objectives 2 Flashcards
teratogenic epileptic drugs
i. Valproate=neural tube defects
ii. Lamotrigdine & carbamazepine=oral/facial clefts
iii. Phenytoin=Fetal hydantoin syndrome
drugs for absence seizures
ethosuximide
lamotrigdine
valproate
drugs for partial seizures
carbamazepine, oxcarb, phenytoin
protocol for status epileptics
- lorazepam 0.1 mg/kg (4-8 mg) IV repeatable in 5-10 minutes if needed,
2, loading with either:
- fosphenytoin 20 phenytoin equivalents (PE)/kg IV, no faster than 150 mg/min,
- phenytoin 20 mg/kg IV, given in saline no faster than 50 mg/min.
LP indications
i. Suspected CNS infection
ii. Suspected demyelinating/inflammatory dz
iii. Suspected SAH
iv. Diagnosing Normal Pressure hydrocephalus and pseudotumor cerebri
v. CSF cytological analysis
contraindications to emergent LP
i. ICP!!! b/c of risk of brain herniation
ii. Coagulopathy (INR>1.5 or platelets <50,000, 6hrs from last Heparin, 5 days from last Clopidogrel).
iii. Spinal cord trauma
iv. Cardiorespiratory compromise
v. Overlying skin lesion/infx
CSF findings in bacterial meningitis
WBC>500-1000 (PMN’s),
Protein ↑
Glucose ↓
CSF findings in viral meningitis
WBC <500 (lympho’s),
Protein ↡/nl,
Glucose nl
CSF findings in TB meningitis
WBC <500 (lympho’s),
Protein ↡,
Glucose ↟
CSF findings in fungal meningitis
Fungus: WBC <500 (lympho’s),
Protein ↡
Glucose ↟
what to for suspected SAH with negative CT?
do tap to r/o low-volume SAH
SAH tap CSF vs traumatic tap
SAH: xanthrochromic and same # of RBC’s in tube 1 and 4
traumatic tap: NOT be xanthochromic, and # of RBC’s will drop from tube 1 to 4
What can reduce edema or herniation from certain cerebral lesions
(tumor, abscess or encephalitis) or spinal cord lesions (metastatic cord compression, myelitis),
IV dex (antinflammatory)
symptoms of herpes simplex encephalitis
aphasia, behavior change, memory deficits
MRI of herpes simplex encephalitis
bilateral/asymmetric involvement of inferior frontal and medial temporal lobes
treatment of herpes simplex encephalitis
IV acyclovir
MS presentation
Most common initial sx involve optic nerves (optic neuritis, INO) or LE motor deficits
Trigeminal neuralgia, (+) Lhermitte’s sign also common
MS timing
starts relapsing/remitting,
later secondary progressive phase w/o full recovery between episodes
MS dx
Multiple signs/sx separated by space and time
i. brain/spinal cord MRI, new/active lesions enhance w/contrast
ii. Oligoclonal bands in CSF (clones of Ab’s), increased Ig synthesis in CSF
MS treatments
i. High dose IV steroids for acute MS attacks
ii. Beta-interferon or Glatiramer acetate reduces severity/frequency of attacks, lessens future
cumulative neuro-disability in some
iii. Calfampridine (K-channel blocker) increases conduction speed, improves sx
iv. Natalizumab: Ab that blocks T-cell adhesion molecules to prevent BBB penetration
Abortive Migraine tx - if migraines are <1-2/month
i. NSAIDs, Analgesics (Tylenol, ASA) for mild migraine
ii. Triptans (can be IM, helpful if pt also has N/V)
iii. Dihydroergotamine (injection, nasal spray)
Prophylactic Migraine tx - for more frequent or more severe neurologic effects
i. Beta-blocker (Propanolol), CCB (Verapamil)
ii. TCA (amytriptyline)
iii. Anticonvulsants (Valproate, Gabapentin, Topiramate)
Tension HA tx:
NSAIDS, analgesics, TCA’s
Eval of HA d/t increased ICP
LP urgently to exclude meningitis, SAH
Get CT first in setting of papilledema to r/o mass lesions (brain tumor, abscess, intraparenchymal hemorrhage) that could cause brainstem herniation
tx for HA due to increased ICP
Mannitol, hypertonic saline to reduce edema,
if there’s an aneurysm, clip or coil it.
Craniotomy to relieve pressure
work up for altered mental status
MMSE
labs: CBC, CMP, TSH, B12
MRI: tumor, infarct, NPH, abscess, etc.
LP if HA/fever
if young –> HIV test
Dx Alzhemeirs
diagnosis of exclusion-
observations from family/friends
Wallerian degeneration:
axons/myelin degenerate distal to crushing/penetrating focal nerve injury
Demyelination caused by
focal compression (carpal tunnel)
GBS, etc.
