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  1. These, in newborn are most commonly linear and simple but may occasionally br depressed without a fracture line, a so-called 'ping-pong' or pond fracture.Q
  2. QGrowing skull fractures (leptomeningeal cysts) usually occur after severe head injuries early in life. The dura matter underlying a linear fracture is torn.
  3. ‘Blow-out’ fracture usually involve the orbital floor with ‘trap-door deformity’ on skull AP view and CT is best technique to study orbital fractures.




1–4% overall

10–20% overall


Associated # in 85-95% cases.

Stretching, tearing of bridging


QLacerated middle meningeal

cortical veins


artery/dural sinus in 70 to 85%



cases & venous "OOZE" or MMA



tear without # in 15% cases only



Between skull & dura. Q Cross dural

Between dura and arachnoid.


attachments but not sutures. 95%

Cross sutures but not dural


supratentorial, 5% bilateral

attachment. 95% supratentorial,



15% bilateral


CT: Biconvex displaced gray-white



interface. 2/3 hyper-dense, 1/3

a) Acute SDH: Crescentic. 60%



hyper-dense, 40% mixed



b) Subacute SDH: May be



nearly isodense with cortex






vessels may enhance.



c) Chronic SDH: Hypodense



with enhancing membrane. May be



loculated. Rehemorrhage



can cause mixed density.



1–2% of very old SDH calcify



Epidural hematoma is a surgical emergency. It is usually caused by an arterial injury (most commonly the middle meningeal artery), often associated with temporal bone fracture, confined by the lateral sutures, and usually lenticular in shape on imaging. Q

Subdural hematoma is usually caused by injury to the bridging cortical veins, is not confined by the lateral sutures, and is usually crescentic in shape on imaging. Q

  1. MR signal characteristics of intracerebral haemorrhage (according to bradley)
Stage Form of haem iron T1-weighted MRI T2-weighted MRI
Hyperacute (first few hours) Oxyhaemoglobin Iso- or hypointense Slightly hyperintense
Acute (1–3 d) Deoxyhaemoglobin Slightly hypointense Hypointense
Early subacute (3–7 d) Intracellular methaemoglobin Hyperintense Hypointense
Late subacute (1–4 weeks) Extracellular methaemoglobin Hyperintense Hyperintense
Chronic Haemosiderin Iso- or hypointense Markedly hyperintense
  1. QCT diagnostic criteria of diffuse axonal injury (DAI):
    1. Single or multiple small intraparenchymal hemorrhages in the cerebral hemispheres (< 2 cm in diameter)
    2. Diffuse cerebral edema with compression of basal cisterns
    3. Intraventricular hemorrhage;
    4. Hemorrhage in the corpus callosum;
    5. Small focal areas of hemorrhage adjacent to the third ventricle (< 2 cm in diameter);
    6. Brain stem hemorrhage.

Q MRI is best for diagnosis of DAI.

  1. Q Ring-enhancing lesions in Brain on CT scan:
    1. Cerebral abscess (73%)
    2. Epidural/subdural empyema
    3. Tuberculoma (regular or irregular ring with or without central/target enhancement is characteristic; however, MRI may be able to differentiate it from neurocysticercosis)
    4. Neurocysticercosis (especially in colloidal and granular-nodular stage)
    5. Toxoplasmosis (especially in HIV)
    6. Metastasis (33%)
    7. Glioblastoma multiforme (48%)
    8. Resolving infarct/hematoma
    9. Adiation necrosis
    10. Lymphoma
    11. Demyelinating disease
    12. Other brain tumors which may show are glioma (high grade), meningioma, leukemia, Craniopharyngioma, acoustic neuroma, abnormal pituitary
  1. Neurocysticercal cysts in brain : 
    CT Brain Axial Postcontrast image : Ring enhancing lesion with enhancing scolex within.

CNS tuberculosis :
  1. Axial MR Postcontrast image :
    1. Diffuse lepto and pachymeningeal enhancement especially in basa cisterns suggestive of meningitis, mostly tubercular.
    2. Multiple ring as well as disc enhancing lesions in brain parenchyma s/o Tuberculomas.


