RPTSpecialists

Cervicogenic headache and the trigeminocervical convergence💡

👉 Cervicogenic headache is pain referred to the head from a source in the cervical spine. Unlike other types of headaches, cervicogenic headache has attracted interest from disciplines other than neurology, in particular manual therapists and interventional pain specialists, who believe that they can find the source of pain among the joints of the cervical spine. https://pubmed.ncbi.nlm.nih.gov/19747657/

Clinical criteria for the diagnosis of cervicogenic headache are: (https://pubmed.ncbi.nlm.nih.gov/11472384/)

▶︎ 1 Unilateral headache without side-shift

▶︎ 2 Symptoms and signs of neck involvement: pain triggered by neck movement or sustained awkward posture and/or external pressure of the posterior neck or occipital region; ipsilateral neck, shoulder, and arm pain; reduced range of motion

▶︎ 3 Pain episodes of varying duration or fluctuating continuous pain

▶︎ 4 Moderate, non-excruciating pain, usually of a non-throbbing nature

▶︎ 5 Pain starting in the neck, spreading to oculo-fronto-temporal areas

▶︎ 6 Anaesthetic blockades abolish the pain transiently provided complete anaesthesia is obtained, or occurrence of sustained neck trauma shortly before onset

▶︎ 7 Various attack-related events: autonomic symptoms and signs, nausea, vomiting, ipsilateral oedema and flushing in the peri-ocular area, dizziness, photophobia, phonophobia, or blurred vision in the ipsilateral eye

👉 Satisfying criteria 1 and 5 qualifies for a diagnosis of possible cervicogenic headache. Satisfying any additional three criteria advances the diagnosis to probable cervicogenic headache.

👉 The mechanism underlying the pain involves convergence between cervical and trigeminal afferents in the trigeminal nucleus caudalis (TNC). (https://pubmed.ncbi.nlm.nih.gov/15062532/)

👉 In this nucleus, nociceptive afferents from the C1, C2, and C3 spinal nerves converge onto second-order neurons that also receive afferents from adjacent cervical nerves and from the first division of the trigeminal nerve (V1), via the trigeminal nerve spinal tract. This convergence has been shown anatomically and physiologically in laboratory animals. (https://pubmed.ncbi.nlm.nih.gov/11403743/, https://pubmed.ncbi.nlm.nih.gov/12077000/, https://pubmed.ncbi.nlm.nih.gov/12821523/, https://pubmed.ncbi.nlm.nih.gov/18494984/)

📘 Piovesan and colleagues describe the trigeminocervical convergence mechanisms under different clinical scenarios. (https://pubmed.ncbi.nlm.nih.gov/38388233/)

✅ A. Nociceptive silence. In healthy individuals, innocuous stimuli that could trigger headaches in patients with migraine (fasting, sleep disturbances) or cervicogenic headache (neck movement, external pressure) do not activate the nociceptive centers.

✅ B. Migraine premonitory phase. Up to 88% of migraineurs report symptoms lasting up to 48 h before the headache and aura. Symptoms and neuroimaging studies suggest the involvement of the hypothalamus (fatigue, yawning) and sensory pathways such as the TNC (neck discomfort, shaded in gray). The activation of nociceptive pathways (ascending), subject to the modulation of centers such as the hypothalamus and periaqueductal gray (descending), seems to be part of the mechanism. (https://pubmed.ncbi.nlm.nih.gov/30074545/)

✅ C. Migraine headache phase. The activation of the trigeminovascular system marks this phase. Nociceptive sensitive structures (meninges, vessels) can originate inputs that travel through V1. The trigeminal tract then projects to the second-order neurons of the TNC and upper spinal cord. This convergence probably accounts for migraine pain in trigeminal (usually frontotemporal, indicated in yellow) and non-trigeminal (occipital and suboccipital) areas. Finally, diffuse projections exist through the entire pain matrix (hypothalamus, thalamus, S1).

