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Thermal Imaging As A Tool In Pain
Management - An 11 Year Study, Part I of II
Hooshang Hooshmand, Masood Hashmi, Eric
Neurological Associates Pain Management
Center, Vero Beach, Florida, USA
The value of
Infrared thermal imaging (ITI) is limited to evaluation of neurovascular
dysfunction. It provides indispensable information regarding neuropathic
pain due to perivascular microcirculatory sympathetic dysfunction. ITI
records superficial, and deep temperature changes. The bilateral cervical
cord temperature modulation demands careful clinical correlation. The ITI
is an objective guide helping the clinician to choose a proper and
harmless treatment protocol, especially avoiding unnecessary surgery.
anatomical tests such as magnetic resonance imaging (MRI), computed
tomography (CT), and physiological tests such as electromyography (EMG)
and nerve conduction velocity (NCV) tests have been the main diagnostic
tools applied in the management of somesthetic (somatic) pain. The above
tests usually are not informative in the diagnosis of neuropathic pain.
The neurovascular involvement in neuropathic pain requires tests such as
Infrared thermal imaging (ITI) and Quantitative sudomotor axon reflex test
(QSART) that address autonomic (e.g., thermal) changes for a more accurate
diagnosis and treatment. This is a study of the role of ITI in the
diagnosis and management of pain. The results were compared with the
information in medical literature.
Scientific Thermal Processor and Agema Cameras were used for this study of
3,265 successive patients. A review of our experience with Infrared
thermal imaging (ITI) and its role in pain management was conducted, and
compared with the recent medical literature. The study was limited to the
role of ITI in the management of complex chronic pain.
technique, and poor background in basic neurophysiologic training, have
contributed to poor utilization and interpretation of ITI. For the ITI to
be accurate and clinically useful, proper technique, standardization, and
proper clinical correlation are the minimal requirements. The basic
physiology of autonomic thermoregulation is outlined in detail to help the
clinician to properly understand and interpret the test. The dysfunction
of thermal sensory nerves in the wall of arterioles cannot be detected by
EMG or NCV and excluding the ITI test may mislead the clinician to
diagnose the condition as "psychogenic" or "functional." Our results were
compatible with the review of current medical literature.
provides useful clinical information when applied with proper technique.
It provides diagnostic and therapeutic information limited to diseases
involving autonomic, neurovascular, and neuroinflammatory changes.
Conversely, it cannot be expected to help diagnose nerve injuries with no
microvascular involvement such as somesthetic nerve injuries. Proper
teaching and understanding of thermoregulation helps the clinician to
obtain indispensable information from this test.
- CRPS, Headache, Sympathectomy ,Thermography.
Infrarotthermographie als Hilfsmittel im Schmermanagement - eine
11 Jahres - Studie. 1. Teil
international 11 / 2 (2001)
This is a
review of our 11-year experience with the application of Infrared
thermal imaging (ITI) in 3,265 patients suffering from chronic pain.
This study focuses on the application of ITI as a diagnostic and
nociceptive pain sensation is divided into two distinct categories:
Neuropathic (Table 1) and somesthetic(somatic) pain. The neuropathic
pain is associated with thermal (vasomotor) changes. These changes
are in response to the afferent noxious impulses of the unmyelinated
sensory (c-thermoreceptors) nerves in the wall of microvasculature
(1). This is in contrast to the common somatic (somesthetic) pain
which is usually not accompanied by circulatory dysfunction.
somesthetic pain is characterized by involvement of afferent
somatic(spinothalamic) nerves usually with no circulatory
disturbance. The somatic pain has a dermatomal pattern (Fig. 1) in
the distribution of nerve roots and nerve trunks. In contrast, the
thermatomal distribution (Fig. 1) of neuropathic pain (2,3) follows
an arterial distribution such as femoral, carotid or brachial
arteries. In pathologic states, hypo-and hyperthermic changes are
recorded by ITI which can be quite helpful in the selection of a
proper treatment protocol.
neuropathic pain, by virtue of involving the neurovascular
structure, is accompanied by circulatory (Thermal) changes leading
to a different type of pain such as causalgia (4), deafferentation
and sensitization (5), as well as abnormally evoked pain: e.g.,
hyperpathic (protopathic) regional pain (6),and allodynic pain
evoked by even minimal tactile stimulation (7). These are
characteristic pains accompanied by neurovascular dysfunction (8) of
any etiology (e.g., post herpetic neuralgia, diabetic mononeuropathy,
Table 1. Disease; in
which neuropathic pain occur.
