Oculomotor nerve palsy in chronic subdural hematoma

Oculomotor nerve palsy in chronic subdural hematoma

Isolated oculomotor nerve palsy is well known as a symptom of microvascular infarction and intracranial aneurysm, but unilateral oculomotor nerve palsy as an initial manifestation of chronic subdural hematoma (CSDH) is a rare clinical condition.

Oculomotor nerve palsy (ONP) usually occurs in chronic subdural hematoma (CSDH) as a common sign of brain herniation that typically is associated with a deterioration of consciousness.


Ninety-eight cases of cSDH were operated over a 6-year period, in which 14 cases were classified as being bilateral. Among these 14 cases, 6 cases showed a rapid and aggressive clinical course. Therefore, complicated risk factors, the initial data on coagulofibrinolytic examination, magnetic resonance imaging appearance, and prognosis were analyzed.

Of the 6 cases, 5 showed a rapid aggravation as they awaited surgery. The period of the aggravation since the initial diagnosis harboring cSDH was 19 to 54 hours. One case was at first neurologically free from any disturbance but 17 hours later experienced a generalized seizure. All 6 cases experienced consciousness disturbance. In addition, 3 of them manifested oculomotor palsy 1).

Case reports

Zavatto et al., reported a bilateral oculomotor palsy after surgical evacuation of chronic subdural hematoma 2).


Corrivetti et al., reported 2 cases of bilateral CSDH who presented with ONP without deterioration of consciousness. An extensive literature reviewrevealed this is an extremely rare finding.

They also investigated all the possible pathogenic mechanisms producing nerve impairment and found a strong association with bilateral subdural hematoma. Vascular compression between posterior circulation arteries and tentorial edge abnormalities also could be involved. Vulnerability of the oculomotor nerve seems to be a necessary condition leading to clinical onset and is caused by predisposing factors to nerve damage, including vascular disease, head trauma, or herpes zoster infection.

Although isolated ONP is a very rare presentation of CSDH, a differential diagnosis is absolutely necessary, because surgical treatment allows good recovery of third nerve palsy in most of the cases 3).


Matsuda et al., reported a rare case of an 84-year-old woman with bilateral CSDH who presented with unilateral oculomotor nerve palsy as the initial symptom. The patient, who had a medical history of minor head injury 3 weeks prior, presented with left ptosis, diplopia, and vomiting. She had taken an antiplatelet drug for lacunar cerebral infarction. Computed tomography (CT) of the head showed bilateral CSDH with a slight midline shift to the left side. She underwent an urgent evacuation through bilateral frontal burr holes. Magnetic resonance angiography (MRA) after evacuation revealed no intracranial aneurysms, but constructive interference in steady-state (CISS) magnetic resonance imaging (MRI) revealed that the left posterior cerebral artery (PCA) ran much more anteriorly and inferiorly compared with the right PCA and the left oculomotor nerve passed very closely between the left PCA and the left superior cerebellar artery (SCA). There is the possibility that the strong compression to the left uncus, the left PCA, and the left SCA due to the bilateral CSDH resulted in left oculomotor nerve palsy with an initial manifestation without unconsciousness. Unilateral oculomotor nerve palsy as an initial presentation caused by bilateral CSDH without unconsciousness is a rare clinical condition, but this situation is very important as a differential diagnosis of unilateral oculomotor nerve palsy 4).


Jalil et al., reported the case of a patient who presented with left oculomotor cranial nerve palsy with an associated large volume left acute on chronic subdural haematoma. Coincidentally, this woman was also found to have a recent history of herpes zoster ophthalmicus 5).


