chronic neuro problems - study this one Flashcards
Functional headaches:
Migraines, tension and cluster headaches
Organic headaches:
(venus and blood vessels cause organic pain)
Originate from pain sensitive areas in the brain:
Venous sinuses, dura mater
Cranial blood vessels
Trigeminal nerve (CNV): Facial nerve (CN VII), glossopharyngeal nerve (CN IX), Vagus nerve (CN X) and the first 3 cervical nerves
primary HA - same 3
cluster, migraine, tension
secondary HA
Sinus infection
Neck injury
Stroke, head trauma
migraines associated with what disorders?
Associated with seizure disorders, stroke, asthma, depression, MI
migraine - Prodrome - 1st (premonitory) - what 3 symptoms (PIF, it’s prodrome)
Prodrome (premonitory): Impending signs of migraine. Hrs to days before the HA. Premonitory symptoms: photophobia, irritability, food cravings
migraine - 2nd Pain phase
: unilateral/throbbing: moderate to severe
migraine - 3rd phase - post drome
After migraine pain subsides.
Sx: fatigue, nausea, sensitivity to light, dizziness, body aches and difficulty concentrating.
TENSION HEADACHE
Bilateral pain in the frontal-occipital region
Pressing, dull and constant, bandlike, non-pulsatile quality
Includes neck pain d/t increased tone of cervical and neck muscle
Photophobia, phonophobia
No premonitory symptoms or n/v
Episodic for weeks, months, years or chronic
Pain usually mild to moderate
tension HA - treatment
Relaxation, massage and hot packs, and correction of faulty posture
Local anesthetic injection
tension HA - meds
Non-opioid analgesics, analgesic combination, muscle relaxants
CLUSTER HEADACHE - common age
. Affects men 3x more than women usually age 20-45
CLUSTER HEADACHE - description - what about lacrimation?
Onset: abrupt and an aura may is present in 14% of people
Unilateral intense excruciating pain described as, boring and non-pulsatile, sharp and stabbing
Lasts minutes to hours
Pain around eyes, radiating to temple, forehead, cheek, nose, gums
Ipsilateral lacrimation, nasal congestion, eyelid edema, miosis, facial flushing or pallor
Agitation, restlessness, inability to relax
cluster HA - treatment
Serotonin receptor agonists: Triptans 1st line of treatment
Oxygen : 100% via non-rebreather mask or high flow nasal cannula 8-10L for 10 min → vasoconstriction
cluster HA - meds
(V has a cluster HA)
verapamil (calcium channel blocker)
Lithium
Corticosteroids
SEIZURES - causes
Metabolic disturbances (acidosis, electrolyte imbalance, hypoglycemia, barbiturate withdrawals, etc)
Involving the CNS (brain tumors, infections of the CNS, ischemic stroke, etc)
Extracranial disorders (heart, lung, liver disease, SLE, DM, HTN, septicemia)
Epilepsy - causes - what neurotransmitter?
Idiopathic Generalized Epilepsy (IGE) -about 1/3 of seizures are idiopathic, with no identifiable cause (IGE believed to be related to genetics)
Birth and congenital defects involving the CNS, infections and inborn metabolic d/o
Later in life, seizures can be provoked by infection, trauma, brain malignancies, strokes
New research implicates glutamate producing astrocytes acting as an excitotoxin in the recurrence of seizures. Scar tissue (gliosis) also plays a role.
Primary Generalized Seizures
(primarily both sides when you’re unconscious)
Primary Generalized Seizures (non-focal)
Involves both sides of the brain
Most people lose consciousness
Focal Seizures (Partial or Partial focal)
(focal is focused)
Focal Seizures (Partial or Partial focal)
Begins in one hemisphere of the brain in a specific region of the cortex
Produces sensory, motor, cognitive or emotional disturbances based on the area of brain involved
Generalized: Absence Seizure - who is affected?
