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Neuro 2 Exam 2 > Peds enhancement neuro > Flashcards

Peds enhancement neuro Flashcards

1
Q

A seizure

A

abnormal, excessive, synchronous discharges of neurons residing primarily in the cerebral cortex.

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2
Q

Epilepsy

A

two or more seizures not due to acute causes.

Etiologies:
Genetic
Structural
Metabolic
Idiopathic
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3
Q

Metabolic and other causes of seizure

A 
*** Hypoglycemia
Hypo or hypernatremia
Hypocalcemia
	PE: Chvostek’s and Trouseau’s
Intoxications/ toxins (lead)
  • FEVER also can be a cause of provoked seizure
  • Toxic- meds
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4
Q
  • Differences in pediatrics
A
  • Generalized seizures are more common in children than adults.
  • Generalized tonic–clonic seizures are rare before 2 yrs of age.

Children older than 6 years old will have seizures similar to that of adults.

Younger children have * less complex behaviors, especially with complex partial seizures.

Can be difficult to determine altered LOC in infants/young children

    • Newborns’ seizures can present in a variety of different ways, and are uncommonly generalized.
  • Apnea, subtle eye deviations, or abnormal chewing movements
  • Differentiating between a newborn who has a seizure and a ‘‘jittery baby’’
  • – Seizures cannot be suppressed by passive restraint
  • – Seizures are not elicited by motion or startling
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5
Q

Seizures in the neonatal period: causes

A 
* Hypoxic ischemic encephalopathy
Intracranial hemorrhage (intraventricular, subdural, subarachnoid)
Ischemic stroke
Infections 
- Bacterial meningitis (E. coli, Listeria, GBS)
- Viral (HSV
Hypoglycemia
Hypo or hypernatremia
Hypocalcemia
Hypomagnesemia
Inborn errors of metabolism
Genetic disorders with seizures
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6
Q

Partial seizures

A

Simple partial seizure
= Focal seizure without impairment of consciousness

Complex partial seizure
= Focal seizure with impaired consciousness

Partial seizures with secondary generalization
= Focal seizure evolving to bilateral convulsive seizure

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7
Q

** Automatisms

A

(stereotypical, repetitive behaviors) present in 50%-75% of cases of Complex partial seizures

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8
Q

Simple partial seizure

A

Focal seizure without impairment of consciousness
Symptoms are referable to the area of the brain involved, no alteration of consciousness
EEG demonstrates unilateral spikes or sharp waves in anterior temporal region; can occasionally by bilateral or multifocal

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9
Q

Complex partial seizure

A

= Focal seizure with impaired consciousness
Partial seizures with alteration of consciousness
Automatisms (stereotypical, repetitive behaviors) present in 50%-75% of cases
EEG with sharp waves or spike discharges in the anterior temporal or frontal lobe, occasionally with multifocal spikes

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10
Q

Partial seizures with secondary generalization

A

= Focal seizure evolving to bilateral convulsive seizure

Partial seizure at onset followed by generalized convulsive activity

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11
Q 
Partial seizures (simple and complex): 
- signs
A

Partial seizures may begin with localized symptoms that the patient is aware of (aura)
May have asymmetric motor symptoms.
*** Postictal state is common, even without convulsive activity.

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12
Q

Types of seizures: generalized (description)

A

Arise from both sides of the brain simultaneously

Quick onset, no aura or warning

Motor activity is symmetrical, whole body

Alteration of consciousness occurs
Primary generalized seizures (grand mal)
Postictal state is common for seizures with convulsions
Absence seizures (petit mal) and myoclonic seizures, atonic seizures, tonic clonic

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13
Q

Neurofibromatosis types 1 and 2

A

café au lait spots
axillary freckling
Lisch nodules (brown spots on iris), optic gliomas
neurofibromas

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14
Q

Tuberous sclerosis

A

Ash leaf macules
Shagreen patch
adenoma sebaceum

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15
Q

Sturge Weber

A
  • portwine stain (V1, V2)
    intellectual disability
    seizures
  • glaucoma
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16
Q

idiopathic seizures

A

in more than half of them we don’t figure out what’s going on

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17
Q

Febrile seizures

A

Most common type of seizure in childhood

Seizure in association with a febrile illness in children between * 6 months and 5 years of age.

