PATH375 Lecture 10 - CNS PDF

PATHOLOGY 375 LECTURE 10: CENTRAL NERVOUS SYSTEM MIKE NIMMO, MD, FRCPC CLINICAL PROFESSOR DEPARTMENT OF PATHOLOGY AND LABORATORY MEDICINE FACULTY OF MEDICINE, UNIVERSITY OF BRITISH COLUMBIA OBJECTIVES 1. Describe the structure and function of the central nervous system. 2. Describe causes and sym...

PATHOLOGY 375 LECTURE 10: CENTRAL NERVOUS SYSTEM MIKE NIMMO, MD, FRCPC CLINICAL PROFESSOR DEPARTMENT OF PATHOLOGY AND LABORATORY MEDICINE FACULTY OF MEDICINE, UNIVERSITY OF BRITISH COLUMBIA OBJECTIVES 1. Describe the structure and function of the central nervous system. 2. Describe causes and symptoms of increased intracranial pressure. 3. Describe causes and clinical presentations of dysraphic developmental disorders, intracranial hemorrhage and cerebrovascular disease. 4. Describe classification of CNS trauma. 5. List causes and characteristics of CNS infections. 6. Describe clinical and pathologic features of multiple sclerosis. 7. Describe metabolic, nutritional and neurodegenerative diseases of the CNS. 8. Describe the neoplasms associated with the central nervous system. 2 STRUCTURE OF THE CNS (BRAIN & SPINAL CORD) • Brain includes cerebrum, cerebellum and brainstem. • Cerebrum (left + right hemispheres). • 4 lobes: • Frontal (motor, behavior, emotions, higher intellectual functions) • Temporal (hearing and smelling). • Parietal (sensory). • Occipital (visual center). • Surface arranged into gyri, invaginations are called sulci. • Basal ganglia: • Group of subcortical nuclei that includes substantia nigra. • Supply inhibitory signal to skeletal muscle, coordinate skeletal muscle contractions. 3 https://medlineplus.gov/ency/imagepages/1074.htm https://www.bioscience.org/2018/v23/af/4586/figures.htm 4 https://neupsykey.com/stroke-7/ STRUCTURE OF THE CNS - BRAIN • Cerebrum cont’d: • Thalamus – center for integrating sensory stimuli and for consciousness. • Hypothalamus – regulates many body functions (temperate, heart rate, blood pressure, thirst, appetite, hormonal regulation). • Cerebellum: • Regulation of motor function, balance, muscle tone. • Brain stem: • Consists of mid brain, pons, medulla oblongata. • Important centers that regulate elementary body functions (e.g. cardiac, vasomotor, respiratory centers located in medulla). 5 http://droualb.faculty.mjc.edu/Lecture%20Notes/Unit%205/chapter_15_the_brain%20Spring%2007with%20figures.htm STRUCTURE OF THE CNS Meninges • Specialized layers of connective tissue surrounding the brain • Dura mater, arachnoid mater, pia mater. Cerebrospinal fluid (CSF) • Circulates through system of channels [ventricles (third, lateral, fourth), subarachnoid space, spinal cord]. • Produced in choroid plexus, reabsorbed by arachnoid granulations. • Serves as cushion, exchange of materials. 6 https://www.smallpocketlibrary.com/2020/07/cranial-meninges.html https://commons.wikimedia.org/wiki/File:1317_CFS_Circulation.jpg Brain histology • Neurons: dendrite, cell body, axon. • Glial (support) cells: • Astrocytes, oligodendroglia (Schwann cells in PNS), microglia, ependymal cells. 7 https://medlineplus.gov/ency/imagepages/18117.htm https://commons.wikimedia.org/wiki/File:Figure_35_01_06.jpg https://en.wikipedia.org/wiki/Grey_matter#/media/File:Grey_matter_and_white_matter_-_very_high_mag.jpg STRUCTURE OF THE CNS – SPINAL CORD • Spinal cord consists of gray and white matter. • Gray matter (Butterfly-like shape): • Anterior/ventral horn (motor neurons). • Contains lower motor tract neurons which gives rise to peripheral nerves  extend to muscles. • Posterior/dorsal horn (sensory neurons). 8 https://courses.lumenlearning.com/ap1x94x1/chapter/the-spinal-cord/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5743665/ STRUCTURE OF THE CNS – SPINAL CORD • White matter: • Consists of myelinated nerve fibers. • Descending motor tracts (e.g. corticospinal tract) contain upper motor neurons. • Ascending sensory tracts (e.g. dorsal column) are axonal extension of neurons located in spinal ganglia. 