External Hydrocephalus

Seen in infants with prominent subarachnoid spaces with little or dilatation of the ventricles.

• Idiopathic: 

                         Benign familial macrocephaly

• Hereditary:

                         Achondroplasia
                         Bechwith syndrome
                         Cerebral gigantism - Soto syndrome
                         Goldenhar syndrome
                         Weaver syndrome 

• Prematurity
• Trauma

                         NAI
                         Head injury - subdural haemtomas                      

• Infection

                         Meningitis

• Systemic

                        Increased venous pressure

Reference:
Maytal J et al. External hydrocephalus: radiologic spectrum and differentiation from cerebral atrophy. AJR June 1, 1987 vol. 148 no. 6 1223-1230

Checklist: Post Rx imaging of head and neck cancers

Clinical information:
Histopathology:
TNM staging:
Surgery: Radical/ modified radical neck dissection, laser, no surgery
Reconstruction surgery: yes/ no
If yes, flap details:
Radiotherapy: yes/ no
If yes, type of radiotherapy

Primary site review:
Residual disease/ recurrence/ post-op change
Radiation induced sarcoma: latent period is 5 years, radiation induces SCC, lymphoma and meningioma

Post RT changes:
Acute post-RT changes (within 2-4 weeks): skin, platysma, neck space edema, enhancing salivary glands, enhancement of mucosal lining, increased attenuation of paralaryngeal fat
Subacute post-RT changes (few months to 18 months): chronic mucositis (polyps), chronic sialadenitis, i.e, loss of volume (virtually in ALL), especially parotids, fibrosis (may or may not enhance, stop enhancing after 18 months), persistent reactive nodes

Radionecrosis:
Sites: larynx, mandible, temporal bone, basisphenoid, maxillary bone
6- 15 months
Sclerosis, fragmentation, mottled appearance, sloughing, break of cartilage and bone with sequestration, pathological fracture, loss of trabeculae. Subluxation/ dislocation (of arytenoids). Soft tissue thickening, abscess, fistula, gas in the soft tissue. Enhancement of the adjacent muscles and fat.

Neurological changes:
Radiation cerebral necrosis: Deep white matter of medial and inferior temporal lobes or frontal lobes (depending on site of RT)
Brainstem encepahlopathy, myelopathy and transverse myelitis
RT induced brachial plexopathy
Traumatic neuroma
Denervation od V, XI and XII nerves





Reference:
Post-treatment imaging appearances in head and neck cancer patients

Staging Sarcoidosis

CXR:
Stage 0: normal
Stage 1: hilar and/or mediastinal lymphadenopathy (resolve in 65%)
Stage 2: hilar and/or mediastinal lymphadenopathy and visible lung disease (resolve in 50%)
Stage 3: Lung disease only (resolve in 20%)
Stage 4: End stage fibrosis (irreversible)

Interstitial lung disease: Simplified approach

Most common ILD: idiopathic interstitial pneumonia (idiopathic pulmonary fibrosis). Always keep sarcoidosis in the differential, before you are fairly sure of other diagnosis. Few ILDs have characteristics (or even pathognomonic) features, although they are rare. Othe rare ones with no typical HRCT features are rare, who cares?

HISTORY:
Get the clue from history, which is unfortunately seldom given on the radiological request form. Dig the history from clinical notes. Clinicians seldom give this information to radiologists.

Exposure related:

Smoking: look for respiratory bronchiolitis-related ILD

Occupuation related:

Farmer: hypersensitivity pneumonitis

Medication related:

Many drugs cause ILD. Refer books if you find long term medication of any drugs to see if they cause ILD.

Connective tissue disorder, arthropathies, inflammaroty bowel disease:

If the referral has come from rheumatologists, the patient is likely to have at lest suspected connective tissue disorder.

