![Schematic model of intervertebral foramens dimensional changes during excessive lateral tilting and backward rotation of the pelvis in patients with calf muscle weakness: Marked decrease in the foraminal height and area in B.2 compared with A.2. Marked decrease in the foraminal width and area in B.3 compared with A.3. Marked decrease in the foraminal height, width and area in B.4 compared with A.4. Marked increase in the disc bulging and facet joint compression in B.2, B.3, and B.4 compared with A.1, A.2, and A.3 respectively. NIVD = normal intervertebral disk, DIVD = degenerated intervertebral disk, SVB = superior vertebral body, IVB = inferior vertebral body, NR = nerve root, LF = ligamentum flavum, FJ = facet joint. A modified figure based on illustration from Takahashi et al. (2022) [14]](https://www.researchgate.net/profile/Efrem-Kentiba/publication/382592001/figure/fig2/AS:11431281263351073@1722032144290/Schematic-model-of-intervertebral-foramens-dimensional-changes-during-excessive-lateral_Q320.jpg)
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1
Ankle Spine Syndrome "Raffet Syndrome II". Ipsilateral Calf
Muscle Weakness Induces Contralateral Lumbar Radiculopathy
Ahmed Raffet1ABCD, Mark Laslett2ABCD, Wolf Schamberger3ABD, Amir Beltagi1ACD, Mohamed M.
ElMeligie4ABD, Efrem Kentiba*5ACD, Noha Khaled1ACD, Hossam Y. Sayed6ABD, Ahmed H.
Omar7ABD, Maged M. Hawana8ACD, Hossam Eddein Fawaz1ABCD
1Department of Biomechanics, Faculty of Physical Therapy, Cairo University, Giza Egypt
2Department of Physical Therapy, Faculty of Medical Sciences, Auckland University, New
Zealand
3Department of Medicine, Division of Physical Medicine and Rehabilitation, University of
British Columbia, Canada
4 Department of Basic Sciences for Physical Therapy, Faculty of Physical Therapy, Ahram
Canadian University, Giza Egypt
5Department of Sports Science, College of Natural and Computational Sciences, Arba Minch
University, Arba Minch Ethiopia
6Department of Anatomy and Embryology, Faculty of Medicine, Cairo University, Giza Egypt
7Department of Neurosurgery, Faculty of Medicine, Cairo University, Giza Egypt;
8Department of Radiology, Faculty of Medicine, Cairo University, Giza, Egypt
DOI: https://doi.org/10.58962/HSR.2026.12.2
Author's contribution; A-Study design; B- Data collection; C- Statistical analysis; D- Manuscript
Preparation; E- Fundus Collection
Corresponding author: Dr. Efrem Kentiba, efre89@gmail.com
How to Cite
Raffet A, Laslett M, Schamberger W, Beltagi A, ElMeligie MM, Kentiba E, Khaled N, Sayed HY, Omar
AH, Hawana MM, Fawaz HE. Ankle Spine Syndrome "Raffet Syndrome II" Ipsilateral Calf Muscle
Weakness Induces Contralateral Lumbar Radiculopathy. Health, Sport, Rehabilitation. 2026;12(2): .
https://doi.org/10.58962/HSR.2026.12.2.
Abstract
Background and Purpose
Lumbar disc herniation and radiculopathy are considered worldwide health conditions. Due to its high prevalence
and recurrence, clinicians should have an understanding of the underlying pathomechanics to prevent permanent
neurological deficits. Although the body is recognized as a kinetic chain, a limited research body explored the
biomechanical impact of a distal problem can have on the spine. This study aimed to describe a new clinical
condition called Ankle Spine Syndrome or “Raffet Syndrome IIˮ by investigating the potential biomechanical
mechanism underlying the radiculopathy contralateral to the side of calf muscle weakness, and to propose the
treatment for this condition in patients with Lumbar disc herniation and radiculopathy.
Material and methods
A study focused on six patients (2 males and 4 females) who suffered from chronic ankle injury and calf muscle
weakness on the side opposite to the lumbar disc herniation and radiculopathy. Initially, the patients underwent
open and closed chain strengthening exercises for the calf muscle, such as double and single leg raises, wall sits
calf raises, and seated calf raises for 6 to 8 weeks. Subsequently, supplementary treatments, including lumbar
2
stabilization exercises, core training, and myofascial release therapy, were added for another 2 to 3 months. The
intensity of perceived pain and disability index were assessed before and after each treatment.
Results
Substantial improvement in back pain, radiculopathy, and functional disability was observed after the initial
treatment. Symptoms were completely resolved with the addition of adjunctive treatment. Furthermore, a follow-
up after six months of a personalized home exercise program showed sustained recovery based on clinical
outcome measures.
Conclusion
Calf muscle weakness can induce contralateral lumbar radiculopathy through a series of abnormal biomechanical
mechanisms affecting the lumbopelvic rhythm and consequently the lumbar spine.
Keywords: Ankle Spine Syndrome, Chronic Low Back Pain, Raffet Syndrome II, Lumbar Disc Herniation,
Contralateral Lumbar Radiculopathy, Calf Muscle Weakness
Анотація
Ахмед Раффет, Марк Ласлетт, Вольф Шамбергер, Амир Бельтаги, Мохамед М. ЭльМелиги, Ефрем
Кентиба, Ноха Халед, Хоссам Ю. Сайед, Ахмед Х. Омар, Магед М. Хавана, Хоссам Эддейн Фаваз. Синдром
гомілковостопного відділу хребта «Синдром Раффета II». Слабкість іпсилатеральних литкових м'язів
викликає контрлатеральну поперекову радикулопатію
Обгрунтування та мета
Грижа поперекового диска та радикулопатія вважаються загальносвітовими захворюваннями. Через його
високу поширеність і рецидиви лікарі повинні мати розуміння основної патомеханіки, щоб запобігти
постійному неврологічному дефіциту. Незважаючи на те, що тіло визнається кінетичним ланцюгом,
обмежена кількість дослідників вивчала біомеханічний вплив дистальної проблеми на хребет. Це
дослідження мало на меті описати новий клінічний стан під назвою «синдром гомілковостопного хребта»
або «синдром Раффета II» шляхом дослідження потенційного біомеханічного механізму, що лежить в основі
радикулопатії, контралатеральної до сторони слабкості литкових м’язів, і запропонувати лікування цього
стану у пацієнтів з грижею міжхребцевого диска поперекового відділу. і радикулопатія.
