Книги по МРТ КТ на английском языке / Neurosurgery Fundamentals Agarval 1 ed 2019

trigeminal nerve, and assessment of bite strength (for portio minor nervi trigemini, the motor branch of the trigeminal nerve). To rule out orbital disease, one should assess extraocular movement function.

The International Classification of Headache Disorders, 3rd edition (ICHD-3) diagnostic criteria for classic TN are as follows9:

•At least three attacks of unilateral facial pain fulfilling criteria b and c.

•Occurring in one or more divisions of the trigeminal nerve, with no radiation beyond the trigeminal distribution.

•Pain has at least three of the following four characteristics:

◦◦ Recurring in paroxysmal attacks lasting from a fraction of a second to

two minutes.

◦◦ Severe intensity.

◦◦ Electric shock-like, shooting, stabbing, or sharp in quality.

◦◦ At least three attacks precipitated by innocuous stimuli to the affected side of the face (some attacks may be, or appear to be, spontaneous).

•No clinically evident neurologic deficit.

•Not better accounted for by another ICHD-3 diagnosis.

Treatment

Medical Therapy

The first-line therapy for TN, carbamazepine, will give initial relief in 69% of patients. If patients fail to respond or become refractory to carbamazepine or oxcarbazepine, second-line agents include baclofen, tricyclic antidepressants, and gabapentinoids. Third-line agents such as phenytoin or benzodiazepines may be tried, but these have a low rate of clinical efficacy.

Surgical Therapy

Surgical referral is recommended for patients that are refractory to or intolerant of medical management.

Ultimately, up to 75% of patients may eventually fail to benefit from medical therapy. Selection of the optimal treatment procedure depends on patient age, distribution of symptoms, prior treatment, and the side effect profile of the treatment modality.10

•Microvascular decompression (MVD):

A microsurgical exploration of the root entry zone is performed via retrosigmoid craniectomy. The vessel that is impinging on the nerve is dissected away and displaced using a nonabsorbable insulator to absorb the pulsations. Internal neurolysis or even intradural retrogasserian trigeminal nerve section may be performed during the MVD if no vascular compression is identified, although with modern imaging techniques, the vascular anatomy is usually delineated preoperatively.

•Ablative procedures:

◦◦ Percutaneous trigeminal rhizotomy: Interruption of pain transmission through selective destruction of the

Aδ and C nociceptive fibers while preserving the Aα and Aβ fibers which mediate touch and other sensory parameters. Methods include radiofrequency thermocoagulation, glycerol injection into Meckel’s cave, and percutaneous microcompression via inflation of a Fogarty catheter balloon.

◦◦ Extradural subtemporal approach: Primarily of historical interest. The approach was used to expose the ganglion and then mildly traumatize it.

◦◦ Stereotactic radiosurgery (SRS):

A small collimator size (4–5 mm) is used to place a 70–90 Gy lesioning dose on the portion of the trigeminal nerve as it enters the brainstem in the root entry zone. There is latency to pain relief, thus SRS is suboptimal for patients needing immediate relief.

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11.3.2  Glossopharyngeal Neuralgia

Pathophysiology

Glossopharyngeal neuralgia may be caused by irritation of the cranial nerve IX. As with TN, there are idiopathic and secondary forms of glossopharyngeal neuralgia. Demyelinating lesions, cerebellopontine angle tumor, peritonsillar abscess, carotid aneurysm, and Eagle syndrome (in which cranial nerve IX is compressed laterally against an ossified stylohyoid ligament) are examples of secondary glossopharyngeal neuralgia.

Vascular compression of cranial nerves IX and X can occur at the nerve root entry zone by the vertebral artery or posterior inferior cerebellar artery.

Signs and Symptoms

Characterized by paroxysmal, severe, stabbing pain involving the ear, tonsillar fossa, base of the tongue, or beneath the angle of the jaw.

Diagnosis

Evaluation includes a thorough history, with emphasis on triggering factors and the presence of nocturnal awakening. A careful intraoral and neck examination should be undertaken to help exclude local disease as a cause for the pain.

