MANAGEMENT OF PX WITH NEUROLOGIC - Onset slow, insidious/ subtle (acute v.s.

TRAUMA chronic)

HEAD INJURY Intracerebral

- Injury to scalp, skull, brain - Bleeding within brain

KINDS: *Head injury guideline

2NDARY GCS 13-15 – minor head injury; GCS 3-12 Major

head injury
- Hrs-days post injury
- 2ndary to
o Cerebral edema
o Bleeding

PRIMARY

- Initial damage to brain

Open HI:

 Scalp injury
 Skull fx

Closed HI: S/s Head Injury

 Concussion - Depends on severeity & location of

o Jarring of brain – loss of injury
consciousness few seconds to - Motor & sensory changes, pupillary
minutes with no structural changes, reduced LOC, seizures
damage - Signs of up ICP
 Contusion (more damage) - Nuchal rigidity (meningeal irritation),
o Bruising to brain airway & breathing irregularities
 Laceration
Head Injury: DIAGNOSIS
o Bleeding into brain tissue
 Skull x-ray
CLOSED HI
 CT scan of head
Epidural hematoma  Cervical spine
 MRI
- Clot between skull & dura
 LP
- Laceration of middle meningeal artery
 Cerebral angiography
- Fast; with loss of consciousness
 EEG
- Then with lucid intervals + loss of
consciousness again Head Injury : TX

Subdural hematoma  Place a cervical collar

 Continuous ICP monitoring
- Clot Between dura and brain
  Neuro check x 72 hrs
 Contusion – neuro function monitored
closely
o If present
o Clots removed surgically
o Hematomas evacuated
o With hydrocephalus – managed
with a drain (VP shunt)
 Monitor VS closely for any up in ICP
 Monitor resp status & maintain airway
o SUCTION PRN
o Note for hypoxemia, up ICP
HI: NURSING MGT
 IVF- slow infusion only ; monitor I & O,
check kidney, DI, SIADH (may put
pressure on the pineal gland)
 Monitor for diabetes insipidus, SIADH
 Provide quiet env
 Seizure precautions
 Bed rest with proper positioning
 Prevent complications of immobility
 Nutritional support
 Emotional support
TRAUMATIC BRAIN INJURY (TBI)
- NEURO/cognitive function affected
after brain injury
- Significant change in px behavior/
cognitive/ personality
TBI: KINDS
Closed (blunt)
- Brain injury, no obvious breakage in the
skull
- Head accelerates, rapidly decelerates or
collide with object
Open brain injury
- Object penetrates skull, brain
CHECK THE CAUSE, INC ICP, neuro check, there
is dec in neuro cognitive, px is confused, so they
are put in a lock unit , should be monitored.
MGMT OF PATIENTS WITH INFECTIOUS
NEUROLOGIC DISORDERS
MENINGITIS:
 Inflammation of meninges (protective
membrane lining brain, SC)
Mode of transmission:
- Droplet
- Discharges from nose, throat
Pathognomonic sign
(+) nuchal rigidity
(+) Kernig’s sign (pain in the posterior
harmstring)
(+) Brudzinski’s sign (pain sa batok and
involuntary flexion of LE)
Meningitis Classification:
Aseptic/ viral meningitis
- Sterile meningitis/ non infectious
- Causes: non bacteria
- Viral or secondary to:
o Lymphoma, leukemia, or brain
abscess
Septic Meningitis (infectious)
- Caused by bacteria
o Neisseria meningitides/
meningococcus (most common)
o Meningococcal meningitis or
bacteria
o Medical ‘E”
o May become comatose
- Haemophilus influenza
- Streptococcus pneumonia
Indicative of meningeal irritation