Figure. 1 - In
neuropathic pain the sensory loss shows thermatomal (vascular)
distribution in contrast to the dermatomal (radicular) distribution
of the somatic pain. Conversely, the malingering sensory loss is
limited to the joints. With permission from Springer-Verlag
ITI exclusively measures temperature changes of the body. Hence, its
diagnostic value is limited to the study of nerve dysfunction with
microvascular involvement (neuropathic pain). The thermal regulation is
achieved by coordination of multiple anatomic areas of central and
peripheral nervous system(PNS). The PNS contribution is modulated by
afferent impulses from microscopic small c-fiber thermoreceptors in the
wall of the microcirculation (arterioles and venules) (9,10,11). Such
minute unmyelinated microscopic nerves cannot be tested with anatomical
tests such as CT and MRI, nor with somatic type of physiological tests
such as electromyography (EMG), and nerve conduction velocity (NCV). The
NCV cannot study the microcirculatory neuropathic function. It studies the
function of the large trunk myelinated nerve fibers which are part of the
somatic (e.g., spinothalamic) nervous system (12). In contrast, ITI
evaluates sympathetic thermoregulatory function more comprehensively than
sweat test. The sweat test e.g., QSART measures the function of a minority
(less than 10%) of cholinergic nerves in the sympathetic system.
In ancient medicine,
physicians were taught to measure temperature by hands. This insensitive
and inaccurate method is still applied by physicians with poor knowledge
of physiology. Approximately Four decades B.C., wet mud salves were used
to detect surface body temperature. Hippocrates advocated the method. By
the end of the 16th century, Galileo devised a "thermoscope" as
a tool in patient care. John Herschel was the first to perform
Thermography by using color filters in a reflecting telescope. By the
early 1950's, thermal recoding was applied by US forces in the Korean war.
Dr. Ray Lawson, and later Professor E.F.J. Ring, and others (13-16)
reported clinical application of thermography. By 1982, thermal imaging
was accepted as a new laboratory test in Japan. At least in 2 states
(California and Florida) the worker’s compensation courts have accepted
the utilization of ITI for the diagnosis of CRPS.
The American Academy
of Neurology (AAN) (17) in 1990 reviewed the utilization of Thermal
imaging in neurologic practice. It emphasized the importance of proper
technique. It found the test not useful for the diagnosis of
radiculopathies, entrapment neuropathies, headaches, stroke, and transient
cerebral ischemia (17). As discussed in the present paper, the ITI is not
useful for diagnosis of transient ischemic attacks, entrapment neuropathy
(18), and disc herniation (19), but can contribute information to
diagnosis and treatment of neuropathic pain due to neurovascular
THE ITI PUZZLE
ITI has been abused, and over -and underused in the past three decades.
Improper technology on one hand, and poor understanding of the basic
anatomy and physiology of the autonomic nervous system (ANS) has
contributed to exclusion of this test, depriving the patient of proper
diagnosis and treatment.
expectation of a single test to identify the cause of a complex clinical
syndrome can lead the physician to deem the test useless. Such a complex
syndrome is properly diagnosed by careful history taking and clinical
correlation rather than by applying a single test. As an example, MRI of
the spine may show an innocuous disc bulging or protrusion unrelated to
the patient’s pain. Whereas only 28-30% of the patients suffering from
chronic back pain are due to disc pathology, over 80% of such patients are
diagnosed as disc disease, leading to unnecessary surgery (20,21).
dynamic state of flux of the sympathetic system plays an important role in
balancing and compensating the external versus internal fluctuations of
body temperature. Accurate recording of this sophisticated temperature
regulation requires impeccable technique, reproducible, consistent
recording, and a controlled laboratory environment. Unfortunately, the
physician rarely enters the laboratory to obtain further, more sensitive,
and accurate pictures than the standard technique done by the technician
(Fig.2). ITI can provide further information leading to correct diagnosis.
The infrared camera
records the infrared electromagnetic spectrum (Table 2). At the short wave
boundary (Table 2 ) the infrared spectrum starts at the visual perception
limit of deep red. At the opposite extreme of long wavelength frequency,
it borders, and blends with, microwave-radio wavelength. The infrared band
international 11 / 2 (2001)
Figure. 2 - Central hyperthermic areas of entrance and exit in electrical
injury. The permanent hyperthermic damage is surrounded by
vasoconstrictive hypothermia. Only after increasing the thermal
sensitivity (right) the lesions were identified. This "button hole" sign
is exclusively seen in electrical injury.
