Pain Surgery Flashcards
A 55-year-old male with known ischemic heartdisease develops a crushing chest pain which radiates into his neck and left arm. The phenomenon of referred pain is best explained by which one of the following mechanisms?
a. Pain transmission along a given afferent nerve is transferred to another afferent pathway due to ephaptic transmission
b. Lateral inhibition of secondary afferent
fibers by a single primary afferent
c. Convergence of primary afferent fibers from a specific part of the body onto second-order neurons that normally receive primary afferents from a different body part
d. Disruption of dorsal root ganglia
e. The blockade of substance P and glutamate in the dorsal horn
A 55-year-old male with known ischemic heartdisease develops a crushing chest pain which radiates into his neck and left arm. The phenomenon of referred pain is best explained by which one of the following mechanisms?
a. Pain transmission along a given afferent nerve is transferred to another afferent pathway due to ephaptic transmission
b. Lateral inhibition of secondary afferent
fibers by a single primary afferent
c. Convergence of primary afferent fibers from a specific part of the body onto second-order neurons that normally receive primary afferents from a different body part
d. Disruption of dorsal root ganglia
e. The blockade of substance P and glutamate in the dorsal horn
Referred pain is a phenomenon in which pain
impulses, usually arising from primary visceral
afferent fibers from one part of the body, terminate on dorsal horn projection neurons that normally receive cutaneous afferents from a different part of the body (such as the arm). It is the convergence of these distinctly different inputs onto the same projection neurons that provides the basis for this phenomenon. However, other theories including central sensitization, thalamic convergence, and hyperexcitability have also been proposed. Pain signaling in the spinal cord dorsal horn is via glutamate (C fibers and A-delta fibers) and substance P (C fibers). The opioid peptides (enkephalin and dynorphin) are released by inhibitory interneurons
in the dorsal horns, medulla, and PAG and inhibit
transmission of pain impulses.
The descending pathway for central control of nociception is best described as involving which one of the following structures?
a. Anterior cingulate cortex fibers that synapse directly on dorsal horn neurons
b. Periaqueductal gray fibers that synapse nucleus raphe magnus neurons, which in turn synapse on dorsal horn neurons
c. Thalamic neurons that synapse upon red nucleus neurons, which in turn synapse upon dorsal horn cells
d. Hypothalamic fibers that synapse upon neurons of the nucleus solitarius that then synapse upon neurons of the dorsal horn
e. Thalamic fibers that synapse upon inhibitory interneurons in the dorsal horn
The descending pathway for central control of nociception is best described as involving which one of the following structures?
a. Anterior cingulate cortex fibers that synapse directly on dorsal horn neurons
b. Periaqueductal gray fibers that synapse nucleus raphe magnus neurons, which in turn synapse on dorsal horn neurons
c. Thalamic neurons that synapse upon red nucleus neurons, which in turn synapse upon dorsal horn cells
d. Hypothalamic fibers that synapse upon neurons of the nucleus solitarius that then synapse upon neurons of the dorsal horn
e. Thalamic fibers that synapse upon inhibitory interneurons in the dorsal horn
Periaqueductal gray stimulation activates
enkephalin-releasing neurons that project to the
nucleus raphe magnus, 5-HT release activates projections to inhibitory interneurons in Laminae II
(substantia gelatinosa). This results in release of
either enkephalin or dynorphin (endogenous opioid neurotransmitters), which bind to mu opioid
receptors on the axons of incoming nociceptive
C and A-delta fibers, inhibiting the release of substance P/glutamate from then and activation of
ascending pain pathways.
