1
Q
Meningitis
- define
A
- infection of connective tissue covering brain
- includes CSF
2
Q
Meningitis - extent of infection
A
- usually include entire subarachnoid space around brain and spinal cord (dt CSF circulation)
- brain itself (encephalitis)
- blood vessels (vasculitis)
- ventricular system (ventriculitis)
3
Q
Etiology of meningitis
A
- bacterial
- viral
- fungal
- protozoa
4
Q
How treat bacterial meningitis
A
- hospital admission with strong IV abx
5
Q
How treat viral meningitis
A
- Usually self limiting, no real treatment
- aseptic meningitis
6
Q
True or false - the different types of meningitis present differently
A
FALSE
- all types are similar in presentation, only way to really differentiate is via lumbar puncture
7
Q
When considering meningitis, what should the presence of focal neurological signs make you think?
A
- NOT infectious etiology
- more likely a stroke
8
Q
Delirium
- describe
A
- temporary condition of confusion usually associated with reversible cause
- Tx by treating underlying issue
9
Q
causes of delirium
A
- hypoglycemia
- hypoxia
- thiamine deficiency
- hypovolemia
- hyponatremia
- chem/drug toxicty
10
Q
How to treat delirium other than tx underlying issue
A
- Rally pack or banana bag and O2
- except for hyponatremia and chem/drug tox
11
Q
Rally pack contents
A
1 L over 4-8 hrs:
- thiamine
- folic acid
- Multivitamin
- magnesium sulfate
12
Q
Dementia
A
- progressive, irreversible process with periods of lucidity
- may be indolent
- interspersed with loss of cognitive ability
13
Q
Two types of Dementia
A
- Alzheimers (most common type)
- Multi-infarct
14
Q
Alzheimers
- onset
- sx
A
- slow onset (but can be fast and early onset too)
- behavior changes
- anxiety, depression, visual hallucinations, paranoia
- don’t sleep at night, nap during the day
15
Q
what is an early sx of Alzheimers
A
Discalculia: lose concept of money
16
Q
Two histologic characteristics found on pathologic exam of brain
A
- plaques
- tangles
Also
- shrunken gyre and exaggerated sulci
- What looks like enlarged ventricles but is actually just loss of cortical mass called hydrocephalus ex-vacuo
17
Q
Multi-infarct dementia
A
- recurrent minor strokes
- seen in pts with cerebral vascular disease
- many small hemorrhages that accumulate and result in reduced function
18
Q
Huntington’s Chorea
- etiology
- main sx
A
- autosomal dominant
- involuntary muscle movements
- facial grimaces
- personality changes
- emotional disturbances
- dementia
- occurs mid-life
19
Q
Huntington’s Chorea
- genetic problem
A
- increased triplet nucleotide repeats in DNA
- causes protein to misfold = loss of gaba neurons
- caudate nucleus degenerates
- more and more repeats in subsequent generations so disease is expressed earlier
20
Q
What is the main neurotransmitter to be lost in:
- Huntingtons
- Parkinsons
A
- Huntingtons: gaba
- Parkinsons: dopamine
21
Q
Parkinsons
- cause
A
- degenerative destruction of substantia nigra = loss of dopaminergic neurons going to forebrain structures (like caudate)
22
Q
Parkinsons sx
A
- pill rolling
- postural changes
- poor balance
- shuffling gate
- flat affect
- 20-50% develop dementia
- bradykinesia which progresses to rigidity
23
Q
Cause of Parkinson’s
A
- elusive
- neurotoxins (MPTP) can cause immediate onset bc they selectively target the substantia nigra
24
Q
What are the two demyleninating disease
A
- ALS
- MS (more common)
25
what are the two diseases that cause loss of neuron cell bodies
- Huntingon's
| - Parkinson's
26
Amyotrophic lateral sclerosis (ALS)
- aka
- describe
- Lou Gehrig's
- degenerative disease with gradual progressive motor weakness leading to respiratory failure in 3-5 years
- maintain complete awareness/consciousness but lose motor function
27
What degenerate in ALS
- upper motoneurons (cerebral cortical cells)
| - lower motor neurons in SC and brain stem
28
ALS etiology
- familial
| - sporadic
29
Multiple Sclerosis
- etiology
- when does it usually occur
- autoimmune reaction against oligodendrocytes, triggered by viral infection
- around age 30 (females more often_
30
Common first presenting complaint of MS
optic neuritis
31
What is diagnoses of MS on a CT?
plaques involving white matter (where myelin is!)
