(7) Surgical Pathology - Diseases of the Central Nervous System 401 - Dr. Baby Lynne Asuncion - October 20-28, 2014

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SURGICAL PATHOLOGY: DISEASES OF THE CENTRAL NERVOUS SYSTEM IIIDr. Baby Lynne Asuncion | October 20-28, 2014

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SALAMAT ATE JAIDI

DEMYELINATING/DEGENERATIVE DISORDERS

CASEA 72-year-old was complaining of difficulty of breathing. On

examination, an apparent tremor of his fingers was seen with expressionless face and monotonous voice. He died after a day. On autopsy, a portion of the brain had a characteristic finding.o Absence of substantia nigra: Parkinson's disease

Part of normal aging process: loss of dopaminergic responses → subsequent decrease in dopamine levels

DEMYELINATING DISEASESo Acquired conditions: myelin damage and axonal preservations

Multiple sclerosis: MC Others:

Neuromyelitis optica/Devic disease Acute disseminated encephalomyelitis (ADEM) Acute necrotizing hemorrhagic encephalomyelitis (ANHE) Central pontine myelinolysis

MULTIPLE SCLEROSISo Females more affected than maleso No age predilectiono Pathophysiology: Immune mediated response: targets the myelin

sheath demyelination Optic nerve, brainstem and spinal cord MC: SC

Common manifestation: paralysis of lower extremities

NEUROMYELITIS OPTICA/DEVIC DISEASEo Immune mediated: antibodies against aquaporin

Seen in optic nerve and spinal cord

ACUTE DISSEMINATED ENCEPHALOMYELITIS (ADEM)o Often follow a viral infectiono One complication associated with postviral vaccination

ACUTE NECROTIZING HEMORRHAGIC ENCEPHALOMYELITIS (ANHE)o Demyelinating symptomatologyo Affect younger adults and childreno Sequelae of viral infection particularly upper respiratory infection o More fatal outcome than ADEM

CENTRAL PONTINE MYELINOLYSIS (CPM)o affect pons (MC): Loss of myelin

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o demyelination associated with severe electrolyte imbalanceo presents as quadriplegia

DEGENERATIVE DISEASEo Diseases of grey mattero Progressive loss of neurons, secondary changes in white matter tractso Resistance of degradation of protein aggregates

Tau protein: tauopathy- Related to Alzheimer’s disease- Protein noted in microtubule and associated with

hyperphosphorylation- Abnormal accumulation presents with cortical dementias

o Groups Symptomatic/anatomic: Cerebral, Basal ganglia, Brainstem,

Spinocerebellum, Motor Neurons- Cerebral: Alzheimer- Basal Ganglia & Brainstem: Parkinson & Huntington’s disease

(AD; abnormal protein: huntingtin)- Spinocerebellum: Friedreich ataxia (MC inherited form of

ataxia, early onset, wheel-bound at age 20)- Motor neurons: ALS

Pathologic - Degenerative diseases that have inclusions/abnormal

structures observed in affected cells

ALZHEIMER DISEASEo MC cause of dementia in elderly patients

65 years: incidence of 2% and doubles every 5 years

o Insidious impairment of higher intellectual function with mood and behavior alterations

o 5-10% hereditary: autosomal dominant

OTHER FINDINGSo Neuritic plaque: spherical collections

of neuritic processes surrounding amyloid beta

o Neurofibrillary tangle Filaments extending (cone-shaped):

Accumulation of tau protein Severe cognitive dysfunction

Granulovacuolar degeneration Black staining granule within

vacuole: argyrophilic granule - silver stain

Hirano bodies Eosinophilic bodies, elongated not

spherical Glassy eosinophilic color Found in pyramidal cells in

hippocampus

Ronald Reagan died of severe pneumonia, a complication of Alzheimer's.


MS PLAQUESMultiple specks of gray to tan color

Irregular lesions: seen in demyelination

Luxol Fast Blue PAS StainNormal: blue color

Unmyelinated: patches of unstained areas

R: Normal brain (healthy brain) vs Alzheimer brain

L: Cortical atrophy: widened cerebral sulci in the frontal, temporal and

parietal lobes

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PARKINSON DISEASE AND SYNDROMEo Loss of pigmented dopaminergic neuronso Manifestations:

Diminished facial expression Rigidity and trembling of head Forward tilt of trunk (stooping

posture) Slow voluntary movement Reduced arm swinging Rigidity and trembling of extremities Shuffling gait with short steps

