T4 Syndrome:
A Case Study
By Eleanor Richardson
BSc (Hons) Physiotherapy MCSP MHPC
Pg Dip Orthopaedic Medicine & Manual Therapy
Assessment findings and clinical hypothesis (see Appendix 1 and 2):
This patient’s description of their pain and parasthesia did not fit the typical dermatomal pattern of
referral one would expect from a cervical or upper thoracic nerve route. In this instance I was lucky
enough to be able to rule out the possibility of multiple level space occupying lesions, or other serious
pathology, as the patient’s MRI scans were normal. Furthermore, the diagnosis of thoracic outlet
syndrome (TOS) had already been ruled out. However, I was aware that although vascular and true
neurological TOS had been excluded, the possibility of “symptomatic TOS” in the absence radiographic
or electro-physical abnormalities – described by Watson et al. (2009) as the most common form of TOS
– could not fully be ruled out at this stage. However, the patient’s subjective findings were not
consistent with the typical clinical manifestations of symptomatic thoracic outlet (Watson et al., 2009).
Although the patient described their pain as insidious in onset I felt it was possibly linked to her sudden
return to swimming after a 2 year gap in her training schedule. This, along with the aggravating factors
and absence of medical findings, led me to believe that the patient’s symptoms may have a mechanical
element. Her poor response to muscle relaxants led me to think that perhaps the mechanical issue
was more arthogenic than myogenic in nature. The absence of increased pain immediately on waking
led me to think that an inflammatory condition was unlikely.
The patient’s subjective reports of parasthesia, altered and extreme temperature perception and
“puffiness” in the glove distribution led me to think that her symptoms were unlikely to be solely somatic
in origin.
These descriptions are recognised in the literature as being typical symptoms of
sympathetically maintained pain in T4 syndrome (Evans, 1997; Fruth, 2006; Jowsey and Perry, 2010).
The outcome of the subjective assessment led me to focus my objective on assessing any possible
mechanical dysfunction of the thoracic and cervical spine as both these structures were clearly
implicated during her aggravating movements. The main objective findings (please refer to highlighted
areas in initial assessment) in this case study are consistent with other author’s reports of T4 syndrome
symptomatology (Conroy and Schneiders, 2005; Fruth, 2006: Evans, 1997). However, this syndrome is
poorly defined in the literature (Conroy and Schneiders, 2005) and much clinical debate exists
regarding whether spinal joints can refer pain or parasthesia to the hands (Jowsey and Perry, 2010).
Consequently I was aware that it would not be possible to fit my patient’s subjective and objective
findings neatly into a clinical syndrome. I therefore adopted an impairment based approach to my
assessment. In this case, and in the absence of a gold standard for diagnosing a poorly understood
condition, I used symptom reproduction with palpation and observation of movement patterns to inform
my primary hypothesis. Performing a central poster-anterior (PA) pressure to the T4 level was the most
comparable sign in the initial assessment. Pain provocation with palpation has been advocated as a
reliable means for identifying symptomatic structures and an important factor in clinical decision making
(Fruth, 2006).
I therefore felt that impaired movement at T4 provided a possible peripheral driver to this patient’s
symptoms. As sympathetic outflow to the upper limb is supplied by levels T2-5 (Evans, 1997); the
sympathetic nervous system could provide a pathway for referral from the thoracic spine to the upper
limb (Conroy and Schneiders, 2005). My primary hypothesis was therefore informed by combining
subjective and objective findings with existing anatomical, theoretical and clinical research.
Treatment selection/progression:
Thoracic joint mobilisation of the T4 level in T4 syndrome has been utilised successfully in a case study
by Conroy and Schneiders (2005). Although the hypoalgesic effects of spinal mobilisation in the
treatment of T4 syndrome are not fully understood, a recent randomised control trial found that a grade
III postero-anterior rotatory mobilisation technique applied to T4 produced a statistically significant
increase in post treatment skin conductance in the hands of 36 healthy subjects (Jowsey and Perry,
2010).
