Cerebral Aneurysm o Endovascular Coiling—to prevent blood

 Localized dilatation that develops secondary to flow in the aneurysm

weakness of the arterial wall  Medical
 Most often occur on the Circle of Willis o Medication:
o 30% occur in the post communicating  Pain relievers
artery  Osmotic diuretics
o 13% in the branching of the middle  Calcium channel blockers
cerebral artery  Anticonvulsants
 Stool softeners/laxatives
Types of Aneurysms
Nursing Management:
A. Saccular Aneurysms (most common)
B. Fusiform Aneurysms  Strict bed rest, HOB 30 degrees
 Deep breathing
Pathophysiology:
 Vital signs, Glasgow coma scale
 Input and output
 Avoid coughing, sneezing, straining—can
increase ICP

Complications: after rupture

 Increased ICP
 Rebleeding
 Cerebral vasospasms
 Hydrocephalus

Neurotransmitters
 Chemical messenger that carries chemical
signals from one neuron to the next target cell
Predisposing Factors: then another nerve cell, a muscle cell or a gland
 High blood pressure Types:
 Smoking
 Congenital  Excitatory: encourage a target cell to take action
 Family history o Norepinephrine
o Serotonin
Symptoms: o Glutamate
 Headache—acute onset with severe pain;  Inhibitory: decrease the chances of target cell
“Worst headache” taking action
 Facial pain o GABA (Gamma Aminobutyric acid)
 Neck pain and stiffness o Glycine
 Alteration in consciousness  Both: Acetylcholine and Dopamine
 Seizures: occurring within 24 hours of onset Remember:
 Autonomic disturbances
o Subarachnoid accumulation of products  Dopamine deficit= Parkinson’s Disease (Rx:
of blood degradation may elicit fever, Antiparkinsonian drugs to increase dopamine)
N/V, sweating, chills, and cardiac  Dopamine excess= Schizophrenia (Rx:
arrhythmias Antipsychotic drugs to decrease dopamine)
 Visual symptoms:  Acetylcholine deficit= Myasthenia gravis (Rx.
o Blurred vision Mestinon to increase ACH)
o Diplopia  Acetylcholine excess= Bipolar disorder (Rx.
o Visual field deficit Lithium to decrease ACH)

Diagnosis: Notice that:

 History of headache—worst headache of the  Neurotransmitter deficit= MedSurg illness

