1. No category

Parsonage-Turner syndrome
Author: Doctor I. Kolev M.D1
Creation Date: December 2002
Update: July 2004
Scientific Editor: Professor Alexis Brice
1
Fédération de Neurologie, Hôpital Salpêtrière, Bâtiment Paul Castaigne 47-83 Bd de l'Hôpital, 75013
Paris, France. ivan.kolev@psl.ap-hop-paris.fr
Abstract
Keywords
Disease name and synonyms
Excluded diseases
Diagnosis criteria / definition
Differential diagnosis
Frequency
Clinical description
Management and treatment
Etiology
Diagnostic methods
Unresolved questions
References
Abstract
Parsonage-Turner is a clinically defined syndrome that is easily confused with other neck and upper
extremity abnormalities. Affected patients present with a characteristic pattern of sudden and acute pain
across the top of the shoulder, lasting a few hours to a fortnight, followed by flaccid paralysis of some
muscles of the shoulder girdle. Features supporting strongly diagnosis of Parsonage-Turner disease
include:
-discrepancy for muscles wasting and denervation between muscles innervated by the same nerve;
-patchwork distribution of muscles denervation for muscles that are innervated by several nerves or nerve
trunk arising from the brachial plexus
-dissociation between sparing of the sensory nerve action potential and muscles denervation depending
from the same mixed nerves.
The incidence has been estimated at approximately 1.64 in 100,000, with a peak rate between the third
and fifth decades and a slight male predominance. Although different precipitating factors, such as
infection, trauma, surgery, immunization, and autoimmune mechanisms, have been suspected and
incriminated in the occurrence of Parsonage-Turner syndrome, the etiology remains unknown. Prognosis
is generally favorable, with about 75% of complete recovery within 2 years. Treatment is symptomatic and
is based on analgesic drugs and physical therapy.
Keywords
Neuralgic amyotrophy – Brachial plexus – Pain – Patchwork amyotrophy and weakness – Symptomatic
treatment – Spontaneous recovery – Unknown etiology.
Disease name and synonyms
Parsonage-Turner disease was first reported
under different names, such as:
• Localised neuritis of the shoulder girdle
(1)
• Seratus magnus paralysis (2)
• Multiple neuritis of the shoulder girdle (3)
• Acute brachial radiculitis (4-5)
In 1948, Parsonage and Turner described similar
conditions and isolated a distinct clinical
Kolev I. Parsonage-Turner syndrome. Orphanet Encyclopedia. July 2004.
http://www.orpha.net/data/patho/GB/uk-Turner.pdf
1
syndrome under the neutral term of "Neuralgic
amyotrophy; the shoulder-girdle syndrome" (6).
Subsequently, further appellations have been
proposed, such as:
-Paralytic brachial neuritis (7-8)
-Acute shoulder neuritis (9)
-Acute scapula-humeral palsy (10)
-Brachial plexus neuropathy (11)
This terminology underlines the persistent lack of
knowledge concerning the pathogenic process
and the localization of lesions in this syndrome.
Nevertheless, the "Parsonage-Turner syndrome"
(12) appellation has the advantage of referring to
a well-recognized and a well-identified clinical
entity, without addressing the issues of
localization or pathogenic process.
Excluded diseases
Hereditary neuralgic amyotrophy (HNA) or
Hereditary brachial plexus neuropathy
(HBPN)
Familial occurrences of the Parsonage-Turner
syndrome led to the individualization of
Hereditary neuralgic amyotrophy (HNA) or
Hereditary brachial plexus neuropathy (HBPN).
Clinical features of HNA are identical to those of
the sporadic form. Family history, a marked
tendency of relapse, cases beginning more
frequently in childhood, and in some cases,
minor dysmorphic features, enable distinguishing
the hereditary forms from the sporadic variety
(13). An autosomal-dominant transmission mode
linked to 17q25 locus is admitted in most HNA
families (14), but recent data tend towards a
genetic heterogeneity (15).
