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MS – NEURO 1.27.22 o Prob: Paresthesias - numbness, tingling

sensation
ANATOMY AND PHYSIOLOGY OF NS
 Occipital Lobe: vision
CNS – Central Nervous System  Temporal Lobe: hearing, memory,
understanding, language
 Brain + Spinal cord
o Wernicke’s area: receptive speech
 Cranial Nerves – 12 pairs
o Global Aphasia: both broca’s *
o Supply head & neck area except CN X
wernicke’s area is affected
(vagus nerve)  up to thorax-abdomen
 supplies 75% of PNS
 Spinal Nerves – 31 pairs
CEREBELLUM
PNS – Peripheral Nervous System
 “little cerebrum”
 Somatic NS – innervates skin & muscles  Responsibility: balance & coordination
 Autonomic NS – innervates body parts for  Ipsilateral innervation (same side)
involuntary processes ex: smooth & cardiac  Problem: ataxia (wide based gait)
muscles, glands  NDx: risk for fall/ injury
o Sympathetic NS – Fight or Flight
o Parasympathetic NS – Rest & Digestion
BASAL GANGLIA

 Group of nuclei that fxn together as 1 

PARTS OF THE CEREBRUM
responsible for fine motor movement/
- Cerebral hemispheres  contralateral coordination
innervation o Caudate nucleus
o Globus pallidus
o Putamen
 Thalamic nuclei: another group
o Thalamus – largest thalamic nucleus,
communicates with cerebrum for
cognitive fxn
o Hypothalamus – endocrine fxn, BP,
appetite, & thirst center
o Subthalamus & Epithalamus – fxn as
relay stations
 Substantia Nigra – dopamine releasing nucleus
 Frontal Lobe: Executive fxns: thinking, planning,  Amygdala – associated w/ hippocampus,
organizing, problem solving, emotional & responsible for memory
behavioral control, & personality
o Motor cortex: movement  supply
skeletal muscles
o Broca’s area: expressive speech 
prob: Aphasia  NDx: Ineffective verbal
communication
 Parietal Lobe: perception, making sense of the
world, arithmetic, spelling
o Sensory cortex: sensations
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o ascending tracts – sensory/ afferent – 6
o ex: spinothalamic tract: pain and temp
from skin  parietal lobe
o descending tract – motor/ efferent – 8
o ex: corticospinal (pyramidal) tract:
motor area  skeletal muscles
 Center of reflex – involuntary response to a
stimulus
o ex: withdrawal reflex
 Origin of ANS
o SNS – thoracic + lumbar nerves
o PNS – cranial + sacral nerves
BRAIN STEM

 Vital center of the brain: respiratory center – NERVE CELLS

pons + medulla; cardiovascular center – medulla
 Origin of cranial nerves  Neurons – functional units
o III + IV = midbrain o Transmits impulses
o V, VI, VII, VIII – pons o Prob: Neuroma
o IX, X, XI, XIII – medulla  Neuroglia – supporting cells
o Except I (olfactory bulb) + II (eyes) o Most numerous, doesn’t transmit
 Parts: o Prob: GLIOMA – most common primary
o Midbrain - Vision, hearing, eye brain tumor
movement, body movement o Types:
o Pons  Astrocytes – support nerve fibers
o Medulla  Ependymal cells – line the ventricles
 CN I: olfactory bulb of the brain
 CN II: eyes  Oligodendroglia/ oligodendrocytes
 CN III, IV, V: extraocular muscles movement – produces myelin sheath (CNS) –
Prob: Multiple sclerosis
 Schwann cells – produces myelin
SPINAL CORD sheath in PNS - Prob: GBS
Fxn:  Microglia – macrophages of NS

 Passageway of tracts:

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 Complications:
o Nutritional imbalance
o Oral infxn  oral care/ gargle with
water based mouthwash
o Anxiety/ depression

BELL’S PALSY

CRANIAL NERVE DISORDERS (Most Common)

