Brachial neuritis, also called neuralgic amyotrophy, has two major clinical symptoms, pain

and muscle weakness from atrophy. It is a multifocal, immune-mediated inflammatory

process that involves the peripheral nerves. Milner reports that up to 80% of patients have a
unilateral onset, and 60% involves the dominant side while only 20% had a bilateral
extremities onset. This activity describes the causes, pathophysiology, presentation, and
diagnosis of brachial neuritis and highlights the role of the interprofessional team in its
management.
Objectives:
 Review the causes of brachial neuritis.
 Describe the history and physical exam of a patient with brachial neuritis.
 Summarize the treatment options for brachial neuritis.
 Outline the importance of improving care coordination among interprofessional team
members to improve outcomes for patients affected by brachial neuritis.
Access free multiple choice questions on this topic.
Go to:

Introduction
Brachial neuritis, also called neuralgic amyotrophy, has two major clinical symptoms, pain
and muscle weakness from atrophy. It is a multifocal, immune-mediated inflammatory
process that involves the peripheral nerves. Milner reports that up to 80% of patients have a
unilateral onset, and 60% involve the dominant side, while only 20% had a bilateral
extremities onset.[1] Upper and middle trunks are more commonly involved. Most lesions are
axonal. However, those caused by demyelination usually carry a better prognosis. Motor
axons are mainly affected. As a result, nerves that carry mostly motor fibers are affected to a
larger degree and more commonly than mixed nerves and pure sensory nerves. Long thoracic,
suprascapular, axillary, musculocutaneous nerves, anterior and posterior interosseous nerves
are the most commonly affected according to a 2014 study by Ferrante et al. This condition
was first reported by Parsonage and Turner in 1948 in a case report, although some records
indicate its documentation in the late 19th century. 
Go to:

Etiology
Brachial neuritis could have a very wide range of etiologies. More common causes that have
been reported in the literature include infection, whether bacterial, parasitic, or viral;
Coxsackie B virus; mumps; variola major and minor; HIV; and parvovirus B19.[2]
Other conditions that predispose patients to developing brachial neuritis are exposure to
surgery, anesthesia, rheumatic diseases such as connective tissue disorders (i.e., Ehlers-
Danlos syndrome), systemic lupus erythematosus, temporal arteritis, and polyarteritis nodosa.
Trauma to the shoulder girdle and stressful exercise are other determining factors.
Additional sources include immunizations, including tetanus toxoid and antitoxin, diphtheria,
pertussis, tetanus (DPT) vaccine, smallpox, swine flu, pregnancy, and childbirth, radiation
therapy, lumbar puncture, pneumoencephalogram, radiologic contrast dye administration, and
allergy desensitization.
The majority of brachial neuritis cases are sporadic, however, there does exist a hereditary
form that is autosomal dominant which is called hereditary neuralgic amyotrophy aka HNA.
[3] Chromosome 17q24 has been linked to this disease. [3] The main feature for the
hereditary cause is that the affected patient will get recurrent attacks that are caused by the
same preceding events as the sporadic form. [3]
Go to:

Epidemiology
It mostly affects middle-aged males, although it can affect patients of both genders and all
age groups. According to a review study by Ferrante et al., 70% of patients were male with an
average age of 41.4 years. Milner described the condition in 2016 as rare, with an incidence
of 2 to 3 cases per 100,000 per year.[1]
Go to:

Pathophysiology
Although the pathophysiology of brachial neuritis is not exactly known, there are 2 theories
to explain the mechanism behind the development of this disease. The first one is that viral
illnesses, one of the most commonly reported cases, will directly affect the brachial plexus
thereby causing the symptoms.[2] The second one is that of an autoimmune cause where the
immune system will attack the virus or the antigen affecting the brachial plexus during the
process.[2]
For diseases with a vasculitic component such as polyarteritis nodosa, lupus, and temporal
arteritis a vascular cause is thought to be responsible for the onset of brachial neuritis.[2] 
For pain that is associated with brachial neuritis, ischemia caused by either a mechanical or
an inflammatory cause is thought to be related to the onset of sudden extreme pain [2] 
Go to:

Histopathology
Although the amount of data is sparse, there has been a report of brachial plexus biopsies
done in patients with sporadic brachial neuritis which shows mononuclear inflammatory
infiltrates.[3] 
Nerve biopsies that were done in postsurgical patients with brachial neuritis demonstrated
neovascularization, perineural thickening, and focal fiber loss suggesting ischemic changes
that point to possible immune pathogenesis [2]
Go to:

