Chapter 20 Diagnostic Nerve Blocks Flashcards

1. Pain relief after local anesthetic blockade does not reliably predict successful neurodestructive surgery, that is, long-lasting analgesia without deafferentation pain. 2. Prognostic local anesthetic blocks may be used to evaluate patients for neurolytic block. A negative response to blockade may be extremely valuable in preventing an unnecessary neurodestructive procedure. 3. Relief of neuropathic pain with intravenous lidocaine appears to predict potential responders to oral mexiletine t

1
Q

differential neural blockade

A

This technique is premised upon the concept of selective
blockade of one neurologic modality without blocking the
others, and is divided into two clinical approaches. The
basis for the anatomic approach is the actual anatomic separation of somatic and sympathetic nervous system fibers, so that an injection of local anesthetic solution
blocks one modality without affecting the others

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2
Q

foundation for differential neural blockade is

A

nerve fiber length and fiber diameter. Nerve fiber length determines relative susceptibilities of a given fiber to local
anesthetic concentrations, and nerve fiber diameter determines the modalities subserved by the fiber

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3
Q

four subclasses of A fibers

A

Aa, Ab, Ag, and
Ad. A-alpha fibers subserve motor function and proprioception.
A-beta fibers subserve touch and pressure

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4
Q

A-gamma fibers

A

subserve muscle spindle tone.

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5
Q

A-delta fibers

A

subserve sharp pain and temperature sensations.

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6
Q

B-fibers

A

thin myelinated, preganglionic autonomic nerves; and the unmyelinated

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7
Q

C-fibers

A

subserve dull pain and temperature. C-fibers are thinner than the myelinated A- and B-fibers and have a lower conduction velocity than the others

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8
Q

differential spinal block

A

attempts to block
separately sympathetic, sensory, and motor systems for the
subsequent determination of the etiology of an individual’s
lower abdominal or lower extremity pain mechanism

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9
Q

Prior to performing lumbar puncture and standard subarachnoid anesthesia

A

obtain informed & written consent, an IV and a crystalloid infusion is begun. noninvasive
hemodynamic monitors is applied and baseline vital signs are recorded.

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10
Q

In the conventional differential spinal block, four solutions are prepared and labeled A, B, C, and D.

A

Solution A contains no local anesthetic (placebo); solution
B contains 0.25% procaine;
solution C contains 0.5% procaine; and solution D contains 5.0% procaine. These solutions are injected sequentially ( the effects of each solution must completely dissipate prior to injecting the subsequent solution in sequence) through a 25- to 27-gauge pencil-point spinal needle, which has been introduced in standard fashion at the L2–L3 or L3–L4 interspace

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11
Q

Four basic interpretations of the differential spinal block

A

Psychogenic pain, Sympathetic pain, Somatic pain, Central pain.

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12
Q

Psychogenic pain

A

If the injection of the placebo solution (solution A) relieves the patient’s pain, the pain is tentatively classified as psychogenic, depending on duration of analgesia. For prolonged or permanent pain
relief, the pain is probably truly psychogenic, whereas
if the pain relief is temporary, the response is likely a
placebo reaction

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13
Q

Sympathetic pain

A

If the patient does not obtain relief following the placebo injection, but experiences relief
from 0.25% procaine (solution B), the mechanism subserving the patient’s pain is likely mediated by the sympathetic nervous system. This presumes that there are clinical signs of complete sympathetic block
(increased skin temperature; psychogalvanic reflex
response, sweat chloride test, etc.) and no detectable
sensory changes

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14
Q

Somatic pain

A

If the patient does not obtain relief following the injection of placebo or 0.25% procaine, but
0.5% procaine provides significant relief, this typically
indicates that the pain is subserved by Ad fibers and/or
C-fibers, and is therefore classified as somatic.

