Thoracic radiculopathy

Thoracic radiculopathy is the pain and resulting symptoms associated with compression on the nerve or nerve roots of the thoracic spine. When the symptoms radiate or refer distally from the spine into the back and outward along the ribs to the anterior chest wall it is considered radiculopathy.

Epidemiology

Thoracic radiculopathy represents an uncommon spinal disorder that is frequently overlooked in the evaluation of spinal pain syndromes 1).

Etiology

Anything that encroaches on, or presses on a nerve, and disrupts its function at the nerve root can be considered a cause of nerve root entrapment.

Degenerative disc disease that results in wear on the intervertebral disc, and a reduction in disc height may result in loss of space at the intervertebral foramen. Herniated discs can place pressure on the nerve in addition to inflammation that irritates the nerve. Degenerative joint disease that results in the formation of bony spurs on the facet joints can narrow the intervertebral space placing pressure on the exiting nerve. Trauma or muscle spasm can put pressure on the peripheral nerve, producing symptoms along that nerve’s distribution path.


The symptoms of thoracic radiculopathy, regardless of the cause, are often not recognized, as there is typically no associated motor deficit. When the etiology is disc herniation or trauma, motor deficit or myelopathy may be observed in the advanced stages.

Furthermore, the typical presentation of band-like thoracic or abdominal pain can mimic a myriad of conditions 2).

With many differential diagnoses to consider, it is not surprising that thoracic radiculopathy is often not discovered for months, or years, after symptoms arise 3).

Rarer causes of thoracic radiculopathy described in the literature include post-thoracotomy, paravertebral mesothelial cyst, and myodil cyst 4).


Thoracic radiculopathy has been reported as a complication of spinal cord stimulation (SCS) paddle lead implantation by several authors and commonly presents as abdominal pain.

Lee et al., from the Houston Methodist Hospital performed a search of all patients who underwent either placement of a new epidural paddle lead electrode or revision of an epidural paddle lead electrode for SCS in the thoracic region from January 2017 to January 2018. They then investigated all cases of immediate postoperative abdominal pain.

They identified 7 patients who had immediate postoperative abdominal pain among 86 cases of epidural SCS procedures. Most patients were discharged on postoperative days 1-3. No patients required revisions or removals of their SCS for any reason.

They conclude that the etiology of immediate postoperative abdominal pain after thoracic paddle lead implantation for SCS is most likely thoracic radiculopathy. They hypothesized that small, transient epidural hematomas could be the cause of this thoracic radiculopathy. They argue that all patients with immediate postoperative abdominal pain and no other neurologic deficits after thoracic paddle lead implantation for SCS should first be treated conservatively with observation and pain management 5).

References

1) , 3)

O’Connor RC, Andary MT, Russo RB, DeLano M. Thoracic radiculopathy. Phys Med Rehabil Clin N Am. 2002 Aug;13(3):623-44, viii. Review. PubMed PMID: 12380552.
2) , 4)

Mammis A, Bonsignore C, Mogilner AY. Thoracic radiculopathy following spinal cord stimulator placement: case series. Neuromodulation. 2013 Sep-Oct;16(5):443-7; discussion 447-8. doi: 10.1111/ner.12076. Epub 2013 May 17. PubMed PMID: 23682904.
5)

Lee JJ, Sadrameli SS, Desai VR, Austerman RJ, Leonard DM, Dalm BD. Immediate Abdominal Pain after Placement of Thoracic Paddle Leads for Spinal Cord Stimulation: A Case Series. Stereotact Funct Neurosurg. 2019 Jan 3:1-6. doi: 10.1159/000495415. [Epub ahead of print] PubMed PMID: 30605913.