Hereditary neuropathy with liability to
pressure palsies (HNPP)
HNPP is a distinct genetic disorder and recurrent
brachial plexopathy might be its only expression
(16).
Diabetic amyotrophy
Proximal diabetic neuropathy, which consists of
muscle-weakness and, exceptionally, wasting in
the proximal part of the lower limbs, involves the
scapulo-humeral region (17).
Neuralgic amyotrophy as a complication of
serotherapy
This entity, known since 1910, is clinically
identical to Parsonage-Turner syndrome, except
that the delay between pain and paralysis is
shorter, and sometimes preceded by generalized
urticaria. This condition is usually considered
distinct from Parsonage-Turner syndrome
because of the well-identified precipitating factor.
However, numerous authors consider it as the
prototypic form of the Parsonage-Turner
syndrome, and use this argument to support the
involvement of an immune mechanism in
Parsonage-Turner syndrome (6-13-18-19-20-2122-48-49).
Neuralgic amyotrophy of the lumbar plexus
Similar conditions involving lumbo-sacral plexus
rather than brachial plexus have been described.
Although the clinical features and evolution are
very similar, pelvis belt neuralgic amyotrophy is
excluded from Parsonage-Turner syndrome (23).
Diagnosis criteria / definition
Parsonage-Turner disease is a rare and clinically
defined syndrome of unknown etiology, which
consists of sudden pain followed by muscleweakness and wasting of the shoulder girdle and
upper arm. Usually "without any constitutional
disturbance, pain starts suddenly across the top
of the shoulder-blade (…) and lasts from a few
hours to a fortnight (…) Then, a flaccid paralysis
of some of the muscles of the shoulder girdle
and often of the arm develops". Sensory
impairment is more often limited to "a patch of
numbness over the outer side of the upper arm.
When the paralysis appears, the severe pain
usually stops" (6).
Differential diagnosis
At the disease onset, the pain around the
shoulder girdle may be a sign leading to
misdiagnosis, as acute pain can occur in
numerous other shoulder affections (13-24),
such as:
• Rotator cuff tears
• Adhesive capsulitis
• Calcific tendonitis
• Shoulder arthritis
• Local bone affection
• Cervico-brachial neuralgia
• Herpes Zoster
When muscles are subsequently affected with
paralysis and wasting, other conditions involving
the second motor neurone can be discussed,
especially:
• Discogenic nerve root compression
• Tumors of the spinal cord or brachial plexus
• Infiltrative tumor of the nerve root or brachial
plexus such as Pancoast-Tobias syndrome
• Outlet syndrome such as neuralgia of the
supra scapular nerve, the long thoracic
nerve, or the thoracic outlet syndrome
• Traumatic compressive nerve injuries
• Cervical artery dissection
• Anterior poliomyelitis
• Amyotrophic lateral sclerosis
The acute onset of pain followed by its rapid
resolution or decrease, as weakness and
paralysis occur, constitute a disease pattern
characteristic of Parsonage Turner syndrome.
Kolev I. Parsonage-Turner syndrome. Orphanet Encyclopedia. July 2004.
http://www.orpha.net/data/patho/GB/uk-Turner.pdf
2
However, electro-physiological and imaging
studies are useful in distinguishing the above
conditions from Parsonage-Turner syndrome (611-13-24).
Frequency
Firstly described in military personnel during the
Second
World
War,
Parsonage-Turner
syndrome seems rare. In the general population
of Rochester, Minnesota, the incidence has been
estimated at about 1.64 in 100,000 (25). Ages of
affected patients range from 3 months to 84
years (26), with the highest incidence occurring
between the third and fifth decades (6-7-11-2728-29-30), and the average age at onset has
been estimated to 38 years from review of
literature series(31). A male predominance is
reported in the civilian population, with a maleto-female ratio ranging from 1.74:1 to 4:1 (11-2526).
Clinical description
Local pain around the shoulder girdle is the
prevalent presenting symptom (6-7-8-10-11). It is
usually sudden and often severe, insufferable,
sometimes awakening patients during the night.