  1. Phakomatosis
    1. Von Hippel–Lindau (VHL) disease is a rare, autosomal dominant genetic condition that predisposes individuals to benign and malignant tumours.
      1. The most common tumours found in VHL are central nervous system and retinal hemangioblastomas, clear cell renal carcinomas, pheochromocytomas, pancreatic neuroendocrine tumours, pancreatic cysts, endolymphatic sac tumors and epididymal papillary cystadenomas VHL results from a mutation in the von Hippel–Lindau tumor suppressor gene on chromosome 3p25.3
    2. Tuberous sclerosis or tuberous sclerosis complex (TSC) is a rare multi-system genetic disease that causes benign tumors to grow in the brain and on other vital organs such as the kidneys, heart, eyes, lungs, and skin.
      1. A combination of symptoms may include seizures, intellectual disability, developmental delay, behavioral problems, skin abnormalities, lung and kidney disease.
      2. TSC is caused by a mutation of either of two genes, TSC1 and TSC2, which code for the proteins hamartin and tuberin respectively. These proteins act as tumor growth suppressors, agents that regulate cell proliferation and differentiation.
Important Features:
  1. Brain: calcified subependymal nodules, cortical tubers, subependymal giant cell astrocytomas
  2. Eyes: astrocytic hamartomas
  3. Heart:rhabdomyomas
  4. Lung:lymphangiomyomatosis
  5. Kidneys: Angiomyolipomas
  1. Sturge-weber syndrome
    1. a congenital disturbance that produces facial cutaneous angiomas with a distinctive and easily recognized appearance, along with intracranial abnormalities such as leptomeningeal angiomas.
    2. Persons with the syndrome may be mentally retarded and often exhibit hemiparesis or hemiatrophy on the side of the body opposite the port-wine nevus.
    3. Both men and women may be affected and seizures may develop in affected persons.
    4. The nevus associated with sturge-weber syndrome usually extends over the sensory distribution of cn #6, the first division of the trigeminal nerve.
    5. The lesion usually stays to one side of the face. Affected persons will usually also have an angioma of the choroid of the eye.
    6. Intracranial angioma is unlikely if the nevus does not involve the upper face. Deficits develop as the person matures and may be a consequence of focal ischemia in the cerebral cortex that underlies the leptomeningeal angioma.
  1. Primary Intracranial Tumors
    Essentials of Diagnosis
    1. Many different cell types; prognosis upon which one; half are gliomasQ
    2. Most present with generalized or focal disturbances of cerebral function: generalized symptoms include nocturnal headache, seizures, and projectile vomiting; focal deficits relate to location of the tumor
    3. CT or MRI with gadolinium enhancement defines the lesion; posterior fossa tumors are better visualized by MRIQ
    4. Biopsy is the definitive diagnostic procedure, distinguishes primary brain tumors from brain abscess and other intracranial spaceoccupying lesions such as metastases
  2. Specific types:
    1. Glioblastoma multiforme:
      1. in strictest sense an astrocytoma, but rapidly progressive with a poor prognosis
    2. Astrocytoma:
      1. More chronic course than glioblastoma, with a variable prognosis
    3. Medulloblastoma:
      1. seen primarily in children and arises from roof of fourth ventricle
    4. Cerebellar hemangioblastoma:
      1. patients usually present with disequilibrium and ataxia, and occasional erythrocytosis
    5. Primary cerebral lymphoma:
      1. Usually in AIDS and other immunodeficient states, though may occur rarely in immunocompetent individuals.
Brain tumors may be seen as a cystic lesion with enhancing mural nodule on ct/mr imaging:
  1. Hemangioblastoma
  2. Ganglioglioma
  3. Pilocytic Astrocytoma
  4. Glioblastoma Multiforme
  5. Pleomorphic Xanthoastrocytoma