Матеріал і методи
Дослідження було зосереджено на шести пацієнтах (2 чоловіки та 4 жінки), які страждали від хронічної
травми гомілковостопного суглоба та слабкості литкового м’яза на стороні, протилежній грижі
міжхребцевого диска та радикулопатії. Спочатку протягом 6–8 тижнів пацієнти проходили вправи для
зміцнення литкового м’яза відкритого та закритого ланцюга, такі як підйоми подвійної та однієї ноги,
підйоми литок сидячи та сидячи. Згодом додаткове лікування, включаючи вправи для стабілізації
поперекового відділу, базове тренування та терапію міофасціального звільнення, було додано ще на 2-3
місяці. Інтенсивність відчутного болю та індекс непрацездатності оцінювали до та після кожного лікування.
Результати
Після початкового лікування спостерігалося суттєве покращення болю в спині, радикулопатії та
функціональної недостатності. Симптоми повністю зникли після додавання додаткового лікування. Крім
того, подальше спостереження після шести місяців індивідуальної домашньої програми вправ показало
стійке одужання на основі вимірювань клінічних результатів.
Висновок
Слабкість литкових м’язів може спричинити контралатеральну поперекову радикулопатію через низку
аномальних біомеханічних механізмів, що впливають на попереково-тазовий ритм і, як наслідок, на
поперековий відділ хребта.
Ключові слова: синдром гомілковостопного хребта, хронічний біль у попереку, синдром Раффета II,
поперекова грижа диска, контралатеральна поперекова радикулопатія, слабкість литкового м’яза
Аннотация
3
Ахмед Раффет, Марк Ласлетт, Вольф Шамбергер, Амір Бельтагі, Мохамед М. ЕльМелігі, Ефрем Кентіба,
Ноха Халед, Хоссам І. Сайєд, Ахмед Х. Омар, Магед М. Гавана, Хоссам Еддін ФавазСиндром нарушенния
инервации голеностопа «Синдром Раффета II». Слабость ипсилатеральных икроножных мышц вызывает
контрлатеральную поясничную радикулопатию
Обоснование и цель
Грыжа поясничного диска и радикулопатия считаются заболеваниями во всем мире. Из-за высокой
распространенности и рецидивов клиницисты должны понимать основную патомеханику, чтобы
предотвратить стойкий неврологический дефицит. Хотя тело признано кинетической цепью, ограниченное
количество исследований изучало биомеханическое воздействие дистальных проблем на позвоночник. Это
исследование было направлено на описание нового клинического состояния, называемого синдромом
голеностопного позвоночника или «синдром Раффета II», путем изучения потенциального
биомеханического механизма, лежащего в основе радикулопатии, противоположной стороне слабости
икроножных мышц, и предложения лечения этого состояния у пациентов с грыжей поясничного отдела
позвоночника. и радикулопатия.
Материал и методы
Исследование было сосредоточено на шести пациентах (2 мужчин и 4 женщины), которые страдали
хронической травмой голеностопного сустава и слабостью икроножных мышц на стороне,
противоположной грыже поясничного диска и радикулопатии. Первоначально в течение 6–8 недель
пациенты проходили упражнения для укрепления икроножных мышц с открытой и закрытой цепочкой,
такие как подъемы на две и одну ногу, подъемы на носки сидя у стены и подъемы на носки сидя.
Впоследствии дополнительные методы лечения, включая упражнения по стабилизации поясницы,
тренировку корпуса и миофасциальную релаксирующую терапию, были добавлены еще на 2–3 месяца.
Интенсивность воспринимаемой боли и индекс инвалидности оценивались до и после каждого лечения.
Результаты
После первоначального лечения наблюдалось существенное улучшение боли в спине, радикулопатии и
функциональной инвалидности. Симптомы полностью исчезли при добавлении дополнительного лечения.
Кроме того, последующее наблюдение после шести месяцев индивидуальной программы домашних
упражнений показало устойчивое выздоровление, основанное на клинических показателях результатов.
Выводы
Слабость икроножных мышц может вызвать контрлатеральную поясничную радикулопатию посредством
ряда аномальных биомеханических механизмов, влияющих на пояснично-тазовый ритм и, следовательно,
на поясничный отдел позвоночника.
Ключевые слова: синдром лодыжки и позвоночника, хроническая боль в пояснице, синдром Раффета II,
грыжа поясничного отдела позвоночника, контралатеральная поясничная радикулопатия, слабость
икроножных мышц.
Introduction
Lumbar disc herniation is the most common cause of radiculopathy, typically leading to radicular
pain due to nerve root compression on the affected side. However, reports of contralateral radiculopathy
in relation to the side of disc herniation are uncommon in the literature [1]. Determining whether the
herniated disc is responsible for the patient’s symptoms becomes more challenging when imaging reveals
the disc herniation on the contralateral side of the symptoms. This poses a complex situation, and spine
surgeons may be hesitant to perform surgery due to the potential risk of treatment failure. While various
potential causes of contralateral lumbar radiculopathy have been suggested, there remains limited
understanding of its incidence, underlying pathomechanics, and optimal management approaches [2].
Core muscle strength is necessary to achieve and maintain functional lumbopelvic stability. As a
group, the core muscles work synergistically to contribute towards adequate lumbopelvic stability, which
is necessary for maintaining correct lumbar and pelvic posture and alignment during movement,
providing efficient biomechanical function, maximizing force generation, and minimizing joint loads in
4
all types of activities [3]. However, core muscles have also been expanded distally beyond the
lumbopelvic region to include the calf muscle [4]. The orchestra must play together; one instrument out of
tune ruins the sound. In other clinical terms, the core muscles must work together to achieve lumbopelvic
stability. One muscle with inappropriate activation may produce lumbopelvic instability or at least
abnormal mechanical rhythm of the lumbopelvic region may arise from the weakness of any of these
muscles [5].
