Gamma Knife radiosurgery for trigeminal neuralgia

Gamma Knife radiosurgery for trigeminal neuralgia

Gamma knife radiosurgery (GKRS) is one of the alternatives for treatment for classical trigeminal neuralgia (TN).

The first use of SRS by Lars Leksell was for the treatment of trigeminal neuralgia. Initially, this was reserved for refractory cases following multiple operations 1).

The Leksell Gamma Knife and the Accuray CyberKnife systems have been used in the radiosurgical treatment of trigeminal neuralgia. The 2 techniques use different delivery methods and different treatment parameters. In the past, CyberKnife treatments have been associated with an increased incidence of treatment-related complications, such as facial numbness.

CyberKnife radiosurgical parameters can be optimized to mimic the dose distribution of Gamma Knife plans. However, Gamma Knife plans result in superior sparing of critical structures (brainstem, temporal lobe,and cranial nerves VII and VIII) and in steeper dose fall off away from the target. The clinical significance of these effects is unknown 2).

Indications

Generally recommended for patients with co-morbidities, high-risk medical illness, pain refractory to prior surgical procedures, or those on anticoagulants (anticoagulation does not have to be reversed to have SRS).

Mechanism

Treatment plan

4 -5 mm isocenter in the trigeminal nerve root entry zone identified on MRI. Use 70–80 Gy at the center, keeping the 80% isodose curve outside of the brainstem.

Results: Significant pain reduction after initial SRS: 80–96% 3) 4) 5) 6) but only ≈ 65% become pain free. Median latency to pain relief: 3 months (range: 1 d-13 months) 7).

Recurrent pain occurs with in three years in 10–25%. Patients with TN and multiple sclerosis are less likely to respond to SRS than those without MS. SRS can be repeated, but only after four months following the original procedure.

Outcome

Repeat Radiosurgery for Trigeminal Neuralgia

Case series

A total of 263 patients contributed by 9 member tertiary referral Gamma Knife centers (2 in Canada and 7 in USA) of the International Gamma Knife Research Consortium (IGKRF) constituted this study.

The median latency period of Facial pain response (PR) after SRS was 1 mo. Reasonable pain control (Barrow Neurological Institute Pain Scale I-IIIb) was achieved in 232 patients (88.2%). The median maintenance period from SRS was 14.1 months (range, 10 days to 10 years). The actuarial reasonable pain control maintenance rates at 1 yr, 2 yr, and 4 yr were 54%, 35%, and 24%, respectively. There was a correlation between the status of achieving BNI-I and the maintenance of facial pain recurrence-free rate. The median recurrence-free rate was 36 mo and 12.2 mo in patients achieving BNI-I and BNI > I, respectively (P = .046). Among 210 patients with known status of post-SRS complications, the new-onset of facial numbness (BNI-I or II) after SRS occurred in 21 patients (10%).

In this largest series SRS offers a reasonable benefit to risk profile for patients who have exhausted medical management. More favorable initial response to SRS may predict a long-lasting pain control 8).

2016

One hundred seventeen patients with medically refractory TN treated by GKRS at the Department of Functional Neurosurgery and Gamma Knife Radiosurgery, and Department of Neurology, Ruber International Hospital, Madrid, Spain were followed up between 1993 and 2011. Mean maximum dose was 86.5 Gy (range: 80-90 Gy; median: 90 Gy). Clinical response was defined based on the Burchiel classification. They considered classes I and II as a complete response. For toxicity, they use the Barrow Neurological Institute Pain Scale. Mean duration of follow-up was 66 months (range: 24-171 months).

Complete response at last follow-up in our patients was 81%, with an excellent response while off medication in 52%. Pain-free rates without medication (class I) were 85% at 3 years (confidence interval [CI]: 78%-94%), 81% at 5 years (CI: 72%-91%), and 76% at 7 years (CI: 65%-90%). Complete response rates (classes I-II) were 91% at 3 years (CI: 86%-97%), 86% at 5 years (CI: 79%-93%), and 82% at 7 years (CI: 72%-93%). Poor treatment response rates differed significantly between patients who had undergone previous surgery and were refractory to management with medication prior to GKRS. New or worsening facial numbness was reported in 32.5% (30% score II and 2.5% score III). No anesthesia dolorosa was reported. Permanent recurrence pain rate was 12%.

