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Pain theory & management
- 1. PAIN THEORY & MANAGEMENT BY DR. MESTET Y. (Neurosurgery resident) 16/16/2020
- 2. Outline • Introduction • Classification • Mechanism • Pathway • Theory • Management 26/16/2020
- 3. Introduction • Pain: defined as ‘an unpleasant sensory and emotional experience associated with actual or potential tissue damage’. 36/16/2020
- 4. Nociception • Is the sensory process of detecting tissue damage. 46/16/2020
- 5. Classification • Fast vs slow: • Acute vs chronic: why? 56/16/2020
- 6. Mechanisms of pain Nociceptive Neuropathic 66/16/2020
- 7. 76/16/2020
- 11. Cartesian Dualistic Theory • Describe pain as a mutually exclusive phenomenon; a result of physical injury or psychological injury. • No synergism. 116/16/2020
- 12. Specificity Theory • States that each sensations are the result of specific energy experienced at an infinite number of receptors. • Contributed for discovery of somatosensory modalities (cold, pain, heat, and touch). 126/16/2020
- 13. Pattern theory • Suggested that each sensation relays a specific pattern or sequence of signals to the brain. • Depending on which pattern the brain reads, correlates with the sensation felt. 136/16/2020
- 15. Neuromatrix Model • Suggests that Central nervous system is responsible for eliciting painful sensations rather than the periphery. Input coming in from the periphery can initiate or influence the neurosignature, but cannot create a neurosignature of their own. Pain can be affected not only by physical factors but by cognitive and emotional factors. Memory formation specific neurosignatures that elicit certain sensations can occur. • Was developed to explain phantom pain. 156/16/2020
- 16. Bio psychosocial Model • Most accepted theory on etiology of pain. • Hypothesizes that pain is the result of interactions b/n the 3 constructs of pain (biological, psychological and sociological factors). • Founded by John Joseph Bonica, father of pain medicine. 166/16/2020
- 17. Management Part 1.Trigeminal neuralgia Part 2. Neurosurgical Mgt of intractable pain 176/16/2020
- 18. Part 1. Trigeminal neuralgia Epidemiology 4/100,000. 2% of patients with MS have TGN. 20x increased risk of TGN in MS. 2x more in F. Typically > 50 (average 63). Causes Compression by SCA at its entry: 80–90%. MS plaque Persistent primitive trigeminal artery Dolichoectatic basilar artery Posterior fossa tumor How? Demyelination induced ephaptic transmission 186/16/2020
- 20. Diagnosis • Mainly clinical. Criteria: A) At least 3 attacks of unilateral facial pain fulfilling criteria B and C. B) Occurring in divisions of the trigeminal nerve, with no radiation beyond its distribution C) Pain has at least three of the following four characteristics: Recurring in paroxysmal attacks lasting from a second to 2 minutes. Severe intensity Electric shock-like, shooting, stabbing, or sharp in quality > 3 attacks precipitated by innocuous stimuli to the affected side D) No clinically evident neurologic deficit E) Not better accounted for by another ICHD-3 diagnosis • IX:MRI/MRA/ 206/16/2020
- 21. DDX • Cephalic neuralgias Atypical (type 2) TGN Atypical facial pain Glossopharyngeal neuralgia Geniculate neuralgia Tic convulsif Occipital neuralgia superior laryngeal neuralgia Herpes zoster postherpetic neuralgia (ram say-hunt syndrome) Supraorbital neuralgia (SON) Trigeminal neuropathic pain Trigeminal deafferentation pain Short-lasting unilateral neuralgiform headache w ith conjunctival injection and tearing (SUNCT) • Ophthalmic pain • Otalgia • Vascular pain syndromes Migraine headaches Cluster H/A Giant cell arteritis • Sinusitis • Dental disease • TMJ dysfunction • Neoplasm 216/16/2020
- 22. Rx I. Medical Rx: acceptable relief in 69% with carbamazepine (mechanism?). 226/16/2020
- 23. Cont’d Surgical Rx: when refractory to medical Rx. ●Microvascular decompression ●Ablative procedures: Rhizotomy with radiofrequency thermocoagulation, mechanical balloon compression, or chemical (glycerol) injection Radiosurgery Peripheral neurectomy and nerve block 6/16/2020 23
- 24. Radiofrequency Rhizotomy • Involves use RF stimulation (alternating electrical field with an oscillating frequency of 500,000 Hz) to cause a thermal lesion in the retrogasserian ganglion. 246/16/2020
