SOMATIC SENSATIONS

LEARNING OUTCOMES
• At the end of this lecture, students should be able to describe
• Pain pathways
• Differences between fast and slow pain ….Herpes zoster
• Double pain sensation after pin prick ……..Tic douloureux
• Pain suppression system/analgesia ---Brown-Sequard syndrome
• Referred pain mechanism …………headache and its types
• Visceral pain pathways ------temperature sensation
• Hyperalgesia and allodynia
PAIN
 Pain refers to unpleasant sensory and emotional
experience associated with actual or potential tissue
damage.
• Special receptors for pain (free nerve endings) A delta & C
• Non adapting in nature
• shows Hyperalgesia----increasing in sensitivity of pain as
pain continues
• Nociception refers to neural encoding of impending or
actual tissue damage.

• A delta and C fibers can also be activated without causing

pain. For instance, gentle stimulation with a fine needle may be
perceived as sharp but not painful.
•PAIN & OTHER SOMATIC DISORDERS
• HYPERALGESIA:
• An exaggerated response to a noxious/toxic stimulus

• ALLODYNIA
A sensation of pain in response to an innocuous stimulus.
e.g. painful sensation from a warm shower when skin is
damaged by sun burn
 PAIN RECEPTORS LOCATION
1. Superficial skin layers
2. Internal tissues
• Periosteum
• Joint surfaces
• Arterial walls
• Falx and tentorium
*Viscera have sensory receptors for no other modalities
besides pain. Visceral pain differs from surface pain
STIMULI FOR PAIN
1. Mechanical
2. Thermal
3. Chemical
• Bradykinin, serotonin, histamine, potassium ions,
proteolytic enzymes, prostaglandin, substance P
4. Electrical
CAUSES OF PAIN
1. Tissue damage
Bradykinin---------------------------------------stimulates pain nerve
endings, mechanism
not clear
Increased potassium ions increase nerve
Increased proteolytic enzymes membrane
(from damaged cells) permeability
Rate of tissue damage α pain intensity
more damage more pain
• 2. Tissue ischemia
• Anaerobic metabolism due to oxygen deficiency
lactic acid concentration
• Bradykinin and other proteolytic enzymes are also released
due to cell damage as a result of ischemia
• lactic acid, bradykinin and proteolytic enzymes stimulate
pain nerve endings
• 3. muscle spasm
i. Direct effect----------stimulate mechanoreceptive pain
receptors
ii. Indirect effect
compression of blood vessels ischemia leading to
pain
 increase rate of tissue metabolism more ischemia
more release of chemicals
Posterior median sulcus

Anterior median fissure

• ORIGINATION OF FIBERS IN SPINOTHALAMIC TRACT
1. Pain fibers: Fibers carrying pain fibers reach the spinal
cord via dorsal roots. Central Axons reach the dorsal horn,
they branch into ascending and descending collaterals,
forming the dorsolateral tract of Lissauer. Axons in
Lissauer's tract run up and down for one or two spinal
cord segments before they penetrate the gray matter of
the dorsal horn.
• Neospinothalamic tract ( A delta fast pain) synapse mainly
in lamina I (lamina marginalis) of dorsal horns where they
excite second order neurons which cross to the opposite
side by passing through anterior commissure.
• ORIGINATION OF FIBERS IN SPINOTHALAMIC TRACT
1. Pain fibers---cont’d

