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Blockk V : Syyndrommatologyy & Symmptomatology
Moduule 2 : Pain andd the Change off Tempe
Coursse Periood : AAcademiic Year 22009 ‐ 22010
3rd Semeester
AAugust 224th – 288th 2009
FacultBrawij
erature
ty of MMedicine jaya Unniversitty 20099
Kelas A Kelas B Kelas BI 1 2 3 4 1 2 3 4 1 2 3 4
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Time Schedule of Modul V (Syndromatology & Symptomatology) ; Module 2 (Pain and the Change of Temperature)
Academic Year 2009‐2010 ; 3rd Semester ; August 24th ‐ 28th 2009
Mandiri 5
Mandiri 4
Mandiri 3
Mandiri 2
Mandiri 1
Overview of Pain and Body Temperature Change
ISHOMA
ISHOMA
ISHOMA
Kelas A Kelas B Kelas BI
24.08.'09 Senin
Tgl Hari Jam Kegiatan Materi Modul
Keynote Speaker
AA
Kuliah 2 Patophisiology of Neuropathic Pain MDH SNK WMS
Kuliah 3 Regulation of Body Temperature in Adult
Kuliah 1 Patophisiology of Nociceptive Pain FB
RI ESW RR
Kuliah 4 Regulation of Body Temperature in Neonatal TAN
RI
EKO LK
25.08.'09 Selasa
Kuliah 5 Hyperthermia, Fever, Chills & Rash ISN KRM WWJ
Kuliah 6 Hypothermia & Frostbite ISN WWJ KRM
26.08.'09 Rabu
27.08.'09 Kamis
Diskusi 1 Modul Task 1 ‐ 3
Diskusi 2 Modul Task 4 ‐6
Diskusi 3 Modul Task 7 ‐ 8
ISHOMA
TANARY DA ISN SMD EA ACA BS SDR AAN RtR LK
28.08.'09 Jum'at
Diskusi 4 Modul Task 9 ‐ 10
Diskusi 5 Modul Task 11 ‐12
Diskusi 6 Modul Task 13 ‐ 14
ISHOMA
AA IDRDAARY SDR RR RtRON SMD EKO ESW BS
I. PJMK : Dr. med. Tommy Alfandy Nazwar, dr.
II. Secretary : Shahdevi Nandar Kurniawan, dr, SpS.
III. Contributors
A. Sub‐Module Pain
1. Department of Anatomy Histology:
a. Andi Ansharullah, dr, DAAK.
b. Dr. med. Tommy Alfandy Nazwar, dr.
2. Department of Physiology:
a. Dr. Retty Ratnawati, dr, MSc.
b. Prof. Dr. M. Rasjad Indra, dr, MS.
3. Department of Neurology:
a. Moch. Dalhar, dr, SpS.
b. Shahdevi Nandar Kurniawan, dr, SpS.
c. Masruroh Rahayu, dr, MKes.
4. Department of Anesthetic:
a. Hari Bagianto, dr, SpAn(K)IC.
b. Karmini Yupono, dr, SpAn.
c. Isngadi, dr, MKes, SpAn.
d. Wiwi Jaya, dr, SpAn.
5. Department of Neurosurgery:
a. Farhad Bal'afif, dr, SpBS.
b. Agus Chairul Anab, dr, SpBS.
B. Sub‐Module Body Temperature Changes
1. Department of Physiology:
a. Dr. Retty Ratnawati, dr, MSc.
b. Prof. Dr. M. Rasjad Indra, dr, MS.
2. Department of Anesthetic:
a. Karmini Yupono, dr, SpAn.
3. Department of Pediatric:
a. R. Aj. Siti Lintang Kawuryan P, dr, SpA(K).
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page i
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page ii
IV. Keynote‐Speakers and Facilitators
Keynote‐Speakers:
AA : Andi Ansharullah, dr, DAAK. EKO : Eko Sulistijono, dr, SpA. ESW : Dr. Endang Sri Wahyuni, dr, MS. FB : Farhad Bal'afif, dr, SpBS. ISN : Isngadi, dr, MKes, SpAn. KRM : Karmini Yupono, dr, SpAn. LK : R. Aj. Siti Lintang Kawuryan P, dr, SpA(K).
MDH : Moch. Dalhar, dr, SpS. RI : Prof. Dr. M. Rasjad I, dr, MS. RR : Dr. Retty Ratnawati, dr, MSc. SNK : Shahdevi Nandar K, dr, SpS. TAN : Dr. med. Tommy A. Nazwar, dr. WMS : Widodo, dr, SpS. WWJ : Wiwi Jaya, dr, SpAn.
Facilitators: AA : Andi Ansharullah, dr, DAAK. AAN : A. Andi Asmoro, dr, SpAn. ACA : Agus Chairul Anab, dr, SpBS. ARY : Arliek Rio Julia, dr, MS, DAHK. BS : Bambang Soemantri, dr, MKes. DA : Danik Agustin P, dr, MKes. EA : Endang Asmaningsih, dr, MS. EKO : Eko Sulistijono, dr, SpA. ESW : Dr. Endang Sri Wahjuni, dr, MS.
IDR : Indriati Dwi Rahayu, dr. ISN : Isngadi, dr, MKes, SpAn. LK : R. Aj. Siti Lintang Kawuryan P, dr, SpA(K). ON : Onggung MH Napitupulu, dr, MKes. RR : Dr. Retty Ratnawati, dr, MSc. RtR : Rita Rosita, dr, MKes. SDR : Sudiarto, dr, MS. SMD : Soemardini, dr, MPd. TAN : Dr. med. Tommy Alfandy Nazwar, dr.
V. Competency Area
This module is a part of the elaboration of the area of competence 3 of the Indonesian
Doctor Competencies i.e. The Scientific‐Base of Medical Sciences.
VI. Competency Component
A. Review of Anatomy Nervous System
B. To apply the Concepts and Principles of :
1. The Pathophysiology of Nociceptive Pain
2. The Pathophysiology of Neuropathic Pain
3. Neonatal Thermoregulation
4. The Regulation of Body Temperature in Adult
5. The Pathophysiology and the Signs and Symptoms of:
a. Hypothermia & Frostbite
b. Hyperthermia, Fever, Chills, & Rash
VII. Clinical Competence
Be able to recognize and place the clinical pictures of the most common diseases related to
Pain and Change of Temperature syndrome and symptoms and knows how to acquire
more information on it
VIII. Learning Objectives
At the end of the Teaching learning Process of this Module, the student should be able to:
A. Understand the pathophysiology of Pain and the changes of temperature
B. Recognize significant signs and symptoms occurred in some diseases associated with
Pain and the changes of Temperature
C. Identify the most common diseases in Indonesia which are related to Pain and the
changes of Temperature.
IX. Lecture Description
This module is a part of Module on Pain and The Change of Temperature integrated
designed for medical student of the 3rd semester through Teaching‐Learning Process in the
3rd Block both in Lecture and Small Group Discussion. This part of Module will facilitate the
student a basic understanding of the neuroanatomy of Pain and Temperature prior to
developing their knowledge on diseases related to Pain and the Changes of Temperature.
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page ii
X. General Concept of Nociceptive Pain
A. Basic Terms
1. Input from the somatosensory systems informs the organism about events impinging
on it.
2. Sensation can be divided into four types: superficial, deep, visceral, and special.
Superficial sensation in concerned with touch, pain, temperature, and two‐point
discrimination. Deep sensation includes muscle and joint position sense
(proprioception), deep muscle pain, and vibration sense. Visceral sensations are
relayed by autonomic afferent fibers, and include hunger, nausea, and visceral pain.
Special senses – smell, vision, hearing, taste, and equilibrium – are conveyed by
cranial nerves.
3. Receptors are specialized cells for detecting particular changes in the environment,
and is divided into: Extroceptors, (refer: Histology) receive stimulus (pain,
temperature, touch, tactile) sensation from the skin, Enteroceptors, receive sensation
from the mucus membrane of the body openings and visceral organs, and
Proprioceptors receive impulse from muscle, joint, and tendons.
4. Connections are a chain of three long neurones and a number of interneuron
conducts stimuli from the receptor or free ending to the somatosensory cortex. First
Order Neuron lies in Ganglion spinals of Radix posterior of the spinal cord, or a
somatic afferents ganglion of cranial nerves. Second Order neuron lies within the
neuro‐axis (spinal cord or brainstem i.e. Nucleus gracilis and Nucleus cuneatus) to
terminate in the thalamus. Third Order Neuron lays in the thalamus, projects to the
sensory cortex, in turn, process information, interpret its location, quality, and
intensity and make appropriate responses.
5. Sensory Pathways are bundle (tractus) of multiple neurons created from the same
type of receptor. This pathway ascending in the spinal cord continues within the
brainstem, to end in the main sensory areas in the cortex (gyrus postcentralis). There
are two major sensory pathways, i.e. the lemniscal (dorsal column) system (funiculus
gracilis/Goll and funiculus cuneatus/Burdach) carries touch, joint sensation, two point
discrimination, and vibratory senses from receptor to the cortex, and the
ventrolateral system (ventral: spino‐reticular pathway relays deep and chronic
somatic pain to brainstem ; lateral: spinothalamicus lateralis relays impulses
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 1
concerning nociceptive stimuli such as pain, crude touch or changes in skin
temperature). Each of the two systems is characterized by somatotopic distribution
with convergence in the thalamus and sensory projection areas of cerebral cortex,
where there is a map like representation of the body surface.
6. The sensory trigeminal fibers contribute to both of the two systems and provide the
input from the face and mucosal membranes.