It is fascinating that while core muscle weakness is commonly associated with chronic low back
pain, it is unexpected that weakness in the calf muscles could cause contralateral radiculopathy and
chronic low back pain. This is part of the lumbar pathomechanics. Therefore, this study aimed to uncover
the potential biomechanical mechanism behind radiculopathy on the opposite side of the calf muscle
weakness and understand how to treat this condition. Consequently, a new medical condition called Ankle
Spine Syndrome or "Raffet Syndrome II" is being described for the first time in the medical literature.
Material and Methods
Participants
This case series examines the patients afflicted with ankle spine syndrome, encompassing six
individuals (2 males and 4 females) with an average age of 32.2 years. The patients displayed calf muscle
weakness contralateral to the side of lumbar disc herniation and radiculopathy. These individuals endured
chronic, unresolved low back pain and radiculopathy that remained unresponsive to prolonged medical
management or physical therapy. The lumbar radicular pain manifested as sharp, shooting, or lancinating
within a narrow band, spanning no more than 5-8 cm and running down the lower limb. This pain was
experienced superficially and deeply. Dynamic activities, such as walking, running, and jogging,
exacerbated their symptoms, while static activities, like standing and sitting improved them, and rest
offered relief.
Ethical policy
Written informed consent was obtained from all patients for publication of their clinical details
and/or clinical images. The study was also approved by the Research Ethical Committee, Faculty of
Physical Therapy, Cairo University (No:P.T.REC/012/004909).
Procedure
Initial treatment intervention was designed for the patients with ankle spine syndrome to target
the weakness of the calf muscle and its consequences on gait then an adjunctive intervention was added to
the initial one to target the lumdopelvic stability. The outcome measures were the intensity of combined
back pain and radiculopathy using the Numerical Pain Rating Scale [6], and the functional level using the
Oswestry Disability Index to evaluate the impact of back pain and radiculopathy on functional activities
[7]. The intensity of perceived pain and disability index were evaluated before and after each intervention.
A 31-year-old international Egyptian football player was the first patient to present with the clinical
manifestations of the current syndrome. He experienced chronic low back pain and radiculopathy
contralateral to the side of calf muscle weakness. In an attempt to explore patients with the same clinical
presentation of the football player, 1000 patients with chronic ankle injuries and calf muscle weakness
were screened. It was found that 700 patients didn’t have chronic low back pain, and 300 patients had
chronic low back pain. Out of these 300 patients, six patients were found to have the clinical
manifestations of the ankle spinal syndrome, and another 50 athletic patients were exhibited facet
arthropathy on the opposite side of calf muscle weakness.
The patients reported severe pain during dynamic activities, with pain intensity scores ranging
between 8 and 10, and experienced no pain during rest. Additionally, they reported functional disability
5
scores ranging from 10 to 22, indicating mild to moderate levels of functional disability. A thorough
examination unveiled calf muscle weakness alongside a history of chronic ankle injuries contralateral to
the side of radiculopathy. Patients 1 to 5 had experienced lateral ankle sprains, while patient 6 had
suffered from a post-traumatic transverse fracture of the distal tibia. Slow-motion mobile camera analysis
revealed that the patients exhibited excessive knee flexion during mid-stance and terminal stance sub-
phases of the gait cycle and a diminished heel rise during terminal stance on the side of calf muscle
weakness. All patients presented normal laboratory values, including Complete Blood Count, Erythrocyte
Sedimentation Rate, C-reactive protein, uric acid, and vitamin D. Patients 4 and 6 demonstrated
diminished knee and ankle jerks on the side affected by radicular pain. A comprehensive examination for
all patients is provided in Table (1). Figure (1) displays the magnetic resonance imaging examination of
patients 3, 4, and 6 with the current syndrome and three additional patients with facet arthropathy.
Table 1
Physical examination of the patients with Ankle Spine Syndrome “Raffet Syndrome II”
Patients
1
2
3
4
5
6
Age (years)
20 y
21 y
38 y
41 y
34 y
39 y
Sex
Male
Mal
e
Female
Female
Female
Female
Onset of Ankle Injury (months)
20
14
11
12
15
24
Onset of Contralateral Radiculopathy (months)
12
6
5
6
8 m
10
Lab (-/+)
-
-
-
-
-
-
Previous Physical Therapy (-/+)
+
+
+
+
+
+
Previous Medication (-/+)
+
+
+
+
+
+
Previous Chronic Ankle Injury (-/+)
+
+
+
+
+
+
Prone Instability Test (-/+)
+
+
+
+
+
+
Passive Lumbar Extension Test (-/+)
+
-
-
-
-
+
Aberrant Movement Patterns
-
-
-
-
-
-
Painful Arc Sign (-/+)
-
-
-
-
-
-
Instability Catch Sign
-
-
-
-
-
-
Hypermobility PA Test (-/+)
-
-
+
+
+
+
Gowers’s Sign (-/+)
-
-
-
-
-
-
Cluster of Laslett (-/+)
-
-
-
-
-
-
Trendelenburg Test (-/+)
-
-
-
-
-
-
Piriformis Provocation Test (-/+)
-
-
-
-
-
-
Calf Raise Test of Affected Ankle (-/+)
+
+
+
+
+
+
Calf Raise Test of Non Affected Ankle (-/+)
-
-
-
-
-
-
Calf Muscle Atrophy of Affected Ankle (-/+)
+
+
+
+
+
+
MRI (-/+)
+
+
+
+
+
+
Neurological Signs (-/+)
+
+
+
+
+
+
NINDS Scale for Knee Jerk (Scale)
+2
+2
+2
+1
+2
+1
NINDS Scale for Ankle Jerk (Scale)
+2
+2
+2
+1
+2
0
Sciatica (-/+)
+
+
+
+
+
+
Straight leg raise test (-/+)
-
-
-
-
-
-
Calf Muscle Strength of Affected Ankle (MMRCS)
3/5
3/5
2/5
2/5
2/5
2/5
Calf Muscle Strength of Non Affected Ankle
(MMRCS)
5/5
5/5
5/5
5/5
5/5
5/5
6
Foot Abnormalities (-/+)
-
-
-
-
-
-
Gait Abnormalities (-/+)
+
+
+
+
+
+
Time for Initial Improvement (weeks)
6 w
6 w
7 w
7 w
7 w
8 w
Time for Final Improvement (months)
2 m
