NEURO-Siezure Concussion Flashcards

1
Q

What is the result of aberrant electrical activity in the brain d/t metabolic, traumatic, infections, tumors, meds/drugs, congenital defects?

A

Seizures

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2
Q

What is the disease characterized by the presence of ​recurrent seizures​?

A

Epilepsy

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3
Q

What detects synchronous firing throughout multiple regions of the brain → disrupts normal brain activity

A
EEG
Normal brain activity
1. activity different places
2. activity different times
3. Does not tell simple vs complex
4. Always need PT HPI
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4
Q

What are the theories behind seizures?

A

● Altered membrane permeability/ ion dysfnx- disruption of ions across cell membrane, d/t genetic mutations

● Changes in neuronal excitability/​ion ​channel activity ​→ would ultimately change the membrane permeability

● Neurotransmitter imbalance- acetylcholine excess or γ-aminobutyric acid GABA inhibitory decreased

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5
Q

EEG show a seizure begin in a specific of ​one​ cerebral hemisphere. Name this classification

A

Focal/Partial seizures​

Simple: ​no impairment of consciousness or awareness 1 hemisphere

Complex: ​Consciousness impaired​; 1 hemisphere

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6
Q

Parital seizure activity that spread across the brain & becomes generalized?

A

Jacksonian march” - manifest up to 120 seconds

Focal/Partial
● MC ​type​ is ​temporal lobe
● MC is ​complex​ partial

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7
Q

What are Partial Seizure DDX? What diagnosis tools help differeinate?

A
● Movement disorders, 
● Migraine HA,
● sleep disorders, 
●syncope, 
●behavioral and psych issues can mimic
● 2nd to brain injury, thorough PMH

For any make sure to get:
○ EEG
○ Laboratory evaluation
○ Imaging

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8
Q

Did trial of AED use for treatment have good outcomes?

A

Partial Seizure: Treatment
● AED
● TX started after second unprovoked seizure- epilepsy ● Type and origins are important
● LTC ​YEARS
● RX ​impair cognition
● Surgical if epileptic established via testing/imaging

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9
Q

EEG shows widespread ​synchronized​ electrical activity on both hemispheres

A

Generalized- travel all over brain

Absence
Myoclonic
Tonic clonic
Tonic
Atonic

MC- young children

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10
Q

What are tips to get a good PMH?

A

difficult to obtain d/t associated with amnesia
● Need solid history of period- ictal and the post-ictal period
● Look for triggers

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11
Q

What trigger lower seizure threshold?

A

fever,
menstruation,
stress,
sleep issues

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12
Q

Ms. Emily has nonconvulsive: very short episodes of conscious detachment, that last 10s-100s times per day

A

AKA petit mal seizures,
children and cease in adulthood
Children school failure
blank stare, and unresponsiveness,
Motion-lip smacking, mild clonic motion eyelids
INC/DEC postural tone-autonomic phenomena.
resume normal activity immediately.

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13
Q

Ms. Jenna had a sudden loss of muscle tone leading to slackening of the jaw, drooping of the limbs, and falling to the ground.

A

Atonic

AKA drop attacks

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14
Q

Mr. Tim had brief involuntary muscle contractions, involving bilateral jerking of muscles, to face, trunk, and legs.

A

Myoclonic

induced by stimuli of cerebral origin.

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15
Q

Ms. Emma has PMH of tonic contraction of the muscles with extension of the extremities and immediate loss of consciousness. What type is this seizure?

A
AKA GRAND Mal
​most common​ major motor seizure. 
vague warning/ focal seizure 
Incontinence of bladder and bowel 
Cyanosis contraction of airway and respiratory muscles. clonic phase-rhythmic bilateral contraction and relaxation of the extremities. 
Tonic- extensor MSK, followed by falling
end of the clonic phase-unconscious until the RAS begins to function again. 
60 to 90 seconds.
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16
Q

What happens at end of clonic phase?

A
POST-ICTAL PERIOD
Brain recovery
RAS begins- growth factor signals protein kinase to active cell growth
suppressed consciousness
confusion
fatigue- lots of damage
improves gradually
17
Q

How to manage seizures?