✅ D. Cervicogenic headache. Conversely, neck structures (joints, vertebrae) can generate nociceptive stimuli transmitted via C1-3. The projections terminate in the upper spinal cord as well as the TNC. This mechanism possibly mediates the pain felt in the anterior (V1) and posterior (C1-3) areas following stimuli in the neck.

V1: 1st branch of the trigeminal nerve; V2: 2nd branch of the trigeminal nerve; V3: 3rd branch of the trigeminal nerve; C1-3: 1st, 2nd and 3rd cervical nociceptive roots; GG: gasserian (trigeminal) ganglion; TNC: trigeminal nucleus caudalis; Hyp: hypothalamus; Th: thalamus; S1: primary sensory cortex.

Supraspinatus Tendon Swelling in Rotator Cuff Tendinopathy 💡

🗯️ There is an ongoing debate, whether the mechanisms of RC tendinopathy are extrinsic, intrinsic or a combination of both. (https://pubmed.ncbi.nlm.nih.gov/20846766/)

👉 Extrinsic factors are defined as those causing compression of the RC tendons, while intrinsic mechanisms are those associated with degeneration of the RC tendon. Neer proposed an extrinsic mechanism to the etiology RC tendinopathy with compression of the RC tendons and associated tissues within the subacromial space under the anterior aspect of the acromion or surrounding structures (https://pubmed.ncbi.nlm.nih.gov/5054450/) and coined this subacromial impingement syndrome (https://pubmed.ncbi.nlm.nih.gov/6825348/). The diagnosis of “subacromial impingement” inherently implies an extrinsic compression mechanism due to narrowing of the subacromial space, which may not accurately represent all RC tendon pathology.

👉 On the other hand, proponents of an intrinsic mechanism stress the importance of tendon changes, i.e. tensile tissue overload, degeneration, beginning primarily articular sided as the most relevant mechanism. (https://pubmed.ncbi.nlm.nih.gov/20846766/.

📌 But there is clearly potential for an interaction between intrinsic and extrinsic mechanisms: McCreesh et al have demonstrated that RC muscle fatigue leads to short-term decrease in acromiohumeral distance (AHD) and swelling of the supraspinatus tendon in people with RC tendinopathy (https://pubmed.ncbi.nlm.nih.gov/29333279/). Porter and colleagues documented a relationship between supraspinatus tendon thickness increase after swimming, immediately and 6 hours afterwards and the likelihood of future shoulder pain (odds ratio (OR) 1,3-2,3, https://pubmed.ncbi.nlm.nih.gov/37946512/).

✅ The enlarged tendon occupies more subacromial space, a phenomenon represented by the subacromial occupation ratio (AHD/supraspinatus thickness), increasing the potential for compression (https://pubmed.ncbi.nlm.nih.gov/23736252/) and the possible development of secondary acromial osteophytes. So, instead of the acromion pushing down on the tendon, an alternative hypothesis would be that a swollen supraspinatus tendon pushes up into the acromion (https://pubmed.ncbi.nlm.nih.gov/34852803/).

💡 By the way, a brand-new study by Dube´ and colleagues (https://pubmed.ncbi.nlm.nih.gov/38762149/) demonstrates that supraspinatus tendon thickness can be normalized by a high load or load exercise program. After the 12-week intervention, the supraspinatus tendon thickness ratio significantly increased back to a normal range for those in the “Degenerative” subgroup (characterized by tendon thinning and/or tearing), while it significantly decreased back to a normal range for those in the “Reactive” subgroup (characterized by tendon thickening, and hypoechoic areas in US imaging) and did not significantly change for those in the “Normal” subgroup (s. table in comments). Normalising tendon thickness might be one mechanism contributing to reducing symptoms. But this must be confirmed in further studies.

📷 Illustration: https://link.springer.com/chapter/10.1007/978-3-319-76153-4_1.

