Syringobulbia in a Pediatric Population

Neurosurgery ◽  
2005 ◽  
Vol 57 (6) ◽  
pp. 1147-1153 ◽  
Author(s):  
Jeremy D.W. Greenlee ◽  
Arnold H. Menezes ◽  
Bryan A. Bertoglio ◽  
Kathleen A. Donovan
Keyword(s):  
Posterior Fossa ◽  
Cranial Nerve ◽  
Fourth Ventricle ◽  
Pediatric Population ◽  
Demographic Data ◽  
Posterior Fossa Decompression ◽  
Radiographic Findings ◽  
Presenting Symptoms ◽  
Cranial Nerve Dysfunction ◽  
Cranial Nerve Palsies

Abstract OBJECTIVE: To better understand the presentation, management, and outcome of syringobulbia in the pediatric age group. METHODS: The University of Iowa pediatric neurosurgery database was searched for patients under the age of 18 with a diagnosis of syringobulbia. The patients' records were retrospectively reviewed for demographic data, chief complaint and presenting symptoms, neurological and radiographic findings, treatment, outcome, and complications. Children with open neural tube defects and Chiari II malformations were excluded. RESULTS: Six pediatric patients were identified as meeting inclusion criteria. The average age at time of surgery was 14.8 years. The chief complaints were vision impairment in three children and numbness, gait instability, and headache worsened with Valsalva in one patient each. Other prominent symptoms included sleep apnea and weakness. All patients showed at least one cranial nerve dysfunction. Radiographs revealed hindbrain herniation and associated syringomyelia in all cases. Two patients had scoliosis. Treatment was posterior fossa decompression with cerebellar tonsillar shrinkage, opening of foramen of Magendie, and duraplasty. Two patients also required concomitant ventral decompression. The cavity of syringobulbia communicated with syringomyelia and the fourth ventricle in most children but was distinct from the fourth ventricle. Two patients received fourth ventricle to subarachnoid shunts. Follow-up averaged 3.2 years, and all patients clinically improved after surgery. Magnetic resonance imaging documented resolution of syringobulbia in all cases, with syringomyelia improving in all cases. There was no permanent morbidity or mortality in the series. CONCLUSION: Syringobulbia is strongly associated with Chiari malformation and syringomyelia, and patients often present because of cranial nerve palsies. Posterior fossa decompression is a safe and effective treatment.

scholarly journals Syringobulbia in pediatric patients with Chiari malformation type I

2018 ◽  
Vol 22 (1) ◽  
pp. 52-60 ◽  
Author(s):  
Arnold H. Menezes ◽  
Jeremy D. W. Greenlee ◽  
Brian J. Dlouhy
Keyword(s):  
Posterior Fossa ◽  
Cranial Nerve ◽  
Chiari Malformation ◽  
Fourth Ventricle ◽  
Pediatric Patients ◽  
Posterior Fossa Decompression ◽  
Type I ◽  
Chiari Malformation Type I ◽  
Presenting Symptoms ◽  
Cranial Nerve Palsies