Typical Absence Seizure (petit mal)
Usually occurs in children and rarely extend beyond adolescence
Generalized: Tonic-Clonic Seizure “Grand mal” - how long is loss of consciousness? and jerking?
Most common of the generalized seizures
Loss of consciousness followed by stiffening of the body (tonic phase lasting 10-20 sec)
Then jerking of extremities (clonic phase for 30-40 secs)
Myoclonic seizure
(my clone is fast)
Myoclonic seizure
Sudden, excessive, forceful jerking or twitching of the body or extremities.
Lasts < a few sec and can occur in clusters
Atonic seizure (aka “akinetic”, “astatic”, “drop”)
(no tone for less than 15 sec)
Atonic seizure (aka “akinetic”, “astatic”, “drop”)
Involves a tonic episode or an acute loss of muscle tone → person falls to ground
Person usually remains conscious. High risk for head injury
Lasts <15 secs
Tonic seizure
(tonic and conscious at 29)
Sudden increase tone of extensor muscle and stiffness. Affects both sides of body. Remains conscious
Lasts < 29 secs
Clonic seizure
Rare
Begins with loss of consciousness and sudden loss of muscle tone followed by limb jerking
PARTIAL SEIZURES: SIMPLE FOCAL SEIZURE
(simply focused and awake)
Person remains conscious and alert
PARTIAL SEIZURES: COMPLEX FOCAL SEIZURE
(complexed by my dreams)
Person has loss of consciousness or alteration in awareness
Their eyes are open but unaware of their actions “dreamlike”. Can be dangerous or embarrassing as people may walk onto oncoming traffic or remove their clothes
→Focal seizures lasts 30 sec to 2 minutes
→ People may feel tired and confused after event
STATUS EPILEPTICUS (SE)
Any seizure lasting >5 min or a series of separate seizures in rapid successions in which the person does not regain consciousness.
Neurons become exhausted and stop functioning → anoxic brain injury
Other complications: respiratory distress, cardiac dysrrhythmias, acidosis, hyperthermia
A neurological emergency
STATUS EPILEPTICUS (SE) - treatments (3 meds)
(your status is AKD)
IV Ativan or Versed, followed by Dilantin (phenytoin), Keppra
Intubation may be required
Last resort anesthesia to entirely suppress neuro activity
SUBCLINICAL SEIZURES
(sub sleep)
A type of epileptic seizure occurring in sedated patients
External physical signs masked by sedative drugs
EEG if subclinical seizures suspected
SEIZURE: MANAGEMENT
Assess pre-ictal symptoms. Ask family and witnesses
Observe seizure characteristics: features and duration
Medical intervention
Treat the underlying cause
Medication management with AEDS (anti-epileptic drugs)
seizure precautions
: O2 ready, suction ready, working IV, padded side rails, bed in lowest position.
Do’s and Don’ts during a seizure
Observe:
Time seizure and characteristics
Do remove objects around patient to prevent injury
Do not stick your finger in mouth to clear airway
Do not attempt to start an IV (you may harm yourself or patient)
Don’t use padded tongue blades
can chip teeth and obstruct airway or get aspirated
seizure = diagnosis
EEG
Labs to rule out metabolic disorder
CT or MRI of head to rule out structural lesion
EPILEPSY AND SEIZURE: TREATMENTS - the weird one
(epilepsy in vagus)
AEDS (Lewis, T58-8): works in 70% of patient. The aim is to maximize seizure control with minimal toxic side effects.
