Radiology | Medicine-3 Dr. Jose P.

Rizal School of Medicine Xavier University – Ateneo de Cagayan

Normal Cranial CT/MRI
Aubrey A. Encong

CT scan
• Technique of choice
– Acute trauma – Acute intracranial hemorrhage – Diseases, base of the skull – With contraindications to MRI

Normal CT scan of the head; this slice shows the cerebellum, a small portion of each temporal lobe, the orbits, and the ethmoid sinuses.

LEGEND: + - border of maxillary sinus, * - maxillary sinus ostium, U - uncinate process, E - ethmoid sinuses, IT- inferior turbinate, MT- middle turbinate, S - septum, C - concha bullosa.

MRI

• Preferred technique for diagnostic evaluation of most pxs with neurologic disease

Axial

sagittal

frontal

Arteries and Veins of the Head
Christine L. Namoc

Arteries of the Head
Common Carotid Artery – divides into:
Internal Carotid Artery supplies the brain
Opthalmic artery Post. Communicating artery Anterior cerebral artery Middle cerebral artery

Arteries of the Head
External Carotid Artery supplies structures external to the skull
Superior thyroid artery Ascending pharyngeal artery Lingual artery Facial artery Occipital artery Posterior auricular artery Superficial temporal artery Maxillary artery

Circle of Willis middle Right
cerebral artery

Ant. Cerebral artery Left middle cerebral artery Ant. Communicating artery Posterior cerebral artery Post. Communicating artery Internal Carotid Artery

Basilar artery
External Carotid arteries Common Carotid Arteries

Veins of the Head
Veins of the brain
Cerebral veins Cerebellar veins Veins of brainstem

Diploic veins Emissary veins

Veins of the sinuses
Superior sagittal Inferior Straight Transverse Sigmoid Occipital Cavernous Superior and inferior petrosal

Veins of the Head
External Jugular Vein
Posterior external jugular vein Superficial cervical vein Suprascapular vein Anterior jugular vein
Internal Jugular Vein
Inferior petrosal sinus Facial vein Pharyngeal veins Lingual vein Superior thyroid vein Middle thyroid vein

Circle of Willis
Anastomosis between branches of 2 internal carotid arteries and the 2 vertebral arteries Arteries involved:
Anterior communicating Anterior cerebral Internal carotid Posterior communicating Posterior cerebral Basilar (formed by junction of 2 vertebral arteries)

Normal MR arteriogram, axial slab, through the circle of Willis

MR arteriogram demonstrating markedly diminished left middle cerebral artery flow as a result of

Normal MR venogram, median sagittal slab

MR venogram demonstrating lack of flow in the superior sagittal and straight sinuses because of dural sinus thrombosis

Cranial Nerves
Kenneth Nomer E. Escalante

Cranial Nerves
I II III IV V Olfactory Optic Occulomotor x Trochlear Trigeminal Opthalmic Maxillary Mandibular Abducens Facial Vestibulocochlear Glossopharyngeal Vagus Spinal Accessory Hypoglossal Cribriform Plate of Ethmoid Optic Canal Superior Orbital Fissure Superior Orbital Fissure Superior Orbital Fissure Foramen Rotundum Foramen Ovale Superior Orbital Fissure Internal Acoustic Meatus Facial Canal Stylomastoid Foramen Internal Acoustic Meatus Jugular Foramen Jugular Foramen Jugular Foramen Hypoglossal Canal

VI VII VIII IX X XI XII

Skull, from the front
Supraorbital foramen Frontal bone Frontal Notch Glabella Nasion

Orbit

Infraorbital margin Infraorbital foramen

Foramen magnum Occipital condyle Jugular foramen

Carotid canal

Foramen lacerum

Palatine bone

Foramen ovale

Foramen spinosum

Foramen ovale

Foramen spinosum

Foramen lacerum

Jugular Foramen

Occipital bone

Parietal bone

Midbrain (Ventral)
Optic Nerve (CN II)

Optic Tract

Optic Chiasma

Mamillary body
(not part of midbrain)

Cerebral peduncle Interpemdicular fossa

Trochlear Nerve (CN IV)

Occulomotor Nerve (CN III)

Pons (Ventral)
Superior pontine sulcus Trigeminal Nerve (CN V) Eminentia pyramidalis Vestibulocochlear Nerve (CN VIII) Sulcus basilaris Facial Nerve (CN VII) Inferior pontine sulcus