"near infrared" (0.75 to 3m m), "middle infrared" (3-6µ
m), "far infrared" (6-15µ
"extreme infrared" (15-100µ
standard ITI units measure the far infrared (FIR) wave length. To
accurately record and measure subtle temperature changes requires a
" blackbody" box. The "blackbody" is an object capable of absorbing
all radiation and equally emitting any wave length (Kirchhoff Law).
thermal imaging laboratory requires minimum space of 3.5x4.5 meters;
Room temperature of 70-72ºF; No shiny (e.g., Linoleum) or smooth
plastic floor to avoid heat and light mirror effect; The interior of
the laboratory should be infrared absorptive. Walls should be
insulated at minium rate of R=19Hr-Ft 2 - ºF/BTU; Room
humidity of 50-70 %. The air conditioner should provide laminar down
flow ranging no more than 1ºF (1.8 ºC) temperature. The patients are
cooled down in a 20-21ºC steady state room for 30 minutes of
equilibration without clothing. No prior smoking for at least 90
minutes, no sun bathing lotion, no application of ice packs or heat,
no acupuncture, laser therapy, EMG needle test, or transcutaneous
electric nerve stimulation (TENS) for at least 48 hours prior to the
thermographic testing. The patient should not wear any type of
jewelry during the test. A standard sensitivity of 24-34ºC is the
usual staring point. Standardization of technique, and consistent
reproduction of the results are essential for accuracy of the test.
A standardized ambient temperature of
Table 2. The
relationship of electromagnetic spectrum to the infrared band.
LW Far Inrared
21-22º C (70-72ºF), a minimum of 2-3 sets of reproducible measurements in
a cool, controlled temperature, no smoking, and no perfumes for at least 1
hour before the test, are the minimal technical requirements (22) to
achieve a reliable comparative side to side (delta T) of ± 0.2 - 0.3º C
(23). The review of ITI done prior to patients being referred to our
clinic have revealed the tendency for inflexible routine baseline
temperature measurements, rather than adjusting the sensitivity gauge to
achieve a more accurate test(1).
The sympathetic nervous system is an integral
part of the comprehensive central and peripheral nervous system playing a
REGULATION of the body (skin and viscera)(24-27),
2. CONTROL OF VITAL
SIGNS ( blood pressure, pulse, and respiration), and
3. MODULATION OF
regulation is achieved by modulating heat loss and heat preservation
through dermal and sub-dermal circulatory (sympathetic) and sweating
(cholinergic) changes. In contrast to the fish, the "warm blooded" animals
can only survive in the stable, narrow - range band of the internal
environment temperature - milieu interne (28). The dermal and subdermal
structures provide a grid style of vertical and horizontal vascular
shunting system which protects the body against excess ambient heat by
wasting the body heat through vasodilation and sweating. The same system
does the opposite in excess ambient cold environment by conserving heat,
and by cooling the skin surface. The deep tissue circulation plays a major
role in the protection of the internal environment (homeostasis). In cold
temperature, skin vasoconstriction increases the deep tissue heat and
circulation to prevent core hypothermia. Chronic pathologic sympathetic
up- regulation causes the vicious circle of persistent dermal
vasoconstriction, and increased deep circulation in bone and muscles,
leading to osteopenia and muscle weakness (29).
system modulates the cellular immune function (30), leading to modulation
of cellular neurogenic inflammation in pathologic conditions (30-45). In
severe and chronic stages of sympathetic dysfunction, neuroinflammation
results in bulbous lesions (33), pelvic inflammatory disease (PID),
interstitial cystitis (46), and sterile abscess (47). The regional
neuroinflammatory edema leads to impingement of the peripheral nerves
mislead the clinician to mistake the disease for conditions such as carpal
tunnel (38,48,49) and Dupuytren’s contracture (50) (Table 3), thoracic
outlet (TOS), tarsal tunnel, and myofascial syndrome (39). The surgical
trauma or repetitive trauma due to sympathetic ganglion blocks (Table 3),
in turn aggravates the inflammation (12,40,51-54), becoming a new source
of neuropathic pain and leading to spread of the disease (42,55). ITI can
spare the patient from unnecessary surgery (12,36,37,38). The primary
afferent sensory neuron plays a major role in modulation of excitatory,
and pro-inflammatory neuropeptides such as substance P (SP) (43,44,56-66),
nitric oxide (NO) (67-87), and calcitonin gene-related peptide (CGRP)
(88), as well as inhibitory hormones such as corticotropin-releasing
hormone, opioid peptides, such as dynorphin (59).
