Acute Nervous System Related Pain
Madelyn K. Craig
Gopal Kodumudi
Devin S. Reed
William C. Bidwell
Alan David Kaye
Introduction
Acute nervous system pain can be broadly divided into central nervous system pain and peripheral nervous system acute pain. Central nervous system acute pain can be further divided into central nervous system pain caused by primary and secondary etiologies. The peripheral nervous system acute pain classification is more dependent on the etiologies of acute pain in the peripheral nervous system.
In this chapter, we review the diverse etiologies and treatments of acute nervous system related pain. In this chapter, we discuss primary and secondary causes of central nervous system pain, the wide variety of etiologies of pain, and pain caused by pathology of the peripheral nervous system. Clinical features and treatments are reviewed for both central and peripheral nervous system acute pain.
Central Nervous System Related Acute Pain
Headaches are a common medical complaint; it is estimated that up to one in seven Americans are diagnosed with migraines.1 Migraine, cluster, and tension-type headaches are the most commonly experienced primary central nervous system acute pain.
Migraine headache can be moderate to severe intensity, is usually unilateral, and is often associated with sensitivity to light and sound. Migraine without aura headache usually lasts for 3-72 hours while migraine with aura typically lasts minutes with unilateral, sensory visual, language, and speech symptoms systems, followed by headache and migraine symptoms. Chronic migraine lasts for more than 15 days in a month for more than 3 months, with features of migraine on a minimum of 8 days in a month.
Cluster Headaches
Cluster headaches are a form of primary headaches that are rare but severe. The headache is unilateral with at least one autonomic ipsilateral symptom. The headaches occur daily for weeks to months with remission periods extending to months and years. The headache can occur several times a day or every other day. A link between pain attack and vasodilatation in cluster headache seems to exist.
Tension-Type Headache
Tension-type headache, also called as muscle contraction headache, is usually bilateral, does not worsen, can last for minutes or weeks, and describes as of a tightening or pressing quality. Photophobia may be present, but nausea or vomiting are typically not seen.
TABLE 17.1 FEATURES OF DIFFERENT TYPES OF HEADACHES | ||||||||||||||||||||||||
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Acute primary headaches can be distinguished by several factors; in Table 17.1, features of each of these primary headaches are explained including location, characteristics, duration, and associated symptoms.
Treatments
Migraine and Tension Type
Nonsteroidal anti-inflammatory drugs (NSAIDs) and acetaminophen have long been the treatment of choice for migraines and tension-type headaches but there are other treatment options available including, triptans, antiemetics, dihydroergotamine, and peripheral nerve blocks. Newer treatments include neuromodulation, calcitonin gene-related peptide (CGRP) antagonists, and lasmiditan. Table 17.2 shows the level of evidence for various pharmacologic treatments. It should be noted that opioids are generally avoided.
Selecting a treatment should be determined by onset, progression, side effects, and duration. A large number of migraines occur in the morning with progression during sleep and are hard to treat by the time they are diagnosed so consider aggressive treatment. Non-oral treatment should be considered for rapidly progressing headaches, long-duration headaches, or headaches associated with nausea and vomiting. Often, the same patient may have variability in their attacks.2 A stepwise approach is not recommended for initiation of therapy, rather stratified care showed better outcomes.
TABLE 17.2 LEVEL OF EVIDENCE FOR VARIOUS PHARMACOLOGIC TREATMENTS | |||||||||||||||||||||||||||||||||||||||||||||
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A nonpharmacologic approach to treatment may be chosen for patients with a poor response, a contraindication to pharmacologic treatment, or because the patient requests an alternate treatment. These options include neuromodulation and peripheral nerve blocks.