Rotator cuff (RC) tendon insertion into the humeral head (legends: SSP supraspinatus, IS infraspinatus, TM teres minor, SSC subscapularis

Anatomy of the Intervertebral Foramen 💡

Each lumbar nerve root exits the thecal sac laterally and emerges from the lateral spinal recess formed by the inferior facet of the rostral vertebrae and the superior facet of the caudal vertebra. Then, the nerve root exists the spinal canal through the intervertebral foramen (singular of foramina, AKA neural foramina), which is present in a teardrop-like shape between every pair of vertebra laterally, one on each side. It allows the passage of some anatomical structures out of and into the vertebral canal (s. figure below, https://link.springer.com/chapter/10.1007/978-3-031-44984-0_3):

👉 Spinal nerve root

👉 Posterior root ganglia (AKA spinal ganglia)

👉 Sinu-vertebral nerve (AKA recurrent meningeal nerve)

👉 Segmental spinal artery (AKA root artery)

👉 Intervertebral veins

👉 Transforaminal ligaments (when present). The transforaminal ligaments are narrow bands of collagen fibres that traverse the outer end of the intervertebral foramen.

👉 Fat (adipose tissue)

✅ The relative size of the spinal nerve and nerve roots within the intervertebral foramen varies from level to level and is important with respect to the risk of spinal nerve and nerve root compression. As an approximate rule, the cross-sectional area of an intervertebral foramen increases from L1–2 to L4–5, but the L5–S1 foramen is conspicuously smaller than the rest, (https://pubmed.ncbi.nlm.nih.gov/6867859/) yet, paradoxically, the L5 spinal nerve is the largest of the lumbar nerves.

✅ Consequently, the L5 spinal nerve occupies about 25–30% of the available area in an intervertebral foramen, while the other lumbar nerves occupy between 7% and 22%, making the L5 nerve the most susceptible to foraminal stenosis. (https://books.google.de/books/about/Clinical_Anatomy_of_the_Lumbar_Spine_and.html?id=UYC_NpoFfAsC&redir_esc=y)

Just published 🔥

The ‘forgotten’ lateral patellofemoral ligament: The known unknown 🦵

👉 Contrary to the well known and extensively studied medial patellofemoral ligament (MPFL), the lateral patellofemoral ligament (LPFL) (s. illustration), a primary medial stabilizer of the patellain extension and early flexion (https://www.sciencedirect.com/science/article/pii/S106018722300062X), remains poorly studied and understood. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6197417/)

📘 In a brand-new paper, Vasiliadis and colleagues describe some interesting facts (https://pubmed.ncbi.nlm.nih.gov/39144577/):

▶︎ The native location of the LPFL is in the second layer of a three‐layer model, between the lateral epicondyle and the patella, within the anterolateral aspect of the knee. (https://pubmed.ncbi.nlm.nih.gov/35162134/, https://www.sciencedirect.com/science/article/pii/S106018722300062X)

▶︎ It originates from an osseous area, on average, 10.8 mm anterior and 2.6 mm distal to the lateral femoral epicondyle (https://journals.sagepub.com/doi/10.1177/26350254211033608, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5718311/). At the same time, it as a broad patellar osseous insertion and a soft tissue insertion on the patellar tendon (https://journals.sagepub.com/doi/10.1177/26350254211033608).

▶︎ Interestingly, LPFL loosens approximately 15 mm when going from 0° to 90° of flexion (https://journals.sagepub.com/doi/10.1177/26350254211033608), with greater changes observed early in flexion (from 0° to 30°). (https://www.sciencedirect.com/science/article/pii/S106018722300062X?via%3Dihub)

▶︎ Scientifically, medial patellar instability with medial subluxation of the patella is commonly described as an iatrogenic complication (>90%) (https://journals.sagepub.com/doi/10.1177/2325967117741439) , mainly due to lateral retinacular release (https://www.sciencedirect.com/science/article/pii/S106018722300062X?via%3Dihub) , followed by overcorrection with medializing tibial tuberosity osteotomy, over‐tightened MPFL reconstruction and detachment of vastus lateralis from the patella. (https://pubmed.ncbi.nlm.nih.gov/24992066/)

🔪 LPFL reconstruction (LPFLr) with different graft sources (autografts and allografts, s. section in infographic below) has been considered the treatment of choice (https://pubmed.ncbi.nlm.nih.gov/35782849/, https://pubmed.ncbi.nlm.nih.gov/24992066/, https://journals.sagepub.com/doi/full/10.1177/26350254211033608), however prospective date assessing functional outcomes after LPFLr are lacking.

