Fisioterapia KARAM

07/12/2024

18/06/2024

📝👀

27/03/2024

Causes of headache and neck pain according to the affected site🤕

https://pubmed.ncbi.nlm.nih.gov/38388233/

👉 Various anatomical structures can cause referred pain in specific head and neck regions. When stimulated, multiple neck structures, such as muscles and their insertions, joint capsules, discs, ligaments, nerves, and nerve roots, are candidates for generating cervicogenic headache [https://journals.lww.com/jonmd/citation/1944/05000/referred_head_pain_and_its_concomitants__report_of.9.aspx, https://pubmed.ncbi.nlm.nih.gov/2402682/, https://pubmed.ncbi.nlm.nih.gov/16109118/, https://pubmed.ncbi.nlm.nih.gov/8059267/, https://pubmed.ncbi.nlm.nih.gov/17894927/] (s. figure).

👉 Dysfunction of the C2-3 zygapophyseal joint has been reported as one of the most common causes of CEH [https://pubmed.ncbi.nlm.nih.gov/9046716/, https://pubmed.ncbi.nlm.nih.gov/1740655/, https://pubmed.ncbi.nlm.nih.gov/8349476/].

▶︎ IS: midline interspinous tissues
▶︎ TP: myofascial trigger point
▶︎ ZA: zygapophyseal joint
▶︎ GON: greater occipital nerve

📷 Illustration: https://pubmed.ncbi.nlm.nih.gov/38388233/

11/03/2024

15/11/2023

Meniscal Tears Wrap-up 🦵
Based on https://pubmed.ncbi.nlm.nih.gov/37874571/ a.o.

👉 Classification
Meniscal tears (ie, separation of fibrous structure) can be classified as traumatic (resulting from excessive shear force) or degenerative (resulting from repetitive forces on a deteriorated meniscus). Tears can also be defined based on pattern and location, which can influence healing (s. illustration, https://pubmed.ncbi.nlm.nih.gov/37874571/).

👉 Epidemiology
According to a Swedish population-wide report from 2014, the annual incidence of clinically diagnosed meniscal tears was 79 (95% CI, 63-94) per 100 000 persons (https://arthritis-research.biomedcentral.com/articles/10.1186/ar4678), whereby acute traumatic tears are most prevalent in active young populations (aged 18-40 years), who engage in sports and often accompany cruciate ligament injuries (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8549477/). Degenerative tears, typically affecting older adults (aged 40 Years or older), are commonly found in patients with knee OA (63% of older adults with symptomatic OA showed a meniscal tear diagnosed by MRI, https://pubmed.ncbi.nlm.nih.gov/18784100/).

But it`s important to be aware of the high rate of asymptomatic, radiologically verified meniscal tears (19% of adults aged 40 years or older, https://pubmed.ncbi.nlm.nih.gov/29886437/).

👉 Risk factors
Risk factors are:
Playing pivoting sports, such as soccer and rugby but nor running for traumatic meniscal tears (https://pubmed.ncbi.nlm.nih.gov/23628788/) and
age (older than 60 years), gender (male), work-related kneeling and squatting, and climbing stairs (greater than 30 flights) were risk factors for degenerative meniscal tears (https://pubmed.ncbi.nlm.nih.gov/23628788/).

👉 Clinical Presentation
Meniscal tears typically present with knee pain localized to the joint line and an accompanying effusion: acute onset, often following a noncontact twisting/rotatory injury for traumatic tears, or insidious onset for degenerative tears.

Clinical tests help diagnose a meniscal tear by provocation of symptoms (s illustration): A meta-analysis of 5 studies (594 participants) suggested that a combination of clinical tests (including McMurray and joint line tenderness) is better than individual findings (positive likelihood ratio, 2.7 [95% CI, 1.4-5.1]; negative likelihood ratio, 0.4 [95% CI, 0.2-0.7], https://pubmed.ncbi.nlm.nih.gov/11585485/). Nevertheless these values imply only a small change to post test probability in diagnosis.

👉 Treatment
There is no evidence that surgical management is superior to rehabilitation-based approaches for most traumatic and degenerative meniscal tears. Evidence-based clinical guidelines recommend most patients with a symptomatic meniscal tear be referred to a physical the ra**st for 3 months or longer of rehabilitation-based care as first-line treatment (https://pubmed.ncbi.nlm.nih.gov/31154847/).

5 RCTs of young adults (mean age, 30-35 years) compared early surgery (arthroscopic partial meniscectomy or meniscal repair) with 12 weeks of exercise therapy (neuromuscular exercises 1-2 times weekly) with the option of surgery later if needed. Both RCTs found that both groups experienced clinically relevant improvements in pain and function with no clinically important differences between groups (https://evidence.nejm.org/doi/full/10.1056/EVIDoa2100038, https://pubmed.ncbi.nlm.nih.gov/35676079/), except with regard to mechanical symptoms (in favour of surgery, https://pubmed.ncbi.nlm.nih.gov/36878666/).

Meniscal repair seems to be associated with a lower progression to knee osteoarthritis at approximately six years of follow-up compared to partial meniscectomy, https://pubmed.ncbi.nlm.nih.gov/37812251/. However, meniscal repair is associated with a 14.8% (95% CI, 11.3%-18.3%) failure rate as reported by a meta-analysis of 38 studies (1358 patients, https://pubmed.ncbi.nlm.nih.gov/34161741/).