External trigeminal neurostimulation/transcutaneous supraorbital neurostimulation stimulates the supraorbital and supratrochlear nerves, and in the acute setting, is used for 60 minutes to alleviate pain. Migraine prevention requires 20 minutes of stimulation nightly. Single pulse transcranial stimulation uses magnetic pulses to the occiput. These pulses may stop spreading depolarizations and inhibit thalamocortical pain pathways. The magnet is pulsed several times for acute pain relief and 4 pulses twice daily as preventative with a max of 17 pulses per day. Vagal nerve stimulation uses a handheld device that inhibits vagal afferents. This inhibits cortical spreading depolarization and thalamocortical pathways. Two cycles of 2 minutes each are used repeated again 15 minutes later if pain persists.3 It should be noted that data for neuromodulation were drawn from small randomized controlled trials, and while neuromodulation is FDA approved for migraines, it does meet the same standards as pharmacologic treatments.
Peripheral nerve blocks that are used for migraine treatment include occipital and sphenopalatine ganglion blocks. The occipital nerve block can be achieved by injecting 5 mL of 0.5% bupivacaine or ropivacaine near the greater and lesser occipital nerve. The sphenopalatine ganglion block is performed by using cotton-tipped pledgets that are soaked in 4% lidocaine. These pledgets are inserted along the superior border of the middle turbinate until it reaches the mucosa.4
Some newer therapies include lasmiditan and CGRP antagonists. Lasmiditan is a selective serotonin 1F receptor agonist. It was FDA approved in 2019 for the acute treatment of migraines. Initial dosing of 50 mg is recommended. On subsequent attacks, dose may be increased to 100-200 mg with no more than 1 dose in 24 hours. Lasmiditan does have many adverse effects including dizziness, fatigue, and nausea.5 CGRP antagonists (ubrogepant and rimegepant) modulate trigeminovascular pain. Rimegepant is given as a single 75 mg/d dose, and ubrogepant is 50-100 mg with a maximum dose of 200 mg/d.6
Cluster headaches are typically unilateral, escalate rapidly, and are associated with autonomic symptoms as outline in Table 17.1. Treatment of cluster headaches begins with oxygen and a triptan (if intranasal, then administered contralateral to headache) as early as possible. Treatment can vary widely and can include many of the therapies for migraines as it is based mainly on empirical data.
Secondary Headache
Any headache with an underlying condition as the cause is termed as secondary headache. The treatment of any secondary headache is aimed primarily at treating the underlying cause.
The most common presenting symptom of giant cell arteritis is headache. It is treated by decreasing the vascular inflammation with prednisone usually 40-60 mg/d (or equivalent steroid) for 2-4 weeks followed by reducing the dose by 10 mg every 2 weeks to 20 mg, then by 2.5 mg every 2-4 weeks to 10 mg, then by 1 mg every 1-2 months if no relapse has occurred.7
Headaches secondary to a space-occupying lesion usually resolve with resection or resolution of the lesion and are usually due to vasogenic, intracellular, osmotic edema, or less commonly a mass effect. Strategies to control edema include osmotic therapy (mannitol), diuretics, glucocorticoids, hypothermia, hyperventilation, fluid restriction, and elevation of the head of the bed. Dexamethasone is the preferred steroid with 4-6 mg every 6-8 hours being the most common dose. If headaches still persist, then conventional headache treatments may be used including opioids.8
Subarachnoid hemorrhage usually presents with a sudden and severe headache and often is described as the worst headache of the patient’s life. Pain control of the headache is usually achieved with a short-acting opioid such as morphine. Other conventional therapies can be
used; however, aspirin is usually avoided until after the aneurysm is secured. Nimodipine 60 mg every 4 hours is used to treat vasospasm. The mechanism of benefit is unknown but has shown improved outcomes.9
used; however, aspirin is usually avoided until after the aneurysm is secured. Nimodipine 60 mg every 4 hours is used to treat vasospasm. The mechanism of benefit is unknown but has shown improved outcomes.9
Idiopathic intracranial hypertension typically displays a pattern of progressive headaches that are severe, are poorly defined, and often are associated with horizontal diplopia. It is seen mainly in young obese females. Treatment consists of weight loss, carbonic anhydrase inhibitors, and topiramate. Serial lumbar punctures can relieve headache and are an option during avoidance of medical therapy or pregnancy but are generally not recommended. Conventional migraine headache treatment is used if above treatments are ineffective.10
Headache related to central nervous system infection is treated primarily by controlling infection. Conventional migraine treatment may be used as support. Headache related to central venous thrombosis is estimated to require bed rest of hospital admission in 14% of patients with central venous thrombosis.11 For patients with elevated intracranial pressure, acute treatment to control intracranial pressure is similar to the treatment outlined in the section on subarachnoid hemorrhage. Severe headache treatment can include topiramate, therapeutic lumbar puncture or even lumboperitoneal shunt.12
Withdrawal headaches can occur from the overuse of many medications but most commonly analgesics. This overuse can be due to treatment of headaches or other therapy. The treatment is rapid withdrawal of the overused medication. The exception to this is with the use of barbiturates, benzodiazepines, opioids, and any medication with a contraindication to sudden discontinuation. These medications must be tapered off. Bridge/withdrawal therapy is usually provided and includes many of the conventional migraine treatment. Choice of bridge therapy must be determined based on the medication to be discontinued usually to avoid the same class of medication.12
Causes of Acute Peripheral Neuropathy
The causes of acute peripheral neuropathy include inflammatory: hereditary, infectious, metabolic, infectious, traumatic, and toxic.