MRI/MRA is indicated in virtually all

­patients to rule out a mass lesion or vascular pathology11,​12; plain skull films may reveal an ossified stylohyoid ligament

(consistent with Eagle syndrome).

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According to the ICHD-3, the diagnosis of glossopharyngeal neuralgia requires all of the following:

•At least three attacks of unilateral pain.

•Pain is located in the posterior part of the tongue, tonsillar fossa, pharynx, beneath the angle of the lower jaw and/ or in the ear.

•Pain has at least three of the following four characteristics:

◦◦ Recurring in paroxysmal attacks lasting from a few seconds to 2 minutes

◦◦ Severe intensity

◦◦ Shooting, stabbing, or sharp in quality

◦◦ Precipitated by swallowing, coughing, talking, or yawning

•No clinically evident neurological deficit.

•Not better accounted for by another ICHD-3 diagnosis.

Treatment

Medical Therapy: See medical treatment section for TN (section 11.3.1). Application of local anesthetics to the oropharynx may also prove diagnostic and therapeutic.

Surgical Therapy: For those who fail medical therapy, procedures include intracranial sectioning of cranial nerve IX plus the upper three to four rootlets of cranial nerve X at the jugular foramen, or vascular decompression.13,​14,​15,​16

11.3.3  Other Craniofacial Neuralgias

Other craniofacial neuralgias include geni­ culate neuralgia (involves a somatic sensory branch of the facial nerve), occipital neuralgia, and supraorbital/supratrochlear neuralgia. All these conditions involve pain in the distribution of the involved nerve and may be treated with medications, nerve blocks, and decompressive surgery/ ablative procedures.

11.3.4  Postherpetic Neuralgia

Following resolution of the rash caused by Varicella-zoster virus (VZV), a variable percentage of patients may continue to experience severe neuropathic pain. Major risk factors include older age, greater acute pain, and greater rash severity.17,​18,​19,​20 The risk is also likely increased with immunosuppression.21,​22 The pain usually resolves 2–4 weeks after the vesicular eruption has healed; when pain persists for more than 1 month, it is called PHN.

Pathophysiology

Acute herpes zoster is caused by reactivation of latent VZV in the dorsal root ganglia of cranial or spinal nerves, often years after resolution of the original infection.

As cellular immunity wanes with age or immunocompromise, the virus is transported along peripheral nerves, producing an acute neuritis.20,​23

Signs and Symptoms

Pain associated with acute zoster infection and PHN can be burning, sharp, or stabbing in character and may be constant or intermittent.24,​25 More than 90% of patients with PHN also have allodynia (pain evoked by normally benign stimuli such as light touch). Patients with PHN often have deficits in thermal, tactile, pinprick, and/ or vibration sensation within the affected dermatomes.26 It usually presents soon after resolution of the rash, but has been reported to occur months to years after the initial event.27

Diagnosis

The diagnosis of PHN is a clinical one, made when pain persists beyond 4 months in the same distribution as a preceding documented episode of acute herpes zoster. Additional supporting diagnostic factors include advanced age, severe prodromal pain and preceding rash with acute zoster, a dermatomal distribution, and the presence of allodynia.28

Rarely, nerve pain in acute zoster may emerge in the absence of a rash, as occurs in a condition called zoster sine herpete or in intercostal neuralgia. Pain in a trigeminal or radicular distribution combined with the detection of VZV by polymerase chain reaction (PCR) in the cerebrospinal fluid (CSF) supports the diagnosis of zoster sine herpete.29

On examination, the areas affected by PHN may be remarkable for scarring related to the vesicular eruption of the preceding acute herpes zoster infection, or by areas of excoriation caused by scratching. The affected skin may display decreased sensation to mechanical and thermal stimuli, hyperalgesia (increased sensitivity to painful stimuli), or allodynia.

