Approximate Normal ADC Values

Gray matter  - 0.85 +/- 0.13 x 10 e-3 mm2 / s

White Matter - 0.80 +/- 0.13 x 10 e -3 mm2/s

CSF   - 3.63 +/- 0.30

DIffusion Restriction Areas ~ 0.60 - 0.65

Proton MR Spectroscopy - ppm of Minor Metabolites

Metabolite                PPM

Valine
Leucine                         --->      0.9 ppm
Isoleucine

Alanine                          --->     1.48 ppm

Acetate                          --->     1.9 ppm

Succinate                      ---->     2.4 ppm

Lipid / Lactate              ---->     0.8 to 1.3 ppm


PS: To differentiate Lipids vs Lactate which occur at the 1.3ppm in the short TE acquisition, and additional TE = 135ms imaging is done in which the lipids do not invert.

       Pic F - Short TE                                           Pic G - Intermediate TE

Distinguishing the Amino acid peaks of Valine, Leucine and Isoleucine at the 0.9ppm and the lactate/lipid at 0.8-1.3ppm is important in distinguishing between Cystic Tumors (Both primary and mets) from Brain Abscesses - by doing the Intermediate TE (135ms) Spectroscopy, which causes the inversion of Aminoacids and lactate peak, but not of lipid.

Image showing the inversion of lipid in intermediate TE..

Fibrodysplasia Ossificans Progressiva

1. Bilateral Hallux Valgus - with malformed first metatarsal and phalanges.

2. Medial cortical thickening with formation of Pseudo-exostosis ( Calcification of Gracilis / Semitendinosus tendons).

3. Shortened first metacarpals

4. Usually the hetrotopic ossification begins in the soft tissues of neck, even after trivial trauma.

5. FNAC is contraindicated as it can result in permanent deforming ossification.

6. F.O.P is an AD disease with complete penetrance,, but with variable expressivity.

7. Can be diagnosed by the HALLUX VALGUS. Genetic testing is available.

8. Small vertebral bodies, enlarged pedicles, small spinal canal may be seen.

9. Starts by 2-5yrs, Death by 3rd decade by recurrent pulmonary infections due to prevention of expansion of thoracic cage (Impairing Respiration).

Causes of CT Bowel Fat Halo Sign

CT Bowel Fat Halo Sign

Seen in 

1. Chronic Inflammatory Bowel Disease

2. Cytoreductive therapy

3. GVHD.

4. Normal patients ~20% of normal, with increased BMI can have this sign positive.

"When seen in both the small and large bowel, the halo sign has been considered specific evidence of Crohn’s disease. When only the colon is affected, the degree and geographic distribution

of bowel wall thickness are signs used to distinguish ulcerative colitis from Crohn’s disease. '

(Gore RM, Balthazar EJ, Ghahremani GG, MillerFH. CT features of ulcerative colitis and Crohn's, AJR, 1996)

Fluid-blood levels in Intracranial Hemorrhage

Excerpt from the Stroke Article
ref: http://stroke.ahajournals.org/content/24/4/554.full.pdf

"The cause of lobar hemorrhage after fibrinolytic treatment remains puzzling. We speculate, but have
proof in only one patient, that the presence of amyloid angiopathy may be an important risk factor. We cannot exclude the possibility, however, of hemorrhage into a prior silent infarction as the mechanism in some of these patients. Long-standing hypertension has been specifically implicated as a risk factor for cerebral
hemorrhage.
However, the site of hemorrhage associated with hypertension is usually in the distribution of perforating vessels, not lobar.
Patients with hypertension alone usually have bleeding into sites such as basal ganglionic, posterior lateral thalamus, pons, and cerebellar hemispheres.
Patients with hypertension and lobar hemorrhages may have amyloid angiopathy as well.

One recent study of surgically treated patients with lobar hematomas indeed suggested that amyloid angiopathy is a major contributing factor. 

In two series of patients with lobar hemorrhage but without anticoagulant or fibrinolytic treatment, hypertension was found in only one third of the patients. Although hemorrhage into the cerebellum has traditionally been linked to hypertension, blood pressure was normal in our one patient with a massive vermis hemorrhage. Furthermore, one study claimed that vermis hemorrhages were relatively frequent in anticoagulated patients."

" We suspect, therefore, that cerebral amyloid angiopathy may be a contributing, if not crucial, factor in

fibrinolysis-associated hemorrhages. Intracerebral lobar hemorrhage is frequently associated with cerebral amyloid angiopathy in patients in the sixth or seventh decade of life. It encompasses multiple, usually superficially located, areas of hemorrhage on CT scans. Frontal or parietal lobe hemorrhages are common, but cerebellar and putaminal locations have been described in association with amyloid angiopathy. Recently, it was also noted that cerebral amyloid angiopathy associated with lobar intracerebral hemorrhage resulted in good outcome in the vast majority of patients."