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NMSP Exam 1 > Cerebrovascular Disease and Infections > Flashcards

Cerebrovascular Disease and Infections Flashcards

1
Q

What deficits are seen in an anterior cerebral artery rupture?

A
  • Upper motor neuron type weakness
  • Cortical type sensory loss
  • Contralateral hemiplegia initially
  • Alien hand syndrome
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2
Q

What is alien hand syndrome? When is it seen?

A
  • Semi Automatic movements of the contralateral arm not under voluntary control
  • Seen in anterior cerebral artery rupture
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3
Q

What deficits are seen in posterior cerebral artery rupture?

A
  • Contralateral homnymous hemianopia
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4
Q

What deficits are seen in middle cerebral artery rupture?

A
  • Aphasia
  • Hemineglect
  • Hemianopia
  • Face-arm or face-arm-leg sensorimotor loss
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5
Q

What is the gaze preference in MCA rupture?

A
  • TOWARD side of lesion
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6
Q

What are lacunes?

A
  • Small deep infarcts involving penetrating branches of MCA or other vessels
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7
Q

What is the difference between hypoxia and ischemia?

A
  • Hypoxia –> decreased oxygen

- Ischemia –> decreased blood supply

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8
Q

What is the ultimate consequence of hypoxia and ischemia?

A
  • Tissue infarction
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9
Q

What are the three major categories of cerebrovascular disease?

A
  1. Thrombosis
  2. Embolism
  3. Hemorrhage
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10
Q

What is a stroke?

A
  • Clinical designation
  • Applies to all classifications of cerebrovascular disease
  • Acute onset and persists longer than 24 hours
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11
Q

What are some of the most common cerebrovascular disorders?

A
  • Global ischemia
  • Embolism
  • Hypertensive intraparenchymal hemorrhage
  • Ruptured aneurysm
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12
Q

What does survival depend on when blood flow is reduced?

A
  • Collateral circulation
  • Duration of ischemia
  • Magnitude and rapidity of flow reduction
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13
Q

What are the two types of reduction in blood flow?

A
  1. Global ischemia

2. Focal ischemia

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14
Q

What are some causes of global ischemia?

A
  • Cardiac arrest
  • Shock
  • Severe hypotension
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15
Q

What are some causes of focal ischemia?

A
  • Embolic or thrombotic arterial occlusions
  • Vasculitides
  • Atherosclerosis in hypertension
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16
Q

What does the damage look like to watershed areas in an infarct?

A
  • Sickle shaped band of necrosis
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17
Q

What can cause damage to the ACA-MCA watershed area?

A
  • Occlusion of internal carotid artery

- Hypotension in patient with carotid stenosis

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18
Q

What symptoms are seen in ACA-MCA watershed infarct?

A
  • Proximal arm and leg weakness

- Transcortical aphasia –> language issues

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19
Q

What symptoms are seen in MCA-PCA watershed infarct?

A
  • Higher order visual processing
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20
Q

What can cause carotid stenosis?

A
  • Atherosclerosis
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21
Q

What could be a consequence of atherosclerosis of the internal carotid artery?

A
  • Thrombi can embolize distally to the MCA, ACA, or ophthalmic artery
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22
Q

What may be some symptoms of a thrombi that embolizes from the carotids?

A
  • Contralateral face-arm or face-arm-leg weakness
  • Contralateral sensory changes
  • Contralateral visual field defects
  • Aphasia or neglect
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23
Q

What are some sites of primary thrombosis?

A
  • Carotid bifurcation
  • Origin of middle cerebral artery (MCA)
  • Either end of basilar artery
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24
Q

What is an atheroma?

A
  • Intimal lesion, lipid core covered by fibrous cap
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25
Q

What happens if the lipid cap ruptures?

A
  • Exposes blood to thrombogenic substance –> thrombosis/clot
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26
Q

What do infarcts look like in the brain?