Which one of the following is not a potential site for ulnar nerve entrapment?
a. Arcade of Struthers
b. Heads of the flexor carpi ulnaris
c. Intermuscular septum
d. Osbourne’s fascia
e. Sublimis arch
a. Arcade of Struthers
b. Heads of the flexor carpi ulnaris
c. Intermuscular septum
d. Osbourne’s fascia
e. Sublimis arch
Ulnar nerve at the elbow lies in the postcondylar
groove, then under the aponeurosis (Osbourne’s
fascia) then under the FCU itself. Initial benefit
following ulnar nerve transposition at the cubital
tunnel may be complicated by kinking at the
arcade of Struthers more proximally, which may
necessitate release at this level. Technique for
ulnar nerve decompression transposition is:
incision, identify, and protect/mobilize medial
antebrachial cutaneous nerve, identify ulnar nerve
proximal to Osbourne’s fascia, decompress distally
through leading edge of FCU (simple decompression); for transposition, extend decompression proximally by cutting intermuscular septum and
arcade of Struthers if present; assess position in full range of motion to ensure no subluxation. Recurrence of symptoms after decompression alone may suggest kinking/tethering at the intermuscular septum (or arcade of Struthers if not divided initially) requiring release
A 43-year-old woman is referred with a 2- year history of sharp, shooting pains radiating into the right side of her jaw. Each attack lasts for a few seconds but they seem to merge together so it can seem like several minutes of pain. After this she may be pain free for several hours. It is often triggered by eating/drinking, brushing her teeth, touching her face, and talking. She denies any tearing, eye/eyelid changes or nasal congestion/rhinorrhea. There is no other past medical or family history. Neurological examination is normal and MRI head was unremarkable. Which one of the following is most appropriate first line therapy?
a. Baclofen
b. Carbamazepine
c. Gabapentin
d. Lamotrigine
e. Pimozide
a. Baclofen
b. Carbamazepine
c. Gabapentin
d. Lamotrigine
e. Pimozide
The history is suggestive of trigeminal neuralgia
(tic douloureux). First line treatment is carbamazepine. Common side effects of CBZ: dizziness, vertigo, ataxia, diplopia, blood disorders, drowsiness, skin reactions. If CBZ not tolerated due to side effects could try oxcarbazepine (higher risk
of hyponatremia), or if allergic start gabapentin.
Other useful drugs include baclofen, phenytoin,
and lamotrigine
A 22-year-old female presents to her GP with a 3-month history of sharp, stabbing jaw pain and blurred vision on the right side. She is about to sit her examinations and is finding it difficult to study because of her symptoms.
Which one of the following would you wish to exclude as a priority?
a. Tolosa-Hunt syndrome
b. Multiple sclerosis
c. Intracranial tumor
d. Classical trigeminal neuralgia
e. Psychogenic pain syndrome
a. Tolosa-Hunt syndrome
b. Multiple sclerosis
c. Intracranial tumor
d. Classical trigeminal neuralgia
e. Psychogenic pain syndrome
While the majority of cases of trigeminal neuralgia are due to vascular compression or idiopathic
(Classical), in a small proportion of cases it may be
the presenting feature of significant underlying
condition such as multiple sclerosis (brainstem
plaque causing ephaptic transmission), basilar
artery aneurysms, acoustic schwannomas, and
posterior fossa meningiomas, all of which may
cause injury to the fifth cranial nerve by compression. Red flag symptoms which should be
excluded include: sensory changes, deafness, difficulty achieving pain control, poor response to
carbamazepine, history of skin or oral malignancy
that could lead to perineural spread, symptoms in
ophthalmic distribution (more likely herpes zoster), under age of 40, symptoms suggestive of
optic neuritis, family history of MS. The
Tolosa-Hunt syndrome is a presumably inflammatory disorder that produces ophthalmoplegia
associated with headache and loss of sensation
over the forehead. Pupillary function is usually
spared, and the site of pathology is believed to
be in the superior orbital fissure or the cavernous
sinus. It is usually not associated with trigeminal
neuralgia.