INFECTIOUS : MENINGITIS DIAGNOSTIC EXAM
 Lumbar puncture
o Inc CSF pressure cloudy or milky
white
o Inc CHON level
o Dec glucose concentration
(pathogen is eating glucose)
o (+) gram stain, C &S (except in
viral)
o CBC: up WBC (more than 10
elev wbc)
o CT scan / skull X-ray: to R/O
underlying cause
o Cultures of blood, urine, nose &
throat secretions
Initial Manifestations MENINGITIS
- Headache, fever
Classical Manifestations:
- Nuchal rigidity (early sign),
- (+) Kernig’s sign, (+) Brudzinski’s sign
- Photophobia
- Petechial rash @trunk, LE, mucous
membranes, conjunctiva, palms of the
hands or soles of feet
o Meningococcal meningitis
Other s/s of Meningitis
 Disorientation, memory impairment
 Lethargy > unresponsiveness > coma
 Seizures
o 2ndary to focal areas of cortical
irritability
 Up ICP
o Accumulation of purulent
exudates
o Dec LOC, focal motor deficits
Infectious: Meningitis
Prevention:
 Vaccination
o Meningococcal polysaccharide
 In contact with meningococcal
meningitis
o Antimicrobial chemoprophylaxis
- Penicillin
- Rifampin, ciprofloxacin, ceftriaxone
Meningitis MGT:
 NEURO status, monitor VS
 Fall & safety precautions (seizure or
altered LOC)
 Preventing complications
 Droplet precaution until 24 hrs. after
initiation of antibx
o Infectious type : bacterial
meningitis
Medications:
Early administration of antiinfectives
- Antifungal (Amphotericin B) – shake &
bake, may cause chills and fever, give
500 mg paracet 25 -50 mg
diphenhydramine/ benadryl
- PCN (Ampicillin, Pi
- Cephalosphorin (Cefotaxime,
ceftriaxone)
- Vancomycin = resistant strains (last
resort to prevent Antimicrobial
resistance)
- Adjunctive therapy (Dexamethasone,
Hydrocortisone) – prevent severity of
cerebral edema & inc ICP
o Given before 1st antibx dose
then q6 hrs (so antx will be
aborbed more effectively)
- Fluid volume expanders
o Tx dehydration, shock
 - Phenytoin sodium (Dilantin) 100-200 INFECTIOUS: Encephalitis
mg
 Severe acute inflammation of brain
INFECTIOUS: BRAIN ABSCESS  Herpes simplex virus
o Most common cause
- Collection of infectious material within
brain tissue CAUSES:
CAUSES: (chronic sinusitis every month- px)  Enterovirus
 HSV (person- person)
- Direct brain invasion
o Trauma/ sx  HIV
 Arboviruses
- Spread of infx from nearby sites
o Sinus, ears, teeth  Animal borne illnesses
- Spread of infx from other organs INFECTIOUS: ENCEPHALITIS
o Lung abscess, infective
endocarditis
- Frontal lobe S/S:
o Most common site
- Fever, headache, confusion, behavioral
INFECTIOUS: BRAIN ABSCESS s/s: changes
- Diagnostic assessment
 Headache
o EEG, CSF analysis
o Usually worse in AM,
- MGT:
o Most prevailing symptom
o Antiviral (acyclovir = zovirax) for
 Vomiting
3 wks
 Focal neurologic signs
o Foscavir (if resistant to Zovirax)
o Weakness of an extremity,
o Check for renal function
decreasing vision, seizures
(Zovirax)
 Change in mental status
o Lethargic, confused, irritable or RABIES
disoriented behavior
 Fever may or may not be present  Viral disease  acute brain
inflammation in humans & warm-
INFECTIOUS: BRAIN ABSCESS MGT: blooded animals
 Neuro status Causes:
 Administering meds
- Lyssaviruses (Greek: Lyssa  goddess of
o Antimicrobial therapy
madness, rage, frenzy)
 PCN, chloramphenicol
- Rabies virus
o Corticosteroids
- Australian bat lyssavirus
o Anti-seizure meds (phenytoin
- ** virus present in nerves & saliva of a
Na, Phenobarbital)
symptomatic rabid animal
 Assessing response to TX
 Fall & safety precautions Transmission