History and Physical

There are usually three phases in brachial neuritis. In phase 1, the patient will complain of
severe pain that is usually unilateral and is described as aching that is sudden in onset and
involves the lateral aspect of the shoulder as seen in axillary nerve involvement, scapular pain
in the suprascapular nerve, the superolateral thoracic wall in long thoracic nerve, antecubital
fossa in anterior interosseous nerve, and lateral arm or forearm in musculocutaneous
nerve. The pain usually is not positional and is worse at night, causing the patient to wake
from sleep. The average time between the trigger and the symptoms is 1 to 28 days; however,
66% of patients report the trigger within seven days. According to van Alfen et al., early
identification permits medical treatment that may repeal the severity of the clinical course.
The acute pain is self-limited and subsides after a few days to weeks. In general, the longer
the pain lasts the longer it will take for the patient to recover. In a typical course, after the
pain resolves, patients will enter phase 2 of the disease and will start to develop weakness
that is painless such as arm and shoulder girdle weakness. The forearm and hands can also be
involved but are much less common. Atrophy of the muscles also starts to occur but there is
usually a slow steady recovery of muscle function afterward following 6 to 18 months known
as phase 3 of the disease.[3]
On physical examination, typically 2 or more nerves will be involved. One unique
characteristic that can differentiate brachial plexus neuritis from other conditions is that in
brachial neuritis there is differential involvement of the different muscles that are innervated
by the same peripheral nerve (pathy paresis). Lower motor neuron signs can be appreciated
later on in the disease course on physical exam (hypotonia, areflexia, atrophy, and
fasciculations) mainly in the upper brachial plexus (C5,6,7). For weakness that occurs after
the acute pain phase, shoulder abduction and external rotation will be decreased signifying
involvement of the deltoids, supraspinatus, and infraspinatus muscles. When the long thoracic
nerve is involved you will get medial scapular winging due to involvement of the serratus
anterior muscle. Sensory changes can also be present in about 78% of patients consisting of
paresthesias and hypoesthesia over the lateral arm, deltoids, and radial forearm. Patients may
not notice sensory changes due to severe severe pain. 
Go to:

Evaluation
It is essential to diagnose brachial neuritis because it can mimic many other diagnoses, such
as rotator cuff, cervical cord compression, or nerve entrapment. If brachial neuritis is
mistaken for one of these conditions, the patient may undergo unnecessary surgery. Although
obtaining a good and thorough history and physical will usually be enough to diagnose
brachial neuritis, the use of imaging is helpful to support the diagnose of this condition as
well as ruling out other conditions. The use of an MRI of the shoulder with a special focus on
the brachial plexus should be used to rule out musculoskeletal disorders.[4] This must be
communicated to the radiologist when ordering the test. For acute stages, the MRI on T2 will
show signal hyperintensity(suggesting edema) within the affected muscles. For chronic
stages, the MRI on T1 will show intramuscular signal intensity(signifying fatty infiltration)
and atrophy of the affected muscles.
Other workups such as CBC and ESR will usually be normal while other labs such as LFTs
and ANA will be abnormal but are inconclusive. Other diagnostic modalities such as plain
radiographs and CSF analysis will usually be normal. Further workup includes tests for
Epstein Barr virus, Varicella-zoster, dengue, and Hepatitis E. Obtaining a detailed
history from the patient regarding recent surgery, childbirth, infection, tetanus vaccine,
influenza vaccine, and recently prescribed medications such as antivirals, antiepileptic, or
botulinum toxins is important as well.
Nerve conduction/EMG is also crucial in the evaluation of these patients. Electrophysiology
studies will show different findings depending on the time of the study and the underlying
pathology. For example, if demyelination is the main pathophysiology, then one will see a
conduction block, demyelination, or Wallerian degeneration that may occur in varying
combinations. Since brachial neuritis is an axonal disorder, nerve conduction velocities and
distal latencies are usually normal while there will be reduced amplitudes. In early findings
such as 3 to 4 weeks after symptoms, the EMG will usually show acute denervation with
fibrillation potentials as well as positive sharp waves for nerve roots and peripheral nerves. In
later stages (3-4 months after symptoms) the EMG will show chronic denervation and
polyphasic motor unit potentials with early reinnervation.  A 1996 study by Fibuch et
al. showed that 25% of patients had a recent viral illness before the symptoms of brachial
neuritis.[5] Ohta et al. found that when emergency situations present in rural areas where
there might not be an EMG or MRI machine, proper utilization of knowledge and skills such
as gathering accurate history, asking the questions mentioned above, and performing physical
examination can lead to the appropriate diagnosis. Newer technology using high-resolution
may be helpful as well in the diagnosis of brachial neuritis.[6] 
Go to:

