Neurologic Disorders Overview
Neurologic Disorders Study Notes
Learning Objectives
Differentiate seizure types and pathophysiology
Consider the pharmacology of various anticonvulsant medications
Identify mechanisms in neurodegenerative diseases
Compare and contrast various neurodegenerative disorders
Describe prototype medications
Prioritize nursing care, safety, and red flags
Brain Structure – Functional Anatomy
Lobes:
Frontal Lobe:
Functions: Executive function, speech.
Temporal Lobe:
Functions: Memory, emotion.
Note: Affected in seizures and Alzheimer's Disease (AD).
Parietal Lobe:
Functions: Sensory processing.
Occipital Lobe:
Functions: Vision.
Basal Ganglia:
Role: Important for movement control.
Note: Affected in Parkinson’s disease.
Brainstem and Reticular Activating System:
Functions: Alertness and consciousness.
Seizure Pathophysiology
Definition of Seizures:
Abnormal or uncontrolled neuronal discharges in the brain.
Often due to foci of neural activity.
Foci:
Damaged area of the brain responsible for abnormal neuronal firing.
Imbalance in Neurotransmitters:
High glutamate (excitatory) and low GABA (inhibitory) contribute to seizures.
Consequences:
Affects consciousness, motor activity, and sensation.
Seizures are usually a symptom of another underlying disorder.
Seizure Types
Focal Seizures:
Localized to one area of the brain.
Patients often stay aware during the seizure.
Generalized Seizures:
Foci spread to the entire brain, resulting in loss of consciousness.
Types include:
Tonic-Clonic Seizures:
Characterized by a clonic phase followed by an ictal phase.
Absence Seizures:
Epilepsy vs Isolated Seizures
Epilepsy:
Defined as two or more unprovoked seizures.
Acute Causes of Seizures:
Fever (common in children).
Trauma.
Alcohol withdrawal.
Hypoglycemia.
Common Seizure Triggers:
Missed doses of seizure medications.
Sleep deprivation.
Stress.
Flashing lights.
Electrolyte imbalances.
Dangers of Seizures
Risks:
Risk for injury.
Aspiration risk.
Hypoxia and apnea.
Long-term neurological damage.
Postictal confusion and paralysis.
Importance of protecting from asphyxiation.
Status Epilepticus:
Defined as a seizure lasting longer than 30 minutes.
Requires treatment of seizures lasting more than 5 minutes to prevent cerebral edema or hypoxia.
Pathophysiology:
Increased metabolic demand leads to acidosis, brain injury, and hypoxia.
Goals of Treatment:
Maintain ventilation.
Correct underlying causes.
Terminate seizure with medications.
Seizure Management
Management Strategies:
Depends on seizure type.
“One-time events”: Treat seizure and observe for future events.
Recurrent seizures:
Medications.
Surgical interventions.
Medication management includes prophylaxis and rescue medications such as benzodiazepines.
Surgical interventions may involve video EEG (VEEG) to map areas with foci and ablation procedures.
Benzodiazepines
Mode of Action:
Potentiate GABA in the brain, increasing inhibition of neurons.
Uses:
Rescue medication to stop active seizures.
Management of alcohol withdrawal.
Prototype Drug:
Lorazepam (Ativan).
Other examples: Diazepam, Midazolam.
Important Considerations:
Monitor for respiratory depression, hypotension, and oversedation.
Barbiturates
Prototype Drug:
Phenobarbital (Luminal).
Mode of Action:
Modify the action of GABA, resulting in sedative effects.
Primary Use:
Control of status epilepticus.
Rarely used due to severe side effects.
Adverse Effects:
Dependence and addiction.
Drowsiness and oversedation.
Potential liver and kidney damage, laryngospasm, and vitamin deficiencies.
Hydantoins: Sodium Channel Blockers
Prototype Drug:
Phenytoin (Dilantin).
Other example: Fosphenytoin.
Mode of Action:
Sodium channel blockers prevent neuronal excitability.
Nursing Considerations:
Very narrow therapeutic range; monitor drug levels closely.
Side Effects:
Ataxia, gingival hyperplasia.
Monitor CBC for blood dyscrasias and assess liver and kidney function.
