CNS Lecture Final 2007

Pathology of the Pathology of the Central Nervous Central Nervous

SystemSystem

Michelle Y. So, M.D.Michelle Y. So, M.D.

Lecture I: Vascular Lecture I: Vascular Diseases of the Diseases of the Central Central Nervous SystemNervous SystemLecture II: Infections of Lecture II: Infections of the Central the Central Nervous Nervous SystemSystemLecture III: Tumors of the Lecture III: Tumors of the Central Central Nervous SystemNervous System

Lecture I Lecture I Vascular Diseases of the Vascular Diseases of the Central Nervous SystemCentral Nervous System

Vascular Diseases of Vascular Diseases of the CNSthe CNS

Diseases of the brain parenchyma Diseases of the brain parenchyma secondary to pathologic alterations of secondary to pathologic alterations of blood vessels supplying and draining the blood vessels supplying and draining the CNSCNS

50% of all neurologic disorders50% of all neurologic disorders Mortality Rate:Mortality Rate: 100/l00,000 population100/l00,000 population Brain infarct Brain infarct - - 5050

Subarachnoid hemorrhage - 10Subarachnoid hemorrhage - 10 Brain hemorrhage - 30Brain hemorrhage - 30

Others Others - 10 - 10

Part I : Hypoxia, Ischemia Part I : Hypoxia, Ischemia & & Infarction InfarctionPart II : Intracranial Part II : Intracranial HemorrhageHemorrhagePart III : Hypertensive Part III : Hypertensive

Cerebrovascular DiseaseCerebrovascular Disease

Part IPart IHypoxia, Ischemia & Hypoxia, Ischemia &

InfarctionInfarction

Hypoxia, Ischemia & Hypoxia, Ischemia & InfarctionInfarction

Brain – 2% of the body weightBrain – 2% of the body weight

15% of the cardiac 15% of the cardiac outputoutput

20% of the oxygen 20% of the oxygen consumptionconsumption


Definition of termsDefinition of terms

1. Hypoxia - reduced oxygen1. Hypoxia - reduced oxygen

2. Anoxia – total absence of 2. Anoxia – total absence of oxygenoxygen

3. Ischemia – reduction or 3. Ischemia – reduction or cessation of blood flowcessation of blood flow

4. Infarction – localized area of 4. Infarction – localized area of ischemic necrosis in an organ or ischemic necrosis in an organ or tissue resulting from sudden loss of tissue resulting from sudden loss of its arterial supplyits arterial supply

Hypoxia, ischemia & Hypoxia, ischemia & InfarctionInfarction

Causes of CNS Hypoxia /AnoxiaCauses of CNS Hypoxia /Anoxia

1.1. Cardiac arrest Cardiac arrest

2.2. Vascular obstructionVascular obstruction

3.3. Decreased ODecreased O22 saturation saturation

4.4. Decreased hemoglobinDecreased hemoglobin

5.5. Histotoxic agentsHistotoxic agents


Brain parenchymal damage due to Brain parenchymal damage due to the varous forms of the varous forms of hypoxia/anoxia is the samehypoxia/anoxia is the same

Hypoglycemia – histologic Hypoglycemia – histologic effects are similar to effects are similar to hypoxia/anoxiahypoxia/anoxia


In clinical practice , there are In clinical practice , there are two general types of acute two general types of acute ischemic injury:ischemic injury:

Generalized – reduced Generalized – reduced cerebral perfusion with cerebral perfusion with widespread bilateral damagewidespread bilateral damage

Focal – severe reduction Focal – severe reduction or cessation of blood flow to a or cessation of blood flow to a localized arealocalized area

Hypoxia, ischemia and Hypoxia, ischemia and InfarctionInfarction

Generalized Generalized HypotensionHypotension

Cardiac arrestCardiac arrest Focal Focal

AtherosclerosisAtherosclerosis ArteriolosclerosisArteriolosclerosis

EmbolismEmbolism VasculitisVasculitis

Morphologic evolution of Morphologic evolution of an infarctan infarct

Hypoxia, ischemia and Hypoxia, ischemia and InfarctionInfarction

Hypotension Hypotension

- “Arterial border zone pattern”- “Arterial border zone pattern”

