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118 Cards in this Set

  • Front
  • Back
Wallerian Degeneration
Interruption of an axon resulting the degeneration of the distal portion. Regeneration of the proximal portion is possible in the PNS and unlikely in the CNS
What are Luxol fast blue-PAS stains used for?
Myelin (aka white matter)
transsynaptic degeneration
Only happens in certain areas of the nervous system. Most often occurs when damage to optic nerve or tract results in degeneration of the lateral geniculate nucleus, due to lack of innervation.
Normal wear and tear pigment in neuron.
Normal wear and tear pigment in neuron
Central chromatolysis
change occuring secondary to disruption of the neuron when cell body swells and nissl substance is lost (RER). Does not imply pending cell death, but this can occur.
Dying back
Axons becoming atrophic with atrophy starting distally and progressing proximally. More typical of PNS nerve axonopathies than CNS.
Axonal spheroids
Focal dilations of axons filled with accumulated organelles (from transport blockage). Can occur after axonal injury or dystrophic axonopathies.
Astrocytosis (gliosis)
Proliferation of, or sometimes hypertrophy of astrocytes. The astrocyte is the primary source of scar tissue in the CNS, which consists of glial filaments within asytrocytic processes.
Rosenthal fibers
Thick, eosiniphilic elongated or globual structures within astrocytic processes in areas of dense gliotic reaction. Can also be seen in certain well-differentiated astrocytomas.
Characteristics of Alzheim type-2 astrocytes?
Pale, severly swollen, astrocytic nuclei with severe hepatic failure and elevated blood amonia levels.
Polyglucosan bodies
Concentric inclusion bodies commonly called corpora amylacea. Not pathological, but increase with age. PAS-positive, pale grey in hematoxylin.
What are oligodendrocytes? What is their principle cell reponse? Do they proliferate?
The myelin-producting cell of the CNS. Cell death is primary response. Have mild proliferative capacity as possibly seen at edges of early MS lesions.
Primary demyelination
Direct loss of myelin sheaths without loss of the axons associated with them. Can be from direct attacks on sheath as in MS or on oligo cell bodies as in the infection multifocal leukoencephalopathy.
Where do ependynmal cells reside?
The ventricles. Regeneration is limited and glial scars are formed when they die.
What is the function of microglial cells? Where do they reside?
The are probably 1) phagocytic, 2) cytokine-producting, 3) antigen-presenting. Located in CNS parenchyma.
What is a rod cell reaction?
The exaggerated elongated rod-like appearance that activated microglial cells take on. Often a component of viral infections in the brain.
What are microglial nodules?
Microglial cells aggregated in to small nodules. Frequently occur around dead neurons where phagocytosis is thought to be taking place. Most often seen as a component of viral or Rickettsial infections.
Where are macrophages in the CNS from?
1) Intrinsic cells (microglia). Seen in smaller or less confluent lesions. or 2) Circulating precursors. Seen in large damage - ie infarcts.
Why can the PNS regenerate in response to injury better?
Is has Schwann cells and basal lamina that invest the PNC axons.
What is segmental demyeliniation?
Loss of myelin sheath in PNS. But regenerates more quickly (days to weeks).
What is the most important demyelination disease in the PNS?
Gullian-Barre syndrome. Characterized by an auto-immune attack on PNS myelin. Mechanism believed to be similar to MS.
How is dying back different in the PNS versus the CNS?
Quicker in PNS. When the neuropathies are sensory, they often result in stocking-glove sensory losses in the feet and hands.
What are the 3 causes of increased cranial pressure?
1) Increase in intracranial tissue mass - ie neoplasm or inflammatory lesion. 2) Increase in intracranial blood, either extravascular or intravascular. 3) Increase in water content. When this occurs in the brain substance , it is called cerebral edema.
What are the 3 types of cerebral edema?
1) cytotoxic - altered ion concentrations causing water to leave blood. Cause by failure of ion pumps from ischemia or hypoxia or a hypo-osmal state as in water intoxication. 2) Vasogenic - structural or functional damage to the blood-brain barrier. Usually seen in tumors and infaracts. Proteins can leak in too. More extensive in white matter. 3) Interstitial - transudation of CSF across the ventricular walls as in chronic hydrocephalus.
What is the most important consequence of increased intracranial pressure?
Herniation from one brain compartment to another.
What are the most clinically significant herniations? What does they result in clinically?
1) Uncal or Transtentorial Herniation. Brain shifts downwards through the tentorial notch. Pinching of oculomotor nerves with pupilary dilation. Usually produces secondary herniations in the brainstem. Usually fatal.