GKRS achieved favorable outcomes compared with surgery in terms of pain relief and complication rates in our cohort of patients, notwithstanding decreasing pain-free survival rates over time. They consider GKRS to be an initial treatment in the management of medically intractable TN in selected patients 9).


In a single-center, retrospective comparative study, 202 patients with MS and concomitant TN were evaluated. A minimum follow-up of 24 months was required. Patients with a history of microvascular decompression or previous intervention were excluded. There were 78 PBC procedures performed and 124 first-dosage GKRS procedures for a total of 202 patients between February 2009 and December 2013. The PBC procedures were successfully completed in all cases. The two groups were compared with regards to initial effect, duration of effect, and rate of complication(s), including the type and severity of the complication(s).

Immediate pain relief resulted in 87% of patients treated with PBC and in 23% of patients treated with GKRS. The Kaplan-Meier plots for the two treatment modalities were similar. The 50% recurrence rate was at 12 months for the PBC and 18 months for the GKRS. The rates of complication (excluding numbness) were 3% for GKRS and 21% for PBC. The difference was statistically significant (Chi-square test, p = 0.03).

PBC and GKRS are effective techniques for the treatment of TN in patients with MS, with GKRS presenting fewer complications and superior long-term relief. For these reasons, we consider GKRS as the first option for the treatment of TN in MS patients, reserving PBC for patients with acute, intractable pain 10).

Case reports

A 72-year-old -female presented with trigeminal neuralgia (TN) and radiological evidence of neurovascular compression on the affected side. She had complete resolution of her pain for 7 years after treatment with GKRS. The patient experienced recurrence and underwent repeat GKRS, this time resulting in another 3 years of pain relief. After the second recurrence, repeat intracranial imaging demonstrated resolution of neurovascular compression.

GKRS is an important treatment option for TN, although the mechanisms behind pain relief from this procedure still remain unclear. While prior histological and radiological studies point to ablative mechanisms for pain relief, this case report suggests that GKRS may result in a decompressive effect in TN due to changes in neurovascular architecture. Despite this finding, TN is known to occur and recur in the absence of neurovascular compression; thus, further work is necessary to understand the etiology of TN and its treatments.

In this case, Moosa et al. demonstrated that vessel-nerve relationships may change over time in TN patients treated with GKRS, which raises the possibility that GKRS could release a neurovascular compression 11).

References

1)

Lunsford LD. Comment on Taha J M and Tew J M: Comparison of Surgical Treatmen ts for Trigemin al Neuralgia: Reevaluation of Radiofrequency Rhizotomy. Neurosurgery. 1996; 38
2)

Descovich M, Sneed PK, Barbaro NM, McDermott MW, Chuang CF, Barani IJ, Nakamura JL, Lijun M. A dosimetric comparison between Gamma Knife and CyberKnife treatment plans for trigeminal neuralgia. J Neurosurg. 2010 Dec;113 Suppl:199-206. PubMed PMID: 21222296.
3)

Brisman R. Gamma knife surgery with a dose fo 75 to 76.8 Gray for trigeminal neuralgia. J Neurosurg. 2004; 100:848–854
4)

Pollock BE, Phuong LK, Foote RL, Sta ord SL, Gorman DA. High-dose trigeminal neuralgia radiosurgery associated with increased risk of trigeminal nerve dysfunction. Neurosurgery. 2001; 49:58–62; discussion 62-4
5)

Kondziolka D, Lunsford LD, Flickinger JC. Stereotact ic radiosurgery for the treatment of trigeminal neuralgia. Clin J Pain. 2002; 18:42–47
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Massager N, Lorenzoni J, Devriendt D, Desmedt F, Brotch i J, Levivier M. Gamma kn ife surgery for idiopathic trigeminal neuralgia performed using a far-anterior cisternal target and a high dose of radiation. J Neurosurg. 2004; 100:597–605
7)

Urgosik D, Liscak R, Novotny J, Jr, Vymazal J, Vladyka V. Treatment of essential trigeminal neuralgia with gamma knife surgery. J Neurosurg. 2005; 102 Suppl:29–33
8)

