Week 3 Neuro Flashcards
In peds, must r/o these severe head injury before dx of minor head injury or mild TBI (concussion):
- skull fracture
- spinal cord injury
- brain bleeds
- moderate-severe TBI
What guideline is used if a CT scan is needed?
PECARN calculator
Glasgow coma scale score 13-15 means
- mild
- no focal deficits
- < 30 minutes LOC
- may have linear skull fractures
Glasgow coma scale score 9-12 means
- moderate
- focal signs
- variable loss LOC
- may have depressed skull fracture or intracranial hematoma
Glasgow coma scale of < 8 means
- severe
- focal signs
- prolonged loss LOC
- depressed skull fractures and intracranial hematoma
Pedi head injury management
- If worried caregiver is not reliable = admit
- Discharge home with close observation:
- Minor head trauma and no LOC
- Brief LOC (< 5 mins) with:
- Normal neuro exam
- No s/sx IICP (vomiting, h/a)
- No s/s basilar skull fracture (raccoon eyes, battle sign)
- With or w/o a head CT
- Wake child every 2-4 hours at night for first 24-48 hrs
- Educating parent s/sx of deterioration
- Not responding to q’s
- Vomiting
- Horrible headache
- Slurring speech
highest risk sport for boys and girls for concussion/mild traumatic brain injury?
boys: football and hockey
girls: soccer and basketball
concussion red flags, bring to ED!
- Weakness, numbness, decreased coordination
- Worsening headaches
- Repeated vomiting or nausea
- Slurred speech
- Anisocoria (unequal pupils)
- Seizures
- very drowsy
- Increasing confusion, agitation, restlessness
- Focal neurological signs
- Problem with nerve, spinal cord, left side face numb / arm numb, paralysis of leg
- Can’t recognize people or places
- Neck pain
- Unusual behavior changes
- Any loss of consciousness, especially if for 30 seconds or more
retrograde amnesia vs anterograde amnesia
retrograde amnesia: very brief, can’t recall events before injury
anterograde amnesia: seconds-minutes, can’t make new memories and can’t recall
which imaging preferred for concussions? and what are the indications?
CT scan
indications:
- Focal neurological findings
- Signs of IICP
- GCS < 15 after 2 hrs OR < 13 at any time
- Seizures r/t to trauma
- Age > 60
- Anticoagulation or coagulopathy
- Intoxication
- Recurrent vomiting
- s/sx skull fracture
- LOC (excessive irritability or lethargy)
- LOC >1 min
- Amnesia
simple concussion
sx’s resolve (brain healed) in 7-10 days without complications
complex concussion
- prolonged healing that is persistent for over 10 days
- may develop post concussive syndrome
- prolonged impaired cognitive function
- repeated concussions
concussion monitoring
repeat neuro exam q 15 mins
if sent home, monitor next 24 hrs:
- Inc drowsiness
- Vomiting > 2x
- Neck pain
- Drainage from ear / nose
- Seizure , fainting
- Unu irritability, personality changes
- h/a getting worse or lasts > 1 day
- Unequal pupils, blurred vision
- Gait abnormalities
When can the child return to play after a concussion?
not until all symptoms have cleared, both at rest and with exertion and without meds
Return to play guidelines after a concussion
- Physical & cognitive rest for the first 24-48 hrs before return to play, 24 hrs or longer each step
- Need to communicate with coach, teachers
- Advance activity slowly (includes screen use, reading, homework, physical activity) with lots of breaks
- 1 - sx limited activity (no sx)
- 2 - light aerobic - no weights
- 3 - sport specific
- 4 - non contacting drills - yes weights
- 5 - full contact practice
- 6 - return to play
- If symptoms return, cannot attempt that activity again for 24 hours
concussion prevention
- Wear helmets when appropriate and properly fitted
- Avoid re-injury before first concussion resolves
What is second impact syndrome?
- Patient sustains a 2nd head injury before the symptoms from the first head injury have resolved
- Days to weeks after the first injury
- LOC is not a requirement; impact may be mild and athlete may appear only dazed initially
- Can cause cerebral edema and herniation, leading to death
*Stress importance with patients that ALL concussion symptoms must be resolved prior to return to activity*
What is post concussive syndrome?
