It is usually seen in the cervical region but can extend into the medulla oblongata and pons or it can reach downward into the thoracic or lumbar segments. Syringomyelia is often associated with type I Chiari malformation and is commonly seen between the C-4 and C-6 levels. The exact development of syringomyelia is unknown but many theories suggest that the herniated tonsils in type I Chiari malformations cause a "plug" to form, which does not allow an outlet of CSF from the brain to the spinal canal. Syringomyelia is present in 25% of patients with type I Chiari malformations. Pathophysiology
The most widely accepted pathophysiological mechanism by which Chiari type I malformations occur is by a reduction or lack of development of the posterior fossa as a result of congenital or acquired disorders. Congenital causes include hydrocephalus, craniosynostosis (especially of the lambdoid suture), hyperostosis (such as craniometaphyseal dysplasia, osteopetrosis, erythroid hyperplasia), X-linked vitamin D-resistant rickets, and neurofibromatosis type I. Acquired disorders include space occupying lesions due to one of several potential causes ranging from brain tumors to hematomas. Traumatic brain injury may cause delayed acquired Chiari malformation, but the pathophysiology of this is unknown. Additionally, ectopia may be present but asymptomatic until a whiplash injury causes it to become symptomatic.Some neurological experts believe that Chiari malformation type I is developed as a result of Filum Disease, an abnormal traction of the spinal cord caused by an excessively tense Filum terminale. This theory was first introduced by Dr. Miguel B. Royo Salvador in 1993.
It also exhibits weak partial agonism of GABAA receptor complexes that contain α6-type monomers; the clinical relevance of this is unknown.Flumazenil does not antagonize all of the central nervous system effects of drugs affecting GABA-ergic neurons by means other than the benzodiazepine receptor (including ethanol, barbiturates, and most anesthetics) and does not reverse the effects of opioids. It will however antagonize the action of non-benzodiazepine z-drugs, such as zolpidem and zopiclone, because they act via the benzodiazepine site of the GABA receptor - it has been used to successfully treat z-drug overdose. Pharmacodynamics
Intravenous flumazenil has been shown to antagonize sedation, impairment of recall, psychomotor impairment and ventilatory depression produced by benzodiazepines in healthy human volunteers. The duration and degree of reversal of sedative benzodiazepine effects are related to the dose and plasma concentrations of flumazenil. Availability
Flumazenil is sold under a wide variety of brand names worldwide like Anexate, Lanexat, Mazicon, Romazicon. In India it is manufactured by Roche Bangladesh Pharmaceuticals and USAN Pharmaceuticals. See also
Benzodiazepine overdose
Benzodiazepine
Bretazenil
Imidazenil
Ro15-4513
GABAA receptor negative allosteric modulators

References
Other
Romazicon product information, Roche USA

External links
 Media related to Flumazenil at Wikimedia Commons
Flumazenil drug label/data at Daily Med from U.S. National Library of Medicine, National Institutes of Health.