2 m
3 m
2 m
2 m
3 m
Time for Discharge (months)
3.5 m
3.5
m
4.75 m
4.75 m
4.75 m
5 m
Time for Follow up (months)
6 m
6 m
6 m
6 m
6 m
6 m
Notes: MMRCS: Modified Medical Research Council scale
Fig. 1. Magnetic resonance imaging of lumbar spine. (A) Transverse image (left) and diagram (right)
show grade I nerve root compression at L4/L5 or L5/S1 (abutment grade). The herniated disc abuts the
nerve root, but the nerve root is in its normal position, causing radiculopathy on the contralateral side of
calf muscle weakness (contralateral radiculopathy). (B) Transverse image (left) and diagram (right) show
narrowing of the facet joints spaces at L4/L5 or L5/S1 on the contralateral side of calf muscle weakness
(contralateral facet arthropathy)
All six patients had previously sought physical therapy for back pain and radiculopathy including;
spinal stabilization, core strength, and stretching exercises in addition to different electrotherapeutic
modalities. The patients’ symptoms showed improvement in the short term and relapsed again during
dynamic activities. Also, these patients consumed medications with minimal and temporary effects on the
pain. In the treatment plan, our initial focus was to address the weakness of the calf muscle and its
impact on walking. We prescribed open and closed-chain strengthening exercises targeting the calf
muscle to achieve this. These included double and single-leg calf raises (with straight and bent knees),
wall-sit calf raises, and seated calf raises, which performed over a period of 6-8 weeks. In addition to
these exercises, gait training was provided to correct abnormal walking patterns, particularly during mid-
stance and terminal stance.
7
Furthermore, each patient received a tailored home exercise program to ensure continued
improvement in calf muscle strength. As part of our combined treatment intervention, an adjunctive
treatment was introduced to address lumbopelvic dysfunction over a period of 2-3 months. This included
lumbopelvic stabilization exercises, core strength training, and lumbar myofascial release therapy.
Throughout the treatment, patients were encouraged to diligently carry out their home exercise programs
to maintain optimal strength in their calf muscles and ensure stability in the lumbopelvic region. As part
of a follow-up plan, this home exercise program was also recommended to be continued for an additional
six months.
Results
After 6 to 8 weeks of the initial treatment intervention, the patients long-term back pain and
contralateral radiculopathy resolved by a mean of 69%. The pain intensity scores were reduced to “mild”
and “moderate” levels and ranged from 1 to 4 as assessed using Numerical Pain Rating Scale (Table 2).
Also, the functional abilities improved by a mean of 67%. The low back functional disability scores
decreased to “no” and “mild” disability levels and ranged from 3 to 9 as assessed using Oswestry
Disability Index (Table 3).
Table 2
Numerical Pain Rating Scale scores in patients with Ankle Spine Syndrome “Raffet Syndrome II”
Patients
1
2
3
4
5
6
Numerical Pain Rating Scale
during static activity (Scale)
0
0
2
4
3
3
Numerical Pain Rating Scale
during dynamic activity
(Scale)
8
Severe
Pain
9
Severe
Pain
8
Severe
Pain
10
Severe
Pain
9
Severe
Pain
10
Severe
Pain
Numerical Pain Rating Scale
after initial intervention
during dynamic activity
(Scale)
1
Mild Pain
2
Mild Pain
3
Mild Pain
4
Moderate
Pain
3
Mild Pain
4
Moderate
Pain
Percent of improvement after
initial intervention (%)
87.5%
77.77%
62.5%
60%
66.66%
60%
Numerical Pain Rating Scale
after combined intervention
during dynamic activity
(Scale)
0
No Pain
0
No Pain
0
No Pain
0
No Pain
0
No Pain
0
No Pain
Percent of improvement after
combined intervention (%)
100%
100%
100%
100%
100%
100%
Notes: No Pain=0; Mild Pain=1-3; Moderate Pain=4-6; Severe Pain=7-10
After 2 to 3 months of the combined treatment intervention, the patients experienced more
improvement. Their long-term back pain and contralateral radiculopathy resolved by 100%. The pain
intensity scores reduced to “no pain” level as all patients scored zero on the Numerical Pain Rating Scale
(Table 2). Also, their functional abilities improved by a mean of 94%. The functional disability scores
decreased to “no disability” level and ranged from 0 to 3 as assessed by the Oswestry Disability Index
(Table 3). After 6-months follow-up of HEPs, the clinical outcome measures were retained.
Table 3
8
Oswestry Disability Index scores in patients with Ankle Spine Syndrome “Raffet Syndrome II”
Patients
1
2
3
4
5
6
Oswestry Disability
Index before treatment
10
Mild
Disability
12
Mild
Disability
19
Moderate
Disability
22
Moderate
Disability
20
Moderate
Disability
20
Moderate
Disability
Oswestry Disability
Index after initial
intervention
3
No
Disability
3
No
Disability
8
Mild
Disability
9
Mild
Disability
5
Mild
Disability
7
Mild
Disability
Percent of
improvement after
initial intervention (%)
70%
75%
57.89%
59.09%
75%
65%
Oswestry Disability
Index after combined
intervention
0
No
Disability
0
No
Disability
2
No
Disability
2
No
Disability
0
No
Disability
3
No
Disability
Percent of
improvement after
combined intervention
(%)
100%
100%
89.47%
90.91%
100%
85%
Notes: No Disability=0-4; Mild Disability=5-14; Moderate Disability=15-24; Severe Disability=25-34; Complete
Disability=35-50
Discussion
This study aimed to describe a new clinical condition called Ankle Spine Syndrome or “Raffet
Syndrome IIˮ by investigating the potential biomechanical mechanism underlying the radiculopathy
contralateral to the side of calf muscle weakness, and to propose the treatment for this condition in
patients with Lumbar disc herniation and radiculopathy. Several authors have reported patients presenting
with contralateral radiculopathy [1, 2, 8- 11]. However, the exact mechanisms underlying this clinical
condition are still not well understood [2]. There is no currently consensus about the pathomechanics of
contralateral radiculopathy, or on which treatment approach may be appropriate [1, 10].