- Sequela of minor head injury
- poorly understood
- at least 3 of these:
- h/a, dizziness, fatigue, irritability, impaired memory/concentration, insomnia, lowered tolerance for noise and lights
- no imaging needed unless red flags
What is Bell’s palsy?
- Acute, isolated peripheral facial paralysis of the 7th cranial nerve
- most common cause: HSV activation
- Other associated viruses are: cytomegalovirus, Epstein–Barr virus, adenovirus, rubella virus, influenza B, coxsackie virus
- Pregnancy
- most spontaneously resolve
What is Bell’s palsy?
- Acute, isolated unilateral peripheral facial paralysis of the 7th cranial nerve
- most common cause: HSV activation
- Other associated viruses are: cytomegalovirus, Epstein–Barr virus, adenovirus, rubella virus, influenza B, coxsackie virus
- Pregnancy
- most spontaneously resolve
Bell’s palsy sx’s
- Sx’s can persist up to 3 months
- Acute onset (w/in 48 hrs) of unilateral of upper and lower facial paralysis
- Weakness of facial muscles
- flattening of the nasolabial fold
- drooping mouth/asymmetrical smile
- Hyperacusis (sounds too loud)
- Posterior auricular pain
- Decreased tearing
- can’t close eyelid = irritation
- Taste disturbances
Bell’s palsy sx’s
- Acute onset (w/in 48 hrs) of unilateral of upper and lower facial paralysis
- Weakness of facial muscles (flattening of the nasolabial fold and drooping of the affected corner of the mouth)
- Hyperacusis (sounds too loud)
- Posterior auricular pain
- Decreased tearing
- Poor eyelid closure
- Taste disturbances
- Otalgia
when are you worried if it’s a central cause/stroke or if it’s Bell’s palsy?
a stroke/central cause would have only 1 area affected (mouth drooping) and other parts of face are still movable like wrinkling forehead and eyes
paralysis from stroke spares forehead
What grading system used for Bell’s palsy?
house and brackmann system
1 = normal
6 = severe paralysis
bells palsy diagnostic criteria
paralysis or paresis of *all* facial nerve muscle groups unilaterally, sudden onset and absence of CNS disease
What other testing to consider in dx for Bell’s Palsy?
Lyme titer (if tick exposure) MRI (if don't recover in 3 months) EEG/EMG (if fail to improve)
Bell Palsy treatment/management
- Corticosteriods/Prednisone w/in 72 hrs of sx onset
- or Acyclovir or valacyclovir in conjunction
- Eye care
- risk for corneal abrasions/ ulcers
- Artificial tears during the day and lubricating ointment at night
- risk for corneal abrasions/ ulcers
- tape or an eye patch for 24–48 hours to help heal a corneal abrasion
Ramsay hunt syndrome
- Peripheral facial nerve weakness caused by varicella zoster
- Same symptoms as Bell’s palsy but:
- rash/vesicles
- Paralysis more severe
- Anterior tongue numbness, ear pain, vertigo, hearing impairment
- Less likely to have a complete recover
Treat early with oral glucocorticoids and antivirals:
- Prednisone and acyclovir
what is the SCAT5?
sport concussion assessment tool 5
- No screen time, no reading, no strenuous activity
- No aspirin or NSAIDs
- Worsening sx’s to seek help
- Enough rest /sleep
- Return in 7-10 days and repeat SCAT test to see
Is imaging indicated with recurring, stable headache with normal neurological exam?
