NEURAL

DISTURBANCES
INCREASE INTRACRANIAL
PRESSURE
 Excessive, prolong increased ICP
anorexia of brain cells & cellular death

permanent damage or death of patient

Etiology
 Head injury
 Cerebral edema
 Inflammation or abscess
 Hemorrhage
 Brain tumor
 Cranial surgery
Signs & Symptoms
 Results from distortion of tissue 2’ to
increased pressure as well as direct
pressure on cerebral contents
 Restlessness
 Headache
 Vomiting
 Pupillary changes
Signs & Symptoms
 Papilledema
 Vital signs changes:
a. Bradypnea
b. Bradycardia
c. Hypertension
d. Increased pulse pressure
e. Hyperthermia
 Brainstem reflex manifestations
Management
 Remove basic cause (drain hematoma,
treat infection, remove tumor)
- medications
- mechanical decompression
 Operative management
- elevate the patient’s head slightly
 Dehydrating regimen
- hypertonic solution
- diuretics
- steroids
TRANSIENT ISCHEMIC ATTACK
 Focal neurologic deficits that can last
from a few seconds to a few hours
transient interruption of blood supply &
oxygenation to a localized area of the
brain
 Recovery w/n 24 hours
 Usual site– Internal carotid artery
Predisposing Factors
 Release of tiny fragments of blood clots,
fused platelets & atheromatous material
from plaques

Occlusion of Intracerebral blood

vessels
Nursing Assessment
 Involvement of Middle Cerebral Artery &
Vertebral basilar system
2. Hemiplegia
3. Hemiparesis
4. Unilateral blindness
5. Disturbance in speech & confusion
6. Syncope accompanied by pallor &
postural slump
7. Numbness
8. Visual impairment headache
Management
 Dilator
 Anticoagulants
 Aspirin
 O2 inhalation
 Surgery:
a. Endarterectomy
b. Patch graft angioplasty
CEREBROVASCULAR ACCIDENT
 Reduction of bllod supply
 Affected side of the body – opposite
affected portion of the brain
Etiology
 Spasm
 Compression
 Thrombosis
 Embolism
Nursing Assessment
 GENERAL FOCAL
 Headache Paralysis
 Vomiting Sensory loss
 Convulsions Language disorder
 Coma Reflex changes
 Nuchal rigidity
 Fever
 HPN
 Confusion
 Mental status changes
HEAD INJURIES
 Mild to extreme damage transmitted to
brain tissue as a result of mechanical
force
injuries
Effects
 Subdural hematoma
 Collectionof blood between dura &
arachnoid in the subdural space
 Prognosis- poor

Extradural hematoma
 Results from tear in the wall of skull; blood
collects in the extradural space separating
dura from the skull
Nursing Care
 Establish an airway
 Check for presence of shock
 Check for evidence of spinal injuries
 Observe for scalp and skull injuries
 Prevent infection
 Rest
 Observe for CSF leakage
 Improve cognitive functioning (orient)
SPINAL CORD INJURIES
 Fracture or displacement of 1 or more
vertebrae damage to SC & nerve roots
neurologic deficits & altered
perception/ paralysis or both

Fracture cut, compress or completely

sever the SC patient is not positioned &
move correctly at the scene of accident
Types of Injury
 Cervical injury
 Quadriphlegia (C1-C8)
 Perspiration (-) at the paralyzed site
 Unable to void, (+) fecal incontinence
 Respiratory failure

 Thoracic injury
 Paraphlegia
 Bladder distention and impacted rectum
 Flaccid paralysis at first but becomes spastic
 Autonomic dysreflexia (above T6 & in cervical
lesions)
Types of Injury
 Lumbar Injury
 Flaccid paralysis of LE, bladder &
rectumculate (loss of sympathetic tone)
 S2-S4 injury damages sympaha & para
 Injury above S2 (+)erection but unable
to eja
 Spinal Tumors
 Same symptoms but development is
slower
Signs and Symptoms
 General
 Loss of sensation below level of injury
 Inability to move
EARLY SYMPTOMS OF SHOCK
 Early symptoms of shock:
f. Absence of reflexes below level of the
lesion
g. Flaccid paralysis (below level of injury)
h. Inability to perspire in affected parts
i. Hypotension
Signs and Symptoms
 LATE SYMPTOMS OF SHOCK
 Reflex hyperexcitability (spastic
paralysis)
 State of diminished reflex excitability
(flaccid paralysis)
 Inability to perspire in affected parts
 Urinary retention
Management
 Maintain vertebral alignment
 Bed rest with supportive device (bed
board)
 Bed rest with total immobilization
 Traction

