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PCCM Fellowship > Neurology > Flashcards

Neurology Flashcards

1
Q

Baclofen Withdrawal

A

Baclofen is a GABA receptor agonist
Intrathecal allows for high CSF levels

Abrupt withdrawal leads to Sx within 1 day
FEVER, autonomic dysfxn, AMS, spasticity, seizures, rhabdo, DIC
Psych (hallucinations, delusions, confusion, agitation, fluctuating LOC, anxiety)

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2
Q

Post-op hydrocephalus

A

Serial HC, serial assessment fontanelle and sutures.
Monitor A’s + B’s

Prefer to wait for shunt placement until >2kg 2o high risk infection in patient population

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3
Q

VP Shunts Risks

A

Frontal catheters ~ weakness passing near genu of internal capsule,CN2.3.6 injuries, ST memory issues from forniceal injury

Peritoneal shunt ~ PTX, hemothorax, bowel perf

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4
Q

Lumbar drains

A

Commonly placed to stop CSF leaks after anterior skull base surgery (check beta transferrin if concerned)
Tx with drain, flat bed rest, furosemide and acetazolamide

Complications: back/leg pain while drain opened.
Tension pneumocephalus (downward herniation of brain 2/2 air entering nose and entering intracranial cavity
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5
Q

Posterior Fossa Syndrome (cerebellar mutism)

A

Caused by spltting the cerebellar vermis (done to visualize post fossa tumours)
Highest risk 7-11y
Risk not being able to extubate, mutism or hypophonia, tremors, titubations - with severe strabismus and abnormal ocular movements

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6
Q

Hypothalamic tumour

A

Post op complications are ischemia related to vasospasm of ACA/MCA, also DI

Encourage papaverine on artery intra-op
Post-op vasospasm can occur when artery that was under severe stretch now spasms as it relaxes.
Waxing/waning neuro exam that is exquisitely sensitive to BP
Keep pos FB and give pressors

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7
Q

First hour checklist in Status Epilepticus

A 
Fingerstick glucose
Obtain IV access + monitors
Labs: Drug levels, CBC, extended chem, HcG in females, tox if suspected
\+/- Head CT
EEG
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8
Q

Toxidromes associated with status epilepticus

A

Isoniazid: Tx w/ benzos + pyridoxine
TCA: evaluate QRS widening, Tx w/ NaHCO3
Theophylline: Tx w/ benzos or barbiturates, consider gastric lavage/charcoal/WBI
Cocaine/sympathomimetics: Tx w/ benzos
Alcohol withdrawal: Tx w/ inc doses of benzo and/or barbiturate
Organophosphates: Tx w/ atropine, midazolam, pralidoxime

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9
Q

What is the time to efficacy of fospheny to phenytoin?

A

Fospheny is a water-soluble prodrug that is converted to phenytoin by plasma esterases.

While fospheny can be administered more quickly (less caustic), it has the same time to effect on seizures ~15 minutes

** Follow free phenytoin levels - highly protein bound, so important in hypoalbuminemic states and if pt is on VPA (displaces phenytoin from albumin)

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10
Q

MOA of AEDs

A

Fospheny/pheny: Slows rate of recovery voltage-gated Na channel - activity-dependent inhibition of action potential firing - peak 15 mins

Phenobarb: GABA activation at a binding site separate from benzos - PB has slow entry into brain, but has inc uptake during sz, and drug may be conc near sz focus - onset 5 mins, peak 15 mins, 1/2life 50-150 hrs

VPA: Modulates Na + Ca currents + activating GABA receptor - effective in myoclonic, absence, lennox-gestaut RSE

Keppra: glutamate + GABA receptors + Ca channels

Pentobarbital: Activation of GABA, inhibition of NMDA, alters Cl, K and Ca ion channels

Inhaled anaesthetics: GABA, nicotinic, glycine, K-gated ion channels

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11
Q

SE od AEDs

A

Fospheny/pheny: hypotension 2/2 propylene glycol formulation. Also has potential for bradycardia and dysrhythmia

VPA: Transaminitis and hyperammonemia, pancreatitis, thrombocytopenia/coagulation issues, SJS. Great HDS profile

PB: Somnolence, resp depression, hypotension

Keppra: Great HDS profile

Pentobarbital: Dilation of venous capacitance vessels = dec preload and CO, WBC dysfunction (Risk PNA), ileus, DI, long half life

Inhaled anaesthetics: dec cerebrovascular resistance = inc CBF + potentially ICP (mild), lower BP, negative inotropy

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12
Q

SE od AEDs

A

Fospheny/pheny: hypotension 2/2 propylene glycol formulation. Also has potential for bradycardia and dysrhythmia

VPA: Transaminitis and hyperammonemia, pancreatitis, thrombocytopenia/coagulation issues, SJS. Great HDS profile

PB: Somnolence, resp depression, hypotension

Keppra: Great HDS profile, fully renally cleared. No hepatic metabolism!