Abducens Nerve (CN VI)

Medulla (Ventral)
Glossopharyngealn erve (CN IX) Inferior pontine sulcus Pyramids Olivary body Post-olivary sulcus Pre-olivary sulcus Hypoglossal nerve (CN XII) Pyramidal decussation Anterior median fissure

Vagus nerve (CN XI)

Spinal accessory nerve (CN XI)

Olfactory Bulb, Nerve

• Originates as the central process of the olfactory receptor nerve cells in the mucus membrane above the superior concha • Bundles of nerve fibers pass through openings in the cribriform plate of Ethmoid • Ends in the Olfactory Bulb in the anterior canial fossa • The Olfactory tract runs from the posterior end of the Olfactory bulb towards the olfactory area in the cerebral cortex

• MRI of the brain pre and post gadolinium demonstrates a T1 dark, T2 intermediate to hyperintense lesion emanating from the anterior cranial fossa into the left nasal region with moderate, homogeneous contrast enhancement. There is also a T1 dark, T2 bright signal present in the left maxillary sinus, sphenoid sinus, and the left frontal ethmoid recess, which demonstrates a peripheral rim of enhancement.

Optic Nerve

• Optic nerve Leaves the orbital cavity through the Optic Canal with the Ophthalmic Artery • Optic nerves on both sides join into the Optic Chiasma • Optic Tract emerges from the lateral sides of the chiasma and passes through the lateral side of the midbrain to the lateral geniculate body and then to the optic radiation • Optic radiation curved backwards to the visual cortex

Optic Schwannoma

Occulomotor, Trochlear, Abducens

• Occulomotor nerve emerges from the anterior midbrain and divides into superior and inferior rami which enter the orbit through the Superior Orbital Fissure • Trochlear nerve emerges from the posterior midbrain, lies below the Occulomotor and enters the orbit through the Superior Orbital Fissure • Abducens emerges from the anterior midbrain and enters the orbit through the Superior Orbital Fissure

Trigeminal

Trigeminal Neurilema

Facial

Vestibulocochlear

Acoustic Schwannoma

• • • • • • •

• •

BrainTF10-Acoustic Schwannoma Clinical Profile: There was a H/O decreased hearing and tinnitus on the left side with headaches.  Findings: There is evidence of an extra-axial mass lesion located in the cerebellopontine angle cistern with an intracanalicular component. This lesion is of intermediate signal intensity on the T1W images and enhances intensely after contrast administration.     Discussion:  They account for approximately 7% to 8% of all primary intracranial tumors. They usually arise from the vestibular portion of the eighth cranial nerve. When bilateral, they are usually associated with neurofibromatosis type II. They usually involve the intracanalicular portion of the nerve (20% do not have an intracanalicular component). A mass may also be seen in the cerebellopontine angle cistern. MRI:     On the T1W images, the lesions are usually hypointense or of intermediate signal and show variable signal pattern on the T2W images. They are usually well demarcated from CSF, more so on the MR cisternogram images. Cystic and hemorrhagic changes are more commonly seen, than in meningiomas. Focal/nodular calcifications may be seen. Widening of the internal auditory canal may be seen. The lesion usually shows homogeneous contrast enhancement. Occasional inhomogeneous contrast enhancement may be seen. Tumors without an intracanalicular component may be difficult to differentiate from a meningioma. 

Glossopharyngeal

Vagus

Spinal Accessory, Hypoglossal

Neural Tube Disorders
Josie Mae N. Taghoy

• Cause: incomplete development of the brain, spinal cord and/or their protective coverings • Occurs when the fetus' spine fails to close properly during the early stages of pregnancy (first 28 days). • Accdng to the Spina Bifida Association of America (SBAA), spina bifida is the most common NTD. • Other types: anencephaly and encephaloceles

• Has the best prognosis • Spine fails to close properly during the first few weeks of pregnancy, causing damage to the nerves and spinal cord. • No cure • Prognosis depends largely on the number and severity of abnormalities • Outlook is poorest for those with complete paralysis, hydrocephalus and other problems.