OBJECTIVESyringobulbia (SB) is a rare entity, with few cases associated with Chiari malformation type I (CM-I) in the pediatric population. The authors reviewed all pediatric cases of CM-I–associated SB managed at their institution in order to better understand the presentation, treatment, and surgical outcomes of this condition.METHODSA prospectively maintained institutional database of craniovertebral junction abnormalities was analyzed to identify all cases of CM-I and SB from the MRI era (i.e., after 1984). The authors recorded presenting symptoms, physical examination findings, radiological findings, surgical treatment strategy, intraoperative findings, and outcomes. SB cases associated with tumors, infections, or type II Chiari malformations were excluded.RESULTSThe authors identified 326 pediatric patients with CM-I who were surgically treated. SB was identified in 13 (4%) of these 326 patients. Headache and neck pain were noted in all 13 cases. Cranial nerve abnormalities were common: vagus and glossopharyngeal nerve dysfunction was the most frequent observation. Other cranial nerves affected included the trigeminal, abducens, and hypoglossal nerves. Several patients exhibited multiple cranial nerve palsies at presentation. Central sleep apnea was present in 6 patients.Syringomyelia (SM) was present in all 13 patients. SB involved the medulla in all cases, and extended rostrally into the pons and midbrain in 2 patients; in 1 of these 2 cases the cavity extended further rostrally to the cerebrum (syringocephaly). SB communicated with the fourth ventricle in 7 of the 13 cases.All 13 patients were treated with posterior fossa decompression with intradural exploration to ensure CSF egress out of the fourth ventricle and through the foramen magnum. The foramen of Magendie was found to be occluded by an arachnoid veil in 9 cases. Follow-up evaluation revealed that SB improved before SM. Cranial nerve palsies regressed in 11 of the 13 patients, and SB improved in all 13.CONCLUSIONSThe incidence of SB in our surgical series of pediatric patients with CM-I was 4%, and all of these patients had accompanying SM. The SB cavity involved the medulla in all cases and was found to communicate with the fourth ventricle in 54% of cases. Posterior fossa decompression with intradural exploration and duraplasty is an effective treatment for these patients.

scholarly journals Hemorrhagic vestibular schwannoma: an unusual clinical entity

1998 ◽  
Vol 5 (3) ◽  
pp. E14 ◽  
Author(s):  
Dean Chou ◽  
Prakash Sampath ◽  
Henry Brem
Keyword(s):  
Vestibular Schwannoma ◽  
Cranial Nerve ◽  
Unusual Case ◽  
Case Reports ◽  
Clinical Entity ◽  
Vestibular Schwannomas ◽  
Presenting Symptoms ◽  
Cranial Nerve Dysfunction ◽  
Nerve Dysfunction ◽  
Management Issues

Hemorrhagic vestibular schwannomas are rare entities, with only a few case reports in the literature during the last 25 years. The authors review the literature on vestibular schwannoma hemorrhage and the presenting symptoms of this entity, which include headache, nausea, vomiting, sudden cranial nerve dysfunction, and ataxia. A very unusual case is presented of a 36-year-old man, who unlike most of the patients reported in the literature, had clinically silent vestibular schwannoma hemorrhage. The authors also discuss the management issues involved in more than 1000 vestibular schwannomas treated at their institution during a 25-year period.

Pseudomyasthenia Resulting from a Posterior Carotid Artery Wall Aneurysm: A Novel Presentation: Case Report

Neurosurgery ◽  
2001 ◽  
Vol 49 (6) ◽  
pp. 1466-1469 ◽  
Author(s):  
Ramachandra P. Tummala ◽  
Andrew Harrison ◽  
Michael T. Madison ◽  
Eric S. Nussbaum
Keyword(s):  
Carotid Artery ◽  
Cranial Nerve ◽  
Cranial Nerve Palsy ◽  
Intracranial Aneurysms ◽  
Nerve Palsy ◽  
Oculomotor Nerve ◽  
Artery Wall ◽  
Carotid Artery Wall ◽  
Cranial Nerve Dysfunction ◽  
Cranial Nerve Palsies

