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Neurologic Adverse Events

Acute Disseminated Encephalomyelitis (ADEM)

Neurologic Adverse EventsADEM is an intense autoimmune disease that produces multiple inflammatory lesions in the brain and spinal cord that damages nerve fibers. ADEM occurs in fewer than 1 (0.8) per 100,000 people per year.

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Brighton Collaboration Case Definition (Level 1)

Focal or multifocal findings referable to the central nervous system, including one or more of the following:

-- Encephalopathy
-- Focal cortical signs (including but not limited to: aphasia, alexia, agraphia, cortical blindness)
-- Cranial nerve abnormality/abnormalities
-- Visual field defect/defects
-- Presence of primitive reflexes (Babinski's sign, glabellar reflex, snout/sucking reflex)
-- Motor weakness (either diffuse or focal)
-- Sensory abnormalities
-- Altered deep tendon reflexes (hypo- or hyperreflexia, asymmetry of reflexes)
-- Cerebellar dysfunction (including ataxia, dysmetria, cerebellar nystagmus)

Magnetic resonance imaging (MRI) findings displaying diffuse or multifocal white matter lesions on T2-weighted, diffusion-weighted (DWI), or fluid-attenuated inversion recovery (FLAIR) sequences (± gadolinium enhancement on T1 sequences). 


Acute disseminated encephalomyelitis (ADEM) is a monophasic inflammatory disease that often occurs after a viral infection or rarely after vaccinations. The inflammatory process causes an acute widespread multifocal demyelinating condition which can affect both the brain and the spinal cord. The proposed pathogenesis is that myelin autoantigens, such as myelin basic protein, share antigenic determinants with those of an infecting pathogen. Antiviral antibodies or a cell-mediated response to the pathogen cross reacts with the myelin autoantigens, resulting in ADEM.

The neurologic signs are variable, multifocal and depend upon the location of the CNS lesions. Motor deficits, impaired consciousness, cranial nerve abnormalities, including optic neuritis with vision impairment, gaze paresis, facial weakness, sensory deficits, and swallowing difficulties occurred frequently. Systemic symptoms like fever, malaise, myalgias, headache, nausea and vomiting can precede the neurological symptoms. Seizures may occur in the acute hemorrhagic form of ADEM. Optic neuritis is often bilateral and transverse myelitis is often complete.

Evidence of inflammation is commonly found in the cerebral spinal fluid. Lymphocytic pleocytosis (up to 1000/mm3) can be seen. Polymorphonuclear leucocytosis may be seen initially. Increased protein concentration is found in the majority of patients. Glucose content is usually normal. Rarely oligoclonal bands can be seen in patients with ADEM. However the CSF can also be normal in some patients. Therefore, neuroimaging is helpful to support the diagnosis of ADEM.

Both computed tomography scanning and magnetic resonance imaging have been widely used in patients suspected of having ADEM. MRI is generally regarded as the superior technique, because, as CT scans can be normal during the initial phase of the disease. Multiple patchy areas of increased signal intensity may be seen on conventional T2 weighted MRI images and fluid-attenuated inversion recovery sequence in the subcortical white matter. Lesions are typically bilateral but asymmetric and tend to be poorly marginated. Almost all patients have multiple characteristic lesions of demyelination in the deep and subcortical white matter. Grey matter, such as basal ganglia, thalami and brainstem may also be affected.

In the past, ADEM commonly followed such childhood infections as measles and chickenpox. However, ADEM in developed countries is now seen most frequently after non-specific viral illnesses. The viruses that have been associated with the disorder include rubella, influenza, Epstein-Barr, coxsackie, coronavirus, HIV, herpes simples, cytomegalovirus, and West Nile virus.

ADEM has a broad differential diagnosis. ADEM, multiple sclerosis, viral encephalitis and vasculitis share similar CSF profile, and similar MRI findings though not necessarily the same clinical course. ADEM tends to present with a more acute, widespread MRI lesions and typically all lesions are of the same age. Viral encephalitis, subcortical arteriosclerotic leukoencephalopathy, neuro-sarcoidosis, progressive multifocal leukoencephalopathy, HIV encephalitis, subacute sclerosing panencephalitis, mitochondrial encephalopathy, and leukodystrophies are also on the differential though the incidence is low.