TRIGEMINAL NEURALGIA – CN V

 Inflammation of CN VII  reversible

 Pons:
o sensory  face
o motor  muscle of mastication
 AKA: Tic doloreux
 Etio: idiopathic
 Cyclic remission and exacerbation
 RF: Autoimmune, viral infxn, family hx, infxn,
muscle twitching  severe unilateral facial
PAIN
 Dx test: hx + PE
 NDx: acute pain
 GOAL:
o To prevent pain – identify + avoid
precipitation factors
o To manage pain
 Neuropathic pain: nerve dysfxn
 pain reliever (narcotics)/
antiseizure drugs  stop pain
sensation in the nerves 
carbamazepine (Tegretol),
Gabapentin
 Nociceptive pain – injury +
inflammation  NSAIDS
o To prevent and manage complications
 Paralysis on one side of the face
 Etio: idiopathic
 RF: infxn, trauma
 GOAL: prevent muscle atrophy
 MNGT:
o Facial muscle exercises
o Facial muscle massage
o TENS – transcutaneous electrical nerve
stimulation  done by therapist
o Steroids  anti-inflammatory effect
o Vit B complex
SEIZURES
 Abnormal and excessive impulse transmission in
the brain
 PRIMARY Sz: Idiophatic  primary seizure
disorder  EPILEPSY
 SECONDARY Sz: Known causes – sign of a
disease  fever, CVA, TBI, brain tumor, inc. ICP
 S/Sx:
o Motor – convulsion
o Blank staring – petit mal (absence)
o Muscle twitching
o Psychomotor – lip smacking
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 SEIZURE CLASSIFICATION
o Unclassified seizures – cannot
determine if general or partial
 STAGES OF SEIZURE
o Preictal Phase
 Aura  secure safety, protect
self  lie down, put something
to open airway, remove sharps/
jewelries/ scarf/ etc
o Ictal Phase
 Secure patient safety
 DO NOT PUT ANYTHING IN
MOUTH; Turn head to side 
prevent aspiration
 Note symptoms (tonic –
naninigas; clonic – nangingisay)
 Time seizure
o Post Ictal Phase
 Adults – confused  reorient
 Children - Asleep  assess
breathing
 DX TESTS:
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o EEG – electroencephalogram
 Clean scalp – so electrodes stick
 Orient  no pain
 Avoid stimulants  ex:
coffee/chocolate in the morning
 cause false positive
 Avoid NS depressant  ex:
alcohol + antiseizure meds the
night before  cause false
negative
 Deprive of sleep  to see
epileptogenic focus
o MRI
o CT Scan
o Transcranial UTZ
o Lumbar puncture  if infxn suspected
 MNGT:
o Safety
o Airway
o Drug therapy (HALLMARK!) 
antiseizures  stops seizure attack
 CNS depressant  monitor RR;
give at night  DO NOT GIVE
WITH OTHER CNS DEPRESSANTS
 Benzodiazepines – ex:
Diazepam
 for acute mgt, status
epilepticus (prolonged
uncontrolled seizure despite
the usual mgt); NOT FOR LONG
TERM TX – may cause rebound
sz
 Barbiturates – ex:
Phenobarbital  long term tx
 Hydantoin – ex: Phenytoin
 Carbamazepine
 Topiramate
 Valproic Acid
 Ethosuximide
SPINAL CORD INJURY
 CAUSE:
o TRAUMA – MVA (most common), sports
injuries, falls, pedestrian accidents
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o Non traumatic – tumor, infxn of entire cord  loss of all spinal cord
 2 types fxn (loss of motor/ sensory/ reflexes) 
o COMPLETE SCI  complete transection SNS dec., PNS inc.--> vasodilation, dec
of the cord  all fxn below injury is lost HR, dec BP  SPINAL SHOCK/
o INCOMPLETE SCI  partial transection neurogenic shock (only type of shock
of the cord  some fxn lost, some without SNS compensation 
retained bradycardia)
o Cranial Nerves + Sacral Nerves = PNS;
Thoracic Nerves + Lumbar Nerves = SNS
o Management is by managing the injury

