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Φυσιοκίνηση Κέντρο Φυσικοθεραπείας Λαμίας Κέντρο Φυσικοθεραπείας - Κινησιοθεραπείας

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31/12/2025

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🧩 𝐓𝐡𝐞 𝐌𝐲𝐬𝐭𝐞𝐫𝐲 𝐨𝐟 𝐭𝐡𝐞 𝐒𝐭𝐫𝐞𝐭𝐜𝐡-𝐒𝐡𝐨𝐫𝐭𝐞𝐧𝐢𝐧𝐠 𝐂𝐲𝐜𝐥𝐞: 𝐌𝐞𝐜𝐡𝐚𝐧𝐢𝐜𝐚𝐥 𝐨𝐫 𝐍𝐞𝐮𝐫𝐚𝐥?

■ In human movement, muscles often perform better when they are actively stretched immediately before they shorten. This phenomenon is known as the Stretch-Shortening Cycle (SSC).

■ A common example is the way we naturally dip down (stretch) before jumping up (shorten).
■ This sequence produces higher force, work, and power compared to a shortening movement that starts from a standstill—a boost known as the SSC effect.
■ While the existence of the SSC effect is well-documented, the exact physiological reasons behind it are debated.

■ Scientists generally group the causes into two categories:

■ ⚙️ Mechanical factors: Changes within the muscle fibers themselves, such as elastic energy return or the engagement of the protein titin.
■ 🧠 Neural factors: Changes in the nervous system, such as reflexes or increased excitability in the spinal cord and motor cortex.

■ A 2025 study by Rissmann et al. sought to determine if the brain and spinal cord modulate their excitability during the shortening phase of the SSC to contribute to this performance boost.

🔬 The Study Design

■ The researchers studied the plantar flexor muscles (calf muscles) of 18 healthy adults.
■ Participants performed two types of movements on a dynamometer, carefully matched to have the same level of muscle activity (EMG):
■ ➡️ Pure Shortening (SHO): The muscle shortened without a prior stretch.
■ 🔁 Stretch-Shortening Cycle (SSC): The muscle was actively stretched immediately before shortening.
■ To measure neural excitability during these movements, the researchers used advanced stimulation techniques:
■ 🧠 Transcranial Magnetic Stimulation (TMS): To measure cortical excitability (how responsive the motor cortex in the brain is).
■ 🧠 Cervicomedullary Electrical Stimulation (CES): To measure spinal excitability (how responsive the spinal cord is).
■ 📈 Electromyography (EMG): To detect stretch reflexes.

📊 Key Findings

■ 1. The SSC Effect is Real but Not Neural
■ As expected, the participants produced significantly more torque (about 12% more) during the SSC contractions compared to the pure shortening contractions.
■ However, when the researchers looked at the nervous system, they found no corresponding boost:
■ 🚫 No Cortical Change: There was no difference in cortical excitability between the SSC and pure shortening conditions.
■ 🚫 No Spinal Change: Similarly, spinal excitability remained unaltered during the shortening phase of the SSC.
■ 🚫 Absent Reflexes: The researchers found almost no stretch reflex activity during the active stretch phase (observed in only 1 out of 15 participants).

■ 2. The Mechanism is Mechanical
■ Because the performance increased (the 12% boost) while the neural drive from the brain and spine remained constant, the authors concluded that the SSC effect in this context is driven by mechanical mechanisms rather than neural ones.
■ This supports the theory that intrinsic properties of the muscle sarcomeres—such as "residual force enhancement" (rFE) and altered cross-bridge kinetics—are responsible for the extra power.

■ 3. Residual Force Depression (rFD)
■ The study also examined what happened after the movement, during a steady isometric hold.
■ Muscles typically produce less force after shortening, a phenomenon called Residual Force Depression (rFD).
■ The study found that steady-state torque was significantly lower following the SSC compared to the reference contractions.
■ Interestingly, just like the shortening phase, this depression in force was not correlated with any changes in cortical or spinal excitability.

