[MIM 162 100]

(Neuralgic amyotrophy, acute brachial plexus neuritis)

Estimated incidence 1/60,000. Most cases are sporadic but there is an autosomal dominant inherited mutation of the SEPT9 gene on 17q25 (50 % of familial cases). The etiology is unknown: there is often a precipitating factor such as a viral infection, trauma, surgery, vaccineation, childbirth or an autoimmune mechanism.

Typically characterized by:

-         sudden severe pain in the shoulder and arm, spontaneous and continuous at the beginning, then triggered by movement. This acute phase lasts from a few hours to several weeks (average: 3 weeks)

-        the second (chronic) phase is characterized by a progressive flaccid paralysis of the involved  or of the territory innervated by brachial plexus

-        full and spontaneous recovery within 2 years following the onset of the disease.

Signs of denervation are heterogenous, and are associated with varying degrees of autonomic and sensory disturbances (hypoesthesia, dysesthesia and paresthesia).

Other anatomical regions can be involved (very rare) as the lower limb (10%), the diaphragm and the vocal cords (5%) or the facial nerve territory.

The risk of recurrence is more important in the inherited form.

Treatment: pain killers, especially those effective against neuropathic pain, gentle physiotherapy.

Anesthetic implications:

neuropathic pain, limb atrophy; it is probably cautious to avoid regional anesthesia and IV lines on the affected limbs. 

References:

-         Hussey AJ, O’Brien CP, Regan PJ. 
Parsonage-Turner syndrome: case report and literature review. 
Hand 2007; 2: 218-21.

-        Sobey JH, Franklin A. 
Management of neuropathic pain in an adolescent with Parsonage-Turner brachial plexitis. 
Reg Anesth Pain  Med 2014; 39: 176

-         Wiser Smith DP, Elliott JA, Helzberg JH. 
Intravenous corticosteroid therapy for bilateral Parsonage-Turner syndrome. 
Reg Anesth Pain Med 2014; 39: 243-7.

Updated: November 2018