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Neuromusculoskeletal & Psychiatry II Exam #2 > Cerebrovascular Disease and Infections > Flashcards

Cerebrovascular Disease and Infections Flashcards

1
Q

What deficits would you expect to see when the anterior cerebral artery is compromised?

What is “alien hand syndrome”?

A

UMN-type weakness and cortical-type sensory loss.
CL hemiplegia initially.
CL leg > arm or face

Semiautomatic movements of the CL arm not under voluntary control.

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2
Q

What deficits would you expect when the posterior cerebral artery is compromised?

A

CL homonymous hemianopia

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3
Q

What deficits would you expect to see when the middle cerebral artery is compromised?

What are lacunes?

A

Aphasia, hemianopia, hemineglect, and face-arm or face-arm-leg sensorimotor loss.
Gaze preference toward side of lesion.

Small, deep infarcts penetrating branches of the MCA (or other vessels).

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4
Q

What are the 2 types of reduction in blood flow and examples of each?

A

Global ischemia - cardiac arrest, shock, severe hypotension.

Focal ischemia - embolic or thrombotic arterial occlusion, or atherosclerosis in HTN.

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5
Q

What region is most susceptible to ischemia and infarction?

What does it produce?

A

The region between 2 vessels.

Sickle-shaped band of necrosis over the cerebral convexity a few cm. lateral to the interhemispheric fissure.

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6
Q

What deficits would you expect in an ACA-MCA watershed compromise?

What are 2 causes?

A

Proximal arm and leg weakness.
Transcortical aphasia - language issues.

Occlusion of the ICA or hypotension in a patient with carotid stenosis.

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7
Q

What deficits would you expect in an MCA-PCA watershed compromise?

A

Higher-order visual processing dysfunction.

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8
Q

What symptoms are seen in a patient with carotid stenosis? (4)

A

CL face-arm or face-arm-leg weakness.
CL sensory changes.
CL visual field defects.
Aphasia

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9
Q

What are the 2 patterns of border zone infarcts?

A
  1. Cortical border zone infarcts - ACA/MCA and MCA/PCA

2. Internal border zone infarctions - MCA/LCA

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10
Q

What are the 3 most common sites of primary thrombosis in the head/neck?

A

Carotid bifurcation
Origin of the MCA
Either end of the basilar a.

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11
Q

What is a marantic emboli?

A

Proteinaceous emboli from marantic (non-bacterial thrombotic) endocarditis (NBTE). It can be the result of hypercoagulable states like advanced malignancy or amniotic fluid emboli (childbirth).

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12
Q

What is “shower emboli”?

A

Fat after long bone fracture

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13
Q

What are 3 heritable coagulation factor disorders?

A

Protein S deficiency
Protein C deficiency
Antithrombin III deficiency

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14
Q

What is the definition of a transient ischemic attack (TIA)?

What duration is most common?

Is it an emergency?

A

Neurological deficit < 24 hrs. due to temporary brain ischemia.

Approx. 10 min. (> 10 min. probably causes some degree of cell death).

Yes, approx. 15% of TIAs will have a stroke causing persistent deficits within 3 mo.; half of them within 48 hrs.

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15
Q

What are the 2 types of stroke?

What are they associated with?

A

Hemorrhagic stroke (red): intra-cerebral or subarachnoid hemorrhage.

  • emboli-associated
  • hemorrhage secondary to reperfusion of damaged vessels

Ischemic (pale, bland, anemic) infarction: bloodless.

  • thrombus-associated, plaque-associated
  • hemorrhagic-conversion: fragile vessels rupture leading to secondary hemorrhage
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16
Q

What are lacunar infarcts?

A

Small vessel infarcts resembling small lakes or “lacunes”. The arteries develop arteriolar sclerosis (usually of the lenticulostriate arteries).

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17
Q

What defects would you seen in the following lacunar infarcts?

Posterior limb of internal capsule
Thalamic lacune
Basal ganglia lacune

A

Posterior limb of internal capsule: pure motor hemiparesis (lenticulostriate aa.)

Thalamic lacune: CL somatosensory deficits

Basal ganglia lacune: hemiballismus

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18
Q

What would be found surrounding a slit hemorrhage?

A

Pigment laden Mo
Mo
Gliosis

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19
Q

What are the following types of hypertensive encephalopathy (malignant HTN)?

