Chapter 55 Painful Peripheral Neuropathies

Question 1

Neuropathy

Answer 1

a general term used to describe disease of

nerve function and structures

Question 2

Neuropathies arise from

many different etiologies

Answer 2

diabetic peripheral neuropathy, postherpetic neuropathy, chemotherapy-induced
peripheral neuropathy, HIV neuropathy, and neuropathy of chronic renal failure) and can be painful or painless. They can affect the central nervous system (CNS), the
peripheral nervous system, or both simultaneously.

Question 3

Neuropathies result from

Answer 3

physical injury, inherited genetic disorders, infection, autoimmune disorders, and most often systemic disease.

Question 4

mononeuropathy

polyneuropathy

Answer 4

Neuropathies can affect solely one single nerve, termed a mononeuropathy, or several separate
nerves, which is termed a polyneuropathy.

Question 5

nociceptive pain

Answer 5

Pain is considered a normal, adaptive, or physiologic response when it results from nociceptors (pain receptors) having been activated by tissue disease or damage

Question 6

neuropathic pain arises

from

Answer 6

spontaneous activity within the nervous system, or

an aberrant response to “normal” sensory stimulation (e.g., fine touch evoking pain).

Question 7

Mononeuropathy multiplex

Answer 7

reflects changes

in multiple single, discreet nerves.

Question 8

Polyneuropathy

Answer 8

reflects changes in sensation in a diffuse, often bilateral, pattern
that is not restricted to discreet nerves

Question 9

Neuritis

Answer 9

a subtype
of neuropathy reserved for an inflammatory process
affecting the nerves.

Question 10

Neuropathic pain

Answer 10

defined as pain initiated or
caused by a primary lesion or dysfunction in the nervous system has been revised to now include “pain arising as direct consequence of a lesion or disease affecting the
somatosensory system

Question 11

Neuropathic pain can result from multiple causes and it can be categorized according to the site of initial injury

Answer 11

(central nervous system, peripheral nervous system, or mixed) and
the condition causing disease.

Question 12

Paresthesias

Answer 12

Abnormal nonpainful sensations that may be spontaneous or evoked (tingling or “pins and needles” sensations

Question 13

Dysesthesias

Answer 13

Abnormal pain that may be spontaneous or evoked

unpleasant tingling

Question 14

Hyperpathia

Answer 14

An exaggerated painful response evoked by a noxious or

non-noxious stimulus

Question 15

Allodynia

Answer 15

A painful response to a normally non-noxious stimulus

e.g., light touch is perceived as burning pain

Question 16

Hyperalgesia

Answer 16

An exaggerated painful response to a normally noxious stimulus

Question 17

Spontaneous pain

Answer 17

Painful sensation with no apparent external

stimulation

Question 18

mechanisms are thought to be responsible for the

development of neuropathic pain

Answer 18

These include changes
in ion channel number and density resulting in central and peripheral sensitization. Other changes include cortical
reorganization and disinhibition of neuronal circuitry, and cellular and molecular changes as a result of the immune
response following the initial nerve damage. The sympathetic nervous system is also thought to play a role in maintaining neuropathic pain

Question 19

Following trauma to a nerve, sodium channels

Answer 19

accumulate in a higher than normal concentration around the area of injury and along the entire axon, resulting in hypersensitivity
of the nerve and ectopic foci

Question 20

nerve injury can result in the release of

Answer 20

neuropeptides that might further cause peripheral sensitization through neurogenic inflammation. Nerve injury also can result in sprouting of sympathetic fibers into the dorsal root ganglia of the affected nerve.

Question 21

The CNS undergoes changes with peripheral nerve injury.

Answer 21

peripheral neuropathy results in reduced input to the CNS (postherpetic neuralgia, diabetic neuropathy).

Question 22

In diabetic neuropathy, there is little evidence

that peripheral sensitization

Answer 22

as might be seen with
increased sodium channels or with ephaptic transmission) occurs; rather the evidence points toward reduced neural input to the CNS.