ABSTRACT OBJECTIVE AND IMPORTANCE Painful oculomotor palsy can result from enlargement or rupture of intracranial aneurysms. The IIIrd cranial nerve dysfunction in this setting, whether partial or complete, is usually fixed or progressive and is sometimes reversible with surgery. We report an unusual oculomotor manifestation of a posterior carotid artery wall aneurysm, which mimicked ocular myasthenia gravis. CLINICAL PRESENTATION A 47-year-old woman developed painless, intermittent, partial IIIrd cranial nerve palsy. She presented with isolated episodic left-sided ptosis, which initially suggested a metabolic or neuromuscular disorder. However, digital subtraction angiography revealed a left posterior carotid artery wall aneurysm, just proximal to the origin of the posterior communicating artery. INTERVENTION The aneurysm was successfully clipped via a pterional craniotomy. During surgery, the aneurysm was observed to be compressing the oculomotor nerve. The patient's symptoms resolved after the operation. CONCLUSION The variability of incomplete IIIrd cranial nerve deficits can present a diagnostic challenge, and the approach for patients with isolated IIIrd cranial nerve palsies remains controversial. Although intracranial aneurysms compressing the oculomotor nerve classically produce fixed or progressive IIIrd cranial nerve palsies with pupillary involvement, anatomic variations may result in atypical presentations. With the exception of patients who present with pupil-sparing but otherwise complete IIIrd cranial nerve palsy, clinicians should always consider an intracranial aneurysm when confronted with even subtle dysfunction of the oculomotor nerve.

Recurrent subarachnoid hemorrhage complicating cerebral arterial ectasia

1981 ◽  
Vol 55 (1) ◽  
pp. 139-142 ◽  
Author(s):  
Steven J. Goldstein ◽  
Phillip A. Tibbs
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cranial Nerve ◽  
Review Of The Literature ◽  
Radiographic Findings ◽  
Content Type ◽  
Clinical Complications ◽  
Cranial Nerve Palsies ◽  
Arterial Ectasia ◽  
Fine Print

✓ A case of subarachnoid hemorrhage (SAH) complicating cerebral arterial ectasia is reported. While ischemia and cranial nerve palsies are commonly associated with this condition, review of the literature reveals that SAH is exceedingly rare. The pathogenesis, radiographic findings, and clinical complications of cerebral arterial ectasia are discussed.

scholarly journals Divergence insufficiency alleviated by posterior fossa decompression with duraplasty in a patient with Chiari type 1.5 malformation

2018 ◽  
Vol 22 (5) ◽  
pp. 504-507 ◽  
Author(s):  
Allison Strickland ◽  
Cordell M. Baker ◽  
R. Michael Siatkowski ◽  
Timothy B. Mapstone
Keyword(s):  
Posterior Fossa ◽  
Chiari Malformation ◽  
Posterior Fossa Decompression ◽  
Chiari Type ◽  
Presenting Symptoms ◽  
Dural Opening ◽  
Adequate Decompression ◽  
Divergence Insufficiency ◽  
Repeat Imaging

The authors present a case of Chiari type 1.5 malformation with the uncommon presenting symptoms of esotropia and diplopia due to divergence insufficiency in a 12-year-old girl. Imaging at initial diagnosis revealed cerebellar herniation with extension of the tonsils to the C2 vertebral body, a retroflexed odontoid, and a small cervical syrinx. The patient was initially treated with an uncomplicated Chiari malformation decompression without dural opening. Repeat imaging revealed an adequate decompression. Three months postoperatively the patient’s diplopia recurred and she underwent repeat posterior fossa decompression with dural opening and duraplasty. Following repeat decompression with dural opening and duraplasty, the patient’s diplopia had not recurred by the 2-year follow-up.https://thejns.org/doi/abs/10.3171/2018.5.PEDS1886

scholarly journals Opioid overdose in a child: case report and discussion with emphasis on neurosurgical implications

2015 ◽  
Vol 16 (6) ◽  
pp. 752-757 ◽  
Author(s):  
Andrew Reisner ◽  
Laura L. Hayes ◽  
Christopher M. Holland ◽  
David M. Wrubel ◽  
Meysam A. Kebriaei ◽  
...  
Keyword(s):  
At Risk ◽  
Case Report ◽  
Young Children ◽  
Posterior Fossa ◽  
Mental Status ◽  
Fourth Ventricle ◽  
Altered Mental Status ◽  
Surgical Decompression ◽  
Opioid Overdose ◽  
Posterior Fossa Decompression