Which one of the following statements regarding surgical treatments for trigeminal neuralgia is LEAST accurate?
a. Microvascular decompression is a favored option for trigeminal neuralgia in MS
b. Radiofrequency thermocoagulation of gasserian ganglion is most likely to cause anesthesia dolorosa
c. Percutaneous destructive techniques directed at the gasserian ganglion may cause a trigemino-cardiac reflex
d. Balloon compression is usually performed under general anesthetic
e. Stereotactic radiosurgery of the trigeminal root only produces pain relief in a delayed fashion
a. Microvascular decompression is a favored option for trigeminal neuralgia in MS
b. Radiofrequency thermocoagulation of gasserian ganglion is most likely to cause anesthesia dolorosa
c. Percutaneous destructive techniques directed at the gasserian ganglion may cause a trigemino-cardiac reflex
d. Balloon compression is usually performed under general anesthetic
e. Stereotactic radiosurgery of the trigeminal root only produces pain relief in a delayed fashion
Microvascular decompression is the gold standard
in good surgical candidates (i.e. classical trigeminal neuralgia, evidence of vascular compression
on MRI, short duration of disease, no previous surgery); pain relief is usually immediate and 60-
70% remaining pain free at 10-20 years. Indications include patients whose pain is no longer
controlled by drugs and whose quality of life has
markedly deteriorated, young patients, side
effects from antiepileptic drugs. The procedure
requires general anesthesia, and its adverse effects
include aseptic meningitis, ipsilateral hearing loss
(in less than 5%), CSF leak, low risk of sensory
loss, and death (0.4%). Stereotactic radiosurgery
targeting the trigeminal root does not require
general anesthesia, but its pain-relieving effects
are not immediate. Adverse effects include facial
numbness, paresthesias, and sensory complications. Percutaneous destructive neurosurgical techniques (radiofrequency thermocoagulation,
glycerol rhizolysis, or balloon compression) can
achieve immediate pain relief and can therefore
be considered for emergency management, but
50% of patients have recurrence at 5 years. Sedation or even GA is required, and it carries a risk of trigeminal-vagal reflex effects on the heart during lesioning and a very small risk of carotid injury or intracranial infection. Balloon compression
carries a risk of temporary trigeminal motor
dysfunction. Adverse effects include a facial
numbness, corneal numbness (risk of keratitis),
dysesthesias, and anesthesia dolorosa.
Gate control theory of pain is best described by which one of the following statements?
a. The thalamus gates pain perception in the cortex
b. The substantia gelatinosa gates nociceptive signals before they reach the thalamus
c. The dorsal root ganglion gates nociceptive signals before they reach the substantia gelatinosa
d. The nociceptive nerve endings gate pain signals by altering the ratio of C and A-delta fibers activated
e. The dorsal columns gate nociceptive signals by ephaptic transmission
a. The thalamus gates pain perception in the cortex
b. The substantia gelatinosa gates nociceptive signals before they reach the thalamus
c. The dorsal root ganglion gates nociceptive signals before they reach the substantia gelatinosa
d. The nociceptive nerve endings gate pain signals by altering the ratio of C and A-delta fibers activated
e. The dorsal columns gate nociceptive signals by ephaptic transmission
The 1965 gate control theory of pain by Melzack
and Wall proposed that there were three spinal
cord systems involved in pain transmission: the
substantia gelatinosa, dorsal column fibers, and
central transmission cells in the DH. The substantia gelatinosa functions as a gate that modulates signals before they reach the brain. Large
diameter fibers have inhibitory effects to “shut
the gate” whereas small diameter fibers carrying
noxious stimuli open the gate to pain transmission. In a simplistic view of this model, rubbing
of the injured area promotes proprioceptive (i.e.
large diameter) fiber input and reduces pain
perception. In the late 1990s, Melzack proposed
the neuromatrix theory, adding higher cortical
functions as key elements of pain transmission
and interpretation. Today, the experience of pain
is described as distributed in three dimensions:
cognitive, affective, and sensory. Frontal and
limbic areas are believed to subserve the
cognitive-evaluative component of pain. Limbic
cortex, cingulum, hypothalamus, thalamus, and various midbrain regions are thought to contribute to the motivational-affective component of
pain. Primary somatosensory cortex, thalamus,
spinothalamic tract, and local nerve endings are
involved in the sensory component of pain.