Some important brain tumors

  1. Meningioma (the most common extra-axial brain tumor)
    1. It is derived from "arachnoid cap cells"
    2. Peak incidence 45 years (30–75 yrs)
    3. M:F = 1:2 to 1:4
    4. Associated with neurofibromatosis type 2 and basal cell nevus syndrome
    5. Histological types:
  • Fibroblastic
  • Transitional
  • Meningothelial / syncitial
  • Angioblastic (malignant)
It can also be classified as:
  1. Globular (most common)
  2. Enplaque
  3. Multicentric
About 90% are supratentorial
  1. Convexities of lateral hemispheres (most common site/type of meningioma)
  2. Parasagital
  3. Sphenoid ridge and middle cranial fossa
  4. Frontobasal at olfactory groove
Imaging features
CT scan
  1. Extraaxial sol (hyperdense/isodense)
  2. Cortical buckling
  3. Calcification (circular/medial pattern)
  4. Hyperostosis of adjacent bone
  5. Intense uniform enhancement on cect
  1. Hypo-to isointense on T1W1 and iso to hyperintense on T2W1
  2. Dural tail sign (curvilinear area of enhancement)
  1. "Mother-in-Maw" sign (contrast media shows up early and stays late into venous phase)
  2. "Sunburst/spoke-wheel" pattern of tumor vascularity with hypervascular cloud like stain.
  1. Vestibular schwannoma
    1. Tumors origination from cranial nerves account for 6-8 % of primary intracranial tumors and most are benign neoplasms arising from schwan cell (schwannomas) of the nerve sheaths.
    2. Vestibular schwannoma arises eccentrically from the sheath and compress the parent nerve rather than invading it.
    3. It is the most common cp angle tumor, followed by meningioma and epidermoid cyst
    4. All cranial nerves except I and II, which are in fact white matter tracts of the cerebrum, have nerve sheaths, but schwannomas usually grow on the sensory nerves, most frequently from the superior vestibular division of vestibulocochlear nerve (acoustic neuroma) and with decreasing frequency, from trigeminal, glossopharyngeal and lower cranial nerves. Pure motor cranial nerves rarely form schwannomas.
    5. Multiple cranial nerve schwannomas are found in neurofibromatosis type 2 and bilateral vestibular schwannomas are pathognomonic (sine qua non) of NF-2. Recently, NF-2 is called as misme complex (multiple inherited schwannomas, meningiomas and ependymomas). Cranial nerve tumors almost invariably show marked contrast enhancement.
    6. Acoustic (vestibular) schwannomas (neuromas) account for 80% of cerebellopontine lesions
  2. Oligodendroglioma
    1.  Uncommon glioma constituting 2–5% of all primary brain tumors
    2.  Peak age to get affected being 35–45 years.
    3.  Frontal lobes are most commonly involved.
    4. Imaging features:
  • It is the most common intracranial tumor to calcify.
  • ‘Nodular or clumped’ calcification is seen in 70 90% of all cases.
  • Heterogeneous partially calcified mixed density
  • Hemispheric mass that often extends peripherally to cortex.
  • Overlying skull may show pressure erosion.
  • Cystic degeneration is common.
  • Necrosis or gross hemorrhage rare.
  • Mild/moderate non-homogenous enhancement is common.
Commonest of CNS Tumours      
Most common primary CNS neoplasm Glioblastoma multiforme
2nd Most common primary CNS neoplasm Meningioma
Most common intracranial germ cell tumor Germinoma
Most common Mixed glioma Oligo-astrocytoma
Most common Site of Schwannoma Vestibular division on VIIIth nerve
Most common Intracranial tumour in neonates Teratoma
Most common primary intracranial neoplasm in sellar / parasellar region Pituitary adenoma
Most common intraaxial posterior fossa tumor in adults Metastasis from extracranial sites
Most common of all primary intracranial neoplasms Glioblastoma multiforme
Most common supratentorial neoplasm in adults Glioblastoma multiforme
Most common intracranial tumour to calcify Oligodendroglioma
Most common site of cellular ependymoma in brain 4th ventricle
Most common nonglial primary brain tumour Meningioma
Most common intracranial extraaxial tumour Meningioma
Most common Spinal extradural neoplasm Metastasis
Most common benign spinal neoplasm Vertebral hemangioma
Most common malignant extradural neoplasm Metastasis
Most common spinal intramedullary tumour in adults Ependymoma
Most common spinal intramedullary tumour in children Astrocytoma

