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PATHOLOGY LABORATORY CNS Objectives: 1. 2. 3. 4. 5.

At the completion of this laboratory, the student will be able to: describe the morphologic, histologic and clinical aspects of the CNS lesions represented by these slides differentiate between the various types of CNS infarcts discuss the normal blood supply and the effects of decreased blood supply to areas of the brain discuss healing in the brain identify common brain tumors

Slide X2-304: This section consists of cerebral cortex with underlying white matter. The gyri are disrupted due to a contusion. This is best seen by examining the slide without the use of the microscope. Notice how the cortex is absent at the center of the tissue. This microscopic pattern is typical for a contusion. The cortex is completely destroyed in the area of the contusion. The outermost layer of the cortex is frequently preserved in an infarct, a differentiating feature. Note the ironcontaining macrophages in the area of damage. In the white matter there is loss of myelin and nerve fibers, and some astrocytic reaction. Necrosis

Hemosiderin Macrophages in Infarct, there is a zone on the periphery where there is viable tissue because cortical vessels, that supply the cortex in contusion, however, the whole area will be affected however, there are many changes occur after death Contusion vs Concussion - both are neurological injuries - concussion - diagnosed by symptoms - contusion - you can see physical evidence of injury, this is more dangerous Questions:

1. Could this slide be due to a fall from a bar-stool two days prior to death? Why? No, it is old; see hemosiderin laden macrophages (these mean there was a hemorrhage..), these are from old injuries. Astrocytic reactions (glioisis) does not occur right away (like a week) and macrophages do not show up for about 3 days. We do not see lots of PMNs. 2. Do you understand the difference between coup and contrecoup lesions? Coup is a brain injury at the sight of impact. Contrecoup is brain injury opposite side of initial injury 3. Would this lesion necessarily leave a residual neurologic deficit? Why? Yes it could if this forms a scar we do not see neuron regenerations in the brain, astrocytic reactions turn to scars. If small enough may not be notable. 4. Would this lesion necessarily be fatal? No, unless the seizes are, cortex damage should not be fatal from a contusion unless swelling and hemorrhage caused intracranial pressure to increase and he should have died by now. If they die, its usually due to subdural hematoma or something that causes widespread damage 5. Could motor seizures be a result of this injury? Yes, contusions can cause permanent damage to the brain with gliosis and scar formation which become sites of future seizure activity, as well as blood on the brain which can induce seizures. depends on where the contussion is - if its in the motor cortex then they could have motor seizures Hemorrhage: Epidural middle meningeal artery Subarachnoid bridging veins

Slide X2-401: This 25-year-old man, Mr. Cal C. Tonin, was seen in the emergency room presenting with fever, severe headache, irritability and photosensitivity. He died 48 hours after admission. This is a slide of a section of his brain.

PMNs Inflammation of the meninges.

Questions: 1. What is your interpretation of this slide (acute or chronic)? Acute meningitis or leptomeningitis, We see PMNs and the person has signs of meningitis photophobia and other signs of infection. 2. Discuss the common etiologic agents associated with this disease in newborns, young adults and the elderly. Meningitis, can be caused by many bacteria including new born S. agalactiae-Group B strep (also ecoli and listeria), N. mengitiis in 2-29 (in groups like dorms or soldiers), young and old is S. pneumo. We can also have a viral pneumonia or aseptic (coxsackievirus, CMV) and those caused by fungi (Crypto neoformans). 3. How are the above agents (question #2) identified in the laboratory?

CSF tap and culture and then gram stain. For a virus do a diagnosis of exclusion see less WBCs and neg gram stain with a normal glucose level. See neutrophils first, then lymphcytes and monos after 48 hours. With both see increased protein. Can do PCR for viruses. Listeria is a gram pos rod, highly motile, only gram pos with endotoxin, reproduces in the cold (commonly asso with eating un-pasturized cheese). If the stuff is yellow indicates pus (grossly). When you take the CSF sample use the last tube for mico since it is the least contaminated (should have 3 tubes, 2 for hemo/chem and last for micro). Look for blood, glucose and protein. In the CSF, normal glucose should be 2/3 of serum glucose. Be careful about diagnosis of increased glucose since diabetic or from an IV (dextrose). If the BBB is compromised see and increase in proteins. Also expect an increase in ICP with infections. With bacterial infections expect increases in C reactive proteins, LDH, and LPS (with gram neg use the hemolymph from horse-shoe crabs it coag in presence of LPS). All these are neg with viral infections. Camp test is used for group B strep Many cases of meningitis follow an URT infection, present with nuchal rigidity Bacterial is more dangerous and almost always fatal whereas viral is almost always reversible - bac kills you because of injury to the brain, swelling, edema, inflammation, increase in intracranial pressure - viral doesnt do as much damage CSF know everything about itI didnt take notes Protein lower than serum o Bacterial will be decreased o Viral may be decreased Glucose 2/3 of serum o Decreased in bacterial and possibly in viral (usually unchanged sometimes increased since the irritated cells release glucose) Neutrophilic response possible within 24 hours bacterial o Lysteria monocytogenes will give a lymphocytic response though! CRP bacterial will be increased, viral will be normal (not specific!) LDH bacterial increased and viral normal (not specific!) Lymphocytic viral, fungi o Early in viral you will likely see a neutrophilic response Many gram stains will not show a positive response because not concentrated enough Bacteria: Neonates Group B strep, e. coli Children Streptococcus pneumonia is #1 in all age groups except neonates!!!! Close quarters (prisons, military) Neisseria meningitides CSF made in choroid plexus out of foramen of luschka and megendie into subarachnoid space Accumulation can be communicating or noncommunicating o Communicating Neisseria meningitides

