Lumbar spinal stenosis diagnosis

Lumbar spinal stenosis diagnosis

Diagnosing lumbar spinal stenosis or herniated intervertebral disc is usually helpful only in potential surgical candidates 1).

Boden et al., performed magnetic resonance imaging on sixty-seven individuals who had never had low back pain, sciatica, or neurogenic claudication. The scans were interpreted independently by three neuro-radiologists who had no knowledge about the presence or absence of clinical symptoms in the subjects. About one-third of the subjects were found to have a substantial abnormality. Of those who were less than sixty years old, 20 per cent had a herniated nucleus pulposus and one had spinal stenosis. In the group that was sixty years old or older, the findings were abnormal on about 57 per cent of the scans: 36 per cent of the subjects had a herniated nucleus pulposus and 21 per cent had spinal stenosis. There was degeneration or bulging of a disc at at least one lumbar level in 35 per cent of the subjects between twenty and thirty-nine years old and in all but one of the sixty to eighty-year-old subjects. In view of these findings in asymptomatic subjects, they concluded that abnormalities on magnetic resonance images must be strictly correlated with age and any clinical signs and symptoms before operative treatment is contemplated 2).


Results of a survey suggested that there are no broadly accepted quantitative criteria and only partially accepted qualitative criteria for the diagnosis of lumbar spinal stenosis. The latter include disk protrusion, lack of perineural intraforaminal fat, hypertrophic facet joint degeneration, absent fluid around the cauda equine, and hypertrophy of the ligamentum flavum 3).

There is still no widely accepted diagnostic or classification criteria for the diagnosis of Lumbar spinal canal stenosis LSS and as a consequence studies use widely differing eligibility criteria that limit the generalizability of reported findings 4).

There are no universally accepted radiographic definitions for the diagnosis of central, lateral recess and foraminal stenosis.


Most studies of Lumbar central canal spinal stenosis diagnosis (LCCSS) rely on criteria published by Verbiest et al. 5). He defined relative spinal stenosis as a diameter between 10 and 12 mm whereas absolute stenosis was a diameter less than 10 mm. This method has been criticized for ignoring the trefoil shape of the LSS and the intrusion of ligamentum flavum and disc material in degenerative stenosis 6).

Magnetic resonance imaging

Magnetic resonance imaging (MRI) is most commonly used for the clinical assessment of degenerative LCCSS. LCCSS is a quantitative diagnosis that is made when the measurement of an individual is outside the range of normal. Thus, the criteria for LCCSS should be compared from an analysis of a normative distribution of measurements 7) 8)

In a meta-analysis, CT and MRI were found to have similar accuracy for the assessment of central stenosis 9).

By using a combination of magnetic resonance imaging (MRI) and computed tomography (CT) of the lumbar spine, it is possible to distinguish between spinal stenosis caused by bone compression and specific soft tissue epidural intraspinal lesions that cause localized spinal canal stenosis and neural compression. Examples include facet cysts and yellow ligament hypertrophy 10).

Because imaging findings of lumbar spinal stenosis (LSS) may not be associated with symptoms, clinical classification criteria based on patient symptoms and physical examination findings are needed 11).

Magnetic resonance imaging (MRI) has replaced myelography, now considered an old-fashioned technique. In selected cases with multilevel lumbar spinal stenosis, functional myelography revealed the highest precision in reaching a correct diagnosis. It resulted in a change in the surgical approach in every fifth patient in comparison with the MRI and proved most helpful, especially in elderly patients 12).

Cross sectional area

Narrowing of the lumbar dural sac cross sectional area (DSCSA) and spinal canal cross-sectional area (SCCSA) have been considered major causes of lumbar central canal spinal stenosis (LCCSS). DSCSA and SCCSA were previously correlated with subjective walking distance before claudication occurs, aging, and disc degeneration. DSCSA and SCCSA have been ideal morphological parameters for evaluating LCCSS.

To evaluate lumbar central canal spinal stenosis (LCCSS) patients, pain specialists should more carefully investigate the dural sac cross-sectional area (DSCSA) than spinal canal cross-sectional area (SCCSA) 13).

Schonstrom et al. showed that neurogenic claudication due to LSS was better defined by the cross-sectional area (CSA) of the dural sac, but that the CSA of the lumbar vertebral canal was unrelated to that of the dural sac 14). From in vitro 15) and in situ 16) studies, the authors postulated that constrictions above the critical size 70 to 80 mm2 would be unlikely to cause symptoms and signs of cauda encroachment. Subsequently, conflicting results have been published concerning the relationship between symptom severity and dural CSA. Even after axial loading, no statistically significant correlations were found in some studies 17). However, in another study, the use of the minimal CSA of the dural sac in central stenosis was found to be correlated with neurogenic claudication assessed measuring the maximum tolerated walking distance 18).

