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PATHOPHYS > 5CNSPathology > Flashcards

5CNSPathology Flashcards

1
Q

Define Leptomeningitis

A

an inflammatory process that is localized to the interfacing surfaces of the pia and arachnoid, where CSF flows

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2
Q

Define Pachymeningitis

A

inflammation of the dura, usually a consequence of contiguous infection, such as chronic sinusitis or mastoiditis. The dura is a barrier to infection, and inflammation is restricted to its outer surface.

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3
Q

What causes bacterial meningitis?

A

The vast majority of meningitis cases are caused by suppurative bacteria and the organism relates to the patients age

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4
Q

List the bacterial meningitis organisms by age

A
  • Neonates: E.coli and Group B Strept. Also Lesteria monocytogenes
  • Infant: (3mo. to 3 yrs) H. influenza.
  • Adult: Strept. pneumococcus.(gram pos diplococcus: purple on gram stain)
  • Military barracks: N. meningitidis. (where people are crowded together, 35% of people harbor this in their sinuses w/o symptoms)
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5
Q

What is the most definitive diagnostic tool of bacterial meningitis?

A

Because most organisms initiate a purulent or suppurative response, the presence of PMN’s in the CSF is the most definitive diagnostic index of meningitis.

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6
Q

what does the presence of lymphocytes indicate when it comes to meningitis?

A

the hallmark of meningitis caused by tuberculosis, viral menigitides, and chronic fungal infections (Cryptococcal meningitis)

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7
Q

What give the arachnoid, the creamy gray or white color , over the convexities as well as the base of the brain in bacterial meningitis? where else can this color be observed?

A

The brain disclosing an exudate of PMNs and fibrin

Because the intracranial and intraspinal subarachnoid space are connected, the exudate passes freely between these compartments.

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8
Q

What prevents the spread of infection in the brain during bacterial meningitis?

A

The pia, although delicate, is an effective barrier against the spread of infection and generally prevents involvement of the underlying brain.

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9
Q

Describe the barrier made by H. influenza and its significance in bacterial meningitis.

A

H. influenza elicits a dense leukocytic exudate, which is rich in fibrin over the convexities. As a result, the exudate becomes loculated, creating a barrier to antibiotics.

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10
Q

What are the clinical signs of bacterial meningitis?

A

H/A, vomiting, and fever are common, and convulsions frequently occur in children. If untreated, coma and death.

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11
Q

What are the classic signs of bacterial meningitis?

A

cervical rigidity, head retraction, pain in the knee when the hip is flexed (Kernig sign), and spontaneous flexion of the knees and hips when the neck is flexed (Brudzinski sign).

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12
Q

Define parkinson disease

A

A neurologic disorder characterized pathologically by the loss of neurons in the Substantia Nigra and clinically by tremors at rest, muscular rigidity, expressionless face and emotional lability.

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13
Q

Parkinson disease epidemiology

A

Typically appears in the 6th to 8th decades of life, and more than 2% of the population in N. America eventually develop the disease.

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14
Q

Who develops Parkinson?

A
  • No sex or racial diff are apparent
  • Genetic factors do not play a role except for a rare autosomal dominant early onset form due to a point mutation of chromosome 4
  • The vast majority of cases are idiopathic, but the disease has been recorded after viral encephalitis (von Economo encephalitis) and after the intake of a toxic chemical (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; MPTP)
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15
Q

What is the substantia nigra? What happens to it with age?

A

relays information to the basal ganglia through dopaminergic synapses. Normal aging is associated with a loss of neurons in the S.N. and a reduction in the dopamine content of that region.

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16
Q

Why is it suggested that parkinson is not an acceleration of normal age related changes?

A

Because there is a decrease in incidence in people over 80

accelerated process of the substantia nigra**

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17
Q

HIstory lesson: Parkinson disease

A

von Economo Encephalitis occurred during the influenza epidemic of 1916 to 1920, and resulted in injury to the substantia nigra.(gross loss of pigmentation)
-Depending on the extent of neuronal damage, the clinical expressions of “postencephalitic parkinsonism”were either immediate or delayed.

