Neurological Conditions
What is a Seizure? : Disruption in electrical brain function
Define Seizure: Electrical dysfunction in the brain. Affects the following
Consciousness
Motor
Sensation
What is a convulsion? : Violent contraction of muscles. Specifically refers to the physical S/S
What is an Epilepsy? Chronic; unprovoked seizure and recurrent. Two or more seizures occurring more than 24 hours a part without identifiable cause
Assessing Seizure Disorders
EEG (nodes into scalp, for abnormal brain waves
CT scan (detailed images of brain)
MRI (soft tissue imaging of brain
Skull Radiography (X-ray imaging of bone structure)
Medical History (triggers, symptoms, family hx, medication related)
What is the difference? What do each look like? S/S
There are many different types of seizures to know
Focal Aware Seizure
Patient remains awake and alert
limbs start switching
weird sensations or strange emotions
Focal Impaired Awareness Seizure
Patient stares blankly and their consciousness is altered
Automatisms means repetitive movements
I.e. lip- smacking, chewing, hand-rubbing
Absence Seizure
Brief blank stare 5-30 seconds
Eyelid fluttering
No movement, falling or jerking (able to stand)
Tonic-Clonic Seizure
Loss of consciousness
Tonic: Body stiffens
Clonic: Limbs jerk rhythmically
Atonic Seizure
Sudden loss of muscle tone
patient limp, drops or falls
Convulsion = physical manifestation; what you SEE and TOUCH
Convulsion S/S
Violent, involuntary jerking or stiffening of muscles
Rhythmic limb movements
Teeth clenching
Loss of bladder/bowel control may happen
Epilepsy
Pattern of seizures over time
Patient history of seizures “I’ve had several seizures over the past year
Recurring episodes
Without obvious trigger
Patient appears normal in between
i.e. A child with absence seizures occurring 10-20 times per day
i.e. An adult with tonic-clonic seizures happening monthly
i.e. Patient with a mix of focal and generalized seizures over months/years

Focal Seizures Slide
What is a focal seizure?
AKA partial seizures
Origin: specific area/group of cells on ONE side of brain
S/S vary depending on region of brain that’s affected
Different types of Focal Seizures
Focal Aware Seizure
Awake and Aware; conscious
Unusual sensations, sudden localized twitching, strange emotions
Focal Impaired Awareness Seizures
Confusion or partial loss of awareness; altered consciousness
Blank stare, automatisms
Focal to Bilateral Seizures
One side of brain then spread to both hemispheres
Generalized seizure, initial focal S/S
Partial Simple Seizure Slide
Localized, fully aware not altered consciousness
Because consciousness is there, pt can describe S/S, use this as assessment documentation
Motor Manifestations
Rhythmic jerking of one limb or face
Tonic stiffening of extremity
Jacksonian march (idk)
Todd’s paralysis (idk)
Sensory/Autonomic Manifestations
Tingling, numbness, burning sensation
Visually disturbed from flashing lights, spots
Auditory or olfactory aura
Means they hear sounds that aren’t there, pt can describe what they’re hearing “Do you hear that?” “What’s that noise?”
Ringing, buzzing, humming, roaring, clicking, popping, voices
Olfactory: burning smell (most common)
Flushing, pallor, piloerection (hairs stand up)
Generalized Seizures Slide
Both hemisphere of brain simultaneously abnormal electrical. Widespread effect of consciousness and motor function. Both sides of body
Tonic-Clonic Seizure
Loss of consciousness
Tonic: Body stiffens
Clonic: Limbs jerky rhythmically
Falls
Absence Seizures
Person stops moving
Blank stare (5-30 seconds), don’t hear their name
Last a few seconds; common children, rare in adults
Atonic Seizures (Drop attack)
Sudden loss of muscle strength; limp
Falls
Myoclonic Seizures
Brief, shock-like muscle jerk or twitches in specific muscle group
Clonic Seizures
Limbs jerky rhythmically
Tonic Seizures
Body stiffens
Falls
Absence Seizures S/S Slide
Form of generalized seizure common w/ children, 5-30 seconds
Commonly mistaken for not paying attention/daydreaming
No aura No postictal phase
Aura
Warning sign BEFORE seizure
Postictal
period AFTER seizure ends
Classic S/S of Absence Seizure
Suddenly stops activity
Blank, fixed stare
Eyelid fluttering (3 Hz)
No falling or convulsions
During Absence Seizure
Unresponsive verbally
Automatisms
May happen multiple times a day
Abrupt onset and offset
Happens without warning (onset)
Stops suddenly like nothing happened (offset)
After Absence Seizure
No postictal confusion
Patient unaware they just had a seizure
Immediately able to return to activity
EEG Hallmark of Absence Seizure
3 Hz spike-and-wave discharges— diagnostic for absence seizure. First-line treatment: Ethosuximide
Treatment for Generalized Seizures
Treatment selection depends on seizure type, patient age, and comorbid conditions
Tonic-Clonic Seizures
Loss of consciousness, muscle rigid, rhythmic jerking movements
Carbamazepine (Tegretol)