NO
indications for imaging for headache include
- Abnormal neuro exam findings
- History suggestive of ICP
- seizures
- Recent onset of severe HA
- Change in type or pattern of HA
- Severe HA with underlying disease that predisposes them to intracranial process (sickle cell anemia, HTN, coagulopathy, history of neoplasm, neurofibromatosis
what is SNOOP and what is it for?
headache warning signs
- systemic symptoms
- fever, muscle pain, weightless
- neoplasm or neurologic sx’s
- onset
- How fast h/a sets in, severely
- older age
- 50+
- pattern, position change, pregnancy, progressive, painful eye
tension headache sx’s
at least 2 of:
- bilateral, band like
- pressing/tighening quality
- mild to moderate intensity
- no aggravation from routine physical activity
both of these:
- NO n/v
- NO photophobia or photophobia
tension headache sx’s
at least 2 of:
- bilateral, band like
- pressing/tighening quality
- mild to moderate intensity
- no aggravation from routine physical activity
both of these:
- NO n/v
- NO photophobia or photophobia
tension headache treatment
- Tylenol, asa, NSAIDS (ibuprofen, naproxen); caffeine [don’t overuse]
- Consider prophylaxis if headaches are frequent (>2/ week), of long duration (> 3-4 hours), or severe enough to cause significant disability or overuse of abortive treatment
- Amitriptyline only proven medication
what medications are NOT helpful with tension headaches?
triptans
barbiturates, opiates
do the majority of migraines have aura or no aura?
80-85% have no aura
15-20% have aura (positive sx’s: flashing lights, scintillation, paresthesia then neg sx’s numbness, aphasia, scotoma (chunk of vision gone))
migraine triggers
- Changes in weather (heat, humidity, high altitude)
- Stress; crying
- Alcohol
- Hunger
- Fatigue / no sleep
- Loud noises
- Flickering lights
- Noxious stimuli
- Foods
- Fried food, red wine, hot dogs (MSG), cheese, chocolate, cured meats & fishes, peanuts
- Exertion
- Nitroglycerin
- Minor head trauma
- Menses
- Surgical menopause
migraine diagnosis
repeated attacks lasting 4-72 hrs, normal exam and no other reasonable cause for headache
at least 2:
- unilateral pain 60%
- throbbing/pulsating pain
- aggravating of movement or activity
- mod-severe
at least 1:
- nausea/vomiting
- photophobia or photophobia
How to treat migraines?
- avoid triggers
- headache diary
- educate: won’t cure but will try controlling
- abortive treatment and preventative treatment
Migraine preventative treatment indications
- > 4 attacks a month
- Consider comorbid conditions when prescribing medications
- Freq long lasting h/a a/s with significant disability
- Contraindication to abortive tx
- Frequ use of abortive tx
- Uncommon migraine (hemiplegic, basilar, migraine with prolonged aura, migrainous infarction)
migraine preventative treatment
- Start low, titrate up for 8–12 weeks (educate results til 8 weeks)
- TAPER OFF if need to d/c!
- Beta blockers [propranolol]
- TCAs [Amitriptyline]
- Valproate [BBW suicide]
- Topiramate
- CCB [verapamil]
- CGRP (monoclonal antibody): a potent vasodilator
- ‘numab’ = monoc. antib
- Erenumab (Aimovig)
- Fremanezumab (Ajovy)
- Galcanezumab (Emgality)
- Eptinezumab (Vyepti): IV
- ‘numab’ = monoc. antib
Migraine abortive treatment
- start ASAP when it comes
- limit abortive use max 2 days per week (rebound analgesic)
mild to moderate: Tylenol, NSAID, allieve, excedrin, triptans
severe (incapacitating; ED): abortive + IV/IM antiemetics (metoclopramide, Benadryl)
pediatric red flags headaches
- < 5- 6 yrs old
- New onset
- Focal neuro signs
- Nocturnal awakening [Tumor]
- Vomiting, papilledema [IICP]
- Loss of cognitive/neuro functioning
- Sig change in existing h/a pattern
- Head trauma with LOC >10 minutes
- Inability to control headache with appropriate tx
Pediatrics: migraine abortive vs preventative treatment
- abortive: early as possible, NSAIDs more effective, sleep, sedative if distressed (dephenhydramine/benzos)
- preventative: NOT recommended but mostly lifestyle, propranolol, topiramate
pediatrics tension headache
mild - analgesics
refer if more severe (analgesics, indomethacin (not for young), combo)
define seizure and epilepsy
seizure: abnormal focal or generalized neuronal discharge with physical manifestations
epilepsy: 2 or more unprovoked seizures
most common secondary identifiable cause of seizures in adults and children?