Primary tumours in the sellar and parasellar region
Tumour Typical features
Pituitary macroadenoma Enlarged sella turcica, strong enhancement, sometimes haemorrhage
Meningioma Broad dural base, enhancement along planum sphenoidale
  Hyperostosis, ‘blistering’ of sphenoid sinus, dural tail sign, mother in law phenomenon
Schwannoma T1-hypo- and T2-hyperintense, strong enhancement but heterogenous
Chordoma Bone destruction on CT, heterogeneous signal and enhancement on MRI, seen in clivus and sacrum
Chondrosarcoma Bone destruction and calcification on CT, T2 hyperintense on MRI
Crangiopharyngioma Calcification, cysts, nodular enhancement
Rathke's cleft cyst T1-hyperintense on MRI, smooth peripheral enhancement
Dermoid Hypodense on CT and T1 hyperintense on MRI
Epidermoid Isodense to CSF on CT and isointense to CSF on T1 and T2 weighting, brighter than CSF on FLAIR and DWI
Tuber cinerum Grey matter isointense on T1 weighting and T2 hamartoma hyperintense
Optic glioma Thickening of chiasm, spread along optic pathways
Germ cell tumours Located in midline, intense enhancement; can be synchronous with pineal germinomas

Spine Imaging:
Low back pain  
  No neurologic deficits   MRI or CT after 4 weeks
  With focal deficits   MRI > CT
  Spinal stenosis   MRI or CT
  Cervical spondylosis   MRI or CT myelography
  Infection   MRI + contrast, CT
  Myelopathy   MRI + contrast > myelography
  Arteriovenous malformation   MRI, myelography/angiography

Quick specifics – CNS
Sutural diastasis
Copperbeaten skull
Raised intracranial tension
Bracket calcification Lipoma of corpus callosum
Dawson fingers on Brain MRI Multiple sclerosis
Tram track / Rail road track gyriform cortical calcifications Sturge weber syndrome
Hyperdense MCA sign
Insular ribbon loss sign
Light bulb sign on MR Diffusion
Acute stroke
Pseudodelta sign
Cortical vein sign
Sugar icing appearance
Zuckerguss appearance
Dural tail sign
Mother-in-law sign
Sunburst / Spoke wheel tumour vascularity
Geographic lytic skull
Vertebra plana
Eosinophilic granuloma
Multiple punched out lesion in skull vault Mutiple myeloma
Hair-on-end skull vault Thallasemia
Picture frame vertebra Paget's disease
Fish mouth vertebra Sickle cell anemia
Bat wing 4th ventricle
Molar tooth sign
Joubert syndrome
Boxcar ventricles Huntington's disease
Clower leaf skull Thanatophoric dysplasia
Cord sign
Empty delta sign
Intracranial dural sinus thrombosis
Corduroy appearance
Polka dot appearance
Intravertebral hemangioma
Eye of the Tiger sign Hollaverden Spatz syndrome
Flat tyre sign
Umbrella sign
Ruptured globe
Figure of 8 appearance Pachygyria
Fish vertebrae Sickle cell disease
Hot cross bun sign Multisystem atrophy
Inverted Napolean hat sign Spondylolisthesis
Scottie-Terrier dog sign Spondylolysis
Mount Fuji sign Tension pneumocephalus
Reversal sign Anoxic brain injury
Salt and Pepper pattern Vascularity in Glomus tumors
Sandwich vertebra Osteopetrosis
Strawberry skull on antenatal USG Trisomy 18
Tau sign Persistent trigeminal artery

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