- Boundary zone – subject to - Boundary zone – subject to reduction in blood reduction in blood flowflow

- If patient dies immediately - If patient dies immediately after – no after – no microscopic changesmicroscopic changes

- After a few days – wedge shaped - After a few days – wedge shaped hemorrhagic hemorrhagic infarctioninfarction


Cardiac arrestCardiac arrest

- “Laminar necrosis”- “Laminar necrosis”

- Diffuse neuronal necrosis of the - Diffuse neuronal necrosis of the cerebral cerebral and cerebellar corticesand cerebellar cortices

- More severe within the sulci than - More severe within the sulci than the the gyrigyri

- Increases in severity from the - Increases in severity from the frontal frontal and temporal to the and temporal to the occipital lobesoccipital lobes

Hypoxia, Ischemia & Hypoxia, Ischemia & infarctioninfarction

- Most vulnerable neurons :- Most vulnerable neurons :

1. 31. 3rdrd layer of the cerebral cortex layer of the cerebral cortex

2. Pyramidal cells of the 2. Pyramidal cells of the hippocampushippocampus

3. Purkinje cells of the 3. Purkinje cells of the cerebellumcerebellum

- Due to differences in the - Due to differences in the intrinsic metabolic requirements of intrinsic metabolic requirements of neuronsneurons

Hypoxia, Ischemia & Hypoxia, Ischemia & infarctioninfarction

- Cerebral white matter is - Cerebral white matter is relatively spared but diminished in relatively spared but diminished in bulk due to the loss of neurons in bulk due to the loss of neurons in the gray matter – enlargement of the the gray matter – enlargement of the ventricles ventricles

- Similar pattern of brain damage - Similar pattern of brain damage

- status epilepticus- status epilepticus

- hypoglycemic brain damage- hypoglycemic brain damage


Focal Focal

AtherosclerosisAtherosclerosis

ArteriolosclerosisArteriolosclerosis

EmbolismEmbolism

VasculitisVasculitis

Morphologic Morphologic evolution of an infarctevolution of an infarct


Focal lesionsFocal lesions1.1. Atheroscleosis Atheroscleosis

- Chief etiologic factor in the - Chief etiologic factor in the production of cerebral infarction – production of cerebral infarction – cause of thrombosis in 90%cause of thrombosis in 90%

- Most commonly affected vessels:- Most commonly affected vessels: Internal carotid and Internal carotid and

vertebral arteries vertebral arteries Basilar and middle cerebral Basilar and middle cerebral

arteriesarteries - Lumen is reduced by up to 90% - Lumen is reduced by up to 90%

before blood flow is impairedbefore blood flow is impaired


2. Arteriolosclerosis (hyaline & 2. Arteriolosclerosis (hyaline & hyperplastic)hyperplastic)

- affects mainly the media of - affects mainly the media of intracerebral arteries with intracerebral arteries with narrowing of the lumennarrowing of the lumen

- associated with diabetes - associated with diabetes and hypertensionand hypertension

Hypoxia, Ischemia & Hypoxia, Ischemia & Infarction Infarction

3. Embolism 3. Embolism

Sources of emboli: Sources of emboli:

- Heart thrombi in post-MI, - Heart thrombi in post-MI, valvulitis valvulitis (RHD), bacterial (RHD), bacterial endocarditisendocarditis

- Aorta and neck vessels: - Aorta and neck vessels: atheromaatheroma

- Peripheral vessels : fat - Peripheral vessels : fat and tumor and tumor emboliemboli

