Exam 1: Chronic Neuro

Question 1

Define seizures:

Answer 1

Transient, superficial neurologic event of sudden/excessive cortical discharges

Question 2

Causes of seizures:

Answer 2

Cerebral injury
Lesions
Metabolic/nutritional disorders
Idiopathic

Question 3

How do antiepileptics work?

Answer 3

Target Na+ or Ca2+ channels or enhance GABA

Question 4

Characteristics of dementia:

Answer 4

Progressive deterioration/decline of memory and cognition

Question 5

Two types of dementia:

Answer 5

Vascular

Alzheimer’s

Question 6

Changes to the brain seen in AD:

Answer 6

Degeneration of frontal/temporal neurons
Brain atrophy
Proteinopathies (amyloid plaques, neurofibrillary tangles)

Question 7

What structure found in AD causes inflammation and neurodegeneration?

Answer 7

Amyloid plaques

Question 8

Protein responsible for AD plaques:

Answer 8

Beta-amyloid (Aβ), specifically Aβ-42

Question 9

Structure of amyloid plaques:

Answer 9

Dense core of Aβ surrounded by inflammatory cells and dystrophic neurites

Question 10

Protein responsible for neurofibrillary tangles:

Answer 10

Tau protein, dissociated and formed into paired helical filaments

Question 11

Testing for Aβ:

Answer 11

CSF (reduced levels)

PET imaging

Question 12

Testing for tau levels:

Answer 12

CSF (increased levels)

Question 13

Biggest risk factor for AD:

Answer 13

ε4 allele of APOE gene

Question 14

Definition of vascular cognitive impairment:

Answer 14

Syndrome with evidence of stroke or subclinical vascular brain injury and cognitive impairment in at least one domain

Question 15

Vascular cognitive injury vs. stroke:

Answer 15

VCI is cumulative tissue damage in the white matter vs. a large focal infarct

Question 16

VCI pathologies:

Answer 16

Amyloid angiopathy
**Microinfarcts** (most common)
Atherosclerosis
Small white matter infarcts
Hyaline substance in vessel walls due to inflammation

Question 17

Manifestations of VCI:

Answer 17

Memory-loss (short-term), cognitive ability, decreased functioning at work/social settings, anxiety, agitation

Question 18

Definition of delirium:

Answer 18

Acute confusional state due to ANS overactivity

Question 19

Two types of delirium:

Answer 19

Excited (SNS) and hypokinetic (PSNS)

Question 20

Pathogenesis of Parkinson’s disease:

Answer 20

Degeneration of dopaminergic neurons in the substantia nigra

Development of Lewy bodies in the residual neurons

Question 21

S/s of Parkinson disease:

Answer 21

Bradykinesia
Tremor
Rigidity
Postural instability
Shuffling gait

Question 22

Types of drugs used in PD:

Answer 22

Dopamine precursors (best results)
Dopamine agonists
MAOIs
Anticholinergics

Question 23

Overview of MS:

Answer 23

Demyelinating autoimmune disease of the CNS affecting young adults

Question 24

Three factors implicated in MS:

Answer 24

Immunologic abnormalities
Genetics
Environmental factors

Question 25

Parts of the CNS preferentially affected by MS:

Answer 25

Optic and oculomotor nerves | Spinal nerve tracts

Question 26

Immune cells involved in MS:

Answer 26

**Macrophages **T lymphocytes **B lymphocytes NK cell Neutrophils

Question 27

CNS cells involved in MS:

Answer 27

Microglia Astrocyte **Oligodendrocyte Neuron

Question 28

Two potential pathogenesis mechanisms for MS:

Answer 28

Myelin sheath damage | Oligodendrocyte damage

Question 29

Two pathways to myelin sheath damage:

Answer 29

Macrophage mediation | Antibody mediation

Question 30

Two pathways to oligodendrocyte damage:

Answer 30

Distal oligodendropathy | Primary oligodendrocyte damage with secondary demyelination

Question 31

Pathogenesis of ALS:

Answer 31

Excitotoxicity (glutamate --> Ca2+ influx) Oxidative stress Mitochondrial dysfunction Neuroinflammation

Question 32

Manifestation highly suggestive of ALS:

Answer 32

Hyperreflexia in weak, atrophied extremities

Question 33

Other manifestations of ALS:

Answer 33

Weakness, atrophy, cramps, stiffness, twitching

Question 34

Diagnosis of ALS:

Answer 34

Clinical s/s EMG MRI Serum labs

Question 35

Only pharmaceutical tx for ALS:

Answer 35

Glutamate inhibitor (riluzole)

Question 36

Spinal shock looks like:

Answer 36

Temporary loss of reflexes (skeletal/ANS) below level of injury Flaccid muscles

Question 37

Neurogenic shock looks like:

Answer 37

Loss of brainstem SNS control Hypotension, bradycardia, circ collapse Respiratory failure

Question 38

Autonomic dysreflexia occurs when injury is located:

Answer 38

T6 or above

Question 39

Triggers for autonomic dysreflexia:

Answer 39

Visceral stimulation (full bladder/bowel) or activation of pain receptors below injury level

Question 40

S/s of autonomic dysreflexia:

Answer 40

Hypertension, headache, bradycardia, flushing *above* level of injury, clammy skin *below* level of injury

Question 41

Treatment of autonomic dysreflexia:

Answer 41

Removal of stimulus | Aggressive BP management

Question 42

Pathogenesis of autonomic dysreflexia:

Answer 42

Stimulus generates sympathetic response/increased BP | Brain activates PSNS to compensate, but without SNS tone below injury, leads to peripheral vasodilation/clamminess

Question 43

Cells that mediate GBS demyelination:

Answer 43

T-cell and B-cell

Question 44

Most common form of GBS in the US:

Answer 44

Acute inflammatory demyelinating polyneuropathy

Question 45

Tx for GBS:

Answer 45

Supportive Plasmapheresis Immunoglobulin to distract the immune system