Electrodiagnostic studies

Patients with symptoms, physical examination and imaging findings consistent with LSS do not require additional testing. Although there is little evidence in the literature, electrodiagnostic evaluation is used in some patients with symptoms and findings that are equivocal or conflicting with imaging results and in whom procedures are being considered. Electrodiagnostic criteria for stenosis have been proposed:(47) mini-paraspinal mapping with a one side score > 4 (sensitivity 30%, specificity 100%), fibrillation potential in limb muscles (sensibility 33%, specificity 88%), absence of tibial H-wave (sensitivity 36%, specificity 92%). Better sensitivity was found for a composite limb and paraspinal fibrillation score (sensitivity 48%, specificity 88%) 19).

Diagnostic Screening

Jensen et al. developed a self-administered diagnostic screening questionnaire for lumbar spinal stenosis (LSS) consisting of items with high content validity and to investigate the diagnostic value of the questionnaire and the items.

The screening questionnaire was developed based on items from the existing literature describing key symptoms of LSS. The screening questionnaire (index test) was to be tested in a cohort of patients with persistent lumbar and/or leg pain recruited from a Danish publicly funded outpatient secondary care spine clinic with clinicians performing the reference test. However, to avoid unnecessary collection of data if the screening questionnaire proved to be of limited value, a case-control design was incorporated into the cohort design including an interim analysis. Additional cases for the case-control study were recruited at two Danish publicly funded spine surgery departments. Prevalence, sensitivity, specificity and diagnostic odds ratio (OR) were calculated for each individual item, and AUC (area under the curve) was calculated to examine the performance of the full questionnaire.

A 13-item Danish questionnaire was developed and tested in 153 cases and 230 controls. The interim analysis was not in favour of continuing the cohort study, and therefore, only results from the case-control study are reported. There was a positive association for all items except the presence of back pain. However, the association was only moderate with ORs up to 3.3. When testing the performance of the whole questionnaire, an AUC of 0.72 was reached with a specificity of 20% for a fixed sensitivity of 95%.

The items were associated with LSS and therefore have some potential to identify LSS patients. However, the association was not strong enough to provide sufficient accuracy for a diagnostic tool. Additional dimensions of symptoms of LSS need identification to obtain a reliable questionnaire for screening purposes 20).

References

1)

Deyo RA, Bigos SJ, Maravilla KR. Diagnostic imaging procedures for the lumbar spine. Ann Intern Med. 1989 Dec 1;111(11):865-7. Review. Erratum in: Ann Intern Med 1989 Dec 15;111(12):1050. PubMed PMID: 2530926.
2)

Boden SD, Davis DO, Dina TS, Patronas NJ, Wiesel SW. Abnormal magnetic-resonance scans of the lumbar spine in asymptomatic subjects. A prospective investigation. J Bone Joint Surg Am. 1990 Mar;72(3):403-8. PubMed PMID: 2312537.
3)

Mamisch N, Brumann M, Hodler J, Held U, Brunner F, Steurer J; Lumbar Spinal Stenosis Outcome Study Working Group Zurich. Radiologic criteria for the diagnosis of spinal stenosis: results of a Delphi survey. Radiology. 2012 Jul;264(1):174-9. doi: 10.1148/radiol.12111930. Epub 2012 May 1. PubMed PMID: 22550311.
4)

Genevay S, Atlas SJ, Katz JN. Variation in eligibility criteria from studies of radiculopathy due to a herniated disc and of neurogenic claudication due to lumbar spinal stenosis: a structured literature review. Spine (Phila Pa 1976). 2010 Apr 1;35(7):803-11. doi: 10.1097/BRS.0b013e3181bc9454. Review. PubMed PMID: 20228710; PubMed Central PMCID: PMC2854829.
5)

Verbiest H. Pathomorphologic aspects of developmental lumbar stenosis. Orthop Clin North Am. 1975 Jan;6(1):177-96. PubMed PMID: 1113966.
6)

Eisenstein S. The trefoil configuration of the lumbar vertebral canal. A study of South African skeletal material. J Bone Joint Surg Br. 1980 Feb;62-B(1):73-7. PubMed PMID: 7351439.
7)