Hypoxia, Ischemia and Hypoxia, Ischemia and InfarctionInfarction

4. Vasculitis4. Vasculitis

- Polyarteritis nodosa- Polyarteritis nodosa

- Giant cell arteritis- Giant cell arteritis

- Granulomatous angiitis- Granulomatous angiitis

Hypoxia, Ischemia and Hypoxia, Ischemia and InfarctionInfarction

Morphologic evolution of an Morphologic evolution of an infarctinfarct

3 Phases3 Phases

Coagulation Coagulation necrosisnecrosis

Liquefaction Liquefaction necrosisnecrosis

CavitationCavitation

Part IIPart IIIntracranial HemorrhageIntracranial Hemorrhage

Part II : Intracranial Part II : Intracranial HemorrhageHemorrhage

Intracerebral Intracerebral (hypertensive)(hypertensive)

Subarachnoid (berry Subarachnoid (berry aneurysm)aneurysm)

Mixed intracerebral and Mixed intracerebral and subarachnoid subarachnoid

(A-V (A-V malformation)malformation)

Intracranial HemorrhageIntracranial Hemorrhage Intracerebral (hypertensive)Intracerebral (hypertensive)Etiology: results from “Charcot-Etiology: results from “Charcot-Buchard” Buchard” microaneurysms that form microaneurysms that form at the at the bifurcation of small bifurcation of small intraparenchymal intraparenchymal arteries. Associated arteries. Associated with age and with age and hypertensionhypertension

Location : 1. Putamen (55%)Location : 1. Putamen (55%) 2. Lobar white matter 2. Lobar white matter (15%)(15%)

3. Thalamus , pons and 3. Thalamus , pons and cerebellar cerebellar cortex (l0% each)cortex (l0% each)

Intracranial HemorrhageIntracranial Hemorrhage

Morphology: Morphology: 1. Small punctate hemorrhages1. Small punctate hemorrhages - fresh round/oval, well-- fresh round/oval, well-circumscribed dark red spotscircumscribed dark red spots

- older lesions – tiny areas - older lesions – tiny areas of softening , brown to golden-of softening , brown to golden-yellow in color (hemosiderin)yellow in color (hemosiderin)

- predilection for the grey - predilection for the grey matter or junction of the cortex matter or junction of the cortex and white matterand white matter


2. “Slit hemorrhages”2. “Slit hemorrhages”

- Slit-like pigment stained areas of - Slit-like pigment stained areas of softeningsoftening

- subcortical lesion- subcortical lesion

3. Gross hemorrhage3. Gross hemorrhage

- one to several cm. in diameter- one to several cm. in diameter

- massive – displacement /disruption of - massive – displacement /disruption of adjacent brain tissue, distortion of the adjacent brain tissue, distortion of the ventriclesventricles

*End result – leave a cystic cavity with *End result – leave a cystic cavity with yellow-orange borders and marginal gliosisyellow-orange borders and marginal gliosis

Intracranial hemorrhageIntracranial hemorrhage

Subarachnoid hemorrhageSubarachnoid hemorrhage

Etiology: results from Etiology: results from rupture of a berry rupture of a berry aneurysm aneurysm (rarely, an A-V mal)(rarely, an A-V mal)

Morphology: subarachnoid Morphology: subarachnoid hemorrhage, hemorrhage, hydrocephalus – hydrocephalus – sudden blockage of sudden blockage of the SAS, the SAS, consequent fibrosisconsequent fibrosis


True aneurysm True aneurysm

- dilatation of the vascular - dilatation of the vascular lumen, yielding all components of lumen, yielding all components of the wallthe wall

- focal absence of the media- focal absence of the media

- aneurysm wall: thickened intima - aneurysm wall: thickened intima

adventitiaadventitia

- 2- 2oo changes changes -atherosclerosis/thrombosis-atherosclerosis/thrombosis


Location : major arteries at the base of Location : major arteries at the base of the brainthe brain

