pressure-induced pain

tenderness to palpation of pericranial

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 Possible Peripheral Mechanism

Myofascial pain Innocuous

(Noxious)
Thin myelinated (A) Thick myelinated(A, A)

C- unmyelinated

Ischemia
Mechanical stimuli Increased Tenderness
Chemical mediators
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 Head & Neck
Muscle contraction Tender Muscle

Accumulation chemical
mediators

Muscle hardness

Manual papation 12
 CENTRAL MECHANISM
1. Spinal/trigeminal sensitization

Supra spinal structures

Trigeminal nerves

Pericranial musculature
Trigeminal nc caudalis
Spinal dorsal horn

Vascular structure

Cervical nerves of neck

and shoulders

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 Continuous suprathreshold signal

Activate second order neuron

Synaptic efficiency

Dorsal horn sensitivity to pain

Threshold activation
Enlargement of peripheral receptive field of
pain

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2. Supra spinal sensitization

Sensitization of third order thalamic neuron or

higher
structure
Wide spread and unspecific nature of
hypersensitivity

CTTH : general pain sensitivity

ETTH : Normal central pain processing

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 Wind up

Repetitive noxious Cumulative activity in

stimuli central pain neuron

Doesnt return to base

line level between
stimuli

Prolonged myofascial
noxious input Sensitization in TTH

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Pain modulation/inihibition :
Serotonergic mechanism

Disturbances in pain-
modulating Altered pain
transmitters perception in CTTH

Celular change in CNS

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Serotonin (5- Hydroxytryptamine, 5-
HT)
Anti nociceptive effects :
Receptors :
5-HT1
5-HT 2
5-HT 3

5-HT Inhibitory
Faclitatory

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5-HT 1A receptors : Inhibitory action on spinal
nociceptive

5-HT Vascular effects

The exact role of 5-HT in pain-modulation
unknown

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Impaired descending inhibition and facilitation

Malfunctioning of supra spinal descending tract

RVM Augmenting inhibition

of the nociceptive reflex

the pain threshold Atenuation of pain

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 RVM
Glu exitation of NMDA
receptors
Electrical stimuli

Nociceptive signal at
Dorsolatera Funiculi
(DLF)

pain threshold Via : -Stimulating

cholinergic
-Monoaminergic
receptors
 Glu stimuli
Electrical Nociceptive
stimuli signal DLF

Threshold
of VLF

Via : - Spinal Serotonergic

-Cholecystokinin
descending pathway

Other
attenuation Endogenous opioid
of pain
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 Novel synapse Exitability of 2nd
ANociceptive DHN order neuron

Central
Sensitization

supra spinal Presynaptic link A

inhibition of A-Fiber Nociceptive DHN due to
to DHN C-Fiber-Induced
activation of spinal
interneuron

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Biochemica
Disturbances of pain
l transmitters (serotonin)

Altered pain
perception in

Cellular changes in CNS

Peripheral
Algogenic
nerves
Serotonin
Anti nociceptive
CNS effects
- C5HT1 - C5HT2
- C5HT3
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 A pathophysiological model for chronic Tension Type
Headache

In healthy subjects, the processing of pain in finely regulated by

multiple pathways the degree of perceived pain is
appropriate for the actual situation
(Fig.2)

The model shows two of pain modulatory structures:

1. PAG in the mid brain inhibitory pathways descending to
the spinal dorsal horn

2. RVM in the brain stem inhibit nociceptive transmission (off

cells) and fascilitate nociceptive transmission (on cells)

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 Figure 2. NORMAL PAIN PROCESSING

Supplementary motor area

Supraspinal Limbic system
Stuctures Sensory cortex
and thalamus PAG RVM motor cortex

Normal
pain Inhibition Facilitation
transmission
Brain stem/ Nociceptive second order
Spinal cord neurons: V, C2 and C3 Motor neurons

Stimulation Inhibition

Pericranial
myofascial A-delta and C A-beta
tissues Muscle fibres
Sensory afferents

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 Figure 3. ABERRANT PAIN PROCESSING

Supplementary motor area

Supraspinal Limbic system
Stuctures Sensory cortex
and thalamus PAG RVM motor cortex
Increased
pain Inhibition Facilitation
transmission

Brain stem/ Sensitized nociceptive second order

Spinal cord neurons: V, C2 and C3 Motor neurons

Stimulation Stimulation

Pericranial
myofascial A-delta and C A-beta
Muscle fibres
tissues
Sensory afferents

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 In the sensitized state the afferent A fibres
that normally inhibit A- and C-fibres by
presynaptic mechanisms in the dorsal horn will
on contrary stimulate the nociceptive second
order neurones
(Fig.3)

The effect of A and C-fibre stimulation of the

nociceptive dorsal horn neurones will be
potentiated and the receptive fields of the dorsal
horn neurones will be expanded

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 CHRONIC TENSION-TYPE
HEADACHE
Continuous nociceptive input from
pericranial myofascial tissues

Induce and maintain

Central sensitization at the level of the spinal

dorsal horn/trigeminal nucleus so that stimuli
that are normally innocuous are misinterpreted
as pain

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Summary

Tension Type Headache is a Multifactorial

disorder with several concurrent
pathophysiological mechanism

Both peripheral & central mechanisms may be

involved in the synthesis and pathophysiology of
TTH

Serotonergic mechanisms in TTH and the

possible synaptic and cellular events in the
dorsal horn/trigeminal nucleus involved in
central sensitization
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Possible mechanism to myofascial pain &
tenderness :
Sensitization of peripheral myofascial
nociceptors

Sensitization of second order neurones at

the level of the dorsal horn/trigeminal
nucleus

Sensitization of supra spinal neurones

Decreased anti nociceptive activity from

supra spinal structures

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Thank You

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