Vascular multi-infarct dementia
Binswanger Dz
Charcot-Bouchard microaneurysms

HTN is a risk factor for which kind of hemorrhages?

A

Vascular multi-infarct dementia: dementia, abnormal gait and pseudobulbar signs.

Binswanger Dz: large area of subcortical white matter with myelin and axon loss.

Charcot-Bouchard microaneurysms: minute aneurysms in the basal ganglia that are associated with HTN.

Deep brain parenchymal hemorrhages.

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20
Q

What kind of hemorrhage can result in beta-amyloid deposition (same as in AD)?

A

Lobar hemorrhage caused by Cerebral Amyloid Angiopathy (CAA) that cause microbleeds.

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21
Q

What is CADASIL?

What is the major symptom(s)?

When is it first detectable?

What gene is implicated?

What are some histopathological changes seen?

A

Cerebral AD arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL).

Recurrent strokes and dementia.

First detectable at approx. 35 y/o.

NOTCH 3 gene

Thickening of media and adventitia
Loss of SM cells
PAS+ deposits

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22
Q

What is the most common cause of a SAH?

A

Rupture of a saccular (Berry) aneurysm

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23
Q

Saccular, mycotic, traumatic and dissection aneurysms are most common in…

Atherosclerotic (fusiform) aneurysms are most common in…

A

Anterior circulation (anterior communicating a., ACA)

The basilar a.

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24
Q

In which patients are saccular aneurysms most likely to rupture?

What is the risk of bleeding per year?

1/3 of ruptures are associated with… (2)

A

Fifth decade, slightly more common in females.

> 10 mm. have about 50% risk of bleeding/year.

Acute increases in ICP

  • straining at stool
  • orgasm
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25
Q

What is the risk a few days after a SAH, regardless of etiology?

A

Increased risk of additional ischemic injury from vasospasm afecting vessels bathed in extravasated blood (esp. if it involves base of brain/CoW).

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26
Q

Where do AVMs exist in the CNS?

What site is most common?

A

Subarachnoid space, and may extend into the brain parenchyma or may be exclusively in the parenchyma.

MCA and posterior branches are most common.

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27
Q

How does infection occur in the 4 principle routes of infection?

Hematogoneous
Direct implantation
Local extension
Peripheral nervous system

A

Hematogoneous: most common! Arterial primarily, but can be due to venous spread via anastomosis with facial vv.

Direct implantation: trauma or congenital malformations (meningomyelocele).

Local extension: sinuses, teeth, cranial or spinal osteomyelitis.

Peripheral nervous system: viruses (Rabies, HZ).

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28
Q

How does tuberculus meningitis develop?

A

Via seeding CSF from subepidural or submeningeal granulomas.

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29
Q

Where are the lymphatics of the CNS?

How does is affect the spread of infection?

A

Epidural space.

Infections of the retropharyngeal, posteriro mediastinal or retroperitoneal spaces may produce epinal epidural abscesses.

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30
Q

What kind of infection does Herpes Simplex and Zoster produce?

Where do they replicate?

A

A latent infection of sensory ganglia.

Replicate in Schwann cells and ascend to the CNS within sensory nerves.

31
Q

How does Rabies invade the CNS?

A

It binds at or near the AChR at the NMJ and ascends to the CNS via motor nerves.

32
Q

What is an important factor in the pathogenesis of CNS infections and the selection of antibiotic therapy?

A

The relative impermeability to Igs, complement and antibiotics due to lack of fenestrations or clefts.

33
Q

What are the causes of the following types of meningitis?

Meningocephalitis
Chemical meningitis
Acute pyogenic meningitis
Aseptic meningitis
Chronic meningitis
A

Meningocephalitis: inflammation of meninges and brain parenchyma.
Chemical meningitis: non-bacterial irritant in the subarachnoid space.
Acute pyogenic meningitis: bacterial.
Aseptic meningitis: acute or subacute viral.
Chronic meningitis: Tb, Spirochetes or Cryptococcus.

34
Q

What will accelerate the development of cerebral edema?

What will slow it?

A

Accelerate - products released by both living bacteria and antibiotic-lysed bactera.

Corticosteroids.

35
Q

What are the locations of Pneumococcal meningitis vs. H. influenzae meningitis?

A

Pneumococcal - convexities near the sagittal sinus.

