Does Subacromial Injection With Glutamate Receptor Antagonist, Ketamine, Attenuate Pain in Rotator Cuff Tendinopathy?
Does Subacromial Injection With Glutamate Receptor (NMDAR) Antagonist, Ketamine, Attenuate Pain in Rotator Cuff Tendinopathy?
The hypothesis of the present study is that in patients with rotator cuff tendinopathy a specific pharmacological blocking of peripheral glutamate-receptor N-methyl-d-aspartate receptor type1 (NMDAR) glutamate receptors will result in pain alleviation. Activated NMDAR1 has been demonstrated to be crucial for pain regulation in various pain disorders, and in biopsies from patients with tendinopathy, NMDAR1 was found to be activated.
To test this hypothesis a specific NMDA receptor antagonist, ketalar (ketamine), will be injected guided by ultrasound into the subacromial space in patients with rotator cuff tendinopathy, and subsequently the pain response will be assessed.
2,5 ml - if well tolerated immediately followed by another 2,5 ml - of an approximately 1 mg/ml ketalar solution (1 ml of ketalar 10 mg/ml + 9 ml of NaCl 9%) injected 2 times with 1-12 weeks between each injection
2,5 ml - if well tolerated immediately followed by another 2,5 ml - of a 9% NaCl solution injected 2 times with 1-12 weeks between each injection
Inclusion Criteria: diagnosis of rotator cuff tendinopathy by exercise-related shoulder pain with positive impingement tests as described by Hawkins and Neers, and MRI findings consistent with tendinopathy. Symptom duration at least 1 year to ensure neuronal ingrowth and NMDAR expression Exclusion Criteria: previous surgery in any shoulder. previous cortisone use, either as injections or orally symptoms or signs of cervicobrachialgia or polyneuropathy full thickness rotator cuff ruptures verified by MRI primary inflammatory mediated pain, hence, patients with glenohumeral arthrosis, glenohumeral arthritis or systemic disorders predisposing for arthritis a central component of pain perception manifested by radiating pain in the involved limb; implying worse outcome after subacromial decompression. pregnancy breastfeeding reduced liver function (Increased serum bilirubin, ASAT or ALAT), decompensated heart failure (NYHA class 3-4) increased intracranial pressure or disease of the central nervous system (CNS) chronic alcoholism epilepsy psychiatric disease, increased intraocular pressure acute intermittent porphyria hyperthyroidism use of thyroid hormones upper respiratory tract infections pneumonia intracranial lesions acute head injuries ocular injuries hydrocephalus risk factors predisposing for intra-articular bleeding increased risk of infection