SPINA BIFIDA

A. Surface of the myelomenigocele has become covered with skin through secondary epithelization from the margins of the defect B. Sagittal T1-weighted MR demonstrates features of untreated myelomeningocele: dehiscence of high signal subcutaneous fat (F), fascia, muscle, and bone in the zone of spina bifida; low position of the spinal cord (C); acute angulation (arrow) of the cord under the last intact lamina at the upper margin of the spina bifida; and posterior herniation of the neural tissue (white arrow-heads) forming the dorsal wall of the cerebrospinal fluid space (S) that protrudes through the spina bifida. This patient also exhibits thoracolumbar kyphos.

Repaired myelomeningocele with epidermoid inclusion, 4 year old child. Sagittal T1-weighted (A) and T2weighted (B) MRI disclose a repaired lumbosacral myelomeningocele. The low-lying spinal cord (c) is tethered inferiorly by a mass (arrowhead) that is nearly isotense to the cord on the T1- and T2-weighted images. Closure of the sac has created dorsal fluid compartments with restricted communication. Such compartments appear brighter on T2-weighted images because of reduced dispersal of signal by the cerebrospinal fluid pulsations and perhaps because of higher protein concentrations within them.

Spina bifida patient with a congenital kyphosis (Gibbus) deformity.

ANENCEPHALY

ENCEPHALOCELE

HYDROCEPHALUS

Chiari Malformation s
(kee-AR-ee)
Paul Carlo P. Araneta Maureen Irish C. Sambaan

What are Chiari malformations?
 Chiari malformations (CMs) are structural defects in the cerebellum  Normally the cerebellum and parts of the brainstem sit in an indented space at the lower rear of the skull, above the foramen magnum  When part of the cerebellum is located below the foramen magnum, it is called a Chiari malformation

How does it develop?
 CMs may develop when the bony space is smaller than normal, causing the cerebellum and brainstem to be pushed downward into the foramen magnum and into the upper spinal canal

What causes these malformations?
 Structural defects in the brain and spinal cord that occur during fetal development – called primary or congenital CM  Later in life if spinal fluid is drained excessively from the lumbar or thoracic areas of the spine either due to injury, exposure to harmful substances, or infection – called acquired or secondary CM  Primary CM is much more common than secondary CM

Classification Type I involves the extension of the cerebellar tonsils (the lower part of the cerebellum) into the foramen magnum, without involving the brainstem Type II, also called classic CM, involves the extension of both cerebellar and brainstem tissue into the foramen magnum Type III is the most serious form of CM.  The cerebellum and brainstem protrude, or herniate, through the foramen magnum and into the spinal cord Type IV involves an incomplete or underdeveloped cerebellum — a condition known as cerebellar hypoplasia

Cephaloceles

Candy T. Cahilog Livey A. Aleria

Cephalocele refers to a defect in the skull and dura with extracranial herniation of intracranial structures.

1-3 in 10,000 live births
• incidence of occipital cephaloceles to be 70 – 90% of all cephaloceles

Development attributed to:
failure of primary neurulation (Van Allen) result of a postneurulation event in which the brain tissue herniates through a defect in the mesenchyme that is to become the cranium and dura (Gluckman, et al)

US - for antenatal diagnosis CT - demonstrates the osseous defect MR- definitive role in demonstrating contents of
the sac

MR venogram - shows the assoc. venous sinus
abn

4 Types based on Contents
Meningoencephaloceles Meningocele Atretic cephaloceles Glioceles

Ultrasound images (sagittal and axial sections) showing a cystic mass placed in the anterior part of the ethmoid bone (arrow).

3D ultrasound view of the fetal face (29 weeks)

Thin axial T2 weighted FSE images shows mixed intensity tissue within the cephalocele.

Axial T2 weighted images of the posterior fossa reveal abnormal band of tissue surrounded by CSF extending from the brainstem to

Corpus Callosum Anomalies
Kelvin C. Nacalaban Yasmin Grace Y. Lao

Agenesis of the Corpus Callosum
• Absence (may be complete or partial) of the corpus callosum • Etiology – Disturbance of embryogenesis in the first trimester of gestation by some unknown insult leads to failure of the callosal axons to pass across the midline.

• Its incidence is usually sporadic; may be increased in patients with Trisomy 8, 13, and 18. • Associated with other diseases: Dandy-Walker Malformations, Lipomas, Arnold-Chiari Malformation, Hydrocephalus, etc.

MRI is the diagnostic imaging of choice

Sagittal T1-weighted MRI of the brain shows complete absence of the corpus callosum.

