Kristin Miller
I. MENINGITIS
A. Inflammation of the protective membranes covering the brain and spinal cord, collectively called the meninges, usually due to the spread of infection.
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Altered consciousness, 780.09 |
Meningitis, 322.9 |
B. Etiology.
1. Infectious.
a. Viral infections–most common cause, usually termed aseptic meningitis when no bacterial cause can be found
• Enteroviruses (90%).
• Herpes simplex virus type 2.
• Varicella zoster virus.
b. Bacterial.
• Newborns to 3 months of age.
i. Group B streptococci.
ii. Escherichia coli.
iii. Listeria monocytogenes.
• Older children.
i. Neisseria meningitidis.
ii. Streptococcus pneumonia.
iii. Haemophilus influenzae type B especially in countries that do not offer vaccinations.
c. Parasitic.
• Angiostrongylus cantonensis.
• Gnathostoma spinigerum.
2. Noninfectious.
a. Cancer.
b. Drugs.
• Nonsteroidal anti-inflammatory drugs (NSAIDs).
• Antibiotics.
• Intravenous immunoglobulin.
c. Inflammatory conditions.
• Sarcoidosis.
• Systemic lupus erythematous.
• Vasculitis.
C. Occurrence.
1. Viruses more likely in late summer and fall.
2. Bacterial: 3 per 100,000.
3. Viral: 10.9 per 100,000.
4. Increased risk with crowding and prolonged exposure such as daycare, military, college dorms, and those with compromised immune systems.
5. Age–most cases occur in children younger than 5 years, but decreased incidence with increased vaccination rates.
6. Race–higher incidence in African Americans than Caucasians.
7. Sex–viral 3 times more likely in males than females.
D. Clinical manifestations.
1. General population.
a. Classic triad of severe headache, nuchal rigidity, high fever.
b. Altered mental status.
• Confusion.
• Extreme irritability.
• Sleepiness
• Abnormal cry.
• Seizures.
c. Sensitivity to light.
E. Physical findings.
1. Signs in newborns.
a. Constant cry.
b. Excessive sleepiness or irritability.
c. Poor feeding.
d. Bulging fontanel (increased ICP).
e. Stiffness of body and/or neck.
f. Difficult to comfort, cries harder when picked up.
2. Positive Kernig's sign or Brudzinski's sign.
F. Diagnostic tests.
1. Lumbar puncture (LP)–definitive test for diagnosis, will see low glucose, increased white blood cells (WBC), increased protein, culture and Gram stain should be done.
2. Complete blood count (CBC), blood culture, C-reactive protein, polymerase chain reaction (PCR), erythrocyte sedimentation rate (ESR).
3. CT or MRI before LP since LP contraindicated with tumor, abscess, or increased intracranial pressure (ICP); MRI often done later to assess complications/sequelae.
G. Differential diagnosis.
|
Brain abscess, 324 |
Head injury, 959.01 |
H. Treatment.
1. Viral.
a. Supportive care–bed rest, fluids, analgesics.
b. Antiviral drugs–acyclovir for herpes simplex and varicella zoster.
c. May need to be admitted to monitor ICP or complications.
2. Bacterial.
a. Early intervention with antibiotics critical.
b. Always treat with antibiotic for most commonly known pathogens until diagnosis confirmed.
c. May need to be admitted to manage ICP, complications, administration of IV fluids and antibiotics.
d. Birth to 6 weeks–ampicillin and third-generation cephalosporin (Cefotaxime or Ceftriaxine).
e. Older than 6 weeks–vancomycin and third-generation cephalosporin.
f. Prophylactic treatment of contacts with patients with Neisseria meningitidis–sulfadiazine or rifampin.
I. Complications.
1. Increased ICP.
2. Deafness–may be prevented with prophylactic steroids.
3. Hydrocephalus.
4. Seizures.
5. Venous or cerebral infarction.
6. Cranial nerve palsies.
7. Up to 70% sustain sequelae from bacterial meningitis.
8. Most children with nonherpetic viral meningitis recover completely.
J. Follow up.
1. Frequent visits when cared for at home.
2. Immediately for any decline in neurological condition or respiratory distress.
3. Shortly after hospitalization to follow neurological status and assess pan for treatment of any sequelae.
K. Education.
1. Importance of prevention via immunizations.
2. Handwashing and infection-control measures, especially in crowded locations.
3. Prophylaxis for certain exposures.
4. Support and coordination of comprehensive services may be needed.
II. ENCEPHALITIS
A. Inflammation of the brain due to a viral infection.
|
Altered consciousness, 780.9 |
Lethargy, 780.79 |
B. Etiology.
1. Primary form: direct viral infection of the brain and spinal cord.
2. Secondary form: viral infection that first occurs elsewhere in the body and travels to the brain.
3. Exposure to viruses through:
a. Breathing in respiratory droplets from infected person.
b. Contaminated food or drink.
c. Insect bites or animal bites (rabies).
d. Specific viruses:
• Arboviruses–most common cause, carried by mosquitoes or ticks.
• Enteroviruses–coxsackievirus, echovirus, poliovirus.
• Others: herpes simplex encephalitis (most common and worst prognosis–10-40% mortality).
• Eastern equine: 70-90% mortality.
• Western equine.
• St. Louis encephalitis: 30% mortality.
• West Nile.
• California and Venezuela equine.
4. Allergic reaction to vaccinations (extremely rare).
5. Effects of cancer and treatments.
6. Autoimmune or immune response problems (immunocompromised, HIV).
C. Occurrence.
1. Seasonal: more common summer and fall.
2. Age: more prevalent or severe in young children and elderly.
3. Higher in those with weakened immune system.
4. Geographic: higher in areas where mosquito-borne viruses are common.
5. Outdoor activities increase risk.
D. Clinical manifestations.
1. Headache.
2. Nausea.
3. Lethargy.
4. Behavioral changes–confusion, disorientation, irritability, personality changes.
5. Joint pain, stiff neck.
E. Physical findings.
1. Fever.
2. Positive Brudzinski's sign or Kernig's sign.
3. Abnormal reflexes.
4. Rash.
5. Emergency symptoms:
a. Low level of consciousness (LOC), poor responsiveness.
b. Muscle weakness or paralysis.
c. Seizure.
d. Sudden change in mental functions.
e. Bulging fontanel.