A
  • Wedge shaped due to distribution
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27
Q

What are some sources of emboli?

A
  • A fib
  • MI
  • Valvular disease
  • Artery-to-Artery emboli
  • Dissection
  • PFO
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28
Q

What is a marantic emboli?

A
  • Proteinaceous emboli from marantic (non-bacterial thrombotic) endocarditis
  • Hypercoagulable states such as advanced malignancy
  • Amniotic fluid emboli –> child birth
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29
Q

Which artery is most likely affected by an emobli?

A
  • MCA
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30
Q

What is a shower emboli?

A
  • Fat after long bone fracture
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31
Q

What is characteristic of bone marrow embolization?

A
  • Widespread white matter hemorrhages
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32
Q

What are some causes of hypercoaguability?

A
  • Heritable coagulation factor disorders
  • Dehydration
  • Adenocarcinomas/malignancies
  • Surgeries, trauma, childbirth
  • DIC
  • Hematologic disorders
  • Vasculitis
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33
Q

What are some common causes of a transient ischemic attack (TIA)?

A
  • Migraines
  • Seizures
  • Non-neurologic conditions (cardiac arrhythmias or hypoglycemia)
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34
Q

How long are TIAs typically? What happens if they are longer?

A
  • Around 10 min

- Anything longer causes some permanent cell death

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35
Q

Why are TIAs so important to recognize?

A
  • They are a neurological emergency

- May have a stroke causing persistent deficits within 3 months

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36
Q

What is the mechanism of TIAs?

A
  • Embolus temporarily occludes then dissolves, in situ thrombus formation and/or vasospasm
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37
Q

What are the two types of stroke?

A
  • Hemorrhagic

- Ischemic

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38
Q

What does a hemorrhagic stroke look like?

A
  • Intracerebral or subarachnoid hemorrhage
  • Emboli associated
  • Hemorrhage secondary to reperfusion of damaged vessels
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39
Q

What does an ischemic stroke look like?

A
  • Bloodless
  • Thrombus associated
  • Hemorrhagic conversion
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40
Q

What is hemorrhagic conversion seen in ischemic stroke?

A
  • Fragile vessels rupture leading to secondary hemorrhage
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41
Q

What are some causes of ischemic stroke?

A
  • Embolic
  • Thrombotic
  • Large vessel
  • Small vessel
  • Lacunar infarcts
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42
Q

What symptoms are seen in lenticulostriate artery infarct?

A
  • Pure motor hemiparesis
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43
Q

What symptoms are seen in thalamic lacune?

A
  • Contralateral somatosensory deficits
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44
Q

What symptoms are seen in basal ganglia lacune?

A
  • Hemiballismus
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45
Q

What are slit hemorrhages?

A
  • Small caliber penetrating vessels –> look like slit like cavities
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46
Q

What surrounds a slit hemorrhage?

A
  • Pigment laden macrophages
  • Macrophages
  • Gliosis
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47
Q

What causes hypertensive encephalopathy?

A
  • Malignant HTN
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48
Q

What is seen in hypertensive encephalopathy?

A
  • Vascular multi-infarct dementia
  • Binswanger disease
  • Charcot-Bouchard microaneurysms
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49
Q

What signs are seen in vascular multi infarct demetia?

A
  • Dementia
  • Gait
  • Pseudobulbar signs
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50
Q

What signs are seen in binswanger disease?

A
  • Large area of subcortical white matter with myelin and axon loss
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51
Q

What signs are seen in charcot-bouchard microaneurysms?

A
  • Associated with chronic hypertension

- Minute aneurysms in the basal ganglia

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52
Q

What is cerebral amyloid angiopathy?

A
  • Lobar hemorrhage

- Same B-amyloid deposited in the walls of vessels (like in Alz disease) producing microbleeds

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53
Q

What is CADASIL?

A
  • Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy
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54
Q

What is seen in CADASIL?

