PAIN SENSATION AND

PATHOPHYSIOLOGY OF HEADACHE

PRESENTER: DR WILLIAM Ramadhan.A

FACILITATOR: DR M A. Njelekela
 OVERVIEW

DEFINITION
TYPE OF PAIN
MECHANISM OF PAIN SENSATION
PAIN PATHYWAY
PATHOPHYSIOLOGY OF HEADACHE
TYPES OF HEADACHE
TREATMENT
REFERENCES
 PAIN

Pain is unpleasant sensation that occur

whenever any tissue are being damaged,
and it causes the individual to react to
remove the pain stimulus.
sign of morbidity and the most prominent
experience that humans judge the
existence of disease within ourselves
 Types of pain.
Fast pain
Slow pain
 FAST PAIN

Fast pain is felt within about 0.1 second

after a pain stimulus is applied,
The fast sharp pain signals are elicited by
either mechanical or thermal pain stimuli;
they are transmitted in the peripheral
nerves to the spinal cord by small
myelinated type Ad fibers
 It is believed that glutamate is the
neurotransmitter substance secreted in
the spinal cord at the type Ad pain nerve
fiber endings.
This is one of the most widely used
excitatory transmitters in the central
nervous system, usually having a duration
of action lasting for only a few
milliseconds.
 SLOW PAIN

slow pain begins only after 1 second or

more and then increases slowly over many
seconds and sometimes even minutes.
the slow-chronic type of pain is elicited
mostly by chemical types of pain stimuli
but sometimes by persisting mechanical or
thermal stimuli.
This slow chronic pain is transmitted to
the spinal cord by unmyelinated type C
fibers.
 suggest that type C pain fiber terminals, entering the
spinal cord secrete both glutamate transmitter and
substance P transmitter. The glutamate transmitter
acts instantaneously and lasts for only a few
milliseconds.
Substance P is released much more slowly, building
up in concentration over a period of seconds or even
minutes.
In fact, it has been suggested that the double pain
sensation one feels after a pinprick might result
partly from the fact that the glutamate transmitter
gives a faster pain sensation, whereas the substance
P transmitter gives a more lagging sensation.
 Regardless of the yet unknown details, it
seems clear that glutamate is the
neurotransmitter most involved in
transmitting fast pain into the central
nervous system, and substance P is
concerned with slow-chronic pain.
 The sharp pain, plays an important role in
making the person react immediately to
remove himself or herself from the
stimulus.
The slow pain tends to become greater
over time. This sensation eventually
produces the intolerable suffering of long
continued pain and makes the person keep
trying to relieve the cause of the pain.
 Mechanism of Pain Sensation

Stimuli mechanical, thermal and chemical

(bradykinin, serotonin, histamine, potassium
ion).
- Prostaglandins and substance P enhance the
sensitivity of pain ending. Do not elicit direct.
Pain Receptor (sensory receptor) are free
nerve end in the skin and other tissues
(periosteum, artery walls, joint surfaces,
meninges, falx and tentorium in the cranial
vault.
- Brain tissue lack pain receptor.
 Pain Pathway

Pain pathway is normally through spinal

nerve, spinal cord to the brain.
two separate pathways for transmitting
pain signals into the CNS.
two pathways mainly correspond to the
two types of pain in peripheral pain fibers
fast-sharp pain pathway - type Ad fibers
slow-chronic pain pathway type C fibers
 On entering the spinal cord, the pain signals take two pathways to
the brain, through (1) the neospinothalamic tract and
(2) the paleospinothalamic tract.
Neospinothalamic Tract for Fast Pain. The fast type Ad pain fibers
transmit mainly mechanical and acute thermal pain. They
terminate mainly in lamina I (lamina marginalis) of the dorsal
horns, and there excite second-order neurons of the
neospinothalamic tract.
These give rise to long fibers that cross immediately to the
opposite side of the cord through the anterior commissure and then
turn upward, passing to the brain in the antero lateral columns.
Neospinothalamic Tract terminate in the Brain Stem and Thalamus.

The fast-sharp type of pain can be localized much more exactly in

the different parts of the body than can slow-chronic pain (why?)
 Paleospinothalamic Pathway

Transmitting Slow-Chronic Pain.

transmits pain mainly from the peripheral slow-chronic type C
pain fibers, although it does transmit some signals from type
Ad fibers as well.
In this pathway, the peripheral fibers terminate in the spinal
cord almost entirely in laminae II and III of the dorsal horns,
which together are called the substantia gelatinosa,
. Most of the signals then pass through one or more additional
short fiber neurons within the dorsal horns themselves before
entering mainly lamina V, also in the dorsal horn.
Here the last neurons in the series give rise to long axons that
mostly join the fibers from the fast pain pathway, passing first
through the anterior commissure to the opposite side of the
cord, then upward to the brain in the anterolateral pathway.
 Localization of pain transmitted by way of the
paleospinothalamic pathway is poor.
For instance, slow-chronic pain can usually be
localized only to a major part of the body, such
as to one arm or leg but not to a specific point
on the arm or leg.
This is in keeping with the multisynaptic, diffuse
connectivity of this pathway. It explains why
patients often have serious difficulty in localizing
the source of some chronic types of pain.
 Termination of Spinothalamic Tract

