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Neurological Dysfunction
MS ALISHA TALWAR
Neurological Dysfunction
 Neurological Dysfunction refers to a disorder of the
Central Nervous System and affects the efficiency of
brain processes.
 It includes-
 Increased Intracranial Pressure
 Headache
 Seizure
 Epilepsy
Intracranial Pressure
 Refers to the pressure contained within the cranial
cavity.
 The normal range is between 5 to 15 mmHg.
 ICP over 20 mm/Hg is considered elevated ICP, also
known as intracranial hypertension.
 Factors that influence ICP
 Arterial pressure
 Venous pressure
 Intra-abdominal and intra-thoracic pressure
 Posture
 Temperature
 Blood gases (CO2 levels)
 The degree to which these factors  ICP
depends on the ability of the brain to
accommodate to the changes
 Skull has three essential
components:
- Brain tissue = 78% or 1400g
- Blood = 12% or 75ml
- Cerebrospinal fluid (CSF) =
10% or 75ml
 Any increase in any of these
tissues causes increased ICP
 These three components of the
cranial vault maintain a state
of equilibrium. Their pressure
and volume determine the
condition of balance.
Monro-Kellie Hypothesis
 The pressure–volume relationship between ICP, volume of CSF, blood, and
brain tissue, and cerebral perfusion pressure (CPP) is known as the
Monro–Kellie doctrine or the Monro–Kellie hypothesis.
 The Monro–Kellie hypothesis states that the cranial compartment is
incompressible and that the volume inside the cranium is fixed.
The cranium and its constituents (blood, CSF, and brain tissue) create a
state of volume equilibrium, such that any increase in volume of one
of the cranial constituents must be compensated by a decrease
in volume of another
Regulation and Maintenance of ICP
If the volume in any one of the components (brain tissue,
blood, and CSF) increases within the cranial vault and the
volume from another component is displaced, the total
intracranial volume will not change.
Normal compensatory adaptations
Alteration of CSF absorption or production
Displacement of CSF into spinal subarachnoid space
Shunting of venous blood out of the skull
Causes of Increase ICP
 Intracranial hemorrhage
 Traumatic brain injury
 Ruptured aneurysm
 Arteriovenous
malformation
 Other vascular anomalies
 Central nervous system
infections
 Neoplasm
 Vasculitis
 Ischemic infarcts
 Hydrocephalus
 Pseudotumor cerebri
Sustained increases in ICP result in brainstem compression
and herniation of the brain from one compartment to
another
Precipitating Factors
Several factors may increase ICP:
 Cerebral edema resulting from infection
 Intracranial or subarachnoid bleeding
 Brain tumor
Neurological condition
Complications
 Death
 Permanent neurological problems
 Reversible neurological problems
 Seizures
 Stroke
Clinical Manifestations
 An altered LOC is usually the earliest sign of increased ICP
 The patient may exhibit partial or total loss of motor and sensory
function
 Pupillary changes may occur, such as unequal size, constriction, dilation,
or reduced or absent responses to light
 Cushing’s triad (bradycardia, bradypnea, and hypertension)is a late sign
of increased ICP
 Other signs and symptoms include changes in respiratory patterns,
headache, seizures, vomiting, and a widening pulse pressure
Assessment and Diagnostic Tools
 Detailed history and Physical examination
 CT scan
 Skull X-rays
 ICP monitoring
ICP Monitoring
Neurological condition
Sites of ICP Monitoring
 Subarachanoid
 Intraventricular
 Epidural
Management
 The goal of treatment is to normalize ICP and avoid complications
 Pressures are carefully monitored by means of epidural monitoring,
subarachnoid screw and bolt, or intraventricular monitoring
 CSF blockage is corrected by surgical placement of shunts
 Drug therapy may include an antibiotic, an anticonvulsant, and a diuretics.
 Hyperventilation therapy
 Metabolic disorders are corrected
 Lumbar puncture is contraindicated in a patient with increased ICP
because it can cause life- threatening herniation (shifting of brain contents into
another compartment)
Nursing Management: Assessment
 Change in level of consciousness
 Changes in vital signs (Cushing triad)
 Ocular signs
 Headache-Often continuous and worse in the morning
 Vomiting- No nausea and Projectile
 Decrease in motor strength and function
 Assess movement and response to stimuli
 Assess for Decerebrate posturing (extensor) & Decorticate posturing
(flexor)
Ocular changes
Neurological condition
Neurological condition
Nursing Diagnosis
 Ineffective Tissue Perfusion (cerebral) related to increased ICP as evidenced
by decreased LOC, sluggish pupil response, papilledema, and posturing
 Keep head of bed slightly elevated and the head in midline (straight). For clients with
a basal skull fracture, keep bed flat.
 Limit movement, space essential nursing tasks, and reduce or eliminate
environmental stimuli (e.g., loud noise, bright lights).
 Avoid extreme hip flexion.
 Keep client quiet. Change position with assistance and use a turning sheet. Avoid
range-of-motion (ROM) exercises until ICP approaches normal unless ordered
otherwise by the physician.
 Administer reduced fluid volumes at an even rate for 24 hours. Give diuretics as
prescribed; note client's response to therapy.
 Hyperventilate the mechanically ventilated client briefly according to
medical orders.
 Suction the airway only when necessary.
 Give 100% oxygen before and after suctioning when it is required.
 Keep suctioning brief, without exceeding 10-15 seconds per pass of the
catheter.
 Administer a prescribed stool softener.
 Ensure that a gastric tube used for decompression or nourishment remains
patent.
 Administer prescribed medications if vomiting or persistent coughing occur.
 Risk for Ineffective Breathing Pattern and Ineffective Airway
Clearance related to diminished LOC and herniation of the brain stem
secondary to increased ICP
 Attach a pulse oximeter to the finger, earlobe, bridge of the nose, or toe.
 Insert an oral airway if client is comatose.
 Administer prescribed oxygen.
 For mechanically ventilated clients, ensure that the ventilator delivers the
prescribed tidal volume at the ordered rate.
 Suction when necessary to clear tracheal secretions or keep endotracheal
tube patent.
 Risk for Infection related to impaired skin and tissue integrity
secondary to surgery, invasive diagnostic or monitoring
procedures, or original head injury
 Keep wounds clean and dry.
 Use aseptic technique when handling any part of the intracranial
monitoring device or changing a dressing applied after surgery.
 Administer antibiotic therapy, if prescribed.
 Risk for Impaired Skin Integrity related to low
capillary blood flow secondary to pressure and
inactivity
 Tilt or turn client from side to side every 2 hours.
 Avoid friction by using a lift sheet.
 Use a pressure-relieving mattress or mechanical bed for
clients whose position cannot be readily changed.
 Keep skin clean and dry.
 Self-Care Deficit (total or specify type) related to
diminished LOC as manifested by inability to follow
directions and impaired neuromuscular function
 Give client complete care, including bathing, oral care,
nutrition, and elimination, until ICP is normal and client can
resume these activities independently.
 Impaired Verbal Communication related to decreased
LOC or endotracheal intubation as evidenced by an
inability to speak
 Look for grimacing or moaning.
 Correct problems that may be causing discomfort, such
as a wrinkled sheet or an object pressing on the skin.
 Provide paper and pencil or a magic slate if client is alert
but intubated.
Headache/Cephalgia
 Headache is pain in any region of the head. Headaches
may occur on one or both sides of the head, be isolated
to a certain location, radiate across the head from one
point.
 A headache may appear as a sharp pain, a throbbing
sensation or a dull ache. Headaches can develop
gradually or suddenly, and may last from less than an
hour to several days.
Classification of Headache
 According to WHO
Migraine
Tension type
Cluster
Medication over use
Primary Headaches
 90% of all headaches are primary headaches.
 Primary headaches usually first start when people are between 20
and 40 years old
 Migraines typically present with pulsing head pain, nausea,
photophobia (sensitivity to light) and phonophobia (sensitivity to
sound).
 Tension-type headaches usually present with non-pulsing
"bandlike" pressure on both sides of the head, not accompanied by
other symptoms
 Cluster headaches- short episodes (15–180 minutes) of severe pain, usually
around one eye, with autonomic symptoms (tearing, red eye, nasal congestion)
which occur at the same time every day. Cluster headaches can be treated with
triptans and prevented with prednisone, ergotamine or lithium.
 Trigeminal neuralgia or occipital neuralgia: shooting face pain
 Hemicrania continua: continuous unilateral pain with episodes of severe pain.
Hemicrania continua can be relieved by the medication indomethacin.
 Primary stabbing headache: recurrent episodes of stabbing "ice pick pain" or
"jabs and jolts" for 1 second to several minutes without autonomic symptoms
(tearing, red eye, nasal congestion). These headaches can be treated
with indomethacin.
 Primary cough headache: starts suddenly and lasts for several
minutes after coughing, sneezing or straining (anything that may
increase pressure in the head).
 Primary exertional headache: throbbing, pulsatile pain which
starts during r after exercising, lasting for 5 minutes to 24 hours.
 Primary sex headache: dull, bilateral headache that starts during
sexual activity and becomes much worse during orgasm
 Hypnic headache: moderate-severe headache that starts a few
hours after falling asleep and lasts 15–30 minutes.
Secondary Headaches
 Headaches may be caused by problems elsewhere in the head or neck. Some
of these are not harmful, such as cervicogenic headache (pain arising from the
neck muscles). Medication overuse headache may occur in those using
excessive painkillers for headaches, paradoxically causing worsening
headaches
 Meningitis: inflammation of the meninges which presents with fever and
meningismus, or stiff neck
 Bleeding inside the brain (intracranial hemorrhage)
 Subarachnoid hemorrhage (acute, severe headache, stiff neck WITHOUT
fever)
 Ruptured aneurysm, arteriovenous malformation, intraparenchymal
hemorrhage (headache only)
 Brain tumor: dull headache, worse with exertion and change in position,
accompanied by nausea and vomiting. Often, the person will have nausea and
vomiting for weeks before the headache starts
 Temporal arteritis: inflammatory disease of arteries common in the elderly
(average age 70) with fever, headache, weight loss, jaw claudication, tender
vessels by the temples, polymyalgia rheumatica
 Acute closed angle glaucoma (increased pressure in the eyeball): headache
that starts with eye pain, blurry vision, associated with nausea and vomiting. On
physical exam, the person will have a red eye and a fixed, mid dilated pupil.
 Post-ictal headaches: Headaches that happen after a convulsion or
other type of seizure, as part of the period after the seizure (the post-
ictal state)
 Gastrointestinal disorders may cause headaches,
including Helicobacter pylori infection, celiac disease, irritable bowel
syndrome, inflammatory bowel disease, gastroparesis, and hepatobiliary
disorders.
Pathophysiology of Migraine
Neurological condition
Pathophysiology of cluster headache
Neurological condition
Comparison of Primary headaches
Neurological condition
Diagnosis of Headaches
 Most headaches can be diagnosed by the clinical history alone. If the symptoms
described by the person sound dangerous, further testing with neuroimaging or
lumbar puncture may be necessary. Electroencephalography (EEG) is not useful
for headache diagnosis
 The first step to diagnosing a headache is to determine if the headache is old or
new.
 A "new headache" can be a headache that has started recently, or a chronic
headache that has changed character
 For example, if a person has chronic weekly headaches with pressure on both
sides of his head, and then develops a sudden severe throbbing headache on
one side of his head, they have a new headache.
Red flag
 It can be challenging to differentiate between low-risk, benign headaches and high-risk, dangerous
headaches since symptoms are often similar. Headaches that are possibly dangerous require further lab
tests and imaging to diagnose.
 The American College for Emergency Physicians published criteria for low-risk headaches. They are as
follows:
 age younger than 30 years
 features typical of primary headache
 history of similar headache
 no abnormal findings on neurologic exam
 no concerning change in normal headache pattern
 no high-risk comorbid conditions (for example, HIV)
 no new concerning history or physical examination findings
The American Headache Society recommends using "SSNOOP", a
mnemonic to remember the red flags for identifying a secondary
headache:
 Systemic symptoms (fever or weight loss)
 Systemic disease (HIV infection, malignancy)
 Neurologic symptoms or signs
 Onset sudden (thunderclap headache)
 Onset after age 40 years
 Previous headache history (first, worst, or different headache)
Management
 Pharmacological-The main classes of drugs to treat headache disorders
include: analgesics, anti-emetics, specific anti-migraine medications, and
prophylactic medications
 Behavioural Treatments-Massages,relaxation training, Meditation,
lying down in a dark and quiet room, hot or cold compresses on the head
and neck and sometimes cognitive behavioural therapy.
 Diversional Therapies- Guided Imagery, Aroma therapy
 Lifestyle changes- Avoid skipping meals, limit alcohol and caffeinated
beverages.
 Complementary therapies- Acupressure, acupuncture,
reflexology, use of several herbs and supplements like-
 ginger
 vitamin B2
 magnesium supplements
 fish oil
Nursing Management (Diagnosis)
1. Acute pain r/t stress and tension, irritation / nerve pressure,
vasospasm, increased intracranial pressures.
2. Ineffective individual coping r/t situations of crisis, personal
vulnerability, not adequate support systems, work overload,
inadequate relaxation, severe pain, excessive threat to himself.