Question 23

potential mechanisms exist for a central contribution to the pain from peripheral neuropathy

Answer 23

Loss of large fiber (A-b) sensory input could result in a reduction in non-nociceptive sensory input, thereby reducing the effectiveness of the “gate.” opioid and GABA receptors (both involved in inhibition of nociceptive transmission in the CNS) are down regulated and the amount of GABA in the dorsal horn is reduced. death of dorsal horn interneurons in lamina II (many of which
are involved in inhibition of nociceptive transmission in the dorsal horn) by overexposure to excitatory amino acids. Cholecystokinin, involved in opioid receptor inhibition, has also been found to be upregulated in the spinal cord following experimental nerve injury

Question 24

Common Conditions Causing Neuropathic Pain Syndromes

Physical Injury/Trauma

Answer 24

Complex regional pain syndrome (CRPS), Type I & II Radiculopathy
Stroke (cerebrovascular accident)
Spinal cord injury

Question 25

Common Conditions Causing Neuropathic Pain Syndromes

Inherited/Genetic

Answer 25

Charcot-Marie-Tooth

Fabry’s disease

Question 26

Common Conditions Causing Neuropathic Pain Syndromes

Infections/Autoimmune

Answer 26

Human immunodeficiency virus
Herpes simplex virus
Acute inflammatory demyelinating polyneuropathy

Question 27

Common Conditions Causing Neuropathic Pain Syndromes

Systemic Disease

Answer 27

Diabetes mellitus
Kidney disorders/renal failure
Vitamin deficiencies (beriberi, alcoholic pellagra,
vitamin B12 deficiency)
Vascular disorders
Chemical toxins (isoniazid, chemotherapy agents)
(platinum, vinca alkaloids, taxanes), arsenic, thallium
Hypothyroidism
Amyloidosis
Multiple myeloma

Question 28

A central mechanism that may explain the allodynia seen

in some peripheral neuropathies involves

Answer 28

A-b fiber sprouting and A-b fiber “phenotypic switching.” A-b fibers
normally synapse in all lamina of the spinal cord except lamina II, where C-fiber input predominates. However, following peripheral C-fiber nerve injury, A-b fiber “sprouting” into lamina II occurs, therefore allowing mechanical non-nociceptive input via the peripheral A-b fibers to trigger second-order pain pathways.

Question 29

A-b fibers in the dorsal horn do not normally express substance P (as seen in C-fibers), but following peripheral nerve injury

Answer 29

they can (phenotypic switching). When this happens, they thereby
allow non-nociceptive input to trigger CNS nociceptive transmission.

Question 30

patient presents with signs and symptoms suggestive of neuropathic pain

Answer 30

allodynia, hypoand/

or hyper-algesia, and paresthesias

Question 31

Focal lesions of peripheral nerves (mononeuropathies) result frequently from

Answer 31

processes that produce localized damage
and include nerve entrapment; mechanical injuries; thermal, electrical, or radiation injuries; vascular lesions; and neoplastic or infectious processes

Question 32

polyneuropathies often result in

Answer 32

a bilateral and symmetric disturbance in function as a result of agents that act diffusely on the peripheral nervous system: toxic substances, deficiency states, metabolic disorders, and immune reactions

Question 33

the most important pieces of historical information

Answer 33

The location of the pain and other symptoms

Question 34

In the patient suspected of having polyneuropathy, the clinician should focus on

Answer 34

sensory evaluation. Strength and deep tendon reflexes are preserved in many patients with
polyneuropathy. In addition to testing vibration, proprioception,
and light touch, the sensory examination should include several special stimuli including light-touch rubbing, ice, single pinprick, and multiple pinpricks.

Question 35

sensory evaluation

Answer 35

Lightly stroking the affected area with a finger will assess for allodynia (pain provoked by non-noxious stimuli). Ice
application will test for both temperature sensation and abnormal sensations such as pain and lingering after sensations. Single pinprick testing may elicit a sensory
deficit or hyperpathia. Repeated pinprick testing may elicit summation (pain growing more intense with subsequent stimuli) or lingering after sensations, both common findings in polyneuropathy

Question 36

Patients suspected of having polyneuropathy can be considered
for what ELECTRODIAGNOSTIC TESTING

Answer 36

electromyography (EMG) and nerve conduction velocity (NCV) studies, which may offer insights into whether the process is a demyelinating (reductions in nerve conduction velocities) or axonal (reductions in the
amplitude of evoked responses) neuropathy.

