Intracranial Neoplasia and Stroke Flashcards

1
Q

in what domestic animals do we see the highest incidence of brain neoplasms?

A
  1. brachycephalic breeds: boxers, bulldogs, boston terriers
    -in these breeds, glial neoplasms most often seen
    -Boxers love meningiomas
  2. usually >7-9 years old (most over 2 years old)
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2
Q

what is the most common metastatic neoplasm?

A

hemangiosarcoma but this and other metastatic neoplasms that spread hematogenously LOVE the lungs so:

when you consider intracranial neoplasia as a differential, you MUST ALSO PERFORM 3 view chest rads

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3
Q

describe extension from adjacent structures as a route of metastasis in intracranial neoplasms

A
  1. extension of primary nasal cavity neoplasms relatively common
  2. neoplasms from middle or inner ear to extend to brain are less common
    -if so: squamous cell carcinoma and adenocarcinoma
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4
Q

what is also seen in nearly all cases of secondary neoplasms that extend into the cranial cavity?

A

clinical signs that reflect the original/primary site

nasal cavity: sneezing, nasal discharge

neoplasms of ear: chronic unilateral OTE/M/I

bone neoplasms of the skull: palpable mass/visible mass

pituitary: endocrine (hyperadrenocorticism, diabetes insipidus/mellitus

metastatic: nonspecific but lethargy, inappetence, weight loss

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5
Q

describe lymphoma

A
  1. usually multicentric (frequent and extensive infiltration of choroid plexus and leptomeninges) but can be primary (intravascular lymphoma, confined to nervous system)
  2. can occur as a mass located over brain surface (hard to distinguish from meningioma)
  3. more common in cats than dogs, esp if the cat FeLV positive
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6
Q

describe clinical signs of primary intracranial neoplasia

A
  1. relate to the area affected! can vary widely
  2. most primary intracranial neoplasms are slow growing, so classic presentation:
    -unilateral/asymmetric chronic, progressive signs
  3. if caudal to the tentorium cerebelli: more sever clinical signs than if in rostral cerebral hemisphere
  4. most primary intracranial neoplasms do NOT metastasize outside the brain (may metastasize along the CNS through CNS through ventricular system/CSF), but most patients do no have systemic signs of illness
  5. most neoplasia in CNS results in vasogenic edema (due to lack of tight junctions)
    -can treat with corticosteroids to improve clinical signs if you KNOW it is vasogenic!
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7
Q

describe diagnosis of intracranial neoplasia

A
  1. requires MRI
    -CT may help if lesions involve bony structures, but MRI preferred and required
  2. but MRI requires general anesthesia, so must obtain minimum database prior and also MUST perform 3-view thoracic rads first
    -MRI of the brain is not considered until thoracic radiographs are performed!!
  3. CSF analysis: rarely definitive and rarely done

-may see protein elevation with normal cell count (albuminocytologic dissociation)
-some meningiomas undergo necrosis and result in neutrophilic pleocytosis

-RISKS: DO NOT do until AFTER imaging!!!!
–if spinal tap a patient with elevated intracranial pressure, removing spinal fluid lowers subarachnoid pressure at site of tap, causing intracranial structures to shift from region of high pressure to low pressure = brain herniation = BAD NEWS BEARS

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8
Q

describe treatment of intracranial neoplasia

A
  1. definitive: combo of sx, RT, chemo
  2. palliative: corticosteroids for vasogenic edema, anticonvulsants to control seizures
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9
Q

describe meningiomas

A
  1. extraparenchymal, arise from dura
    -the most commonly reported brain neoplasm in cats! also very common in dogs
  2. most commonly in cats >9 and dogs >7
    -commonly in doliocephalic breeds: boxers, goldens, dovbies, scottish terriers, old english sheepdogs
  3. since from meninges, tend to be located over brain convexities
    -in goldens: commonly in olfactory/frontal lobes
    -also convexities of cerebrum and floor of cranial cavity ventral to brainstem
    -can also be in optic nerves (mass effect in orbit), or spinal cord or paranasal sinuses in dogs
  4. biologic behavior:
    -benign (rarely metastasize)
    -but presence in cranial cavity = malignant effect
    -can invade parenchyma in dogs, not likely in cats
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10
Q

describe diagnosis of meningiomas

A
  1. definitive: histopath when dead
  2. hyperostosis: thickening of bone
  3. CT or MRI:
    -broad based attachment
    -extra-axially located
    -uniformly contrast enhancing
    -dural tail sign: trailing off of neoplasm at the neoplasm margins
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11
Q