Treatment

Herpes Zoster: Pain associated with the acute attack of herpes zoster may be treated with epidural or paravertebral somatic block (intercostal) (See section on pain procedures).30 Oral antiherpetic drugs include acyclovir (Zovirax), valacyclovir (Valtrex), and famciclovir (Famvir). These drugs reduce the incidence of PHN but may cause thrombotic thrombocytopenic purpura/hemolytic­ uremic syndrome when used in severely immunocompromised patients at high doses.

PHN: It is suggested to initiate therapy with lidocaine skin patches since this modality has the lowest potential for

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serious side effects. Most drugs useful for TN are less effective for PHN. First-line drug treatments include tricyclic antidepressants, gabapentin, and pregabalin. These treatments along with opioids have proven more effective than placebo in systematic reviews.31,​32,​33,​34 Since the pain of PHN can be chronic, long-term therapy is often required, however, the long-term benefits of most therapies are uncertain, and side effects are common.35

•Tricyclic antidepressants (TCA):

Amitriptyline, nortriptyline.

◦◦ Recommended as initial treatment for those with moderate-to-severe PHN pain. Exceptions include patients with heart disease, epilepsy, or glaucoma.

◦◦ Should be used cautiously in older patients especially those with cognitive impairment/dementia due to anticholinergic effects.

•Antiepileptic drugs: Gabapentin, oxcarbazepine, zonisamide.

◦◦ Recommended for patients with moderate-to-severe PHN with contraindications to or intolerance of TCAs.

◦◦ Side effects include dizziness, som- nolence, ataxia, peripheral edema, confusion, and depression.

•Topical treatment: Capsaicin, lidocaine patch 5%.

◦◦ Recommended for patients with mild-to-moderate localized pain from PHN who do not desire systemic therapy with TCAs.

•Intrathecal steroids:

◦◦ An option for patients who continue to have intractable pain despite the above measures. These do not work for pain in the trigeminal nerve distribution.

•Surgical treatment:

◦◦ No operation is uniformly successful in treating PHN. Procedures include nerve blocks, rhizotomy, cordotomy,

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sympathectomy, neurectomies, acupuncture, dorsal root entry zone (DREZ) lesions, spinal cord stimulation (SCS), and motor cortex stimulation (for facial PHN). See procedures section.

11.3.5  CRPS/Causalgia

The term causalgia was introduced by Weir Mitchell in 1864 to describe a rare syndrome that followed a minority of partial peripheral nerve injuries in the American civil war. The syndrome is characterized by regional pain, limited range of motion, swelling, skin changes, vasomotor instability, and patchy bone demineralization, usually in the distal limb. It frequently begins following a fracture, soft tissue injury, or surgery. The syndrome has subsequently been reclassified as “complex regional pain syndrome” (CRPS).

Two subtypes of CRPS have been recognized36,​37:

•Type I akareflexsympatheticdystrophy or causalgia minor: Corresponds to patients with CRPS without evidence of peripheral nerve injury and represents about 90% of clinical presentations.

•Type II formerly termed causalgia:

Refers to cases in which objective peripheral nerve deficits are present.

Pathophysiology

The pathogenesis of CRPS is unknown. Early theories invoked ephaptic transmission between sympathetic and afferent pain fibers although this theory is rarely cited these days. Some studies have found that patients with CRPS have

significant increases in proinflammatory cytokines in affected tissue as well as in plasma and CSF.38,​39,​40,​41 The release of inflammatory mediators and pain-pro- ducing peptides by peripheral nerves has therefore been implicated as a possible mechanism.42,​43,​44 Central sensitization, whereby increased activity in nociceptive afferents leads to increased synaptic transmission at somatosensory neurons in the dorsal horn of the spinal cord, is another possible explanation for pain and allodynia in CRPS.42 Another more recent postulate involves excessive norepinephrine release at sympathetic terminals together with catecholamine hypersensitivity, which may explain autonomic manifestations of CRPS.45