Sciatica- a Patient's perspective 💡

👉 The term sciatica refers to pain that radiates from the spine to the thigh, calf and sometimes the foot. Although the area of pain corresponds to the area supplied by the sciatic nerve, there is rarely an actual lesion/disease of the nerve. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10348639/)

👉 A patient page published in JAMA (s. infographic below) aims to help patients and front-line clinicians create a stepped, multimodal treatment plan aimed at improving pain and function. (https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2811335)

📘 Btw…a brand-new study by Dove and colleagues examined the prevalence of subjective reports of leg weakness versus objective leg weakness (

Internal Snapping Hip and the Iliopsoas 💡

👉 Snapping hip syndrome (SHS), alternatively known as “coxa saltans,” is a common musculoskeletal complaint seen in 5–10% of the general population and is characterized by an audible or palpable snap of the hip (https://pubmed.ncbi.nlm.nih.gov/27679733/).

👉 The phenomenon can be bilateral or unilateral, painful or painless, idiopathic, or post-traumatic (ttps://pubmed.ncbi.nlm.nih.gov/27679733/). There is no significant difference in gender, although these symptoms are more common in elite athletes (i.e. dancers), especially with hip flexion beyond 90 degrees (https://pubmed.ncbi.nlm.nih.gov/16325091/). Generally, pain associated with this syndrome is aggravated by activities including flexion and rotation (https://pubmed.ncbi.nlm.nih.gov/17021311/).

🔊Hip snapping is classified by pathology, whether intra- or extra-articular. Intra-articular pathology, such as a labral tear, cartilage defect, loose body, or osseous fragment can present with audible snapping that accompanies hip movement (https://pubmed.ncbi.nlm.nih.gov/8657916/). Extra-articular sources of pathology that present similarly include either the iliotibial (IT) band or iliopsoas (IP) tendon. The IT band “snaps” as it moves over the lateral hip or greater trochanter of the femur, while the IP tendon audibly snaps as it moves, most commonly, over the pectineal eminence of the anterior pelvis (https://pubmed.ncbi.nlm.nih.gov/23015936/). Most studies report a sudden “jerky” movement and audible or palpable snap of the iliopsoas over the iliopectineal eminence as the hip is brought from a position of flexion, abduction, and external rotation (FABER) to extension and neutral (https://pubmed.ncbi.nlm.nih.gov/27343394/).

💡 The IP tendon is more than just a source of hip snapping. A systematic review by Hirase and colleagues confirms the role of the iliopsoas as a dynamic anterior femoral head stabilizer from 0 to 15 degrees of hip flexion (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7754519/, https://pubmed.ncbi.nlm.nih.gov/11956980/)

🤸‍♂️ The primary flexor function of the IP muscle is described in hip flexion angles from 45 to 60 degrees of flexion. When injured or inflamed, the iliopsoas tendon can be a source of snapping and/or discomfort, and due to its anatomic relation to hip structures, irritation, tightness, or contracture can be symptomatic (s. Figure, https://link.springer.com/article/10.1007/s00256-018-3083-5). Chronic IP pathology, wear, or compromise can also contribute to atraumatic hip instability (https://link.springer.com/chapter/10.1007/978-1-4939-2645-9_31). Therefore, IP involvement in snapping hip requires evaluation and potential intervention.