2) Heriation of the cerebellary tonsils in to the foramen magnum. Fatal compression of the medullary center resulting in cardiorespiratory failure.
What is hydrocephalus? What the causes?
Dilation of the ventricular system. Increased production of CSF (less common) or decreased reabsorption of CSF (more common) in the arachnoid granulations.
What is a noncommunicating hydrocephalus? What are 2 causes?
When an obstuction does not allow CSF to leave the ventricular system. 1) Stenosis of the cerebral aqueduct and 2) tumors in the ventricles.
What is a communnicating hydrocephalus? What is a frequent cause? For what group of patients is this of particular concern?
When obstruction to flow of CSF is in the subarachnoid space. Frequently caused by scarring of the arachnoid granulations and subarachnoid space following a healed meningitis or subarachnoid hemorrhage.

Important in premature infants recovering from intraventricular hemorrhages that have extended in to the subarachnoid space around the base of the brain and have resulted in fibrosis of subarachnoid space near the foramina of the 4th ventricle.
What are the 3 causes of CVEs?
1) locally occlusive vascular disorders, 2) reduction in systemic perfusion or exygenation, 3) hemorrhage
What are important sites of anastomoses in the cerebral arterial circulation?
1) Circle of Willis - Presence/absence of posterior communicating arteries, anterior cerebral arteries

2) An interblock can result in a external to internal carotid via opthalmic from internal and orbital from external.

3) Leptomeningeal vessels - between branches of the major cerebral arteries

4) Anastamoses within brain parchyma are NOT important in preventing ischemia
Are watershed regiong more vulnerable to specific vascular blockages or generalized decreases in cerebral blood flow?
More vulnerable to generalized decreases. Anastamoses sometimes can receive collateral flow between major arterial distributions.
Are venous anatamoses numerous or rare?
Numerous - both in intracranial and extracranial. This is why venous infarction is relatively rare.
What does the anterior spinal artery supply?
1) Anterolateral white matter and 2) Nearly all grey matter.
Are infarcts of the spinal cord common or rare?
Rare due to abundant collaterals both between levels and within each level. But are extensive when they do occur.
What are the 7 types of arterial cerebral infarction?
1) Thrombotic, 2) Embolic, 3) Arterial dissection, 4) Hypertension-related ischemia, 5) External factors producting compromise of the arterial lumen, 6) Non-occlusive decreases in perfusion or energy substrate, 7) Increased intracranial pressure
What are the important factors in thrombotic occlusions? How are they characterized?
Atherosclerosis - most important. Usually in large vessels, near branch poins, extracranial portion of the int carotid. Infarcts are large frequently. CNS atherosclerosis generally is corresponds with systemic disease. Collaterals have time to form.

2) Vasculitis (arteritis) - Much less common cause. Usually in small to medium arteries. Multiple, smaller infarcts. Often associated with collagen vascular disease (eg polyarteritis nodosa, lupus), meningitis, etc. Granulomatous angitis (Primary CNS vasculitis) is a form restructed to CNS.

