Spontaneous spinal subdural hematoma

Spontaneous spinal subdural hematoma

Spontaneous spinal subdural hematomas are extremely rare.

A nontraumatic acute spontaneous spinal subdural hematoma (sSDH) is a rare complication after spinal surgery. Although an sSDH is often associated with anticoagulation therapy, vascular malformations, or lumbar puncture, the pathogenesis of nontraumatic spontaneous sSDH remains unclear 1)

In the majority of cases, spontaneous hematomas are idiopathic. However, when attributed to anticoagulation therapy coumarins are more common than direct factor Xa inhibitors such as apixaban. Previous reports have linked direct factor Xa inhibitors with intracranial subdural hematomas much more frequently than spinal subdural hematomas. The manifestation of severe neurological deficits, such as sensorimotor disturbances and loss of sphincter control, is common and is considered a surgical emergency 2).


An 82-year-old patient with a history of ischemic heart disease and atrial fibrillation under acenocoumarol was admitted to emergency department with sudden onset of paraplegia and intense back pain associated with urinary incontinence and anal sphincter disorder. On examination his lower limb power was MRC grade 0 out of 5 in all ranges of movement bilaterally and a complete bilateral anesthesia reaching the T12 dermatome was noted. Biological test results showed an International Normalized Ratio at 10. Magnetic resonance imaging revealed a posteriorly located spinal hematoma at T12 level, measuring 36 mm with spinal cord compression. After correction of hemostasis disorders the patient was admitted to the operating room for a T11-L1 laminectomy with evacuation of the subdural hematoma. Muscle power showed a gradual improvement in the lower limbs estimated at 3/5 with regression of sphincter disorders but unfortunately a sequellar sensory impairment persisted.

SSH is a rare situation of acenocoumarol bleeding incident, it should be evoked in any patient treated by this molecule with signs of spinal cord compression 3).


A case of a patient with a spontaneous spinal thoracic subdural hematoma secondary to apixaban use with loss of sphincter control and paraplegia. After 6 months of follow-up, the patient recovered completely 4).

Spinal subdural hematoma (S-SDH) rarely occurs after aneurysmal subarachnoid hemorrhage (SAH). Little information is known regarding the management and prognosis of patients with both S-SDH and SAH. Here, we present an illustrative Case and provide a systematic review of S-SDH in the setting of SAH. METHODS:

A systematic literature review using PRISMA guidelines revealed 11 previous cases of concurrent intracranial SAH and spinal SDH, which are presented with our new reported Case. RESULTS:

Intracranial sources of spontaneous SAH included 8 aneurysms, 1 pseudoaneurysm, and 3 angiogram negative cases. Hunt Hess grade ranged from 1-4, mean time between SAH and S-SDH was 5.8 days, and S-SDH presented most frequently in the lumbar spine. 8 patients showed significant to complete clinical recovery, 2 had continued plegia of the lower extremities, and 2 expired. Modified Rankin score ranged from 0-6, with mRS > 2 for 4 out of 12 patients. Patients with a poor clinical outcome (mRS > 2) had an initially negative cerebral angiogram, earlier presentation with less time between SAH and S-SDH (0.8 vs 7.6 days), use of antithrombotic medication, no diversion of CSF, and cervical or thoracic S-SDH. CONCLUSION:

S-SDH is an uncommon occurrence in the setting of aneurysmal SAH with better outcomes associated with lumbar location, delayed presentation, CSF diversion, and lack of antithrombotic use. Conservative treatment may be sufficient in cases with delayed S-SDH and lack of significant neurological deficits. More reported cases will allow greater understanding of this clinical entity 5).

Surgical intervention is recommended in patients presenting with severe neurologic deficits. Conservative treatment is a reasonable option for asymptomatic patients 6).