H. influenzae - basal location.

36
Q

What occurs in focal cerebritis?

A

Inflammatory cells infiltrate the walls of veins and extend into the brain substance.

37
Q

Phlebitis from meningitis may lead to…

Leptomeningeal fibrosis may lead to…

A

Venous thrombosis and hemorrhagic infarction of the underlying brain.

Hydrocephalus

38
Q

Pneumococcal meningitis can cause what complications?

A

Chronic adhesive arachnoiditis

39
Q

What syndrome is a complication of bacterial meningitis?

A

Friedman-Waterhouse syndrome (adrenal hemorrhage)

40
Q

What are the presumptive bacterial IDs of the following Gram stain results?

G- diplococci
G+ diplococci
G- pleomorphic
G+ cocci
G- bacilli
A 
G- diplococci: N. meningitidis
G+ diplococci: S. pneumoniae
G- pleomorphic: H. influenzae
G+ cocci: S. aureus or S. epidermidis
G- bacilli: E. coli
41
Q

What lab changes to the CSF would you expect to see in bacterial meningitis?

Pressure
Gross appearance
Neutrophils
Lymphocytes/monocytes
Glucose
Protein

Aside from most of the changes above, which 4 values would be markedly different in a viral etiology?

A 
Pressure: >20 cm H2O (NL = 7-20 cm H2O)
Gross appearance: cloudy, turbid.
Neutrophils: > 100/ml (NL = 0)
Lymphocytes/monocytes: > 5/ml (NL = 0-5)
Glucose: < 50 mg/dl (NL = 50-80 mg/dl)
Protein: 50-1000 mg/dl (NL = 15-45 mg/dl)

Viral:

  • Glucose levels will be normal in a viral infection.
  • The gross appearance is clear/colorless in a viral infection.
  • Protein content is much less in a viral infection.
  • Lymphocytes/monocytes will be more elevated in a viral infection.
42
Q

Which cells are dominant in viral meningitis?

Bacterial meningitis?

Fungal?

A

Early: PMNs
Late: lymphocytes

PMNs

Early: PMNs
Late: lymphocytes

43
Q

Common bacterial pathogens indicated in the following meningitis age groups:

Neonatal

3 mo. - 2 y/o (not vaccinated)

Adolescent and young adult

Elderly

A

Neonatal - E.coil, Grp. B strep.

3 mo. - 2 y/o (not vaccinated) - H. influenza type B

Adolescent and young adult - N. meningitidis

Elderly - S. pneumoniae, Listeria monocytogenes

44
Q

What are 4 predisposing factors/conditions for development of a brain abscess?

A

Acute bacterial endocarditis -> multiple abscesses.

Congenital heart disease: right to left shunt removes pulmonary filtration of organisms.

Chronic pulmonary sepsis (bronchiectasis)

Systemic disease w/ immunosuppression

45
Q

What is the presentation of a patient with a brain abscess?

What changes are seen on evaluation of the CSF?

What complications can ensue?

What is the treatment?

A

Progressive focal neurological deficits, signs of increased ICP may also develop.

High WBC ct., high protein, normal glucose.

Abscess rupture with ventriculitis or meningitis
Venous sinus thrombosis

Surgical drainage and Abx (< 10% mortality w/ treatment).

46
Q

What is the cause of a subdural empyema?

What is a classic association?

What are the symptoms and CSF findings?

A

Bacterial or fungal infection of skull bones/sinuses spread to the subdural space (usually no involvement of arachnoid or subarachnoid spaces).

Thrombophlebitis of bridging vessels leading to infarct.

Similar to abscess: high WBC ct., high protein, normal glucose.

47
Q

What is associated with an extradural abscess?

Extradural abscesses of the spine can lead to…

A

Osteomyelitis

Cord compression and prompt a neurosurgical emergency.

48
Q

Which populations are at an elevated risk for N. meningitidis infection?

What is the presentation?

What is the major complication?

A

Crowded populations - prisons, colleges, military, etc.

Rapidly progressive sepsis with fever, hypotension, DIC and petechial/purpuric lesions.

Hemorrhagic infarction of adrenals: W-F syndrome

49
Q

What is purpura fulminans?

A

Hemorrhagic skin lesions which progress to gangrene that occur in the distal portion of the limbs.

50
Q

What are symptoms of chronic meningitis?

What changes are seen in the CSF?