🧠 Conclusion

■ The results of this study indicate that the performance benefits of the stretch-shortening cycle—at least during submaximal, controlled movements—are not associated with modulations in cortical or spinal excitability.
■ The nervous system does not appear to "ramp up" its responsiveness to facilitate the movement.
■ Instead, the boost is derived from mechanical factors triggered during the active stretch, which persist to enhance force during the subsequent shortening phase.

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⚠️Disclaimer: Sharing a study or a part of it is NOT an endorsement. Please read the original article and evaluate critically.⚠️

Link to Article 👇

31/12/2025

📊 Research Summary: Spinal manipulation alone did not differ from guideline-based medical care for disability or pain in adults with increased risk for chronic low back pain.

https://ja.ma/4jglgPj

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30/12/2025

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📚 December’s Article of the Month — Reliability of the Short Physical Performance Battery (SPPB): a systematic review with meta-analysis

This systematic review and meta-analysis, published in European Geriatric Medicine, examines the reliability of the Short Physical Performance Battery (SPPB), one of the most widely used tools to assess physical performance in older adults. 🧓📊

🔍 Why it matters: The findings confirm that the SPPB total score demonstrates good intra- and inter-rater reliability across different settings and populations. This reinforces its robustness and usefulness in both clinical practice and research when evaluating physical function and monitoring functional change over time.

📖 Read the full article: https://bit.ly/44M2323

30/12/2025

Kaplan Fibers of Iliotibial Band: “The ITB and associated anatomical structures in the right knee, the superior lateral genicular artery passes anteriorty to the distal KF, ALL, anterolateral ligament; FCL, fibular collateral ligament; GT, lateral gastrocnemius tendon; ITB, iliotibial band; LE, lateral epicondyle; PLT, popliteus tendon.”

- Godin et al.'s article: 'A Comprehensive Reanalysis of the Distal Iliotibia Band: Quantitative Anatomy, Radiographic Markers, and Biomechanical Properties.' AmJ Sports Med., 2017 Sep:45:2595-603 with permission from SAGE Publications under STM Permissions Guidelines (11).

Image Credit: Authors

EFORT

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http://www.secretlifeoffascia.com/

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28/12/2025

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💪 Arthrogenic Muscle Inhibition is a game-changer in ACL care. In a large multicenter cohort, over half of ACL-injured patients showed AMI—yet most cases were reversible when properly identified. The validated SANTI classification now offers clinicians a simple tool to detect and treat AMI before surgery, improving outcomes and preventing stiffness. Read more here: https://doi.org/10.1002%2Fksa.12790

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28/12/2025

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𝗧𝗵𝗲 𝗚𝘂𝘁-𝗗𝗶𝘀𝗰 𝗔𝘅𝗶𝘀: 𝗛𝗼𝘄 𝗬𝗼𝘂𝗿 𝗠𝗶𝗰𝗿𝗼𝗯𝗶𝗼𝗺𝗲 𝗠𝗮𝘆 𝗕𝗲 𝗖𝗮𝘂𝘀𝗶𝗻𝗴 𝗬𝗼𝘂𝗿 𝗕𝗮𝗰𝗸 𝗣𝗮𝗶𝗻

⬛ 𝙊𝙫𝙚𝙧𝙫𝙞𝙚𝙬

🔹 Low back pain (LBP) is a leading cause of disability worldwide, with Intervertebral Disc Degeneration (IDD) widely regarded as its primary driver
🔹 While mechanical stress, age, and genetics are traditional suspects, recent research has unveiled a surprising culprit: the trillions of microorganisms living in your digestive tract
🔹 This connection is now known as the gut-disc axis
🔹 The following post details how the gut microbiome influences spinal health, challenging the long-held belief that intervertebral discs are sterile environments