Signs and Symptoms

The primary clinical manifestations of CRPS are pain, sensory changes, motor impairments, autonomic symptoms, and trophic changes in the affected limb.46 The onset generally occurs within 4–6 weeks of the inciting event.46,​47 The initial symptoms usually include pain, erythema, and swelling of the affected limb.43 Pain is typically the most prominent and debilitating symptom and is described as a stinging, burning, or tearing sensation that is felt deep inside the limb in most cases. Sensory abnormalities include hyperalgesia, allodynia, or hypesthesia (diminished capacity for physical sensation) and usually occur in the distal limb.48 Limb movement may be limited by edema, pain, or contractures. Trophic changes may include increased hair growth, increased or decreased nail growth, contraction and fibrosis of joints and fascia, and skin atrophy. These symptoms may spread over time to involve adjacent areas of the affected limb or other ipsilateral or contralateral limbs.49,​50

Diagnosis

The diagnosis of CRPS is based upon history and physical examination, using the following features48:

•Symptoms develop after limb trauma, usually within 4–6 weeks.

•Symptoms no longer fully explained by the initial trauma.

•Symptoms affect the distal limb, go beyond the region involved in the trauma, or extend beyond the territory innervated by a single nerve or nerve root.

In the absence of an agreed upon pathophysiology, no “gold-standard” diagnostic criteria have been developed. Tests that have been proposed include thermography, three-phase bone scan, osteoporosis on X-ray, response to sympathetic block and autonomic testing, but none of these has demonstrated adequate specificity.

Treatment

A multidisciplinary approach is suggested for the management of CRPS, and treatment is more effective when started early in the course of the disease.51,​52 For patients with early CRPS, it is suggested to start with one or more of the following: nonsteroidal anti-inflammatory drugs (NSAIDs), an anticonvulsant (gabapentin or pregabalin), a TCA or other antidepressant drug effective for neuropathic pain (typically amitriptyline or nortriptyline), bisphosphonate treatment, or topical lidocaine/capsaicin cream. Medical therapy is usually ineffective. Other proposed treatments include:

•Sympathetic blocks (18–25% have satisfactory long-lasting relief).

•Intravenous regional sympathetic block: Particularly for upper extremity CRPS although not better than placebo in several trials.53,​54

•Surgical sympathectomy: Some purport this relieves pain in greater than 90% of

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patients. Other studies have shown this to be no more effective than placebo.55

•SCS: Some success reported.

•Dorsal root ganglion stimulation.

11.3.6  Peripheral Nerve

Pathophysiology

Peripheral nerve syndromes may be caused by compression of nerve segments such as in carpal tunnel syndrome but can also occur proximally at the root level such as when a herniated cervical disc compressed the spinal root. Pathology may be caused less commonly by transection, nerve ischemia, radiation, inflammation, degeneration, and metabolic problems.

Diagnosis and Treatment

Nerve conduction studies and electrodiagnostic studies such as electromyogram and are the most effective means of identifying and classifying peripheral nerve disorders.

MRI is also used to identify cervical spine disease, disc herniation, degeneration, and compression. Treatments include medication, splinting, steroid injections, and surgery for nerve decompression or transposition.

Syndromes

Carpal Tunnel

•Most common entrapment syndrome; involves median nerve in the wrist.

•Symptoms include hand tingling that is worse at night.

•Tinels (tapping of wrist) and Phalen’s (flexion of wrist) tests are used to diagnose.

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•Electrodiagnostic studies are the most sensitive for diagnosis.

Anterior Interosseous

•Rare, pure motor neuropathy with occasional reported dull forearm pain.

•Patient fails to make OK sign (flexion of thumb interphalangeal and index finger distal interphalangeal joint impaired).

•Can diagnose with pinch test (patient cannot pinch paper between thumb and index finger) as well as on ultrasound and MRI.

Posterior Interosseous

•Compression causes gradual onset of weakness of extension of the digits and wrist. Pain is not a primary feature and no sensory deficit.

•MRI can identify muscle signal changes indicating denervation.

Ulnar

•Can be compressed above elbow, at elbow, at cubital fossa, or Guyon’s canal at the wrist.

