A 54-year-old woman was initially diagnosed with left breast cancer 11
years ago. Based on left lumpectomy, axillary lymph node dissection and imaging
she was staged as cT2N1M0. Her tumor was ER/PR negative and HER2-neu low. She
received adjuvant chemotherapy with doxorubicin and cyclophosphamide followed
by paclitaxel. She received radiation to left breast, supraclavicular and
intramammary lymph nodes.
At the end of 2008, she presented with persistant left shoulder pain
despite conservative management. A shoulder MRI showed diffuse edema of the
pectoralis major and minor muscles, deltoid muscle and mild arthosis of the
acromioclavicular joint. A few weeks later she developed tingling numbness and
weakness in the left upper extremity. PET/CT was ordered and showed an
asymmetric soft tissue with hazy infiltration of the adjacent fat. It was deep
to the left pectoralis muscles and extended into the left axilla.
On corresponding functional images, there was mild increased metabolic
activity in this region, with a maximum SUV of about 3.4. There was also
atrophy of the left pectoralis major, pectoralis minor, deltoid muscle, and
infraspinatus muscle. Given her remote history of surgery and radiation
therapy, the pattern was felt to represent recurrent breast carcinoma and not
A core needle biopsy of the left chest wall soft tissue mass was
nondiagnostic. At the same time an EMG done by neurology showed brachial
plexopathy. A MRI spine and brachial plexus showed mass in the left
supraclavicular fossa with involvement of brachial plexus. The plexus were
extensively clumped and demonstrated abnormal contrast enhancement. Abnormal
thickening and enhancement extended medially along the trunks to involve the
root at the C6/C7 level, where it continued along the left lateral aspect of
the spinal canal.
This enhancing soft tissue contacted the left side of the spinal cord
with slight cord flattening without frank cord compression. The pattern was
highly suggestive of recurrent breast carcinoma with perineural spread. A brain
MRI was negative for metastases. Her screening mammogram from three months ago
On a follow-up visit, she had persistant left shoulder pain and weakness
in the left upper extremity. Due to the location and progressive symptoms
repeat biopsy was not attempted. Given the absence of other lesions or
hypermetabolic activity on the imaging studies, this could represent either a
recurrent or primary breast cancer with brachial plexus involvement. She
received radiation; however, the dose was limited due to prior treatment. She
was started on palliative chemotherapy pending HER2-neu testing by FISH.
1: Clockwise from upper left CT, PET, maximum intensity projection
(MIP) PET, and PET/CT fusion images. The axial CT image demonstrates asymmetric
infiltration of the neurovascular bundle and fat in the left supraclavicular
region compared to the right. This is associated with mild increased FDG uptake
with a maximum SUV of 3.4. This infiltration was noted to extend from deep to
the pectoralis muscles to the axilla.
Figure 2: LEFT Precontrast T1 weighted MR image
demonstrates asymmetric infiltration of the neurovascular bundle and fat in the
left supraclavicular region as was shown on the PET/CT. RIGHT
Postcontrast fat suppressed T1 weighted MR image demonstrates diffuse
enhancement of the infiltrating lesion.
Figure 3: Postcontrast fat suppressed T1 weighted MR
images demonstrate abnormal thickening and enhancement of the C7 nerve root as
well as enhancing soft tissue contacting the left side of the spinal cord with
slight cord flattening. This finding was also seen involving the C6 nerve root
to a lesser extent.
Source: M. Ghesani
Brachial plexus syndrome, with regards to oncological etiology, can be
either from neoplastic process or radiation-induced injury. Neoplastic etiology
can be either primary tumors (schwanommas or neurofibromas) or metastatic
disease (lung, breast, lymphoma, thyroid). Metastatic diseases most commonly
involve the lower trunks with radicular pain being the most common complaint,
and motor weakness or reflex abnormalities being the most common physical
finding. Although radiation-induced plexopathy is usually seen a few weeks to
months after radiation and exact etiology is unclear, clinically these patients
have less pain and more paresthesias and weakness than neoplastic brachial
FDG-PET was done in 19 patients with breast cancer and symptoms
referable to brachial plexus involvement; 14 patients had increased uptake
within brachial plexus, one patient had increased uptake in the chest wall and
four patients had a normal study. When a CT was done in nine patients with
increased 18-FDG uptake in the brachial plexus, only three patients had clear
involvement of brachial plexus. PET is useful in identifying malignancy
involving brachial plexus; however, a larger sample is required to confirm
these findings. EMG study is helpful in localizing the trunk involvement. An
MRI is more sensitive than a CT in imaging brachial plexus. Treatment of
brachial plexopathy from neoplastic etiology is radiation, physical therapy and
optimal pain control.
The above case illustrates low uptake of 18FDG in the area of brachial
plexus several years after surgery and radiation therapy, favoring recurrent
breast carcinoma rather than post-therapy changes. This was further supported
by presence of an associated soft tissue mass on MRI, and evidence of
perineural spread outside the radiation therapy field.
Vamsee Torri, MD, is a Fellow in Hematology/Oncology at St.
Lukes-Roosevelt Hospital Center.
Neilesh Gupta, MD, is a Radiology Resident at St.
Lukes-Roosevelt Hospital Center.
Munir Ghesani, MD, is Associate Clinical Professor of Radiology at
Columbia University College of Physicians and Surgeons and Attending
Radiologist at St.Lukes-Roosevelt Medical Center.
For more information:
- Ahmad A. Br J Cancer. 1999;79:478-482.
- Braverman AS. J Clin Oncol. 2005 ASCO Annual Meeting
Proceedings. Vol 23, No. 16S, Part I of II (June 1 Supplement), 2005:748.
- Jaeckle KA. Semin Neurol. 2004;24:385-393.
- Kori SH. Oncology. 1995;9:756-760.
- J Clin Oncol. 2005:748.