Non-orthopaedic causes of shoulder pain: what the shoulder expert must remember.

Aim of this review is to underline some specific patterns of shoulder pain that are not related to musculoskeletal diseases but are manifestations of gastrointestinal, neurological, cardiological or rheumatological diseases. The most important pathologies (like gallstones, myocardial ischaemia and Parsonage-Turner syndrome...) that can manifest with shoulder pain will be presented by specialty doctors and elements for differential diagnosis will be discussed. Orthopaedic shoulder surgeons should always suspect other causes of pain, different from those related to bone, tendons and joint. If there is something unfair, patients should be referred to family doctor for further investigations in order to exclude major systemic diseases.

Sensory ataxic neuropathy and esophageal achalasia in a patient with Sjogren's syndrome.

We describe a patient who developed an ataxic sensory syndrome associated with xerophthalmia and progressive dysphagia with regurgitation. Electrophysiological findings were consistent with an axonal sensory neuropathy, and superficial peroneal nerve biopsy showed a reduction in number of myelinated fibers with epineurial inflammation. Rheumatoid factor, anti-SSA/SSB and antinuclear antibodies were positive and a diagnosis of Sjogren's syndrome was made. An endoscopic investigation revealed esophageal achalasia. We suggest that there may be a common autoimmune mechanism directed to different targets on the basis of this rare association.

Clinical and electrophysiological correlations in type 2 diabetes mellitus at diagnosis.

The purpose of this study was to evaluate, in newly diagnosed type 2 diabetes mellitus (DM): (1) the prevalence and staging of peripheral neuropathy, as well as its possible relationship with metabolic profile; (2) the clinical value of both the Diabetic Neuropathy Index (DNI) and the Diabetic Neuropathy Score (DNS), and their reciprocal concordance, as a screening method for neuropathy. Thirty-nine newly diagnosed DM subjects underwent: neurological examination, nerve conduction studies (NCS), quantitative sensory system and cardiovascular autonomic function assessments. Peripheral neuropathy was observed in 72% of the subjects (its staging was similar to that of patients with longer disease history), while another 10% of them showed a borderline neuropathy. The Deep Breathing test was abnormal in 28% of the patients; postural hypotension was found in 6%. The same proportion (82%) of subjects who scored positively on the DNI showed altered NCS, while the quantitative sensory system assessments had a low sensitivity in order to detect the neuropathy. No correlation was found between metabolic indexes and DNI/DNS parameters. The high prevalence of peripheral and autonomic function alterations suggests that each newly diagnosed diabetic subject should be screened for neuropathy by the DNI, to reduce the negative prognostic influence of this complication.

Electrophysiological findings of peripheral neuropathy in newly diagnosed type II diabetes mellitus.

This study was aimed at assessing the electrophysiological signs of peripheral neuropathy in diabetes mellitus (DM) type II patients at diagnosis. Nerve conduction studies (NCS) of median, ulnar, peroneal, tibial and sural nerves were performed in 39 newly diagnosed DM subjects and compared to those of 40 healthy controls. Metabolic indices were also investigated. Electrophysiological alterations were found in 32 (82%) of the DM patients, and more than half of them (62.2%) showed multiple (two to five) abnormal parameters. Because most of the subjects (84.4%) had from two to five nerves involved, these alterations were widespread in the seven nerves evaluated. Forty-two percent of the patients had NCS alterations suggestive of distal median mononeuropathy, implying that metabolic factors in DM make the median nerve more susceptible to focal entrapment. A reduced sensory nerve action potential (SNAP) amplitude was observed in the median nerve in 70% of the patients, in the ulnar in 69% and in the sural nerve only in 22%. In the presence of a decrease in the SNAP amplitude of the ulnar or median nerve, the SNAP amplitude of the sural nerve was normal in 82 or 80% of the subjects, respectively. This finding may be in keeping with a distal involvement of the sensory fibres, as explored by routine median or ulnar NCS. No correlation was found between metabolic indices and NCS parameters. In conclusion, a high percentage of newly diagnosed DM patients show signs of neuropathy, and upper limb nerve sensory NCS seem to be more sensitive in detecting it than lower limb NCS.

Subclinical electrophysiological alterations of phrenic nerve in chronic inflammatory demyelinating polyneuropathy.

Alterations of the phrenic nerve (PN) and pulmonary function tests (PFTs) have been described in patients with chronic inflammatory demyelinating polyneuropathy (CIDP). This study was aimed at assessing the relationship between PN and respiratory function in CIDP patients without clinical signs of respiratory failure. Bilateral PN and right median nerve conduction studies were carried out along with blood gas analysis and PFTs: maximal inspiratory pressure; maximal expiratory pressure; forced vital capacity. The amplitude of the compound muscle action potential of the PN was seen to be altered in 19/24 (79%) patients and latency in 22 (92%). Eighteen patients (75%) showed at least one abnormal PFTs or CO2 partial pressure value. Electrophysiological alterations of the PN were observed in a high percentage of the CIDP patients studied. No statistically significant correlation was observed between PN and PFTs alterations.