Moon et al., reported two cases of Kernohan’s notch phenomenon secondary to chronic subdural hematoma detected by MRI. In the first case, the patient was drowsy with an oculomotor palsy and a hemiparesis ipsilateral to the chronic subdural hematoma. MRI in the post-operative period showed no abnormal signal or deformity of the crus cerebri. The neurological signs immediately resolved after trephination. In the second case, the patient was admitted with progressive decrease in their level of consciousness and ipsilateral hemiparesis with the chronic subdural hematoma. MRI on admission revealed an abnormal signal in the contralateral crus cerebri against the chronic subdural hematoma. After surgery, the mental state gradually recovered to normal with some degree of residual hemiparesis. In patients with chronic subdural hematoma, a compressive deformity of the crus cerebri, without abnormal signal on MRI, may predict a better neurological recovery in patients with Kernohan’s notch phenomenon 6).


Mishra et al., reported a 50-year old male patient with complaints of drooping of the right upper eyelid, for the past 1 day. He also gave a history of generalized mild headache for the past 1 week. There was no history of any injury, vomiting, fever, seizures, loss of consciousness, slurred speech, numbness, weakness, diplopia or any other major systemic illnesses like hypertension or diabetes. The patient also gave no history of any cardiovascular disorder. Patient was not a known alcoholic and neither was he on any anti coagulant or anti platelet therapy. On examination the patient was conscious and well oriented in time and space. His vitals were all within normal limits. Neurological examination was strictly unremarkable. Blood test revealed a normal blood count, urea, creatinine and electrolytes and was also negative for HIV antibodies. Ocular examination of the right eye revealed a vision of 6/9, improving to 6/6 with pin hole. There was severe ptosis with the marginal reflex distance 1 (MRD1) < −0.5 mm and a poor levator function (<4 mm). The eyeball too was displaced outwards and downwards (infraducted and abducted). The ocular movements were severely affected, with an absence of adduction and elevation; however abduction was full with mild residual depression. Depression was accompanied by intorsion, maximally when the eye was abducted. The pupil was dilated (6 mm) and un-reactive to light (vs. 3 mm and reactive in the left eye). Fundus was essentially normal. The left eye was uninvolved. A provisional diagnosis of isolated unilateral oculomotor nerve palsy, right eye, was made and the suspected site of involvement of the nerve was clinically deduced to be around the fascicular subarachnoid portion. This is because the fascicles of the third cranial nerve exit the mid brain through the medial aspect of the cerebral peduncles and are not near any other cranial nerves at this point. So isolated third cranial nerve palsy occurs from lesions in this location. Aneurysm is the most common lesion to affect the third cranial nerve in the subarachnoid space. The fact that the pupil too was involved pointed towards a posterior communicating artery aneurysm. A provisional diagnosis of a posterior communicating artery aneurysm with or without overt subarachnoid haemorrhage was made and the patient was sent for an urgent computed tomography (CT scan) of the brain and orbits, which revealed a CSDH in the right fronto-temporo-parietal lobe, causing mass effect in the form of compression of the right lateral ventricle and a midline shift of 16.5 mm. The patient was immediately transferred to a higher neurological centre where he underwent evacuation of the haematoma via a right frontal burr hole surgery. Post operative period was uneventful and the patient was put on anti epileptics (tablet dilantin 300 mg once daily), observed for 2 months and then sent on 04 weeks sick leave. His oculomotor nerve palsy gradually recovered completely and CT scan brain repeated on his return from sick leave showed a complete resolution of the haematoma. He was finally discharged back to his unit with no residual adverse effects whatsoever 7).


Cortes-Franco et al.,published in 2006 a Isolated IIIrd nerve palsy as the only sign of chronic subdural haematoma 8).


Ortega-Martínez et al., reported a patient with a chronic subdural hematoma that presented with a complete third nerve palsy and normal consciousness. Complete recovery was achieved after surgical evacuation. Rebleeding within the hematoma cavity, most possibly favored by antiaggregating agents, was considered responsible for this rare presentation. In these cases expeditious surgical evacuation is indicated 9).