Raymaekers et al. presented the case of an intradural hematoma after an extraforaminal surgery through the Wiltse approach for an extraforaminal disk herniation at L5/S1. This 58-year-old woman experienced hypoesthesia and progressive motor dysfunction in the left leg several hours postoperation. Urgent magnetic resonance imaging revealed an intradural hematoma at the L1/L2 to L2/L3 level in the ventral dural sac proximal to the surgical level. Surgical decompression was performed. There was no evidence of trauma, coagulopathy, or anticoagulation therapy. To our knowledge, this case is the first to report an acute sSDH proximal to the surgery level after an extraforaminal spinal surgery through the Wiltse approach for an extraforaminal disk herniation. It illustrates that attentive postoperative neurologic monitoring, even in the absence of intraoperative irregularities, remains important to diagnose and treat this complication at the early stage 7)


A 55-year-old woman without malignancy or coagulopathy history presented with progressive low back pain for the past 2 weeks. Progressive bilateral leg weakness happened 1 week ago. On the day she called for help, she presented with bilateral leg grade 2 muscle power and generalized back pain. There was no headache or meningeal sign. An absent bilateral knee reflex was found. Magnetic resonance imaging showed a space-occupying lesion at the T2-T6 and T12-L1 levels in the ventral and dorsal spinal canal, leading to cord compression. Due to rapid neurologic function deterioration, emergent T12-L1 laminectomy was performed. We found a T12-L1 tense dura sac with subdural hematoma ventral to the cord. Removal of the SDH was performed. T2-T6 levels were treated conservatively. She returned ambulant 1 week after operation. Magnetic resonance images at 3 months and 1 year later showed the SDH being absorbed and replaced by adhesive arachnoid cysts along the whole T and L spine. However, these lesions are asymptomatic for at least 2 years 8).


Sanchez et al. reported a case of Reverse Takotsubo Cardiomyopathy in an otherwise healthy 23-year-old man presenting with back pain, urinary retention, bradycardia, and hypertension. Troponin levels and brain natriuretic peptide (BNP) were elevated, and echocardiogram revealed an ejection fraction (EF) of less than 20%. In addition, MRI demonstrated a spinal subdural hematoma from T1-S1 with no cord compression. Repeated echocardiogram demonstrated an EF of 20-25% with a reverse Takotsubo pattern of cardiomyopathy. With supportive care, his clinical picture improved with normalization of cardiac enzyme and BNP values. This case represents a r-TTC presenting as heart failure in a young, apparently healthy male likely incited by a spinal subdural hematoma. To our knowledge, it is the first of its kind reported 9).


A 7-yr old girl presented to Neurology Department, Mofid Hospital, ShahidBeheshti University of Medical Sciences, Tehran, Iran with limping and pain in lower extremities and acute paraplegia without history of direct trauma. The patient had muscle weakness in lower limbs and was unable to bear weight. Deep Tendon Reflexes (DTR) in lower extremities had increased. Her MRI showed spinal subdural hematoma we reextended from T2 to T6. We performed laminectomy from T2 to T5 and about 70 cc of subdural hematoma was evacuated. One month after the surgery, the patient’s neurological deficit resolved completely. The results showed the pivotal role of attention to clinical manifestation in acute spinal subdural hematoma and early diagnosis to prevent irreversible neurologic complication 10)


Spinal subdural hematoma in pediatric nonaccidental trauma 11)


A case of spontaneous, atraumatic subdural hematoma involving the thoracic region in an 80-year-old woman on warfarin is reported. The patient presented with gross motor and sensory loss, delayed onset of incontinence, and no other symptoms. An MRI suggested an epidural hematoma concentrated around the T4-T9 levels. She was taken emergently to the OR approximately 30 hours after the initial onset of symptoms for a T3-T11 laminectomy. No epidural hematoma was noted. However, discoloration and bulging of the thecal sac were noted, and the dura was incised longitudinally from T2 to T10 revealing an expansive jelly-like blood clot which was evacuated. Postoperatively, the patient had regained 1/2 sensory function in the bilateral lower extremities. At the 2-week mark, the patient was still incontinent and showed 2/2 sensory and 2/5 motor functions in select muscle groups in her bilateral lower extremities. Completely nontraumatic, spontaneous subdural hematomas of the spine are very rare, and early surgical decompression within 24 hours from symptom onset may allow neurological recovery. Large extensive laminectomies up to 10 thoracic levels have been shown to be safe and effective in a few cases, including our case 12).


Acute lumbar spinal subdural hematoma inducing paraplegia after lumbar spinal manipulation 13).