32
How to diagnose MS
Diagnosis of exclusion unless plaques on the CT
33
MS
| - progression
- subtle sx like urinary incontinence
- sx progress to blindness, incontinence, ataxia, paraplegia
- episodic exacerbations and remissions
34
Acute idiopathic polyneuritis
- aka
- describe
- Guillain-Barre Syndrome
- ascending motor paralysis affecting both spinal and cranial nerves (get to C4 affects diaphragm = ventilator)
- post-infectious autoimmune disorder
35
Two common triggers for Acute idiopathic polyneuritis
- campylobacter jejuni
| - vaccinations
36
Acute idiopathic polyneuritis
| - recovery
- gradual
- w/o residual defect
- recover from top down
37
Acute idiopathic polyneuritis tx
- admit to hospital
| - often tx with steroids to reduce inflammation
38
Inborn errors of metabolism
- gene prevents normal enzymatic pathway
- often related to low IQ, developmental issues
- usually die young
39
Two metabolic diseases
- Tay-Sachs
| - Riemann-Pick disease
40
Tay-Sachs
- describe
- inheritance pattern
- common in what population
- deficit of ganglioside lipids important in cellular membranes, esp. in nervous tissue in brain
- autosomal recessive
- Ashkenazi jews
41
neoplastic disease of the CNS
| - clinical manifestations
Depend on both
- local effects: irritative, compressive, destructive
- generalized effects: increased pressure, edema, hemorrhage, etc.
42
neoplastic disease of the CNS
| - metastasis
- all are potentially malignant but extra neural metastasis is rare (usually don't live long enough for mets to occur)
43
neoplastic disease of the CNS
| - how does age affect risk?
- risk increases with age
BUT also
- second most common group of childhood tumors
44
Astrocytoma
- where in brain
- when in life
- sx
- prognosis
- white matter
- 3rd and 4th decades peak risk
- seizures, ICP, motor deficits, mental changes
- slow growing, lots of time to get it out
45
Glioblastoma
- where in brain
- when in life
- how common
- sx
- usually frontal or temporal lobes
- 5th or 6th decade
- most common type of brain tumor in adults
- same sx as other astrocytomas but more rapid progression/deterioration
46
Glioblastoma
| - life expectancy
- untreated 14 weeks
| - treated 10-11 months
47
Metastatic tumors of the brain
- how common
- sx
- where in brain
- 15-30% intracranial tumors
- HA, seizure, motor deficits, mental change - all due to local expansion/edema
- usually in cortex at gray-white junction
48
5 most common primary sites that cause brain mets in order of most frequent
```
Lung
Breast
Melanoma
Kidney
GI
```
49
Muscle diseases
| - how related to neuro
- caused by lesions of anterior horn, peripheral axons, neuromuscular junction
50
Most common type of muscle disease related to neuro
- muscular dystrophies
| - Duchenne is most common
51
Muscular dystrophy
| - describe
- genetic
| - regressive alterations in muscle fibers = weakness
52
Duchenne type muscular dystrophy
- degeneration of muscles, have extreme weakness
- usually of trunk/pelvis
- classic description of kid who gets off teh floor with arms, not "normal" way
53
Duchenne type muscular dystrophy
| life expectancy
- not great
- usually die in 20-30s
- commonly dt pulmonary complications
54
Duchenne type muscular dystrophy
| - gastrocnemius
- may appear enlarged dt pseudohypertorphy (fatty infiltrate between muscle fibers)
55
Myasthenia gravis
- etiology
- when does it show up
- presentation
- autoimmune, antibody to Ach receptor on muscles that impairs the neuromuscular junction
- early adulthood
- abnormal muscular fatigue and weakness
56
Myasthenia gravis tx
- Cholinergic meds or meds that block Ach-esterase
| - if don't treat diaphragm won't work - die
57
How to test for myasthenia gravis
- blink a bunch of times, lids will tire
- give tensilon, Ach burst will let them blink again
- test for antibodies
58
Prion
| - define
- proteinaceous and infectious
- "ion" ending as analogy to virion
- small proteinaceous infectious particles that resist inactivation by procedures that modify nucleic acids
- everyone has prion proteins, they are not dangerous until they misfold
59
What is crazy about prions
- defy convention
- "replicate" without DNA
- not a true replication, induces a conformational change in other prions
60
Common way to transfer prions
eat misfolded prion from someone/something else
61
Name for prion diseases, why?
- spongiform encephalopathy
| - prions kill neurons, produces vacuoles/holes in cortex
62
Prion diseases
- how dangerous
- cure
- cause
- what is protein resistant to?
- all are fatal
- no cure for any
- misfolded prion proteins accumulate in cytosol
- resistant to heat, proteases, anti-invectives, UV irradiation, etc.
63
Prion disease MC 3 sx
- dementia
- ataxia
- myoclonus
64
Prion disease other sx other than three MC
- progressive loss of motor function
- loss of speech
- hallucinations
- seizures
- visual agnosia
65
List 6 common prion diseases
1. Scrapie in sheep
2. Bovine spongiform encephalopathy (aka BSE or mad cow disease)
3. Chronic wasting syndrome (white tailed deer, elk, moose)
4. Feline spongiform encephalopathy
5. Kuru - New Guinea women
6. Creutzfeldt-Jakob disease
66
Iatrogenic transmission of prion disease
- human growth hormone injections in France 2009
- dura grafts
- corneal transplants
- neurosurgical instruments up to 2 years after autoclaved (now all disposable)
67
Creutzfeldt-Jakob disease
| - etiology
- mostly sporadic, can be iatrogenic, variant, familial
68
Familial defect in prion gene
Fatal familial insomnia
- 35 families
- symptomatic in 40s, can't sleep
- die from insomnia
Neurology
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