CHAPTER 4

Nursing Care of Children with Neurological Disorders

NEUROLOGICAL SYSTEM OF CHILDREN AND ADULTS

Anatomical and Physiological Differences

INTELLIGENCE QUOTIENT (IQ)

• IQ development occurs rapidly from 0 to 3 years, laying the foundation for future intelligence.
• Continued cognitive development from 4 to 6 years is influenced by environment and education.
• Long-term memory development progresses from limited capacity in early childhood to mature capabilities in adolescence.

PRIMITIVE REFLEXES AND THEIR TRANSFORMATION INTO MATURE MOTOR DEVELOPMENT

• Primitive reflexes are automatic, stereotypical movements present in infants, typically integrating into voluntary movements by 6–12 months.
• This process occurs through:
• Integration
• Maturation
• Synaptic pruning

ABNORMAL RESPONSES

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• Absence or diminished reflexes during the expected age period indicate abnormal neurological function.
• Persistence or re-emergence of primitive reflexes beyond the normal integration age suggests neurological issues or developmental delays.
• Retained primitive reflexes reduce the brain’s ability to efficiently process sensory information.

REFER TO BOOK

PAGE NO. :- 181

Table 2: Impact of retained primitive reflexes on child development and associated neurological condition

CONCEPT OF ICP AND CSF PRESSURE

NEUROLOGICAL ASSESSMENT IN CHILDREN

• This guide provides an overview of age-specific neurological assessment techniques, examination methods, and developmental milestones for children from birth to 12 years.

• Age-Specific Neurological Assessment
• Pediatric GCS

Decorticate and decerebrate posture

NEURAL TUBE DEFECTS

Definition

• NTDs are congenital anomalies resulting from incomplete closure of the neural tube during embryonic development.

• Types
• There are two main types:

• Spina bifida aperta (SBA) or open spina bifida, also known as spina bifida cystica, is visible at birth, with exposed neural tissue or a protruding sac.

Spina bifida cystica. (A) Note the anatomical defect and (B) original lumbosacral defect in a child

• Spina bifida occulta (SBO) or closed spina bifida

Fig:-A sacral dimple that is a sign of possible spina bifida occulta

Fig:-A tuft of hair is a sign of possible spina bifida occulta

Fig:-Anencephaly

Fig.:-Encephalocele

Infectious Factors

• Other infections (CMV, toxoplasmosis)

• Maternal rubella infection

Nutritional Factors

• Maternal folate deficiency impairs neural tube closure by disrupting DNA synthesis and repair, increasing NTD risk.

Environmental Factors

• Exposure to pesticides and insecticides alters neural tube development through neurotoxicity.

Maternal Factors During Pregnancy

• Advanced maternal age (>35 years)
• Multiple gestations
• Previous history of miscarriage or stillbirth

Maternal Health Conditions

• Diabetes mellitus
• Obesity
• Epilepsy and anticonvulsant use
• Hyperthermia

Socioeconomic Factors

• Limited access to prenatal care and nutrition education.
• Poor dietary quality and inadequate folate intake.

Geographic and Ethnic

• Factors NTD prevalence varies geographically and ethnically due to genetic predisposition, dietary patterns, nutrient deficiencies, and environmental exposures.

Clinical Manifestations

Spina Bifida Occulta Clinical Manifestations

• Asymptomatic in 70–80% of cases
• Cutaneous anomalies (e.g., dimples, lipomas, or haemangiomas) over the spine

Spina Bifida Cystica Clinical Manifestations

• A visible sac or cyst protruding from the spine

• Hydrocephalus and increased intracranial pressure

Pathophysiology

Diagnostic Evaluation

• Prenatal diagnosis is primarily achieved through
• Postnatal diagnosis involves

Complications

• Short-Term Complications

• Infection
• Cardiovascular instability
• Hydrocephalus

• Long-Term Complications

• Neurological deficits
• Cognitive impairment
• Orthopaedic issues

• Psychological and Social Complications

• Emotional distress
• Behavioral problems
• Social isolation

• Complications Specific to NTD Types

• Anencephaly
• Encephalocele

• Management

• Supportive Care

• Respiratory Care
• Pain Management
• Wound Care
• Nutritional Support

Emotional Support

• Families of infants with NTDs experience significant emotional distress, necessitating comprehensive emotional support.

Surgical Management

• The primary goal of surgical management in NTDs is to prevent further neurological deterioration, improve functional outcomes, and enhance quality of life.