⬛ 𝙏𝙝𝙚 𝙋𝙖𝙧𝙖𝙙𝙞𝙜𝙢 𝙎𝙝𝙞𝙛𝙩: 𝙏𝙝𝙚 𝘿𝙞𝙨𝙘 𝙞𝙨 𝙉𝙤𝙩 𝙎𝙩𝙚𝙧𝙞𝙡𝙚

🧫 Historically, the medical community viewed the intervertebral disc (IVD) as a sterile organ
🧫 Recent studies using advanced sequencing have identified bacteria within these discs
🧫 There is a significant overlap in bacterial species found in the gut and those found in the IVD, suggesting that the two environments "talk" to one another

⬛ 𝙈𝙞𝙘𝙧𝙤𝙗𝙞𝙤𝙩𝙖 𝙋𝙧𝙤𝙛𝙞𝙡𝙚𝙨

🟢 Healthy Discs ▪ Tend to contain an abundance of Firmicutes, Actinobacteria, and Saccharopolyspora
▪ These are associated with strong intestinal barriers and antibacterial protection
🔴 Degenerated/Herniated Discs ▪ Show higher levels of pathogenic bacteria such as Pseudomonas veronii, Streptococcus anginosus, and notably Propionibacterium acnes (P. acnes)
▪ P. acnes is a bacteria strongly associated with bone and joint infections

⬛ 𝙃𝙤𝙬 𝙩𝙝𝙚 𝙂𝙪𝙩 𝘿𝙚𝙨𝙩𝙧𝙤𝙮𝙨 𝙩𝙝𝙚 𝘿𝙞𝙨𝙘: 𝙏𝙝𝙧𝙚𝙚 𝙈𝙚𝙘𝙝𝙖𝙣𝙞𝙨𝙢𝙨

1. Bacterial Translocation (The "Leaky" Barrier) 🚧 When the gut microbiome is unbalanced, the intestinal epithelial barrier becomes permeable
▪ Invasion:
▫ Bacteria escape the gut, enter the bloodstream, and reach the IVD
▪ The Perfect Hiding Spot:
▫ Because the interior of a disc lacks oxygen (anaerobic) and has limited immune surveillance (it is "immune-privileged"), it becomes an ideal breeding ground for anaerobic bacteria like P. acnes
▪ Destruction:
▫ Once established, these bacteria release toxins and trigger inflammation
▫ This leads to the ingrowth of blood vessels and nerves into the disc, destroying its structure and amplifying pain signals sent to the brain

2. Immune System Regulation 🛡 The gut microbiome acts as a "training ground" for the body's immune system
▪ Systemic Inflammation:
▫ Dysbiosis weakens the gut lining, causing immune cells to release pro-inflammatory cytokines (such as IL-6 and TNF-α) into the circulation
▪ Remote Damage:
▫ These inflammatory molecules migrate to the spine
▫ They stimulate disc cells to degrade their own structural matrix (collagen and aggrecan), leading to herniation and degeneration
▪ Pain Sensitization:
▫ The influx of immune cells stimulates the production of nerve growth factor (NGF)
▫ This causes pain-sensing nerve fibers to grow into the disc, causing chronic back pain

3. Metabolite and Nutrient Regulation 🧪

Gut bacteria are responsible for metabolizing food into chemical signals, including Short-Chain Fatty Acids (SCFAs) like propionate and butyrate
▪ Bone Remodeling:
▫ While SCFAs generally support bone health by regulating osteoclasts, their diffusion into the IVD can have mixed effects
▫ In degenerated discs, the presence of these metabolites and specific receptors may contribute to calcification of the disc and cartilage endplates
▪ Barrier Maintenance:
▫ A healthy mucus layer in the gut, maintained by specific bacteria and mucins (like MUC2), is essential to prevent toxic metabolites from entering the bloodstream and reaching the spine

⬛ 𝙍𝙚𝙡𝙖𝙩𝙚𝙙 𝘽𝙞𝙤𝙡𝙤𝙜𝙞𝙘𝙖𝙡 𝘼𝙭𝙚𝙨

🔗 Gut-Bone Marrow Axis
▪ Gut dysbiosis can damage the bone marrow niche
▪ Since the spine consists of vertebral bodies containing marrow, inflammation here can lead to aberrant immune cell formation within the spine itself, contributing to systemic inflammation and pain