- Infected animal scratches or bites

another animal or human
 - Saliva from an infected animal can also
transmit rabies if the saliva comes into
contact with the mouth, nose or eyes
Rabies cause:
 Dogs ( 99%)
 Bat bites (USA)
 Rodents (rare)
 Cats
**rabies animals - Exceptionally aggressive, may
attack without provocation
DX:
- Fluorescent antibody test (FAT)
o A immunohistochemistry
procedure
o Rabies-specific antibody
RABIES S/S
Incubation period:
- 1-3 mos; <1 wk to more than 1 yr
- ** depends on travel distance of virus
to CNS via PNS
EARLY :
 Fever
 Tingling at the site of the exposure
LATE:
- Violent movements, uncontrolled
excitement, (hydrophobia) fear of
water, an inability to move body parts,
confusion, loss of consciousness
- Death (2-10 days post s/s)’
RABIES MGT:
 Prevention
o Animal control
 Vaccination programs
o Recombinant vaccine (V-RG)
o Human diploid cell rabies
vaccine
o Four doses of rabies vaccine
over a 14-day period
- Day 1  three, seven, 14 after the first (
4 shots)
- Received pre-exposure vaccine  post
– exposure vaccinations on days 0 & 2
- Adult: IM deltoid NOT gluteal ADM
- Pedia: IM lateral thigh
RABIES MGT:
 Washing bites & scratches for 15
minutes with soap & H20, povidone
iodine or detergent
 Tetanus prophylaxis
o Heavy & painful
 Debridement of affected area
 Analgesics PRN
 Milwaukee protocol/ Wisconsin
protocol (2004)
o Chemically induced coma
(ketamine + midazolam) +
antiviral drugs (ribavin +
amantadine)
o Extensive rehab
POLIO
 Poliomyelitis/ infantile paralysis
 Infectious disease caused by poliovirus
 ** virus entry to host cell has not been
firmly established
DX:
 Stool sample or a swab of pharynx
 Serum antibodies to poliovirus
 CSF analysis : up WBCH + CHON
POLIO S/S:
 90-95 %
o Of infections cause no
symptoms
 5-10 %
o Minor symptoms
 o Fever, headache, vomiting,
diarrhea, neck stiffness and
pains (arms, legs)
 0.5 %
o Muscle weakness  inability to
move
o Few hrs to few days
 ** back to normal within one or two
wks
POLIO: muscle weakness
 Weakness most often legs
 But may less commonly involve muscles
of the head, neck, diaphragm
 Not all people fully recover
 2-4 % of children die
 15-30 % of adults die
 Post polio syndrome
o May occur yrs after
POLIO TRANSMISSION:
 Infected feces entering mouth
 By contaminated food or water
 Less commonly from infected saliva
 ** spread disease even if no symptoms
are present for up to six weeks
MGT:
 Prevention
o Polio vaccine/ immunizations
o Polio vaccination boosters
 NO CURE
 Prophylactic antibx at weakened muscle
 Analgesics
 OT, PT, orthotic devices (long TX)’
 Moderate exercise
 Nutritious diet
MANAGEMENT OF PX WITH NEUROLOGIC
AUTOIMMUNE DISORDERS
MULTIPLE SCLEROSIS
- Chronic degenerative progressive
demyelinating disease of CNS
Incidence:
- Young adults 20-40 y/o
- Women
- Whites
Cause: idiopathic, viral infection, defective
immune system, autoimmune
NO CURE
- Myelin sheath responsible for nerve
impulse
PATHOPHYSIOLOGY
Sensitized T-cells remain in CNS  promote
infiltration of other agents  damaged immune
system  inflammation  destroys myelin &
oligodendroglial cells (secretes myelin) 
demyelination  plaques on the axon of
neuron  slows/interrupts/distorts/blocks flow
of nerve impulses  irreversible damage to
axon
AUTOIMMUNE: Multiple Sclerosis
- Mild, s/s are visual, headache, several
yrs to downgrade to severe
Clinical manifestion – relate to region most
directly affected by lesions:
 Blurred vision
o Visual disturbances (diplopia)
o Most common initially
 Scotoma (patchy blindness)
 Blindness
 Muscle spasm
 Weakness
 Numbness
 Fatigue
  Up susceptibility to infection  Glucocorticoids
 Emotional instability o Prednisone, dexamethasone
 Euphoria during remissions o Dec inflammation
 Dysphagia  Amantadine (Symmetrel)
o Tx fatigue
AUTOIMMUNE: Multiple Sclerosis
o Antimalarial
Nursing Mgt:  Methylphenidate (Ritalin)
o CNS stimulant reduces fatigue
 Eye patch – tx diplopia
o Give only during the day
 Well balanced diet, high fiber
o Px is awake
o Immobilized px
 Fluoxetine (Prozac) ; Amitriptyline
o Tx & prevent constipation
(Elavil)
 Minimize spasticity, contractures
o Antidepressant
 ADLs functioning
 Tegretol (Carbamazepine)
 PT, OT , ST consults
o Anticonvulsant
 Fall & safety precautions
 ***steroids
 B/B programs
o Prevent edema formation at
 Plasmapheresis
sclerotic plaques
o Reinfusion of FFP
o Tx for acute exacerbations
o Px Have defected immune
 Vit B
system
o Supports cell replication
o Cleansing of the plasma of the
o Enhances metabolic function
defected antibody
 Immunomodulating agents:
o Removal of plasma and
o “ABC”: Avonex, Betaseron,
reinfusion of new
Copaxone
o > 24 hr procedure
o Reduction in antibodies
o TX exacerbation
AUTOIMMUNE: MYASTHENIA GRAVIS
 Hot baths avoided (burns)
o Px with MS – numb and this - Autoimmune disorder
may lead to burns - Antibodies bind to Ach receptors
(responsible for muscle contractions)
PLASMAPHERESIS
- If receptors are impacted = weakness 
 Plasma & components removed paralysis
 Blood cells & antibody containing -  loss of Ach receptors
plasma separated -  loss of response @ neurotransmitter
 Cells & plasma substitute are reinfused - Incidence:
 Results reduction in circulating o Women (more) 20-40 yrs
antibodies o Men above 40 yrs (60-70 yrs)
- S/S:
AUTOIMMUNE: Multiple Sclerosis MGT: o Early s/s: ptosis, diplopia
 Muscle relaxants: (double vision)
o Baclofen o Weakness, fatigued skeletal
muscles
 o Dysphagia, dyspnea
Myasthenia gravis:
- Weakness that worsen that worsen
with activity & relieved by rest
- Give med on time AC 30 min-1 hr
before meals (mestinon)
o When eating u need ur muscles
to eat and swallow
o So give med prior, do not miss
meds, missing may lead to
unable to move/breath
MG TX: Acetylcholinesterase inhibitors
- Cause accumulation of Ach @ synaptic
cleft
- To stimulate remaining Ach at the
neurons
Examlples:
 Edrophonium (Tensilon)
o 10-20 min effect only
o Used as a diagnostic agent for
myasthenia gravis
o Weakness is gone away
 Neostigmine (Prostigmine)
o 2-4 hr effect
 Pyridostigmine (Mestinon)
o 3-6 hr effect
Cholinergic Crisis (cholinergic overdose)
- Extreme muscle weakness, increased
salivation, tears, miosis/ pupillary
constriction
- Antidote: Atropine Sulfate
(anticholinergic)
o Block PSNS
o Can make the weakness go
away
Myasthenic crisis (underdosing)
- Not much acetylcholine
- Extreme muscle weakness, respiratory
difficulty
- Tx: up dosing (mestinon)
- To see which one – give tensilon first
and check,
- if muscle weakness go away
myasthenia crisis
- If muscle weakness increases 
cholinergic crisis
Autoimmue: Myasthenia Gravis S/S
 Muscle weakness:
o Dyspnea, dysphagia, decreased
p
o Ptosis
o physical activity
 fatigue
 diplopia
 impaired speech
 strabismus
 “snarl smile” (forced smile on one side)
 Mask like facial expression
 Drooling
 Resp difficulty, diminished breath
sounds
Autoimmue: Myasthenia Gravis MGT:
 Patent airway
 Aspiration precaution (chin tuck, double
swallow 90 deg)
 Fall & safety precaution
 Start meal with cold beverages (induce
muscle contraction)
 Adequate ventilation
 Reverse isolation
 Adequate rest with activity
 Observe for mysasthenic & cholinergic
crisis
 Plasmapheresis
o FFP transfusion
 Thymectomy
o It shrunks, T-lymphocytes are
one that destroys Ach
 o Removal dec symptoms  Prevent complications of immobility:
 Glucocorticoids (immunosuppresants) TED stockings
 Antacids  Plasmapheresis
o Anti ulcer drugs (proton pump  IV immune globulin (IVIG)
inhibitor) o Fresh antibodies is introduced
o To prevent GI ulceration  Continuous ICG monitoring
 Anticoagulant
AUTOIMMUNE: GUILLAIN-BARRE SYNDROME
 Alpha-adrenergic blockers
- Attack of peripheral nerve myelin o HTN
- PERIPHERAL NERVE SYSTEM  IVF – hypotension
DEMYELINIZATION  Steroids
- “infectious polyneurithis”  Fall & safety precautions
- “acute idiopathic polyneurithis”  Aspiration precautions
- “Landry’s paralysis”
- Acute rapid segmental demyelination of
peripheral nerves MANAGEMENT OF PX WITH PNS DISORDERS
- Producing ascending weakness
- Predisposing factors: Trigeminal Neuralgia: TIC DOULOUREUX
o Resp/ GI infection “Painful Twitch”
o SX - 5th CN
o Vaccination - Unilateral paroxysms of pain
o Pregnancy - Occurs in 2nd, 3rd branches of trigeminal
nerve
Autoimmune : GBS S/S
- Trigeminal nerves controls:
 LE muscle weakness & diminished o Corneal reflex
reflexes o Facial sensation
 Quadriplegia o Mastication muscles
 Neuromuscular resp failure - Abrupt shooting, stabbing unilateral
 Paresthesia of hand, feet pain
o Very fast / short period of time
PATHOPHYSIOLOGY Trigeminal Neuralgia: TIC
o Can be in hours
DOULOUREUX
o Rapid
 Pain related to demyelination of - Cause not certain
sensory fibers - Suggested causes:
 Blindness o Chronic decompression or
 Dysphagia irritation of trigeminal nerve
 Instability of CV system (CN V)