3) Hyperviscosity (eg sickle cell anemia and polycethmia) and Coagulopathy (eg DIC and TTP)
What is Granulomatous angitis?
aka Primary CNS vasculitis. It's a form of vasculitis restricted to the CNS. Probably autoimmune and usually granulomatous.
Where do embolic occulsions usually occur?
MCA and PCA. Often are multiple and involve the gray-white junction.
What are the 2 places embolic occulsions usually arrise from?
Thomboemboli usually from 1) thrombus already formed in 2) proximal vessel or heart.
What are 3 characteristics of embolic infarcts?
1) Often smaller than thrombotic infarcts. 2) Often hemorrhagic - due to reperfusion. 3) Can manifest as Transient Ischemic Attacks.
What is the mechanism by which embolic infarcts usually cause hemorrage?
Reperfusion into ischemically damaged areas after clot lysis.
What is the usual cause of an arterial discesstion infact? What is the mechanism of infarction?
Trauma - sometimes mild. Occlusion of true lumen due disecting blood compressing luminal space.
What are lacunar infarcts characteristic of? Where do they usually occur? Mechanism by which they occur?
Hypertension-related ischemia infarction. Typically in basal ganglia and pons - pontine perforating arteries or lenticulo striate atrteries. Usually small, cavitary (<1.5cm). Hypertension causes changes that predispose to thrombus.
What are the 2 extrinsic factors producing compromise of the arterial lumen?
1) Vasospasm 2) Compression of PCA after tentorial herniation, results in medial occipital lobe infarcts.
What is a significant complication of a subarachnoid hemorrhage due to rupture of a saccular aneurysm?
Vasospasm with infarction.
What are the 2 causes of non-occlusive causes of arterial cerebral infarction?
1) Systemic hypotention or cardiac arrest 2) Hypoxia and hypoglycemia
What are the characteristics of systemic hypotention cerebral arterial infarcts?
1) Watershed infarcts 2) Laminar necrosis of cerebral cortex and selective neuronal cells loss (most sensitive - purkinje cells, CA1 region of hippocampus) 3) Global ischemic neuronal necrosis is most severe manifestation
What are the characteristics of hypoxia and hypoglycemia related cerebral arterial infarcts?
1) Usually with some hypotention 2) Selective neuronal loss - purkinje and hippocampal cells, excitoxicity cell death - from less exictory amino acid transmitters
What cerebral arterial infarcts are typically the largest? Whare are of most variable size? What are seen with a watershed distribution?
Atherosclerotic are large. Embolic are variable (usually smaller). Hypotensive show watershed etiology.
What are the 3 factors that determine extent of cerebral arterial infarction?
1) Site - proximal (larger) vs distal (smaller). 2) Rapidity of occlusion - due to possibility of collateral formation. 3) Presence of naturally-occuring collaterals.
Which are pale and which are hemorrhagic - thombotic and embolic?
Thombotic - pale. Embolic - usually hemorrhagic (depends on reperfusion)
What are lacunar infarcts due to? Where are they usually found?
Hypertensive changes. Basal ganglia and pons.
Appearance of recent, subacute, remote infarcts?
Recent - softened, dusky color, edematous. Subacute - liquefaction, destruction. Remote - scarring, cavitation, atophy of tracts (wallerian).
What are the usual causes of death in the period soon after an cerebral infarction and later?
Prompt causes - 1) Secondary to edema with herniation. 2) Cardiac arrhythmia