This provides some evidence that spinal mobilisation directed at T4 can produce
sympathoexcitatory effects and supports the idea that neurophysiological mechanisms produce
hypoalgesic effects mediated by the pathways of the sympathetic nervous system (Bialosky, 2009;
Jowsey and Perry, 2010).
Appling an impairment based approach to manual therapy, I used this research and the patient’s
irritability to inform the grade at which to begin (see movement diagram in Appendix 2). During the first
treatment session I applied a grade III central PA to T4 for a relatively short duration so I could evaluate
the patient’s individual response to treatment and any possible latent effects. I then sequentially
increased the duration and grading as irritability and symptoms allowed, whilst using my objective
markers and subjective findings to monitor progress. Once a positive effect to mobilisations was
established I introduced a home exercise programme consisting of localised T4/5 thoracic
flexion/extension exercises. This was to target the movement dysfunction found at that motion
segment.
Once symptoms were alleviated during normal activities I was then able to assess the patient’s
technique whilst swimming - something she had not tried for approximately 2 months. The outcome of
this functional demonstration allowed me to modify treatment to address her residual movement
impairment (see Appendix 2, 19.10.10). Arm elevation has been shown to influence thoracic posture
(Edomson and Singer, 1997: Crawford and Jull, 1993) and I applied this biomechanical knowledge to
inform treatment progression. Using Maitland’s concept of technique being the “brainchild of ingenuity”
(Maitland et al., 2005), I was able to progress my treatment into a more functionally relevant position for
this individual patient.
Implications for future practice:
Although my primary hypothesis was T4 syndrome, I am in agreement with Evans (1997) who states
the term “upper thoracic syndrome” may be more appropriate as symptoms may not just be derived
from the T4 segment. Had this patient’s most comparable sign been palpation of T2 for example, I
would still have utilised an impairment based approach to manual therapy, only directed at this level
rather than T4.
This patient has taught me the importance of determining whether movement impairments are
associated with a patient’s symptoms and whether these can be addressed by manual therapy or
exercises. Prior to critically evaluating the evidence base, my knowledge of the possible presentations
for patients with sympathetically maintained pain was limited and consequently my primary hypothesis
may have been different. This case study, in conjunction with the evidence base surrounding upper
thoracic dysfuntction, has highlighted the importance of establishing a hypothesis regarding the pain
mechanisms behind a patient’s symptoms at initial assessment and allowing this to inform subsequent
treatment and progression.
Bibliography
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Appendix 1
Subjective Assessment: A 31 year old female presents with a 3 month history of intermittent posterior
thoracic pain (NRS 5-10/10) and bilateral glove parasthesia of gradual, insidious onset. However, the
patient revealed that she resumed open water swimming 3-4 months ago after a 2 year break. Patient
also describes occasional sensations of hot/cold and “puffiness” in both hands. She was referred to a
vascular consultant by her GP 2 months ago with the provisional diagnosis of thoracic outlet syndrome:
all investigations negative. She was then referred to a neurologist and underwent MRI scanning of her
brain, neck, thoracic and lumbar spine - all were normal. The neurologist referred her to physiotherapy.
Her pain is worsening and she has now stopped all swimming training. No past medical history to
note.
Aggravating factors:
→ swimming (medley – i.e. all strokes, not stroke specific)
→ prolonged sitting at desk/computer > 1 hour (patient works as an IT consultant)
→ laying at night with pillows under head (most comfortable completely flat)
24 hour pattern:
→ begins within 2 hours of waking then depends on activity throughout the day. Worse last thing at
night
Easing factors:
→ Tramol and diazepam for the first 3 days then no effect (stopped taking these 2 month ago)
→ hot bath/ shower and massage to shoulders gives temporary relief only
Objective Assessment:
→ increased cervical lordosis and cervico-thoracic kyphosis
→ flattened upper thoracic spine (T2-7)
→ minimal thoracic movement during single arm elevation to either side
→ all thoracic movements pain free but restricted, most noted into flexion where there was minimal
movement from below T3
→ symptoms reproduced++ with central PA on T4
→ ULTT 1 limited on both sides by pain across upper thoracic spine
Clinical Hypothesis: “T4 syndrome”
Appendix 2: Patient Notes
(see attached noted in separate PDF document)