Developmental Support

• Infants with NTDs require multidisciplinary developmental support to optimize growth and development.

Nursing Management

• Nursing Assessment

• Neurological status
• Spinal cord function
• Developmental milestones

HYDROCEPHALUS

Introduction

• Hydrocephalus is a neurological disorder characterized by the accumulation of CSF in the brain, leading to increased intracranial pressure and potentially life-threatening complications.

Etiology

• Congenital Causes

• Neural tube defects (e.g., spina bifida, encephalocele)
• Dandy-Walker malformation
• Chiari II malformation

• Acquired Causes

• Infections (e.g., encephalitis, brain abscess, meningoencephalitis)
• Traumatic brain injury
• Tumors (e.g., brainstem gliomas, medulloblastoma)

Risk Factors

• Maternal infection (e.g., Zika virus)
• Premature birth

Types

• Based on the Cause

• Congenital hydrocephalus
• Acquired hydrocephalus

• Based on CSF Flow

• Communicating hydrocephalus
• Non-communicating hydrocephalus
• Normal pressure hydrocephalus (NPH)

Other Types

• Hydrocephalus ex vacuo

Pathophysiology

Flow of cerebrospinal fluid

Clinical Manifestations

• General Clinical Manifestations

• Hydrocephalus presents with a range of clinical manifestations due to increased ICP and CSF accumulation .

Common symptoms include:

• Headache, nausea, vomiting
• Cranial nerve palsies (III, IV, VI).
• Sensory disturbances

• Visual disturbances
• Auditory disturbances
• Motor disturbances
• Other sensory changes

Age-specific Clinical Manifestations

• Infants (0–12 months): Infants with hydrocephalus exhibit macrocephaly (enlarged head circumference).

• Children (1–5 years): Children with hydrocephalus display headache, nausea, vomiting, papilledema, diplopia,

• Older children (6–18 years): Older children with hydrocephalus experience headaches (worsening in the morning).

Radiological Signs

• Periventricular lucency (PVL)
• Ventricular enlargement

Diagnostic Evaluation

• Clinical evaluation includes medical history, focusing on developmental delays, microcephaly, and neurological symptoms.
• Cranial ultrasound
• Electroencephalogram (EEG)

Management

• Surgical Management

Types of shunts used in hydrocephalus

Valves present in the shunts

Medical Management

• Acetazolamide (Diamox), a carbonic anhydrase inhibitor, reduces CSF production and is administered at 20–30 mg/kg/day divided every 8 hours.

Nursing Management

• Assessment

• Collect health history on hydrocephalus diagnosis, etiology, shunt type, placement date, associated medical conditions, and allergies.

General Measures

• Follow the discharge instructions regarding post operative care and medication.
• Monitor temperature and maintain a chart of dairy.

Prevent Infection

• Report any signs of infection (redness, swelling, discharge) or shunt malfunction.

Feeding

• Avoid heavy or greasy foods.
• Encourage fluids to prevent dehydration.

Mobility

• Avoid bending the head of the child.
• For older children, encourage gentle movements (e.g., stretching, walking).

Sleeping

• Place the child on their back or side with a pillow supporting their head.
• Avoid placing the shunt site directly on the mattress.

Complications

• Developmental delays

• Vision and hearing problems

• Seizures

• Cerebral hemorrhage

Shunt-related complications:

• Shunt malfunction
• Shunt infection

MENINGITIS

• Meningitis, an inflammation of the protective membranes (meninges) surrounding the brain and spinal cord, is a serious and potentially life-threatening infection affecting children worldwide.

Causes of Meningitis in Children

• Bacterial meningitis is caused by pathogens such as Streptococcus pneumoniae, Haemophilus influenzae type b (Hib), and Neisseria meningitidis.

Bacterial Causes

• Streptococcus pneumoniae (40-50%)

• Haemophilus influenzae type b (Hib) (20-30%)

Viral Causes

• Enteroviruses (EV), herpesviruses (HSV-1, HSV-2, VZV)

Fungal Causes

• Cryptococcus neoformans, Candida species.

Parasitic Causes

• Naegleria fowleri (primary amebic meningoencephalitis)

High-Risk Groups

• Premature infants, low birth weight

• Infants

• College students living in dormitories

• Travel to endemic areas.

Risk Factors for Tubercular Meningitis (TBM)

• Young age (<5 years)
• Family history of tuberculosis
• Delayed or inadequate treatment of tuberculosis.

