Middle meningeal artery embolization for chronic subdural hematoma

Middle meningeal artery embolization for chronic subdural hematoma

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Chronic subdural hematoma is fundamentally a disorder of the meningeal blood vessels.

Embolization of the middle meningeal artery (MMA) has recently been proposed as a curative treatment for chronic subdural hematoma (cSDH), but evidence for the indication and timing is not definitive.

Fiorella and Arthur reviewed the potential role for the endovascular management of cSDH within the context of a discussion of the epidemiology, pathophysiology, and conventional management of this disease 1).

Trials

Systematic Reviews

The goal of a study was to review the evidence on MMAE in cSDH to assess its safety, feasibility, indications and efficacy. We performed a systematic review of the literature according to PRISMA guidelines using multiple electronic databases. Our search yielded a total of 18 original articles from which data were extracted. A total of 190 patients underwent MMAE from which 81.3% were symptomatic cSDH. Over half (52.3%) of the described population were undergoing antithrombotic therapy. Most (83%) procedures used polyvinyl alcohol (PVA) particles and no complications were reported regarding the embolization procedures. Although the definition of resolution varied among authors, cSDH resolution was reported in 96.8% of cases. MMAE is a feasible technique for cSDH, but the current body of evidence does not yet support its use as a standard treatment. Further studies with a higher level of evidence are necessary before MMAE can be formally recommended 2).


Three double-arm studies comparing embolization and conventional surgery groups and 6 single-arm case series were identified and analyzed. Hematoma recurrence rate was significantly lower in the embolization group compared with conventional treatment group (2.1% vs. 27.7%; odds ratio = 0.087; 95% confidence interval, 0.026-0.292; P < 0.001; I2 = 0%); surgical complication rates were similar between groups (2.1% vs. 4.4%; odds ratio = 0.563; 95% confidence interval, 0.107-2.96; P = 0.497; I2 = 27.5%). Number of patients with modified Rankin Scale score >2 in the embolization (12.5%) versus conventional treatment (9.1%) group showed no statistical difference (P = 0.689). A composite hematoma recurrence rate of 3.6% was found after summing the 6 case series. Composite recurrence and complication rates in the embolization cohorts of the double-arm studies and the case series were lower than literature values for conventional surgical treatments.

MMA embolization is a promising treatment for chronic subdural hematoma. Future randomized clinical trials are needed 3).

Case series

A review was registered with the International prospective register of systematic reviews (PROSPERO). Public/Publisher Medline (PubMed), Cumulative Index to Nursing and Allied Health Literature (CINAHL), Excerpta Medica dataBASE (EMBASE) and the Cochrane Library were searched using Medical Subject Headings (MeSH) terms for MMA embolization and CSDH from January 2000 through November 2018. All articles in the English language literature describing MMA embolization for CSDH were included, irrespective of study design. Consecutive patients who underwent MMA embolization at our hospital from January 2017 through June 2018 comprised our clinical experience.

Fifteen studies with 193 procedures were included in the review. Ninety-five (49.2%) cases involved primary MMA embolization; 88(45.6%) embolization for recurrent CSDH, and 10(5.2%) were performed for prophylaxis after surgical evacuation. Recurrence after MMA embolization requiring further treatment occurred in 7(3.6%) cases. All other patients had symptomatic relief with no further recurrence. No procedure-related complications were reported. Polyvinyl alcohol was the most commonly used material. Our series included 8 patients treated with Onyx (Medtronic). All had symptom relief and significant reduction in hematoma size; no recurrences or procedure-related complications were observed 4).


Nakagawa et al., retrospectively assessed data from 381 consecutive patients who underwent burr hole irrigation for CSDH between 2009 and 2017. Recurrent symptomatic ipsilateral CSDH in 71 (18%) patients was treated by a second burr-hole irrigation and 20 of them had a further symptomatic CSDH recurrence thereafter. Those with persistent ipsilateral CSDH recurrence were treated by MMA embolization. Before the MMA embolization procedures, the amount of hematoma membrane enhancement determined using superselective MMA angiography-DynaCT imaging was classified into three stages.

Embolization of the MMA proceeded without perioperative complications or further CSDH recurrence. The interval between recurrence and the amount of hematoma membrane enhancement significantly correlated (first to second and second to third treatments: p = 0.012 and p = 0.017, respectively). The frequency of bilateral CSDH was significantly higher and the recurrence interval between the first and second treatments was significantly shorter in repeated recurrences group compared with recurrence group (p = 0.023 and p = 0.006, respectively).

