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2. Neuro exam 2 > Martin: Intro, CV disease, & Infection > Flashcards

Martin: Intro, CV disease, & Infection Flashcards

1
Q

Which cell type is evident 12-24 hrs after acute CNS hypoxic/ischemic insult?

A

Red neurons (“red dead guys”)

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2
Q

Morphology of red neurons

A
  • Shrinkage of cell body
  • Pyknosis of nucleus
  • Dissapearance of nucleolus
  • Loss of nissl substance
  • Intense eosinophilia of the cytoplasm
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3
Q

What are the hallmarks of subacute and chronic neuronal injury (i.e., degeneration)?

A
  • Cell loss —> Apoptosis

- Reactive gliosis

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4
Q

What is gliosis?

A

Proliferation of astrocytes in response to brain injury

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5
Q

What is the axonal reaction?

Best seen where?

A
  • Change observed in cell body during regeneration of the axon
  • Best seen in anterior horn cells of SC when motor axons cut
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6
Q

Most important histopathologic indicator of CNS injury regardless of etiology?

Characterized by what 2 things; what cell?

A
  • Gliosis
  • BOTH hypertrophy and hyperplasia of astrocytes
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7
Q

Which cells of the CNS are most sensitive to insult?

A
  • Pyramidal neurons (hippocampus)
  • Neocortical Betz cells
  • Cerebella purkinje cells
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8
Q

Intracellular inclusions seen in herpes, rabies and cytomegalovirus?

Where specifically in the cell is each seen?

A
  • Cowdry body (intranuclear): herpes
  • Negri body (intracytoplasmic): rabies
  • Both nucleus and cytoplasm: CMV
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9
Q

Intracytoplasmic inclusions seen in Alzheimer’s and Parkinson disease?

A
  • Neurofibrillary tangles: Alzheimer’s disease
  • Lewy bodies: Parkinson’s disease
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10
Q

__________ act as the metabolic buffers and detoxify the brain; also contributing to the BBB (foot processes)

A

Astrocytes

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11
Q

What is the intermediate filament found in Astrocytes and can be stained for?

A

GFAP

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12
Q

Gliomas are positive for which stain?

A

GFAP

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13
Q

What type of astrocyte is seen in pt’s with long-standing hyperammonemia due to chronic liver disease (will have flapping tremor of hands with extension of the wrist, asterixis), Wilson disease, or hereditary metabolic disorders of the urea cycle?

A

Alzheimer Type II Astrocyte

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14
Q

What type of cytoplasmic inclusion bodies are characteristic of Pilocytic Astrocytoma and also found in regions of long standing gliosis?

A

Rosenthal fibers

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15
Q

Which heat-shock proteins are found in Rosenthal Fibers?

A
  • αB-crystallin
  • hsp-27

*Also ubiquitin

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16
Q

What is Alexander disease and what cellular changes are seen in this disease?

A
  • Leukodystrophy due to mutation in GFAP
  • Rosenthal fibers, but more commonly seen are corpora amylacea (aka polyglucosan bodies)
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17
Q

Corpora amylacea (aka polyglucosan bodies) are positive for which stain?

A

PAS positive

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18
Q

______ are mesoderm derived phagocytic cells that serve as resident macrophages of the CNS

A

Microglia

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19
Q

Which round, faintly basophilic, concentrically lamellated structures increase with age and are though to represent degenerative changes in the astrocyte?

A

Corpora amylacea (aka polyglucosan bodies)

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20
Q

What are the cell surface markers of Microglia?

A

CR3 and CD68

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21
Q

What are 4 ways microglia respond to injury?

A

1) Proliferation
2) Dev. elongated nuclei (rod cell), as in neurosyphillis
3) Microglial nodules: microglia aggregate around small foci of necrosis
4) Neuronophagia: microglia congregate around cell bodies of dying neurons

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22
Q

How does the myelination ability of oligodendrocytes differ from schwann cells?

A
  • Oligodendrocytes myelinate numerous internodes on multiple axons
  • Schwann cells in peripheral nerve, has a one-to-one correspondance between cells and internodes
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23
Q

Injury or apoptosis of __________ cells is a feature of acquired demyelinating diseases and leukodystrophies?