In the ankle spine syndrome, the authors described a novel clinical condition, and discussed the
root cause and treatment for this condition in the light of the previous literature. A better understanding of
the underlying pathomechanics of contralateral radiculopathy may help researchers, physiotherapists, and
clinicians in developing effective and efficient rehabilitation programs for the patients with this
syndrome. This syndrome was reported in 6 patients with a previous history of chronic ankle injuries
associated with calf muscles strength deficits. The patients suffered from unresolved chronic low back
pain with radiculopathy contralateral to their calf muscles weakness, which didn’t respond to prolonged
physical therapy or medication.
Calf muscle weakness has a significant impact on the mechanics of gait. Generally, inability of
the calf muscle to effectively control the anterior advancement of the tibia is a major cause of inadequate
knee extension in mid-stance and terminal stance. The lack of sufficient calf muscle strength allows the
tibia to fall forward excessively as the body vector advances. As a result, the tibia advances faster than the
femur, causing continued knee flexion. Although borderline weakness of the calf muscle is difficult to
detect with traditional manual muscle testing, excessive knee flexion may be an initial indicator of calf
muscle weakness to the clinician. The quadriceps may have adequate strength to support the flexed knee
but cannot reestablish the knee extension because the soleus cannot stabilize the tibia to give a near stable
base for the quadriceps to work. As the quadriceps draws the proximal femur forward for knee extension,
it also advances the body mass over the hip joint. Consequently, the entire proximal body mass (i.e.,
9
center of gravity (COG)) moves forward, shifts the body vector (i.e., line of gravity (LOG)) farther
anterior to the ankle joint and increases the demand torque at the ankle, which the weak soleus cannot
resist. Hence, the whole limb rather than just the femur advances and knee extension remains inadequate
[12]. If the soleus response is inadequate, the mid-stance advancement of the tibia over the foot will
fall into excessive dorsiflexion (exaggerated heel rocker). Unfortunately, any attempt from gastrocnemius
(through its knee flexion effect) to compensate for the weakness of the soleus can accelerate the anterior
tibial advancement, producing further knee flexion [12]. Terminal stance heel raise is also lost with soleus
weakness. This may occur even if the patient had a normal dorsiflexion control in mid-stance, because the
force exerted by the calf muscle during terminal stance is approximately double compared to that required
during mid-stance, which makes any deficit in calf muscle strength more obvious in terminal stance. This
delay of heel raise at the beginning of terminal stance is a more significant sign of a weak soleus than its
occurrence at the end of this phase. In late terminal stance, the mere trailing position of the limb will lift
the heel once the ankle reaches the end of its passive dorsiflexion range [12].
The calf muscle is conceptualized as a “hidden core muscle” with substantial consequences on the
mechanics of lumbopelvic rhythm. During gait, the concept of contra-directional lumbopelvic rhythm
describes the movement in which the pelvis and lumbar spine rotate in opposite directions. The
importance of this rhythm is to remain supra-lumbar trunk (i.e., the part of the body located above the
imaginary supra-lumbar line, directly above the first lumbar vertebra) nearly stationary as the pelvis
rotates over the femurs during gait. In other words, the lumbar spine acts as a mechanical decoupler
allowing the pelvis and the supra-lumbar trunk to move independently. In this manner, the position of the
supra-lumbar trunk region including the head and eyes remains relatively fixed in space, regardless of
pelvic rotation [13]. As per the authors’ knowledge, most literature reported this kinematic decoupling
mechanism in the sagittal plane (i.e., anterior pelvic tilt causes lumbar extension while posterior pelvic tilt
causes lumbar flexion). This classical expression of the decoupling mechanism is far away from what the
authors would like to portray for the patients with this syndrome.
Normally, the pelvis moves in three planes of motion; arc of 8° of pelvic tilt (4° anterior tilt and
4° posterior tilt) in sagittal plane, arc of 10° of pelvic rotation (5° forward and 5° backward) in transverse
plane, and 4° of pelvic drop in coronal plane [12]. All these pelvic motions are not transferred to supra-
lumbar trunk region due to the presence of this mechanical decoupling mechanism of the lumbar spine.
Moreover, this mechanism takes the burden of absorbing all these pelvic motions by moving the lumbar
spine in a direction opposite to the pelvic motion in three planes, and keeps the supra-lumbar trunk region
mechanically unaffected by multidirectional pelvic motions. The decoupling mechanisms in transverse
and frontal planes are what the authors would like to highlight strongly during normal walking and unfold
the pathological consequences of the disruption or exaggeration of these mechanisms on the spine
biomechanics in patients with calf muscle weakness (Figure 2).
