Neurological Disorders medsurge

Seizure

Sudden, uncontrolled electrical discharge of neurons in the brain • Disrupts normal brain function • May occur alone or with other conditions

Astrocyte dysfunction affects recurrence

• focus localization critical for surgery

Not classified as _____disorder if caused by reversible systemic/metabolic issue

Prodromal Phase of a Seizure

Early signs (hours/days before)

Aural Phase of a Seizure

Sensory warning

Ictal Phase of a Seizure

Active seizure phase

Postictal Phase of a Seizure

Recovery period

Myoclonic Seizures

Generalized-Onset Seizures

Quick, rhythmic jerks (arms or eyelids); 3 per second is typical. • Short duration: 10–60 seconds. • Eyelid myoclonia is a specific variant.

Tonic Clonic (formerly Grand mal)

Generalized-Onset Seizures

Sudden loss of consciousness, followed by tonic phase (stiffening), then clonic phase (jerking movements).

May include: Cyanosis, drooling, incontinence, biting of tongue/cheek

• Postictal phase: fatigue, soreness, possible confusion; patient often sleeps and has no memory of event.

Typical Absence Seizure

Generalized-Onset Seizures – Nonmotor

Common in children, rarely continues into adulthood. • Brief staring, <10 seconds, patient appears unresponsive. • May be misinterpreted as daydreaming.

Atypical Absence Seizure

Generalized-Onset Seizures – Nonmotor

• Longer than 10 seconds, continues into adulthood.

• Includes eye blinking, lip movements, or other motor signs.

Focal-Onset Seizures

Begins in one hemisphere of the brain. • Manifestations depend on location: can be motor, sensory, cognitive, or emotional.

Focal-Onset Seizures Types by Awareness

Focal Aware Seizures: Patient is alert and may describe odd sensations (smells, sounds, emotions).

• Focal Impaired Awareness: Altered consciousness—may appear awake but cannot interact. May display automatic movements (e.g., undressing, walking into danger). Often no memory after event.

Focal-Onset Seizures: Motor activity

tonic, clonic, atonic, automatisms

Focal-Onset Seizures: Nonmotor activity

emotional changes, sensory disturbances

Generalized Seizures

Start in both sides of the brain

• Always affect awareness

• May cause staring, jerking, or loss of muscle tone

• Person usually doesn’t remember it

• Absence: Brief staring, unresponsive

Tonic-Clonic: Stiffening → jerking, full loss of consciousness Myoclonic: Quick jerks (arms/face), person may remain aware

Focal Seizures

Start in one part of the brain

• Awareness may be preserved or impaired

• Symptoms depend on location in brain

• Focal Aware: Person is awake, may feel strange sensations Focal Impaired: Person can’t respond normally, may do automatic behaviors (e.g., lip smacking)

Psychogenic Nonepileptic Seizures (PNES)

Look like seizures, but are not caused by abnormal brain activity.

• Triggered by psychological stress or trauma. • Often misdiagnosed as epilepsy. •

Proper diagnosis requires video-EEG to confirm absence of electrical changes.

• History may include abuse, PTSD, or emotional trauma.

Status Epilepticus

Neurologic Emergency

Continuous seizure activity or back-toback seizures without return to consciousness

• Lasts longer than 5 minutes • Can occur with any type of seizure

Complications: • Brain uses more oxygen and glucose than it receives • Neurons become exhausted, risk of permanent brain damage

Convulsive Status Epilepticus

Most common type: prolonged tonicclonic

• Can cause: • Respiratory failure, hypoxia

• Acidosis, hyperthermia, dysrhythmias

Nonconvulsive Status Epilepticus

Often with focal impaired awareness seizures

Refractory (RSE) Status Epilepticus

Ongoing seizures despite treatment with first-line & second-line drugs

Epilepsy

a chronic neurological condition causing recurring seizures due to abnormal electrical activity in the brain