A case of a 41-year-old man with a 1-month history of postural headache due to spontaneous intracranial hypotension (SIH). His MRI revealed bilateral chronic subdural hematoma (CSH) and diffuse dural enhancement after gadolinium infusion. Indium-111 radionuclide cisternography revealed a CSF leak from the cervico-thoracic junction and rapid accumulation of radioisotope in the bladder. Postural headache failed to resolve with prolonged bed rest. The patient became restless and suffered recent memory disturbance. We therefore decided to treat the CSF leak with an epidural blood patch. After the procedure, the patient’s headache resolved completely. However one day later, left oculomotor nerve palsy developed. MRI revealed enlargement of the left CSH with mass effect and midline shift. After hematoma drainage, the patient became alert and oculomotor palsy recovered gradually. To treat cases of CSH with SIH, the best method is to repair the CSF leakage and treat subdural hematoma at the same time. If the patient shows depressed consciousness, we recommend initial drainage of the subdural hematoma, because, following the repair of CSF leakage, mass effect such as uncal herniation may occur 10).


An 85-year-old male presented with bilateral chronic subdural hematomas (CSDHs) resulting in unilateral oculomotor nerve paresis and brainstem symptoms immediately after removal of both hematomas in a single operation. Initial computed tomography on admission demonstrated marked thick bilateral hematomas buckling the brain parenchyma with a minimal midline shift. Almost simultaneous removal of the hematomas was performed with the left side was decompressed first with a time difference of at most 2 minutes. However, the patient developed right oculomotor nerve paresis, left hemiparesis, and consciousness disturbance after the operation. The relatively marked increase in pressure on the right side may have caused transient unilateral brain stem compression and herniation of unilateral medial temporal lobe during the short time between the right and left procedures. Another factor was the vulnerability of the oculomotor nerve resulting from posterior replacement of the brain stem and stretching of the oculomotor nerves as seen on sagittal magnetic resonance (MR) images. Axial MR images obtained at the same time demonstrated medial deflection of the distal oculomotor nerve after crossing the posterior cerebral artery, which indicates previous transient compression of the nerve and the brain stem. Gradual and symmetrical decompression without time lag is recommended for the treatment of huge bilateral CSDHs 11).


In 1994 Phookan and Cameron published a bilateral chronic subdural haematoma with isolated oculomotor nerve palsy 12).


Crone et al published in 1985 a patient with adult-onset diabetes mellitus who developed an oculomotor palsy with pupillary sparing. Five days after her initial evaluation, she presented in a confused state with a complete oculomotor palsy. Computed cranial tomography revealed a chronic subdural hematoma. They recommend that noninvasive radiographic intracranial investigation be considered in elderly patients with adult-onset diabetes mellitus who present with headache and pupil-sparing oculomotor palsy 13).

References

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Kurokawa Y, Ishizaki E, Inaba K. Bilateral chronic subdural hematoma cases showing rapid and progressive aggravation. Surg Neurol. 2005 Nov;64(5):444-9; discussion 449. PubMed PMID: 16253697.
2)

Zavatto L, Marrone F, Allevi M, Ricci A, Taddei G. Bilateral oculomotor palsy after surgical evacuation of chronic subdural hematoma. World Neurosurg. 2019 Apr 10. pii: S1878-8750(19)31035-6. doi: 10.1016/j.wneu.2019.04.043. [Epub ahead of print] PubMed PMID: 30980981.
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Corrivetti F, Moschettoni L, Lunardi P. Isolated Oculomotor Nerve Palsy as Presenting Symptom of Bilateral Chronic Subdural Hematomas: Two Consecutive Case Report and Review of the Literature. World Neurosurg. 2016 Apr;88:686.e9-12. doi: 10.1016/j.wneu.2015.11.012. Epub 2015 Nov 14. Review. PubMed PMID: 26585722.
4)