A

protect head
Dont control movements
Roll to side if poss.
Gabapentin, Pregabalin- affects calcium channel, dec ions d/t Ca affect n enzymes. Lowerr calcium, DEC activity. DEC seiz

18
Q

What Drug MOA acts on Na+ channels

A
Phenytoin
Carbamazeipine
Oxcarbamazeipine
Lamotrigine
Lacosoame
Sonisamid
19
Q

What Drug MOA act on GABA receptors

A

Benzo
Barbiturates
DEC GABA uptake

20
Q

What occurs with a concussion?

A

Physiological
NOT structural damage +/-
brain floats freely in the CSF,
blunt force to the head accelerates the brain within the skull, shearing tissue, bleeding, inflammation

Direct brain hits inside skull- coup
Opposite damage of force Rebound from hit forward- contercoup

21
Q

What is single most important protective?

A

Helmet

Youth Leading cause of TBI
Auto accidents
Sports

Multiple +/- permanent damge
Tau protein
N- aceytlaspartate
Cholin

22
Q

Mr. Jacob c/c HA, dizziness, insomnia, irritability, fatigue, impaired memory, lowered tolerance to light and noise after hit on field. What is workup?

A

Concussion- TBI

Labs- SCAT2, post IMPACT
Neruo exam
CT

23
Q

Continuation of 3 mild symptoms: headache, irritability, insomnia, poor concentration, memory, fatigue, impaired memory, lowered tolerance to light and noise may persist for months

A

Post-concussion syndrome

HA- MHA, tensio, opthalmic migraine, cluster

CN signs: dizziness, vertigo, tinnitus, blurred vision, diplopia, photophobia

TX: cognitive retraining, medications, or
psychological support-anxiety, irritability, insomnia, depression, decreased libido, fatigue

Complete brain rest
NO school
NO activity

24
Q

What correlates to severity of concussion>

A

duration of retrograde amnesia

25
Q

What is protective brain mechanism and reason to support being out from school?

A

Brain metabolism slowed for ​weeks​ after TBI

○ Any​brain metabolic activity puts strain on the organ

26
Q

What are stepwise progression of concussion?

A

Initial Treatment​: No activity until asymptomatic, cell phones, school, sports OUT

● Step 1​: Short periods of reading, focusing or school attendance
● Step 2​: When full school day tolerated: Low impact activity – walking, bike, increase intensity as
tolerated
● Step 3​: Aerobic activity specific to sport OK
● Step 4​: Non-contact drills
● Step 5​: Full contact OK in practice setting

Progress
● Symptoms free each stage,
● if stage induces symptoms, 24 hr rest, then fall back to prev stage.

27
Q

Does Concussion cause ALS

A

ALS = Amyotrophic lateral sclerosis, a.k.a. Lou Gehrig’s disease
● Probably not
● TDP-43 at lower brain levels in ALS

28
Q

What can chronic concussion lead to?

A

Chronic Traumatic Encephalopathy ​(CTE)

● Abnormal buildup of tau protein in brain and spinal cord

29
Q

This pressure is the minimum threshold BP need to maintain adequate brain perfusion.

A

60mmHg

30
Q

A Pt present to you office complaining of a HA. They also admit that they’ve had changes in the vision, n/v, irritability and difficulty walking. This term is causing the HA associate with your probable Dx.
Bonus point: if the ICP becomes to high ths could happen.

A

Mass effect – growth of tumor is taking up limited space in the skull resulting in pressure on the meninges causing the HA.
Bonus: Uncal Herniation – pushing of brain stem through the foramen magnum.

31
Q

You’re at a picnic with your family and talking with your nephew. While talking you notice that he all of sudden stops talking and just stares into space for a minute. When you ask him about it he has no idea what you’re talking about. You tell his mother to take him in for a check up because you think he had this.

A

Petite maul or absence seizure

32
Q

A Pt comes into the ER with left sided weakness, slurred speech, and ptosis. Ct scan shows no hyperattenuation. On a pathophysiological level these metabolic changes are happening in the affected portion of the brain.

A

Loss of ATP production and increased production of lactic acid. (Causing denaturation of proteins.)

33
Q

A hemorrhagic stroke can still result in this in that section of the brain from the pressure the bleed is creating.

A

Ischemia