Cases of non-traumatic spinal subdural hematoma accompanied by intracranial hemorrhage are even more rare. There are a few reports of spontaneous spinal subdural hematoma with concomitant intracranial subdural or subarachnoid hemorrhage, but not with intracerebral hemorrhage. Especially in a case of Lee et al., the evaluation and diagnosis were delayed because the spontaneous intracerebral hemorrhage accompanying the unilateral spinal subdural and subarachnoid hemorrhages caused hemiplegia. They reported a case of spinal subdural and subarachnoid hemorrhage with concomitant intracerebral hemorrhage, for the first time, with a relevant literature review 14).


A 76-year-old woman with a spinal subdural hematoma (SDH) was presented with severe back pain without headache. Magnetic resonance imaging (MRI) performed 4 days after onset showed SDH extending from Th2 to L3. She was diagnosed with spontaneous SDH without neurological manifestation, and conservative treatment was selected. Transient disturbance of orientation appeared 7 days after onset. Small subarachnoid hemorrhage (SAH) was detected on head CT, and strict antihypertensive therapy was started. Symptoms changed for the better. Back pain disappeared 4 weeks after onset. On follow-up MRI at 6 months after onset, the SDH had been resolved spontaneously. Although adhesive arachnoiditis was observed at Th4-6, the recurrence of clinical symptoms was not observed at one year and a half after onset. Spinal subdural space is almost avascular; a hematoma in a subdural space is considered to come from a subarachnoid space when it is a lot. A hemorrhage in subarachnoid space was flushed by cerebral spinal fluid; hematoma or arachnoiditis was not formed in general. In this case, hemorrhage was a lot and expansion of SDH was large enough to cause cranial SAH and arachnoiditis. But longitudinally expanded SDH did not show neurological manifestation and resolved spontaneously 15).


A 38-year-old male patient presented with sudden lower back and bilateral leg pain.

A magnetic resonance imaging (MRI) scan on the third day after the onset of symptoms revealed a subdural hematoma from L1 to S1, presenting as hyperintensities on T1 weighted sequences and hypointensities to isointensities on T2 weighted sequences.

Laminectomy and subdural evacuation were performed immediately.

An abnormal ligamentum flavum was observed intraoperatively. A histological examination revealed extravasation of blood in the degenerated ligamentum flavum. Postoperatively, the lower limb pain improved immediately. At the 6-month follow-up, the pain and numbness of the lower limb disappeared, and the muscle strength of both legs recovered completely with normal gait.

Spontaneous SSDH with ligamentum flavum hematoma was caused by a sudden increase of intravenous pressure, resulting from a marked surge in the intra-abdominal or intrathoracic pressure. Consecutive MRI scans provided valuable information, leading to a diagnosis of spontaneous SSDH 16).


Oh et al. presented a case of acute nontraumatic SSDH presenting with transient left hemiplegia for 4 hours. A magnetic resonance imaging study of cervical spine confirmed SSDH with C3-6 cervical cord compression at the left side. The patient had conservative management without recurrence. Although hemiplegia is an unusual clinical manifestation of SSDH, it should be differentiated from that of cerebrovascular origin promptly. Conservative management may be an alternative therapeutic option for selective cases with transient neurological deficits 17).


1) , 7)

Raymaekers V, Beck T, Goebel S, Janssens F, Van den Branden L, Menovsky T, Plazier M. An Acute Spinal Intradural Hematoma after an Extraforaminal Wiltse Approach: A Case Report and Review of the Literature. J Neurol Surg A Cent Eur Neurosurg. 2020 Oct 21. doi: 10.1055/s-0040-1714432. Epub ahead of print. PMID: 33086421.
2) , 4)

Ardebol J, Cahueque M, Lopez W, Azmitia E. Spontaneous thoracic spinal subdural hematoma associated with apixaban therapy. J Surg Case Rep. 2019 Apr 27;2019(4):rjz115. doi: 10.1093/jscr/rjz115. eCollection 2019 Apr. PubMed PMID: 31044059; PubMed Central PMCID: PMC6486654.
3)

Aissa I, Elkoundi A, Andalousi R, Benakrout A, Chlouchi A, Moutaoukil M, Laaguili J, Bensghir M, Balkhi H, Lalaoui SJ. Unusual localization of bleeding under acenocoumarol: Spinal subdural hematoma. Int J Surg Case Rep. 2019;59:15-18. doi: 10.1016/j.ijscr.2019.04.053. Epub 2019 May 10. PubMed PMID: 31100481; PubMed Central PMCID: PMC6522769.
5)

