Strong & Soft

10/01/2026

Sarcopenic obesity isn’t just “fat + muscle loss;" It’s a self-reinforcing biological loop. Poor diet, inactivity, and aging don’t act independently, they converge to reprogram metabolism, muscle, and adipose tissue at the same time.

What the system looks like ⬇️

🍔 Energy excess + inactivity
↑ Visceral & ectopic fat
↑ Insulin resistance
↓ Metabolic rate & anabolic hormones

🧠 Adipose tissue becomes inflammatory
↑ Cytokines
↑ Leptin resistance
↓ Protective signaling

💪 Muscle becomes metabolically impaired
↑ Myostatin & altered myokines
↑ Mitochondrial dysfunction
↑ Oxidative stress & anabolic resistance
This fat–muscle cross-talk accelerates decline rather than compensating for it.

Downstream consequences'

❤️ Higher cardiovascular risk
🧬 Increased cancer incidence
🩸 Greater diabetes risk
🦴 More fractures & frailty
🏥 Higher hospitalization, morbidity, mortality
♿ Reduced independence and quality of life

This isn’t just a weight problem. It’s a signaling problem. Sarcopenic obesity represents failure of muscle and adipose tissue to communicate properly, and treating one without the other rarely works.

Muscle is not just for movement.
Adipose tissue is not just storage.
Both are endocrine organs — and when their signals break, the system follows.

doi: 10.3389/fendo.2023.1185221

05/01/2026

GLUTEAL PAIN / SCIATIC PAIN

03/01/2026

🎊🌲Between Christmas and the beginning of the new year, we traditionally publish our ‘Best of’ series featuring the most influential posts of the year that is coming to an end.

📣 Today 🥇 # rank 9 in 2025

𝗕𝗲𝘆𝗼𝗻𝗱 𝗡𝗲𝗿𝘃𝗲 𝗘𝗻𝘁𝗿𝗮𝗽𝗺𝗲𝗻𝘁: 𝗔 𝗡𝗮𝗿𝗿𝗮𝘁𝗶𝘃𝗲 𝗥𝗲𝘃𝗶𝗲𝘄 𝗼𝗳 𝗠𝘂𝘀𝗰𝗹𝗲–𝗧𝗲𝗻𝗱𝗼𝗻 𝗣𝗮𝘁𝗵𝗼𝗹𝗼𝗴𝗶𝗲𝘀 𝗶𝗻 𝗗𝗲𝗲𝗽 𝗚𝗹𝘂𝘁𝗲𝗮𝗹 𝗦𝘆𝗻𝗱𝗿𝗼𝗺𝗲

▶️ Sciatica-like pain is frequently attributed to lumbar disc herniation or spinal stenosis, but in many patients, symptoms persist despite treatment of spinal causes, suggesting extraspinal etiologies (Guedes et al., 2020). Deep Gluteal Syndrome (DGS), first described by McCrory and Bell (1999) as sciatic nerve entrapment, has emerged as a significant source of nondiscogenic buttock and leg pain.

▶️ Prevalence estimates suggest that up to 17% of patients presenting with sciatica may have DGS (Kizaki et al., 2020). Traditionally viewed as a nerve entrapment disorder, more recent evidence highlights the contribution of muscular and tendinous pathologies—particularly enthesopathies of the deep external rotators and hamstring origin—as primary pain generators (Martin et al., 2015; De Lorenzis et al., 2023).
▶️ This evolving perspective necessitates a redefinition of DGS that integrates muscle–tendon pathology with neural mechanisms.

📘 In a brand-new narrative review Yoon et al. (2025, https://www.mdpi.com/2075-4418/15/19/2531 -diagnostics-15-02531) expand the conceptual framework of Deep Gluteal Syndrome beyond sciatic nerve entrapment, emphasizing muscle- and tendon-related pathologies as central contributors.

✅ Pathogenesis: In addition to sciatic nerve compression, pathologies such as ischiofemoral impingement, proximal hamstring tendinopathy, and enthesopathy of the deep external rotators can directly generate pain or secondarily irritate neural structures.