90% - internal carotid system90% - internal carotid system

anterior communicating anterior communicating arteryartery

junction of the carotid and junction of the carotid and posterior communicatingposterior communicating

bifurcation of the middle bifurcation of the middle cerebral cerebral arteryartery

l0% - vertebral-basilar systeml0% - vertebral-basilar system


Rupture : 90% - 30 to 70 years oldRupture : 90% - 30 to 70 years old Events leading to rupture (?)Events leading to rupture (?) - (+) hypertension- (+) hypertension - many are normotensive- many are normotensivePrognosis: Prognosis: First hemorrhage – fatal in 30%First hemorrhage – fatal in 30% 70% survive – 20 to 30 % will 70% survive – 20 to 30 % will have a fatal recurrence in 6 monthshave a fatal recurrence in 6 months


Mixed intraparenchymal and Mixed intraparenchymal and subarachnoid hemorrhagesubarachnoid hemorrhage

Etiology: arteriovenous Etiology: arteriovenous malformation – network of malformation – network of thick-walled vessels of various thick-walled vessels of various diameters, neither purely diameters, neither purely arterial nor purely venous arterial nor purely venous (“arterialized veins”) (“arterialized veins”)

Part III.Part III. Hypertensive Hypertensive

Cerebrovascular DiseaseCerebrovascular Disease

Hypertensive Hypertensive Cerebrovascular DiseaseCerebrovascular Disease

Pathologic changes Resultant CNS Pathologic changes Resultant CNS lesionlesion

in blood vesselsin blood vessels

Atherosclerosis Atherosclerosis Major infarctMajor infarct

Multiple Multiple small infarctsmall infarct

ArteriolosclerosisArteriolosclerosis LacunaeLacunae

Binswanger’s DiseaseBinswanger’s Disease

MicroaneurysmMicroaneurysm Intracerebral hemorrhageIntracerebral hemorrhage


LacunaeLacunae

- “Little lakes”- “Little lakes”

- Collection of multiple - Collection of multiple small 2-15 mm, small old small 2-15 mm, small old cavitary infarctscavitary infarcts

- located in the basal - located in the basal ganglia and thalamusganglia and thalamus

- usually asymptomatic- usually asymptomatic


Binswanger’s DiseaseBinswanger’s Disease - Subcortical leukoencephalopathy- Subcortical leukoencephalopathy - Patchy or diffuse degeneration - Patchy or diffuse degeneration of the white of the white mattermatter

- demyelination , irregular loss - demyelination , irregular loss of both axons of both axons and myelinand myelin

- widespread gliosis- widespread gliosis - due to decreased perfusion of - due to decreased perfusion of the deep white the deep white mattermatter

- progressive deterioration of - progressive deterioration of mental capacity - mental capacity - dementiadementia

Lecture IILecture IIInfections of the Central Infections of the Central

Nervous SystemNervous System

Part I : MeningitisPart I : MeningitisPart II: Part II:

EncephalitisEncephalitis

Infections of the CNSInfections of the CNS

Routes of infection:Routes of infection:

1. Bloodstream – most common1. Bloodstream – most common

2. Direct implantation – 2. Direct implantation – iatrogenic and iatrogenic and traumatictraumatic

3. Local extension – from 3. Local extension – from infected air infected air sinusessinuses

4. Peripheral nervous system 4. Peripheral nervous system – viral – viral infections infections

MeningitisMeningitis

Signs and symptoms:Signs and symptoms:

HeadacheHeadache

Neck stiffnessNeck stiffness

VomitingVomiting

Mental confusionMental confusion

(-) Focal neurologic signs(-) Focal neurologic signs

MeningitisMeningitis CSF findingsCSF findings Bacterial Viral Bacterial Viral TB TB

PMN’sPMN’s

LymphocytesLymphocytes

ProteinProtein

GlucoseGlucose NN NN//

Part I. MeningitisPart I. Meningitis

1. Acute pyogenic 1. Acute pyogenic (bacterial)(bacterial)

2. Acute lymphocytic 2. Acute lymphocytic (viral)(viral)

3. Subacute/chronic (TB, 3. Subacute/chronic (TB, fungal)fungal)


1. Acute pyogenic meningitis1. Acute pyogenic meningitis Etiology: Escherichia coli – Etiology: Escherichia coli – neonateneonate