🧑‍🤝‍🧑 Many people experience benign, asymptomatic snapping on an infrequent basis, and for this, no treatment is necessary. If the snapping becomes symptomatic, a program of conservative management is attempted first (https://www.ncbi.nlm.nih.gov/books/NBK448200/, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4961351/).

👨‍⚕️ The intervention focus should be an impairment-oriented hip mobilization and strengthening program (https://journals.lww.com/nsca-scj/fulltext/2015/10000/snapping_hip_syndrome__a_review_for_the_strength.13.aspx, https://pubmed.ncbi.nlm.nih.gov/37289915/). However, there is currently no high-quality evidence for this recommendation

📷 Illustration: https://link.springer.com/article/10.1007/s00256-018-3083-5

A plantar intrinsic foot muscles exercise program for older adults to improve mobility related outcomes 🦶

👉 Among fall prevention interventions, those involving a functional exercise program aimed at improving mobility (i.e., gait, balance, coordination and functional task training (https://pubmed.ncbi.nlm.nih.gov/21586143/) seem to be most effective, reducing the rate of falls by 23% (https://pubmed.ncbi.nlm.nih.gov/31792067/).

👉 Functional exercise programs, including fall preventive exercise interventions, are established without noticeable understanding of the plantar intrinsic foot muscles (PIFMs), while there are indications that these muscles have a role in fall related aspects of mobility. The PIFMs stabilize and stiffen the foot (https://pubmed.ncbi.nlm.nih.gov/32446178/, https://pubmed.ncbi.nlm.nih.gov/24478287/) and consequently contribute to balance and propulsive gait (https://pubmed.ncbi.nlm.nih.gov/30655349/, https://pubmed.ncbi.nlm.nih.gov/21864955/). Weakness of the PIFMs in older adults may thus have a detrimental effect on mobility and fall risk. Indeed, it was found that toe flexor weakness predicts falling in older adults (https://pubmed.ncbi.nlm.nih.gov/19751956/, https://pubmed.ncbi.nlm.nih.gov/34979512/).

📘 Therefore, Willemse and colleagues (https://pubmed.ncbi.nlm.nih.gov/39033125/) developed a PIFM strengthening exercises. The training consists of both isolated and functional foot exercises, of which the intensity gradually increases based on the participant’s progression, to be executed 5 days a week for 12 weeks (1 x supervised session, 4 x self-training/week).

📷 The figure below shows exercises included in the training, together with the number of repetitions, the contraction time and pose for the easiest intensity level of the training.

👉 At the onset of the training, each participant starts the exercises at the easiest level. When the participant perceives the exercise without any difficulty for 5 consecutive training sessions and the trainer scores maximum motor performance using a 3-point scale, modified from Fraser and Hertel (https://pubmed.ncbi.nlm.nih.gov/29364026/), , the trainer sets the level of intensity to the next level (s. comments for the corresponding exercise progressions)..

Motor performance is scored as:
0️⃣ : no movement or position cannot be maintained
1️⃣ : exercise can be partially completed or with difficulty or compensation
2️⃣ : exercise can be completed with typical performance

👉 In an upcoming RCT, the authors intend to investigate the effect of this PIFM strengthening training on mobility related outcome variables (maximum gait speed (primary outcome measure), capacity and strength of the plantar intrinsic foot muscles, foot and ankle biomechanics during gait, and various other fall risk-related variables) in older adults.

👉 The most recent systematic review found low-certainty evidence that PIFM strengthening exercises improve foot function during gait and very low-certainty evidence for its favorable effect on dynamic balance control (https://pubmed.ncbi.nlm.nih.gov/35057831/).

💡So, don`t forget PIFM exercises to improve gait, balance control and possibly fall prevention in older adults!