B. Pain Pathways
The free nerve endings in peripheral and cranial nerves responsible to be specific
receptors for pain are called Nociceptors which are sensitive to mechanical, thermal, or
chemical stimuli. The pain fibers in peripheral nerves are smaller than in the cranial
nerves and are readily affected by local anesthetics. The thinly myelinated A‐delta fibers
convey discrete, sharp, short lasting pain. The unmyelinated C fibers transmit chronic,
burning pain. These nociceptive axons arise from neurons located within Ganglion spinals
of radix posterior spinal cord and Ganglion trigeminus.
Injured tissue may release prostaglandins or other neuroactive molecules (such as
serotonin, histamine, and bradykinin), which lower the threshold of peripheral
nociceptors and thereby increase the sensibility to pain (hyperalgesia). Aspirin and other
nonsteroidal anti inflammatory drugs inhibit the action of prostaglandins and act to
relieve pain (hypalgesia/analgesia).
C. Pain Systems
The central projections of nociceptive primary sensory neurons impinge on
second‐order neurons within superficial of cornu posterior on the spinal cord.
According to the gate theory of pain, the strength of synaptic transmission at
these junctions is decreased when large axons within the nerve are excited (“the gate
closes “). Conversely, the strength of synaptic transmission is increased when there is no
large‐fiber input.
There is some evidence for long‐lasting changes, which may underlie chronic pain
syndromes, in the cornu posterior after nerve injury. For example, after injury to C fibers,
these fibers may degenerate and vacate their synaptic target sites on superficial second‐
order neurons within the cornu posterior. This central sensitization may produce
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 2
Allodynia that is perception of innocuous stimulus as painful or Hyperpathia that is
perception of a mildly unpleasant stimulus as very painful.
The central ascending pathway for pain sensation consists of two systems: the
Tractus spinothalamicus lateralis which conducts the sensation of sharp, stabbing pain,
and the Tractus spino‐reticulo‐thalamicus which conveys deep, poorly localized, burning
pain. Both pathways are interrupted when the ventrolateral quadrant of spinal cord is
damaged by trauma or in surgery (cordotomy), deliberately performed to relive pain;
contralateral loss of all pain sensation results below the lesion.
D. Referred Pain
Pain arising from a viscous such as the stomachache varies from dull to severe;
however the pain is poorly localized; it radiates to the dermatome level that receives
sensory fibers from the organ concerned.
The cells in columna posterior that receive noxious sensations from afferents in
the skin also receive input from nociceptors in the viscera. When visceral afferents
receive a strong stimulus, the cortex may misinterpret the source. For example, referred
pain in the shoulder caused by gallstone colic; the spinal segments that relay pain from
the gall‐bladder also receive afferents from the shoulder region (convergence theory).
Similarly, pain in the heart caused by myocardial infarct is conducted by fibers that reach
the same medulla spinals segments where pain afferents from N. ulnaris (lower arm
area) synapse. Other theory is Facilitation theory; in which visceral pain facilitates input
from a somatic structure, has not been proved conclusively.
E. Descending Systems and Pain Control
Certain neurons within the brain, particularly of the grey matter of the midbrain,
send descending axons to medulla spinalis. One of the descending axon is relayed in the
medulla oblongata and continued to the medulla spinalis as serotonergic pathway. The
other, is relayed and continued too to the medulla spinalis as cathecolaminergic
pathway. These two descending pathways act as inhibitory pathways, suppress the
transmission of pain signals and can be activated with endorphins and opiate drugs.
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 3
XI. General Concept of Neuropathic Pain
A. Overview
Neuropathic pain is the 14th most common pain complaint seen in general
practice. Despite the availability of many well‐tolerated therapies, patients like Mrs.
Showalter often receive inadequate care. A recent survey of patients with neuropathic
pain showed that the majority was undertreated. In this survey, 73% of respondents
reported inadequate pain control. In addition, 25% had never been treated with
standard therapy, including antiepileptic drugs (AEDs), antidepressants, or opioids.
Despite the widespread acceptance of AEDs and antidepressants as effective, first‐line
therapy, 72% of patients with neuropathic pain had never been treated with an AED and
60% had never been treated with a tricyclic antidepressant. Neuropathy frequently
accompanies a variety of general medical conditions, including diabetes, RA, and thyroid
disease. Neuropathy may also occur as a consequence of peripheral nerve injury.
Historical identification of conditions with frequent neuropathic co morbidity raises the
index of suspicion of neuropathy as the cause of chronic pain, especially extremity pain.
B. Definition
Neuropathic pain is characterized by altered, unpleasant sensations. Several
adjectives used to describe pain are more commonly used by patients with neuropathic
pain. Textbook descriptions of neuropathy often focus on numbness. Patients, however,
are generally less disturbed by the absence of normal sensation (or numbness) and are
more concerned with new abnormal sensations perceived in the numb area, including
burning, prickling, heat, cold, or a perception of swelling. Patients may also refer to the
affected area as feeling “wooden” or “dead.” Although the painful area may become
insensible to normal touch stimuli, patients will often describe the presence of intense
sensations over the neuropathic area. Generally, these perceptions are greatest when
the damaged area is stimulated (e.g., by wearing clothing, using bedclothes, or being
exposed to the wind). Patients may occasionally report that the neuropathic area feels
misshapen, deformed, or alien, although the external appearance may be quite normal.
The presence of hyperalgesia and allodynia effectively discriminate neuropathic
from non‐neuropathic pain. Occasionally, the examiner may notice that the painful area
is cool to the touch. Rarely, the same area may be warm and red.
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 4
C. Pathophysiology of Neuropathic Pain
Advances in the neuroscience of pain have significantly helped our understanding
of the mechanisms underlying symptoms and signs of neuropathic pain. Descriptions of
pain after nerve injury and dysfunction date as far back as the late eighteenth century
and have been described in greater detail in the late nineteenth century. Pathologic
studies of human peripheral nerves demonstrating preferential loss of nerve fibers in
certain painful neuropathies, such as postherpetic neuralgia, laid the groundwork for
theories postulating the loss of myelinated fibers as the precursor of neuropathic pain.
These ideas subsequently formed the basis for the gate‐ control theory of pain. However,
pathologic studies demonstrating the loss of other fiber types as well, including small
unmyelinated fibers, called for additional explanations for the underlying
pathophysiology of neuropathic pain. After an extensive review of this topic, Scadding
concluded that the loss of a particular fiber size did not predispose patients to develop
pain, nor did it prevent them from developing pain as part of peripheral neuropathy.
Human psychophysical studies performed in the first half of the twentieth
century set the stage for the developing concept of sensitization of neurons in the
peripheral and central nervous system (CNS). It was, however, the introduction of animal
models that dramatically enhanced our understanding of the pathophysiology
mechanisms of such abnormal phenomena as allodynia and hyperalgesia, both of which
are common symptoms of neuropathic pain.
D. Pathophysiology Mechanisms Underlying Abnormal Sensations
The primary pathology in peripheral neuropathies is in the peripheral nervous
system, so that primary pathophysiology mechanisms are those of the peripheral
nervous system. However, it is overwhelmingly clear from basic science research that the
CNS undergoes changes when the peripheral nervous system is injured and
dysfunctional. The concept that has been evolving is that peripheral generators of
abnormal activity are responsible for chronic pain symptoms. Consequently, efforts
should be made to correct the abnormalities in the peripheral nervous system to
improve overall symptomatology.
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 5
A large number of human laboratory and clinical studies, as well as animal
research on sensory symptoms and signs of neuropathic pain syndromes, point to the
many peripheral and central mechanisms whose interactions lead to the manifestation
of neuropathic pain. Enough experimental and clinical evidence exists from peripheral
nervous system research to suggest some common mechanisms as a cause for
neuropathic pain. These mechanisms include receptor sensitization and spontaneous
afferent activation. On the other hand, all symptoms cannot be explained by peripheral
pathophysiology. An increasing body of basic science information suggests that CNS
mechanisms play a significant role, and central sensitization is the best example of how
CNS mechanisms lead to the development of chronic neuropathic pain. An exciting
development has been the realization that peripheral sensitization can initiate and
maintain central mechanisms of neuropathic pain.
A large body of research exists on peripheral mechanisms of neuropathic pain
and associated phenomena. Sensitization of nociceptors has been documented even in a
human patient, and it is probable that this sensitization occurs as a result of the release
of many chemical mediators of inflammation, the so‐called inflammatory soup.
Sensitization of primary afferents has been documented in animal and human research
and it presents with ectopic generation of nerve impulses at the site of injury caused by
increased sensitivity of adrenergic receptors. Continuous spontaneous activity of
sensitized primary afferents is the probable mechanism of ongoing pain. Up regulation of
sodium channels is possibly a more specific explanation of mechanical allodynia and
hyperalgesia. Hyperalgesia to heat appears to be mediated by sensitized small fiber
nociceptors. Sympathetic catecholamine sensitization of the primary afferents may be
the mechanism by which the sympathetic nervous system adversely affects primary
afferents resulting in hyperalgesia and allodynia. Ephaptic transmission between the
sympathetic nervous system and primary afferents has been suggested. Activation of
silent nociceptors could explain ongoing pain and pressure pain. Ectopic discharges of
dorsal root ganglion cells have been documented in animal models of neuropathic pain
and could also explain ongoing pain.
