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R



Radial Nerve



Keywords


Radial nerve, Saturday night palsy, Radial tunnel syndrome, Compressive neuropathy, Tinel sign, De Quervain’s tenosynovitis


Anatomy


The radial nerve is formed by axons from C5 to T1 roots and is branched off the lateral cord of the brachial plexus. Axons pass through several structures including the spiral groove of humerus, fibrous arch attachment of triceps to humerus, lateral intermuscular septum below deltoid insertion, and arcade of Frohse. Above the elbow, it branches off to innervate triceps, anconeus, brachioradialis, extensor carpi radialis longus/brevis, and posterior cutaneous nerves of the arm and forearm. At or below the elbow, branches are divided so that they come off either before or after the arcade of Frohse. Branches that come off the radial nerve before the arcade of Frohse include the superficial radial nerve, which supplies sensory innervation to dorsolateral hand and the first 31/2 digits, and the posterior interosseus nerve, which innervates the extensor carpi radialis brevis and supinator. Branches below the arcade of Frohse are the terminal motor branch of the posterior interosseus nerves, which innervate finger/thumb extensor, extensor carpi ulnaris, abductor pollicis longus, and articular branches to the wrist joint. Radial nerve injury is the least affected nerve among the three major nerves (median, ulnar, and radial) in the upper extremities. Radial nerve compression or injury may occur at any point along the anatomic course, ranging from proximally, involving brachial plexus, to distally, involving the radial aspect of the wrist, and may have varied causes (Table 110). The most frequent site of compression is in the proximal forearm in the area of the supinator muscle and involves the posterior interosseous branch.



Table 110




















Radial Nerve Lesion: Location Versus Etiology
Location of Lesion Etiology
Axilla Pressure palsy; often occurs in sedated patient
Upper arm Pressure,a fracture of humerus,b injection and neonatal
Posterior interosseus Radial fracture, soft tissue mass, laceration, supinator syndromec
Superficial radial Rupture, synovial effusion, compression, trauma, surgery, injection, and nerve tumor

a Pressure on medial arm compressing against humerus; often seen in sleep paralysis (Saturday night palsy), during anesthesia, and with tourniquet.


b Holstein-Lewis fracture, mid-third humerus fracture.


c Related to repetitive pronation-supination movement. Sometimes mistakenly referred to as “resistant tennis elbow.” Maximum tenderness located 4 to 5 cm distal to lateral epicondyle.


Syndromes



  1. I. Radial tunnel syndrome is characterized by pain over the anterolateral proximal forearm in the region of the radial neck. This syndrome often appears in individuals whose work requires repetitive elbow extension or forearm rotation. It is sometimes mistakenly referred to as “resistant tennis elbow.” The maximum tenderness is located 4 to 5 fingerbreadths distal to the lateral epicondyle, as compared with lateral epicondylitis (seen in tennis elbow), in which maximum tenderness is usually directly over the epicondyle. Symptoms are intensified by extending the elbow and pronating the forearm. In addition, resisted active supination and extension of the long finger cause pain. Weakness and numbness usually are not demonstrated.
  2. II. Posterior interosseous syndrome: The etiology of posterior interosseous nerve syndrome is similar to that of radial tunnel syndrome. Compression is thought to occur after takeoff of the branches to the radial wrist extensors and the sensory branches. After emerging from the supinator, the nerve may be compressed before it bifurcates into medial and lateral branches, causing a complete paralysis of the digital extensors and dorsoradial deviation of the wrist secondary to paralysis of the extensor carpi ulnaris. If compression occurs after the nerve bifurcates, selective paralysis of muscles occurs, depending on which branch is involved. Compression of the medial branch causes paralysis of the extensor carpi ulnaris, extensor digiti quinti, and extensor digitorum communis. Compression of the lateral branch causes paralysis of the abductor pollicis longus, extensor pollicis brevis, extensor pollicis longus, and extensor indicis proprius. Most commonly, entrapment occurs at the proximal edge of the supinator.
  3. III. Wartenberg syndrome: Patients with the diagnosis of Wartenberg syndrome complain of pain over the distal radial forearm associated with paresthesia over the dorsal radial hand. They frequently report symptom magnification with wrist movement or when tightly pinching the thumb and index digit. These individuals demonstrate a positive Tinel sign over the superficial radial sensory nerve and local tenderness. Hyperpronation of the forearm can cause a positive Tinel sign. A high percentage of these patients reveal physical examination findings consistent with De Quervain’s tenosynovitis.