Table 3. The role of
ITI in selection of treatment modalities.
Identification of "Virtual Sympathectomy". ( Permanent
hyperthermia due to damage from repetitive ganglion block needle
insertion). ITI spares the patient from further blocks.
Alpha-receptor supersensitivity to circulating Nor-ep shows diffuse
hypothermia indicating the futility of any other chemical,
radiofrequency, or surgical procedures.
identifies the permanent hyperthermia in the injured extremity. The
apex, central part of permanent sympathetic nerve damage is
surrounded by hypothermia. Any form of needle insertion, nerve
block, or topical Clonidine skin patch application to the damaged
nerve area aggravates and enlarges the lesion. The treatments should
be applied proximally at epidural and paravertebral levels of spine
corresponding to the area of nerve damage.
evidence of neurovascular instability on ITI proves advanced stage
of sympathetic dysfunction non- responsive to sympathetic ganglion
block or sympathectomy.
identifies referred-pain focal hypothermic area. Massage or nerve
block in this focus relieves the pain.
international 11 / 2 (2001)
Figure. 3 - Cervical neuropathic pain represented with hypothermia on ITI
in the paravertebral area. Gentle pressure exerted over the cervical spine
(Left) revealed reactive release of inflammatory chemicals and blushing of
the skin in the hypothermic area. Treatment with paravertebral nerve
blocks (Right) provides pain relief, and dissemination of irritative
substances (SP, NO, etc). Massage therapy after block enhances the
chronic stage, the referred pain such as seen in shoulder-hand
syndrome, results in antidromic spread (89) of the inflammatory
substances (59) causing secondary involvement of the paravertebral
sensory nerves. The sympathetic dysfunction leads to inflammatory
response in the extremity, as well as in the epidural and
paravertebral regions of spine. ITI helps identify these
inflammatory changes. Epidural (90) and paravertebral (91) nerve
blocks in these regions help relieve the inflammation (Fig. 3). Such
blocks achieve pain relief, as well as anti-inflammatory effect
through injection of minute (2.5 to 10 mg) doses of depo-medrol® (methylprednisolone)
CENTRAL REGULATION OF
sympathetic system participates in regulating the core body
temperature within a narrow band. The normal blood flow to the skin
is 200 ml/mm which is 4% of the cardiac output (93). This output far
exceeds the baseline oxygen and nutrient requirements of skin. The
rich arteriovenous anastomoses in acral areas of the palm of hands,
feet, and axilla, allow a large volume of blood to flow through the
skin. This leads to hyperthermia and heat emission. The parallel
anatomical structure of large arteries and veins in the extremities
allows countercurrent exchange of heat leading to superficial
vasoconstriction, and simultaneous shunting of blood from the
superficial to the deep venous systems, leading to surface heat
NERVOUS SYSTEM THERMOREGULATION
changes in blood circulation are detected by neurons in the preoptic
nuclei of the hypothalamus(94). The thermoreceptors for cold - and
warmth sensations in the skin and perivascular areas play an
important role in this temperature detection (94). The posterior
hypothalamus modulates proper heat-generation or dissipation
mechanisms. The inhibition of sympathetic output results in
cutaneous vasodilation and heat loss (94). Moreover, the same
inhibition results in more cholinergic sweating (by 1/10 of nerve
fibres in the efferent
sympathetic nerves ).
On the opposite extreme, cold
exposure stimulates increased sympathetic output from posterior
hypothalamus leading to vasoconstriction, and heat conservation (94). The
shunting of blood into the deep venous system acts as an insulator in the
subcutaneous fat layers between the blood and the cold ambient
temperature. The protective effect of subcutaneous fat is important. The
obese individuals can maintain a higher internal temperature on cold
exposure. They also have chronically cooler skin temperature (95,96). The
above multiple factors contribute to maintenance of a constant core
temperature of approximately 37º
C against a range of external temperature fluctuations-usually between 15º
C and 54º C (60º
F- 128º F) (97).