9 https://courses.lumenlearning.com/ap1x94x1/chapter/the-spinal-cord/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5743665/ Sensory tracts (ascending) Motor tracts (descending) 10 https://open.oregonstate.education/aandp/chapter/14-5-sensory-and-motor-pathways/ Peripheral nerve histology • Axons that pass out of brain stem or spinal cord are myelinated by Schwann cells. • Anterior spinal roots join with posterior roots to form peripheral nerve trunks. • Motor nerves end peripherally at muscle end plates and sensory nerves are associated with peripheral sensory endings. 11 https://www.frontiersin.org/articles/10.3389/fncel.2017.00347/full https://upload.wikimedia.org/wikipedia/commons/a/ac/1319_Nerve_StructureN.jpg OBJECTIVES 1. Describe the structure and function of the central nervous system. 2. Describe causes and symptoms of increased intracranial pressure. 3. Describe causes and clinical presentations of dysraphic developmental disorders, intracranial hemorrhage and cerebrovascular disease. 4. Describe classification of CNS trauma. 5. List causes and characteristics of CNS infections. 6. Describe clinical and pathologic features of multiple sclerosis. 7. Describe metabolic, nutritional and neurodegenerative diseases of the CNS. 8. Describe the neoplasms associated with the central nervous system. 12 IMPORTANT CONCEPTS REGARDING CNS PATHOLOGY • CNS function is highly organized and localized: • Localized lesion produces localized symptoms. • CNS is contained within a closed space, with fixed internal volume: • Increase volume results in herniation. • Blood brain barrier maintains constant environment. • Brain and spinal cord surrounded by cerebrospinal fluid (CSF): • Alterations in CSF composition provides information as to disease. • Neurons are incapable of division: • Loss of neurons not replaced. • Neural cell tumors occur in children. • Glial cells are dividing cells: • Brain tumors in adults are gliomas. • Unique CNS diseases (neurotropic organisms, neurodegenerative diseases). 13 PATHOLOGY OF THE CNS - SYMTPOMS • CNS consists of highly specialized functional units. • Lesion in certain region results in predictable functional defect(s). • Eg. injury to: • Occipital lobe (visual center)  blindness. • Precentral gyrus (motor area of cerebral cortex)  motor defects (paralysis). • Symptoms result from dysfunction of, or loss function of neurons. 14 INCREASED INTRACRANIAL PRESSURE (ICP) • CNS is contained within a closed space, with fixed internal volume. • Intracranial contents: • Brain parenchyma, CSF, blood. • ICP is pressure of CSF. • Increased ICP is life threatening condition. • Causes: • Brain parenchyma: tumor, cerebral edema. • CSF outflow obstruction • Alterations in cerebral blood volume: intra-cerebral hemorrhage, hematoma. 15 INCREASED ICP • Symptoms include headache, vomiting, vision change, loss of consciousness, death. • If pressure is not relieved may get herniation of brain. • Brain herniation = movement of brain tissue from normal intracranial compartment to another. • Different types of herniation depending on where brain moves to (extracranial, subfalcine, transtentorial and tonsillar). • Death may result from compression of vital centers (eg. compression of medulla oblongata from tonsillar herniation). 16 https://en.wikipedia.org/wiki/Falx_cerebri#/media/File:Falxcerebri.jpg https://pubs.rsna.org/doi/full/10.1148/rg.2019190018 PATHOLOGY OF THE CNS - SYMTPOMS • Space occupying lesions: • Specific deficits depending on location. • Symptoms may result from: • Loss of neurons  Alzheimer’s. • Abnormal function of neurons  Parkinson’s. • Abnormal excitation of neurons  Epilepsy (seizures) • Psychiatric disease: • Eg. Schizophrenia, bipolar psychosis. • Caused by abnormal function of brain cells. • Exact nature of dysfunctions unknown and not described in pathologic terms. 17 OBJECTIVES 1. Describe the structure and function of the central nervous system. 2. Describe causes and symptoms of increased intracranial pressure. 3. Describe causes and clinical presentations of dysraphic developmental disorders, intracranial hemorrhage and cerebrovascular disease. 4. Describe classification of CNS trauma. 5. List causes and characteristics of CNS infections. 6. Describe clinical and pathologic features of multiple sclerosis. 7. Describe metabolic, nutritional and neurodegenerative diseases of the CNS. 8. Describe the neoplasms associated with the central nervous system. 