Repeatedly recurrent CSDH can be safely treated and cured by MMA embolization. Hematoma membrane enhancement pattern using DynaCT images can predict repeated recurrences CSDH. 5)


Five patients with symptomatic chronic SDHs underwent MMA embolization using PVA microparticles. Size of SDH was recorded in maximum diameter and total volume.

Four patients underwent unilateral and 1 underwent bilateral MMA embolization successfully. All cases had significant reduction in total volume of SDH at longest follow-up scan: 81.4 to 13.8 cc (7 wk), 48.5 to 8.7 cc (3 wk), 31.7 and 88 to 0 and 17 cc (14 wk, bilateral), 79.3 to 24.2 cc (8 wk), and 53.5 to 0 cc (6 wk). All patients had symptomatic relief with no complications. Histologic analysis of the chronic SDH membrane in a separate patient that required surgery revealed rich neovascularization with many capillaries and few small arterioles.

MMA embolization could present a minimally invasive and low-risk initial treatment alternative to surgery for symptomatic chronic SDH when clinically appropriate 6).


MMA embolization was performed using angiography, selective microcatheterization of the MMA, and infusion of polyvinyl alcohol particles. Outcomes were assessed clinically and with interval imaging studies at 1 d, 2 wk, and 6 wk postprocedure, and additional intervals as indicated.

MMA embolization was performed successfully on 60 total SDHs in 49 patients. This includes upfront treatment for new (not previously treated) SDH in 42, for recurrence in 8, and prophylaxis (soon after surgical evacuation) in 10. There were 3 mortalities (unrelated to the procedure), and no procedural complications. Of the 50 nonprophylactic cases, there were 4 (8.9%) cases of recurrence requiring surgical evacuation, and 31 (68.9%) that had resolution or reduction in size >50% of SDH at longest follow-up. Overall, 41 (91.1%) were stable or decreased in size and able to avoid surgery.

MMA embolization may represent a minimally-invasive alternative to surgery for new or recurrent chronic SDH, or as prophylaxis to reduce the risk of recurrence after surgery. Given our encouraging results with a 91% long-term success rate, a large scale clinical trial is warranted 7).


Link TW, Schwarz JT, Paine SM, Kamel H, Knopman J. Middle Meningeal Artery Embolization for Recurrent Chronic Subdural Hematoma: A Case Series. World Neurosurg. 2018 Oct;118:e570-e574. doi: 10.1016/j.wneu.2018.06.241. Epub 2018 Jul 6. PubMed PMID: 30257310.


Five patients with symptomatic chronic SDHs underwent MMA embolization using PVA microparticles at our institution. Size of SDH was recorded in maximum diameter and total volume.

Four patients underwent unilateral and 1 underwent bilateral MMA embolization successfully. All cases had significant reduction in total volume of SDH at longest follow-up scan: 81.4 to 13.8 cc (7 wk), 48.5 to 8.7 cc (3 wk), 31.7 and 88 to 0 and 17 cc (14 wk, bilateral), 79.3 to 24.2 cc (8 wk), and 53.5 to 0 cc (6 wk). All patients had symptomatic relief with no complications. Histologic analysis of the chronic SDH membrane in a separate patient that required surgery revealed rich neovascularization with many capillaries and few small arterioles.

MMA embolization could present a minimally invasive and low-risk initial treatment alternative to surgery for symptomatic chronic SDH when clinically appropriate 8).


Seventy-two prospectively enrolled patients with CSDH underwent MMA embolization (embolization group; as the sole treatment in 27 [37.5%] asymptomatic patients and with additional hematoma removal for symptom relief in 45 [62.5%] symptomatic patients). For comparison, 469 patients who underwent conventional treatment were included as a historical control group (conventional treatment group; close, nonsurgical follow-up in 67 [14.3%] and hematoma removal in 402 [85.7%] patients). Primary outcome was treatment failure defined as a composite of incomplete hematoma resolution (remaining or reaccumulated hematoma with thickness > 10 mm) or surgical rescue (hematoma removal for relief of symptoms that developed with continuous growth of initial or reaccumulated hematoma). Secondary outcomes included surgical rescue as a component of the primary outcome and treatment-related complication for safety measure. Six-month outcomes were compared between the study groups with logistic regression analysis. Results Spontaneous hematoma resolution was achieved in all of 27 asymptomatic patients undergoing embolization without direct hematoma removal. Hematoma reaccumulation occurred in one (2.2%) of 45 symptomatic patients receiving embolization with additional hematoma removal. Treatment failure rate in the embolization group was lower than in the conventional treatment group (one of 72 patients [1.4%] vs 129 of 469 patients [27.5%], respectively; adjusted odds ratio [OR], 0.056; 95% confidence interval [CI]: 0.011, 0.286; P = .001). Surgical rescue was less frequent in the embolization group (one of 72 patients [1.4%] vs 88 of 469 patients [18.8%]; adjusted OR, 0.094; 95% CI: 0.018, 0.488; P = .005). Treatment-related complication rate was not different between the two groups (0 of 72 patients vs 20 of 469 patients [4.3%]; adjusted OR, 0.145; 95% CI: 0.009, 2.469; P = .182). Conclusion MMA embolization has a positive therapeutic effect on CSDH and is more effective than conventional treatment 9).