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15
Q

The caveat of somatic pain

A

The caveat, of course, is that the patient did exhibit signs of
sympathetic nervous system blockade following the
injection of 0.25% procaine, and that the pain relief from 0.5% procaine is accompanied by analgesia or anesthesia in the areas of concern. This is important because of the variability in Cm for B-fibers that is known to exist. If the patient has an elevated Cm for B-fibers, pain relief from 0.5% procaine might be due to a sympathetic block rather than a sensory block

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16
Q

Central pain

A

If the injections of solutions A, B, and C fail to resolve the patient’s pain, 5% procaine (solution D) is then injected to block all modalities, including motor function. If solution D does relieve the pain, the mechanism is still considered to be somatic, and it is presumed that the patient has an elevated Cm for Ad and C-fibers. However, if there is no relief following the injection of the 5% solution, the pain is classified as central in origin.

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17
Q

modified differential spinal block

A

In the modified block, only solutions A and D are injected
through the spinal needle. If the patient obtains no or only
partial relief following the injection of solution A (placebo),
then 2 ml of 5% procaine (solution D) are injected
through the spinal needle. The needle is then removed,
and the patient is placed supine.

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18
Q

proposed interpretation of the modified differential spinal

If the patient’s pain is relieved after injection of solution A

A

the interpretation is the same as in the conventional

differential spinal technique

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19
Q

proposed interpretation of the modified differential spinal

If the patient does not obtain relief following the injection
of solution D (5% procaine)

A

the diagnosis is considered to be the same as in the conventional approach whereby the patient fails to get relief following injection of all solutions (A through D)

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20
Q

proposed interpretation of the modified differential spinal

If the patient obtains complete pain relief after injection of solution D,

A

the pain is considered to be
somatic and/or sympathetic in nature. At this point the regression of blockade becomes important, as 5% procaine blocks motor, sensory, and sympathetic fibers. Therefore, the patient is queried as to the return of his or her pain concomitant with the regression of, first, motor block, followed by sensory block regression, and, ultimately, by sympathetic block regression

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21
Q

proposed interpretation of the modified differential spinal

If the pain returns when the patient again appreciates
a pinprick as sharp (recovery from analgesia), the mechanism is considered to be

A

somatic (subserved by Ad fibers and/or C-fibers)

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22
Q

proposed interpretation of the modified differential spinal

If the pain relief persists for a prolonged period after
recovery from analgesia, the mechanism is considered
to be mediated

A

by the sympathetic nervous system (mediated by B-fibers)

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23
Q

differential epidural block

A

developed in an effort to circumvent the possibility of producing post– lumbar puncture headache from the differential spinal block
and to allow for better assessment of incident pain if a catheter is placed

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24
Q

differential epidural block technique

A

the technique relying on
placement of a standard 18- or 20-gauge Tuohy-type epidural
needle into the epidural space at L2–L3 or L3–L4.Four
solutions are sequentially injected, with solution A a placebo (typically normal saline solution), and solution B containing 0.5% lidocaine, presumed to be the mean sympathetic blocking concentration of lidocaine in the epidural space. Solution C is 1% lidocaine, presumed to be
the mean sensory blocking concentration of lidocaine, and
solution D is 2% lidocaine, a concentration intended to
block all modalities (sympathetic, sensory and motor).

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25
Q

two shortcomings of the differential epidural block technique

A

First, because of the delay in onset of blockade of each modality using the epidural approach (as compared with subarachnoid administration of local anesthetic), a significantly longer period would be required between injections, thus increasing the time-intensive nature
of the procedure.
Second, if local anesthetics occasionally fail to give discrete end points when administered in the subarachnoid space, they do so even more frequently when administered epidurally, therefore tending to further “muddy the waters” in assessing the response of patients to each subsequent
injection

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26
Q

anatomic approach to differential block

A

The anatomic approach relies on three injections: a placebo, a sympathetic nerve block, and a somatic sensory and motor block

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27
Q

the anatomic

approach certainly has applicability for

A

head and neck and

upper extremity pain

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28
Q

differential epidural approach

may be preferred for

A

thoracic pain to minimize the likelihood of pneumothorax resulting from thoracic paravertebral blocks used in the anatomic approach