• Paleospinothalamic tract (slow pain)carrying mainly type C

slow pain fibers and some fast A delta fibers
synapse/terminate mainly in lamina II and III of dorsal
horns (substantia gelatinosa). Then signals pass through
additional neurons before entering lamina V. from here last
neuron in series give long axons which cross to the opposite
side and join neospinothalamic tract.
• 2. Thermal fibers
• Upon entering the spinal cord, the thermal signals travel for
a few segments upward or downward in the tract of
Lissauer and then terminate mainly in laminae I, II, and III
of the dorsal horns—the same as for pain. After a small
amount of processing by one or more cord neurons, the
signals enter long, ascending thermal fibers that cross to
the opposite anterolateral sensory tract
• Termination of the Anterolateral tract
• (NEOSPINOTHALAMIC TRACT)
• A few fibers of the neospinothalamic tract terminate in the
reticular areas of the brain stem
• Most of the pain fibers from neospinothalamic tract pass all the
way to the thalamus without interruption, terminating in the
ventrobasal complex along with the dorsal column–medial
lemniscal tract.
• A few fibers also terminate in the posterior nuclear group of the
thalamus. From these thalamic areas, the signals are
transmitted to other basal areas of the brain, as well as to the
somatosensory cortex.
• Termination of Anterolateral tract
• PALEOSPINOTHALAMIC TRACT
• The slow-chronic paleospinothalamic pathway terminates widely in
the brain stem. Only one tenth to one fourth of the fibers pass all
the way to the thalamus. Instead, most terminate in one of three
areas: (1) the reticular nuclei of the medulla, pons, and
mesencephalon; (2) the tectal area of the mesencephalon deep to
the superior and inferior colliculi; or (3) the periaqueductal gray
region surrounding the aqueduct of Sylvius.
• From the brain stem pain areas, multiple short-fiber neurons relay
the pain signals upward into the intralaminar and ventrolateral
nuclei of the thalamus and into certain portions of the
hypothalamus and other basal regions of the brain.
• TERMINATION OF FIBERS OF SPINOTHALAMIC TRACT

• Tactile signals in anterolateral tract terminate mainly into

the ventrobasal complex of thalamus where dorsal column
fibers terminates. From here signals are transmitted to the
somatosensory cortex
• Termination of Anterolateral tract
• Thermal signals
• terminate in both (1) the reticular areas of the brain stem
and (2) the ventrobasal complex of the thalamus.
• A few thermal signals are also relayed to the cerebral
somatic sensory cortex from the ventrobasal complex.
• Compare and contrast between neospinothalamic and
paleospinothalamic pathways.
• Differentiate between fast and slow pain.
• Define Referred pain. Describe its mechanism.
• What are two pathways by which visceral pain is
transmitted?
• Describe analgesia system.
• Inhibition of pain transmission by tactile stimulation
(Gate control theory)
• Describe sensory and motor changes occurring in Brown-
Sequard syndrome.
• What is herpes zoster?
• What is Tic douloureux?
• Name the intracranial and extracranial causes of headache?
• Name the temperature receptors, mechanism of
stimulation of receptors, adaptation, spatial summation
and pathway of transmission.
FAST PAIN VERSUS SLOW PAIN
• FAST PAIN SLOW PAIN
1. Also called sharp pain, 1. also called burning pain, aching
pricking pain, acute or electric pain , nauseous and chronic pain
pain
2. Stimuli 2. Stimuli
Mechanical and Thermal mechanical, thermal and chemical

3. Receptors 3. Receptors
Free nerve endings Free nerve endings
FAST PAIN VERSUS SLOW PAIN
• FAST PAIN
4. Perception time
• 0.1 sec after stimulation
5. Body parts involved
Usually skin
SLOW PAIN
4. perception time
1 sec or more then increases
slowly over many sec or
minutes
5. body parts involved
skin and deep tissues
FAST PAIN VERSUS SLOW PAIN
• FAST PAIN SLOW PAIN
6. Duration 6. Duration
• for short time for long time
7. Neurotransmitter 7. Neurotransmitter
• glutamate Substance P
8. localization of pain source 8. localization of pain source
• highly localized enhanced diffuse, poorly localized
• by tactile receptors because of multi synaptic
stimulation connections
9. Non adapting in nature 9. Non adapting in nature
FAST PAIN VERSUS SLOW PAIN
• FAST PAIN SLOW PAIN
10. Transmission 10. Transmission
A delta fibers mainly type C fibers; A delta as well
Neospinothalamic tract Paleospinothalamic tract
Transmission velocity Transmission velocity
6-30 m/sec 0.5-2 m/sec

11. synapse in lamina I of dorsal 11. synapse in lamina II & III of dorsal horn
horn (lamina marginalis) (substantia gelatinosa)
Excite second order neurons signals through short fiber neurons to
Whose axons cross to opposite side lamina V, last axon cross to the opposite
side
FAST PAIN VERSUS SLOW PAIN
• FAST PAIN SLOW PAIN