Ativan, Versed, Keppra (levetiracetam), Dilantin, Topamax (topiramate), Trileptal (oxcarbazepine), Depakene
Vagal nerve stimulation (VNS) – works by sending regular mild electrical signals to the brain “pacemaker for the brain”. Used as an adjunct to drug therapy or when drug therapy fails
Surgery: When patient is refractory to drug therapy and VNS
epilepsy - nursing management
Medication education: Continue medication even when seizures are well controlled
For patients on dialysis, need to adjust time of medication or take supplemental dose (consult with treating provider)
MS - three pathological processes
(Sue is a demon, scarred by inflammation)
chronic inflammation
demyelination
gliosis (scarring) in the CNS
Myelin initially regenerates and symptoms improve
Ongoing inflammation affects nearby oligodendrocyctes limiting myelin to regenerate
Inflammation → to axons replaced by glial scar tissue and sclerotic plaques throughout the white matter → decreased electrical conduction
MS - symptoms - just the weird one
(Sue is an electrical hermit)
Paresthesia and tremors; pain to low thoracic and abd, Lhermitte’s sign – electrical sensation down spine, Cognitive decline in approx. 50% of people
MS death
usually PNA or suicide
MS - diagnosis (think of YY) and how many attacks?
At least 2 inflammatory demyelination lesions in MRI
Sx attacks occurring at different times > a month apart
All other possible dx ruled out
MS: PSEUEDO-EXACERBATION - most common trigger
(Sue has a UTI)
MS exacerbation not caused by worsening MS
Temporary worsening of symptoms without actual myelin inflammation or damage
Brought on by triggers such as UTI (most common), infection, stress, exercise
MS: NURSING MANAGEMENT - what type of diet?
Help patient identify triggers and exacerbations
Educate on self-catheterization for urinary retention
Avoid exposure to heat
Promote high protein diet, fluid intake, bowel regimen program
Wear eye patch if diplopia present
Prevent complications d/t immobility during acute attack
Prevent infections
Emotional support
PARKINSONISM - causes
(Fox has too much water)
Illicit and pharmacologic drug- induced
Hydrocephalus
Strokes, tumors
PARKINSON’S DISEASE - patho
(parkinson’s in niagra)
Damage to the Dopamine (DA) producing neurons of the Substancia Nigra (Black substance) of the midbrain. Lewy body (clumps of protein) found in substantia nigra
Sx do not occur until 80% of neurons in substantia nigra are loss
PARKINSON’S DISEASE - Early stage of the disease - one side or both?
Early stage of the disease
Unilateral involvement
Mild tremor
Slight limp
Decreased arm swing
PARKINSON’S DISEASE - As the disease progresses
(Fox and arthur are late in the game)
Shuffling propulsive gait
Dysarthria (abnormal speech caused by muscle weakness)
Loss of postural reflex → poor adjustments to balance
PARKINSON’S DISEASE: COMPLICATIONS - high risk for what?
Impaired motor functions e.g. dyskinesia
Neurologic disorders – e.g. dementia (assoc. with a high mortality rate)
Neuropsychiatric – depression, isolation, hallucination, psychosis
Dysphagia – malnutrition and aspiration risk
**High risk for falls
PARKINSON’S DISEASE: TREATMENT - what is the med called?
(Fox is a dope)
Dopaminergic: Levodopa/carbidopa (Sinemet)
PARKINSON’S DISEASE: OTHER THERAPIES
(fox needs brain stimulation)
Deep brain stimulation (DBS) an implanted device like a pacemaker, Ablation
MYASTHENIA GRAVIS (MG)
(my muscles get weak)
Weakness increases with muscle use
MYASTHENIA GRAVIS (MG) - patho
(low sneezes in my grave)
Auto-antibodies attack acetylcholine receptors (AChR) → ↓ in the number and effectiveness of Ach receptors.
MYASTHENIA GRAVIS - clinical manifestations - when is weakness the worst?
Primary features: Fluctuating weakness
Muscles strongest in the morning then weaken with continued activity
Varies from mild weakness of the ocular muscles to rapidly developing generalized weakness that may lead to death.