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29
Q

Interpretations of result during anatomic approach to differential block

A

If the patient obtains pain relief following the injection of saline, the pain is considered to be of “psychogenic” origin, with the same considerations applying as previously mentioned. If pain
disappears following the chloroprocaine injection, the pain is considered to be either sympathetic or somatic. The pain is considered to be somatic if it returns once the sensory block dissipates; but if pain relief persists after the sensory block dissipates, it is considered to have a sympathetic nervous
system origin. If the patient continues to experience pain,
even in the face of complete sensory and motor block, the
pain is considered to be central, with the same considerations as previously mentioned for differential spinal block

30
Q

TABLE 20–3

A

Anatomic Differential Block: Procedural Sequence

31
Q

Diagnostic Blocks: Limitations

Potential limitations due to altered primary afferent nerve activity:

A
  • Receptor sensitization by tissue factors
  • Spontaneous discharge from dorsal root ganglion (DRG) proximal to injury
  • Propagation of antidromic activity distal to site of nerve injury
  • Sympathetic influences on receptor sensitization, inflammation, or neuroma firing
32
Q

Diagnostic Blocks: Limitations

Potential limitations due to altered spinal processing:

A
  • Peripheral nerve block alters balance of large fiber and C-fiber input to dorsal horn
  • Spinal block of superficial fibers of descending inhibitory system
  • Acute activation of descending inhibitory tracts by stress of nerve block procedure
  • Presence of conditioned descending stimulatory modulation, which may persist
  • Pain dependent on converging inputs from two sources, not both apparent
33
Q

Diagnostic Blocks: Limitations

Potential limitations due to central plasticity:

A
  • Unpredictable response to block of conditioning afferent input with central sensitization
  • Block of afferents may normalize dorsal horn responsiveness, leading to prolonged relief
  • Block of adjacent uninjured nerve may relieve pain in its area if altered central processing
  • Block of injured nerve may not relieve deafferentation pain if there is DRG receptive field expansion
34
Q

Diagnostic Blocks: Limitations

Potential limitations due to local anesthetic effects:

A
  • Relief after sympathetic block may be due to subtle undetected somatic block
  • Intended profound somatic blocks typically less than complete neural block
  • Differential pharmacologic block by local anesthetics is unpredictable, with varying degrees of overlapping partial block of each sensory modality
  • Systemic effects of absorbed local anesthetics on neuropathic pain
35
Q

The use of a nerve block to identify a nerve pathway that is the source of an individual’s ongoing pain assumes three potentially
false premises:

A

(1) pathology causing pain is located in an exact peripheral location and impulses from this site travel via a unique and consistent neural route,
(2) injection of a local anesthetic totally and selectively abolishes sensory function of intended nerves, and
(3) relief of pain following
local anesthetic block is due solely to block of the target neural pathway.

36
Q

Diagnostic Nerve Blocks: Questions To Be Addressed

A
  1. Anatomic location and source of pain
  2. Visceral versus somatic origin of trunk pain
  3. Sympathetic versus somatic origin of peripheral pain
  4. Identify referred pain syndromes
  5. Segmental levels of nociceptive input
  6. Painful muscle spasm versus fixed contracture deformity
  7. Diagnosis of central pain states
37
Q

Facet joint diagnostic blockade is probably most accurately

performed by

A

medial branch nerve block.

38
Q

The diagnosis of third occipital nerve headache after whiplash injury in cases where there is no distinguishing feature on history or physical examination is typically
made by

A

local anesthetic C2–C3 facet joint blocks

39
Q

in the chest, abdomen, or pelvis

a somatic source may be confirmed by

A

injections into costochondral tissue, truncal muscles, or intercostal nerves

40
Q

If it can be established that pain is visceral in origin, treatment may be directed towards

A

exploration of abdominal or pelvic organs, or towards denervation of
visceral structures, if an untreatable malignancy is encountered

41
Q

techniques employed in the diagnosis of painful states involving the viscera and the trunk

A

Celiac plexus block, hypogastric plexus

block, intercostal nerve block, or local infiltration

42
Q

Diagnostic sympathetic

blocks

A

These include the cervicothoracic and lumbar sympathetic chain.