(festinating) Very characteristic: pill rolling

o Disease: idiopathico Syndrome: with causative factors like

infection, vascular condition, toxic insults particularly in the substantia nigra

TREATMENT: Give DOPAMINE (LEVODOPA) FOR LIFEo Common in patients with multiple injury to head

Muhammad Ali diagnosed at age 42 Michael J. Fox diagnosed at 30

AMYOTROPHIC LATERAL SCLEROSIS (ALS)o Amyotrophic: no muscle nourishmento Lateral: affected nerves (lateral area of SC or

brain)o Sclerosis: diffuse fibrosiso Loss of LMN in SC and BSo Loss of UMN in CSTo Missense mutation: gain of functiono Males more than femaleso 5th decade of life or even latero Progressive degeneration early onset of deatho Motor neurons die inability of brain to initiate

and control muscle movements Respiratory arrest Paralysis

o Asymmetric hand weakness, fasciculations, progressive muscle atrophy

Why Ice bucket challenge?o Numbness of entire body (main manifestation of ALS): NUMB

ALL OVER

“Lou Gehrig’s disease”Lou Gehrig, a famous baseball player for the New York Yankees had this disease


MidbrainL: Normal substantia nigraR: Depigmented (pallor of substantia nigra) Parkinson’s disease

Top: Lewy bodyRound, pink inclusion: 2 parts- Inner area (dense core)- Outer area (pale halo)Accumulation of alpha-synuclein

Very thinned out anterior nerve roots (very

characteristic of ALS) L: Spinal cord with

unstained areas Loss of myelinated fibers associated with degeneration

R: Bunina bodies noted within the neurons (Make

use of PAS stain)

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READ ON : one case daw dito…

MULTIPLE SYSTEM ATROPHY (MSA)o Presence of glial cytoplasmic inclusions, typically within the cytoplasm

of oligodendrocyteso Different patterns of clinical presentationo Dominant symptoms:

Parkinsonism (MSA-P: striatonigral degeneration) Cerebellar dysfunction (MSA-C: olivopontocerebellar atrophy)

- Least frequently observed Autonomic dysfunction (MSA-A: Shy-Drager Syndrome)

o Gross Morphology: Cerebellar forms: atrophy of cerebellum, including the cerebellar

peduncles, pons (basis pontis), medulla (inferior olive) Parkinsonian: atrophy of substantia nigra and striatum (putamen) Autonomic: usually no gross findings Atrophic brain regions show evidence of neuronal loss and variable

numbers of neuronal cytoplasmic and nuclear inclusionso Microscopic:

Diagnostic glial cytoplasmic inclusions in oligodendrocytes with silver impregnation

Contain alpha-synuclein, ubiquitin, alpha-beta-crystallin Inclusions are ultrastructurally distinct from other

neurodegenerative disease Similar inclusions may also be found in the cytoplasm of neurons,

neuronal and glial nuclei, and in axonso Pathogenesis:

The relationship between glial cytoplasmic inclusions and disease is supported by the observation that the inclusions are present in low numbers at earliest stages of MSA and increase in abundance as the disease progresses, although they eventually disappear as cells die in the final stages

Glial cytoplasmic inclusions can occur in the absence of neuronal loss, suggesting that they may represent a primary pathologic event

Several studies: no up-regulation of alpha-synuclein expression- Suggest protein is acquired secondarily by oligodendrocytes

from injured or dying neurons

HUNTINGTON'S DISEASE (13!)o ADo Progressive movement disorders and dementiao Degeneration of striatal neuronso Jerky, hyperkinetic, sometimes dystonic movements involving all parts

of the body (chorea) are characteristico May later develop parkinsonism with bradykinesia and rigidityo Relentlessly progressive, ave. course of about 15 years to deatho Microscopic:

Small brain and shows striking atrophy of the caudate nucleus, and less markedly at early stages, the putamen

Globus pallidus may be atrophied secondarily, and the lateral and 3rd ventricles are dilated

Atrophy is frequently seen in the frontal lobe, less in parietal lobe and occasional in the entire cortex

Severe loss of striatal neurons - Most marked changes in caudate nucleus, especially in tail and

portions nearer the ventricle- Putamen: later stages of disease- Nucleus accumbens: best preserved portion of the striatum

Two populations of neurons spared:- Diaphorase positive neurons that contain nitric oxide synthase- Large cholinesterase positive neurons

