NEUROPATHIES

Mrs. KEERTHANA.B
ASSISTANT PROFESSOR
MSN, PSG CON
 BELL’S PALSY

PERIPHERAL FACIAL PARALYSIS,

ACUTE BENIGN CRANIAL POLYNEURITIS
Definition
Bell’s Palsy is a disorder characterized by inflammation of the facial nerve
(CN III) on one side of the face in the absence of any other disease such as stroke.

It is an acute, Peripheral facial paresis.

Etiology

Viral infection such as Viral meningitis

Activation of herpes simplex virus (HSV1)

Associated with flu-like illness, headaches, chronic middle ear

infection, hypertension, diabetes, sarcoidosis, tumors, Lyme disease
and trauma.
Pathophysiology
Etiological factors

Inflammation

Pathophysiology
Edema

Ischemia

Demyelination of
Nerve

Pain, alteration in motor

and sensory function
 CLINICAL MANIFESTATION
Pain around and behind the ear
Fever
Tinnitus
Hearing deficit
Flaccidity of the affected side of the
face with drooping of the mouth
accompanied by drooling
Inability to close the eyelid with an
upward movement
Widened palpebral fissure
Flattening of the nasolabial fold
Inability to smile, frown or whistle
Decreased muscle tone may alter
chewing ability
Loss of tearing or excessive tearing
Lower eyelid to turn out
DIAGNOSTIC TEST

 Electromyography (Testing percutaneous nerve excitability)

 Management of Bell’s Palsy
Moist heat application

Gentle Massage

Electrical stimulation of the nerve

Exercises

Drug: Corticosteroids (Prednisone, tapered over two weeks period)

Acyclovir

Other antiviral agents: Valacyclovir, Famciclovir

 Nursing Management
Mild analgesics
Hot wet pack application
Good Nutrition
Oral Hygiene
Dark glasses
Artificial tears
Ointment and impermeable eye shield
Facial Sling
Reassurance
 GUILLAIN BARRE
SYNDROME
POSTINFECTIOUS POLYNEUROPATHY
ASCENDING POLYNEUROPATHIC PARALYSIS
GUILLAIN BARRE SYNDROME
DEFINITION

It is an acute, rapidly progressing and potentially fatal form of

polyneuritis.

It is characterized by ascending, symmetric paralysis that usually

affects cranial nerves and the peripheral nervous system
 ETIOLOGY

Immune system stimulation from a viral infection

Trauma
Surgery
Viral immunization
Campylobacter jejuni gastroenteritis
 PATHOPHYSIOLOGY
Cellular and Humoral immune mechanisms directed at the nerves

Demyelination , Edema and inflammation of affected nerves

Transmission of nerve impulses is stopped or slowed down

Muscles innervated by the damaged peripheral nerves undergo denervation and

atrophy

Remyelination occurs slowly neurologic function returns in a proximal to

distal pattern
 CLINICAL MANIFESTATION
Weakness of the lower extremities (occurs over hours to days to weeks peeks about fourteenth day)

Paresthesia

Hypotonia

Areflexia

Autonomic Nervous system dysfunction

 Orthostatic hypotension

 hypertension

 Abnormal vagal responses (Bradycardia heart block, asystole)

Bowel and bladder dysfunction

Facial flushing

Diaphoresis

Cranial nerve involvement (facial weakness, extraocular involvement

difficulties, dysphagia and paresthesia of face)
Pain (Paresthesia, muscular aches, cramps and hyperesthesia)
 DIAGNOSTIC STUDIES

History and Clinical signs

CSF normal at initial days

CSF Protein increases 7-10 days (Normal : 15 – 45 mg/dL)

EMG shows reduced nerve conduction velocity

 MANAGEMENT OF GBS

1. Plasmapheresis
2. IV administration high dose immunoglobulin
3. Corticosteroids
4. Airway Management (Ventilatory support)
NURSING MANAGEMENT
Assessment
Routine assessment
Monitor ascending paralysis
Assess respiratory function
Monitor ABG
Assess gag, swallowing and corneal reflexes
Monitor Blood pressure, cardiac rate and rhythm
Intervention
 Airway Management (may need ventilatory support)
 If fever develops, antibiotic therapy may be needed
 Nutritional needs (Enteral / Parenteral)
 Support and encouragement to patient and caregiver
TRIGEMINAL
NEURALGIA
DEFINITION
Trigeminal neuralgia is sudden, usually unilateral, severe, brief, stabbing, recurrent
episodes of pain in the distribution of the trigeminal nerve.