Question 37

Quantitative sensory testing (QST) may be the most useful in

Answer 37

the assessment and longitudinal monitoring of painful peripheral neuropathies. While large fibers are assessed through the use of sensory thresholds to vibration, small fibers can be assessed by
threshold for detection of heat, painful heat, cold, and painful cold stimuli.

Question 38

cause of diabetic neuropathy

Answer 38

has not been determined
with certainty. Current hypotheses focus on the
possibilities of metabolic and ischemic nerve injury.
Pathologic examination of nerves taken from diabetic
patients has shown evidence of microvascular disease supporting
the ischemic nerve theory

Question 39

Metabolic abnormalities of diabetic neuropathy

include

Answer 39

(1) accumulation of sorbitol in diabetic nerve as excess glucose is converted to sorbitol by the enzyme
aldose-reductase,
(2) autooxidation of glucose resulting in
reactive oxygen molecules, and
(3) inappropriate activation
of protein kinase C.

Question 40

Diabetic neuropathy can be divided by the pattern of distribution of involved nerves

Answer 40

Mononeuropathy

• Cranial mononeuropathy
• Compression mononeuropathy

Mononeuropathy multiplex - Proximal motor neuropathy
- Truncal neuropathy

Polyneuropathy

• Distal symmetric polyneuropathy
• Painful diabetic neuropathy
• Autonomic polyneuropathy

Question 41

distal symmetric

polyneuropathy

Answer 41

most common form of diabetic neuropathy. It is predominantly a sensory disturbance. Patients often present with gradual onset of paresthesias
and pain in the legs and feet. Symptoms begin in the toes and gradually ascend over months to years to involve more
proximal levels. The fingertips and hands become involved later, usually when symptoms in the lower extremities have ascended to the knee level. Allodynia and burning pain are common and are often worse
at night.

Question 42

in Diabetic neuropathy
distal symmetric
polyneuropathy
Examination shows

Answer 42

graded distal sensory loss

predominantly affecting vibration and position sensation. Reflexes may be diminished or absent.

Question 43

in Diabetic neuropathy
distal symmetric
Electrophysiologic testing shows

Answer 43

a decrease in the amplitude of evoked
responses to a greater degree than reduction in nerve conduction velocities as the neuropathy progresses. This reflects primarily axonal damage rather than demyelination

Question 44

Severe sensory loss may allow repeated trauma to go unnoticed, resulting in

Answer 44

development of foot ulcers and diabetic

neuroarthropathy (Charcot’s joints)

Question 45

syndrome of acute painful diabetic neuropathy

Answer 45

characterized by the rapid onset of severe pain in the distal lower extremities characterized by constant burning in the feet, dysesthesia, allodynia, and lancinating leg pains.

Question 46

In syndrome of acute painful diabetic neuropathy Examination shows

Answer 46

little or no sensory loss with preserved reflexes. Electrophysiologic testing shows decreased amplitude or absent sensory potentials, but may also be normal. This type of neuropathy often remits within a year after blood sugars are controlled

Question 47

Autonomic neuropathy

Answer 47

Symptomatic autonomic neuropathy most often occurs as a component of distal symmetric polyneuropathy. Autonomic nervous system abnormalities include postural hypotension, impaired heart rate control (resting
tachycardia and fixed heart rate), esophageal dysmotility, gastroparesis, and erectile dysfunction.

Question 48

Lower extremity proximal motor neuropathy

Answer 48

an uncommon painful disorder associated with diabetes. It is characterized by acute or subacute onset of moderate to marked weakness and wasting of the pelvifemoral muscles
accompanied by back, hip, and thigh pain with preserved sensation in the regions of pain. The condition may be
painless or accompanied by pain described as a constant, severe, deep ache.