  • Simple febrile seizure is single, brief (<15 minutes), and generalized

Complex febrile seizure is much less common (approximately 20%) and is recurrent in a single illness, prolonged (>15 minutes), and focal.

3-6% of those with febrile seizures will develop afebrile seizures or epilepsy

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18
Q

Febrile seizures- LP indicated if:

A

Infant under 12 months
Prolonged complex febrile seizure
** Children who have been partially treated with antibiotics

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19
Q

Absence seizures

A

Short (5-20 sec) lapses in consciousness, speech, or motor activity
Often daily or multiple times a day
No postictal drowsiness
EEG: 3 cycles per second generalized spike and wave activity
Tx: ethosuximide

20
Q

Myoclonic seizure

A

Spasm of a muscle or group of muscles

Brief, repetitive, symmetrical muscle contractions

  • Juvenile myoclonic epilepsy (JME)
  • Is an idiopathic generalized epileptic syndrome characterized by myoclonic jerks, generalized tonic-clonic seizures (GTCSs), and sometimes absence seizures
  • Presents in adolescence
  • Generalized polyspike and wave discharges at 4-6Hz
  • Lifelong risk of seizures
  • Tx: valproic acid
21
Q

Benign Rolandic Epilepsy

A

with centrotemporal spikes (BECTS)

Onset between 3-10, with seizures during sleep or at night
Facial twitching, salivation
Normal development
Low seizure frequency: ¼ of patients have only one seizure
* Spontaneously remits

22
Q

Atonic-akinetic seizure (drop attack)

A

Sudden loss of postural tone

23
Q

Infantile spasms

A

Seizure that involves * spasms of the muscles of the neck, trunk, and extremities

Unclear if focal or generalized, so categorized as unknown type

Any disorder that can produce brain damage can be associated with infantile spasms – tuberous sclerosis, HIE (=hypoxic ischemic encephalopathy)

2% of childhood epilepsies but 25% of epilepsy with onset in the first year of life.

EEG shows * hypsarrhythmia (high amplitude disorganized background, multifocal discharges)

  • Long-term overall prognosis for patients with infantile spasms is poor. Associated with cognitive impairment.

Tx: ACTH, or for tuberous sclerosis: vigabatrin

West syndrome = severe epilepsy syndrome with

  1. Infantile spasms
  2. Hypsarrhythmia on EEG
  3. Developmental regression/mental retardation
24
Q

asking about precipitating events

A 
Start with open ended question
Precipitating events (pre-ictal)
  • Position, activity, awake or asleep, * trigger: illness, medications, flashing lights, hyperventilation, being overtired/sleep deprivation (stress?)
    Was there any warning before the spell: abdominal discomfort, fear, other, any associated symptoms?
25
Q

Description of the episode (ictal)

A

LOC: was the child responsive during the episode
Amnesia of episode?
Repetitive behaviors: lip smacking, pulling at clothing
Body movements
* Loss of continence?
Skin color, perioral * cyanosis?
Prior episodes, frequency?

26
Q

Physical Examination-

A
  • Fever or other abnormal vital signs

Ht/wt/FOC (= head circumference)

Head size, skin abnormalities (hypo/hyperpigmented areas), meningismus, asymmetry of the face or the extremities, enlarged organs, dysmorphic features

Alteration of mental status, cranial nerve abnormalities, motor tone or strength or reflex changes, gait abnormalities, ataxia, sensory abnormalities.