Pentobarbital: Dilation of venous capacitance vessels = dec preload and CO, WBC dysfunction (Risk PNA), ileus, DI, suppression of brain stem reflexes, long half life

Inhaled anaesthetics: dec cerebrovascular resistance = inc CBF + potentially ICP (mild), lower BP, negative inotropy

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13
Q

What neurotransmitter is primarily responsible for excitotoxic cell death in brain injury?

A

Glutamate

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14
Q

What is the equation for Cerebral Perfusion Pressure?

A

CPP = MAP - ICP

If CVP >ICP then CPP = MAP - CVP

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15
Q

What is the equation for cerebral metabolic rate?

A

CMRO2 = CBF x AVDO2

where AVDO2 = CaO2 - SjvO2
note: SjvO2 can be directly measured with fibreoptic catheter placed cephalad into jugular bulb

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16
Q

By how much does cerebral blood flow change with each mmHg change in PaCO2?

A

CBF changes by 3% for every mmHg change in PaCO2

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17
Q

Is CBF regulated by oxygen concentration?

A

CBF is generally not regulated by oxygen concentration when PaO2 >60mmHg

Whereas PaO2 <60mmHg results in profound increase in CBF in an effort to offset ischemia

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18
Q

Normal cerebral blood flow value (ml/100g brain/min) are highest at which age of life?

A

4 years of age

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19
Q

What are the components of the brain death examination?

A

Patient must be normotensive and normothermic (>35o)
First exam to be performed 24h post-injury

Interval examinations:
7d = unable to perform exam
Term NB - 30d = 24h
31d - 18y = 12h

Clinical Exam:
Absence of motor responses
Absence of pupillary light responses
Absence of corneal reflexes
Absence of caloric responses
Absence of gag reflex
Absence of coughing in response to tracheal suctioning
Absence of sucking and rooting reflexes
Absence of respiratory drive at a PaCO2 60mmHg or 20mmHg above normal baseline
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20
Q

Describe the pathway for pupillary light response

A

Impulse –> optic nerve –> optic chiasm –> nerves decussate (lateral retina continue on same side, medial fibres cross) –> synapse in pretectal nuclei of midbrain –> project bilaterally to Edinger-Westphal nuclei –> efferent fibres carried to pupillary sphincter muscles of ipsilateral eye via CN3

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21
Q

Describe the pathway for corneal reflex

A

Corneal sensory fibers (V1 of CN5) –> end in ipsilateral sensory nucleus of CN5 pons –> neurons project to both motor nuclei of CN7 (also located in pons)–> CN7 travels ipsilaterally to orbicularis oculi muscle = blink

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22
Q

Describe response to light for lesions in (1) retina, prechiasm CNII, (2) symmetrical brainstem process, (3) isolated CNIII

A

(1) Retina, prechiasm CNII:
- No response B/L when light directed towards ipsilateral eye, constriction B/L when light directed towards unaffected eye

(2) Symmetrical brainstem process
- No response B/L

(3) Isolated CNIII
- No constriction if ipsilateral eye when light directed towards either eye

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23
Q

Describe pathology of corneal reflex if pathology to (1) CN5 V1, (2) Pons, (3) Motor nucleus of CN5 or peripheral CN7

A

(1) CN5 V1 - no response B/L when affected eye touched, normal response when unaffected eye touched
(2) Pons - No response B/L
(3) Motor nucleus of CN5 or peripheral CN7 - No blink on affected side to stimulation B/L

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24
Q

Describe absent doll’s eye reflex

A

Turn head briskly from midline to one side

Absence = Eyes turn with head and never deviate back to midline

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25
Q

Describe Ice water caloric testing

A

Cold water cools endolymph = inc density = downward migration = mimics horizontal rotation of head

4 responses:
1. Normal caloric nystagmus (fast COWS): cold water opposite, warm water sam side