At what point is the diagnosis made?

What 3 bugs can cause this?

A

Fever, HA, lethargy, confusion, N/V and neck stiffness.

Elevated protein, lymphocytic pleocytosis, and sometimes a reduced glucose level.

If symptoms and CSF changes are persistant or progress for > 4 wks.

Tb, Neuroborreliosis, Neurosyphilis.

51
Q

Where does chronic meningitis due to Tb infect?

What kind of exudate does it produce?

What vascular change may occur?

Which symptoms are pronounced?

What is a tuberculoma?

A

Subarachnoid space, base of brain (arachnoiditis) and obliterates cisterns and encases CNs.

Gelatinous or fibrous exudate.

Obliterative endarteritis: inflammation infiltrates vessel walls; intimal thickening; arterial occlusion and infarction.

CN symptoms are pronounced; hydrocephalus.

Well-circumscribed intraparenchymal mass with central caseous necrosis. Inactive lesions may calcify.

52
Q

What is the presentation of chronic meningitis due to Borrelia Burgdorferi (Lyma Dz)?

What is found within the CSF? How is it tested for?

What complication can ensue?

A

Neurological symptoms follow the rash by about 4 wks.
CN palsies and peripheral neuropathies can be characteristic.

Antibodies - tested w/ PCR.

Antibodies may cross-react with other diseases/infections: Mono, RA, SLE, syphilis, etc.

53
Q

Neurosyphilis is a complication of what infection?

What is meningovascular neurosyphilis?

What is paretic neurosyphilis? What is seen on histology?

What is granular ependymitis?

A

Tertiary stage of untreated syphilis (Treponema pallidum).

MN: chronic meningitis involving the base of the brain leading to communicating hydrocephalus.

PN: insidious, but progressive menatl deficits associated with delusions of grandeur that terminate in severe dementia (general paresis of the insane).
Perivascular iron deposits.

GE: proliferation of subependymal glia under damaged ependymal lining with associated hydrocephalus.

54
Q

What is tabes dorsalis?

What symptoms exist?

What parts of the spinal cord are affected?

A

Damage to sensory nerves (loss of myelin/axons) in the dorsal roots.

Impaired joint position sense and ataxia. There is also loss of pain sensation, joint damage (Charcot lesions) and “lightening pains” (absense of DTRs).

Gracile fasciculus and cuneate fasciculus.

55
Q

How is aseptic (viral) meningitis diagnosed?

Most cases are caused by what?

What changes are seen in the CSF?

What is the course of treatment?

A

Absence of a recognizable organism with meningeal irritation, fever and alternations of consciousness with a relatively acute onset.

80% are due to enteroviruses.

Lymphocytic pleocytosis, moderately elevated protein; glucose near normal.

Treated symptomatically - course is usually self-limited.

56
Q

How does viral meningitis spread to the CNS (encephalitis)?

What does the brain due in response?

A

Hematogenous dissemination of viruses or through nerves (CN 1 and CN 5).

Brain mounts an inflammatory response with a population of lmyphocytes sensitized by the virus. May remain latent!

57
Q

What is the cause of arthropod-borne viral encephalitis?

What changes are seen to the CSF?

What morphological changes are seen?

A

West Nile involving the spinal cord and causes a polio-like syndrome with paralysis.

Slight increase in pressure, increased protein; normal glucose.

Multiple foci of necrosis in both white and gray matter.
Neuronophagia: single-cell neuronal necrosis with phagocytosis (by Mo) of debris.
Microglial nodules: small aggregates around foci of necrosis.

58
Q

HSV-1 has a predilection for which populations?

What kind of infection does it cause?

Where does it predominantly infect?

A

Children and young adults.

Necrotizing and hemorrhagic.

Inferior and medial temporal lobes.

59
Q

What is the outcome of half of neonates born via vaginal delivery to women with an active HSV-2 infection?

A

They develop severe encephalitis

60
Q

Where does the latent phase of Herpes Zoster infect?

What is the reactivation called?

What is persistent post-herpetic neuralgia syndrome?

A

Sensory neurons of dorsal root or trigeminal ganglia.

Shingles - painful vesicular skin eruption limited to a single or limited dermatome.

Persistent pain as well as painful sensation following a non-painful stimulus.

61
Q

Who is at risk for CMV infection?

What is the progression of infection?