🔗 Gut-Bone Axis
▪ Hormones secreted by the gut after eating (like GIP and GLP-1) regulate bone remodeling
▪ If the gut environment is compromised, it can lead to decreased bone mineral density in the vertebrae, which correlates with low back pain

⬛ 𝙁𝙪𝙩𝙪𝙧𝙚 𝘿𝙞𝙧𝙚𝙘𝙩𝙞𝙤𝙣𝙨 𝙞𝙣 𝘿𝙞𝙖𝙜𝙣𝙤𝙨𝙞𝙨 𝙖𝙣𝙙 𝙏𝙧𝙚𝙖𝙩𝙢𝙚𝙣𝙩

🧬 Diagnostics
▪ Physicians may eventually use stool or blood samples to analyze microbiome diversity using 16S rRNA sequencing
▪ This may help detect biomarkers for disc degeneration

💊 Therapeutics

▪ Treatments could shift from purely mechanical interventions (like surgery) to biological ones
▪ Targeting the gut microbiome may inhibit the cascade of inflammation that destroys the disc

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⚠️Disclaimer: Sharing a study or a part of it is NOT an endorsement. Please read the original article and evaluate critically.⚠️

Link to Article 👇

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18/12/2025

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𝗨𝗻𝗱𝗲𝗿𝘀𝘁𝗮𝗻𝗱𝗶𝗻𝗴 𝗣𝗮𝘁𝗲𝗹𝗹𝗼𝗳𝗲𝗺𝗼𝗿𝗮𝗹 𝗣𝗮𝗶𝗻 𝗦𝘆𝗻𝗱𝗿𝗼𝗺𝗲: 𝗔 𝗖𝗼𝗺𝗽𝗿𝗲𝗵𝗲𝗻𝘀𝗶𝘃𝗲 𝗖𝗹𝗶𝗻𝗶𝗰𝗮𝗹 𝗚𝘂𝗶𝗱𝗲

Patellofemoral Pain Syndrome (PFPS) is a prevalent and often persistent condition, frequently referred to as "runner's knee," though it affects a much broader population. It is defined as an umbrella term for pain arising from the patellofemoral joint (where the kneecap meets the thigh bone) or adjacent soft tissues.
This guide explores the anatomy, causes, diagnosis, and evidence-based management of PFPS.

🦴 1. 𝗧𝗵𝗲 𝗔𝗻𝗮𝘁𝗼𝗺𝘆 𝗼𝗳 𝘁𝗵𝗲 𝗣𝗿𝗼𝗯𝗹𝗲𝗺

■ To understand the pain, one must understand the mechanics. The knee consists of two major joints, but PFPS is localized to the patellofemoral joint.
■ The Mechanism: The patella (kneecap) sits within the trochlear groove of the femur. In a healthy knee, the patella glides smoothly over the femoral cartilage, lubricated by synovial fluid.
■ Stability: The joint relies on a complex system for stability. The joint capsule and medial collateral ligament provide structural support, while the retinaculum (ligamentous bands) and patellofemoral ligaments ensure proper tracking during movement.

❓ 2. 𝗪𝗵𝘆 𝗗𝗼𝗲𝘀 𝗜𝘁 𝗛𝗮𝗽𝗽𝗲𝗻? (𝗘𝘁𝗶𝗼𝗹𝗼𝗴𝘆)

■ PFPS is rarely caused by a single event. It is typically multifactorial, resulting from a combination of overuse, anatomical abnormalities, and muscular imbalances.
■ The Core Issue: Patellar Maltracking
Abnormal tracking causes excessive stress on the cartilage and is often described as the patella being pulled too far laterally.

■ Contributing Factors

■ Muscle Imbalance: Weakness in the Vastus Medialis Obliquus (VMO) combined with a tight or dominant Vastus Lateralis pulls the patella laterally, increasing pressure on the joint surface.
■ The Hip Connection: Patients often demonstrate weak hip abductors and external rotators, causing thigh adduction and internal rotation during activities, altering knee mechanics.
■ Tight Structures: A tight iliotibial (IT) band, hamstrings, or calf muscles can increase posterior force on the knee or pull the patella laterally.