  1. Conjugate deviation: slow deviation of eyes toward cold stimulus = intact brainstem function but cortical compromise (GA, supratentorial lesion, metabolic comas)
  2. Dysconjugate deviation = early brain stem compression or MLF stroke
  3. Absent response = severe brainstem compromise
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26
Q

Describe gag reflex

A

Touching each side of posterior pharynx = elevation of both sides of pharyngeal musculature

CN9 stimulus –> solitary nucleus in medulla –> B/L projections from each solitary nucleus to nucleus ambiguous of CN10 –> completed efferent limb back to pharyngeal muscles B/L

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27
Q

Describe the abnormal respiratory pattern if pathology occurs rostral to caudal

A

Cheyne-Stokes –> Hyperventilation/ataxic breathing –> Apneustic/Apnea

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28
Q

Describe posterior cord syndrome

A

Injury to dorsal columns = Impaired proprioception and vibration

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29
Q

Describe anterior cord syndrome

A

Due to injury of anterior 2/3 of spinal cord = Intact proprioception and vibration, but loss of pain and temperature

May also leads to motor impairment and sphincteric dysfunction due to involvement of ventral horn carrying LMN and lateral corticospinal tracts

30
Q

Describe central cord syndrome

A

Motor deficits worse in UE>LE, loss of pain and temperature sensation in a cape-;like distribution and possible bowel/bladder dysfunction

Due to syringomyelia or edema to cervical spinal cord

31
Q

Describe Brown-Sequard syndrome

A

loss of ipsilateral voluntary motor function and proprioception, with loss of pain, temperature, and tactile sense on C/L side of injury

32
Q

Describe a normal and abnormal ICP waveform

A

P1 = Percussion wave (first and tallest peak ~systolic BP wave travelling through cerebral arterial system, choroid plexus and ultimately transmitted to ventricular system

P2 = Tidal wave (reflective of rebound pulsations after percussion wave ~ surrogate of compliance
- If high ICP and poor compliance, this wave will predominate over P1!!!

P3 = Dicrotic wave (reflects venous pulsations after AoV closure)

33
Q

Describe Lundberg A and B waves

A

A waves = plateau waves = ICP amplitude increases up to 50mmHg over baseline for 5-20 minutes –> when resolves, baseline now reset to higher baseline
–> reflects inappropriately high cerebral blood volume due to heterogenous disruption in autoregulation and decreased intracranial compliance. Also results in decreased CPP and ischemia/worsening edema

B waves = ICP amplitude increases 10-20mmHg above baseline for only 1-2minutes
–> reflective of vasomotor instability, but may also be due to worsening intracranial compliance. Also seen in abnormal respiratory patterns

34
Q

Name 6 contraindications to lumbar puncture

A
  1. Clinical evidence of inc ICP (flexing neck can obstruct cerebral venous return)
  2. Cardiopulmonary instability
  3. PLT<50
  4. INR>1.4 (risk spinal epidural hematoma)
  5. Overlying skin infections
  6. Cervical cord lesions (don’t want to flex head
35
Q

Name 6 contraindications to lumbar puncture

A
  1. Clinical evidence of inc ICP (flexing neck can obstruct cerebral venous return)
  2. Cardiopulmonary instability
  3. PLT<50
  4. INR>1.4 (risk spinal epidural hematoma)
  5. Overlying skin infections
  6. Cervical cord lesions (don’t want to flex head)
36
Q

What is a normal CSF glucose and protein level?

A

Glucose should be 1/2 to 1/3 serum glucose

Protein level 5-40 in a child (65-150 in preterm)

37
Q

Draw the pressure volume curve of ICP (Monroe Kellie Doctrine)

A

Volume can regulate to a large degree before ICP exponentially increases
Normal ICP for child ~10, for adults ~15

38
Q

What is the earliest protective mechanism of increased ICP?

A

Displacement of CSF down craniospinal axis

39
Q

Draw the brain’s autoregulation curve

A

CBF vs MAP - BP range of 50-150mmHg can be regulated by arteriolar vasodilation/vasoconstriction

In chronic intracranial hypertension, their autoregulation curve will shift to the right. Don’t bring the BP down quickly bc theyre CBF will acutely decrease

40
Q

What is the cause of seizures in PRES/RPLS?

A

Dysregulation of CBF
Subcortical edema without infarction preferentially of parietal and occipital lobes, associated with cyclosporine and tacrolimus
Poor sympathetic innervation of posterior circulation

41
Q

What are the two indication for steroids in brain pathology?

A

Brain tumours and tuberculous meningitis.