Xu Z, Mathieu D, Heroux F, Abbassy M, Barnett G, Mohammadi AM, Kano H, Caruso J, Shih HH, Grills IS, Lee K, Krishnan S, Kaufmann AM, Lee JYK, Alonso-Basanta M, Kerr M, Pierce J, Kondziolka D, Hess JA, Gerrard J, Chiang V, Lunsford LD, Sheehan JP. Stereotactic Radiosurgery for Trigeminal Neuralgia in Patients With Multiple Sclerosis: A Multicenter Study. Neurosurgery. 2019 Feb 1;84(2):499-505. doi: 10.1093/neuros/nyy142. PubMed PMID: 29688562.
9)

Martínez Moreno NE, Gutiérrez-Sárraga J, Rey-Portolés G, Jiménez-Huete A, Martínez Álvarez R. Long-Term Outcomes in the Treatment of Classical Trigeminal Neuralgia by Gamma Knife Radiosurgery: A Retrospective Study in Patients With Minimum 2-Year Follow-up. Neurosurgery. 2016 Dec;79(6):879-888. PubMed PMID: 27560193.
10)

Alvarez-Pinzon AM, Wolf AL, Swedberg HN, Barkley KA, Cucalon J, Curia L, Valerio JE. Comparison of Percutaneous Retrograsserian Balloon Compression and Gamma Knife Radiosurgery for the Treatment of Trigeminal Neuralgia in Multiple Sclerosis: A Clinical Research Study Article. World Neurosurg. 2016 Oct 15. pii: S1878-8750(16)31016-6. doi: 10.1016/j.wneu.2016.10.028. PubMed PMID: 27756676.
11)

Moosa S, Wang TR, Mastorakos P, Sheehan JP, Elias WJ. Gamma Knife Radiosurgery for Trigeminal Neuralgia Reduces Neurovascular Compression: A Case Report after 11 Years. Stereotact Funct Neurosurg. 2019 Sep 5:1-5. doi: 10.1159/000501624. [Epub ahead of print] PubMed PMID: 31487732.

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)

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.
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.
7)

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.
8)

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.
9)

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.
10)

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.
11)

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.
12)

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.
13)

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.
14)

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.
15)

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.

Head fixation device complications in pediatric neurosurgery

Head fixation device complications in pediatric neurosurgery

Head Fixation in pediatric neurosurgery is associated with complications.

They are widely used among pediatric neurosurgeons in patients younger than 5 years old. Guidelines for their safe use are not well defined despite common use and experience of significant complications associated with such devices 1).


Variability in the thickness of the developing cranium necessitates age-specific considerations to reduce the risk of adverse events. To suggest possible guidelines for the use of cranial fixation pins in children, Berry et al. surveyed neurosurgeons treating pediatric patients regarding their experience with such devices.

An Institutional Review Board-approved, 30-item multiple choice survey was provided by electronic mail to 605 neurosurgeons treating pediatric patients. The survey included specific questions regarding their experience with cranial fixation pins with respect to age ranges of patients, selection of pin size, type of pin pressure applied, and complications encountered.

One hundred sixty-four (27%) responses were received. One hundred fifty-eight of the 164 (96%) neurosurgeons reported using cranial fixation pins in their pediatric practice. Forty-four of the 164 (27%) apply fixation pins in patients aged 1 to 2 years. Eighty-two (50%) apply pins in patients aged 2 to 3 years, and 89 (54%) apply pins in patients aged 3 to 4 years. For patients aged 2 to 5 years old, the majority of responders use between 10 and 40 pounds of pressure, whereas for those older than 5 years of age, most use between 30 and 40 pounds of pressure. After age 10, patients are treated as adults. Eighty-nine of the 164 (54%) responders reported complications directly related to the use of cranial fixation pins, including cranial fracture, epidural or subdural hematoma, scalp laceration, or cerebrospinal fluid leak. One hundred fifty-four of the 164 (94%) neurosurgeons responded that they are not aware of any standard guidelines for cranial fixation pin use in pediatric patients. Seven (4%) who stated that they were aware of guidelines did not describe where they obtained those guidelines.

Cranial fixation pins are widely used among pediatric neurosurgeons in patients younger than 5 years old. Guidelines for their safe use are not well defined despite common use and experience of significant complications associated with such devices. 2).


