7,8-Dihydroxyflavone accelerates recovery of Brown-Sequard syndrome in adult female rats with spinal cord lateral hemisection.

BACKGROUND: 7,8-Dihydroxyflavone (DHF) mimicks the physiological action of brain-derived neurotrophic factor (BDNF). Since local BDNF delivery to the injured spinal cord enhanced diaphragmatic respiratory function, we aimed to ascertain whether DHF might have similar beneficial effects after Brown-Sequard Syndrome in a rat model of spinal cord lateral hemisection (HX) at the 9th thoracic (T9) vertebral level. METHODS: Three sets of adult female rats were included: sham+vehicle group, T9HX+vehicle group and T9HX+DHF group. On the day of surgery, HX+DHF group received DHF (5 mg/kg) while HX+vehicle group received vehicle. Neurobehavioral function, morphology of motor neurons innervating the tibialis anterior muscle and the transmission in descending motor pathways were evaluated. RESULTS: Adult female rats received T9 HX had paralysis and loss of proprioception on the same side as the injury and loss of pain and temperature on the opposite side. We found that, in this model of Brown-Sequard syndrome, reduced cord dendritic arbor complexity, reduced cord motoneuron numbers, enlarged cord lesion volumes, reduced motor evoked potentials, and cord astrogliosis and microgliosis were noted after T9HX. All of the above-mentioned disorders showed recovery by Day 28 after surgery. Therapy with DHF significantly accelerated the electrophysiological, histological and functional recovery in these T9HX animals. CONCLUSIONS: Our data provide a biological basis for DHF as a neurotherapeutic agent to improve recovery after a Brown-Sequard syndrome. Such an effect may be mediated by synaptic plasticity and glia-mediated inflammation in the spared lumbar motoneuron pools to a T9HX.

Indomethacin responsive headache syndromes: chronic paroxysmal hemicrania and Hemicrania continua. How they were discovered and what we have learned since.

In the indomethacin responsive headaches (IRHs), chronic paroxysmal hemicrania (CPH) and Hemicrania continua (HC), the indomethacin (INDO) response is swift, absolute, and permanent, with moderate doses. Traditionally, CPH has been linked to cluster headache (CH) due to clinical similarities: unilaterality, intensity, and some autonomic phenomena. However, other clinical features differ essentially between these two headaches: sex ratio, mean attack frequency (CPH: 13.6 versus CH: 1.7 attacks/day), and duration of attacks. The therapeutic profile in CPH (indomethacin effect: ++; triptan effect: generally non-existent) is reversed in CH. The autonomic phenomena also differ clearly, a forehead supersensitivity sweating pattern and Horner-like pupil being present only in CH. The chronic/non-chronic stage ratio is 3.9 in CPH, against 0.14 in CH, a >25 times difference. Conversely, CPH and HC are very similar, clinically speaking. Accordingly, we should probably sever the link between CH and CPH and favour, instead, a linking together of CPH and HC, the two principal IRHs.

Cervical epidural abscess presenting with Brown-Sequard syndrome in a patient with type 2 diabetes.

An 80-year-old woman with type 2 diabetes was admitted due to right-handed muscle weakness. The patient presented with Brown-Sequard syndrome, with complete paralysis of the right lower limb along with a loss of pain and temperature sensations in the left lower limb. Magnetic resonance imaging revealed a cervical epidural abscess, and accompanying edema or inflammation of the right side of the spinal cord at the C5 level. She underwent drainage and evacuation of the spinal abscess, followed by intravenous antibiotic administration. These interventions ameliorated the neurological deficits. The present case suggests the importance of epidural abscess as a rare pathogenetic cause of Brown-Sequard syndrome in type 2 diabetes.

Paraspinal muscle impingement causing acute Brown-Sequard syndrome after posterior cervical decompression.