Pathophysiology

Clinical Manifestations

• Neonates (0–1 Month)
• Subtle symptoms:

• Lethargy

• Refusal to feed

• Older Children
• Hyperacute presentation (1–2 days, less common)

• Rapid onset fever

• Shock 3

Acute Presentation (2–7 Days, More Common)

• Nonspecific findings: Fever, anorexia, poor feeding, headache

• Manifestations of meningeal irritation

• Increased ICP symptoms: Headache, vomiting, bulging fontanel or diastasis of sutures, oculomotor

Diagnostic Evaluation

CSF profile in CNS infections

Complications

• Seizures (20–30%),

• Hydrocephalus (10–20%),

Cognitive Impairment

• Memory loss or difficulties with memory consolidation
• Attention deficits and decreased focus

Behavioral Problems

• Hyperactivity and impulsivity

• Emotional regulation difficulties (e.g., anxiety, depression)

Medical Management

• Initial assessment and stabilization: Initial management involves rapid assessment and stabilization of vital functions.

Supportive Care

• Maintain fluid and electrolyte balance.
• Monitor for seizures and manage with anticonvulsants (e.g., phenytoin or levetiracetam).

Medical Management for Bacterial Meningitis

• Antibiotic therapy: Start empiric antibiotic therapy as soon as possible, ideally within 1 hour of presentation.

Adjunctive Therapy

• Dexamethasone (0.6 mg/kg/day divided q6h for 2–4 days) to reduce inflammation and cerebral edema.
• Acyclovir (20 mg/kg/dose q8h) if HSV encephalitis is suspected.

Medical Management for Tubercular Meningitis

ENCEPHALITIS

Introduction

• Encephalitis, an inflammation of the brain, is a serious neurological disorder that affects children worldwide.

Etiology

• Viral infections (80–90%)
• Bacterial infections (5–10%)
• Post-infectious encephalitis
• Autoimmune disorders

Pathophysiology

Clinical Manifestations

• Fever (50–70%)

• Headache (30–50%)

• Vomiting (20–40%)

Diagnostic Evaluation

• Detailed medical history and physical examination
• Laboratory tests
• Imaging studies

Medical Management

Antimicrobial Therapy

• Acyclovir (HSV
• Ceftriaxone (for bacterial encephalitis)

Complications

• Long-term cognitive impairment
• Epilepsy
• Behavioral changes

Prognosis

• Prognosis varies depending on etiology, severity, and promptness of treatment. Mortality rates range from 5–30%. Long-term sequelae occur in 20-50% of survivors.

Nursing Management of Children with Meningitis and or Encephalitis

• General Care

• Rest
• Medication
• Temperature control

Specific Precautions

• Avoid strenuous activities (e.g., sports, heavy lifting)

• Limit screen time (TV, tablets, smartphones)

• Avoid loud noises

Visitor Restrictions

• Limit visitors to immediate family members and caregivers.
• Isolate the child from siblings or other household members with infectious diseases.

Home Hygiene

• Regularly clean and disinfect: High-touch surfaces (e.g., doorknobs, light switches), toys and play areas, bathrooms, and kitchen

SEIZURE DISORDERS

• Seizure disorders, also known as epilepsy, affect approximately 1% of children worldwide.
• Seizures can significantly impact a child’s quality of life.

Types of Seizure Disorders

• Seizures in children can be classified into several types, each with distinct characteristics (Table 8).

Etiology

Provoked Seizures

• Traumatic brain injury
• Metabolic disorders
• Structural brain abnormalities

Unprovoked Seizures

The causes are as follows:

• Genetic predisposition
• Developmental disorders
• Idiopathic epilepsy

Other Factors

• Premature birth, low birth weight due to low brain volume
• Medications
• Perinatal asphyxia (oxygen deprivation damages brain tissue, potentially leading to seizures).

Clinical Manifestations

• Specific Symptoms

• Aura: It is a warning sign before a seizure.
• Children who can express aura symptoms

Age-Specific Manifestations of Seizure

• Infants (0–12 months)
• Toddlers (1–3 years)
• Children (4–12 years)

Diagnostic Evaluation

• Medical history
• Physical examination
• Laboratory tests
• Imaging studies

Complications

• Status epilepticus
• Behavioral problems
• Social isolation

Medical Management

• Acute Seizure Management

• Intranasal midazolam spray
• Buccal midazolam
• Rectal diazepam

Unprovoked Seizures Chronic Treatment

• First-line: Oral valproate
• Second-line: Oral carbamazepine

Nursing Management

• History taking:-Seizure onset, frequency, type, medications, allergies
• Physical assessment: Vital signs, neurological examination, developmental assessment.