*people that died from the Spanish flu usually died due to pneumonia(staph aureus)

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18
Q

What does gross anatomy reveal with Parkinson disease?

A

a loss of pigmentation in the Substantia Nigra and Locus Ceruleus.

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19
Q

What do you find microscopically with Parkinson disease?

A

pigmented nuerons are scarce with small extracellular deposits of melanin, from necrotic neurons.
-Residual atrophic nerve cells contain spherical, granular,eosinophilic cytoplasmic inclusions called Lewy Bodies(displace the nucleus)

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20
Q

What does the midbrain look like?

A

Mickeymouse :)

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21
Q

What is the clinical presentation of Parkinson disease?

A
  • Characterized by a slowness of all voluntary movements and a muscular rigidity throughout the entire range of movement, and most patients have a course tremor of the distal extremities. (pill-rolling)
    • This tremor is present at rest and disappears with voluntary movement.
  • The face is expressionless (mask-like) and a reduced rate of swallowing leads to drooling
  • Hypertonia produces muscular rigidity referred to as “cog-wheel rigidity,” and spontaneous movement is diminished (akinesia). The posture is char. stooped
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22
Q

What do Parkinson’s patients have a higher incidence of?

A

Depression and dementia (they live a long time)

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23
Q

Levodopa and Parkinson

A

In early Parkinsonism, substitution therapy with Levodopa (Carbidopa, Sinemet) is beneficial.
-This therapy does not rectify the underlying disorder and with the passage of several years, becomes ineffective (refractory)

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24
Q

What are some other causes of Parkinson like symptoms?

A
  1. Drugs: Phenothiazines and Haldol
    1. CO or Manganese poisoning.
    2. Bilateral infarcts of Basal Ganglia
    3. Hydrocephalus
      5 Tumors near the Basal Ganglia
    4. Cerebral Trauma
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25
Q

Define Alzheimer disease

A

An insidious and progressive neurological disorder characterized by loss of memory, cognitive impairment, and eventual dementia

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26
Q

Who was the term Alzheimer disease restricted to in the past, who is it used on today?

A

The term was originally restricted to patients younger than 65 years in whom dementia was associated with neuropathological alterations (presenile dementia).
-Today, the term Alzheimer disease is used generically for all ages and identifies a specific morphological corollary of dementia.

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27
Q

What is the most common cause of dementia in the elderly worldwide?

A

Alzheimers

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28
Q

Prevelance of alzheimers relating to age/sex/familial?

A

before age 65: 1-2%
after age 85: 10%
women are affected twice as often as men

The vast majority of cases are sporadic, but a familial variant is recognized (5-10%).(chromosome 21)

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29
Q

Plaques and Alzheimer disease?

A

Beta-protein amyloid deposition in senile plaques.

- These plaques are located in areas of the cerebral cortex and are linked to intellectual function and are a constant feature of AD.
- Beta-protein amyloid is also found in the walls of cerebral blood vessels and may be the origin of the deposits in the brain.
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30
Q

Neurofibrillary tangles and Alzheimer disease

A
  • Neurofibrillary tangles, which are paired helical filaments that consist of an abnormal form of a normally occurring microtubule-associated protein, which is normally responsible for proper axonal transport.
  • This abnormal form destabilizes the microtubules, causing axonal degeneration, and the paired helical filaments, which occupy the cytoplasm of pyramidal cells in Alzheimer disease.
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31
Q

Gross finding in Alzheimer disease

A
  • The loss of neurons and neuritic processes, the gyri narrow, the sulci widen, and bilateral cortical atrophy becomes apparent in the frontal, temporal,parietal and hippocampal cortices.
  • The brain loses approximately 200 gms in an interval of 3-8 years.
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32
Q