CNS plasticity changes, particularly in neuropathic pain, play a significant part in
the development and maintenance of chronic pain syndromes and their symptoms and
signs. The symptoms and signs related to the phenomenon of central sensitization were
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 6
recognized in the late 1930s and have been well characterized in human laboratory
models. Clinical research has confirmed what the laboratory models had demonstrated:
Neuropathic pain phenomena, such as ongoing pain, allodynia, and hyperalgesia, are to a
significant degree the result of central mechanisms. Research in animal models
contributed significantly to the understanding of some of the basic mechanisms. The
phenomenon of wind‐up at the dorsal horn level was recognized as early as 1966, but
received much deserved attention only over the 1990s. Physiologic and pharmacologic
studies of spinal cord neuroplasticity changes after neuropathic injuries have contributed
to a better understanding of wind‐up and central sensitization. It was found that
excitatory amino acid neurotransmitters, in particular N‐methyl‐D‐aspartate (NMDA)
receptor‐related activity, play a crucial role in the genesis and maintenance of chronic
neuropathic pain and associated symptoms and signs. Our understanding of
pathophysiologic mechanisms underlying neuropathic pain has advanced considerably,
and it is becoming clear that neuropathic pain is a complex biological phenomenon with
many components. A better understanding of the pathologic mechanisms of neuropathic
pain and its components should contribute to a better evaluation and treatment of
patients with neuropathic pain, including painful neuropathies.
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 7
E. Epidemiology of Common Neuropathic Pain Syndromes
Neuropathy is a common accompaniment of a variety of common medical
conditions. The etiology of the neuropathy is usually identified based on a history of
comorbid medical illnesses or previous nerve injury. Patients with evidence of peripheral
neuropathy should be screened for these common medical conditions.
F. Diabetic Neuropathy
Neuropathy occurs in approximately 23 to 28% of patients with diabetes. The risk
of developing neuropathy increases with type 2 diabetic, aging, duration of diabetes, and
medical consequences of diabetes (e.g., renal and cardiovascular disease). Peripheral
neuropathy is common in older patients with diabetes, even when the blood sugar is
well controlled. Peripheral neuropathy occurs in more than 50% of patients with type 2
diabetes who are older than 60 years.
G. Postherpetic Neuralgia
Postherpetic neuralgia is defined as pain that persists for more than 1 month
after the onset of herpes zoster. Postherpetic neuralgia occurs in approximately 30% of
patients following acute zoster and lasts 1 year in approximately 10% of patients.
Persistence of postherpetic neuralgia increases with aging and pain severity.
Interestingly, despite the focal nature of postherpetic neuralgia pain complaints, patients
with these conditions report significant impairment in both physical and emotional
quality of life. Interestingly, quality of life for all eight domains of the Medical Outcome
Health Survey (SF‐36) is lower in patients with postherpetic neuralgia versus patients
with acute herpes zoster.
H. Complex Regional Pain Syndromes
Complex regional pain syndrome (CRPS) develops following an identified injury or
period of limb immobilization (e.g., casting). CRPS may be categorized as type 1
(occurring in the absence of a nerve injury; formerly called reflex sympathetic dystrophy)
or type 2 (occurring after injury to a specific large nerve; formerly called causalgia). The
terms “sympathetically maintained pain” and “sympathetically mediated pain” were also
formerly used to describe this syndrome. Failure to achieve relief using sympathetic
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 8
blocks, particularly in patients with long‐standing complaints, led to the discontinuation
of these terms. CRPS patients are readily identified in the clinic by seemingly
exaggerated guarding of the painful extremity, often holding the arm in a splinted
posture and avoiding movement. They may also shroud the extremity with a cover to
limit sensory exposure or, alternatively, hold the extremity away from the body as
though trying to continually demonstrate the painful area to onlookers. Some patients
will place an affected arm across the doctor’s desk for history taking, often to the
surprise of the examiner. These behaviors serve to reduce normal movement of or
contact with the painful limb. The patient history reveals a persistently painful extremity
with pain severity that is disproportionately in excess of that caused by any preceding
injury. Patients typically report changes in temperature in the painful limb, as well as
intermittent redness and swelling. These findings may or may not be evident at the time
of evaluation because they are generally transient (see Box 2). Interestingly, subjective
patient reports of CRPS changes (allodynia, edema, and sweating/color/temperature
abnormality) have greater diagnostic sensitivity and specificity than objective clinical
examination findings for the same conditions. On examination, patients with CRPS
excessively guard the painful limb, often splinting it and restraining an examiner from
touching it. “Motor neglect” has also been described in some patients with CRPS, who
have reported an inability to move the extremity, to move an extremity without mentally
focusing on the extremity, or a perception that the extremity is no longer part of the
person’s body.
Objective motor findings are rarely present in CRPS, but may include restricted
range of motion, weakness, or tremor. Motor findings typically are seen with very long‐
standing, untreated CRPS. Ten or 20 years ago, it was common to see patients with end‐
stage CRPS, with contracted joints, as well as abnormal skin, hair, and nail growth. Better
identification of this syndrome and an emphasis on rehabilitation and maintaining
function in the painful limb has resulted in current patients typically displaying evidence
of only early, more reversible disease stages, such as color and temperature changes and
avoidance of movement by voluntary splinting. A Mayo Clinic survey identified the
prevalence of CRPS types I and II, respectively, as 0.02 and 0.004%. Patients with CRPS
type I were predominantly female (female : male ratio = 4 : 1). Pain typically affected
an upper extremity in patients with either type I and II. The most common precipitating
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 9
events for CRPS type I was fracture (46%) and sprain (12%). CRPS type I symptoms
resolved in 74% of cases, with a mean time to resolution of 1 year. In this sample, clinical
signs and symptoms were similar. In clinical practice, however, symptoms reported by
patients are usually not observed during the initial visit or visits but may be noted over
time when multiple opportunities to observe the extremity have occurred.
I. Cancer‐Related Neuropathy
Cancer‐related neuropathy may occur as a consequence of compressive
neuropathy, direct injury from surgery, chemotherapy, or nutritional deficits.
Management of cancer‐related neuropathy with standard analgesics and neuropathic
medications is effective in most patients. A survey of 213 cancer patients with
neuropathy showed satisfactory to good efficacy with standard neuropathic treatment in
79 to 91% of patients.
J. HIV‐Related Neuropathy
Distal sensory polyneuropathy (with complaints of painful feet) is the most
common neuropathy seen in human immunodeficiency virus (HIV)‐infected patients and
may be caused by immunological dysfunction related to the infection itself, as well as the
toxicity of antiretroviral drugs. Sensory neuropathy does occur in HIV‐infected patients
prior to treatment with antiretroviral medications. A recent survey of HIV patients who
had never been treated with antiretroviral drugs showed symptomatic neuropathy in
35%,, with a 1‐year incidence rate for symptomatic distal sensory neuropathy of 36%.
The risk for neuropathy increases with antiretroviral therapy, with combination
dideoxynucleoside therapy having synergistic effects on neurotoxicity and symptomatic
neuropathy
K. Evaluation of Neuropathic Pain
Peripheral neuropathy is best recognized by the identification of symmetrical,
distal dysesthesia, and sensory loss, such as a stocking or sock distribution of numbness
or burning pain. Historical reports of hyperalgesia and allodynia, along with a history of
predisposing medical conditions, establish a probable diagnosis for peripheral
neuropathy. Diagnosis becomes more obvious as neuropathy severity increases and
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 10
sensory loss becomes more dense. Other types of chronic neuropathic pain, such as
postherpetic neuralgia and CRPS, are identified by eliciting a history of inciting events In
patients with painful feet, other common causes of chronic foot pain need to be ruled
out. Unique pain locations and symptoms with nonneuropathic syndromes can help the
clinician distinguish them from peripheral neuropathy. Morton’s neuroma produces a
unilateral pain that is located in the ball of the foot with weight bearing. Plantar fasciitis
is an excruciating pain in the heel of one or both feet that occurs after taking the first
steps on rising from bed or a prolonged sitting position. Tarsal tunnel syndrome
produces a diffuse pain over the medial ankle and sole, caused by compression of the
tibial nerve. The tibial nerve travels behind the medial malleolus, immediately posterior
to the tibial artery. Both travel into the foot beneath the flexor retinaculum, a fibrous
band between the medial malleolus and the calcaneous.
Nerve impingement in the tarsal tunnel is similar to but less common than
compression of the median nerve in the carpal tunnel of the wrist. Loss of vibratory and
joint position sensations is a good marker of early peripheral neuropathy. Except in cases
of severe nerve impairment, when vibratory testing is no longer necessary because of
marked loss of tactile sense, most patients with neuropathy will still perceive vibration
from a tuning fork that has been struck hard enough to produce audible sound.
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 11
Detection of early neuropathy requires a comparison of the level of tuning fork vibration
that is perceived in the toe of the healthy examiner. Elderly patients and patients with
diabetes who lack significant neuropathy should be able to sense the level of vibration
that is just perceived in the healthy examiner’s great toe when the tuning fork is
immediately placed on the patient’s lateral malleolus.
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 12
XII. General Concept of Temperature (Regulation of Body Temperature)
A. Normal Body Temperature
As a homeothermic living creature, normal value for the morning oral
temperature of young adults is 36.3‐37.1 oC (97.3‐98.8 oF). Various parts of the body
are at different temperature, and the magnitude of the temperature different between
the parts varies with the environment temperature. The extremities are generally
cooler than the rest of the body. The temperature of the scrotum is carefully regulated
at 32 oC. The rectal temperature is representative of the temperature at the core of the
body and varies least with changes in environmental temperature. The oral
temperature is normally 0.5 oC lower than the rectal temperature, but it is affected by
many factors, including ingestion of hot or cold fluid, gum‐chewing, smoking, and
mouth breathing.