3. Deficient knowledge : about the condition and treatment needs r/t
lack of recall, did not know the information, cognitive limitations
Seminar of Nervous System
Seizures
Terminology
 Seizures-A seizure is an abnormal electrical discharge that occurs in your brain.
Usually brain cells, or neurons, flow in an organized fashion along the surface of
your brain. A seizure occurs when there is an excess of electrical activity.
 Seizure Disorder-A seizure disorder is a medical condition (one of about 40)
characterized by episodes of uncontrolled electrical activity in the brain, thus
producing symptoms that include two or more seizures.
 Convulsions-An abnormal, involuntary contraction of the muscles. A person
having convulsions appears to be shaking rapidly and without control
 Tremors- An involuntary (unintentional) rhythmic movement of muscles of
limb(s). It’s usually due to an anomaly in the motor part (movement controlling
part) of the brain.
Seizure Disorder
 Definition- Seizures are episodes of abnormal motor,
sensory, autonomic or psychic activity (or combination of
these) that result from sudden excessive discharge from
cerebral neurons
Etiology
 The underlying cause is an electrical disturbance( dysrhythmia) in the nerve
cells in one section of the brain: these cells emit abnormal, recurring,
uncontrolled electrical discharges
 The specific causes of seizures are varied and can be categorized as idiopathic
(genetic, developmental defects) and acquired.
 Cerebrovascular diseases
 Hypoxemia
 Fever (childhood)
 Head Injury
 Hypertension
 CNS Infections
 Metabolic and toxic conditions (Renal failure,
hyponatremia, hypocalcemia, hypoglycemia, pesticide
exposure)
 Brain tumors
 Drug and alcohol withdrawal
 Allergies
Clinical Manifestations
 Associated loss of consciousness, excess movement or
loss of muscle tone or movement, and disturbances of
behaivour, mood, sensation, and perception may also
occur.
Epilepsy
 The term “epilepsy” refers to recurrent, unprovoked
seizures from known or unknown causes. The term
“ictus” describes the period in which the seizure occurs,
and the term “postictal” refers to the period after the
seizure has ended but before the patient has returned to
his or her baseline mental status.
Classification
Partial seizures
Partial seizures arise from a localized area in the brain and
cause specific symptoms.
Partial seizures include simple partial (Jacksonian motor-
type and sensory-type), complex partial (psychomotor or
temporal lobe), and secondarily generalized partial
seizures.
Simple partial(Jacksonian motor-type)
 A simple partial seizure begins as a localized motor seizure, which is
characterized by a spread of abnormal activity to adjacent areas of
the brain.
 Stiffening or jerking in one extremity, accompanied by a tingling
sensation in the same area. For example, the seizure may start in the
thumb and spread to the entire hand and arm.
 The patient seldom loses consciousness, although the seizure may
secondarily progress to a generalized tonic-clonic seizure.
Neurological condition
Simple partial (sensory-type)
seizure
 Perception is distorted in a simple partial seizure.
 Symptoms can include hallucinations, flashing lights, tingling
sensations, a foul odour, vertigo, déjà vu (the feeling of having
experienced something before) or the opposite feeling—something
seems unfamiliar even though it is familiar in some way (called
jamais vu).
Complex partial (psychomotor
or temporal lobe) seizure
 Includes purposeless behaviour
 The patient may experience an aura and exhibit overt signs,
including a glassy stare, picking at his clothes, aimless wandering,
lip-smacking or chewing motions, and unintelligible speech.
 The seizure may last for a few seconds or as long as 20 minutes.
Neurological condition
Generalized seizures
 Generalized seizures cause a generalized electrical
abnormality in the brain.
 They include several distinct types, including absence
(petit mal), myoclonic, generalized tonic-clonic (grand
mal), and akinetic.
Absence (petit mal) seizure
 An absence seizure commonly occurs in children but also may affect
adults.
 It usually begins with a brief change in the level of consciousness,
indicated by blinking or rolling of the eyes, a blank stare, and slight
mouth movements. The patient retains his posture and continues
pressurise activity without difficulty.
 seizure lasts from 1 to 10 seconds.
Myoclonic seizure
 A myoclonic seizure—also
called bilateral massive
epileptic myoclonus
 Involuntary muscular jerks
of the body or extremities,
which may occur in a
rhythmic manner, and a brief
loss of consciousness
Generalized tonic-clonic (grand mal)
seizure
 Begins with a loud cry, precipitated by air rushing from the lungs through the
vocal cords.
 The patient falls to the ground, losing consciousness. The body stiffens (tonic
phase) and then alternates between episodes of muscle spasm and relaxation
(clonic phase).
 Tongue biting, incontinence, labored breath- ing, apnea, and subsequent
cyanosis may also occur. The seizure stops in 2 to 5 minutes, when abnormal
electrical conduction of the neurons is completed. The patient then regains
consciousness but is somewhat confused and may have difficulty talking. If he
can talk, he may complain of drowsiness, fatigue, headache, muscle soreness,
and arm or leg weakness. He may fall into a deep sleep after the seizure
Neurological condition
Akinetic seizure
 An akinetic seizure is characterized by a general loss of postural tone
and a temporary loss of consciousness.
 This type of seizure occurs in young children. Sometimes it’s called a
drop attack because it causes the child to fall.
Neurological condition
Management
 Anticonvulsants
• Blockers of repetitive activation of the sodium channel:
Phenytoin, carbamazepine, oxcarbazepine, eslicarbazepine, lamotrigine,
topiramate
• Enhancers of slow inactivation of the sodium channel:
Lacosamide, rufinamide
• Gamma-aminobutyric acid (GABA)–A receptor enhancers:
Phenobarbital, benzodiazepines, clobazam
• N -methyl-D-aspartic acid (NMDA) receptor blockers: Felbamate
• Alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid
(AMPA) receptor blockers: Perampanel, topiramate
• T-calcium channel blockers: Ethosuximide, valproate
• N- and L-calcium channel blockers: Lamotrigine, topiramate, zonisamide,
valproate
• H-current modulators: Gabapentin, lamotrigine
• Blockers of unique binding sites: Gabapentin, levetiracetam, perampanel
• Carbonic anhydrase inhibitors: Topiramate, zonisamide
• Neuronal potassium channel (KCNQ [Kv7]) opener: Ezogabine
Other Potential treatment therapies
 Vagus nerve stimulation
 Ketogenic diet
 Deep brain stimulation
 Responsive neurostimulation
 Continuous stimulation of the seizure onset zone (subthreshold
stimulation)
 Minimally invasive surgery
 Stereotactic laser ablation or radiosurgery
Surgical Approaches
 Hemispherectomy
 corpus callosotomy
Nursing management
(Assessment)
 Obtain seizure history, including prodromal signs and symptoms, seizure
behavior, postictal state, history of status epilepticus.
 Document the following about seizure activity
 Circumstances before attack, such as visual, auditory, olfactory, or
tactile stimuli; emotional or psychological disturbances; sleep;
hyperventilation
 Description of movement, including where movement or stiffness
started; type of movement and parts involved; progression of
movement; whether beginning of seizure was witnessed
 Position of the eyes and head; size of pupils
 Presence of automatisms, such as lip smacking or repeated swallowing
 Incontinence of urine or feces
 Duration of each phase of the attack
 Presence of unconsciousness and its duration
 Behavior after attack, including inability to speak, any weakness or
paralysis (Todd’s paralysis), sleep
 Investigate the psychosocial effect of seizures.
 Obtain history of drug or alcohol abuse.
 Assess compliance and medication-taking strategies.
Nursing Diagnosis
 Ineffective breathing pattern related to neuromuscular impairment
secondary to prolonged tonic phase of seizure or during postictal
period as evidenced by abnormal respiratory rate, rhythm, and or
depth
 Ineffective Tissue Perfusion (cerebral) related to seizure activity.
 Risk for Injury related to seizure activity
 Ineffective Coping related to psychosocial and economic
consequences of epilepsy
Status Epilepticus
 Status epilepticus is a series of generalised seizures that occur without
full recovery of consciousness between attacks.
 The term has been broadened to include continous clinical or electrical
seizures (on EEG ) lasting atleast 30 minutes, even without impairment
of consciousness.
 It is considered as medical emergency.
 Vigourous muscular contractions impose on a heavy metabolic demand
and can interfere with respirations. Repeated episodes of cerebral
anoxia and edema may lead to irreversible and fatal brain damage.
Spinal Cord Injuries
Spinal cord Injuries
 A spinal cord injury (SCI) is damage to the spinal cord that
causes changes in its function, either temporary or permanent.
These changes translate into loss of muscle function, sensation,
or autonomic function in parts of the body served by the spinal cord
below the level of the lesion.
 There are approximately 12,000 new cases of spinal cord injury
each year in the United States.
 They are most common in white males.
Types of SCI
 Incomplete spinal cord injuries: With incomplete injuries, the cord is
only partially severed, allowing the injured person to retain some
function. In these cases, the degree of function depends on the extent of
the injuries.
 Complete spinal cord injuries: By contrast, complete injuries occur
when the spinal cord is fully severed, eliminating function. Though, with
treatment and physical therapy, it may be possible to regain some
function.
Neurological condition
Incomplete/Partial Spinal Cord Injuries
Anterior cord syndrome
 Injury to the front of
the spinal cord,
damages the motor and
sensory pathways in
the spinal cord.
Sensation may return,
but struggle with
movement.
Central cord syndrome
 Injury to the central of the cord, and
damages nerves that carry signals from the
brain to the spinal cord. Loss of fine motor
skills, paralysis of the arms, and partial
impairment—usually less pronounced—in
the legs are common. Some survivors also
suffer a loss of bowel or bladder control, or
lose the ability to sexually function.
Posterior cord syndrome
 Posterior cord syndrome is damage to the posterior
gray and white matter of the spinal cord; it usually
results from an extension injury and impairs vibratory
sensation, light touch (motor function, pain, and
temperature sensation remain intact)
Brown-Sequard syndrome
 Damage to one side of the
spinal cord. The injury may
be more pronounced on one
side of the body; for
instance, movement may be
impossible on the right side,
but may be fully retained on
the left.
Horner syndrome
 It occur as part of Brown-
Séquard syndrome or result
from damage to the midbrain
and causes anhidrosis (lack
of sweat), ptosis, and
pupillary contraction on the
affected side of the face
Complete Spinal cord Injuries
 Tetraplegia: damage to the cervical spinal cord, producing varying
degrees of paralysis of all limbs. Sometimes known as quadriplegia,
tetraplegia
 Paraplegia: Injury to lower half of the body, including the legs. These
injuries are the product of damage to the thoracic spinal cord.
 Triplegia: Triplegia causes loss of sensation and movement in one arm
and both legs, and is typically the product of an incomplete spinal cord
injury.
 Hemiplegia: It is a form of paralysis that affects just one side of the
body, often just one arm and one leg
Neurological condition
Neurological condition
 Injuries below the lumbar spinal cord do not typically produce symptoms
of paralysis or loss of sensation.
 They can produce nerve pain, reduce function in some areas of the body
 Injuries to the sacral spinal cord can interfere with bowel and bladder
function, cause sexual problems, and produce weakness in the hips or
legs.
Etiology
 Motor vehicle accidents- Auto and motorcycle accidents are the leading cause of
spinal cord injuries, accounting for almost half of new spinal cord injuries each year.
 Falls-A spinal cord injury after age 65 is most often caused by a fall. Overall, falls
cause more than 15 percent of spinal cord injuries.
 Acts of violence- Around 12 percent of spinal cord injuries result from violent
encounters, often involving gunshot and knife wounds.
 Sports and recreation injuries- Athletic activities, such as impact sports and diving
in shallow water, cause about 10 percent of spinal cord injuries.
 Alcohol- Alcohol use is a factor in about 1 out of every 4 spinal cord injuries.
 Diseases- Cancer, arthritis, osteoporosis and inflammation of the spinal cord also can
cause spinal cord injuries.
Risk factors
 Being male. Spinal cord injuries affect a disproportionate amount of men. In
fact, females account for only about 20 percent of traumatic spinal cord injuries
in the United States.
 Being older than 65. Falls cause most injuries in older adults.
 Engaging in risky behavior. Diving into too-shallow water or playing sports
without wearing the proper safety gear or taking proper precautions can lead to
spinal cord injuries. Motor vehicle crashes are the leading cause of spinal cord
injuries for people under 65.
 Having a bone or joint disorder. A relatively minor injury can cause a spinal
cord injury if you have another disorder that affects your bones or joints, such
as arthritis or osteoporosis.
Signs and symptoms
 Difficulty in breathing
 Problems with bladder and
bowel function
 Bedsores
 Chronic pain
 Headaches
 Changes in mood or personality
 Loss of libido or sexual function
 Loss of fertility
 Nerve pain
 Chronic muscle pain
 Pneumonia
Diagnosis
 History and Physical Examination
 Radiological Imaging- CT scans, MRI
 EMG
 Myelography
Level of spinal cord injury
 C-1 to C-3: Tetraplegia with total loss of muscular/respiratory function.
 C-4 to C-5: Tetraplegia with impairment, reduced pulmonary capacity, complete
dependency for ADLs.