Injury & Death: • Risk increases with loss of consciousness and falling during seizures

have a 2–3x higher mortality rate

SUDEP (Sudden Unexpected Death in Epilepsy): • Cause unknown • Often associated with tonic-clonic seizures • May occur during sleep, without a witnessed seizure

Diagnostic Studies for Seizures

history and seizure description

Primary Diagnostic Tool – EEG (Electroencephalogram): • Evaluates electrical activity in the brain • Helps determine seizure type and location (focus) • Note: First EEG may appear normal – doesn’t rule out epilepsy

MEG (Magnetoencephalography): • Used with EEG for greater sensitivity

Lab Tests: • CBC, electrolytes, liver/kidney function, UA • Rule out metabolic or systemic

imaging Studies – to detect structural or vascular causes:

• CT or MRI – first-line for new-onset seizures

• Cerebral angiography – views blood vessels

• SPECT – shows blood flow to detect seizure focus

• MRS, MRA, PET – used in specialized or unclear case

Antiseizure Medications

Prevent seizures, minimize side effects • Not a cure

Common Drug Classes & Examples

• Hydantoins – Phenytoin (Dilantin)

• Iminostilbenes – Carbamazepine (Tegretol)

• Valproates – Valproic acid (Depakene), Divalproex (Depakote)

• Barbiturates – Phenobarbital • Benzodiazepines – Lorazepam (Ativan), Diazepam (Valium) (used for status epilepticus)

• Newer Agents – Levetiracetam (Keppra), Lamotrigine (Lamictal), Topiramate (Topamax)

Common CNS Side Effects • Diplopia (double vision) • Drowsiness • Ataxia (impaired coordination) • Mental slowness/cognitive changes

~30% of patients don’t respond to drugs • Older Adults: • More sensitive to lower doses • Drugs like phenytoin or phenobarbital may affect cognition or liver function

Status Epilepticus treatment

rapid IV lorazepam (Ativan) or diazepam (Valium)

Surgical option for seizure

Temporal Lobe Resection

• 80% seizure-free at 5 years; 72% at 10 years • Requires: diagnosis, failed drug trial, and defined seizure pattern

Other seizure treatment options

• Vagal Nerve Stimulation (VNS): sends mild pulses to brain

• Responsive Neurostimulation (RNS): detects & stops seizure via EEG feedback

• Ketogenic Diet: high-fat, low-carb – ketones fuel brain

• Biofeedback: teaches brainwave regulation

Common Triggers for seizures

• Metabolic imbalance (acidosis/alkalosis)

• Electrolyte disturbances: ↑K, ↓K, ↓glucose

• Dehydration

• Water intoxication

During a Seizure

Ensure airway & safety (pad rails, clear area)

• Do not restrain

• Loosen clothing, stay with patient

• Administer IV meds: lorazepam, diazepam, Dilantin

• Prepare for suction, O2, or intubation if needed • Observe and document seizure

Headache

Most Common Pain Complaint

Most are functional (non-lifethreatening)

Structures that can cause the pain include:

• Venous sinuses, dura mater, and cranial blood vessels

• Nerve pathways

Primary headaches

(not caused by another condition): • Tension-type, Migraine, Cluster

Secondary headaches

(result from another issue): • Sinus infection, neck injury, brain tumor

Tension-Type Headache

Known as stress headaches; most common

Pain Description:Bilateral, dull, tight, or band-like pressure

Diagnosis: • Based on history, tenderness, resistance to movement • EMG for muscle tension

Treatment: • Symptomatic: NSAIDs, acetaminophen, aspirin, muscle relaxants

• Preventive: Tricyclic antidepressants, antiseizure meds, stress management

Migraine Headaches

Recurring; typically unilateral (on one side), pulsating/throbbing pain

•Onset: 25–55 years; more common in women

•Categories: • With aura (visual, sensory, or speech changes)

• Without aura (more common)

•Pathophysiology:

• Genetic and vascular-neuro triggers • Involves brain inflammation, vasodilation, hyperexcitability •Triggers: • Hormones, sleep changes, certain foods, barometric pressure, alcohol, stress

Symptoms: • Nausea, photophobia, phonophobia, fatigue, difficulty concentrating

Treatment: • Symptomatic: NSAIDs, caffeine combos, aspirin • Moderate-Severe: Triptans (cause vasoconstriction and reduce neurogenic inflammation) • Preventive: • Antiseizure meds (Topiramate, valproate) • Beta blockers, CGRP antagonists, Botox (for chronic migraines)

Cluster Headaches

Most severe primary headache •Affects trigeminal nerve; more common in men and smokers

Pain: • Intense, sharp, stabbing around one eye; may radiate

• Occurs in "clusters" (several per day for weeks)

•Autonomic symptoms: • Tearing, nasal congestion, facial flushing, miosis

•Triggers: • Alcohol, heat, strong odors, tyraminerich foods

Treatment: • Symptomatic: • 100% oxygen at 7–12 L/min for 15–20 minutes • Triptans (contraindicated in some with vascular disease)

• Preventive: • High-dose verapamil • Invasive options: nerve blocks, deep brain stimulation

Medication Overuse Headache (MOH)

Rebound headaches due to excessive analgesic use

• Common culprits: NSAIDs, triptans, opioids, butalbital, ergotamine

Multiple Sclerosis (MS)

Chronic, progressive CNS disorder

•Caused by demyelination of nerve fibers in brain and spinal cord

•Onset: 20–50 years

•Symptoms often begin 30–35 years

•More progressive if diagnosed after 50

•More common in temperate climates

•Linked to environmental exposure before puberty • Cause unknown, but may include: • Infections, smoking, trauma, stress, pregnancy, genetics

Three Key Processes: 1.Chronic inflammation 2.Demyelination 3.Gliosis (scarring) in CNS

• an autoimmune disorder driven by activated T cells

MS Progression & Clinical Course

Demyelination affects impulse speed, not the nerve itself

• Impulses still occur, but are slowed

• Myelin may regenerate = remission phase

Over time: regeneration stops → permanent damage • Impulse transmission fails • Function is lost

• Gradual onset, vague symptoms over months/years • Often missed early • May experience: • Progressive deterioration • Remissions and exacerbations • Overall trend: worsening neurologic function

MS Clinical Manifestations

Early signs: •Blurred/double vision, red-green distortion, vision loss

•Motor: Weakness, spasticity, scanning speech

•Sensory: Numbness, pain, tinnitus, hearing loss

•Cerebellar: Ataxia, dysarthria, dysphagia, nystagmus (rapid involuntary movements of the eyes)

•Bladder/Bowel:

•Constipation •Spastic (overactive) or flaccid (underactive) bladder

•Cognitive: Short-term memory, planning, word finding

•Emotional: Anger, depression, euphoria

•Fatigue is very common

Diagnosis of MS

No definitive single test

•Based on: •History, symptoms, and imaging:

•MRI: plaques, inflammation, atrophy

•CSF analysis: ↑ IgG, oligoclonal bands

•Evoked potentials: delayed responses (vision/hearing)

•Diagnosis requires: •2+ demyelinating lesions in 2+ CNS locations •Occurrence at different times •Exclusion of other conditions

Parkinson ’s Disease (PD)

Chronic, progressive neurodegenerative disorder

• Cause: Unknown • Linked to genetics + environmental exposures (e.g., pesticides, rural areas) • Family history in 15% of cases

• Patho Key Points: • Loss of dopamine-producing neurons in the substantia nigra • Results in imbalance with acetylcholine • Leads to motor issues: tremor, rigidity, slowed movement • Lewy bodies = abnormal protein clumps (can cause Lewy body dementia)

PD Cardinal Motor Symptoms

“TRAP”

Tremor • Often first sign; resting “pill-rolling” tremor • Increases with stress/concentration