MYASTHENIA GRAVIS - diagnosis
(test the cold in my grave)
EMG to test for muscle weakness
Ice pack test: Ptosis (drooping eye) improves when cold applied to eye. (Colddecreases Ach breakdown)
MYASTHENIA GRAVIS: TREATMENTS - meds
(my grave is a mest)
anti-cholinesterase agents -pyridostigmine (Mestinon)
Corticosteroid- prednisone to suppress immune system
Immunosuppressive- Tacrolimus, Cyclosporine, Imuran
MYASTHENIA GRAVIS: - surgery
(thymus in the grave)
Thymectomy
Plasmapheresis: removes circulating AChR antibodies
IV immunoglobulin (IVIG): related to decrease antibody production
MYASTHENIA GRAVIS: NURSING CARE
Adequate ventilation
Assess level of fatigue
space out activity to prevent over fatigue
Test for gag and cough
mysanthyic crisis
mysanthyic crisis - exacerbation of sx due to under medication of ach meds.
AMYOTROPHIC LATERAL SCLEROSIS (ALS) - what age
(Al is old)
Characterized by loss of motor neurons in the brain and spinal cord for unknown reason
Onset: 55-75 yrs of age; more common in men
Leads to death in 2-5 years from time of diagnosis due to respiratory failure.
ALS: AKA LOU GEHRIGS DISEASE - is cognition affected?
No cure
Patient remains cognitively intact while the body is wasting away
ALS -Early onset
(al is drooling and slurring early in the night)
Early onset: tripping, drooling, extremities fatigue, slurred speech, muscle cramps and twitch
ALS -cause of death
Death usually results from respiratory tract infection 2/2 respiratory dysfunction
ALS: AKA LOU GEHRIGS DISEASE - treatment
(Al is ruzie)
Riluzole (Rilutek) reduces the release of glutamate (excitatory neurotransmitter) in the brain and spinal cord thought to cause nerve damage
ALS - nursing interventions
Emotional support
Implement interventions to prevent infections (UTIs, PNA, PU, etc.)
Discuss advance directives
HUNTINGTON’S DISEASE - what area of the brain?
(growing basal in huntington)
Involves the basal ganglia and extrapyramidal motor system
HUNTINGTON’S DISEASE - s/sx
(Corey is spazzing in huntington)
Abnormal and excessive involuntary movement (chorea). Writhing, twisting movements of limbs, face and body
Cognitive and psychiatric manifestations usually precede motor dysfunction
Eventually all psychomotor functions fail including eating and talking
HUNTINGTON’S DISEASE - cause of death
PNA and suicide
3 Most common cognitive disorders in adults are:
Depression
Dementia
Delirium (acute confusion)
ALZHEIMER’S DISEASE - moderate
Self care deficit, poor concentration, short and long-term memory loss, poor judgement
Behavior changes (irritability, aggression, wandering)
Dysphasia (loss of language comprehension and speech)
Apraxia( inability to manipulate objects or perform purposeful acts)
Visual agnosia (inability to recognize objects by sight)
Dysgraphia (inability to use written language)
Eventually loses ability to recognize family members
ALZHEIMER’S DISEASE - severe
Complete self care and ADL loss (requires total care)
Communication loss
Severe brain involvement
alzheimers meds
Acetylcholinesterase inhibitors (donepezil)
Memantine (Namenda) – decreases excessive release of glutamate and neurotoxins
delirium - causes
(delirious from no O2)
Poor O2 supply and impaired O2 usage to brain, neurotransmitter abnormalities, and proinflammatory cytokines
delirium
Hypo or hyperactive or mixed type
Disorganized thinking, irritability, insomnia, poor appetite, hallucinations
Key differences between delirium and dementia is that delirium presents with sudden cognitive change
Simple absence seizure - how long?