Other Seizure Medications
Valproate (Valproic Acid):
Mechanism: Desensitizes sodium channels.
Effective for a wide range of seizures, but hepatotoxic.
Side effects: CNS depression, vertigo, ataxia, visual disturbances.
Carbamazepine (Tegretol):
Monitor for blood dyscrasias.
Levetiracetam (Keppra):
Widely used for seizure prophylaxis, fewer side effects and interactions.
Considerations for Seizure Management
Important to monitor plasma drug levels closely.
Promoting patient adherence to medication regimens is critical.
Risks associated with medication discontinuation include rebound seizures and increased suicidal ideations.
Pregnancy and Seizures:
Many medications are dangerous for fetal health, but seizures also pose risks to the baby.
Valproic acid is highly teratogenic, associated with neural tube defects and cleft palate.
Phenytoin and phenobarbital require careful evaluation of risks versus benefits.
Neurodegenerative Diseases
Overview:
Neurodegenerative disorders are chronic and progressive diseases affecting the nervous system.
Commonly affect motor function, cognition, or both.
Currently no cure; focus on treatment includes symptom relief, preserving function, and improving quality of life.
Examples of Disorders:
Parkinson’s disease
Alzheimer’s disease
Multiple sclerosis
Lewy-Body dementia
Frontotemporal dementia
Parkinson’s Pathophysiology
Location:
Substantia nigra in the basal ganglia.
Imbalance:
Shortage of dopamine, responsible for initiating movement.
Excess acetylcholine inhibits movement.
Pathophysiology of Parkinson’s Disease:
Acetylcholine dominance causes characteristic motor symptoms.
The disease is progressive and currently has no cure.
Medication Management Strategies:
Increase dopamine levels and inhibit acetylcholine activity using drugs like Levodopa/Carbidopa and anticholinergics.
Parkinson’s Symptoms
Motor Control Symptoms:
Tremors, rigidity, bradykinesia.
Increased fall risk and difficulties with eating.
Non-Motor Symptoms:
Sleep disturbances, constipation, drooling, and depression.
Levodopa/Carbidopa
Components:
Levodopa: Crosses the blood-brain barrier as dopamine.
Carbidopa: Prevents premature breakdown of levodopa, allowing higher levels to reach the CNS.
Considerations:
Gold standard for early treatment; timing of administration is crucial.
“Wearing Off” and Dyskinesias
“Wearing Off”:
Refers to when medications stop being effective during the day, causing “off periods” with symptoms such as freezing and bradykinesia.
Dyskinesias:
Occur during “on periods” when medications are working effectively.
Considerations:
Timing of doses is very important; adjustments may be required.
Anticholinergics (Benztropine)
Prototype Drug:
Benztropine.
Uses:
Reduces tremors and rigidity in Parkinson’s.
Nursing Considerations:
Assess for anticholinergic effects: dry mouth, constipation, photophobia, urinary retention.
Caution in elderly due to potential confusion and fall risk.
Alzheimer’s Disease Overview
Prevalence:
Leading cause of dementia in 70% of all cases.
Symptoms:
Progressive cognitive decline, memory loss, confusion affecting cognition and behavior.
Changes to the Brain:
Cerebral atrophy (brain shrinkage).
Decrease in acetylcholine affecting the hippocampus and cerebral cortex.
Presence of amyloid plaques and tau tangles associated with cerebral inflammation.
Medication Management for Alzheimer’s Disease
Current Treatment Status:
No completely effective treatments exist, but options can slightly slow progression.
Cholinesterase Inhibitors:
Increase acetylcholine in the CNS.
Prototype drug: Donepezil; other drugs include Rivastigmine.
Side effects: Cholinergic effects such as bradycardia, drooling, tearing, syncope, and diarrhea.
Atropine: Antidote for overdosage.
Memantine (Namenda)
Mechanism of Action:
Regulates glutamate levels; used for moderate to severe Alzheimer's disease.
Effects:
May slow progression slightly.
Adjuvant medications also used to manage Alzheimer's symptoms include atypical antipsychotics, anxiolytics, and mood stabilizers.