o Noncommunicating Base of brain Tumors effecting ventricles Soap Bubble Lesion Pathonogmonic for Cryptococcus neoformans o Occurs in immunocompromised Slide X2-901: Mrs. Ariel Dyte is a 48 year old female who presented to the local emergency room following a minor fender bender. Her car was witnessed to leave the roadway and impact with a light pole. EMS personnel found her to be conscious but slightly confused. She could not recall the accident. Examination revealed only a superficial laceration with surrounding contusion on her forehead; therefore a head CT was ordered to rule out skull fracture or closed head injury. Below is an image of the CT findings.

CT findings Slide X2-901 is of the stereotactic biopsy of the lesion.

Differential: - seizure - would explain the loss of conciousness, accident, memory loss - stroke - would not be concious after stroke, usually paralyzed - TIA - usually gives you a focal neurological defeicit and then recover completely within 24 hours - CV problem such as arrythmia can cause a sudden loss and gain of conciousness 1. Describe the histologic features? Hypercellular. See pink neuropil in background. See hemorrhage, which usually accompanies necrosis. Probably would see mitoses. Microvascular hyperplasia or proliferation. Also, looking for palisading necrosis. 2. What is the diagnosis? Glioblastoma multiforme, which is a grade IV astrocytoma. If unsure, could you stains to check. 3. Who is usually affected? What is the usual progression with this tumor? 40-60 yos, very aggressive, worst prognosis, microscopic extensions spread at the time of diagnosis, so even if you remove the tumor it might already have mets to other parts of the brain. much more extension often through the corpus callosum to the other lobes - this is why this is fatal and has such poor prognosis Astrocytomas: Juvenile Pilocytic o Good prognosis Glioblastoma multiforme o Can extend beyond the o Hemorrhage, necrosis, mitotic figures, pleomorphism Anaplastic astrocytoma Differentiating benign or malignant: Necrosis, hemorrhage Mitotic figures Pleomorphism Pendamomas (?) Meduloblastomas Meningiomas Psammoma bodies o Papillary cystadenocarcinomas, papillary thyroid carcinoma

Slide X2-904: Mr. Neiman Pick, is a 60 year old scientist who presents with increasing headaches and dizziness. His past medical history is remarkable for colon cancer six years ago. He was treated with colectomy and several rounds of chemotherapy. He does not recall the stage of his cancer and was treated in another state, so the records are not readily available. A CT of the head shows a large mass in the right cerebellum and one in the left frontal lobe. Radiation : it is contraindicated in the colon because small intestine can not stand radiation and its in the way - rectal cancer, you can use radiation. His cancer is stage III - because he has colectomy and got chemo not stage IV - because can not be resected because already has already mets. a person is not a candidate for cholectomy in stage IV because it would not cure him Why not stage I or II ? - there is no reason to do adjuvant chemotherapy in ppl with cancer only in mucosa and submucosa - stage I and II - so chemo only helps with Stage III and beyond Slide X2-904 is from the frontal lobe lesion.

1. Describe the histologic features? There are glands and these should not be in the brain, so abnormal tissue to be in brain, suggests mets. GI adenocarcinomas tend to get dirty necrosis. A lot of debris and junk in the center, so would tend to suggest colon CA primary, even without the history. 2. Is this a primary or metastatic process? One way to differentiate is by looking for multiple tumors (more suggestive of mets) and metastatic tumors are most often found on the border of the gray and white matter and often near the middle cerebral artery where the cells can gain access. 3. Are there any histologic features to suggest a primary origin? You can do a scrape prep and cells will stream out like thin stringy cells if glial in origin and thus primary. 4. How might the pathologist confirm the origin? CEA Mets are most common tumor of the brain Lungs Melanomas breast colon is actually pretty rare There is a reason why we can't treat mets to the brain - blood brain barrier interferes with chemotherapy, you can destroy too much tissue in the brain with radiation without causing problems - clone that is selected for and grows in the brain has certain advantages and resistance - so biologically and physically hard to treat -