A

Oligodendroglial cells

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24
Q

What are Ependymal cells and where are they found in the CNS?

A

Ciliated columnar epithelial cells lining the ventricles

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25
Q

Disruption of the ependymal lining and prolferation of subependymal astrocytes produces what on ventricular surfaces?

A

Ependymal granulation

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26
Q

Which agent may produce extensive ependymal injury, with viral inclusions in ependymal cells?

A

CMV

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27
Q

What is the response of microglia to neuronal injury?

A

Proliferate and accumulate during CNS injury

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28
Q

What is Vasogenic edema and is often seen following what?

A
  • Increased EXTRAcellular fluid due to BBB disruption and increased vascular permeability
  • Fluid shifts from INTRAvascular compartments to INTERcellular spaces
  • Can be either localized (i.e., adjacent to neoplasms or inflammation) or generalied often follows ischemic injury
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29
Q

What is Cytotoxic edema and when is it seen?

A
  • Increase in INTRAcellular fluid secondary to neuronal, glial, or endothelial cell membrane injury
  • Generalized hypoxic/ischemic insult or w/ metabolic derangment
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30
Q

What is the most common cause of noncommunicating (obstructive) hydrocephalus in the neonate/infant?

A

Aqueductal stenosis

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31
Q

Enlargement of the entire ventricular system (“symmetric dilation”) due to accumulation of CSF not being properly absorbed at the dural sinus level is known as?

A

Communicating (“non-obstructive”) hydrocephalus

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32
Q

What 2 congenital conditions cause ventricular system obstruction?

A

1) Acqueductal stenosis
2) Dandy-Walker malformation

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33
Q

What is Hydrocephalus Ex-Vacuo?

Whom is it seen in?

What is the CSF pressure?

A
  • Compensatory increase in ventricular volume secondary to loss of brain parenchyma
  • Atrophy with increasing age, stroke or other injury, chronic neurodegenerative disease
  • CSF pressure is NORMAL!!!
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34
Q

Herniation is displacement of brain tissue due to _____ or ______

A

Mass effect or Increased intracranial pressure

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35
Q

Subfalcine herniation involves displacement of the _______ under the _______

A

Cingulate gyrus under the falx cerebri

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36
Q

Subfalcine herniations can compress which vessel?

A

Anterior cerebral artery

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37
Q

Transtentorial (uncinate, mesial temporal) herniation occurs when?

Which specific part and of which lobe?

A

MEDIAL aspect of the TEMPORAL lobe is compressed against the free margin of the tentorium

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38
Q

What are 3 possible consequences of progression of transtentorial herniations?

A

1) Compression of CN III —> pupillary dilation; eye is “down and out” (ipsilateral to lesion)
2) Compression of PCA —> ischemia of primary visual cortex
3) Large herniation may compress contralateral cerebral peduncle —> hemiparesis ipsilateral to side of herniation = Kernohan notch = “false localizing sign”

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39
Q

What are Duret hemorrhages and are a result of what?

A
  • Progression of transtentorial herniation producing secondary hemorrhagic lesions in the midbrain and pon

- “Flame-shaped” lesions

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40
Q

What are congenital causes of hydrocephalus?

A
  • Intrauterine infections (TORCH)
  • Agenesis/atresia/stenosis
  • Arnold chiari malformations
  • Dandy walker syndrome
  • Cranial defects: Achondroplasia and Craniostenosis
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41
Q

What is the most common parasitic nervous system disease in the world and can lead to hydrocephalus?

A
  • Cysticercosis
  • Taenia Solium (pork tapeworm)
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42
Q

What are the characteristic of normal pressure hydrocephalus and who is it seen in?

A
  • Symmetric type usually occuring in adults >60
  • Develops slowly over time; drainage of CSF is blocked gradually
  • Wet (incontinence), Wacky (dementia), Wobbly (ataxia)
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43
Q

A right hemisphere trans-tentorial herniation, causes a Kernohan’s notch in the _____ cerebellar peduncle, which results in ________ motor impairment.