Chatha DS, Schweitzer ME. MRI criteria of developmental lumbar spinal stenosis revisited. Bull NYU Hosp Jt Dis 2011;69:303–7.
8)

Premchandran D, Saralaya VV, Mahale A. Predicting lumbar central canal stenosis—a magnetic resonance imaging study. J Clin Diagn Res 2014;8:RC01–4.
9)

Kent DL, Haynor DR, Larson EB, Deyo RA. Diagnosis of lumbar spinal stenosis in adults: a metaanalysis of the accuracy of CT, MR, and myelography. AJR Am J Roentgenol. 1992 May;158(5):1135-44. PubMed PMID: 1533084.
10)

Jacobson RE, Granville M, Hatgis DO J. Targeted Intraspinal Radiofrequency Ablation for Lumbar Spinal Stenosis. Cureus. 2017 Mar 10;9(3):e1090. doi: 10.7759/cureus.1090. PubMed PMID: 28413736; PubMed Central PMCID: PMC5388364.
11)

Genevay S, Courvoisier DS, Konstantinou K, Kovacs FM, Marty M, Rainville J, Norberg M, Kaux JF, Cha TD, Katz JN, Atlas SJ. Clinical classification criteria for neurogenic claudication caused by lumbar spinal stenosis. The N-CLASS criteria. Spine J. 2017 Oct 12. pii: S1529-9430(17)31052-5. doi: 10.1016/j.spinee.2017.10.003. [Epub ahead of print] PubMed PMID: 29031994.
12)

Morgalla M, Frantz S, Dezena RA, Pereira CU, Tatagiba M. Diagnosis of Lumbar Spinal Stenosis with Functional Myelography. J Neurol Surg A Cent Eur Neurosurg. 2018 Jan 18. doi: 10.1055/s-0037-1618563. [Epub ahead of print] PubMed PMID: 29346832.
13)

Lim YS, Mun JU, Seo MS, Sang BH, Bang YS, Kang KN, Koh JW, Kim YU. Dural sac area is a more sensitive parameter for evaluating lumbar spinal stenosis than spinal canal area: A retrospective study. Medicine (Baltimore). 2017 Dec;96(49):e9087. doi: 10.1097/MD.0000000000009087. PubMed PMID: 29245329; PubMed Central PMCID: PMC5728944.
14)

Schonstrom NS, Bolender NF, Spengler DM. The pathomorphology of spinal stenosis as seen on CT scans of the lumbar spine. Spine (Phila Pa 1976). 1985 Nov;10(9):806-11. PubMed PMID: 4089655.
15)

Schönström N, Bolender NF, Spengler DM, Hansson TH. Pressure changes within the cauda equina following constriction of the dural sac. An in vitro experimental study. Spine (Phila Pa 1976). 1984 Sep;9(6):604-7. PubMed PMID: 6495030.
16)

Schönström N, Hansson T. Pressure changes following constriction of the cauda equina. An experimental study in situ. Spine (Phila Pa 1976). 1988 Apr;13(4):385-8. PubMed PMID: 3406845.
17)

Lohman CM, Tallroth K, Kettunen JA, Lindgren KA. Comparison of radiologic signs and clinical symptoms of spinal stenosis. Spine (Phila Pa 1976). 2006 Jul 15;31(16):1834-40. PubMed PMID: 16845360.
18)

Ogikubo O, Forsberg L, Hansson T. The relationship between the cross-sectional area of the cauda equina and the preoperative symptoms in central lumbar spinal stenosis. Spine (Phila Pa 1976). 2007 Jun 1;32(13):1423-8; discussion 1429. PubMed PMID: 17545910.
19)

Genevay S, Atlas SJ. Lumbar spinal stenosis. Best Pract Res Clin Rheumatol. 2010 Apr;24(2):253-65. doi: 10.1016/j.berh.2009.11.001. Review. PubMed PMID: 20227646; PubMed Central PMCID: PMC2841052.
20)

Jensen RK, Lauridsen HH, Andresen ADK, Mieritz RM, Schiøttz-Christensen B, Vach W. Diagnostic Screening for Lumbar Spinal Stenosis. Clin Epidemiol. 2020;12:891-905. Published 2020 Aug 19. doi:10.2147/CLEP.S263646

Craniosynostosis diagnosis

Craniosynostosis diagnosis

Commonly, craniosynostosis is present at birth, but it is not always diagnosed when mild. Usually it is diagnosed as a cranial deformity in the first few months of life. The diagnosis relies on physical examination and radiographic studies, including plain radiography and computed tomography (CT). Clinical history should include complications of pregnancy, duration of gestation, and birth weight 1).

