Neurology

# Neurology v Parkinson's Disease (PD), Alzheimer's Disease (AD) v Seizures v CVA/Stroke (Ischemic & Hemorrhagic) v Guillain-Barré (GB) v Bell Palsy

Parkinson's Disease (PD)

Pathophysiology

  • Also known as: Paralysis Agitans

  • Nature of Disease: Progressive, degenerative disease of the nervous system commonly seen in older adults.

  • Misdiagnosis: Often misdiagnosed as Huntington's disease (HD) in younger populations due to overlapping early symptoms and atypical presentations.

  • Motor Function: Disease affects the body's motor function.

  • Types of PD:
      - Primary (idiopathic) PD: Cause is unknown but linked to genetic and environmental factors.   - Secondary PD: Results from identifiable external or underlying factors such as medications, stroke or vascular diseases, head trauma, infections (e.g., encephalitis), and environmental toxins (e.g., CO, manganese).

Causes (Etiology)

  • Exact Cause: Unknown, but attributed to a combination of age, environment, and heredity.

  • Factors:   - Environmental factors: Exposure to chemicals, metals, and well water.   - Age: Over 40 years.   - Genetic factors.

  • Incidence:   - ~1 million affected in the US.   - ~60,000 Americans diagnosed yearly.   - >10 million people worldwide live with PD.   - Incidence increases with age; ~4% diagnosed before age 50, with few at age 30.   - Men are 1.5 times more likely to have PD than women.

Assessment: Recognize Cues

Expected Findings in History (Risk Factors)

  • Time and progression of symptoms.

Expected Findings in Assessment
Physical Symptoms

  • Motor Symptoms:   - Resting tremors (usually unilateral first)   - Bradykinesia   - Muscle rigidity   - Postural instability.

  • Non-Motor Symptoms:   - Drooling   - Forgetfulness   - Urinary urgency   - Loss of sense of smell   - Constipation.

  • Clinical Pearl: Nearly all patients with PD will experience at least one non-motor symptom, often preceding motor symptoms.

Rigidity Types (present in all stages)

  1. Cogwheel: Rhythmic interruption of muscle movement.

  2. Plastic: Mild restrictive movement.

  3. Lead pipe: Total resistance to movement.

Autonomic Nervous System Manifestations

  • Drooling

  • Excessive perspiration

  • Orthostatic hypotension

  • Bladder and bowel issues.

Emotional and Cognitive Impairments

  • Depression (most common), apathy, anxiety, insecurity, mood changes, insomnia, dementia, and psychosis.

Complications

  • Impaired mobility and adverse effects of drugs.

Labs and Diagnostics

  • Diagnosis based on clinical findings and the presence of 2 of the 4 classic symptoms (resting tremors, muscle rigidity, postural instability).

  • Low dopamine levels can be measured in cerebrospinal fluid (CSF).

  • Levodopa Trial: Diagnostic test to see if motor symptoms improve; a positive result is >30% improvement in motor scores.

Plan and Implementation

Goal

  • Promote mobility, safety, and self-esteem; manage symptoms with minimal adverse effects; and prevent complications.

Management Strategies

  • Medications:   - Levodopa: Most effective agent and mainstay of treatment. Benefits pronounced in the first 2 years, followed by dyskinesia and psychiatric complications over time.   - Carbidopa: Added to levodopa to avoid metabolism prior to reaching the brain; reduces gastrointestinal side effects.   - Dopamine Agonists: (e.g., ropinirole) mimic dopamine, lesser risk of dyskinesias.   - COMT Inhibitors: (e.g., entacapone) extend levodopa's action.   - Monoamine Oxidase Type B Inhibitors: (e.g., rasagiline).   - Anticholinergics: (e.g., benztropine) for resting tremors.

  • Surgical Options:   - Deep Brain Stimulation: Involves implanting electrodes to relieve tremors and rigidity.   - Stereotactic Pallidotomy: Creates a lesion to reduce abnormal signaling.

Long-Term Management Strategies

  • Drug Tolerance Management: Establish a baseline cognitive level, modify drug frequencies, and consider drug holidays to prevent toxicity.

  • Wearing-off Phenomenon: Characterized by motor fluctuations, requiring timely medication adjustments.