Diagnosis


Plain x-ray can be obtained to rule out fracture, dislocation, bone tumor, and arthrosis. Magnetic resonance imaging (MRI) can be used to look for soft tissue lipoma, ganglioma, aneurysm, and synovitis. Electromyography (EMG) can also be really useful in determining the location, the timing (acute, subacute, or chronic), and the severity (demyelination or axon lost) of the nerve injury. However, EMG can be normal in the acute setting before Wallerian degeneration occurs, which usually takes about 3 to 7 days. High-resolution ultrasound evaluation of focal neuropathies may also be used in delineating nerve entrapment.


Treatment


A period of immobilization and anti-inflammatory medication may diminish swelling and improve symptoms. In addition, functional splints help prevent contracture and improve function as signs of nerve healing follow. Surgical approach, especially for radial tunnel syndrome, is highly controversial. However, surgical approach would be warranted if the nerve injury is caused by structure compression (i.e., bone tumor, lipoma).



Radiation injury



Keywords


Radiation injury, focal cerebral necrosis, acute encephalopathy, transient myelopathy, radiation-induced tumors, vasculopathy


Radiation injury to the nervous system occurs either as a result of treatment of CNS tumors, when nervous tissue falls into the field of treatment of another organ system or exposure to radiation accidentally, or in warfare. Radiation can damage the cerebral cortex, spinal cord, peripheral nerves, and cerebrovascular system and induce new tumors.


Cerebral injury



  1. I. Acute encephalopathy

    • Presentation and diagnosis: Occurs during the first few days of radiotherapy with headache, fever, nausea, depressed sensorium, and worsening of previous focal deficit. It is more frequent and severe in patients with large brain masses or those receiving daily dose fractions higher than 300 cGy of whole-brain irradiation. It is probably caused by an increase in preexisting cerebral edema but may not be apparent on neuroimaging.
    • Treatment: It responds well to increased doses of dexamethasone or pretreatment with corticosteroid 24 to 72 hours before radiotherapy in large or multiple brain tumors.

  2. II. Early delayed encephalopathy

    • Presentation and diagnosis: Occurs from a few weeks up to 12 to 18 months after irradiation presenting with headache, somnolence, nausea, irritability, fever, and transient papilledema. It usually resolves after several weeks to months. Early delayed encephalopathy occurs in 50% of children who receive prophylactic whole-brain irradiation for leukemia. It is more severe in children younger than 3 years old. Magnetic resonance imaging (MRI) shows worsening edema and contrast enhancement in up to one-third of patients with gliomas within a few months after fractionated radiation therapy, and in 5% to 20% of patients following stereotactic radiosurgery for brain metastases or meningioma.
    • Treatment: Corticosteroids may offer symptomatic relief and hasten recovery.