- 25. Stereotactic Radiosurgery • The least invasive procedure. • For patients with High-risk medical illness, Pain refractory to prior surgical procedures, or Those on anticoagulants (anticoagulation does not have to be reversed to have SRS). Patients with MS. 256/16/2020
- 26. MVD • Offers long-term pain relief. Indications: • Ideal for young healthy patients with 1. Failed medical mgt with ≥ 5 yrs anticipated survival 2. Intractable pain and fail PTR 3. Tic involving V1 for whom the risk of exposure keratitis due to corneal anesthesia would be unacceptable (e.g. already blind in contralateral eye) 4. Patients with MS are usually not candidates for MVD due to low response rate 266/16/2020
- 28. Predictors of worse outcome • Type of TGN: most significant predictor • Compression by multiple artery. • Venous compression: b/c of regrowth of veins. 286/16/2020
- 29. Post-lesion (MVD) assessment 1. Sensation in all 3 divisions of CN 5 2. Corneal reflex bilaterally 3. EOM function 4. Masseter muscle strength 5. Pterygoid muscle strength. Wean off carbamazepine gradually. 296/16/2020
- 30. 306/16/2020
- 31. Part 2: Neurosurgical Management of Intractable Pain 316/16/2020
- 33. Peripheral Nerve Stimulation for Neuropathic Pain • MECHANISM: gate-control theory of pain • TECHNIQUE The PNS device is made up of electrodes inserted along the desired peripheral nerve and a generator system that is buried subcutaneously some distance away. • R/o nerve entrapment first. 336/16/2020
- 34. Spinal Cord Stimulation MECHANISM: 1.The gate control theory of pain transmission. How? Large fibers have a lower threshold for depolarization by an electrical stimulus. Large-diameter sensory fibers within peripheral nerves are segregated into the dorsal columns, hence, more selective activated by electrical stimulation of dorsal columns of the spinal cord. 2. Supraspinal center stimulation. 3. SCS increases GABA and serotonin levels 4. High-frequency stimulation related conduction block. TECHNIQUES: place electrodes in the epidural space: Via hemilaminectomy or percutaneously with a needle Generator 346/16/2020
- 35. Indications 1. Pain Failed Back Surgery Syndrome (most common indication, especially if LE pain > back), Complex regional pain syndrome (CRPS) Post thoracotomy pain (intercostal neuralgia), Multiple sclerosis, diabetic neuropathy and Postherpetic neuralgia (sometimes ) 2. Refractory angina pectoris 3. Painful limb ischemia from inoperable PAD 4. Function al: spastic hemiparesis, dystonia, bladder dysfunction 5. Not used for cancer pain or for patients with limited life expectant. 356/16/2020
- 36. DBS • Include stimulation of somatosensory thalamus, hypothalamus, PVG-PAG and MCS. • Stimulation sites depends on the pain xcr. • Nociceptive and paroxysmal neuropathic pain: PVG-PAG stimulation. • Continuous neuropathic pain: sensory thalamus (nucleus ventrocaudalis). • The affective component of pain: anterior cingulate. • Mechanism: 366/16/2020
- 37. CNS narcotic administration Intraspinal narcotics • Administered epidurally or intrathecally for pain relief. • Usually be achieved for pain below the neck. • Less s/e over systemic narcotics • Effectiveness limited to ≈ 1 year and is not indicated for chronic benign pain. • Intraventricular narcotics • Used for cancer pain (especially head and neck) unresponsive to other methods in patients with a life expectancy < 6 mos. 376/16/2020
- 38. Cordotomy • Interruption of the lateral spinothalamic tract fibers in the spinal cord. • Procedure of choice for unilateral pain below the C5 dermatomal level. • Percutaneous vs open cervical cordotomy (schwartz technique). • Do not go posterior to the dentate ligament (to avoid corticospinal tract). 386/16/2020
- 39. Commissural myelotomy • Interrupts pain fibers crossing in the anterior commissure on their way to the lateral spinothalamic tract. • For bilateral or midline pain, primarily below the thoracic levels. Technique • Laminectomy 3 levels above the highest dermatome involved in pain. • Dura is opened longitudinally • Midline sulcus identified with operating microscope . • Midline incision with blade cephlocaudally for 3–4 cm. 396/16/2020
Editor's Notes
- Pain The International Association for the Study of Pain defines this as ‘an unpleasant sensory and emotional experience associated with actual or potential tissue damage’ (Merskey & Bogduk 1994, p. 209).