12. Termination 12. Termination

A few fibers terminate in 1/10th to 1/4th of fibers pass all the
Reticular areas of brain stem, way to thalamus. But most of fibers
Most of them ascend to terminates widely in the brain stem
ventrobasal complex of Thalamus (reticular nuclei of medulla, pons
Along posterior nuclear group. and mesencephalon), tectal area
Then to other basal areas and of mesencephalon,
periaqueductal gray region
Somatosensory cortex From brain stem areas, multiple
FAST PAIN VERSUS SLOW PAIN
• FAST PAIN SLOW PAIN

12. Termination 12. Termination

short fiber neurons relay the pain
signals upward into intralaminar
and ventrolateral nuclei of
thalamus and into certain portions
of the hypothalamus and other
basal regions of the brain
Glutamate is secreted in the spinal cord at the A delta pain nerve fiber
endings. Type C pain fiber terminals entering the spinal cord release
both glutamate and substance P transmitter
Why double pain sensation occurs after a pin
prick??

• A delta pain fibers release glutamate at the synapses in the

spinal cord. Glutamate acts instantaneously and last for only
a few milliseconds. This glutamate neurotransmitter is
involved in transmitting fast pain into the CNS.
• While Substance P is released much more slowly, building up
in concentration over a period of seconds or even minutes.
Substance P is concerned with transmission of slow pain into
CNS
Function of the Reticular Formation, Thalamus, and
Cerebral Cortex in the Appreciation of Pain
complete removal of the somatic sensory areas of the
cerebral cortex does not prevent pain perception. It means
that pain Perception is principally function of lower centers
brain stem reticular formation, the thalamus, and other
lower brain centers cause conscious perception of pain.
electrical stimulation of cortical somatosensory areas does
cause a human being to perceive mild pain from about 3
percent of the points stimulated.
Cortex plays an important role in interpreting pain quality
BRAIN AROUSAL SYSTEM--- role of pain signals
• Electrical stimulation in the reticular areas of the brain
stem and in the intralaminar nuclei of the thalamus, the
areas where the slow-suffering type of pain terminates, has
a strong arousal effect on nervous activity throughout the
entire brain. In fact, these two areas constitute part of the
brain’s principal “arousal system,”
PAIN SUPPRESSION /
ANALGESIA SYSTEM OF BRAIN & SP. CORD
• Three major components
• (1) The periaqueductal gray and periventricular areas of the
mesencephalon and upper pons surround the aqueduct of
Sylvius and portions of the third and fourth ventricles.
Neurons from these areas send signals to
• (2) the raphe magnus nucleus, a thin midline nucleus
located in the lower pons and upper medulla, and the
nucleus reticularis paragigantocellularis, located laterally in
the medulla.
• From these nuclei, second-order signals are transmitted
down the dorsolateral columns in the spinal cord to.
• (3) a pain inhibitory complex located in the dorsal horns of
the spinal cord. At this point, the analgesia signals can block
the pain before it is relayed to the brain
• Neurotransmitters:
• Many nerve fibers derived from the periventricular nuclei and from
periaqueductal gray area secrete enkephalin at their endings.
• Fibers originating from Nucleus Raphe magnus and nucleus
reticularis paragigantocellularis area send signals to the dorsal horns
of the spinal cord to secrete serotonin at their endings.
• The serotonin causes local cord neurons to secrete enkephalin as
well.
• The enkephalin is believed to cause both presynaptic and
postsynaptic inhibition of incoming type C and type Aδ pain
fibers where they synapse in the dorsal horns.
 1----Periaqueductal gray
And periventricular areas
of Midbrain & upper Pons
Secrete Enkephalin

2----Nucleus Raphe magnus &

reticularis Paragiganto-cellularis
In lower Pons & upper medulla
Secrete serotonin

3----- Pain inhibitory complex

in the dorsal horn of Spinal cord
Local release of enkephalin
Causes pre and post synaptic
Inhibition of the pain fibers
ANALGESIA SYSTEM OF BRAIN & SP. CORD
PAIN SUPPRESSION /
ANALGESIA SYSTEM OF BRAIN & SP. CORD