Fibrillary gliosis that is more extensive than in the usual neuronal loss

Protein aggregates containing HUNTINGTIN can be found in the neurons in the striatum and cerebral cortex

o Direct relationship: degree of degeneration in the striatum and severity of symptoms

o Pathogenesis: Loss of medium spiny striatal neurons lead to dysregulation of the

basal ganglia circuitry that modulates motor input- Normal function: dampen motor activity- Degeneration results in increased motor output

(choreoathetosis) Cognitive changes probably related to neuronal loss from cerebral

cortex Huntingtin:

- Little evidence to suggest that the disease is caused by haploinsufficiency related to a mutated allele

o Clinical features:


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Onset: MC in 4th and 5th decade Related to length of CAG repeat in the HD gene Motor symptoms often precede cognitive impairment Movement disorder: choreiform, with increased and involuntary

jerky movements of all parts of the body- Writhing movements of extremities are typical

Early symptoms of higher cortical dysfunction:- Forgetfulness, thought and affective disorders, progression to a

severe dementia Increased risk of suicide Intercurrent infection: MC natural cause of death

FREIDRICH ATAXIAo Spinocerebellar degeneration, AR progressive illnesso Beginning in the 1st decade of life with gait ataxia, followed by hand

clumsiness and dysarthriao DTR are absent or depressed,

Extensor plantar reflex is typically presento Joint position and vibratory sense are impairedo Sometimes, loss of pain and temperature sensation and light toucho Most develop pes cavus and kyphoscoliosiso High incidence of cardiac arrhythmia and CHFo Concomitant diabetes found in 10% of patientso Most: wheel-bound within about 5 years of onseto Cause of death: intercurrent pulmonary infections and cardiac diseaseo Extremely low levels of FRATAXIN

Normally in inner mitochondrial membrane Role in iron regulation

- Mutation: generalized mitochondrial dysfunctiono Morphology:

SC shows loss of axons and gliosis in posterior columns, distal portions of CST, and spinocerebellar tracts

Degeneration of neurons in SC (Clarke column), BS (CN nuclei VIII, X, XII), cerebellum (dentate nucleus & Purkinje of superior vermis), Betz cells of motor cortex

Decreased large dorsal root ganglion neurons- Secondary degeneration of myelinated axons

o Heart is enlarged and may have pericardial adhesions Multifocal destruction of myocardial fibers with inflammation and

fibrosis is detectable in half of individuals in autopsy

ATAXIA TELANGIECTASIAo ARo Characterized by ataxic-dyskinetic syndrome beginning in childhood,

with subsequent development of telangiectasia in the conjunctiva and skin; and immunodeficiency

o ATM gene encodes a kinase with a critical role in orchestrating the cellular response to double-stranded DNA breaks

o Increased sensitivity to X-ray induced chromosome abnormalities Cells continue to replicate the damaged DNA

o Carrier: 1% Mutated ATM allele may underlie an increased risk of cancer

(breast Ca)o Mutation in ATM results in failure to remove cells with DNA damage

from developing nervous system, predisposing to degenerationo Morphology:

Predominantly in the cerebellum, with loss of Purkinje and granule cells

Degeneration of dorsal columns, spinocerebellar tracts, and anterior horn cells

Peripheral neuropathy Telangiectatic lesions:

- In CNS, conjunctiva, skin of face, neck, arms Cells in many organs show a bizarre enlargement of nucleus to 2-

5x normal size- Schwann cells on dorsal root ganglia and peripheral nerves,

endothelial cells, pituicytes- Referred to as amphicytes

LN, thymus, gonads are hypoplastico Clinical Features

Relentlessly progressive, with death early in second decade Recurrent sinopulmonary infections and unsteadiness in walking Speech becomes dysarthric Eye movement abnormalities Many develop lymphoid neoplasms, often T-cell leukemias, gliomas

and carcinomas


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METABOLIC DISEASESCASEA 62-year-old chronic alcoholic was seen confused and wandering. He had peripheral neuropathy, diplopia, nystagmus, and difficulty in walking. He expired after few days to lobar pneumonia. On autopsy, the brain showed this finding

DIAGNOSIS: Wernicke's encephalopathyo Thiamine deficiency, rapid

GENETIC METABOLIC DISEASESo Neuronal storage disease

Autosomal recessive: enzyme deficiency- Tay-Sachs' disease

o Leukodystrophies Myelin abnormalities either in synthesis or turnover

- Progressive degeneration of myelinated white matter of the brain

- Metachromatic leukodystrophy: Krabbe's diseaseo Mitochondrial encephalomyopathies