Note: Inflammatory cascade in bacterial meningitis may lead to tissue damage and exacerbate neuro sequelae via bacterial lysis and endotoxin release. RedBook - dexamethasone may be beneficial in Hib meningitis and may be considered in strep pneumo if <6wks old

42
Q

What is the cause of seizures in PRES/RPLS?

A

Dysregulation of CBF
Subcortical vasogenic edema without infarction preferentially of parietal and occipital lobes, associated with cyclosporine and tacrolimus
Poor sympathetic innervation of posterior circulation

43
Q

What is the difference between vasogenic and cytotoxic edema?

A

Vasogenic: vascular congestion leads to interstitial leak (PRES/RPLS)
Cytotoxic: astrocytes and endothelial swell (HIE)

44
Q

What is the MCC of refraftory status epilepticus (>60 minutes)

A

Viral encephalitis

45
Q

Describe 6 characteristics of the ideal AED

A
  1. Both GABAergic and NMDA antagonistic properties
  2. Fast acting
  3. Cross the BBB
  4. Short half life
  5. Neuroprotective properties
  6. Favourable risk profile with low to no side effects
46
Q

What are the 5 P’s of stroke management?

A
  1. Parenchyma (limit infarct size)
  2. Pipes (improve compromised flow)
  3. Perfusion (avoid hypotension and dehydration)
  4. Penumbra (vulnerable but salvageable area)
  5. Prevent complications (fever, glycemic control, DVT/aspiration precautions, bowel reg, early mobilization/rehab)
47
Q

What is the timing of complications following subarachnoid hemorrhage?

A

Rebleeding (0-2d) –> Obstructive hydrocephalus (2-4d) –> vasospasm (>3-4d) –> hyponatremia (>5d)

48
Q

What is the MCC of hydrocephalus in term infants?

A

Aqueductal stenosis

49
Q

What is the innervation of the autonomic nervous system?

A

Sympathetic - CNS –> Ach/nicotinic AchR –> NE on organs
or - CNS –> Ach/nicotinic AchR of adrenal gland –> epinephrine into blood –> epinephrine on organs

Parasympathetic - CNS –> Ach/nicotinic AchR –> Ach/muscarinic AchR on organs
Somatic - no synpase; CNS –> acetylcholine on nitoinic AchR on skeletal muscle

Note: ALL pre ganglionic neurons go to nicotinic AchR

50
Q

What part of the LMN does West Nile Virus affect?

A

Anterior horn cell

As does enterovirus, polio

51
Q

What part of the neuron does SMA affect?

A

Anterior horn cell
SMN gene (Survivor Motor Neuron gene usually halts apoptosis)
AR condition
Heart is not involved

52
Q

What part of the neuron does GBS affect? Discuss etiology and presentation

A

Peripheral nerve
Symmetric ascending paralysis, demyelinating disease
May have sensory parasthesia (stocking-glove) and ataxia

Etiology: Mycoplasma and campylobacter
- antigenic mimicry (sialic acid)

Miller-Fischer variant: ophthalmoplegia, ataxia and areflexia with relative little weakness

Autonomic dysfunction is a major risk factor for mortality (cardiac)

Dx: albumino-cytologic dissociation (elevated protein in absence of pleocytosis, delayed EMG conduction found LATE

53
Q

What are the indications for intubation of patients with neuromuscular disease?

A

Forced Vital Capacity <15-20cc/kg (normal ~70cc/kg)
Max NIF 20)
Consider for retention of secretions and weakness of protective airway reflexes
Avoid depolarizing NMB (succinylcholine)

54
Q

Name 4 toxins acting pre-synaptically (Ach doesn’t get released)

A

Black widow spider venom
Scorpion venom
Tick paralysis
Botulism (weakness top/down starting with eyes)

55
Q

Name a toxin acting post-synaptically (Ach blocked from working at receptor)

A

Toxic nerve agents

56
Q

What is the pathophys of tick paralysis?

A

Disorder of Ach release from axonal terminals to neurotocin that inhibits depol
Max toxin production 5-6 days (usually pregnant female)
Weakness, loss of coordination and sometime an ascending paralysis like GBS

57
Q

What is the pathophys of tetanus?

A

Bacteria enter would and create tetanospasmin –> travels to CNS via retrograde axonal transport –> enters presynaptic neurons and inhibits release of GABA = can’t release muscles
Tx: Benzos! (GABA agonism), could try Mg, baclofen, paralysis, human tetanus Ig (only neutralizes circulating toxin, not bound)

58
Q

What is the pathophys of myasthenia gravis?

A

Post-synaptic issue! Abs to AchR
Release of Ach is normal, but don’t have enough AchR available
EMG is more diagnostic than Bx - decremental response to repetitive nerve stimulation, motor nerve conduction normal

Dx: Sleepy after tensilon!! Give edrophonium (anticholinesterase) will bombard receptors with Ach since it won’t get broken down. Cant have upward gaze or lift head off bed

Note: May need to block muscarinic effects (diarrhea, abdo cramps, inc secretions, cardiac arrhythmias) of edrophonium by giving atropine (bc only want nicotinic receptors affected
Tx: neostigmine, pyridostigmine (cholinesterase inhibitors)

59
Q

How do you tell difference between cholinergic crisis and myasthenia crisis?

A

Pupils will be pinpoint in cholinergic crisis!
Overdose of Ach causes pupillary constriction

Myasthenic crisis = pupil constriction is normal

60
Q

What is the pathophys of organophosphates?

A

Binds irreversibly to acetylcholinesterase enzymes and PREVENTS degradation of Ach

Crisis ensues at both muscarinic and nicotinic receptors
Rx: Atropine to prevent muscarinic effects
Pralidoxime (prevents enzyme from being broken down post binding to toxin)

61
Q

What is the presentation of a cholinergic crisis?

A 
SLUDGE
Salivation
Lacrimation
Urinary retention
Defecation
GI cramps
Emesis/edema
62
Q

What is the pathophys of Duchenne’s muscular dystrophy?

A

X linked, absence of dystrophin on Xp21 locus
Dystroglycan is also decreased (needed for normal brain development - may have ID)
Must fix scoliosis before age ten or else they lose vital capacity by 4-10%/year

63
Q

What are safe levels of serum osmolality for 3% and mannitol use?

A

<360mOsm/L for 3%; also leads to better volume status and less interventions to maintain ICP
<320mOsm/L for mannitol - risk ATN and ARF

Note: BBB is nearly impermeable to both
Mannitol decreases ICP acutely by decreasing blood viscosity, later acts as an osmotic diuretic

64
Q

Where are subdural hemorrhages most often located?

A

Inter-hemispheric fissures along tentorium and posterior fossa

Due to tearing of bridging veins
Have worse prognosis due to assoc. underlying brain injury

65
Q

What is the difference between critical illness myopathy (CIM) and critical illness polyneuropathy (CIP)?

A

Stretch reflexes are usually intact in CIM

CIM ~ steroid use, NMB and asthma
CIP ~ sepsis and multi-organ failure

In CIP, sensation to pain and proprioception are reduced in distal extremities

66
Q

Describe the pathophys of Eaton-Lambert syndrome

A

Impaired release of Ach as auto-Abs form against presynaptic VG-Ca channels.

Compared to myasthenia, there is improved muscle function with activity due to accumulation of presynaptic Ca and improved release of Ach

67
Q

Describe Train of Four testing. What TOF ratio is most indicative of no residual motor weakness?

A

4 supramaximal stimuli (>50mA) given at 2Hz

In absence of NMB there will be 4 contractions of equal response. If NMB present there will be a decremental response

A dec in T4 requires 75% of AchR to be blocked
A dec in T1 requires 80%
Abolishment of all 4 twitches = 98%

A ToF ratio of 0.7 is evidence of adequate NMB recovery

68
Q

What muscles are most and least resistant to NMB

A

Most resistant - diaphragm and larynx

Least resistant - upper airway muscles and masseters

69
Q

What are the CNS respiratory centers?

A

Medulla - integrates multiple inputs

  • Dorsal resp group: sends insp signal to diaphragm and ICs
  • Ventral resp groups: coordination of inspiration and exhalation; airway muscle tone; respiratory pacemaking

Pons - integrates other sensory inputs and fine tunes medullary resp activity

70
Q

Where is the brains response to inc CO2

A

Medullary chemoreceptor centers - stimulated directly by inc H+ ions

Intact BBB is impermeable to passive diffusion of H+ and HCO3, but CO2 moves across freely –> hydrolyzed to H+ in CSF
This stimulates inc ventilation rate to clear CO2 and ultimately decrease H+

71
Q

Where are peripheral chemoreceptors located>

A 
Carotid bifurcation (glossopharyngeal nerve) and Ao arch (vagus nerve)
Sensitive to pH, PaO2 and PaCO2

NOT affected by bound O2

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