•Most evident finding is first dorsal interosseous wasting. Other interossei wasting may occur.

•Results in claw deformity and decreased sensation over little finger and ulnar side of ring finger.

•Evaluate with electrodiagnostic studies and ultrasound.

11.4  Procedures for Pain

Medical therapy should be maximized before a patient becomes a candidate for a pain procedure. In general, nonablative procedures are exhausted before resorting to ablative procedures.

11.4.1  Electrical Stimulation

Peripheral Nerve

Peripheral nerve stimulation (PNS) is a technique in which electrodes are placed along the course of peripheral nerves to control pain. PNS utilizes the previously mentioned gate control theory to suppress pain by stimulating the non-noxious sen- sory pathway (large myelinated Aβ nerve fibers). A temporary trial electrode is left in place for a week or so to determine if PNS is helpful followed by implantation of a permanent electrode if the trial is successful.

Dorsal Root Ganglion

The dorsal root ganglion contains the cell bodies of first-order afferent neurons. It occupies a predictable location in the neural foramen, and an epidurally inserted wire can be inserted under fluoroscopic guidance in order to provide relief within the dermatome innervated by that level. Adjacent dermatomes can also be stimulated via the rami communicantes (nerve fibers which run between nearby spinal levels).

Spinal Cord Stimulation

SCS involves the insertion of electrodes into the posterior epidural space in order to interrupt pain transmission ( Fig. 11.5). The exact mechanism of action of SCS is undetermined, but likely involves both anterograde and retrograde modulation of sensory pathways, particularly the activity of wide dynamic range neurons in the dorsal horn of the spinal cord.

The most common indication for SCS is postlaminectomy pain syndrome or failed back syndrome; a condition characterized by persistent pain following back surgeries. SCS is also effective in CRPS type 1,56

as well as post-thoracotomy pain, multiple sclerosis, diabetic neuropathy, refractory angina pectoris, painful limb ischemia from inoperable peripheral vascular disease, and sometimes PHN.

Following electrode placement, an external generator trial over several days determines if SCS is effective, in which case an implantable pulse generator is placed subcutaneously and connected to the electrodes. Complications of SCS include infection (3.5% incidence with plate electrodes), electrode migration, lead breakage, CSF leak, radicular pain, interference with cardiac pacemakers, and weakness. The success rate in pain control is approximately equal to 50% improvement in 50% of patients in experienced hands at specialized centers where multidisciplinary approach is available.57

Deep Brain Stimulation

Deep brain stimulation (DBS) may be used to treat a variety of conditions including movement disorders, epilepsy, and pain syndromes. Deafferentation pain syndromes such as anesthesia dolorosa (pain felt in an area that is completely numb to the touch), pain from spinal cord injury, or thalamic pain syndromes may benefit from stimulation of sensory thalamus (ventral posteromedial or ventral posterolateral). DBS for chronic neuropathic pain produces a 40–50% reduction in pain in about 25–60% of patients.58 Anecdotal reports of DBS and motor cortex stimulation have also been described for the treatment of intractable severe persistent pain states.56

Nociceptive pain syndromes are more likely to benefit from stimulation of periventricular gray matter or periaqueductal gray matter. The Food and Drug Administration (FDA) has failed to approve these devices for pain due to response rate of only about 20%.59

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Transcranial Magnetic

In transcranial magnetic stimulation (TMS), electromagnetic coils held against the scalp influence underlying cortical firing. Studies have shown that repetitive TMS of the motor cortical area corresponding to the painful area may have some efficacy to induce long-lasting pain relief that could have therapeutic potential.60

11.4.2  Drug Delivery

Intraspinal Narcotics

Spinal narcotics can be administered intrathecally or epidurally for pain relief. In intrathecal drug delivery, the subarachnoid space is usually accessed from the lumbar region and medications are infused through a drug delivery system comprised of a pump and catheter. Prior to

implantation of an infusion pump, patients undergo an initial trail where medication is delivered through the catheter for a variable period of time depending on how long it takes to achieve an optimal dosage level. The pump is then implanted under the skin, usually in the abdomen, in a “pocket” between skin and muscle tissue.