The normal human core temperature undergoes a regular circadian
fluctuation of 0.5‐0.7 oC. In individual who sleep at night and are awake during the day,
it is lowest at about 6 AM and highest in the evenings. It is lowest during sleep, is
slightly higher in the awake but relaxed state, and rises with activity. In women, an
additional monthly cycle of temperature variation is characterized by a rise in basal
temperature at the time of ovulation. Temperature regulation is less precise in young
children, and they may normally have a temperature that is 0.5 oC or so above the
established norm for adult.
B. Body Temperature is Controlled by Balancing Heat Production Against Heat Loss
In the human body, heat is produced by: 1) muscular activity, 2) assimilation of
food, and 3) all the vital processes that contribute to the basal metabolic rate. It is lost
from the body by: 1) radiation, 2) conduction and convection, 3) vaporization of water
in the respiratory passages and on the skin, and 4) by urination and defecation. The
balance between heat production and heat loss determines body temperature.
Because the speed of chemical reaction varies with the temperature and
because the enzyme systems of the body have narrow temperature ranges in which
their function is optimal, normal body function depends on a relatively constant body
temperature.
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 13
During exercise, the heat produced by muscular contraction accumulates in the
body, and the rectal temperature normally rises as high as 40 oC (104 oF). Body
temperature also rises slightly during emotional excitement, probably due to
unconscious tensing of the muscles. It is chronically elevated by as much as 0.5 oC when
metabolic rate is high, as in hyperthyroidism, and lowered when the metabolic rate is
low, as in hypothyroidism.
A variety of basic chemical reaction contributes to body heat production at all
times. Ingestion of food increases heat production because of the specific dynamic
action of the food, but the major source of heat is the contraction of the skeletal
muscle. Heat production can be varied by endocrine mechanism in the absence of food
intake or muscle exertion. Epinephrine and nor‐epinephrine produce a rapid but short‐
lived increase in heat production, while thyroid hormone produces a slowly developing
but prolonged increase. Furthermore, sympathetic discharge decrease during fasting
and is increased by feeding.
The reflex thermoregulatory responses in human involve autonomic, somatic,
endocrine, and behavioral changes. One group of responses increases heat loss and
decreases heat production; the other decrease heat loss and increases heat production.
C. The body response to cold:
Increasing heat production by: shivering, hunger, increase voluntary activity, and
increase secretion of nor‐epinephrine and epinephrine. Decreasing of heat loss causes
by: coetaneous vasoconstriction, curling up, and horripilate.
D. The body response to heat:
Increasing heat loss by: coetaneous vasodilatation, sweating, and increase respiration.
Decreasing of heat production causes by: anorexia, apathy and inertia.
E. Role of the Hypothalamus in Regulating the Body Temperature
Thermoregulatory adjustments involve local response as well as general reflex
responses. When coetaneous blood vessels are cooled, they become more sensitive to
catecholamine and the arterioles and venules constrict. This mechanism directs blood
away from the skin. Another heat‐conserving mechanism in human living in cold
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 14
environment is countercurrent exchange. Heat transfers from arterial to venous blood
in the limbs. The deep veins (vena concomitant) run alongside the arteries supplying
the limbs, and heat is transferred from the warm arterial blood going to the cold
venous blood coming from the extremities.
The hypothalamus is said to integrate body temperature information from
sensory receptors (primarily cold receptors) in the skin, deep tissues, spinal cord, extra
hypothalamic portions of the brain, and hypothalamic itself. Each of these five inputs
contributes about 20% of the information that is integrated. There are threshold core
temperatures for each of the main temperature‐regulating responses, and when the
threshold is reached, the response begin. The threshold is 37 oC for sweating and
vasodilatation, 36.8 oC for vasoconstriction, 36 oC for non shivering thermogenesis, and
35.5 oC for shivering.
F. Heat Loss
Heat is transferred from deeper organ and tissues to the skin, where it is lost to the air
and other surrounding.
G. Insulator System of the body
The skin; subcutaneous tissues and especially the fat of the subcutaneous tissue act
together as a heat insulator for the body. The insulation beneath the skin is an effective
means of maintaining normal internal core temperature.
H. Blood flow to the Skin from the Body Core Provide Heat Transfer
1. Blood vessels are distributed profusely beneath the skin. Especially important is a
venous plexus that is supplied by inflow of blood from the skin capillaries. In the
most exposed area of the body (the hand, feet, and ear) blood is also supplied to the
plexus directly from the small arteries through highly muscular arteriovenous
anastomoses. The rate of blood flow into the venous plexus can vary tremendously
(Almost zero è 30 % Cardiac output).
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 15
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Pain and The Changes of Teemperature; AAcademic Year 2009-2010 Page 166 Module -
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Pain and The Changes of Teemperature; AAcademic Year 2009-2010 Page 177 Module -
XIII. General Concept of Neonatal Thermoregulation
A. Introduction
Thermoregulation is the balance between heat loss and body heat production.
The main goal is to maintain the neonatal environment in neutral thermal environment
state and minimize energy expenditure.
Newborn normal temperature : 36,5‐37,5 °C
Hypothermia : Body temperature less than 36,5°C
Hyperthermia : Body temperature more than 37,5 °C
Neutral thermal environment : the range of thermal environment in which the body
temperature is normal, oxygen and caloric
consumption is minimal and the least amount of
metabolic energy is expended.
B. Thermoregulation mechanism
Heat production came from nor epinephrine release causing brown fat deposits
metabolism and oxygen and glucose consumption. At birth, body temperatures
suddenly fall and cold stress occurs.
NOTE: Since newborns cannot shiver, they depend on thermo genesis without
shivering or chemical mechanism to produce heat.
Heat loss can happen very drastic over newborns ability to produce heat and maintain
balance.
There are four mechanisms by which heat is loss in newborns:
Evaporation : Heat loss by water evaporation from wet skin or mucous
Conduction : Heat loss by transfer from body molecules to molecules from a cold
surface that contact with the newborn body. It happens when the
newborn baby placed in a cold and solid surface.
Radiation : Heat loss by electronic waves transfer to other objects that are not in
direct contact.
Convection : Heat loss from body/skin molecules to the surrounding air caused by air
flow.
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 18
All of these mechanisms are problems found in all neonatal care wards. When
the air temperature is very warm, newborns can obtain heat, especially from radiation
and convection process.
NOTE: Sick or preterm newborns are unable to raise their body temperature (by
increasing the body metabolism rate) and have less brown and subcutaneous
fat than term newborns.
C. Pathophysiology of Thermoregulation
1) Hypothermia
• Condition related to hypothermia
Cold environment
Incorrect neonatal nursery after birth ;
‐ inadequate drying process
‐ insufficient clothing
‐ Separating from the mother
‐ Insufficient warming process (before and during transfer)
‐ Sick and stress baby
• Sign and Symptoms
Measuring the newborns body temperature might not be sufficient to detect
early change from cold stress. Newborns are able to use their energy savings to
maintain their body temperature (central temperature) at early stage. Early signs
that might be found are:
Cold feet
Weak sucking ability or feeding intolerance
Lethargy
Skin color change from pale and cyanotic to cutis marmorata or plethora
Tachypnea and tachycardia
Late signs might be found when hypothermia continues :
‐ Lethargy, weak cry
‐ Apneu and bradycardia
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 19
‐ High risk of hypoglycemic, metabolic acidosis, respiratory distress,
abnormality of bleeding factors (DIC, intra ventricular bleeding, pulmonary
hemorrhage)
2) Hyperthermia
• Condition related to hyperthermia:
High environment temperature
Dehydration
Intra Cranial Bleeding
Infection
NOTE: Incubator needs to be observed closely to maintain the temperature.
• Sign and Symptoms
Warm skin, at early reddish or pinkish skin then become pale
The inability to sweat in the newborns is a big part of the problem
Same patterns as hypothermia: increasing metabolism rate, irritability,
tachycardia and tachypnea
Dehydration, intra cranial bleeding, heat stroke and death
D. Management
1) Temperature control
• At delivery room:
Give warm environment free from air flow
Dry the newborns immediately
Mother‐baby contact. Blanketing mother and newborns altogether or cover
with cloth
Covering newborns head with cap
• Use of radiant warmer if contact with the mother is not possible (the mother
underwent post natal complication)
Undress newborns except for diapers and place under radiant warmer
Place temperature probe flat to skin, usually in the abdominal area (right
hypochondria region)
Servo temperature set on 36,5 °C
Measure the body temperature every 30 minutes
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 20
• Procedures need to be followed during incubator period:
Make sure all persons involved in the newborns care are able to use incubator
properly, monitoring the newborns temperature, and adjust the incubator
temperature to maintain neutral environment temperature
Enough continuous power supply, trained maintenance staff and available
spare parts for the incubator
Placed incubator far from opened window. The neonatal ward temperature
must be adequate and minimize opening incubator
NOTE: Direct contact to the sun or phototherapy procedure is able to induce
overheat, therefore body temperature should be monitored closely and
incubator temperature often needs to be adjusted.
• When newborns need incubator care, parents should be encouraged to visit and
carry their baby as often as possible to stabilize the body temperature.