F. Diagnostic tests.
1. LP with CSF exam may show hemorrhagic component and increase WBC.
2. Electroencephalogram (EEG)–periodic sharp waves at 2- to 3-second intervals on a background of diffuse or lateralized slowing if characteristic but nonspecific.
3. MRI–often abnormal, showing limited or massive areas of inflammation and necrosis.
4. PCR and blood antibodies–can show positive DNA for viruses.
5. CBC, toxicology screen.
G. Differential diagnosis.
|
Autoimmune disorder, 279.4 |
Intracranial hemorrhage, 432.9 |
H. Treatment.
1. Antiviral medications.
a. Acyclovir–herpes encephalitis or varicella zoster virus.
b. Ganciclovir–cytomegalovirus (CMV).
2. Antibiotics if bacterial cause.
3. Seizure medications as needed.
4. Steroids to reduce swelling.
5. Acetaminophen for fever and headache.
6. Rest and fluids.
I. Complications.
1. Acute phase lasts 1-2 weeks, may take several months to fully recover.
2. Permanent brain damage can occur in severe cases–can affect hearing, memory, muscle control, sensation, speech, vision.
3. Outcomes vary–high recovery (Rocky Mountain spotted fever), high morbidity (herpes encephalitis) definite mortality, especially if untreated (rabies).
J. Follow up.
1. Emergency for sudden fever or other symptoms of encephalitis.
2. Call for decline in neurological condition.
3. 2-4 weeks to assess for sequelae.
K. Education.
1. Importance of vaccinations: measles-mumps-rubella (MMR), varicella, meningococcal.
2. Immunizations specific for foreign travel.
3. Take steps to prevent genital herpes.
4. Avoidance of mosquitoes.
a. Apply DEET products, not on face, hands, or infants younger than 2 months.
b. Remove sources of standing water.
c. Wear long-sleeve shirts and pants when outside, especially at dusk.
5. Avoidance of ticks.
a. Avoid woods, clear brush in yard, and keep grass mowed.
b. Inspect body after return inside.
c. Avoid contact with vector/host animals.
6. Thoroughly cook meat and wash fruits/vegetables, especially in endemic areas.
III. HEAD INJURY
A. Any trauma that leads to injury to scalp, skull, or brain.
|
Alterations in consciousness, 780.09 |
Nausea, 787.02 |
B. Etiology.
1. Trauma from motor vehicle accident (MVA), physical assaults, falls, accidents at home, work, outdoors, or while playing sports.
2. Common causes include biking, skating, skateboarding, and contact sports.
3. Types.
a. Closed head–did not break the skull, more common.
b. Penetrating or open–break in skull where objects enter brain (50% mortality rate).
c. Focal brain injury–acute epidural, subdural, or subarachnoid hemorrhage.
C. Occurrence.
1. 1.7 million people sustain traumatic brain injury (TBI) annually. Majority are concussions or other forms of mild traumatic brain injury.
2. Contributes to substantial number of deaths and causes of permanent disability.
3. Range from mild with brief change in mental status or consciousness to severe with extended period of unconsciousness.
4. Falls cause 50% of TBI in children age 0 to 14 years.
5. Strike by moving or stationary object causes 25% of TBI in children ages 0 to 14 years.
6. Males more often sustain TBI (59%).
7. High-risk age groups–0 to 4 years and 15 to 19 years.
D. Clinical manifestations.
1. Occur immediately or over several hours to days.
2. Minor head injury symptoms:
a. Headache.
b. Dizziness.
c. Impaired concentration, thinking, and memory.
d. Blurred vision.
e. Distractibility.
f. Noise sensitive.
g. Depression.
h. Anxiety.
3. Severe head injury symptoms:
a. Impaired hearing, smell, taste, or vision.
b. Irritability, personality changes, unusual behavior.
c. Severe headache.
E. Physical findings.
1. Minor head injuries.
a. Unsteadiness.
b. Fatigue.
c. Irritability.
2. Severe head injuries.
a. Changes in or unequal pupils.
b. Convulsions.
c. Fracture in skull or face, bruising of face, swelling at site of injury.
d. Inability to move one or more limbs.
e. Loss of consciousness, confusion, drowsiness.
f. Restlessness, clumsiness, lack of coordination.
g. Stiff neck or vomiting.
F. Diagnostic tests.
1. Important to obtain history of exact details of injury.
2. Glasgow Coma Scale.
3. Head CT to identify significant contusion, hemorrhage, and swelling.
4. Skull and cervical plain films to evaluate skull or neck trauma.
5. Angiogram to evaluate blood vessels in cases of bleeding.
6. Certain cases may require CBC, comprehensive metabolic panel (CMP), blood alcohol level, drug screen, prothrombin time (PT), partial thromboplastin time (PTT), fibrinogen.
G. Differential diagnosis.
|
Brain tumor, 191.9 |
Meningitis, 320.9 |
H. Treatment.
1. Mild head injury–treated at home as long as someone available to monitor.
2. Acetaminophen for pain. No aspirin or ibuprofen due to increased risk of bleeding.
3. Do not:
a. Wash head wound that is deep or profusely bleeding.
b. Remove any object sticking out of wound.
c. Move the person unless absolutely necessary.
d. Shake the person to arouse.
e. Remove helmet if you suspect a serious head injury.
f. Pick up a fallen child with any sign of head injury.
4. Apply ice to reduce swelling.
5. Roll on side if vomiting.
6. Cover bleeding area with clean cloth, only press firmly if no concern for skull fracture.
7. Always treat as if spinal injury if patient unconscious, keep head midline and immobile.
8. Maintain airway and vital signs, CPR if needed.
9. Admit to hospital for severe injury, monitor for progression of symptoms or concern for increased ICP.
I. Complications.
1. Increased ICP.
2. Surgery to remove objects, control hemorrhage, or decompress brain.
3. Seizures.
4. Resulting focal deficits.
a. Weakness, aphasia, personality and intellectual changes, depression, anxiety, aggression, loss or change in: sensations, hearing, vision, taste, smell, speech, or language.