Autoimmune : GBS MGT Diagnostic Method

 Medical “E” : ICU mgt  Based on characteristic behavior

 Assess changes in motor weakness &  Avoiding stimulating trigger points
resp function
Trigeminal Neuralgia: TIC DOULOUREUX S/S:
 Resp therapy/ mechanical ventilation
  Pain
o Felt on skin
o More severe over lip, chin,
nostrils, in teethc
o Drafts of cold air, direct
pressure against nerve may
cause pain
 Paroxysms
o Stimulation of affected nerve
endings
o Triggered by Washing face,
shaving, brushing teeth, eating,
drinking
Trigeminal Neuralgia: TIC DOULOUREUX MGT:
 Anticonvulsive agents
o Carbamazepine (Tegretol)
o Phenytoin (Dilantin)
o Gabapentin (Neurontin),
Lioresal (Baclofen)
 Surgery:
o Trigeminal gangliolysis
-microvascular decompression
of trigeminal nerve
Trigeminal Neuralgia: TIC DOULOUREUX MGT:
 Recognize trigger factors facial pain
o Use cotton pads & room temp
water
 Rinse mouth if toothbrushing causes
pain
 Take food, fluids at room temp, chew
on unaffected side, ingest soft foods
 Perform personal hygiene during pain
free interval
 Monitor : Phenytoin SE
o Bone marrow depression,
gingival hyperplasia
 Provide post op care
CRANIAL DISORDER: BELL’S PALSY (Facial
Paralysis) CN VII
 Disease of 7th cn (Facial – movtor
movement/expression)
 Unilateral or bilateral facial weakness or
paralysis
 Spontaneous recovery 3-5 wks
o Make sure to exercise to
prevent muscle atrophy
CRANIAL VII DISORDER: BELL’S PALSY (Facial
Paralysis)
Cause unknown:
- Result from: infection, hemorrhage,
tumor, meningitis, local trauma
- Inflammatory reaction at 7th CN
-  produces conduction block
-  inhibits neural stimulation to muscle
- By motor fibers of facial nerve
How Long Does Bell’s Palsy Last?
- Complete recovery of Bell’s palsy may
be noted within 3-6 mos with or
without treatment
CRANIAL VII DISORDER: BELL’S PALSY (Facial
Paralysis) S/S
 Face distortion
 Up lacrimation
 Painful sensations: face, behind ear, in
eye
 Diminished blink reflex
o Eye patch
o May cause dryness
 Speech difficulties
 Dysphagia
CRANIAL VII DISORDER: BELL’S PALSY (Facial
Paralysis) MGT:
 Maintain facial muscle tone
 Eye care/ eye patch
 Steroid therapy (prednisone) –
immunosuppressant
 Analgesic
 Heat therapy
 o Comfort,blood flow  Loss of dopamine secreting cells
 Electrical stimulation (TENS) - Responsible for muscle control,
o Prevent muscle atrophy movement, speech, posture
 Surgical exploration of facial nerve - A lot of ACh
- Characterized by (BRT):
PERIPHERAL NEUROPATHY o Bradykinesia (slow to start
- AFFECT peripheral motor, sensory, or movement)
autonomic nerves o Rigidity (stiffness)
- 2ndary to hypoxia  atrophy of nerves o Tremors
- Pins & needle sensation initially before - Affects any age (esp. middle age 60s or
numb older) 20s - atypical
- Cause not known, no known cure
Causes: - Drug tx:
- DM, ETOH abuse, occlusive vascular dse o Anticholinergics
- Dec blood flow o Dopaminergics