 DX TESTS:
o MRI – most definitive
o Myelography – used less common
 MNGT:
o Immobilize – call for help
o Protect the neck
o Massive doses of steroids: Anti-
inflammation  avoid shock (DOC:
METHYLPREDNISOLONE)
 LEVELS OF INJURY
o Vasopressors  increases BP
o C4 – tetraplegia/ high quadriplegia
o Anticholinergic drugs (ATROPINE
 C3 + C4 – origin of phrenic
SULFATE)  block PNS effect  inc. HR
nerve  diaphragm 
o Surgery – Laminectomy 
respiratory paralysis  use of
decompresses spinal cord
mech vent
o Post op: LOG ROLLING – move px as
o C6 – tetraplegia/ low quadriplegia
one unit
 No respiratory paralysis
o Rehabilitation
o T6 – high paraplegia
o L1 – low paraplegia
o ALL OF THESE HAVE:
 Bladder dysfxn AUTONOMIC DYSREFLEXIA
 Bowel dysfxn  Life threatening condition
 Sexual dysfxn  Happen within 6 months after px survives spinal
 SPINAL SHOCK shock
o Usually happen if injury is at T6 and  Aka autonomic hyperreflexia – exaggerated
above autonomic response (high BP, low HR) to a
o Primary Injury/ trauma  inflammation stimulus  noxious or any stimulus not
 bleeding/ swelling (secondary injury)
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necessarily noxious  usually bladder and MOST COMMON TYPES:
bowel distention
 Swelling is only on the injury and below it 
SNS + PNS is now functional but susceptible to
exaggerated response  stimuli (ex: bladder
distention)  SNS stimulation 
vasoconstriction, diaphoresis  inc BP 
baroreceptors  brain can’s send signal back to
bladder, stimulates PNS  head and neck area
will have vasodilation  flushing of face,
headache, nasal congestion, dec HR  can lead
to stroke/ heart attack

 Cannot immediately know type injury d/t

inflammation

 MNGT:
o Prevention: bladder/ bowel training
o Elevate HOB – high folwers  blood
goes down, decongests upper body
o Remove stimulus - Empty bowel,
bladder
o Antihypertensive drugs
o Anticholinergic drugs
INCOMPLETE LESIONS OF THE SPINAL CORD
CENTRAL CORD SYNDROME
 d/t Hyperextension of c-spine injury - most
common
 More paralysis in the upper than the lower
extremities  “Walking paralyzed”
 S/Sx:
o Disproportional greater UL weakness
o Sensory loss is usually minimal
o Some control over the bowel & bladder
o Recovery is possible

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ANTERIOR CORD SYNDROME
 Injury to anterior cord usually d/t hyperflexion
 Loss of voluntary motor, pain, & temp
perception below injury
 Retains posterior column fnx  sensations, of
touch, position, vibration, motion
LATERAL CORD SYNDROME – aka BROWN-SEQUARD
SYNDROME
 Most common cause: trauma  blast injury
(gunshot/ stab wounds)
 Half of spinal cord is affected
 Loss of pain, temp, & light touch on opposite
side
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 Loss of motor fxn, & vibration, position, & deep
touch sensation on same side
POSTERIOR CORD SYNDROME (Not common)
 Damage towards the back of the spinal cord
 Good muscle power, pain & temp sensation
 Difficulty in coordinating movement of the limbs
 Common causes: trauma, compression from
posteriorly located tumors, MS
 Dorsal column lesion (bilateral): bilateral loss of
light touch, vibration, & position sense,
generalized below lesion level
Summary of incomplete spinal cord injuries
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o Inc. Intraabdominal pressure  avoid
Valsalva maneuver, straining, coughing,
vomiting
 EARLY S/SX:
o Changes in LOC: confusion,
disorientation, irritation  EARLIEST!
o Papilledema: swelling of the optic disc –
use ophthalmoscope
o Headache
o Changes in speech
o Vomiting
o Seizure
INTRACRANIAL PRESSURE (ICP) o dizziness
 LATE S/SX:
 Pressure exerted by the cranial contents against o Pupillary changes (unreactive, unequal)
the skull
o Impaired eye movement
 Normal ICP: 10-20 mmhg
o Posturing: decerebrate, decorticate,
 Measured directly by opening the cranium,
flaccid
inserting catheter connected to ICP monitor
o Comatose
 Roles of RN:
o Cushing’s triad
o Identify px at risk
 Widening pulse pressure (inc.
o Identify s/sx of inc. ICP
systolic pressure)
 ICP affects other pressures in the body  Bradypnea
o CCP – cerebral perfusion pressure  Bradycardia
 CPP = MAP – ICP
 N: 70-100 mmhg
o Main arterial pressure (MAP)
 MAP = [systolic pressure + (2 x
diastolic pressure)] / 3
N: 60-100mmhg