In environments in which opioids are increasingly abused for recreation, children are becoming more at risk for both accidental and nonaccidental intoxication. In toxic doses, opioids can cause potentially lethal acute leukoencephalopathy, which has a predilection for the cerebellum in young children. The authors present the case of a 2-year-old girl who suffered an accidental opioid overdose, presenting with altered mental status requiring cardiorespiratory support. She required emergency posterior fossa decompression, partial cerebellectomy, and CSF drainage due to cerebellar edema compressing the fourth ventricle. To the authors’ knowledge, this is the first report of surgical decompression used to treat cerebellar edema associated with opioid overdose in a child.

Intracranial Tumor

2018 ◽  
Author(s):  
Rebecca S. Isserman ◽  
Justin L. Lockman
Keyword(s):  
Postoperative Complications ◽  
Intracranial Hypertension ◽  
Posterior Fossa ◽  
Hemodynamic Instability ◽  
Cerebrospinal Fluid Flow ◽  
Solid Malignancy ◽  
Presenting Symptoms ◽  
Cranial Nerve Palsies ◽  
Complications Of Surgery ◽  
Symptoms And Signs

Intracranial tumors are the most common solid malignancy in pediatrics, with the majority found in the posterior fossa. In these patients, presenting symptoms and signs are frequently related to intracranial hypertension due to obstruction of cerebrospinal fluid flow. Specific cranial nerve palsies and ataxia may also be presenting signs, with or without intracranial hypertension. The anesthesia for surgical resection is nuanced by management of intracranial hypertension, the potential for hemodynamic instability, and postoperative complications resulting from damage to critical brainstem structures. This chapter discusses signs, symptoms, and differential diagnosis; tumor classification; anesthetic induction; and intraoperative and postoperative complications of surgery for a posterior fossa tumor.

scholarly journals Complete 3rd cranial nerve dysfunction postdeflation/ excision of an encasing pituitary macroadenoma intrasellular cyst: A Case Report

2016 ◽  
Vol 30 (3) ◽  
pp. 382-386
Author(s):  
C. S. Ng ◽  
S. Norlela
Keyword(s):  
Cranial Nerve ◽  
Cranial Nerves ◽  
Fluid Pressure ◽  
Residual Tumour ◽  
Pituitary Macroadenoma ◽  
Cystic Fluid ◽  
First Case ◽  
Cranial Nerve Dysfunction ◽  
Cystic Component ◽  
Cranial Nerve Palsies

Abstract Central nervous system injury in particular cranial nerve palsy has been reported to be as high as 2%. Such prevalence of palsy generally attributed to surgical manipulation at the cavernous sinus, especially incurring the abducens nerve. We report the first case of acute oculomotor nerve sequel to the release of cystic fluid wrapping the nerve following a transsphenoidal excision of pituitary macroadenoma in a 57-year-old woman. She attended with the presentation of acute excruciating headache associated with partial drooping of right eye. The computed tomography and magnetic resonance imaging (MRI) were consistent with pituitary apoplexy of an underlying pituitary macroadenoma. Urgent transsphenoidal hypophysectomy was done. Intra-operatively, cystic fluid was aspirated during pituitary tumour dissection. At the same time, curettage was employed to removal residual tumour after the tumour biopsy. Immediate post-operative assessment noted complete right eye ptosis, with clinical evidence of complete right third and fourth nerve palsies. MRI was repeated a week later in view of such palsy non-resolution. However, no local compression or edema noted. Observation and monitoring were opted versus surgical revision. Propitiously the aforementioned cranial nerve palsies persist for a month and subsequently subsided. In this case, we highlight the potential deleterious impact of aspirating cystic component and curettaging during pituitary surgery. Likely postulated accounts for such occurrence include sudden release of fluid pressure with resultant cystic traction on its enfolding cranial nerves and subsequent neuropraxia. We aim to invite comments that could enlighten us on this gray area.

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