Neuro Flashcards
nervous system is divided into two sections:
central nervous system: brain and spinal cord
peripheral nervous system: cranial/spinal nerves and the autonomic nervous system
two basic types of cells in nervous system
neuron: primary functional unit; doesn’t divide (generally) or replace themselves
neuroglia: more numerous and supportive to neuron; can replicate
when neurons are destroyed, generally replaced by neuroglia cells
types of neuroglia and function
oligodendrocytes: produce the myelin sheath in the CNS and make up white matter of brain
Shwann cells: myelinate the nerve fibers in the periphery
Astrocytes: provide structural support to neurons and form BBB; found in gray matter of brain
migraines
an episodic neurologic disorder that’s characterized by a HA that lasts between 4-72 hrs
diagnosis of migraine
two features must occur:
- unilateral head pain
- throbbing pain
- worsens with activity
- moderate/severe pain
AND one of these:
- N/V
- photophobia
- phonophobia
classification of migraines
aura present - visual, sensory, or motor sxs
aura not present
chronic - 15 days/month for 3 months
risk factors of migraines
family hx
estrogen and progesterone
genetic and env. factors (triggers)
migraine triggers
fatigue oversleeping missed meals overexertion weather change stress hormonal changes bright lights or strong smells
patho of migraines
change in neurotransmitter levels in CNS
blood vessel tone
not completely understood; changes in brain metabolism and blood flow, dilation of blood vessels
clinical phases of migraines
premonitory phase
- 1/3 have fatigue, irritability, loss of concentration, stiff neck, food cravings
Migraine aura
- up to 1/3 have aura sxs lasting up to an hr
Headache phase
- throbbing pain
- fatigue, N/V, dizziness, hypersensitivity to touch on head
- lasts 4-72 hrs
Recovery phase
- irritability, fatigue, or depression
- this phase can linger b/t hrs to days
sumatriptan
Imitrex
serotonin 1B/1D receptor agonists
sumatriptan
MOA
constrict intracranial blood vessels
suppress release of inflammatory neuropeptides
block brain pathways for pain
sumatriptan
SE
injection site rx, *chest pressure, *flushing, *weakness, HA, bad taste (nasal)
- more frequent with subcut route
contra: ischemic stroke, heart disease, angina
rimegepant
Nurtec
Calcitonin Gene-related peptide (CGRP)
this class is used when pts can’t take triptan due to contraindications, etc.
rimegepant
CGRP antagonist
used to treat acute migraines
mediates pain transmission
SE: GI upset (dyspepsia, abd. pain, N)
CYP substrate
migraine preventive therapy
beta blockers
tricyclic antidepressants
antiepileptic drugs
estrogens
multiple sclerosis
chronic, inflammatory, autoimmune disorder
potentially disabling; loss of myelin sheath
characteristics:
- inflammation (white matter of brain and spinal cord)
- demyelination
- scar development (gliosis)
MS etiology
unknown
may be triggered by infection
genetic predisposition
MS risk factors
age: 20-40
gender: women
location: moderately cool climate (northern US)
race: caucasian
genetics: family hx
men may have a more, severe progressive form
possible MS risk factors
smoking
vitamin d deficiency
obesity
infection (incl. epstein barr)
MS patho
autoimmune attack against the myelin sheath ending in axon destruction
types of progression of MS
benign: no disability with a return to baseline b/t attacks
relapsing-remitting: 80-90% of cases; always end of up a little weaker after each exacerbation
primary-progressive: steady increase in disability w/o attacks
secondary-progressive: initial RRMS that suddenly begins to decline w/o pds of remission
progressive-relapsing: steady decline; still declining even during remissions
clinical manifestations of MS
dependent on what nerves are impacted
numbness, tingling fatigue walking difficulty (increases risk for falls) pain muscle spasms emotional changes urinary incontinence cog fog sexual issues
interferon beta-1a/b
varying trade names
(Avonex) 1a
used to treat MS
naturally occurring substance
MOA: inhibit pro-inflammatory WBCs from crossing BBB