  3. III. Focal cerebral necrosis (radiation necrosis)

    • Presentation and diagnosis: This may develop several months to 10 years (peak onset of 15 to 18 months) after focal or whole-brain irradiation for brain tumors and head and neck cancers. It also occurs in patients who receive other forms of radiotherapy including brachytherapy, hyperfractionated radiation therapy, and stereotactic radiosurgery. Incidence is 3% to 10% after receiving 5000 cGy of daily fractionated radiation, 0% to 15% after stereotactic radiosurgery, and up to 50% of patients treated with interstitial brachytherapy. Patients usually present with a subacute space-occupying lesion. CT or MRI reveals edema and a patchy or ring-enhancing mass lesion. Positron emission tomography (PET), single photon emission computed tomography (SPECT), and several MRI techniques including MR spectroscopy, perfusion-sensitive MRI, and diffusion-weighted imaging may help to differentiate radiation necrosis from tumor recurrence and may be useful for identification of a “hot spot” for a stereotactic biopsy. Radiation necrosis occurs around the tumor and primarily involves the white matter, mostly sparing of cortex and deep gray structures, with demyelination, loss of oligodendrocytes, axonal injury, calcification, fibrillary gliosis, and mononuclear perivascular infiltrate. The most constant pathologic feature is fibrinoid vascular necrosis.
    • Treatment: Corticosteroids frequently provide improvement, albeit temporary. Hyperbaric oxygen treatment and high-dose vitamin E (2000 IU/day) may be of benefit in some cases. Surgical debulking of necrotic lesions may be necessary in some patients.

  4. IV. Diffuse cerebral injury

    • Presentation and diagnosis: This most frequent (2% to 19%) delayed effect of radiation therapy occurs in adults with primary brain tumors receiving 4000 to 6000 cGy of whole-brain irradiation and occurs in up to 50% of children with primary brain tumors following 2500 to 4000 cGy whole-brain radiation therapy. It becomes evident as moderate to severe cortical dysfunction, progressive dementia, and gait disturbance. Initial signs include memory, attentional, and visuospatial difficulties (especially in children younger than 4 or 5 years of age), ataxia, and focal motor deficits. Children with radiation therapy and concomitant methotrexate have higher risk of developing neurocognitive impairment. MRI may show enlarged ventricles, widening sulci, areas of calcification (especially basal ganglia), and diffuse hyperintense T2 signal abnormalities. Pathologic study shows multifocal white matter destruction, especially in the centrum semiovale and periventricular white matter, dystrophic calcification of the lenticular nuclei, and mineralizing microangiopathy.
    • Treatment: Methylphenidate, acetylcholinesterase inhibitors, and other psychostimulants have been used in both children and adults with attention or cognitive deficits from radiation treatment.

Spinal cord injury



  1. I. Transient myelopathy

    • Presentation and diagnosis: The most common radiation-induced spinal injury, usually occurring 1 to 30 months after radiotherapy, with peak at 4 to 6 months. It occurs in 10% to 15% of patients receiving mantle field radiation therapy for Hodgkin disease. Lhermitte sign (paresthesias radiating down the spine and limbs, precipitated by neck flexion) is often present, and myelopathic signs are usually absent. CT, MRI, and myelography results are normal.
    • Treatment: The syndrome resolves gradually over 1 to 9 months without risk of developing delayed, severe radiation myelopathy.

  2. II. Delayed progressive myelopathy

    • Presentation and diagnosis: This has a peak time of onset of 9 to 18 months after radiotherapy, with a frequency of 1% to 12%. Risk is correlated with the dose and schedule; risk is less than 5% with total doses of 4500 cGy in daily fractions of 180 cGy. Delayed progressive myelopathy usually begins with hypoesthesias or dysesthesias in lower extremities, then weakness and sphincter dysfunction. Pain is not a prominent symptom. The level of dysfunction ascends up to the area irradiated. Symptoms progress over weeks to months, with paraplegia or quadriplegia in approximately 50%. MRI may show focal or diffuse fusiform spinal cord enlargement with intrinsic cord signal abnormalities. Cerebrospinal fluid (CSF) may show high levels of protein or white blood cells. Pathologic study shows coalescing foci of demyelination, axonal degeneration, and fibrinoid vascular necrosis.
    • Treatment: Patients may show improvement or stabilization of symptoms spontaneously or following corticosteroids, hyperbaric oxygen, or warfarin.