 C-6 to C-7: Tetraplegia with some arm/hand movement allowing some
independence in ADLs.
 C-7 to T-1: Tetraplegia with limited use of thumb/fingers, increasing
independence.
 T-2 to L-1: Paraplegia with intact arm function and varying function of intercostal
and abdominal muscles.
 L-1 to L-2 or below: Mixed motor-sensory loss; bowel and bladder dysfunction.
Complications
Spinal Shock
 Spinal shock is caused by sudden, severe spinal cord damage and initially
produces flaccid paralysis; areflexia below the level of the lesion and loss
of cutaneous and proprioceptive sensations occur in the first few hours
and may last for weeks
 Recovery occurs over time; reflex activity returns in 3 to 6 weeks; flexion
spasms affect paralyzed limbs 6 to 16 weeks after injury.
Autonomic dysreflexia
 Autonomic dysreflexia is a complication of complete spinal cord injury
 Injury occurring at the T8 level
 It is a clinical emergency and is caused by stimulation of the autonomic reflexes below
the level of the lesion
 It causes decreased heart rate, pallor, pilomotor spasm (goose bumps and hair
erection), and severe, persistent hypertension, blotchy skin, diaphoresis, flushing,
nasal congestion, pounding headache, and vasodilation above the lesion
 It can be precipitated by various sensory stimuli, including a full bladder or rectum,
painful stimuli (such as pressure on the skin, pressure ulcers, and surgical incisions),
other skin stimulation (such as pressure on the glans penis or perianal or periurethral
area), and visceral contractions (such as bladder spasms and uterine contractions of
pregnancy)
Pathophysiology
 Injury results from primary & secondary insults
 Primary injury occurs at the time of the traumatic insult
 Secondary injury occurs over hours to days as a result of a complex
inflammatory process, vascular changes and intracellular calcium changes
leading to oedema and ischemia of the spinal cord. Irreversible damage
occurs to nerve cells leading to permanent disability
 Spinal cord injury may occur without evidence of bony injury on Xray or
CT. Injuries are more commonly associated with injury to ligaments discs
and growth plates
Management
Emergency care
 Airway management - The cervical spine must be maintained in neutral
alignment at all times
 clearing of oral secretions and/or debris is essential to maintaining airway
patency and preventing aspiration
 Hypotension - May be hemorrhagic and/or neurogenic in acute spinal cord
injury
 Neurogenic shock - Judicious fluid replacement with isotonic crystalloid
solution to a maximum of 2 L is the initial treatment of choice
 Maintain adequate oxygenation and perfusion of the injured spinal cord,
supplemental oxygenation and/or mechanical ventilation may be required
 Head injuries - Amnesia, external signs of head injury or basilar skull fracture,
focal neurologic deficits, associated alcohol intoxication or drug abuse, or a
history of loss of consciousness mandates a thorough evaluation for intracranial
injury, starting with non-contrast head CT scanning
 Ileus - Placement of a nasogastric (NG) tube is essential
 Antiemetics should be used.
 Pressure sores - To prevent pressure sores, turn the patient every 1-2 hours,
pad all extensor surfaces, undress the patient to remove belts and back pocket
keys or wallets, and remove the spine board as soon as possible
 Pulmonary management
 Treatment of pulmonary complications and/or injury in patients with
spinal cord injury includes supplementary oxygen for all patients and
chest tube thoracostomy for those with pneumothorax and/or
hemothorax.
 Surgical decompression
 Emergent decompression of the spinal cord is suggested in the setting of
acute spinal cord injury with progressive neurologic deterioration, facet
dislocation, or bilateral locked facets.
 To prevent further injury, the spine is immobilized with a cervical collar, cervical traction or
cervical tongs
 A steroid is administered for the first 24 hours after the injury to reduce edema and inflammatory
response
 An analgesic and an opioid may be administered to control pain
 A muscle relaxant is given to reduce muscle spasm
 An antacid and an antihistamine are given to prevent gastric ulcers (traumatic events, such as
spinal cord injury, can precipitate gastric ulcer formation)
 Anticoagulant therapy is initiated to prevent deep vein thrombosis; therapy may include low doses
of heparin, thigh-high antiembolism stockings (which compress superficial veins and prevent
periph- eral blood pooling), and sequential pneumatic compression devices (which massage the
veins, mimic muscle action, and prevent peripheral blood pooling and thrombus formation)
 Rehabilitative management includes surgical release of tendons for
persistent muscle spasm of paralyzed muscles and surgical correction for
cervical support (laminectomy and spinal fusions)
 Rehabilitation referrals include those for occupational and physical
therapies, nutritional counseling, social services, and psychiatric
evaluation and assistance
Nursing Management
 Risk for Ineffective Breathing Pattern
 Risk for Trauma
 Impaired Physical Mobility r/t Limitation in independent, purposeful
physical movement of the body or of one or more extremities
 Acute Pain r/t tissue damage
 Constipation r/t change in activity levels
 Impaired Urinary Elimination r/t disturbance in urinary pattern
 Risk for Autonomic Dysreflexia
 Risk for Impaired Skin Integrity r/t pressure ulcers
 Deficient Knowledge r/t disease condition
 Risk for Disuse Syndrome—paralysis/mechanical immobilization.
 Autonomic Dysreflexia—bladder/bowel distension, skin irritation, lack of
caregiver knowledge.
 Self-Care deficit—neuromuscular impairment, decreased strength/endurance,
pain, depression.
 Nutrition: imbalanced risk for—dysfunctional eating pattern,
excessive/inadequate intake in relation to metabolic need.
 Role Performance, ineffective/Sexual dysfunction—situational crisis and
transition, altered body function.
 Interrupted Family Process—situational crisis and transition.
References
 http://nursingcrib.com/pathophysiology/increased-intracranial-pressure/
 http://www.umm.edu/ency/article/000793all.htm
 http://en.wikipedia.org/wiki/Intracranial_pressure
 http://cncplan.blogspot.com/2012/06/nursing-intervention-for-icp-increased.html
 image courtesy of ADAM via
http://assets0.scripps.org/encyclopedia/graphics/images/en/9453.jpg
 https://amy47.com/quick-notes/neuro-nursing-diagnosis/#comment-92
 https://www.rnpedia.com/nursing-notes/medical-surgical-nursing-
notes/increased-intracranial-pressure/
Thank You
Neurological Infections
Meningitis
Meningitis
 Meningitis is an inflammation of the subarachnoid space
and meninges
 It can be classified as septic (caused by bacterial
infection) or aseptic (caused by viral infection) Exudate
formation causes meningeal irritation and increased ICP
Types of Meningitis
 Bacterial Meningitis
 Viral Meningitis
 Fungal Meningitis
 Amebic Meningitis
 Parasitic Meningitis
 Non Infectious Meningitis
Viral Meningitis
 Viral Meningitis-Viral meningitis is the most common type of
meningitis. Viruses in the Enterovirus (Non Polio) category cause 85
percent of cases. These are more common during the summer and fall,
and they include:
 coxsackievirus A, coxsackievirus B, echoviruses
 Other viruses can cause meningitis. These include:
 West Nile virus, influenza, mumps, HIV, measles, herpes viruses,
Coltivirus, which causes Colorado tick fever.
Bacterial Meningitis
 Bacterial Meningitis-Bacterial meningitis is contagious and caused by infection from certain
bacteria. It’s fatal if left untreated. Between 5 to 40 percent of children and 20 to 50 percent of
adults with this condition die. This is true even with proper treatment.
 The most common types of bacteria that cause bacterial meningitis are:
 Streptococcus pneumoniae, which is typically found in the respiratory tract, sinuses, and
nasal cavity and can cause “pneumococcal meningitis”
 Neisseria meningitidis, which is spread through saliva and other respiratory fluids and
causes “meningococcal meningitis”
 Haemophilus influenza, which can cause not only meningitis but infection of the blood,
inflammation of the windpipe, cellulitis, and infectious arthritis
 Listeria monocytogenes, which is a foodborne bacteria
 Tuberculous meningitis is a bacterial infection caused by Mycobacterium tuberculosis; it’s
generally self-limiting and benign
Fungal Meningitis
 Fungal meningitis is rare and usually caused by fungus spreading through
blood to the spinal cord. Although anyone can get fungal meningitis,
people with weakened immune systems, like those with an HIV infection
or cancer, are at increased risk.
 The most common cause of fungal meningitis for people with weak
immune systems is Cryptococcus. This disease is one of the most
common causes of adult meningitis in Africa
 Parasites can cause a rare form of meningitis called eosinophilic meningitis,
eosinophilic meningoencephalitis, or EM, with increased levels of
eosinophils (a type of white blood cell) in the fluid around the brain and spinal
cord (the cerebrospinal fluid; CSF). EM also can be caused by other types of
infections (not just by parasites) and can have non-infectious causes, such as
medications.
 The three main parasites that cause EM in some infected people are:
 Angiostrongylus cantonensis (neurologic angiostrongyliasis)
 Baylisascaris procyonis (baylisascariasis; neural larva migrans)
 Gnathostoma spinigerum (neurognathostomiasis)
Amebic Meningitis
 Primary amebic meningoencephalitis (PAM) is a very rare form of
parasitic meningitis that causes a brain infection that is usually fatal. PAM
is caused by the microscopic ameba (a single-celled living
organism) Naegleria fowleri when water containing the ameba enters the
body through the nose.
Non-Infectious Meningitis
Non–infectious meningitis causes include:
 Cancers
 Systemic lupus erythematosus (lupus)
 Certain drugs
 Head injury
 Brain surgery
This type of meningitis is not spread from person to person.
Clinical Manifestations
In Adults
 Fever
 Headache
 Stiff neck
 Sensitivity to bright light
 Sleepiness or trouble waking up
from sleep
 Nausea
 Vomiting
 Lack of appetite
 Lethargy (a lack of energy)
 Nausea
 Vomiting
 Photophobia (increased sensitivity
to light)
 Altered mental status (confusion)
 Positive Kernig and Brudzinski’s
Signs
In Newborns and infants may show these signs:
 High fever
 Constant crying
 Excessive sleepiness or irritability
 Inactivity or sluggishness
 Poor feeding
 A bulge in the soft spot on top of a baby's head (fontanel)
 Stiffness in a baby's body and neck
Complications
 Hearing loss
 Memory difficulty
 Learning disabilities
 Brain damage
 Gait problems
 Seizures
 Kidney failure
 Shock
 Death
Diagnostic Tests
 Blood cultures. Blood samples are placed in a special dish to see if it grows
microorganisms, particularly bacteria. A sample may also be placed on a slide
and stained (Gram's stain), then studied under a microscope for bacteria.
 Imaging. Computerized tomography (CT) or magnetic resonance (MR) scans
of the head may show swelling or inflammation. X-rays or CT scans of the
chest or sinuses may also show infection in other areas that may be
associated with meningitis.
 Spinal tap (lumbar puncture). For a definitive diagnosis of meningitis,
you'll need a spinal tap to collect cerebrospinal fluid (CSF). In people with
meningitis, the CSF often shows a low sugar (glucose) level along with an
increased white blood cell count and increased protein.
Management
 Bacterial meningitis must be treated immediately with intravenous
antibiotics and, more recently, corticosteroids. This helps to ensure recovery
and reduce the risk of complications, such as brain swelling and seizures.
 Symptomatic Management
 Viral Meningitis- Antibiotics can't cure viral meningitis, and most cases
improve on their own in several weeks. Treatment of mild cases of viral
meningitis usually includes:
 Bed rest
 Plenty of fluids
 Over-the-counter pain medications to help reduce fever and relieve body
aches
 Antifungal medications treat fungal meningitis and a combination of
specific antibiotics can treat tuberculous meningitis.
 Noninfectious meningitis due to allergic reaction or autoimmune disease
may be treated with corticosteroids. In some cases no treatment may
be required, because the condition can resolve on its own. Cancer-
related meningitis requires therapy for the individual cancer.
Nursing Management (Diagnosis)
 Ineffective cerebral tissue perfusion r/t increased ICP and cerebral
edema
 Altered Thermoregulation (Hyperthermia) r/t infection
 Acute pain and discomfort r/t meningeal irritation
 Decreased sensory perceptions r/t altered level of consciousness
 Deficient of Knowledge r/t disease condition
Nursing Interventions
◆ Perform neurologic examinations, and check vital signs hourly; early
detection of increased ICP, hyperthermia, hydrocephalus, and shock can
help prevent complications
◆ Implement isolation techniques if the causative agent is highly
contagious; bacterial meningitis is transmitted by direct and sometimes
indirect contact with respiratory droplets from infected people and carriers
◆ Monitor fluid intake and output to prevent overhydration, which can
lead to cerebral edema and increased ICP
◆ Provide nutritional support to maintain immune response and fluid and
electrolyte balance; enteral feedings may be required
◆ Provide proper positioning, skin care, and ROM exercises to prevent
complications of immobility, such as contracture deformities, muscle
wasting, pneumonia, and pressure ulcers
◆ Provide a comfortable, quiet, dimly lit environment to help prevent
seizures and to reduce the dis- comfort of photophobia
◆ Give emotional support to the patient and family
Brain Abscess
 A brain abscess is a collection of pus, immune cells, and other material
in the brain, usually from a bacterial or fungal infection. brain abscess is
a collection of pus, immune cells, and other material in the brain,
usually from a bacterial or fungal infection.
