Brainstem Vascular Malformation Research Articles

Horner’s syndrome and epidural anesthesia in labor and cesarean section

Homer's syndrome (HS) is based on dysfunction of symphathetic nervous system at the cervical canal. The signs of the syndrome occur on the same side as the lesion of the sympathetic trunk and include: a constricted pupil, a weak-droopy eyelid, apparent decreased sweating, and with or without inset eyeball. HS has been observed as a rare complication of epidural anaesthesia in obstetrics during labour or cesarean section. In parturients, it warrants further investigation as other serious causes must be excluded, such as pancoast tumours, thoracic aortic aneurysms, carotid dissection, neuroblastoma, and brainstem vascular malformation. Management involves early diagnosis of the underlying benign condition while treatment is based on appropriate conservative observation, as most often the syndrome resolves spontaneously. However in very rare cases immediate medical or surgical management is needed.

Acquired progressive ataxia and palatal tremor: Importance of MRI evidence of hemosiderin deposition and vascular malformations

Oculopalatal tremor is frequently accompanied by progressive ataxia. In symptomatic oculopalatal tremor the ataxia frequently is delayed in onset. Progressive ataxia is a defining clinical feature of superficial siderosis. We report 5 cases with palatal tremor and ataxia. Four cases had evidence of intraparenchymal hemosiderin deposition on T2-gradient-echo imaging. Three cases had a brainstem vascular malformation. In two cases the hemosiderin deposition was likely due to prior trauma. The significance of these associations and possible similarities between ataxia related to superficial siderosis and ataxia and intraparenchymal hemosiderin is discussed.

Microsurgery for brainstem vascular malformation:report of 19 cases

Objective To investigate the microsurgical treatment of brainstem vascular malformation and evaluate the surgical outcome. Method Brain stem vascular malformations in 19 cases were resected by microsurgical techniques. Six cases of cavernous malformations ( CM ) in the dorsal of pons and medulla underwent operations via through the base of the forth ventrical approach. Another nine cases of CM in lateral and ventral lateral pons were treated via suboccipito - retrosigmoid approach. Three cases of arteriovenous malformation(AVM) in cerebellomedullary fissure were treated via telovelar approach. One case of AVM in the dosal medulla were resected via transvermian approach. Results All the lesions were totally resected. Pathologic diagnosis were CM( 15 cases) and AVM(4 cases). The diameter of all the CM were less than 1 centimeter. One AVM was 1.5 centimeter in diameter, the other two lesions was 2. 0 centimeter, the last one was 2. 5 centimeter. The functional disorders were improved after operation in 13 cases. Complications appeared in five patients, which improved between one week and three months. One patient died of sever pneumonia. During two months to six years after operation, the brainstem vascular malformation didn't recrudesce and re - bleed. No one patient appeared new syndromes. Conclusions The microsurgical management of brainstem vascular malformation can effectively prevent re - bleeding. Selecting different surgical approach basing on the locations can reduce the neurofunction damage. In order to accelerate the recovery of damaged brainstem, early surgery should be choosen for the patients with surgical indications. Basing on the correct choice of surgical indications, using the extensive knowledge of microanatomy,new concept of minimal invasive surgery and skillful microsurgical techniques, the surgical results of brainstem vascular malformation are satisfactory. Key words: Brain Stem; Central nervous system vascular malformations; Hemangioma,cavernous,central nervous system; Intracranial arteriovenousmalformations; Microsurgery

Brainstem capillary telangiectasias in a pacient with central vestibular syndrome

Capillary telangiectasias represent one of the four types of brainstem vascular malformations, characterized by multiple thin-walled vascular channels, interposed between normal brain parenchyma of unknown etiology. They are most of the time an incidental radiologic finding, almost all patients being asymptomatic. We present the case of a 65 years old male, admitted to our clinic for recurrent episodes of horizontal diplopia to lateral gaze on the left side, dizziness and unsteadiness of gait. The cerebral MRI showed imaging features characteristic for capillary telangiectasias in the brainstem and the cerebral angiography was normal.

Pediatric Horner syndrome

Introduction: The purpose of this study was to define the etiologies of Horner syndrome in the pediatric population. Methods: A retrospective review was performed of the medical records of all pediatric Horner syndrome patients (<18 years old) examined by the pediatric ophthalmology services at two large referral centers. Results: Seventy-three pediatric Horner syndrome patients were identified. Of these, 31 (42%) were congenital, 11 (15%) were acquired without surgical intervention, and 31 (42%) were acquired after a surgical procedure of the thorax, neck, or central nervous system. Of the congenital Horner syndrome patients, a history of delivery with the use of forceps, vacuum extraction, shoulder dystocia, fetal rotation, or postterm delivery was elicited in 16 patients (53%). Concomitant brachial plexus injury was identified in only 3 patients. Two patients had congenital varicella syndrome and 1 patient was diagnosed with neuroblastoma. This patient had a palpable supraclavicular mass and stridor. Diagnosis of the patients with acquired Horner syndrome included neuroblastoma (2), trauma (1), rhabdomyosarcoma (1), brainstem vascular malformation (1), disseminated sclerosis (1), and not determined (5). Conclusion: In children with congenital Horner syndrome, a history of forceful manipulation of the infant during birth may reduce the need for extensive systemic evaluation. Without such history, a decision to proceed with further evaluation is made with consideration of the relative incidence of neuroblastoma by age and the physical findings. All acquired pediatric Horner syndrome patients without a known etiology require thorough evaluation because of the frequent association of serious underlying disease.