Extending the straight leg raise test 🤓

👉 The straight leg raise test (SLR, here a figure from the renowned New English Journal of Medicine) is traditionally considered a classic test in orthopedics for the inclusion or exclusion of a compressive event (classically a herniated disc) in the lumbar spine. If a radiating pain occurs below the knee joint with a flexion of the leg between 30°-70° (the information here is very variable), a positive test result was assumed.( https://pubmed.ncbi.nlm.nih.gov/25806916/, https://pubmed.ncbi.nlm.nih.gov/10788860/, https://pubmed.ncbi.nlm.nih.gov/38771839/)

👉 However, it should be known that the SLR is quite well suited to rule out such a herniated disc (imaging or findings during surgery) with regard to the presence of a herniated disc (imaging or findings during surgery) (https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD007431.pub2/full, but its specificity is low in this respect. https://pubmed.ncbi.nlm.nih.gov/29253501/, https://books.google.de/books/about/Netter_s_Orthopaedic_Clinical_Examinatio.html?id=RJ0MEAAAQBAJ&redir_esc=y)

👉 It must be mentioned that in a modern understanding, the SLR not only indicates a stretching of the nerve root via space-occupying intervertebral disc material (see figure), but also an increased mechanosensitivity in general.( https://pubmed.ncbi.nlm.nih.gov/29385943/, https://pubmed.ncbi.nlm.nih.gov/32766466/). For example, neuritis, inflammation without axonal damage or radiculitis without nerve compression could also cause a positive SLR, as increased mechanosensitivity is also to be expected here. (https://pubmed.ncbi.nlm.nih.gov/11585565/, https://pubmed.ncbi.nlm.nih.gov/16154692/, https://pubmed.ncbi.nlm.nih.gov/8235812/)

👉In addition, it should be borne in mind that many asymptomatic people have herniated discs on images, so that the reference standard "imaging" appears questionable in this respect (so-called verification bias). (https://pubmed.ncbi.nlm.nih.gov/25430861/, https://pubmed.ncbi.nlm.nih.gov/34548049/)

👉 Nevertheless, the validity of the SLR for herniated discs or nerve root compression can be significantly improved by structural differentiation, some of which has already been used in the past: Pesonen et al. propose the following differentiation as an extension of the SLR (ESLR) in several studies. (s. pictures in comments)

In the respective hip flexion position (if below 90°), in which the patient's problems occur or intensify, structural differentiation is carried out. The SLR is considered positive if:

📍 1. Symptoms of SLR occur and
📍 2. through the appropriate structural differentiation (distal →in proximal symptoms, proximal →in distal) an intensification of symptoms occurs. (see illustration in the comments)

📍So if the patient reports distal symptoms, then an internal rotation of the hip differentiates structurally, i.e. neural vs. non-neural.

📍 If, on the other hand, the patient describes proximal symptoms, then dorsiflexion in the upper ankle joint is used as a corresponding differentiation. (https://pubmed.ncbi.nlm.nih.gov/33761924/, https://pubmed.ncbi.nlm.nih.gov/34548049/)

👉Compared to traditional SLR, the authors were able to determine a significantly higher likelihood ratio (i.e. higher diagnostic accuracy, background s. https://flexikon.doccheck.com/de/Likelihood-Quotient) for nerve root compression on MRI (2.4 (p = 0.34) vs. 5.6 (p < 0.05). A positive ESLR increased the chance of a herniated disc or nerve root compression by a factor of 8. (https://pubmed.ncbi.nlm.nih.gov/34548049/)

Proximal Median Nerve Entrapment (PMNE) 💡

👉The primary symptom associated with PMNE is pain in the proximal volar area of the forearm.

✍️ Many patients report an increase in pain severity with an increase in activity. Other symptoms may include weakness in the forearm and the hand (such as a decrease in grip strength), cramping in the hand (writer’s cramp), and paresthesia or numbness in the first 3 digits. (https://pubmed.ncbi.nlm.nih.gov/1613038/, https://pubmed.ncbi.nlm.nih.gov/15552706/, https://pubmed.ncbi.nlm.nih.gov/8463605/, https://pubmed.ncbi.nlm.nih.gov/1313546/, https://pubmed.ncbi.nlm.nih.gov/11494839/)

🤚Nocturnal symptoms are not as common for PMNE as they are for carpal tunnel syndrome.