Which one of the following is the commonest vessel thought to cause compression of the trigeminal root in cases of trigeminal neuralgia?
a. Anterior inferior cerebellar artery
b. Basilar artery
c. Dandy’s vein
d. Posterior inferior cerebellar artery
e. Superior cerebellar artery
f. Vertebral artery
a. Anterior inferior cerebellar artery
b. Basilar artery
c. Dandy’s vein
d. Posterior inferior cerebellar artery
e. Superior cerebellar artery
f. Vertebral artery
Neurovascular compression is found in 88% of
cases on imaging, but an average of 7% of explorations reveal no pathology intraoperatively. The superior cerebellar artery is the most common
(70-80%), and is usually compressing the rostral
and anterior portion of the nerve in patients with
V2 or V3 symptoms. The anterior inferior cerebellar artery is the compressive vessel in 10% of
cases and occurs in the caudal and posterior portion of the nerve closest to nerve VI, while veins
impact the nerve in 5-13% of cases. Microvascular decompression involves separating offending
vessels from the nerve and inserting a synthetic
sponge or Teflon felt between them to maintain
the separation. The trigeminal nerve must be
carefully and circumferentially inspected along
its entire intracranial course from the root entry
zone to its entrance laterally into Meckel’s cave.
This procedure ordinarily provides pain relief
without any facial sensory loss and has a greater
potential for producing long-lasting pain relief.
Interestingly, tic pain does not always stop immediately following a microvascular decompression, and nerve manipulation by itself (e.g. where no offending vessel found, or without moving the artery) transiently stops the tic pain although it will soon recur thereafter.
Which one of the following statements regarding intrathecal drug delivery systems is LEAST accurate?
a. The intrathecal route results in higher subarachnoid drug concentrations, lower absolute drug doses, and avoidance of side effects associated with systemic dosing
b. Ziconotideis exclusivelyintrathecal analgesic which blocks a N-type calcium channel
c. Development of an catheter tip granuloma is particularly associated with morphine
d. Intrathecal baclofen has a potent analgesic effect
e. Indications for intrathecal drug delivery
do not include patient preference
a. The intrathecal route results in higher subarachnoid drug concentrations, lower absolute drug doses, and avoidance of side effects associated with systemic dosing
b. Ziconotideis exclusivelyintrathecal analgesic which blocks a N-type calcium channel
c. Development of an catheter tip granuloma is particularly associated with morphine
d. Intrathecal baclofen has a potent analgesic effect
e. Indications for intrathecal drug delivery
do not include patient preference
The continuous administration of analgesics via
the intrathecal route results in higher subarachnoid drug concentrations, lower absolute drug doses, and avoidance of side effects associated with systemic dosing (especially at high doses).
Additionally, concerns about opiate diversion
and analgesic compliance are reduced. Indications for intrathecal drug delivery for pain
control:
1. An established pain diagnosis has been
made classifying the symptoms as neuropathic, nociceptive, or mixed.
2. Pain is chronic or both chronic and progressive in nature owing to either a malignant or nonmalignant cause.
3. Pain should be present throughout nearly
the entire day.
4. Patients have failed to achieve analgesia
with conservative nonpharmacologic
modalities.
5. Patient is refractory or intolerant to orally
administered analgesics.
6. Corrective treatment addressing the pain
generator is not warranted.
7. Surgical contraindications to implanting
prosthetic hardware and accessing the
intrathecal space are absent (e.g. bacteremia, anticoagulation).
Although several agents are commonly used for
chronic intrathecal delivery, only three medications currently have FDA approval for long-term
intrathecal use: baclofen, morphine, and ziconotide. Ziconotide is exclusively intrathecal form of ω-conotoxin MVIIa that blocks a N-type
calcium channel on small myelinated and unmyelinated nociceptive afferents that are primarily localized in the superficial Rexed laminae (I and II). Intrathecal baclofen, a GABA-B agonist,
is primarily used to treat spasticity but may help
with pain associated with spasticity and dystonias.