Hemophilus influenza – Hemophilus influenza – infants infants and childrenand children

Neisseria meningitidis Neisseria meningitidis – – adolescents and adolescents and young young adultsadults

Pneumococcus – very young Pneumococcus – very young and and very old very old


Microscopic :Microscopic :

PMN’s in the subarachnoid PMN’s in the subarachnoid space , space , especially especially around blood vesselsaround blood vessels

Complications:Complications:

Vasculitis --- infarctionVasculitis --- infarction

Adhesive arachnoiditis --- Adhesive arachnoiditis --- obliterated obliterated SAS --- SAS --- hydrocephalushydrocephalus


2. Acute lymphocytic (viral) 2. Acute lymphocytic (viral) meningitismeningitis

2/3 cases – (+) organism 2/3 cases – (+) organism identified – identified – mumps, EB mumps, EB virus, HS IIvirus, HS II

Less fulminant clinical Less fulminant clinical coursecourse

Self-limitingSelf-limiting

MeningitisMeningitis 3. Subacute or chronic meningitis3. Subacute or chronic meningitis A. Mycobacterium tuberculosisA. Mycobacterium tuberculosis Basal exudateBasal exudate

Tubercle formation with Tubercle formation with caseation caseation necrosis, necrosis, langhan’s giant cellslanghan’s giant cells

Complications:Complications: Vasculitis – infarctionVasculitis – infarction Arachnoiditis – Arachnoiditis –

hydrocephalus hydrocephalus *more commonly seen in *more commonly seen in TB than TB than pyogenicpyogenic


B. Cryptococcus neoformans B. Cryptococcus neoformans

SASSAS

Mild/marked chronic or Mild/marked chronic or granulomatous granulomatous inflammation inflammation

Indolent or fulminantIndolent or fulminant

Part 2. Part 2. EncephalitisEncephalitis

1.Bacterial1.Bacterial

2. Viral2. Viral

3. Fungal3. Fungal


1. Bacterial encephalitis1. Bacterial encephalitis

May occur as an extension from meningitisMay occur as an extension from meningitis

““meningoencephalitis”meningoencephalitis”

Primary parenchymal infection --- focal Primary parenchymal infection --- focal cerebritis--- abscesscerebritis--- abscess

*Focal deficits*Focal deficits

*Increased intracranial *Increased intracranial pressurepressure

* Ruptures – ventriculitis, * Ruptures – ventriculitis, meningitis, sinus meningitis, sinus thrombosisthrombosis

EncephalitisEncephalitis A. TuberculomaA. Tuberculoma B. Brain abscessB. Brain abscess Produced by:Produced by: - direct implantation – traumatic- direct implantation – traumatic - local extension – mastoiditis- local extension – mastoiditis - hematogenous – from infections in the - hematogenous – from infections in the heart heart & lungs (ex. acute bacterial & lungs (ex. acute bacterial endocarditis)endocarditis) * Fibrosis with collagen production – * Fibrosis with collagen production – capsulecapsule

* Fibroblasts derived from blood vessels* Fibroblasts derived from blood vessels

EncephalitisEncephalitis C. NeurosyphilisC. Neurosyphilis Meningitic neurosyphilisMeningitic neurosyphilis Paretic neurosyphilisParetic neurosyphilis - diffuse parenchymal invasion - diffuse parenchymal invasion with with microglial microglial proliferation and gliosisproliferation and gliosis

Tabes dorsalisTabes dorsalis - loss of axons and myelin in the - loss of axons and myelin in the

dorsal (sensory) rootsdorsal (sensory) roots*Obliterative endarteritis*Obliterative endarteritis* Perivascular inflammation – plasma * Perivascular inflammation – plasma

cellscells


2. Viral encephalitis2. Viral encephalitis

Perivascular and Perivascular and parenchymal parenchymal mononuclear infiltratemononuclear infiltrate

Glial nodulesGlial nodules

Neuronophagia – clusters Neuronophagia – clusters around foci of around foci of necrosisnecrosis