Blocks sodium channels
Common Side effects
Dizziness, drowsiness, and nausea
Monitor
CBC and liver function
Risk of aplastic anemia
Phenytoin (Dilantin)
Stabilizes neuro membranes
Monitor
drug levels closely; narrow therapeutic range
S/S of toxicity
Nystagmus (rapid eye movement; involuntary)
Ataxia (“drunk” loss of coordination)
Gingival Hyperplasia (inflamed gums, swollen)
Valproic Acid (Depakene)
Increases GABA activity
Monitor
Liver Function Tests (LFTs)
Amylase/Lipase
Common Side Effects
GI upset
Tremors
Weight gain
S/S of toxicity
Hepatotoxicity & Pancreatitis
Myoclonic Seizures
Brief jerks of muscle groups, occurs in clusters
Valproic Acid (Depakene)
First-line for myoclonic seizures
Enhances inhibitory neurotransmission
increases the activity of chemicals that SLOW DOWN brain activity
S/S of toxicity
Hepatotoxicity & Pancreatitis
Treatment for Status Epilepticus Slide
Life threatening. More than 5 minute seizure or recurrent seizures without recovery in between. Can lead to permanent brain damage, respiratory failure, death
Immediate Assessment (1)
Airway & administer oxygen
Establish IV access
Monitor Vital Signs
First-line treatment (2)
Administer Benzodiazepines (Lorazepam or Diazepam IV)
to stop seizure
Second-line treatment (3)
If seizure continues even after benzodiazepines
Phenytoin or Fosphenytoin IV loading dose under cardiac monitoring
Ongoing Management (4)
ICU admission; continue to monitor EEG
Identify and treat underlying cause and prevent complications
AEDs (Antiepileptic Drugs) Key Side Effects Slide
High risk drugs with significant side effects. Monitor closely and educate patient. Routine labs required. Following are side effects of each drug
Nurse Priority: Teach patient never to abruptly discontinue AEDs — can lead to status epilepticus (seizure that doesn’t stop)
Phenytoin (Dilatin)
Gingival Hyperplasia (swollen, inflammation of gums)
Ataxia (“drunk” loss of coordination)
Nystagmus (rapid eye movement; involuntary)
Diplopia (you see two images of the same object)
Steven-Johnson syndrome (rare) (red patches of skin)
Monitor: Serum levels, CBC, LFTs
Carbamazepine (Tegretol)
Aplastic Anemia (bone marrow stops making RBCs)’
Agranulocytosis (bone marrow stops making WBCs, specifically neutrophils)
SIADH (Too much ADH hormone; retain too much water)
Hyponatremia (too much water; blood too diluted)
(Mild) N&V, headache, confusion, weakness → (severe) seizure, coma, cerebral edema, death
Diplopia (you see two images of the same object)
Dizziness
Monitor: Serum levels, CBC, sodium
Valproic Acid (Depakote)
Hepatotoxicity (toxic to liver) — monitor LFTs
Thrombocytopenia (low platelet count; can’t clot properly)
Teratogenic (cause birth defects)
Weight gain, hair loss, tremors
Levetiracetam (Keppra)
Behavioral changes; irritability, aggression
Somnolence, dizziness
Mood disorders / depression
Relatively favorable safety profile
Brain & Cerebellar Disorders
Different parts of brain affected affects different things
Cerebellum
motor control
Balance
Posture
Cerebral cortex
Cognition
Planning
Voluntary movement
Clinical Signs (Cerebellum & Cerebral cortex)
Abnormal movement
Cognitively challenged
Autonomic issues (things body does w/o thinking)
Breathing, sweating, digesting, etc.
Parkinson’s Disease
Movement disease. Brain cells that make dopamine DIE. Progressive and degenerative. NOT curable but treatable
4 Main Symptoms
Resting Tremor
W/O dopamine, muscles twitch and shake
Being still makes hand shake looks like you’re rolling a small pill — usually starts in one hand
Bradykinesia
Brady = slow
Kinesia = movement
Hard to START moving (biggest problem) & moving slower
Rigidity
Muscles tight all the time
Postural Instability
Not upright, cannot balance well, wobbly, high fall risk
Neurotransmitter Balance Theory Slide
Imbalance between Dopamine & Acetylcholine
Dopamine ↓ Acetylcholine ↑
Dopaminergic loss (neurons that make dopamine die) (1)
Reduced Dopamine (2)
Relative Acetylcholine Excess (3)
Treatment implications (4)
Treatment Options for Parkinson’s Disease
Levodopa (L-dopa)
Converted to dopamine by dopadcarboxylase. Dietary protein can affect absorption
Crosses Blood Brain barrier
GOLD STANDARD
Increased functional independence
Motor symptoms increases
Enhanced quality of life
Effective across all stages
Cons
Delayed Therapeutic Response (6 months)
High rate of dyskinesias (involuntary movement) (80% of people)
Amantadine (Symmetrel)
Promotes release of dopamine that’s already stored
Anticholinergic (blocks acetylcholine) & Antiviral properties
Uses
Mild PD S/S
Drug induced Parkinsonism
Side effect of a medication that causes Parkinson’s-like symptoms but not actually having Parkinson’s disease
I.e. tremors (resting), bradykinesia, rigidity (muscle stiffness)
Pharmacokinetics of Levodopa
L-Dopa is absorbed so fast in small intestine that it is converted to dopamine before it reaches the brain.