A

A right hemisphere trans-tentorial herniation, causes a Kernohan’s notch in the left cerebellar peduncle, which results in right-sided motor impairment.

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44
Q

What is a tonsillar herniation and why is it life threatening?

A
  • Displacement of the cerebellar tonsils through the foramen magnum
  • Can can brainstem compression and compromises vital respiratory and cardiac centers in the medulla
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45
Q

_______ refers to a diverticulum of disorganized brain tissue extending through a defect in cranium; most often occurring in the posterior fossa

A

Encephalocele (sometimes misleadingly referred to as a “nasal glioma”)

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46
Q

Malformation of the anterior end of the neural tube leading to a “frog-like” apperance of a fetus is known as?

A

Anencephaly

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47
Q

The cause of Microcephaly is linked to?

A
  • Chromosomal abnormalities
  • Fetal alcohol syndrome
  • HIV-1 acquired in utero
  • Zika
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48
Q

What is Lissencephaly and the 2 general patterns observed?

A
  • Reduction in the # of gyri; sometimes agyria = NO gyri
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49
Q

What term describes neurons in innaprpriate places?

A

Neuronal heterotopia: assc w Epilepsy

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50
Q

Which forebrain anomaly is characterized by small, unusually numerous, irregularly formed cerebral convolutions? Leads to extra thick cortex

A

Polymicrogyria

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51
Q

What is Holoprosencephaly? Severe forms produce which abnormalities?

A
  • Incomplete separation of the cerebral hemispheres across the midline
  • Cyclopia from midline abn
  • Arrhinencephaly from absence of olfactory CNs
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52
Q

Holoprosencephaly is associated with what disease and signaling mutation?

A
  • Trisomy 13
  • Sonic hedgehog signaling pathway
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53
Q

Radiologic imaging showing a “bat wing” deformity is associated with that condition?

A

Agenesis of the corpus callosum

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54
Q

What is an Arnold-Chiari Type II malformation and what other abnormalities is it associated with?

A
  • Type 2 = more severe
  • Vermis extends down into foramen magnum
  • Assc w hydrocephalus and myelomeningocele
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55
Q

What is an Arnold-Chiari Type I malformation?

A
  • Type 1 = less severe & sometimes asymptomatic
  • Cerebellar tonsils extend down vertebral canal
  • May present w HA’s if CSF flow is impaired
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56
Q

Which condition is associated with an enlarged posterior fossa, absence of cerebellar vermis w/ replacement by a large midline cyst representing an expanded roofless 4th ventricle?

A

Dandy-Walker Malformation

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57
Q

Which condition has hypoplasia of the cerebellar vermis, elongation of the cerebellar peduncle and an altered shape of brainstem; together giving a ‘molar tooth sign’ on imaging?

A

Joubert syndrome

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58
Q

Syringomyelia is associated with what other condition; how does it present?

What part of the spinal cord is involved?

A
  • Associated w/ Arnold-Chiari Malformations
  • S/s: pain & temp loss of both UE (cape-like syrinx)
  • Central canal of spinal cord grows, interrupting the fibers in the anterior white commisure
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59
Q

Expansion of the ependyma-lined central canal of the spinal cord is known as ________.

A

Hydromyelia

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60
Q

What is Cerebral Palsy and what are the clinical manifestations of this disease?

Occurs due to insults during which period?

A
  • Non-progressive neurologic motor deficits characterized by combination of spasticity, dystonia, ataxia/athetosis, and paresis
  • Pre-natal and perinatal periods (are present from birth)
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61
Q

What type of hemorrhage is seen in the germinal matrix of premature infants?

A
  • Intraparenchymal hemorrhage
  • Junction between thalamus and caudate nucleus
  • May extend into ventricles —> subarachnoid space —> hydrocephalus (obstructive)
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62
Q

Infarcts may occur in the supratentorial white matter of premature infants and are known as?

Characteristic finding?

A
  • Periventricular leukomalacia
  • Chalky yellow plaques = white matter necrosis and calcification
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63
Q

Extensive ischemic damage of both white and gray matter leading to large cystic lesions during the perinatal period is known as?