Axial T1-weighted MRI shows that the lateral ventricles are parallel to each other and do not come into contact with each other as they normally should.

Sagittal T1-weighted MRI of the brain. Parasagittal section through the lateral ventricle shows dilatation of the atrium and occipital horn (colpocephaly).

Axial nonenhanced CT of the brain shows colpocephaly due to dilated atria and occipital horns of the lateral ventricle. Lateral ventricles are parallel in configuration.

genu

anterior body

Sagittal T1-weighted MRI of the brain shows partial agenesis of the corpus callosum. The genu and anterior body of the corpus callosum are visualized, while the posterior body, splenium, and the rostrum are absent.

body spleniu m

Sagittal T1-weighted MRI of the brain shows apparent atypical callosal dysgenesis in lobar holoprosencephaly. The body and splenium of the corpus callosum are well formed while the genu and rostrum are hypoplastic.

A patient with Dandy-Walker malformation. The corpus callosum is present but thinned.

• a progressive neurological disease characterized by corpus callosum demyelination and necrosis and subsequent atrophy • Alcoholism is the greatest risk factor • MBD is dintinguished from other diseases that may affect the CC (ischemic stroke, lymphoma, etc) by lesions that are symmetrical and located at the anterior portion

Marchiafava-Bignami Disease (MBD)

Multiple T1 dark and T2 bright lesions within the corpus callosum and frontal lobe

Multiple T1 dark and T2 bright lesions within the corpus callosum and frontal lobe

Severe atrophy of the body and splenium of the corpus callosum

FLAIR shows periventricular white matter degeneration

Sagittal T1-weighted MR image shows corpus callosum atrophy (short arrow), which is characteristic of chronic form. Involvement of central layers of corpus callosum, indicated by hypointensity, with sparing of dorsal and ventral layers results in the sandwich sign (long arrow).

Other Diseases with Involvement of the Corpus Callosum
LIPOMA

Coronal T1-weighted MR image shows large well-defined homogeneous midline mass lesion in region of corpus callosum with characteristic bright signal of lipoma. Note associated dysgenesis of corpus callosum.

PILOCYTIC ASTROCYTOMA

Sagittal T1-weighted MR image shows wellcircumscribed hypointense lesion in body of corpus callosum.

MULTIPLE SCLEROSIS

Sagittal fluid-attenuated inversion recovery paramedian image obtained through corpus callosum shows multiple ovoid hyperintense lesions (arrow).

Sagittal T2-weighted MR image shows multiple hyperintense lesions in corpus callosum.

HYDROCEPHALUS

Sagittal T1-weighted MR image shows well-defined cystic lesions (arrows) of corpus callosum.

Axial T2-weighted MR image shows abnormal signal throughout corpus callosum, which has persisted for many years.

Holoprosencephal y

Adlee W. Hassannoor Vincent Mari Angelo W. Laguardia

• denotes an incomplete or absent division of the embryonic forebrain (prosencephalon) into distinct lateral cerebral hemispheres Epidemiology:
– US: 1 in 10,000-20,000 neonates at birth Internationally: similar to that in the US – At birth, the ratio of females to males is 2:1 – Age of onset: 3-4 weeks of gestation

Pathogenesis

Types (from most severe to least):
(1)alobar (2) semilobar (3) lobar

Facial phenotypes (from most severe to least):
(1)cyclopia (2)ethmocephaly (3)cebocephaly (4)ocular hypotelorism and midline clefting (5) milder facial dysmorphic features in combination or in isolation

Most severe

Wide spectrum of HPE phenotypes

Mild

Alobar HPE

MRI: Coronal fluid-attenuated inversion recovery image showing alobar holoprosencephaly

Fetal MRI shows alobar holoprosencephaly

Early fetal MRI shows alobar holoprosenscephaly

Semilobar HPE

Lobar HPE

A

B

C

D

Dorsal Lobar

HPE

Dandy Walker Complex and Posterior Fossa Malformations
Chrismarie Joy L. Bugayong Ahliah E. Ibrahim

Dandy-Walker Complex
• Dandy-Walker malformation • Dandy-Walker variant • Mega cisterna magna
Precisely differentiating the malformations may not be possible using imaging methods!