Newborns temperature must be measured every 4 hours or according to the
doctor’s instructions to maintain the body temperature between 36, 5 °C –
37,5 °C
Open incubator portholes only when necessary and for brief periods
2) Temperature Measurement
• Axillary temperature
Benefits: able to detect decrease of body temperature fast, accurately, and
hygiene
Place the thermometer in the middle of the armpit and hold it with the infant
arm at the body side for 5 minutes
Skins in this location are not reacted to low body temperature with
vasoconstriction
Even though the axillary temperature will be lower than the real body
temperature, but any change of axillary temperature will be the same as the
change of body temperature
• Rectal temperature
It is an invasive procedure and not always reliable
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 21
Body temperature from the lower extremities can affect the rectal
temperature
When peripheral vasoconstriction happens, newborns will concentrate their
circulation, therefore cold blood from both lower extremities will reduce the
rectal temperature
• Environment temperature
Each room must be equipped with wall thermometer
Maintain the room temperature between 24‐26 °C
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 22
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Signs And Symptoms Associated With The Changes Of Temperature
1. Fever – Hyperthermia – Fever And Rash
1. FEVER
Fever is an elevation of body temperature that exceeds the normal daily variation
and occurs in conjunction with an increase in the hypothalamic set point (e.g., from 37°C to
39°C). This shift of the set point from "normothermic" to febrile levels very much resembles
the resetting of the home thermostat to a higher level in order to raise the ambient
temperature in a room. Once the hypothalamic set point is raised, neurons in the
vasomotor center are activated and vasoconstriction commences. The individual first
notices vasoconstriction in the hands and feet. Shunting of blood away from the periphery
to the internal organs essentially decreases heat loss from the skin, and the person feels
cold. For most fevers, body temperature increases by 1°–2°C. Shivering, which increases
heat production from the muscles, may begin at this time; however, shivering is not
required if heat conservation mechanisms raise blood temperature sufficiently.
Nonshivering heat production from the liver also contributes to increasing core
temperature. In humans, behavioral adjustments (e.g., putting on more clothing or bedding)
help raise body temperature by decreasing heat loss.
The processes of heat conservation (vasoconstriction) and heat production
(shivering and increased nonshivering thermogenesis) continue until the temperature of the
blood bathing the hypothalamic neurons matches the new thermostat setting. Once that
point is reached, the hypothalamus maintains the temperature at the febrile level by the
same mechanisms of heat balance that function in the afebrile state. When the
hypothalamic set point is again reset downward (in response to either a reduction in the
concentration of pyrogens or the use of antipyretics), the processes of heat loss through
vasodilation and sweating are initiated. Loss of heat by sweating and vasodilation continues
until the blood temperature at the hypothalamic level matches the lower setting. Behavioral
changes (e.g., removal of clothing) facilitate heat loss.
A fever of >41.5°C (>106.7°F) is called hyperpyrexia. This extraordinarily high fever
can develop in patients with severe infections but most commonly occurs in patients with
central nervous system (CNS) hemorrhages. In the preantibiotic era, fever due to a variety
of infectious diseases rarely exceeded 106°F, and there has been speculation that this
natural "thermal ceiling" is mediated by neuropeptides functioning as central antipyretics.
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 26
In rare cases, the hypothalamic set point is elevated as a result of local trauma,
hemorrhage, tumor, or intrinsic hypothalamic malfunction. The term hypothalamic fever is
sometimes used to describe elevated temperature caused by abnormal hypothalamic
function. However, most patients with hypothalamic damage have subnormal, not
supranormal, body temperatures
2. HYPERTHERMIA
Although most patients with elevated body temperature have fever, there are
circumstances in which elevated temperature represents not fever but hyperthermia
Hyperthermia is characterized by an uncontrolled increase in body temperature that
exceeds the body's ability to lose heat. The setting of the hypothalamic thermoregulatory
center is unchanged. In contrast to fever in infections, hyperthermia does not involve
pyrogenic molecules (see "Pyrogens," below). Exogenous heat exposure and endogenous
heat production are two mechanisms by which hyperthermia can result in dangerously high
internal temperatures. Excessive heat production can easily cause hyperthermia despite
physiologic and behavioral control of body temperature. For example, work or exercise in
hot environments can produce heat faster than peripheral mechanisms can lose it.
A. Causes of Hyperthermia
1) Heat stroke
In association with a warm environment may be categorized as exertional or
nonexertional. Exertional heat stroke typically occurs in individuals exercising at
elevated ambient temperatures and/or humidities. In a dry environment and at
maximal efficiency, sweating can dissipate ~600 kcal/h, requiring the production of >1
L of sweat. Even in healthy individuals, dehydration or the use of common
medications (e.g., over‐the‐counter antihistamines with anticholinergic side effects)
may precipitate exertional heat stroke. Nonexertionalheat stroke typically occurs in
either very young or elderly individuals, particularly during heat waves.
2) Drug‐induced hyperthermia
It has become increasingly common as a result of the increased use of prescription
psychotropic drugs and illicit drugs. Drug‐induced hyperthermia may be caused by
monoamine oxidase inhibitors (MAOIs), tricyclic antidepressants, and amphetamines
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 27
and by the illicit use of phencyclidine (PCP), lysergic acid diethylamide (LSD),
methylenedioxymethamphetamine (MDMA, "ecstasy"), or cocaine.
B. Pathogenesis of Fever
1) Pyrogens
The term pyrogen is used to describe any substance that causes fever. Exogenous
pyrogens are derived from outside the patient; most are microbial products,
microbial toxins, or whole microorganisms. The classic example of an exogenous
pyrogen is the lipopolysaccharide (endotoxin) produced by all gram‐negative bacteria.
Pyrogenic products of gram‐positive organisms include the enterotoxins of
Staphylococcus aureus and the group A and B streptococcal toxins, also called
superantigens.
2) Pyrogenic Cytokines
Cytokines are small proteins (molecular mass, 10,000–20,000 Da) that regulate
immune, inflammatory, and hematopoietic processes. For example, the elevated
leukocytosis seen in several infections with an absolute neutrophilia is the result of
the cytokines interleukin (IL) 1 and IL‐6. Some cytokines also cause fever; formerly
referred to as endogenous pyrogens, they are now called pyrogenic cytokines. The
pyrogenic cytokines include IL‐1, IL‐6, tumor necrosis factor (TNF), ciliary neurotropic
factor (CNTF), and interferon (IFN) . (IL‐18, a member of the IL‐1 family, does not
appear to be a pyrogenic cytokine.) Other pyrogenic cytokines probably exist. Each
cytokine is encoded by a separate gene, and each pyrogenic cytokine has been shown
to cause fever in laboratory animals and in humans. When injected into humans, IL‐1
and TNF produce fever at low doses (10–100 ng/kg); in contrast, for IL 6, a dose of 1–
10 g/kg is required for fever production.
A wide spectrum of bacterial and fungal products induce the synthesis and release of
pyrogenic cytokines, as do viruses. However, fever can be a manifestation of disease
in the absence of microbial infection. For example, inflammatory processes, trauma,
tissue necrosis, or antigen‐antibody complexes can induce the production of IL‐1,
TNF, and/or IL‐6, which—individually or in combination—trigger the hypothalamus to
raise the set point to febrile levels.
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 28
3) Elevation of the Hypothalamic Set Point by Cytokines
During fever, levels of prostaglandin E2 (PGE2) are elevated in hypothalamic tissue and
the third cerebral ventricle. The concentrations of PGE2 are highest near the
circumventricular vascular organs (organum vasculosum of lamina terminalis)—
networks of enlarged capillaries surrounding the hypothalamic regulatory centers.
Destruction of these organs reduces the ability of pyrogens to produce fever. Most
studies in animals have failed to show, however, that pyrogenic cytokines pass from
the circulation into the brain itself. It appears that both exogenous and endogenous
pyrogens interact with the endothelium of these capillaries and that this interaction is
the first step in initiating fever—i.e., in raising the set point to febrile levels.
The key events in the production of fever are illustrated below. As has been
mentioned, several cell types can produce pyrogenic cytokines. Pyrogenic cytokines
such as IL‐1, IL‐6, and TNF are released from the cells and enter the systemic
circulation. Although the systemic effects of these circulating cytokines lead to fever
by inducing the synthesis of PGE2, they also induce PGE2 in peripheral tissues. The
increase in PGE2 in the periphery accounts for the nonspecific myalgias and
arthralgias that often accompany fever. It is thought that some systemic PGE2 escapes
destruction by the lung and gains access to the hypothalamus via the internal carotid.
However, it is the elevation of PGE2 in the brain that starts the process of raising the
hypothalamic set point for core temperature.
3. Fever of Unknown Origin ( FUO )
Fever of unknown origin (FUO) was defined by Petersdorf and Beeson in 1961 as (1)
temperatures of >38.3°C (>101°F) on several occasions; (2) a duration of fever of >3 weeks;
and (3) failure to reach a diagnosis despite 1 week of inpatient investigation. While this
classification has stood for more than 30 years, Durack and Street have proposed a new
system for classification of FUO: (1) classic FUO; (2) nosocomial FUO; (3) neutropenic FUO;
and (4) FUO associated with HIV infection.
A. Diseases associated with Fever and Rash
This chapter reviews rashes that reflect systemic disease, but it does not include
localized skin eruptions (i.e., cellulitis, impetigo) that may also be associated with fever .
Rashes are classified herein on the basis of the morphology and distribution of lesions.
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 29
For practical purposes, this classification system is based on the most typical disease
presentations. However, morphology may vary as rashes evolve, and the presentation
of diseases with rashes is subject to many variations For instance, the classic petechial
rash of Rocky Mountain spotted fever may initially consist of blanchable erythematous
macules distributed peripherally; at times, the rash associated with RMSF may not be
predominantly acral, or it may not develop at all.
Diseases with fever and rash may be classified by type of eruption: centrally distributed
maculopapular, peripheral, confluent desquamative erythematous, vesiculobullous,
urticarial, nodular, purpuric, ulcerated, or eschar.
B. Approach to the Patient with Fever and Rash
A thorough history of patients with fever and rash includes the following relevant
information: immune status, medications taken within the previous month, specific
travel history, immunization status, exposure to domestic pets and other animals, history
of animal (including arthropod) bites, existence of cardiac abnormalities, presence of
prosthetic material, recent exposure to ill individuals, and exposure to sexually
transmitted diseases. The history should also include the site of onset of the rash and its
direction and rate of spread.
