This is a one month-old female with congenital hypothyroidism, hypoplasia of the thyroid gland, elevated TSH (eight times normal value), elevated FSH and LH (four times normal values), normal GH, without diabetes insipid. She is now being treated for the hypothyroidism, and we are waiting for hormonal follow-up; MRI follow-up in three to six month follow-up.
Has anyone an explanation for the focal bright spot on T1-weighted images in the cranial portion of the pituitary stalk, just down the median eminence, in the presence of a normal neurohypophysis?
Is it an “ectopic” adenohypophysis?
Is this a thin pituitary stalk in pituitary gland hypoplasia?
What will happen at follow-up?
It is the start of an infiltrative disease?
…It is simply that I do not know the normal and physiological behavior of the pituitary gland?…
Best regards to all of You!…
We have recently presented (AJNR 2009, Letter to the Editor) the regression of a dilated PVS in the temporal stem, after surgery of a pituitary nonfunctioning macroadenoma. We have other two cases, both in the temporal stem, one after pituitary apoplexy (most likely in macroadenoma but no surgical confirmation), and the other one after surgical resection of a cranial vault meningioma invading the superior sagittal sinus (far away from the dilated temporal stem PVS). We are trying to publish these last two cases.
Has anyone other cases? Which is the frequency of regression of dilated PVS? Is it frequent, and we simply do not look for this?
Best regards to all of you.…
This is a case for Prof. Dr. Dillon.
It is in press by our neurosurgeons and us, for the use of Duragen.
Idiopathic herniation of the thoracic spinal cord: a case report and technique note.
Ulivieri S.1, Oliveri G.1, Petrini C.1, D’Elia F.2, Cuneo G.L.3, Cerase A.4
Units of 1Neurosurgery, and 4Neuroradiology, “Santa Maria alle Scotte” Hospital, Siena, Italy
2Unit of Radiology, and 3Section of Neuroradiology, Department of Neurology, “San Donato” Hospital, Arezzo, Italy
A 35-year-old man presented with insidiously progressive and disabling pain in the left leg. There was no history of trauma or surgery; neurological examination revealed features suggestive of thoracic level Brown-Séquard syndrome.
The patient underwent a thoracic laminectomy at T9–T10. The dura was opened under the microscope and an atrophic spinal cord displaced to the left was visible. The spinal cord was incarcerated through a 2.5 cm wide anterolateral dural defect and had an exophytic edematous appearance. In order to perform an anterior untethering, the dentate ligament was transected and the nerve roots were preserved. The spinal cord was gently mobilised out of the dural defect. Notably, there were no major adhaesions and thus there was no need to manipulate the cord. Then, it was decided to position hemostatic material (Spongostan®) and glue (Tissucol®) around the defect and finally a sheet of collagenous membrane (DuraGen®) anterior to the spinal cord. The wound was closed in layers without external cerebrospinal fluid drainage. No spinal cord monitoring was used. The initial post-operative neurological deficit was unchanged and there was no sign of cerebrospinal fluid leakage. The patient was discharged seven days after surgery to rehabilitation.
Best regards to all of you.
ISCH Cerase (.ppt)…