43
Q

How to establish the presence of a sympathetically maintained pain state?

A

Confirmation of pain relief and complete sympathetic block on two occasions with different local anesthetics. Failure to obtain relief is consistent with sympathetically independent
pain (SIP).

44
Q

REFERRED PAIN STATES

A

medial branch blocks for facet syndrome relieve distal buttock and thigh pain, or when injection of active trigger points
for myofascial pain provides relief of distant somatic referred pain.

45
Q

Central pain

A

arises from the brain or spinal cord. It may occur after a central lesion or as a result of abnormal
central modulation of nociceptive and non-nociceptive input

46
Q

The classic response seen with a central pain state is

A

inadequate analgesia after multiple peripheral blocks.
Inadequate pain relief is expected after epidural anesthesia to a segmental level that supplies the painful area, as well as poor analgesia with systemic or intraspinal
opioids.

47
Q

Psychogenic pain

A

Failure to relieve pain with complete sensory and motor block of the segmental levels associated with the painful area suggests the presence of supraspinal mechanisms. It does not in
and of itself allow the specific diagnosis of either central pain or a psychogenic pain syndrome. Temporary pain
relief after a placebo block is a common phenomenon

48
Q

PROGNOSTIC BLOCKS

A

Local anesthetic blocks may be used to evaluate patients with cancer pain as potential candidates for neurolytic blocks, such as celiac plexus block for the visceral pain of pancreatic cancer. Opioid or local anesthetic injections
help predict the response to an implanted apparatus for intraspinal drug administration in similar patients with cancer pain.Failure to obtain adequate analgesia will prevent an unnecessary operation or intervention.

49
Q

positive prognostic blocks do not

reliably predict long-lasting analgesia, without

A

deafferentation pain, after neurodestructive procedures in patients
with chronic nonmalignant pain.

50
Q

Pain relief following sacroiliac joint injection may be related to
.

A

infiltration of the sacroiliac joint ligament or sacrospinalis muscle, thus giving the incorrect impression that the joint
is the source of the pain. Groin pain seems to be a distinguishing characteristic of patients who respond favorably
to sacroiliac joint injection.

51
Q

Downfall of sacroiliac joint injection

A

intra-articular spread
of local anesthetic is necessary to achieve efficacy, and this is rarely achieved without adjacent spread of the injectate
to nontargeted tissues and nerves, including the second, third, and fourth sacral nerves (roots of the pudendal nerve).

52
Q

discography may be a useful technique for determining

A

Pain may arise from the annulus of the intervertebral disc, and discography may be a useful technique for determining the internal structure of the disc

53
Q

lumbar sympathetic nerve block

LSNB

A

Lumbar sympathectomy may be performed to relieve lower extremity ischemic pain due to advanced peripheral
vascular disease. This therapeutic intervention may be preceded by a prognostic lumbar sympathetic nerve block
(LSNB) using a local anesthetic agent

54
Q

Following LSNB, what is observed to supports performance of a therapeutic lumbar sympathectomy (by radiofrequency lesion or by neurolytic blockade

A

The presence of an
acceptable increase in skin temperature following LSNB further supports performance of a therapeutic lumbar
sympathectomy (by radiofrequency lesion or by neurolytic
blockade) designed to increase blood flow to the
ischemic extremity.

55
Q

The purpose of diagnostic sympathetic block

A

is to selectively interrupt sympathetic nervous
system control of vasculature, while leaving somatic pathways
unchallenged

56
Q

Stellate ganglion blockade (SGB) may fail to produce sympathetic denervation of the upper extremity due to

A

the multiple sites of sympathetic nerve activity that bypass the ganglion. Production of Horner’s syndrome is no
guarantee that sympathetic flow to the hand has been interrupted

57
Q

What is the rationale for using sympathetic blocks as a treatment modality in established cases of CRPS.?

