Neuro Five Flashcards

1
Q

MS signs

A

Motor and sensory from spinal cord
Ataxia and nystagmus
Frequency of relapses decrease during course but steady neurologic deterioration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Central pontine myeloysis

A

Symmetric demyelination

Myelin loss no inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Parkinson histo

A

Loss of pigmentation substantia nigra

Lewy body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

ALS time

A

Fifty or older

SODone is on chromosome twenty one get gain of function alanine to valine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Btwelve defiency

A

Anemia
Or neurologic which presents a few weeks as numbness, tingling, slight ataxia in LE
Rapid progression:spastic weakness of LE
Complete paraplegia

Replacement can improve unless complete paraplegia has developed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Histo Btwelve defiency

A

Swelling of myelin layers make vacuoles
Axons of ascending and descending tracts degenerate

SuBACute combined degeneration of SPC spinal cord

Axons of both are degenerated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Corneal stroma

A

No blood vessels or lymphatics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Why get corneal vasculrization

A

Chronic corneal edema

Inflammation scarring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Risk factor glaucoma

A

DM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Cytotoxic edema can lead to

A

Hernation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Vasogenic edema follows what

A

Ischemic injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Thrombosis is mainly due to

A

Atherosclerosis

Rupture , ulceration or erosion of plaque exposes blood to thrombogenic substance get clot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Tia transient ischemic attack

A
One hour smal infarct
One day function lost
Neurologic emergency 
Fifteen perfect have a stroke causes persistent deficits within three months, 
Half within first forty eight hours

MOA embolus temporarily occluded then dissolves , get thrombosis formation or vasoaspasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Hypertension and brain

A

Lacune
Slit hemorrhages

Hypertensive encephalopathy
-deep brain
Vascular multi infarct dementia-dementia gait and pseudobulbar signs
Binswanger disease-large area of subcortical white matter with myelin and axon loss

Charcot Bouchard-microaneurysms associate with chronic HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Bacterial meningitis complication

A

Seizure, encephalitis, hearing loss, blindness, paralysis

Fulminant with meningococcemia, rash
Adrenal hemorrhage->death
Waterhouse friderichsen syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Bacterial meningitis

A
Pressure over 10
Cloudy turbid
Neutrophils over 100
Lymph over 5 ml
Glucose less than 50
Protein 50-1000
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Virus meningitis

A

Clear colorless, no neutrophils, lymph mono 0-5
Glucose 50-80
Protein 15-45

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Neisseria meningitidis

Epidemiology

A

Colonized the oropharynx and rhinopharynx of asymptomatic carriers and spreads by direct contact with respiratoy secretions

Higher in crowded populations like dorms prisons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

N meningitidis clinical manifestations

A

Rapidly progressive septicemia with fever, hypotension DIC, petechial and purpuric lesions
Purpura fulimans:hemorrhagic skin lesions which progress to gangrene;occurs in distal portions of limbs

Hemorrhagic infarction of adrenal glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Chronic meningitis symptoms

A

Fever, headache, lethargy, confusion, nausea, vomiting, stiff neck

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

CSF chronic meningitis

A

Elevated protein concentration, predominantly lymphocytic pleocytosis, sometimes a low glucose level

TB, neuroborreliosis, neurosyphilis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Diagnose chronic meningitis

A

Diagnosis is made if symptoms and CSF persist or progress for a period of at least 4 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Treponema pallidus

A

Neurosyphilis

Meningovascular neurosyphilis

Paretic neurosyphilis

Tabes dorsalis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Neurosyphilis

A

Tertiary stage: only about 10% of untreated PTs develop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Meningovascular neurosyphilis

A

Chronic meningitis involving base of the brain (variable convexities and spinal leptomeninges)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Paretic neurosyphilis

A

Insidious but progressive mental deficits associated with mood alterations (delusions of gradeur0 that terminate in severe dementia (general paresis of the insane ) perivascular iron deposits

Granular ependymomas:proliferation of subependymal glia under damaged ependymal linings associated with hydrocephalus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Tables dorsalis

A

Damage to the sensory nerves (loss of myelin and axons) in the dorsal roots; impaired joint position sense and resultant ataxia (locomotor ataxia);loss of pain sensation (Charcot joints) lightening pains;absence of DTR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Herpes

A

Chickenpox cutaneous

Latent phase:in sensory neurons of dorsal root or trigeminal ganglia

Reactivation(shingles) painful ) vesicular skin eruption limited to a single or limited dermatome

Persistent postherpetic neuralgia syndrome:perstent pain as well as painful sensation following nonpainful stimuli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Rabies

A

Incubation period 1-3 months depends on distance of wound to the brain

Infection ascends along peripheral nerves fromt he wound site

Nonspecific symptoms (malaise HA, fever) with local paresthesia around wound (diagnostic)