🔍 3. 𝗜𝗱𝗲𝗻𝘁𝗶𝗳𝘆𝗶𝗻𝗴 𝗣𝗙𝗣𝗦: 𝗦𝘆𝗺𝗽𝘁𝗼𝗺𝘀 𝗮𝗻𝗱 𝗗𝗶𝗮𝗴𝗻𝗼𝘀𝗶𝘀

■ PFPS is characterized by a gradual, non-traumatic onset of pain located around or behind the kneecap (peripatellar or retropatellar).

■ Common Clinical Signs

■ The "Cinema Sign": Pain experienced when sitting with the knees flexed for long periods.
■ Activity-Related Pain: Symptoms worsen with stair climbing, squatting, running, or kneeling.
■ Pain Behavior: Walking downhill often loads the joint more than walking uphill, provoking pain. Conversely, pain walking uphill may indicate gluteal impairment or tight calves.

■ Diagnosis

■ Diagnosis is primarily a process of exclusion — ruling out other pathologies like patellar tendinopathy or meniscal tears.
A diagnosis is supported if there is:
■ Retropatellar or peripatellar pain.
■ Reproduction of pain during squatting or activities that load the joint in a flexed position.

💪 4. 𝗠𝗮𝗻𝗮𝗴𝗲𝗺𝗲𝗻𝘁 𝗮𝗻𝗱 𝗥𝗲𝗵𝗮𝗯𝗶𝗹𝗶𝘁𝗮𝘁𝗶𝗼𝗻

The gold standard for treating PFPS is exercise therapy. Combining hip and knee exercises is superior to knee exercises alone.

🧱 A. The Rehabilitation Pillars

■ Quadriceps Strengthening: Strengthening the quads is essential. Exercises must be pain-free.
■ VMO Focus: Rehabilitation should aim to improve firing speed and endurance. VMO exercises are most effective in the range of 0 to 30 degrees of flexion. Pain and swelling can inhibit the VMO, making pain reduction necessary.

■ Hip Strengthening: Targeting hip abductors and lateral rotators leads to better functional outcomes and reduced pain.

■ Proprioceptive & Functional Training: Patients often have decreased proprioception. Functional strength training and proprioceptive drills improve neuromuscular control and are highly recommended.

🔄 B. Open vs. Closed Kinetic Chain

■ Both Open Kinetic Chain (foot free) and Closed Kinetic Chain (foot fixed) exercises are effective.
■ Open Chain: Should be performed in a pain-free range, typically between 40° and 90° of flexion.
■ Closed Chain: More functional but requires careful load management.

➕ C. Adjunct Therapies

■ Foot Orthoses: Prefabricated orthoses can enhance functional performance and may help prevent osteoarthritis in the long term.
■ Taping: Patellar taping is recommended as an adjunct to exercise to help manage pain and alignment.
■ Electrotherapy: Generally not recommended as a primary treatment. However, specific electrical stimulation of the VMO may be considered to address neuromuscular imbalances.

■ 🚫 5. 𝗪𝗵𝗮𝘁 𝘁𝗼 𝗔𝘃𝗼𝗶𝗱

■ Painful Exercises: Pain inhibits muscle function (specifically the VMO) and prolongs the condition.
■ Ignoring the Hips: Treating only the knee often results in suboptimal outcomes.

🚆 𝗦𝘂𝗺𝗺𝗮𝗿𝘆 𝗔𝗻𝗮𝗹𝗼𝗴𝘆

■ The patellofemoral joint is like a train on a track.
■ The patella is the train, and the femoral groove is the track.
■ Muscular imbalances act like a mechanical failure pulling the train off-center, creating grinding and pain.
■ Rehabilitation focuses on fixing not just the train but the control systems — the hips and thigh muscles — to ensure smooth movement.

08/12/2025

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