Management of Brain-Stem Vascular Malformations: Advances in Surgical Technique and Long-Term Results

Summary: The therapeutic options for brain-stem vascular malformations have expanded, and postoperative morbidity has declined, with renewed interest in skull base surgery, surgical lasers, electrophysiologic stimulation of cranial nerve nuclei, intraoperative ultrasound, and intraoperative angiography. This article reviews experience (1984–1993) in evaluating the long-term results of 63 patients with brain-stem vascular malformations; 27 patients were treated surgically, and 36 were observed. There were 45 cavernous angiomas, 13 arteriovenous malformations (AVMs), five capillary telangiectasias, and nine associated venous angiomas. Forty-one (65%) of 63 were located in the pons. Hemorrhage was the initial presentation in 54 (86%) patients; 23 (42.5%) suffered repeat hemorrhages. Surgery was performed when the malformation was near the brain-stem surface, when the neurologic status deteriorated, and in cases of repeat hemorrhage. Resection of venous angiomas was avoided. Of 27 surgical patients, 15 (56%) had transient worsening of their neurologic status and five (18.5%) suffered permanent neurologic deficits that included truncal ataxia, internuclear ophthalmoplegia, abducens palsy, paralysis of upward gaze, and nuclear facial weakness. Two patients (13.5%) suffered a recurrent hemorrhage from residual malformation. There was no mortality. Neurologic improvement occurred in 23 (85%) surgical patients, and 24 (89%) returned to independent living with functional neurologic capacity. Results improved with surgical experience and technical advances, leading the authors to conclude that surgical treatment is the best option for brain-stem vascular malformations. Observation is reserved for deep-seated and asymptomatic cavernous angiomas; stereotactic radiosurgery is preferred for intraparenchymal AVMs and unruptured AVMs of the tectum and ventral brain stem.

Contralateral trochlear nerve palsy and facial sensory change due to a probable brainstem vascular malformation

Brainstem vascular malformation is a rare cause of trochlear nerve palsy. The authors report a patient who presented with a rightsided trochlear nerve palsy and ipsilateral facial paresthesia. Magnetic resonance imaging disclosed a small, linear vascular malformation in the left midbrain. Involvement of the trochlear fascicles and trigeminal second order neurons is suggested as a possible pathogenic mechanism.

Cerebellar venous angioma associated with angiographically occult brain stem vascular malformation. Report of two cases

We studied two patients with angiographically documented cerebellar venous angioma (malformation) and angiographically occult vascular malformation of the brain stem. One patient had recurrent hemorrhage in the pontine tegmentum. The second patient had recurrent hemorrhage in the midbrain. None had hemorrhage originating from the abnormal cerebellar venous channels. The more benign nature of angiographic venous malformations is supported by the cases we are presenting, as well as from a review of the literature, which includes an autopsy study of similar cases. The management of multiple vascular brain lesions is contingent on the verification of symptomatic pathological blood vessels. It is emphasized that angiographically occult vascular malformation could possibly exist in the vicinity of angiographic venous malformation when the patient with intracerebral hemorrhage, especially in the posterior fossa, was diagnosed as having venous malformation.

Surgical management of brain stem vascular malformations

Vascular malformations of the brain stem are a histologically heterogenous collection of lesions which most often present with sudden and progressive neurologic deficit related to haemorrhage. Since 1987 the authors have treated eleven cases of brain stem vascular malformation. Seven of the patients were treated with complete surgical extirpation of the haematoma and malformation because of progressive neurologic deficit. Four additional patients made a full neurologic recovery and are being carefully observed for signs suggestive of the need for surgical treatment. Complete surgical excision of brain stem vascular malformations is mandatory for patients with progressive neurologic deficit related to recurrent haemorrhage.

Magnetic resonance appearance of slow flow vascular malformations of the brainstem.

Twelve patients with slow flow brain stem vascular malformations had magnetic resonance scans performed on a 1.5 Tesla scanner using T1 (TR = 400-800 ms, TE = 25 ms) and T2 (TR = 2000 ms, TE = 20, 25, 80 ms) weighted scans. Eight patients (70%) had solitary brainstem vascular malformations while 4 (30%) had multiple lesions both supra and infratentorially. Five patients had venous angiomas demonstrated by angiography and MR. There were 26 lesions seen on MR of which only 14 were identified by CT. These lesions demonstrated a specific MR image pattern indicative of subacute or chronic parenchymal hematoma. It was characterized by an iso to hyperintense central signal surrounded by a well defined thin band of low signal intensity. The central zone could appear to be single or multilocular. In multilocular lesions the hemorrhages within different cells could be of different ages. One patient did not have findings of a chronic hematoma but exhibited only low signal secondary to calcification and a venous angioma. None of these lesions had surrounding edema. Despite the variable etiologies of slow flow vascular malformations of the brainstem, their MRI manifestations seem to indicate a final common pathway of chronic hematoma. These lesions are quite distinct from MS or tumor, the usual clinical considerations in the differential diagnosis.