STUDY DESIGN: A case report. OBJECTIVE: To present a previously unreported cause of neurologic compromise after cervical spine surgery. SUMMARY OF BACKGROUND DATA: Several different causes of postoperative neurologic deficit have been reported in the literature. The authors present a case of acute postoperative paralysis after posterior cervical decompression by a mechanism that has not yet been reported in the literature. METHODS: A 54-year-old muscular, short-statured man underwent posterior cervical laminectomy from C3-C5 without instrumentation and left C5 foraminotomy. Within hours of leaving the operating room, he began to develop postoperative neurologic deficits in his extremities, which progressed to a classic Brown-Sequard syndrome. Magnetic resonance imaging revealed regional kyphosis and large swollen paraspinal muscles impinging on the spinal cord without epidural hematoma. Emergent operative re-exploration confirmed these findings; large, swollen paraspinal muscles, a functioning drain, and no hematoma were found. RESULTS: The patient was treated with immediate corticosteroids at the time of initial diagnosis, and emergent re-exploration and debulking of the paraspinal muscles. The patient had complete recovery of neurologic function to his preoperative baseline after the second procedure but required a third procedure in which anterior discectomy and fusion at C4-C5 was performed, which led to improvement of his preoperative symptoms. CONCLUSION: When performing posterior cervical decompression, surgeons must be aware of the potential for loss of normal lordosis and anterior displacement of paraspinal muscles against the spinal cord, especially in muscular patients.

Brown-Sèquard syndrome caused by type III odontoid fracture: a case report and review of the literature.

STUDY DESIGN: Case report. OBJECTIVE: To present the second case of Brown-Sèquard syndrome (BSS) produced by type III odontoid fracture managed by conservative treatment. SUMMARY OF BACKGROUND DATA: The occurrence of BSS due to odontoid fracture is scarce. So far 6 cases have been reported, and only 1 is produced by type III odontoid fracture. The possible pathophysiology, clinical course and treatment outcome have been rarely discussed. METHODS: A 39-year-old man presented with weakness of his left arm and leg, mild neck pain, and impaired proprioceptive and light touch sensations below the left C2 dermatome. There were decreased pain and temperature sensations below the right C4 dermatome too. Computerized tomography showed odontoid type III fracture with posterior displacement at that level. Magnetic resonance imaging presented focal hyperintensity around the C2 vertebral level. High dose of prednisolone, close reduction with Gardner-Wells tong skull traction, following external stabilization by Halo-Vest and rehabilitation therapy were applied. RESULTS: Complete resolution of neck pain and significant improvement of motor and sensory functions, i.e., light touch and proprioception, were shown 2 months after spinal injury. Impaired temperature discrimination persisted, however. CONCLUSION: BSS is rarely caused by type III odontoid fracture and this is the second report. Conservative intervention is advantageous for both type III odontoid fracture and BSS which is consistent with previous results.

Brown-Sequard syndrome after thoracic endovascular aortic repair.

A 76-year-old female had suffered from distal arch aortic aneurysm and chronic DeBakey IIIB type dissecting aneurysm. The patient underwent thoracic endovascular aortic repair (TEVAR). After TEVAR the patient had a motor and proprioceptive loss on the left side and a pain and body temperature loss on the right side below the level of T7. At diagnosis of Brown-Sequard syndrome, corticosteroid and free radical scavenger were administered soon afterwards. Her neurological deficits gradually improved and the patient was discharged with the aid of a walking stick three months after TEVAR.

[MRI features of spinal neurosarcoidosis associed with cervical spondylosis]. / Myélopathie sarcoïdosique associée à un canal cervical rétréci : aspects IRM.

INTRODUCTION: Spinal neurosarcoidosis is rare and exceptionally inaugural. OBSERVATION: A 49-year-old African woman developed a progressive left Brown-Sequard syndrome. Magnetic resonance imaging (MRI) scans of the cervical spinal cord revealed an intramedullary lesion from C2 to T1 with intense pial enhancement after administration of contrast material associated with cervical spondylosis. The diagnostic of sarcoidosis was confirmed by liver biopsy which demonstrated noncaseating granulomas. CONCLUSIONS: MRI features of spinal neurosarcoidosis were reviewed by the authors with focus on differential diagnosis.

Delayed onset of Brown-Sequard syndrome involving upper extremity pain.

