Exam 1: Chronic Neuro Flashcards
Define seizures:
Transient, superficial neurologic event of sudden/excessive cortical discharges
Causes of seizures:
Cerebral injury
Lesions
Metabolic/nutritional disorders
Idiopathic
How do antiepileptics work?
Target Na+ or Ca2+ channels or enhance GABA
Characteristics of dementia:
Progressive deterioration/decline of memory and cognition
Two types of dementia:
Vascular
Alzheimer’s
Changes to the brain seen in AD:
Degeneration of frontal/temporal neurons
Brain atrophy
Proteinopathies (amyloid plaques, neurofibrillary tangles)
What structure found in AD causes inflammation and neurodegeneration?
Amyloid plaques
Protein responsible for AD plaques:
Beta-amyloid (Aβ), specifically Aβ-42
Structure of amyloid plaques:
Dense core of Aβ surrounded by inflammatory cells and dystrophic neurites
Protein responsible for neurofibrillary tangles:
Tau protein, dissociated and formed into paired helical filaments
Testing for Aβ:
CSF (reduced levels)
PET imaging
Testing for tau levels:
CSF (increased levels)
Biggest risk factor for AD:
ε4 allele of APOE gene
Definition of vascular cognitive impairment:
Syndrome with evidence of stroke or subclinical vascular brain injury and cognitive impairment in at least one domain
Vascular cognitive injury vs. stroke:
VCI is cumulative tissue damage in the white matter vs. a large focal infarct
VCI pathologies:
Amyloid angiopathy **Microinfarcts** (most common) Atherosclerosis Small white matter infarcts Hyaline substance in vessel walls due to inflammation
Manifestations of VCI:
Memory-loss (short-term), cognitive ability, decreased functioning at work/social settings, anxiety, agitation
Definition of delirium:
Acute confusional state due to ANS overactivity
Two types of delirium:
Excited (SNS) and hypokinetic (PSNS)
Pathogenesis of Parkinson’s disease:
Degeneration of dopaminergic neurons in the substantia nigra
Development of Lewy bodies in the residual neurons
S/s of Parkinson disease:
Bradykinesia Tremor Rigidity Postural instability Shuffling gait
Types of drugs used in PD:
Dopamine precursors (best results)
Dopamine agonists
MAOIs
Anticholinergics
Overview of MS:
Demyelinating autoimmune disease of the CNS affecting young adults
Three factors implicated in MS:
Immunologic abnormalities
Genetics
Environmental factors
Parts of the CNS preferentially affected by MS:
Optic and oculomotor nerves
Spinal nerve tracts
Immune cells involved in MS:
**Macrophages
**T lymphocytes
**B lymphocytes
NK cell
Neutrophils
CNS cells involved in MS:
Microglia
Astrocyte
**Oligodendrocyte
Neuron
Two potential pathogenesis mechanisms for MS:
Myelin sheath damage
Oligodendrocyte damage
Two pathways to myelin sheath damage:
Macrophage mediation
Antibody mediation
Two pathways to oligodendrocyte damage:
Distal oligodendropathy
Primary oligodendrocyte damage with secondary demyelination
Pathogenesis of ALS:
Excitotoxicity (glutamate –> Ca2+ influx)
Oxidative stress
Mitochondrial dysfunction
Neuroinflammation
Manifestation highly suggestive of ALS:
Hyperreflexia in weak, atrophied extremities
Other manifestations of ALS:
Weakness, atrophy, cramps, stiffness, twitching
Diagnosis of ALS:
Clinical s/s
EMG
MRI
Serum labs
Only pharmaceutical tx for ALS:
Glutamate inhibitor (riluzole)
Spinal shock looks like:
Temporary loss of reflexes (skeletal/ANS) below level of injury
Flaccid muscles
Neurogenic shock looks like:
Loss of brainstem SNS control
Hypotension, bradycardia, circ collapse
Respiratory failure
Autonomic dysreflexia occurs when injury is located:
T6 or above
Triggers for autonomic dysreflexia:
Visceral stimulation (full bladder/bowel) or activation of pain receptors below injury level
S/s of autonomic dysreflexia:
Hypertension, headache, bradycardia, flushing above level of injury, clammy skin below level of injury
Treatment of autonomic dysreflexia:
Removal of stimulus
Aggressive BP management
Pathogenesis of autonomic dysreflexia:
Stimulus generates sympathetic response/increased BP
Brain activates PSNS to compensate, but without SNS tone below injury, leads to peripheral vasodilation/clamminess
Cells that mediate GBS demyelination:
T-cell and B-cell
Most common form of GBS in the US:
Acute inflammatory demyelinating polyneuropathy
Tx for GBS:
Supportive
Plasmapheresis
Immunoglobulin to distract the immune system