Where does radiculoneuritis occur in these patients?

What cellular changes are seen on histology?

A

Fetuses and immunosuppressed (AIDS).

In utero: periventricular necrosis -> severe brain destruction -> microcephaly and periventricular calcification.
Localizes in paraventricular subependymal regions.

Inflammation of lower spinal cord and roots.

Prominent enlarged cells with intranuclear and intracytoplasmic inclusions.

62
Q

What symptoms are seen acutely in poliomyelitis?
What may it progress to?

What is post-polio syndrome?

A

Flaccid paralysis caused by mononuclear cell perivascular cuffs and neuronophagia of the anterior horn motor neurons of the spinal cord.

It is the resolution of the illness that occurs 25-35 yrs. after initial illness. It is characterized by decreased muscle mass and pain.

63
Q

What is the incubation period for Rabies?

What is the clinical diagnostic characteristic?

What are the prominent symptoms? (4)

A

1-3 mo. Depends on distance of wound to brain.

Nonspecific symptoms (malaise, fever, HA*) with local paresthesias around the wound (diagnostic).

Extraordinary CNS excitability
Flaccid paralysis
Respiratory center failure
Hydrophobia due to contracture of pharyngeal muscles that produce aversion to swallowing

64
Q

What kind of meningitis does HIV cause?

What morphological changes are seen acutely vs. chronically?

What changes occur to the white matter?

What changes are seen to the iris?

What 2 diseases can HIV meningitis lead to?

A

Aseptic meningitis within 1-2 wks. of seroconversion.

Acute: perivascular inflammation.
Chronic: microglial nodules with multinucleated giant cells.

Myelin pallor, axonal swelling and gliosis.

Deterioration after starting antiviral therapy which leads to a paradoxical exacerbation of symptoms from opportunistic infections.

HIV-associated dementia
Primary CNS lymphoma

65
Q

What is the major cause of PML?

What does it infect?

It is almost exclusively seen in which patients?

What is seen morphologically?

A

JC polyomavirus - primary infection asymptomatic, reactivation during immunosuppression.

Oligodendrocytes causing demyelination.

Immunosuppressed (HIV+)

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

66
Q

What causes subacute sclerosing panencephalitis (SSPE)?

What symptoms is it characterized by?

Which patients does it infect?

What changes are seen on histology?

A

Paramyxovirus

Cognitive decline, limb spasticity and seizures.

Children (non-immunized) moths or years following infection of measles (rubeola).

Widespread gliosis and myelin degeneration, viral inclusions and neurofibrillary tangles.

67
Q

What are the disease associations for the following:

Mucormycosis

Cryptococcus meningitis

Mucormycosis, Aspergillosis, Candida

How are these infections spread?

A

Mucormycosis: DM

Cryptococcus meningitis: AIDS

Mucormycosis, Aspergillosis, Candida: Vasculitis

Hematogenous dissemination

68
Q

What stain is used to detect Cryptococcus neoformans?

What antigen is seen in the CSF?

A

India ink stain

Cryptococcal polysaccharide antigen

69
Q

What should you associated with a Toxoplasmosis gondii infection?

What does it cause?

How is it detected?

A

HIV and pregnancy.

Brain abscesses.

Free tachyzoites and encysted bradyzoites at periphery of necrotic zones.

70
Q

What are the 2 protozoa than can cause cerebral amebiasis?

A

N. fowleri - “brain-eating ameba”. Infects via contaminated freshwater (lakes, rivers, etc.) and infects through the nose.

Acanthamoeba: chronic granulomatous meningitis.

71
Q

What protozoan can cause cerebral malaria?

A

P. falciparum: results in long-term cognitive defects in survivors.

72
Q

What are the symptoms of prion disease (CJD)?

What protein is seen in serum?

What is spongiform change?

A

Rapidly prgressive neurodegenerative disorders (dementia).

PrP

Intracellular vacuoles in neurons and glia.

73
Q

What exposure is seen in vCJD?

What is seen on histology?

A

Bovine spongiform encephalopathy.

Kuru plaque: + Congo red and + PAS stain.

74
Q

What is fetal familial insomnia?

What genetic change is seen?

What is the outcome?

A

A kind of prion disease.

Asp. substitution at codon 129.

Less than a 3-year survival.

Neuromusculoskeletal & Psychiatry II Exam #2 (15 decks)

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