A
  • Recurrent strokes and dementia
  • Thickening of the media and adventitia
  • Loss of smooth muscle cells and basophilic PAS+ deposits
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55
Q

When is CADASIL detected?

A
  • Around 35 years old and infarcts typically occur 10-15 years later
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56
Q

What gene is seen in CADASIL?

A
  • Auto Dom –> NOTCH 3 gene
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57
Q

What are some stroke risk factors?

A
  • HTN
  • Diabetes
  • Hypercholesterolemia
  • Cigarette smoking
  • Pos family history
  • Cardiac disease
  • Prior history of stroke
  • Hypercoagulability
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58
Q

What should you think if there is a stroke in a young patient?

A
  • Arterial dissection (like in marfan)
  • PFO or hypercoagulability
  • Sickle cell
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59
Q

What is the most frequent cause of a significant subarachnoid hemorrhage?

A
  • Rupture of saccular (berry) aneurysm –> begins as basilar SAH
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60
Q

What aneurysms are seen in the anterior circulation?

A
  • Saccular
  • Mycotic
  • Traumatic
  • Dissection
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61
Q

Where in the circle of willis are saccular aneurysms found?

A
  • Majority in ACA

- Secondary location in MCA

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62
Q

How can saccular (berry) aneurysms be treated?

A
  • Clipping due to having a neck
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63
Q

When do aneurysms usually rupture?

A
  • Fifth decade and slightly more in females
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64
Q

What increases the likelihood of ruptured aneurysms?

A
  • Increased intracranial pressure –> straining at stool or sexual orgasm
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65
Q

What are some hereditary diseases that have increased incidence of aneurysms?

A
  • If first degree relative is affected
  • Infantile polycystic kidney disease
  • Ehlers-Danlos type IV
  • NF1
  • Marfan
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66
Q

How do people present with a ruptured aneurysms?

A
  • Worse headache they have ever had

- Repeat bleeding is common

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67
Q

What are people most at risk for a couple of days after SAH?

A
  • Additional ischemic injury from vasospasm affecting vessels bathed in extravasated blood
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68
Q

What are the four groups of vascular formations?

A
  • Arteriovenous malformations (AVM)
  • Cavernous malformations/hemangiomas
  • Capillary telangiectasias
  • Venous angiomas
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69
Q

What do cavernous malformations look like?

A
  • Distended, loosely organized vascular channels arranged back to back
  • ** THERE IS NO BRAIN PARENCHYMA***
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70
Q

What regions of the brain are affected by cavernous malformations?

A
  • Cerebellum
  • Pons
  • Subcortical regions
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71
Q

What is seen in cavernous malformations?

A
  • Foci of old hemorrhage
  • Infarction
  • Calcification seen in surrounding area
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72
Q

Who is most likely affect by AVMs?

A
  • Males more than females in their 10-30s
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73
Q

What are some symptoms of AVMs?

A
  • Seizure

- Intracerebral hemorrhage or SAH

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74
Q

What do AVMs look like?

A
  • Tangle, worm like vascular channels with prominent pulsatile arteriovenous shunting with high blood flow
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75
Q

Where are AVMs most commonly seen?

A
  • MCA and posterior branches (subarachnoid space)
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76
Q

What mutation is associated with AVMs?

A
  • KRAS oncogene
77
Q

What are some causes of multifocal vascular disease?

A
  • Cerebral atherosclerosis
  • Vessel thrombosis/emboli from carotid or heart
  • Cerebral arteriosclerosis from chronic hypertension
78
Q

What is seen in vascular dementia?

A
  • Multiple, bilateral gray matter and white matter infarcts
79
Q

What are the four principal routes of infection?

A
  1. Hematogenous
  2. Direct implantation
  3. Local extension
  4. PNS
80
Q

How does tuberculous meningitis develop?

A
  • Seeding CSF from subepidural or submeningeal granulomas
81
Q

How does herpes simplex and zoster infections spread?