Report of a case: A 60-year-old white male with a history of C3-C4 spinal cord injury with subsequent C3-C4 fusion complained of right upper extremity painful spasms of 2 years duration with associated hyperspasticity, motor weakness and poor positional and vibrational sense. The patient was diagnosed with Brown-Sequard syndrome (BSS) and treated with botulinum toxin type A injections distributed into the affected muscle groups that provided substantial and lasting relief. This case is unique in that the patient's trauma occurred 28 years before the development of the BSS suggesting a slow evolution of the condition.

Neurological improvement associated with resolution of irradiation-induced myelopathy: serial magnetic resonance imaging and positron emission tomography findings.

We document serial magnetic resonance imaging (MRI) and [(18)F] 2-fluoro-2-deoxyglucose (FDG)-positron emission tomography (PET) findings in the process of improvement from delayed radiation necrosis of the spinal cord. A 61-year-old woman underwent radiotherapy for an oral carcinoma. Forty-six months later she developed a left-sided Brown-Séquard syndrome, suggesting incomplete cervical cord transection below the cervico-thoracic junction. Two months after starting steroid therapy, she had gradual clinical improvement, which continues 8 years after the termination of radiotherapy. Neurological improvement was associated with gradual resolution of an extensive high-intensity area within the cervico-thoracic spinal cord on MRI. Initially, the FDG-PET showed linear and uniform increase in FDG uptake throughout the cervical spinal cord with standardized uptake value of 2.68 +/- 0.16 (mean +/- SD), but it returned to normal value (1.90 +/- 0.14) at final follow-up. Considering that the normalization of FDG uptake correlated with neurological recovery, the uniform- and diffuse-increased FDG uptake noted in the initial course of myelopathy could reflect the metabolic activity of the compromised spinal cord.

Factors associated with improved neurologic outcomes in patients with incomplete tetraplegia.

STUDY DESIGN: Retrospective review of 412 patients with traumatic, incomplete, cervical spinal cord injuries, and an average follow-up period of 2 years. OBJECTIVES: To determine what patient characteristics, injury variables, and management strategies are associated with improved neurologic outcomes. In particular, the effects of intravenous steroids (NASCIS II protocol), early definitive surgery (<24 hours after injury), early anterior decompression for burst fractures or disc herniations (<24 hours after injury), and surgical decompression for stenosis without fracture were assessed. SUMMARY OF BACKGROUND DATA: Controversy surrounds the pharmacologic and surgical management of patients with spinal cord injuries. METHODS: Neurologic data were collected retrospectively and classified using American Spinal Injury Association guidelines. This information was recorded at the time of injury, on admission to rehabilitation, on discharge from rehabilitation, and at 1, 2, and final year of follow-up evaluation. Outcome measures included change in motor score, change in sensory score, final motor score, and final sensory score. The SPSS v10.0.7 statistical software package was used for data analysis. RESULTS: Neurologic recovery was not related to the following factors: gender, race, type of fracture, or mechanism of injury. Neurologic recovery also was not related to the following interventions: high-dose methylprednisolone administration, early definitive surgery, early anterior decompression for burst fractures or disc herniations, or decompression of stenotic canals without fracture. Improved neurologic outcomes were, however, noted in younger patients ( = 0.002), and those with either a central cord or Brown-Sequard syndrome ( = 0.019). CONCLUSIONS: The most important prognostic variable relating to neurologic recovery in a patient with a spinal cord injury is the completeness of the lesion. When an incomplete cervical spinal cord lesion exists, younger patients and those with either a central cord or Brown-Sequard syndrome have a more favorable prognosis for recovery. In this study, no evidence was found to support high-dose steroid administration, routine early surgical intervention, or surgical decompression in stenotic patients without fracture.

Recovery after high-dose methylprednisolone and delayed evacuation: a case of spinal epidural hematoma.