The lumbar puncture is essential to the ADEM workup. Titers for various bacteria, viruses, or other agents can assist in distinguishing ADEM from various forms of infectious meningoencephalitis.

The immune profile is also helpful in distinguishing ADEM from MS. The IgG index or oligoclonal bands are positive in more than two thirds of all first clinically recognized MS bouts and in 90-98% of individuals who have experienced multiple MS bouts. One or more of these studies is positive in no more than 10% of ADEM cases.


Treatment of ADEM attempts to suppress a presumed aberrant immune response to an infectious agent or a vaccination and so ADEM is often treated with high-dose intravenous corticosteroids. One common protocol is 20 mg/kg/d of methylprednisolone (maximum dose of 1 g/d) for 3-5 days.

Approximately two thirds of the patients who are treated early with steroids have cessation of further progression of their symptoms, reduction in the duration of neurological symptoms, and a decrease in the severity of long term sequelae.

However, when steroids fail, intravenous immune globulin (IVIG) or plasmapheresis have been reported to improve symptoms and speed recovery. IVIG is believed to treat conditions associated with inflammation and immune dysregulation by neutralizing circulating myelin antibodies, by down-regulating proinflammatory cytokines, blocking Fc receptors on macrophages, suppressing inducer T and B cells and augmenting suppressor T cells, and by blocking the complement cascade. A total of 2 g/kg of IVIG for 2-3 days is recommended. IVIG may be preferable when meningoencephalitis cannot be excluded. IVIG is easier to administer and has fewer complications than plasma exchange. The cost and efficacy of the two treatments are comparable. There is no convincing evidence that treatment with the combination of intravenous corticosteroids and IVIG confers any advantage.

To reduce the risk of potential anaphylaxis, it is recommended to check serum IgA level before infusing IVIG. Infusions may increase risk of thromboembolic events, migraine attacks, aseptic meningitis (10%), urticaria, pruritus, or petechiae (2-30 days postinfusion). There is increased risk of renal tubular necrosis in elderly patients and in patients with diabetes, volume depletion, and preexisting kidney disease.

Case Example

20 year old white male was in his usual state of good health until the day prior to presentation, 2 weeks post-vaccination, when he noticed a bilateral, ascending, circumferential numbness in his lower extremities. His symptoms progressed within 24 hours to lower extremity muscle weakness causing difficulty with walking and standing and an inability to urinate. On physical exam there was decreased sensation to pin prick and light touch to the mid-chest, and lower extremity weakness (left > right and distal > proximal). Reflexes 3+/4 at the bicep, triceps and patella, 2+/4 at ankles with 3-4 beat clonus. Patient had sluggish pupils and absent corneal reflexes. There was no diplopia, loss of vision, dysphagia, or dysarthria. Within hours, the patient developed acute shortness of breath and was intubated. There were no recent upper respiratory tract infections, diarrhea, rashes, animal or insect bites.

MRI of brain, C-spine and T-spine showed multifocal diffuse T2 hyperintensity throughout brain and spinal cord. Cerebral spinal fluid had 27WBC, 40RBC, protein of 113, and glucose of 80. 

Transverse Myelitis

Acute transverse myelitis (ATM) is acute inflammation of gray and white matter across both sides of one or more adjacent spinal cord segments. Damage will affect function at that segment and segments below it. The cause of ATM is unknown.

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Brighton Collaboration Case Definition (Level 1)

-- Myelopathy (development of sensory, motor, or autonomic dysfunction attributable to the spinal cord, including upper- and/or lower-motor neuron weakness, sensory level, bowel and/or bladder dysfunction, erectile dysfunction).

-- Cerebrospinal fluid (CSF) pleocytosis (>5WBC/mm3 in patients >2 months of age).