• ACTIVATION OF Analgesia system by

i. nervous signals entering the periaqueductal gray area
and periventricular areas by periventricular nuclei in the
hypothalamus adjacent to 3rd ventricle & Medial
forebrain bundle in hypothalamus or
ii. Inactivation of pain pathways by morphine like drugs
can almost totally suppress many pain signals entering
through the peripheral nerves
Analgesia signals from electrical stimulation in the peri
aqueductal gray area or raphe magnus nucleus can block the
pain signals entering in the spinal cord before they are relayed
to the brain. They also block local cord reflexes resulting from
pain i.e. withdrawal reflexes
Stimulation of higher areas of brain {( Hypothalamus
(periventricular nuclei in the hypothalamus adjacent to 3rd
ventricle & Medial forebrain bundle in hypothalamus} that
excite the periaqueductal gray area can also suppress pain

NEUROTRANSMITTER SUBSTANCES INVOLVED IN ANALGESIA

SYSTEM are ENKEPHALIN & SEROTONIN
Analgesia by Brain‘s Opiate System
• Opiate like substances found at different points in the brain
are the break down products of pro-opiomelanocortin,
proenkephalin & prodynorphin these are
• Enkephalins
• Are found in brain stem and spinal cord
• Βeta-endorphin,
are present in hypothalamus & pituitary
• met-enkephalin, leu-enkephalin & dynorphin
are present in brainstem & spinal cord
• The analgesic actions of opioid drugs are mediated at
multiple sites of action including the dorsal horn of the
spinal cord, and sites within the brain such as the brainstem
and midbrain.
Inhibition of Pain Transmission by
Simultaneous Tactile Sensory Signals
• stimulation of large-type Aβ sensory fibers from peripheral tactile
receptors can depress transmission of pain signals from the same
body area. This effect presumably results from local lateral
inhibition in the spinal cord (gate control hypothesis)
• Examples
• rubbing the skin near painful areas
• liniments are often useful for pain relief.
• Acupuncture relieve pain by Tactile receptors stimulation plus
psychogenic excitation of the Analgesia system
PAIN CONTROL BY TACTILE RECEPTOR STIMULATION
Tactile
stimulation
STRESS INDUCED ANALGESIA

• Soldiers wounded in the heat of battle feel no pain until the

battle is over . This is stress induced analgesia.
• mediated by activation of the descending inhibitory pain
pathway.
Treatment of Pain by Electrical Stimulation
• Stimulating electrodes are placed on selected areas of the skin or,
on occasion, implanted over the spinal cord, supposedly to
stimulate the dorsal sensory columns.
• In some patients, electrodes have been placed discretely in
appropriate intralaminar nuclei of the thalamus or in the
periventricular or periaqueductal area of the diencephalon. The
patient can then personally control the degree of stimulation.
Dramatic relief has been reported in some instances. Also, pain
relief has been reported to last for as long as 24 hours after only a
few minutes of stimulation.
Surgical Interruption of Pain Pathways
1. In case of Severe and intractable pain (sometimes resulting from
rapidly spreading cancer)
• Partial cordotomy in the anterolateral quadrant on the side
opposite to the pain -----------to interrupt the anterolateral sensory
pathway
• Usually done in the thoracic region of the spinal cord
• often relieves the pain for a few weeks to a few months

2. cauterize specific pain areas in the intralaminar nuclei in the

thalamus, which often relieves suffering types of pain while leaving
intact one’s appreciation of “acute” pain, an important protective
mechanism
Surgical interruption of pain pathways
(cont’d)
A cordotomy is not always successful in relieving pain for two
reasons.
1. many pain fibers from the upper part of the body do not cross to
the opposite side of the spinal cord until they have reached the
brain, and the cordotomy does not transect these fibers.
2. pain frequently returns several months later, partly as a result of
sensitization of other pathways that normally are too weak to be
effectual (e.g., sparse pathways in the dorsolateral cord).
Neurotransmitter receptors that directly gate ion channels are
called
Act through second messenger system-----
Tactile receptors that detect movement of objects over surface
Of skin and low frequency vibration are called-------
Tactile receptors detecting pressure-------
Receptors for pain
Neurotransmitter for fast pain is
Synaptic fatigue is due to
Synaptic delay ?
Dorsal column carries ?
 Visceral Pain