✅ Diagnosis: Clinical differentiation from lumbar radiculopathy is critical. Provocative maneuvers (FAIR, piriformis stretch, Pace’s test) and imaging (high-resolution MRI, MR neurography, dynamic ultrasonography) aid in distinguishing nerve-dominant from tendon-dominant subtypes. This differentiation might be a crucial factor in clinical reasoning.

✅ Treatment: A stepwise strategy is recommended—beginning with conservative care (load management, progressive tendon loading exercises , neural mobilization/desensitization), depending on tendon involvement or neural mechano-hypersensitive with refractory cases reserved for surgery. But, current evidence largely comprises case series and expert opinion underscoring the need for randomized controlled trials.

💡 Conclusion:

DGS should be reframed as a heterogeneous syndrome involving both neural entrapment and muscle–tendon pathology. Recognition of tendon-dominant and mixed subtypes allows for more precise diagnosis and tailored treatment strategies. Future work must focus on validating classification systems and establishing high-level evidence for emerging therapies.

📷 Illustration: Anatomy of the subgluteal space according to Koh (2021) https://pubmed.ncbi.nlm.nih.gov/33827758/

Diagram of the deep muscles of the subgluteal space, with the gluteus maximus muscle removed.

The sciatic nerve (1) typically emerges from beneath piriformis muscle (P), passing over the obturator internusegemellus tendon and muscle complex, quadratus femoris (QF) muscle and lateral to the hamstring origin (H).

Note that the gemellus muscles lie superior (SG) and inferior (IG) to the obturator internus tendon within the subgluteal space; the obturator internus muscle belly lies deep to the subgluteal space within the pelvis (not drawn).

Medial to the sciatic nerve lies the PCNT (2). The inferior gluteal nerve (3) and pudendal nerve (4) emerge from below piriformis further medially within the subgluteal space.

The superior gluteal nerve (5) is seen superiorly within the subgluteal space, passing superior to the piriformis muscle and adjacent to the SI joint.

📚 References

Battaglia, P.J., Mattox, R., Haun, D.W., Welk, A.B., & Kettner, N.W. (2016). Dynamic ultrasonography of the deep external rotator musculature of the hip: A descriptive study. PM&R, 8(7), 640–650. https://doi.org/10.1016/j.pmrj.2015.11.001

De Lorenzis, E., Natalello, G., Simon, D., Schett, G., & D’Agostino, M.A. (2023). Concepts of entheseal pain. Arthritis & Rheumatology, 75(3), 493–498. https://doi.org/10.1002/art.42299

Guedes, F., Brown, R.S., Lourenço Torrão-Júnior, F.J., Siquara-de-Sousa, A.C., & Pires Amorim, R.M. (2020). Nondiscogenic sciatica: What clinical examination and imaging can tell us? World Neurosurgery, 134, e1053–e1061. https://doi.org/10.1016/j.wneu.2019.11.083

Hauser, R.A., Lackner, J.B., Steilen-Matias, D., & Harris, D.K. (2016). A systematic review of dextrose prolotherapy for chronic musculoskeletal pain. Clinical Medicine Insights: Arthritis and Musculoskeletal Disorders, 9, 139–159. https://doi.org/10.4137/CMAMD.S39160

Hernando, M.F., Cerezal, L., Pérez-Carro, L., Abascal, F., & Canga, A. (2015). Deep gluteal syndrome: Anatomy, imaging, and management of sciatic nerve entrapments in the subgluteal space. Skeletal Radiology, 44(7), 919–934. https://doi.org/10.1007/s00256-015-2112-6

Kizaki, K., Uchida, S., Shanmugaraj, A., Aquino, C.C., Duong, A., Simunovic, N., Martin, H.D., & Ayeni, O.R. (2020). Deep gluteal syndrome is defined as a non-discogenic sciatic nerve disorder with entrapment in the deep gluteal space: A systematic review. Knee Surgery, Sports Traumatology, Arthroscopy, 28(10), 3354–3364. https://doi.org/10.1007/s00167-020-05966-x