- Pain may be experienced in the absence of nociception. Eg. ‘thalamic syndrome’ (after stroke) cause pain despite no any injury, probably due to the loss of descending inhibitory signals from the thalamus.
- Why chronic? Wind-up phenomenon, temporal & spatial summation & central sensitization b/c of neuroplasticity of 2nd order neurons. the hypo activity of the endogenous pain inhibitory neurons may or may not be the cause. Chronic back pain vs fibromyalgia
- brain was not the homogenous object that but instead a complex structure with various components. In addition to the identification of specific pathways for different sensory inputs, Bell also postulated that the brain was not the homogenous object that Descartes believed it was, but instead a complex structure with various components.[13] individual sensations were the result of specific energy experienced at certain receptors. Furthermore, Muller believed that there was an infinite number of receptors in the skin, and this surplus of receptors accounted for the ability of an individual to discriminate between different sensations.[14]
- According to the gate-control theory of pain, large A delta and small C nerve fibers carry normal and painful sensations, respectively, to the substantia gelatinosa, where stimulatory and inhibitory neurons are activated to transmit sensory messages to the brain. Pain perception is allowed to pass through this gate only when small nerve fibers are triggered; stimulation by signals from both types of fibers suppresses the nociceptive input at the spinal cord level and reduces the signals to the sensory cortex. The gate control theory of pain transmission proposed by Melzack and Wall3 in 1965 describes a balance between small and large sensory fibers, with positive and negative feedback loops controlling the activity of the dorsal horn cells of the spinal cord. The theory postulates that a predominance of small-diameter sensory fiber activity opens “gates” within the dorsal horn of the spinal cord and that predominance of large-diameter fiber activity closes them. The gate control theory of pain states that when a stimulus gets sent to the brain, it must first travel to three locations within the spinal cord. These include the cells within the substantia gelatinosa in the dorsal horn, the fibers in the dorsal column and the transmission cells which are located in the dorsal horn as well.[18] The substantia gelatinosa of the spinal cord's dorsal horn serves to modulate the signals that get through, acting similar to a “gate” for information traveling to the brain.[19] The sensation of pain that an individual feels is the result of the complex interaction among these three components of the spinal cord. Simply stated, when the “gate” closes, the brain does not receive the information that is coming from the periphery to the spinal cord. However, when the signal traveling to the spinal cord reaches a certain level of intensity, the “gate” opens. Once the gate is open, the signal can travel to the brain where it is processed, and the individual proceeds to feel pain. The information mentioned above accounts for the physical component of pain, but as stated earlier, the Gate Control Theory was one of the first to acknowledge that psychological factors contributed to pain as well. In more recent times, researchers have postulated that these cortical control centers are responsible for the effects of cognitive and emotional factors on the pain experienced. Current research has also suggested that a negative state-of-mind serves to amplify the intensity of the signals sent to the brain as well.[21] For example, somebody who is depressed has a “gate” that is open more often, allowing more signals to get through, increasing the probability that an individual will experience pain from an otherwise normal stimulus. Also, there are reports that certain unhealthy lifestyle choices will also result in an “open gate,” which in turn leads to pain that is disproportionate to the stimulus.[22] The gate control theory has proven to be one of the most significant contributions to the study of pain throughout history. The concepts that Melzack and Wall introduced to the study of pain are still utilized by researchers today. Even though this theory initiated the idea that pain wasn’t solely a result of physical injury but rather a complex experience, influenced by cognitive and emotional factors, there was still additional research necessary to comprehend the mechanisms and etiology of pain completely. This need precipitated the introduction of the following two philosophies regarding pain.