-- Neuroimaging findings demonstrating acute inflammation (± meninges), or demyelination of the spinal cord of variable lesion length. No brain lesions.


Acute transverse myelitis (ATM) is acute inflammation of gray and white matter across both sides of one or more adjacent spinal cord segments. Damage will affect function at that segment and segments below it. The cause of ATM is unknown, but most evidence supports an autoimmune process. Approximately one third of patients with ATM report a febrile illness (flu-like illness with fever) in close temporal relationship to the onset of neurologic symptoms. Transverse myelitis may be a relatively uncommon manifestation of several autoimmune diseases including systemic lupus erythematosus, Sjogren's syndrome, and sarcoidosis. Myelitis has rarely been reported secondary to vaccinations. The spinal cord often may be the site of involvement of the first attack of multiple sclerosis. The symptoms and signs of ATM depend upon the level of the spinal cord involved and the extent of the involvement of the various long tracts. Symptoms include bilateral weakness, tingling, numbness of the feet and legs, and difficulty voiding that may develop over hours to a few days. The arms are involved in a minority of cases. Deficits may progress over several more days to a complete transverse sensorimotor myelopathy, causing paraplegia, loss of sensation below the lesion, urinary retention, and fecal incontinence. Almost all patients will develop leg weakness of varying degrees of severity. Sensation is diminished below the level of spinal cord involvement in the majority of patients. Because of the acuteness of the process, signs of spinal shock may be evident, in which the lower limbs will be flaccid and areflexic, rather than spastic and hyperreflexic as they should be in upper motor neuron paralysis. However, within several days, this spinal shock will disappear and signs of spasticity will become evident. Pain in the neck, back, or head, and/or pain in the distribution of a single spinal nerve may occur. Guillain-Barré syndrome can be distinguished because it does not localize to a specific spinal segment.

Incidence is estimated at approximately 0.1 to 0.5 per 100,000 persons with peaks between 10 and 19 years and 30 and 39 years of age.

Diagnosis often requires MRI, CSF analysis, and/or blood tests. The first concern of the physician who evaluates a patient with complaints and examination suggestive of a spinal cord disorder is to rule out a mass-occupying lesion that might be compressing the spinal cord. Potential lesions include tumor, herniated disc, stenosis, and abscess. Therefore, an MRI of the appropriate levels of the cord should be obtained urgently to evaluate for spinal cord compression. MRI examination of the brain is also commonly ordered to rule out acute disseminated encephalomyelitis or Multiple Sclerosis, both of which can present with ATM-like features. In ATM, the MRI typically shows inflammatory lesion(s) within the cord and/or cord swelling. Tests for treatable causes as directed by the H&P may include chest x-ray; PPD; a comprehensive metabolic screen, HbA1c, serologic tests for mycoplasma, Lyme disease, HIV, Herpes simplex virus-2, Cytomegalovirus, Epstein-Barr virus, Varicella-zoster virus, Human herpes viruses 6 and 7; vitamin B12 and folate levels; ESR; tests for SLE and Sjogren's syndrome, Hgb A1c, thyroid profile, urine heavy metals, and CSF and blood for syphilis. A specific antibody marker for neuromyelitis optica (NMO-IgG), which distinguishes neuromyelitis optica from multiple sclerosis, is available. Cerebral spinal fluid usually contains monocytes, protein content is slightly increased, and IgG index is elevated (normal, ≤ 0.85). CSF cultures, immunoglobulin level, and protein electrophoresis may also be indicated.

Generally, the more rapid the progression is, the worse the prognosis. About 1/3 of patients recover, 1/3 retain some weakness and urinary urgency, and 1/3 are bedridden and incontinent. Multiple sclerosis eventually develops in about 10 to 20% of the patients. Recovery generally begins within 1 to 3 months and may continue for up to 2 years. Most patients with ATM show good to fair recovery. While a small percentage of patients may suffer a recurrence, other diagnoses such as MS, SLE, or antiphospholipid syndrome should be sought should symptoms recur.


