Virchow-Robin spaces producing visual field defect

Abstract

However, immediate improvement in syringomyelia and relatively short history indicate congenital predisposition aggravated by growth spurt. Tension related to tethering of the bottom or middle of the spinal cord probably leads to stretch injury that can obstruct the flow of fluid within the central canal or produce fluid cavitation per se. This type of syrinx is unlikely to benefit from foramen magnum decompression, and best treated with surgery to untether the spinal cord. The remarkable improvement in clinical symptoms and radiology indicates the magnitude of tension within the whole of cord, with re-establishment of CSF dynamics. Though there have been isolated reports of sectioning of filum terminale benefitting Chiari or syringomyelia, [4] holocord syringomyelia improving after detethering of cord has not been reported previously. Holocord syringomyelia with tethered cord indicates caudal traction as the primary etiology, and so requires mere detethering of cord. Foramen magnum decompression is not needed even in presence of tonsillar descent. However, individual cases need to be evaluated carefully before deciding treatment.

Enlarged tumefactive perivascular, or Virchow-Robin, spaces and hydrocephalus: do we need to treat? Illustrative cases

“…Therefore, surgical treatment in these cases is rarely performed and has only been reported once in a case of type 1 and four times in cases of type 2 GTPVS. [16][17][18][19] Depending on its size and location, a type 3 GTPVS can become apparent through a wide range of neurological deficits such as hemiparesis, tremors, oculomotor nerve palsy, parkinsonism, or cerebellar ataxia. 6,7 In other cases, they cause symptoms due to obstructive hydrocephalus.…”

Tumefactive Virchow-Robin spaces

“…One of these patients was temporarily treated with medication for dementia without improvement [52]. In three other patients, the presenting symptoms of intermittent hemianopsia [14], quadrantanopsia [79], and temporary unilateral weakness and numbness [77] were attributed to the mass effect of more focally located tumefactive VRs; the first patient underwent endoscopic cystoventriculostomy of periventricular tumefactive VRs near the optic radiation, postoperative MRI showed tumefactive VRs reduction and intermittent hemianopsia was resolved [14]; the latter patient underwent tumefactive VRs resection in the medial frontal lobe, no postoperative outcome data were given [77]. In yet another patient, hydrocephalus symptoms were caused by tumefactive VRs between the left temporal lobe and supraventricular area compressing the foramen of Monro [49].…”