Premature fusion of the cranial sutures restricts cranial growth perpendicular to the affected suture with compensatory overgrowth along the other patent sutures. This results in the characteristic skull shape deformities noted in craniosynostosis. Diagnostic imaging is necessary to confirm the fused suture and to assess the accompanying skull deformities, intracranial pathology and other complications. A prematurely fused suture shows perisutural sclerosis, linearity, reduced serration, bony bridging or the absence of the suture on a plain skull radiography or CT image. Secondary signs of increased ICP, such as a “copper-beaten” appearance, are also observed in severe cases 2).

Soboleski et al. 3) reported the ultrasonographic findings of craniosynostosis as follows : 1) the loss of the hypoechoic fibrous gap between hyperechoic body plates; 2) an irregular, thickened inner sutural margin; 3) the loss of a beveled edge; and 4) asymmetric fontanels. On “Black Bone” MRI, the affected fused sutures are demonstrated as absence of suture 4).


A normal patent suture is demonstrated as a radiolucency, serrated and nonlinear line on plain skull radiography and 3D-CT images 5) 6) 7) 8).

Ultrasonography shows a normal patent suture as an uninterrupted hypoechoic fibrous gap between hyperechoic cranial bones with an end-to-end appearance on a transverse scan of the sagittal sinus and a beveled appearance on a transverse scan of the coronal and lambdoid suture9) 10) 11)


Conventional MRI has typically been unreliable in identifying sutures individually. However, Eley et al. described a novel gradient echo MRI sequence (“Black Bone”) that minimizes soft tissue contrast to enhance the bone-soft tissue boundaries and can demonstrate normal patent cranial sutures as hyperintensity distinguished from the signal void of the cranial bones 12).


Proisy et al. from Rennes first described a high-resolution sonography technique and its limitations. They then analyzed the reliabilityeffectiveness and role of ultrasonography in routine practice using a PubMed literature review.

Ten studies reported excellent correlations between ultrasonography and 3D-CT. Cranial US for the diagnosis of a closed suture had 100% sensitivity in 8 studies and 86-100% specificity before the age of 12 months. Negative findings mean imaging investigation can be stopped. If ultrasonography confirms diagnosis, neurosurgical consultation is required. Thus, 3D-CT can be postponed until appropriate before surgery.

Cranial suture ultrasound is an effective and reliable technique for the diagnosis of craniosynostosis. It has many advantages: it is fast and non-irradiating, and no sedation is required. It should be used as first-line imaging in infants below the age of 8-12 months when craniosynostosis is clinically suspected. 13).

References

1)

Panchal J, Uttchin V. Management of craniosynostosis. Plast Reconstr Surg. 2003;111:2032–48.
2)

Kim HJ, Roh HG, Lee IW. Craniosynostosis : Updates in Radiologic Diagnosis. J Korean Neurosurg Soc. 2016 May;59(3):219-26. doi: 10.3340/jkns.2016.59.3.219. Epub 2016 May 10. Review. PubMed PMID: 27226852; PubMed Central PMCID: PMC4877543.
3) , 11)

Soboleski D, Mussari B, McCloskey D, Sauerbrei E, Espinosa F, Fletcher A. High-resolution sonography of the abnormal cranial suture. Pediatr Radiol. 1998;28:79–82.
4) , 12)

Eley KA, Watt-Smith SR, Sheerin F, Golding SJ. “Black Bone” MRI : a potential alternative to CT with three-dimensional reconstruction of the craniofacial skeleton in the diagnosis of craniosynostosis. Eur Radiol. 2014;24:2417–2426.
5)

Badve CA, K MM, Iyer RS, Ishak GE, Khanna PC. Craniosynostosis : imaging review and primer on computed tomography. Pediatr Radiol. 2013;43:728–742. quiz 725-727.
6)

Branson HM, Shroff MM. Craniosynostosis and 3-dimensional computed tomography. Semin Ultrasound CT MR. 2011;32:569–577.
7)

Kirmi O, Lo SJ, Johnson D, Anslow P. Craniosynostosis : a radiological and surgical perspective. Semin Ultrasound CT MR. 2009;30:492–512.
8)

Nagaraja S, Anslow P, Winter B. Craniosynostosis. Clin Radiol. 2013;68:284–292.
9)

Regelsberger J, Delling G, Helmke K, Tsokos M, Kammler G, Kränzlein H, et al. Ultrasound in the diagnosis of craniosynostosis. J Craniofac Surg. 2006;17:623–625. discussion 626-628.
10)

Soboleski D, McCloskey D, Mussari B, Sauerbrei E, Clarke M, Fletcher A. Sonography of normal cranial sutures. AJR Am J Roentgenol. 1997;168:819–821.
13)

Proisy M, Bruneau B, Riffaud L. How ultrasonography can contribute diagnosis of craniosynostosis. Neurochirurgie. 2019 Oct 2. pii: S0028-3770(19)30231-0. doi: 10.1016/j.neuchi.2019.09.019. [Epub ahead of print] PubMed PMID: 31586456.