Epidemiology:

Twice common among women than men

Age over 40
ETIOLOGY
RISK FACTORS:
◦ Multiple Sclerosis

◦ Hypertension

Other Causes:
◦ Herpesvirus infection

◦ Infection of the teeth and Jaw

◦ Brain stem infarct

 PATHOPHYSIOLOGY
Trigeminal nerve is the fifth cranial nerve (CN V) has both motor and sensory
branches

Blood vessels especially the superior cerebellar artery, become compressed

Chronic irritation of the trigeminal nerve at the root entry zone

Increased firing of the afferent or sensory fibers

 CLINICAL MANIFESTATION
Paroxysms of excruciating pain described as a burning, knife-like, or lightning-like shock in
the lips, upper or lower gums, cheek, forehead, or side of the nose.
Intense pain, twitching, grimacing and frequent blinking and tearing of the eye occur during
the acute attack.
The attacks are usually brief, lasting only seconds to 2-3 minutes and are generally
unilateral.
Occurs several times a day or weeks or months apart
Clustering (Cycle of pain and refractoriness).
Triggered by mechanism of light touch
Precipitating stimuli include chewing, tooth brushing, feeling a hot or cold blast of air on the
face, washing the face, yawning or even talking.
 DIAGNOSTIC STUDIES

Neurologic assessment

Computed tomography (CT Scan)

Magnetic Resonance Imaging (MRI)

To rule out any lesions (MS), tumors or vascular abnormalities.
MANGEMENT OF TRIGEMINAL NEURALGIA
DRUG THERAPY:
◦ Antiseizure drug (reduce pain by stabilizing neuronal membrane and block
nerve firing)
◦ Carbamazepine, Oxcarbazepine, topiramate, clonazepam, phenytoin,
lamotrigine and divalproex
◦ Gabapentin or baclofen

◦ Tricyclic antidepressants such as amitriptyline or nortriptyline (treat constant

burning or aching pain)
Conservative therapy
◦ Nerve blocking with local anesthesia

◦ 6-18 months

Alternative therapies:

Acupuncture, biofeedback, vitamin therapy, nutritional therapy and

electrical simulation of the nerves
Surgical therapy
Glycerol rhizotomy

Percutaneous radiofrequency rhizotomy

Microvascular decompression

Gamma knife radiosurgery

 NURSING MANAGEMENT
Assessment:
◦ Triggering factors

◦ Characteristics

◦ Frequency

◦ Pain management techniques

◦ Nutritional status

◦ Hygiene

◦ lifestyle
Nursing intervention
Pain management

Environmental management

Nutrition

Hygiene

Pre operative management

Post operative management

Post operative management
Ice application
Comparing pain level pre operative level
Follow up
Chew on unaffected side
Avoid hot beverages
Check oral cavity and hygiene
Protect extreme temperatures at face
Use an electric razor
Wear a protective eye shield
Examine eye regularly
Complication
Respiratory failure
UTI
Paralytic ileus
Muscle atrophy
DVT
Pulmonary emboli
Skin breakdown
Orthostatic hypotension
Nutritional deficiencies
MYASTHENIA
GRAVIS
DEFINITION
Myasthenia gravis is an autoimmune disease of the neuromuscular junction
characterized by the fluctuating weakness of certain skeletal muscle groups.