Advantages over systemic narcotics include less medication requirement, less sedation and/or confusion, less constipation, and possibly less nausea and vomiting. Increasing doses are required with time due to the development of tolerance and/ or progression of disease.61 Complications include meningitis and respiratory failure (rare). CSF fistula and spinal headache may also occur and dislodgement/disconnection of the catheter tip may occur but can

usually be surgically corrected. Long-term use of intrathecal or epidural opioids may cause formation of catheter-associated granulomas, inflammatory masses at the tip of intrathecal catheters that can possibly lead to neurological deficit and/or catheter revision. Cancer pain is significantly improved in up to 90% and success rates for neuropathic pain range from 25 to 50%.

Currently, the only medications approved by the FDA for intrathecal administration are morphine, ziconotide, and baclofen.

11.4.3  Spinal Ablative Procedures

Fig. 11.6 demonstrates the central and peripheral nervous systems with the

Fig. 11.6  Illustration of the central and peripheral nervous systems with

potential lesional procedures segregated at each level of pain processing. DREZ, dorsal root entry zone. (Reproduced from Harbaugh R, Shaffrey C, Couldwell W et al, Neurosurgery Knowledge Update: A Comprehensive Review, 1st edition, ©2015, Thieme Publishers, New York.)

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various lesional procedures that will be discussed below.

Dorsal Root Entry Zone

DREZ lesions appear most effective in treating deafferentation pain from nerve root avulsion, spinal cord injuries, PHN, and postamputation phantom limb pain. During the procedure, the DREZ is identified under microscope and lesions are created ipsilateral to the avulsed nerve roots by radiofrequency current or selective incisions.

Sympathectomy

Surgical sympathectomy is indicated for a variety of conditions including essential hyperhidrosis, primary Raynaud disease, shoulder-hand syndrome, and intractable angina. The procedure may also be used to treat the symptoms of causalgia major. Lumbar sympathectomy is indicated for causalgia major of the lower extremity and preoperative lumbar sympathetic blocks may be utilized to evaluate the patient for response. Removal of the L2 and L3 sympathetic ganglion is usually adequate to remove sympathetic tone from the lower extremities.

Cordotomy

Cordotomy involves interruption of the lateral spinothalamic tract fibers in the spinal cord. This is the procedure of choice for unilateral pain below the C5 dermatome level in a terminally ill patient and may be performed open or percutaneously at the C1–C2 interspace. If any contralateral pain exists, it tends to be magnified following the procedure.

Bilateral cervical cordotomies carry the risk of a loss of automaticity of breathing (Ondine’s curse).

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A second procedure should be staged after normal respiratory function and CO2 responsiveness are verified following the first procedure if bilateral cordotomies are desired.

With percutaneous cordotomy, radio­ frequency current is used to lesion the lateral spinothalamic tract. In experienced hands, 94% will achieve significant pain relief at the time of discharge although this number drops to 60% at 1 year and 40% at 2 years. Complications include ataxia, bladder dysfunction, ipsilateral paresis, dysesthesia, sleep induced apnea, and death from respiratory failure.

Commissural Myelotomy

This procedure interrupts pain fibers crossing in the anterior commissure on their way to the lateral spinothalamic tract. Indications include bilateral or midline pain, primarily below the thoracic levels. About 60% of patients have complete pain relief, 28% have partial, and 8% have none. Complications include lower extremity weakness (8%), dysesthesias, bladder dysfunction, sexual dysfunction, and injury to the anterior spinal artery (rare).

11.4.4  Intracranial Ablative Procedures

Stereotactic Mesencephalotomy

This is used for unilateral head, neck, face, and/or upper extremity pain. MRI guidance is used to create a lesion 5 mm lateral to the Sylvian aqueduct at the level of the inferior colliculus. The main complication is diplopia due to interference with vertical eye movement (often transient).