👌Inability to produce an “OK” sign may be noted (s. picture below right)

🤚 Physical signs include tenderness in the forearm over the pronator teres muscle and along the median nerve distribution. Unlike median entrapment at the carpal tunnel, if weakness is present, it should involve muscles supplied by the median nerve both above and below the wrist.

👉 The Tinel sign (paresthesias radiating in a median nerve distribution with pressure or tapping over the median nerve in the forearm) may be present, but by itself is not specifically diagnostic of PMNE. A positive Phalen sign (paresthesias radiating in a median nerve distribution with sustained flexion of the wrist) or Tinel sign with tapping over the wrist more likely indicates carpal tunnel syndrome, rather than PMNE.

👉Three provocative tests have been described to help confirm the site of compression for PMNE.( https://pubmed.ncbi.nlm.nih.gov/1910654/). The tests are based on creating maximal tension on the anatomic sites that can contribute to PMNE:

1️⃣ The pronator teres muscle is implicated if symptoms are reproduced upon resisted pronation of the forearm in neutral position with the elbow extended.

2️⃣ The lacertus fibrosis (bicipital aponeurosis) is implicated if symptoms are reproduced upon resisted elbow flexion at 120° to 130° flexion with the forearm in
maximal supination.

3️⃣ The flexor digitorum superficialis is implicated if symptoms are reproduced upon resisted flexion of the proximal interphalangeal joint to the long finger (“middle finger flexion test”). (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8461194/, https://pubmed.ncbi.nlm.nih.gov/11494839/, https://pubmed.ncbi.nlm.nih.gov/1910654/)

Illustration: https://pubmed.ncbi.nlm.nih.gov/26231964/

The anatomy of radial nerve entrapment 💡

👉 When it occurs in relation to work, radial nerve entrapment (RNE) usually refers to 1 of 2 syndromes: radial tunnel syndrome or posterior interosseous nerve syndrome (PINS). [https://thejns.org/view/journals/j-neurosurg/104/5/article-p766.xml, https://pubmed.ncbi.nlm.nih.gov/10829184/]

👉Although RNE may occur from compression at any point along the course of the radial nerve owing to acute trauma (eg, humerus fracture, Saturday night palsy), space-occupying lesion (eg, lipoma, ganglion), or local edema or inflammation, radial tunnel syndrome and PINS are more common from repetitive work activities.

👉 Radial tunnel syndrome and PINS have been described to occur at 1 of 5 potential sites. These sites, from proximal to distal, include the fibrous bands of the radiocapitellar joint, radial recurrent vessels (the leash of Henry), the tendinous edge of the extensor carpi radialis brevis, the arcade of Frohse, and the distal edge of the supinator. Most cases of RNE have been described at the arcade of Frohse. [https://pubmed.ncbi.nlm.nih.gov/26231964/]

👉 PIN entrapment may be confused with tennis elbow because the clinical symptoms, as well as the location and severity of the pain, are often alike [https://link.springer.com/article/10.1007/s00264-023-05805-x]. The most frequent compression site of the PIN is the arcade of Frohse, which is a fibrous arch formed by the proximal edge of the superficial head of the supinator muscle [https://pubmed.ncbi.nlm.nih.gov/19297265/].