Treatment / Management
There is no specific treatment for neuralgic amyotrophy; it is a self-limiting condition that
resolves on its own. Initially, the severe pain should be treated with analgesics, such as opioid
medications and/or NSAIDs. Although neuropathic pain medications, such as tricyclic or
antiepileptic agents would initially make sense, this is not recommended due to the fact that
these medications have a slow onset [3]. Since the acute pain phase is typically short in
duration, a relatively fast-acting analgesic is needed. Corticosteroids may also help in the
acute phase and have been shown to lead to a faster resolution of the acute pain but do not
overall influence the overall prognosis of brachial neuritis[3]. Immobilization of the affected
extremity is also important during the acute pain phase but afterward, strengthening and
stretching exercises are very important once the pain is under control. During the acute phase,
acupuncture and transcutaneous electrical nerve stimulation (TENS) can be tried. In patients
that have superimposed cervical degenerative joint disease where imaging is suggestive of
nerve root-level compression, a cervical epidural injection may be helpful to distinguish
between pain due to cervical radiculopathy and brachial neuritis. The patient should use the
affected extremity as soon as possible and consider a shoulder stabilizer with nonsurgical
management. Strengthening exercises are not recommended for completely denervated
muscles, and the role of electrical stimulation is controversial but should be considered when
the denervated state is for more than 4 months. As a follow-up, EMG could be done of the
involved muscles which can show the extent of reinnervation.[7] This bit of information can
help one assess which muscles can tolerate a higher level of strengthening and at what time in
treatment. For chronic patients, there is evidence that immunotherapy, such as IVIG, may be
used but this is still lacking data.[8]
Go to:

Differential Diagnosis
The wide list of possible conditions that brachial neuritis could resemble include diseases of
the musculoskeletal systems or other conditions such as cervical root lesion, mononeuritis
multiplex, multifocal motor neuropathy, tumors of brachial plexus, transverse myelitis,
amyotrophic lateral sclerosis, Herpes zoster, adhesive capsulitis, acute calcific tendinitis,
superior sulcus tumor, complex regional pain syndrome, myocardial infarction, and
pulmonary embolism.
Go to:
Prognosis
If pain control, corticosteroids, and an appropriate exercise plan with physical therapy
has been prescribed, Ferrante et al. reported 89% of patients recovered within three years,
75% within two years, and 36% within the first year. Recent studies show that many of these
patients will continue to have pain and some functional limitation, however, full recovery of
strength is possible and can take up to 8 years. As seen in the Van Alfen et al. study, per-
sistent pain was experienced by 30% of patients and functional limitations by 66% after a
mean of 2.5 years. [9]
Some factors associated with poorer prognosis are female gender, persistent pain as well as
lack of motor recovery by three months, lower trunk involvement (upper trunk involvement
has better prognosis), and hereditary cases (idiopathic cases have rare recurrence rate whereas
hereditary cases have much more common recurrence rates). 
Go to:

Complications
Although the majority of patients do recover from brachial neuritis, complications are not
uncommon. Because of the atrophy and weakness that is associated, patients can have the
positions of their joints shifted slightly such as in the shoulders, wrist, and hands. Because of
this, the risk of subluxation or impingement is higher. Adhesive capsulitis of the shoulder
could also result which will cause pain and a limited range of motion to the shoulders.
Patients with persistent residual pain and weakness can also have trouble doing everyday
tasks such as reaching or lifting objects or doing repetitive tasks with their shoulders and/or
arms. Patients who have repeat episodes of brachial neuritis, such as those who have the
hereditary form, are also at a higher risk of getting these complications. 
Go to:

Deterrence and Patient Education

For many patients, their symptoms will start to resolve in a few months but it is not
uncommon for it to take much longer. Patience is key. The best thing that one can do is to
adequately control their pain with medications prescribed by their doctors. After their pain
resolves, physical therapy will be crucial in addressing the weakness that will typically
present after the pain subsides. Although there is no guarantee in preventing brachial neuritis,
the best advice is to prevent shoulder or arm injuries since that can potentially predispose
them to the condition. Otherwise, there is not much else that one can do to prevent the
condition. 
As with other types of peripheral neuropathies, avoiding cigarettes and alcohol, eating a
healthy diet along with regular exercises can certainly help with this condition. 
Not surprisingly, this condition can cause a lot of anxiety and emotional stress. Patients are
encouraged to participate in relaxation techniques like yoga which can reduce their stress
levels. EMG follow-up studies can also be done since these tests can show early signs of
recovery before clinical signs of recovery thereby helping to relieve patient's anxieties[2].
Go to:

Enhancing Healthcare Team Outcomes

An interprofessional team manages brachial neuritis. The diagnosis is often difficult, and
delay in treatment is common. Besides the orthopedic and hand surgeon, other team members
may include a neurologist, physical therapist, pharmacist, pain specialist, and specialty
trained nurses in neurology and pain management. There are a variety of treatments for
brachial neuritis, but physical therapy is the first-line treatment. Pharmacists should evaluate
medications prescribed, drug-drug interactions, and patient compliance and communicate
with the team. Specialty trained nurses assist with the education of the patient and their
family and report issues to the team.
The outcomes of patients with brachial neuritis are guarded. No treatment works reliably, and
relapse is common. The disorder can affect the quality of life. Hence a mental health
consultation should be obtained. [10][11]
Go to:

Review Questions
 Access free multiple choice questions on this topic.
 Comment on this article.
Go to:

References
1.
Milner CS, Kannan K, Iyer VG, Thirkannad SM. Parsonage-Turner Syndrome:
Clinical and Epidemiological Features From a Hand Surgeon's Perspective. Hand (N
Y). 2016 Jun;11(2):227-31. [PMC free article] [PubMed]
2.
Feinberg JH, Radecki J. Parsonage-turner syndrome. HSS J. 2010 Sep;6(2):199-
205. [PMC free article] [PubMed]
3.
Gonzalez-Alegre P, Recober A, Kelkar P. Idiopathic brachial neuritis. Iowa Orthop
J. 2002;22:81-5. [PMC free article] [PubMed]
4.
Sneag DB, Rancy SK, Wolfe SW, Lee SC, Kalia V, Lee SK, Feinberg JH. Brachial
plexitis or neuritis? MRI features of lesion distribution in Parsonage-Turner
syndrome. Muscle Nerve. 2018 Sep;58(3):359-366. [PubMed]
5.
Fibuch EE, Mertz J, Geller B. Postoperative onset of idiopathic brachial
neuritis. Anesthesiology. 1996 Feb;84(2):455-8. [PubMed]
6.
Herraets IJT, Goedee HS, Telleman JA, van Asseldonk JH, Visser LH, van der Pol
WL, van den Berg LH. High-resolution ultrasound in patients with Wartenberg's
migrant sensory neuritis, a case-control study. Clin Neurophysiol. 2018
Jan;129(1):232-237. [PubMed]
7.
Feinberg JH, Nguyen ET, Boachie-Adjei K, Gribbin C, Lee SK, Daluiski A, Wolfe
SW. The electrodiagnostic natural history of parsonage-turner syndrome. Muscle
Nerve. 2017 Oct;56(4):737-743. [PubMed]
8.
Morishima R, Nagaoka U, Nagao M, Isozaki E. Chronic Brachial Plexus Neuritis
That Developed into Typical Neuralgic Amyotrophy and Positively Responded to
Immunotherapy. Intern Med. 2018 Apr 01;57(7):1021-1026. [PMC free article]
[PubMed]
9.
van Alfen N, van Engelen BG. The clinical spectrum of neuralgic amyotrophy in 246
cases. Brain. 2006 Feb;129(Pt 2):438-50. [PubMed]
10.
Calvo-Lobo C, Unda-Solano F, López-López D, Sanz-Corbalán I, Romero-Morales
C, Palomo-López P, Seco-Calvo J, Rodríguez-Sanz D. Is pharmacologic treatment
better than neural mobilization for cervicobrachial pain? A randomized clinical
trial. Int J Med Sci. 2018;15(5):456-465. [PMC free article] [PubMed]
11.
Clarke CJ, Torrance E, McIntosh J, Funk L. Neuralgic amyotrophy is not the most
common neurologic disorder of the shoulder: a 78-month prospective study of 60
neurologic shoulder patients in a specialist shoulder clinic. J Shoulder Elbow
Surg. 2016 Dec;25(12):1997-2004. [PubMed]