NEURO-Siezure Concussion Flashcards
What is the result of aberrant electrical activity in the brain d/t metabolic, traumatic, infections, tumors, meds/drugs, congenital defects?
Seizures
What is the disease characterized by the presence of recurrent seizures?
Epilepsy
What detects synchronous firing throughout multiple regions of the brain → disrupts normal brain activity
EEG Normal brain activity 1. activity different places 2. activity different times 3. Does not tell simple vs complex 4. Always need PT HPI
What are the theories behind seizures?
● 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
EEG show a seizure begin in a specific of one cerebral hemisphere. Name this classification
Focal/Partial seizures
Simple: no impairment of consciousness or awareness 1 hemisphere
Complex: Consciousness impaired; 1 hemisphere
Parital seizure activity that spread across the brain & becomes generalized?
Jacksonian march” - manifest up to 120 seconds
Focal/Partial
● MC type is temporal lobe
● MC is complex partial
What are Partial Seizure DDX? What diagnosis tools help differeinate?
● 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
Did trial of AED use for treatment have good outcomes?
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
EEG shows widespread synchronized electrical activity on both hemispheres
Generalized- travel all over brain
Absence Myoclonic Tonic clonic Tonic Atonic
MC- young children
What are tips to get a good PMH?
difficult to obtain d/t associated with amnesia
● Need solid history of period- ictal and the post-ictal period
● Look for triggers
What trigger lower seizure threshold?
fever,
menstruation,
stress,
sleep issues
Ms. Emily has nonconvulsive: very short episodes of conscious detachment, that last 10s-100s times per day
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.
Ms. Jenna had a sudden loss of muscle tone leading to slackening of the jaw, drooping of the limbs, and falling to the ground.
Atonic
AKA drop attacks
Mr. Tim had brief involuntary muscle contractions, involving bilateral jerking of muscles, to face, trunk, and legs.
Myoclonic
induced by stimuli of cerebral origin.
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?
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.
What happens at end of clonic phase?
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
How to manage seizures?
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
What Drug MOA acts on Na+ channels
Phenytoin Carbamazeipine Oxcarbamazeipine Lamotrigine Lacosoame Sonisamid
What Drug MOA act on GABA receptors
Benzo
Barbiturates
DEC GABA uptake
What occurs with a concussion?
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
What is single most important protective?
Helmet
Youth Leading cause of TBI
Auto accidents
Sports
Multiple +/- permanent damge
Tau protein
N- aceytlaspartate
Cholin
Mr. Jacob c/c HA, dizziness, insomnia, irritability, fatigue, impaired memory, lowered tolerance to light and noise after hit on field. What is workup?
Concussion- TBI
Labs- SCAT2, post IMPACT
Neruo exam
CT
Continuation of 3 mild symptoms: headache, irritability, insomnia, poor concentration, memory, fatigue, impaired memory, lowered tolerance to light and noise may persist for months
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
What correlates to severity of concussion>
duration of retrograde amnesia
What is protective brain mechanism and reason to support being out from school?
Brain metabolism slowed for weeks after TBI
○ Anybrain metabolic activity puts strain on the organ
What are stepwise progression of concussion?
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.
Does Concussion cause ALS
ALS = Amyotrophic lateral sclerosis, a.k.a. Lou Gehrig’s disease
● Probably not
● TDP-43 at lower brain levels in ALS
What can chronic concussion lead to?
Chronic Traumatic Encephalopathy (CTE)
● Abnormal buildup of tau protein in brain and spinal cord
This pressure is the minimum threshold BP need to maintain adequate brain perfusion.
60mmHg
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.
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.
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.
Petite maul or absence seizure
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.
Loss of ATP production and increased production of lactic acid. (Causing denaturation of proteins.)
A hemorrhagic stroke can still result in this in that section of the brain from the pressure the bleed is creating.
Ischemia
