ANTERIOR INTERCOSTAL COMPRESSION SYNDROME:

Anterior Intercostal Compression Syndrome (AICS) was first described by Dr. Deepak Sebastian as a differential screen for anterior chest and thoracic pain. It is a condition where the intercostal space is compromised resulting in anterior chest and thoracic pain. While intercostal neuralgia exists as a clinical entity, several other structures within the intercostal space are speculated to be potential pain mediators. In the presence of AICS the exact structures however, are difficult to specify. When visceral mediation has been ruled out and in the absence of neuralgic radiating pain, AICS may be considered. Forward head posture with protracted scapulae can cause cervical, thoracic and shoulder dysfunction.

The consequence of a forward head posture on the ribs, is worth mentioning. The upper ribs assist respiration by moving in a pump handle fashion assisted by the pectoralis minor which narrows the intercostal space. Rib widening or the bucket handle movement is assisted by the serratus anterior which helps widen the intercostal space (Brand, 2008). This is accomplished with a fixed scapula whilst stabilizing the ribs from an excessively anterior displacement (Flynn, 1996). Dysfunctional states as in a prolonged forward head and scapula protraction, can render the pectoralis minor tight and the serratus anterior weak in addition to other factors (subcranial, cervical and thoracic dysfunction). This can cause a relative approximation of the intercostal space resulting in pain. In the absence of intercostal neuralgia, the structures within the intercostal space that are speculated to cause pain are the periosteum of the ribs, intercostal muscles, and the intercostal artery and vein.

Management should hence address all components of a forward head but more specifically pectoralis minor stretching, mobilizing the intercostal space into opening and serratus anterior strengthening. Differentials include intercostal muscle cramp or tear, rib fractures, costochondritis, Tietze syndrome, rib infection or metastasis in rare cases, and post-operative thoracic surgery, particularly coronary artery bypass.

References:
Brand, R. A. (2008). "Origin and Comparative Anatomy of the Pectoral Limb". Clinical Orthopaedics and Related Research 466 (3): 531.

Flynn TW. ed. The Thoracic Spine and Chest Wall. Boston, MA: Butterworth-Heinemann; 1996.

Sebastian D. Anterior Intercostal Compression Syndrome. (In differential screening of regional pain in musculoskeletal practice 2015; Jaypee Bros, New Delhi, London, Philadelphia, Panama.

THE CERVICAL EXTENSOR ENDURANCE TEST (CEET):

The CEET was first described by Dr. Deepak Sebastian as a screen exam to identify the presence of weakness of the neck extensors and differentiate the presence of weakness of the superficial versus the deep neck extensors. With the patient lying prone and head and neck past the edge of the table and the cervico-thoracic junction stabilized, the ability of the individual to sustain a chin tuck position in neutral for 20 seconds is evaluated (fig. a). A positive finding for weakness of the deep neck extensors is the ‘chin length’ increasing with neck extension, as observed on the inclinometer, indicating a dominance of the superficial extensors of the neck (fig. b). Weakness of both deep and superficial neck extensors is identified by the presence of neck flexion indicating an inability to hold the head up (fig. c). 30 individuals with neck pain were examined by 2 raters for reproducibility, with the study yielding ‘good’ inter-rater reliability, (k=0.800, SE of kappa = 0.109, 95% CI).

References:
Sebastian D, et, al. The cervical extensor endurance test: A reliability study. J Bodyw Mov Ther. 2015 Apr;19(2):213-6