• Viscera have sensory receptors for pain

• Localized damage seldom causes pain. Excitation of pain
nerve endings in diffuse areas of the viscera can cause severe
pain.
• Visceral pain in thoracic and abdominal cavities is
transmitted through small type C pain fibers and can
transmit slow suffering type of pain
 CAUSES OF VISCERAL PAIN
Ischemia- Acidic metabolic i.e. lactic acid or tissue
degeneration end products such as bradykinin,
proteolytic enzymes stimulate pain endings

Chemical stimuli- Proteolytic acidic gastric juice may

leak from ruptured gastric or duodenal ulcer--
widespread digestion of parietal peritoneum--pain
 CAUSES OF VISCERAL PAIN
Spasm of hollow viscus – causes pain by mechanical
stimulation of pain endings, spasm causes diminished blood
flow combined with muscle’s increased metabolic need for
nutrients.
Pain from spastic viscus occurs in the form of cramps
e.g. appendicitis, menstruation, parturition.
Over distension of a hollow viscus -– over stretch of
connective tissue and collapse of blood vessels---ischemia
A visceral disease causes visceral pain & parietal pain
Viscera insensitive to pain:
Parenchyma of the liver and alveoli of lungs
However
• Liver capsule is extremely sensitive to both direct
trauma and stretch and bile ducts are also sensitive
to pain.
• In the lungs, both bronchi and parietal pleura are
very sensitive to pain
DUAL PAIN PATHWAY OF VISCERAL PAIN
Sensations from abdomen and thorax are transmitted
through two pathways to the central nervous system
TRUE VISCERAL PATHWAY
• Visceral pain is transmitted by pain sensory fibers in
autonomic nerve bundle and is referred to surface area of
body far from the painful organ
PARIETAL PATHWAY
• Parietal sensations are conducted directly into local spinal
nerves and are localized directly over the painful area
Because of dual pain pathway, Pain from the viscera is
localized to two surface areas of the body at the same time
1. Referred pain to the surface of the body localizes in the
dermatomal segment from which the visceral organ
originated in the embryo e.g. Visceral pain from heart,
• From stomach
• From appendix

• While their parietal component is directly over irritated the

peritoneum
True visceral pain ----referred to
surface area of same dermatomal
origin
Pain impulses pass first from the
inflamed appendix through visceral
pain fibers located within sympathetic
nerve bundles and then into the
spinal cord at about T10 or T11;
this pain is referred to an area around
the umbilicus and is of the aching,
cramping type.
2. Parietal pain---localized
Then as the inflamed appendix
involves the parietal peritoneum, pain
impulses from inflamed peritoneum
causes sharp type pain
directly over the irritated peritoneum
in the right lower quadrant of the
abdomen Rebound tenderness +ve
In right iliac fossa
 REFERRED PAIN

Feeling of pain in a part of the body that is far from

the tissue causing pain is referred pain
• Localized damage to the viscera seldom causes pain

DERMATOMAL RULE
• Visceral pain is referred to the structure which has
same dermatomal origin as that of the visceral
organ in which Pain originates
 REFERRED PAIN

• Heart originated in neck and upper thorax

(between C3 and T5). Heart pain is referred to side
of neck, over the shoulder, over pectoral muscles,
down the left arm and into the substernal area of
the upper chest. These areas send their sensory
fibers into C3 to T5
• Why heart pain is frequently referred to the left
side-??----
As left part of the heart is more frequently involved
than right
 REFERRED PAIN
WHY VISCERAL PAIN IS REFERRED TO THE SURFACE AREA??
MECHANISM
Branches of visceral pain fibers synapse on the same 2nd order
neurons that receive pain signals from the skin of same
dermatome
When the visceral pain fibers are stimulated, pain signals from
the viscera are conducted through at least some of the same
neurons that conduct pain signals from the skin, and the person
has the feeling that the sensations originate in the skin.
*Referred pain mechanism is also called Convergence
-Projection theory*
ALSO CALLED AS CONVERGENCE-PROJECTION THEORY
PHANTOM LIMB
• A phantom limb is the sensation that an amputated or
missing limb is still attached. Approximately 80 to 100% of
individuals with an amputation experience sensations in their
amputated limb. However, only a small percentage will
experience painful phantom limb sensation.
• Reasons: 2 theories
i. Remapping of the somatosensory cortex
ii. Reorganization of brain if sensory input is cut off e.g in ventral
posterior thalamic nucleus
•PAIN & OTHER SOMATIC DISORDERS
• HYPERALGESIA:
• An exaggerated response to a noxious/toxic stimulus

