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Essentials of Pain Medicine > Chapter 53 Central Pain States > Flashcards

Chapter 53 Central Pain States Flashcards

KEY POINTS 1. Central pain states are common sequelae of SCI and stroke. 2. Pathophysiology of central pain is not understood. 3. Alterations in several neurotransmitters occur, including glutamate, GABA, norepinephrine. 4. Involvement of the spinothalamocortical pathway is strongly supported by animal models, but the precise pathway in humans is unknown. 5. The three components of central pain (steady dysesthetic, intermittent neuralgic, and evoked) must all be treated. In central pain o

1
Q

Central pain

A

a term used to describe the pain associated
with a wide range of disorders of the central nervous system
(CNS).

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2
Q

The International Association for the Study of Pain (IASP) defines central pain as

A

pain initiated or caused by a primary lesion or dysfunction of the CNS.

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3
Q

disorders of central pain include

A

poststroke, spinal
cord injury (SCI), traumatic brain injury, and multiple sclerosis
(MS).

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4
Q

The leading cause of central pain originating in the brain is

A

stroke

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5
Q

Dejerine-Roussy

syndrome

A

extrathalamic lesions. These pain-generating lesions extend from the first synapse of the
dorsal horn, or trigeminal nuclei, to the cerebral cortex.

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6
Q

etiology

A

The predominant etiology is vascular in origin, accounting for 90% of brain central pain (supratentorial 78% and infratentorial 12%). Extrathalamic sites are involved in 50% to 75% of cases

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7
Q

Chronic poststroke

pain more commonly occurs in the presence of

A

right-sided

thalamic lesions

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8
Q

Central pain of spinal origin is predominantly the result of

A

trauma

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9
Q

Many central pain patients maintain their ability to

A

touch, vibration, and joint movements. This supports the belief that the central pain involves the
spinothalamic tract and its thalamocortical projections.

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10
Q

The highest prevalence of central pain is reported in cases of lesions in the

A

spinal cord, medulla, and ventroposterior part

of the thalamus.

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11
Q

spinal cord injury (SCI) pain is broadly divided into

A

nociceptive and neuropathic with subclassification into

second and third tiers based on the anatomic structures involved, site of pain, and etiology.

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12
Q

Nociceptive pain may be

A

musculoskeletal or visceral in nature. The former may be secondary to overuse of certain parts of the body to compensate for regions of paresis or result from secondary changes in bone or joints.

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13
Q

Neuropathic pain usually seen in areas of

A

sensory abnormalities

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14
Q

Neuropathic pain has been

subdivided on the basis of

A

region, into at-level (radicular or central), above-level, and below-level pain to indicate the
presumed site of the lesion responsible for pain generation.

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15
Q

Taxonomy of Spinal Cord Injury Pain

Nociceptive Musculoskeletal

A 
Bone, joint, muscle trauma or
inflammation
Mechanical instability
Muscle spasm
Secondary overuse syndromes
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16
Q

Taxonomy of Spinal Cord Injury Pain

Nociceptive
Visceral

A

Renal calculus, bowel
dysfunction, sphincter
dysfunction, etc.
Dysreflexic headache

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17
Q

Taxonomy of Spinal Cord Injury Pain

Neuropathic: Above level

A

Compressive
mononeuropathies
Complex regional pain
syndromes

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18
Q

Taxonomy of Spinal Cord Injury Pain

Neuropathic: At level

A 
Nerve root compression
(including cauda equina)
Syringomyelia
Spinal cord trauma/ischemia
Dual level cord and root
trauma
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19
Q

Taxonomy of Spinal Cord Injury Pain

Neuropathic: Below level

A

Spinal cord trauma/ischemia

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20
Q

neuropathic pain definition outlined by the IASP was

A

“pain initiated or caused by a primary lesion or

dysfunction in the nervous system

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21
Q

Grading System for Neuropathic Pain

A

Criteria to be evaluated for each patient
1. Pain with a distinct neuroanatomically plausible distribution*
2. A history suggestive of a relevant lesion or disease affecting the
peripheral or central somatosensory system†
3. Demonstration of the distinct neuroanatomically plausible
distribution by at least one confirmatory test‡
4. Demonstration of the relevant lesion or disease by at least one
confirmatory test

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22
Q

Central pain states likely result from pathophysiologic

changes caused by

A

irritation of, or damage to, central pain pathways.