- The neuromatrix model denotes that there are four components within the central nervous system responsible for creating pain. The four components are the “body-self neuromatrix, the cyclic processing, and synthesis of signals, the sentinel neural hub, and the activation of the neuromatrix.”[24] According to Melzack, the neuromatrix consists of multiple areas within the central nervous system that contribute to the signal, which allows for the feeling of pain. These areas include the spinal cord, brain stem and thalamus, limbic system, insular cortex, somatosensory cortex, motor cortex, and prefrontal cortex.[25] The signal that these areas of the central nervous system work together to create is responsible for allowing an individual to feel pain, and he referred to as the “neurosignature.” Furthermore, this theory states that input coming in from the periphery can initiate or influence the neurosignature, but these peripheral signals cannot create a neurosignature of their own.[26] This idea that peripheral signals can alter the neurosignature is an important concept when considering the effect that nonphysical factors have on an individual’s experience with pain. Melzack’s theory claimed that not only are there specific neurosignatures that elicit certain sensations, but when there is alteration in a certain signal, this allows for memory formation of these particular experiences. If the same circumstances occur again in the future, it is this memory that allows for the same sensation to be felt.[27]
- Th ere is no correlation with h erpes sim plex infection
- Neurologic exam must be intact (only exception: mild sensory loss)
- The International Classification of Headache Disorders, 3rd edition (ICHD-3) diagnostic criteria for classic TN Neuroimaging — Neuroimaging with head MRI (or CT if MRI is not an option) is useful for identifying the small proportion of patients who have a structural lesion (eg, tumor in the cerebellopontine angle, demyelinating lesions including multiple sclerosis) as the cause of painful trigeminal neuropathy [37,38]. In addition, high resolution MRI and magnetic resonance angiography (MRA) may be useful for identifying vascular compression as the etiology of classic TN, but the utility of these studies has not been established. We recommend obtaining brain MRI with and without contrast to rule out a causative structural brain lesion for all patients presenting with suspected TN. High-resolution MRI with thin cuts through the region of the trigeminal ganglion and heavy T2 weighting (eg, a constructive interference in steady-state [CISS] fusion study), is the preferred imaging modality if available. Patients with trigeminal sensory loss, bilateral symptoms, and those younger than 40 years may have a higher risk of secondary TN (ie, painful trigeminal neuropathy). It help pick multiple sclerosis if present.
- Patients with true TGN initially responded to carbam azepine, none with AFP did Tic convulsif=geniculate neuralgia with hemi facial spasm Superior laryngeal neuralgia: a branch of the vagus atypical trigeminal neuralgia or trigeminal neuralgia type 2:meets ICHD-3 criteria for classic TN except it has concomitant persistent facial pain
- Figure 172-1. The radiofrequency needle is inserted into the cheek at a point 2.5 cm from the corner of the mouth, 1 cm below the occlusal plane. The trajectory is the intersection of two planes: one directed to the midpupil and the other to a point 3 cm anterior to the tragus. During needle insertion, the surgeon’s index finger is inserted into the patient’s mouth lateral to the teeth to prevent intraoral penetration and to ensure that the needle is not directed lateral to the maxilla. In the operating suite, the patient is placed supine on the operating table. Intravenous access is secured. The patient is then placed with the head extended to about 30 degrees to obtain a clear submental-vertex view of the foramina ovale and spinosum, located on the greater wing of the sphenoid bone, of the affected side. Biplanar fluoroscopy can be used if available. Usually a portable C-arm digital fluoroscope is sufficient. Magnification (2×) of the fluoroscopic image may be required to visualize the foramen clearly.