Toximetabolic causes of polyneuropathies almost always cause
axonal degeneration, with secondary demyelination
Multiple mononeuropathies can be d/t
systemic illness like SLE, Sarcoid, or
Leprosy
Non-acute Polyneuropathy causes
**DM
but can be metabolic, autoimmune,cancerous, infectious
what testing can elucidate which type of neuropathy?
EMG
If EMG + clinical picture suggests inflammatory, immune-mediated, or vasculitic cause, get ____ biopsy to confirm dx
sural nerve
neuropathy treatments
i. Chronic weakness: Braces/splints/cane/walker
ii. Chronic pain: Topical capsaicin or lidocaine patches
iii. Pain:
- Anticonvulsants (Gabapentin, Pregabalin, Carb),
- Antidepressants (Duloxetine, Amitriptyline)
trigeminal neuralgia tx
Anticonvulsants like gabapentin and carbamazepine prevent the nerve from misfiring and producing the shock-like pain.
postherpatic neuralgia tx
acylcovir asap!
for pain sxs: Topical capsaicin or lidocaine
Topical capsaicin MOA
depletes substance P, a pain mediator
radiculopathy (dorsal root inflamm) tx
Surgical removal of the inflammatory insult (if possible) is obviously the best way
Otherwise, analgesics, anti-inflammatory meds (steroids), and nerve block procedures help
Polymyositis diagnosis
clinical: (“I am having difficulties climbing up stairs”, “I have troubles
with reaching to grab something off the top shelf”…aka proximal weakness).
Confirmed with an EMG, muscle biopsy showing inflammatory cells amongst necrotic/regenerating m. fibers.
Polymyositis treatment
corticosteroids
myasthenia gravis dx
clinical: (ptosis, dysarthria, dysphagia, diplopia all extremely common).
Tensilon test (pretty outdated though).
LOOK FOR THE AUTOANTIBODIES (anti-AChR).
MG treatment
immunosuppression (steroids), AChE inhibitors (pyridostigmine), thymectomy
ALS dx
clinical diagnosis (combined UMN+LMN, often unilateral to start off, purely motor deficits, fasciculations).
ALS treatment
not much except RILUZOLE (NMDA-R antag.)
myasthenia graves crisis presentation
profound weakness/quadriplegia and inability to speak, swallow or breathe
triggers: acute stressors like severe infection.
myasthenia crisis management
Neuro emergency, admit to ICU, maintain on ventilator.
Treat current infection, immunosuppress if indicated.
GBS (guillan barre syndrom) emergency presentation
Ascending paralysis that can often involve diaphragm.
GBS management
Neuro emergency, admit to ICU, ventilator.
immunosuppression
spinal cord syndrome management
Evaluate UMN, LMN signs to localize.
Evaluate dermatomal sparing to
determine intramedullary (suspended sensory level, sacral sparing, etc) or extramedullary (sacral
involvement) etiology.
Remove cause of compression if possible.
Parkinsons pathophys
Progressive loss of dopaminergic neurons from SNc.
This means loss of direct pathway “stimulation” of the VL thalamus and increase in indirect pathway
“inhibition” of the VL thalamus.
Parkinson best treatment and MOA
Levodopa + Carbidopa
(prevent peripheral DOPA decarboxylase
conversion)
treatment of essential tremor
beta blockers (also barbs and booze, but don't do it)
CJD on EEG
periodic sharp wave discharge
neurological criteria for brain death
a. Known severe cause
b. No improvement despite treatment for over ~6 hours (extended for younger folk)
c. unresponsive to painful stimuli
d. All CNs/brainstem reflexes must be absent
e. No spontaneous respirations
what test can confirm brain death?
RADIOISOTOPE BRAIN SCAN:
the absence of cerebral blood flow over a 10 min period.
supportive care for ALS
oxygen, CPAP, BiPAP mask.
Aggressive = mechanical ventilation via trach
tube.
Many patients opt for death by respiratory failure or pneumonia at home…relief of anxiety of dyspnea = BENZOS.
managing end-stage dementia
Constantly monitor behavioral changes. Constantly address nutrition, dressing, hygiene
acute hemorrhage on T2 MRI
center of an acute hemorrhage is brighter,
with a darker periphery, which changes as the hematoma ages.
acute infarction seen faster on which imaging?
MRI
is acute infarction bright or dark on MRI and CT?`
MRI: bright
CT: dark
edema is dark or bright on MRI and CT?
MRI: bright
CT: dark
do abscesses, encephalitis, and myelitis dark or bright on T2 MRI?
bright
MRI of meningitis description
contrast enhancement of leptomeninges
metastatic brain tumors presentation
often multiple,
with surrounding edema,
usually found at the gray-white junction
Epidural spinal cord metastases often arise from ______ and expand toward ____
vertebral bone
spinal cord
MS plaques appear bright or dark in T2 MRI?
bright
Degenerative spine disease (spondylosis, disc herniations, and central canal stenosis) and its relation to the spinal cord and nerve roots are best seen with…
MRI
second place: CT with intrathecal contrast