18 DYSRAPHIC MALFORMATIONS • Group of congenital malformations characterized by incomplete closure of the neural tube, or bones protecting CNS. • Cranial (incomplete formation of cranium) Figures from genetics/developmental disorders lecture • Destruction of brain in utero with resulting anencephaly. • Spinal dysraphism (incomplete closure of posterior spine) • Spina bifida occulta: • Defects in vertebral bones, but not opening or sac. • Meningocele: • Defect in bone with opening/sac in back (protrusion of meninges through defect). • Myelomeningocele: • Defect in bone with opening/sac in back containing parts of spinal. https://commons.wikimedia.org/wiki/File:Anencephaly-web.jpg https://www.cdc.gov/ncbddd/spinabifida/facts.html https://commons.wikimedia.org/wiki/File:Spina-bifida.jpg 19 INTRACRANIAL HEMORRHAGE • Classified into 4 groups based on location. • Epidural hematoma: • Arterial hemorrhage: space between skull and dura. • Usually due to trauma (MVA), not immediately apparent, takes several hours to form. • If unrecognized, lethal. • Subdural hematoma: • Venous hemorrhage: space between dura and arachnoid. • Symptoms slower onset than epidural hematoma (present within 48 hours of injury). • Falls in patients with cerebral atrophy (alcoholics, elderly). Pediatrics in Review September 2019, 40 (9) 468-481 20 INTRACRANIAL HEMORRHAGE • Subarachnoid hemorrhage • Hemorrhage into space between arachnoid and pia (brain surface). • Usually due to trauma, also rupture of aneurysms (Berry aneurysms). • Intracerebral hemorrhage • Hemorrhage into substance of the brain from intracerebral vessels x • Causes: • Traumatic. • Non-traumatic: stroke, tumor. Pediatrics in Review September 2019, 40 (9) 468-481 21 CEREBROVASCULAR DISEASE • Secondary to disease of blood vessels supplying the CNS. • Clinical manifestation of CVD is stroke (aka ‘brain attack’). • • Categorized as: ischemic (85%) or hemorrhagic (15%). Need to act F.A.S.T (ideally treatment started within a few hours of symptoms). • • F – Face (is it drooping). • A – Arms (can both arms be raised). • S – Speech (is it slurred or jumbled) • T – Time to call 911 if any of above signs present. Ischemic: • Related to atherosclerosis of cerebral arteries or thromboembolic occlusion of cerebral arteries. • CNS is susceptible to localized or global ischemia. 22 Fig 21-6. Cerebral infarcts. Pathology for the Health Professions, 2012 CEREBROVASCULAR DISEASE • Global ischemia: • Generalized reduction of oxygen supply. • Two major patterns of injury: • Multiple small foci of ischemic necrosis. • May occur due to atherosclerosis, results in multiinfarct dementia (progressive mental deterioration). • Hypoperfusion from cardiac failure or any form of shock. • Mechanisms of shock: • Pump failure  Cardiogenic shock • Loss of fluid  Hypovolemic shock • Loss of peripheral vascular tone  Hypotonic shock • Region furthest from blood supply most susceptible to hypotension (watershed zone). 23 Fig 21-6. Cerebral infarcts. Pathology for the Health Professions, 2012 CEREBROVASCULAR DISEASE • Focal ischemia: • Ischemic necrosis of localized part of cerebral cortex. • Usually thromboembolic origin. • Either from mural thrombus after myocardial infarct. • Or embolus from cardiac valve (endocarditis). • Pathologic changes  liquefactive necrosis: • Necrosis characterized by dissolution of tissue. • Necrotic area is soft and filled with fluid. • Brain surrounding infarct is edematous  profound neurologic deficits (depend on site of occlusion). • May get partial resolution as edema subsides. • Physical and occupational therapy important to long term rehabilitation. 24 CEREBROVASCULAR DISEASE • Hemorrhagic stroke: • Strokes resulting from rupture of blood vessel, no occlusion. • Causes: • Hypertension: • Chronic severe systemic hypertension is most common cause. • Usually occur in the basal ganglia. • Cerebral amyloid angiopathy. • Cerebral arteriovenous malformation. • Intracranial aneurysm. https://www.bioscience.org/2018/v23/af/4586/figures.htm https://medicine.tamu.edu/class-files/webpath16/tutorial/stroke/stroke011.htm 25 OBJECTIVES 1. Describe the structure and function of the central nervous system. 2. Describe causes and symptoms of increased intracranial pressure. 3. Describe causes and clinical presentations of dysraphic developmental disorders, intracranial hemorrhage and cerebrovascular disease. 4. Describe classification of CNS trauma. 