5. Paralysis.
6. Chronic headaches.
J. Follow up.
1. Seek care immediately for:
a. Vomiting more than once.
b. Confusion.
c. Drowsiness, unable to awaken.
d. Weakness or inability to walk.
e. Severe headache.
f. Severe head trauma or fall from more than height of the person.
g. LOC for > 1 minute.
h. Stops breathing.
i. Severe head or facial bleeding.
2. Follow up in 1 week after injury and every few weeks to monitor for and manage any sequelae.
K. Education.
1. Wear helmets for biking, skating, and other similar sports.
2. Wear proper sports equipment, and make sure in good condition.
3. Wear seat belts, use age-appropriate car seats.
4. Prevent falls by childproofing home–stairs, bathtubs, rugs, furniture.
5. Be visible and obey traffic laws when biking.
6. Safe areas to play.
7. Know signs and symptoms of head injury/concussion and know when to seek medical care.
IV. CONCUSSION
A. Alteration in mental status after a blow to the head, consciousness may or may not occur.
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Altered consciousness, 780.09 |
Confusion, 298.9 |
B. Etiology.
1. Type of traumatic brain injury caused from: bump, blow, or jolt to the head.
2. Blow to body can cause head and brain to move rapidly back and forth, resulting in head injury.
3. Results from falls, MVA, and players that collide with each other, ground, or obstacles.
C. Occurrence.
1. 135,000 sports- and recreation-related TBIs come to emergency departments (EDs) each year (includes concussions in children age 5-18 years).
2. Athletes who have had a concussion are at increased risk for another.
3. Children and teens are more likely to get a concussion and take longer to recover than adults.
4. More than 2 million concussions happen per year, 85% never diagnosed.
5. 50% of football players may experience one concussion per year.
D. Clinical manifestations.
1. Hallmark signs–confusion and amnesia that may occur immediately or several minutes after injury occurs.
2. Early (minutes and hours) symptoms experienced:
a. Headache.
b. Dizziness or vertigo.
c. Lack of awareness of surroundings.
d. Nausea or vomiting.
3. Late (days to weeks) symptoms experienced:
a. Persistent low-grade headache.
b. Light-headedness.
c. Poor attention and concentration.
d. Memory dysfunction.
e. Easy fatigability.
f. Irritability and low frustration tolerance.
g. Intolerance to bright light or loud noises.
h. Anxiety or depressed mood.
E. Physical findings.
1. Vacant stare.
2. Delayed verbal and motor responses.
3. Confusion and inability to maintain focus.
4. Disorientation.
5. Slurred or incoherent speech.
6. Incoordination.
7. Memory deficits.
8. Emotional.
9. Any period of unconsciousness.
10. Grade 1 concussion.
a. Transient confusion.
b. No loss of consciousness.
c. Concussion symptoms or mental status abnormalities resolve in less than 15 minutes.
11. Grade 2 concussion.
a. Transient confusion.
b. No loss of consciousness.
c. Concussion symptoms or mental status abnormalities last more than 15 minutes.
12. Grade 3 concussion.
a. Any loss of consciousness, either brief (seconds) or prolonged (minutes).
F. Diagnostic tests.
1. Sideline/immediate evaluation.
a. Orientation–to time, place, person, and situation.
b. Concentration–digits backward, months of year in reverse.
c. Memory–recall 3 words or objects, details of contest, names.
d. Physical tests–40-yard sprint, pushups, knee bends.
• Any associated symptoms with these tests are abnormal findings.
e. Neurological tests.
• Pupils, coordination, sensation.
2. Head CT–for Grade 2 concussion with symptoms that worsen or last longer than 1 week and for Grade 3 concussions.
3. Immediate post-concussion assessment and cognitive testing (ImPACT) testing to assess cognitive functioning, done soon after concussion and before return to activities, mostly for Grade 3 concussions.
G. Differential diagnosis.
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Migraine, 346.9 |
H. Treatment.
1. Remove from contest.
2. Monitor for progressive neurological changes.
3. ED for Grade 3 concussions.
4. When to return to play: need to be asymptomatic with normal neurological assessment at rest and with exertion.
a. Grade 1–after 15 minutes same day.
b. Multiple Grade 1–1 week.
c. Grade 2–1 week.
d. Multiple Grade 2–2 weeks
e. Grade 3 with brief LOC–1 week.
f. Multiple Grade 3–1 month or longer.
I. Complications.
1. Seizures.
2. Second impact syndrome–repeat concussion that occurs before the brain recovers from the first, can slow recovery or increase likelihood of long-term problems including brain damage, brain swelling, and even death.
3. Depression–not being able to participate in their sport.
4. Rare case for development of blood clot on brain.
J. Follow up.
1. See return to sports guidelines above, need to be cleared first.
2. Call or go to ED for:
a. Unequal pupils.
b. Drowsy and cannot awaken.
c. Worsening headache.
d. Weakness, numbness.
e. Repeated vomiting.
f. Seizure.
g. Slurred speech.
h. Increased confusion.
i. Unable to recognize people or places.
j. LOC.
K. Education.
1. Use protective equipment that fits properly and is well maintained.
2. Practice safe playing techniques/good sportsmanship.
3. Know signs and symptoms of concussion, when to sit out and when to return.
V. STATUS EPILEPTICUS
A. 30 minutes or more of continuous seizure activity or a series of seizures without return to full consciousness between seizures.
|
Alteration in consciousness, 780.09 |
Status epilepticus, 345.3 |
B. Etiology.
1. Idiopathic.
2. Central nervous system (CNS) neoplasms, stroke, infections, electrolyte abnormalities, trauma, metabolic disorders, toxic ingestion, hypoxic insult.
3. History of epilepsy.
4. Noncompliance with antiepileptic medications.
5. History of injury–MVA, fall.
C. Occurrence.
1. 50,000–200,000 cases per year.