Spinal epidural hematoma (SEH) is rare and not without serious sequelae. We report a patient who developed Brown-Séquard syndrome from SEH after fluoroscopic-guided cervical steroid injection and favorable response to methylprednisolone (MP). A 56-year-old man reported immediate sharp shooting pain to the upper extremities on introduction of epidural toughy needle. A total of 5 mL of 0.2% ropivacaine and 120 mg methylprednisolone acetate suspension was administered at the C6-7 interspace. Within half an hour, a neurologic deficit occurred at C7-8 and right Brown-Séquard syndrome developed. Once SEH was suspected (3 hours after onset of neurologic deficit), a protocol of high-dose MP intravenous infusion was initiated. Immediate incomplete recovery of motor, sensory, and sphincteric functions was noted within 30 minutes of infusion. Emergency spinal C6-T2 bilateral decompressive laminectomies and evacuation SEH were performed within an expected delay (10 hours from the onset of neurologic deficit). Fluoroscopic guidance does not take the place of adherence to meticulous technique. An unexplained neurologic deficit after invasive spinal procedures should raise the concern for SEH. Early recognition and emergent evacuation remain the mainstay management for SEH. This case suggests some neuroprotection from MP in cases of cervicothoracic cord compression secondary to traumatic SEH. When potential risks for SEH exist, it is advisable not to administer local anesthetic so as not to interfere with neurologic assessment and delaying the diagnosis.

Brown-Sequard syndrome associated with Horner's syndrome after a penetrating trauma at the cervicomedullary junction.

STUDY DESIGN: Case report of a 21-year-old man that had concurrence of Brown-Sequard syndrome and Horner's syndrome after a penetrating trauma in the neck. OBJECTIVES: This report analyzes the location of lesions that cause a combination of Horner's and Brown-Sequard syndrome. It is important to know the anatomic structure of spinal cord and the sympathetic nerve chain. SETTING: Spinal Cord Unit, Department of Physical Medicine and Rehabilitation, Hospital La Fe, Valencia, Instituto Oftalmologico de Alicante, Alicante, Spain. METHODS: Description of a single patient case report. RESULTS: The clinical findings and MRI showed a good correlation. The Horner's syndrome was confirmed with a 4% cocaine test. The patient received a conservative treatment with high-dose steroid therapy (NASCIS-3). CONCLUSION: The patient presented with Brown-Sequard syndrome and Horner's syndrome. Clinical examination and MRI made a quick and correct diagnosis. The patient recovered completely after the conservative treatment.

Brown-Sequard syndrome caused by a Kirschner wire as a complication of clavicular osteosynthesis.

A case of spinal cord injury caused by delayed migration of a Kirschner wire is reported. Some cases of distant injuries caused by bone wires, and acupuncture needles have been published, but this is the first reported case of delayed thoracic spinal cord damage caused by the migration of a clavicular wire. A 22-year-old male patient was admitted with a clinical picture of spinal shock after performing physiotherapeutic exercises. Two months prior to this, the patient had undergone surgical treatment for a clavicular fracture in a different clinical center. Imaging showed a clavicular wire had migrated into the spinal canal. An early prescription of a spinal cord methyl-prednisolone protective treatment (NASCIS II), the surgical extraction of the foreign body and the rehabilitation exercises were the keys to a quick recovery.

[Brown-Séquard syndrome after closed injury of the cervical spine]. / Syndrome de Brown-Séquard après traumatisme fermé du rachis cervical.

The case of a Brown-Séquard syndrome at the C5 level, in a 21-year-old young man after a traffic accident is reported. Initially, the symptoms of spinal injury were concealed by those related to head and face trauma. The neurologic assessment showed a hemiplegia located in the same side as the medullar injury with a controlateral thermo-algesic anaesthesia. X-rays, CT-scan and MRI of the cervical spine confirmed the diagnosis. The treatment included the immobilization of the spine combined with i.v. methylprednisolone (bolus of 30 mg.kg-1 followed by a continuous infusion at a rate of 5 mg.kg-1.h-1 for 23 hours). The outcome was favourable. Six weeks later, the patient was again able to walk. However the thermo-algesic anaesthesia remained unchanged. This case report underlines the necessity of a careful and complete neurologic assessment of trauma patients and reminds of the possibility of occurrence of a Brown-Séquard syndrome in them.