Risk Factors
 A compromised immune system due to HIV or AIDS
 Cancer and other chronic illnesses
 Congenital heart disease
 Major head injury or skull fracture
 Meningitis
 Immunosuppressant drugs, such as those used in chemotherapy
 Chronic sinus or middle ear infections
Clinical Manifestations
Symptoms usually develop slowly over several weeks, but they can also
come on suddenly. Symptoms you should watch for are:
 Differences in mental processes, such as increased confusion, decreased
responsiveness, and irritability
 Decreased speech
 Decreased sensation
 Decreased movement due to loss of muscle function
 Changes in vision
 Changes in personality or behavior
 Vomiting
 Fever
 Chills
 Neck stiffness, especially when it occurs with fevers and chills
 Sensitivity to light
In babies and young children, most of the symptoms are similar. However, your
child may show other symptoms of a brain abscess. The soft spot on top of your
baby’s head, called the fontanelle, may be swollen or bulging. Other symptoms in
children can include:
 Projectile vomiting
 High-pitched crying
 Spasticity in the limbs
Diagnostic Evaluation
 History of infections
 CBC- Elevated WBCs
 EEG
 A chest x-ray to determine whether there is a lung infection
 Imaging scans, such as an MRI or a CT scan, in which an abscess
will show up as one or more spots
 A CT-guided aspiration, a type of needle biopsy in which a sample
of pus is taken for analysis.
Prevention
 To prevent brain abscess, otitis media, mastoiditis,
rhinosinusitis, dental infections, and systemic infections
should be treated promptly.
Management
 The goal is to eliminate the abscess.
 Treatment modalities include antimicrobial therapy, surgical
incision, or aspiration (CTguided stereotactic needle).
 Medications used include corticosteroids to reduce the
inflammatory cerebral edema and antiseizure medications for
prophylaxis against seizures (phenytoin, phenobarbital).
 Abscess resolution is monitored with CT scans.
Nursing Management
 Nursing interventions should support the medical treatment, as do patient
teaching activities that address neurosurgical procedures.
 Patients and families need to be advised of neurologic deficits that may remain
after treatment (hemiparesis, seizures, visual deficits, and cranial nerve palsies).
 Frequently assess neurologic status, especially LOC, speech and sensorimotor
and cranial nerve functions.
 WOF signs of increased ICP: decreased LOC, vomiting, abnormal pupil response
and depressed respirations.
 The nurse assesses the family’s ability to express their distress at the patient’s
condition, cope with the patient’s illness and deficits, and obtain support.
 Always provide safety measures.
Encephalitis
 Encephalitis is an acute inflammation (swelling) of the brain usually
resulting from either a viral infection or due to the body's own immune
system mistakenly attacking brain tissue.
 The most common cause is a viral infection. The brain becomes inflamed
as a result of the body's attempt to fight off the virus.
 Encephalitis generally begins with fever and headache. The symptoms
rapidly worsen, and there may be seizures (fits), confusion, drowsiness,
and loss of consciousness, and even coma.
Neurological condition
Types
Different types of encephalitis have different causes.
 Japanese encephalitis is spread by mosquitoes
 Tick-borne encephalitis is spread by ticks
 Rabies can be spread through a bite from a mammal
 There is also primary or secondary encephalitis.
 Primary or infectious encephalitis can result if a fungus, virus, or bacterium
infects the brain.
 Secondary, or post-infectious, encephalitis is when the immune system responds
to a previous infection and mistakenly attacks the brain.
Causes
 Encephalitis can develop as a result of a direct infection to the brain by a virus,
bacterium, or fungus, or when the immune system responds to a previous infection
Primary (infectious) encephalitis can be split into three main categories of
viruses:
 Common viruses, including HSV (herpes simplex virus) and EBV (Epstein-Barr virus)
 Childhood viruses, including measles and mumps
 Arboviruses (spread by mosquitoes, ticks, and other insects), including Japanese
encephalitis, West Nile encephalitis, and tick-borne encephalitis
Secondary encephalitis: could be caused by a complication of a viral infection.
Symptoms start to appear days or even weeks after the initial infection. The patient's
immune system treats healthy brain cells as foreign organisms and attacks them
Signs and Symptoms
 The patient typically has a fever, headache, and photophobia (excessive
sensitivity to light). There may also be general weakness and seizures.
Less common symptoms
 The individual may also experience nuchal rigidity (neck stiffness), which can
lead to a misdiagnosis of meningitis. There may be stiffness of the limbs, slow
movements, and clumsiness. The patient may also be drowsy and have a
cough.
 In serious cases headaches, nausea, vomiting, confusion, disorientation,
memory loss, speech problems, hearing problems, hallucinations, as well as
seizures and possibly coma may occur. In some cases, the patient can
become aggressive
In infants and young children, signs and symptoms might also include:
 Bulging in the soft spots (fontanels) of an infant's skull
 Nausea and vomiting
 Body stiffness
 Poor feeding or not waking for a feeding
 Irritability
Diagnostic Evaluation
 Brain imaging. MRI or CT images can reveal any swelling of the brain or another condition
that might be causing your symptoms, such as a tumor.
 Spinal tap (lumbar puncture). A needle inserted into your lower back removes
cerebrospinal fluid (CSF), the protective fluid that surrounds the brain and spinal column.
Changes in this fluid can indicate infection and inflammation in the brain. Sometimes samples
of CSF can be tested to identify the virus or other infectious agent.
 Other lab tests. Samples of blood, urine or excretions from the back of the throat can be
tested for viruses or other infectious agents.
 Electroencephalogram (EEG). Electrodes affixed to your scalp record the brain's electrical
activity. Certain abnormal patterns may indicate a diagnosis of encephalitis.
 Brain biopsy. Rarely, a small sample of brain tissue might be removed for testing. Brain
biopsy is usually done only if symptoms are worsening and treatments are having no effect.
Prevention
• Loss of memory - especially among those who had herpes simplex
virus encephalitis
• Behavioral or personality changes - such as mood swings, bouts of
frustration and anger, and anxiety
• Epilepsy
• Aphasia - language and speech problems
Management
 Bed rest
 Plenty of fluids
 Anti-inflammatory drugs — such as acetaminophen, ibuprofen— to relieve headaches
and fever
 Antiviral medications commonly used to treat encephalitis -Acyclovir (Zovirax)
 Breathing assistance, as well as careful monitoring of breathing and heart function
 Intravenous fluids to ensure proper hydration and levels of essential minerals
 Anti-inflammatory drugs, such as corticosteroids, to reduce swelling and pressure
within the skull
 Anticonvulsant medications, such as phenytoin (Dilantin), to stop or prevent seizures
Nursing Diagnosis
 Ineffective Cerebral Tissue Perfusion related to inflammatory
processes, increased ICP.
 Risk for injury related to disorientation, seizures, and the unfamiliar
environment.
 Altered thought processes related to changes in the level of
consciousness
 Imbalanced Nutrition: Less Than Body Requirements related to
anorexia, fatigue, nausea, and vomiting
 Acute pain related to irritation
Cranial Nerve Disorders
Trigeminal Neuralgia
Trigeminal neuralgia
 Trigeminal neuralgia is inflammation of the trigeminal nerve, causing
intense facial pain. It is also known as tic douloureax because the
intense pain can cause patients to contort their face into a grimace and
cause the head to move away from the pain. The obvious movement is
known as a tic.
 The pain of trigeminal neuralgia is intense and may be an isolated
episode or may be occur every few hours, minutes, or seconds.
Etiology
 Idiopathic
 There are some instances when the nerve can be compressed by
nearby blood vessels, aneurysms, or tumors.
 There are inflammatory causes of trigeminal neuralgia because of
systemic diseases including multiple sclerosis, sarcoidosis, and Lyme
disease. There also is an association with collagen vascular diseases
including scleroderma and systemic lupus erythematosus
Signs and Symptoms
 Episodes of severe, shooting or jabbing pain that may feel like an electric shock
 Spontaneous attacks of pain or attacks triggered by things such as touching the face, chewing,
speaking or brushing teeth
 Bouts of pain lasting from a few seconds to several minutes
 Episodes of several attacks lasting days, weeks, months or longer — some people have periods
when they experience no pain
 Constant aching, burning feeling that may occur before it evolves into the spasm-like pain of
trigeminal neuralgia
 Pain in areas supplied by the trigeminal nerve, including the cheek, jaw, teeth, gums, lips, or
less often the eye and forehead
 Pain affecting one side of the face at a time, though may rarely affect both sides of the face
 Pain focused in one spot or spread in a wider pattern
 Attacks that become more frequent and intense over time
Management
 Idiopathic trigeminal neuralgia most often is treated with good success using a
single anticonvulsant medication such as carbamazepine.
 Gabapentin, baclofen and phenytoin may be used as second line drugs, often in
addition to carbamazepine. In many patients, as time progresses,
carbamazepine becomes less effective and these drugs can be used in
combination to control the pain.
 Should pain persist and medication fail to be effective, surgery or radiation
therapy may be other treatment options.
 Lamotrigine may be prescribed for multiple sclerosis patients who develop
trigeminal neuralgia.
Nursing Diagnosis
 Pain (acute / chronic) r / t trigeminal nerve compression and inflammation of the
temporal artery.
 Imbalanced Nutrition : Less than Body Requirements r / t pain during chewing.
 Ineffective individual coping r / t severe pain, excessive threat to the self-alone.
 Knowledge Deficit: on the condition and needs medication r / t cognitive limitations.
 Anxiety r / t prognosis of disease and changes in health.
 Ineffective management of therapeutic regimen r / t less knowledge about the
prevention of stimulus triggers pain.
 Risk for injury to the eyes r / t the risk factors: possible reduction in corneal sensatio
Bell’s Palsy
 Bell’s palsy is a condition that causes a
temporary weakness or paralysis of the muscles
in the face. It can occur when the nerve that
controls your facial muscles becomes inflamed,
swollen, or compressed.
 The condition causes one side of your face to
droop or become stiff.
Etiology
 Bell's palsy occurs when the seventh cranial nerve becomes swollen or
compressed, resulting in facial weakness or paralysis. The exact cause of
this damage is unknown, but many medical researchers believe it’s most
likely triggered by a viral infection
The viruses that have been linked to the development of bell’s palsy include:
 Herpes simplex, which causes cold sores and genital herpes
 HIV, which damages the immune system
 Sarcoidosis, which causes organ inflammation
 Herpes zoster virus, which causes chickenpox and shingles
 Epstein-barr virus, which causes mononucleosis
Clinical Manifestations
 The symptoms of Bell’s palsy can develop one to two weeks after you
have a cold, ear infection, or eye infection. They usually appear abruptly,
 Bell’s palsy is marked by a droopy appearance on one side of the face
and the inability to open or close your eye on the affected side. In rare
cases, Bell’s palsy may affect both sides of the face.
Other signs and symptoms of Bell’s palsy include:
 Drooling
 Difficulty eating and drinking
 An inability to make facial expressions, such as smiling
or frowning
 Facial weakness
 Muscle twitches in the face
 Dry eye and mouth
 A headache
 Sensitivity to sound
Diagnostic Evaluation
 History
 Physical examination
 CT scan
 MRI
 EMG
Complications
 Misdirected re-growth of nerve fibers: Nerve fibers re-grow in an irregular way.
This can result in involuntary contractions of some muscles. A patient may
involuntarily close one eye when trying to smile. The problem might be the other way
round - when the person closes one eye, the side of the mouth lifts involuntarily.
 Ageusia: Chronic loss of taste.
 Gustatolacrimal reflex: Also known as crocodile tear syndrome. While the patient is
eating, their eye will shed tears. It eventually goes away. In some rare cases, the
problem can be longer lasting.
 Corneal ulceration: When eyelids cannot completely shut, the protective and
lubricating tear film of the eye may become ineffective. This can result in corneal
drying. The risk of corneal drying is even higher if Bell's palsy has also caused a
reduction in tear production. Corneal ulceration can result in infection of the cornea,
which can lead to severe loss of vision.
Management
 Corticosteroid drugs, which reduce inflammation
 Antiviral medication, which may be prescribed if a virus caused your bell’s palsy
 Over-the-counter pain medications, such as ibuprofen or acetaminophen, which can help
relieve mild pain
 Using eye drops and an eye patch (for your dry eye)
 Placing a warm, moist towel over your face to relieve pain
 Massaging your face
 Doing physical therapy exercises to stimulate your facial muscles
 Additional modalities may include electrical stimulation applied to the face to prevent muscle
atrophy, or surgical exploration of the facial nerve.
 Surgery may be performed if a tumor is suspected, for surgical decompression of the
facial nerve, and for surgical rehabilitation of a paralyzed face.
Nursing Diagnosis
 Body image disturbance related to alteration in
structure and function for vision secondary to Bell’s
Palsy
 Disturbed sensory perception: Visual
Nursing Management
 Patients need reassurance that a stroke has not occurred and that spontaneous recovery occurs
within 3 to 5 weeks in most patients. Teaching patients with Bell’s palsy to care for themselves at
home is an important nursing priority.