S/S Degenerative Parkinson’s Disease:

- Loss of sensation - Progressive, degenerative disorder

- Paresthesia caused by dopamine depletion in basal
- Weakness, pain ganglia (neurotransmitter)
- Muscle atrophy - Generalized decline in muscular
- Neurpathic pain function
o Stabbing - 3rd – 4th most common
o Burning neurodegenerative dse
o Electric-shock like - No known cause
- Unlike in musco - Incidence: 50 + yrs
o Tenderness, achiness, stiffness Dopamine (less in Parkinson)
Diagnostic Assesment: - Inhibitory effect (moderator)
 EMG, somatosensory evoked studies - Coordination of impulses & responses
(motor, intellectual)
MGT:
Ach
 Local corticosteroids
 ASA, codeine/ tramadol - Stimulating effect
o Relieve pain - Nerve & muscle communication
- Inc in Parkinson
 Gabapentin (Neurontin)
 Pregabalin (Lyrica) Pathophysiology

Destruction of dopaminergic neuronal cells in

MANAGEMENT OF PATIENTS WITH
DEGENERATIVE NEUROLOGIC DISORDERS
PARKINSON’S DISEASE
the substantia nigra in the basal ganglia 
depletion of dopamine stores  degeneration
of the dopaminergic nigrostrial pathway 
imbalance of excitatory (Ach) & inhibiting
dopamine) neurotransmitters in the corpus
striatum  impairment of extrapyramidal tracts
controlling complex body movements 
tremors, rigidity, bradykinesia
STAGES OF PARKINSON’S
- Flexion of affected arm
- Px leans toward the unaffected side
- Slow shuffling gait
- Px has inc difficulty walking and
requires assistance
- Profound disability, with wheelchair
DEGENERATIVE PARKINSON’S DSE
Lab & DX Findings:
 PET scan
o Evaluate levels of levodopa
uptake & conversion
o Levodopa – precursor of
dopamine
o If u are a dopamine, brain will
not let u in, cannot cross BBB .
so u need levodopa which can
cross BBB
o Dec uptake
 Presence of 3 cardinal s/s (BRT)
o Bradykinesia, muscle rigidity,
tremor
CLINICAL MANIFESTATIONS: DEGENERATIVE
PARKINSON’S DSE
DEGENERATIVE PARKINSON’S DSE
NURSING MGT:
 Up mobility through daily exercise
 Enhance self-care activities
 Up bowel elimination
 Up nutrition by maintaining normal
weight
 Diet : hi CHON, hi caloric, hi fiber, soft
 Fluids 2 L/day
SX MGT:
 Neural transplantation of adrenal
medullary tissue
o Restore normal dopamine
release
 Deep brain stimulator (DBS)
o Pacemaker like brain implants
o Electrode placed on thalamus
to pulse generator SQ
subclavicular/ abd pouch
o Block nerve pathways that
cause tremors
DG TX FOR PARKINSON’S DSE: DOPAMINERGICS
: EXAMPLES
 Levodopa (Dopar)
o Mainstay TX; precursor of
Dopamine
o Always in combination with
carbidopa (Sinemet)
o Precursor to enter BBB
o On-off syndrome (freezing
mode)
 o On- you can move/have energy; DEGENERATIVE : HUNTINGTON’S DISEASE MGT:
off- freeze move, cannot move
 PT, OT, ST consults
(put them on bed)
 Aspiration precaution
o Avoid B6
o Blenderized meals (if with
- Grains, brans (wheat), eggs, chicken,
chewing probs)
nuts, vit supplements
 Skin precaution
- 25 / 100 mg – 25 mg levodopa and 100
o Paddings
carbidopa
 Fall & safety precaution
ANTICHOLINERGICS:  Do not interact stiffness or sudden
turning away of head as a means of
Benztropine ( Cogentine ) – oral, IV, IM
saying no
Bipedirden (Akineton) – oral IM
o Caused by involuntary
Diphenhydramine (Benadryl) Trihexyphenidyl
movement
(Artane) Procyclidine (Kemadrin) – oral
 Learn how px expresses his emotion
Dopa
DEGENERATIVE : HUNTINGTON’S DISEASE
- Inc dopamine concentration by S/S
providing more precursor, more
dopamine leads to inc inhibiting effects  Chorea (ABN involuntary movements)
o Constant writing, twisting
Amantadine  Intellectual & cognitive decline
- Inc dopamine release o Hallucinations
o Dementia
o Emotional disturbance
DEGENERATIVE : HUNTINGTON’S DISEASE o Suicidal depression, anxiety,
euphoria, psychosis
Also called:  Speech affected
- Huntington’s chorea, hereditary chorea,  Chewing difficulty(dysphagia)
chronic progressive chorea, adult  Disorganized gait
chorea DEGENERATIVE : HUNTINGTON’S DISEASE
- Degeneration of cerebral cortex and MGT:
basal ganglia
- Chronic hereditary dse of nervous  Haloperidol decanoate (Haldol)
system o Blocks dopamine receptors
- Lack of GABA & Ach o Improves chorea in px
-  progressive involuntary choreiform o Can make rigid px
(dance-like) movements +dementia  Antiparkinson meds (levodopa)
o Leads to weakness/paralysis o TX for EPS s/s
- Predisposing Factors: o Tremors
o Genetics, 35-45 yrs  Antidepressants
- NO TX  Antipsychotics
- DX: MRI  atrophy basal ganglia
- Px looks angry