2. Mortality rate 20%, mostly from underlying case of brain injury.
3. Can occur in all age groups, more in elderly.
4. Males and females affected equally.
D. Physical findings.
1. Absence status.
a. Confusion, lethargy.
b. EEG with continuous or intermittent but frequent spikes and slow wave discharges.
2. Focal motor status.
a. Continuous jerking of restricted muscle groups.
3. Complex partial status.
a. Confused, dazed, automatisms often present.
b. Most often series of seizures, remaining confused between seizures.
4. Generalized tonic-clonic status.
a. Continuous convulsions or repetitive convulsions without resolution of postictal depression between episodes.
E. Diagnostic tests.
1. EEG.
2. Head CT initially, may do MRI later if warranted.
3. CMP (focus on glucose, Na+, Ca++), toxicology screen, WBC.
4. LP if CNS infection in differential.
F. Differential diagnosis.
|
Encephalitis, 323.9 |
Stroke/ischemia, 434.91 |
G. Treatment.
1. Maintain vital signs and ABCs.
2. Administer DIASTAT AcuDIAL after 5 minutes of seizure activity. Call 911 if seizure continues.
3. Ativan IV: 0.1 mg/kg at 2 mg/min.
4. Diazepam IV: 0.3-0.5mg/kg at 2 mg/min.
5. Fosphenytoin, phenobarbital, phenytoin (Dilantin), divalproex sodium (Depakote IV). Monitor for respiratory depression.
6. Correct any abnormal laboratory findings.
7. Treat any underlying infection.
H. Complications.
1. Respiratory failure.
2. Aspiration.
3. Hypotension.
4. Acidosis.
5. Hyperthermia.
I. Follow up.
1. Coordinate with specialists for any associated injuries or complications.
2. See neurologist in 2 weeks.
3. Start maintenance antiepileptic medication, call for any side effects or further seizures.
J. Education.
1. Know signs and symptoms and when and how to give DIASTAT AcuDIAL.
2. Medication information and compliance.
3. Avoidance of any seizure triggers: sleep deprivation, alcohol.
4. Seizure safety: no tub baths unsupervised, monitor closely with swimming, helmets appropriate for sports, no driving until seizure free for 6 months, what to do during a seizure–lay on side on ground, do not put anything in mouth, time event, and keep safe.
VI. CONFUSIONAL MIGRAINE
A. Characterized by a typical migraine aura, headache, and confusion.
|
Confusion, 298.9 |
Irritability, 799.22 |
B. Etiology.
1. Idiopathic.
2. Triggered by head trauma.
C. Occurrence.
1. Rare, only 5% of migraine patients.
2. Single attacks are most common, multiple attacks are rare.
3. May evolve into typical migraine episodes.
D. Clinical manifestations.
1. Inattention
2. Distractibility.
E. Physical findings.
1. Impaired speech and motor activities.
2. Can last 10 minutes to 20 hours. A more profound, disturbed level of consciousness may lead to migraine stupor, which can last hours up to 5 days.
3. Confusional state is usually followed by sleep.
F. Diagnostic tests.
1. Complete neurological exam.
2. MRI and MRA to evaluate arteries within the brain.
3. History may include family history, history of trauma, and classic symptoms.
G. Differential diagnosis.
|
Acute psychosis, 298.9 |
Metabolic encephalopathies (Reye's |
H. Treatment.
1. Sleep.
2. Typical migraine-abortive medications.
I. Follow up.
1. Reoccurrence of episodes.
2. Change in neurological status (resulting from any head trauma).
J. Education.
1. Avoidance of migraine triggers.
2. Keep a headache/episode diary.
3. Limit use of over-the-counter analgesics.
4. Keep a regular schedule: meals, sleep, hydration, exercise, and minimize stress.
VII. HEADACHES: MIGRAINES
A. Episodic headache disorder characterized by various combinations of neurological, gastrointestinal, psychophysiological, and autonomic changes.
|
Benign paroxysmal vertigo, 386.11 |
Migraine, 346.9 |
B. Etiology.
1. Generally inherited disorder, 70-80% familial.
2. Leading hypothesis for origin–neurovascular disturbance triggered by multiple stimuli and affecting serotonin transmission in the CNS.
3. Episodic brain malfunction–a central nervous system disorder of primarily the brain and nerves, and secondarily of the blood vessels. Malfunction is caused in part by changes in the level of circulating neurotransmitters and involving serotonin in particular.
4. Head trauma.
5. Illness and infection.
6. Environmental and emotional factors.
7. Certain foods and beverages.
C. Occurrence.
1. Mean age of onset is 7.2 years for boys and 10.9 years for girls.
2. 3% of children age 3-7 years.
3. 4-11% for children age 7-11 years.
4. 8-23% for children age 11-15+ years.
5. Risk factors:
a. Children who have a family history of headaches or migraines.
b. Boys before they reach puberty.
c. Girls after they reach puberty.
d. Children over age 10 years.
D. Clinical manifestations.
1. Pounding or throbbing head pain. In children, pain usually affects the front or both sides of the head. In adolescents, pain usually affects one side of head.
2. Pallor or paleness of skin.
3. Irritability.
4. Phonophobia or sensitivity to sound.
5. Photophobia or sensitivity to light.
6. Loss of appetite.
7. Nausea and/or vomiting, abdominal pain.
8. Dizziness.
E. Physical findings.
1. May have none if not experiencing migraine at time of exam.
2. Due to pain, may see increase in heart rate or blood pressure.
3. Look of discomfort in facial expressions and demeanor.
4. Wanting to lie down in quiet, dark room.
F. Diagnostic tests.
1. Most important aspect of diagnosing migraine is the headache history.
a. Description of current and previous headaches, when started.
b. Headache frequency, duration, and associated symptoms.
c. What medications have been taken and are currently being taken.
d. Family and medical history.
e. Pain location, quality, and severity–how disabling?
f. Social history–psychological symptoms.
g. Precipitating factors.
2. Complete neurological exam–including fundoscopic exam to rule out papilledema.
3. Head CT.
a. Recent/new onset.
b. Evolution or change in headaches.