decrease relapse by up to 30%
AE: flu-like rx, liver toxicity, bone marrow suppression (monitor blood counts), depression, drug interactions
glatiramer acetate
Copaxone
treat MS
MOA: increased production of anti-inflammatory T-cells which cross BBB and suppress inflammation
similar efficacy as interferons
AE:
- injection site rxs
- post-injection rxs: flushing, palpitations, chest pain, rash laryngeal constriction (all are transient and no treatment is necessary unless severe constriction)
fingolimod
Gilenya
oral agent
retain lymphocytes in the lymph nodes, preventing them from crossing BBB therefore decreasing inflammation
RRMS
dimethyl fumarate
Tecfidera
oral agent
developed specifically for MS
thought to inhibit immune cells and may have antioxidant properties
natalizumab
(Tysabri)
infusion
MOA: prevents circulating T cells from leaving the vasculature and crossing BBB
treats MS and Crohn’s
monotherapy only; relapsing form of MS
natalizumab
AEs
HA, fatigue (these most common)
Black Box: progressive multifocal leukoencephalopathy; risk increased when combined with other immunosuppresants
drug only available through the TOUCH program
hepatotoxic (monitor LFTs), hypersensitivity
other infusion meds used to treat MS
alemtuzumab (Lemtrada)
- reserved for pts with poor response to 2 or more MS meds
mitoxantrone (Novantrone)
- secondary progressive
- progressive-relapsing
- worsening RRMS (w/o complete remission)
treating an acute relapse of MS
preferred
- high dose glucocorticoid
IV gamma globulin
- pts intolerant to glucocorticoids
ACTH (H.P. Acthar Gel)
- unable to tolerate steroids or have not been effective
managing MS sxs
urinary frequency - anticholinergics urinary retention - cholinergics constipation - bulk-forming laxative, stay hydrated fatigue - amantadine, need more rest muscle spasms - muscle relaxants cognitive dysfx - donepezil (Aricept)
myasthenia gravis (MG)
autoimmune disease; almost the opposite of parkinson’s except it’s autoimmune mediated by antibodies at the Ach receptors at the neuromuscular junction
characterized by fluctuating weakness of certain muscle groups
course of disease is variable
MG risk factors
age: 10-65
gender: women
MG patho
antibodies attack Ach receptors
this prevents Ach molecules from attaching and stimulating muscle contraction
myasthenia gravis clinical manifestations
often first appear during pregnancy, post-partum or after anesthesia
- insidious onset
- fluctuating weakness of skeletal muscle
- strength comes back after resting
- muscles involved:
eyes/eyelids, facial, speaking, breathing
at risk for impaired nutrition, aspiration and impaired ventilation
myasthenic crisis
can develop as disease progresses
acute exacerbation of muscle weakness
triggered by a stressor:
infection, surgery, emotional distress, pregnancy, menses, inadequate pharmocotherapy (or noncompliant)
major complication:
- breathing muscle weakness leading to possible resp. arrest
MG pharmacotherapy
immunosuppressants (steroids)
cholinesterase inhibitors - prevent inactivation of ACh by cholinesterase; give 30-45 minutes prior to eating to strengthen swallowing muscles
neostigmine
Prostigmin
cholinesterase inhibitor
uses: MG and profound constipation
MOA: enhances cholinergic action by facilitating transmission of impulses across neuromuscular junctions; affects both muscarinic and nicotinic receptors
nicorinic receptors
adrenal
skeletal muscles
muscarinic receptors
glands
sweat
neostigmine
AEs
muscarinic:
- increased secretions, GI motility
- urinary urgency
- bradycardia
- bronchial constriction
- miosis (pupil constriction), near-sightedness
nicotinic (neuromuscular):
- increased muscle contraction
- toxic doses - reduced contraction
toxicity could lead to cholinergic crisis
cholinergic crisis
extreme muscle weakness or paralysis s/s of excessive muscarinic stimulation treatment: mechanical ventilation antidote: atropine pt should wear med alert bracel AAT
MG crisis v. cholinergic crisis
ends are the same
MG - not enough ACh, muscle weakness, resp failure
cholinergic - too much ACh or nystigmine, overstimulation of muscles, wear out, resp failure
differentiating between MG and cholinergic crisis
Give endrophonium which is a short acting cholinesterase inhibitor
will improve if MG crisis
worsen if cholinergic
amyotrophic lateral sclerosis (ALS) aka Lou Gehrig’s disease
rare, progressive neuro disorder characterized by the loss of motor neurons (upper and lower)
death usually occurs around 3 years after diagnosis
unknown etiology
ALS risk factors
age: 40-70
gender: male
genetics: 10%
smoking
ALS patho
motor neurons in the brainstem and spinal cord gradually degenerate
excitotoxicity hypothesis
excessive levels of glutamate intitiate a cascade of events that lead to neuron death
ALS clinical manifestations
weakness of upper extremities (sometimes begins in legs), muscle wasting, spasticity
dysarthria, dysphagia, drooling
cognitive and behavioral changes
constipation
sleep problems
breathing - most common cause of death is resp. failure
riluzole
Rilutek
glutamate inhibitor
only drug approved for ALS
MOA: glutamate antagonist; reduces damage to motor neurons
SE: dizziness, GI upset, hepatotoxic
increases life expectancy 3-6 months
Guillain-Barre Syndrome (GBS)
autoimmune disorder that causes demyelination
myelin sheath is damaged by autoantibodies
onset: days to weeks following a viral infection
GBS clinical manifestations
weakness/tingling in lower extremities that ascends up the body
severity of sxs increases over hrs or weeks
potentially life threatening if resp muscles are involved
recovery: descends down the body
GBS clinical manifestations
uncoordinated movements - loss of strength - difficulty walking - increased risk of falling numbness and decreased sensations - as it ascends loss of bladder/bowel control blurred vision - often presents early, doesn't follow ascending pattern difficulty breathing, swallowing, chewing
GBS pharm
no known cure
some only get once, others have reoccurences
Goal of Rx: reduce severity & accelerate recovery
high dose steroid therapy, then taper
high-dose immunoglobulin therapy
meningitis
acute inflammation of the meningeal tissues of the brain and spinal cord
etiology: infection (lungs or bloodstream) or penetrating wounds
Streptococcus pneumoniae and Neisseria meningitidis
Enteroviruses
fungi, parasites and toxins
meningitis risk factors
older adults > 40
college students, military bases, prisoners
spread through resp. droplet, contaminated saliva
often follows an ear or sinus infection or in the immunocompromised
some people are carriers
occurs in the pia mater and the subarachnoid space with CSF
meningitis classic triad
fever
headache
stiff neck
meningitis other clinical manifestations
N/V photophobia altered mental status (d/t increased ICP) -drowsiness - coma - seizures meningococcus - skin rash - petechiae or purpuric rash
Positive Kernig sign
indicative of meningitis
flex knee and hip and then begin to extend leg toward ceiling, will cause pain in neck
Positive Brudzinski sign
indicative of meningitis
pt lying supine, begin to flex chin towards chest, this will cause pt to flex the knees and hips
bacterial meningitis
more deadly than viral
can cause long term effects such as hearing loss, seizure, brain damage, emboli causing loss of digits and limbs
treatment for bacterial meningitis
start abx immediately aggressive antibiotics IV, often multiple drugs ceftriaxone, vancomycin acyclovir (just in case it's viral) steroid therapy prophylaxis vaccines
encephalitis
acute inflammation of the brain
almost always viral
west nile encephalitis, measles, chicken pox, mumps, HSV
encephalitis clinical manifestations
signs appear on day 2 or 3 of infection range from mild changes in mental status to coma other sxs: - fever - HA - N/V - other CNS changes
encephalitis pharm
acyclovir is used for HSV infection only seizure disorders d/t increase in ICP - antiseizure meds Supportive care - fluids - acetominophen - antiemetics
brain abscess
accumulation of pus within the brain tissue
etiology: local or systemic infection
most common: ear, tooth, mastoid, or sinus infection
strep or staph usually