Gobran Taha Alfotih reported 14 cases http://www.roneurosurgery.eu/atdoc/AlfotihGobran_Embolization.pdf

Case reports

A case of a 74-year-old male on aspirin with a history of recurrent symptomatic chronic right-sided subdural hematoma treated successfully with a SEPS and right middle meningeal artery embolization with poly vinyl alcohol (PVA) microparticles. The patient initially presented to the emergency department with headaches, difficulty walking, and left sided hemiparesis. CT Head showed a large chronic right-sided subdural hematoma measuring 2.7 cm thick with 1 cm of leftward shift. Patient underwent placement of a right-sided SEPS and the subdural hematoma decreased in size to 1.0 cm with 2 mm of leftward shift. The patient had resolution of headaches and neurological symptoms and was discharged home. Three months later, the patient returned to the emergency department with headache and left hand numbness. CT Head showed an acute on chronic right-sided subdural hematoma measuring 1.4 cm with 3 mm of leftward shift. Patient underwent right-sided SEPS placement. Repeat CT Head showed reduction in the subdural hematoma to 1.2 cm. The SEPS was removed and the patient had resolution of neurological symptoms. The patient then had a diagnostic cerebral angiogram with PVA microparticle embolization of the right middle meningeal artery. A SEPS was placed at the time of the angiogram to further reduce the size of the subdural hematoma.

Repeat CT Head after SEPS and middle meningeal artery embolization showed decrease in size of the subdural hematoma. Follow-up CT Head showed stability of the subdural hematoma and patient had no further neurological symptoms. Patient was discharged home.

Middle meningeal artery embolization is a useful endovascular technique for reducing the arterial supply to the membranes in chronic subdural hematomas. Middle meningeal artery embolization can reduce the recurrence rate of subdural hematomas 10).

References

1)

Fiorella D, Arthur AS. Middle meningeal artery embolization for the management of chronic subdural hematoma. J Neurointerv Surg. 2019 Feb 23. pii: neurintsurg-2019-014730. doi: 10.1136/neurintsurg-2019-014730. [Epub ahead of print] Review. PubMed PMID: 30798265.
2)

Court J, Touchette CJ, Iorio-Morin C, Westwick HJ, Belzile F, Effendi K. Embolization of the Middle meningeal artery in chronic subdural hematoma – A systematic review. Clin Neurol Neurosurg. 2019 Aug 10;186:105464. doi: 10.1016/j.clineuro.2019.105464. [Epub ahead of print] Review. PubMed PMID: 31600604.
3)

Srivatsan A, Mohanty A, Nascimento FA, Hafeez MU, Srinivasan VM, Thomas A, Chen SR, Johnson JN, Kan P. Middle Meningeal Artery Embolization for Chronic Subdural Hematoma: Meta-Analysis and Systematic Review. World Neurosurg. 2019 Feb;122:613-619. doi: 10.1016/j.wneu.2018.11.167. Epub 2018 Nov 24. PubMed PMID: 30481628.
4)

Waqas M, Vakharia K, Weimer PV, Hashmi E, Davies JM, Siddiqui AH. Safety and Effectiveness of Embolization for Chronic Subdural Hematoma: Systematic Review and Case Series. World Neurosurg. 2019 Mar 13. pii: S1878-8750(19)30678-3. doi: 10.1016/j.wneu.2019.02.208. [Epub ahead of print] Review. PubMed PMID: 30878752.
5)

Nakagawa I, Park HS, Kotsugi M, Wada T, Takeshima Y, Matsuda R, Nishimura F, Yamada S, Motoyama Y, Park YS, Kichikawa K, Nakase H. Enhanced hematoma membrane on DynaCT images during middle meningeal artery embolization for persistently recurrent chronic subdural hematoma. World Neurosurg. 2019 Feb 27. pii: S1878-8750(19)30485-1. doi: 10.1016/j.wneu.2019.02.074. [Epub ahead of print] PubMed PMID: 30825631.
6) , 8)