It worsens progressively for some hours or even
two days. Described as a constant severe ache
associated with tenderness of the muscles, the
pain is not affected by coughing. However, it is
accentuated by arm movements and muscular
pressure, but almost unaltered by movements of
the neck. The pain is commonly distributed
across the back of the scapula and the tip of the
shoulder. It often radiates down the outer side of
the arm and up along the neck, and seldom
spreads down as far as the outer side of the
forearm, below the elbow. There is no exact
correlation between the localisation of the pain
and the distribution of the subsequent muscle
paralysis. However, in general, pain radiating
below the elbow is associated with involvement
of the biceps or triceps, and radiation into the
neck involves the sternocleidomastoid and
trapezius. Similarly, most of the patients with
bilateral paralysis also initially suffer from
bilateral pain. Usually the severe pain lasts from
a few hours to three weeks, and then disappears
rather suddenly while the muscular wasting and
weakness occur. A less severe pain may persist
considerably
longer.
Severe
pain
may
sometimes last days or even weeks after
appearance of the weakness. Occasionally,
muscular
weakness
and
pain
occur
simultaneously. Although lack of pain is
extremely uncommon in Parsonage-Turner
syndrome, it has been already reported in the
original series of Parsonage and Turner(6).
As the pain subsides, flaccid paralysis of some
muscles of the shoulder girdle, and often of the
arm, develops (6-7). Usually, muscle weakness
appears suddenly, but sometimes gradually
increases over two or three days, or even one
week in rare cases. Paralysis is of lower motor
neurone type, with flaccidity and rapid wasting of
the affected muscles. Tendon reflexes might be
affected, depending on the severity and extent of
muscular paralysis and wasting. Hypoactive
reflexes are frequently encountered, and
fasciculations are occasionally seen (6-7-8-1011).
Depending on the supposed anatomical site of
the lesion, several patterns of weakness are
reported: weakness involving muscles that are
innervated by either one peripheral nerve,
several peripheral nerves, one or several nerveroot, or a combination of nerve-roots and
peripheral nerves. The most frequent pattern of
weakness corresponds to the involvement of
several peripheral nerves, among which axillary,
suprascapular,
long
thoracic
and
musculocutaneous nerves are the most
commonly affected (6-7-8-10-11). Radial (11-7),
anterior interosseous (7-10-33-36), and median
nerves (37), are also occasionally reported to be
affected. The involvement of the phrenic nerve,
resulting in diaphragm paralysis with dyspnea is
rarely, but classically, reported. This involvement
is probably underestimated, as it is frequently
associated with asymptomatic presentation.
Regarding nerve-root involvement pattern, C5
and C6 are the most commonly affected; C4 and
C7 are also involved, but more rarely.
Accordingly, the weakness will affect the deltoid,
which is the muscle the most frequently involved,
and the supraspinatus, infraspinatus, serratus
anterior, biceps, triceps, and wrist and finger
extensors (6-7-8-11-38-39). Muscle involvement
is
usually
unilateral,
although
bilateral
involvement is not uncommon, with an
asymmetrical pattern of affected muscles.
Weakness and pain area do not coincide
perfectly. Muscular atrophy occurs rapidly in
different degrees of severity. The resulting
clinical feature is a patchwork of weakness and
atrophy in one or several muscles, principally
around the shoulder blade.
In the early stages of the affection, many
patients report a localised numbness, although
there is no residual sensory impairment at the
later stages when weakness has already
appeared (6-7). Sensory impairment at the later
stages is usually mild and the most commonly
involved area is a small strip over the outer side
of the upper arm, corresponding to the
distribution of the circumflex nerve. Nerve-root
distribution of muscle weakness is usually
associated with sensory impairment occurring
down the outer side of the arm and forearm in
Kolev I. Parsonage-Turner syndrome. Orphanet Encyclopedia. July 2004.
http://www.orpha.net/data/patho/GB/uk-Turner.pdf
3
the C5-C6 cases, and extending to the neck side
when C4 root is involved. In fact, areas of
sensory impairment correspond to the
distribution of the nerve or nerve-root
supposedly affected, which is itself based on
distribution of weakness. However, in several
cases, the degrees of sensory impairment and
weakness corresponding to the distribution of
the same nerve do not correlate (6-7-8-10-1125-26-28-31).