  3. III. Motor neuron syndrome

    • Presentation and diagnosis: Beginning 4 to 14 months after radiotherapy, this rare lower motor neuron syndrome becomes evident as subacute, diffuse leg weakness, asymmetric atrophy, fasciculations, depressed deep tendon reflexes, and flexor plantar responses without sensory or sphincter involvement. Symptoms gradually progress over several months and then stabilize without improvement. Electromyography (EMG) shows diffuse denervation in affected limb and lumbar paraspinal muscles. CSF may be normal or have increase in protein. This syndrome may result from damage to lumbosacral anterior horn cells, motor axons, or nerve roots.
    • Treatment: Therapy is supportive.

Peripheral nerve damage


Radiation plexopathy of the brachial or lumbosacral plexi must be distinguished from recurrent tumor in neighboring structures such as breast or lung. Radiation plexopathy tends to produce less pain but more weakness than tumor invasion. Paresthesias and edema are common. EMG may show myokymic discharges. Contrast-enhanced CT, MRI, and PET often help in differentiating radiation plexopathy from other compressive lesions.


Cerebrovascular disease


Extracranial carotid disease, with transient ischemic attacks or strokes, may develop 6 months to 50 years (median, 10 to 20 years) after radiation therapy for head and neck cancers. Vascular studies show disease limited to the field of radiation, including such unusual sites as proximal common carotid artery and internal carotid artery distal to the common carotid bifurcation. Occlusive disease of the intracranial arteries may follow irradiation of optic gliomas, pituitary, or suprasellar tumors (2 to 20 years later; median, 5 years). The most frequent finding on arteriography is narrowing or occlusion of the supraclinoid internal carotid artery and proximal middle cerebral artery. Vasculopathy following radiation therapy in early childhood (usually for suprasellar tumors) frequently shows a “moyamoya” pattern. Radiation-induced stenosis is better treated with stenting than open surgery.


Radiation-induced tumors


In order of decreasing frequency, meningiomas, gliomas, and sarcomas may occur after radiation therapy. Meningiomas have a latency of 15 to 50 years (mean, 36 years) after irradiation, and gliomas may develop approximately 10 years after irradiation.



Radiculopathy



Keywords


Radiculopathy, cauda equina syndrome, conus medullaris syndrome


Radiculopathy is the result of any process that causes damage to or irritation of the nerve root. The spinal roots may be injured by compression (disk disease, spondylosis, hypertrophied ligaments, epidural abscess), trauma, or nondegenerative causes such as diabetes, vasculitis, tumor, infection (i.e., herpes zoster and Lyme disease), and demyelination. Cervical and lumbosacral regions are the two most commonly involved areas.


Clinical presentation


Radiculopathy presents as radicular pain. Radicular pain is characteristically lancinating, electrical, burning, abrupt, referred to a particular dermatome, and aggravated by maneuvers that stretch the dorsal nerve root, such as coughing or sneezing, or the Valsalva maneuver. There may be sensory changes and weakness in the affected dermatome and myotome, respectively. Exam findings comprise hypesthesia or anesthesia confined to the involved dermatome; due to overlap of cutaneous innervation, there may be little or no sensory loss on exam. Weakness may occur in the appropriate myotomal distribution. Fasciculations may be present. Hyporeflexia or areflexia are restricted to the muscles supplied by the involved root (Table 111). Straight leg raising sign and Spurling sign (limb pain or paresthesia following extension and rotation of the neck to the side of the pain) may be present in cases of lumbar and cervical radiculopathy, respectively. Crossed straight leg raising usually indicates a larger lesion. Improvement of the radicular symptoms with shoulder abduction may also be present in cervical radiculopathy (shoulder abduction relief test). Central lumbar lesions may result in cauda equina syndrome or conus lesion (Table 112).



Aug 12, 2020 | Posted by in NEUROLOGY | Comments Off on R
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