General Care

• Monitor and record seizures (frequency, duration, type). Maintain a seizure diary.
• Administer medications as prescribed

Safety Precautions

• Pad side rails of bed, chair, staircase at home and remove hazardous objects
• Use seizure precautions (e.g., helmet, padding)

Medication Management

• Understand medication side effects and interactions
• Administer medications at the same times daily.

Response to a Seizure Event at Home

• Stay calm and avoid crowding around the child
• Turn the child onto the side (recovery position)
• Note the time and duration of seizure duration

Dietary Considerations

• Maintain a balanced diet. Focus on whole foods, fruits, vegetables, whole grains, lean proteins, and healthy fats.
• Encourage plenty of water intake.

Emotional Support to Older Children

• Encourage open communication
• Offer emotional reassurance

Emergency Preparedness

• Keep emergency contact numbers handy
• Know the nearest hospital location

Travel Precautions

• Consult healthcare provider before travel
• Pack emergency medications
• Make the child carry an identification card/ ID band in the form of an attractive wristlet mentioning the disease condition of the child.

CEREBRAL PALSY (CP)

• CP is a group of permanent, non-progressive disorders of movement, posture, and muscle tone caused by abnormal brain development or damage to the developing brain, typically occurring before birth, during birth, or in early childhood.

Risk Factors

• Prenatal Risk Factors (~70–80%)
• Perinatal Risk Factors (~10–20%)
• Neonatal Risk Factors (~5–10%)

Types of Cerebral Palsy

Types of cerebral palsy

Pathophysiology

Classification Based on Functional Limitations

Pathophysiology

Clinical Manifestations

• General signs include delayed milestones, such as sitting, crawling, or walking; impaired muscle tone, posture, and movement.

Spastic Cerebral Palsy

• Clonus (involuntary muscle contractions).

• Scissoring (crossing) of legs.

Dyskinetic Cerebral Palsy

• Involuntary movements (choreoathetosis).

• Dystonia (abnormal postures).

Ataxic Cerebral Palsy

• Impaired coordination and balance.

• Wide-based gait.

Mixed Cerebral Palsy

• Combination of spastic, dyskinetic, and ataxic features.

Other Manifestations

• Gastrointestinal issues (constipation, reflux), sleep disturbances, behavioral challenges (ADHD, anxiety), and orthopedic deformities (scoliosis, contractures).

Diagnostic Evaluation

• A physical examination assesses muscle tone, reflexes, posture, and movement patterns.
• Laboratory tests
• Genetic testing

Complications

• Pain

• Epilepsy

• Intellectual disability

Nutritional Management

• Children with CP require special nutritional care to ensure they grow and develop properly.
• This is because CP affects their ability to eat, digest, and absorb nutrients.

Oral Feeding Strategies

• Positioning
• Three-finger method

Three-finger method of holding and supporting oral feeding in CP child

Alternative Feeding Methods

• Nasogastric tube (NGT) feeding
• Gastrostomy tube (G-tube) feeding

Medical Management

• Muscle Relaxants and Spasticity Management
• Anticholinergics for Dystonia and Athetosis
• Anticonvulsants for Seizure Control
• Orthopedic and Pain Management

Surgical Management

• Surgical management of cerebral palsy (CP) aims to improve mobility, reduce spasticity, and enhance the overall quality of life.

Physical Therapy (PT)

• Physical therapy (PT) is a key component of treatment across all ages, aiming to improve mobility, strength, and balance.

Neurodevelopmental Treatment (NDT)

• Enhances motor control and function and reduces spasticity and contractures.
• Techniques include handling, positioning, and movement facilitation to promote relaxation, flexibility, and coordinated movement.

Physical Therapy (PT) at Home

• Passive stretching
• Active exercises
• Balance training
• Mobility aids

Occupational Therapy (OT) at Home

• Sensory integration
• Fine motor skills
• Adaptive equipment

Sensory Integration Therapy at Home

• Deep pressure
• Tactile Stimulation

Facilitating Communication

• Children with cerebral palsy (CP) often face communication challenges that hinder their ability to express needs, emotions, and thoughts.
• Technology such as electronic communication devices and text-to-speech software can further support communication.

Government of India Initiatives

• The Indian government has launched several initiatives and financial assistance programs for the rehabilitation of cerebral palsy.