DEGENERATIVE : AMYOTROPHIC LATERAL  Voice assumes a nasal sound
SCLEROSIS (ALS)  Paralysis (late)
 Mind is still sharp
“ Lou Gehrig’s Disease”, ice bucket challenge
DEGENERATIVE: ALS MGT:
- Neuron degeneration in upper, lower
motor neuron > muscle atrophy Nursing MGT:
- No known cause
- Risk factors  Resp status & resp support
o Men 50-60 yrs  Prevent contractures
- Life expectancy: 3 yrs from s/s onset  Decision making (end to life decisions)
- Cause of death: Pharmacologic Mgt:
o Infx, resp failure, aspiration
- Symptomatic TX only  Riluzole (Rilutek)
- Lab tests: o Glutamate antagonist
o EMG (Reduction of functional o Slows deterioration of motor
motor units of muscles – neurons
sarcomeres)  Muscle relaxant / antispasmodic
o MRI (high signal intensity in o Baclofen (lioresal) (inserted in
corticospinal tracts) abdomen, pump)
- Excessive glutamate, defective o Dantrolene sodium
antibodies, faulty genes, damage to o Dantrium or diazepaman
cells, free radicals  degeneration of (Valium)
motor system
ALZHEIMER’S DISEASE
- Too much glutamate causing
degeneration - Chronic progressive degenerative
- Glutamate amino acid, irreversible neuro dementia
neurotransmitter allowing neuron to - Profound effects on memory, cognition,
talk to each other, whenever self care
transmitted supposed to be vacuumed - Atypical for some
out by cell membrane protein but in - DX: MRT/ CT brain => accelerated
ALS, it remains there marked cerebral atrophy
- Rilotec – drug slowing production of - Cause unknown:
glutamate o Genetic tendency
o Down syndrome
DEGENERATIVE: ALS S/S
o Reduced synthesis of
 Fatigue neurotransmitter Ach
 Progressive muscle weakness - Involves diff stages:
 Cramps o Simple memory loss to
 Incoordination vegetative state
 Muscle atrophy (arms, trunks, legs) - Onset: 40-50 yrs (typical) early for
 Spasticity atypical
 DTR brisk & overactive
ALZHEIMER’S DISEASE
 Dysarthria, dysphagia
 Dyspnea Early S/S:
  Forgetfulness, subtle memory loss
Other s/s
 Inappropriate impulsive behavior
 Personality changes
 Decline in speech
 Terminal stage
- Sometimes they have paranoia, after a
blink of an eye- feels in different
place/don’t know where she is
- Do not approach them at the back
- No memory loss – hrs/ many days later
ALZHEIMER’S DISEASE :
 Fall & safety precautions
 Orientation & validation TX (for
moderate to severe type) ( don’t tell
that you are going to school (pag yung
98 yrs old sinabi yan) – (tell her oh
really, what is the name of your mom –
validation tx)  this calms them
 Self care
 B/B continence
 Drug Tx:
Cholinesterase inhibitor:
o Denepezil (Aricept) – used if
memory is still intact,
Memantine (Namenda), Exelon,
Reminyl, rivastigmine,
Galantamine (Razadyne)
o Antidepressants
o Psychotropic drugs
MANAGEMENT OF PX WITH ONCOLOGIC
NEUROLOGIC DISORDERS
Spinal Cord Tumor
Brain Tumor
 Malignant or benign
 Primary
o Meningiomas
 2ndary
o Breast, colon, lungs
 Gliomas
 Astrocytomas, glioblastomas
o Fatal within 2 yrs with
treatment & often within weeks
if untreated
 Compress or invade adjacent tissuess
 Destruction of neurons
 Up ICP + displacement of brain
structures
S/S:
 According to cell type & location of
tumor
 S/S of up ICP
o DIZZINESS, HA, altered LOC,
mental changes, seizures
Diagnosis:
- CT scan, EEG, MRI, skull xray
TX:
- Sx
- Radiation, chemotherapy
- Drugs or shunting of CSP
o Decompression of up ICP
NURSING MGT:
- Assess neuro status
- Maintain patent airway
- Seizure precautions, monitor temp
- Turning, repositioning
- Emotional support
CEREBRAL ANEURYSM
Circle of Wllis
- Anterior cerebral artery
- Anterior communicating artery
Risk factors:
- Congenital
- HTN
- Atherosclerosis
Can be saccular, fusiform, pseudoaneurysm
TX :
 Surgical clipping
 Hypotensive TX
 Endovascular coiling
o Within 24 hrs of aneurysm
o Occlude ruptured aneurysm
- Result of contusion tear injury
- Nerve fibers swell & disintegrate
PATHOPHYSIOLOGY
Damage to cord  contusion, laceration or
compression of cord  cord edema occurs 
compromised capillary circulation & venous
return > ischemia then necrosis of cord 
destruction of myelin & axons  total sensory,
motor paralysis, loss of reflex act below level of
injury

Aseptic meningitis – non infectious

MANAGEMENT OF PX WITH SCI

SPINAL CORD INJURY (SCI)

- From mild flexion-extension “whiplash”

injuries to complete transection of cord
w/ quadriplegia
- Incidence:
o 16-30 yrs
o Males
o ETOH, drug abuse
o Motor vehicle accidents, falls,
violence
- Sites: Common
o C5-7, T12, L1