describe treatment and prognosis of meningiomas

A
  1. definitive: combo of surgery (often sole therapy in cats), radiation, chemotherapy
  2. palliative:
    -corticosteroids
    -anticonvulsive therapy

prognosis:
-dogs with palliative: 2-6 months

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12
Q

describe gliomas

A
  1. arise from glia, hard to tell which cell specifically
  2. appear as intraparenchymal mass within the brain (glial cells make up parenchyma)
  3. definitive diagnosis: biopsy (rarely performed)
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13
Q

describe ependymomas

A
  1. rare, derived from epithelial lining of ventricles and central canal of spinal cord
  2. more common in brachycephalics
  3. bc intraventricular, can cause obstructive hydrocephalus
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14
Q

describe choroid plexus neoplasms

A
  1. relatively common in dogs; no breed predilection; rare in cats
  2. most commonly from 4th ventricle, but can be from any ventricle
  3. most classified as papillomas bc extremely well differentiated
  4. diagnosis made only when metastasis within the nervous system or if there is microscopic criteria of malignancy
  5. exfoliation of papillomas (both benign and malignant may occur and result in dissemination to other areas of brain or spinal cord via CSF pathways
  6. hydrocephalus often also seen
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15
Q

describe pituitary neoplasms

A
  1. relatively common in dogs, most often recognized by finding an endocrine disorder
  2. either endocrinologically active or non-functional (no endocrine disorder)
  3. hyperadrenocorticism commonly seen in dogs as a result
    -PU/PD, panting, restless
  4. in cats: acromegaly = excessive GH secretion, resulting in hepatic production of IGF-1, so most common issue is uncontrolled diabetes mellitus (IGF-1 antagonizes insulin)
  5. microadenomas (more common) or macroadenomas
    -macroadenomas can result in neuro: behavior abnormalities or seizures
  6. as grow dorsally, affect appetite center, so seeing a Cushing dog that becomes less hungry or even anorexic may be the first sign of an enlarging pituitary neoplasm
  7. involvement of hypothalamus and median eminence may result in central diabetes insipidus
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16
Q

describe diagnosis and treatment of pituitary neoplasms

A

diagnosis: MRI!!
-no significant difference in endocrine tests when compare dogs with visible pituitary mass to those without

treatment:
-radiation therapy, gives longer survival times but does not control endocrinopathy so also endocrine therapy

17
Q

define stroke

A

pathologic reduction in blood flow to brain parenchyma

can be:
-ischemic: reduction or lack of blood supply related to blocked vasculature, more common
-hemorrhagic: rupture of a vessel

18
Q

compare and contrast ischemia, infarct, and ischemic penumbra

A

ischemia: any reduction below normal or what the cell needs to maintain normal function

infarct: ischemia so severe it results in cell death

ischemic penumbra: the tissue between the necrotic core of an ischemic infarct and the surrounding normal tissues; if can help the cells here, can positively impact patient outcome!

19
Q

describe clinical presentation of strokes

A
  1. peracute, nonprogressive, asymmetric; dramatic signs!
    -asymmetric due to the lack of overlap in the area supplied by each vessel in the brain
  2. the vessels that most commonly cause ischemic stroke:
    -middle cerebral artery and distal tributaries: result in prosencephalic signs
    -rostral cerebellar artery: vestibulocerebellar signs
20
Q

describe the pathophysiology of strokes

A
  1. breed disposition:
    -greyhound: racing = altered vasculatur
    -cavalier king charles spaniel: macroplatelets = coagulation
  2. thrombosis usually underlies vascular obstruction, so think of hypercoagulable state:
    -endocrinopathies: hyperadrenocorticism, PLN, HW, neoplasia
    -hypertension: kidney disease, hyperadrenocorticim, hyperthyroid (cat)
    -altered lipid metabolism: diabetes, hypothyroid
  3. ischemia = less blood supply to tissue and cells = energy deprivation = failure of Na+/K+ ATPase pump = Na+ and + plus flow into cell and pull fluid in with them = cytotoxic edema!!
    -corticosteroids, mannitol, hypertonic saline not effective like for vasogenic edema
21
Q

describe diagnosis of strokes

A
  1. signalment, history, anatomic localization = suspicious
  2. supported by finding evidence of hypercoagulable state
  3. definitive: MRI!
    -well-demarcated T2-hyperintense area of brain tissue with little to no swelling
    -use diffusion weighted imaging to differentiate between vasogenic and cytotoxic edema
22
Q

describe treatment and prognosis of strokes

A
  1. no specific!
    -supportive care: correct any other abnormality that would impact blood supply/perfusion to brain
  2. treat underlying disorder if present