Matsuda R, Hironaka Y, Kawai H, Park YS, Taoka T, Nakase H. Unilateral oculomotor nerve palsy as an initial presentation of bilateral chronic subdural hematoma: case report. Neurol Med Chir (Tokyo). 2013;53(9):616-9. PubMed PMID: 24067774; PubMed Central PMCID: PMC4508681.
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Jalil MF, Tee JW, Han T. Isolated III cranial nerve palsy: a surprising presentation of an acute on chronic subdural haematoma. BMJ Case Rep. 2013 Jun 19;2013. pii: bcr2013009992. doi: 10.1136/bcr-2013-009992. PubMed PMID: 23784767; PubMed Central PMCID: PMC3702887.
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Moon KS, Lee JK, Joo SP, Kim TS, Jung S, Kim JH, Kim SH, Kang SS. Kernohan’s notch phenomenon in chronic subdural hematoma: MRI findings. J Clin Neurosci. 2007 Oct;14(10):989-92. PubMed PMID: 17823049.
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Mishra A, Shukla S, Baranwal VK, Patra VK, Chaudhary B. Isolated unilateral IIIrd nerve palsy as the only sign of chronic subdural haematoma. Med J Armed Forces India. 2015 Jul;71(Suppl 1):S127-30. doi: 10.1016/j.mjafi.2013.07.009. Epub 2013 Sep 26. PubMed PMID: 26265807; PubMed Central PMCID: PMC4529560.
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Cortes-Franco S, García-Marín VM, Pacheco-Abreu EM, Roldán Delgado H. [Isolated IIIrd nerve palsy as the only sign of chronic subdural haematoma]. Med Clin (Barc). 2006 Sep 30;127(12):479. Spanish. PubMed PMID: 17040640.
9)

Ortega-Martínez M, Fernández-Portales I, Cabezudo JM, Rodríguez-Sánchez JA, Gómez-Perals LF, Giménez-Pando J. [Isolated oculomotor palsy. An unusual presentation of chronic subural hematoma]. Neurocirugia (Astur). 2003 Oct;14(5):423-5; discussion 425. Spanish. PubMed PMID: 14603390.
10)

Mikawa S, Ebina T. [Spontaneous intracranial hypotension complicating subdural hematoma: unilateral oculomotor nerve palsy caused by epidural blood patch]. No Shinkei Geka. 2001 Aug;29(8):747-53. Review. Japanese. PubMed PMID: 11554093.
11)

Okuchi K, Fujioka M, Maeda Y, Kagoshima T, Sakaki T. Bilateral chronic subdural hematomas resulting in unilateral oculomotor nerve paresis and brain stem symptoms after operation–case report. Neurol Med Chir (Tokyo). 1999 May;39(5):367-71. PubMed PMID: 10481440.
12)

Phookan G, Cameron M. Bilateral chronic subdural haematoma: an unusual presentation with isolated oculomotor nerve palsy. J Neurol Neurosurg Psychiatry. 1994 Sep;57(9):1146. PubMed PMID: 8089699; PubMed Central PMCID: PMC1073157.
13)

Crone KR, Lee KS, Davis CH Jr. Oculomotor palsy with pupillary sparing in a patient with chronic subdural hematoma. Surg Neurol. 1985 Dec;24(6):668-70. PubMed PMID: 4060048.

Chronic subdural hematoma neuroendoscopy

Chronic subdural hematoma neuroendoscopy

Some authors recommend the endoscopic treatment of chronic subdural hematomas, especially the septated ones 1) 2).

Fibrin membranes and compartmentalization within the subdural space are a frequent cause of failure in the treatment of chronic subdural hematomas (CSH). This specific subtype of CSH classically requires craniotomy, which carries significant morbidity and mortality rates, particularly in elderly patients.

Under local scalp anesthesia, a rigid endoscope is inserted through a parietal burr hole in the subdural space to collapse fibrin septa and cut the internal membrane. It also allows cauterization of active bleedings and the placement of a drain under direct visualization.

The endoscopic treatment of septated CSH represents a minimally invasive alternative to craniotomy especially for the internal membranectomy 3).

Treatment of loculated chronic subdural hematoma using neuroendoscopy combined with closed system drainage is a minimally invasive method and a therapeutic alternative to the craniotomy-membranectomy technique 4).

The application of visualization features of soft neuroendoscopy in the treatment of CSDH can significantly improve hematoma clearance, shorten the time of drainage tube, reduce postoperative complications and recurrence rate, and improve surgical outcomes 5).