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23
Q

Injury to the CNS may result in

A

anatomic, neurochemical,
inflammatory, and excitotoxic changes that result in a sensitized
and hyperexcitable CNS

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24
Q

Several neurotransmitters are involved in the processing of

noxious input along the pain pathway

A

glutamate, gammaaminobutyric
acid (GABA), norepinephrine, serotonin, histamine,
and acetylcholine

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25
Q

The shift in firing

from a rhythmic burst to a single spike is determined by

A

noradrenergic, serotonergic, and cholinergic input to the

reticular and relay cells of the thalamus

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26
Q

excitatory amino acids, such as glutamate, are released in the region of
SCI and may lead to

A

neuronal hyperexcitability.

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27
Q

At the spinal cord level, substance P and cholecystokinin (CCK)
might play an additional role by

A

influencing the voltage gated sodium and calcium channels.

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28
Q

Potassium channels

play a critical role in

A

setting the resting membrane potential

and controlling the excitability of neurons

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29
Q

Central pain in SCI may result from

A

a combination of
deafferentation-induced plastic changes in supraspinal areas along with abnormal input from a pain generator in the spinal cord

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30
Q

In SCI, NMDA receptor activation might trigger

A

the intracellular cascade leading to the upregulation of neuronal activity/ excitability that results in spontaneous and evoked neuronal
hyperactivity/hyperexcitability and causes abnormal pain perception.

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31
Q

important mechanisms might be a loss of

endogenous inhibition, including

A

reduced GABA-ergic,

opioid, and monoaminergic inhibition.

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32
Q

Central glutamate

levels

A

Central glutamate
levels are known to increase in response to pain in healthy humans, and patients with fibromyalgia are known to have elevated central glutamate levels that
directly correlate with response to painful stimuli

33
Q

Patients with fibromyalgia are also known to have

decreased

A

dopamine and opioid receptor availability in

the forebrain.

34
Q

Patients with complete SCI are known to have

A

a postinjury reorganization
of the somatosensory cortex that correlates with
pain intensity

35
Q

Proposed mechanism of central
pain in spinal cord injury. Input from primary
afferents can be distorted by two mechanisms.

FIGURE 53-3

A

The spinothalamic tract projection neurons from
below the spinal injury may be lesioned and give rise to deafferentation hyperexcitability in higher-order neurons including the thalamus. Second-order neurons in the dorsal horn at the rostral end of the spinal lesion may become hyperexcitable as a
consequence of excitotoxic changes and
disinhibition from damaged GABA-ergic neurons at the level of injury. Abnormal input from these second-order neurons in the rostral end of the spinal cord lesion may propagate via the
propriospinal system to the deafferentated thalamic neurons resulting in pain referred to areas below injury level

36
Q

explain why pain occurs more often in patients with partial lesions than in those with complete
cord and thalamic injuries.

A

Lesions in the spinothalamocortical pathways can cause ectopic discharges in various neurons of the spinal cord and brain. Such ectopic neuronal discharges create
an illusion of noxious input because of the imbalance
between the lateral (inhibitory) and medial (excitatory) STT

37
Q

explain why pain occurs more often in patients with partial lesions than in those with complete
cord and thalamic injuries

A

It appears that severe CNS
lesions, with total destruction of ascending sensory systems, do not lead to a central pain syndrome and that
mild, moderate, or severe disruption of the anterolateral ascending system, with partial or complete preservation
of the dorsal column/medial lemniscus functions, is most
frequently associated with central pain syndrome

38
Q

central pain frequently develops weeks or months
after development of the lesion and is associated with sensory changes involving the spinothalamic pathways, especially changes in temperature perception

A

Sensory stimuli act on neural systems that have been modified by previous inputs, the “memory” of which
significantly influences pain behavior. The fact that a memory is not activated by the development of a lesion
might explain the long delay in the onset of central pain in some patients. The long-term potentiation that is
important for this memory might be mediated by NMDA receptors and their influence on calcium conductance.

39
Q

Microglia

A

the macrophages of the
brain and spinal cord that release inflammatory mediators in the event of injury or infection. The activation of microglia and subsequent inflammation is thought to precipitate a cycle of further inflammation and activation of astrocytes.