Problem in the mitochondria Disorders of oxidative phosphorylation

- MELAS: Mitochondrial Encephalomyopathy and lactic acidosis and stroke like episodes Manifest like stroke + progressive muscle weakness

because of lactic acidosis (encephalo: brain & myopathy: muscles)

- Ragged red fibers: associated with myoclonic epilepsy

TOXIC AND ACQUIRED METABOLIC DISEASESo Hypoglycemia or hyperglycemia

Same manifestation: altered consciousness

Hypoglycemia : target pyramidal neurons of cerebral cortex, Sommer section of Hippocampus and Purkinje cells of Cerebellum- Cells also commonly affected by hypoxia

Hyperglycemia : DKA or HONK- MC manifestation: Severe cerebral edema

o Hepatic encephalopathy Accumulation of ammonia reactive gliosis and neuronal loss

o Carbon Monoxide Poor delivery of oxygen to the brain Neuronal layer 3, 5 of cerebral cortex, Sommer section of

hippocampus and Purkinje cells of cerebellum (same cells affected by hypoxia)- Carbon monoxide competes with oxygen in the blood

o Combined methotrexate and radiation-induced injury Common in patients in chemotherapy Manifests with drowsiness, confusion, ataxia Necrosis of white matter: axonal degeneration and surrounding

reactive gliosiso Radiation

High doses coagulative + liquefactive necrosis with subsequent edema

Neuronal loss, reactive gliosis altered mental statuso Methanol

Occupational exposure (factories); usually analytic grade Target retinal ganglion cells blindness Focal necrosis of white matter


Small area with mamillary bodies punctate hemorrhages

Very characteristic finding

Left: Cerebellar degeneration in ethanol toxicityAcute onset: reversible symptomsChronic: Wernicke Korsakoff encephalopathy Atrophic: widening of cerebellar

vermis Common manifestation: ataxia,

unsteady gait, nystagmus

Right: Bergmann gliosisLoss of Purkinje cells No layering Predominating small blue dots: glial

Cyanocobalamin (B12) deficiency Subacute combined degeneration of

the spinal cord Degeneration: patches of

unmyelinated areas (Luxol Fast Blue PAS)

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CNS TUMORSCASEA 3-year-old boy was brought by his parents to a physician due to loss of balance. His speech is more slurred now. He had a wide-based gait. He was also seen bobbing his head. A midline tumor was noted

Problem in balance: affectation of cerebellum Microscopy:o Small round blue cells (blastic), highly cellular

neoplasm, proliferation of small hyperchromatic cells

o See Homer-Wright rosettes

DIAGNOSIS: Medulloblastomao Commonly presents as cerebellar dysfunctiono Primitive cells tend to have the same features irregardless of locationo Associated with high incidence of hydrocephalus (push the pathways of

CSF)

GENERALITIESo Found intracranial, slow and subtle onseto Malignant > benigno 15% SC and 85% braino Primary malignancy > metastasis

Gliomas: MC primary malignancy

MANIFESTATIONSo Headache, seizures, mental changes, increased ICP symptoms, focal

neurologic symptomso Depend on size: benign tumors can be fatal due to brain compression

LOCATION OF CNS TUMORSo Tentorium cerebelli: extension of dura matter dividing cerebellum and

inferior portion of occipital lobe

Supratentorial: above the tentorium- Commonly seen in tumors of adults- Cerebrum, basal ganglia,

thalamus and hypothalamus

Infratentorial: below the tentorium- Tumors of children- Cerebellum, midbrain and

brainstem

MC NEOPLASMSo Adults

Astrocytoma Glioblastoma [multiforme]

- MC primary intracranial malignancy in adults Meningioma: 2nd MC

- 3rd MC: Schwannoma Metastasis

o Children Astrocytoma Medulloblastoma: MC Both glioblastoma and medulloblastoma are aggressive tumors:

diagnosed in their late stages

STAGING OF CNS TUMORS

TUMOR SIZE STAGE

Most ImportantSUPRATENTORIAL INFRATENTORIAL

T1 </= 5 cm, unilateral <= 3 cm, unilateralT2 >5 cm, unilateral >3 c, unilateralT3 Invades the ventricular systemT4 Crosses the midline/invades supra- or infratentorially

GRADING OF CNS TUMORSMost important basis for prognosis and treatment

WHO Grading

GRADING T1 T2 T3 T4I IA IB IVII IIA IIBIII IIIA IIIBIV IV


Thiamine (B1) deficiency Pinpoint hemorrhages and areas of

necrosis in mamillary bodies (near the hypothalamus)