patient associated with stiff neck  Neurotransmitter excess= Psych illnesses
 CT scan, MRI
Myasthenia Gravis
 Lumbar puncture (not recognize by CT scan)  Failure in the transmission of electrical impulses
o To identify blood in CSF that runs in the to muscle cells due to decrease supply of
Subarachnoid spaces Acetylcholine at the Myoneural junction
 Angiography  Extreme muscle weakness especially during
Management: activity or exertion
 Characterized by remission and exacerbation
 Surgical: to repair the aneurysm
Craniotomy: Pathophysiology:
o Clipping of aneurysm—at the neck of Decrease Acetylcholine; Increase Cholinesterase—
the aneurysm so no more blood flowing >impaired transmission of the nerve impulses to muscles
in the area, prevent rupturing at myoneural junction
  Cause: unknown but can be an autoimmune
o The antibodies destroy ACH receptor
Nursing responsibilities: While on Anticholinesterase
site at the neuromuscular junction
 Two peaks of onset:  Give meds exactly on time
o Early onset for female: 20-40 y.o  Give milk and crackers
o Late onset for male: 50 y.o  Monitor the effectiveness of the drug by
 Common in women assessing the muscle strength before and after
medication
Signs and symptoms:
 Observe side effect: N/V, Abdominal cramps,
 Ptosis—initial sign increase salivation
 Diplopia Management:
 Expressionless face
 Dysphagia  Provide comfort
 Decrease symptoms (drugs)—
Complications: Anticholinesterase (long acting); Pyridostigmine
 Respiratory muscle weakness leading to bromide (Mestinon) and Neostigmine
respiratory arrest (Prostigmine)
 15-20% of patient with MG have Thymoma—  Have antidote ready at bedside for cholinergic
enlargement of thymus gland; secrete more t- crisis—atropine sulfate
cells Myasthenic crisis Cholinergic crisis
Diagnosis: Abrupt onset; severe, Similar to MC + side
general muscle effects anticholinesterase
 Based on clinical manifestation weakness;
 Confirmed by testing the client’s response to Inability to swallow, Excess salivation, Abd.
speak, decrease RR Pain, N/V, diarrhea,
Acetylcholinesterase drugs (short acting)
fasciculations
 Tensilon test/Edrophonium HCL
o Short acting anti-cholinesterase
Salivation
o Only used for diagnostic purposes Lacrimation
o Tensilon of 10mg is administered via IV Urination
push Defecation
o 2mg (adults) is injected first
o If no untoward reaction such as Cause: undermedication Cause: overdosage
increased weakness, change in RR, Tensilon test: improves Tensilon test: worsens
nausea, and abdominal cramps Have antidote ready at
o Then remaining 8mg is injected bedside
Ventilation assistance Ventilation assistance
o If patient has MG, symptoms will be
temporarily relieved for 3-5 minutes
o Children older than a year: test dose Surgery
should 0.5 mg, followed by 1mg. several
minutes apart to a maximum total dose  Thymectomy in clients less than 60
of 5mg
Collaborative management:
o Children and Adolescents: test dose of
1mg and subsequent doses of 1-2mg  Plasmapheresis (Plasma exchange)
 Administered several minutes
apart to a maximum total dose Parkinson’s Disease
of 10mg  Associated with decreased levels of dopamine
 CSF analysis: reveals elevated cholinesterase resulting from destruction of pigmented
levels neuronal cells in substantia nigra in the basal
 EMG: the amplitude of motor potentials ganglia
decreases with each test reflecting fatigue  Affects older adults mostly at age 50-60 years
Interventions: old and above. Males
 Causes: unknown; hereditary
Medications:
Pathophysiology:
 Anticholinesterase—blocks action of
cholinesterase and increase levels of
acetylcholine at neuromuscular junction
o Neostigmine (Prostigmin)
o Pyridostigmine (Mestinon)
o Given: in the morning; Antecebum (AC)
1 hour before eating; 30 minutes before
meals
 Immunosuppression medications
o Glucocorticoids
o Corticosteroids (Prednisone) Manifestations: TRAP
o Cyclosporineor azathioprine (Imuran)
  Tremor—initial sign  Avoid constipation
o At rest with pill rolling position of thumb
Avoid the following:
and fingers
o Worsens with stress and anxiety  Drugs
o Progressive impairment affecting ability o Phenothiazines
to write and eat o Pyridoxine
 Rigidity o Reserpine
o Involuntary contraction of skeletal o Monoamine Oxidase
muscles  Marplan
o Cogwheel rigidity: intermittent jerking  Parnate
movement  Nardil
 Bradykinesia to Akinesia—slowed or delayed  Food:
movement that affects chewing, speaking, eating o Vitamin B6
 Bradykinesia and rigidity—expressionless mask o Tyramine rich foods
like face
 Poor posture
o Involuntary flexion of head and
shoulders, stooped leaning forward
position
o Equilibrium problems causing falls, and
short, accelerated steps
o Shuffling gait/propulsive gait

Manifestations:

 Autonomic nervous system

o constipation and urinary hesitation or
frequency
o orthostatic hypotension, dizziness with
position change
o depression and dementia, confusion,
disorientation, memory loss, slowed
thinking
o inability to change position while
sleeping, sleep disturbance

Triad Symptoms:

 Rigidity
 Tremors
 Bradykinesia

Diagnostic exam: No specific test; Physical examination;

Signs and symptoms

Medications:

 Antiparkinsonian: Levodopa (Larodopa)—to

increase the levels of dopamine;
 Taken with food; dark urine and sweat, Avoid
Vitamin B6 (block the effects)
 Carbidopa with Levodopa (Sinemet)—long
acting
o S/E: Hypokinesia and Hyperkinesia
 Amantadin (Symmetrel)—prevent tremors;
o Give with milk to prevent GI upset
 Anticholinergics—Benztropine Mesylate
(Cogentin) to reduce rigidity and some of the
tremors

Nursing Intervention:

 Increase mobility:
o Physical therapy, Assistive devices, Self-
care
o Broad-based gait, raise feet while
walking
 Safety:
o Side rails, grab bars, no scatter rugs
 Read aloud, enunciate syllable clearly