Characteristic HRCT features:
Sarcoidosis: bilateral symmetrical mediastinal and/or hilar lymph nodes and/or fissural beading
Asbestosis: calcified and non-calcified pleural plaques with bibasal ILD
Lymphangioleiomyomatosis/ tuberous sclerosis: child bearing woman with numerous diffuse cystic areas!
Pulmonary alveolar protenosis: diffuse mosaic ground glass crazy paving pattern without fibrosis.
Chronic hypersensitivity pneumonitis: UIP pattern with centrilobular nodules, sparing the lung bases

Typical patterns in CTDs:
Most common pattern in CTD: NSIP, next UIP
Rheumatoid arthritis: UIP, less common - NSIP
Scleroderma/ systemic sclerosis: fibrotic NSIP
Polymyositis: NSIP or organising pneumonia
Sjogren's: LIP
Dermatomyositis/ polymyositis: NSIP, less common - organising pneumonia
Mized collagen vascular disorder: NSIP

Diagnosis to be considered in a smoker:
Never miss a lung tumor on HRCT!
Histiocytosis: centrilobular fine nodules of 1-10mm and cysts in upper zones with relative sparing of lower zones. Stop smoking = good prognosis
RB-ILD:
Histopathological diagnosis on HRCT!:
UIP/ IPF: Bibasal zones peripheral reticulation, honeycombing, fibrosis. Ground glass is less than reticulation. UIP pattern is seen in asbestosis, CTD (especially RA), drug toxicity, sarcoid, chronic hypersensitivity pneumonitis (centrilobular nodules and sparing of bases)
NSIP: Bibisal peripheral symmetric ground glass opacity. Honeycombing uncommon.
COP: Non-smokers more than smokers! subpleural, peribronchial and/or perilobular consolidation. Air bronchogram. ground glass opacity. Smooth well defined "reverse halo" nodules (reverse halo is also seen in Wegeners').
AIP: patchy bilateral anteroposterior increasing ground glass opacity with lobular sparing. Looks similar to ARDS, but clinically not.
RB-ILD: Occurs always in smokers. Cntrilobular nodules, pathcy ground glass, bronchial wall thickening, with added centrilobular emphsema.
DIP: Rare. Common in smokers. Bilateral ground glass predominantly mid and lower zones. Reticulations and honeycombing may be seen.
LIP: a/w Sjogren's, PBC. Bilateral groound glass, thin preivascular cysts, centrilobular nodules, mild reticulations.

Reference: 
1.  Interstitial lung disease, Seminars in roenthenology volume 45, no 1

Diffusion weighted images

Basics:
Bright signal on DWI (B=1000) means restricted diffusion and/or T2 effect.
On ADC, low signal in the same region means restricted diffusion, and bright or isointense signal means T2 shine through effect.
On T2,  the same area may appear bright or isointense.

Pathologies with restricted diffusion:
Acute stroke, acute stroke, acute stroke... (repeat this 10 times before proceeding to next)
Infection: Herpes encephalitis, Pyogenic infection, CJD, meningoencephalitis
Epidermoid (ADC usually cannot be calculated)

Diffuse axonal injury
Oxyhemoglobin (intracellular and hyperacute) (extracellular methHb shows increased signal on both DWI and ADC!)

A few acute MS lesions
Post-ictal
Susceptibility artefact: in inferior frontal and temporal regions should not be mistaken for restricted diffusion


Non-restricted diffusion:
Infection: HIV encepahlopathy
Tumor: primary or secondary, arachnoid cyst
Inflammation: most acute MS lesions
Chronic lesions: chronic stroke, gliosis, neuronal loss
Others: hypertensive encephalopathy, clyclosporin toxicity, hyperperfusion after endartertectomy

List of diseases involving Hoffa's fat

Hoffa's disease
Intracapsular chondroma
Localized nodular synovitis
Post artthroscopy fibrosis
Shear injury
Intraarticular loose bodies
Meniscal cyst
Ganglion cyst
Cylops (arthrofibrosis)
PVNS
Hemophilia
Synovial hemanagioma
Synovial chonromatosis
Lipoma arborescens
Synvoial proliferation in inflammatory arthritis

Stable vs unstable fracture of the vertebrae

Unstable:
neurologic deficit
loss of 50% of vertebral body height
fracture dislocation
angulation of the thoracolumbar junctionmore than 20 degree
canal comprimisemore than 30 percent

Stable:
neurologically intact
posterior arch remains intact