Extraordinary CNS excitability;violent motor responses progressing to convulsions

Flaccid paralysis , respiratoy center failure

Hydrophobia dopamine at the mouth due to contracture of pharyngeal muscles that produce an aversion to swallowing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

CJD

A

90% prion seventh decade

Iatrogenic transmission:corneal transplant, brain implant or electrodes and HGH

Rapidly progressice dementia with startle myoclonus 7 months

So rapid , little if any gross evidence of brain atrophy (spongiform changes microscopic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

VCJD

A

UK young adults

Behavioral changes early in DZ
Slower progression
Exposure to bovine spongiform encephalopathy
Kuru plaque : extracellular deposits of aggregated ABN protein +Congo red and +PAS
Cerebellum of VCJD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

FFI fatal familial insomnia

A

Sleep disturbances initially less than three year survival

Aspartate substitution at 129
Ataxia, autonomic disturbances, stupor and coma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Most cases of AD are

A

Sporadic@
5-10% familial

Pathological examination necessary for definitive diagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Treat parkinson

A

L DOPA replaced with Carbidopa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Huntington

A

4p16.3
CAG normal 10-36 get adult onset with 40-50
Juvenile over 60

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

ALS early sign

A

Drop objects muscle strength and bulk dismissed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Fasciculations ALS

A

Involuntary muscle contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Respiratoy infections ALS

A

Respiratoy muscle involved

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Progressive Muscl atrophy

A

LMN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Progressive bulbar palsy

A

Lower brainstem and cranial motor nuclei early and prognosis rapidly
2 year dead

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

ALS

A

2 year dead

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Pilocytic astrocytoma

A

First two decades of life
Cerebral hemispheres or cerebellumNF1 predisposes, espicially optic tumors

Functional loss of neurofibromin in tumor

Well circumscribed often cystic with a ural nodule
Radiology discrete, contrast enhancement, lack or surrounding edema, cyst

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Pilocytic astrocytoma

A

Biphasic pattern:loose glial with cystic changes and dense piloted. Tissue

Hair like cells with long bipolar processes

Rosenthal fibers

Eosinophilia granular bodies (EGBs)

Extension into subarachnoid space is common (not sign of aggressiveness) espicially with optic nerve lesions
GFAP positive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Glioblastoma (IV/IV)

A

Most common primary brain neoplasm

Primary vs secondary neoplasms

Primary-later in like (older patient, no precursor lesion (EGFR and PTEN)

Secondary-preceded by lower grade lesions (TP53), IDH1 (R132 H mutation has better prognosis) and IDH2 typically younger

Throughout brain

Contrast ring enhancing hypodense central necrosisi

Cells follow fiber tracts and extend well beyond imaging

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Glioblastoma histology

A

Necrosis : serpentine pattern of necrosis in hypercellular areas

Pseudo-palisading of cells around necrosis

Vascular/endothelial proliferation

  • VEGF produced by malignant astrocytes in response to hypoxia is responsible
  • tufts of cells pile up and bulge into vascular lumen
  • glomeruloid body: MKD proliferation produces a ball like structure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Oligodendroglioma

A

10-15% of all gliomas, primarily adults

Primary cerebral hemispheres

Calcification usually restricted to the cortex, curving around or gyriform distribution

Histology:perineuronal satellitosis, perivascular aggregation and subpial accumulation of tumor cells
Perinuclear halos fried eggs

Delicate anastomsing capillaries chicken wire

Most are well differentiate grade II, IV

IDH1 and IDH2 isocitrates dehydrogenase genes, most common mutation in oligodendrocytes (90%) favorable prognosis

1p19q loss favorable prognosis

Anaplastic oligo II/Iv-vascular hypertrophy and necrosis, often retains geometric vascularity often retains geometric vascularity

Increased grease with increased N;C, mitosis and cellularity

Often these features found in nodules located within a IIIV tumor

Poor prognosis similar to glioblastoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Four molecular groups

A

Malignant embryonal tumor in children (20% of brain tumors in kids)

  • 4 molecular GRPS
  • WNT: older kids, monosomy CHR 6, B catenin, 5 YR survival 90%
  • SHH: sonic hedgehog, infants-young adults, nodular desmoplastic morph, MYCN AMP, prognosis intermediate between WNT and GRPS 3 and4)

Group 3:MYC AMP 17(i17Q) infants, kids-classic or LG cell, worst prognosis

Group 4 17Q, NO MYC or MYCN, intermediate, 17Q poor prognosis, classic or LG cell morphology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Medulloblastoma