*** Evidence of trauma: Battle’s sign, raccoon eyes, clear rhinorrhea = basilar skull fracture

Evidence of increased ICP

  • Brudzinski’s or Kernig’s would suggest meningitis
27
Q

Differential diagnosis

A

Syncope

  • Syncopal seizures may have tonic stiffening, clonic jerking and/or post-ictal confusion
  • Vasovagal (fear, heat, stress, noxious stimuli): nausea, pallor, diaphoresis
  • Orthostatic (dehydration, autonomic disease)
  • Cardiogenic (arrhythmia, structural)

Parasomnias

  • Sleepwalking
  • Night terrors
Hyperventilation/ panic attack
Benign sleep myoclonus
Benign positional vertigo
Complicated migraine
Tics
Narcolepsy
Confusional migraine
Staring spells, daydreaming
* Breath holding spell
Aspiration
Decorticate posturing
Sandifer’s syndrome (GERD related)
28
Q

Differential Diagnosis: Seizure versus syncope

A

Position- seizures may occur in any position, *syncope usually occurs when sitting or standing

Eye movements- eyes are usually closed or partially open during a syncopal episode, more likely to be * open during a seizure. The presence of * deviation of the eyes to one side or another suggests a partial seizure.

Seizures that affect one side of the body more than the other are likely to be focal in origin. Syncopal episodes are usually symmetrical.

Precipitating factors
Seizures may be precipitated by flashing lights, hyperventilation, illness or being overtired (stress?)
Syncope is precipitated by standing up, being overheated, sight of blood, frightening event
State of alertness- syncope doesn’t occur in sleep, seizures may occur in sleep or wakefulness. Parasomnias only occur in sleep.

29
Q
  • Staring spells
A

Occur when the patient is passive, listening to a teacher, or parent or watching TV
Indeterminate length
Interruptible by voice or touch.

30
Q
  • Absence seizures can
A 
Occur in the midst of activity
Last only 10-20 seconds
May  have eye blinking/fluttering or subtle head movements
Recovery is quick 
Incontinence may occur.
31
Q

Acute stabilization

A

Airway, breathing, and circulation and stopping the seizure.

The patient should be positioned to allow for an open airway, and if necessary, an oral or nasal airway should be inserted.

Oxygen should be administered and further equipment for assisted ventilation should be at the bedside.

Intravenous (IV) access should be established promptly.

The actively convulsing patient should also be protected from self-inflicted trauma.

*** A rapid glucose level determination should be performed at the bedside
Naloxone for suspected drug exposure

32
Q

Todd’s paralysis

A

temporary paralysis after seizure
Partial or complete but usually occurs on *just one side of the body
Average of 15 hours, at which point it resolves completely.
May also affect speech and vision.

33
Q

Stevens Johnson Syndrome

A

terrible allergic reaction to a drug, e.g. antibiotic and anti seizure drugs

34
Q

treatment vs not?

A
  • If 1st seizure with lower risk of recurrence, consider no treatment.

Use of rectal valium as a “rescue measure”

If decision to treat, choose a medication based on seizure type, age of patient and side effect profile.

Monotherapy is generally preferable, especially in first line treatment.

Dietary treatment

  • Ketogenic diet
  • Modified Atkins diet

Surgical treatment

  • Vagal nerve stimulator
  • Surgical removal of seizure focus
35
Q

Hertz

A

3 hertz- absence seizure

4-6 hz- Juvenile myoclonic epilepsy

2 Hz-Lennox-Gastaut Syndrome

36
Q

Pathophysiology of head injury

A

Primary injury: mechanical damage sustained immediately at the time of trauma

Secondary injury: ongoing derangement of neuronal cells not initially injured during the traumatic event

** Hypoxia, hypoperfusion, e.g.

37
Q

Why kids are more at risk for head trauma

A

Developing brain is more sensitive to concussion injury than an adult athlete.

  • Developing brain is not able to recover as quickly as teen or adult brain.
  • Axons in pediatric brain are not as well myelinated – more vulnerable to injury.
  • Younger have less well-developed cervical and shoulder muscles, less stability to absorb impact.

May not use proper techniques to reduce risk for injury.