ITI RECORDING OF DEEP
in medicine addresses the thermal variations in superficial and deep
structures of the body (Fig. 2). Even though the old literature has
claimed that ITI studies the surface skin temperature, as claimed by the
U.S. Federal Register (98), to a depth of 6 mm. The research conducted by
Elam, et al (99) has shown the test to be informative in evaluating deep
temperature changes as well. The skin is an almost perfect radiator of the
deep heat. This radiator helps prevent hyperthermia and damage to internal
organs (specifically the brain). This radiator, with 98% emissive
efficiency, allows the deep heat to radiate and dissipate in the ambient
environment (99). This heat radiation is recorded by ITI (Fig. 2). The ITI
records pathological temperatures at least as deep as 27 mm (Fig. 2) in
the extremities, and even deeper in the breast. Different methods have
been applied to study superficial and deep circulation (e.g.,
scintigraphic bone scanning, and ITI)(100). The first clinical application
of ITI was to record the thermal changes of deep structures such as breast
cancer (101,102), and arthritis (103-105). ITI in Paget’s disease has
shown pathological hyperthermia in deep structure of vertebral bodies. The
ITI in Paget’s disease showed direct correlation with improvement and
reversal of osteopenia and pain after proper treatment (106). This is
another example of the sensitivity of ITI in identifying the deep tissue
The ITI provides
accurately measurable information regarding subtle thermal changes(100).
The ITI shows any old or new sympathetic nerve damage or dysfunction, thus
confusing the examiner and demanding careful and proper clinical
correlation. The examiner interprets the old lesion as the main pathology.
The confusing results due to multiple old and new life time injuries may
mislead the physician to end up losing faith in ITI. Only proper history
taking and interpretation can solve such a problem. However, in a double
blind study the above example of ITI will be tagged as invalid.
Another source of confusion is
spread of the thermal changes to the contralateral extremity - making it
difficult to compare the delta T between the two extremities. As the
disease becomes chronic and the sympathetic thermal dysfunction becomes
bilateral (1,61,107), the ITI shows identical bilateral temperature
changes causing difficulty in diagnosis. This is true both in standard ITI,
and in cold stress tests (108,109). The bilateral representation of
central sympathetic temperature regulation is modulated at the following
centers: The first center is at the chain of sympathetic ganglia on each
side of spine. These ganglia relay the transmission of pain or thermal
impulses horizontally and vertically(21,110) (Fig. 3). This bilateral
integration of the impulses at the sympathetic chain level serves the
purpose of transmitting the stressful impulses to the rest of the body,
and coordinating the sympathetic stress regulation (21). The second center
is at the spinal cord level (61) where the temperature modulation is
exerted symmetrically and bilaterally with side to side temperature
variation (delta-T) of ± 0.2 - 0.3º
C (23). This explains the spread of thermal changes to the contralateral
side (1). The next relay center for neuropathic afferent nerves and
temperature regulation is the hypothalamic modulation centers (107).
Finally, at the cerebral hemispheric level, the Central autonomic network
(CAN) exerts its influence on vasomotor, visceromotor, neuroendocrine,
cardiovascular, and pain modulation. The CAN includes the limbic
system-specifically the mesial frontal and insular cortex, amygdala, stria
terminalis hypothalamus, and nucleus solitarius (111,112).
SIGNIFICANCE OF HYPERTHERMIC REGIONS
stage of nerve dysfunction, the involved area is hyperthermic due to
release of destructive cytokines (21,47). After a few weeks, the
hyperthermic area shrinks.
international 11 / 2 (2001)
Figure. 4 - A
previously undiagnosed right leg arteriovenous malformation (AVM)over
27mm deep, complicated by CRPS (RSD) . ITI identified the deep
lesion and spared the patient from the scheduled sympathectomy.
Vascular surgery corrected the condition.
Figure. 5 -
The paravertebral chain of ganglia transmit the neuropathic pain and
abnormal sympathetic dysfunction vertically (e.g., from foot to hand
and vice versa), and horizontally (from side to side). This explains
the remote symptoms and thermal manifestations of CRPS patients.
With permission from Springer-Verlag Publishers (1).
Figure. 6 -
CRPS nerve damages to right toes after "neuroma exploration". The
sympathectomy did nothing for the pain. ITI spared the patient from
the scheduled chemical sympathectomy. The left foot showed
compensatory hypothermia after sympathectomy.
Figure. 7 -
"Virtual sympathectomy" secondary to repeated stellate ganglion
nerve blocks leading to permanent sympathetic nerve damage and
hyperthermia (heat leakage) in upper extremities. The ITI spared the
patient from further sympathetic nerve blocks.
some cases (47) the hyperthermia persists due to permanent damage to the
thermosensory nerve fibers (1) (Fig. 4). This bodes a poor prognosis.