Later causes - 1) Debilitation 2) Aspiration Pneumonia
In a cerebral infarction, what is the time course of Cell necrosis, PMN invasion, mononuclear invastion, gliosis, and cavitation?
1-2 days: Cell necrosis and PMN infiltrate. 3-5 days: Mononuclear infiltrates. 2nd week: Gliosis (astrocyte proliferation and hypertrophy). Caviation can take years.
What is the cause of venous cerebral infarction? What are the risk factors?
Thrombosis. Must be extensive because of large collateral circulation. 1) Hypercoagulbility and 2) venous infection.
What do venous cerebral infarcts looks like grossly and microscopicly?
Gross - densely hemorrhagic.
Micro - Severly hemorrhagic with venous congestion.
What are the etiologies of cerebral hemorrhage?
1) Subarachnoid hemorrhage secondary to rupture of sacuular (berry) aneurysms 2) Hypertensive intracerebral hemorrhage 3) Vascular malformations 4) Amyloid angiopathy 5) Hemorrhage in to neoplasms 6) Blood dyscrasias 7) Mycotic aneuysms 8) Duret Hemorrhage 9) Trauma
Where do subarachnoid hemorrhages secondary to rupture of saccular (berry) aneurysms occur? Mechanism by which they occur? Pathological features?
Saccular aneurysms occur in bifurcation of large subarachnoid arteries - circle of willis and proximal MCA in 90%. They may be multiple - 15% to 20% of cases. From weakening of wall - are pseudoanuerysms.

Pathology: subarachnoid hemorrhage. Rebleeding common. Intracerebral hemorrrhages can result from rupture directly into parenchyma. Secondary infarction can occur from vasospasm due to blood constricting meingeal vessels. Arachnoid fibrosis possibly leading to hydrocephalus.
Where to hypertensive intracerebral hemorrhages usually occur? What is the pathology?
Short circumfrential arteries. Supratentorial sites (70% to 80%) include basal ganglia (lenticulostriates), thalamus (thalamostriates), cerebral hemispheric white matter. Hemorrhages into the pons are almost always fatal.

Pathology: Large hematomas, sometimes in to ventricles. Mass effect due to edema and hematoma often leading to herniation. Can leave behind relatively little tissue injury.
What are vascular malformation intracerebral hemorrages?
Hemorrhages due to ateriovenous malformations - direct shunts. May present with seizures from local ischemic damage. May be intraparenchymal, subarachnoid, or both.
How do amyloid angiopathies result in intracerebral hemorrhages?
Often associated with Alzheimier's disease. Primarily affects meningeal and corticol vessels, so usually superficial. Often smaller than hypertensive hemorrhages and more survivable. Common cause of intracerebral hemorrhage in elderly.
What is a common cause of intracerebral hemorrhage in the elderly?
Amyloid angiopathy.
What are 2 primary tumors that frequently bleed and cause intracerebral hemhorrages? What are 3 metastatic?
Primary - glioblastoma and oligodendroglioma (rarely clinically signifcant).

Secondary - Melanoma, renal cell carcinoma, choriocarcinoma.
Severe thrombocytopenia or very elevated WBCs are associated with what form of intracerebral hemmorhage?
Blood dyscasias. Usually in cerebral hemispheric white matter.
Rupture of the meningeal arteries results in what form of hematoma?
Epidural hematoma. From trauma.
Venous rupture or rupture of bridging veins (between dural sinuses and cortical vessels) in subdural space results in what form of hematoma?
Subdural hematoma. From trauma.
Subarachnoid hemorrages also be due to trauma in addition to rupture of saccular aneurysms? What features on brain are they often coupled with?
Yes. Contusion on brian surface.
What are intraparenchymal hemorrhages due to trauma cause by?
Shearing or contusive injury. The same forces than can induce axonal shearing.
Do CNS tumors frequently or rarely metastisize?
What are the most common type of intra-axial (within CNS parenchyma) tumors?
Astrocytomas. Most intra-axial have glial differentiation or origins.
Is MRI or CT more sensitive for imaging neoplasms?
MRI - and T2 or FLAIR images are particularly useful.
Do most extra-axial tumors in the CNS have a unfavorable or favorable prognosis?
What are the majority of extra-axial neoplasms within the CNS compartment?
tumors or meningeal or peripheral nerve (Schwann cell) origin.
What is the mass effect? Does it occur in intra-axial, extra-axial, or both type of neoplasms?
A space-occupying lesion increase intracranial volume, leads to herniation. Also, abnormally permeable tumor vessels can contribute to cerebral edema (more T2 or FLAIR signal) and worsen the mass effect.

