Sunday, 8 July 2018

Pituitary stone

Clinically a known case of pituitary macro adenoma, prolactinoma as lab reports were showing high levels of prolactin. Under regular treatment of Bromocriptine.
CT SAG REFORMATTED IMAGE
CT SAG REFORMATTED IMAGE
MRI BRAIN SAGITTAL T2W IMAGE
Pituitary stone

Also known as pituitary lithiases or pituitary calculus.
A very rare entities defined as extensive calcifcation in the sella turcica.

There is inconsistency regarding what pituitary stones actually are. Some authors suggest the term be used only for calcifications in the sella turcica that occur in the absence of any other pituitary pathology, others use this term more liberally to describe excessive calcification from any cause, such as pituitary adenoma.

Epidemiology
Although the exact incidence is unknown, this entity is generally considered to be very rare as there are only 1 to 6 case reports of idiopathic calcifications so far. However, calcification in pituitary adenoma is considered more common which is approximately 10%.

The aetiology of 'primary' de-novo pituitary stones remains an enigma but is thought to be secondary to an unknown inflammatory process, subclinical haemorrhage, or cartilaginous metaplasia.
In cases secondary to other pathologies, most commonly pituitary adenomas, especially in prolactinomas, is thought to be a sequelae of fibrosis secondary to haemorrhage.

Other secondary causes rare and include Pituitary tuberculosis, metabolic imbalances like hypercalcaemia, sequel of pituitary apoplexy.

Clinical presentation varies significantly, may be entirely asymptomatic or endocrinopathies such as hypopituitarism, hyperprolactinaemia from an underlying pituitary adenoma or hemorrahge.

Imaging
CT is the modality of choice, best demonstrated on sagittal reformatted images as in this case, where they appear as well defined hyperdense nodule in the sella turcica. On MRI, signal changes are consistent with calcification that is low signal on T1, T2 as well as GRE without enhancement on post contrast.

Treatment and prognosis
Presence of stone in a macro adenoma not going to change line of management, treatment should be directed towards underlying cause. It should be left alone if idiopathic and asymptomatic.

Differential diagnosis off course in absence of macroadenoma should include calcified Rathke cleft cyst, calcified meningioma and calcified aneurysm in pituitary region. 

Vit B12 deficiency MRI brain findings


Lab report showed low level of Vit B12 levels.
Patient improved with Vit B12 supplements.

Hemangioblastoma MRI

PC CT BRAIN
FLAIR
T1
DW
GRE
T2
T1 PC
PC T1
PC T1
Hemangioblastoma

A highly vascular tumor.
An intra axial posterior fossa mass with cyst and an enhancing mural nodule is a diagnostic clue.
Currently classified as meningeal tumor of uncertain histogenesis (WHO, 2000)

Locaion:
90% posterior fossa (m/c) in that 80% cerebellar hemispheres, 15% Vermis, 5% in other places  fourth ventricle, medulla.
10% Supratentorium.
In ~ 60% of cases mass present as cyst + mural nodule and in ~ 40% of cases only as a solid nodule.

Imaging findings:
Cyst is clear, density on CT and signal intensity on MRI same as that of Csf, non enhancing thin imperceptible wall.
Mural nodule on CT may be iso to hyper dense, intense and homogenous enhancement. On MRI hypo to iso intense on T1, hyperintense on T2 and FLAIR. May see flow voids within the nodule with adjacent vascular feeders on T2w images, intense and homogenous enhancement on T1 images implies to its highly vascular nature. May show low signal intensity hemosiderin staining on GRE if associated to with any bleed.

Presentation is usually with headache, dysequilibrium, dizziness may be due to its mass effect and hydrocephalus.
Age : for sporadic: 40-60 yr and for familial : can occur at younger age. Slight male predominance.

Closest DD is Pilocytic Astrocytoma; mural nodule show mild to moderate enhancement not this intense, not characterized by flow voids and feeders. Seen in relatively younger age group.

Posterior cortical atrophy MRI

Clinically : progressive dementia, not responding to Csf drainage. 
Here is MRI BRAIN compared to previous MRI. 
FOLLOW UP MRI
PREVIOUS MRI DATED 8 JULY 2014
Salient feature of this MRI is bilateral posterior cortical atrophy.
There is moderate grade Atrophy involving bilateral parietal lobes, appears to be progressive as it has increased compared to previous MRI dated 8 July 2014. An associated marked mid brain atrophy. No obvious signal abnormality on diffusion weighted images.

Differential Diagnosis:
Benson's syndrome, an atypical variant of Alzheimer's disease.
Levy body dementia.

CJD.

Crossed cerebellar diaschisis MRI




Crossed cerebellar diaschisis

Refers to a depression in function, metabolism and perfusion affecting the cerebellar hemisphere as a result of contralateral supratentorial lesion.
This disturbance occures in a portion of the brain at a distance from the original site of injury but connected via white matter tracts.
Initially this phenomenon was defined as being caused by an acute lesion but now considered being related to a lesion of any temporal duration.
Other than neurological deficits and clinical features associated with the contralateral supratentorial lesion, this condition is generally asymptomatic.
This is a well-recognised phenomenon following cerebral infarction, although it can be a sequela of any significant supratentorial lesion like tumours, intracerebral haemorrhage, encephalitis , Dyke-Davidoff-Masson syndrome, Radiation necrosis etc.
There is no treatment for this phenomenon other than management of the supratentorial insult and prevention of further insults.