Acute Diabetic Peripheral Neuropathy
Painful diabetic peripheral neuropathy is a common painful neuropathy.13 Painful diabetic neuropathy can be seen in about 90% of patients with both type I and type II diabetes.14 Foot ulceration, nephropathy, and retinopathy are often associated with painful diabetic neuropathy.15 The acute painful neuropathy is mainly by exclusion, and treatment involves tight glycemic control prophylactically and also by medications for pain. These medications include first-line anticonvulsant treatment with gabapentin or pregabalin and antidepressants such as duloxetine and venlafaxine, which prevent the uptake of noradrenaline and serotonin. Opioids have also been used to treat painful diabetic neuropathy with some clinical evidence.16
Medication such as topical medication such as the lidocaine patch and capsaicin has also been used and has reported efficacy data. The pathophysiological mechanisms for painful diabetic neuropathy or diabetic neuropathic pain are not completely understood. A relationship with hyperglycemia has been noted.17
Presence of allodynia or pain to touch suggests that central nervous system can also be affected by DPN. Painful allodynia, mood changes, and depression can cause decreased quality of life and make the management of this condition even more challenging.14
Herpes Zoster, Postherpetic Neuralgia Acute Peripheral Neuropathy
Acute pain related to nerve involvement can occur in herpes zoster and in postherpetic neuralgia. Herpes zoster occurs annually in about one million persons in the United States with 10%-15% developing postherpetic neuralgia. There is a lifetime prevalence of one in three people getting shingles and that is why getting a vaccine is so important to minimize the likelihood of having this painful disease. Herpes zoster is more common in patients who are immunocompromised from diseases such as leukemia, Hodgkin disease, systemic lupus erythematosus, rheumatoid arthritis, and organ transplants.18
Primary sensory neurons are affected by the varicella-zoster infection. They have ectopic pacemaker sites, which are hyper excitable. These ectopic hyper excitable sites can cause pain in both herpes zoster and in postherpetic neuralgia. The central nervous system can exacerbate the peripheral input that is maintained by ectopic activity.19 Herpes zoster is a reactivation of the virus causing the infection with varicella-zoster. A complication of herpes zoster infection is postherpetic neuralgia (10%-15% incidence, eg, 100 000-150 000 new cases in the United States per year). Treatment with analgesics and antiviral drugs within first 72 hours is helpful to decease the severity and complications in both herpes zoster and postherpetic neuralgia.19
Medications for treatment of pain in herpes zoster and postherpetic neuralgia include anticonvulsant medications such as gabapentin and pregabalin; tricyclic antidepressants topical analgesics such as capsaicin, tramadol, and opioids; and oral analgesics.20 Postherpetic neuralgia occurs because of reactivation of latent varicella-zoster. There are now extended-release formulations of gabapentin (eg, Gralise) and pregabalin, which reduce the likelihood of sedation and dizziness.
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