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Fibrocartilaginous embolism (FCE) is a rare and probably under diagnosed cause of spinal cord infarction presumably due to acute embolization of nucleus pulposus fragments into the spinal circulation. Concomitant cerebral involvement is much rarer and often asymptomatic. Although the definitive diagnosis is histologic, certain criteria have been proposed to support the diagnosis in living patients, such as absence of vascular risk factors, acute onset or antecedent of valsalva maneuver before the episode and the exclusion of potential differential diagnoses. A 56 years-old patient, without any medical history was referred for sudden back pain while carrying heavy load at work. Clinical examination showed a Brown-Sequard syndrome. Brain and spine MRI disclosed spinal cord infarction at the C4-C5 level associated with brain infarctions involving exclusively the vertebrobasilar circulation. The exhaustive etiological assessment was normal. In our case, the acute symptoms onset, the clinical and imaging data and lack of evidence for other plausible diagnoses in the setting of a valsalva-like maneuver are highly suggestive of FCE diagnosis.

Brown-Séquard syndrome (BSS) is a rare syndrome and is often described in association with spinal cord injury resulting from hemisection of the spinal cord. BSS due to cervical disc herniation is rare with often delayed diagnosis. The importance of early recognition with imaging cannot be over-emphasized, as the prognosis is better when compared to traumatic and vascular etiologies of BSS. We report a rare case of BBS in an 86-year-old man secondary to cervical disc herniation who had dramatic improvement after surgical intervention. This case highlights the unusual presentation from a very common spinal pathology along with a review of the pertinent literature.

We report a 28-year-old woman who presented with a partial Brown-Sequard syndrome 18 months after a fall from a horse. Investigation revealed the cause of her symptoms to be a spinal cord herniation at the level of T6. A review of previously reported cases of posttraumatic spinal cord herniation was undertaken. Six of the cases reported have clear evidence of injury at the site of subsequent herniation; the remaining five cases may be related to trauma or may be spontaneous spinal cord herniation, with an unrelated history of trauma.

Brown–Sequard Syndrome (BSS) caused by cervical spondylosis (CS) is rare. About 70% of patients with CS presenting with BSS show lesion-dermatome discrepancy, which may be due to spinal cord lamination. From the clinical point of view, this discrepancy should be carefully evaluated and these patients should be treated as an emergency.

Spinal cord herniation is a rare condition that has become increasingly recognised in the last few years. The authors report a case of idiopathic spinal cord herniation in a 33 year old woman who presented with progressive Brown-Sequard syndrome. The diagnosis was made on MR imaging. After repairing the herniation the patient made a gradual improvement. Potential causes are discussed, including the possible role of dural tethering. In conclusion, idiopathic spinal cord herniation is a potentially treat able condition that should be more readily diagnosed with increased awareness and newer imaging techniques such as high resolution MRI.

Idiopathic spinal cord herniation (ISCH) is a rare condition presenting as progressive Brown-Sequard syndrome in 66% of patients [1]. Other presentations include symmetrical spastic paraparesis (30%) or less commonly, pure sensory or motor deficits. The spinal cord protrudes through a ventral or ventrolateral dural defect, causing unilateral distortion to the lateral funiculus and giving rise to progressive neurological symptoms. The mean age at presentation is 53 years with a 2:1 female preponderance. First described by Wortzmann in 1974, there are now over 120 cases reported in the literature, however its pathogenesis remains unknown [1]. Postulated pathogenic mechanisms include both congenital dural abnormalities and acquired dural injury leading to cord herniation, exacerbated by cerebrospinal fluid pulsations during the cardiorespiratory cycle. The progressive nature of symptoms may be explained by the intra-operative observation of tethering of the cord at the margins of the dural defect [1–3]. The anatomy of the thoracic spinal cord is thought to contribute to the predisposition of ISCH to the thoracic cord. The thoracic kyphosis and the natural ventral position of the cord in themid-thoracic levels, combined with repeated flexion and extension movementare believed to aggravatedural injury in the thoracic region [4]. Diagnosis of ISCH ismadebyMRI.Diagnostic features includeventral displacementor ‘‘kinking’’ of the spinal cordat the level of thedural defect, enlargement of the dorsal subarachnoid space, cord signal changes and atrophic changes with thinning of the cord. Phase contrast MRI can be helpful in differentiating from an arachnoid cyst [5]. Surgical management of this patient involved a T6–T7 laminectomy and durotomy (Fig. 1). The herniated cord was gently retracted and the hernial orifice obliterated using a dural patch. At discharge on post-operative day 4, weakness was markedly improved with nearly full power, and sensation and reflexes were normal. The patient returned 3 months post-operatively for follow-up MRI (Fig. 2).