5. List causes and characteristics of CNS infections. 6. Describe clinical and pathologic features of multiple sclerosis. 7. Describe metabolic, nutritional and neurodegenerative diseases of the CNS. 8. Describe the neoplasms associated with the central nervous system. 26 CNS TRAUMA • Concussion: • Syndrome of altered consciousness secondary to head injury. • Transient neurologic dysfunction (loss of consciousness, temporary respiratory arrest, loss of reflexes). • No significant macroscopic or microscopic brain changes. • Contusion (analogous to bruising of soft tissue): • Secondary to disruption of blood vessels due to trauma. • Contusion at site of impact = Coup injury (from direct force) • Contusion at opposite site of impact = Contrecoup injury (from deceleration of brain). • Laceration (analogous to tearing of of soft tissue): • Typically caused by open trauma disrupting integrity of brain. • Severe form of injury with tearing of brain. 27 https://commons.wikimedia.org/wiki/File:Contrecoup.svg CNS TRAUMA • Spinal cord injuries: • Spinal cord protected by vertebrae (cervical, thoracic, lumbar, sacrum, coccyx). • Cervical spinal cord is most vulnerable due to greatest mobility. • Hyperextension injury, a force to the forehead forces head backwards. • Hyperflexion injury, impact on the occiput forces head forwards. • May cause ligament rupture, compression of spinal nerves, transection of spinal cord. 28 OBJECTIVES 1. Describe the structure and function of the central nervous system. 2. Describe causes and symptoms of increased intracranial pressure. 3. Describe causes and clinical presentations of dysraphic developmental disorders, intracranial hemorrhage and cerebrovascular disease. 4. Describe classification of CNS trauma. 5. List causes and characteristics of CNS infections. 6. Describe clinical and pathologic features of multiple sclerosis. 7. Describe metabolic, nutritional and neurodegenerative diseases of the CNS. 8. Describe the neoplasms associated with the central nervous system. 9. Describe the structure and function of the skin. 10. Describe different types of external injury to skin and grading of burns. 11. Describe idiopathic and immune skin disorders. 12. Describe features of common skin neoplasms. 29 CNS INFECTIONS • Infections can be acquired by: • Hematogenous/vascular spread (most common). • Direct extension from adjacent structures. • Ascending neural route (eg. Rabies). • Forms of CNS infections: • Myelitis is inflammation of spinal cord parenchyma (poliomyelitis). • Encephalitis is inflammation of cerebral parenchyma (viral). • Meningitis is inflammation of the meninges. • Cerebral abscess (bacteria) – localized suppurative infection. 30 CNS INFECTIONS – MENINGITIS • Usually caused by infection. • Broadly classified into: • Acute pyogenic (bacterial) meningitis: • Group B streptococci (neonates). • Neisseria meningitides (children). • Streptococcus pneumoniae (adults). • Aseptic (viral) meningitis: • Misnomer, term referring to absence of recognizable organism. • Etiologic agent can be identified in only minority of cases. • Chronic meningitis: • Tuberculosis, Fungal infections, lyme disease, syphilis. • Meningoencephalitis = meningeal and brain parenchymal inflammation. 31 CNS INFECTIONS – VIRUSES • Usually cause encephalitis. • CNS may be involved in systemic viral infections (herpes, measles, rubella). • Some viruses selectively attack the CNS (rabies, tick borne viruses). • The immunocompromised are at increased risk of viral CNS infections. • HIV affects the CNS  causes AIDS related encephalopathy. • HIV infects T lymphocytes, which ‘import’ virus to CNS. • Secretion of cytokines, some are toxic to neurons  consequence = AIDS related dementia. • HIV patients increased risk for opportunistic infections (Toxoplasma and Cryptococcus). 32 CNS INFECTIONS • Prions • Small infectious protein particles (do not contain DNA or RNA). • Prions infect nervous system selectively. • Most common diseases is Creutzfeldt-Jakob disease (CJD). • Bovine spongiform encephalopathy is prion disease in cows. • Brain undergoes spongiform degeneration (prion disease is also known as transmissible spongiform encephalopathy). • Protozoa • Toxoplasmosis occurs as an opportunistic infection in AIDS. • Fungi • Candida, Aspergillus, and Cryptococcus may cause CNS infections in immunocompromised individuals. 