A

Malignant embryonal tumor in kids (20% of brain tumors in kids)0

Cerebellum, midline, occlude CSF flow-sheets of anaplastic cells, abundant mitosis, homer wright rosettes, drop metz:disseminate thru CSF to Cauda equina

  • exquisitely radiosensitive: total excision pls XRT-?75% 5 year survival
  • CNS supratentorial PNET (primitive neuroectodermal tumor)
49
Q

Paraneoplastic syndromes

A

Subacute cerebellar degeneration

Limbic encephalitis

Eye movement DOs

Lambert Eaton myasthenic syndrome

50
Q

Subacute cerebellar degeneration

A

PCA-1 antibody anti yo

Destruction of purkinje cells, gliosis and milked chronic inflammatory infiltrate

Women with ovarian , uterine, or breast carcinoma

51
Q

Limbic encephalitis

A

ANNA-1 antibody:neuronal nuclei (CNS and PNS):small cell carcinoma of lung

NMDA receptor”hippocampal neurons:ovarian teratomas

VGKC-complex antibody:voltage gated K channel, periph neuropathy, SX in Limbic encephalitis often appear before any malignancy is suspected

52
Q

Eye movement DO

A

Opsoclonus, neuroblastoma in kids

53
Q

Lambert Eaton myasthenic syndrome

A

Voltage gated calcium channels

54
Q

Treat paraneoplastic syndromes

A

Immunotherapy to remove circulating ABs remove tumor

55
Q

NF1 associated lesion

A

Pheochromocytoma

56
Q

Features NF2

A

Neurofibromatosis cafe au late optic nerve glioma

57
Q

Von hipped lindau associated lesion

A

Pheochromocytoma , paraganglia

58
Q

Other features of Von hipped lindau

A

Renal cell carcinoma
Hemangioblastomas
Pancreatic endocrine neoplasm

59
Q

Cowden gene

A

PTEN AD 10q23

60
Q

Cowden

A

Lipid phosphatse/benign follicular appendage tumors (trichilemmonas):internal adenocarcinoma (breast or endometrial)

61
Q

Tuberous sclerosis

A

TSC1/hamartin

TSC2/tuberin

62
Q

What do TSC1 and TSC2 do

A

Work together in a complex that negatively regulates mTOR

In absence angiofibromas and mental retardation

63
Q

NF1 gene

A

17q11 neurofibromin

64
Q

NF2 gene

A

Merlin

65
Q

What does Merlin do

A

Integrates cytoskeletal signaling

66
Q

VHL

A

AD 3p25.3 tumor suppressor

Involved in regulating expression of erythropoietin ->polycythemia

Hemangioblastomas of the CNS (cerebellum and retina)

Cysts of pancreas
Renal cell carcinoma

Pheochromocytoma

67
Q

NF1

A
Common AD
Neurofibromas
Optic nerve gliomas
Lisch nodules
Cafe au last 
HYPERPIGMENTED cutaneous nodules
68
Q

NF2

A

Less common
Bilateral schwannomas
Increased meningiomas and ependymomas

69
Q

Rosenthal fibers

A

Pilocytic astrocytoma thick elongated eosinophilia irregular structures that occur with astrocytes processes

Ab crystalin and ubiquitin

70
Q

What is pilocytic astrocytoma

A

Low grade non infiltrating neoplasm in kids

71
Q

Alexander disease

A

Leukodystrophy from GFAP

Abundant rosenthal fibers

72
Q

Corpora amlacea

A

Common in old people from degeneration of astrocytes
CAG polymers with HSP and ubiquitin
Wherever there are atrocities end processes
PAS
Basophils

73
Q

Alford bodies

A

Myoclonic epilepsy

74
Q

Microglia

A

CR3 and 68

Get long nuclei gamma is neurosyphilis granulomas

75
Q

What is global cerebral ischemia

A

Generalized reduction of cerebral perfusion (cardiac arrest, shock, and severe hypotension)

76
Q

Respirator brain

A

Brain dead left on ventilator laminar necrosis and gradual liquefication

77
Q

Linear parasagittal infarction

A

Sickle cerebral convexity a few centimeters lateral to interhemispheric fissure
Between ACA MCA
Hypoxic/hypoglycemic stress
After hypotensive events

78
Q

Bone marrow embolism after trauma

A

Widespread white matter hemorrhages characteristic of embolization of non emarrow after trauma

79
Q

What may cause luminal narrowing

A

Infectious vasculitis

Polyarteritis nodosa

Primary angiitis

80
Q

What is contraindicated in hemorrhagic infarcts

A

Thrombolytic therapy

81
Q

In hemorrhagic and non hemorrhagic infarct, __ and __ mater are unaffected and do not contribute to the healing process

A

Pia arachnoid

82
Q

Where are Charcot Bouchard most common

A

Small vessels within the basal ganglia , saccular berry aneurysms occur in larger intracranial vessels in the subarachnoid space

83
Q

CAA histology

A

No fibrosis

Only the leptomeningeal and cerebral cortical arterioles

84
Q

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy

A

AS NOTCH3 misfolds and in vascular smooth muscle

Recurrent strokes and dementia

35 changes and infarcts 40
Loss of smooth muscle cells

Infarct or hemorrhage
Hematoma

85
Q

Pathogenesis of saccular aneurysm

A

Absence of smooth muscle or intimal elastic lamina at birth

Smooth muscle defects are congenital and aneurysms are subsequently acquired

86
Q

Rupture of berry and chronis adhesice arachnoiditis

A

After rupture a non communicating hydrocephalus results from organization of the subarachnoid hemorrhage occluding foramina of luschka and magendie

87
Q

AVM

A

Cerebral hemispheres young adult
Vessels in subarachnoid or brain
Tangled vessels that shunt-bypass capillary bet
Can be respected

Males
Seizures, intracranial hemorrhage, subarachnoid hemorrhage, MCA common sot
CHF due to shunt effects

88
Q

How do infectious agents spread

A

Hematogenous

89
Q

Adolescent meningitis

A

N meningitidis

90
Q

Old people meningitis

A

Strep p and listeria monocytogenes

91
Q

Immune suppressed meningitis

A

Klebsiella

92
Q

Acute aseptic meningitis

A

Enterovirus no bacteria but have meningitis

Self limited asymptomatic

93
Q

Bacterial meningitis

A

EXUDATE within leptomeninges pia and arachnoid

Neutrophils

94
Q

Bacterial meningitis adhesive arachnoiditis

A

Capsular polysaccharide of the microbe can make gelatinous exudate that promotes arachnoid fibrosis from SCARRING

95
Q

Abscesses

A

Focus necrosis of brain tissue with inflammation that is usually caused by bacteria

96
Q

What do abscess look like

A

Ring enhancement
Bacterial organisms granulation tissue with fibrosis is typical healing inflammatory response reaction to a cerebral abscess LUNG INFECTION

97
Q

Most common bacteria in brain abscesses of non immunosuppressed patients

A

Strep and staph

98
Q

Clinical presentation Brian abscesses

A

Progressive focal neuro deficit

99
Q

Negri bodies

A

Found in pyramidal neurons of the hippocampus and purkinje cells of cerebellum

Rabies

100
Q

PML

A

Demyelination is its principle pathological effect
Immune compromised

JC polymoavirus

Glassy amphophilic viral inclusions

101
Q

Subacute sclerosing panencephalitis

A

Kids or young adults months or years after an initial infection by measles virus

102
Q

Toxoplasmosis

A

AIDS CNS abscesses

Protozoa

103
Q

Prions protective

A

Heterozygosity at 129 protective

104
Q

CJD

A

Rapidly progressive dementia

105
Q

Gerstmann straussler scheinker syndrome

A

Progressive cerebellar ataxia

106
Q

Presentation CJD

A

Subtle changes in memory and behavior followers by rapid dementia and startle myoclonus

107
Q

VCJD

A

129 MET MET

Heterozygous protective

108
Q

CJD morphology

A

Congo red PAS positive

Kuru plaques
Status spongiosus cyst like

109
Q

FFI

A

Sleep disturbances initially
PRNP gene
3 years
Get ataxia, autonomic disturbances, stupor, and coma
NO spongiform pathology
-neuronal loss and reactive gliosis int he nation rventral and dorsomedial nucleus of the thalamus

110
Q

FFI vs CJD

A

Asparagins at 178 and methionine at 129–FFI

Asparagine at 178 and valine at 129 CJD

111
Q

MELAS

A

Lactic acidosis
Stroke like reversible deficits do not correspond with discrete vascular areas

No cytochrome c oxidase

MTTL1

112
Q

MERRF

A

Maternal

Myoclonus myopathy ragged red fibers in muscles and ataxia

113
Q

Hypoglycemia

A

Initially injury to large pyramidal neurons

114
Q

Hyperglycemia

A

Severe dehydration that leads to confusion, stupor and coma

Rehydration must be slow of get edema

115
Q

Methanol

A

Kidd retinal ganglion cells becomes formic acid and formaldehyde

Formate

116
Q

CO

A

CA1 purkinje cells
Inhibits cytochrome C in os phos
Lays II and sommers secto

117
Q

Ethanol

A

Atrophy and loss of granule cells in anterior vermis of the cerebellum loss of purkinje cells and proliferation of adjacent astrocytes

118
Q

Radiation

A

Coagulation necrosis, sclerosis ,