Epidemiology:

Both gender

Women: childbearing years

Men: 50 – 70 years
Etiology and Pathophysiology

Autoimmune problem (When immune system mistakenly attacks healthy tissue)

Antibodies are proteins that attack foreign, harmful substance, attack the
neuromuscular junction (acetylcholine receptors)

Damage to the neuromuscular membrane reduces the effect of the neurotransmitter

substance acetylcholine, which is crucial substance for communication between
nerve cells and muscles

Prevents stimulating muscle contraction and Muscle weakness

Clinical manifestation

Fluctuating weakness of skeletal muscle

Muscles involved: used for moving the eyes and eyelids, chewing, swallowing,
speaking, and breathing

Muscles strong in the morning becomes weak during continued activity.

Facial mobility and expression can be impaired.

Speech is affected and voice often fades after a long conversation

Peek sign
 Precipitating factors for MG
exacerbations
Emotional stress Aminoglycoside
Pregnancy Antibiotics
Menstruation Beta-adrenergic blockers
Trauma Procainamide
Illness
Quinidine
Temperature extremes
Phenytoin
Hypokalemia
Psychotropic drugs (Lithium carbonate, phenothiazines,
benzodiazepines, tricyclic antidepressants)
 MYASTHENIA CRISIS

Is an acute exacerbation of muscle weakness triggered by infection, surgery,

emotional distress, drug overdose or inadequate drugs.
Diagnostic Studies
History and Physical Examination
EMG – decreased response to repeated stimulation of the hand muscles.
Tensilon test (IV anticholinesterase agent edrophonium chloride)
Atropine, a cholinergic antagonist
Chest CT scan.
MANAGEMENT OF MYASTHENIA GRAVIS

Drug therapy:
◦ Anticholinesterase drugs (enhancing neuromuscular junction)

◦ Alternate day corticosteroids (suppress the immune system)

◦ Immunosuppressants

◦ Azathioprine, mycophenolate, cyclosporine

Surgical therapy

◦ Thymectomy

Other therapies:

Plasmapheresis

IV Immunoglobulin G
NURSING MANAGEMENT
Assessment:
Fatigability
Severity
Coping Abilities
Vital signs
Saturation
ABG
PFT
Muscle strength
Nursing Diagnosis
Ineffective airway clearance related to intercostal muscle weakness and
impaired cough and gag reflex

Impaired verbal communication related to weakness of larynx, lips, mouth,

pharynx and jaw

Activity Intolerance related to muscle weakness and fatigability

Disturbed body image related to inability to maintain usual lifestyle and role
responsibilities.
Nursing Intervention
Maintaining adequate ventilation
Continuing drug therapy
Side effects
Myasthenia crisis and Cholinergic crisis
Easily chewed and swallowed foods (Semi solids)
Diversional activities
Education on complication
MULTIPLE
SCLEROSIS
Definition
Multiple Sclerosis (MS) is a chronic, progressive, degenerative disorder of the CNS
characterized by disseminated demyelination of nerve fibers of the brain and spinal cord.

Epidemiology:

20 – 50 years of age

Women are affected two to three times more often than men.

India: 0.5 to 2 per 100,000.

Etiology
Unknown

Environmental exposure like an infection

Multiple genes are believed to be involved

Precipitating factors:

Infection, smoking, physical injury, emotional stress, excessive fatigue, pregnancy and
poor state of health.
 PATHOPHYSIOLOGY
Chronic inflammation, demyelination and gliosis in the CNS

The primary neuropathologic condition is an autoimmune process orchestrated

by activated T cells.

An environmental factor or virus in genetically susceptible individuals may

initially trigger this process

The activated T cells in the systemic circulation migrate to the CNS, disrupting
the blood brain barrier
 This is the initial event in the development of Multiple sclerosis

Antigen-antibody reaction within the CNS activates the inflammatory response

and leads to the demyelination

Initially attacks on the myelin sheaths of the neurons in the brain and spinal cord
results in damage to the myelin sheath

Transmission of nerve impulses still occurs, though transmission is slowed

Impairment of function occurs

Myelin can regenerate and symptoms disappear, the patient experiances a

remission
 Ongoing inflammation occurs, nearby oligodendrocytes are affected and the
myelin loses the ability to regenerate.