Link TW, Boddu S, Marcus J, Rapoport BI, Lavi E, Knopman J. Middle Meningeal Artery Embolization as Treatment for Chronic Subdural Hematoma: A Case Series. Oper Neurosurg (Hagerstown). 2018 May 1;14(5):556-562. doi: 10.1093/ons/opx154. PubMed PMID: 28973653.
7)

Link TW, Boddu S, Paine SM, Kamel H, Knopman J. Middle Meningeal Artery Embolization for Chronic Subdural Hematoma: A Series of 60 Cases. Neurosurgery. 2018 Nov 9. doi: 10.1093/neuros/nyy521. [Epub ahead of print] PubMed PMID: 30418606.
9)

Ban SP, Hwang G, Byoun HS, Kim T, Lee SU, Bang JS, Han JH, Kim CY, Kwon OK, Oh CW. Middle Meningeal Artery Embolization for Chronic Subdural Hematoma. Radiology. 2018 Mar;286(3):992-999. doi: 10.1148/radiol.2017170053. Epub 2017 Oct 10. PubMed PMID: 29019449.

Chronic Subdural Hematoma Surgical Technique

Chronic Subdural Hematoma Surgical Technique

Till 1970s, craniotomy was the most commonly used method. Burr hole trephination for chronic subdural hematoma became the most preferred method from 1980s. In 1977, Twist drill craniotomy for chronic subdural hematoma was introduced. Closed system drainage after a Burr hole (BH) or a Twist drill (TD) became the most frequently used surgical method 1).

The duration of procedure was significantly more in Burr-Hole Craniostomy BHC than in Twist-Drill Craniostomy TDC. In postoperative outcome, there was no significant difference in the GCS score, motor power improvement, motor power deterioration, overall clinical improvement, and improvement in CT scans of both the groups. Postoperative residue requiring reoperation was significantly more in TDC group. There was no significant difference in the development acute SDH, reoperation rate, complications, death, and hospital stay in both the groups. Avoiding the complications of general anesthesia and giving the equal postoperative improvement and complications of BHC, the TDC is considered as an effective alternative to the BHC in the surgical management of CSDH 2)

Although nonsurgical treatment is often successful, trephination has more advantages, such as rapid resolution of the symptoms and short period of hospitalization. Nonsurgical treatment is possible in asymptomatic patients with a small CSDH. For the symptomatic patients with CSDH, trephination is the treatment of choice, either by BH or TD. In gray zone between surgery and medical treatment, shared decision making can be an ideal approach. For chronic subdural hematoma recurrences, repeated trephination is still effective for patients with a low risk of recurrence. If the risk of recurrence is high, additional management would be helpful. For the refractory CSDHs, it is necessary to obliterate the subdural space 3).


Chronic subdural hematoma treatment in the elderly include observation, operative burr holes or craniotomy, and bedside twist drill drainage. The decision on which technique to use should be determined by weighing the comorbidities and symptoms of the patient with the potential risks and benefits.

Chronic subdural hematoma are ideally treated with surgical drainage. Despite this common practice, there is still controversy surrounding the best surgical procedure. With lack of clear evidence of a superior technique, surgeons are free to base the decision on other factors that are not related to patient care.

Originally, CSDHs were treated by open craniotomy 4) 5) 6) 7). Later burr hole trephination (BHT) was adopted because it was less invasive with lower morbidity and recurrence rates when compared with standard craniotomy 8) 9) 10) 11) 12) 13).

The traditional methods include evacuation via a burr hole with closed system drainage with or without irrigation, two burr-hole craniostomy with closed system drainage with irrigation or craniotomy, with subdural drain or without drain placement.

Minicraniotomy (MC) emerged as an attractive alternative to BHT as it allows better visualisation of the subdural cavity, enabling better haemostasis and resection of membranes.

Although bedside twist drill evacuation may avoid operating room costs and anesthetic complications in an elderly patient population and allow earlier anticoagulation resumption treatment if necessary, there is also a risk of morbidity if uncontrolled bleeding is encountered or the patient is unable to tolerate the bedside procedure. However, bedside twist drill craniostomy is a reasonable and effective option for the treatment of subacute/chronic SDH in patients who may not be optimal surgical candidates 14).


Subperiosteal vs Subdural Drain After Burr-Hole Drainage of Chronic Subdural Hematoma: A Randomized Clinical Trial (cSDH-Drain-Trial) 15).