Teaching Eye Care
 Because the eye usually does not close completely, the blink reflex is diminished, so the eye
is vulnerable to injury from dust and foreign particles. Corneal irritation and ulceration may
occur. Distortion of the lower lid alters the proper drainage of tears. Key teaching points
include the following:
 Cover the eye with a protective shield at night.
 Apply eye ointment to keep eyelids closed during sleep.
 Close the paralyzed eyelid manually before going to sleep.
 Wear wrap around sunglasses or goggles to decrease normal evaporation from the eye.
Teaching About Maintaining Muscle Tone
 Show patient how to perform facial massage with gentle
 upward motion several times daily when the patient can tolerate the
massage.
 Demonstrate facial exercises, such as wrinkling the forehead,
 blowing out the cheeks, and whistling, in an effort to prevent muscle
atrophy.
 Instruct patient to avoid exposing the face to cold and drafts
Neurological condition

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Neurological condition

  • 2. Neurological Dysfunction  Neurological Dysfunction refers to a disorder of the Central Nervous System and affects the efficiency of brain processes.  It includes-  Increased Intracranial Pressure  Headache  Seizure  Epilepsy
  • 3. Intracranial Pressure  Refers to the pressure contained within the cranial cavity.  The normal range is between 5 to 15 mmHg.  ICP over 20 mm/Hg is considered elevated ICP, also known as intracranial hypertension.
  • 4.  Factors that influence ICP  Arterial pressure  Venous pressure  Intra-abdominal and intra-thoracic pressure  Posture  Temperature  Blood gases (CO2 levels)  The degree to which these factors  ICP depends on the ability of the brain to accommodate to the changes
  • 5.  Skull has three essential components: - Brain tissue = 78% or 1400g - Blood = 12% or 75ml - Cerebrospinal fluid (CSF) = 10% or 75ml  Any increase in any of these tissues causes increased ICP  These three components of the cranial vault maintain a state of equilibrium. Their pressure and volume determine the condition of balance.
  • 6. Monro-Kellie Hypothesis  The pressure–volume relationship between ICP, volume of CSF, blood, and brain tissue, and cerebral perfusion pressure (CPP) is known as the Monro–Kellie doctrine or the Monro–Kellie hypothesis.  The Monro–Kellie hypothesis states that the cranial compartment is incompressible and that the volume inside the cranium is fixed. The cranium and its constituents (blood, CSF, and brain tissue) create a state of volume equilibrium, such that any increase in volume of one of the cranial constituents must be compensated by a decrease in volume of another
  • 7. Regulation and Maintenance of ICP If the volume in any one of the components (brain tissue, blood, and CSF) increases within the cranial vault and the volume from another component is displaced, the total intracranial volume will not change. Normal compensatory adaptations Alteration of CSF absorption or production Displacement of CSF into spinal subarachnoid space Shunting of venous blood out of the skull
  • 8. Causes of Increase ICP  Intracranial hemorrhage  Traumatic brain injury  Ruptured aneurysm  Arteriovenous malformation  Other vascular anomalies  Central nervous system infections  Neoplasm  Vasculitis  Ischemic infarcts  Hydrocephalus  Pseudotumor cerebri Sustained increases in ICP result in brainstem compression and herniation of the brain from one compartment to another
  • 9. Precipitating Factors Several factors may increase ICP:  Cerebral edema resulting from infection  Intracranial or subarachnoid bleeding  Brain tumor
  • 11. Complications  Death  Permanent neurological problems  Reversible neurological problems  Seizures  Stroke
  • 12. Clinical Manifestations  An altered LOC is usually the earliest sign of increased ICP  The patient may exhibit partial or total loss of motor and sensory function  Pupillary changes may occur, such as unequal size, constriction, dilation, or reduced or absent responses to light  Cushing’s triad (bradycardia, bradypnea, and hypertension)is a late sign of increased ICP  Other signs and symptoms include changes in respiratory patterns, headache, seizures, vomiting, and a widening pulse pressure
  • 13. Assessment and Diagnostic Tools  Detailed history and Physical examination  CT scan  Skull X-rays  ICP monitoring
  • 16. Sites of ICP Monitoring  Subarachanoid  Intraventricular  Epidural
  • 17. Management  The goal of treatment is to normalize ICP and avoid complications  Pressures are carefully monitored by means of epidural monitoring, subarachnoid screw and bolt, or intraventricular monitoring  CSF blockage is corrected by surgical placement of shunts  Drug therapy may include an antibiotic, an anticonvulsant, and a diuretics.  Hyperventilation therapy  Metabolic disorders are corrected  Lumbar puncture is contraindicated in a patient with increased ICP because it can cause life- threatening herniation (shifting of brain contents into another compartment)
  • 18. Nursing Management: Assessment  Change in level of consciousness  Changes in vital signs (Cushing triad)  Ocular signs  Headache-Often continuous and worse in the morning  Vomiting- No nausea and Projectile  Decrease in motor strength and function  Assess movement and response to stimuli  Assess for Decerebrate posturing (extensor) & Decorticate posturing (flexor)
  • 22. Nursing Diagnosis  Ineffective Tissue Perfusion (cerebral) related to increased ICP as evidenced by decreased LOC, sluggish pupil response, papilledema, and posturing  Keep head of bed slightly elevated and the head in midline (straight). For clients with a basal skull fracture, keep bed flat.  Limit movement, space essential nursing tasks, and reduce or eliminate environmental stimuli (e.g., loud noise, bright lights).  Avoid extreme hip flexion.  Keep client quiet. Change position with assistance and use a turning sheet. Avoid range-of-motion (ROM) exercises until ICP approaches normal unless ordered otherwise by the physician.  Administer reduced fluid volumes at an even rate for 24 hours. Give diuretics as prescribed; note client's response to therapy.
  • 23.  Hyperventilate the mechanically ventilated client briefly according to medical orders.  Suction the airway only when necessary.  Give 100% oxygen before and after suctioning when it is required.  Keep suctioning brief, without exceeding 10-15 seconds per pass of the catheter.  Administer a prescribed stool softener.  Ensure that a gastric tube used for decompression or nourishment remains patent.  Administer prescribed medications if vomiting or persistent coughing occur.
  • 24.  Risk for Ineffective Breathing Pattern and Ineffective Airway Clearance related to diminished LOC and herniation of the brain stem secondary to increased ICP  Attach a pulse oximeter to the finger, earlobe, bridge of the nose, or toe.  Insert an oral airway if client is comatose.  Administer prescribed oxygen.  For mechanically ventilated clients, ensure that the ventilator delivers the prescribed tidal volume at the ordered rate.  Suction when necessary to clear tracheal secretions or keep endotracheal tube patent.
  • 25.  Risk for Infection related to impaired skin and tissue integrity secondary to surgery, invasive diagnostic or monitoring procedures, or original head injury  Keep wounds clean and dry.  Use aseptic technique when handling any part of the intracranial monitoring device or changing a dressing applied after surgery.  Administer antibiotic therapy, if prescribed.
  • 26.  Risk for Impaired Skin Integrity related to low capillary blood flow secondary to pressure and inactivity  Tilt or turn client from side to side every 2 hours.  Avoid friction by using a lift sheet.  Use a pressure-relieving mattress or mechanical bed for clients whose position cannot be readily changed.  Keep skin clean and dry.
  • 27.  Self-Care Deficit (total or specify type) related to diminished LOC as manifested by inability to follow directions and impaired neuromuscular function  Give client complete care, including bathing, oral care, nutrition, and elimination, until ICP is normal and client can resume these activities independently.
  • 28.  Impaired Verbal Communication related to decreased LOC or endotracheal intubation as evidenced by an inability to speak  Look for grimacing or moaning.  Correct problems that may be causing discomfort, such as a wrinkled sheet or an object pressing on the skin.  Provide paper and pencil or a magic slate if client is alert but intubated.
  • 29. Headache/Cephalgia  Headache is pain in any region of the head. Headaches may occur on one or both sides of the head, be isolated to a certain location, radiate across the head from one point.  A headache may appear as a sharp pain, a throbbing sensation or a dull ache. Headaches can develop gradually or suddenly, and may last from less than an hour to several days.
  • 31.  According to WHO Migraine Tension type Cluster Medication over use
  • 32. Primary Headaches  90% of all headaches are primary headaches.  Primary headaches usually first start when people are between 20 and 40 years old  Migraines typically present with pulsing head pain, nausea, photophobia (sensitivity to light) and phonophobia (sensitivity to sound).  Tension-type headaches usually present with non-pulsing "bandlike" pressure on both sides of the head, not accompanied by other symptoms
  • 33.  Cluster headaches- short episodes (15–180 minutes) of severe pain, usually around one eye, with autonomic symptoms (tearing, red eye, nasal congestion) which occur at the same time every day. Cluster headaches can be treated with triptans and prevented with prednisone, ergotamine or lithium.  Trigeminal neuralgia or occipital neuralgia: shooting face pain  Hemicrania continua: continuous unilateral pain with episodes of severe pain. Hemicrania continua can be relieved by the medication indomethacin.  Primary stabbing headache: recurrent episodes of stabbing "ice pick pain" or "jabs and jolts" for 1 second to several minutes without autonomic symptoms (tearing, red eye, nasal congestion). These headaches can be treated with indomethacin.
  • 34.  Primary cough headache: starts suddenly and lasts for several minutes after coughing, sneezing or straining (anything that may increase pressure in the head).  Primary exertional headache: throbbing, pulsatile pain which starts during r after exercising, lasting for 5 minutes to 24 hours.  Primary sex headache: dull, bilateral headache that starts during sexual activity and becomes much worse during orgasm  Hypnic headache: moderate-severe headache that starts a few hours after falling asleep and lasts 15–30 minutes.
  • 35. Secondary Headaches  Headaches may be caused by problems elsewhere in the head or neck. Some of these are not harmful, such as cervicogenic headache (pain arising from the neck muscles). Medication overuse headache may occur in those using excessive painkillers for headaches, paradoxically causing worsening headaches  Meningitis: inflammation of the meninges which presents with fever and meningismus, or stiff neck  Bleeding inside the brain (intracranial hemorrhage)  Subarachnoid hemorrhage (acute, severe headache, stiff neck WITHOUT fever)
  • 36.  Ruptured aneurysm, arteriovenous malformation, intraparenchymal hemorrhage (headache only)  Brain tumor: dull headache, worse with exertion and change in position, accompanied by nausea and vomiting. Often, the person will have nausea and vomiting for weeks before the headache starts  Temporal arteritis: inflammatory disease of arteries common in the elderly (average age 70) with fever, headache, weight loss, jaw claudication, tender vessels by the temples, polymyalgia rheumatica  Acute closed angle glaucoma (increased pressure in the eyeball): headache that starts with eye pain, blurry vision, associated with nausea and vomiting. On physical exam, the person will have a red eye and a fixed, mid dilated pupil.
  • 37.  Post-ictal headaches: Headaches that happen after a convulsion or other type of seizure, as part of the period after the seizure (the post- ictal state)  Gastrointestinal disorders may cause headaches, including Helicobacter pylori infection, celiac disease, irritable bowel syndrome, inflammatory bowel disease, gastroparesis, and hepatobiliary disorders.
  • 44. Diagnosis of Headaches  Most headaches can be diagnosed by the clinical history alone. If the symptoms described by the person sound dangerous, further testing with neuroimaging or lumbar puncture may be necessary. Electroencephalography (EEG) is not useful for headache diagnosis  The first step to diagnosing a headache is to determine if the headache is old or new.  A "new headache" can be a headache that has started recently, or a chronic headache that has changed character  For example, if a person has chronic weekly headaches with pressure on both sides of his head, and then develops a sudden severe throbbing headache on one side of his head, they have a new headache.
  • 45. Red flag  It can be challenging to differentiate between low-risk, benign headaches and high-risk, dangerous headaches since symptoms are often similar. Headaches that are possibly dangerous require further lab tests and imaging to diagnose.  The American College for Emergency Physicians published criteria for low-risk headaches. They are as follows:  age younger than 30 years  features typical of primary headache  history of similar headache  no abnormal findings on neurologic exam  no concerning change in normal headache pattern  no high-risk comorbid conditions (for example, HIV)  no new concerning history or physical examination findings
  • 46. The American Headache Society recommends using "SSNOOP", a mnemonic to remember the red flags for identifying a secondary headache:  Systemic symptoms (fever or weight loss)  Systemic disease (HIV infection, malignancy)  Neurologic symptoms or signs  Onset sudden (thunderclap headache)  Onset after age 40 years  Previous headache history (first, worst, or different headache)
  • 47. Management  Pharmacological-The main classes of drugs to treat headache disorders include: analgesics, anti-emetics, specific anti-migraine medications, and prophylactic medications  Behavioural Treatments-Massages,relaxation training, Meditation, lying down in a dark and quiet room, hot or cold compresses on the head and neck and sometimes cognitive behavioural therapy.  Diversional Therapies- Guided Imagery, Aroma therapy  Lifestyle changes- Avoid skipping meals, limit alcohol and caffeinated beverages.