(simply blank for 10 seconds)
Simple absence seizure – blank stare “day dreaming” for 10 sec
Complex absence seizure
(complex and blank at 20)
Complex absence seizure – blank stare accompanied by some form of body movement (chewing, blinking, etc) for up to 20 sec
Atypical absence sz
(atypical into adulthood)
Atypical absence sz – similar to complex absence seizure but continue into adulthood
May occur >100x a day; easy to overlook
*Very important to diagnose and treat these as they may progress to tonic-clonic grand mal seizures
tonic clonic - symptoms
(the tonic is blue)
Cyanosis, excessive salivation, incontinence, biting of tongue/cheek common
tonic clonic - Postictal:
Postictal: fatigue, confusion, amnesia, muscle soreness
MS - pseudo exaccerbation - Uhthoff’s phenomenon
(sue is huffing heat)
Uhthoff’s phenomenon (extreme heat that worsen’s MS symptoms
Once trigger resolves symptoms usually subside within 24 hrs
masythenia gravis - Initial mild Sx
(my grave blinks in the beginning)
Initial mild Sx: ocular palsie, ptosis, diplopia, incomplete eye closure. In 20% of people, MG does not progress beyond ocular muscle involvement
masythenia gravis - more severe symptoms - and which muscles are affected?
More severe: Dysarthria (can’t speak), dysphasia, breathing difficulty. Proximal muscle weakness of neck, shoulder and hip. Distal muscles less affected
masythenia gravis - does not include
(normal reflexes at the grave)
Does not include: sensory loss, has normal reflexes, muscle atrophy rare
MG disease highly variable. May have short term remissions, stabilize or severe and progressive.
masythenia gravis - Does not include
sensory loss, has normal reflexes, muscle atrophy rare
MG disease highly variable. May have short term remissions, stabilize or severe and progressive.
masythenia gravis - test
(tension tests my sneeze at the grave)
Tensilon (Edrophonium) test – an IV Acetyl cholinesterase inhibitor that improves muscle contractility after administration
Serology test to identify for specific antibodies
CT to evaluate for thymoma
huntingtons disease - patho
(huntington is Fox’s opposite)
Results in: Excessive dopamine, deficiency of Ach and GABA
Dysphasia
Dysphasia (loss of language comprehension and speech)
Apraxia
(ape can’t use a fork)
Apraxia( inability to manipulate objects or perform purposeful acts)
Visual agnosia
Visual agnosia (inability to recognize objects by sight)
Dysgraphia
Dysgraphia (inability to use written language)
tonic clonic - do they remember?
No memory of seizure
simple focal seizure - what do they feel?
(simply focused anger)
Sudden unexplained emotions: joy, anger, sadness or nausea
May hear or smell things that aren’t real
how to diagnose parkinsons
TRAP and asymetrical onset
TRAP
tremors (pill rolling), rigidity (cogwheel), Akinesia (loss of movement, blinking, increased salivation, mask face), postural instability
complex focal seizure can lead to what?
May spread across the brain and evolve to become tonic-clonic type
mysanthyic crisis - symptoms
(ptosis in the grave)
increased skeletal muscle weakness, ptosis, dypnea, may need intubation. sx better after IV cholinesterase
cholinergic crisis
acute exacerbation due to OVER medication of ACH meds, maybe after thyriodectomy
cholinergic crisis - sx
(cole is flaccid and drooling)
flaccid paralysis, respiratory failure, increased salivation, miosis
cholinergic crisis - after IV cholenesterase?
worse, have atropine available
ALS patho
(Al has too much gluten)
prob too much glutamate
frontal lobe damage
speech
lumbar puncture in what vertebrae?
3 - 4
patient can hear but not understand
receptive aphasia - Wernicke’s area
guillain barre syndrome - treatment
(Guillian and ferris have plasma)
plasma ferrous ? take out antibodies from plasma and put the blood back without the antibodies
EMG
(EMG, it’s gillian)
EMG to confirm dx (progressive weakness of >1 limb and diminished/absent reflexes
parkinson’s diagnosis- TRB
is made when 2 of the 3 characteristic signs of the Classic Triad or characteristic signs (You will be tested on this):
Tremor
Rigidity
Bradykinesia – slow or retarded movement
Dementia occurs in up to 40 % of clients. Ultimate confirmation is a positive response to antiparkinsonian meds.
where is broca’s area located?
frontal lobe
brain stem - parts
(pmm brainstem)
midbrain, pons, medulla oblogata
PSN - dorsal root
travels afferent path - carries sensory info from peripheral to CNS