How do neoplasms affect the nervous system?
1) Mass effect 2) Infiltration of normal substances (often in intra-axial tumors)
Is location, histological type, or grade the most important prognostic consideration?
Where are most childhood tumors located?
80% are in the posterior fossa (infratentorial). CNS tumors are also the most common solid tumors of childhood.
Where are most adulthood tumors located?
80% are supratentorial. The likelihood of anaplastic change in glial tumors increases with age.
What are the majority of primary tumors in the CNS?
Gliomas (aka glial tumors).
How do gliomas present usually?
Signs of increased intracranial pressure (headache, papilledema), focal deficits, new onset seizures.
Most gliomas are of what type?
Astocytic neoplasms.
What are the 3 histological categories of astrocytic neoplasms?
1) Astrocytoma (well differentiated) 2) Astrocytoma with anaplastic features 3) Glioblastoma multiforme (highly malignant)
What are key features of a Fibrillary Astrocytoma?

What features result in classification of a 'astrocytoma with anaplastic features'?
Aka astrocytoma. Neoplastic cells typically have histologic features of fibrillary astrocytes. Peak incidence in 3rd to 4th decade, common in hemispheres.

increased cellularity, pleomorphism, increased mitotic rate, vascular proliferation. Necrosis is absent.
Is necrosis present in astrocytoma with anaplastic features?
No. Would need to advance to glioblastoma.
What are the key features of a glioblastoma multiforme?
Falls under astrocytic neoplasm category, which are gliomas. Over 50% of all gliomas are this kind. Common in 5th to 6th decades, but occur at all ages. "Ring enhancement" seen on imaging is due to central necrosis. Highly anaplastic. Most malignant of all gliomas.
What neoplasm is characterized by ring enhancement?
Glioblastoma multiforme
What is one of the most common tumors of childhood and often occurs as a grossly cytic tumor in the cerebellum and is curable by surgery? What are it's pathology?
Juvenile Pilocytic Astrocytoma. Is a variant of astrocytoma with a much better prognosis that the typical diffuse astrocytomas.

Alternating patterns of densely packed 'pilocytic' astrocytes and loosely arranged astrocytes with a spongy appearance, often forming microcysts.
What is the classification and key features of oligodendromas?
15-20% of all gliomas. Uniform cells with "fried-egg" perinuclear clearing oligodendroglial appearance. Tends to be more circumsized than astocytoma. May be heavily calcified. Slow-growing but infiltrating, some with very long survivals.
What is the classification and characteristics of a ependymoma? What ventricles are they most commonly found in?
5% of gliomas. Majority in 4th ventricle, may arrise in conjuction with lateral ventricles. Pathology: perivascular pseudorosettes possible. Pretty well circumscribed, but less favorable prognosis.
What tumors are characterized by perivascular pseudo rosettes?
What tumors are characterized by "fried-egg" perinuclear clearing?
What are most mixed-gliomas?
What are primitive neuroectodermal tumors? What is the most common type?
Embryonal tumors. Medulloblastoma is by far the most common and is the only one we really deal with.
40 to 45% of primary CNS tumors in children and of what kind?
What are key characteristics of medulloblastomas?
Primative cell (probably neuronal) neoplasm. By definition in cerebellum. 40 to 45 % of primary CNS tumors in children.

Propensity to spread widely throughout neuroaxis by way of the CSF. Highly cellular, malignant cells. Highly invasive - including leptomeninges.
Which tumor has the propensity to spread widely throughout the neuroaxis by way of the CSF?
What are the key features of meningiomas?
15% of primary intracranial tumors. Globular, encapsulated mass attached to dura. Compress brain without invasion. Nests and whorls are common. Nearly always bening, but can recur.
What tumors compress the brain without invasion and commonly have nests and whorls of cells?
What are the 3 tumors of the peripheral nerves?
Schwannoma, Neurofibroma, Neurofibromatoses
What are the key characteristics of the schwannoma?
Occurs anywhere in PNS, but most important sites are intracranial (cerebello-pontine angle) and intraspinal. Are 8% of primary intracranial tumors, most are CN 8 origin (acoustic schwannoma). 30% of tumors in spinal canal.