Question 49

Diabetic lumbosacral radiculoplexus neuropathy (DLRPN)

Answer 49

referred to as diabetic amyotrophy, proximal
diabetic neuropathy, diabetic polyradiculopathy, Bruns- Garland syndrome, or diabetic lumbar plexopathy. It usually affects individuals with diabetes mellitus Type II
over the age of 50 years, and presents as an asymmetric weakness associated with pain in the legs that appears subacutely and progresses over weeks to months. Although motor function recovery is slow and often incomplete, the
pain usually resolves.

Question 50

Diabetic truncal neuropathy involves

Answer 50

acute or gradual
onset of unilateral pain in the chest or abdomen and may mimic myocardial infarction, intra-abdominal pathology, or spinal disorders. Examination shows marked allodynia
and hyperpathia in the distribution of pain. EMG typically demonstrates denervation in the abdominal or intercostal musculature

Question 51

Cranial mononeuropathies

Answer 51

involving the oculomotor,
abducens, trochlear, and facial nerves may occur in diabetic patients. The most common of these is oculomotor neuropathy that is manifest as ophthalmoplegia and ptosis. The eye is deviated laterally and has impaired movement
vertically and medially

Question 52

Entrapment neuropathies are believed to occur more frequently in patients with diabetes mellitus

Answer 52

Carpal tunnel syndrome is believed to occur more than twice as frequently as in the nondiabetic population.

Question 53

Amyloidosis

Answer 53

a disease caused by extracellular deposition of amyloid, a fibrous protein. Amyloidosis can be primary, familial, or
associated with other conditions such as multiple myeloma,
chronic infectious or inflammatory states, aging, and longterm hemodialysis.

Question 54

characterize painful peripheral neuropathy in amyloidosis.

Answer 54

Deep aching and occasional shooting pains, distal sensory

loss, and autonomic and motor involvement

Question 55

Treatment of

neuropathy associated with amyloidosis is aimed at

Answer 55

the underlying condition when such is identifiable

Question 56

Multiple myeloma

Answer 56

due to malignant plasma cell growth. Painful neuropathy can appear in myeloma with or without
amyloid deposition. The neuropathy is extremely variable in severity and rate of progression, ranging from a mild, predominantly sensory neuropathy to a complete tetraplegia. Pain in myeloma often declines with successful treatment
using chemotherapy, radiation therapy (especially for isolated
plasmocytomas), or plasmapheresis.

Question 57

untreated hypothyroidism may develop painful sensorimotor neuropathy

Answer 57

present with longstanding pain in either the hands
or the feet accompanied by weakness in the distal limb musculature.
The neuropathy often resolves with successful
replacement of thyroid hormone.

Question 58

Thiamine deficiency seen in

Answer 58

alcoholics, chronic dialysis

patients, and people on restrictive diets

Question 59

Thiamine deficiency

lead to beriberi

Answer 59

consists of heart failure, vasodilatation, and peripheral neuropathy. Hand foot, and calf pains with allodynia, decreased sensation, and motor involvement characterize the neuropathy.

Question 60

Alcoholic neuropathy is characterized by

Answer 60

motor and sensory deficits, often accompanied by pain.
The pain consists of aching in the legs or feet with intermittent
lancinating pains. The upper limbs are rarely
involved. Burning of the soles and allodynia may also occur.

Question 61

Alcoholic neuropathy occurs only after

Answer 61

chronic and severe alcohol abuse and is invariably accompanied
by severe nutritional deficiency. Treatment
consists of abstinence and thiamine supplementation.

Question 62

Pellagra

Answer 62

caused by niacin deficiency and is rarely
seen in developed countries. Signs and symptoms include dermatitis, gastrointestinal complaints, neurasthenia, and spinal cord dysfunction. Pellagra is associated with a mixed, painful polyneuropathy similar to that seen with
beriberi.

Question 63

In Pellagra a predominant feature of the sensorimotor neuropathy
is

Answer 63

spontaneous pain in the feet and lower legs,
with tenderness of the calf muscles and cutaneous hyperesthesia
of the feet

Question 64

Treatment of pellagra

Answer 64

with niacin often results in resolution of all symptoms except the peripheral neuropathy.