Microscopic finding in Alzheimers disease

A
  1. Senile (neuritic) Plaques: discrete spherical masses of silver-staining neuritic processes surrounding a central amyloid core. Found predominantly in the hippocampus and amygdala, as well as the cortex. (silver stain)
    1. Neurofibrillary Tangles: bundles of paired, helical filaments in the cytoplasm of cortical neurons or hippocampal pyramidal cells that displace or encircle the nucleus (flame cells).
      - Are dramatically demonstrated on silver stains and are commonly found in the cortex, hippocampus, and the amygdala.
    2. Amyloid Angiopathy: found within cerebral blood vessels seen with congo red stains.
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33
Q

How is Alzheimer disease diagnosed?

A

Although pathologic examination of brain tissue is necessary for the definitive diagnosis, the combination of clinical assessment and modern radiologic methods allow accurate diagnosis in 80-90% of cases

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34
Q

where else are alzheimer pathological changes seen?

A

The pathologic changes seen are identical to almost all patients with trisomy 21 who survive beyond 45 years of age and a decline in cognition can be clinically demonstrated.

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35
Q

What happens with the progression of alzheimer disease?

A
  • Clinically, patients come to medical attention because of a gradual loss of memory and cognitive function, difficulty with language, and changes in behavior.
  • The disease is progressive and in the late stages, previously intelligent and productive persons are reduced to pitiful demented, mute, incontinent, and bedridden patients.
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36
Q

What do people with Alzheimer disease usually die of?

A

Terminal bronchopneumonia

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37
Q

Define Multiple sclerosis

A

A chronic, demyelinating disease of the CNS in which there are numerous patches of demyelination throughout the white matter.

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38
Q

What is the prevelance of MS?

A

It is the most common demyelinating disorder, with a prevalence of 1 in 1000.

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39
Q

Does MS affect sensory or motor functions?

A

The disease affects both sensory and motor functions and is characterized by exacerbations and remissions over a period of several years.

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40
Q

Where does MS mostly occur?

A

Principally a disease of temperate climates, and is rare in the tropics.

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41
Q

What is the prevelance of MS by age/sex

A

Acquired at a mean age of 30 years and is rare before 14 and after 60.
Women are afflicted almost twice as often.

42
Q

What is the etiology of MS?

A

The etiology is unknown: experimental and clinical studies have pointed to a possible genetic, immune, and infectious etiology

43
Q

MS and genetic factors

A

Genetic factors suggest a familial aggregation of the disease with an increased risk in 2nd and 3rd degree relatives.
-Monozygotic twins shows a 25% concordance for MS (2% for dizygotics).

44
Q

Immune factors are related to the histologic appearance of lesions: MS

A

perivascular lymphocytes and macrophages, with numerous CD4+ and CD8+ T-cells.

CD4: T helper cells
CD8: suppressor cells

45
Q

Viruses and MS

A
  • A wide variety of viruses have been implicated at one time or another, including mumps, rubella, herpes and measles.
  • To date, no direct evidence exists for the involvement.
  • JC virus recently has been studied, due to its role in initiating demyelination in the CNS. (agent causing -Progressive Multifocal -Leukoencephalopathy (PML).
46
Q

What is the hallmark of MS? and where is it found?

A
  • The plaque is the hallmark of the disease.
  • Variable size with smooth rounded contour
  • Usually situated in the white matter, but occasionally breech the gray-white junction
  • Exhibits a preference for the optic nerves and chiasm and uniformly localizes to the periventricular white matter. Can also involve the cerebellum, brainstem and SC
47
Q

What happens during MS(to the tissues)?

A
  • Histologically, there is selective loss of myelin in a region of axonal preservation.
  • Perivascular inflammation of lymphocytes and macrophages with focal edema.
  • As the plaque ages, it becomes more discrete and the edema regresses.
  • Astrocytes traverse the aging plaque and the tissue becomes dense with glial processes
48
Q

When does MS usually begin?