The sitting active and prone passive lag test (SAPLT) was first described by Dr. Deepak Sebastian to identify the presence of an active or a passive terminal extension lag at the knee joint. The lack of terminal extension and its consequences in the knee have been previously described. The terms flexion deformity or contracture have been used and their occurrence has been mostly associated with post-operative knee surgery, neurological sequelae and osteoarthritis. Additional causes described are arthrogenic muscle inhibition (AMI) secondary to trauma to the knee, inadequate cortical representation, tightness of the posterior knee capsule, tightness of the gastrocnemius, popliteus and hamstrings and injury to the knee extensor mechanism. Terminal extension in the knee is a pre-requisite for adequate stability and load distribution during the stance phase of gait and weight bearing function. The lack of full extension at the knee can result in a greater force of quadriceps contraction and energy expenditure. It can also result in slower walking velocity, abnormal gait mechanics, overloading the ipsilateral patello-femoral joint and the contra-lateral limb, resulting in pain and dysfunction. This includes, but not limited to patello-femoral pain, gait abnormalities, lower extremity muscle imbalances, leg length discrepancy and back pain. Residual flexion contractures after have been associated with poorer functional scores and outcomes. While some flexion contractures are obvious others can be subtle and missed. Additionally it may ‘not’ be a contracture but a diminished efficiency of the knee extensor mechanism. The may still result in a lack or lag of terminal knee extension, with instability and consequences therein. This simply means that a lack in terminal knee extension may be secondary to an active or a passive restraint. Although the prevalence has not been studied, in clinical practice we observed the presence of a knee extension lag in most patients with a knee dysfunction. Since the presence and consequences of a lack in terminal knee extension is obvious, a reliable test to appropriately identify its presence led to the description of the APLT. Additionally, the test was able to differentiate an active versus as passive restraint, suggesting the type of intervention needed.

Methods: 56 patients with a diagnosis of knee pain were randomly assigned and independently examined by two physical therapists at a time, to determine the presence of an active or a passive extension lag at the knee. An active lag was determined by the inability of the erectly seated subject to actively extend the involved knee in maximally dorsiflexion of the ankle to the same level as the normal knee held in maximal extension and ankle in maximal dorsiflexion, as seen by the levels of the toes. A passive lag was determined by placing the subject prone with the knees just past the edge of the table and determining the high position of the heel in a fully resting extension position compared to the heel on the normal side. Results: For the sitting active lag test, the inter-rater reliability was ‘good’ (Kappa 0.792, SE of kappa 0.115, 95% confidence interval). For the prone passive lag test, the inter-rater reliability was ‘good’ (Kappa 0.636, SE of kappa 0.136, 95% confidence interval). Conclusion: The SAPLT may be incorporated as a simple yet effective test to determine the presence of a knee extension lag. It identifies the type of restraint, active, passive or both, and is suggestive of the most appropriate management.
 

References:
Sebastian D, et al. The sitting active and prone passive lag test: An inter rater reliability study. J Bodyw Mov Ther. 2014 Apr;18(2):204-9.

T2 RADICULOPATHY:

T2 radiculopathy was first described by Dr. Deepak Sebastian as a differential screen for radicular pain in the upper extremity. It is a condition where the second thoracic nerve is entrapped in the intervertebral foramen between T2T3 resulting in upper extremity radicular pain.

The anterior divisions of the thoracic spinal nerves from T1 to T11 are the intercostal nerves. They exit from the thoracic spinal column beneath their corresponding vertebra ( O Connor RC, 2002 ). Each nerve is connected with the adjoining ganglion of the sympathetic trunk by a gray and a white ramus communicans. The intercostal nerves are distributed chiefly to the thoracic pleura and abdominal peritoneum and differ from the anterior divisions of the other spinal nerves in that each pursues an independent course without plexus formation. Lateral cutaneous branches are derived from the intercostal nerves, about midway between the vertebræ and sternum; they pierce the Intercostales externi and Serratus anterior, and divide into anterior and posterior branches. The lateral cutaneous branch of the second intercostal nerve which exits between T2T3, does not divide like the other thoracic nerves, into an anterior and a posterior branch; but midway anterior to the axilla, gives off a branch, the intercostobrachial nerve (ICBN. It pierces the intercostalis externus, the serratus anterior, crosses the axilla to the medial side of the arm, and joins with a filament from the medial brachial cutaneous nerve. It then pierces the fascia, and supplies the skin of the upper half of the medial and posterior part of the arm, communicating with the posterior brachial cutaneous branch of the radial nerve which supplies the lateral forearm (Loukas M 2006). A second intercostobrachial nerve is frequently given off from the lateral cutaneous branch of the third intercostal which supplies filaments to the axilla and medial side of the arm (Fig). One can assume that the ICBN is the communicating link between T2 spinal nerve and the upper extremity. Thus the sequence of events resulting in a T2 radiculopathy involve the T2 spinal nerve, adjoining intercostobrachial nerve, medial antebrachial cutaneous nerve and the posterior brachial cutaneous branch of the radial nerve.