Rigidity • Jerky, “cogwheel” resistance to movement • Muscle soreness, fatigue

Akinesia / Bradykinesia • Loss/slowness of voluntary movements • Masked face, drooling, shuffling gait

Postural Instability • Balance issues, risk for falls • Test: Pull patient backwards gently

Progression of Motor symptoms of PD

• Early: Mild tremor, ↓ arm swing

• Later: • Shuffling, propulsive gait with arms flexed

• Speech issues (hypokinetic dysarthria—quiet/monotone) • Loss of automatic movements: • Stooped posture, masked face, festination (short steps)

Progression of Non motor Symptoms of PD

• Neuropsych: Depression, anxiety, apathy

• Autonomic: • Constipation, urinary retention • Erectile dysfunction

• Cognitive: Memory changes, dementia risk

• Sleep problems: • Insomnia, daytime drowsiness

• REM sleep behavior disorder (acting out dreams)

PD Complications

Dementia, depression, hallucinations

• Dysphagia → risk for aspiration & malnutrition

• Debilitation → pneumonia, UTIs, skin breakdown

• Orthostatic hypotension → increased falls

PD Diagnosis

• No specific test

• Based on TRAP symptoms and history

• Positive response to antiparkinsonian drugs = confirmation

Drug Therapy in Parkinson’s Disease

Primary Treatment: Levodopa-Carbidopa (Sinemet)

Levodopa crosses the blood-brain barrier and converts to dopamine (DA). • Carbidopa prevents levodopa breakdown before it reaches the brain

Start with one drug → fewer side effects, easier to adjust.

Wearing Off" Phenomenon (Hypomobility) • Symptoms return as medication wears off. • Often begins 3–5 years after starting treatment.

Surgical Options for Advanced PD

When Used: • For patients not responding to medication or with severe motor issues.

Deep Brain Stimulation (DBS) • Most common surgical treatment. • Reversible and programmable. • Decreases abnormal brain activity from DA loss. • Benefits: improves movement, reduces dyskinesia, lowers medication needs.

Other Surgical Interventions • Ablation surgery: Targets and destroys overactive brain areas causing symptoms.

• Neural transplantation (experimental): Fetal neural tissue transplanted into basal ganglia to replace DA-producing cells.

Nutritional Therapy in PD

Goals: Prevent malnutrition and constipation.

Tips for Dysphagia & Bradykinesia: • Choose soft, easy-to-swallow, appetizing foods.

• Ensure adequate fiber and fruits.

• Prefer 6 small meals over 3 large ones for energy conservation.

Medication Considerations: • Levodopa absorption reduced by high-protein diets and vitamin B6—plan meals around dosing.

Plan meals carefully to minimize frustration and maximize intake.

Amyotrophic Lateral Sclerosis (ALS)

Progressive, fatal neurological disease affecting motor neurons (voluntary movement). •

No cure; treatment is symptomatic and collaborative. • Motor neurons degenerate, disrupting brain-to-muscle communication.

Signs & Symptoms • Early: Dropping objects, tripping, slurred speech.

• Progressive: Muscle weakness, fasciculations, spasticity, dysarthria, dysphagia, drooling, hyperreflexia.

• Fatigue, pain, respiratory compromise, emotional lability, and memory changes possible.

• Death usually due to respiratory failure from aspiration, paralysis, or infection.

ALS Nursing Interventions

Educate patient and family on disease progression.

• Support communication, mobility, and respiratory function.

• Reduce aspiration and fall risk.

• Promote ROM to limit spasticity.

• Administer medications for: Pain, excessive salivation, muscle cramps, constipation, depression

. • Provide emotional and anticipatory grief support.

Refer to OT, PT, speech therapy, home care, and hospice services.

Myasthenia Gravis

Autoimmune neuromuscular disease affecting voluntary muscle transmission.