Udayakumaran et al. applied a headband made of Plaster of Paris (POP) around the head and then applying the fixation pins of the fixation frame directly on to the POP.

They used this technique of head fixation successfully for infants with no complications 3).


Agrawal et al. described an extremely simple technique of head fixation for image-guided neurosurgery in young children in whom standard pin fixation cannot be used.

This involves positioning the head on a horseshoe headrest and using a ‘U-drape’ to fix the head to the headrest.

Over the last 5 years, this technique of head fixation (in conjunction with Stealthstation) has been used for various neurosurgical procedures in more than ten infants successfully 4).


Rubber plugs (usually used for antibiotic bottles) pierced by the skull pins are used to avoid intracranial penetration of the pins. The upper surface of the rubber plugs attached to the scalp contributes to support of the head. Four infants were successfully treated in a prone position with this technique 5).


Gupta adapted a standard Mayfield horseshoe headrest and cranial fixation system to allow simultaneous use of the headrest and three-point pin fixation. The system is compatible with most neuronavigational systems.

The combined horseshoe and pin system was used successfully in more than 30 patients ranging in age from 6 months to 14 years. No complications were encountered.

Rigid immobilization is achievable in the pediatric population, facilitating intracranial and frameless stereotaxy procedures 6).

Case series

Five of 766 children (0.65%) undergoing craniotomies with pin fixation of the head had depressed skull fractures and/or epidural hematomas from the pin fixation. Age ranged from 2.6 to 7.5 years; all fractures were temporal and occurred during posterior fossa craniotomies 7).


Lee et al. examined complications over the past 6 years, and encountered 5 children with depressed skull fractures secondary to the application of a skull clamp fixation device. There were 3 boys and 2 girls with ages ranging from 3 to 8 years (mean 5.8 years). Two patients had brainstem gliomas, 2 patients had hypothalamic gliomas and 1 patient had a medulloblastoma. Four of the children required separate cranial procedures for the exploration and elevation of the depressed fractures. There were no sequelae associated with the depressed fractures. We conclude that skull clamp fixation devices are safe, but should be used with caution in the pediatric patient. In addition, we present several modifications of existing skull clamps which may decrease the risk of depressed skull fractures 8).

Case reports

An 11-year-old girl diagnosed with non-communicating hydrocephalus, caused by a posterior fossa tumor. During the surgery, complications were found in the form of acute epidural hematoma due to head fixation pins. So, the operation was stopped. An emergent CT scan was carried out and showed a bilateral skull fracture and a massive right-sided epidural hematoma. An emergency craniotomy for clot removal was performed and five days later, a second surgery was carried out uneventfully for the residual tumor. The patient fully recovered after the second surgery.

Complications due to the use of a pinhead fixation are easier to occur in pediatric patients because the bones are thinner and need a more careful strategy when pinning. With prompt identification of any complications and earlier treatment, a good outcome will be achieved.

Parenrengi et al. compared this case report with published literature in order to suggest a way to prevent this complication.

Skull fractures and associated epidural hematomas in pediatric patients need to be considered as possible complications of the pin-type head fixation application. The head fixation devices in pediatric need to be used with great caution and knowing the risk factors, safe technique for application and management of complications will prevent a worse outcome 9).


A 4-year-old girl who sustained a depressed skull fracture by penetration of a pin of the head holder. The fracture was noted at the end of the surgery performed for treatment of a cerebellar astrocytoma and was managed conservatively.

Several factors seem to be involved in the production of this complication as are faulty application of the pins, excessive pin pressure, skull thinning, young patient’s age, and pathological conditions that evolve with long-standing raised intracranial pressure 10).


A 5-month-old girl with a growing lesion in the right thalamus and basal ganglia underwent stereotactic biopsy, which disclosed an anaplastic astrocytoma. To avoid insertion of the four stereotactic frame fixation pins through the infant’s skin and into bone, the pins were advanced into the hollowed end of rubber tops obtained from Vacutainer blood sampling tubes. The pressure applied to the skin was diffused through the rubber onto a wide skin surface, obviating skin puncture or bone deformation. This technique provided firm head fixation, and target accuracy was confirmed on postoperative imaging. This technique is safe and should permit the use of conventional stereotactic techniques in young infants 11).

References

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