Illustration: https://pubmed.ncbi.nlm.nih.gov/37874571/

18/09/2023

Continuum Model of Tendon Pathology 💡

👉 Jill Cook et al. proposed the continuum pathology model in 2008, which has been widely recognized [https://pubmed.ncbi.nlm.nih.gov/18812414/, https://pubmed.ncbi.nlm.nih.gov/27127294/]. This model suggested that management may be optimized by tailoring interventions to the stage of pathology.

👉 They suggested that overload is the core factor driving tendinopathy and divided tendinopathy into three stages: reactive tendinopathy, tendon dysrepair and degenerative tendinopathy (s. graphic, https://pubmed.ncbi.nlm.nih.gov/37637777/).

1⃣ In the reactive tendinopathy, overload induced non-tendinogenic differentiation and proliferation of tendon cells [https://pubmed.ncbi.nlm.nih.gov/15336929/]. The production of large proteoglycans (e.g., aggrecan, versican and hyaluronan), which have a strong ability to bind water, increases. At this stage, Col (collagen) arrangement and vascularization do not change significantly. Patients may complain of pain and tendon swelling associated with acute overload, which can be completely relieved with adequate rest. The rounded and enlarged tendon cells, increased extracellular matrix (ECM), and confined space lead to increased intratendinous resting pressure [https://pubmed.ncbi.nlm.nih.gov/19371780/]. The accumulation of hydrophilic glycoproteins and proteoglycans reduces matrix permeability, which increases the intra-tendinous dynamic pressure [https://pubmed.ncbi.nlm.nih.gov/36323498/].

2⃣ Persistent overload leads to further increase of proteoglycan production as well as Col structure destruction and Col arrangement disorder. The inflammatory response caused by overload induces angiogenesis [https://pubmed.ncbi.nlm.nih.gov/28119539/]. This stage is called tendon dysrepair. Soreness and stiffness may occur in the morning or after being still for a longer period of time. Imaging may reveal focal structural abnormalities (e.g., thicking) with or without increased vascularization. If the load is optimized, this stage is still considered reversible. If not optimized, overload may impair vascularization and cause hypoxia, which led to leaking vessel and negative feedback increased intratendinous pressure [https://pubmed.ncbi.nlm.nih.gov/36323498/].

3⃣ Finally, the transformation of tendon tissue into scar-like tissue, accompanied by tendon cells exhaustion and significant matrix abnormalities, marks the stage of degenerative tendinopathy. The tendon may have one or more focal nodules, with or without diffuse thickening. If the tendon is under high load or the lesion is extensive enough, it may rupture.

06/09/2023

5⃣ Reasons Why Some Herniated Intervertebral Discs are Painless

👉 Despite clear findings of an herniated intervertebral disc (HIVD) on MRI or CT, many HIVDs do not cause pain. Jensen et al reported that only 36% of 98 asymptomatic patients had normal discs at all levels on MRI, with 52% showing a bulging disc at least at one level and 27% with a disc herniation. https://pubmed.ncbi.nlm.nih.gov/8208267/

💡 Shin & Chang propose five reasons why some HIVDs do not induce pain. https://www.dovepress.com/five-reasons-why-some-herniated-intervertebral-discs-are-painless-peer-reviewed-fulltext-article-JPR

1⃣ Chemical inflammation around the sinuvertebral nerve and nerve root is the main mechanism of pain in an HIVD, together with direct mechanical compression of these nociceptive nerves. https://pubmed.ncbi.nlm.nih.gov/12616153/. An HIVD can be painless if compression and inflammation are insufficient to cause pain.

2⃣ Although rare, motor weakness or sensory deficits without pain may develop following HIVDs. Painless weakness or sensory deficits following HIVDs suggest less of a transient, inflammatory component and more of an established mechanical component. Compression of nerve tissue in the absence of inflammation results in painless loss of motor or sensory function. https://www.sciencedirect.com/science/article/pii/S1040738315001008

3⃣ Secondary change in gene expression within the dorsal root ganglia (DRG) after HIVDs might be attributed to painless HIVDs. Gene expression within the DRG dynamically changes after an HIVD has developed, which alters the level of protein production of certain factors related to the inflammation process and nociception (ie pro-inflammatory, pro-apoptotic, and pro-nociceptive factors). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6404509/ If gene expression within the DRG changes in a way that prevents persistent inflammation through natural adaptation processes or treatments, there may be no pain even in the presence of an HIVD.

4⃣ Reorganisation of neural circuits within laminae I–III of the spinal dorsal horn could be the cause of a painless HIVD. Inhibitory and excitatory interneurons in these laminae play an important role in the nociceptive signalling pathway through modulating the activity of wide dynamic range neurons and nociceptive-specific neurons in the spinal dorsal horn. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6703564/ During reorganisation because of neuroinflammation, when inhibitory synapses are greatly increased compared with excitatory synapses, the secretion of neurotransmitters involved in the transfer of nociceptive signals is significantly reduced. In such situations, patients may not experience pain, even in the presence of an HIVD.

5⃣ An HIVD can be painless in patients with an effective pain coping strategy. Pain is a complex sensory and emotional experience that involves both physiological and psychological factors. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7680716/ Coping strategies can influence pain perception and the level of pain experienced by patients. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4957813/ Additionally, people with effective coping strategies may have a higher tolerance for pain, and their bodies may release pain-relieving chemicals that mask any discomfort from pain.

31/08/2023

Parte del proceso de rehabilitación en Tendinopatia bicipital.