A
  • Produce latent infection of sensory ganglia
  • Replicate in schwann cells
  • Ascend to the CNS within sensory nerves
82
Q

How does rabies infections spread?

A
  • Bind at or near Ach receptors at the NMJ

- Ascend to the CNS via motor nerves

83
Q

What is the CNS response to infection?

A
  • Widespread infection –> involving all tissue elements, characteristic of bacterial meningitis and many viral encephalitides
  • Functional specialization of different cell populations and of specific neuro-anatomical regions determine the characteristic neurological syndromes
84
Q

What accelerates the development of cerebral edema?

A
  • Accelerated by products released by both living bacteria and antibiotic lysed bacteria
85
Q

What slows the development of cerebral edema?

A
  • Slowed and reversed by corticosteroids
86
Q

What are the symptoms of acute meningitis?

A
  • Headache
  • Meningeal irritation signs (Kernig/Brudzinski)
  • High fever
  • Confusion
  • Coma
87
Q

When do symptoms of acute meningitis develop?

A
  • Within several days; however may develop over a few hours with a fulminant course
88
Q

Where is the exudate in pneumococcal meningitis?

A
  • Convexities near sagittal sinus
89
Q

Where is the exudate in H. influenzae meningitis?

A
  • Basal location
90
Q

What is ventriculitis?

A
  • Fulminant infection

- Inflammation may extend into ventricles

91
Q

What is focal cerebritis?

A
  • Inflammatory cells infiltrate walls of the veins and extend into the brain substance
92
Q

What are some systemic signs that are caused by acute meningitis?

A
  • Ventriculitis
  • Focal cerebritis
  • Phlebitis –> may lead to venous thrombosis and hemorrhagic infarction
  • Leptomeningeal fibrosis –> hydrocephalus
93
Q

What are the complications seen in bacterial meningitis?

A
  • Seizures
  • Encephalitis
  • Hearing loss, blindness, paralysis
  • Fulminant –> esp. with meningococcemia (will see adrenal hemorrhage causing death)
94
Q

What is the gram neg diplococci causing meningitis?

A
  • N. meningitidis
95
Q

What is the gram pos diplococci causing meningitis?

A
  • S. pneumoniae
96
Q

What is the gram neg pleomorphic causing meningitis?

A
  • H. influenzae
97
Q

What is the gram pos cocci causing meningitis?

A
  • S. aureus or s. epi

- Streptococci

98
Q

What is the gram neg bacilli causing meningitis?

A
  • E. coli or other gram neg
99
Q

Where in the spine is the best place to do a lumbar puncture?

A
  • Between 3rd and 4th lumbar vertebrae
100
Q

How does the CSF differ between bacterial cause and viral cause?

A
  • Bacterial: Cloudy, high neutrophil, low glucose, very high protein levels
  • Virus: clear, no neutrophils, high lymphocytes, normal glucose, increased protein levels
101
Q

What are some risk factors for meningitis?

A
  • Age <5 and >60
  • DM
  • Immunosuppression
  • Contiguous infections
  • IVDA
  • Bacterial endocarditis
  • Sickle cell
102
Q

What organisms are most likely to cause meningitis in neonates?

A
  • E. coli

- Grp B strep

103
Q

What organisms are most likely to cause meningitis in unvaccinated children under 2yo?

A
  • H. influenzae type B
104
Q

What organisms are most likely to cause meningitis in adolescents and young adults?

A
  • N. meningitidis
105
Q

What organisms are most likely to cause meningitis in elderly?

A
  • S. pneumoniae

- Listeria monocytogenes

106
Q

What organisms are most likely to cause meningitis in immunocompromised individuals?

A
  • S. pneumoniae
  • N. meningitidis
  • L. monocytogenes
  • P. aeruginosa
107
Q

What organisms are most likely to cause meningitis in a basilar skull fracture?