A

Clinically, MS has its onset during the 3rd or 4th decades, with periods of exacerbations, which is the expression of the formation of new plaques of demyelination, and remissions.
Some patients exhibit a relentless course without any remissions.

49
Q

What are the first symptoms of MS?

A

The disease typically begins with symptoms related to lesions of the optic nerves, brainstem or spinal cord.

- Blurred vision, or the loss of vision in one eye, is often the presenting complaint.
- When the initial lesion is in the brainstem, the most troubling early symptoms are double vision and vertigo.
50
Q

What are the symptoms of MS when plaques are on the spinal cord?

A

weakness of one or both legs and sensory symptoms in the form of numbness in the lower extremities.

51
Q

Are MS symptoms reversible?

A
  • Many of the initial symptoms are partially reversible within a few months
  • Unfortunately, in most patients, the disease recurs and thereafter follows a chronic relapsing and remitting course
52
Q

What is the degree of functional impairment in MS patients?

A

Variable, ranging from minor disability to severe incapacity, with widespread paralysis, dysarthria, severe visual defects, incontinence and dementia.

53
Q

How long do MS pt typically live and what do they usually die from?

A

Patients usually die of respiratory paralysis or UTI’s in terminal coma.
Most pt’s survive 20-30 yrs after the onset of symptoms

54
Q

What is a Berry aneurysm

A

Caused by arterial defects that originate during embryonic development, when the bifurcation of an artery creates a Y-shaped configuration.

55
Q

What is the most common reason for berry aneurysms?

A
  • The circumferential muscular layer of the parent vessel, may fail to interdigitate to the two branches, creating a point of congenital muscular weakness, bridged only by endothelium, the internal elastic lamina, and the slender adventitia.
  • Reason for over 90% of Berry’s occuring at branch points in the Circle of Willis
56
Q

What happens with time to a berry aneurysm? (before rupture)

A
  • The bloodstream from the parent vessel exerts relentless pressure on the crotch of the Y, and with time, the endothelium and internal elastic membrane degenerates and fragments.
  • A saccular aneurysm evolves, its walls being formed only by adventitia.
57
Q

How many people over the age of 55 have undetected berry’s?

A

25%

58
Q

Where are berry aneurysms found?

A
  1. Anterior Cerebral Artery and the Anterior Communicating Artery.
    1. The complex of the Internal Carotid Artery-Posterior Communicating Artery-Anterior Cerebral Artery.
    2. The trifurcation of the Middle Cerebral Artery
59
Q

How many people present with multiple berry’s?

A

In 20% of cases, multiple berry aneurysms are present.

60
Q

What happens when a berry ruptures and what are the mortality rates?

A
  • Rupture of a berry aneurysm causes a life-threatening subarachnoid hemorrhage, with a 35-50% mortality during the initial hemorrhage.
  • In 1/3 of patients, the rupture can cause either an intracerebral of intraventricular hemorrhage
  • Large aneurysms of the internal carotid complex can produce palsies of the 3rd, 4th, and 6th cranial nerves and seizures initiated by the compression of the medial aspect of the temporal lobe.
61
Q

What is the first sign of a subarachnoid hemorrhage after a berry rupture?

A

A sudden severe headache heralds the onset of the SAH and may be followed by coma

62
Q

What happens to pt who survive the berry rupture?

A

Patients who survive for 3-4 days often manifest a progressive decline in consciousness, due to arterial spasm and consequent cerebral ischemia and infarction
Survivors of the initial episode may rebleed, in which case the prognosis is worse.

63
Q

Hypertension-Associated Aneurysms: what is it and how does it develop?

A
  • The integrity of cerebral arterioles is compromised by hypertension through the deposition of lipid and hyaline material in their walls (lipohyalinosis).
  • The resulting weakening of the walls leads to the formation of Charcot-Bouchard aneurysms, small fusiform dilatations located on the trunk of a vessel, rather than at a bifurcation, and are predisposed to rupture, causing hypertensive cerebral hemorrhage.
64
Q

Hypertension-Associated Aneurysms AKA?