• Enlarged posterior fossa

Dandy-Walker Complex

• High position of tentorium with upward displacement of the lateral sinuses • Torcular herophili associated with varying degrees of vermian aplasia or hypoplasia • Cystic dilatation of the fourth ventricle that nearly fills the entire posterior fossa

Dandy-Walker Malformation
• Rare congenital malformation (US: 1/ 35,000 live births) • Accounts for approximately 1-4% of hydrocephalus cases • Nature and cause of the insult are unknown • Characterized by:
– Agenesis or hypoplasia of the cerebellar vermis – Cystic dilatation of the fourth ventricle – Enlargement of the posterior fossa

Magnetic Resonance Picture Imaging 1. Sagittal T1-

weighted MRI in a 5-yearold girl shows: • Large posterior fossa cyst elevating the torcular herophili and sinus rectus (blue arrow) • Hypoplastic vermis is everted over the posterior fossa cyst (yellow arrow) • Cerebellar hemispheres and brainstem (b) are hypoplastic • Thinned occipital squama

b

Magnetic Resonance Imaging Picture 2. Axial T2weighted MRI shows: • Hydrocephalus • Large cerebrospinal fluid cyst in the posterior fossa

C

C

• Thinned occipital bone (arrows) • Hypoplastic cerebellar hemispheres with a winged appearance (c)

Magnetic Resonance Imaging Picture 3. Axial T1weighted MRI shows: • Ventriculomegaly • Superiorly displaced posterior fossa cyst

Dandy-Walker variant
• More likely to present in adulthood than in infancy or childhood • Consist of:
– Vermian hypoplasia – Cystic dilatation of the fourth ventricle – Without enlargement of the posterior fossa

Magnetic Resonance Imaging 4. Dandy-Walker Picture
variant in a 13-year-old girl with thoracal scoliosis. Sagittal T1-weighted MRI shows: • Agenesis

of the corpus

callosum • Hypoplastic inferior vermis • Fourth ventricle slightly enlarged • Posterior fossa typically normal in size

Mega Cisterna Magna
• Consist of:
– normal cerebellar vermis and fourth ventricle – enlarged posterior fossa 2o to enlarged cisterna magna

Magnetic Resonance Imaging
• Large

Picture 6. Sagittal T1weighted MRI shows:

retrocerebellar cerebrospinal fluid collection • Normal fourth ventricle and vermis

Posterior Fossa Arachnoid Cysts
• Displacement of the fourth ventricle and cerebellum anteriorly • Produces significant mass effect

Sagittal (left) and axial (right) MR views of the brain revealing a large posterior fossa arachnoid cyst and caudal displacement of the cerebellar tonsils

CT scan of an infratentorial posterior fossa arachnoid cyst with obstructive hydrocephalus.

Neurofibromato sis
Lathefa L. Pescadero Jeanette A. Venancio

• Group of neurocutaenous syndromes primarily affecting tissues derived fro the neural crest • Consists primarily of distinct neuroectodermal disorders (phakomatoses) which are inherited as autosomal dominant traits

EPIDEMIOLOGY
Incidence NF-1:
1:2500 live births

Prevalence 1:5,000

Age Always present at birth, in number during late childhood and adolescence Symptoms begin in teens or early twenties, but occa. as early as 1st and as late as 7th decade of life

NF-2:

1:33,000 live births

1:210,000

CLASSIFICATION

Neurofibromatosis 1 ( NF-1 )
• More common type • AKA Peripheral neurofibromatosis and von Recklinghausen’s Neurofibromatosis • The skull and brain manifestations are protean and highly variable penetrance • Classic skull malformations include hypolplasia of the sphenoid bone  poorly separated orbit and middle cranial fossa and to sutural defects • Optic gliomas are common, as are other low-grade gliomas and hammartomas in the white matter and basal ganglia

Left, Plain radiograph of the left forearm in a 15-year-old boy shows hypoplasia and deformity of the radius and ulna. Note the intramedullary sclerotic streaks within the radius and periosteal dysplasia. Right, Compare these findings with the normal right forearm, and note the unrelated exostosis of the distal radius.

T1-weighted MRI in a 7-year-old girl with a family history for the disease and who had been blind for 18 months shows bilateral optic nerve gliomas (arrows) (same patient as in Image 12).

A 7-year-old girl with a family history of neurofibromatosis type 1 had been blind for 18 months. T2-weighted transaxial MRI shows bilateral optic nerve gliomas (arrows).