A
  • S. pneumoniae
  • H. influenzae
  • Grp A beta-hemolytic strep
108
Q

How do patients present with an abscess?

A
  • Progressive focal neurological deficits

- Signs of increased intracranial pressure may also develop

109
Q

What does the CSF look like in an abscess?

A
  • High WBC
  • High protein
  • Normal glucose
110
Q

What are some complications seen in ascesses?

A
  • Herniation
  • Abscess rupture with ventriculitis or meningitis
  • Venous sinus thrombosis (patient dies)
111
Q

What is the treatment for most brain abscesses?

A
  • Surgical drainage and antibiotics
112
Q

What does a brain abscess look like on CT?

A
  • Edema surrounding liquefactive necrosis
113
Q

What is subdural empyema?

A
  • Bacteria or fungus infection of skull bones or sinuses spread to subdural space
114
Q

What is the treatment of subdural empyema?

A
  • Surgical drainage
115
Q

What is associated with an extradural abscess?

A
  • Osteomyelitis
116
Q

Where does N. meningitidis colonize?

A
  • Oropharynx and rhinopharynx
117
Q

What agar is used to grow N. meningitidis?

A
  • Chocolate agar
118
Q

What are the clinical manifestations of N. meningitidis?

A
  • Rapidly progressive septicemia with fever, hypotension, DIC, petechial and purpuric lesions
  • Purpura fulminans
  • Hemorrhagic infarction of adrenal glands
119
Q

What is purpura fulminans?

A
  • Hemorrhagic skin lesions which progress to gangrene

- Occurs in distal portion of limbs

120
Q

What are the symptoms of chronic meningitis?

A
  • Fever
  • Headache
  • Lethargy
  • Confusion
  • N/V
  • Stiff neck
121
Q

What does the CSF look like in chronic meningitis?

A
  • Elevated protein
  • Predominantly lymphocytic pleocytosis
  • Sometimes low glucose
122
Q

What are some causes of chronic meningitis?

A
  • TB
  • Neuroborreliosis
  • Neurosyphilis
123
Q

What is seen in mycobacterium tuberculosis diffuse meningoencephalitis?

A
  • Gelatinous or fibrinous exudate in subarachnoid space

- Obliterative endarteritis –> inflammation infiltrates vessel walls with intimal thickening

124
Q

Where is the predilection in mycobacterium tuberculosis diffuse meningoencephalitis?

A
  • Base of brain –> CNs could be affected

- Obliterated Cisterns and encases CNs

125
Q

What is needed to diagnose mycobacterium tuberculosis diffuse meningoencephalitis?

A
  • Culture AND smear to increase chance of positive
126
Q

What symptoms are seen in borrelia meningitis?

A
  • Cranial nerve palsy and peripheral neuropathies

- CSF with antibodies

127
Q

How is borrelia meningitis diagnosed?

A
  • CSF PCR
128
Q

What is meningovascular neurosyphillis?

A
  • Chronic meningitis involving base of the brain

- Causes communicating hydrocephalus

129
Q

What is seen in meningovascular neurosyphilis?

A
  • Obliterative endarteritis = Heubner arteritis
130
Q

What is paretic neurosyphilis?

A
  • Insidious, but progressive mental deficits associated with mood alterations (delusions of grandeur) that terminate in severe dementia
  • Perivascular iron deposits
  • Glandular ependymitis –> proliferation of subependymal glia under damaged ependymal lining
131
Q

What is tabes dorsalis?

A
  • Damage to sensory nerves in the dorsal roots
132
Q

What symptoms are seen in tabes dorsalis?

A
  • Impaired joint position sense and resultant ataxia
  • Loss of pain sensation
  • Joint damage
  • Lightening pains
  • Absence of deep reflexes
133
Q

What is the main cause of aseptic meningoencephalitis?

A
  • Enteroviruses
134
Q

What does the CSF look like in aseptic meningoencephalitis?