Damage occurs to the underlying axon

Nerve impulse transmission is disrupted, resulting in the permanent loss of nerve

function

As inflammation subsides, glial scar tissue, leading to the formation of hard,

sclerotic plaques

Plaques found throughout the white matter of the CNS.

Clinical Manifestation
Insidious and gradual

Chronic progressive deterioration in some patients

Remission and exacerbation in others

Clinical manifestations vary with each patient according to the CNS area involved
 Patterns of Multiple Sclerosis
Category Characteristics
Relapsing-remitting Clearly defined relapses with full recovery or sequelae and residual deficit
on recovery
85%
Primary Progressive Slowly worsening neurologic function from the beginning with no distinct
relapses or remissions
10%
Secondary- A relapsing-remitting initial course, followed by progression with or
Progressive without occasional relapses, minor remissions and plateaus
50%
Progressive- Progressive disease from onset, with clear acute relapses, with or without
Relapsing full recovery. Periods between relapses are characterized by continuing
progression.
5%
Clinical Manifestation

Motor problems

Sensory Problems

Cerebellar Problems

Emotional Problems
Motor Problems

Weakness or paralysis of the limbs, the trunk or the head

Diplopia

Scanning speech

Spasticity of the muscles that are chronically affected

Sensory Problems
Numbness and tingling and other paresthesias
Patchy blindness (scotomas)
Blurred vision
Vertigo
Tinnitus
Decreased hearing
Chronic neuropathic pain
Lhermitte’s sign
Cerebellar signs
Nystagmus
Ataxia
Dysarthria
Dysphagia
Severe fatigue (aggravated by heat, humidity, deconditioning and medication side effects)
Bowel and bladder function (Constipation or incontinence)
A flaccid (hypotonic) bladder
Sexual dysfunction
Problems of Cognitive function
Emotional Problems
Anger
Depression
Euphoria
 Diagnostic studies

History and Physical Examination

MRI of the brain and spinal cord – plaques, inflammation, atrophy, tissue breakdown and destruction

CSF Analysis: an increase in immunoglobulin G and presence of oligoclonal banding

Confirmatory factors:

1. Evidence of at least two inflammatory demyelinating lesions in at least two different locations within the CNS

2. damage or an attack occurring at different times

3. all other possible diagnoses rules out

 MANAGEMENT OF MULTIPLE
SCLEROSIS
DRUG THERAPY:

◦ Immunomodulators (to modify the disease progression and prevent relapses)

◦ Beta-Interferon
◦ Glatiramer acetate
◦ Teriflunomide
◦ Immunosuppressants
◦ Mitoxantrone dimethyl fumarate
◦ Sphingosine 1-phosphate Receptor Modulator
◦ Fingolimod
◦ Monoclonal Antibody
◦ Natalizumab
Corticosteroids
◦ ACTH
◦ Prednisone
◦ Methylprednisone
Cholinergics Muscle Relaxants

◦ Bethanacol ◦ Diazepam

◦ Neostigmine ◦ Baclofen

◦ Dantrolene
Anticholinergics
◦ Tizanidine
◦ Propantheline

◦ Oxybutynin Nerve Conduction enhancer

◦ Dalfampridine
Other therapies
Neurectomy
Rhizotomy
Cardotomy
Dorsal-column electrical stimulation
Intrathecal baclofen
Thalamotomy or deep brain stimulation
Physical and speech therapies
Exercise
Water exercise
Nursing Management
Assessment:

◦ Pain
◦ Medication
◦ Family history
◦ Nutritional history
◦ Elimination
◦ Activity exercise
◦ Cognitive perceptual
◦ Sexuality
◦ Coping stress tolerance
Nursing Diagnosis
Impaired physical mobility related to muscle weakness or paralysis and muscle
spasticity

Impaired urinary elimination related to sensorimotor deficits

Ineffective self-health management related to knowledge deficit regarding management

of Multiple sclerosis
Nursing Intervention
Assist in identifying triggers

Assist to deal with anxiety due to diagnosis of MS

Intervention to promote physical mobility and prevent pressure sore

Encourage vigorous and early treatment

Good balance of exercise and rest

Teach treatment regimen and side effects

Support to caregiver of MS