4. Head MRI.
a. Papilledema present.
b. Focal neurological signs–abnormal exam, hemiparesis.
c. Complicated migraine–examine blood vessels that supply the brain.
5. Evaluation as needed if concern for infectious cause.
a. LP if concern for increased intracranial pressure/papilledema present; generally need to do head MRI prior to LP.
G. Differential diagnosis.
|
Brain tumor, 239.6 |
Papilledema, 377 |
H. Treatment.
1. Treat underlying pathology if present.
a. Diamox for pseudotumor cerebri.
2. Goals of treatment.
a. Reduce attack frequency, severity, and duration.
b. Improve responsiveness to treatment of acute attacks.
c. Improve function, reduce disability, and improve quality of life.
3. Nonpharmacologic treatments.
a. Relaxation techniques, biofeedback, stress management.
b. Rest, quiet dark room, applying ice packs to forehead or neck.
c. Lifestyle/behavioral interventions.
• Maintain routine sleep pattern with adequate sleep hours.
• Regular routines, meal, exercise, school attendance.
• Staying hydrated.
• Avoidance/discontinuation of caffeine.
• Avoidance/discontinuation of overuse of abortive medications.
• Stress reduction.
4. Acute medication treatment.
a. Medication should not be used more than 2, or at most, 3 days a week to prevent development of rebound headaches.
b. Prevents or stops progression of headache.
c. Use medication as early as possible to prevent escalation and to increase the drug's effectiveness.
d. Mild to moderate pain: ibuprofen (NSAIDs with or without caffeine) or acetaminophen (Tylenol).
e. Moderate to severe pain: triptans (contraindicated for migraine variant such as hemiplegic or basilar migraine), ergotamine, dihydroergotamine (DHE).
f. Antiemetics to help relieve pain, nausea, vomiting.
g. Steroid dose pack to break migraine status, prolonged migraine.
5. Preventative medication treatment.
a. Use when:
• Recurring migraine that interferes with daily routine despite acute treatment (two or more attacks/month that produce disability and can last up to 3 days or more).
• Failure, contraindication, or side effects from acute medications.
• Overuse of acute medications.
• Frequent headaches (more than 2/week) with risk for rebound headache syndrome.
b. Medication options:
• Antidepressants: amitriptyline (Elavil), fluoxetine (Prozac), duloxetine (Cymbalta).
• Beta blockers: propranolol (Inderal).
• Antihistamines: cyproheptadine (Periactin) (most effective in toddlers).
• Calcium channel blockers: verapamil.
• Anticonvulsants: valproic acid (Depakote), topiramate (Topamax).
I. Follow up.
1. Assess medication effectiveness, monitor for any possible side effects.
2. When abortive medications do not elevate migraine, may need IM or IV abortive medications and fluids such as ketorolac (Toradol) or promethazine (Phenergan).
3. Any neurological changes or progression in headaches.
J. Complications.
1. Comorbid anxiety and/or depression.
2. Medication side effects.
3. Acute vascular disorder.
4. High incidence of motion sickness.
5. Sleep disturbance.
6. Drop in school performance due to missed days, and inability to concentrate with a headache.
K. Education.
1. Migraine diagnosis and treatment (medications/possible side effects).
2. Keep a headache diary, look for headache triggers.
3. Know symptoms and when to treat headache.
4. Limit use of abortive medications.
5. Behavioral modifications, follow routine schedule.
6. Daily school attendance.
7. Reduce stress and avoid triggers.
8. Empower patient and family to be involved and take control of their headaches and treatment.
VIII. TENSION-TYPE HEADACHES
A. Headache that presents with pressure/tightening quality and lacks migraine criteria.
|
Headache, 784 |
Pain, neck, 723.1 |
B. Etiology.
1. Behavioral.
2. Muscular.
3. Vascular.
4. May coexist with otherwise typical migraine headaches.
C. Occurrence.
1. Most common benign headache disorder.
2. 10-25% prevalence in childhood and adolescence.
3. Boys and girls tend to suffer equally until age 11 or 12 when female preponderance occurs.
D. Clinical manifestations.
1. Episodic headaches occur less than 15 days/month.
2. Chronic headaches occur more than 15 days/month.
3. Can last 30 minutes to 7 days.
4. Pain is mild to moderate (not severe).
5. Pain is bilateral and described as pressing or tightening, may occur in a hat band distribution.
6. Pain not aggravated by physical activity (unlike migraine).
7. No nausea or vomiting.
8. May have photophobia or phonophobia, but not both.
E. Physical findings.
1. Normal neurological exam, worrisome if abnormal.
2. May see signs of pain: facial expressions, demeanor, increased heart rate and blood pressure.
3. May be misdiagnosed as sinus headache.
F. Diagnostic tests.
1. Same as migraine.
2. History/complaints consistent with tension-type headache criteria.
G. Differential diagnosis.
|
Allergies, 995.3 |
Sinusitis, 473.9 |
H. Complications.
1. Depression.
2. Poor academic performance, difficulty concentrating, missed school days and other activities.
I. Treatment.
1. Nonpharmacologic treatments.
a. Healthy habits.
• Adequate routine sleep schedule.
• Balanced meals.
• Regular exercise.
• No caffeine.
b. Psychophysiological therapy.
• Reassurance.
• Counseling.
• Stress management.
• Relaxation therapy.
• Biofeedback.
• Treatment of anxiety and/or depression.
2. Pharmacotherapy.
a. Acute treatment–not to be used more than 2 days/week.
• NSAIDs.
• Acetaminophen.
b. Preventative treatment.
• Amitriptyline (Elavil).
• Selective serotonin reuptake inhibitors (SSRIs).
• Muscle relaxers (tizanidine [Zanaflex]).