• Rehabilitation Schemes include:

• GHARAUNDA (Group Home for Adults)
• NIRAMAYA (Health Insurance Scheme)
• Assistance to persons with disabilities for purchase/fitting of aids/appliances (ADIP scheme)

Nursing Management

Nursing Assessment

• A nurse should assess the following for a child with cerebral palsy.

Physical Assessment

• Muscle tone (spasticity, hypotonia)

• Range of motion (ROM)

• Mobility (gross motor skills)

Neurological Assessment

• Cognitive function (developmental milestones)

• Level of consciousness

Developmental Assessment

• Gross motor skills (e.g., sitting, walking)

• Fine motor skills (e.g., grasping, manipulating)

Nutritional Assessment

• Feeding difficulties (e.g., aspiration, dysphagia)

Emotional and Social Assessment

• Emotional well-being (e.g., anxiety, depression)

• Social interactions (e.g., family, peers)

Environmental Assessment

• Home environment (e.g., accessibility, safety)

• School or daycare setting

Medication and Treatment Assessment

• Current medications

• Treatment plans (e.g., PT, speech therapy)

Risk Assessment

• Aspiration pneumonia

• Pressure ulcers

• Contractures

• Falls

• Seizure-related injuries.

HEAD INJURY/TRAUMATIC BRAIN INJURY (TBI)

• Head injury, defined as an external physical force-induced trauma to the brain, can cause diminished or altered consciousness, leading to impaired cognitive abilities and physical functioning.

Causes of Head Injury

• Non-inflicted Causes
• Inflicted Causes

Risk Factors

• Age
• Urban residence
• Poor caregivers’ supervision
• Lack of safety measures

Classification of TBI Based on Severity

• Mild TBI (mTBI)
• Uncomplicated
• Complicated
• Moderate TBI
• Severe TBI

Various Forms of Head Injury

• Subarachnoid hemorrhage (SAH)
• Epidural hematoma (EDH)
• Subdural hematoma (SDH)

Pathophysiology

Pathophysiology of brain injury

Clinical Manifestations

Physical

• Changes in bowel and bladder function
• Changes in level of consciousness, ranging from brief loss of consciousness to coma.

Sensory-Perceptual

• Auditory and Vestibular
• Visual

Cognition

• Attention
• Executive Functioning

Language

• Pragmatic/Social Communication
• Spoken Language
• Speech

Voice

• Aphonia/dysphonia resulting from intubation, tracheostomy, or use of mechanical ventilator.

Feeding and Swallowing

• Oral and/or pharyngeal dysphagia

Behavioral and Emotional

• Changes in affect—overemotional, over-reactive, emotionless (flat affect)

Cranial Nerve Signs

• A low score on the GCS in total and in individual components.

Pupillary Signs

• Anisocoria (unequal pupils), hippus (pupillary oscillations), and fixed pupils.

Signs of Increased ICP

• Headache

• Cushing’s reflex (bradycardia, hypertension).

Focal Neurological Deficits

• Hemiparesis

• Hemisensory loss

Clinical Manifestations Among Infants and Toddlers with TBI

• Irritability, persistent crying, and inability to be consoled
• Changes in eating or nursing habits (not breastfeeding, drooling)

Diagnostic Evaluation

• Physical assessment
• X-rays—Evaluate skull fracture

Complications

• Infection: Brain abscess, Meningitis

• Seizures—Post-traumatic epilepsy

• Post-concussion Syndrome—Headache—Fatigue— Irritability pneumonia, deep venous thrombosis, and pulmonary embolus due to prolonged immobility.

Management

• Supportive Management

• Airway management
• Fluid management
• Seizure prophylaxis

Management of Increased ICP

• Prolonged elevations of ICP greater than a threshold of 20 mm Hg are associated with poor neurologic outcomes in the pediatric population.

Surgical Management

• Craniotomy
• Decompressive hemicraniectomy

Nursing Management

• Level of consciousness (LOC)
• Respiratory assessment
• Neurological assessment

BRAIN ABSCESS

Introduction

• Brain abscess is a serious and potentially life-threatening infection that affects approximately 1–2 children per 100,000 annually.