• ALLODYNIA
A sensation of pain in response to an innocuous stimulus.
e.g. painful sensation from a warm shower when skin is
damaged by sun burn
PAIN & OTHER SOMATIC DISORDERS
HYPERALGESIA
(1) excessive sensitivity of the pain receptors, which is called
primary hyperalgesia, and
(2) (2) facilitation of sensory transmission, which is called
secondary hyperalgesia.
• example primary hyperalgesia
extreme sensitivity of sunburned skin, which results from
sensitization of the skin pain endings by local tissue
products from the burn—perhaps histamine, prostaglandins,
and others.
Secondary hyperalgesia frequently results from lesions in
the spinal cord or the thalamus
 Herpes zoster (Shingles)

Herpes virus Herpes zoster is

affects dorsal root reactivation of
ganglion Varicella zoster virus.
Severe pain and Same virus
skin eruption in Which causes
the affected chicken pox
dermatome
• Herpes Zoster
• The cause of the pain is presumably infection of the pain
neuronal cells in the dorsal root ganglion by the virus. In
addition to causing pain, the virus is carried by neuronal
cytoplasmic flow outward through the neuronal peripheral
axons to their cutaneous origins. Here the virus causes a
rash that vesiculates within a few days and then crusts over
within another few days, all of this occurring within the
dermatomal area served by the infected dorsal root.
TIC DOULOUREUX
Trigeminal neuralgia or glossopharyngeal neuralgia
Tic Douloureux
• Lancinating or stabbing type of pain occasionally occurs in
some people over one side of the face in the sensory
distribution area (or part of the area) of the fifth or ninth
nerves; this phenomenon is called tic douloureux (or
trigeminal neuralgia or glossopharyngeal neuralgia
• Triggering factors: movement of jaw while eating
• treatment ----pain is blocked by cutting the peripheral nerve
from the hypersensitive area or sensory portion of fifth
nerve is sectioned inside the cranium or sensory nucleus
ablation
 BROWN SEQUARD SYNDROME

Condition associated with Hemi section of the spinal

cord resulting in paralysis and loss of dorsal column
sensation ipsilateral and loss of spinothalamic
sensations contralateral below the level of
transection
• At the level of lesion
Ipsilateral lower motor neuron lesion
And loss of all cutaneous sensations (dorsal, spinothalmic
and spinocerebellar tracts)
on Contralateral side--- no sensory or motor loss

Above the level of lesion

Ipsilateral no motor loss and probably hperalgesia
On contralateral side---- no sensory or motor loss
 BROWN SEQUARD SYNDROME
a) below the level of transection

• Ipsilateral upper motor neuron lesion

• Ipsilateral loss of sensations carried by Dorsal
Column Medial Lemniscus
• Ipsilateral dystaxia (loss of coordination of
movements d/t damage to dorsal spinocerebellar)
• Contralateral loss of sensations transmitted by
spinothalamic tract 2-3 segments below the level of
lesion
• Contralateral dystaxia d/t damage to ventral
spinocerebellar tract
HEADACHE
INTRACRANIAL ORIGIN
• Headache of Meningitis
• Caused by Low CSF pressure
• Migraine headache
• Alcoholic headache
EXTRACRANIAL ORIGIN
• Resulting from muscle spasm
• Caused by irritation of nasal structures
• Caused by eye disorders
CAUSES of INTRACRANIAL HEADACHE
1. Tugging on venous sinuses around the brain
2. Damage to tentorium
3. Stretching the Dura at the base of the brain
4. Damage to the blood vessels of the meninges
Supratentorial pain stimuli refer headache to front
half of head supplied by somatoS portion of 5th nerve
SUBTENTORIAL pain impulses via glossopharyngeal,
vagus and 2nd cervical are referred to the posterior
part of the head/ Occipital headache
Types of Intracranial Headache