Wernicke-Korsakoff encephalopathy Memory disturbances, psychosis, eye

problems (diplopia or nystagmus) Chronic alcoholism

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M1

FOUR BASESo Nuclear atypia (pleomorphism)o Mitotic activityo Necrosis o Vascular endothelial hyperplasiao **If see 4 features: high-grade tumor

PROGNOSISo Correlates well with grading of tumoro Associated with response of patient with treatment protocol,

particularly radiationo Consider age when tumor was diagnosed

GRADE OVERALL PICTURE

<50 Y/O >50 Y/O

I 50% survive - -II 4 years 5.5 years 0.5 yearsIII 1.6 years 2.5 years 0.7 yearsIV 0.7 years 1 year 0.5 years

***Grade III in > 50y/o: already symptomatic easy to diagnose immediate treatment

Grade I: Don't usually show symptomsGrade II: HeadacheGrade III: mental dysfunctionGrade IV: severe

HISTOLOGIC CLASSIFICATIONo Gliomas

Infiltrating fibrillary astrocytoma: largest group of gliomas- Main presentation: based on size, location- Prognosis: depends on WHO grading

Other glial tumors: oligodendroglioma, ependymoma, choroid plexus papilloma

o Others Neuronal tumors: ganglioma Primitive tumors: medulloblastoma Other tumors: meningioma, peripheral nerve tumors, metastatic

tumors, paraneoplastic syndromeo Treatment protocol: increase survival rate by 25%

Gliomas: 5 YSR GBM: less than 5 YSR

PILOCYTIC ASTROCYTOMAo WHO Grade 1o Good prognosiso Benign behavioro Affects growing children and young adultso Picture

Cystic space, well-circumscribed Cerebellum (MC), floor and walls of third ventricles, optic

nerves and cerebrum Like gelatin in consistency

o Glial fibrillary acidic protein + (MC stain used to identify astrocytomas) Eosinophilic granular bodies: characteristic of tumor Pinkish Hair-like extensions: Rosenthal fibers

o Treatment: Resection

DIFFUSE ASTROCYTOMAo WHO Grade IIo Capacity to grow exponentiallyo Subtle onset but could have progressive manifestation aggressiveo Grossly: poorly defined tumor

Similar to pilocytic astrocytoma: gelatinous surfaceo Microscopically

Higher cellularity Differentiation in sizes of fibrillary structures Positive for GFAP: brown color

GEMISTOCYTIC ASTROCYTOMAo WHO Grade IIIo Gemistocytes: Astrocytes that have pleomorphic appearanceo Abundance of eosinophilic cytoplasm push nuclei towards one side

ANAPLASTIC ASTROCYTOMAo WHO Grade IIIo Difficult to differentiate with other astrocytomao More dense cellular pattern o Variability of sizes and shapes of astrocyteso Mitotic figures present

GLIOBLASTOMA [MULTIFORME]o WHO Grade IVo High-grade tumor due to presence of necrosis

Hemorrhagic ill-defined area, necrotic center paler than periphery o Microscopically

Pseudopalisading pattern of tumor cells Surrounds pinkish areas: necrotic areas Increased in vascular endothelial proliferation (normal: single lined)

- See tufting of vascular supply: glomeruloid-like body


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Presence of mitotic figures Vascular proliferation

OLIGODENDROGLIOMAo WHO Grade II/IIIo 4th to 5th decadeo Common location: white matter of cerebrumo Gross: Gelatinous surface, well circumscribed, often with cystic space

With associated hemorrhage, calcificationso Microscopically

Grade II : sheets of similar fried egg looking cells- Very cellular: closely packed proliferating oligodendrocytes

Grade III : nuclear pleomorphism- Denser, anaplastic, pleomorphic appearance, - Prominence of vascular supply, proliferation of endothelial

lining

EPENDYMOMAo WHO Grade II/IIIo MC intramedullary tumor (within the spinal cord)o Often noted at 1st decade of life (ventricles)o Adult onset (spinal cord)o Grossly

Warty projections: finger like papillary masses extended into ventricular surface

o Microscopically GRADE II

- Regular round cells surrounding a vascular channel: ependymal rosettes

- Pinkish area devoid of nucleus: fibrillary extension of ependymal cells

- Perivascular pseudorosettes GRADE III

- Glandular structures- Pseudorosettes- Tubular acinar structures- Increased cellularity- Predominance of necrosis and mitosis- Poorer prognosis