From the observation of few cases in which
sensory impairment was absent and the pattern
of muscles affected by weakness did not
correspond to any peripheral nerve or nerve root
distribution, Parsonage and Turner (6)
suggested that the lesion could probably also
affect the spinal cord (anterior horn cells).
Management and treatment
Prognosis is generally good, since recovery of
strength
and
sensation
usually
begins
spontaneously, as early as 1 month after
symptoms onset, with about 75% of complete
recovery within 2 years (11). However, the
period of time for complete recovery is very
variable, ranging from 6 months to 5 years (724). It seems that the delay in recovering
strength depends on the severity and duration of
pain, weakness, or both (6-8-11-39).
Furthermore, patients with involvement of
proximal and upper trunk lesions have the most
rapid recovery(11). Although not very common,
relapse might nevertheless occur within a few
months to several years after full recovery (6-78-11-38-40-41). In general, complete restoration
to normal strength and function usually occurs
within five years.
However, prognosis is influenced by the duration
of the resulting incapacity, some patients having
experienced impairment persisting sometimes
thirty years after the onset (31). The occurrence
of diaphragmatic forms must be taken into
account in the diagnostic approach of dyspnea.
No specific treatment has yet been proved
efficient in Parsonage-Turner syndrome. In the
early stages, pain may require treatment.
Common analgesic drugs are usually sufficient.
However, in many cases, high pain intensity
requires morphine administration.
Corticosteroids administration does not provide
any significant benefit, with the exception of a
few patients who experienced some pain relief
(11). Rest is recommended (42), and
immobilization of the affected upper extremity
may be helpful in relieving the pain and in
preventing stretching of the affected muscles
(10-43).
As pain subsides, physical therapy is
recommended. Passive range of motion
exercises of the shoulder and elbow (38-43) are
suggested to maintain full range of motion.
Active rehabilitation is undertaken only when
some recovery of the affected muscle(s) is
already obtained. Furthermore, all the upper
body muscles should undergo rehabilitative
exercises, and not only those presenting clinical
weakness (42). It is also recommended that
strength recovery reaches a plateau before
patient returns to sports (44).
However, the recovery delay does not seem to
be improved by these physical therapies (11).
Surgical stabilization of the scapula to the
thorax, or tendon transfers have been performed
with benefit in patients who did not achieve
recovery (43).
Etiology
The exact cause of brachial neuritis remains
unknown. Numerous authors have proposed
various precipitating events or factors. These
factors, suggested to contribute to the
development of brachial neuritis, are found in
approximately 30 to 85% of the cases (1-6-7-811-26-28-35), 3 to 14 days preceding the onset
of pain. The most frequently reported factors are
infection, viral diseases, trauma, heavy exercise,
surgery,
immunization,
and
autoimmune
mechanisms (vaccinations, serotherapy, foreign
serum injection, subcutaneous injections of
allergens, immunogenic substances, pregnancy)
(6-7-8-10-11-13-27-28-30-32-33-34-45).
Although commonly admitted, the contributing
role of these factors has not been proved and
remains hypothetical.
The particular case of post-serotherapy
neuralgic amyotrophy (18-19-20-21-22) must be
underlined. This well-known condition is an
occasional complication of serum injection.
Although
incompletely
elucidated,
the
physiopathology of this process lies in the
occurrence of perineural oedema, similar to the
mechanism involved in urticaria in serum
sickness (6). Several authors consider that
neuralgic amyotrophy following foreign serum
injection should not be distinguished from the
Parsonage-Turner syndrome (48-49).
In a way similar to post-serotherapy neuralgic
amyotrophy, and on the basis that numerous
immune events are recognized as precipitating
factors for Parsonage-Turner disease, an allergic
or hypersensitivity reaction mechanism is
commonly suggested in the etiology of the
disorder (6-9-28-45). Rare cases reported in
anatomo-pathological studies are suggestive of
an inflammatory-immune pathogenesis (50).