Burr hole trephination for chronic subdural hematoma

Twist drill craniotomy for chronic subdural hematoma

Subdural drain for chronic subdural hematoma

Subdural evacuating port system for chronic subdural hematoma

Subgaleal drain for chronic subdural hematoma

Craniotomy for chronic subdural hematoma

Neuroendoscopy

References

1) , 3)

Lee KS. How to Treat Chronic Subdural Hematoma? Past and Now. J Korean Neurosurg Soc. 2019 Mar;62(2):144-152. doi: 10.3340/jkns.2018.0156. Epub 2018 Nov 30. PubMed PMID: 30486622; PubMed Central PMCID: PMC6411568.
2)

Thavara BD, Kidangan GS, Rajagopalawarrier B. Comparative Study of Single Burr-Hole Craniostomy versus Twist-Drill Craniostomy in Patients with Chronic Subdural Hematoma. Asian J Neurosurg. 2019 Apr-Jun;14(2):513-521. doi: 10.4103/ajns.AJNS_37_19. PubMed PMID: 31143272; PubMed Central PMCID: PMC6516027.
4)

Ernestus R, Beldzinski P, Lanfermann H, Klug N. Chronic subdural hematoma: surgical treatment and outcome in 104 patients. Surg Neurol 1997;48:220–5.
5)

McKissock W, Richardson A, Bloom WH. Subdural hematoma: a review of 389 cases. Lancet 1960;1:1365–9.
6)

Tyson G et al. The role of craniectomy in the treatment of chronic subdural hematomas. J Neurosurg 1980;52:776–81.
7)

Putnam IJ, Cushing H. Chronic subdural hematoma. Its pathology, its relation to pachymeningitis hemorrhagica, and its surgical treatment. Arch Surg 1925;11:329–93.
8)

Chronic Almenawer S et al. Subdural hematoma management: a systematic review and meta-analysis of 34829 patients. Ann Surg 2014;259(3):449–57.
9)

Lee J, Ebel H, Ernestus R, Klug N. Various surgical treatments of chronic subdural hematoma and outcome in 172 patients: is membranectomy necessary? Surg Neurol 2004;61:523–5528.
10)

Ducruet A et al. The surgical management of chronic subdural hematoma. Neurosurg Rev 2012;35:155–69.
11)

Leroy H et al. Predictors of functional outcomes and recurrence of chronic subdural. J Clin Neurosci 2015;22:1895–900.
12)

Regan J, Worley E, Shelburne C, Pullarkat R, Burr Watson J. Hole Washout versus craniotomy for chronic subdural hematoma: patient outcome and cost analysis. PLoS One 2015;10(1):1–8.
13)

Mondorf Y, Abu-Owaimer M, Gaab M, Oertel J. Chronic subdural hematoma – Craniotomy versus burr hole trephination. Br J Neurosurg 2009;23(6):612–6.
14)

Garber S, McCaffrey J, Quigley EP, MacDonald JD. Bedside Treatment of Chronic Subdural Hematoma: Using Radiographic Characteristics to Revisit the Twist Drill. J Neurol Surg A Cent Eur Neurosurg. 2016 Jan 25. [Epub ahead of print] PubMed PMID: 26807616.
15)

Agrawal A, Pacheco-Hernandez A, Moscote-Salazar LR. Letter: Subperiosteal vs Subdural Drain After Burr-Hole Drainage of Chronic Subdural Hematoma: A Randomized Clinical Trial (cSDH-Drain-Trial). Neurosurgery. 2019 Aug 6. pii: nyz289. doi: 10.1093/neuros/nyz289. [Epub ahead of print] PubMed PMID: 31387117.

Spontaneous spinal subdural hematoma

Spontaneous spinal subdural hematoma

Spontaneous spinal subdural hematomas are extremely rare.

Surgical intervention is recommended in patients presenting with severe neurologic deficits. Conservative treatment is a reasonable option for asymptomatic patients 1).

Spontaneous spinal subdural hematoma after anticoagulation therapy

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 sphinctercontrol, 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).

Aneurysmal Subarachnoid Hemorrhage with Spinal Subdural Hematoma

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).

Case reports

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 6).


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 7).


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 8)


Spinal subdural hematoma in pediatric nonaccidental trauma 9)


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 10).


Acute lumbar spinal subdural hematoma inducing paraplegia after lumbar spinal manipulation 11).


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 12).


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 13).


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 14).


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 15).

References

1) , 6)

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