Question 65

Isoniazid

Answer 65

is a frequently used antituberculous drug.
Chronic administration in individuals with slow metabolism of the drug (slow acetylators) is associated with the
development of painful neuropathy.

Question 66

Isoniazid neuropathy Initial symptoms

Answer 66

distal numbness and tingling paresthesias are later accompanied by pain, which may be felt as a deep ache or burning.
The calf muscles are painful and tender, and walking often aggravates symptoms. Symptoms may be particularly
troublesome at night.

Question 67

Isoniazid neuropathy treatment

Answer 67

Prophylactic coadministration of

pyridoxine (vitamin B6) prevents development of neuropathy; however, it is not therapeutic once the neuropathy develops

Question 68

most common neurologic complication of cancer treatment is

Answer 68

chemotherapy-induced peripheral neuropathy
(CIPN), a common adverse effect of treatment with
platinum-derived, taxane, and vinca alkaloid chemotherapeutic
compounds. These chemotherapeutic agents exert their cytotoxic effect by binding to DNA and producing interstrand and intrastrand cross-linkage,
thus impairing DNA synthesis and transcription.

Question 69

The development

of CIPN is the most common reason a

Answer 69

platinum- based chemotherapy regimen is changed to another agent, administered at a lower dose, or given in fewer or
less frequent cycles of therapy.

Question 70

chemotherapy-induced peripheral neuropathy

(CIPN) earliest manifestations of neuropathy

Answer 70

decreased vibration
sense in the toes and loss of ankle jerk reflexes. At larger doses, paresthesias may appear and progress to severe dysesthesias. The neuropathy is reversible, but recovery may take more than a year after discontinuation of the agent.

Question 71

Charcot-Marie-Tooth (CMT) disorders are subdivided into

Answer 71

demyelinating and

axonal forms, depending on EMG conduction studies

Question 72

Most common symptoms in Charcot-Marie-Tooth

Answer 72

include lower extremity
motor symptoms (foot deformity, difficulty ambulating), hyporeflexia, and sensory loss.

Question 73

infectious neuropathies are very common

Answer 73

Mycobacterium leprae, although quite uncommon
in North America and Europe, is among the leading cause. It usually affects the skin and nerves, but there also exists a pure neural leprosy in about 4% to 10%40 of all leprosy
cases. Symptoms are found primarily in the form of mononeuritis
or mononeuritis multiplex.

Question 74

The sensory neuropathies associated
with HIV (HIV-SN) include

Answer 74

distal sensory polyneuropathy
(DSP) due to the viral infection and antiretroviral toxic neuropathy (ATN) due to the medical treatment of
the viral illness.

Question 75

The onset of DSP can occur in either

Answer 75

the subacute or chronic phases, or following the

development of an AIDS-defining illness

Question 76

The clinical

manifestation of antiretroviral toxic neuropathy (ATN)

Answer 76

can appear within the first week to 6 months of the initiation of antiretroviral therapy and may subside after its cessation. The painful peripheral
neuropathy results from both direct neuronal inflammatory injury to the nerve itself (DSP) and the treatment using HAARTs leading to mitochondrial dysfunction

Question 77

The clinical features of HIV-SN

Answer 77

are dominated by painful
dysesthesia, allodynia, and hyperalgesia. Onset is
often gradual and most commonly begins with bilateral lower extremity involvement. The neuropathy progresses
in a length-dependent fashion with a worsening
gradient of disease from distal structures to those more proximal.

Question 78

HIV-SN symptoms

Answer 78

The dysesthesias commonly first involve
the soles of the feet and progress proximally; when the symptoms encompass the dermatomes of the knee the patient will often report finger involvement. The first symptoms noted are often numbness or burning sensation following a diurnal cycle with the pain worse
at night. Shortly thereafter, patients will report allodynia and hyperalgesia of the involved structures.

Question 79

In HIV- SN, as a result, wearing shoes and walking become

Answer 79

painful and the patient’s

gait becomes antalgic.

Question 80

In HIV- SN motor involvement

Answer 80

There is minimal subjective or objective motor involvement and it is generally limited to the intrinsic muscles of the foot. Physical examination
shows a diminution or loss of ankle reflexes in
addition to the sensory findings.

Question 81

Reactivation of a latent infection of varicella zoster virus (human herpes virus-3) in the trigeminal ganglia or the dorsal root ganglia can result in

Answer 81

facial or peripheral pain in
the dermatomal distribution of the affected nerves. The resulting condition herpes zoster or “shingles” can be
excruciatingly painful and can result in a chronic pain condition called postherpetic neuralgia (PHN).

Question 82

risk factors for the

development of PHN.

Answer 82

Advanced age, greater severity of the rash, and presence and severity of a painful prodrome preceding the rash

Question 83

clinical presentation of PHN

Answer 83

common in the thoracolumbar region, following a single or multiple dermatomes with a prodromal period followed by the eruption of a maculopapular vesicular rash. The pain is most often described as burning, stabbing, and/or
throbbing and is commonly associated with cutaneous allodynia of the region.

Question 84

Prevention of PHN

in patients who had a herpes zoster reactivation was successful in those

Answer 84

who received acyclovir

Question 85

Acute inflammatory demyelinating polyradiculoneuropathy
(AIDP) caused by Guillain-Barré syndrome (GBS) is
characterized by

Answer 85

areflexic and ascending motor paralysis with sensory paresthesias. It is often preceded by an infection, generally an upper respiratory tract infection or gastroenteritis.
Most frequently, if an agent is identified, EBV,
CMV, Mycoplasma pneumoniae, and Campylobacter jejuni are found

Question 86

Guillain-Barré syndrome (GBS) symptoms

Answer 86

The onset of symptoms develops over several days, or more frequently, weeks. Pain is a common early symptom; weakness, usually in the legs, may progress to respiratory failure requiring mechanical ventilation. Sensory symptoms include paresthesias often
in the presence of decreased sensation in a glove-stocking
distribution. Autonomic dysfunction is also commonly evidenced by tachycardia and orthostatic hypotension.

Question 87

Guillain-Barré syndrome (GBS) pain

Answer 87

The pain is principally
an ache, strain, or deep burning sensation in the
thigh or buttocks and can be quite severe. While pain in AIDP may be severe, it is usually transient. Pain is usually worse at night.

Question 88

Guillain-Barré syndrome (GBS) diagnosis and treatment

Answer 88

Nerve conduction studies and lumbar puncture aid the diagnosis. General therapy for AIDP (Acute inflammatory demyelinating polyradiculoneuropathy) is supportive along with plasmapheresis and IVIG. Glucocorticoids and other immunosuppressants have not been clearly shown to be helpful.

Question 89

IDIOPATHIC SMALL-FIBER NEUROPATHY

Answer 89

This condition usually presents with painful feet in patients over age 60. It can be defined as the presence of paresthesias (usually painful) with the
absence of significant large-fiber dysfunction (atrophy, loss of vibratory sense, or loss of reflexes). Diagnosis is often confirmed through tests of autonomic function, quantitative sensory testing, or skin biopsy

Question 90

antidepressants treatment of peripheral neuropathic pain

Answer 90

TCAs (amitriptyline, nortriptyline, desipramine,
imipramine) are the best studied and most efficacious, followed
by SNRIs (duloxetine, venlafaxine) and then SSRIs (citalopram, paroxetine).

Question 91

The side effect profile of the TCAs, primarily anticholinergic effects, limits their widespread
application, especially in patients with

Answer 91

autonomic neuropathy, glaucoma, cardiac arrhythmias, and urinary
hesitation.

Question 92

Anticonvulsants are used very frequently and successfully

Answer 92

gabapentin and pregabalin, structural
analogs to (GABA), are considered first-line agents and are used in the treatment of a
multitude of neuropathic pain syndromes including radiculopathy,
CRPS Type I and II, diabetic neuropathy, postherpetic
neuralgia, and mixed neuropathic pain conditions.