Rothrock RJ, Li AY, Rumsey J, Fifi JT, Kellner CP, Roonprapunt C. Aneurysmal Subarachnoid Hemorrhage with Spinal Subdural Hematoma: A Case Report and Systematic Review of the Literature. World Neurosurg. 2019 May 16. pii: S1878-8750(19)31343-9. doi: 10.1016/j.wneu.2019.05.069. [Epub ahead of print] Review. PubMed PMID: 31103768.
6) , 8)

Gan CW, Chen SY, Chang CS, Liu JD. Spontaneous Spinal Subdural Hematoma: Case Report of 2 Years’ Clinical and Radiologic Findings. World Neurosurg. 2019 Jul;127:275-278. doi: 10.1016/j.wneu.2019.04.063. Epub 2019 Apr 13. PubMed PMID: 30986583.
9)

Sanchez K, Glener S, Esplin NE, Okorie ON, Parikh A. A Case of Reverse Takotsubo Cardiomyopathy Incited by a Spinal Subdural Hematoma. Case Rep Neurol Med. 2019 Jul 22;2019:9285460. doi: 10.1155/2019/9285460. eCollection 2019. PubMed PMID: 31428488; PubMed Central PMCID: PMC6679891.
10)

Farzan A, Pourbakhtyaran E, Moosavian T, Moosavian H. Spinal Subdural Hematomas in a Normal Child without Trauma History: A Case Report. Iran J Child Neurol. 2019 Summer;13(3):121-124. PubMed PMID: 31327977; PubMed Central PMCID: PMC6586447.
11)

Hong CS, Camara-Quintana J, Kundishora AJ, Diluna ML, Kahle KT. Teaching NeuroImages: Spinal subdural hematoma in pediatric nonaccidental trauma. Neurology. 2019 Jul 30;93(5):e522-e523. doi: 10.1212/WNL.0000000000007869. PubMed PMID: 31358679.
12)

Arain AR, Moral M, Shams S, Desai K, Kalsa K. Atypical Presentation of Atraumatic Spinal Subdural Hematoma Associated with Warfarin: A Case Report and Review of the Literature. Case Rep Orthop. 2019 May 20;2019:4037916. doi: 10.1155/2019/4037916. eCollection 2019. PubMed PMID: 31236299; PubMed Central PMCID: PMC6545747.
13)

Benyaich Z, Laghmari M, Lmejjati M, Aniba K, Ghannane H, Benali SA. Acute lumbar spinal subdural hematoma inducing paraplegia after lumbar spinal manipulation: A case report and literature review. World Neurosurg. 2019 May 9. pii: S1878-8750(19)31275-6. doi: 10.1016/j.wneu.2019.05.002. [Epub ahead of print] PubMed PMID: 31078801.
14)

Lee Y, Lim J, Han S, Choi SW, Youm JY, Koh HS. Spontaneous Spinal Subdural and Subarachnoid Hemorrhage with Concomitant Intracerebral Hemorrhage: A Case Report. Korean J Neurotrauma. 2019 Apr 19;15(1):34-37. doi: 10.13004/kjnt.2019.15.e7. eCollection 2019 Apr. PubMed PMID: 31098347; PubMed Central PMCID: PMC6495584.
15)

Go T, Tsutsui T, Iida Y, Fukutake K, Fukano R, Ishigaki K, Tsuchiya K, Takahashi H. A Case of Spontaneous Spinal Subdural Hematoma Complicated by Cranial Subarachnoid Hemorrhage and Spinal Adhesive Arachnoiditis. Case Rep Orthop. 2019 Mar 13;2019:7384701. doi: 10.1155/2019/7384701. eCollection 2019. PubMed PMID: 31001442; PubMed Central PMCID: PMC6436331.
16)

Li X, Yang G, Wen Z, Lou X, Lin X. Surgical treatment of progressive cauda equina compression caused by spontaneous spinal subdural hematoma: A case report. Medicine (Baltimore). 2019 Mar;98(12):e14598. doi: 10.1097/MD.0000000000014598. PubMed PMID: 30896615.
17)

Oh SH, Han IB, Koo YH, Kim OJ. Acute spinal subdural hematoma presenting with spontaneously resolving hemiplegia. J Korean Neurosurg Soc. 2009 Jun;45(6):390-3. doi: 10.3340/jkns.2009.45.6.390. Epub 2009 Jun 30. PubMed PMID: 19609426; PubMed Central PMCID: PMC2711240.