Internal jugular vein stenosis

Internal jugular vein stenosis (IJVS) is gaining increasing attention from clinical researchers due to a series of confounding symptoms that impair the quality of life in affected individuals but cannot be explained by other well-established causes. In a study of Zhou et al.,from the Xuanwu Hospital, aimed to elucidate the clinical features, neuroimaging characteristics and pathogenesis of IJVS, and explore their possible correlations, in attempt to provide useful clues for clinical diagnosis and treatment. Forty-three eligible patients with unilateral or bilateral IJVS confirmed by contrast-enhanced magnetic resonance venography of the brain and neck were enrolled in a study. Magnetic resonance imaging along with magnetic resonance angiography or computed tomography angiography was applied to identify the radiological pattern of parenchymal or arterial lesions. Cerebral perfusion and metabolismwere evaluated by single-photon emission computed tomography (SPECT). Of the 43 patients (46.0 ± 16.0 years old; 30 female), 14 (32.6%) had bilateral and 29 had unilateral IJVS. The common clinical symptoms at admission were tinnitus (60.5%), tinnitus cerebri (67.6%), headache(48.8%), dizziness (32.6%), visual disorders (39.5%), hearing impairment (39.5%), neck discomfort (39.5%), sleep disturbance (60.5%), anxiety or depression (37.5%) and subjective memory impairment (30.2%). The presence of bilateral demyelination changes with cloudy-like appearance in the periventricular area and/or centrum semiovale was found in 95.3% (41/43) patients. SPECT findings showed that 92.3% (24/26) patients displayed cerebral perfusion and metabolism mismatch, depicted by bilaterally and symmetrically reduced cerebral perfusion and increased cerebral glucose consumption. IJVS may contribute to alterations in cerebral blood flow and metabolism, as well as white matter lesion formation, all of which may account for its clinical manifestations. 1).


Fifteen consecutive patients were screened from 46 patients suspected as IIH and were finally confirmed as isolated IJV stenosis. The stenotic IJV was corrected with stenting when the trans-stenotic mean pressure gradient (∆MPG) was equal to or higher than 5.44 cmH2 O. Dynamic magnetic resonance venography, computed tomographic venography and digital subtraction angiography of the IJV, ∆MPG, ICP, Headache Impact Test 6 and the Frisén papilledema grade score before and after stenting were compared.

All the stenotic IJVs were corrected by stenting. ∆MPG decreased and the abnormal collateral veins disappeared or shrank immediately. Headache, tinnitus, papilledema and ICP were significantly ameliorated at 14 ± 3 days of follow-up (all P < 0.01). At 12 ± 5.6 months of outpatient follow-up, headache disappeared in 14 out of 15 patients (93.3%), visual impairments were recovered in 10 of 12 patients (83.3%) and tinnitus resolved in 10 out of 11 patients (90.9%). In 12 out of 15 cases, the Frisén papilledema grade scores declined to 1 (0-2). The stented IJVs in all 15 patients kept to sufficient blood flows on computed tomographic venography follow-up without stenting-related adverse events.

Non-thrombotic IJV stenosis may be a potential etiology of IIH. Stenting seems to be a promising option to address the issue of intracranial hypertension from the etiological level, particularly after medical treatment failure 2).


Previous magnetic resonance imaging studies have shown abnormalities of the internal jugular veins in patients with thoracic outlet syndrome (TOS), but this finding has largely been ignored. We, thus, prospectively performed diagnostic brachiocephalic venograms in all patients with diagnosed neurogenic TOS from April 2008 to December 2011 (mean age, 42.6; r, 16-68; 77.8% women and 22.2% men). Stenosis of the left internal jugular vein, left subclavian vein, right internal jugular vein, and right subclavian vein were assessed, and significant stenoses of these vessels were seen in 63.49%, 65.08%, 60.32%, and 68.25% of patients, respectively. Internal jugular vein stenosis was not present in 23.81%, present unilaterally in 28.57%, and present bilaterally in 47.62% of patients. Subclavian vein stenosis was not present in 17.46%, present unilaterally in 28.57%, and present bilaterally in 53.97% of patients. Phi coefficients of correlation were 0.067 between left internal jugular vein and left subclavian vein stenoses, 0.061 between right internal jugular vein and right subclavian vein stenoses, and 0 between any internal jugular vein and any subclavian vein stenoses, indicating there is no correlation between jugular vein stenosis and subclavian vein stenosis in these patients. We conclude that right and left internal jugular vein stenosis is common in patients with neurogenic TOS symptoms. Treatment of internal jugular vein stenosis could potentially benefit these patients, and the implications of these findings warrant further study 3).