Practice Q: BP 120/80; ICP 30

MAP= [120 + (2 x 80)] / 3 = (120 + 160)/3 = 280/3 = 93
CPP = MAP – ICP = 93 – 30 = 63mmhg
 CCP is inversely proportional to CCP  inc. ICP =
dec. CPP  NDx: ineffective cerebral tissue
perfusion
 CAUSE OF INCREASED ICP MUNRO KELLIE HYPOTHESIS - Compensatory
o Brain  d/t inc. brain tissue (tumor) mechanism when ICP increases
o Blood d/t bleeding
o CSF  d/t inc. CSF (hydrocephalus)  Displacement of CSF
o CVA, TBI, Infxn o Normal production: 500ml / day
o Inc. PCO2 o Normal amount: 150 ml  75ml in
o Inc. intrathoracic pressure brain, 75ml in spinal cord
 Decreased blood in the brain

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o Increase venous return  help by o Pupil reactivity score is subtracted to
positioning px at low fowlers – HOB 30- total GCS score
40 degrees o GCS score has evolved over the last 44
o Decreased arterial blood flow  years and now includes new
decrease CPP terminology and an expanded GCS-P
 Brain herniation  compression of the brain score
stem – VERY DIFFICULT TO REVERSE o Sternal rub & retromandibular pressure
o Inc ICP  brain gets pushed downwards are not recommended
to the foramen magnum (where spine o Do not include a combined score when
attaches to the skull) one of the elements of the scale is non-
o Compression of brain stem  midbrain testable
(CN III, IV)  s/sx: o While the GCS-P should not be used as
 Unequal, nonreactive pupils the sole decision instrument in TBI, it
 Absent EOMs (Doll’s eye appears to be a useful tool in our
maneuver) decision-making arsenal when
o Inc. systolic pressure  inc. MAP  inc. combined w/ clinical judgement
CPP o GCS may be even more predictive if you
o Compression of the pons + medulla  incorporate px age & CT findings (GCS-P
respiratory + cardiovascular centers  A CT)
dec. RR + dec. HR (LATE SIGN)
Scor Motor Verbal Eye Pupil
ASSESSMENT: e response respons opening reactivity
e (pupil
 Early signs: headache, vomiting, dizziness, GCS – unreacti
use SPERM ve to
o Sensorium – alert, awake, lethargic light?)
o Pupils – both reactive to light, L/R is 0 - - - Neither
nonreactive, unequal size pupil
o EOMs – Doll’s eye maneuver – “follow 1 None None None 1 pupil
my finger w/ eyes w/o moving head 2 Extension To To Both
o Respiration – RR is 25, irregular sound pressure pupils
3 Abnormal Words To speech -
breathing
flexion
o Motor – strength, resistance
4 Withdraw Confuse Spontaneo -
al d us
5 Localizing Oriente - -
d
6 Obeying - - -
command
s

 GCS – P  latest
o Developed in 1974  changed 2014

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Common conditions that causes of increased ICP

 CVA
 TBI
 Brain Tumor
 Meningitis

CVA – CEREBROVASCULAR ACCIDENT

 Stroke = brain attack, dec O2 to the brain

(ischemia)