Post lumbar puncture spinal hematoma

Post lumbar puncture spinal hematoma

Lumbar puncture is a useful diagnostic and treatment tool. Although serious events are seldom, they can be detrimental. A precaution not to underestimate such events in practicing lumbar, especially in patients with suboptimum coagulation state. Image-guided procedure can be useful and should be considered in appropriately selected patients 1).


In a Danish cohort study, risk of spinal hematoma following lumbar puncture was 0.20% among patients without coagulopathy and 0.23% among those with coagulopathy. Although these findings may inform decision-making about lumbar puncture by describing rates in this sample, the observed rates may reflect bias due to physicians selecting relatively low-risk patients for lumbar puncture 2).


It is estimated that approximately 4% of symptomatic spinal hematomas are related to traumatic LP. They are commonly located inclusively with the epidural space in 75% of the cases, whereas subarachnoid hemorrhage and spinal subdural hematoma can be found in 15.7% and 4.1%, respectively. Multi-compartmental spinal hematomas are rare and thought to present in 0.33% 3).


In clinical practice, few carry out postprocedural investigation for spinal hematoma unless the patient reports sensory or motor changes after the procedure. In a meta-analysis, approximately 85% of symptomatic spinal hematomas required surgical intervention 4)


Surgery is indicated for symptomatic patients with reported complete neurological recovery in almost 40%. The timing of surgery is vital and associated with improved neurological outcome when done in less than 36 hours 5).


Nevertheless, symptomatic spinal hematoma is a critical condition and we emphasize that surgical intervention should be considered at a low threshold for urgent decompression to optimize overall clinical outcome. Coagulopathy is an important risk factor that should not be underestimated in planning for LP. The presence of pre-existing coagulopathy was found to be a significant poor prognostic factor regardless of surgical intervention. Therefore, an early investigation with spinal MRI should be obtained to rule out an evolving spinal hematoma. Mortality was reported high in patients with compressive cervical spinal epidural hematomas and cardiovascular disease 6).

Case reports

A case for a patient with Burkitt lymphoma who presented with mild neuroaxial symptoms. An urgent cerebrospinal fluid sample was required which was taken after correcting his platelets count to 53.4 × 109/L. He developed a massive multi-compartmental thoracolumbar hematoma with acute cauda equine syndrome requiring surgical intervention. Despite aggressive management, he remained permanently paraplegic with functional status that negatively affected his overall outcome 7).

References

1) , 7)

Al Jishi A, Murty N. Massive lumbar spine hematoma post-spinal tap. Surg Neurol Int. 2017 Dec 6;8:293. doi: 10.4103/sni.sni_351_17. PMID: 29285409; PMCID: PMC5735427.
2)

Bodilsen J, Mariager T, Vestergaard HH, Christiansen MH, Kunwald M, Lüttichau HR, Kristensen BT, Bjarkam CR, Nielsen H. Association of Lumbar Puncture With Spinal Hematoma in Patients With and Without Coagulopathy. JAMA. 2020 Oct 13;324(14):1419-1428. doi: 10.1001/jama.2020.14895. PMID: 33048155.
3)

Groen RJ, van Alphen HA. Operative treatment of spontaneous spinal epidural hematomas: a study of the factors determining postoperative outcome. Neurosurgery. 1996 Sep;39(3):494-508; discussion 508-9. doi: 10.1097/00006123-199609000-00012. PMID: 8875479.
4) , 6)

Kreppel D, Antoniadis G, Seeling W. Spinal hematoma: a literature survey with meta-analysis of 613 patients. Neurosurg Rev. 2003 Jan;26(1):1-49. doi: 10.1007/s10143-002-0224-y. Epub 2002 Sep 24. PMID: 12520314.
5)

Evans RW. Complications of lumbar puncture. Neurol Clin. 1998 Feb;16(1):83-105. doi: 10.1016/s0733-8619(05)70368-6. PMID: 9421542.

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
WhatsApp WhatsApp us
%d bloggers like this: