17 Jan 24 Flashcards

1
Q

Generalized convulsive status epilepticus

A

> 5mins of gen convusive seizure
Or
2 generalized convulsive seizures without interval recovery of consciousness

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2
Q

GCSE RF

A

Nonadherence to AEDs
Structural brain abnormalities (tumor)
Metabolic abnormalities
Infection
Drug withdrawal

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3
Q

GCSE ttt

A

🍔 stabilize circulation, airway and breathing
🍔 BZ (repeat administration until termination of seizure activity
🍔 begin antiepileptics
🍔 EEG monitoring for refractory status epilepticus or failure to regain consciousness.

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4
Q

GCSE patient who is persistently unresponsive

A

Patients with GCSE regain consciousness after 10-20 mins
persistently unresponsive state mayb due to:

🧠 sedation due to persistent effects of BZ. Or
🧠 ongoing seizure activity without physical manifestations (non convulsive status epilepticus )

Ttt: Do EEG (to diff between them 2)
Continue BZ and AED
Propofol/ phenobarbital for refractory cases

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5
Q

GCSE complications

A

Neuronal injury and death.
Hence immediate seizure cessation is warranted.

We dont do MRi as GCSE is emergency
As seizure cessation is priority

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6
Q

Breath holding spell Cyanotic vs pallid

A

Cyanotic:
Triggered by vigorous crying leading to breath holding , cyanosis , LOC with rapid return to baseline.

Pallid BHS :
After minor trauma
No crying
Pain and fear causes slow HR and breat holding , child becomes pale , diaphoretic , limp .
Brief LOC
Sometimes sleepy and confused for a short period after.

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7
Q

Management of BHS

A

Last < 1min
Clinical dx no workup needed
Screen for iron def anemia
Iron therapy shows improvement
Monitoring shows bradycardia before LOC in BHS

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8
Q

Fibromyalgia Ttt

A

TCA

Alternates in refratory cases
Duloxetine
Milnacipran
Pregablin

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9
Q

Ttt of TN

A

Carbamezipine
Oxcarbazepine(better tolerated)

Side effects:
Hyponatremia (due to inc sensitivity to ADH)
Leukopenia
NV

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10
Q

Trigeminal neuralgia workup

A

MRA / MRI of brain with contrast

If not clear
Nerve conduction (trigeminal reflex) testing

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11
Q

Blepharospasm MECH

A

Recurrent forceful contraction of eyelid muscles
Form of focal dystonia
🤡BL and symmetric
If Ass with spasm of lower face and jaw
(Meige syndrome)
💩affected by sensory input
BRIGHT LIGHTS , may trigger muscle contraction
🦬 sensory trick ;
Touching and brushing the skin around eye may terminate the spasm.

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12
Q

Management of blepharospasm

A

🐊Wear dark glasses to block bright lights
🐊Botulism toxin inj

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13
Q

Workup for first time seizure

A

🚨Glucose CBC eectrolytes renal function liver function urine drug screen
🚨CT (acutely) MRI (elective)
🚨LP (if fever , nuchal rigidity)
🚨EEG
🚨if LOC do ECG for arrythmia

For unprovoked seizures do EEG and MRI. Otherwise dont.

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14
Q

Indications to start antiepileptics

A

Abnormal EEG or imaging
Nocturnal seizures
Focal deficits

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15
Q

Paroxysmal sympathetic hyperactivity

A

Sudden episodes of excessive sympathetic activity

Ass with severe TBI

Mech : damage to cortical areas resp for modulating and imhibiting sympathetic centers.

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16
Q

Paroxysmal sympathetic hyperactivity triggers and S/S

A

External stimuli like bathing and repositioning.

S/S:
Tachycardia
Hypertension
Tachypnea
Fever
Diaphoresis

Last for 20-30 mins.

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17
Q

Management of PSH

A

Avoid triggers
Treat fever
Medicines. Opiods GABA a2agonists
Opioids improve symptoms via gen reduction of symp tone.

18
Q

Mechanism of diffuse Axonal injury

A

▶️Head trauma
▶️Accleration- deceleration or rotational shearing forces on axons (at gray white matter junction)

19
Q

Management of DAI

A

Supportive
Manage incr ICP

20
Q

CF of DAI

A

⛱ severe neurologic impairment (GCS<8)
⛱impairment greater than imaging findings
⛱ MRI:
🧠Punctate hemorrhages in white matter
🧠Blurring of gray-white matter junction

21
Q

Why CT is normal in DAI?