Case series

Between January 2012 and October 2016, eight patients diagnosed with multi-lobular CSDH using computed tomography(CT)imaging underwent endoscopic evacuation. First, we established a 3×3cm craniotomy at a position where a rigid endoscope and aspiration tube would be able to reach as much of the hematoma cavity as possible in the longitudinal plane. Second, after identifying and removing the outer membrane of the CSDH with the scope, we evacuated the hematoma longitudinally, keeping the inner membrane intact. We also applied monopolar diathermy to any obvious bleeding points and the capillary network on the outer membrane of the CSDH, using the aspiration tube.

The mean duration of surgery was 42 minutes. Follow-up CT scan revealed no recurrence in any of the cases, and neurologic function improved in all patients postoperatively.

A multi-lobular CSDH can be drained quickly and effectively using a rigid endoscope and aspiration tube through a small craniotomy. In a cohort of eight patients, postoperative neurologic recovery was observed in all cases with no evidence of recurrence. This technique could be used in any facility with ready access to CT imaging and a rigid endoscope 6).

Case reports

A two-month-old male infant presented with a bulging and tense fontanel, a reduced level of consciousness, bradycardia, and significant macrocephaly. Computed tomography (CT) demonstrated massive bilateral, low attenuation subdural fluid collections, reaching a diameter of 4.5 cm. Emergency burr hole washout and insertion of subdural drains was performed. Despite prolonged drainage over 10 days, the protein level remained at 544 mg/dl and the mean erythrocyte count at 6,493/µl. Continuous drainage was required to avoid clinical deterioration due to raised intracranial pressure; however, the fluid condition was still considered incompatible with permanent subdural-peritoneal shunting. We, therefore, performed an endoscopic subdural lavage with a careful evacuation of residual blood deposits. No complications were encountered. Postoperatively, mean protein level was 292 mg/dl and mean erythrocyte count was 101/µl. Endoscopic lavage could be safely performed in a case of extensive subdural low attenuation fluid collections, where conventional burr hole drainage failed to improve protein and cellular contents as a prerequisite for successful permanent shunting. We conclude that adaptation of this technique can be helpful in selected cases as an alternative procedure 7).


A 78-year-old Japanese man with a history of colon cancer was referred to our department of neurosurgery for the management of asymptomatic left chronic subdural hematoma (CSDH). He was receiving bevacizumab therapy for colon cancer, and the size of the CSDH increased or decreased depending on bevacizumab administration. Simple drainage was performed because of the risk of a critical increase in the size of CSDH during bevacizumab therapy, but since the CSDH was organized and firm, the drainage was insufficient. Therefore, neuroendoscope-assisted craniotomy was performed, and the organized CSDH was almost completely removed. The present case indicates the possible involvement of bevacizumab in the occurrence of CSDH and the efficacy of the neuroendoscopic approach in the surgical treatment of organized CSDH 8).

References

1)

Rodziewicz GS, Chuang WC. Endoscopic removal of organized chronic subdural hematoma. Surgical Neurology. 1995 Jun;43:569–573.
2)

Smely C, Madlinger A, Scheremet R. Chronic subdural haematoma — a comparison of two different treatment modalities. Acta Neurochirurgica. 1997;139:818–826
3)

Berhouma M, Jacquesson T, Jouanneau E. The minimally invasive endoscopic management of septated chronic subdural hematomas: surgical technique. Acta Neurochir (Wien). 2014 Dec;156(12):2359-62. doi: 10.1007/s00701-014-2219-1. Epub 2014 Sep 16. PubMed PMID: 25223748.
4)

Hellwig D, Heinze S, Riegel T, Benes L. Neuroendoscopic treatment of loculated chronic subdural hematoma. Neurosurg Clin N Am. 2000 Jul;11(3):525-34. PubMed PMID: 10918025.
5)

