PAGE LIST

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

Clinically young female with psychiatric complaints like altered behaviors and generalized weakness.

MRI FLAIR images of brain shows bilateral fronto parietal and temporal peri ventricular confluent T2 hyper intensities. DDs given were Viral encephalitis like HIV encephalitis, ADEM, Toxic Metabolic encephalopathy. MRI screening of spine shows no obvious spinal cord involvement.

Lab report showed significantly low level of Vit B12 suggestive of isolated brain involvement in B12 deficiency. Patient improved with Vit B12 supplements.

Vitamin B12 deficiency 

Vitamin B12 or Cobalamin deficiency causes a wide range of hematological, gastrointestinal, psychiatric and neurological disorders.
Neuropsychiatric symptoms may precede hematologic signs and are represented by myelopathy, neuropathy, dementia and visual loss due to optic nerve atrophy. 

Causes 
A strict vegetarian diet contains very little cobalamin. There is clear evidence of abnormal cobalamin metabolism in vegetarians and hyper-homocysteinemia is a risk factor, especially for stroke and vascular dementia, vegetarians are advised to take cobalamin supplements lifelong.
In developed countries, the diet is rich in meat and cobalamin-rich foods; thus, malabsorption is the most common cause of cobalamin deficiency. 
Infants born to vegetarian mothers are at risk of cobalamin deficiency and may present with megaloblastic anemia.

Clinical and Hematological Manifestations ranges from incidental increased mean corpuscular volume and neutrophils hypersegmentation in otherwise asymptomatic patients to symptoms due to severe anemia, such as angor, dyspnea on exertion, fatigue or symptoms related to congestive heart failure, such as ankle edema, orthopnea and nocturia. 

Neuroimaging
Vitamin B12 deficiency may affect both the central (brain, spinal cord and optic nerve) and the peripheral (peripheral nerves) nervous system.
The spinal cord involvement is associated with the most frequent manifestation of vitamin B12 deficiency, namely subacute combined degeneration (SCD), is characterized by symmetric dysesthesia, disturbance of position sense and spastic paraparesis or tetraparesis. The most consistent MRI finding is a symmetrical abnormally increased T2 signal intensity, commonly confined to posterior columns in cervico dorsal spinal cord ' inverted V' configuration. 

Isolated brain involvement has also been reported in B12 deficiency but is rare in adults. 
MRI shows confluent T2 high-intensity signal in periventricular white matter.
Isolated brain involvement is common in children with inherited cobalamin-related diseases characterized by white matter loss with delayed myelination.
In infants with nutritional cobalamin deficiency MRI has revealed delayed myelination.

Therapy is definitely Vitamin B12 supplements oral or intra muscular. 

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.

For similar case : Click here