A
  • Multicystic encephalopathy
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64
Q

Diastatic fracture

A

Fracture that crosses a suture

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65
Q

Clinical term for altered consciousness secondry to a head injury typically brough about by a change in momentum of the head

A

Concussion

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66
Q

What is the morphology of a brain contusion?

A
  • Wedge shaped w/ a broad base lying along the surface at the point of impact
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67
Q

What term describes an old traumatic lesion?

Term for contusion at point of impact and the opposite of that?

A
  • Plaque Jaune: old lesion. Yellow/brown patches.
  • Coup: contusion at point of impact
  • Contrecoup: contusion on opposite of side impact bc of sudden decel
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68
Q

Diffuse axonal injury is best demonstrated using what lab techniques/stains?

A
  • Silver impregnantion (silver stain)
  • Immunoperoxidase stains for amyloid precursor protein and α-synuclein
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69
Q

Sudden onset of severe headache (“worst headache of my life”), often with rapid neurologic deterioration is consistent with a _________ hemorrhage

A

Subarachnoid

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70
Q

Secondary injury associated seen in subarachnoid hemorrhage is often associated with what?

A

Vasospasm

71
Q

A patient presents after a direct blow to the head which initially knocked him unconscious, after 1hr he begins to exhibit neurological deterioration, what do you suspect?

A

Epidural hematoma = rapid neuro sx develop

Assc w skull fracture

72
Q

What type of hematoma is associated with rupture of the bridging veins?

A

Subdural hematoma

73
Q

Which patient populations are at higher risk for subdural hematomas?

A
  • Elderly w/ brain atrophy due to increased stretching of the bridging vein
  • Infants due to thin-walled bridging veins
74
Q

What is seen in the brains of individuals with CTE (dementia pugilistica) during a post-mortem autopsy?

A
  • Atrophic w/ enlarged ventricles
  • Accumulation of tau-containing neurofibrillary tangles
  • Characteristic pattern involving superficial frontal and temporal lobe cortex
75
Q

Border zone (“watershed”) infarcts are usually seen after ________ episodes

A

Hypotensive

76
Q

What are the subacute changes seen 24 hours to 2 weeks after global ischemia?

A
  • Tissue necrosis
  • Influx of Macrophages and Reactive gliosis (10 days)
  • Vascular proliferation
77
Q

Global cerebral ischemia occurs after which events?

A

Cardiac arrest, shock, or severe hypotension

78
Q

Which artery is most frequently affected by embolic infarction?

A

MCA — direct extension of the internal carotid artery

79
Q

Widespread hemorrhagic lesions involving the white matter are characteristic of embolization of _______ after trauma

A

Bone marrow

Aka shower emboli

80
Q

Most common sites for thrombotic occlusions in the brain

A
  • Carotid bifurcation
  • Origin of MCA
  • Either end of Basilar artery
81
Q

Thrombolytic therapy following an infarct is contraindicated in?

A

Hemorrhagic infarcts –> may cause extensive intracerebral hematomas

82
Q

Infarcts are often initially nonhemorrhagic, but secondary hemorrhage can occur from ______ injury

A

Ischemia-reperfusion

83
Q

What are the most common locations for lacunar infarcts?

A
  • Lenticular nucleus
  • Thalamus
  • Internal capsule
  • Deep white matter
84
Q

How can HTN lead to the development of lacunar infarcts?

A

Cerebral vessels develop arteriolar sclerosis and may become occluded —> Lacunes aka small lakes

85
Q

Small slit like cavity that is surrounded by a brownish discoloration after reabsorption of a hemorrhage is known as what?

A

Slit hemorrhage

86
Q

Hypertensive encephalopathy is a consequence of?

A

Malignant hypertension

Assc w deep brain parenchymal hemorrhages

87
Q

Patients who have bilateral gray and white matter infarcts over many months and years may develop what distinct clinical syndrome characterized by dementia, gait abnormalities, pseudobulbar signs and other focal neuro deficits?

