Parsonage-Turner Syndrome: Rehabilitation Case #131

The answer is written in the order of events, and the order is the differentiating feature of this condition: severe shoulder pain first, then weakness as the pain subsides. That biphasic sequence is the acute pattern in about 70 percent of cases, and it is unlike anything a mechanical shoulder does. A torn tendon is weak from the moment it tears; a stiffening capsule hurts more as it stiffens, not less. Here the pain and the weakness trade places over a fortnight, which is what an inflammatory insult to nerves looks like once the acute phase passes and the denervation declares itself. The character of the pain supports it long before any test: constant, burning, worst at night, unrelieved by simple analgesia, and spread over the outer shoulder, the scapula and the antecubital fossa — a distribution no single joint or tendon owns. The most useful single examination finding is the one in clue 2 rather than the dramatic one in clue 3. Full, painless passive range in every plane removes adhesive capsulitis from the table immediately, because the whole definition of that condition is a capsule that will not let the arm move even when someone else moves it. Once passive range is full, a weak arm is a neurological arm. Clue 3 then supplies the anatomy. Medial scapular winging on a wall push-off means the long thoracic nerve, and the long thoracic nerve is nowhere near the rotator cuff. Set that beside weak abduction and external rotation, which implicate deltoid, supraspinatus and infraspinatus by way of the axillary and suprascapular nerves, and the lesion is already scattered across nerves that share no common trunk and no single root. The named nerves this condition picks off are exactly these — axillary, suprascapular, anterior interosseous, long thoracic and musculocutaneous — in a patchy rather than uniform distribution. The vaccination eleven days earlier is not incidental. More than half of cases follow an identifiable precipitant: infection, surgery, immunisation, trauma or intense upper-body exercise, with hepatitis E identified in about 10 percent and heavy exercise in another 10 percent. It is a trigger, not a cause to be argued about, and asking for one is part of the history. Clue 5 confirms what clues 3 and 4 imply. Fibrillation potentials and positive sharp waves in supraspinatus, infraspinatus, deltoid and serratus anterior cross three nerve territories and more than one root, which is a pattern no single radiculopathy and no single entrapment can produce. A normal cervical MRI removes the compressive explanation, and the hourglass constriction on nerve ultrasound is the positive imaging correlate. The timing of these studies is itself worth knowing: nerve conduction can take about a week to become abnormal and needle electromyography about four weeks, so a study done in the painful first days is normal in a patient who has the condition, and that normal result has misdirected many people. What the therapist has to say next is the hard part, and it should be accurate. Most nerve function recovers over two to three years, but more than 70 percent of people retain some weakness or other residual symptoms; at three years only 7.7 percent had recovered completely and 26.7 percent were still unable to work. For a heating engineer whose job is overhead, that conversation belongs at the start of rehabilitation rather than the end, alongside scapular stabilisation and graded return-to-work planning.