ISCHEMIC STROKE  thrombotic/ embolic, most

common CVA

 Thrombotic – thrombus formation in the

cerebral vessel
o Atherosclerosis
o More common ischemic stroke
 Embolic – thrombus developed outside the
cerebral vessels  dislodged  blocks the
cerebral vessels
 S/Sx:
o Initial: diffused  s/sx of inc. ICP
o Swelling subsides  focal sx (depends
on part of brain affected)

FRONTAL LOBE OCCIPITAL LOBE

-hemiplegia -visual disturbances
 MANAGEMENT for increased ICP: -hemiparesis -cerebellum
o Position – low fowlers  promote -broca’s aphasia -ataxia, imbalance
-behavioral disturbances
venous return (PRIORITY!)
-temporal lobe
o O2 administration
TEMPORAL LOBE  -wernicke’s aphasia
o Reduce cerebral metabolism
PARIETAL LOBE  -paresthesia
 Fever – manage BASAL GANGLIA  -movement disorders
 Low dose, short acting sedative -tremors
o Transient hyperventilation -ballismus
 To cause vasoconstriction (dec  VISUAL FIELD DEFECT
blood in brain)
 Dec. pCO2 (30-40mmHg)
o Mannitol (osmotic diuretic) – for
cerebral edema
o Steroids – hydrocortisone –
antiinflammatory
o Manage the cause, risk factors
o Rehabilitation  bring to optimum
level of fxn
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 MNGT:  Dizziness
o Manage inc. ICP  Confusion
o Manage Risk Factors  Difficulty understanding
o Manage Symptoms (palliative)  Trouble speaking
o Thrombolytics drugs given within 3 days  Numbness
 to dissolve thrombus  Weakness
 USA: Urokinase, Streptokinase,  Trouble walking
Alteplase  Lack of balance
o Anti-thrombotic drugs  prevent  DX TESTS:
further thrombus formation o CT Scan
 Antiplatelet – aspirin, o MRI
clopidogrel o Cerebral angiography – use of dye in
 Anticoagulant – heparin, cerebral vessels  Xray to see blockage
warfarin  MNGT:
o Rehabilitation o Manage inc. ICP
 “MILD STROKE”  may lead to ischemic attack o Manage Risk Factors (esp. HPN)
o TIA – Transient Ischemic Attack o Manage Symptoms (palliative)
 Neurologic deficits resolving o Supportive treatment – nutritional, fluid
w/in 24 hrs (bc. You can only wait for bleeding to
o RIND – Reversible Ischemic Neurologic stop or else  craniotomy
Disorder o Craniotomy
 Neurologic deficits resolving  to stop bleeding
beyond 24 hrs  to remove big clot
o Lacunar Stroke o Rehabilitation

HEMORRHAGIC STROKE TBI – Traumatic Brain Injury

 Rupture of blood vessel  Mechanisms of injury

 Cause: o Concussion – (+) neuro decifits but no
o Uncontrolled HPN findings on MRI/ CT scan
o Aneurysm – cerebral
o AV malformation
 S/Sx:
o Diffused – inc. ICP
o Focal sx
o FAST
 Face – one side of face is
drooping
 Arm – weakness
 Speech – difficulty
 Time – time to call for
ambulance o Contusion – hematoma in the brain
o 10 s/sx: tissue
 Severe headache o Open head Injury – (+) penetration to
 Vision changes the skull

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o Closed head injury – (-) penetration;
blunt trauma; usually d/t

 DX TEST:
o CT scan
o MRI
o Skull Xray
 MNGT:
o Manage inc. ICP
o Supportive treatment
o Craniotomy
 To control bleeding
 To remove clot
o Rehabilitation

BRAIN TUMORS
o Coup + Counter Coup Injury – Whiplash
 2 types:
o Primary brain tumor – tumor arises
from brain tissue itself
o Secondary brain tumor – tumor
metastasized to the brain

o Basilar Skull fracture – S/Sx: Racoon

eyes (bruise around eyes), battle sign
(bruise behind ears), rhinorrhea/
otorrhea  collect fluid + test for
glucose; if in linen – (+) halo signs