A

Vascular (multi-infarct) dementia

88
Q

What is the risk factor most commonly associated with deep brain parenchymal hemorrhages?

A

HTN

89
Q

What causes Charcot-Bouchard microaneurysms?

A

Chronic HTN

90
Q

What is a Charcot-Bouchard microaneurysm vs. Saccular (berry) aneurysm?

Where is each most commonly seen?

A
  • Charcot-Bouchard occur in vessels less than 300 um in diameter; most often within basal ganglia from lenticulostriate arteries
  • Saccular (berry) aneurysms occur in branch points of anterior circulation and cause SAH
91
Q

What is the risk factor most commonly associated with lobar hemorrhages?

A

Cerebral amyloid angiopathy (CAA)

92
Q

What is the mutation associated with Cerebral Autosomal Dominant Arteriopathy w/ Subcortical Infarcts and Leukoencephalopathy (CADASIL)?

A

NOTCH3

93
Q

Cerebral Autosomal Dominant Arteriopathy w/ Subcortical Infarcts and Leukoencephalopathy (CADASIL) is characterized clinically how?

A

Recurrent strokes (usually infarcts, less often hemorrhages) and dementia

94
Q

Most frequent cause of clinically significant subarachnoid hemorrhage is rupture of?

A

Saccular (berry) aneurysm

95
Q

There is an increased incidence of saccular (berry) aneursyms in people with what disorders?

A
  • AD polycystic kidney disease
  • Ehlers-Danlos type IV
  • NF1

*Smoking and HTN are risk factors

96
Q

What is the most common site for Arteriovenous Malformations?

A

MCA; particularly its posterior branches

97
Q

Who is most at risk for Arteriovenous Malformations?

How does it present?

A
  • Males twice as frequently; between ages 10-30
  • Presents as seizure disorder, intracerebral hemorrhage, or subarachnoid hemorrhage
98
Q

Morphology of Arteriorvenous Malformations

A

Tangled vessels (“worm-like”) that show prominent, pulsatile arteriovenous shunting with high blood flow – bypass a capillary bed

99
Q

Waterhouse-Friderichsen syndrome results from?

Occurs most commonly due to meningitis caused by?

A
  • Meningitis-associated septicemia w/ hemorrhagic infarction of the adrenal glands and cutaneous petechiae
  • Meningococcal and pneumococcal meningitis
100
Q

What is chemical meningitis?

A

Nonbacterial irritant introduced into the subarachnoid space

101
Q

How can hydrocephalus result from pyogenic meningitis?

Particularly with what organism?

A
  • Capsular polysaccharide of pneumococcal meningits produces a gelatinous exudate that promotes arachnoid fibrosis
  • Referred to as chronic adhesive arachnoiditis
102
Q

What are predisposing conditions for the development of a brain abscess?

A
  • Acute bacterial endocarditis
  • Congenital heart disease (w/ right to left shunting)
  • Immunosuppression
103
Q

Discrete lesions in the brain with central liquefactive necrosis surrounded by brain edema is characteristic of?

A

Brain Abscess

104
Q

Most common bacteria in brain abscesses of non-immunosuppressed patients?

A
  • Streptococci
  • Staphylococci
105
Q

Extradural abscess are commonly associated with?

A

Osteomyelitis

106
Q

What are the common causes of chronic bacterial meningoencephalitis?

A
  • Mycobacterium tuberculosis
  • Treponema pallidium
  • Borrelia species
107
Q

The most serious complications of chronic tuberculosis meningitis are ________ producing hydrocephalus, and ________ producing arterial occlusion and infarction of underlying brain

A

The most serious complications of chronic tuberculosis meningitis are arachnoid fibrosis producing hydrocephalus, and obliterative endarteritis producing arterial occlusion and infarction of underlying brain

108
Q

What stain is used to look for TB infection?

A

Acid-fast

109
Q

Which form of neurosyphilis involves the base of the brain and may cause communicating hydrocephalus?

A

Meningovascular neurosyphilis

110
Q

How does paretic neurosyphilis clinically manifest?