A

Skin perfusion does increase on the ipsilateral
hand following SGB as measured by laser Doppler fluxmetric
hand perfusion studies, however, and does so in a
manner inversely related to the duration of symptoms of CRPS. This implies that although the use of these blocks
for diagnostic purposes may be somewhat controversial,

58
Q

Intravenous regional blocks (IVR) using bretylium and guanethidine have been administered to patients with

A

suspected sympathetically mediated pain syndromes

59
Q

bretylium and guanethidine mechanism of action

A

inhibit release of norepinephrine from nerve terminals, and guanethidine depletes tissues of it

60
Q

Intravenous lidocaine hydrochloride has been used in the diagnosis of

A

neuropathic pain states. there is selective peripheral and central analgesia produced by
intravenous lidocaine in neuropathic pain states

61
Q

Patients who respond

favorably to IV lidocaine infusions may be placed on

A

oral congeners of lidocaine, notably mexiletine or tocainide for
prolonged management

62
Q

Mechanism of action of lidocaine and mexiletine

A

suppress the excitability of dorsal horn neurons
by blocking Na+ and K+ channels, as well as persistent sodium currents in sensory axons of individuals suffering from neuropathic pain syndromes

63
Q

Phentolamine,

A

an a-adrenergic blocking agent, has been
administered intravenously in an attempt to determine
if a patient’s pain is sympathetically mediated

64
Q

Response to IV phentolamine should indicate

A

patients who might expect positive response to systemic or transdermal sympatholytic
agents

65
Q

PREREQUISITES FOR OPTIMAL

DIAGNOSTIC BLOCK

A

A comprehensive history should include a pain diary,
a history of the present pain, and all previous diagnostic workup and therapy information. A complete neurological
and general physical examination including a
functional evaluation should be undertaken. Results of diagnostic studies and psychological evaluations are reviewed

66
Q

modifications to regional anesthesia
procedures may improve the reliability of diagnostic nerve
block:

A
  • Limit the use of preprocedure sedatives and analgesics to ensure that the patient remains communicative at all
    times.
  • Limit the volumes of local anesthetics to minimize the
    likelihood of spread to adjacent, unwanted sites.
  • Make liberal use of radiography including fluoroscopy, CT scans, contrast material, ultrasonography, and plain
    film x-rays to improve accuracy.
  • Employ a peripheral nerve stimulator with a variable output to locate target nerves precisely for plexus and peripheral nerve block.
67
Q

modifications to regional anesthesia
procedures may improve the reliability of diagnostic nerve
block:

A
  • Repeat positive blocks with a local anesthetic of different duration, if the first block is successful, in an attempt to correlate the duration of pain relief to that of the expected duration of the local anesthetic.
  • Maintain detailed observations and records of the effects of the diagnostic block.
  • Record the patient’s pain scores at rest and with function, as well as vital signs, sensory and motor examination findings, signs of sympathetic nervous system function, and the presence of pain behaviors both before and after the diagnostic block.
  • Ask the patient to maintain records of neurologic symptoms, degree of pain relief, pain scores, activity levels, and analgesic intake following discharge
68
Q

False-positive results may occur due to a

A

placebo response, systemic effects of local anesthetics, spread of agent to adjacent tissues or
nerves, unreliable patient report of block effects, and temporary alterations in central processing due to lack of normal afferent input

69
Q

False-negative responses may occur

A

when a block fails to
relieve pain. This may result from an incomplete block, the presence of alternative pain pathways, unappreciated referred pain syndromes, unreliable patient report of block
effects, and diagnostic testing performed at inappropriate times

70
Q

back and leg pain may be due to

A

lumbar disc herniation or degeneration, or to piriformis muscle syndrome, facet joint disease, sacroiliac joint dysfunction, ligamentous strain or tear, or myofascial pain, requiring radically different diagnostic somatic blocks to be performed