Dopamine can’t cross the blood brain barrier. less than 1% of L-dopa actually reaches CNS.Reaminer is metabolized and excreted by kidneys
Oral absorption (very fast in small intestine)
Peripheral metabolism (enzymes break down L-dopa too before crossing BBB)
Dopamine in blood stream leads to adverse effects → nausea & orthostatic hypotension
BBB transfer ( less than 1% is actually absorbed)
Renal Excretion (remaining 99% excreted)
Carbidopa (Lodosyn)
Prescribed along side Levodopa
Mechanism
Blocks the enzyme (decarboxylase) that converts L-dopa to dopamine prematurely
Carbidopa (lodosyn) cannot cross BBB so it doesn’t interfere with L-dopa effects
Advantages
L-dopa availability to CNS 10 fold → reduces l-dopa dose by 75%
Decreases side effects
Faster therapeutic effect
What is a stroke?
Cerebrovascular accident (CVA) blood flow in brain interrupted
Ischemic Stroke (87%)
Blood vessels in brain get blocked → ischemic brain, brain cells die
due to blood clot or traveling embolus (i.e blood clot from leg → brain)
Thrombotic Stroke
Most common ischemic stroke
Blood clot in the brain artery; typically athersclerotic plaque buildup in brain
Embolic Stroke
Blood clot forms elsewhere
Commonly in heart (atrial fibrillation) → travels to brain artery
Hemorrhagic Stroke (13%)
Blood vessels burst → bleeding into brain tissue → brain cell damaged through compression and toxic effects
Higher mortality rate
Transient Ischemic Attack (TIA)
Mini stroke
Temporary symptoms less than 24 hours
Evaluate immediately to prevent full stroke
Spot a Stroke FAST
F - Face Drooping
smile droops to one side or feel numb, uneven, lopsided
A - Arm Weakness
one arm weaker after goes down after lifted both up
S - Speech Difficulty
slurred speech, difficult to understand, unable to speak
T - Time to call 911
note when S/S began for treatment decision
Stroke Warning Signs
Sudden
Confusion
Numbness or weakness (one side of limb weak/numb)
Vision problems (Can’t see one or both eyes, blurred, double vision)
Trouble walking (loss of balance, coordination, dizziness)
Severe headache (worst headache of my life)
Risk Factors of Stroke
Hypertension
Sedentary lifestyle
Obesity
Smoking
Poor diet
Excessive alcohol
Chronic stress
High cholesterol
Atrial fibrillation
Depression
Cerebrum & Stroke
Two hemispheres, four lobes. each affect different parts
Frontal
Motor function, speech, executive function, personality
Parietal
Sensory, spatial awareness, temperature, pain
Temporal
Hearing, speech comprehension, memories
Occipital
Visual processing and interpretation
Right CVA
Stroke affecting right hemisphere. Right CVA pts often lack awareness of their deficits, close monitoring, fall precautions, frequent reorientation
Left sided Hemiplegia or Hemiparesis
Means left side body weakness/paralysis
Left arm, left leg, left face
Right Hemisphere Stroke → affects LEFT side of body
Difficulty judging distances, sizes, positions, ignoring left side of environment
Impulsivity and poor judgment
Left CVA
Stroke affecting left hemisphere. Left CVA often experience language barriers, easily irritated. Provide ample time for communication, use simple sentences, visual aid and expression
Right sided Hemiplegia or Hemiparesis
Means right side body weakness/paralysis
right arm, right leg, right face
Aphasia (language deficit)
Speech is hard, forming words, understanding commands
Slow and cautious behavior
Patients may be overly scared, taking risks, slow at actions
Stroke Prevention and Treatment
Distinguish if ischemic or hemorrhagic. Based on type of stroke and timing
Before Stroke Prevention (1)
Antiplatelet Drugs: Aspirin
Anticoagulant: Warfarin (Coumadin)
Antihypertensives: Blood pressure control (most effective)
After Ischemic Stroke (Acute Treatment)
tPA: clot buster, must be within 3-4.5 hours of stroke symptom onset
Verify onset time
Contraindications (recent surgery, bleeding disorders), neuro status q15m
After Hemorrhagic Stroke
No FDA-approved targeted therapy
Focus on controlling bleeding, blood pressure, intracranial pressure
Contraindications: anticoagulants and thrombolytics (worsens bleeding)
Life After Stroke
As soon as medically stable
Stroke Rehab
Physical Therapy
Speech Therapy
Psychological Support