adults: stroke, vascular disease, neurocysticercosis (tapeworm in brain)
children: idiopathic
causes of seizures in neonates (< 1 month)
- Perinatal hypoxia and ischemia
- Intracranial hemorrhage and trauma
- Acute CNS infection
- Metabolic disturbances (hypoglycemia, hypocalcemia, hypomagnesemia)
- Drug withdrawal
- Developmental disorders
- Genetic disorder
causes of seizures: infant and children (1 month - 12 yrs)
- Febrile seizures
- CNS infection
- Trauma
- Genetic disorders (metabolic, degenerative, primary epilepsy syndromes)
- Idiopathic
causes of seizures in adolescents (12-18 yrs)
- Trauma
- Genetic disorders
- Infection
- Brain tumor
- Illicit drug use
- Idiopathic
causes of seizures in young adults
- Trauma
- Alcohol withdrawal
- Illicit drug use
- Brain tumor
- Idiopathic
causes of seizures in older adults > 35 yrs
- Cerebrovascular disease (embolic stroke, hemorrhagic, thrombotic stroke)
- Brain tumor
- Alcohol withdrawal
- Metabolic disorders (hepatic failure, hypoglycemia, uremia, hyponatremia)
- Idiopathic
generalized tonic clonic/grand Mal seizure
- most dramatic and most common generalized epilepsy
- May begin as a cry as the result of air moving across the glottis from sudden tonic muscle contraction
- Tonic phase: stiffening of limbs bilaterally
- Clonic phase: rhythmic jerking, will become slower in frequency as seizure is coming to an end
absence seizures/petit mal seizure
- Momentary loss of awareness
- May not realize the seizure has occurred
- Few seconds
- NO post-ictal period
- Typically begin in childhood, often noticed first by school teachers
- Misdiagnosed with ADHD
myoclonic seizures
- Brief episodes of sudden motor contraction, often flexion of the upper extremities; muscle jerks
- difficult to tell if LOC occurs or not
- Most commonly occur in the morning just after awakening, or when awakening from a nap
atonic seizures
- drop attacks
- Brief episodes that are characterized by a sudden increase or decrease in muscle tone
- dramatic falls
- Wear protective head gear
simple partial seizures
simple partial: sensory complaints: metallic taste in mouth, rising sensation in stomach, déjà vu
- Others are generally unaware the patient is having a seizure unless the patient tells someone
- Gelastic seizures: bursts of uncontrollable laughter not associated with anything funny, typically only seen with hypothalamic hamartomas (rare)
complex partial seizures
- may seem alert and responsive, but patient is not aware of what is going on
- can talk but doesn’t make sense
- May have automatisms [non purposeful movements (picking at clothing, lip smacking, nose wiping)]
non epileptic seizures/psychogenic seizures
- Paroxysmal events that have NO electrographic correlate
- Very similar to true epileptic seizures
- Patients are NOT faking; they are unaware these are not true ictal events
- Often associated with psychiatric disorders such as depression, anxiety, borderline personality disorder, OCD, PTSD
- Hx of physical, emotional or sexual abuse
- May have both epileptic and non-epileptic seizures
- Diagnosis: Capture an event on video
- EEG monitoring
Epileptic seizure (vs Non ES)
- LOC with generalized motor activity
- Eyes are generally open
- Mouth generally open
- Tongue bite on the lateral edges
- Tongue falls when on side
- No response to painful stimuli
- Sternal rub to test
- Episode is short-lived (< 5 minutes)
Non epileptic seizures (vs ES)
- Awake, alert
- Forced eye closure
- Forced mouth closure
- Tongue bite on the tip of the tongue
- Normal response with painful stimuli
- Episode can wax and wane for hours
seizure (vs syncope)
- LOC quick
- Can have cyanosis
- motor manifestations lasting >30 seconds
- post-ictal disorientation, muscle soreness, and sleepiness
- Accompanied by an aura
- Duration of tonic-clonic movements is usually 30–60 seconds
- TIME!