Clinical trials

References

1)

Zhou D, Ding J, Asmaro K, Pan L, Ya J, Yang Q, Fan C, Ding Y, Ji X, Meng R. Clinical Characteristics and Neuroimaging Findings in Internal Jugular Venous Outflow Disturbance. Thromb Haemost. 2019 Jan 3. doi: 10.1055/s-0038-1676815. [Epub ahead of print] PubMed PMID: 30605919.
2)

Zhou D, Meng R, Zhang X, Guo L, Li S, Wu W, Duan J, Song H, Ding Y, Ji X. Intracranial hypertension induced by internal jugular vein stenosiscan be resolved by stenting. Eur J Neurol. 2018 Feb;25(2):365-e13. doi: 10.1111/ene.13512. Epub 2017 Dec 7. PubMed PMID: 29114973.
3)

Ahn SS, Miller TJ, Chen SW, Chen JF. Internal jugular vein stenosis is common in patients presenting with neurogenic thoracic outlet syndrome. Ann Vasc Surg. 2014 May;28(4):946-50. doi: 10.1016/j.avsg.2013.12.009. Epub 2014 Jan 21. PubMed PMID: 24462538.

Mastoid cells

A section of the mastoid process of the temporal bone of the cranium shows it to be hollowed out into a number of spaces, the mastoid cells, which exhibit great variety in their size and number.

MAC: mastoid air cells; SH: spine of Henle; SMC: suprameatal crest.

At the upper and front part of the process they are large and irregular and contain air (a form of skeletal pneumaticity), but toward the lower part they diminish in size, while those at the apex of the process are frequently quite small and contain marrow; occasionally they are entirely absent, and the mastoid is then solid throughout. At birth the mastoid is not pneumatized, but becomes aerated over the first year of life. Poor pneumatization is associated with eustachian tube dysfunction.


Lin et al., from the Guangdong Second Provincial General Hospital, analyzed treatment of microvascular decompression using the retrosigmoid approach (RA) in primary trigeminal neuralgia and hemifacial spasm using preoperative images combined with intraoperative microscopic navigation to avoid unnecessarily opening the mastoid air cells (MACs).

Ten patients with primary trigeminal neuralgia and 20 patients with hemifacial spasm (test group) were treated using retrosigmoid approach (RA) for microvascular decompression. Preoperative head magnetic resonance angiography and temporal bone computed tomography were performed and the images registered using SPM12 and fused with MRIcron to determine the relationship between mastoid air cells (MACs) and sigmoid sinuses. An O-arm was used for navigation, and the transverse sinussigmoid sinus was projected under a microscope to guide RA. A control group comprised 139 patients who had the same surgical procedure as the test group but without image processing or intraoperative navigation.

The relationship between mastoid air cells (MACs) and the ipsilateral sigmoid sinus was classified as follows: I, MACs did not exceed the lateral edge of the ipsilateral sigmoid sinus (10/60); II, MACs exceeded the ipsilateral lateral edge of the sigmoid sinus but did not exceed the medial edge (42/60); and III, MACs exceeded the medial edge of the ipsilateral sigmoid sinus (8/60). Test and control groups showed significant differences in the incidences of opening MACs (P = 0.003). There was no cerebrospinal fluid leakage or scalp and intracranial infection at follow-up.

Image processing and intraoperative microscopic navigation can avoid unnecessarily opening MACs and might reduce postoperative cerebrospinal leakage and scalp infection after RA craniotomy 1).

1)

Lin J, Zhang Y, Peng R, Ji X, Luo G, Luo W, Wang M, Zhu M, Sun X, Zhang Y. Preoperative Imaging and Microscopic Navigation During Surgery Can Avoid Unnecessarily Opening the Mastoid Air Cells Through Craniotomy Using the Retrosigmoid Approach. World Neurosurg. 2019 Jan;121:e15-e21. doi: 10.1016/j.wneu.2018.08.181. Epub 2018 Sep 3. PubMed PMID: 30189308.
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