👉 The anatomy of RNE is illustrated in the following figure [https://pubmed.ncbi.nlm.nih.gov/26231964/]

Hot off the press 🔥

Neuroinflammation in osteoarthritis. From pain to mood disorders

👉 Osteoarthritis (OA) is the most frequent form of musculoskeletal disease and affects millions of people in the world, especially the elderly. Thus, considering the increase in life expectancy, the number of subjects suffering from this pathology is growing every year. (https://ard.bmj.com/content/73/7/1323, https://www.sciencedirect.com/science/article/pii/S1521694214000059?via%3Dihub)

👉As pain intensity in OA shows no direct correlation has to structural joint damage (https://bmcmusculoskeletdisord.biomedcentral.com/articles/10.1186/1471-2474-12-144), various authors suggest the existence of a neuropathic or nociplastic component (https://link.springer.com/article/10.1007/s11926-012-0279-x, https://www.nature.com/articles/nrrheum.2014.47, https://pubmed.ncbi.nlm.nih.gov/38524267/)-

📘 In a recent review paper, Amodeo et al. (https://pubmed.ncbi.nlm.nih.gov/38556026/) describe the role of neuroinflammation in osteoarthritic pain and its interaction with mood disorders: Several studies have shown that, following injury or infections, the nervous system exhibits the typical features of inflammation, named neuroinflammation (https://www.mdpi.com/1420-3049/27/10/3194), a localized form of inflammation that occurs in PNS (nerves and ganglia) and CNS (spinal cord and brain, https://pubs.asahq.org/anesthesiology/article/129/2/343/18003/Neuroinflammation-and-Central-Sensitization-in).

💡 Numerous factors, such as trauma or the normal aging process, contribute to neuroinflammation. It is also a major cause and the driver of the progression of several neurodegenerative and neuropsychiatric diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), and depression (https://onlinelibrary.wiley.com/doi/10.1111/ejn.14720, https://www.mdpi.com/1422-0067/23/11/5938). In addition, neuroinflammation is associated with different types of pain involving the CNS, such as central neuropathic pain, but also quite unexpectedly with other pain conditions, such as OA pain.

👉Indeed, it is now clear that some painful conditions for a long time considered as being exquisitely peripheral (e.g., OA pain or chronic constriction injury of the sciatic nerve) also manifest typical features of centrally driven pain, including signs of neuroinflammation in the PNS and CNS. (https://pubmed.ncbi.nlm.nih.gov/38556026/))

👉 Primary afferent fibers innervating the joint project to several spinal cord segments and terminate in both the superficial and deeper laminae, where they make synapse with second-order dorsal horn neurons (https://pubmed.ncbi.nlm.nih.gov/17678850/), which become hyperexcitable following pathological changes in the joint, with a reduction of their firing threshold and an enhancement of their responses to joint stimulation (https://pubmed.ncbi.nlm.nih.gov/38556026/). Furthermore, sensitized dorsal horn neurons expand their receptive fields, a mechanism that underlies the spread of hypersensitivity from the knee joint to adjacent areas (https://www.nature.com/articles/s41598-018-25581-8). Thus, neuroinflammation in the spinal cord is a distinctive sign of persistent pain (https://journals.lww.com/anesthesia-analgesia/fulltext/2019/04000/microglial_modulation_as_a_target_for_chronic.19.aspx).

👉 Continuous nociceptive inputs from the joint by significantly elevated proinflammatory cytokines such as IL-1ß, IL-6 and TNF alpha driven by activated Schwann cells, satellite glial cells (SGCs) and infiltrating macrophages express specific markers, and release pro-inflammatory cytokines, thus contributing to the generation and maintenance of an inflammatory environment. affect the activation of non-neuronal cells, primarily microglia and less consistent astrocytes in the spinal cord and brain.

🧠 Neuroinflammation is further characterized by vascular changes resulting in increased blood–brain barrier (BBB) permeability, which leads to increased invasion of leukocytes, activation of glial cells, and eventually production of inflammatory mediators, including cytokines and chemokines (https://pubs.asahq.org/anesthesiology/article/129/2/343/18003/Neuroinflammation-and-Central-Sensitization-in).

🤔 The authors therefore hypothesize that an efficacious control of the neuroinflammatory components during OA (i.e. by new drugs like microglia inhibitors) and/or transdiagnostic interventions like exercise therapy, https://www.sciencedirect.com/science/article/pii/S0361923016300557 may represent a promising strategy to counteract both pain and related comorbidities.