- Tongue biting, incontinence, and post-ictal headache
syncope (vs seizure)
- Provoked by acute pain, anxiety, or occurred immediately after rising from a lying or sitting position
- Stereotyped transition to unconsciousness that includes tiredness, sweating, nausea, and tunnel vision
- Can have convulsive movements if remains upright after losing consciousness due to sustained decreased cerebral perfusion (such as in a dentist chair)
- may have incontinence
- Tonic-clonic movements < 15 seconds
- Rarely see tongue biting or post-event headache; can have incontinence (not common)
treatment for seizures
- 1st line: anti epileptic medications
- surgery: implantable devices
treatment for epilepsy
- start med after 2nd seizure
- 1st line: anti epileptic medications
- don’t sub to generic brand (dilantin and phenytoin)
- surgery
- temporal lobectomy
- lesionectomy
- multiple subpial transection
- corpus callosotomy
- hemispherectomy
- implantable devices
- vagal nerve stimulator (under clavicle)
- NeuroPace (pacemaker for brain)
- Deep brain stimulator
hormonal birth control and AED meds
- Counsel oral contraceptives will be less effective and they may need to use a back-up method
- phenytoin, phenobarbital, carbamazepine, topiramate, oxcarbazepine, and lamotrigine
- Lamotrigine makes BC less effective and BC makes lamotrigine less effective
- phenytoin, phenobarbital, carbamazepine, topiramate, oxcarbazepine, and lamotrigine
- need at least 50 mcg of estrogen to overcome interaction (use backup)
- Efficacy of the morning-after pill is decreased
- Interaction with BC hormones (NuvaRing, Mirena, etc.)
-
Folate should be prescribed in all women of childbearing age taking AEDs.
- Tegretol reduces folate in body
- AEDs OK in pregnancy
- risk of tonic-clonic seizure during pregnancy greatly outweighs fetal risk
- Valproic acid considered the most teratogenic of all the AED
- 10% risk of congenital malformation (cleft lip and cleft palate)
childhood absence epilepsy
- Girls 60–78%
- Peak: 6-7 years years old
- Tend to occur in developmentally normal children
- seizures are brief, often lasting 5–10 seconds; they start and stop suddenly
- NOOO post-ictal period
- 10–100x/day
- May also see eye fluttering, eyes rolling upwards (tonic movements of the eye), lip smacking, and autonomic symptoms such as flushing and tachycardia
- EEG can be normal, though can show interictal spike and wave discharges
- Children may become seizure free (33–80%) though some will go on to develop GTC seizures (40%)
- May develop problems with cognition, social adaptation, or behavior
- Usually well controlled with ethosuximide
- or valproate
- or lamotrigine
infantile spasms (west syndrome)
- Rare, very dramatic form of epilepsy mostly in 1st year of life
- Triad of
- infantile spasms
-
EEG pattern of hypsarrhythmia
- continuous multifocal spike and slow waves with high amplitude on ECG
- developmental delay
- Any disorder that produces brain damage can be associated with infantile spasms (prenatal, perinatal, postnatal disorders)
- underlying structural cause!!
- Diminish/disappear by the 4-5th year of life
- Underdeveloped psychomotor development from the spasms in 70–90%
- Milestone loss
- Spasms begin with a sudden, rapid, tonic contraction of the trunk and limbs that gradually relaxes over 0.5–2 seconds •
- Intensity may vary form subtle head nodding to a powerful contraction of the body
- Goals: best quality of life with few seizures, the fewest side effects from treatment, and the least number of medications
- treatment:
- ACTH, vigabatrin, vitamin B6 and prednisone are mainstays of treatment
- benzos, valproic acid, lamotrigine, topiramate, zonisamide, and levetiracetam
- ACTH, vigabatrin, vitamin B6 and prednisone are mainstays of treatment
- Ketogenic diet
- poor prognosis
Lennox Gastaut syndrome criteria and causes
- Having multiple seizure types: tonic and atonic seizures, include absence and myoclonic seizures and non-convulsive status epilepticus
- Developmental Delay or regression with or without other neurologic abnormalities;
- Causes
- Genetic disorders
- Neurocutaneous syndromes (tuberous sclerosis
- Encephalopathies following hypoxic-ischemic insults
- Trauma at birth
- Meningitis
- Head injuries
- 40% have cryptogenic etiology; these children are commonly found to have genetic disorders
Lennox gastaut syndrome treatment
- No drug very effective
- Rufinamide first approved and clobazam
- Valproic acid, lamotrigine, topiramate, rufinamide, felbamate, clobazam
- Carbamazepine/tegretol can worsen drop attacks
- Ketogenic diet
- Corpus callosotomy
- Vagus nerve stimulation
juvenile myoclonic epilepsy
- typically a healthy young teenager with one or more of the following seizures:
- Absence seizures
- Myoclonic jerks
- Generalized convulsions
- Myoclonus and generalized seizures often occur shortly after awakening in the morning
- control with AED
- Valproic acid, lamotrigine, topiramate, levetiracetam, and clonazepam
- Lifelong disorder, treatment indefinitely
- Good prognosis, normal cognitive development, seizures generally respond well to treatment
ketogenic diet
- high fat, protein causing ketosis = anti seizure effect
- 4 parts fat: 1 part protein and carbs
- need supervision by dietician
- better in children than adults
- don’t do longer then 2 years
- complications:
- GI
- metabolic acidosis
- osteopenia (need Ca and vitamin D supplements)
when is surgery considered with epilepsy?