A

Charcot-Bouchard aneurysms

65
Q

Hypertensive Intracerebral Hemorrhage: where do they occur(top 3)

A
  1. The Basal Ganglia-Thalamus (75%)
  2. The Pons (15%)
  3. The Cerebellum (10%)
66
Q

Charcot-Bouchard aneurysms: locations

A

Associated with long-standing HTN, occurs in a geographic distribution that closely corresponds to the pattern of intracerebral hemorrhage and argues strongly for a relationship between them.

67
Q

Hypertensive Intracerebral Hemorrhage: symptoms/prognosis

A
  • The onset of symptoms is abrupt, and weakness usually dominates.
  • When the hemorrhage is progressive, and it usually is, death occurs within hours to days
  • As the hematoma enlarges, it may cause death by transtentorial herniation, or it may rupture into a lateral ventricle and initiate massive intraventricular hemorrhage.
68
Q

Intraventricular Hemorrhage

A
  • Rupture of a small vessel into a ventricle rapidly distends the entire ventricular system with blood, with expansion of the 4th ventricle.
  • The rush of blood through the ventricular system seemingly causes death by distention of the 4th ventricle and the compression of vital centers in the medulla
69
Q

Cerebellar Hemorrhage

A
  • Bleeding into the cerebellum causes abrupt ataxia, usually accompanied by a severe occipital headache and vomiting.
  • The expanding hematoma threatens life acutely through compression of the medulla, either directly or as a consequence of the herniation of the cerebellar tonsils through the foramen magnum
70
Q

Cerebral Infarction

A

Cerebrovascular occlusive disease remains a major cause of morbidity and mortality.

Cerebral infarcts are designated as “Hemorrhagic” or “Bland”, and in general, infarcts caused by embolization are the sites of hemorrhage, whereas those initiated by thrombotic occlusion are largely ischemic and therefore bland.

71
Q

Cerebral Infarction: Antherosclerosis

A

Atherosclerosis predisposes to vascular thrombosis and embolic events, both of which results in localized ischemia and subsequent cerebral infarction.

72
Q

Cerebral Infarction: patho

A
  • An embolus occludes vascular flow abruptly, after which the ischemic region undergoes necrosis.
  • The blood vessels that traverse the area of infarction also becomes necrotic and leak blood into that region.
  • Because thrombosis in-situ progresses more slowly, the collateral vessels also thrombose, thereby guarding against secondary hemorrhage
73
Q

Cerebral Infarction: aftermath

A
  • A recent infarct of the brain transforms the cerebral tissue into a liquefactive, necrotic putty-like debris which is ultimately phagocytized by macrophages.
  • Cerebral infarcts are not repaired by fibroblasts, and as an early response, capillaries proliferate at the margin of the lesion and become numerous by the 5th day.
  • Within months, the necrotic area is excavated by phagocytosis and a permanent cyst is formed, and at the same time the neovascularity regresses.
74
Q

TUMORS OF THE CNS

A
  • Intracranial tumors constitute only 2% of all aggressive neoplasms, and Gliomas (tumors of neuroectodermal origin) account for 60% of primary intracranial neoplasms.
    • Meningiomas account for 20%
    • All others (i.e. craniopharyngiomas, lymphomas, schwannomas, etc.) account for the last 20%.
75
Q

3 things to remember about the brain and tumors

A
  1. Brain is very acceptable to other tumors of the body. Brain is not very giving(metastasis stays within brain and spinal cord)
  2. Primary brain tumors in adults anterior, kids post brain cerebellum
  3. All tumors increase intercranial pressure= increased risk of seizures
76
Q

TUMORS IN THE CNS: etiology

A

15 per 100,000 persons.

20% of all cancers of childhood.