Guan F, Peng WC, Huang H, Dai B, Zhu GT, Mao BB, Xiao ZY, Lin ZY, Hu ZQ. [Efficacy analysis of soft neuroendoscopic techniques in the treatment of chronic subdural hematoma]. Zhonghua Yi Xue Za Zhi. 2019 Mar 5;99(9):695-699. doi: 10.3760/cma.j.issn.0376-2491.2019.09.012. Chinese. PubMed PMID: 30831620.
6)

Ishikawa T, Endo K, Endo Y, Sato N, Ohta M. [Neuro-Endoscopic Surgery for Multi-Lobular Chronic Subdural Hematoma]. No Shinkei Geka. 2017 Aug;45(8):667-675. doi: 10.11477/mf.1436203572. Japanese. PubMed PMID: 28790212.
7)

Beez T, Schmitz AK, Steiger HJ, Munoz-Bendix C. Endoscopic Lavage of Extensive Chronic Subdural Hematoma in an Infant After Abusive Head Trauma: Adaptation of a Technique From Ventricular Neuroendoscopy. Cureus. 2018 Mar 2;10(3):e2258. doi: 10.7759/cureus.2258. PubMed PMID: 29725561; PubMed Central PMCID: PMC5931418.
8)

Takahashi S, Yazaki T, Nitori N, Kano T, Yoshida K, Kawase T. Neuroendoscope-assisted removal of an organized chronic subdural hematoma in a patient on bevacizumab therapy–case report. Neurol Med Chir (Tokyo). 2011;51(7):515-8. PubMed PMID: 21785247.

Chronic subdural hematoma recurrence

Chronic subdural hematoma recurrence

Epidemiology

In 2 large cohorts of US patients, approximately 5% to 10% of patients who underwent surgery for nontraumatic SDH were required to undergo repeated operation within 30 to 90 days. These results may inform the design of future prospective studies and trials and help practitioners calibrate their index of suspicion to ensure that patients are referred for timely surgical care 1).

Recurrence rates after chronic subdural hematoma (CSDH) evacuation with any of actual techniques twist drillcraniostomy (TDC), burr hole craniostomy, craniotomy range from 5% to 30%. 2).

Risk factors

In the series of Han et al. independent risk factors for recurrence were as follows: age > 75 years (HR 1.72, 95% CI 1.03-2.88; p = 0.039), obesity (body mass index ≥ 25.0 kg/m2), and a bilateral operation 3).

Chon et al. shown that postoperative midline shifting (≥5 mm), diabetes mellitus, preoperative seizure, preoperative width of hematoma (≥20 mm), and anticoagulant therapy were independent predictors of the recurrence of chronic subdural hematoma.

According to internal architecture of hematoma, the rate of recurrence was significantly lower in the homogeneous and the trabecular type than the laminar and separated type 4).


The recurrence rate of chronic subdural hematoma cSDH seems to be related to the excessive neoangiogenesis in the parietal membrane, which is mediated via vascular endothelial growth factor (VEGF). This is found to be elevated in the hematoma fluid and is dependent on eicosanoid/prostaglandin and thromboxane synthesis via cyclooxygenase-2 (COX-2).

Anticoagulant therapy

Antiplatelet therapy

Antiplatelet therapy significantly influences the recurrence of CSDH 5).

Pneumocephalus

Remaining pneumocephalus is seen as an approved factor of recurrence 6) 7).

Septation

Jack et al.found a 12% reoperation rate. CSDH septation (seen on computed tomogram scan) was found to be an independent risk factor for recurrence requiring reoperation (p=0.04). Larger post-operative subdural haematoma volume was also significantly associated with requiring a second drainage procedure (p<0.001). Independent risk factors of larger post-operative haematoma volume included septations within a CSDH (p<0.01), increased pre-operative haematoma volume (p<0.01), and a greater amount of parenchymal atrophy (p=0.04). A simple scoring system for quantifying recurrence risk was created and validated based on patient age (< or ≥80 years), haematoma volume (< or ≥160cc), and presence of septations within the subdural collection (yes or no).

