V Syndro Sy Module 2 Pain and the Change of …v1.fk.ub.ac.id/id/pu/BlockV_Module2 TA_2009-2010_Student...Module - Pain and The Changes of Temperature; Academic Year 2009-2010 Page

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


ISHOMA

TANARY DA ISN SMD EA ACA BS SDR AAN RtR LK

28.08.'09 Jum'at


Diskusi 5 Modul Task 11 ‐12


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


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.


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.


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.


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


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.


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


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


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


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.


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.


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.


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


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).


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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.


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


‐ 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


• 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


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





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.


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


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.


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.


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


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


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.


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


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.


(a) Frostbite Frostbite with vesiculation


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.




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.



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.


http://www.aafp.org/afp

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


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.


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 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)


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


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


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


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‐


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.


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:


– 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.



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.

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