 Astrocytomas – most common in adults (in

cerebrum) + children (in the cerebellum)
 Initial symptoms are focal
 Enlarging tumor  diffused symptoms d/t ICP
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 May be resectable or not  remove  chemo  nuchal rigidity
+ rad  Kernig’s sign
 DX TEST: CT scan, MRI  Brudzinski’s sign
 MNGT: o Petecchial rashes (esp if d/t meningo
o Manage inc ICP coccimia)
o Manage symptoms (palliative)  Dx test:
o Surgery – craniotomy o Culture and sensitivity
 Cerebrum – supratentorial o CBC
 Cerebellum – infratentorial o Lumbar puncture
 Post op: remain flat on bed; o CT scan/ MRI
assess for inc. ICP o CSF analysis
o Rehabilitation  MNGT:
o Manage inc. ICP
o Supportive treatment
MENINGITIS
o Massive anti-infective therapy
 Cause: bacterial/ fungal infection (antibacterial/ antifungal)
 RF: immunocompromised, direct opening in the
meninges
 S/Sx:
o Inc. ICP – diffused
o S/sx of meningeal irritation

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AUTOIMMUNE DISEASES

Myasthenia Gravis Multiple Sclerosis Guillain Barre Syndrome

Where is Neuro mascular junction  Central Nervous System – Peripheral Nervous System
prob? destruction of acetylcholine demyelination + destruction of demyalination; schwann cells
receptors (by antibodies) oligodendrocytes not destroyed
Earliest Muscle weakness + Paralysis  Demyelination of optic nerve  Ascending paralysis + loss of
manifestatio pstosis (muscle around the visual disturbances reflexes, numbness/ paresthesia
n eyes)
Etiology -thymoma Idiopathic Idiopathic
-idiopathic
Risk Factors Viral infxn Viral, hormonal, females Viral  Epstein Barr Virus,
cytomegalovirus,
Campylobacter jejuni
S/sx Respiratory paralysis Charcot’s triad Respiratory paralysis
-scanning speech
-intention tremors
-nystagmus

MYASTHENIA GRAVIS

Dx Tests: Mngt:

 Tensilon Test  Support respiratory fxn

o anticholinesterase drug  inc  Support nutrition
acetylcholine in the junction   ROM exercises
temporary improvement in muscle fxn  Prevent complications from immobilization
(most definitive test)  Surgery:Thymectomy
 EMG – electromyography  Drug therapy: anticholinesterase drugs
 Nerve conduction test o Long acting – lasts: 20-30mins after
 MRI/ CT scan - to identify thymoma intake to 4-6hrs
o Ex: Neostigmine, Physostigmine,
Pyridostigmine

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MULTIPLE SCLEROSIS

Dx Tests: Mngt:

 MRI  Palliative care (relieve s/sx)

 CT scan – only useful when changes are already  Provide safe environment
severe  Prevent complications
 CSF analysis  Muscle relaxants – for spasticity
 Antidepressant drugs
 *Plasmapheresis
o Separates antibodies from the blood
o Cons may outweigh pros here

GUILLAIN-BARRE SYNDROME

Dx Test:

 MRI Mngt:
 CSF analysis – identifying more proteins/
 Support respiratory fxn
immunoglobulins in CSF
 Support nutrition
 EMG – electromyography – nerve conduction
 Prevent complications from immobilization
test
 ROM exercises
 NCT – nerve conduction test
 Promote safety
 Prevent aspiration

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 Plasmapheresis o Given per kg body wt
 IV-Ig – Intravenous immunoglobulins PRIORITY!