Categories:

Primary SCI

- Initial insult/ trauma; usually

permanent

2ndary SCI
 - C4- Upper quad
- C6- lower quad
- T6 – high para (ans dysreflexia)
- L1 – low para
FACTORS THAT AFFECT VERTEBRAL INJURY
 Position of person’s head, neck trunk at
time of injury
 Magnitude, rate of application, duration
of injuring force
 Point of application of injuring force
ASIA IMPAIRMENT SCALE (American Spinal
Injury Assoc)
A= complete
- No motor/ sensory functions that will
be coming back
- Numb, cannot move
B -= incomplete
- Sensory function preserved; not motor
C = incomplete
- Motor function preserved below neuro
level + more than ½ muscles with
muscles with muscle grade less than 3
(can go against gravity, u can lift arm
but if u put weight on it, you cannot
move it)
o ROM, no gravity
D = incomplete
- Motor function below preserved neuro
level; have muscle grade 3 or more
E = Normal
CLASSIFICATION OF SCI ( after spinal shock –
saka malalaman if complete or incomplete)
COMPLETE LESION
- Total permanent functional disruption
of spinal cord
INCOMPLETE LESION
- Not totally disrupted at level of injury
- Some ascending/ descending fibers/
both remain intact, continue to function
- More common
CLASSIFICATION OF SCI
Level of injury
1. Quadriplegia/ tetraplegia
- Paralysis (complete or incomplete) of
UE , LE
- C4, C6 injury
2. Paraplegia
- Paralysis of LE
- T6, L1 injury
*QUADRIPARESIS, PARAPERESIS
- DENOTE weakness rather than total paralysis
SCI: INCOMPLETE LESIONS: Cervical
Cervical cord syndrome: (common)
- Motor, sensory deficits UE
- Cause: injury/ edema central cord
Brown Sequard syndrome (lateral cord
syndrome)
- Ipisilateral paresis/ paralysis with
ipisilateral loss of touch, pressure
- Contralateral loss of pain, temp
- Cause: transverse hemisection or ½
injury to SC
Anterior cord syndrome
- Loss of pain + temp, motor function
nipple down
- Touch, vibration sensation intact
- Damage to white & gray matter anterior
SC
- Hyperflexion injuries
Posterior cord syndrome
 - Opposite, have sensation of pain and o Autonomic dysreflexia common
temp and motor but sensation of touch (“E”)
and vibration are gone o Brain does not know what is
happening below the level of
ASSESSMENT OF SCI
injury
- Depends on level of cord injury o ANS will try to vasoconstriction
- Motor, sensory changes below injury = HTN
- Loss of reflexes below level of injury
SC
- Loss of bowel, bladder control
Lateral Horn
CERVICAL INJURIES
- Thoracic region
C1-C4 breathing
- Give rise to ANS
C2-C3
LUMBAR-SACRAL INJURIES
- Usually fatal
- Loss of movement , sensation of LE , B &
C4 B, sexual dysfunctions
- S2- S3 center of micturition
- Major innervation to diaphragm via
o Injury @ this level, bladder will
phrenic nerve
contract but not empty
Above C4 (neurogenic bladder)
- Injury above S2:
- Resp difficulty, paralysis of all 4
o In males = have an erection but
extremities
no ejaculation (SNS damage)
C5 or below - Injury S2-S4
o No erection nor ejaculation
- May have movement in shoulder (damages SNS & PSNS)