10
Fig. 2. Decoupling mechanism of lumbar spine. (A) Lumbar decoupling mechanism in the transverse
plane; the lumbar vertebrae rotate in a direction opposite to the direction of pelvis rotation, allowing the
supra-lumbar trunk region to remain relatively stationary in space despite the pelvis’ movement. The facet
joints compressed on the rotatory sides and opened in non-rotatory sides. (B) Lumbar decoupling
mechanism in the frontal plane; the lumbar spine bends in a direction opposite to the direction of lateral
pelvic tilting
Weakness of the calf muscle found in the patients with the current syndrome led to ipsilateral
excessive knee flexion during mid-stance and terminal stance, and delayed heel raise that normally
happens at the beginning of terminal stance. Consequently, the patients showed relative functional
shortening of the ipsilateral limb, especially during terminal stance, and excessive displacement of center
of gravity during gait. As a compensatory mechanism, the lower limb length was gained again by
excessive dropping (in the frontal plane) and backward rotation (in the transverse plane) of the pelvis on
the ipsilateral side [12, 14]. These pelvis compensations are a fairly abrupt motion that accompanies
persistent heel contact in a person who has a weakness of calf muscle during terminal stance [12] (Figure
3).
11
Fig. 3. Schematic model of calf muscle and pelvis during gait. (A) Normal calf muscle during standing.
The pelvis is in a neutral position. (B) Normal calf muscle during terminal stance. Functional lengthening
of the lower limb occurs when the heel leaves the ground, and the knee is fully extended. (C) Weak calf
muscle during terminal stance. Relative functional shortening of the lower limb occurs due to lack of heel
raise, excessive anterior displacement of the tibia, excessive ankle dorsiflexion, and excessive knee
flexion. The lower limb length is restored by excessive dropping and backward rotation of the pelvis on
the weak side.
These compensations are considered a mechanical advantage to the ipsilateral limb, cause a
functional lengthening to this limb, and prevent excessive abnormal displacement of center of gravity
during gait. However, they are also considered a mechanical disadvantage on other hand to the lumbar
spine structure as it exaggerates the kinesiological decoupling mechanism in frontal and transverse planes.
In the frontal plane, the weakness of the calf muscle produced excessive pelvic drop toward the
ipsilateral limb during gait. This excessive motion of the pelvis was compensated by excessive side
bending of the lumbar spine contra-laterally through the exaggerated decoupling mechanism of the
lumbar spine. This compensatory movement of the lumbar spine reduced the dimensions of neural
foramina, lateral recess, and facet joints spaces at the bending side of lumbar spine. In the transverse
plane, the weakness of the calf muscle produced excessive backward rotation of the pelvis toward the
ipsilateral limb during gait. This excessive motion of the pelvis was compensated by excessive axial
rotation of lumbar spine contra-laterally through the exaggerated decoupling mechanism of the lumbar
spine. This compensatory movement of the lumbar spine reduced the dimensions of neural foramina,
lateral recess, and facet joints spaces at the rotatory side of lumbar spine.
The exaggerated lumbar decoupling mechanism is considered a mechanical advantage to the
supra-lumbar trunk and gaze stability in people with ipsilateral calf muscle weakness, as the supra-lumbar
trunk region may not be affected by excessive downward and backward rotations of the pelvis. However,
the exaggerated decoupling mechanism of interest led to serious pathological consequences. Therefore, it
could be a mechanical disadvantage to the lumbar spine itself by overloading all structures at the bending
and rotation sides of lumbar spine during gait, which led to excessive facet compression, impingement of
nerve root by narrowing of intervertebral foramen, or impingement of nerve root by asymptomatic disc
12
bulge, which may elicit back pain and contralateral radiculopathy (Figure 4). As a novelty biomechanical
mechanism, this elucidated why the patients’ symptoms were aggravated by dynamic activities (walking,
running, and jogging) while relieved completely by rest.
Fig. 4. Schematic model of intervertebral foramens dimensional changes during excessive lateral tilting
and backward rotation of the pelvis in patients with calf muscle weakness: Marked decrease in the
foraminal height and area in B.2 compared with A.2. Marked decrease in the foraminal width and area in
B.3 compared with A.3. Marked decrease in the foraminal height, width and area in B.4 compared with
A.4. Marked increase in the disc bulging and facet joint compression in B.2, B.3, and B.4 compared with
A.1, A.2, and A.3 respectively. NIVD = normal intervertebral disk, DIVD = degenerated intervertebral
disk, SVB = superior vertebral body, IVB = inferior vertebral body, NR = nerve root, LF = ligamentum
flavum, FJ = facet joint. A modified figure based on illustration from Takahashi et al. (2022) [14]
The research by Wang et al. [15] demonstrates that the intervertebral foramina of the lumbar
spine undergo significant changes during lumbar flexion, extension, lateral bending, and axial rotation.
They observed a notable decrease in foraminal width, height, and area on the side where the lumbar spine
bends, while these dimensions increased significantly on the opposite side. Similarly, there was a
significant decrease in foraminal width and area on the side where the lumbar spine rotates, with an
increase on the opposite side. Furthermore, the collaborative efforts of Lorenc et al. [16] and Yadesa et al.
[17] have significantly advanced our understanding of the effects of lumbar spine motion on neural
foramina and its implications for chronic low back pain. Lorenc et al. [16] found a direct correlation
between the anteroposterior diameter of the neural foramen and the degree of axial rotation of the lumbar
vertebra at the same level. They concluded that axial rotation of the lumbar vertebra may cause back pain,
radiculopathy, and sensory deficiency in the lower extremities. Additionally, Blankenbaker et al. [17]
reported a significant association between axial rotation in each lumbar motion segment and chronic low
back pain (CLBP) or radiculopathy, as identified through discography. This collaborative research is a
testament to the power of collective knowledge in advancing our understanding of complex medical
conditions. These findings suggest that the induced stress on the adjacent connective tissue [18] and the
narrowed neural foramen (lateral spinal stenosis) [17, 19] at the bending and rotation sides of the lumbar
spine may explain the link between excessive side bending and axial rotation of the lumbar spine and
chronic low back pain (radiculopathy). Therefore, congruent with these findings and from a
biomechanical standpoint, the restoration of calf muscle strength and normal gait pattern was followed by
a marked improvement in all symptoms of chronic low back pain and contralateral radiculopathy.