J. Follow up.
1. Assess medication effectiveness and any possible side effects.
2. Any neurological change or headache progression.
K. Education.
1. As with migraines.
IX. COMMON MEDICATIONS TO TREAT HEADACHES IN CHILDREN
A. Preventative:
1. Cyproheptadine (Periactin): 0.25-0.4 mg/kg or 2-4 mg daily bid.
2. Amitriptyline: start 10 mg at bedtime. Up to 1-2 mg/kg at bedtime.
3. Propranolol (Inderal): 1-2 mg/kg/day up to 4 mg/kg/day bid. Unless using LA form.
4. Tizanidine (Zanaflex): 2-4 mg at bedtime up to 12 mg. Monitor hepatic panel at 1, 3, and 6 months.
5. Valproic acid (Depakote): 10-20 mg/kg bid up to 60 mg/kg.
6. Topiramate (Topamax): titrate to 50 mg bid.
7. Verapamil: 40 mg tid or SR 120 mg, 180 mg, 240 mg daily.
B. Abortive:
1. Sumatriptan (Imitrex NS): 5-10 mg (1-2 sprays). Oral 25 mg up to 100 mg.
2. Rizatriptan (Maxalt): 5 -10 mg tab.
3. Dihydroergotamine mesylate (Migranal): 1 spray each nostril, may repeat in 15 minutes.
4. Zolmitriptan (Zomig): 2.5-5 mg tab; 5 mg NS.
5. Eletriptan (Relpax): 20-40 mg tab.
6. Metoclopramide (Reglan): 0.1-0.2 mg/kg/dose up to 4 times a day.
7. Promethazine (Phenergan): 0.25 mg/kg/dose (max 25mg) up to 4 times a day.
8. Ibuprofen: 15 mg/kg/dose every 6 hours.
9. Acetaminophen (Tylenol): 10 mg/kg/dose every 4 hours.
X. FEBRILE SEIZURES
A. Seizure in association with a febrile illness in the absence of central nervous system infection or acute electrolyte imbalance in children older than 3 months of age without a prior afebrile seizure.
|
Altered level of consciousness, 780.09 |
Fever, 780.6 |
B. Etiology.
1. Benign age-dependent epilepsy syndrome, seizure in early life in presence of fever without intracranial infection.
2. Genetic disposition–two to three times more common among family members of affected children than general population.
C. Occurrence.
1. 2-5% of children will have a febrile seizure.
2. Most common between ages of 6 months to 3 years, with peak incidence at 18 to 24 months of age.
3. Risk factors.
a. High peak temperature during illness.
b. Family history of febrile seizures in a first- or second-degree relative.
c. Developmental delay.
d. Neonatal nursery stays longer than 30 days.
e. Attendance at daycare.
D. Physical findings.
1. Temperature of at least 39°F.
2. Simple febrile seizure.
a. Generalized tonic-clonic movements.
b. Eyes roll back.
c. Loss of consciousness.
d. Last few seconds to minutes (less than 15 minutes).
e. Postictal depression is brief.
3. Complex febrile seizures.
a. Last longer than 15 minutes.
b. May reoccur within the same day.
c. Prolonged period of postictal drowsiness or neurological abnormalities.
d. Focal seizure manifestations.
E. Diagnostic tests.
1. Simple febrile seizure.
a. Extensive history taking.
b. Evaluation for cause of fever, CBC.
c. LP for infants younger than 6 months of age.
2. Complex febrile seizure.
a. CSF evaluation.
b. Head CT if warranted.
c. EEG if concerned.
F. Differential diagnosis.
|
Encephalitis, 323.9 |
Metabolic disorder, 277.9 |
G. Treatment.
1. Control fever with antipyretic medication.
2. Antibiotics appropriate for any bacterial infections.
3. Treat cause of fever, fluids.
4. Diazepam rectally or lorazepam (Ativan) IV for seizures lasting longer than 5 minutes.
5. No need for anticonvulsant medication.
H. Complications.
1. Rare, no neurological sequelae.
2. Fewer than 10% of patients experience severe or recurrent attacks.
3. Likelihood of developing epilepsy less than 5%.
4. Possible complications if septic nature is cause for fever and seizure.
5. Risk for reoccurrence.
a. Neurological or developmental abnormality.
b. Positive family history.
c. Onset of febrile seizures before age 1 year.
d. Low peak temperature at onset of seizure.
e. Duration of fever.
I. Follow up.
1. Any seizure without fever.
2. As needed for treatment of cause of fever.
J. Education.
1. Reassurance of the benign nature.
2. First aid during a seizure.
3. When to call the doctor or go to the emergency room: Need to find and treat cause of fever, to stop seizure that continues past 5 minutes and does not stop with diazapam rectal (Diastat).
XI. GENERALIZED SEIZURES
A. Seizure in which the first clinical changes indicate initial involvement of both hemispheres.
|
Absence seizure, 345 |
Seizure, 780.39 |
B. Etiology.
1. Up to 80% have unclear etiology.
2. Hereditary.
3. Perinatal: infectious, hypoxia, trauma.
4. Metabolic, toxic, nutritional.
5. Infectious.
6. Vascular.
7. Neoplastic.
C. Occurrence.
1. Children account for about 15% of all epilepsy cases.
2. Generalized seizures account for one-third of all epilepsies.
3. Most often start in childhood or adolescence.
D. Clinical manifestations.
1. Generalized tonic-clonic (grand mal).
a. Starts suddenly with stiff muscles (tonic phase) and then rhythmic contractions (clonic phase).
b. Impaired consciousness.
c. Loss of bladder control common.
d. Can last a few minutes.
e. Postictal phase that can include drowsiness, confusion, and headache.
2. Atonic seizure (drop attack).
a. Sudden drop to the floor, head may nod/drop.
b. Brief episode, loss of consciousness brief.
c. Injuries are common.
3. Absence seizures.
a. Abrupt sudden loss of consciousness with cessation of all motor activity.
b. Brief periods of staring blankly into space.
c. Ends abruptly, no postictal state.
d. Can be induced by hyperventilation.
e. May see lip smacking, chewing, eye fluttering.
4. Myoclonic.
a. Brief contraction of a muscle group.
b. Can drop objects.
c. Recovery is immediate and often maintains consciousness.