A
  • Lymphocytic pleocytosis
  • Moderate increase protein
  • Glucose near normal
135
Q

How do most viruses infect the CNS?

A
  • Through nerves
136
Q

What is the inflammatory response to viruses in the brain?

A
  • Lymphocytes
137
Q

What are some symptoms of arthropod borne viral encephalitis?

A
  • Generalized neuro deficits

- Focal signs

138
Q

What does west nile look like?

A
  • Involves spinal cord and gives a polio like syndrome with paralysis
139
Q

What does the CSF look like in arthropod borne viral encephalitis?

A
  • Colorless
  • Slight increase in pressure
  • Increased protein
  • Normal glucose
140
Q

What is seen in the brain during arthropod borne viral encephalitis?

A
  • Multiple foci of necrosis in both gray and white matter
  • Neuronophagia
  • Microglial nodules
141
Q

What are the symptoms of HSV-1 encephalitis?

A
  • Alterations in mood, memory, and behavior
142
Q

What does HSV-1 encephalitis do to the brain?

A
  • Necrotizing and hemorrhagic
143
Q

What parts of the brain are most affected by HSV-1 encephalitis?

A
  • Inferior and medial temporal lobes (cingulate gyrus destroyed)
  • Orbital gyri of frontal lobes
144
Q

What inclusions are seen in HSV-1 encephalitis?

A
  • Cowdrey type A
145
Q

How do neonates get HSV-2 encephalitis?

A
  • Born by vaginal delivery to women with active primary HSV infection
146
Q

What happens with the herpes zoster infection?

A
  • Latent phase in sensory neurons of dorsal root or trigeminal ganglia
147
Q

What happens when herpes zoster is reactivated?

A
  • Shingles –> painful vesicular skin eruption limited to a single or limited dermatome
  • Postherpetic neuralgia syndrome
148
Q

What is postherpetic neuralgia syndrome seen in reactivated herpes zoster infection?

A
  • Persistent pain as well as painful sensation following nonpainful stimuli
149
Q

Who is most likely affected by CMV?

A
  • Fetuses and immunocompromised ind.
150
Q

What happens to the brain in a CMV infection?

A
  • Periventricular necrosis causing severe brain destruction (mainly parenchyma)
  • Microcephaly
  • Periventricular calcification
151
Q

Where does CMV localize in the brain?

A
  • Paraventricular subependymal regions –> severe hemorrhagic necrotizing ventriculo encephalitis and choroid plexitis
152
Q

Where does poliomyelitis attack?

A
  • Mononuclear cell perivascular cuffs

- Neuronophagia of the anterior horn motor neurons of the spinal cord

153
Q

What symptoms are seen in poliomyelitis?

A
  • Flaccid paralysis

- Associated with muscle wasting and hyporeflexia

154
Q

What is the incubation period of rabies?

A
  • 1-3 months
155
Q

How does rabies infect?

A
  • Ascends along peripheral nerves from the wound site
156
Q

What are some symptoms of a rabies infection?

A
  • Paresthesias around wound
  • Extraordinary CNS excitability –> violent motor responses progressing to convulsions
  • Flaccid paralysis
  • Hydrophobia
157
Q

What happens in acute HIV aseptic meningitis?

A
  • Mild lymphocytic meningitis
  • Perivascular inflammation
  • Some myelin loss
158
Q

What happens in chronic HIV aseptic meningitis?

A
  • Microglial nodules with multinucleated giant cells
159
Q

What happens to the vessels in HIV aseptic meningitis?

A
  • Abnormal prominent endothelial cells and perivascular foamy or pigment-laden macrophages
160
Q

What happens to the white matter in HIV aseptic meningitis?

A
  • Multifocal or diffuse areas of myelin pallor, axonal swelling, and gliosis
161
Q

What is IRIS?

A
  • Immune reconstitution inflammatory syndrome
162
Q

What is seen in IRIS?