A
  • T. pallidum (spirochete)
  • Progressive cognitive impairment associated with mood alterations (including delusions of grandeur)
  • Terminates in severe dementia (general paresis of the insane)

**will see perivascular iron deposits

111
Q

Tabes dorsalis results from damage to?

A

Dorsal column medial lemniscus system (posterolateral columns, fasciculus cuneatus and gracilis)

112
Q

Which condition presents with widened gait, impaired joint position sense and ataxia, loss of pain sensation leading to skin and joint damage (Charcot joints), characteristic “lightning pains,” and absence of DTRs?

A

Tabes dorsalis

113
Q

What are the neurologic symptoms associated w/ Neuroborreliosis (Lyme Disease)

A

Lyme pie to the FACE

F- facial nerve plasy

A- arthritis

C- cardiac block

E- erythema migrans

**develop 4wks after rash (bell’s and peripheral neuropathy)

114
Q

Which virus is an important cause of epidemic encephalitis, especially in tropical regions of the world?

A

Arbovirus

115
Q

Involvement of the spinal cord in West Nile encephalitis can lead to ________ syndrome w/ paralysis

A

Polio-like syndrome w/ paralysis

116
Q

HSV-1 has a tropism for which lobes of the brain; what type of injury is seen when infected?

A
  • Temporal lobes and orbital gyri of the frontal lobe
  • Hemorrhagic lesions w/ Cowdry type A intranuclear viral inclusion bodies within neuron and glia
117
Q

What does HSV-2 cause particularly in neonates born by vaginal delivery to a woman with active primary HSV genital infections?

A

Severe encephalitis

118
Q

In immnosuppressed individuals, CMV most commonly causes?

A

Subacute encephalitis

119
Q

Periventricular leukomalacia is characteristc of infection by which virus?

A

CMV

120
Q

Poliovirus has a tropism for which neurons of the spinal cord?

A

Anterior horn motor neurons

121
Q

CMV infection is confirmed by?

A

Immunohistochemistry

122
Q

How does CNS infection by poliovirus present initially and what are the CSF findings?

A
  • Meningeal irritation
  • CSF consistent w/ aseptic meningitis (pleocytosis of lymphocytes, moderately elevated protein, nearly normal glucose)
123
Q

What is post-polio syndrome?

A
  • Happens to pt’s 25-35 years after the resolultion of initial illness
  • Characterized by progressive weakness and decreased muscle mass and pain in the affected area
124
Q

Negri bodies associated with rabies infection are found where in the brain?

A
  • Pyramidal neurons of the hippocampus
  • Purkinje cells of the cerebellum

*Sites usually devoid of inflammation

125
Q

Which symptoms/findings are virtually diagnostic for rabies infection?

A

Malaise, headache and fever in conjunction w/ local paresthesias around the wound

126
Q

What is seen during the acute phase of HIV infection of the CNS?

A

Mild lymphocytic meningitis, perivascular inflammation, and some myelin loss

127
Q

What are the only CNS cell type to express both the CD4 coreceptor and the chemokine receptors (CCR5 or CXCR4) that are required in combination for efficient infection by HIV?

A

Microglia

128
Q

What is immune reconstitution inflammation syndrome (IRIS)?

A
  • Seen in AIDS patients
  • Paradoxical deterioration after starting therapy and consists of an exuberant “reconstituted” inflammatory response while on antiretroviral therapy
  • Intense inflammation w/ influx of CD8+ lymphocytes
129
Q

What type of encephalitis is associated with widely distributed microglial nodules, often containing macrophage-derived multinuclated giant cells?

A

HIV encephalitis

130
Q

Which virus causes Progressive Multifocal Leukoencephalopathy (PML)?

This virus has tropism for which cell, and what is its principle pathologic effect?

A
  • JC polyomavirus
  • Tropism for oligodendrocytes —> demyelination is its principal pathologic effect
131
Q

Progressive Multifocal Leukoencephalopathy (PML) occurs almost exclusively in who?

A

Immunosuppressed individuals

132
Q

Which encephalitis is characterized by patches of irregular, ill-defined white matter injury w/ enlarged oligodendrocyte nuclei containing glassy amphopilic viral inclusions?