A

DAI is on microscopic level hence not apparent on CT.

MRI is more sensitive and shows minute punctate hem in white matter (axons) and blurring of gray white interface (due to edema).

22
Q

Pediatric TBi when to do CT without contrast in age <2

A

High risk features age <2

AMS/fussy
LOC
Severe mech of injury (fall>3m, high impact , MVC)
Non frontal scalp hematoma
Palpable skull fracture

23
Q

TBI CT indication in age >2-18

A

AMS(somnolence, agitation)
LOC
Sever injury( fall>5m, high impact, MVC)
Vomiting , severe headache
Basilar skull fracture signs ( CSF rhinorrhea )

24
Q

Signs of basilar skull fracture

A

CSF rhinorrhea
Periorbital hematoma
CSF otorrhea
Post auricular ecchymosis (battle sign)

25
Indications for CT scan in concussion
Amnesia for events >30mins prior to injury Focal deficits Signa of skull fracture
26
Concussion CF
👹Transient neurologic disturbance Dizziness Disorientation Amnesia After mild TBI 👹No structural intracranial injury
27
Ttt of concussion
🚑 remove from same day physical play 🚑 neurologic evaluation 🚑 rest for >24h 🚑 gradual return to normal activity (1 week) if symptoms do not worsen 🛖 physical : light aerobic exercise , non contact sports , contact sports 🛖 limit screen time , frequent breaks , shortened days.
28
Concussion mechanism
Transient disturbance of normal neuronal function due to: Widespread neuron depolarisation Dec CBF Localised lactic acidosis
29
Concussion vs DAI
Concussion is transient neuronal functional disturbance DAI is severe trauma causing tearing of white matter tracts. Pts are severely obtunded or comatose Shaken baby Head impact car collision
30
Epidural hematoma
Trauma to sphenoid bone with tearing of middle meningeal artery
31
Epidural hematoma ttt
Urgent surgical evacuation
32
Epidural hematoma CF
Brief LOC followed by lucid interval Hematoma expansion causing; Inc ICP Uncal herniation
33
Intervention to reduce Cerebral blood flow to dec ICP
Head elevation to ⬆️ venous outflow Sedation to ⬇️ metabokic demand Hyoerventilation to ⬇️ PaCO2 resulting in vasoconstriction
34
Subfalcine herniation
Cingulate gyrus is displaced under falx cerebri Does not cause pupillary involvement IL anterior cerebral artery compression leading to CL leg weakness
35
Mechanism of tranexamic acid in fall pt?
Prevents intracranial hemorrhage
36
Manangement of TBI
▶️Main cerebral perfusion pressure ▶️Prevent Intracranial hemorrhage ▶️Other measures Prevent seizure (levetitacetam) Control blood sugar (insulin target 140-160) Maintain normothermia (antipyretics , surface cooling devices )
37
How to maintain Cerebral perfusion pressure ?
CPP= MAP-ICP Maintain MAP: Isotonic fluids Vasopressor therapy Reduce ICP. : Head elevation Sedation (propofol , midazolam) Osmotic therapy (hypertonic saline, mannitol) Decompressive ttt (craniectomy, CSF removal)
38
How to prevent ICH in TBI
Tranexamic acid(antifibrinolytic) Reversal of anticoagulation
39
Acute traumatic coagulopathy in TBI
TBI pts are at risk of sec traumatic coagulopathy Severe tissue injury leads to uncontrolled coagulation and consumption of coagulation factors ; Hypocoagulability Hyperfibeinolysis (breaking down necessary clots. Ttt: tranexamic acid (within 3hrs reduces mortality)
40
Central herniation
🛞Caudal displacement of diencephalon and brainstem 🛞Rupture of paramedian basilar artery branches 🛞BL midposition & fixed pupils (loss of sympathetic & parasympathetic innervation 🛞Decorticate (flexor) ➡️ decerebrate (extensor) posturing
41
Ttt of central herniation
🚨Dec ICP 🚨Correct underlying etiology(Hemorrhage evacuation) to prevent tonsillar herniation which compresses medulla and cause cardiac and resp arrest.