CT scan through the orbits in a patient with the disease shows a right optic glioma.

A 66-year-old woman with neurofibromatosis type 1 presented with paresthesia down the right arm. T1-weighted transaxial MRI through the cervical spine shows a low-signal-intensity mass extruding through the left foraminal canal at vertebral level C5-6; the mass appears to be eroding the vertebral body. The final diagnosis was a neurofibroma.

Neurofibromatosis 2 ( NF-2 )
• Less common type • AKA central neurofibromatosis • Bilateral acoustic neuroma • Characterized by bilateral 8th cranial nerveschwannomas as well as schwannomas of other cranial nerves and multiple meningiomas

Axial and coronal T1-weighted images with gadolinium demonstrating bilateral acoustic schwannomas.

Coronal T1 with gadolinium showing extra-axial meningioma located in right frontal cortex (left) and sagittal T1 with gadolinium showing small enhancing lesion on the posterior aspect of the medulla (right).

Sagittal T1-weighted postcontrast image in a patient with known neurofibromatosis type 2 that demonstrates 2 midline meningiomas (arrowheads), one over the convexity and one along the vein of Galen. The enhancing mass in the medulla (arrow) most likely is an ependymoma.

Axial postcontrast T1-weighted image demonstrates a large enhancing sellar meningioma surrounding both internal carotid arteries in this case of neurofibromatosis type 2 (NF2) (black arrows). Enhancing tissue in the ethmoid air cells also represents a meningioma extending through the cribriform plate. Meningiomas in patients with NF2 can be more aggressive and invasive than spontaneous meningiomas. Note the small, round, enhancing extra-axial mass posterior to the tectum (white arrows). Although this could represent another meningioma, the shape and location suggest it is a trochlear (CN IV) schwannoma instead.

Sagittal T1-weighted postcontrast image of the thoracic spine demonstrates an enhancing extraaxial meningioma (arrow) anterior to the cord with a complex enhancing mass (arrowheads) that represents a conus ependymoma filling the spinal canal in the lower thoracic spine.

Intracranial Hemorrhage
Mary Claudette M. Abad Melissa A. Corinales

• the pathological accumulation of blood within the cranial vault • occurs when a blood vessel in the head is ruptured or leaks • from physical trauma (head injury) or nontraumatic causes (hemorrhagic stroke) such as a ruptured aneurysm

Intracranial Hemorrhage

Subdural Hemorrhag

Subdural Hemorrhage
• form of traumatic brain injury in which blood collects between the dura (the outer protective covering of the brain) and the arachnoid (the middle layer of the meninges) • arise from bleeding from small veins between the dura and the brain • occur when physical injury results in the development of shearing forces

Acute subdural hematoma. Note the bright (white) image properties of the blood on this noncontrast cranial CT scan.

MR examination shows bilateral fluid collections as a result of chronic bilateral subdural hematomas and new subdural hematomas in the right frontal and posterior interhemispheric region.

Subarachno id

Subarachnoid Hemorrhage area • bleeding of an artery in the
between the brain and the thin tissues that cover the brain • may arise due to trauma or spontaneously, and is a medical emergency which can lead to death or severe disability • most frequent cause of subarachnoid hemorrhage is bleeding from an aneurysm

• CT scan of the brain showing subarachnoid hemorrhage as a white area in the center

The pathological accumulation of blood within the cranial vault. Epidemiology  ICH accounts for 8-13% of all strokes  30-day mortality rate of 44%. Age:  - >55 years and doubles with each decade until age 80 years. Sex: slight male predominance Race: higher incidence in Asian countries

Pathophysiology
 hypertensive damage to blood vessel walls  Hypertension  eclampsia  drug abuse  arteriopathy  cerebral amyloid angiopathy  moyamoya
 altered hemostasis

 thrombolysis  autoregulatory dysfunction with excessive cerebral  anticoagulation blood flow  bleeding diathesis  reperfusion injury  hemorrhagic necrosis  hemorrhagic  tumor transformation  infection  cold exposure  rupture of an aneurysm or arteriovenous malformation (AVM)  Nonpenetrating and penetrating cranial trauma  venous outflow obstruction  cerebral venous thrombosis

CT scan of right frontalintracerebral hemorrhage complicating thrombolysis of an ischemic stroke

Fluid-attenuated inversion-recovery, T2-weighted, and gradient echo MRI illustration of intracerebral hemorrhage associated with a right frontal arteriovenous malformation.