Intrathecal delivery of medications can result
in several potential adverse events including
sedation, cognitive impairment, nausea, vomiting, pruritus, urinary retention, constipation,
hormonal dysfunction, and edema. The development of an inflammatory mass (granuloma) is particularly associated with morphine and increasingly hydromorphone, with high drug concentrations combined with low flow rate increase the risk of granuloma development. Presentation is with loss on pain control or newonset pain complaints or progressive myelopathy.
CT myelography or MRI with gadolinium contrast of the catheter tip region is necessary to confirm the diagnosis. In asymptomatic and
nonprogressive patients, weaning of intrathecal
medications and initiation of saline infusion can
produce spontaneous disintegration of the mass.
In patients with progressive or severe neurologic
compromise, urgent surgical decompression and
excision are recommended.
Which one of the following statements regarding motor cortex stimulation for pain is LEAST accurate?
a. Electrodes may be placed in the subdural or extradural space
b. Subdural placement of electrodes may be required to achievelowerlimb pain coverage
c. Risk of seizures is highest intraoperatively and during programming
d. Is appropriate for deafferentation pain
syndromes
e. Is not indicated in patients with multiple sclerosis related chronic pain syndromes due to high seizure risk
a. Electrodes may be placed in the subdural or extradural space
b. Subdural placement of electrodes may be required to achievelowerlimb pain coverage
c. Risk of seizures is highest intraoperatively and during programming
d. Is appropriate for deafferentation pain
syndromes
e. Is not indicated in patients with multiple sclerosis related chronic pain syndromes due to high seizure risk
Chronic stimulation of the precentral gyrus
below the threshold to produce a motor response
is able to alleviate certain types of deafferentation
pain and MCS has shown efficacy for a number of
deafferentation pain syndromes (e.g. trigeminal,
central post-stroke pain, anesthesia dolorosa,
post-herpetic neuralgia, multiple sclerosis, phantom limb pain, and spinal cord injury). The mechanism of action has been attributed to modulation of deafferentation-induced pathologic hyperactivity in thalamic relay nuclei and/or increased sensitivity of higher order pain pathway neurons.
Intraoperatively, the central sulcus is localized using SSEPs and a contact paddle electrode is placed in the epidural space overlying the facial or upper extremity region of the motor cortex. The electrode is then used for motor evoked potentials with electromyography to confirm motor activity. Iced saline is prepared for irrigation if a seizure is
induced. The minimum thresholds for motor activity and any seizure activity are noted. After confirmation, a paddle electrode is sutured to the dura over the precentral gyrus over the motor area that corresponds to the patient’s pain distribution. Subdural placement is associated with greater energy efficiency, but also an increased rate of complications, including subdural hematomas and a higher reported rate of seizures. However, opening of the dura may be necessary anyway for coverage of lower extremity pain, which requires placement of an electrode along the medial part of the hemisphere. MCS has an overall complication rate of about 5%: wound breakdown or infection (5.1%),
hardware breakage from trauma, and seizures
(12%). Stimulation of the motor cortex is known
to be associated with the potential to induce seizures, and most seizures observed during MCS
occur during programming sessions.
An unpleasant abnormal sensation, whether
spontaneous or evoked.
Sensory disturbances:
a. Allodynia
b. Analgesia
c. Anesthesia dolorosa
d. Causalgia
e. Dysesthesia
f. Hyperesthesia
g. Hyperalgesia
h. Hyperpathia
i. Hypoesthesia
j. Hypoalgesia
k. Neuropathic pain
l. Nociceptive pain
m. Paresthesiae
e. Dysesthesia
A painful syndrome characterized by an abnormally painful reaction to a stimulus, especially a repetitive stimulus, as well as an increased threshold.