Martin, H.D., Reddy, M., & Gómez-Hoyos, J. (2015). Deep gluteal syndrome. Journal of Hip Preservation Surgery, 2(2), 99–107. https://doi.org/10.1093/jhps/hnv029

McCrory, P., & Bell, S. (1999). Nerve entrapment syndromes as a cause of pain in the hip, groin and buttock. Sports Medicine, 27(4), 261–274. https://doi.org/10.2165/00007256-199927040-00005

Yen, Y.S., Lin, C.H., Chiang, C.H., & Wu, C.Y. (2024). Ultrasound-guided sciatic nerve hydrodissection can improve the clinical outcomes of patients with deep gluteal syndrome: A case-series study. Diagnostics, 14(4), 757. https://doi.org/10.3390/diagnostics14040757

Yoon, Y.H., Hwang, J.H., Lee, H.W., Lee, M., Park, C., Lee, J., Kim, S., Lee, J., de Castro, J.C., Lam, K.H.S., et al. (2025). Beyond nerve entrapment: A narrative review of muscle–tendon pathologies in deep gluteal syndrome. Diagnostics, 15(19), 2531. https://doi.org/10.3390/diagnostics15192531

03/01/2026

03/01/2026

Benign Sensory Trigeminal Neuropathy is a recognized clinical diagnosis characterized by persistent or recurring numbness (and sometimes tingling) in one or more divisions of the trigeminal nerve, without an identifiable structural, infectious, or systemic cause and without the characteristic lancinating pain of trigeminal neuralgia.

It is a diagnosis of exclusion, but an important one to consider.

Key Characteristics:

· Pure Sensory Deficit: The hallmark is isolated numbness (hypoesthesia) or altered sensation (paresthesia) in the face. There is no associated weakness of the masticatory muscles (innervated by the motor root of V3).

· Absence of Pain (or Minimal Pain): It lacks the severe, paroxysmal, electric shock-like pain of Trigeminal Neuralgia (TN). Patients may report a dull ache or discomfort, but the primary complaint is numbness.

· Chronic but Stable/Non-Progressive: Symptoms persist for months to years but typically do not worsen significantly and do not spread beyond the trigeminal territory.

· Commonly Affects V2 and/or V3: The maxillary (V2) and mandibular (V3) divisions are most often involved, sometimes in isolation.

Pathophysiology:

The exact cause is unknown. Leading theories include:

· Post-viral or Post-inflammatory Neuropathy: A prior subclinical viral infection (e.g., herpes simplex) may have caused localized nerve inflammation and demyelination.

· Immune-Mediated: A localized, benign autoimmune process targeting the trigeminal nerve or ganglion.

· Compressive Microvascular Loop: Similar to classic TN but causing a pure sensory deficit rather than pain, due to a "gentler" compression.

Diagnosis (A Diagnosis of Exclusion):

1. Clinical History: Chronic, stable, painless numbness in a trigeminal distribution.

2. Normal Neurological Exam: Aside from the sensory deficit in the affected division(s), the exam is normal. Corneal reflex is often preserved.

3. Negative MRI: A high-resolution MRI of the brain and cranial nerves is mandatory to rule out all other causes (MS plaque, tumor, vascular compression, etc.). The MRI in benign sensory trigeminal neuropathy is normal.

4. Negative Lab Work: Blood tests (e.g., for Lyme, autoimmune disease, vitamin B12 deficiency, diabetes) are typically negative.

Management:

Since it is benign and self-limiting in many cases, management is conservative and supportive.

1. Reassurance and Education: This is the cornerstone of treatment. Explaining the diagnosis, its benign nature, and excellent long-term prognosis alleviates significant anxiety for the patient.