  • 48.  Complementary therapies- Acupressure, acupuncture, reflexology, use of several herbs and supplements like-  ginger  vitamin B2  magnesium supplements  fish oil
  • 49. Nursing Management (Diagnosis) 1. Acute pain r/t stress and tension, irritation / nerve pressure, vasospasm, increased intracranial pressures. 2. Ineffective individual coping r/t situations of crisis, personal vulnerability, not adequate support systems, work overload, inadequate relaxation, severe pain, excessive threat to himself. 3. Deficient knowledge : about the condition and treatment needs r/t lack of recall, did not know the information, cognitive limitations
  • 52. Terminology  Seizures-A seizure is an abnormal electrical discharge that occurs in your brain. Usually brain cells, or neurons, flow in an organized fashion along the surface of your brain. A seizure occurs when there is an excess of electrical activity.  Seizure Disorder-A seizure disorder is a medical condition (one of about 40) characterized by episodes of uncontrolled electrical activity in the brain, thus producing symptoms that include two or more seizures.  Convulsions-An abnormal, involuntary contraction of the muscles. A person having convulsions appears to be shaking rapidly and without control  Tremors- An involuntary (unintentional) rhythmic movement of muscles of limb(s). It’s usually due to an anomaly in the motor part (movement controlling part) of the brain.
  • 53. Seizure Disorder  Definition- Seizures are episodes of abnormal motor, sensory, autonomic or psychic activity (or combination of these) that result from sudden excessive discharge from cerebral neurons
  • 54. Etiology  The underlying cause is an electrical disturbance( dysrhythmia) in the nerve cells in one section of the brain: these cells emit abnormal, recurring, uncontrolled electrical discharges  The specific causes of seizures are varied and can be categorized as idiopathic (genetic, developmental defects) and acquired.  Cerebrovascular diseases  Hypoxemia  Fever (childhood)  Head Injury  Hypertension  CNS Infections
  • 55.  Metabolic and toxic conditions (Renal failure, hyponatremia, hypocalcemia, hypoglycemia, pesticide exposure)  Brain tumors  Drug and alcohol withdrawal  Allergies
  • 56. Clinical Manifestations  Associated loss of consciousness, excess movement or loss of muscle tone or movement, and disturbances of behaivour, mood, sensation, and perception may also occur.
  • 57. Epilepsy  The term “epilepsy” refers to recurrent, unprovoked seizures from known or unknown causes. The term “ictus” describes the period in which the seizure occurs, and the term “postictal” refers to the period after the seizure has ended but before the patient has returned to his or her baseline mental status.
  • 59. Partial seizures Partial seizures arise from a localized area in the brain and cause specific symptoms. Partial seizures include simple partial (Jacksonian motor- type and sensory-type), complex partial (psychomotor or temporal lobe), and secondarily generalized partial seizures.
  • 60. Simple partial(Jacksonian motor-type)  A simple partial seizure begins as a localized motor seizure, which is characterized by a spread of abnormal activity to adjacent areas of the brain.  Stiffening or jerking in one extremity, accompanied by a tingling sensation in the same area. For example, the seizure may start in the thumb and spread to the entire hand and arm.  The patient seldom loses consciousness, although the seizure may secondarily progress to a generalized tonic-clonic seizure.
  • 62. Simple partial (sensory-type) seizure  Perception is distorted in a simple partial seizure.  Symptoms can include hallucinations, flashing lights, tingling sensations, a foul odour, vertigo, déjà vu (the feeling of having experienced something before) or the opposite feeling—something seems unfamiliar even though it is familiar in some way (called jamais vu).
  • 63. Complex partial (psychomotor or temporal lobe) seizure  Includes purposeless behaviour  The patient may experience an aura and exhibit overt signs, including a glassy stare, picking at his clothes, aimless wandering, lip-smacking or chewing motions, and unintelligible speech.  The seizure may last for a few seconds or as long as 20 minutes.
  • 65. Generalized seizures  Generalized seizures cause a generalized electrical abnormality in the brain.  They include several distinct types, including absence (petit mal), myoclonic, generalized tonic-clonic (grand mal), and akinetic.
  • 66. Absence (petit mal) seizure  An absence seizure commonly occurs in children but also may affect adults.  It usually begins with a brief change in the level of consciousness, indicated by blinking or rolling of the eyes, a blank stare, and slight mouth movements. The patient retains his posture and continues pressurise activity without difficulty.  seizure lasts from 1 to 10 seconds.
  • 67. Myoclonic seizure  A myoclonic seizure—also called bilateral massive epileptic myoclonus  Involuntary muscular jerks of the body or extremities, which may occur in a rhythmic manner, and a brief loss of consciousness
  • 68. Generalized tonic-clonic (grand mal) seizure  Begins with a loud cry, precipitated by air rushing from the lungs through the vocal cords.  The patient falls to the ground, losing consciousness. The body stiffens (tonic phase) and then alternates between episodes of muscle spasm and relaxation (clonic phase).  Tongue biting, incontinence, labored breath- ing, apnea, and subsequent cyanosis may also occur. The seizure stops in 2 to 5 minutes, when abnormal electrical conduction of the neurons is completed. The patient then regains consciousness but is somewhat confused and may have difficulty talking. If he can talk, he may complain of drowsiness, fatigue, headache, muscle soreness, and arm or leg weakness. He may fall into a deep sleep after the seizure
  • 70. Akinetic seizure  An akinetic seizure is characterized by a general loss of postural tone and a temporary loss of consciousness.  This type of seizure occurs in young children. Sometimes it’s called a drop attack because it causes the child to fall.
  • 72. Management  Anticonvulsants • Blockers of repetitive activation of the sodium channel: Phenytoin, carbamazepine, oxcarbazepine, eslicarbazepine, lamotrigine, topiramate • Enhancers of slow inactivation of the sodium channel: Lacosamide, rufinamide • Gamma-aminobutyric acid (GABA)–A receptor enhancers: Phenobarbital, benzodiazepines, clobazam • N -methyl-D-aspartic acid (NMDA) receptor blockers: Felbamate
  • 73. • Alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor blockers: Perampanel, topiramate • T-calcium channel blockers: Ethosuximide, valproate • N- and L-calcium channel blockers: Lamotrigine, topiramate, zonisamide, valproate • H-current modulators: Gabapentin, lamotrigine • Blockers of unique binding sites: Gabapentin, levetiracetam, perampanel • Carbonic anhydrase inhibitors: Topiramate, zonisamide • Neuronal potassium channel (KCNQ [Kv7]) opener: Ezogabine
  • 74. Other Potential treatment therapies  Vagus nerve stimulation  Ketogenic diet  Deep brain stimulation  Responsive neurostimulation  Continuous stimulation of the seizure onset zone (subthreshold stimulation)  Minimally invasive surgery  Stereotactic laser ablation or radiosurgery
  • 76. Nursing management (Assessment)  Obtain seizure history, including prodromal signs and symptoms, seizure behavior, postictal state, history of status epilepticus.  Document the following about seizure activity  Circumstances before attack, such as visual, auditory, olfactory, or tactile stimuli; emotional or psychological disturbances; sleep; hyperventilation  Description of movement, including where movement or stiffness started; type of movement and parts involved; progression of movement; whether beginning of seizure was witnessed
  • 77.  Position of the eyes and head; size of pupils  Presence of automatisms, such as lip smacking or repeated swallowing  Incontinence of urine or feces  Duration of each phase of the attack  Presence of unconsciousness and its duration  Behavior after attack, including inability to speak, any weakness or paralysis (Todd’s paralysis), sleep  Investigate the psychosocial effect of seizures.  Obtain history of drug or alcohol abuse.  Assess compliance and medication-taking strategies.
  • 78. Nursing Diagnosis  Ineffective breathing pattern related to neuromuscular impairment secondary to prolonged tonic phase of seizure or during postictal period as evidenced by abnormal respiratory rate, rhythm, and or depth  Ineffective Tissue Perfusion (cerebral) related to seizure activity.  Risk for Injury related to seizure activity  Ineffective Coping related to psychosocial and economic consequences of epilepsy
  • 79. Status Epilepticus  Status epilepticus is a series of generalised seizures that occur without full recovery of consciousness between attacks.  The term has been broadened to include continous clinical or electrical seizures (on EEG ) lasting atleast 30 minutes, even without impairment of consciousness.  It is considered as medical emergency.  Vigourous muscular contractions impose on a heavy metabolic demand and can interfere with respirations. Repeated episodes of cerebral anoxia and edema may lead to irreversible and fatal brain damage.
  • 81. Spinal cord Injuries  A spinal cord injury (SCI) is damage to the spinal cord that causes changes in its function, either temporary or permanent. These changes translate into loss of muscle function, sensation, or autonomic function in parts of the body served by the spinal cord below the level of the lesion.  There are approximately 12,000 new cases of spinal cord injury each year in the United States.  They are most common in white males.
  • 82. Types of SCI  Incomplete spinal cord injuries: With incomplete injuries, the cord is only partially severed, allowing the injured person to retain some function. In these cases, the degree of function depends on the extent of the injuries.  Complete spinal cord injuries: By contrast, complete injuries occur when the spinal cord is fully severed, eliminating function. Though, with treatment and physical therapy, it may be possible to regain some function.
  • 85. Anterior cord syndrome  Injury to the front of the spinal cord, damages the motor and sensory pathways in the spinal cord. Sensation may return, but struggle with movement.
  • 86. Central cord syndrome  Injury to the central of the cord, and damages nerves that carry signals from the brain to the spinal cord. Loss of fine motor skills, paralysis of the arms, and partial impairment—usually less pronounced—in the legs are common. Some survivors also suffer a loss of bowel or bladder control, or lose the ability to sexually function.
  • 87. Posterior cord syndrome  Posterior cord syndrome is damage to the posterior gray and white matter of the spinal cord; it usually results from an extension injury and impairs vibratory sensation, light touch (motor function, pain, and temperature sensation remain intact)
  • 88. Brown-Sequard syndrome  Damage to one side of the spinal cord. The injury may be more pronounced on one side of the body; for instance, movement may be impossible on the right side, but may be fully retained on the left.
  • 89. Horner syndrome  It occur as part of Brown- Séquard syndrome or result from damage to the midbrain and causes anhidrosis (lack of sweat), ptosis, and pupillary contraction on the affected side of the face
  • 90. Complete Spinal cord Injuries  Tetraplegia: damage to the cervical spinal cord, producing varying degrees of paralysis of all limbs. Sometimes known as quadriplegia, tetraplegia  Paraplegia: Injury to lower half of the body, including the legs. These injuries are the product of damage to the thoracic spinal cord.  Triplegia: Triplegia causes loss of sensation and movement in one arm and both legs, and is typically the product of an incomplete spinal cord injury.  Hemiplegia: It is a form of paralysis that affects just one side of the body, often just one arm and one leg
  • 93.  Injuries below the lumbar spinal cord do not typically produce symptoms of paralysis or loss of sensation.  They can produce nerve pain, reduce function in some areas of the body  Injuries to the sacral spinal cord can interfere with bowel and bladder function, cause sexual problems, and produce weakness in the hips or legs.
  • 94. Etiology  Motor vehicle accidents- Auto and motorcycle accidents are the leading cause of spinal cord injuries, accounting for almost half of new spinal cord injuries each year.  Falls-A spinal cord injury after age 65 is most often caused by a fall. Overall, falls cause more than 15 percent of spinal cord injuries.  Acts of violence- Around 12 percent of spinal cord injuries result from violent encounters, often involving gunshot and knife wounds.  Sports and recreation injuries- Athletic activities, such as impact sports and diving in shallow water, cause about 10 percent of spinal cord injuries.  Alcohol- Alcohol use is a factor in about 1 out of every 4 spinal cord injuries.  Diseases- Cancer, arthritis, osteoporosis and inflammation of the spinal cord also can cause spinal cord injuries.
  • 95. Risk factors  Being male. Spinal cord injuries affect a disproportionate amount of men. In fact, females account for only about 20 percent of traumatic spinal cord injuries in the United States.  Being older than 65. Falls cause most injuries in older adults.  Engaging in risky behavior. Diving into too-shallow water or playing sports without wearing the proper safety gear or taking proper precautions can lead to spinal cord injuries. Motor vehicle crashes are the leading cause of spinal cord injuries for people under 65.  Having a bone or joint disorder. A relatively minor injury can cause a spinal cord injury if you have another disorder that affects your bones or joints, such as arthritis or osteoporosis.
  • 96. Signs and symptoms  Difficulty in breathing  Problems with bladder and bowel function  Bedsores  Chronic pain  Headaches  Changes in mood or personality  Loss of libido or sexual function  Loss of fertility  Nerve pain  Chronic muscle pain  Pneumonia
  • 97. Diagnosis  History and Physical Examination  Radiological Imaging- CT scans, MRI  EMG  Myelography
  • 98. Level of spinal cord injury  C-1 to C-3: Tetraplegia with total loss of muscular/respiratory function.  C-4 to C-5: Tetraplegia with impairment, reduced pulmonary capacity, complete dependency for ADLs.  C-6 to C-7: Tetraplegia with some arm/hand movement allowing some independence in ADLs.  C-7 to T-1: Tetraplegia with limited use of thumb/fingers, increasing independence.  T-2 to L-1: Paraplegia with intact arm function and varying function of intercostal and abdominal muscles.  L-1 to L-2 or below: Mixed motor-sensory loss; bowel and bladder dysfunction.