Furthermore, some authors underline that the
particular
evolution
of
Parsonage-Turner
disease, i.e. sudden pain onset and
spontaneous recovery, is similar to the
Kolev I. Parsonage-Turner syndrome. Orphanet Encyclopedia. July 2004.
http://www.orpha.net/data/patho/GB/uk-Turner.pdf
4
inflammatory dysimmune process of the delayed
over-sensitiveness type (30).
Several studies provide additional evidence for
an allergic or autoimmune mechanism. Sierra et
al (51) showed that blood lymphocytes in
patients with neuralgic amyotrophy are
specifically sensititized to brachial plexus nerves.
In addition, Vriesendorp et al (52) determined
that complement-fixing antibodies to peripheral
nerve myelin and terminal complement activation
products are increased in serum of patients in
the acute phase of neuralgic amyotrophy.
Diagnostic methods
The Parsonage-Turner disease is a clinical
syndrome and there is no existing diagnostic
study providing a specific result that allows
diagnosis confirmation. The results of most of
laboratory studies are normal, and their aim is to
eliminate conditions in differential diagnosis.
There is no evidence for an inflammatory or
infectious process. Cerebrospinal fluid is usually
normal or might show a slight increase in the
total protein (8-11-28). Imaging studies such as
brachial plexus and cervical MRI are helpful in
eliminating any local pathological process, which
is associated with a differential diagnosis
condition. High intensity signals on T2-weighted
images in shoulder muscles before development
of muscle atrophy have been described, but are
not specific (46).
Electromyographical studies are more useful as
they give the precise pattern of muscles
involvement, and subsequently the hypothetical
localisation of the nerve lesion(s). They can also
be helpful in detecting sub-clinical involvement of
unsuspected muscles, or in ruling out a
traumatic or compressive nerve or trunk lesion.
In neuralgic amyotrophy, electromyographical
findings usually reveal acute denervation
resulting from an axonal neuropathy. However,
some rare studies reported evidence of proximal
conduction block, suggesting focal proximal
demyelination (47).
The following features are highly suggestive of
Parsonage-Turner disease diagnosis:
-discrepancy
for
muscles
wasting
and
denervation between muscles innervated by the
same nerve;
-patchwork distribution of muscles denervation
for muscles that are innervated by several
nerves or nerve trunk arising from the brachial
plexus;
-dissociation between sparing of the sensory
nerve action potential and muscles denervation
depending from the same mixed nerves.
Similarly, diaphragmatic denervation supports
also diagnosis of Parsonage-Turner disease
(31). Diaphragmatic involvement may also be
revealed by radiography or ultrasonography
imaging of the thorax, even if there is no clinical
evidence for a diaphragmatic weakness.
Unresolved questions
Although some arguments are in favor of a
possible
immune
mechanism,
the
etiopathogenesis of Parsonage-Turner disease
remains unknown. Furthermore, the rare cases
of conduction block reported suggest a possible
focal demyelination (47-53), which may occur
during the early stage of the affection, when
electromyographical
studies
are
rarely
performed. Moreover, the precise location of the
lesion on the nerve root, either among the
brachial plexus, or in the nerve trunk is also
uncertain. Particularly, the cases with distal
muscles involvement may result from a partial
plexus trunk lesion or a distal terminal nerve
lesion (31). Thus, the diversity of appellations
for Parsonage-Turner diseases reflects entirely
these uncertainties as to the localization and the
pathogenic process.
More recently, many cases of clinical variations
of Parsonage-Turner disease have been
reported (37-54). These variants forms include
focal and distal forms, sensory isolated forms,
and some involve cranial nerves (31). Therefore,
it seems that the nosographic framework of
neuralgic amyotrophy is widening, and that the
condition should be considered as a multifocal
neuropathy involving mostly, but not only, nerves
of the upper extremity.
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