** On the other hand, a recent study showed that younger kids may recover more quickly than adolescents with concussion.

38
Q

Emergent head CT is recommended if:

A

Penetrating injury
* GCS under or = 14, or other evidence of altered mental status
* Depressed or basilar skull fx
* Worsening HA
LOC prolonged
Clinical deterioration or worsening symptoms
Pre-existing risk factors (ex. - bleeding disorder)

Also, for age under 2:

Concerns for abuse
	Irritability
	Bulging fontanel
	Persistent vomiting
	*** Large boggy nonfrontal scalp hematomas in 		children under 1 yr old
	Definite LOC
39
Q

Concussion

A

by immediate and transient post traumatic impairment of neural function due to CNS involvement

Approach to management:
RECOGNITION 
RESPONSE 
REHABILITATION 
RETURN
40
Q

Colorado’s Senate Bill 40

A

Re: concussions

  1. Required training for coaches
  2. Removal from play (“when in doubt, sit them out”)
  3. Notify parent
  4. Medical clearance before return to play

Special consideration: the pushy parent

41
Q

Management (cont’d) -When to send concussion patient to ED

A

Acute head trauma
Seizures or focal neurological deficits
History of prolonged LOC: > 30 seconds
Suspicion of Skull Fracture
Severe Headache (9-10/10)
Slurred speech
Significant drowsiness
Repetitive Vomiting
Altered mental status morethan 30 minutes

Subacute head trauma (1-5 days)
Increasing severity of headache
Sudden onset of vomiting, especially if headache is relieved by vomiting
New severe symptoms

42
Q

Concussion Management

A

Day of Injury:
* No same-day return to play!
* No driving.
Do not leave injured athlete unattended for first 24 - 48 hours.
** Emphasize physical and cognitive rest! Consider limiting…
TEXTING * VIDEO GAMES * INTERNET * TV * LOUD MUSIC Educate parents that some symptoms may worsen over 1st 24 – 48 hours (but child should not have worsening LOC, 3-4 episodes of vomiting, etc)

Second Impact Syndrome
* Catastrophic event which may occur when a second concussion occurs while the athlete is still symptomatic and healing from a previous concussion.

Can cause cerebral blood flow increase and rapid swelling around the brain, rarely resulting in severe neurological damage or death.
Rare; All reported cases < 24 years old

Imaging: * CT without contrast if neuro exam findings are abnormal*

** Premature return to play may confer increased risk to the athlete
Physical and Cognitive Rest: 1st few days ( no “cocooning)
* Step-wise Return To Play protocol
Same for child & adolescent athletes.
Individualized
Additional management tools: neuropsychological (=NP) testing, balance assessment, neuroimaging
Home management of mild concussions: observation
No need to wake them frequently
Pharmacotherapy
Headache: Naproxen (Aleve)
110 lbs: Rx for 500mg tab po q AM & q PM
<110 lbs: OTC 220mg tab po q AM & q PM
Take with breakfast/dinner (food and drink)
Limit use to 5 days on, 2 days off, repeat x 1.

43
Q

return to play

A 
generally at least 24 hours for each step.  
 no activity
1. Light exercise
2. sport specific exercie (no impact)
3. non contact training
4. full contact practice
5. Return to play
44
Q

*Concussion Management Summary

A

Concussion prevention

Properly fitted helmet
Cervical musculature strengthening
Play clean (good sportsmanship)

Appropriate recognition and diagnosis

Educate players, parents, and coaching staff about signs and symptoms so they quickly recognize
Close monitoring over initial hours to identify catastrophic response
Proper healthcare evaluation prior to return sports
Specialty follow-up when an athlete has not returned to normal within expected recovery times (i.e., 2-3 weeks)

Management should be more conservative in younger patients!

45
Q

majority of concussion patients are better in

A

7-10 days

important to refer when recovery is not proceeding as expected after concussion (ie, relatively quick 1-2 week symptom resolution) – if symptomatic after 3 wks

Neuro 2 Exam 2 (19 decks)

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