• Caused by antibodies attacking acetylcholine receptors (AChR) at the neuromuscular junction.

Pathophysiology: • Blocks acetylcholine → reduced muscle contraction.

• Weakness increases with use, improves with rest.

Key Features: • Onset often starts with eye and facial muscles (ptosis, diplopia, masklike appearance).

• Can progress to involve swallowing, speech, and respiratory muscles.

Diagnostic Tools Myasthenia Gravis

History & Physical: Muscle weakness, fatigue with gaze

. • Tensilon Test: Short-term improvement confirms it

• EMG: Decreased response to repeated stimulation.

Myasthenic Crisis

(too little medication): Weakness, respiratory failure. Improves with IV anticholinesterase.

Cholinergic Crisis (Myasthenia Gravis)

(too much medication): Muscarinic symptoms (salivation, cramps, diarrhea). Triggered by excess anticholinesterase drugs.

Interventions: Myasthenia Gravis

Keep tracheostomy kit at bedside during hospitalization.

• Administer meds as prescribed; stress medication timing.

• Conserve energy: morning activities, rest periods.

• Teach importance of Medic Alert bracelet.

• Avoid fatigue and stress (physical, emotional, spiritual).

• Encourage easy-to-swallow foods and frequent hydration.

Encourage coughing & deep breathing every 4–6 hr to prevent infection.

• Monitor for recurrent respiratory and bladder infection

Priority Nursing Diagnoses for Myasthenia Gravis

• Ineffective airway clearance

• Risk for injury and aspiration

• Impaired physical mobility • Risk for imbalanced nutrition

Trigeminal Neuralgia

Primary Cause: typically caused by compression of the trigeminal nerve (cranial nerve V) by an artery or vein, leading to nerve irritation. This compression can result in demyelination, which makes the nerve more susceptible to pain signals.

Secondary Causes: • Less commonly, it may be caused by tumors, multiple sclerosis (which can damage the myelin sheath), or other abnormalities affecting the nerve.

Trigeminal Neuralgia Clinical Manifestations

• Pain: The hallmark symptom is severe, sudden, sharp, stabbing or electric shock -like pain that affects one side of the face. The pain typically follows the distribution of the trigeminal nerve, often affecting the jaw, cheek, or forehead.

• Trigger Zones: The pain can be triggered by routine activities like chewing, speaking, brushing teeth, or even touching the face.

• Duration: Pain episodes are usually brief, lasting a few seconds to a couple of minutes, but can occur in rapid succession. There may be periods of remission where the pain subsides.

Trigeminal Neuralgia Diagnostic

Clinical Diagnosis: Based on the characteristic pain pattern and response to certain triggers.

• MRI: Often performed to rule out secondary causes, such as tumors or vascular abnormalities, that could be compressing the trigeminal nerve.

Medication for trigeminal neuralgia

Anticonvulsants: Carbamazepine is the most commonly prescribed medication as it helps stabilize nerve activity.

Other options include oxcarbazepine, gabapentin, and lamotrigine

. • Muscle Relaxants: Baclofen may be used in combination with anticonvulsants.

Surgical Options: trigeminal neuralgia

Percutaneous Radiofrequency Rhizotomy: A procedure where a needle is inserted through the cheek to reach the trigeminal nerve. Radiofrequency energy is then used to damage the nerve fibers selectively, reducing the transmission of pain signals. •

Microvascular Decompression (MVD): A surgical procedure to relieve pressure on the trigeminal nerve by moving or removing the blood vessels that are compressing it. This procedure has a higher success rate in providing long-term relief.

Bell ’s Palsy

Primary Cause: inflammation of the facial nerve (cranial nerve VII), leading to temporary paralysis or weakness of the muscles on one side of the face. The exact cause is unknown, but it is often linked to viral infections, such as herpes simplex virus (HSV), which can reactivate and cause nerve inflammation.

Other Triggers: Other potential triggers include upper respiratory infections, stress, or a compromised immune system.