A thorough physical examination entails close attention to the rash, with an assessment
and precise definition of its salient features. First, it is critical to determine the type of
lesions that make up the eruption. Macules are flat lesions defined by an area of
changed color (i.e., a blanchable erythema). Papules are raised, solid lesions <5 mm in
diameter; plaques are lesions >5 mm in diameter with a flat, plateau‐like surface; and
nodules are lesions >5 mm in diameter with a more rounded configuration. Wheals
(urticaria, hives) are papules or plaques that are pale pink and may appear annular
(ringlike) as they enlarge; classic (nonvasculitic) wheals are transient, lasting only 24–48
h in any defined area. Vesicles (<5 mm) and bullae (>5 mm) are circumscribed, elevated
lesions containing fluid. Pustules are raised lesions containing purulent exudate;
vesicular processes such as varicella or herpes simplex may evolve to pustules.
Nonpalpable purpura is a flat lesion that is due to bleeding into the skin; if <3 mm in
diameter, the purpuric lesions are termed petechiae; if >3 mm, they are termed
ecchymoses. Palpable purpura is a raised lesion that is due to inflammation of the vessel
wall (vasculitis) with subsequent hemorrhage. An ulcer is a defect in the skin extending
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 30
at least into the upper layer of the dermis, and an eschar (tâche noire) is a necrotic
lesion covered with a black crust.
2. HYPOTHERMIA
1. Hypothermia
Accidental hypothermia occurs when there is an unintentional drop in the body's core
temperature below 35°C (95°F). At this temperature, many of the compensatory physiologic
mechanisms to conserve heat begin to fail. Primary accidental hypothermia is a result of the
direct exposure of a previously healthy individual to the cold. The mortality rate is much
higher for those patients who develop secondary hypothermia as a complication of a serious
systemic disorder.
A. Causes
1) Primary accidental hypothermia is geographically and seasonally pervasive. Although
most cases occur in the winter months and in colder climates, it is surprisingly
common in warmer regions as well. Multiple variables make individuals at the
extremes of age, the elderly and neonates, particularly vulnerable to hypothermia.
The elderly have diminished thermal perception and are more susceptible to
immobility, malnutrition, and systemic illnesses that interfere with heat generation or
conservation. Dementia, psychiatric illness, and socioeconomic factors often
compound these problems by impeding adequate measures to prevent hypothermia.
Neonates have high rates of heat loss because of their increased surface‐to‐mass
ratio and their lack of effective shivering and adaptive behavioral responses. In
addition, malnutrition can contribute to heat loss because of diminished
subcutaneous fat and because of depleted energy stores used for thermogenesis.
2) Individuals whose occupations or hobbies entail extensive exposure to cold weather
are at increased risk for hypothermia. Military history is replete with hypothermic
tragedies. Hunters, sailors, skiers, and climbers also are at great risk of exposure,
whether it involves injury, changes in weather, or lack of preparedness.
3) Ethanol causes vasodilatation (which increases heat loss), reduces thermogenesis and
gluconeogenesis, and may impair judgment or lead to obtundation. Phenothiazines,
barbiturates, benzodiazepines, cyclic antidepressants, and many other medications
reduce centrally mediated vasoconstriction. Up to 25% of patients admitted to an
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 31
intensive care unit because of drug overdose are hypothermic. Anesthetics can block
the shivering responses; their effects are compounded when patients are not covered
adequately in the operating or recovery rooms.
4) Several types of endocrine dysfunction can lead to hypothermia. Hypothyroidism—
particularly when extreme, as in myxedema coma—reduces the metabolic rate and
impairs thermogenesis and behavioral responses. Adrenal insufficiency and
hypopituitarism also increase susceptibility to hypothermia. Hypoglycemia, most
commonly caused by insulin or oral hypoglycemic drugs, is associated with
hypothermia, in part the result of neuroglycopenic effects on hypothalamic function.
Increased osmolality and metabolic derangements associated with uremia, diabetic
ketoacidosis, and lactic acidosis can lead to altered hypothalamic thermoregulation.
5) Neurologic injury from trauma, cerebrovascular accident, subarachnoid hemorrhage,
or hypothalamic lesions increases susceptibility to hypothermia. Agenesis of the
corpus callosum, or Shapiro syndrome, is one cause of episodic hypothermia,
characterized by profuse perspiration followed by a rapid fall in temperature. Acute
spinal cord injury disrupts the autonomic pathways that lead to shivering and
prevents cold‐induced reflex vasoconstrictive responses.
6) Hypothermia associated with sepsis is a poor prognostic sign. Hepatic failure causes
decreased glycogen stores and gluconeogenesis, as well as a diminished shivering
response. In acute myocardial infarction associated with low cardiac output,
hypothermia may be reversed after adequate resuscitation. With extensive burns,
psoriasis, erythrodermas, and other skin diseases, increased peripheral blood flow
leads to excessive heat loss.
B. Clinical Presentation
In most cases of hypothermia, the history of exposure to environmental factors, such as
prolonged exposure to the outdoors without adequate clothing, makes the diagnosis
straightforward. In urban settings, however, the presentation is often more subtle and
other disease processes, toxin exposures, or psychiatric diagnoses should be considered.
After initial stimulation by hypothermia, there is progressive depression of all organ
systems. The timing of the appearance of these clinical manifestations varies widely.
Without knowing the core temperature, it can be difficult to interpret other vital signs.
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 32
For example, a tachycardia disproportionate to the core temperature suggests secondary
hypothermia resulting from hypoglycemia, hypovolemia, or a toxin overdose. Because
carbon dioxide production declines progressively, the respiratory rate should be low;
persistent hyperventilation suggests a central nervous system (CNS) lesion or one of the
organic acidosis. A markedly depressed level of consciousness in a patient with mild
hypothermia should raise suspicion of an overdose or CNS dysfunction due to infection
or trauma.
C. Physiologic Changes Associated with Accidental Hypothermia
Severity Body
Temperature
Central Nervous System
Cardio vascular
Respiratory Renal and Endocrine
Neuro muscular
Mild 35°C (95°F)–32.2°C (90°F)
Linear depression of cerebral metabolism; amnesia; apathy; dysarthria; impaired judgment; maladaptive behavior
Tachycardia, then progressive bradycardia; cardiac‐cycle prolongation; vasoconstriction; increase in cardiac output and blood pressure
Tachypnea, then progressive decrease in respiratory minute volume; declining oxygen consumption; bronchorrhea; bronchospasm
Diuresis; increase in catecholamines, adrenal steroids, triiodothyronine and thyroxine; increase in metabolism with shivering
Increased preshivering muscle tone, then fatiguing
Moderate <32.2°C (90°F)–28°C (82.4°F)
EEG abnormalities; progressive depression of level of consciousness; pupillary dilatation; paradoxical undressing; hallucinations
Progressive decrease in pulse and cardiac output; increased atrial and ventricular arrhythmias; suggestive (J‐ wave) ECG changes
Hypoventilation; 50% decrease in carbon dioxide production per 8°C drop in temperature; absence of protective airway reflexes
50% increase in renal blood flow; renal autoregulation intact; impaired insulin action
Hyporeflexia; diminishing shivering‐induced thermogenesis; rigidity
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 33
Severity Body
Temperature
Central Nervous System
Cardio vascular
Respiratory Renal and Endocrine
Neuro muscular
Severe <28°C (82.4°F)
Loss of cerebrovascular autoregulation; decline in cerebral blood flow; coma; loss of ocular reflexes; progr essive decr ease in EEG EEG
Progressive decrease in blood pressure, heart rate, and cardiac output; re‐entrant dysrhythmias; maximum risk of ventricular fibrillation; asystole
Pulmonic congestion and edema; 75% decrease in oxygen consumption; apnea
Decrease in renal blood flow parallels decrease in cardiac o.p; extreme oliguria; poi kilothermia; 80% decr in basal metab olism
No motion; decreased nerve‐ conduction velocity; peripheral areflexia; no corneal or oculocephalic reflexes
2. Frostbite
Peripheral cold injuries include both freezing and nonfreezing injuries to tissue. Tissue
freezes quickly when in contact with thermal conductors such as metal or volatile solutions.
Other predisposing factors include constrictive clothing or boots, immobility, or
vasoconstrictive medications. Frostbite occurs when the tissue temperature drops below
0°C. Ice crystal formation subsequently distorts and destroys the cellular architecture. Once
the vascular endothelium is damaged, stasis progresses rapidly to microvascular
thrombosis. After the tissue thaws, there is progressive dermal ischemia. The
microvasculature begins to collapse, arteriovenous shunting increases tissue pressures, and
edema forms. Finally, thrombosis, ischemia, and superficial necrosis appear. The
development of mummification and demarcation may take weeks to months.
A. Clinical Presentation
1) The initial presentation of frostbite can be deceptively benign. The symptoms always
include a sensory deficiency affecting light touch, pain, and temperature perception.
The acral areas and distal extremities are the most common insensate areas. Some
patients complain of a clumsy or "chunk of wood" sensation in the extremity.
2) Deep frostbitten tissue can appear waxy, mottled, yellow, or violaceous‐white.
Favorable presenting signs include some warmth or sensation with normal color.
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 34
(a) Frostbite Frostbite with vesiculation
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 35
Reference
A. Anatomy and Pathophysiology of Nociceptive Pain
1. Drake, Richard L; Vogl, Wayne; Mitchell, Adam W.M. (2005) Gray’s Anatomy for Students.
1stEd. Elsevier Churchill Livingstone. p.782‐787.