5. Infantile spasms.
a. Clusters of seizures involving flexion jerk of the neck, trunk, and extremities.
b. Range from subtle head drop or shoulder shrug to more violent action.
c. Decreased responsiveness may follow spasms.
d. Spasms are brief, lasting just a few seconds.
E. Physical findings.
1. Seizure rare to happen in office to observe, can have family video episodes.
2. May be “normal” between seizures.
3. Low-grade fever, up to 101°F may occur after seizure.
4. Injuries possible, especially with atonic seizures.
F. Diagnostic tests.
1. EEG in awake and sleep states.
2. MRI if focal spike on EEG or abnormal neuro exam.
3. May do CMP, CBC if concerned abnormalities might be a cause.
4. EKG for concern for cardiac disorder (syncope).
5. Prolonged EEG to catch episodes if warranted.
G. Differential diagnosis.
|
Apnea, 786.03 |
Hyperventilation, 786.01 |
H. Treatment.
1. Anticonvulsant medication.
a. Absence seizures–ethosuximide (Zarontin), lamotrrgine (Lamictal), divalproex (Depakote).
b. Generalized–divalproex (Depakote), lamotrigine (Lamictal), topiramate (Topamax), levetiracetam (Keppra), felbamate (Felbatol), zonisamide (Zonegran).
c. Infantile spasms–ACTH, topiramate (Topamax), Vigabitrin (Sabril).
2. 70% of patients with epilepsy will gain seizure freedom with medications.
3. Vagal nerve stimulator or ketogenic diet for intractable seizures.
I. Follow up.
1. Medication management, anticonvulsant therapeutic levels, and possible need for CMP, liver functions, CBC for some medications.
2. Medication side effects.
3. Continued seizures.
J. Complications.
1. High risk for depression in epilepsy patients.
2. Medication side effects.
3. Developmental delay.
4. Anxiety, intellectual underachievement.
K. Education.
1. Seizure/epilepsy etiology and prognosis.
2. Seizure safety.
3. Psychosocial comorbidities.
4. Medication management and possible side effects.
5. Reevaluation parameters.
XII. PARTIAL SEIZURES
A. Seizure, electrical disturbance, arising from one area of the brain; consciousness may or may not be preserved. Can spread to become generalized.
|
Autonomic phenomena, 337.9 |
Partial simple seizure, 345.5 |
B. Etiology.
1. Idiopathic (most common in children).
2. Brain injury/trauma.
3. Developmental brain abnormality.
4. Tumors (rare).
5. Infectious or hypoxic injuries.
C. Occurrence.
1. Most common type of seizure experienced by people with epilepsy.
2. Risk factors–developmental and brain abnormalities.
D. Clinical manifestations.
1. Depends on which part and how much of the brain is affected.
2. Virtually any movement, sensory, or emotional symptom can occur.
3. Simple partial.
a. No loss of consciousness.
b. Motor signs.
• Focal nature.
• Postural.
• Phonatory (vocalizations or arrest of speech).
• Eye or truncal deviations.
c. Somatosensory symptoms.
• Visual.
• Auditory.
• Olfactory.
• Gustatory.
• Vertiginous.
d. Autonomic symptoms.
• Epigastric sensations.
• Pallor.
• Sweating.
• Flushing.
• Papillary dilation.
4. Complex partial.
a. Impairment of consciousness.
b. Can start as simple and evolve to loss of consciousness.
c. May also progress to generalized seizure (partial seizure that secondarily generalizes).
E. Physical findings.
1. Generally none on office exam, unless cause of seizure leaves or is cause of a neurological deficit.
F. Diagnostic tests.
1. As with generalized seizures, but head MRI warranted.
G. Differential diagnosis.
|
Abnormal involuntary movements, 781 |
Myoclonus, 345.1 |
H. Treatment.
1. Anticonvulsant medications.
a. Oxcarbazepine (Trileptal), or broad-spectrum anticonvulsant medication.
2. Surgical intervention if intractable to medications.
3. Vagal nerve stimulator or ketogenic diet.
I. Follow up.
1. As with generalized seizures.
J. Complications.
1. As with generalized seizures.
K. Education.
1. As with generalized seizures.
XIII. COMMON ANTICONVULSANT MEDICATIONS FOR CHILDREN
A. Divalproex (Depakote): Start 10-20 mg/kg/day given bid, liquid tid; maintenance dose 30-60 mg/kg/day. Monitor CBC with platelets and liver enzymes every 6 months for liver failure, thrombocytopenia.
B. Levetiracetam (Keppra): Start 10-20 mg/kg/day bid; maintenance dose 30-60 mg/kg/day.
C. Lamotrigine (Lamictal): Titrate slowly over 8-12 weeks to starting dose. Risk for Stevens-Johnson syndrome. Maintenance dose 5-15 mg/kg/day bid; lower dose when on enzyme inducer anticonvulsant.
D. Topiramate (Topamax): Start 1 mg/kg/day bid; maintenance 3-9 mg/kg/day. Monitor bicarb for metabolic acidosis.
E. Oxcarbazepine (Trileptal): Start 10 mg/kg/day bid; maintenance 30-60 mg/ kg/day.
F. Ethosuximide (Zarontin): Start 10-15 mg/kg/day bid; maintenance dose 15-40 mg/kg/day. Monitor CBC for leucopenia, aplastic anemia.
G. Zonisamide (Zonegran): Start 1-2 mg/kg/day daily or bid; maintenance dose 5-8 mg/kg/day.
XIV. GLOBAL DEVELOPMENTAL DELAY
A. Subset of developmental disabilities defined as significant delay in two or more of the following developmental domains: gross/fine motor, speech/language, cognition, social/personal, and activities of daily living.
|
Abnormal brain development, 742.2 |
Language disorder, 315.31 |
B. Etiology.
1. Genetic abnormalities.
2. Early environmental deprivation.
3. Metabolic abnormalities.
4. Abnormal CNS/brain development.
5. Idiopathic/unknown.
C. Occurrence.
1. Developmental disabilities of early onset affect 5-10% of children.
2. Refers to younger children younger than 5 years of age.
3. 1-3% of children younger than 5 years of age are affected.