40
Q

neuropathic component of central pain quality of the pain may be

A

burning, aching, shooting,
pricking, and tingling. The discomfort is generally constant but may wax and wane and often has a deep and/or a superficial component.

41
Q

can provoke or exacerbate spontaneous pain

A

Nonpainful tactile, thermal, vibratory,

auditory, visual, olfactory, and visceral stimuli

42
Q

Patients with classic Dejerine-Roussy

syndrome have a

A

a rapidly regressing hemiparesis and a sensory deficit to touch, temperature, and pain. Allodynia, hyperalgesia, and spontaneous severe paroxysmal pain on
the hemiparetic side also often occur. These patients can exhibit hemiataxia, hemiastereognosia, and choreoathetoid movements.

43
Q

Organic signs on sensory examination of patients

with thalamic lesions include

A

the so-called thalamic

midline split for sensory loss and pain.

44
Q

Patients with a history of spontaneous or evoked dysesthesia,
hyperesthesia, or paresthesia should undergo

A

specific but simple bedside testing.

45
Q

Sensory testing in the region where the pain is localized usually shows a

A 
paradoxic hypoalgesia (decreased sensitivity to painful stimulus).
The region where the patient feels the pain often has decreased sensitivity to thermal stimuli, especially to cold.
46
Q

Testing for disturbed

temperature sensation can be accomplished with

A

a cold metal instrument, ice, or ethyl chloride spray.

47
Q

Touch can be tested with

A

cotton wool, while pinprick sensation should be assessed using the contralateral side as a control.

48
Q

Chronic poststroke pain patients have an intact

A

vibration sensation

49
Q

Chronic poststroke pain patients may exhibit mitempfindung (with sympathy)

A

a phenomenon in which stimulation in one area of the
body results in a simultaneous sense of the provoked sensation
in another part of the body

50
Q

Chronic poststroke pain patients may exhibit alloesthesia

A

in which a sensory stimulus on one

side of the body is perceived on the other side

51
Q

Testing for autonomic dysfunction may be important in

patients with SCI.

A

Lesions above the sixth thoracic level

(splanchnic outflow) are often associated with autonomic dysreflexia.

52
Q

Dysreflexia characterized by

A

sudden dramatic increases in blood pressure, high or low heart rate, and headache after sensory input such as a full bladder.

53
Q

Dysreflexia becomes especially important in SCI patients having surgery where

A

below the level of their lesion, including
minor operations of the urinary (i.e., cystoscopy)
or gastrointestinal (i.e., colonoscopy) systems where the viscera will be stimulated.

54
Q

the goal of therapy is to

A

improve function and reduce pain without

creating intolerable side effects

55
Q

options available for managing central

pain include

A

pharmacotherapy, behavioral therapy,
physical therapy, neuromodulation, other interventional
therapies, and ablative neurosurgery

56
Q

The mainstay of central pain

A

antidepressants that possibly act by modulating the thalamic burst firing activity via its actions on locus coeruleus
noradrenergic neurons and the serotoninergic cells in the dorsal raphe

57
Q

Amitriptyline is often effective in

A

central poststroke control and SCI pain. Amitriptyline’s benefit derives, in part, from its ability to prevent reuptake of noradrenaline
and serotonin.

58
Q

Tricyclic antidepressants (TCAs) dose

A

should be titrated to 50 to 100 mg/day

59
Q

a good regimen to control the common, steady, burning, dysesthetic component of this syndrome

A

a combination of a TCA (e.g., amitriptyline),

clonazepam, a benzodiazepine, and a (NSAID)

60
Q

Antiepileptic drugs (AEDs) are useful for

A

the treatment of neuropathic pain. Currently, the most commonly prescribed
AEDs are gabapentin and pregabalin. Both gabapentin and pregabalin appear to be effective in treating
central pain

61
Q

Opioids

A

may benefit some patients; however, it is not first-line therapy. Patients who respond to a trial of opioid infusion may be prescribed long-acting opioids, such as the slow-release formulations or the transdermal preparation.

62
Q

Central Pain Treatment Algorithm

Step 1. Identify problems.