Alzheimer's Disease (AD)

Pathophysiology

  • Nature: Sub-type of dementia characterized by a gradual decline in brain function over time.

  • Symptoms: Difficulty learning new information; leads to impairments in memory, language, judgment, behavior, and ultimately functional ability.

  • Aging Effects: As the brain ages, it weighs less and takes up less cranial space, with dementia hastening age-related changes.

  • Etiology: Uncertain exact cause, usually attributed to genetic and environmental factors causing a pathological cascade.

Stages / Classifications

  1. By Age of Onset:    - Early-Onset (EOAD): Before age 65, often genetic.    - Late-Onset (LOAD): After age 65, associated with aging.

  2. By Disease Stage:    - Preclinical Stage: Brain changes begin, asymptomatic.    - Symptomatic Pre-Dementia (MCI): Early cognitive decline without complete loss of function.    - Dementia Phase:      - Early Stage: Progressive memory loss, mild mood changes.      - Moderate Stage: Worsening confusion, increased assistance required.      - Severe Stage: Severe cognitive decline, total dependence for care.

Disease Pathology

  • Characterized by neurofibrillary tangles, amyloid plaques, and vascular degeneration affecting memory areas of the brain.

  • Neuronal degeneration leads to atrophy, particularly in the hippocampus and cerebral cortex.

Assessment: Recognize Cues

Expected Findings in History (Risk Factors)

  • Chemical Imbalances: History of TBI, infections, etc.

  • Physical Assessment: Memory impairment is usually the first symptom noticed, changes in behavior.

Labs & Diagnostics

  • AD diagnosed by excluding other conditions; tests include blood work, imaging, etc.

  • Neuropsychological Tests: MMSE, MoCA, etc.

Analysis: Nursing Priorities

  • Patient safety, symptom management, cognitive support are core focus areas, ensuring independence while preventing injury.

Management

  • Pharmacological Management: Includes cholinesterase inhibitors, NMDA antagonists, and monitoring for behavioral symptoms.

  • Behavioral Management: Reality orientation, cognitive stimulation, and adequate nutrition.

Seizures

Pathophysiology

  • Result from an imbalance between excitatory and inhibitory processes in the brain, leading to abnormal electrical discharges.

  • Epilepsy: A chronic condition characterized by repeated unprovoked seizures.

Assessment: Recognize Cues

Expected Findings in History

  • Recent physical activity, stress, and prior seizure history.

Summary of Seizure Types

  1. Generalized Seizures: Involve both hemispheres.    - Tonic-Clonic: Loss of consciousness, rhythmic jerking.    - Absence: Brief impaired consciousness.

  2. Partial Seizures: Begin in one hemisphere, can be simple or complex.

Management

  • Seizure Precautions: Protect from injury, maintain airway, and monitor vital signs during seizures.

  • Drug Therapy: Administer anticonvulsants to manage seizures and monitor for side effects.

Cerebrovascular Accident (CVA)/Stroke

Pathophysiology

  • Interruption of blood supply leads to death of brain tissue, categorized into ischemic and hemorrhagic strokes.

Types of Stroke

  1. Ischemic Stroke: Most common, includes thrombotic and embolic strokes.

  2. Hemorrhagic Stroke: Involves bleeding into brain tissue, most often due to hypertension.

Assessment

Symptoms

  • Sudden confusion, weakness on one side, difficulty seeing, severe headache, and loss of balance.

Management

  • Immediate Care: Ensure airway, breathing, circulation.

  • Drug Therapy: Use thrombolytics for ischemic stroke within proper timeline; monitor for complications.

Guillain-Barre Syndrome (GBS)

Pathophysiology

  • An autoimmune disorder leading to demyelination of peripheral nerves, often following viral or bacterial infections which cause ascending paralysis.

Management

  • Monitor respiratory function closely and intervene early if respiratory efforts deteriorate.

  • Therapies: IVIG and plasmapheresis to reduce autoimmunity effects.

Bell's Palsy

Pathophysiology

  • Acute unilateral facial paralysis due to lower motor neuron involvement of facial nerve (CNVII), often resolving with time but may leave lasting effects.

Management

  • Corticosteroids within 72 hours of symptom onset are key.

  • Emphasize eye protection and facial exercises to facilitate recovery and prevent complications.