  • 99. Complications Spinal Shock  Spinal shock is caused by sudden, severe spinal cord damage and initially produces flaccid paralysis; areflexia below the level of the lesion and loss of cutaneous and proprioceptive sensations occur in the first few hours and may last for weeks  Recovery occurs over time; reflex activity returns in 3 to 6 weeks; flexion spasms affect paralyzed limbs 6 to 16 weeks after injury.
  • 100. Autonomic dysreflexia  Autonomic dysreflexia is a complication of complete spinal cord injury  Injury occurring at the T8 level  It is a clinical emergency and is caused by stimulation of the autonomic reflexes below the level of the lesion  It causes decreased heart rate, pallor, pilomotor spasm (goose bumps and hair erection), and severe, persistent hypertension, blotchy skin, diaphoresis, flushing, nasal congestion, pounding headache, and vasodilation above the lesion  It can be precipitated by various sensory stimuli, including a full bladder or rectum, painful stimuli (such as pressure on the skin, pressure ulcers, and surgical incisions), other skin stimulation (such as pressure on the glans penis or perianal or periurethral area), and visceral contractions (such as bladder spasms and uterine contractions of pregnancy)
  • 101. Pathophysiology  Injury results from primary & secondary insults  Primary injury occurs at the time of the traumatic insult  Secondary injury occurs over hours to days as a result of a complex inflammatory process, vascular changes and intracellular calcium changes leading to oedema and ischemia of the spinal cord. Irreversible damage occurs to nerve cells leading to permanent disability  Spinal cord injury may occur without evidence of bony injury on Xray or CT. Injuries are more commonly associated with injury to ligaments discs and growth plates
  • 102. Management Emergency care  Airway management - The cervical spine must be maintained in neutral alignment at all times  clearing of oral secretions and/or debris is essential to maintaining airway patency and preventing aspiration  Hypotension - May be hemorrhagic and/or neurogenic in acute spinal cord injury  Neurogenic shock - Judicious fluid replacement with isotonic crystalloid solution to a maximum of 2 L is the initial treatment of choice  Maintain adequate oxygenation and perfusion of the injured spinal cord, supplemental oxygenation and/or mechanical ventilation may be required
  • 103.  Head injuries - Amnesia, external signs of head injury or basilar skull fracture, focal neurologic deficits, associated alcohol intoxication or drug abuse, or a history of loss of consciousness mandates a thorough evaluation for intracranial injury, starting with non-contrast head CT scanning  Ileus - Placement of a nasogastric (NG) tube is essential  Antiemetics should be used.  Pressure sores - To prevent pressure sores, turn the patient every 1-2 hours, pad all extensor surfaces, undress the patient to remove belts and back pocket keys or wallets, and remove the spine board as soon as possible
  • 104.  Pulmonary management  Treatment of pulmonary complications and/or injury in patients with spinal cord injury includes supplementary oxygen for all patients and chest tube thoracostomy for those with pneumothorax and/or hemothorax.  Surgical decompression  Emergent decompression of the spinal cord is suggested in the setting of acute spinal cord injury with progressive neurologic deterioration, facet dislocation, or bilateral locked facets.
  • 105.  To prevent further injury, the spine is immobilized with a cervical collar, cervical traction or cervical tongs  A steroid is administered for the first 24 hours after the injury to reduce edema and inflammatory response  An analgesic and an opioid may be administered to control pain  A muscle relaxant is given to reduce muscle spasm  An antacid and an antihistamine are given to prevent gastric ulcers (traumatic events, such as spinal cord injury, can precipitate gastric ulcer formation)  Anticoagulant therapy is initiated to prevent deep vein thrombosis; therapy may include low doses of heparin, thigh-high antiembolism stockings (which compress superficial veins and prevent periph- eral blood pooling), and sequential pneumatic compression devices (which massage the veins, mimic muscle action, and prevent peripheral blood pooling and thrombus formation)
  • 106.  Rehabilitative management includes surgical release of tendons for persistent muscle spasm of paralyzed muscles and surgical correction for cervical support (laminectomy and spinal fusions)  Rehabilitation referrals include those for occupational and physical therapies, nutritional counseling, social services, and psychiatric evaluation and assistance
  • 107. Nursing Management  Risk for Ineffective Breathing Pattern  Risk for Trauma  Impaired Physical Mobility r/t Limitation in independent, purposeful physical movement of the body or of one or more extremities  Acute Pain r/t tissue damage  Constipation r/t change in activity levels  Impaired Urinary Elimination r/t disturbance in urinary pattern  Risk for Autonomic Dysreflexia  Risk for Impaired Skin Integrity r/t pressure ulcers  Deficient Knowledge r/t disease condition
  • 108.  Risk for Disuse Syndrome—paralysis/mechanical immobilization.  Autonomic Dysreflexia—bladder/bowel distension, skin irritation, lack of caregiver knowledge.  Self-Care deficit—neuromuscular impairment, decreased strength/endurance, pain, depression.  Nutrition: imbalanced risk for—dysfunctional eating pattern, excessive/inadequate intake in relation to metabolic need.  Role Performance, ineffective/Sexual dysfunction—situational crisis and transition, altered body function.  Interrupted Family Process—situational crisis and transition.
  • 109. References  http://nursingcrib.com/pathophysiology/increased-intracranial-pressure/  http://www.umm.edu/ency/article/000793all.htm  http://en.wikipedia.org/wiki/Intracranial_pressure  http://cncplan.blogspot.com/2012/06/nursing-intervention-for-icp-increased.html  image courtesy of ADAM via http://assets0.scripps.org/encyclopedia/graphics/images/en/9453.jpg  https://amy47.com/quick-notes/neuro-nursing-diagnosis/#comment-92  https://www.rnpedia.com/nursing-notes/medical-surgical-nursing- notes/increased-intracranial-pressure/
  • 113. Meningitis  Meningitis is an inflammation of the subarachnoid space and meninges  It can be classified as septic (caused by bacterial infection) or aseptic (caused by viral infection) Exudate formation causes meningeal irritation and increased ICP
  • 114. Types of Meningitis  Bacterial Meningitis  Viral Meningitis  Fungal Meningitis  Amebic Meningitis  Parasitic Meningitis  Non Infectious Meningitis
  • 115. Viral Meningitis  Viral Meningitis-Viral meningitis is the most common type of meningitis. Viruses in the Enterovirus (Non Polio) category cause 85 percent of cases. These are more common during the summer and fall, and they include:  coxsackievirus A, coxsackievirus B, echoviruses  Other viruses can cause meningitis. These include:  West Nile virus, influenza, mumps, HIV, measles, herpes viruses, Coltivirus, which causes Colorado tick fever.
  • 116. Bacterial Meningitis  Bacterial Meningitis-Bacterial meningitis is contagious and caused by infection from certain bacteria. It’s fatal if left untreated. Between 5 to 40 percent of children and 20 to 50 percent of adults with this condition die. This is true even with proper treatment.  The most common types of bacteria that cause bacterial meningitis are:  Streptococcus pneumoniae, which is typically found in the respiratory tract, sinuses, and nasal cavity and can cause “pneumococcal meningitis”  Neisseria meningitidis, which is spread through saliva and other respiratory fluids and causes “meningococcal meningitis”  Haemophilus influenza, which can cause not only meningitis but infection of the blood, inflammation of the windpipe, cellulitis, and infectious arthritis  Listeria monocytogenes, which is a foodborne bacteria  Tuberculous meningitis is a bacterial infection caused by Mycobacterium tuberculosis; it’s generally self-limiting and benign
  • 117. Fungal Meningitis  Fungal meningitis is rare and usually caused by fungus spreading through blood to the spinal cord. Although anyone can get fungal meningitis, people with weakened immune systems, like those with an HIV infection or cancer, are at increased risk.  The most common cause of fungal meningitis for people with weak immune systems is Cryptococcus. This disease is one of the most common causes of adult meningitis in Africa
  • 118.  Parasites can cause a rare form of meningitis called eosinophilic meningitis, eosinophilic meningoencephalitis, or EM, with increased levels of eosinophils (a type of white blood cell) in the fluid around the brain and spinal cord (the cerebrospinal fluid; CSF). EM also can be caused by other types of infections (not just by parasites) and can have non-infectious causes, such as medications.  The three main parasites that cause EM in some infected people are:  Angiostrongylus cantonensis (neurologic angiostrongyliasis)  Baylisascaris procyonis (baylisascariasis; neural larva migrans)  Gnathostoma spinigerum (neurognathostomiasis)
  • 119. Amebic Meningitis  Primary amebic meningoencephalitis (PAM) is a very rare form of parasitic meningitis that causes a brain infection that is usually fatal. PAM is caused by the microscopic ameba (a single-celled living organism) Naegleria fowleri when water containing the ameba enters the body through the nose.
  • 120. Non-Infectious Meningitis Non–infectious meningitis causes include:  Cancers  Systemic lupus erythematosus (lupus)  Certain drugs  Head injury  Brain surgery This type of meningitis is not spread from person to person.
  • 121. Clinical Manifestations In Adults  Fever  Headache  Stiff neck  Sensitivity to bright light  Sleepiness or trouble waking up from sleep  Nausea  Vomiting  Lack of appetite  Lethargy (a lack of energy)  Nausea  Vomiting  Photophobia (increased sensitivity to light)  Altered mental status (confusion)  Positive Kernig and Brudzinski’s Signs
  • 122. In Newborns and infants may show these signs:  High fever  Constant crying  Excessive sleepiness or irritability  Inactivity or sluggishness  Poor feeding  A bulge in the soft spot on top of a baby's head (fontanel)  Stiffness in a baby's body and neck
  • 123. Complications  Hearing loss  Memory difficulty  Learning disabilities  Brain damage  Gait problems  Seizures  Kidney failure  Shock  Death
  • 124. Diagnostic Tests  Blood cultures. Blood samples are placed in a special dish to see if it grows microorganisms, particularly bacteria. A sample may also be placed on a slide and stained (Gram's stain), then studied under a microscope for bacteria.  Imaging. Computerized tomography (CT) or magnetic resonance (MR) scans of the head may show swelling or inflammation. X-rays or CT scans of the chest or sinuses may also show infection in other areas that may be associated with meningitis.  Spinal tap (lumbar puncture). For a definitive diagnosis of meningitis, you'll need a spinal tap to collect cerebrospinal fluid (CSF). In people with meningitis, the CSF often shows a low sugar (glucose) level along with an increased white blood cell count and increased protein.
  • 125. Management  Bacterial meningitis must be treated immediately with intravenous antibiotics and, more recently, corticosteroids. This helps to ensure recovery and reduce the risk of complications, such as brain swelling and seizures.  Symptomatic Management  Viral Meningitis- Antibiotics can't cure viral meningitis, and most cases improve on their own in several weeks. Treatment of mild cases of viral meningitis usually includes:  Bed rest  Plenty of fluids  Over-the-counter pain medications to help reduce fever and relieve body aches
  • 126.  Antifungal medications treat fungal meningitis and a combination of specific antibiotics can treat tuberculous meningitis.  Noninfectious meningitis due to allergic reaction or autoimmune disease may be treated with corticosteroids. In some cases no treatment may be required, because the condition can resolve on its own. Cancer- related meningitis requires therapy for the individual cancer.
  • 127. Nursing Management (Diagnosis)  Ineffective cerebral tissue perfusion r/t increased ICP and cerebral edema  Altered Thermoregulation (Hyperthermia) r/t infection  Acute pain and discomfort r/t meningeal irritation  Decreased sensory perceptions r/t altered level of consciousness  Deficient of Knowledge r/t disease condition
  • 128. Nursing Interventions ◆ Perform neurologic examinations, and check vital signs hourly; early detection of increased ICP, hyperthermia, hydrocephalus, and shock can help prevent complications ◆ Implement isolation techniques if the causative agent is highly contagious; bacterial meningitis is transmitted by direct and sometimes indirect contact with respiratory droplets from infected people and carriers ◆ Monitor fluid intake and output to prevent overhydration, which can lead to cerebral edema and increased ICP
  • 129. ◆ Provide nutritional support to maintain immune response and fluid and electrolyte balance; enteral feedings may be required ◆ Provide proper positioning, skin care, and ROM exercises to prevent complications of immobility, such as contracture deformities, muscle wasting, pneumonia, and pressure ulcers ◆ Provide a comfortable, quiet, dimly lit environment to help prevent seizures and to reduce the dis- comfort of photophobia ◆ Give emotional support to the patient and family
  • 130. Brain Abscess  A brain abscess is a collection of pus, immune cells, and other material in the brain, usually from a bacterial or fungal infection. brain abscess is a collection of pus, immune cells, and other material in the brain, usually from a bacterial or fungal infection.