A

Determine existing problems and potential adverse sequelae.
Identify biologic and psychological contributors to pain and their influence on the individual’s pain experience.
Determine the impact of pain on the patient’s function.
Determine how well the patient has adjusted to the disorder causing their central pain (SCI, stroke, MS).
Determine the risk of and/or presence of additional consequences of pain and the disorder underlying the central pain (i.e., pressure sores,
contractures, adverse drug effects).

63
Q

Central Pain Treatment Algorithm

Step 2. Determine reasonable objectives/goals for patient and treating physician

A

Pain relief/reduction.
Treatment of spasm—decrease frequency and/or severity.
Increase exercise tolerance and improve function.
Achieve independent living.
Return to work

64
Q

Central Pain Treatment Algorithm

Pharmacologic

A

First line :AEDs (gabapentin and pregabalin)
Second line: TCAs, SNRIs
Combinations with AED
Third line: Opioids, SSRI
Fourth line: Ketamine infusion, Lidocaine infusion

65
Q

Central Pain Treatment Algorithm

Interventional

A 
Specific to condition
Limited evidence
Mainly for refractory cases
Neuromodulation
Spinal cord stimulation (SCS)> DBS, MCS deep brain or motor cortex
stimulation
Intrathecal therapy
Baclofen, Morphine, Clonidine, Ziconotide
Acupuncture
Ablative therapies (DREZ,
cordotomy)
66
Q

Central Pain Treatment Algorithm

Physical and Occupational Therapy

A 
Structured therapy and home exercises
Postural re-education
Spasticity treatment
Bowel/bladder management
Braces and devices to assist in home and work
function
Home/work remodeling
Speech therapy
67
Q

Central Pain Treatment Algorithm

Psychosocial

A 
Psychiatric therapy
Pharmacologic
Counseling
CBT
Pain coping skills
Relaxation
Family support and
education
68
Q

Transcutaneous

electrical nerve stimulation (TENS) provides

A

long-term benefits to patients with central poststroke pain and those with incomplete SCI

69
Q

poor candidates for SCS

A

Patients with anesthesia dolorosa (pain in an anesthetic area) and patients with incomplete lesions are poor candidates. Patients who experience more than 50% pain relief during trial stimulation are potential candidates for an implant. In patients with treatment failure, deep brain stimulation (DBS) of the tactile relay nucleus of
the thalamus or the lemniscal radiations offers hope.

70
Q

For brain-origin central pain

A

The neuralgic component is the component sometimes responsive to ablative neurosurgery. SCS is of no benefit for brain-origin central pain, although patients might report relief during a trial. Paresthesia producing DBS and motor cortex stimulation are appropriate
for the steady component of the pain.

71
Q

The most commonly administered medications in Intrathecal pumps are

A

opioids
(morphine, hydromorphone, and fentanyl), clonidine, and
bupivacaine

72
Q

Baclofen

A

a GABA agonist, has antinociceptive effects,
and its intrathecal administration reduces allodynic responses
of neurogenic central pain

73
Q

Intrathecal
baclofen can be helpful in treating pain and spasticity
multiple types of central pain, including

A

post-stroke, SCI

and MS pain

74
Q

Ablative surgery includes

A

cordotomy, cordectomy, and dorsal root entry zone (DREZ) lesioning.

75
Q

The goal of cordotomy and cordectomy

A

interruption of STTs

76
Q

Cordectomy, the simplest destructive procedure, can benefit patients

A

with complete lesions.

It is not acceptable to most patients because it obviates their hope for eventual restoration of spinal cord function.

77
Q

Percutaneous/open cordotomy

A

achieves the same
results as cordectomy and is offered to patients with incomplete lesions, but carries the risk of aggravating bladder dysfunction and inducing ipsilateral limb paresis.

78
Q

dorsal root entry zone (DREZ)

A

equally effective for the neuralgic and the
evoked elements of spinal-origin central pain. most useful for the relief of end-zone pain (pain starting at the level of injury and extending distally). Pain extending diffusely, often sacrally distributed, and remotely distributed pain, described as phantom or diffuse burning pain, do not
respond well to DREZ.

79
Q

dorsal root entry zone (DREZ) side effects

A 
Although the procedure preserves the hope for future spinal cord function and avoids risk of limb paresis, it can interfere with residual bladder
function and requires a laminectomy and considerable skill.

Essentials of Pain Medicine (80 decks)

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