Fluid-attenuated inversion-recovery, T2-weighted, and gradient echo MRI depiction of left temporal intracranial hemorrhage due to sickle cell disease

EDH occurs in the potential space between the dura and the cranium. Epidemiology  As many as 10-20% of all patients with head injuries are estimated to have EDH.  Approximately 17% of previously conscious patients who deteriorate into coma following a trauma have EDH.

Pathophysiology
 Mainly caused by structural disruption of the dural and skull vessels commonly associated with calvarial fractures.
 Most common etiology – lacerationof the middle meningeal artery

 In the posterior fossa
 Disruption of dural venous sinuses (eg, transverse or sigmoid sinus) by fracture may lead to EDH  Disruption of the superior sagittal sinus may cause vertex EDH.

 In the absence of trauma
 infectious diseases of the skull  vascular malformations of the dura mater  metastasis to the skull

 Spontaneous EDH
 Px’s with coagulopathies associated with other primary medical problems
– end-stage liver disease – chronic alcoholism – other disease states associated with dysfunctional platelets

CT scan of an acute left-sided epidural hematoma. Note the typical convex or lens-shaped appearance. The hematoma takes this shape as the dura strips from the undersurface of the cranium, limited by the suture lines. A midline shift of the ventricular system is present. This hemorrhage requires immediate surgical evacuation.

Nontraumatic epidural hematoma in a young woman. The grey area in the top left is organizing hematoma, causing midline shift and compression of the ventricle.

Craniocerebr al Trauma
Jan Idrian C. Algar Mark Renier B. Rebolos

 Injuries related to skull fracture:
 Scalp injuries  Axonal injury  General penetrating injuries  Missile wounds  Stab wounds  Nonaccidental trauma

 Intracranial hemorrhages related to skull fracture:
 Extradural hemorrhage  Subdural hemorrhage  Subarachnoid hemorrhage  Intracerebral hemorrhage

 Frequency: >60% are simple linear  Sex: Men twice likely to have injury  Risk of head injury: Peaks at 15-30 years old  Head trauma: Most common cause of morbidity and
mortality in infants

 Preferred examination: CT is the modality of choice
in evaluating head injuries

Occipital Skull Fracture in Nonaccidental Injury

Linear Temporoparietal Fracture

Baseball bat assault:

Depressed fracture

Intracranial injury from a golf club

Stab wound to the head from a large knife

Gunshot wound to the right temporoparietal region

Open comminuted fracture with underlying extradural hematoma

Multiple fractures, soft tissue swelling, air in cranial cavity, contusional hemorrhage

Multiple fractures, soft tissue swelling, air in cranial cavity, contusional hemorrhage

Bilateral contusion and intracerebral hematoma

Penetrating injury from a low velocity bullet

Plastic bullet

Left subfrontal subdural hematoma with active hemorrhage

Extracranial hematoma and intracranial extradural hematoma

Right frontal extradural hematoma

8-week-old baby after forceps delivery

Ax attack with open midline frontal fracture

Missile injury through the frontal bone

Missile injury through the frontal bone with intracerebral hematoma/infarction

Astrocytom a
& Variants
Grystel G. Gadian Ma. Florelyn S. Datu

ASTROCYTOMA
• CNS neoplasms • Derived from an immortalized astrocyte • Etiology: – associations with various disorders and exposures – genetic • Two classes of astrocytic tumors – narrow zones of infiltration – diffuse zones of infiltration

ASTROCYTOMA
PATHOPHYSIOLOGY • compression, invasion, and destruction of brain parenchyma • Disruption of normal parenchymal function • Mediation of secondary clinical sequelae • perturbation of CNS function – Neurological signs and symptoms – Focal neurological deficits and seizures

ASTROCYTOMA
variants

NARROW ZONES OF INFILTRATION ASTROCYTOMA
• pilocytic astrocytoma • subependymal giant cell astrocytoma • pleomorphic xanthoastrocytoma

PILOCYTIC ASTROCYTOMA

• Benign tumor of childhood • Cerebellum (MC), brainstem, hypothalamic region, optic pathways, cerebral hemispheres and the spinal cord • Peak incidence is 5-14 years • Grade I