- Recurrence and re-treatment: 5% to 43% Incomplete radiation effects on the targeted tissues.
- Surgical treatments for TN other than MVD generally involve intentional production of a lesion within the trigeminal nerve.
- Asterion: junction of lambdoid, occipitomastoid and parietomastoid sutures. Usually lies within a few m illim eters of the posterior-inferior edge of the junction of th e transverse and sigm oid sinuses (not always reliable – m ay overlie either sinus). burr hole: a) 1 cm inferior and 1 cm medial to the asterion 70 (p 60) b) if the asterion is not easily identified or if there are concerns about the reliability of the asterion as a landmark for the junction of the transverse and sigmoid sinuses,71 place th e burr hole directly over the m astoid em issary vein w hich drains superolaterally into th e sigm oid sinus 3. craniotom y: top of bon e opening as close as possible to transverse sinus. The position of the transverse sinus can be approxim ated by a line draw n from the posterior base of the zygomatic process to the inion, or roughly ≈ 2 finger-breadths above the upper end of the m astoid notch. Lateral limit of bone opening is sigmoid sinus. A triangular bony opening with a leg along each sinus works well. Craniectomy diam eter needs to be only ≈ 3 cm . Apply bon e wax liberally (blocks any possible opening into the mastoid air cells) 4. dural opening: either a curvilinear with each end at a sinus and the convexity away from th e jun ction (Jannetta) or an inverted “T” (with one incision tow ards each sinus and the third tow ards jun ction of sinuses) 5. minim al or no retraction of cerebellum is usually required 6. allow CSF to drain before proceeding: this m ay require gentle advancem ent of a cottonoid in the CPA. A lum bar drain should be placed if CSF cannot be drained 7. follow the junction of tentorium with temporal bon e deep. Place a retractor that both medially displaces the cerebellum and slightly “lifts” th e cerebellum towards the surgeon (m edial displacem ent alone is not as e ective) 8. petrosal vein: coagulate and divide th e petrosal vein complex (usually 2–3 veins connecting to the tentorial dura). If the vein is torn, the dural side is tam ponaded (som etim es up to 30 m inutes is needed) w hile th e free end is coagulated 9. V is deeper than the VII/VIII complex, w hich should not even be seen with this approach. If VII/ VIII are seen, m ove the retractor superiorly as even gentle traction m ay cause h earing loss. The operative field is liberally irrigated, retractors are removed, and a Valsalva-like maneuver is performed with the ventilator by the anesthesiologist to ensure there is no bleeding. The dura is closed in a watertight manner with continuous or interrupted braided 4-0 sutures to prevent subsequent leakage of CSF.
- High-frequency stimulation (in the kHz range) has been demonstrated experimentally to achieve pain relief through conduction block. High-frequency stimulation is unique in providing paresthesia-free analgesia by stimulating beyond the physiologic frequency range.
- post laminectomy pain syndrome (Failed Back Surgery Syndrome): Chronic neuropathic pain is most commonly located in the back and legs. Of patients undergoing lumbosacral spine surgery for treatment of this pain, 10% to 40% eventually have persistent or recurrent pain.11 Failed back surgery syndrome is the most common indication for SCS and has the most evidence supporting its use.
- PVG-PAG stimulation activate endogenous opioid systems. MCS is used primarily for treatment of neuropathic pain syndromes and might be particularly effective for certain varieties of intractable facial pain (e.g., trigeminal neuropathic pain). Because of the somatotopic distribution of leg sensation in the interhemispheric fissure, MCS is usually restricted to face and/ or arm pain. for pain of nonmalignant origin, such as pain associated with FBSS, neuropathic pain following central or peripheral nervous system injury, trigeminal pain, and cluster headache. Not FDA approved. periventricular-periaqueductal gray (PVG-PAG)
- A life expectancy of > 3 m onths is recom m ended for im plantable pum ps (if shorter longevity is anticipated, an external pump m ay be used). Naloxone needed to be A t hand in doing it.