Clinical Manifestations:Bell’s Palsy

Facial Weakness or Paralysis: Sudden onset of weakness or paralysis on one side of the face, making it difficult to close the eye, smile, or wrinkle the forehead on the affected side.

• Drooping: Drooping of the mouth, causing drooling and difficulty with speech and eating.

• Eye Issues: Inability to close the eye on the affected side, leading to dry eye, irritation, or excessive tearing.

• Taste Changes: Altered taste sensation on the front two -thirds of the tongue.

• Ear Pain: Some patients may experience pain around the ear or increased sensitivity to sound on the affected side.

Bell’s Palsy Diagnostics

Clinical Diagnosis: is primarily diagnosed based on the sudden onset of facial weakness or paralysis and exclusion of other conditions (e.g., stroke, tumors)

. • Imaging: MRI or CT scans may be performed to rule out other causes of facial nerve paralysis.

• Electromyography (EMG): Can be used to assess the extent of nerve damage and prognosis.

Treatment: Bell’s Palsy

Corticosteroids: Prednisone is typically prescribed to reduce inflammation and swelling of the facial nerve, especially if started within 72 hours of symptom onset.

• Antiviral Medications: May be used if a viral cause, like herpes simplex, is suspected.

• Eye Care: Important to protect the eye on the affected side, as blinking may be impaired. This may include using lubricating eye drops, wearing an eye patch, and taping the eye closed at night.

• Physical Therapy: Facial exercises may help maintain muscle tone and improve recovery.

Overview of Guillain-Barré Syndrome (GBS)

Occurs: A few days or weeks after viral or bacterial infection.

• Cause: Unknown, but immune response (cellular and humoral) is believed to play a role.

• Result: Myelin sheath or nerve axon damage leading to weakness, pain, and other neurological impairments.

Pathophysiology • Nerve Transmission: Slowed or stopped, leading to flaccid paralysis, muscle atrophy, and denervation.

• Maximum Weakness: Reached in 4 weeks.

• Recovery: Slow remyelination in a proximalto-distal pattern.

• Triggering Infections

• Viral/Bacterial infections: • Cytomegalovirus (most common virus) • Campylobacter jejuni (most common bacteria) • Other triggers include Epstein-Barr, Mycoplasma pneumoniae, and Zika virus.

Guillain-Barré Syndrome Clinical Manifestations

Main Features:

• Rapidly progressing, symmetric weakness (starts from hands/feet and moves upwards).

• Early Symptoms: • Weakness • Paresthesia (numbness, tingling) • Hypotonia (decreased muscle tone) • Decreased reflexes in affected limbs.

• Maximal Weakness: Occurs at 4 weeks.

Guillain-Barré Syndrome Complications

• Autonomic Nervous System Dysfunction:

• Orthostatic hypotension • Hypertension (HTN) • Abnormal vagal response (bradycardia, heart block) • Loss of consciousness, bowel/bladder dysfunction, and facial flushing.

• Pain: • Paresthesia, muscle aches, cramps, and hyperesthesia (increased sensitivity to touch). • Pain is worse at night.

• Respiratory and Other Complications • Most Serious: Respiratory failure (paralysis progresses to thoracic nerves, requiring mechanical ventilation).

• Other Risks: • Respiratory infections, UTIs • Paralytic ileus, muscle atrophy, VTE, orthostatic hypotension, decreased nutrition.

Recovery & Prognosis in GBS

Recovery begins around day 28

• 80% regain ability to walk independently by 6 months
• 60% achieve full recovery within 1 year

Prognosis Influenced By: • Age • Presence of GI infection • Rapid onset of symptoms • Hospital stay > 11 days • Need for mechanical ventilation

tonic phase

stiffening

clonic phase

jerking movements

Glascow Coma Scale
• Level Of Consciousness

Normal GCS= 15
Mild impairment= 13-14
Moderate impairment= 9-12
Major impairment= <8