Sensory disturbances:
a. Allodynia
b. Analgesia
c. Anesthesia dolorosa
d. Causalgia
e. Dysesthesia
f. Hyperesthesia
g. Hyperalgesia
h. Hyperpathia
i. Hypoesthesia
j. Hypoalgesia
k. Neuropathic pain
l. Nociceptive pain
m. Paresthesiae
h. Hyperpathia
A syndrome of sustained burning pain, allodynia, and hyperpathia after a traumatic nerve lesion, often combined with vasomotor and sudomotor dysfunction and later trophic changes
Sensory disturbances:
a. Allodynia
b. Analgesia
c. Anesthesia dolorosa
d. Causalgia
e. Dysesthesia
f. Hyperesthesia
g. Hyperalgesia
h. Hyperpathia
i. Hypoesthesia
j. Hypoalgesia
k. Neuropathic pain
l. Nociceptive pain
m. Paresthesiae
d. Causalgia
Pain in an area or region which is anesthetic.
Sensory disturbances:
a. Allodynia
b. Analgesia
c. Anesthesia dolorosa
d. Causalgia
e. Dysesthesia
f. Hyperesthesia
g. Hyperalgesia
h. Hyperpathia
i. Hypoesthesia
j. Hypoalgesia
k. Neuropathic pain
l. Nociceptive pain
m. Paresthesiae
c. Anesthesia dolorosa
Pain due to a stimulus that does not normally provoke pain.
Sensory disturbances:
a. Allodynia
b. Analgesia
c. Anesthesia dolorosa
d. Causalgia
e. Dysesthesia
f. Hyperesthesia
g. Hyperalgesia
h. Hyperpathia
i. Hypoesthesia
j. Hypoalgesia
k. Neuropathic pain
l. Nociceptive pain
m. Paresthesiae
a. Allodynia
A 58-year-old presents with paroxysmal attacks of stabbing pain in the throat which occasionally shoots to her right ear, usually lasting less than 1 min. She experiences some relief with cocainization of the right tonsil.
Craniofacial pain syndromes:
a. Anesthesia dolorosa
b. Cluster headache
c. Geniculate neuralgia
d. Glossopharyngeal neuralgia
e. Migraine
f. Occipital neuralgia
g. Persistent idiopathic facial pain
h. Temporomandibular joint disorder
i. Tension-type headache
j. Trigeminal neuralgia
d. Glossopharyngeal neuralgia
Brief paroxysms of pain felt deep in the auditory canal. A trigger area is present in the posterior wall of the auditory canal. May benefit from transection of nervus intermedius.
Craniofacial pain syndromes:
a. Anesthesia dolorosa
b. Cluster headache
c. Geniculate neuralgia
d. Glossopharyngeal neuralgia
e. Migraine
f. Occipital neuralgia
g. Persistent idiopathic facial pain
h. Temporomandibular joint disorder
i. Tension-type headache
j. Trigeminal neuralgia
c. Geniculate neuralgia
Pain attacks of severe or very severe unilateral orbital, supraorbital, and/or temporal pain lasting 15-180 min if untreated. May be accompanied by ipsilateral conjunctival injection and/or lacrimation, nasal congestion, and/or rhinorrhea, eyelid edema, forehead and facial sweating, miosis and/or ptosis and a sense of restlessness or agitation. Attacks have a frequency from 1 every
other day to 8 per day.
Craniofacial pain syndromes:
a. Anesthesia dolorosa
b. Cluster headache
c. Geniculate neuralgia
d. Glossopharyngeal neuralgia
e. Migraine
f. Occipital neuralgia
g. Persistent idiopathic facial pain
h. Temporomandibular joint disorder
i. Tension-type headache
j. Trigeminal neuralgia
b. Cluster headache
Persistent or recurring low back pain, with or without sciatica, after one or more spine surgeries
Spine and peripheral pain syndromes:
a. Brachial plexus avulsion
b. Chronic low back pain
c. CRPS
d. Diabetic peripheral neuropathic pain
e. Failed back surgery syndrome
f. Phantom limb pain
g. Post-herpetic neuralgia
h. Post-spinal cord injury
i. Post-thoracotomy pain syndrome
j. Post-traumatic pain
e. Failed back surgery syndrome
Pain after acute rash has healed accompanied by pain, allodynia, paresthesia, or dysesthesia. The pain usually affects a single
dermatome.