Septations within CSDHs are associated with larger post-operative residual haematoma collections requiring repeat drainage. When septations are clearly visible within a CSDH, craniotomy might be more suitable as a primary procedure as it allows greater access to a septated subdural collection. The proposed scoring system combining haematoma volume, age, and presence of septations might be useful in identifying patients at higher risk for recurrence 8).

Membranectomy

Opening the internal hematoma membrane does not alter the rate of patients requiring revision surgery and the number of patients showing a marked residual hematoma six weeks after evacuation of a CSDH 9).

In the study of Lee et al, an extended surgical approach with partial membranectomy has no advantages regarding the rate of reoperation and the outcome. As initial treatment, burr-hole drainage with irrigation of the hematoma cavity and closed-system drainage is recommended. Extended craniotomy with membranectomy is now reserved for instances of acute rebleeding with solid hematoma 10).

Diabetes

Surgeons should consider informing patients with diabetes mellitus that this comorbidity is associated with an increased likelihood of recurrence

11) 12) 13).


Balser et al. report 11% recurrence, which included individuals who recurred as late as 3 years after initial diagnosis 14).

Close imaging follow-up is important for CSDH patients for recurrence prediction. Using quantitative CT volumetric analysis, strong evidence was provided that changes in the residual fluid volume during the ‘self-resolution’ period can be used as significantly radiological predictors of recurrence 15).

A structural equation model showed a significant association between increased antiinflammatory activity in hematoma fluid samples and a lower risk of recurrence, but this relationship was not statistically significant in venous blood samples. Moreover, these findings indicate that anti-inflammatory activities in the hematoma may play a role in the risk of a recurrence of CSDH 16).

Irrigation with artificial cerebrospinal fluid (ACF) decreased the rate of CSDH recurrence 17).

Treatment

There is no definite operative procedure for patients with intractable chronic subdural hematoma (CSDH).

Most recurrent hematomas are managed successfully with burr hole craniostomies with postoperative closed-system drainage. Refractory hematomas may be managed with a variety of techniques, including craniotomy or subdural-peritoneal shunt placement 18).

Although many studies have reported risk factors or treatments in efforts to prevent recurrence, those have focused on single recurrence, and little cumulative data is available to analyze refractory CSDH.

Matsumoto et al. defined refractory CSDH as ≥2 recurrences, then analyzed and compared clinical factors between patients with single recurrence and those with refractory CSDH in a cohort study, to clarify whether patients with refractory CSDH experience different or more risk factors than patients with single recurrence, and whether burr-hole irrigation with closed-system drainage reduces refractory CSDH.

Seventy-five patients had at least one recurrence, with single recurrence in 62 patients and ≥2 recurrences in 13 patients. In comparing clinical characteristics, patients with refractory CSDH were significantly younger (P=0.04) and showed shorter interval to first recurrence (P<0.001). Organized CSDH was also significantly associated with refractory CSDH (P=0.02). Multivariate logistic regression analysis identified first recurrence interval <1 month (OR 6.66, P<0.001) and age <71 years (OR 4.16, P<0.001) as independent risk factors for refractory CSDH. On the other hand, burr-hole irrigation with closed-system drainage did not reduce refractory CSDH.

When patients with risk factors for refractory CSDH experience recurrence, alternative surgical procedures may be considered as the second surgery, because burr-hole irrigation with closed-system drainage did not reduce refractory CSDH 19).

Implantation of a reservoir 20) 21) 22).

Subdural-peritoneal shunt 23).

Middle meningeal artery embolization

Embolization of the MMA is effective for refractory CSDH or CSDH patients with a risk of recurrence, and is considered an effective therapeutic method to stop hematoma enlargement and promote resolution 24) 25) 26) 27) 28) 29).

A pilot study indicated that perioperative middle meningeal artery (MMA) embolization could be offered as the least invasive and most effectual means of treatment for resistant patients of CSDHs with 1 or more recurrences 30).