Traditionally, hyperthermic areas recorded on ITI have been ignored due to
the universal old and partially true dictum emphasizing the importance of
hypothermic foci as the main sign of sympathetic dysfunction. This has
resulted in the examiner usually not paying attention to hyperthermic foci
which are equally significant. Usually, the hyperthermic areas point to
either irreversible damage to the sympathetic system in the traumatized
focus, or a referred pain area undergoing a backlog of neural transmission
of the antidromic afferent sensory nerve fibers (88) to the spinal cord in
the form of algogenic chemicals such as nitric oxide (NO) (67-87,113,114),
SP ( 43,44,56-58,60), CGRP (44,115), and oxidative stress agents (116)
(Fig. 5). These algogenic pro-inflammatory chemicals play a major role in
the function of immune regulation, and when accumulated in large doses
cause movement disorders such as tremor, and pro-inflammatory referred
pains such as headaches, neck pain, back pain (12,113). Traumatic
procedures such as surgical exploration(12), needle insertion in hands or
feet for nerve blocks, or EMG needle insertion should not be applied to
the damaged hyperthermic area in the extremity which may lead to further
deterioration and aggravation of the condition (22,117,118). On the other
hand, the above treatment should be applied to the referred pain areas in
cervical, thoracic and lumbar regions which have undergone no focal nerve
damage but are reflecting the backlog and accumulation of cytokines in the
path from the distal extremity nerve damage to the dorsal horn of the
spinal cord (88) (Fig. 3). This identification of hyperthermic nerve
injury is a major therapeutic contribution of ITI.
Physiologic hyper -
and hypothermia are the reflection of the dynamic function of sympathetic
system(22) to achieve homeostasis. These changes are the end-results of
multiple factors such as hyperthermia due to damage to thermoregulatory
sympathetic nervous system (117,118) (Fig. 2). The up-regulation of the
sympathetic system leads to vasoconstriction and hypothermia. The
down-regulation or damage of this system leads to a dermal hyperthermic
focus surrounded by a compensatory hypothermia (1) (Fig. 6 ).
The referred pain
phenomenon may be accompanied by hypo - or hyperthermia in paravertebral
regions (Fig.3). This form of hyperthermia is due to accumulation of
pro-inflammatory cytokines outlined above. These cytokines play a major
role in development of inflammation (42,55), movement disorder (119-122),
and immune regulation (44,59,113). In contrast, in chronic late stages,
the hyperthermic area becomes more focal and quite small in size
surrounded by compensatory hypothermia of the rest of the region (12). The
contralateral normal side also undergoes compensatory hypothermia. The end
result is two cold extremities with no statistically significant thermal
difference (delta T). This problem can only be solved by proper clinical
dysfunction causes sympathetic up-regulation and regional hypothermia.
This phenomenon has been blamed as Alpha-receptor supersensitivity to
circulatory norepinephrine (NE) after prolonged denervation(24,25). This
phenomenon is usually seen in the sympathectomized limb. The limb, instead
of being warm, becomes colder after surgery due to end - organ
supersensitivity to alpha receptors (24,25,123) (Fig. 6). This is a major
cause of sympathectomy failure (Fig. 6). ITI identifies this form of
hypothermia, sparing the patient from further harmful surgical
treatment(12) (Fig. 6). In this regard, ITI points to the futility of
sympathectomy. Commonly, as the sympathetic system becomes chronically
dysfunctional, the prolonged pathologic vasoconstriction yields to
inconsistent tonus of the vasomotor nerves. This leads to the development
of neurovascular dysfunction, mottling, and instability (124). This refers
to blotching, and fluctuation of skin temperature. ITI identifies this
condition more accurately, and spares the patient from sympathectomy and
ganglion nerve blocks (Fig. 6) which cannot be expected to help an
unstable and failed stage of sympathetic dysfunction (1,12).
THE ROLE OF ITI IN
identification of hyper - and hypothermic areas guides the clinician in
management of pain, more accurate diagnosis, and avoidance of further
traumatizing the already damaged nerves by avoiding unnecessary surgical
procedures (51-53),(Fig. 7), or improper nerve blocks. ITI can identify
these areas of nerve dysfunction in paravertebral regions of the spine
(91) in form of hypothermic foci. Epidural nerve blocks (with bupivacaine
and depo-medrol) in these regions provide both somatic and sympathetic
pain relief (12,21,91). According to Stein (88) the cytokines and
inflammatory chemicals are transmitted via spinal nerves to the spinal
cord and vice versa, modulating the spinal cord function of nociception.
The therapeutic effect of these blocks lasts 8-12 weeks (1,12,21) versus
ganglion blocks which last a few hours or days.
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