Encapsulated mass compresses nerve at margin of tumor. 2 alternating patterns of growth - Antoni type A (densely compacted spindle cells) and Antoni type B (hypocellular, loosely arranged cells). Bening.
What neoplasm often presents with a hearing deficit and has two alternating patterns of growth?
What are the key features of the neurofibroma?
Biphastic tumor of schwann cell and fibroblast-like cells. Often associated with von Recklinghausen's disease. Ill defined capsule, fusiform mass. Myelinated or unmyelinated axons run through the tumor. 5 to 10% lifetime chance of malignant degeneration of at least one neurofibroma into a neurofibrosarcoma.
What are neurofibromatoses? What are the 2 types?
Multiple nerve sheath tumors (schwannoma and/or neurofibromas). Mendialian dominant.

NF-1 (von Recklinhausen's diease) - peripheral form with multiple schwannomas, peripheral and cutaneous neurofibromas, cafe-au-lait spots.

NF-2 - central form from multiple cranial nerve and spinal nerve root schwannomas (bilateral acoustic schwannomas).
What are the most common sites of metastatic tumors to the CNS? In decreasing frequency.
Lung, Breast, GI Tract (usually colon), kidney, melanoma.
What are the key feature of metastatics tumors to the CNS?
Often multiple. Edema of surrounding white matter - "ring enhancement". Location determined by vascular supply. Frequent necrosis.
What tumors have a high incidence in immunodeficiency disorders and are often deep in hemispheres?
Primary CNS Lymphomas
What are the characteristics of primary CNS lymphomas?
<1% of intracranial tumors. Higher incidence in immunodeficiency disorders (post-transplant or chemo). 6% of CNS complications in AIDS (via EBV). Majority deep in cerebrum, multiple, and deep in hemispheres. Most are B-cell.
How do secondary lymphomas usually present? Are these usually caught first in the CNS?
No, CNS involvement usually happens in patient previously diagnoses with systemic lymphoma. More common in leptomeninges and dura.
What are the 3 tumors of the region of the sella turcica (ie near pituitary gland)?
1) craniopharyngioma 2) germ cell tumors 3) pituitary adenomas
What are the characteristics of a craniopharyngioma?
Arises in squamous epithelial rests in pituitary stalk. 3% of intracranial tumors at all ages. 50% of supratentorial tumors in children. May invade the overlying hypothalamus. Can present with endocrine symptoms or symptoms of optic chiasm compression (bilateral temporal hemianopsia). Benign in growth rate, but may be difficult to eradicate.
A tumor arising from squamous epithial the rests in the pituitary stalk is...?
What are characteristics of a germinoma?
Undifferentiated germ cell tumor. >50% of pineal gland tumors are this kind. Malignant, invasive, looks like testicular seminoma, T-cell infiltrate, large cells. Pure germinomas are highly radiosensitive and curable. In the pineal gland - 95% are in males, but only 50% of suprasellar germinomas are in males.
What are the 2 types of germ cell tumors? Which is poorly differentiated and which is differentiated?
germinoma - undifferentiated GCT and teratoma - differentiated GCT
What are the characteristics of a teratoma?
Nearly always in the pineal region. Various types of differentiated tissue elements. >90% in males.
What are the characteristics of pituitary adenomas?
Arise within the sella, but may expand into the intracranial compartment, the sella is enlarges. Hormone-producing tumors may present with hormonal effect (PPL - amenorrhea, ACTH - Cushing's disease, HGH - acromegaly). Endocrinologically silent tumors are more likely to present as intracranial mass lesions extending out of the sella.