33 OBJECTIVES 1. Describe the structure and function of the central nervous system. 2. Describe causes and symptoms of increased intracranial pressure. 3. Describe causes and clinical presentations of dysraphic developmental disorders, intracranial hemorrhage and cerebrovascular disease. 4. Describe classification of CNS trauma. 5. List causes and characteristics of CNS infections. 6. Describe clinical and pathologic features of multiple sclerosis. 7. Describe metabolic, nutritional and neurodegenerative diseases of the CNS. 8. Describe the neoplasms associated with the central nervous system. 34 MULTIPLE SCLEROSIS • Autoimmune demyelinating disease. • Characterized by chronic relapsing and remitting course. • Most common immunologic CNS disease, usually 25 to 45 yo patients. • Pathogenesis not known: • More prevalent in colder climates. • Genetic component. • Immunologic studies reveal: • T lymphocytes in MS lesion belong to a few clones, likely sensitized to some component of myelin. • B lymphocyte clones respond to some unidentified antigen. 35 MULTIPLE SCLEROSIS • Pathology: • Demyelinating disease that typically involves white matter. • Demyelination leads to typical plaques (common in white matter of brain, spinal cord, optic nerve). • Both sensory and motor symptoms • Limb weakness, loss of sensation with tingling, blurred vision. • Clinical criteria to establish diagnosis. • MRI highlights areas of demyelination • Unpredictable course. • Most physically incapacitated over 20-30 year period. 36 https://neuropathology-web.org/chapter6/chapter6aMs.html OBJECTIVES 1. Describe the structure and function of the central nervous system. 2. Describe causes and symptoms of increased intracranial pressure. 3. Describe causes and clinical presentations of dysraphic developmental disorders, intracranial hemorrhage and cerebrovascular disease. 4. Describe classification of CNS trauma. 5. List causes and characteristics of CNS infections. 6. Describe clinical and pathologic features of multiple sclerosis. 7. Describe metabolic, nutritional and neurodegenerative diseases of the CNS. 8. Describe the neoplasms associated with the central nervous system. 37 METABOLIC DISEASES • Inborn errors of metabolism: • Group of diseases characterized by deficiency in enzymes essential for maintenance of myelin and cell membranes of neurons. • Examples include Tay-Sachs and Niemann-Pick disease (both autosomal recessive genetic disorders). • Tay-Sachs disease: • Hexosaminidase A deficiency results in accumulation of gangliosides in neurons leading to toxicity. • Typically seen in infants < 6 months of age. • Niemann-Pick disease: • Sphingomyelinase deficiency results in accumulation of sphingomyelin in neurons leading to toxicity. 38 NUTRITIONAL DISEASES • Deficiencies of certain vitamins cause CNS lesions. • Most important deficiencies affecting brain: • Thiamine (vitamin B1) deficiency: • Presets as Wernicke’s encephalopathy (disturbance of ocular function, gait, mental function) or Korsakoff syndrome (amnesia and confabulation). • Vitamin B12 deficiency: • Causes uncoordinated movement, sensorimotor peripheral neuropathy. • Nicotinic acid (vitamin B3) deficiency: • Causes: dermatitis, diarrhea, delirium (3 D’s). 39 ALCOHOLISM • Alcohol has profound effects on brain. • Small amounts cause euphoria, lack of inhibition. • Large amounts depress brain functions, if excessive  neurotoxin  death. • Indirect affects of chronic alcoholism: • Nutritional and metabolic disturbance (eg. thiamine deficiency). • Repeated head trauma (subdural hematomas) from falling while inebriated. • Direct affects of chronic alcoholism : • Atrophy (cerebellar or cortical)  likely related to loss of neurons from neurotoxic effects of alcohol. • Cerebellar atrophy  accounts for uncoordinated movements. • Cortical atrophy  progressive mental deterioration. • Myleopathy and sensory-motor neuropathy  sensory deficiency, tremor and fatigability of muscles. 