Neuro Slides 2

Front 1

Central Nervous System:
Consists of

Back 1

brain and spinal cord

Front 2

Peripheral Nervous System
Consists of

Back 2

somatic or voluntary
–autonomic or involuntary

Front 3

Nervous System
Function

Back 3

is control of all motor, sensory, autonomic, cognitive, and behavioral activities

Front 4

Disruption in NS causes

Back 4

increased intracranial pressure, expansion places pressure on vital centers, which can cause permanent neurologic deficits or brain death.

Front 5

Coma:

Back 5

clinical state of unarousable, unresponsiveness, no purposeful responses to internal or external stimuli.

Front 6

Persistent vegetative state:

Back 6

a condition in which the unresponsive patient resumes sleep-wake cycles after coma but is devoid of cognitive or affective mental function.

Front 7

Locked-in syndrome:

Back 7

results from a lesion affecting the pons and results in tetraplegia and inability to speak. Vertical eye movements and lid elevation remain intact and are used to indicate responsiveness.

Front 8

most important indicator of the patient’s condition.

Back 8

Level of responsiveness and consciousness

Front 9

Increased ICP causes

Back 9

decreases cerebral perfusion, stimulates further swelling and may shift brain tissue through openings in the rigid dura, resulting in herniation.

Front 10

Decreased cerebral blood flow

Back 10

•Cause: increased ICP
•Resulting in ischemia and cell death
•Early stages; vasomotor centers are stimulated and the systemic pressure rise to maintain cerebral blood flow. **bounding pulse and resp irregularities.
•Increased CO2 causes cerebral vasodilation, leading to increased blood flow and ICP. Decreased PaCO2 is vasoconstrictive, limiting blood flow to the brain. Decreased venous outflow may also increase cerebral blood volume and ICP

Front 11

Cushing’s triad:

Back 11

bradycardia, hypertension and bradypnea. A Grave sign!

Front 12

Increased ICP and lumbar puncture

Back 12

Lumbar puncture ** avoided in patients with increased ICP. can cause brain herniation

Front 13

Decreasing cerebral edema:

Back 13

osmotic diuretics such as Mannitol my be administered to dehydrate the brain tissue and reduce edema. Important to monitor u/o for diuresis.

Front 14

CSF drainage
Caution

Back 14

excess drainage can collapse ventricles and herniation.

Front 15

Intra cranial sgy
preop management

Back 15

CT; demonstrate lesion, degree of edema, ventricular size and any displacement.

Front 16

Brain tumor: tx of edema

Back 16

may be to reduce edema if the patient has a brain tumor. (Decadron)

Front 17

Todd’s paralysis

Back 17

Secondary generalized seizure may result in a transient residual neurologic deficit postictally

Front 18

Generalized
Seizures

Back 18

•Involve both sides of the brain and are characterized by bilateral synchronous epileptic discharges in the brain from the onset of the seizure.

Front 19

Tonic-clonic

Back 19

•most common, formerly grand mal.
•Characterized by loss of cons and falling to the ground, stiffening (tonic) for 10-20 seconds and subseq jerking of the extremities (clonic) for another 30-40 seconds. Cyanosis, excessive salivation, tongue or cheek biting, and incontinence may accompany. Postictal phase; muscle soreness, very tired, and may sleep for several hours or days. No memory of seizure.

Front 20

Absence seizures

Back 20

•Formerly petit mal
•Occurs only in children, rarely continues beyond adolescence.
•May resolve with age or change type of seizure.
•Manifest; brief staring spell that last only a few seconds
•Extremely brief loss of consciousness
•Untreated may occur up to 100x a day
•Can often be precipitated by hyperventilation and flashing lights.

Front 21

Simple partial seizures (no impairment of consciousness).

Back 21

–With motor signs
–with sensory symptoms
–With autonomic symptoms
–with psychic symptoms

Front 22

•Complex partial seizures (impairment of consciousness).

Back 22

–Simple partial onset followed by impaired cons.
–Impairment of cons at onset
–With automatisms

Front 23

Atypical absence seizures:

Back 23

characterized by a staring spell accompanied by other signs and symptoms.
–Includes brief warnings, peculiar behavior during the seizure, or confusion after the seizure.

Front 24

Myoclonic:

Back 24

characterized by a sudden, excessive jerk of the body or extremities. The jerk may be forceful enough to hurl the person to the ground. Very brief and may occur in clusters.

Front 25

Atonic:

Back 25

“drop attack” involves either a tonic episode or a paroxysmal loss of muscle tone and begins suddenly with the person falling to the ground. Consciousness usually returns by the time the person hits the ground, and normal activity can be resumed immediately.
–Great risk of head injury

Front 26

Clonic:

Back 26

begins with loss of consciousness and sudden loss of muscle tone, followed by limb jerking that may or may not be symmetric.

Front 27

Tonic:

Back 27

involves a sudden onset of maintained increased tone in the extensor muscles. Patients often fall.

Front 28

Complications Seizures
•Status epilepticus:

Back 28

a state of continuous seizure activity or a condition in which seizures recur in rapid succession without return to consciousness between seizures. A neuro emergency.
•

Front 29

Seizures:
Most dangerous type

Back 29

Tonic-clonic is the most dangerous; can cause vent insufficiency, hypoxemia, cardiac dysrhythmias, hyperthermia and systemic acidosis, all can be fatal.

Front 30

Vagal nerve stimulation:

Back 30

an electrode is placed around the left vagus nerve in the neck. Programmed to deliver an intermittent elec stimuli to the brain to reduce the frequency and intensity of seizures.
–Used in only a small number of pts.
–Side effects: cough, hoarseness, dyspnea and tingling in the neck.