• Headache of Meningitis. Meningitis----inflammation of all

the meninges, including the sensitive areas of the dura and
the sensitive areas around the venous sinuses.
• extreme pain referred over the entire head.
• Headache Caused by Low Cerebrospinal Fluid Pressure.
• Brain is floating in a fluid inside the skull i.e. cerebrospinal
fluid. Removing the CSF even as little as 20 ml can cause
severe intracranial headache as the weight of the brain
stretches and otherwise distorts the various dural surfaces
and thereby elicits the pain that causes the headache.
Migraine Headache
• A recurrent throbbing headache that typically affects one
side of the head and is often accompanied by nausea and
disturbed vision.
• It often begins with various prodromal sensations,
• such as nausea,
• loss of vision in part of the field of vision,
• visual aura, and other types of sensory hallucinations.
Ordinarily, the prodromal symptoms begin 30 minutes to 1
hour before the beginning of the headache.
• genetic predisposition to migraine headaches
positive family history for migraine has been reported in 65 to 90%of
cases.
• Twice as frequently in women as in men
• Theories of migraine headaches
• Prolonged emotion or tension reflex vasospasm of some of the
arteries of the head, including arteries that supply the brain. The
vasospasm theoretically produces ischemia of portions of the brain,
which is responsible for the prodromal symptoms. Then, as a result of
the intense ischemia, something happens to the vascular walls,
perhaps exhaustion of smooth muscle contraction, to allow the blood
vessels to become flaccid and incapable of maintaining normal
vascular tone and pulsate with blood flow for 24 to 48 hours.
• The blood pressure in the vessels causes them to dilate and pulsate
intensely, and it is postulated that the excessive stretching of the
walls of the arteries—including some extracranial arteries, such as the
temporal artery—causes the actual pain of migraine headaches.

• Other theories of the cause of migraine headaches include spreading

cortical depression, psychological abnormalities, and vasospasm
caused by excess local potassium in the cerebral extracellular fluid.
• Alcoholic Headache. As many people have experienced, a
headache often follows excessive alcohol consumption. It is
likely that alcohol, because it is toxic to tissues, directly
irritates the meninges and causes the intracranial pain.
Dehydration may also play a role in the “hangover” that
follows an alcoholic binge; hydration usually attenuates but
does not abolish headache and other symptoms of hangover.
Extracranial Types of Headache
• Headache Resulting from Muscle Spasm
• Headache Caused by Irritation of Nasal and Accessory Nasal
Structures
• Headache Caused by Eye Disorders
•TEMPERATURE SENSATION
• three types of sensory receptors:
• cold receptors,
• warmth receptors, and
• pain receptors stimulated by “freezing cold” and “burning hot”
sensations
• receptors are located immediately under the skin at discrete
separated spots.
• 3 to 10 times as many cold spots as warmth spots in the body and
the number varies
• 15 to 25 cold spots/cm2 in the lips to
3 to 5 cold spots /cm2 in the finger
to less than 1 cold spot /cm2 in some broad surface areas of the trunk
• Warm receptor-----free nerve endings (type C nerve fibers )
0.4 to 2 m/sec
• Cold receptor------Aδ myelinated nerve ending
about 20 m/sec
some free nerve endings also carry cold
sensations
• extreme degrees of both
cold and heat can be painful
• freezing cold and burning
hot sensations feel almost
alike
Thermal receptors adaptation
• Thermal receptors show adaptation
• becomes strongly stimulated at first, but this stimulation
fades rapidly during the first few seconds and progressively
more slowly during the next 30 minutes or more.
• thermal receptor “adapts” to a great extent, but never 100
percent

• thermal senses respond markedly to changes in

temperature, in addition to being able to respond to steady
states of temperature
MECHANISM OF STIMULATION OF THERMAL
RECEPTORS
• There is no direct physical effects of heat or cold on the
nerve endings
• but both cold and warmth receptors are stimulated by
changes in their metabolic rates as temperature alters the
rate of intracellular chemical reactions more than twofold for
each 10°C change (chemical stimulation of nerve endings)
SPATIAL SUMMATION OF THERMAL SENSATIONS

• it is difficult to judge MINUTE gradations of temperature

when small skin areas are stimulated AS low as 0.01 C.
However, when a large skin area is stimulated all at once, the
thermal signals from the entire area summate