40 NEURODEGENERATIVE DISEASES • Group of diseases of unknown etiology limited to CNS. • Diagnosis of exclusion (need to exclude all other brain disease that could cause symptoms). • Each disease preferentially involves various parts of brain: • Alzheimer’s disease: atrophy of frontal and occipital cortical gyri. • Huntington’s disease: basal ganglia and frontal cortex. • Parkinson’s disease: loss of dopaminergic neurons in the substantia nigra. • ALS: motor neurons of anterior horn of spinal cord, brainstem and frontal cortex. 41 Neural Regen Res 2020;15:838-42 ALZHEIMER’S DISEASE • Form of dementia of unknown etiology, possible genetic factors (5-10% familial, majority sporadic). • Most common cause of dementia in elderly. • Insidious impairment. • Impairment of higher intellectual functions. • Later, progressive disorientation, memory loss, aphasia. • Eventually profoundly disabled, mute, immobile. • Atrophy of brain (narrow gyri, wide sulci) due to loss of neurons. • Histological changes include neurofibrillary tangles and neuritic plaques. https://webpath.med.utah.edu/CNSHTML/CNS088.html https://commons.wikimedia.org/wiki/File:Histopathology_of_Alzheimer%27s_disease.jpg 42 PARKINSON’S DISEASE • Subcortical neurodegenerative disease of unknown etiology. • Decreased dopaminergic neurons in the substantia nigra. • Present with TRAP symptoms: • Tremor, Rigidity, Akinesia, and Postural instability. • Pathologic changes: • Palor of substantia nigra (brainstem). • Histology: loss of melanin rich neurons, remaining neurons contain Lewy’s bodies (inclusion composed of proteins). 43 https://en.wikipedia.org/wiki/File:Paralysis_agitans_(1907,_after_St._Leger).png https://edoc.ub.uni-muenchen.de/11787/ HUNTINGTON DISEASE • Autosomal dominant neurodegenerative disease. • Mutation of gene called huntingtin (HTT) gene (codes for huntingtin protein). • Expansion of CAG trinucleotide repeat in gene causes mutant protein to form. • Characterized by involuntary, gyrating movements and progressive dementia. • Atrophy of basal ganglia and frontal cortex. • Onset of symptoms by age 40. • Most are mentally incapacitated and die within 20 years of onset of symptoms. 44 AMYOTROPHIC LATERAL SCLEROSIS (ALS) Motor tracts • Aka Lou Gehrig’s disease. • Progressive, fatal motor neuron disease of unknown etiology. • 10% familial forms. • Characterized by motor weakness and progressive wasting of muscles in extremities leading to generalized muscle loss and death. • Loss of motor neurons in spinal cord, midbrain and cerebral cortex. • Most prominent is loss and sclerosis of lateral corticospinal tracts (hence, term ALS). • Death due to paralysis of respiratory muscles. 45 OBJECTIVES 1. Describe the structure and function of the central nervous system. 2. Describe causes and symptoms of increased intracranial pressure. 3. Describe causes and clinical presentations of dysraphic developmental disorders, intracranial hemorrhage and cerebrovascular disease. 4. Describe classification of CNS trauma. 5. List causes and characteristics of CNS infections. 6. Describe clinical and pathologic features of multiple sclerosis. 7. Describe metabolic, nutritional and neurodegenerative diseases of the CNS. 8. Describe the neoplasms associated with the central nervous system. 46 CNS NEOPLASMS • ~50% are primary neoplasms: • Gliomas. • Meningiomas. • ~50% are secondary neoplasms (metastases). • General points regarding primary CNS neoplasms. • Rare, but important because of high mortality. • Usually no identifiable risk factor. • Some hereditary syndromes (neurofibromatosis, multiple endocrine neoplasia – MEN) are associated with increased risk of meningiomas. 47 CNS NEOPLASMS - GLIOMAS • Tumors arising from glial cells: • Astrocytes: astrocytoma. • Oligodendroglial cells: oligodendroglioma. • Ependymal cells  ependymoma. • Astrocytic tumors: astrocytoma and glioblastoma. • Account for 80% of glial tumors. • Malignant neoplasms with appearance of astrocytes. • Different types, different prognoses. • Glioblastoma (multiforme). • Highly aggressive, poor prognosis (mean survival 1 yr). • Irregularly infiltrative lesion. 48 https://www.webpathology.com/image.asp?case=741&n=12 https://www.spandidos-publications.com/10.3892/ol.2019.10179 CNS NEOPLASMS – MENINGIOMA. • Neoplasm arising from meninges. • Usually benign. • But may cause death if in vital location. • Good prognosis. • Most arise in midline impinging cerebral hemispheres from the outside. https://webpath.med.utah.edu/CNSHTML/CNS116.html 49