Question 93

Anticonvulsants side effects

Answer 93

sedation, dizziness, GI complaints, and lower extremity edema

Question 94

Other antiepileptics shown to bring symptomatic relief

such as in

Answer 94

HIV neuropathy (lamotrigine), painful diabetic neuropathy (lacosamide), and postherpetic neuralgia (valproic acid)

Question 95

Other oral medications that have shown beneficial effects but are generally employed in refractory cases or as second-line agents, include

Answer 95

opioids such as morphine or tramadol

Question 96

treatment options that

have shown improvement in neuropathic pain include topical agents such as

Answer 96

lidocaine patches (postherpetic neuralgia,
post-traumatic neuralgia) or in experimental studies,
high-concentration (8%) capsaicin creams (HIV neuropathy, postherpetic neuralgia

Question 97

treatment of patient without significant relief of their neuropathic
pain.

Answer 97

In these circumstances, various alternative options
exist, including sympathetic nerve blocks, neurolytic sympathetic blocks, spinal cord stimulation (SCS), deep
brain stimulation (DBS), transcutaneous electrical nerve stimulation (TENS), and repetitive transcranial magnetic stimulation (rTMS).

Question 98

The use of spinal cord stimulation is well established in

Answer 98

neuropathic pain
conditions including postlaminectomy syndrome, CRPS
Type I, and diabetic peripheral neuropathy

Question 99

Gabapentin

Answer 99

Start Dose:100–300 mg/day
Maximum Dose: 3600 mg/day
Documented Effect: PHN, PDN, HIV, mixed
neuropathic pain
Side Effects: Sedation, dizziness, edema

Question 100

Pregabalin

Answer 100

Start Dose: 50–150 mg/day
Maximum Dose: 300 mg/day, (600 mg/day
fibromyalgia)
Documented Effect: PHN, PDN, mixed neuropathic
pain, fibromyalgia, central pain
Side Effects: Sedation, dizziness, edema

Question 101

Tricyclic
antidepressants (Nortriptyline, Desipramine
Trazadone)

Answer 101

Start Dose: 10–25 mg/day
Maximum Dose: 50–150 mg/day
Documented Effect: PHN, PDN, central pain,
mixed neuropathic pain
Side Effects: Cardiac, anticholinergic,
sedation

Question 102

Specific serotonergic
and noradrenergic
reuptake inhibitors (Venlafaxine, Duloxetine)

Answer 102

Start Dose: 37.5 mg/day
20 mg/day
Maximum Dose: 25–375 mg/day, 60 mg/day
Documented Effect: PHN, PDN, fibromyalgia
Side Effects: Sedation

Question 103

Carbamazepine

Answer 103

Start Dose: 300 mg/day
Maximum Dose: 1200–1800 mg (1/3 higher
dose for oxcarbazepine)
Documented Effect: Trigeminal neuralgia
Side Effects: Sedation, dizziness, ataxia,
blood dyscrasias

Question 104

Tramadol

Answer 104

Start Dose: 50–150 mg/day
Maximum Dose: 400 mg/day
Documented Effect: PHN, PDN
Side Effects: Sedation, dizziness, seizure

Question 105

Lamotrigine

Answer 105

Start Dose: 25 mg/day
Maximum Dose: 400–600 mg/day
Documented Effect: Trigeminal neuralgia,
poststroke central pain, HIV
Side Effects: Sedation, tremor, rash

Question 106

Opioids

Answer 106

Start Dose: 5–10 mg/day; titrate and substitute with
long-acting opioids
Maximum Dose: Variable, 100–200 mg (OME)/day
Documented Effect: PHN, PDN, post–amputation
pain
Side Effects: Sedation, dizziness, tolerance, drug abuse, misuse

Question 107

Lidocaine patch

Answer 107

Start Dose: 5%
Maximum Dose: 3 patches/day
Documented Effect: PHN, traumatic nerve injury
Side Effects: Allergic reaction

Question 108

Capsaicin cream

Answer 108

Start Dose: 0.025% and 0.075%
Maximum Dose: N/A
Documented Effect: PHN, PDN, HIV