SUBEPENDYMAL GIANT CELL ASTROCYTOMA

• • • •

Benign large subependymal nodule (SEN) Lateral ventricle, attached to caudate head Children, young adults Grade I

PLEOMORPHIC XANTHOASTROCYTOMA

• • • •

Cerebral hemispheres, meninges and spinal column (rare) Affect males and females equally Children and young adults (peak 20 years) Grade II-III

PLEOMORPHIC XANTHOASTROCYTOMA

DIFFUSE ZONES OF INFILTRATION ASTROCYTOMA
• low-grade astrocytoma • anaplastic astrocytoma • glioblastoma multiforme

LOW-GRADE ASTROCYTOMA

• • • • •

Slow growing primary tumor Brain and spinal cord Slight male predominance (1.18:1) Peak incidence 30-40 years Grade II

ANAPLASTIC ASTROCYTOMA

• Rapidly growing tumor • Cerebral hemispheres (MC), thalamus and hypothalamus, cerebellum and brain stem • Male predominance (1.87:1) • Children and adults • Grade III

GLIOBLASTOMA MULTIFORME

• MC and most malignant • Cerebral hemispheres (adults, MC), brain stem (children) and spinal cord • Primary (>50 years) and secondary (<45 years) • Any age (peak incidence 45-70 years) • Male predominance (3:2) • Grade IV

GLIOBLASTOMA MULTIFORME GLIOBLASTOMA MULTIFORME

GLIOBLASTOMA MULTIFORME GLIOBLASTOMA MULTIFORME

Nonastrocyti c Glial Tumors
Lucio V. Temonio, Jr. Melissa T. Sy

Melissa T. Sy

Oligodendroglioma
• 7% of supratentorial gliomas • Found in middle-aged adults, 45 y.o. • Slow growing tumor • Duration of symptoms before dx = 11 yrs

Oligodendroglioma

• Calcifications in plain skull radiograph

• Lesion occur at: cerebral hemisphere, white matter • MC: frontal lobe

• Calcification within the tumor • Frequently occur but a non-specific sign

Calcium = coarse, irregular strands

COMPARATIVE STUDY

2000

2005

2006

EPENDYMOMA

Lucio Temonio Jr.

Ependymoma
• from cells lining the ventricles (fluid filled spaces w/in the brain) OR spinal cord’s central canal • Duration of symptoms before dx= <1 yr • Arise in children & young adults – Infratentorial ependymomas – Supratentorial ependymomas

• Isodense/ slightly hyperdense

• w/ scattered small/ punctuate Ca deposits

• Lines the ventricle

Primitive Neuroepitheli al Tumors
Wilhema M. Villan Marco Po D. Dela Cruz

• Applied to a tumor that cannot be sharply differentiated from other embryonal cell types • Includes neuroblastoma, pineoblastoma, ependymoblastoma, polar spongioblastoma, & medulloblastoma • Incidence: common CNS tumor in children
– 25% of all intracranial tumors

• Age & gender: Majority - < age of 5 years
– Males = Females

• Location: MC in posterior fossa

• Imaging:
– Computed Tomography
• Large, irregular, heterogeneous mass deep in the cerebral white matter • Solid component of mass is usually hyperdense • Necrosis, cyst formation, calcification, & hemorrhage seen • Enhancement is seen & may be heterogeneous / ringlike

– Magnetic Resonance Imaging
• Large, heterogeneous mass w/ necrosis. Cyst formation, calcification, / hemorrhage • Solid component of mass is slightly hypointense on T1-weighted images & slightly to moderately hyperintense on T2-weighted images

Cerebellar medulloblastoma. This MRI (axial view, T2-weighted image) demonstrates the heterogeneity of the tumor.

Cerebellar medulloblastoma. This axial view CT scan with contrast shows a partially enhancing mass arising in the midline from cerebellum and filling the fourth ventricle.

Medulloblasto ma. Axial T2 weighted image reveals a predominantly isointense mass to grey matter with small foci of cystic changes

T1-weighted sagittal MRI of an 8-year-old boy who presented with nausea and vomiting reveals an enhancing tumor within the fourth ventricle. The child underwent a suboccipital craniotomy and resection of his medulloblastoma.

pineoblastoma

Radiology | Medicine-3 Dr. Jose P. Rizal School of Medicine Xavier University – Ateneo de Cagayan © SY 2007-2008