Slide: Contusion Right side has lost a lot of density, could be edematous, loss of tissue Is this recent or old? Older b/c contains iron in macrophages Inflammatory cells are scarcely present RBC are present which would contradict age and maybe think its recentbut its not Brain heals itself via gliosis after liquifactive necrosis Slide: Contusion high power PMN (inflammatory cells) present Slide: Contusion again Notice Red neurons, they appear as an aftermath of ischemia You can easily have ischemia with contusion or concussion Hard to tell if a slide is contusion or ischemic event you should use history and gross observation rather than slide Slide: Meningitis Autopsy Notice pus and hemorrhaging If you have a pt that has sx of meningitis (HA, photophobia, stiffness in neck) you should do a spinal tap o Always draw 4 tubes o Tube 1 is usually always contaminated from skin flora use for hematology o 2 or 3rd tube to micro o 4th tube used for special agglutinations or TB testing o Normal spinal fluid looks like H2O cause its clear o Normal cell count: less than 5 WBC and all mononuclear (NO PMNs) Bacterial Meningitis will have 100s of WBC and cloudy appearance o Glucose: decreased always in bacterial o Protein: elevated in bacterial and sometimes viral o Lymphocytosis always present in viral meningitis o Herpes and mumps may first show neutrophilia and then lymphocytosis o Gram stain to cover all common organisms o Group B strep have narrower, clearer zone of Beta hemolysis (hemolytic patterns are different for Group A and Group B, but both have beta hemolytic patterns). CAMP test, and serological antibody markers can also be done. o Use blood agar, chocolate agars to cover common organisms o Lysteria is gram + rod, grows in the cold, can do a cold enhancement where put in fridge, it grows, others dont. o If you need a quicker resultuse cold agglutination assays that include heamophilis, group B strep, nisseria meningitis, Cryptococcus, pneumococcus Spinal fluid formed by choroids plexus in lateral 3rd ventricle TB and N. meningitis tend to affect base of brain hydrocephalis (non-comm) Pneumo affects arachanoid villi communicating hydrocephalis Hydrocephalis causes Increased cranial pressure

ICP caused by obstruction from tumor also, also caused by cerebral edema o 2 types of cerebral edema: intracellular vs. extracellular o different types of herniation Congenital hydrocephalis: non-communicating cause no drainage Viral meningitis: see soap bubble lesions. Cryptococcus meningitis, no longer use India ink stain because only positive 20-50% of time. Now do serological stuff. This is a yeast so grow on blood agar.

Slide: PMNs in bacterial meningitis Slide: Smear of spinal fluid Gram negative pleomorphic rods: haemophilus influenzae Slide: PMS in Peripheral blood stream Gram negative diplo: N. meningitis Spread into blood stream and disseminated septicemia Autopsy: adrenals affected water house friderichson disease hemorrhagic necrosis of adrenals Almost any gram negative can cause water house disease Slide: gram positive rod Listeria monocytogenes o Only gram positive that has LPS o Get lymphocytic response (hence the name monocytogenes), only bacteria to do this o Contaminant in unpastuerized cheese o Pathogenic and can proliferate in cold (hence the cheese lives on in the fridge) Group B strep are gram positive cocci Slide X2-301: This is the section of the caudate nucleus from a 48-year-old man, Mr. Artie Phishal, with an occluded carotid artery. Note the ependymal lining. Beneath the ependymal layer is a layer of intact gray matter with large neurons and relatively normal astrocytes and oligodendroglia. Beneath the zone of relatively normal caudate is an area of complete acute necrosis. In the central nervous system, necrosis is usually of the liquefaction type with complete destruction of the tissue with failure of the tissue to regenerate or scar. Note the decrease in density of the white matter, as well as a marked neutrophilic infiltrate. The neuronal changes include shrinkage and eosinophilia, although the age of the slide may preclude a proper evaluation of the cytoplasmic change. Some sections may have thrombi in the vessels.

Red neurons are indicator of ischemic damage, see shrinkage, eosinophilic and loss of nuclei. Questions: 1. What ventricle does the ependyma in this slide line? Lateral ventricle (near the caudate). 2. Is this an anemic or a hemorrhagic infarct? This is an anemic (pale colored), this is due to ischemia and a final cerebral infact, we do not see hemorrhagic (bloody) evidence here. Liquafactive necrosis is most often associated with ischemic strokes, while intracerebral bleeds are hematomas due to rupture of a blood vessel. In this the tissue is destroyed by hydrolytic enzymes and the area is infiltrated by PMNs with conversion of the area to an abscess. 3. Do you think this infarct is minutes old, hours old, days old, weeks old, months old, or years old? Why? 12-24 hours, we see eosinophilia and neutrophils. This means it is acute. 12-24 you see red neurons and these are not chronic and we see them so it should be acute. Also see acute inflammatory exudates coming in. 4. Name possible clinical symptoms and signs, which could arise from this lesion. Basal ganglia is important in controlling voluntary movements and establishing postures. When they are altered - say in disorders like Huntington disease or Wilson disease - the person has unwanted movements, such as involuntary jerking movements of an arm or leg or spasmodic movement of facial muscles. We would expect similar sx in the case of an infarct in this area, however: Depends on location and size, cerebral anastomoses, rapidity Stupor/Coma, convulsions, speech, localizing findings may be more pronounced Diagnosis Clinical Presentation CT Scan, MRI Note: Parkinsons also affected by Basal ganglia dysfunction, cant make it go 5. Assuming this man lived for one year, what would a histologic section from this area look like? The infact would be converted to a cystic cavity which only has blood vessels. Astrocytes would move in and replace the neurons leaving a fibrotic scar (no regeneration of brain tissue occurs).

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