Treatment is directed at the cause or associated disorder, but is otherwise symptomatic and supportive. High-dose intravenous methylprednisolone and/or immunoglobulin, sometimes followed by plasma exchange have been used because the cause may be autoimmune. However, efficacy of such a regimen is uncertain. Following initial therapy, the most critical part of the treatment for this disorder consists of keeping the patient's body functioning while awaiting either complete or partial recovery of the nervous system.

Case Example

A 19 y/o white male healthy basic trainee received multiple routine vaccinations. He recalled no preceding illness and no immediate adverse local or systemic reactions. He denied fever, chills, myalgia, rash, pulmonary or GI symptoms, back trauma, or known exposure to infectious disease. Approximately four weeks following his vaccinations, the patient noted the onset of mid-back pain and parethesia of his toes bilaterally. Examination at the time showed no motor dysfunction. Straight leg raises and DTR were normal and symmetrical. Over the next day, his parethesia w/o numbness progressed to involve his lower legs and thighs. Walking became difficult with perceived weakness in his knees. Within two days he was unable to move his legs. Evaluation noted UE strength to be 5/5, while RLE strength was 2- proximally and 2/5 distally and 3- on the left. There was decreased sensation to all modalities in the legs. Reflexes were 2+ in the UEs and 3+ in the LEs. Creatine Kinase was elevated at 565 (57-374). CSF: Glu 69, Protein 44, (15-45), Myelin Basic Protein 353 (0.07-4.1). There was also documented mild bowel and bladder dysfunction. MRI of brain was normal, but C-Spine showed an abnormal signal from C7 to at least T2.


Transverse Myelitis, National Institute for Neurologic Disorders and Stroke (NIH)

Jacob A, Weinshenker B, An Approach to the Diagnosis of Acute Transverse Myelitis, Semin Neurol 2008;28:105-120

Guillain-Barré Syndrome (GBS)

GBS is a rare disorder in which the body's immune system attacks the nerves to the legs and arms. GBS occurs in about 1 or 2 people per 100,000. It usually presents as a weakness in the legs that spreads upwards to the arms, chest, and the face. Guillain-Barré is one of the leading causes of non-trauma-induced paralysis.

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Brighton Collaboration Case Definition (Level 1)

-- Acute onset of bilateral and relatively symmetric flaccid weakness/paralysis of the limbs with or without involvement of respiratory or cranial nerve-innervated muscles.

-- Decreased or absent deep tendon reflexes at least in affected limbs.

-- Monophasic illness pattern, with weakness nadir reached between 12 hours and 28 days, followed by clinical plateau and subsequent improvement, or death

-- Cerebrospinal fluid (CSF) with a total white cell count <50 cells/mm3 (with or without CSF protein elevation above laboratory normal value)

-- Electrophysiologic (NCS/EMG) findings consistent with GBS


Guillain-Barré syndrome (GBS) is an acute polyneuropathy often triggered by inflammatory and probably autoimmune mechanisms. The illness is typically characterized by the subacute onset of progressive, symmetrical distal paralysis and lower limb weakness. Weakness may progress to upper limbs and there is often pain in the long lower limb and dorsal region muscles. There are decreased or absent deep tendon reflexes in affected limbs. Sensory abnormalities, involvement of cranial nerves, and paralysis of respiratory muscles also can occur. GBS may as well cause dysphagia and autonomic nervous system dysfunction resulting in tachycardia, and arrhythmias. When severe, the patient is almost totally paralyzed, and GBS can interfere with breathing and, at times, with blood pressure or heart rate. In these cases the disorder is life threatening and is considered a medical emergency. Most patients, however, recover from even the most severe forms of Guillain-Barré syndrome, although some continue to have a certain degree of weakness. Both sexes are equally prone to Guillain-Barré syndrome and its variants. It can strike all ages, but with peaks in young adulthood (15-35 yrs) and in elderly persons (50-75 yrs). While the syndrome is rare, afflicting between 1and 3 persons in 100,000, GBS is the most common cause of acute flaccid paralysis in the United States. In about 2/3 of cases, Guillain-Barré is preceded by a few days or weeks (up to two months) by symptoms of a respiratory or gastrointestinal viral infection. Infectious agents related to GBS include cytomegalovirus, Epstein-Barr virus, Campylobacter jejuni, Mycoplasma pneumoniae and Haemophilus influenzae. An increased risk of GBS may be also related to vaccination, but with presently used vaccines this increase remains below one case of GBS per one hundred thousand doses for most populations. Despite its association with the 1976 Swine Influenza vaccine, there is evidence that, in general, influenza vaccination decreases the risk of acquiring Guillain-Barré syndrome.