D. Clinical manifestations.
1. Two standard deviations or more below the mean on age-appropriate standardized norm-referenced testing.
E. Physical findings.
1. Not walking independently by 18 months of age.
2. Poor/clumsy fine motor skills.
3. No two-word sentences by 2 years of age.
4. Does not follow two-step commands at age 2 years.
5. Does not know 6 body parts by 2 years of age.
6. Unable to feed, dress, or do activities of daily living.
7. May see poor feeding, poor weight gain, dysmorphic features, cardiac or liver, kidney, bowel abnormalities.
F. Diagnostic testing.
1. Obtain detailed history and examination.
2. Refer for auditory and ophthalmologic screening.
3. Consider metabolic studies/T4 if newborn screening not done.
4. EEG if history suspects seizures.
5. If close family member with global developmental delay due to a known cause, test for that disorder and obtain cytogenetic screen.
6. Head MRI.
7. Lead screen.
8. Complete metabolic panel.
9. Lactic acid.
10. High resolution chromosomes, fragile X, Rett syndrome.
11. Urine genetic screen.
12. Microarray if other tests negative.
13. Mitochondrial testing, muscle biopsy, if suspected and other testing inconclusive or negative.
G. Differential diagnosis.
|
Autism, 299 |
Genetic syndrome, 759.89 |
H. Treatment.
1. Therapy–speech, physical, occupational, developmental, and/or nutritional.
2. Medications as needed for any underlying cause.
3. Genetic counseling.
I. Follow up.
1. Discussion of test results.
2. For any regression or loss of developmental milestones.
3. Every 3 months to assess progression/development.
4. To obtain further recommendations for testing in step-wise approach.
5. For need for additional resources: referral to genetics, metabolism, developmental pediatrics, therapies, psychiatry, neurology, and other services as needed.
J. Complications.
1. Progressive loss of skills or lack of progression if untreated.
2. Seizures.
3. Behavioral disturbances.
4. Some disorders may affect systemic organs/systems.
K. Education.
1. Explaining test results, possible outcomes, prognosis.
2. Possible complications.
3. Medications if needed/treatment plan.
4. Resources.
5. Genetic and other counseling.
XV. TOURETTE SYNDROME
A. Neurobiological disorder characterized by tics–involuntary, rapid, sudden movements and/or vocal outburst that occur repeatedly.
|
Involuntary movements, 781 Tourette syndrome, 307.22 |
B. Etiology.
1. No known cause has yet been established.
2. Evidence points to abnormal metabolism of dopamine.
3. Genetic studies indicate that Tourette syndrome is inherited as a dominant gene.
C. Occurrence.
1. Estimated that 200,000 people in United States are affected–up to 18% of children.
2. Often undiagnosed or misdiagnosed.
3. 50% chance of affected parent passing to child.
4. Sons are 3 to 4 times more likely to be affected than daughters.
5. Peak severity of symptoms between 8-12 years and adolescents.
6. Can occur as early as 2 years of age, mean age of onset 6-7 years.
7. More common in males.
8. Exacerbated by anxiety, excitement, anger, fatigue, tension, stress.
9. Can decrease with relaxation or concentrating on an absorbing task.
D. Clinical manifestations.
1. Motor tics–involuntary rapid repetitive stereotyped movements of muscle groups.
a. Simple–involves one muscle group: eye blinking, facial grimacing, head jerking, shoulder shrugging.
b. Complex–involves either a cluster of simple movements or more coordinated sequence of movements: hopping, clapping, tensing arm or neck muscles, touching people or objects.
2. Vocal tics–transient vocalizations, meaningless sounds or noises or even words or phrases.
a. Simple vocaltics: sniffing, humming, clearing throat, coughing, squeaking.
b. Rare, complex vocal tics:
• Echolalia–repeating others' words.
• Palilalia–repeating one's own words.
• Coprolalia–obscene words.
3. Symptoms vary in children by type of specific tic and degree of severity.
E. Physical findings.
1. May or may not see tics exhibited on exam while in office because some children can temporarily suppress them, but still have urge.
2. May complain of muscle pain due to frequent motor tics.
F. Diagnostic testing.
1. Based on observing symptoms and evaluating history.
2. Must meet Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) criteria:
a. Both motor and vocal tics must be present at same time.
b. Tics occur many times a day (usually in bouts) nearly daily or intermittently for more than 1 year without a tic-free period of 3 months or more.
c. Tics cause marked distress or significant impairment in social or daily functioning.
d. Onset is before age 18.
e. Tics are not due to physiological effects of medication or underlying medical condition.
G. Differential diagnosis.
|
Akathisia, 781 |
Meige syndrome, 333.82 |
H. Treatment.
1. None if tics are not disruptive to patient/child.
2. Teach coping skills and relaxation techniques.
3. Maintain adequate sleep hours and routine.
4. Treat with medication if disruptive, causes pain, decreases self-esteem, child is teased, child is frustrated, interferes socially or academically.
a. Guanfacine (Tenex)–low side effects, but effective only 50% of time.
b. Clonidine–sedating.
c. Haloperidol (Haldol).
d. Risperidone (Risperdal)–can cause weight gain.
e. Pimozide (Orap)–monitor EKG for prolonged QT interval.
f. Topiramate (Topamax)–limited studies, but can be effective.
I. Follow up.
1. To monitor progression of symptoms to see if they become disruptive.
2. For education and assessment of comorbidities.
3. Medication management.
J. Complications.
1. ADHD: seen in up to 70% of patients who have tics/Tourette syndrome.
2. Obsessive compulsive disorder: seen in up to 50% of patients who have tics/Tourette syndrome.
3. Depression.
4. Anxiety.
5. Muscle pain.
K. Education.
1. Explanation of tics and Tourette syndrome, no known specific cause and no harm to brain, most often “normal” child and IQ.
2. Do not criticize child or draw attention to tics.
3. Be sensitive to child's feelings, child unable to fully stop tics.
4. Teach coping skills and relaxation techniques.
5. Most children have tics for only a few months or less.
6. One-third of children will outgrow Tourette syndrome.
7. Discuss possible complications and when to treat.
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