A

Progressive Multifocal Leukoencephalopathy (PML)

133
Q

Which encephalitis is characterized by widespread gliosis and myelin degeneration; viral inclusions, largely within the nuclei of oligodendrocytes and neurons; variable inflammation of white and gray matter; and neurofibrillary tangles?

A

Subacute Sclerosing Panencephalitis (SSPE)

134
Q

How do most fungi reach the brain; what is another way they may invade?

A
  • Most by hematogenous dissemination
  • Direct extension may also occur, particularly mucormycosis in the setting of diabetes mellitus
135
Q

What are the 3 main forms of injury to the CNS caused by fungal infections?

A

1) Chronic meningitis
2) Vasculitis
3) Parenchymal invasion

136
Q

Vasculitis associated with fungal infections is most frequently seen with what organisms?

A

Mucormycosis and Aspergillosis

137
Q

What are the most commonly encountered fungi that invade the brain?

A

Candida and Cryptococcus

138
Q

Gelatinous material within the subarachnoid space and small cysts within the parenchyma (“soap bubbles”), especilly within the basal ganglia are characteristic of what type of infection?

A

Chronic meningitis associated w/ cryptococcal infection

139
Q

What may be seen on CT with cerebral toxoplasmosis infection?

A

Ring enhancing lesions

140
Q

What is the morphology of cerebral toxoplasmosis abscesses; most often seen where?

A
  • Mostly affect the cerebral cortex (near the gray-white junction) and deep gray nuclei
  • Central necrosis, petechial hemorrhage surrounded by acute and chronic inflammation, macrophage infiltration, and vascular proliferation
141
Q

Which stain is used for Naegleria species to confirm a diagnosis of cerebral amebiasis?

A

PAS or Methenamine silver

142
Q

Cerebral malaria is a rapidly progressing encephalitis caused by what organism?

A

Plasmodium falciparum

143
Q

What are the clinical implications of infection with Taenia Solium causing cysticercosis?

A
  • Form cysts within the subarachnoid space
  • May obstruct CSF flow, leading to life threatening hydrocephalus
  • Hemiplegia, severe headaches, and papilledema
144
Q

Heterozygosity at which codon is protective against the development of diseases associated with prion protein (PrP)?

A

129

145
Q

What are the clinical manifestations of Creutzfeldt-Jakob Disease (CJD)?

A

Subtle changes in memory/behavior followed by a rapidly progessing dementia, often associated with pronounced involuntary jerking muscle contractions on sudden stimulation (startle myoclonus)

146
Q

Creutzfeldt-Jakob Disease (CJD) has a peak incidence during what decade?

How is it transmitted?

Average survival time?

A
  • During the seventh decade
  • Iatrogenic transmission, notably by corneal transplantation, deep implantation of electrodes in the brain, and administration of contaminated preparations of naturally derived GH
  • Average survival = 7 months
147
Q

Onset of the variant form of CJD is linked to consumption of?

A

Bovine spongiform encephalopathy agent in contaminated foods or blood transfusion

148
Q

How does vCJD differ clinically from CJD?

A
  • Behavioral changes early in the disease
  • Slower progression of neurologic symptoms
149
Q

What is seen on electron microscopy with CJD and vCJD?

How are they stained?

A
  • Kuru plaques: extracellular deposits of aggregated abnormal protein (will have halo of spongiform in vCJD); usually seen in the cerebellum, but are abundant in the cerebral cortex in cases of vCJD

- Congo red and PAS-positive

150
Q

Fatal Familial Insomnia (FFI) is caused by what specific mutation in the PRNP gene?

A

Aspartate substitution at residue 129 or PrPc

151
Q

What is the characteristic morphology of Fatal Familial Insomnia (FFI)?

A
  • Neuronal loss and reactive gliosis in the anterior ventral and dorsomedial nuclei of the thalamus
  • Neuronal loss is also prominent in the inferior olivary nuclei
152
Q

What are the clinical manifestations of Fatal Familial Insomnia (FFI)?