2. Moore, Keith L; Agur. Anne M.R. (2007) Essential Clinical Anatomy. 3rdEd. Lippincott
Williams and Wilkins. p.81,101,184‐191,507.
3. Moore, Keith L; Dalley, Arthur F. (2006) Clinically Oriented Anatomy. 5thEd. Lippincott
Williams and Wilkins. p.886‐932.
4. Waxman, Stephen G. (2003) Clinical Neuroanatomy. 25thEd. A Lange Medical Book. Mc
Graw‐Hill. p.51‐58,202‐207.
B. Anatomy and Pathophysiology of Neuropathic Pain
1. Marcus, Dawn. (2005) Chronic Pain A Primary Care Guide to Practical Management.
Humana Press.
2. Loeser, John D; Butler, Steven H; Chapman, C. Richard; Turk, Dennis C. (2001) Bonica’s
Management of Pain. 3rdEd. Lippincott Williams & Wilkins.
3. http://www.cgmh.org.tw/cgmj/2809/280901.pdf
4. http://bja.oxfordjournals.org/cgi/reprint/87/1/12
C. Headache
1. Baehr & Frotscher; Duus’. (2005) Topical Diagnosis in Neurology. 4thEd. Thieme Stuttgart
New York.
2. Collins. (2008) Differential Diagnosis in Primary Care. 4thEd. Lippincott Williams & Wilkins.
3. Gallagher. Weiner’s Pain Management : Primary Headache Disorders.
4. Loeser J.D. (2001) Bonica’s Management of Pain.
5. Mumenthaler. (2006) Fundamentals of Neurology An Illustrated Guide.
D. Neck Pain
1. Marcus, Dawn A. (2007) Headache and Chronic Pain Syndromes, The Case‐Based Guide to
Targeted Assessment and Treatment. Humana Press.
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 36
2. Loeser, John D; Butler, Steven H; Chapman, C. Richard; Turk, Dennis C. (2001) Bonica’s
Management of Pain. 3rdEd. Lippincott Williams & Wilkins.
3. Boswell, Mark V. and Cole, B. Eliot. WEINER’S Pain Management: A Practical Guide for
Clinicians. (2006) 7thEd. Taylor & Francis.
E. Chest Pain
1. Fauci, A.S; Kasper, D.L; Longo, D.L; Braunwald, E; Hauser, S.L; Jameson, J.L; Loscalzo.
(2008) Harrison's Principles of Internal Medicine. 17thEd. The McGraw‐Hill Companies.
2. Loeser, John D; Butler, Steven H; Chapman, C. Richard; Turk, Dennis C. (2001) Bonica’s
Management of Pain. 3rdEd. Lippincott Williams & Wilkins.
F. Abdominal Pain
1. Baehr & Frotscher; Duus’. (2005) Topical Diagnosis in Neurology. 4thEd. Thieme Stuttgart
New York.
2. Collins. (2008) Differential Diagnosis in Primary Care. 4thEd. Lippincott Williams & Wilkins.
3. Gallagher. Weiner’s Pain Management: Primary Headache Disorders.
4. Loeser, J.D. (2001) Bonica’s Management of Pain.
5. Mumenthaler. (2006) Fundamentals of Neurology An Illustrated Guide.
G. Dysmenorrhoea
1. Carol P; Gaspard K. (2003) Alterations in the Male and Female Reproductive Systems in
Essential Pathophysiology. Lippincott Williams & Wilkins.
2. Costanzo L.S. (2007) Reproductive Physiology in Physiology. 3rdEd. Elsevier.
3. French L. (2005) Dysmenorrhea. American Physician Family. 71(2):285‐291.
4. Downloaded from http://www.aafp.org/afp on 4 June 2008.
5. Proctor, M; Farquhar, C. (2006) Diagnosis and Management of Dysmenorrhoea.
BMJ332:1134‐1138. Downloaded from bmj.com on 4 June 2008.
6. Spark, R.A. (2005) Dysmenorrhea. In: Family Medicine Ambulatory Care & Prevention.
4thEd. McGraw‐Hill. p.108‐112.
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 37
H. Low Back Pain
1. Marcus, Dawn A. (2007) Headache and Chronic Pain Syndromes, The Case‐Based Guide to
Targeted Assessment and Treatment. Humana Press.
2. Loeser, John D; Butler, Steven H. C; Chapman, Richard; Turk, Dennis C. (2001) Bonica’s
Management of Pain. 3rdEd. Lippincott Williams & Wilkins.
3. Boswell, Mark V. and Cole, B. Eliot. (2006) WEINER’S Pain Management, A Practical Guide
for Clinicians. 7thEd. Taylor & Francis.
I. Hyperthermia, Hypothermia, Frostbite, Fever And Rash
1. Fauci, A.S; Kasper, D.L; Longo, D.L; Braunwald, E; Hauser, S.L; Jameson J.L; Loscalzo.
(2008) Harrison's Principles of Internal Medicine. 17thEd. The McGraw‐Hill Companies.
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 38
Teaching‐Learning Process
a. Student should work with this Module prior to any lectures on this Topic.
b. This Module will be collected before Small Group Discussion.
c. Student should discuss the module tasks they have already done before.
d. The on duty Facilitators make notes on things the student discuss which need to clarify at
the end of each session or in lecture.
The Assessment
a. The Formative Evaluation will be assessed through Observation Sheets elaborating the
Learning Skill and Content Mastery.
b. The Summative Evaluation will be assessed together with the other modules in Middle
Semester Test and or End Semester Test scheduled.
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 39
MODULE TASK Find out your answers to the following tasks by yourself after discuss it
with your group or after reading the suggested references below.
1. Describe in brief the Spinal Pain and Temperature Pathways
A series of three neurons transmits fast pain and temperature impulses from the
receptors in the periphery to the cerebral cortex where these sensations are perceived.
First Order neurons :
Pain and temperature stimulus are received by receptors in the periphery , carried by the
spinal nerves thorug dorsal root of the spinal cord to the Spinal Ganglion then trasmitted
through the dorsal fasciculus ( Tract of Lissauer ) to the posterior horn of the spinal cord
Second Order Neurons :
From the posterior horn the impuls the second neurons decussate in the ventral white
comissure. After crossing to the contralateral side, the secondary neurons pass the lateral
funicuulus as the spinothalamic tract which is then ascends to terminate in the thalamus.
Third Order Neurons :
The third neurons transmitting the Pain and temperature impuls to terminate in the
sensory centers in ths postcentral gyrus of the cerebral cortex
2. Describe the pain resulted from injury to Pleurae. Why are there any differences
between pain resulted from injury to the visceral pleura and the parietal pleura.
Explain also the referred pain may exist in this case.
The visceral pleura insensitive to pain because its innervation is autonomic (motor and
visceral afferent) . The visceral pleura receives no nerves of general sensation.
The parietal pleura is sensitive to pain , particularly the costal pleura , because it is richly
supplied by branches OF Nn.intercostales and N.phrenicus.
Irritation of the parietal pleura produces local pain and referred pain to the areas sharing
innervation by the segments of medulla spinalis.
Irritation of the costal and peripheral parts of diaphragmatic pleura results in local pain
and referred pain along the Nn.intercostaes to the thoracic and abdominal walls.
Irritation of the mediastinal and central diaphragmatic areas of the parietal pleura results
in pain that is referred to the root of neck and over the shoulder (C3‐C5 dermatomes)
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 40
3. Explain following term:
a. Pain d. Dysesthesia g. Hyperpathia
b. Allodynia e. Paresthesia h. Neuropathic pain
c. Causalgia f. Hyperalgesia
4. Describe peripheral and central mechanism of neuropathic pain.
Peripheral effect:
• Ectopic and spontaneous discharge
• Emphatic conduction
• Alterations in ion channel expression
• Collateral sprouting of primary afferent neurons
• Sprouting of sympathetic neurons into the DRG
• Nociceptors sensitization
Central effects:
• Central sensitization
• Spinal reorganization
• Cortical reorganization
• Charges in inhibitory pathways
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 41
5. What do you know about “Chest Pain“. Describe the anatomical aspect of this Pain.
Ischemia and the accumulation of metabolic products stimulate pain endings in the
myocardium The affrent pain fibers run in the cervical branches of the truncus
sympathicus. The axons of these primary sensory neurons enter spinal cord segments T1‐
T4 or T5 especially of the left side.
Cardiac referred pain is a phenomenon whereby noxious stimuli originating in the heart
are perceived by the person as pain arising from a superficial part of the body – the skin
on the medial aspect of the left upper limb , for example.
Visceral pain is trasmitted by visceral afferent fibers with cell bodies in the same spinal
ganglion, and central processes that enter the spinal cord through the same posterior
roots.
6. Describe the nature of “Headache“ as it commonly are Dural Origin of Headache
The dura is sensitive to pain, especially where it is related to the dural venous sinuses and
meningeal arteries. Although the cause of Headache are numerous, distension of the
scalp or meningeal vessels ( or both ) is believed to be one cause of headache.
Many headaches appear to be dural in original, such as headache occuring after a lumbar
spinal puncture for removal of CSF. These headaches are thought to result from
stimulation of sensory nerve ending in the dura. When CSF is removed, the brain sags
sligthly, pulling on the dura, this may cause pain and headache.