Chihara et al. have treated three cases of CSDH with MMA embolization to date, but there was a postoperative recurrence in one patient, which required a craniotomy for hematoma removal and capsulectomy. MMA embolization blocks the blood supply from the dura to the hematoma outer membrane in order to prevent recurrences of refractory CSDH. Histopathologic examination of the outer membrane of the hematoma excised during craniotomy showed foreign-body giant cells and neovascular proliferation associated with embolization. Because part of the hematoma was organized in this case, the CSDH did not resolve when the MMA was occluded, and the development of new collateral pathways in the hematoma outer membrane probably contributed to the recurrence. Therefore, in CSDH with some organized hematoma, MMA embolization may not be effective. Magnetic resonance imaging (MRI) should be performed in these patients before embolization 31).

Case series

Case reports

References

1)

Knopman J, Link TW, Navi BB, Murthy SB, Merkler AE, Kamel H. Rates of Repeated Operation for Isolated Subdural Hematoma Among Older Adults. JAMA Netw Open. 2018 Oct 5;1(6):e183737. doi: 10.1001/jamanetworkopen.2018.3737. PubMed PMID: 30646255.
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Escosa Baé M, Wessling H, Salca HC, de Las Heras Echeverría P. Use of twist-drill craniostomy with drain in evacuation of chronic subdural hematomas: independent predictors of recurrence. Acta Neurochir (Wien). 2011 May;153(5):1097-103. doi: 10.1007/s00701-010-0903-3. Epub 2010 Dec 31. PubMed PMID: 21193935.
3)

Han MH, Ryu JI, Kim CH, Kim JM, Cheong JH, Yi HJ. Predictive factors for recurrence and clinical outcomes in patients with chronic subdural hematoma. J Neurosurg. 2017 Nov;127(5):1117-1125. doi: 10.3171/2016.8.JNS16867. Epub 2016 Dec 16. PubMed PMID: 27982768.
4)

Chon KH, Lee JM, Koh EJ, Choi HY. Independent predictors for recurrence of chronic subdural hematoma. Acta Neurochir (Wien). 2012 Sep;154(9):1541-8. doi: 10.1007/s00701-012-1399-9. Epub 2012 Jun 1. PubMed PMID: 22653496.
5)

Wada M, Yamakami I, Higuchi Y, Tanaka M, Suda S, Ono J, Saeki N. Influence of antiplatelet therapy on postoperative recurrence of chronic subdural hematoma: a multicenter retrospective study in 719 patients. Clin Neurol Neurosurg. 2014 May;120:49-54. doi: 10.1016/j.clineuro.2014.02.007. Epub 2014 Feb 24. PubMed PMID: 24731576.
6)

Mori K, Maeda M (2001) Surgical treatment of chronic subdural hematoma in 500 consecutive cases: clinical characteristics, surgical outcome, complications, and recurrence rate. Neurol Med Chir (Tokyo) 41:371–381
7)

Stanišić M, Hald J, Rasmussen IA, Pripp AH, Ivanović J, Kolstad F, Sundseth J, Züchner M, Lindegaard KF (2013) Volume and densities of chronic subdural haematoma obtained from CT imaging as predictors of postoperative recurrence: a prospective study of 107 operated patients. Acta Neurochir 155:323–333
8)

Jack A, O’Kelly C, McDougall C, Max Findlay J. Predicting Recurrence after Chronic Subdural Haematoma Drainage. Can J Neurol Sci. 2015 Jan 5:1-6. [Epub ahead of print] PubMed PMID: 25557536.
9)

Unterhofer C, Freyschlag CF, Thomé C, Ortler M. Opening the Internal Hematoma Membrane does not Alter the Recurrence Rate of Chronic Subdural Hematomas – A Prospective Randomized Trial. World Neurosurg. 2016 May 2. pii: S1878-8750(16)30210-8. doi: 10.1016/j.wneu.2016.04.081. [Epub ahead of print] PubMed PMID: 27150644.
10)

Lee JY, Ebel H, Ernestus RI, Klug N. Various surgical treatments of chronic subdural hematoma and outcome in 172 patients: is membranectomy necessary? Surg Neurol. 2004 Jun;61(6):523-7; discussion 527-8. PubMed PMID: 15165784.
11)

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