Inclusion bodiesInclusion bodies


“ “Tropism”Tropism”

Herpes zoster – dorsal root Herpes zoster – dorsal root ganglionganglion

Poliomyelitis – anterior hornPoliomyelitis – anterior horn

Rabies – neuronsRabies – neurons

Herpes simplex – inferior Herpes simplex – inferior frontal and frontal and temporal lobes temporal lobes

Cytomegalovirus - ependymaCytomegalovirus - ependyma


“ “Latency”Latency”

Reactivated months / years Reactivated months / years after initial infectionafter initial infection

EncephalitisEncephalitis Subacute Sclerosing Panencephalitis Subacute Sclerosing Panencephalitis (SSPE)(SSPE)-Measles virus; months/years after -Measles virus; months/years after infectioninfection-Children-Children-Progressive deterioration – -Progressive deterioration – personality changes and involuntary personality changes and involuntary movementsmovements-Gliosis and demyelination; viral -Gliosis and demyelination; viral inclusions in the nucleus of inclusions in the nucleus of oligodendrocytesoligodendrocytes


Progressive Multifocal Progressive Multifocal EncephalopathyEncephalopathy

-Polyomavirus-Polyomavirus

-Demyelination with bizarre -Demyelination with bizarre giant astrocytesgiant astrocytes

-Viral inclusions in the -Viral inclusions in the nucleus of oligodendrocytesnucleus of oligodendrocytes


Transmissible Spongiform Transmissible Spongiform Encephalopathies (Prion Diseases)Encephalopathies (Prion Diseases)-”Spongiform changes” in the grey -”Spongiform changes” in the grey matter with vacuole formationmatter with vacuole formation-Prion protein (PrP) – normal -Prion protein (PrP) – normal cellular protein in neurons which cellular protein in neurons which undergoes conformational change undergoes conformational change from its normal alpha-helix to an from its normal alpha-helix to an abnormal B pleated sheetabnormal B pleated sheet


A. “Crutzfeld – Jacob Disease “ A. “Crutzfeld – Jacob Disease “ (CJD)(CJD)

- Most common- Most common

- Cortex- Cortex

- Mode of transmission – corneal - Mode of transmission – corneal transplants, electrodes, growth transplants, electrodes, growth hormone extractshormone extracts

- Dementia- Dementia

- Uniformly fatal – survival of 7 - Uniformly fatal – survival of 7 months to a few yearsmonths to a few years


B. KuruB. Kuru

- Papua, New Guinea- Papua, New Guinea

- Cerebellum- Cerebellum

- Dementia ; ataxia – terminal- Dementia ; ataxia – terminal

- Mode of transmission - - Mode of transmission - cannibalismcannibalism


3. Fungal Encephalitis3. Fungal Encephalitis

- Immunocompromised patients- Immunocompromised patients

AIDSAIDS

Terminal casesTerminal cases

- Vasculitis esp. with Mucor and - Vasculitis esp. with Mucor and Aspergillus -----thrombosis -----Aspergillus -----thrombosis -----infarctioninfarction

- Parenchymal invasion – Candida - Parenchymal invasion – Candida and Cryptococcusand Cryptococcus

Demyelinating DiseaseDemyelinating Disease

Multiple SclerosisMultiple Sclerosis

- Between 20 and 40 years old- Between 20 and 40 years old

- Relapsing and remitting ; - Relapsing and remitting ; progressiveprogressive

- Paresthesia; motor and sensory - Paresthesia; motor and sensory deficits, incoordination, deficits, incoordination, paraplegia, ataxia, mental paraplegia, ataxia, mental dysfunctiondysfunction

- Irregular areas of demyelination - Irregular areas of demyelination “plaques”“plaques”

Degenerative DiseasesDegenerative Diseases

Parkinsons DiseaseParkinsons Disease

- Stooped posture, slowness of - Stooped posture, slowness of voluntary movements, festinating voluntary movements, festinating gait, rigidity,tremorsgait, rigidity,tremors