- children who are medically refractory, meaning failed 3 or more trials of medications
- severe
- well localized epilepsy respond best to remove
febrile seizures criteria
benign condition
- > 38°C (100.4°F)
- 6 months to < 5 years of age
- No CNS infection or inflammation
- No acute systemic metabolic abnormality that may produce convulsions
- No previous afebrile seizures
simple febrile seizure
- Most common type of febrile seizure
- Seizures that last < 15 minutes
- No focal features
- If they occur in a series, last less than 30 minutes
complex febrile seizure
- Last > 15 minutes
- Have focal or post-ictal paresis
- If the occur in a series, last more than 30 minutes
febrile seizure management
- Antipyretics, AED = not useful
- Possible causes: any viral or bacterial illness or rarely an immunization, HSV 6 commonly causes febrile seizures, likely d/t high fever), MMRV vaccine 1 week afterwards & family hx of seizures
- If the child has focal or prolonged seizures, generalized or focal EEG abnormalities, repeated episodes of febrile convulsion during a febrile illness (complicated febrile seizures), or seizures associated with fever and without fever = sus more serious underlying cause (i.e., bacterial meningitis, encephalitis)
risk factors for recurrence of febrile seizure
- 1st one before 18 months
- low degree temp during seizure
- fever occurs AFTER seizure
- family hx of febrile seizures
multiple sclerosis
- autoimmune inflammatory and neurodegenerative disorder of CNS; demyelination of the brain, the spinal cord, optic nerves
- Ages 20 to 50
- Unknown cause; autoimmune; genetic and environmental influence.
- further from equator = higher risk
- Silent lesions that may be seen on an MRI; no symptoms.
- women> males.
multiple sclerosis sx’s
- non-specific
- most common: visual distrubances/eye pain, paresthesias or weakness of limbs, or facial pain
- if lesions in brain stem = see double vision, facial paralysis, numbness, vertigo.
- cerebellum = poor coordination or tremors
- optic nerve = impaired vision
- pain with movement
- very vague complaints
- fatigue
- depression
- pain, paresthesia
- sexual dysfunction
- spasticity
- tremor
- weakness
- ataxia
- spinal cord lesions = limb weakness, decrease in sensation, and possibly bowel and bladder symptoms
if think it’s MS, get
CBCs, ESR, LFTs, renal function panel, calcium, glucose, thyroid panel, B12, zinc. HIV or Lyme titer
Gold standard diagnosis: MRI (or LP)
MS differentials
- vascular, metabolic things, infections, or neoplasm.
- inflammatory processes like lupus or vascular disorders like a stroke.
- metabolic disorders, like B12 or zinc, and then infection.
- Lyme, HIV
MS treatment
- care team (OT, PT, PA, neurologist, social workers, psych)
- DMT (decrease exacerbation, MRI activity, slow disability rate)
- start asap with 1st sx
- vitamin D
- immunosuppressive
- monoclonal antibody (-zumab)