  • 131. Risk Factors  A compromised immune system due to HIV or AIDS  Cancer and other chronic illnesses  Congenital heart disease  Major head injury or skull fracture  Meningitis  Immunosuppressant drugs, such as those used in chemotherapy  Chronic sinus or middle ear infections
  • 132. Clinical Manifestations Symptoms usually develop slowly over several weeks, but they can also come on suddenly. Symptoms you should watch for are:  Differences in mental processes, such as increased confusion, decreased responsiveness, and irritability  Decreased speech  Decreased sensation  Decreased movement due to loss of muscle function  Changes in vision  Changes in personality or behavior
  • 133.  Vomiting  Fever  Chills  Neck stiffness, especially when it occurs with fevers and chills  Sensitivity to light In babies and young children, most of the symptoms are similar. However, your child may show other symptoms of a brain abscess. The soft spot on top of your baby’s head, called the fontanelle, may be swollen or bulging. Other symptoms in children can include:  Projectile vomiting  High-pitched crying  Spasticity in the limbs
  • 134. Diagnostic Evaluation  History of infections  CBC- Elevated WBCs  EEG  A chest x-ray to determine whether there is a lung infection  Imaging scans, such as an MRI or a CT scan, in which an abscess will show up as one or more spots  A CT-guided aspiration, a type of needle biopsy in which a sample of pus is taken for analysis.
  • 135. Prevention  To prevent brain abscess, otitis media, mastoiditis, rhinosinusitis, dental infections, and systemic infections should be treated promptly.
  • 136. Management  The goal is to eliminate the abscess.  Treatment modalities include antimicrobial therapy, surgical incision, or aspiration (CTguided stereotactic needle).  Medications used include corticosteroids to reduce the inflammatory cerebral edema and antiseizure medications for prophylaxis against seizures (phenytoin, phenobarbital).  Abscess resolution is monitored with CT scans.
  • 137. Nursing Management  Nursing interventions should support the medical treatment, as do patient teaching activities that address neurosurgical procedures.  Patients and families need to be advised of neurologic deficits that may remain after treatment (hemiparesis, seizures, visual deficits, and cranial nerve palsies).  Frequently assess neurologic status, especially LOC, speech and sensorimotor and cranial nerve functions.  WOF signs of increased ICP: decreased LOC, vomiting, abnormal pupil response and depressed respirations.  The nurse assesses the family’s ability to express their distress at the patient’s condition, cope with the patient’s illness and deficits, and obtain support.  Always provide safety measures.
  • 138. Encephalitis  Encephalitis is an acute inflammation (swelling) of the brain usually resulting from either a viral infection or due to the body's own immune system mistakenly attacking brain tissue.  The most common cause is a viral infection. The brain becomes inflamed as a result of the body's attempt to fight off the virus.  Encephalitis generally begins with fever and headache. The symptoms rapidly worsen, and there may be seizures (fits), confusion, drowsiness, and loss of consciousness, and even coma.
  • 140. Types Different types of encephalitis have different causes.  Japanese encephalitis is spread by mosquitoes  Tick-borne encephalitis is spread by ticks  Rabies can be spread through a bite from a mammal  There is also primary or secondary encephalitis.  Primary or infectious encephalitis can result if a fungus, virus, or bacterium infects the brain.  Secondary, or post-infectious, encephalitis is when the immune system responds to a previous infection and mistakenly attacks the brain.
  • 141. Causes  Encephalitis can develop as a result of a direct infection to the brain by a virus, bacterium, or fungus, or when the immune system responds to a previous infection Primary (infectious) encephalitis can be split into three main categories of viruses:  Common viruses, including HSV (herpes simplex virus) and EBV (Epstein-Barr virus)  Childhood viruses, including measles and mumps  Arboviruses (spread by mosquitoes, ticks, and other insects), including Japanese encephalitis, West Nile encephalitis, and tick-borne encephalitis Secondary encephalitis: could be caused by a complication of a viral infection. Symptoms start to appear days or even weeks after the initial infection. The patient's immune system treats healthy brain cells as foreign organisms and attacks them
  • 142. Signs and Symptoms  The patient typically has a fever, headache, and photophobia (excessive sensitivity to light). There may also be general weakness and seizures. Less common symptoms  The individual may also experience nuchal rigidity (neck stiffness), which can lead to a misdiagnosis of meningitis. There may be stiffness of the limbs, slow movements, and clumsiness. The patient may also be drowsy and have a cough.  In serious cases headaches, nausea, vomiting, confusion, disorientation, memory loss, speech problems, hearing problems, hallucinations, as well as seizures and possibly coma may occur. In some cases, the patient can become aggressive
  • 143. In infants and young children, signs and symptoms might also include:  Bulging in the soft spots (fontanels) of an infant's skull  Nausea and vomiting  Body stiffness  Poor feeding or not waking for a feeding  Irritability
  • 144. Diagnostic Evaluation  Brain imaging. MRI or CT images can reveal any swelling of the brain or another condition that might be causing your symptoms, such as a tumor.  Spinal tap (lumbar puncture). A needle inserted into your lower back removes cerebrospinal fluid (CSF), the protective fluid that surrounds the brain and spinal column. Changes in this fluid can indicate infection and inflammation in the brain. Sometimes samples of CSF can be tested to identify the virus or other infectious agent.  Other lab tests. Samples of blood, urine or excretions from the back of the throat can be tested for viruses or other infectious agents.  Electroencephalogram (EEG). Electrodes affixed to your scalp record the brain's electrical activity. Certain abnormal patterns may indicate a diagnosis of encephalitis.  Brain biopsy. Rarely, a small sample of brain tissue might be removed for testing. Brain biopsy is usually done only if symptoms are worsening and treatments are having no effect.
  • 145. Prevention • Loss of memory - especially among those who had herpes simplex virus encephalitis • Behavioral or personality changes - such as mood swings, bouts of frustration and anger, and anxiety • Epilepsy • Aphasia - language and speech problems
  • 146. Management  Bed rest  Plenty of fluids  Anti-inflammatory drugs — such as acetaminophen, ibuprofen— to relieve headaches and fever  Antiviral medications commonly used to treat encephalitis -Acyclovir (Zovirax)  Breathing assistance, as well as careful monitoring of breathing and heart function  Intravenous fluids to ensure proper hydration and levels of essential minerals  Anti-inflammatory drugs, such as corticosteroids, to reduce swelling and pressure within the skull  Anticonvulsant medications, such as phenytoin (Dilantin), to stop or prevent seizures
  • 147. Nursing Diagnosis  Ineffective Cerebral Tissue Perfusion related to inflammatory processes, increased ICP.  Risk for injury related to disorientation, seizures, and the unfamiliar environment.  Altered thought processes related to changes in the level of consciousness  Imbalanced Nutrition: Less Than Body Requirements related to anorexia, fatigue, nausea, and vomiting  Acute pain related to irritation
  • 150. Trigeminal neuralgia  Trigeminal neuralgia is inflammation of the trigeminal nerve, causing intense facial pain. It is also known as tic douloureax because the intense pain can cause patients to contort their face into a grimace and cause the head to move away from the pain. The obvious movement is known as a tic.  The pain of trigeminal neuralgia is intense and may be an isolated episode or may be occur every few hours, minutes, or seconds.
  • 151. Etiology  Idiopathic  There are some instances when the nerve can be compressed by nearby blood vessels, aneurysms, or tumors.  There are inflammatory causes of trigeminal neuralgia because of systemic diseases including multiple sclerosis, sarcoidosis, and Lyme disease. There also is an association with collagen vascular diseases including scleroderma and systemic lupus erythematosus
  • 152. Signs and Symptoms  Episodes of severe, shooting or jabbing pain that may feel like an electric shock  Spontaneous attacks of pain or attacks triggered by things such as touching the face, chewing, speaking or brushing teeth  Bouts of pain lasting from a few seconds to several minutes  Episodes of several attacks lasting days, weeks, months or longer — some people have periods when they experience no pain  Constant aching, burning feeling that may occur before it evolves into the spasm-like pain of trigeminal neuralgia  Pain in areas supplied by the trigeminal nerve, including the cheek, jaw, teeth, gums, lips, or less often the eye and forehead  Pain affecting one side of the face at a time, though may rarely affect both sides of the face  Pain focused in one spot or spread in a wider pattern  Attacks that become more frequent and intense over time
  • 153. Management  Idiopathic trigeminal neuralgia most often is treated with good success using a single anticonvulsant medication such as carbamazepine.  Gabapentin, baclofen and phenytoin may be used as second line drugs, often in addition to carbamazepine. In many patients, as time progresses, carbamazepine becomes less effective and these drugs can be used in combination to control the pain.  Should pain persist and medication fail to be effective, surgery or radiation therapy may be other treatment options.  Lamotrigine may be prescribed for multiple sclerosis patients who develop trigeminal neuralgia.
  • 154. Nursing Diagnosis  Pain (acute / chronic) r / t trigeminal nerve compression and inflammation of the temporal artery.  Imbalanced Nutrition : Less than Body Requirements r / t pain during chewing.  Ineffective individual coping r / t severe pain, excessive threat to the self-alone.  Knowledge Deficit: on the condition and needs medication r / t cognitive limitations.  Anxiety r / t prognosis of disease and changes in health.  Ineffective management of therapeutic regimen r / t less knowledge about the prevention of stimulus triggers pain.  Risk for injury to the eyes r / t the risk factors: possible reduction in corneal sensatio
  • 155. Bell’s Palsy  Bell’s palsy is a condition that causes a temporary weakness or paralysis of the muscles in the face. It can occur when the nerve that controls your facial muscles becomes inflamed, swollen, or compressed.  The condition causes one side of your face to droop or become stiff.
  • 156. Etiology  Bell's palsy occurs when the seventh cranial nerve becomes swollen or compressed, resulting in facial weakness or paralysis. The exact cause of this damage is unknown, but many medical researchers believe it’s most likely triggered by a viral infection The viruses that have been linked to the development of bell’s palsy include:  Herpes simplex, which causes cold sores and genital herpes  HIV, which damages the immune system  Sarcoidosis, which causes organ inflammation  Herpes zoster virus, which causes chickenpox and shingles  Epstein-barr virus, which causes mononucleosis
  • 157. Clinical Manifestations  The symptoms of Bell’s palsy can develop one to two weeks after you have a cold, ear infection, or eye infection. They usually appear abruptly,  Bell’s palsy is marked by a droopy appearance on one side of the face and the inability to open or close your eye on the affected side. In rare cases, Bell’s palsy may affect both sides of the face. Other signs and symptoms of Bell’s palsy include:  Drooling  Difficulty eating and drinking
  • 158.  An inability to make facial expressions, such as smiling or frowning  Facial weakness  Muscle twitches in the face  Dry eye and mouth  A headache  Sensitivity to sound
  • 159. Diagnostic Evaluation  History  Physical examination  CT scan  MRI  EMG
  • 160. Complications  Misdirected re-growth of nerve fibers: Nerve fibers re-grow in an irregular way. This can result in involuntary contractions of some muscles. A patient may involuntarily close one eye when trying to smile. The problem might be the other way round - when the person closes one eye, the side of the mouth lifts involuntarily.  Ageusia: Chronic loss of taste.  Gustatolacrimal reflex: Also known as crocodile tear syndrome. While the patient is eating, their eye will shed tears. It eventually goes away. In some rare cases, the problem can be longer lasting.  Corneal ulceration: When eyelids cannot completely shut, the protective and lubricating tear film of the eye may become ineffective. This can result in corneal drying. The risk of corneal drying is even higher if Bell's palsy has also caused a reduction in tear production. Corneal ulceration can result in infection of the cornea, which can lead to severe loss of vision.
  • 161. Management  Corticosteroid drugs, which reduce inflammation  Antiviral medication, which may be prescribed if a virus caused your bell’s palsy  Over-the-counter pain medications, such as ibuprofen or acetaminophen, which can help relieve mild pain  Using eye drops and an eye patch (for your dry eye)  Placing a warm, moist towel over your face to relieve pain  Massaging your face  Doing physical therapy exercises to stimulate your facial muscles  Additional modalities may include electrical stimulation applied to the face to prevent muscle atrophy, or surgical exploration of the facial nerve.  Surgery may be performed if a tumor is suspected, for surgical decompression of the facial nerve, and for surgical rehabilitation of a paralyzed face.
  • 162. Nursing Diagnosis  Body image disturbance related to alteration in structure and function for vision secondary to Bell’s Palsy  Disturbed sensory perception: Visual
  • 163. Nursing Management  Patients need reassurance that a stroke has not occurred and that spontaneous recovery occurs within 3 to 5 weeks in most patients. Teaching patients with Bell’s palsy to care for themselves at home is an important nursing priority. Teaching Eye Care  Because the eye usually does not close completely, the blink reflex is diminished, so the eye is vulnerable to injury from dust and foreign particles. Corneal irritation and ulceration may occur. Distortion of the lower lid alters the proper drainage of tears. Key teaching points include the following:  Cover the eye with a protective shield at night.  Apply eye ointment to keep eyelids closed during sleep.  Close the paralyzed eyelid manually before going to sleep.  Wear wrap around sunglasses or goggles to decrease normal evaporation from the eye.
  • 164. Teaching About Maintaining Muscle Tone  Show patient how to perform facial massage with gentle  upward motion several times daily when the patient can tolerate the massage.  Demonstrate facial exercises, such as wrinkling the forehead,  blowing out the cheeks, and whistling, in an effort to prevent muscle atrophy.  Instruct patient to avoid exposing the face to cold and drafts