- Degeneration of dopaminergic - Degeneration of dopaminergic neurons in the substantia nigra neurons in the substantia nigra --- decreased dopamine--- decreased dopamine

- Pallor of substantia nigra- Pallor of substantia nigra

Degenerative DiseasesDegenerative Diseases

Alzheimer’s DiseaseAlzheimer’s Disease– More than 50 years oldMore than 50 years old– Progressive disorientation, Progressive disorientation, memory loss and aphasiamemory loss and aphasia

– Cortical atrophyCortical atrophy– Microscopic: neurofibrillary Microscopic: neurofibrillary tangles, senile plaques, amyloid tangles, senile plaques, amyloid angiopathy, vacuolar degeneration angiopathy, vacuolar degeneration

Lecture 3: Tumors of the Lecture 3: Tumors of the Central Nervous SystemCentral Nervous System

Tumors of the CNSTumors of the CNS Primary – 50%Primary – 50% Secondary – 50%Secondary – 50% 70% of tumors in childhood are 70% of tumors in childhood are infratentorial (posterior infratentorial (posterior fossa)fossa)

70% of tumors in adults are 70% of tumors in adults are supratentorialsupratentorial

(cerebral hemispheres)(cerebral hemispheres)

Tumors of the CNSTumors of the CNS

Incidence of intracranial tumorsIncidence of intracranial tumors

PRIMARY NEOPLASMS 50%PRIMARY NEOPLASMS 50%

GliomasGliomas 80% 80%

Glioblastoma Glioblastoma

Astrocytoma Astrocytoma

METASTATIC METASTATIC 50% 50%


Clinical manifestationsClinical manifestations

HeadacheHeadache

Disturbance of mentationDisturbance of mentation

Motor weaknessMotor weakness

Visual field defectsVisual field defects

Cranial nerve palsiesCranial nerve palsies

SeizuresSeizures


Laboratory evaluationLaboratory evaluation

MRIMRI

CT ScanCT Scan

Tumor biopsy – diagnosis is Tumor biopsy – diagnosis is important for important for prognosis and prognosis and managementmanagement


ManagementManagement

SurgerySurgery

RadiotherapyRadiotherapy

ChemotherapyChemotherapy


MeningiomasMeningiomas

- Attached to the dura, arising from - Attached to the dura, arising from meningothelial cellsmeningothelial cells

- Female predominance ; - Female predominance ;

(+) progesterone receptors(+) progesterone receptors

- “Papillary” variant – tends to - “Papillary” variant – tends to recurrecur

- Malignant meningiomas – show brain - Malignant meningiomas – show brain invasion, atypia , mitoses and invasion, atypia , mitoses and necrosisnecrosis


AstrocytomasAstrocytomas

Well-differentiated – Grades 1 Well-differentiated – Grades 1 and 2and 2

Anaplastic – Grade 3Anaplastic – Grade 3

Glioblastoma multiforme – Grade Glioblastoma multiforme – Grade 44


Grading systemGrading system

A A – Anaplasia– Anaplasia

MM – Mitoses – Mitoses

EE – Endothelial cell – Endothelial cell proliferationproliferation

N N - Necrosis- Necrosis


Metastatic TumorsMetastatic Tumors

Five most common primary sites Five most common primary sites – 80%– 80%

1. Lung1. Lung

2. Breast2. Breast

3. Skin (melanoma)3. Skin (melanoma)

4. Kidney4. Kidney

5. GIT5. GIT


Microscopic: well-demarcated Microscopic: well-demarcated masses of masses of carcinoma cellscarcinoma cells

““It is evident at the It is evident at the conclusion of this broad conclusion of this broad overview of diseases of overview of diseases of the central nervous the central nervous

system, that in number and system, that in number and in diversity, they rival in diversity, they rival the wondrous complexities the wondrous complexities of the central nervous of the central nervous

system itself.”system itself.”

The EndThe End

CNS Lecture Final 2007

Documents

Transcript of CNS Lecture Final 2007