Front 31

Pathophys
Major Head Trauma

Back 31

Pathophysiology
•Diffuse axonal injury (DAI) is widespread axonal damage occurring after mild, moderate or severe TBI.
–Process takes 12 to 24 hours to develop and may persist longer.
–Clinical signs: decreased LOC, increased ICP, decortication or decerebration, and global cerebral edema.
–90% of patients remain in a persistent vegetative state.

Front 32

Epidural hematoma;

Back 32

results from bleeding between the dura and the inner surface of the skull.
–Neurologic emergency
–Can be venous or arterial bleed
–Assoc with linear fx involving a vessel
–Sym: decrease LOC, headache, n/v, focal findings.
–Surgical intervention to evacuate hematoma

Front 33

Subdural hematoma:

Back 33

bleeding between the dura mater and the arachnoid layer of the meninges.
–Injury to the brain tissue and parenchymal vessels.
–Acute; signs within 48hrs, decreased LOC and headache.
–Subacute; within 2 to 14 days
–Chronic; over weeks to months
–Size of hematoma dictates s/s
–May be missed in elderly due to mimic of other health problems; somnolence, confusion, lethargy, memory loss

Front 34

Intracerebral hematoma:

Back 34

bleeding within the parenchyma and occurs in approx. 16% of head injuries.
–Usually occurs in frontal or temporal areas
–Rupture of intracerebral vessels
–Size and location of hematoma is key to outcome

Front 35

Clinical Manifestations
Brain tumors

Back 35

•Dependent on location and size.
•Headache is a common; worse at night and awakens patient. Dull and constant.
•Seizures are common with gliomas and mets.
•n/v with increased ICP
•Symptoms may clearly indicate the location of the tumor.

Front 36

Multiple Sclerosis
def

Back 36

Demyelination refers to the destruction of myelin, the fatty and protein material that surrounds certain nerve fibers in the brain and spinal cord.

Front 37

MS
Clincal manifestations

Back 37

Most common S/S:
–Fatigue, depression, weakness, numbness, difficulty in coordination, loss of balance, and pain.
–Visual: blurring, diplopia, patchy blindness and total blindness.

Front 38

Spasticity;

Back 38

extremities and loss of the abdominal reflexes
Symptom of MS

Front 39

Gerontologic considerations
MS

Back 39

Monitor closely for adverse and toxic effects of MS medications and for osteoporosis.

Front 40

Fatigue: MS tx of

Back 40

amantadine, pemoline or fluoxetine

Front 41

Ataxia: MS tx of

Back 41

beta-adrenergic blockers, antiseizure, and benzodiazepines.

Front 42

Bladder/bowel: MS tx of

Back 42

anticholinergics, alpha-adrenergic blockers, anti-spasmodic.

Front 43

UTI; MS tx of

Back 43

Vitamin C, antibiotics

Front 44

Myasthenic crisis:

Back 44

an acute exacerbation of muscle weakness.

Front 45

Myasthenia Gravis
Def

Back 45

•An autoimmune disorder affecting the myoneural junction
•Characterized by varying degrees of weakness of the voluntary*(skelatal) muscles.
•Approx 60,000 people in the US
•Purely a motor disorder with no effect on sensation or coordination.

Front 46

Myasthenia Gravis
at risk pop

Back 46

•Women more than men
•Women age 20 to 40 vs men 60 to 70

Front 47

Myasthenia Gravis
Clinical Manifestations

Back 47

•Initiallly; ocular muscles; diplopia and ptosis are common.
•weakness of the face and throat (bulbar) and generalized weakness.
•Laryngeal: dysphonia and increase risk of choking and aspiration.
•General: all extremities and the intercostal muscles resulting in decreasing vital capacity and resp failure.

Front 48

Myasthenic crisis:

Back 48

an acute exacerbation of muscle weakness.

Front 49

Myasthenia Gravis
Nursing Considerations

Back 49

Major complication result from muscle weakness in areas that affect swallowing and breathing. Monitor for: Aspiration, resp insufficiency and resp infection, SOB

Front 50

Myasthenia Gravis
Management

Back 50

Pyridostigmine bromide (Mestinon)-first line, dose is gradually increased. Adverse effects: fasciculations, abdominal pain, diarrhea, and increased oropharyngeal secretions.

Front 51

Guillain-Barre’ Syndrome
Def

Back 51

•Autoimmune attack on the peripheral nerve myelin.
•Acute, rapid segmental demyelination of peripheral and some cranial nerves.
•An antecedent event most often a viral infection precipitates clinical presentation.

Front 52

Guillain-Barre’ Syndrome
clinical manifestations

Back 52

•Produces ascending weakness with dyskinesia, hyporeflexia, and paresthesias.

Front 53

Guillain-Barre’ Syndrome
medical management

Back 53

•Medical emergency: risk of resp failure
•Monitor changes in muscle strength and resp function alert to needs and progression.
•Preventing complications due to immobility
–Anticoagulation, compression stockings
•Plasmapheresis and IVIG are used to affect directly the peripheral nerve myelin antibody level. Decrease circulating antibodies.
•Continuous EKG; autonomic dysfunction, due to labile symptoms medications are used with caution.

Front 54

Parkinson’s Disease
Def

Back 54

•Disorder of the central and peripheral nervous system; neurodegenertive.

Front 55

Parkinson’s
Clinical Manifestations

Back 55

Tremor
Rigidity
Bradykinesia-most common.
Postural Instability-
Excessive and uncontrolled sweating
•Paroxysmal flushing
•Orthostatic hypotension
•Gastric and urinary retention
•Constipation
•Sexual dysfunction
•depression, dementia, sleep disturbances, and hallucinations.
•Hypokinesia-appears after tremor
•Micrographia –small handwriting
•Face mask like, blinking decreases
•Dysphonia-speech, soft, slurred
•Dysphagia-risk for choking