13
In addition, 50 athletic patients were reported with localized back pain located at the contralateral
side of calf muscle weakness during dynamic activities. They had facet arthropathy at L4/L5 and/or L5/S1
contralateral to the side of calf muscle weakness (contralateral facet arthropathy). These findings may
enhance the validity of the current syndrome, and reinforce the biomechanical proposition through the
exaggerated decoupling mechanism of the lumbar spine, which could be partially responsible for
excessive facet joints compression and loading at the bending and rotatory sides of lumbar spine (Figure
5). These 50 athletic patients received the same designed treatment plan, and showed significant
improvement and returned to their recreational sports without pain.
Fig. 5. Schematic model of facet joints changes during decoupling mechanism of lumbar spine: A1, A2, and A3
show the facet joints from posterior view while B1, B2, and B3 show the facet joints from axial view. In normal
decoupling mechanism: A2 and B2 show the facet joints compressed on the bending and rotatory sides while opened
on the other sides. In exaggerated decoupling mechanism: A3 and B3 show the facet joints closed on the bending
and rotatory sides (leading to facet joints arthropathy) and separated on the other sides
It is worth noting that there were two patients who had performed magnetic resonance imaging on
the lumbar spine two years before their ankle incidents, and the magnetic resonance imaging showed the
same grade of Lumbar disc herniation without any previous complain of radiculopathy that was reported
later. This indicated an old asymptomatic disc herniation that turned into symptomatic and provoked
radiculopathy on the opposite side of calf muscle weakness. The patients with asymptomatic disc
herniation may have risk of developing radiculopathy if they experienced contralateral calf weakness.
This may depend on the severity and chronicity of the calf muscle weakness, and the efficiency of the
musculoskeletal system in absorbing the biomechanical faults during gait, starting from the ankle joint
and ending with lumbopelvic region.
The authors would like to propose a new classification of lumbar radiculopathy based on the
direction of the underlying cause, ipsilateral and contralateral lumbar radiculopathy. Ipsilateral lumbar
radiculopathy is the radicular pain on the same side of the underlying cause, most commonly the nerve
compression that is caused by a herniated disc [20- 22]. The discogenic cause accounts for around 90% of
cases of ipsilateral radiculopathy [22], but other causes are also possible [23, 24]. The contralateral
lumbar radiculopathy is the radicular pain on the opposite side of the underlying cause. It is uncommon
compared with ipsilateral lumbar radiculopathy [10], and can be attributed to several causes such as a
herniated disc [25- 28], or other causes [1, 11, 29, 30]. In this study, the lumbar radiculopathy symptoms
were located on the same side of the lumbar herniated discs, and on the opposite side of the weak calf
14
muscles. The asymptomatic disc herniation turned into symptomatic disc, causing radiculopathy, due to
the weakness of the contralateral calf muscle (contralateral radiculopathy).
It is worth pointing out to some important points. Firstly, the authors would like to focus on
another classification for sciatica; static and dynamic sciatica. Static sciatica is sciatica that is primarily
caused by a defect in one of the spinal components (i.e., sciatica that occurred during rest, static, or even
dynamic activities). Dynamic sciatica is sciatica that is primarily caused by a defect in the locomotor
system rather than a defect in one of the spinal components (i.e., sciatica that aggravated by dynamic
activity, improved by static activity, and relieved by rest) and this type of sciatica which was introduced
in the current study. Secondly, it is recommended for clinicians to categorize sciatica as static sciatica and
dynamic sciatica to find out the root cause of sciatica instead of limiting the assessment and intervention
to the lumbar spine. Thirdly, it is also recommended to include the gait analysis to the assessment for the
patients with sciatica. Fourthly, despite the weak capabilities of gait analysis utilized in this study, there is
no doubt now that the calf muscle weakness can induce the contralateral radiculopathy. Finally, it is
important to direct the attention of the clinicians to examine the spine in more dynamic and functional
activities, rather than limiting examination to x-rays, MRIs, and special tests, which may be insufficient to
describe the clinical picture properly.
Conclusion
The weakness of the calf muscle could be a cause for inducing chronic low back pain and
contralateral radiculopathy, by putting extra strain on the lumbar spine and disturbing the proper
biomechanical relations of lumbopelvic rhythm. Significant recovery of all symptoms of chronic low back
pain and radiculopathy was observed after reconditioning of calf muscle strength and normal gait pattern.
The clinicians may need to look beyond the lumbar spine to identify other possible predisposing factors
of chronic low back pain and radiculopathy. This allows establishing efficient prevention and
rehabilitation programs for the patients with ankle spine syndrome.
Conflict of interests
No potential conflict of interest relevant to this study.