A
  • Sleep disturbances in the initial stages
  • Ataxia, autonomic disturbances, stupor, and finally coma
153
Q

Polymorphisms at which codon influence the development of prion diseases?

A

Codon 129 encoding either Met or Val

154
Q

How does FFI differ from the other prion diseases, morphologically?

A

Does not show spongiform pathology

155
Q

Where are the densest amounts of exudate found with acute meningitis caused by P**neumococcal meningitis and H. influenzae?

A
  • P. meningitis: often densest over convexities near sagittal sinus
  • H. influenzae: usually basal location
156
Q

What might have caused this on MRI?

Flat brain w surrounding hydrocephalus

A

Choroid Plexus Papilloma

157
Q

Which skull fracture will cause orbital and mastoid hematomas?

A

Basilar skull fracture

158
Q

Define chronic traumatic encephalopathy? (CTE)

What are these pt’s more susceptible to?

A

A brain disease linked with repeated head blows

Inc risk of: AD, PD, atrophy

159
Q

How do we ID Shaken Baby Syndrome?

A

Shaking a baby stops the crying bc brain damage

ID with prussian blue stain to look for iron

Also may see: SAH, retinal hemorrhage, subdural hematoma

160
Q

Epidural hematomas are caused by which vessel generally?

A
  • Caused by middle meningeal artery usually 2nd to skull fracture
  • S/s: rapid deterioration, transtentorial herniation, CN3 palsy

Imaging: smooth contours of hematoma

161
Q

What are the 2 assc with Berry Aneurysms?

A

ADPKD

Ehler-Danlos

NF1

Marfan

162
Q

What are the clinical sx assc w loss of ACA?

A

ACA

  • Contralat hemiplegia: leg more than arm/face
  • Alien hand syndrome: contra arm not under voluntary control
163
Q

What are the clinical sx assc w loss of PCA?

A

PCA = Contralat homonymous hemianopia with macular sparing

***affects Occipital lobe

164
Q

What are the clinical sx assc w loss of MCA?

A

MCA = most common place for infarcts and ischemia

  • Aphasia, hemineglect, hemianopia, face-arm sensorimotor loss
  • Gaze preference TO side of lesion
165
Q

What shape indicates a water-shed infarct?

A

Sickle shaped band of necrosis

166
Q

What causes ACA-MCA infarction?

What are the assc sx?

A
  • Cause = occlusion of the internal carotid artery OR hypotension w carotid artery stenosis
  • S/s: proximal arm/leg weakness & transcortical aphasia
167
Q

What are the sx of MCA-PCA infarction?

A

Loss of higher order visual processing

168
Q

What is significant about TIAs?

A

TIAs are a warning sign for larger ischemic event (15% of pt in 3mo)

Neurological emergency & all pt should be emergently admitted

169
Q

Hemorrhagic vs Ischemic infarction

A
  • Hemorrhagic: emboli assc.
    • Bleeding 2nd to reperfusion
    • Cause: A fib, carotid stenosis, DVT w PFO, endocarditis
  • Ischemic: thrombus assc.
    • Clot forms at site of occlusion
170
Q

Where do most saccular aneurysms happen?

What is the underlying defect

A

Anterior ciruclation: ACA and AComm

No media of vessel at branch points - more susceptible to stretch

171
Q

What are the 4 routes of CNS infection?

A
  1. Hematogenous: most common
  2. Direct implantation
  3. Local extension: teeth, sinus
  4. Peripheral NS: rabies, herpes

CSF exchange happens q3-4hrs, so brain is washed in bacteria

172
Q

What is the cause of subdural empyema?

What is a possible complication?

A

Subdural empyema caused by infection of skull bones or sinus infection spreading to subdural space

May cause thrombophlebitis is veins – leads to infarction

173
Q

What are CSF findings with brain abscess?

A

High WBC, High protein, Nml glucose

174
Q

What will be in the CSF of a pt w Lyme disease?

A

CSF = ab

**ab can cross-react w other infectious agents: mono, RA, SLE, syphylis

2. Neuro exam 2 (16 decks)

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