Causative Organisms

• Bacterial infections (Streptococcus, Staphylococcus, E. coli)

• Parasitic infections (Toxoplasma, Taenia solium)

Risk Factors

• Congenital heart disease

• Immunodeficiency (e.g., HIV/AIDS, cancer)

• Chronic lung disease (e.g., cystic fibrosis)

Clinical Manifestations

• Headache (70–90%)

• Fever (50–70%)

• Vomiting (40–60%)

Pathophysiology

Pathophysiology of brain abscess

Diagnostic Evaluation

• CT scan/MRI
• Lumbar puncture (LP)
• Blood cultures

Complications

• Common Complications include seizures, hydrocephalus, cerebral edema, meningitis, cognitive, motor.

Medical Management

• Amphotericin B (0.5–1 mg/kg/ day) for broad-spectrum coverage, Fluconazole (5–10 mg/kg/day) for Candida species.

Surgical Management

• Stereotactic aspiration
• Open craniotomy
• Endoscopic drainage

Nursing Management

• Assessment
• Nursing Interventions
• Immediate Post-discharge Care (First 2–4 Weeks)
• General Care

INTRACRANIAL SPACE-OCCUPYING LESIONS

• Intracranial space-occupying lesions (ICSOL) are abnormal growths or masses within the skull that compress or displace surrounding brain tissue.

Types

• Tumors

• Astrocytomas
• Craniopharyngiomas

• Cysts

• Arachnoid cysts
• Epidermoid cysts

• Vascular Lesions

• Arteriovenous malformations (AVMs)

Etiology/Risk Factors

• Genetic predisposition

• Environmental factors (e.g., radiation exposure)

Clinical Manifestations

• Headache

• Vomiting

Diagnostic Evaluation

• Neuroimaging: CT, MRI, angiography

• Lumbar puncture (LP)

Complications

• The common complications associated with increased ICP such as hydrocephalus, cerebral edema.

Medical Management

• Corticosteroids, such as dexamethasone (0.5–1.5 mg/ kg/day IV/PO divided six hourly), reduce edema and inflammation.

Surgical Management

• The surgical management for pediatric intracranial space occupying lesions involves craniotomy for tumor resection.

Rehabilitation

• Rehabilitation plays a crucial role in restoring functional abilities and improving the quality of life for children with intracranial space-occupying lesions.

Nursing Management

• Assessment priorities include neurological status, vital signs, and fluid balance by maintaining a strict intake output chart.
• Medications, such as corticosteroids and anticonvulsants, are administered as prescribed.

REYE’S SYNDROME

• Reye’s syndrome is a rare but life-threatening neurological disorder that primarily affects children and adolescents.

Etiology

• Reye’s syndrome typically occurs after a viral infection, such as influenza, varicella (chickenpox), or RSV.

SALICYLATE EXPOSURE

↓

MITOCHONDRIAL DYSFUNCTION

↓

IMPAIRED FATTY ACID Β-OXIDATION

↓

↓ ATP + ↑ ROS

↓

OXIDATIVE STRESS & LIPID PEROXIDATION

↓

HEPATIC MITOCHONDRIAL INJURY

↓

MICROVESICULAR STEATOSIS (FATTY LIVER)

↓

↑ AMMONIA + BBB DISRUPTION

↓

CEREBRAL EDEMA

↓

ENCEPHALOPATHY

(CONFUSION → SEIZURES → COMA)

Pathophysiology

Clinical Manifestations

• Reye’s syndrome typically presents with vomiting, confusion, lethargy, seizures, and coma.

Stages

• Seizures and coma

• Respiratory failure

• Personality changes (Irritability, restlessness, confusion, disorientation, lethargy, agitation, and disorientation)

Management

• Initial Management

• Supportive care
• Fluid management

• Pharmacological Management

• Corticosteroids
• Anticonvulsants

• Supportive Therapy

• Mechanical ventilation
• Parenteral nutrition

Nursing Management

• Monitor and manage fluid and electrolyte balance.
• Implement seizure precautions.
• Support respiratory function with oxygen therapy and mechanical ventilation as needed.
• Activate emergency protocols for seizure activity or respiratory distress and administer emergency medications as prescribed.

NEUROMUSCULAR DISORDERS: GUILLAIN BARRÉ SYNDROME AND MYASTHENIA GRAVIS

• Guillain-Barré Syndrome (GBS) and Myasthenia Gravis (MG) are both neuromuscular disorders that involve muscle weakness and impairments in nerve-muscle communication.

summary of key features, classifications, pathophysiology, clinical manifestations, and management strategies for both conditions and Comparison of Guillain-Barré Syndrome (GBS) and Myasthenia Gravis (MG)

REFER TO BOOK ON PAGE NO. 230

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