77
Q

TUMORS IN THE CNS: distribution

A

The distribution of intracranial tumors usually have predictable locations, depending on the age of the patient.
-Astrocytomas occur predominantly in the cerebral hemispheres in adults; in children, the cerebellum and pons are involved.

78
Q

TUMORS IN THE CNS: Space

A

Within the rigidly defined volume of the intracranial compartment, a new growth comprises space.
-If it displaces the brain, as is the case in a Meninigioma, the mass may consume space proportional to the tumor growth, and in this case, this relatively benign tumor, depending on the location, can be as devastating as a high-grade Astrocytoma

79
Q

TUMORS IN THE CNS: Space

A

Within the rigidly defined volume of the intracranial compartment, a new growth comprises space.
-If it displaces the brain, as is the case in a Meninigioma, the mass may consume space proportional to the tumor growth, and in this case, this relatively benign tumor, depending on the location, can be as devastating as a high-grade Astrocytoma

80
Q

TUMORS IN THE CNS: malignant tumors what they do

A

Malignant tumors infiltrate and destroys brain tissue (i.e.Glioblastoma multiforme), resulting in rapid growth and are fatal in a relatively short time.
-Their mass effect within the intracranial compartment is determined by the balance between tissue destruction and tumor growth.

*glioblastoma multiforme: worst brain one! rapid growth fatal over short time

81
Q

Astrocytomas: define

A

Glial neoplasms derived from Astrocytes, star-shaped cells distributed throughout the nervous system, with a role of support of neurons and response to tissue injury.

82
Q

Astrocytomas: who has them and where?

A

75-80% of adult primary brain tumors.
Usually seen in late middle age or older.
Usually found in the cerebral hemispheres in adults and cerebellum and the pons in kids.

83
Q

Grade I Astrocytoma

A
  • Composes 20% of primary intracranial neoplasms.
  • Poorly demarcated and infiltrates the cortex, with an indistinct margin. Can also be seen in the pons and cerebellum (children) and cervical spinal cord (young adults).
  • Life expectancy approximates about 5 yrs.
  • Transformation to a higher degree of anaplasia, often to Glioblastoma multiforme, occurs in 10% of cases and shortens life expectancy.
84
Q

Anaplastic (Grade II) Astrocytoma

A
  • Distinguished from well-differentiated astrocytoma by its greater cellularity, cellular pleomorphism, and anaplasia.
  • The distribution parallels that of grade I Astrocytomas.
  • The growth of the tumor is rapid, and life expectancy averages 3 years.
85
Q

Glioblastoma Multiforme (GBM)

A
  • Accounts for about 40% of primary intracranial neoplasms, predominates in the later decades of life, and life expectancy is about 18 months.
  • Infiltrates extensively in the cortex, frequently crossing the corpus callosum with bilateral extension into the white matter of both hemispheres, with both mottled red (recent hemorrhage) and yellow (remote hemorrhage), likened to a butterfly on gross examination
86
Q

Oligodendroglioma

A
  • In accordance with its cell of origin, arises in the white matter, predominantly in the cerebral hemispheres in adults.
  • Constitute 5-15% of gliomas.
  • Well-circumscribed, gelatinous, grey masses, often with cysts, focal hemorrhage and calcifications (seen in 90% of tumors).
  • The slow growth of these tumors is reflected by an absence of mitotic figures and necrosis, and therefore they have a better prognosis than patients with astrocytomas (survival for 5-10 years)
  • Patients have several years of neurologic complaints, including seizures.
87
Q

Ependymoma: what is the most common one and where do they occur in children and adults?

A

Glial tumor most common in the fourth ventricle, producing obstruction and resulting in Hydrocephalus.

  • Ependymal tissue lines the ventricles and the central canal of the spinal cord.
  • In the first two decades of life, they occur near the 4th ventricle (5-10% of primary brain tumors of this age group).
  • In adults, the spinal cord is their most common location.
  • Second only to Astrocytoma as a tumor of the spinal cord, where it arises from the central canal of the filum terminale, (myxopapillary ependymoma) at the lumbosacral level.
88
Q

Medulloblastoma: define and how many peeps get it?