COMPLICATIONS SCI

1. Spinal shock
- Post traumatic areflexia (reflex act
depression)
- Immediately psot trauma / injury
- Last for days- months- years
- BP decreases – spinal shock, hypo
- Check bladder
- Indications that spinal shock is resolving
o Return of reflexes
o Hyperreflexia (spasm) rather
than flaccidity
THORACIC INJURIES
o Return of reflex emptying of
- Loss of movement of chest, trunk, bladder
bowel, bladder, LE depending on injury
- T6 & above
 - Spinal shock usually lasts for days or o Tight clothing loosened
wks after sci and the ave duration is 4- o Noxious stimulus is found,
12 wks removed
o Nitrates, Nifedipine,
SPINAL SHOCK S/S:
Hydralazine PO (last option)
 Flaccid paralysis  Distended bladder
 Loss of reflexes below lesion level o Catheterization with xylocaine
 Bradycardia gels to prevent triggering AD
 Hypotension  Impacted feces
 Paralytic ileus (not always) o Removed with anesthetic
2. Autonomic dysreflexia ointments (1-2 % lidocaine/
- Injury above T6 xylocaine gel)
- If u have full bladder, constipation, hurt 3. Spasticity
down, will trigger brain sympa but it - Up tone or contraction of muscles = stiff
cannot process something is happening movements
– will cause vasoconstriction – so BP - Treatment:
down o ROM exercises
- Occur for up to 6 yrs after injury o Muscle relaxants Baclofen
- Exaggerated response to unpleasant (Lioresal), Dantrolene Na
stimuli (bladder & bowel distention; (Dantrium)
pressure ulcers, spasms, pain, pressure 4. Long-term pain
on penis, uterine contractions, tight
clothing) TX:
- HOB elev- to down BP, loosen down - Nonnarcotic analgesis
clothing, emptying bladder - Gabapentin
- Make sure BP is decreasing 5. Neurogenic bladder
- Xylocaine – should bring down the BP if - Occurs w. both upper, lower motor
not effective  niphedipene neuron lesions
Autonomic Dysreflexia S/S: *UMN disorders = spastic or reflex bladder
(urine is leaking out)
 Severe HTN
 Bradycardia *LMN disorders = flaccid bladder ( urine is
 Flushing retaining)
 Sweating anxiety
TX:
 Severe headache
 Nasal stuffiness - Intermittent catheterization program
(ICP)
COMPENSATORY BRADYCARDIA px will have diz
- Bethanecol (Urecholine), Tamsulosin
to lower blood pressure
(can induce hypotension, check BP first
AUTONOMIC DYSREFLEXIA TX: no if 90/60) (Flomax/ Harnal)-
- Urine acidifying agents (urine retention
 To prevent cerebral bleeding or seizures
– UTI, kidney stones)
or HTN crisis:/ ruptured aneurysm
o Cranberry juice, vit c
o HOB is elevated (1st step)
6. Neurogenic bowel
TX:
- Sufficient fluid, fiber intake
- Stool softeners, bulk laxatives
- Daily bowel program (Dulcolax sup/
glycerin sup)
7. Respiratory Dysfunction
TX:
- Incentive spirometer
- Diaphragmatic breathing
- “quad cough” – assisted cough
8. Ortho hypotension
- When being moving from lying to sitting
up – drop in BP
- ABD binder + TED stocking prior OOB
o Prevent orth hypo
- ProAmatine (Midodrine)
o Vasopressor  supine HTN
o When giving, make sure to get
the px OOB to prevent shooting
up BP
o Let the px sit down to normalize
BP
o Alpha adrenergic agonist
- Brace compliance (TLSO)
9. Pressure ulcers
10. DVT
11. Sexual dysfunction
a. Depends on location of lesion:
Erection- UMN lesions
Reflex erections – LMN lesions
Ejaculation – LMN lesions,
lesion is more caudal
Treatment:
- Psychological counseling
- Education
- SX: suprapubic catheter
“E” MGT SCI
 Patent airway (priority)
- Jaw thrust; suction
- Resp assistance PRN
- Chin lift is not done – due to presence
of sci – you don’t want to move that
- Cervical collar is applied
 Resp assess
 Assess sensation
 Motor ability
 CV
 “E” care = autonomic dysreflexia
PHARMACOLOGIC MGT: SCI
 Methylprednisolone
o High doses started w/in 8 hrs of
injury to prevent edema of
further compression
o Motor, sensory function
improved
 Anti-infectives, anticoagulants,
laxatives, antispasmodics
SURGICAL MGT SCIE:
Decompressive laminectomy:
- For complete SCI
- Removal of vertebral lamina
o To minimize pressure on SC,
allows for cord expansion from
edema
- To release pressure
Surgical fusion (spinal fusion, rod insertion)
 - Insertion of metal plates, screws & / or o 10% HNP
use - Lumbosacral discs
of o Forces of gravity
o L4-L5, L5-S1
- Middle aged older men
o Strenuous physical act

bone grafts

Halo traction

- Wrench @front vest

New TX for Para/ Quadriplegics

Risk Factors:
- Rewalk , robotics, rehand exoskeleton
- Use of sliding board

DISC HERNIATION OR HERNIATED NUCLEUS

PULPOSUS (slipped disc)

NUCLEUS PULPOSUS – buffer portion of the SC

Definition:

- Part or all of soft, gelatinous central

portion of an intervertebral disc
(nucleus pulposus) is forced through a
weakened part of disk
- Resulting in back pain, nerve root HNP PATHOPHYSIOLOGY
irritation Herniation
Incidence: Annulus is usually torn extrusion of nucleus
- 80 % low pulposus  compression of Spinal nerve roor &
back pain cord  pain (radiculopathy)  weakness or
paralysis of innervated muscle group

ASSESSMENT : HNP

 Thorough health history

 PE
 Straight leg raise test
 o (+) nerve root irritation
o Raise leg & flex foot at 90 deg
o  back pain or leg pain
(positive result)
DIAGNOSTICS: HNP
CONSERVATIVE THERAPY:
Restrictive activity:
 Limitation of extremes of spinal
movement
o Brace, corset or belt
 Bedrest (to straighten SP, FOB)
o Initial 1 or 2 days
 Antiembolic stockings used
o Periodic flexion & extension of
feet
o Supine w/ pillows under legs
o Lateral on unaffected side w/
thin pillow bet knees
o Measure the circumference of
the biggest thigh
o Then the gastrocnemius
 Medications:
o Analgesics, NSAIDS, muscle
relaxants (baclofen, dantrolene)
 Local heat (first , 20 min) or ice
 PT consult
 Ultrasound & massage (by PT)
 Traction
o Pelvic girdle/ head halter
traction
o Help muscle spasm but does
reduce the HNP
 Transcutaneous electrical nerve
stimulation
o Small electric current to skin
ONCE SYMPTOMS SUBSIDE:
- Initiating life-long regiments
- Strengthening muscles of the back
maintain
o Back strengthening exercise 2x
a day
o Swimming (allows gravity relief)
- Assess/ educate about proper body
mechanics
o Proper lifting techniques
o Shifting of positions
o At the level of the trunk/mid
part (when carrying)
o Bend thru the knees
SURGICAL THERAPY HNP
 Laminectomy (w/ or w/o spinal fusion)
o Most common
o Surgical excision of post arch of
vertebra
 Discectomy
o Removal of herniated
fragments of intervertebral disk
o Decompress nerve root