After the first clinical manifestations of the disease, the symptoms can progress over the course of hours, days, or weeks. Untreated, the illness has a mean time to the nadir of clinical function of 12 days with 98% of patients reaching a nadir by 4 weeks. A plateau phase of persistent, unchanging symptoms then ensues followed days later by gradual symptom improvement. Most patients (up to 85%) with GBS achieve a full and functional recovery within 6-12 months. Recovery is maximal by 18 months after onset. Patients may have persistent weakness, areflexia, imbalance, or sensory loss. The reported incidence of some form of permanent neurologic sequelae ranges between 10% and 40%. Approximately 7-15% of patients have permanent bilateral foot-drop, intrinsic hand muscle wasting, sensory ataxia, and dysesthesia. Recent studies report that patients with Guillain-Barré syndrome may exhibit long-term differences in pain intensity, fatigability, and functional impairment compared with healthy controls.

Despite intensive care in tertiary care centers with a team of medical professionals who are familiar with GBS management, there may be up to a 20% incidence of prolonged morbidity and an approximately 8% mortality. Most cases of mortality are due to adult respiratory distress syndrome, sepsis, pneumonia, pulmonary emboli, cardiac arrest, or severe autonomic instability.


Only intravenous immune serum globulin (IVIG) and plasma exchange (PE) therapy have proven effective for Guillain-Barré syndrome. Both therapies have been shown to shorten recovery time by as much as 50%. IVIG is easier to administer and has fewer complications than plasma exchange. The cost and efficacy of the two treatments are comparable.

Randomized trials in severe disease show that IVIG started within 4 weeks from onset hastens recovery as much as plasma exchange. Combining plasma exchange and IVIG neither improved outcomes nor shortened the duration of illness. Additionally, IVIG is the preferential treatment in hemodynamically unstable patients and in those unable to ambulate independently.

Corticosteroids are ineffective as monotherapy. Limited evidence shows that oral corticosteroids significantly slow recovery from GBS. Substantial evidence shows that intravenous methylprednisolone alone does not produce significant benefit or harm. In combination with IVIG, intravenous methylprednisolone may hasten recovery but does not significantly affect the long-term outcome. The dose of IVIG is 2gm/kg infused over 3 days.

To reduce the risk of potential anaphylaxis, it is recommended to check serum IgA level before infusing IVIG. Infusions may increase risk of thromboembolic events, migraine attacks, aseptic meningitis (10%), urticaria, pruritus, or petechiae (2-30 days postinfusion). There is increased risk of renal tubular necrosis in elderly patients and in patients with diabetes, volume depletion, and preexisting kidney disease.

Case Example

An 18-year-old white male with no chronic medical problems, 7 days post vaccination, noted numbness of his toes bilaterally. One week later, both feet felt numb. Three days later, his legs felt numb. He went to the Military Treatment Facility for evaluation and was told his extremity numbness was due to his boots. Three days later, he developed tingling of both his legs that was associated with painful cramps in the calves and tingling of his fingertips. The pain in the calves was at a level of 7/10 and worsened with walking and improved with rest. He could not walk up stairs. He also noticed difficulty getting on and off his bunk due to weakness in the arms.