A
  • Accounts for 20% of brain tumors in children, and arises exclusively in the cerebellum.
  • The most common intracranial primitive neuroblastic tumor, derived from undifferentiated cells of the cerebellum.
    - considered one of the small, round, blue cell tumors of childhood. (i.e. Neuroblastoma, Retinoblastoma, Ewing’s Sarcoma, PNET, Burkitts Lymphoma, and Rhabdomyosarcoma).
89
Q

Medulloblastoma: define and how it attacks

A
  • Accounts for 20% of brain tumors in children, and arises exclusively in the cerebellum.
  • The most common intracranial primitive neuroblastic tumor, derived from undifferentiated cells of the cerebellum.
    - considered one of the small, round, blue cell tumors of childhood. (i.e. Neuroblastoma, Retinoblastoma, Ewing’s Sarcoma, PNET, Burkitts Lymphoma, and Rhabdomyosarcoma).
  • The tumor infiltrates the -vermis of the cerebellum aggressively, and frequently disseminates through the CSF.
90
Q

Medulloblastoma: how does it work?

A

The tumor infiltrates the -vermis of the cerebellum aggressively, and frequently disseminates through the CSF.

91
Q

Medulloblastoma: What does it look like grossly and what is the most common genetic alteration?

A

Grossly, the tumor is well-circumscribed, gray and friable.

The most common genetic alteration is loss of material from the short arm of chromosome 17.

92
Q

Meningioma: Define and where are they found?

A

Intracranial tumors that arise from the arachnoid villi and produce symptoms by compressing brain tissue.

Most common in the parasagittal areas, convexities of the cerebral hemispheres, the olfactory groove and the lateral wing of the sphenoid.

**Has a propensity to erode contiguous bone.(only about 2%)

93
Q

Meningioma: etiology

A
  • Account for 20% of intracranial tumors.
  • Peak incidence is in the 4th-5th decades.
  • Slightly more common in females (60:40)
94
Q

Meningioma: what causes them?

A
  • The majority arise sporadically, and exhibit either a deletion or mutation of chromosome 22.
  • Can also be induced by cranial radiation and is related to dosage, and usually involves a latent period of 10-15 years.
95
Q

Meningioma: Gross appearance?

A

Grossly, they appear as well-circumscribed, firm, bosselated masses of variable size.
-Cut section reveals a gray, fibrous pattern

96
Q

Meningioma: Tumors in diff regions cause what effects?

A

Tumors of the olfactory groove produce anosmia, and those in the suprasellar region can lead to visual defects. H/A’s are common.

97
Q

Meningioma: Clinical appearance

A

Clinically, depending upon the location, seizures rather than neurologic deficits characterize the patient, due to lesions positioned in the parasagittal and over the convexities of the hemispheres

98
Q

Meningioma: what happens if it is not completely removed?

A

Those not completely excised tend to recur, and a typical meningioma doubles in size every 2 years.

99
Q

Acoustic Neuroma

A
  • Intracranial Schwannoma restricted to the 8th cranial nerve, found in the cerebellar pontine angle.
  • The occurrence of the lesion causes tinnitus, and deafness, and depending on the size, can compress other cranial nerves.
  • Malignant change is extremely rare, although local recurrence can occur with incomplete excision.
100
Q

Metastatic Tumors to Brain

A
  • Reach the intracranial compartment through the bloodstream, generally in patients with advanced carcinoma.
  • Tumors of different organs vary in their incidence of intracranial metastasis.
    • Disseminated Melanoma has a greater than 50% likelihood of metastasis, whereas breast and lung are approx. 35%, and kidney and colon have a 5% chance. Prostate, liver and sarcomas rarely spread
  • Most lesions seed to the gray-white junction.

PATHOPHYS (5 decks)

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