For this reason, patients are asked to keep their heads down after lumbar puncture to
minimize the pull on the dura, reducing the chance of headache
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 42
7. Describes and mention the Head structures which are pain sensitive and insensitive
Investigations on humans undergoing intracranial surgery under local anesthesia have
shown that the following structures are pain sensitive: (a) all of the extracranial
structures, especially the arteries; (b) the great venous sinuses and their tributaries from
the surface of the brain; (c) parts of the dura at the base of the brain; (d) the meningeal
arteries and big cerebral arteries at the base of the brain; and (e) the fifth, ninth, and
tenth cranial nerves and the upper three cervical nerves. The cranium (including the
diploic and emissary veins), the parenchyma of the brain, some of the dura, almost all of
the piaarachnoid, and the ependymal lining of the ventricles and the choroid plexus are
insensitive to mechanical, thermal, electrical, or chemical stimuli.
Stimulation of pain‐sensitive structures on or above the superior surface of the tentorium
cerebelli causes pain in parts of the head anterior to a line drawn from the ears across the
top of the head, whereas stimulation of structures on or below the inferior surface of the
tentorium cerebelli generally causes pain behind the aforementioned line, but certain
sites may project to the brow or behind the eyes. It has been further demonstrated that
nociception from the supratentorial structures is mediated by the trigeminal nerve,
whereas nociceptive impulses from stimulation of the infratentorial structures are
transmitted by afferent fibers in the fifth, ninth, and tenth cranial nerves and the upper
three cervical nerves.
The intracranial vessels also are supplied by afferent fibers, which run in the ophthalmic
division of the trigeminal nerve and terminate in the trigeminal ganglion. In addition, the
arteries are surrounded by dense networks of nerves containing a variety of
neuropeptides.
Cranial bones are not pain sensitive, but stretch or other sensation of the periosteum,
which surrounds them, evokes pain locally. The scalp, of course, is pain sensitive, as are
the arteries that supply it (i.e., the supraorbital, frontal, superficial temporal, posterior
auricular, and occipital arteries). The first three arteries are supplied by the trigeminal
nerve, whereas the posterior auricular and occipital arteries are supplied by branches of
the upper cervical nerves. The external carotid artery and its branches are also supplied
by afferent fibers that are a part of the nerve plexuses surrounding these vessels and
eventually reach the spinal dorsal horn or the trigeminal nucleus caudalis via the sensory
roots of the upper four thoracic spinal nerves or the trigeminal nerve. The nerve fibers
containing neuropeptides play a role both in nociception and in the regulation of vascular
tone
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 43
8. Described the pathophysiology and characteristic pain and of migraine with aura
Migraine
Pathogenesis of Migraine
Multiple factors contribute to the generation of a migraine attack:
Vascular and Humoral Factors
It has long been presumed that, in the first phase of migraine, vasoconstriction
produces focal cortical ischemia (accounting for the neurologic deficits seen in
migraine accompagn´ee). Recent measurements of intracranial blood flow, however,
have cast some doubt on this hypothesis. In the second phase, vasodilatation occurs.
Dilatation of the large extracranial vessels causes typically unilateral, often pulsating
pain. The patient appears pale, because the facial capillaries are constricted; only in
cluster headache are they dilated, producing a red face. The third phase,
characterized by edema of the periarterial tissue, manifests itself in a dull, continuous
pain.
These vascular changes are partly due to, and accompanied by, humoral processes of
various kinds; serotonin seems to be the most important transmitter substance
involved. For unexplained reasons (perhaps because of exogenous factors), serotonin
is released at the onset of a migraine attack from stored reserves in the intestinal
wall, the brain, and, most of all, the blood platelets and mast cells. Serotonin at high
concentration in the bloodstream then induces, not only the initial intracranial
vasoconstriction, but also (in concert with histamine released from mast cells) an
increase in capillary permeability. This, in turn, promotes transudation of a type of
plasma kinin called neurokinin, which acts to lower the pain threshold. The
concentration of serotonin in the blood then declines, which induces the
vasodilatation and pain of the second phase. Serotonin is degraded through the
enzymatic action of monoamine oxidases and excreted in the urine as 5‐
hydroxyindoleacetic acid.
CNS Factors
These factors have recently drawn increased attention. Impulses arising in the
diencephalon are thought to be responsible for the episodic character, accompanying
vegetative signs, epileptiform EEG changes, and unilaterality of migraine headache. A
decisive role is played by excitatory processes mediated by fibers of the trigeminal
nerve.
Genetic factors play a role; in some patients, for example, there are well‐
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 44
documentedion channel abnormalities. Many patients report a history of migraine in
their relatives, particularly on the maternal side.
Abnormal neural excitation in the diencephalon, particularly in the thalamic zone
representing the trigeminal area, also plays a role in the pathogenesis of migraine.
Events occurring in this nuclear area are responsible for the triggering of (unilateral)
migraine attacks by peripheral stimuli or emotional factors.
The pathogenetic role of so‐called “spreading depression” is unclear. This is a
phenomenon, known from animal research, in which a stimulus delivered locally to
the occipital cortex induces a wave of excitation that spreads toward the frontal lobe.
The excitation is then followed by reduced excitability (“depression”). It is an
established fact that the speed of this disturbance, as it moves from back to front,
correlates precisely with the speed of a scintillating scotoma moving across the visual
field in an attack of ophthalmic migraine. The common Aura of migraine is visual
aura.
This most common form of complicated migraine is characterized by visual
manifestations preceding the headache, and is thus equivalently termed migraine
with (visual) aura. About one‐third of patients with migraine have this form of
migraine.
A typical type of visual aura is the scintillating scotoma, in which the patient first sees
a bright, colored, lightning‐like figure with a zigzag border proceeding from the center
to the periphery of the homonymous visual field (fortification specter). The figure
reaches the periphery in 5–15minutes and leaves a transient visual field defect behind.
Horizontal visual field defects due to retinal ischemia are less common, and transient
monocular blindness (amaurosis fugax) as a manifestation of retinal migraine is quite
rare.
Scintillating scotomata of this type are followed by a headache episode of the type
described above, usually on the side opposite the homonymous visual field defect. In
rare cases, the scintillating scotoma remains the only manifestation of migraine, and
the headache or other manifestations never develop. A permanent visual field defect
may be present in such cases. A small number of patients with ophthalmic migraine
who, for various reasons, underwent surgical repair of a right‐left intracardiac shunt
went on to have attacks at lower frequency, or no attacks at all. It thus seems that
this type of anomaly may rarely be of pathogenetic importance.
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 45
9. Described the clinical manifestation Tension Type Headache
Tension‐Type Headache
Terminology
Tension‐type headache, earlier known as “cephalea vasomotorea,” is also somewhat
confusingly called “common migraine.” The International Headache Society’s
definition recognizes two types of tension‐type headache, episodic and chronic,
which are distinguished according to the following criteria.
Episodic Tension‐Type Headache:
A : At least 10 earlier episodes fulfilling criteria B–D, occurring fewer than 180 days
per‐year.
B : Headache episodes last 30 minutes to 7 days.
C : At least two of the following pain characteristics are present:
– pressing, not pulsatile,
– mildtomoderate intensity, not impairing everyday activities,
– bilateral,
– not exacerbatedby exertion, walking, or climbing stairs.
D : Both of the following characteristics:
– no nausea or vomiting,
– no or very rare photophobia or phonophobia.
E : At least one of the following is true:
– The history and physical findings are not consistent with another known type
of headache; or
– other types of headache can be excluded with ancillary tests; or
– another type of headache, if present, is different from and not correlated with
the tensiontype headache.
Chronic Tension‐Type Headache:
A : Moderately frequent headaches (15 or more days/month) for at least 6 months,
fulfilling criteria B through D.
B : The pain has at least two of the following characteristics:
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 46
– pressing,not pulsatile,
– mildtomoderate intensity, without impairment of daily activities,
– bilateral,
– not exacerbated by exertion, walking, or climbing stairs.
C : Both of the following characteristics:
– no vomiting,
– no nausea, photophobia, phonophobia (or at most one of these phenomena).
D : At least one of the following is true:
– The history and physical are not consistent with another known type of
headache; or
– other types of headache can be excluded with ancillary tests; or
– another type of headache, if present, is different from and not correlated with
the tension‐type headache.
10. What is cervicogenic headache?
Cervicogenic headache describes head pain that occurs as a result of an abnormality in
the neck. The word genesis means “to come from,” so cervicogenic literally means the
pain comes from a problem in the neck or cervical area. Typically, cervicogenic headache
is experienced as a pain in the neck that moves to the back of the head. Generally, this
pain affects just one side of the head. Sometimes the pain may radiate over the side or
top of the head. Cervicogenic headache episodes usually occur after moving the neck into
certain positions or holding the head in one position for a long time. Often, people find
that certain neck movements will also relieve the neck and head pain. A variety of neck
abnormalities may result in neck pain, with pain also in the head. These may include
trauma or degenerative conditions, such as arthritis.
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 47
Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page 48
11. What is a cervical radiculopathy?
Nerves can be pinched when they leave the spine to go into the arm. The area
where nerves are pinched is called the root. In Latin, radicitus means “by the roots.”
Therefore, when the root of a nerve is pinched, it is called a radiculopathy. When this
happens, you may experience pain, numbness, and/or weakness in the arm. This is called
a cervical (or neck) radiculopathy.
The most common causes of pinched nerves are calcium deposits from arthritis or
a herniated disc. The disc is a sponge‐like cushion that acts like a shock absorber between
the bones in the spine. Sometimes, this sponge can shift backward or to the side, causing
the nerve to be pinched. With aging, this sponge dries out and can be surrounded by
calcium deposits. This causes the spaces between the bones to shrink, which is called disc‐
space narrowing. Although the smaller spaces themselves do not cause problems, this is
often associated with arthritis changes that can pinch a nerve. Pinching these nerves
typically results in pain in the neck and arm, along with numbness in the arm or hand.