2. Observation/Monitoring: Many cases require no active treatment. Regular follow-up
to ensure stability is appropriate.

3. Symptomatic Treatment (if needed):

· For bothersome paresthesias or dysesthesia (unpleasant tingling), a trial of low-dose neuropathic pain medications may be considered (e.g., gabapentin, pregabalin, or amitriptyline).

· Note: These are for symptom control, not to alter the disease course.

4. Avoid Unnecessary Procedures: There is no role for surgical interventions like microvascular decompression or rhizotomy in this condition, as the risks outweigh the benefits.

Prognosis:

· Generally Excellent. The numbness may:

· Resolve completely over months to a few years.

· Persist but remain stable and non-bothersome.

· Rarely, it may have minor fluctuations.

· Progression to classic Trigeminal Neuralgia is uncommon but possible.

Key Differential to Rule Out:

· Numb Chin Syndrome (Mental Neuropathy): Isolated V3 numbness can be a sign of systemic malignancy (e.g., breast cancer, lymphoma metastasis). A full systemic work-up is crucial.

· Trigeminal Sensory Neuropathy from Connective Tissue Disease (e.g., Sjögren's, Scleroderma).

· Post-Herpetic Neuralgia (without active rash).

· Compressive Lesions (as previously discussed).

In summary, Benign Sensory Trigeminal Neuropathy is a favorable diagnosis made after excluding all serious causes. It is managed primarily with reassurance, occasional symptomatic medication, and routine follow-up to confirm its non-progressive nature.

03/01/2026

Arthritis is not a single disease but a group of conditions that cause joint pain, swelling, stiffness, and reduced movement. Each type has a different cause, pattern, and treatment, which is why correct diagnosis is so important.

🔍 Common Types of Arthritis Explained:

🔹 Osteoarthritis (OA)
The most common form, caused by wear and tear of cartilage. Commonly affects the knees, hips, spine, and hands, leading to pain and stiffness that worsens with activity.

🔹 Rheumatoid Arthritis (RA)
An autoimmune disease where the immune system attacks joint lining. It usually affects joints symmetrically and causes prolonged morning stiffness, swelling, and fatigue.

🔹 Psoriatic Arthritis
Seen in people with psoriasis. It can cause swollen fingers or toes (sausage digits), nail changes, and joint pain along with skin rashes.

🔹 Gout
A metabolic arthritis caused by uric acid crystal deposition in joints. It often begins suddenly in the big toe, with severe pain, redness, and swelling.

🔹 Ankylosing Spondylitis
A chronic inflammatory arthritis mainly affecting the spine and sacroiliac joints, leading to back pain, stiffness, and in advanced cases, spinal fusion.

🔹 Juvenile Idiopathic Arthritis (JIA)
Occurs in children under 16 years, causing joint swelling, pain, and stiffness. Early treatment is crucial to prevent growth and joint problems.

🔹 Septic (Infectious) Arthritis
Caused by infection in the joint. It presents with severe pain, swelling, fever, and requires urgent medical care.

03/01/2026

El entramado nervioso que da vida a tus movimientos y sensibilidad.

Lo que ves en esta imagen es el plexo braquial, una red compleja de nervios que se origina en la médula espinal, específicamente entre las vértebras cervicales C5 y torácica T1, y que se ramifica para dar sensibilidad y fuerza a todo el miembro superior.

Cada movimiento de tu hombro, cada contracción de tu brazo, cada sensación en tu mano, depende de esta intrincada conexión. El plexo braquial funciona como un “centro de distribución eléctrica” del cuerpo: de él nacen nervios tan importantes como el nervio mediano, cubital, radial, axilar y musculocutáneo, responsables de acciones tan finas como escribir, tocar un instrumento o simplemente sostener un objeto.

Un daño en este plexo, ya sea por un traumatismo, una compresión o una lesión quirúrgica, puede cambiar radicalmente la vida de una persona, afectando la movilidad, la fuerza o la sensibilidad del brazo.

Este sistema nervioso no solo es anatomía: es la base silenciosa de cada gesto y cada caricia que damos con nuestras manos.

La información presentada tiene carácter académico y educativo.

31/12/2025