The vulnerability of the upper thoracic spine to mechanical dysfunction is described by various sources (Arana E 2004). As is the case with the lumbar and cervical spine, degeneration of the posterior spinal elements of the thoracic spine is an inherent source of axial back pain and radiculopathy. (Vanichkachorn JS, and Vaccaro AR) suggest generators of thoracic radicular pain to be musculoskeletal, neurological, infectious, visceral, metabolic and congenital. Among the musculoskeletal causes, spondylosis, disc disease and somatic causes have been mentioned. (Edmondston et al) investigated the influence of whole body sitting posture on cervico-thoracic posture, mechanical load and extensor muscle activity in 23 asymptomatic adults. They concluded that the more neutral sitting postures reduce the demand on the cervical extensor muscles and modify the relative contribution of cervical and thoracic extensors to the control of head and neck posture. They suggest postures that promote these patterns of muscular activity may reduce posture related pain suggesting muscle weakness and imbalances to be contributors of neck and upper thoracic pain.

Somatic dysfunction in the upper thoracic region may be postural, or acquired secondary to systemic disorders e.g. asthma. The key contributor to dysfunction is the forward head posture, which comprises upper cervical extension, lower cervical flexion, upper and lower thoracic kyphosis. This could lead to considerable hypomobility of the thoracic spine ( Lounardi AC 2011). The forward head posture is typically associated with weakness of the deep cervical flexors and the thoracic extensors ( Watson Trott 1993). The above factors collectively favor the presence of degenerative and mechanical dysfunction of the upper thoracic region. While upper thoracic spine is vulnerable for degenerative and mechanical dysfunction, the potential for irritation of the intercostobrachial nerve exists, if the T1T2, T2T3 segments are involved, resulting in upper extremity radicular pain. Complaints of upper thoracic pain with pain radiating into the arm, the presence of upper thoracic somatic dysfunction, restricted cervical mobility (especially extension) and pressure mechanosensitivity over the lateral aspect of the thoracic vertebrae causing radiating pain into the arm, may be diagnostic indicators.

References:
Sebastian D. T2 radiculopathy: A differential screen for upper extremity radicular pain. Physiother Theory Pract. 2013 Jan;29(1):75-85.

TRIANGULAR INTERVAL SYNDROME:

Triangular Interval Syndrome (TIS) was first described by Dr. Deepak Sebastian as a differential diagnosis for radicular pain in the upper extremity. It is a condition where the radial nerve is entrapped in the triangular interval resulting in upper extremity radicular pain. The triangular interval is the space that is triangular in shape, situated between the long head and lateral head of the triceps brachii and the teres major.

The radial nerve and profunda brachii pass through the triangular interval and are hence vulnerable. The triangular interval has a potential for compromise secondary alterations in thickness of the teres major and triceps (McClelland 2007). They described based on cadaveric studies that fibrous bands were commonly present between the teres major and triceps. When these bands were present, rotation of the shoulder caused a reduction in cross sectional area of the space. Normal resting postures of humeral adduction and internal rotation with scapular protraction may be speculated as a precedent for teres major contractures owing to the shortened position of this muscle in this position. In addition, hypertrophy of this muscle can occur secondary to weight training and potentially compromise the triangular interval with resultant entrapment of the radial nerve (ABY Ng et al 2003).
Shoulder dysfunctions have a potential for shortening and hypertrophy of the teres major. Shoulders that exhibit stiffness, secondary to capsular tightness, contribute to contracture and hypertrophy of the teres major (Jiu-jenk Lin 2006). Hence, restricted external rotation can encourage adaptive shortening and thickening of the internal rotators of the shoulder principally the teres major and subscapularis. One may speculate that the lateral arm pain presented in shoulder dysfunctions may be of a nerve origin secondary to adverse neural tension of the radial nerve.