 Surgery
 Straight alignment of spine
 Log rolling from mattress
 Keep back straight
 Mechanical ventilation if needed
DEGENERATIVE DISEASES
MULTIPLE SCLEROSIS
 Chronic, slowly progressive, non-
contagious
 Breakdown of myelin or demyelination of
the NS
 Affects the white matter of CNS
Incidence
 Greater in cold environment
 Common in age group 20-40 years
 Clinical course extends over 10 – 20
years
Signs and Symptoms
 Spastic weakness of extremities
 Nystagmus
 Intentional tremors- motor weakness in
coordination
 Scanning speech
 Visual disturbance
 Euphoria & emotional hyperexcitable
 N/V
 Bladder & bowel incontinence
 Ataxia
 Anesthesia/numbness
 Paralysis
Medications
 Corticosteroids
 Immunosuppressants
 Baclofen
 Carbamazepine
 Propranolol
 Betanechol
 Oxybutinin Chloride
MYASTHENIA GRAVIS
 Nueuromuscular weakness characterized
by marked weakness & abnormal fatigue
of voluntary muscles
 Muscles supplied by bulbar nuclei are
commonly involved
 Clients with MG have high incidence of
thymus abnormalities & frequently have
SLE
Nursing Management
 Monitor respiratory status
 Maintain suction & “E” equipments at
bedside
 Monitor speech and swallowing
 Instruct client to avoid stress, infection &
fatigue
Pathophysiology
 Defect in transmission of nerve impulses
at the myoneuronal junction
Signs and Symptoms
 Muscle involvement usually progresses
from ocular to facial, proximal muscles,
respiratory muscles
 No muscle atrophy
 With periods of exacerbation &
remissions
 Muscles generally strongest in the
morning
Diagnosis
 Tensilon test in which an injection of
Edrophonium is given
 Tensilon test determine if myasthenic
crisis or cholinergic crisis
 Inc muscle strength myasthenic crisis
 Weakness become severe cholinergic
crisis (atrophine Sulfate)
Management
 Anticholinesterase
b. Neostigmine/Pyridostigmine
c. Tensilon
 Side effects: related to the effects of increased
Ach
 Excessive dose– cholinergic crisis
give atrophine sulfate 30 mins before
meals with milk
h. Steroids
i. Avoid: Streptomycin; Kanamycin and
Neomycin
Cholinergic crisis
 Produced by excessive dosage of
anticholinesterase
 May cause generalized weakness,
presence of fasciculations & tightness,
dysphagia & respiratory weakness,
excessive salivation, sweating abdominal
cramps, diarrhea
 Symptoms worse with Tensilon
Myasthenic crisis
 Acute exacerbation of disease due to
rapid unrecognized progression of
disease, failure of medications,
infections, fatigue
 S/Sx: weakness, dysphagia,
restlessness,
 Tensilon relieves symptoms
 Mgt: thymectomy, respiratory support
GUILLAIN-BARRE
SYNDROME
 Disorder in which a person’s immune
response attacks the myelin sheath
 Clinical syndrome of uknown cause
ivolving the PNS & CN
 Paresthesia, muscle weakness or
paralysis
Pathophysiology
 Anti-ganglioside antibodies highly
associated with C. jejuni infection–
attack the normal ganglioside found in
peripheral neuaral tissues at the nodes
of Ranvier--- ineffective transmission of
impulses
Signs and Symptoms
 Paresthesia of LE
 Muscle weakness of legs- progress to
ascending paralysis involving the trunk,
upper extremities and facial muscles
(complete paralysis)
 Difficulty chewing, swallowing & talking
(CN involvement)
 Loss of sensation & sphinceter
disturbance of bladder & rectum
Management
 Support respiration
 Watch for breathlessness, shallow
irregular breathing
 Assist in Mechanical ventilator
 Minitor for dysphagia
 Monitor for cardiac arrhythmias
 Prevent Cx of immobility
 Physical therapy to prevent tightening of
muscles & to preserve joint & muscle
function
 Corticosteroids
Management
 Plasmapharesis
HUNTINGTON’S DISEASE
 Genetically transmitted degenerative
neurologic disease characterized by
abnormal movements, intellectual
decline & emotional disturbance
 Men & women equally affected
 30- 40 years
 Autosomal dominant (chromosome 4)
Pathophysiology
 D striatum in degeneration of basal
ganglia GABA, Ach, substance P
relative inc concentration of other NT
(dopa & NE) excessive movement in
HD
Signs and Symptoms
 Emotional disturbance (suspicious,
negative, irritable, mental deterioration
procedes abnormal movements
 Depression, psychosis
 Temper outburst
 Decline in cognition, dementia,
incontinence
 Rapid, jerky choreiform movements
Signs and Symptoms
 Behivioral & personality changes
 Weight loss, anorexia, insomnia,
malaise, dizziness
 Early: progressive memory loss, visual
impairment & dysphagia
 Progressive dementia
 Mycoclonus (twitching)
 Rapid deterioration– 90% fatal