A
  • Paradoxical deterioration after starting antiviral therapy
  • Exuberant inflammatory response
  • Paradoxical exacerbation of symptoms from opportunistic infections
163
Q

What is seen in HIV-associated neurocognitive disorders?

A
  • Mild to florid cognitive changes

- Persisting despite effective HIV treatment

164
Q

What virus causes progressive multifocal leukoencephalopathy (PML)?

A
  • JC Polypomavirus
165
Q

What does the JC polyomavirus affect?

A
  • Oligodendroglial cells

- Demyelination principle pathologic effect

166
Q

What occurs in PML?

A
  • Irregular, ill-defined destruction of white matter

- Subcortical area of demyelination with lipid-laden macrophages in the center with decreased number of axons

167
Q

What causes subacute sclerosing panencephalitis (SSPE)?

A
  • Paramyxovirus

- Seen in children months-years following early age acute infection with measles

168
Q

What symptoms are seen in SSPE?

A
  • Cognitive decline
  • Spasticity of limbs
  • Seizures
169
Q

What happens in the brain during SSPE?

A
  • Widespread gliosis and myelin degeneration
  • Viral inclusions
  • Variable inflammation of white and gray matter
  • Neurofibrillary tangles
170
Q

What organisms are the biggest causes of fungal meningoencephalitis?

A
  • Candida albicans
  • Mucor
  • Aspergillus
  • Cryptococcus neoformans
171
Q

Which meningitis causing fungus is most likely found in people with diabetes?

A
  • Mucormycosis
172
Q

Who is most likely to develop chronic meningitis by cryptococcus neoformans?

A
  • People with immune dysfunction –> Immunosuppressed
173
Q

Where is cryptococcus gattii likely to cause chronic meningitis?

A
  • Immunocompetent ind.
174
Q

What is used to prep the CSF in cryptococcus meningitis?

A
  • India ink prep
175
Q

How is cryptococcus meningitis diagnosed?

A
  • Look at CSF for the cryptococcal polysaccharide antigen and culture
176
Q

What does toxoplasmosis gondii do to the brain?

A
  • Brain abscess
177
Q

Where is the brain abscess due to toxoplasmosis located?

A
  • Near gray-white junction of cerebral cortex and deep gray nuclei
178
Q

What does a toxoplasmosis brain abscess look like on CT?

A
  • Ring enhancing lesion
179
Q

What does the histology look like for toxoplasmosis?

A
  • Central foci of necrosis
  • Petechial hemorrhages surrounded by acute and chronic inflammation
  • Macrophage infiltration and vascular proliferation
  • Free tachyzoites and encased bradyzoites
180
Q

How does naegleria fowleri (brain eating ameba) get into the brain?

A
  • Through the nose when contaminated water goes through cribiform
  • Located in warm freshwater
181
Q

What does the brain look like in rocky mountain spotted fever?

A
  • Starry sky on diffusion weighted imaging
182
Q

What is the cause for prion diseae?

A
  • PrP prion protein
183
Q

What symptoms are seen in prion disease?

A
  • Rapidly progressive neurodegenerative disorders
184
Q

What does prion disease do to the brain?

A
  • Microscopic spongiform change –> intracellular vacuoles in neurons and glia
185
Q

How does someone get CJD?

A
  • Corneal transplant
  • Brain implantation of electrodes
  • HGH
186
Q

What are the symptoms of CJD?

A
  • Rapidly progressive dementia with startle myoclonus

- Only about 7 months

187
Q

How is the vCJD in the UK different than CJD?

A
  • Kuru plaque –> extracellular deposits of aggregated abnormal protein
  • Congo red + and PAS+
188
Q

What is fatal familial insomnia?

A
  • Sleep disturbances initially

- Aspartate substitution

189
Q

What symptoms are seen in fatal familial insomnia?

A
  • Ataxia
  • Autonomic disturbances
  • Stupor
  • Finally coma

NMSP Exam 1 (12 decks)

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