Other Types of Dementia
Lewy-Body Dementia:
Characterized by the presence of Lewy bodies in neurons, displaying Parkinsonian symptoms and hallucinations.
Many medications are ineffective or exacerbate symptoms.
Vascular Dementia:
Results from impaired blood flow to the brain.
Frontal-Temporal Dementia:
Early age onset dementia, a rare and familial degenerative disease that is irreversible and progressive.
Multiple Sclerosis Pathophysiology
Definition:
Autoimmune attack on myelin in the central nervous system (CNS).
Autoantibodies target and destroy myelin and axons.
Diagnosis:
Based on plaques observed on MRI and lumbar puncture findings.
Disease Course:
Varies widely:
Relapsing-Remitting:
Flares followed by partial or full recovery (most common at 85%).
Other forms progressively worsen with little to no relapsing.
Multiple Sclerosis Symptoms
Associated Symptoms:
Fatigue, heat sensitivity, neuropathic pain, spasticity, impaired cognitive function, balance and gait issues, bowel and bladder dysfunction, sexual dysfunction, dizziness, vertigo, visual impairment, and slurred speech.
Medication Management of MS
Treatment Goals:
Treat flares early and reduce severity and frequency of flares.
Preserve intact neurological function.
Short-term Treatment of Flares:
Steroids: Prednisone, hydrocortisone.
Long-term Management:
Interferons, glatiramer acetate, and new biologics under development.
Amyotrophic Lateral Sclerosis (ALS)
Definition:
Motor neuron degenerative disease with no cognitive impairment.
Symptoms:
Progressive muscle paralysis leading to respiratory failure, weakness, atrophy, and spasticity.
Treatment:
No cure; Riluzole may provide modest life extension.
Guillan-Barre Syndrome
Pathophysiology:
Demyelination in the peripheral nervous system (PNS) post-viral infection.
Autoantibodies result in ascending paralysis.
Symptoms are usually reversible, but relapses can occur.
Treatment Options:
IVIG, plasmapheresis.
Importance of monitoring respiratory status and autonomic dysfunction.
Myasthenia Gravis
Definition:
Autoimmune condition characterized by autoantibodies to acetylcholine receptors at the neuromuscular junction.
Symptoms:
Weakness leading to paralysis, with a danger of respiratory paralysis.
Treatment:
Pyridostigmine (an acetylcholinesterase inhibitor) to reverse effects.
Cholinergic effects, along with IVIG and steroids, may be required.
Respiratory support may be necessary in a myasthenia crisis.
Knowledge Check 1: Autoimmune Disorders
Characteristics Comparison:
Clinical Characteristics:
Presence of autoantibodies, risk for respiratory failure, untreated paralysis, treatment with IVIG, potential for permanent neurological damage, and neuromuscular junction impact.
Disorders Analyzed: 1. Multiple Sclerosis 2. Myasthenia Gravis 3. Guillan-Barre Syndrome
Knowledge Check 2: Neurocognitive Disorders
Clinical Characteristics:
Progressive memory loss, affects motor movement, tremors/muscle rigidity, spasticity or flaccid paralysis, severe neurological decline, cognition impact, leads to respiratory failure.
Disorders Analyzed: 1. Alzheimer’s Disease 2. Parkinson’s Disease 3. Amyotrophic Lateral Sclerosis (ALS)
Knowledge Check 3: Antiseizure Medications
Clinical Properties:
Severe sedation potential, best for stopping status epilepticus, daily for seizure prophylaxis, unsafe for pregnancy long-term, potential rebound seizures from discontinuation, need for regular lab value monitoring.
Medications Analyzed: 1. Diazepam 2. Phenytoin 3. Phenobarbital 4. Valproic Acid
Final Reflection Questions
Which topic from the lecture felt the most complex or unfamiliar?
Which neurological disorder would be most challenging to care for as a nurse?
How might you support a patient who is cognitively intact but losing physical function, such as with ALS?
References
Adams, M., Holland, N., & Urban, C. (2020). Pharmacology for Nurses: A Pathophysiologic Approach. 6th Ed. Pearson.
Huether, S., McCance, K, & Brashers, V. (2020). Understanding Pathophysiology. Elsevier.