Neurology Flashcards
Acute disseminated postinfectious encephalomyelitis
multifocal periventricular inflammation and demyelination after infection (VZV and measles common), or certain vaccinations (rabies, smallpox)
Charcot- Marie- TOoth
hereditary motor AND sensory neuropathy (HMS), progressive hereditary nerve disorder due to defective neuronal proteins in volved in structure and function of peripheral nerve and/or myelin sheath. AD inhetirance, scoliosis and foot deformities are common.
Krabbe
galactoverebrosidase deficiency leads to galactocerebroside build up in the myelin sheath.
findings: peripheral neuropathy, developmental delay, optic atrophy, globoid cells
Metachromatic leukodystrophy
AR lysosomal storage disease, commonly due to arylsulfatase A deficiency. Sulfatides build up and impair production. destroy myelin sheath. Central and peripheral demyelination result with ataxia and dementia
Progressive multifocal leukoencephalopathy
Demyelination of CNS due to destruction of oligodendrocytes. Associated with JC virus. Seen in 2-4% of AIDS patients (reactivation of latent viral infection. Rapidly progressive and usually fatal. Increased risk associated with natalizumab, rituximab.
Pricking pain (fast, myelinated)
A-delta fibers
Burning or dull pain and itch (slow, unmyelinated)
C- polymodal fibers
vibration and pressure, rapid adapting
Pacinian corpuscle
dynamic/ changing light, discriminatory touch, superficial
Meissner corpuscle
static/ unchanging light touch, superficial
Merkel receptor
propioception, muscle length monitoring
muscle spindle
propioveption, muscle tension monitoring
Golgi tendon organ
CSF changes in Guillain Barre
normal cell count with increase in protein
Guillain Barre syndrome
symmetric ascending mucle weakness (Schwann cells affected), facial paralysis, preceded by infection (campylobacter usually), sensation intact
Parkinson disease
tremor- resting or pill- rolling tremor rogidity- cogwheel rigidity akinesia or hypokinesia postural instability mask- like facies festinating gait
Neurotransmitters in Huntington
decreased ACh
decreased GABA
increased dopamine
treat glaucoma
prostaglandins, beta blockers, alpha agonists, carbonic anhydrase inhibitors, cholinergic agonists
alternate routes for mediation of voluntary movement
reticulospinal and rubrospinal tracts
pain and temperature sensation
lateral spinothalamic tract
important for postural adjustments and head movements
vestibulospinal tract
propioceptive information to the cerebellum
dorsal and ventral spinocerebellar tracts
BPPV
debris, otoliths in vestibular apparatus. Dx Hallpike, Epley for treatment
Meniere triad
imbalance of fluid and electrolyte composition of endolymph. triad:
vertigo
tinnitus
hearing loss
central vertigo
brainstem and cerebellar lesions damaging the vestibular nuclei. or posterior fossa tumor
How is hair transmitted?
tympanic membrane vibrates with sound waves, and the vibration is transmitted to the cochlea via middle ear ossicles.
cholinergic signals in the olivocochlear bundles stiffen the outer hair cells, thereby sensitizing the inner hair cells to a partiular frequency. Outer hair cells are where aminoglycosides (streptomycin, gentamicin) cause damage.
Hair cells and cochlea turn the sound signal into a nercous impluse, which travels from the cell body to the cochlear gangion,
to cochlear nuclei in brainstem
decussation to contralateral superior olivary nucleus
to lateral lemniscus
to inferior colliculus
to medial geniculate body
to primary auditory cortex in the temporal lobe
pathogens most commonly associated with AOM
strep pneumo
h. influenza
m. catarrhalis
most commonly associated with acute otitis externa
p. aeruginosa
cholesteatoma
noncancer, non- cholesterol overgrowth of desquamated keratin debris within the middle ear space that may eventually erode the ossicular chain and the mastoid air cells.
may be 2/2 neg middle ear pressure (chronic retraction pocket), 2/2 eustachian dysfunction or direct growth of epithelium through a TM perforation
commonly associated with chronic middle ear infection
Tx- surgical removal via tympanomastoidectomy and reconstruction of the ossicular chain.
intranuclear inclusions seen in HSV encephalitis
Cowdry type A
cytoplasmic inclusions pathognomonic of rabies
negri bodies
neuronal inclusions characteristic of Parkinson Disease
Lewy bodies
Cytoplasmic inclusion bodies associated with aging
Lipofuscin granules
Dark cytoplasmic pigment in neurons of the substantia nigra and locus coruleus, not seen in patients with Parkinson
melanin
Eosinophilic, rod- like inclusions in hippocampus of Alzheimer patients
Hirano bodies
Diagnosis of AD
Neurofibrillary plaques and tangles
Filamentous inclusions that stain with silver, do not survive neuronal death
Pick bodies
Filamentous inclusions that stain with PAS and ubiquitin
Lewy bodies
dementia plus visual hallucinations
Lewy Body dementia
dementia plus progressive aphasia
FTD (Pick)
dementia plus ataxia and loss of pupillary light reflex
tertiary syphilis
dementia plus megaloblastic anemia and peripheral neuropathy
B12 deficiency
dementia plus resting tremor and bradykinesia
LBD or Parkinson
dementia plus uninhibited social behavior
frontotemporal lobe dementia
dementia plus urinary incontinence and magnetic gait
NPH
dementia plus syncopal episodes
LBD
dementia plus dysarthria and liver disease
Wilson disease
dementia plys myoclonus
CJD
delirium
visual hallucinations fluctuating level of consciousness acute onset disturbances in sleep-wake cycle decreased attention span decreased level of arousal acute changes in mental status disorganized thinking usually reversible (unlike dementia) abnormal EEG
Causes:
drugs especially with anticholinesterase function, UTI,
dementia workup
RPR HIV TSH Vit B12 deficiency MRI of brain
CBC, etc
Down syndrome and AD
Trisomy 21. APP gene on chromosome 21
Drugs that treat AD mechanisms
Cholinesterase inhibitors (prolong ACh) Memantine is an antagonist at the NMDA glutamate receptor
most common cause of dementia
AD
second most common cause of dementia
Vascular dementia
Extracellular amyloid deposits in the grey matter
AD
Intracellular deposits of hyperphosphorylated tau protein
AD
Intracellular spherical aggregates of tau protein seen on silver stain
These are PICK bodies, and this is FTD
multiple sclerosis presenting symptoms
scanning speech intention tremor nystagmus bowel and bladder incontinence internuclear opthalmoplegia optic neuritis
diseases that affect the anterior motor horn
polio, WNV, ALS, Werdnif- Hoffman disease (spinal muscle dystrophy)