He again presented to sick call for evaluation for his numbness of the feet and upper extremity weakness and tingling of the finger tips. He denied headache, nausea /vomiting, abdominal pain or generalized weakness. He denied fever, chills, and insect bites, and had no history of STDs. On physical exam his sensory exam was abnormal, motor strength was reduced (3/5 w/ SLR, 3/5 heel to shin, unable to toe raise), gait and stance were abnormal, and the deep tendon reflexes were absent or diminished. His EMG/NCV showed "electrophysiologic evidence of generalized sensorimotor polyradiculopathy with mixed axonal and acquired demyelinating features."

Cerebral spinal fluid was clear. Protein was elevated at 179.0 (12-60). There were 3 (0-8) WBCs and 2 (0) RBCs noted.

Brachial Plexus Neuritis

Acute brachial plexus neuritis is an uncommon inflammatory condition of the nerves in the shoulder that leads to severe shoulder and upper arm pain followed by marked upper arm weakness. Brachial neuritis occurs in about 1 to 2 cases per 100,000 persons, but this figure is probably low because many cases may be misdiagnosed, or the symptoms are mild and clinically unrecognized.

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Acute brachial plexus neuritis, neuralgia amyotrophy, or Parsonage Turner syndrome, is a clinically defined syndrome that consists of sudden severe, acute, sharp, throbbing, or burning pain in the shoulder girdle and upper arm with no apparent cause. The pain usually is constant, but it is exacerbated by movements of the shoulder. Movements of the neck, coughing, and/or sneezing usually do not worsen the pain. After days or weeks, the pain subsides, to be followed by weakness (within about 2 weeks of onset) and even muscle wasting in the upper arm. The weakness is usually maximal at onset but can progress over 1 or more weeks. Numbness may occur, depending on the particular nerves affected, and usually is found in the nerve distribution corresponding to maximal muscle weakness. However, numbness is rarely a prominent complaint.

The pathophysiology of brachial neuritis is unknown, but the condition is generally thought to be an immune-mediated inflammatory reaction against nerve fibers of the brachial plexus. Studies have suggested that various infections (viral [particularly of the upper respiratory tract] or less commonly, bacterial [pneumonia, diphtheria, typhoid]) precede the onset of acute brachial plexus neuritis in as many as 25% of cases. Up to 15% of cases have been reported to occur following vaccinations. Other possible causal factors such as surgery, trauma (not related to the shoulder), childbirth, medical investigative procedures (lumbar puncture, radiologic dye), and systemic illness (e.g., polyarteritis nodosa, lymphoma, systemic lupus erythematosus, temporal arteritis, Ehlers-Danlos syndrome) have been less commonly implicated. In 30-85% of the cases, a suspected precipitating factor can be found 3-14 days before the initial onset of the pain.

The disorder is often mistaken for other disorders affecting the shoulder region, including cervical radiculopathy, adhesive capsulitis, shoulder arthritis, calcifying tendonitis, or other rotator cuff problems, or Herpes Zoster. Disorders causing muscle wasting or weakness, especially nerve root compression, spinal cord or brachial plexus tumors, anterior poliomyelitis or amyotrophic lateral sclerosis should also be considered in the differential diagnosis.

Evaluation with electrodiagnostic and radiographic studies is useful in confirming the diagnosis and excluding alternative disorders. MRI of the clinically weak muscles may reveal high signal intensity of the affected muscles on the T2 study. These changes may appear within days following the onset of symptoms and persist for months. An MRI scan of the plexus and muscles of the shoulder girdle or upper arm is seldom required to establish a diagnosis, but it may be useful if an early, specific diagnosis would be beneficial. A cervical spine MRI can aid in the diagnosis of suspected cervical radiculopathy.

Electromyographic testing in patients with acute brachial plexus neuritis yields variable data, depending on the severity of neural damage and the timing of the examination.

Most cases of acute brachial plexus neuritis occur between 20 and 60 years of age. The male-to-female ratio ranges from 2:1 to >10:1. The incidence has been estimated as 1-2 cases per 100,000 persons, but this figure is probably low as many cases are misdiagnosed, or the symptoms are mild and clinically unrecognized.