DEGENERATIVE DISEASE OF THE CNS

Parkinson’s Ds Alzheimer’s Ds Huntington’s Ds ALS – Amyotropic

Lateral Sclerosis (aka
Lou Gerigh’s Ds)
What Substantia nigra Cells of cerebral cortex Cells of cerebral cortex All motor neurons
degenerates? (dopamine) + basal ganglia
Etio: Unknown Unknown Hereditary – autosomal Overexcitation of NT
Imbalance of Pathogenesis: dominant  50% called glutamate 
neurotransmitters 1.Precipitation of chance of inheriting degenerate motor
Ach vs Dop abnormal protein neurons (upper, lower,
Inc excitatory (Ach): called amyloid corticobulbar – motor
dec inhibitory (Dop) 2.destruction of ach neurons of cranial
receptors in the nerves w/ motor fxn)
neuronal junction
Risk Factors Age (geria), Family Hx, Age (geria), Family Hx,
Exposure to chemicals Stress
Cardinal 1.Tremors 1.Dementia - Recent 1. Dementia Muscle weakness +
signs 2.Bradykinesia memory 2. Cognitive dysfxn paralysis  respiratory
3.Rigidity 2. Cognitive dysfxn 3. Emotional paralysis
3. Emotional disturbances
disturbances 4. Chorea
PARKINSON’S DISEASE o Regular exercise
o Provide good nutrition
o Assist in self care/ ADLs
o Provide with adaptive utensils
o Prevent complications
 Drug therapy:
o Dopaminergic drugs
 Dopamine precursor – ex:
Levodopa – blood brain barrier
(BBB) – dopamine
 + carbidopa  destroy dopa
decarboxylase – enzyme that
destroy levodopa when it pass
 NDX: risk for injury, fall, aspiration; selfcare the BBB
deficit  Amantadine – inc. release of
 Dx: Hx + PE dopamine from subs. Nigra
 *Movement disorder only but tx may cause (used in the beginning only)
cognitive disfxn  Bromocriptine – dopamine
 Movement disorder only but tx may cause agonist
cognitive problems as well o Anticholinergic drugs
 Mngt:  Benadryl
o Provide safe + unhurried environment  Akineton
o Prevent aspiration  Artane

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 ENCARNADO, 2022
 Cogentin o Serum electrolyte level – decreased Na
may also cause CNS symptoms
 MNGT:
ALZHEIMER’S DS o Provide safe + unhurried environment
o Present reality
o Provide good nutrition
o Keep busy with simple tasks
o Exercise
 Drug therapy
o Anticholinesterase drugs (anti
alzheimers- can pass BBB)
 Rivastigmine
 Donepezil
 Tacrine
o Antipsychotic drugs  may cause
movement disorders
o Antidepressant drugs

HUNTINGTON’S DISEASE

Movement disorder

 Chorea athetosis, ballism & dystonia

o Non-rhythmic involuntary movement
o <ay be combinations of fragments of
purposeful movements & abnormal
postures
 All d/t imbalance of activity in the complex
basal ganglia circuits
 STAGES OF ALZHEIMERS o Sometime aka “extrapyramidal
o Initial stage disorders:
 Have lucid intervals o Primarily conditions r/t excessive
 Lasts 2-3 yrs dopaminergic activity in the basal
o Confusion stage ganglia
 Sundown syndrome – confusion
at dusk  hallucinations,
delusions
 Usually lasts 10 yrs
o Terminal stage
 Total dependence on caregiver
 DX Test – to rule out other diseases
o MRI
o CT scan
o Thyroid fxn test – hypothyroidism also
cause same symptoms

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 ENCARNADO, 2022
 Dx Tests:
o Muscle biopsy
o EMG
o Nerve conduction test
 MNGT:
o Support respiratory fxn
o Prevent aspiration
o Provide safety
o Prevent complication from
immobilization
 Drug therapy
o Glutamate antagonist – Riluzole - not
curative, only slows down progression

 Dx: Family Hx
 Onset of S/Sx – middle adult years (35-45 y/o)
 Genetic counselling  genetic test for
Huntington
 MNGT:
o Provide safe and unhurried
environment
o Prevent aspiration
o Prevent complications
o Antipsychotics
o Antidepressants
o Muscle relaxants – PRN
o Regular exercises  irregular
movement disappears during exercise

LOU GEHRIG’S DISEASE (ALS – Amyotrophic Lateral

Sclerosis)

 Overexcitation of NT called glutamate

 Life span: ~5yrs from dx

ENCARNADO, 2022