Both Neo and paleospinothalamic Tract

terminate in the Brain Stem and Thalamus.
A few fibers of the neospinothalamic tract
terminate in the reticular areas of the
brain stem, but most pass all the way to
the thalamus without interruption,
terminating in the ventrobasal complex.
In paleospinothalamic tract, Only one
tenth to one fourth of the fibers pass all
the way to the thalamus.
 Subcortical Perception

Complete removal of the somatic sensory areas of the

cerebral cortex does not destroy an ability to perceive
pain.
it is likely that pain impulses entering the brain stem
reticular formation, the thalamus, and other lower brain
centers cause conscious perception of pain.
This does not mean that the cerebral cortex has nothing
to do with normal pain appreciation,
it is believed that the cortex plays an especially
important role in interpreting pain quality, even though
pain perception might be principally the function of lower
center.
 HEADACHE

Headaches are a type of pain referred to

the surface of the head from deep head
structures
Headache is one of the most common
complain reported by pts to health workers.
80% of pop. will suffer from headaches in a
given year in developed countries. Half of
them will have severe and disabling
headaches.
 Types of Headache

Tension headache
Migraine headache
Cluster headache
Cranial neuralgia
Traction and Inflammatory
 Common types of headaches

Tension headache.
- Its most common type of headache,
- tend to be on both sides of the head.
- They often start at the back of the head
and spread forward
- due to muscle contraction in the
shoulders, neck, scalp, and jaw.
- They are often related to stress,
depression, or anxiety.
 Migraine headache.
- familial disorder characterized
- By recurrent attacks of headache
widely variable in intensity,
frequency, and duration presumed to
be due genetically determined
hypersensitivity of the brain and
trigeminovascular system to internal
or external stimuli.
- They may tend to begin on one side of the
head, although the pain may spread to both
sides.
may have an "aura" (warning symptoms that
start before your headache)
Headache episode for 4-72 hrs with
Two of one of
-Unilateral nausea/vomiting
-Throbbing photophobia
- Aggravated by movement
- Moderate/severe pain
 Cluster headache.
- are sharp, extremely painful headache
- occur in series for several days-months
- they are far less common than migraine or
tension headaches.
Traction and inflammatory: 2ry to CVD,
brain tumours, infection, inflammation,
change in ICP
Cranial neuralgia: trigeminal,
glossophrary, atypical facial pain,
temporomandibular joint syndrome
 Pathophysiology of headache

Local pathology of pain-sensitive

structures (in &outside of cranium)
- tugging on the venous sinuses around the
Brain.
- damaging the tentorium,
- stretching the dura at the base of the brain,
- stretching stimulus to the blood vessels of
the meninges
- Skin , periosteum , extra cranial vessels
 Pathophysiology of headache

Psychogenic e.g. prolonged Emotion or tension

- contraction of muscles of the head, especially those muscles
attached to the scalp and the neck muscles attached to the
occiput.
- pain of the spastic muscles is referred to the overlying areas of
the head
- Theories: leads to vasospasm of arteries of head include those
supply brain ,produces ischemia of portions of the brain,
- this is responsible for the prodromal symptoms.
- Rebound vasodilatation and cause stretching of the walls of
the arteriesincluding some extra cranial arteries, such as the
temporal arterycauses the actual pain of migraine
headaches.
 Migraine may be initiated by afferent stimulation
from central centers in cortex, thalamus,
hypothalamus. Or externally food, drinks

Trigeminal / spinal nucleus( 5HT,1D receptors) on

the peripheral branches of TGN and central
ramifications in the T Nucleus.neuronal inhibition
of these receptors may abort acute attack eg
triptans
Parasympathetic dilation of Internal & External C.A.
(5 HT IB receptors. Inhibition of theses receptors
causes vasoconstriction and may abort acute attack
eg triptans
 Diagnosis in headaches

History is the vital tool in the diagnosis and

management( FH, onset, frequency, location,
duration, severity, trigger factors, associated
symptoms, PH. ect.)
Examination: a. general - fever, B/P, skin, neck
b. local tenderness
c. Neurological and other

systems
Diagnostic tests: general- ESR,
Local Imaging studies
 Treatment of migraine

Acute attack therapies

1. Non-specific: asa, paracet.,NSAIDs
2. Specific: a. ergot derivatives: ergotamine
b.Triptans: sumatriptan, naratri. rizatr.
Prophylaxis strategies
Pizotifen, propranolol, tricyclics, valporate
Non-pharmacological
help pt identify situations that make the problem
worse and encourage modification and control of
lifestyle adjustments: regular sleep, exercises,
meals, work habits and time for relaxation
 Treatment of CH

Acute attack treatments

1. Oxygen inhalation (100%) at 10-
12l/min for 15mins
2. Parental Sumatriptan 6mg or ? nasal
spray
Preventive treatments
1. Verapamil(chronic)
2. Short course of prednisolone(episodic)
3. Valproate (episodic/chronic)
 References

Guyton book. 11th ed

Ganong physiology book. 11th ed
www.wikipedia.com
THANKS FOR LISTENING