Intracerebral hemorrhage diagnosis

Intracerebral hemorrhage diagnosis

Computed tomography

Noncontrast computed tomography (NCCT) is the gold standard to detect intracerebral hemorrhage (ICH) in patients presenting with acute focal syndromes.

Although CT remains important in the acute setting, MR imaging has proved invaluable for diagnosis and characterization of intracranial hemorrhage.

Non-contrast head CT, given its availability and high sensitivity in detecting blood products, is frequently the first tool to readily detect ICH; however, different types of hemorrhages may share a common appearance on CT and the optimal therapeutic approach varies depending on etiology. An additional diagnostic work-up is frequently indicated to make the final diagnosis and to assist in urgent patient management. CT- and MR angiography, and digital angiography can diagnose vascular anomalies, CT venography can reveal cerebral vein thrombosis, diffusion-weighted MRI (DWI) may show hemorrhagic transformation of an infarct, and susceptibility-weighted MRI (SWI) may detect hypertensive and amyloid angiopathy-related microbleeds. MR also has a major role in revealing underlying etiologies such as cavernoma, primary brain tumor or metastases. These imaging tools assist in determining the cause of ICH, and also in assessing the risk of deterioration. Prognostic factors such as size, location, mass effect, and detection of the “spot sign” all play an important role in foreseeing possible deterioration, thus allowing prompt intervention 1).


Intracerebral hemorrhage volume is a powerful predictor of 30-day mortality after spontaneous intracerebral hemorrhage (ICH). Kothari et al., compared a bedside method of measuring CT ICH volume with measurements made by computer-assisted planimetric image analysis 2).

MRI

Diffusion weighted magnetic resonance imaging (DW-MRI) may be considered as the initial screening tool for imaging patients presenting with focal neurologic symptoms suggestive of stroke.

DW-MRI at b1000 has a diagnostic yield similar to noncontrast computed tomography (NCCT) for detecting ICH and superior to NCCT for detecting ischemic stroke (IS). Therefore, DW-MRI may be considered as the initial screening tool for imaging patients presenting with focal neurologic symptoms suggestive of stroke 3).

Biomarkers

Results indicated that circulating miR-181b, miR-223, miR-155 and miR-145 in plasma samples could be served as a potential noninvasive tool in ICH detection 4).

References

1)

Eliahou R, Auriel E, Gomori M, Sosna J, Honig A. [SPONTANEOUS PARENCHYMAL INTRACRANIAL HEMORRHAGE – A DIAGNOSTIC CHALLENGE]. Harefuah. 2018 Mar;157(3):158-161. Hebrew. PubMed PMID: 29582945.
2)

((Kothari RU, Brott T, Broderick JP, Barsan WG, Sauerbeck LR, Zuccarello M, Khoury J. The ABCs of measuring intracerebral hemorrhage volumes. Stroke. 1996 Aug;27(8):1304-5. PubMed PMID: 8711791.
3)

Keigler G, Goldberg I, Eichel R, Gomori JM, Cohen JE, Leker RR. Diffusion-weighted Imaging at b1000 for Identifying Intracerebral Hemorrhage: Preliminary Sensitivity, Specificity, and Inter-rater Variability. J Stroke Cerebrovasc Dis. 2014 May 1. pii: S1052-3057(14)00065-2. doi: 10.1016/j.jstrokecerebrovasdis.2014.02.005. [Epub ahead of print] PubMed PMID: 24795096.
4)

Gareev I, Yang G, Sun J, Beylerli O, Chen X, Zhang D, Zhao B, Zhang R, Sun Z, Yang Q, Li L, Pavlov V, Safin S, Zhao S. Circulating MicroRNAs as a Potential Non-invasive Biomarkers of Spontaneous Intracerebral Hemorrhage. World Neurosurg. 2019 Sep 13. pii: S1878-8750(19)32446-5. doi: 10.1016/j.wneu.2019.09.016. [Epub ahead of print] PubMed PMID: 31525485.
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