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Information about the authors
Ahmed Raffet
https://orcid.org/0009-0004-7161-7400
ahmed.raffet@pt.cu.edu.eg
Department of Biomechanics, Faculty of Physical Therapy, Cairo University, Giza Egypt
Mark Laslett
https://orcid.org/0000-0002-9187-754X
drmarklaslettprofessional@gmail.com
Department of Physical Therapy, Faculty of Medical Sciences, Auckland University, New Zealand
Wolf Schamberger
https://orcid.org/0009-0000-1566-2128
wolfschamberger@shaw.ca
Department of Medicine, Division of Physical Medicine and Rehabilitation, University of British Columbia, Canada
Amir Beltagi
https://orcid.org/0000-0002-1414-1707
amirbeltagi@pt.cu.edu.eg
Department of Biomechanics, Faculty of Physical Therapy, Cairo University, Giza Egypt
Mohamed M. ElMeligie
https://orcid.org/0000-0002-3090-5252
mohamed.elmeligie@acu.edu.eg
Department of Basic Sciences for Physical Therapy, Faculty of Physical Therapy, Ahram Canadian University, Giza
Egypt
Efrem Kentiba
https://orcid.org/0000-0001-7013-2605
efre89@gmail.com
Department of Sports Science, College of Natural and Computational Sciences, Arba Minch University, Arba Minch
Ethiopia
Noha Khaled
https://orcid.org/0000-0002-1648-9141
17
noha.khaled@pt.cu.edu.eg
Department of Biomechanics, Faculty of Physical Therapy, Cairo University, Giza Egypt
Hossam Y. Sayed
https://orcid.org/0009-0001-0442-894X
omhelgendy@gmail.com
Department of Anatomy and Embryology, Faculty of Medicine, Cairo University, Giza Egypt
Ahmed H. Omar
https://orcid.org/0009-0005-3760-2405
ahmed-hussein@kasralainy.edu.eg
Department of Neurosurgery, Faculty of Medicine, Cairo University, Giza Egypt
Maged M. Hawana
https://orcid.org/0009-0005-0382-0172
maged.mostafa@cu.edu.eg
Department of Radiology, Faculty of Medicine, Cairo University, Giza Egypt
Hossam Eddein Fawaz
https://orcid.org/0009-0009-8477-2561
drhfawaz@yahoo.com
Department of Biomechanics, Faculty of Physical Therapy, Cairo University, Giza Egypt
Інформація про авторів
Ахмед Раффет
https://orcid.org/0009-0004-7161-7400
ahmed.raffet@pt.cu.edu.eg
Кафедра біомеханіки, факультет фізичної терапії, Каїрський університет, Гіза, Єгипет
Марк Ласлетт
https://orcid.org/0000-0002-9187-754X
drmarklaslettprofessional@gmail.com
Кафедра фізичної терапії, Факультет медичних наук, Оклендський університет, Нова Зеландія
Вольф Шамбергер
https://orcid.org/0009-0000-1566-2128
wolfschamberger@shaw.ca
Департамент медицини, Відділ фізичної медицини та реабілітації, Університет Британської Колумбії, Канада
Амір Белтагі
https://orcid.org/0000-0002-1414-1707
amirbeltagi@pt.cu.edu.eg
Кафедра біомеханіки, факультет фізичної терапії, Каїрський університет, Гіза, Єгипет
Мохамед М. ЕльМелігі
https://orcid.org/0000-0002-3090-5252
mohamed.elmeligie@acu.edu.eg
Кафедра фундаментальних наук для фізичної терапії, факультет фізичної терапії, Канадський університет Ахрама, Гіза,
Єгипет
Єфрем Кентиба
https://orcid.org/0000-0001-7013-2605
efre89@gmail.com
18
Департамент спортивних наук, Коледж природничих і обчислювальних наук, Університет Арба Мінча, Арба Мінч,
Ефіопія
Ноха Халед
https://orcid.org/0000-0002-1648-9141
noha.khaled@pt.cu.edu.eg
Кафедра біомеханіки, факультет фізичної терапії, Каїрський університет, Гіза, Єгипет
Хоссам Ю. Саєд
https://orcid.org/0009-0001-0442-894X
omhelgendy@gmail.com
Кафедра анатомії та ембріології, медичний факультет, Каїрський університет, Гіза, Єгипет
Ахмед Х. Омар
https://orcid.org/0009-0005-3760-2405
ahmed-hussein@kasralainy.edu.eg
Кафедра нейрохірургії, медичний факультет, Каїрський університет, Гіза, Єгипет
Магед М. Гавана
https://orcid.org/0009-0005-0382-0172
maged.mostafa@cu.edu.eg
Кафедра радіології, медичний факультет, Каїрський університет, Гіза, Єгипет
Хоссам Еддейн Фаваз
https://orcid.org/0009-0009-8477-2561
drhfawaz@yahoo.com
Кафедра біомеханіки, факультет фізичної терапії, Каїрський університет, Гіза, Єгипет
Информация об авторах
Ахмед Раффет
https://orcid.org/0009-0004-7161-7400
ahmed.raffet@pt.cu.edu.eg
Кафедра биомеханики, факультет физиотерапии, Каирский университет, Гиза, Египет
Марк Ласлетт
https://orcid.org/0000-0002-9187-754X
drmarklaslettprofessional@gmail.com
Кафедра физиотерапии, факультет медицинских наук, Оклендский университет, Новая Зеландия
Вольф Шамбергер
https://orcid.org/0009-0000-1566-2128
wolfschamberger@shaw.ca
Медицинский факультет, Отделение физической медицины и реабилитации, Университет Британской Колумбии, Канада
Амир Бельтаги
https://orcid.org/0000-0002-1414-1707
amirbeltagi@pt.cu.edu.eg
Кафедра биомеханики, факультет физиотерапии, Каирский университет, Гиза, Египет
Мохамед М. ЭльМелиджи
https://orcid.org/0000-0002-3090-5252
mohamed.elmeligie@acu.edu.eg
Кафедра фундаментальных наук физиотерапии, факультет физиотерапии, Канадский университет Ахрама, Гиза, Египет
19
Ефрем Кентиба
https://orcid.org/0000-0001-7013-2605
efre89@gmail.com
Департамент спортивных наук, Колледж естественных и вычислительных наук, Университет Арба Минч, Арба Минч,
Эфиопия
Ноха Халед
https://orcid.org/0000-0002-1648-9141
noha.khaled@pt.cu.edu.eg
Кафедра биомеханики, факультет физиотерапии, Каирский университет, Гиза, Египет
Хосам Ю. Сайед
https://orcid.org/0009-0001-0442-894X
omhelgendy@gmail.com
Кафедра анатомии и эмбриологии медицинского факультета Каирского университета, Гиза, Египет
Ахмед Х. Омар
https://orcid.org/0009-0005-3760-2405
ahmed-hussein@kasralainy.edu.eg
Кафедра нейрохирургии, медицинский факультет, Каирский университет, Гиза, Египет
Магед М. Гавана
https://orcid.org/0009-0005-0382-0172
maged.mostafa@cu.edu.eg
Кафедра радиологии, медицинский факультет, Каирский университет, Гиза, Египет
Хосам Эддейн Фаваз
https://orcid.org/0009-0009-8477-2561
drhfawaz@yahoo.com
Кафедра биомеханики, факультет физиотерапии, Каирский университет, Гиза, Египет
This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0)
Received: 2024-06-17 Accepted: 2024-07-18 In press: 2024-07-25 Published: 2026-06-18