Spine and peripheral pain syndromes:
a. Brachial plexus avulsion
b. Chronic low back pain
c. CRPS
d. Diabetic peripheral neuropathic pain
e. Failed back surgery syndrome
f. Phantom limb pain
g. Post-herpetic neuralgia
h. Post-spinal cord injury
i. Post-thoracotomy pain syndrome
j. Post-traumatic pain
g. Post-herpetic neuralgia
Presentwith severe pain thatis disproportionate to the inciting event, most commonly affecting the hand or foot but that can spread to other body regions.The affected body parts may display sensory disturbances, temperature changes, abnormal patterns of sweating, edema, reduced joint range of motion, movement abnormalities such as weakness, tremor, or dystonia, trophic changes such as skin
atrophy or altered hair and nail growth, and localized osteoporotic changes.
Spine and peripheral pain syndromes:
a. Brachial plexus avulsion
b. Chronic low back pain
c. CRPS
d. Diabetic peripheral neuropathic pain
e. Failed back surgery syndrome
f. Phantom limb pain
g. Post-herpetic neuralgia
h. Post-spinal cord injury
i. Post-thoracotomy pain syndrome
j. Post-traumatic pain
c. CRPS
Involves disconnection of the anterior commissure
Surgical procedures for pain:
a. Anterolateral cordotomy
b. Cingulotomy
c. Deep brain stimulation
d. DREZ lesions
e. Intrathecal morphine
f. Midline myelotomy
g. Mesencephalic tractotomy
h. Motor cortex stimulator
i. Spinal cord stimulation
j. Sympathectomy
k. Thalamotomy
f. Midline myelotomy
Involves lesioning Lissauer’s tract
Surgical procedures for pain:
a. Anterolateral cordotomy
b. Cingulotomy
c. Deep brain stimulation
d. DREZ lesions
e. Intrathecal morphine
f. Midline myelotomy
g. Mesencephalic tractotomy
h. Motor cortex stimulator
i. Spinal cord stimulation
j. Sympathectomy
k. Thalamotomy
d. DREZ lesions
Involves a cord lesion just anterior to the dentate ligament
Surgical procedures for pain:
a. Anterolateral cordotomy
b. Cingulotomy
c. Deep brain stimulation
d. DREZ lesions
e. Intrathecal morphine
f. Midline myelotomy
g. Mesencephalic tractotomy
h. Motor cortex stimulator
i. Spinal cord stimulation
j. Sympathectomy
k. Thalamotomy
a. Anterolateral cordotomy
Involves a lesion of extralemniscal pathways lateral to the spinothalamic tract
Surgical procedures for pain:
a. Anterolateral cordotomy
b. Cingulotomy
c. Deep brain stimulation
d. DREZ lesions
e. Intrathecal morphine
f. Midline myelotomy
g. Mesencephalic tractotomy
h. Motor cortex stimulator
i. Spinal cord stimulation
j. Sympathectomy
k. Thalamotomy
g. Mesencephalic tractotomy*
Aims to treat the motivational-affective component of pain that contributes to fear, suffering, and anxiety
Surgical procedures for pain:
a. Anterolateral cordotomy
b. Cingulotomy
c. Deep brain stimulation
d. DREZ lesions
e. Intrathecal morphine
f. Midline myelotomy
g. Mesencephalic tractotomy
h. Motor cortex stimulator
i. Spinal cord stimulation
j. Sympathectomy
k. Thalamotomy
b. Cingulotomy