The triceps brachii has a potential to entrap the radial nerve in the triangular interval secondary to hypertrophy. The presence of a fibrous arch in the long head and lateral head further complicates the situation. Repeated forceful extension seen in weight training and sport involving punching may be a precedent to this scenario (Manske 1977, Prochaska 1993, Ng 2003). The radial nerve is vulnerable as it passes through this space, for all of the reasons mentioned above. Awareness of the potential existence of this condition may assist clinicians in their clinical decision making process.
 

References:
Sebastian D. Triangular Interval Sydrome. A differential diagnosis for upper extremity radicular pain. Physiother Theory Pract. 2010 Feb;26(2):113-9.

THE LOWER THORACIC SYNDROME

Lower Thoracic Syndrome was first described by Dr. Deepak Sebastian as a differential screen for back pain occurring in the lower thoracic region and flank area. A history of a vertical compression injury as in a fall on the buttock may favor it’s presence. The lower thoracic region, unlike the upper and mid thoracic region, is infrequently described as a source of musculoskeletal pain and dysfunction. The two clinical entities described to cause pain in this region are intervertebral disc herniation and thoracolumbar junction syndrome. The T11, T12 vertebra has been described to be vulnerable for injury, the mechanisms which include vertical compression and flexion compression. These however are described to cause stable or unstable fractures of the vertebra. While the vulnerability of the T11, T12 vertebra for fractures has been adequately presented, traumatic vertical compression injuries that do not result in a fracture are remotely described. The need being obvious secondary to the common occurrence of slips and falls on the buttock in slippery conditions. It is suggested that when bony disruption does not occur in a traumatic event, the structures of the vertebral motion segment which includes the facet joint, exiting nerve root and supporting muscles and ligaments are subjected to stress, consequently resulting in dysfunction. Thus several structures in the lower thoracic region, especially when the mechanism of injury is a vertical compression, are susceptible. They are, the vertebral motion segments of the lower thoracic spine, the thoracoabdominal nerves, the 12th rib, the quadratus lumborum and the serratus posterior inferior. They are speculated to be potential symptom mediators and collectively identified as vulnerable structures in lower thoracic syndrome.

VULNERABLE STRUCTURES IN NON TRAUMATIC VERTICAL COMPRESSION

References:
Sebastian D. Lower Thoracic Syndrome-a differential screen for back pain following vertical compression injury: a case report. J Bodyw Mov Ther. 2014 Oct;18(4):545-52.

THE SCAPULA BACKWARD TIPPING TEST (SBTT):

The Scapula Backward Tipping Test (SBTT) was first described by Dr. Deepak Sebastian to identify the presence of forward tipping of the scapula. Forward tipping of the scapula has been described to encourage shoulder dysfunction and a reliable method to identify it’s presence is hence mandatory. The attributes to this dysfunction are tightness of the coraco-clavicular ligaments, pectoralis minor and teres major. The subject is placed prone with the head and neck supported and palms in the anatomical position. The examiner places one hand on the inferior angle of the scapula and the fingers of the other hand hook under the coracoid process. A gentle pull is imparted in the upward direction to sense tightness. Care is taken to not hook the fingers under the clavicle as this may encourage over stretching of the acromio-clavicular joint. Comparison is made with the non-symptomatic side to improve sensitivity of the testing procedure. This test has been found to be reproducible between examiners and sensitive to the symptomatic side, thereby improving it’s diagnostic utility.
 

References:
Sebastian D, Chovvath R, Malladi R. The scapula backward tipping test: An inter-rater reliability study. Journal of Bodywork & Movement Therapies. 2017; 21: 69-73.

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DEPENDENT HEAD POSTURE DIZZINESS SYNDROME (DHPDS):

Dependent head posture dizziness syndrome was first described by Dr. Deepak Sebastian and Dr. Van Chockalingam. The structural and functional correlation of the semicircular canals of the inner ear and cervical facets have been described for the first time. While the importance of segmental cervical mobility in maintaining ocular- cervical equilibrium has been highlighted, the importance of cervical mobility and alignment in preventing dislodgement of degenerating otoconia during dependent head postures is also outlined. The importance of restoring functional cervical mobility during routine vestibular rehabilitation is emphasized. 

References:

Sebastian D, Chockalingam S, Patel C. Dependent head posture dizziness syndrome: a case report. Int Phys Med Rehab J. 2022; 7(2): 56-65.              

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