MYXOPAPILLARY EPENDYMOMAo WHO Grade II/IIIo Filum terminale of spinal cordo Myoid background: see more of vacuolationo Myxomatous change: mucinous background or slimy surfaceo Cuboidal cells lining vascular channels interspersed vacuolated areaso Form around the vascular channelso Prognosis depends on grading

Young patient with hydrocephalus: 5YSR is 50%

CHOROID PLEXUS PAPILLOMAo WHO Grade Io Children: lateral ventricleo Adult: fourth ventricleo Common manifestation: hydrocephalus due to obstruction of flowo Transformation to malignant tumor seen more in children than in

adultso Papillary growth simulating normal choroid plexuso Microscopically: finger like projections

Papillae supported by very thin fibroconnective tissue Lined by ependymal cells (cuboidal to columnar)

GANGLIOGLIOMAo WHO Grade Io MC location: temporal lobeo Composed of irregular clusters of ganglion cellso Similar to astrocytoma

Difference: ganglioglioma has no mitosis, necrosis, positive reaction to chromogranin or synaptophysin

MEDULLOBLASTOMAo WHO Grade IVo MC CNS tumor arising from a primitive neuroepitheliumo Mass seen near cerebellum

Children: midline location Adult: lateral location

o MC manifestation: hydrocephaluso Grade IV but radiosensitiveo Microscopic:

Proliferation of small, round tumor cells: from primitive neuroepithelium

Very characteristic: tendency to form pseudorosettes called Homer-Wright - Lumen: with glial processes

Flexner-Wintersteiner: in retinoblastoma - Empty lumen

MENINGIOMAo WHO Grade 1o MC benign tumor of adulto MC extramedullary tumor: outside the spinal cord but within the

dura matero Gross

Fixed in meninges Well-circumscribed round mass Compress adjacent brain tissue

o Morphologic patterns Whorling: Syncytial meningothelial Calcified: Psammomatous/Psammoma bodies


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- Starts syncytial then become calcified No prognostic significance

ATYPICAL MENINGIOMAo WHO Grade IIo Higher recurrence rate, more aggressive than the usual meningiomao Radiation therapyo No usual syncytial or psammomatous arrangemento Increase cellularity, pleomorphism and mitosis noted

ANAPLASTIC MENINGIOMAo WHO Grade IIIo Highly aggressive tumoro Course similar to sarcomatous lesiono See multilayer of cells surrounding a vascular coreo Aka “Papillary meningioma”

SCHWANNOMAo WHO Grade 1o “Neurilemmoma”o Arising from cells derived from neural crest: Schwann cellso Located in cerebellopontine angleo Attached to CN VIII: “Acoustic neuroma”o Tendency to compress adjacent structure: brain stem and SCo Benign lesion with fatal outcomeo Well-circumscribed lesion, encapsulated (very thin)

On cut section: cystic structureo Antoni A: cellular

Verocay bodies: absence in central area; palisading processes surrounding central area

o Antoni B: hypocellular

NEUROFIBROMAo WHO Grade 1o Discretely delineated masso Seen on the skin or attached to a nerveo One component of Neurofibromatosiso Microscopic:

Snake-like/S-like cells that are wavy or eosinophilic More compact appearance of spindle cells

o Treatment: resection

OTHER TUMORSo Paraneoplastic syndromes

Immune response against tumor antigens that cross react with antigens in CNS/PNS

o Familial tumor syndromes Usually AD

o Metastatic tumors

NEUROFIBROMATOSIS TYPE Io Lisch nodule: marked melanin deposition in affected eye (iris)o Café-au-lait spots: marked melanin deposition on skin

TUBEROUS SCLEROSISo Mushroom like masses within the ventricular systemo Manifests as hydrocephalus

METASTATIC TUMORS o 25-50% of intracranial tumorso 80%: Lungs, Breast (Lung: MC)o Others: melanoma, kidney, GIT, choriocarcinomao 50% extracranial: meninges (dura)

Extradural: site of metsGrosso Presence of multifocal/multiple lesions

Microscopico See vacuolated larger tumor cells: more of epithelial origin due to

vacuolation

PRIMARY METASTATICPoorly circumscribed Well-circumscribed

Usually single Often multipleLocation varies and depend on

specific typeUsually located at the junction

between the white and gray matter

Pictures to follow

Pagdating sa Patho: Pagdating padin sa patho:


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~ FIN ~


Documents

(7) Surgical Pathology - Diseases of the Central Nervous System 401 - Dr. Baby Lynne Asuncion - October 20-28, 2014