The usual abnormality on physical examination is a brachial plexus lesion, as indicated by involvement of two or more nerves. Weakness commonly occurs in the supraspinatus, infraspinatus, deltoid and/or the biceps muscles.

Brachial plexus neuritis following immunization against smallpox, tetanus toxoid, diphtheria, tetanus and pertussis (DTP), influenza, and hepatitis B have been reported. The exact etiology of post-vaccination brachial plexus neuritis is unknown. Direct injury to the nerve is unlikely because often the not-injected limb can be involved. Moreover, an injection in the deltoid muscle can lead to an axillary nerve injury, but, in many cases larger parts of the brachial plexus are involved.

The course of the neuritis is usually one of gradual improvement and recovery of muscle strength in 3 to 4 months. Some patients, however, experience several years of muscle weakness or a slight permanent weakness. In general, 80% of patients with brachial neuritis recover functionally within 2 years; 90% recover functionally within 3 years. 


Brachial neuropathy is treated conservatively and largely symptomatically. While the pain is present, pain relievers (analgesics) should be freely given. The pain may be severe enough for chronic (weeks of) narcotic therapy. A short course of high-dose oral steroids is often recommended, however immunosuppressive therapy (e.g., steroids, immunoglobulin, plasma exchange) has not been shown to be beneficial.

Physical therapy for 3 to 8 weeks should be focused on the maintenance of full range of motion in the shoulder and other affected joints. Passive and active range of motion exercises should begin as soon as the patient's pain has been adequately controlled; these should be followed by regional conditioning of the affected areas. Strengthening of the rotator cuff muscles and scapular stabilization may be indicated. Passive modalities (eg, heat, cold, transcutaneous electrical nerve stimulation) may be useful as adjunct pain relievers.

Profound weakness in the shoulder muscles may require the use of a sling; however, unless absolutely necessary, it is generally advised to avoid constantly supporting the arm in a sling because of the risk of complicating recovery by the development of adhesive capsulitis ("frozen shoulder").

Although neither direct trauma nor localized inflammation due to IM or SQ vaccine injection is thought causative of brachial plexitis, it is empirically recommended that, if possible, subsequent vaccinations not be given in the affected arm. 

Case Example

30 y/o white male received a vaccination in his left deltoid. He was asymptomatic until about 17 days later he experienced left shoulder pain (2/10) with no decrease in his range of motion (ROM), no decrease in sensation, no paresthesias, and no weakness. Over the next 10 days the pain progressed to a steady 4/10 pain. Within a few days, he had difficulty lifting objects, but noted no decrease in the ROM. However, on examination about 1 month post-vaccination, his pain was 6/10, he noted decreased ROM, and there was left shoulder scapular winging. On exam, there was marked asymmetry with atrophy of left traps, marked drooping of left shoulder, and weak and asymmetric shoulder shrug on left. He was able to abduct to about 90 degrees, but with scapular stabilization, he was able to abduct to about 130 degrees. He reported occasional brief paresthesias in his 4th and 5th digits, but otherwise denied lasting paresthesias or numbness. He denied any preceding infectious illness.

His EMG revealed abnormalities of the trapezius muscle, though clinically, serratus anterior is also involved which is innervated by the long thoracic nerve of brachial plexus origin. MRI of his cervical spine was essentially normal.

He was treated symptomatically with Neurontin tid and Vicodin prn. Three months after onset of symptoms, constant dull pain persisted in left trapezius and scapula regions. This pain intermittently increased to 3 or 4/10 (about 10 times per day) which lasted from 5 minutes to 3 hours. The patient required narcotics 1-2 nights per week for difficulty with sleeping due to pain. At 8 months after onset of symptoms, he was about 50 percent better and continues to improve. 


Debeer P, et al., Brachial plexus neuritis following HPV vaccination, Vaccine (2008) Am Fam Physician 2000;62:2067-72

Last Updated: August 26, 2022
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