Truelearn cerebrovascular all wrong Flashcards

1
Q

Treatment for infantile spasm in patients without tuberous sclerosis and with tuberculosis sclerosis

A

Without ACTH
With Vigabatrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Perinatal strokes
Term arterial or venous more common?

Preterm arterial or venous more common?

A

Term: arterial

Preterm: venous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Embryonal tumor (aka PNET) with multilayered rosettes is associated with … amplification on chromosome …

A

C19MC amplification on chromosome 19.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Where is serotonin produced?

A

Raphe Nucleus in brainstem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Where is dopamine produced?

A

substantia nigra pars compacta (SNc)

and

ventral tegmental area (VTA) (reward/pleasure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Where is histamine produced?

A

tuberomammillary nucleus (TMN) of posterior hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Where is acetylcholine produced?

A

Nucleus basalis of Meynert in substantia innominata in basal forebrain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Where is norepinephrine produced?

A

locus coeruleus in the pons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Where is GABA produced?

A

substantia nigra reticulata

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which three antiemetics are best for migraine?

Which anti-emetic has least evidence to help migraine?

A

Metoclopramide, chlorpromazine, and prochlorperazine
are antiemetic dopamine receptor
antagonists that can be used as monotherapy for acute migraine headache.

Ondansetron is also commonly used for migraine, there is minimal evidence-based data
supporting its use in this setting. In fact, some evidence has instead found that ondansetron has a
relatively high incidence of headache as an adverse effect.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Metoclopramide, chlorpromazine, and prochlorperazine can cause what side effects? What reduces this risk?

List 3

Chlorpromazine is classified as a low-potency typical antipsychotic. Low-potency antipsychotics have more anticholinergic side effects, such as dry mouth, sedation, and constipation, and lower rates of extrapyramidal side effects, while high-potency antipsychotics (such as haloperidol) have the reverse profile.[16]

A

Diphenhydramine (antihistamine Benadryl) to prevent akathisia (restless, agitated, need to move) and acute dystonia (involuntary muscle contractions)

Also risk of QT-interval prolongation and torsades de pointes.

Metoclopramide: dopamine receptor antagonist, rx N/V
Chlorpromazine: low potency FGA, dopamine receptor antagonist (and also antagonist to other receptors: serotonin, histamine, adrenergic, muscarinic)
Prochlorperazine: rx nausea, migraines (3x better than metocloperamide), psychosis, anxiety, RX vomiting from chemo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is MOA of ondansetron?

A

5HT-3 Serotonin receptor antagonist in area postrema on fourth ventricle floor (chemoreceptor trigger zone)

Acts both centrally and peripherally to prevent and treat nausea and vomiting.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Moderate Diffuse Axonal Injury (DAI) definition and prognosis

A

LOC > 24 hrs
days of post-traumatic amnesia
mild to moderate memory deficits
chance of good recovery at 3 months is about 40%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Mild Diffuse Axonal Injury (DAI) definition and prognosis

A

LOC 6-24 hrs
hours of post-traumatic amnesia
mild to moderate memory deficits
chance of good recovery at 3 months about 60%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Post-stroke fatigue is associated with …

A

impaired processing speed and memory

adrenergic / dopaminergic drugs such as modafinil may help

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Ocrelizumab rx MS, MOA?

A

depletion of B cells with cell surface antigen CD20

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Rituximab rx MS, MOA?

A

depletion of B cells with cell surface antigen CD20

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Ofatumumab rx MS, MOA?

A

depletion of B cells with cell surface antigen CD20

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Ublituximab rx MS, MOA?

A

depletion of B cells with cell surface antigen CD20

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Natalizumab rx MS, MOA?

A

blocks integrin-adhesion molecule interactions and inhibits T cell entry into CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

FIngolimod rx MS, MOA?

A

blocks sphingosine 1-phosphate receptor (S1PR) keeping lymphocytes in lymph nodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Siponimod rx MS, MOA?

A

blocks sphingosine 1-phosphate receptor (S1PR) keeping lymphocytes in lymph nodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Glatiramer acetate rx MS, MOA?

A

skews T cell response to non-inflammatory phenotype in part by inactivating T regulatory cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

interferon beta rx MS, MOA?

A

skews T cell response to non-inflammatory phenotype in part by inactivating T regulatory cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Dimethyl fumarate rx MS, MOA?

A

activates transcription factor Nrf2

rx: RRMS and psoriasis

Nrf2 is a key regulator of antioxidant responses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Alemtuzumab rx MS, MOA?

A

lymphocyte depletion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Cladribine rx MS, MOA?

A

impairs DNA synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Teriflunomide rx MS, MOA?

A

impairs DNA synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Early infantile epileptic encephalopathy (EIEE) or Ohtahara syndrome: age of presentation, type of seizures, typical EEG

A

first three months of life
tonic seizures, focal seizures,
EEG showing a burst suppression pattern consistent in wake and sleep w periodicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is central cord syndrome and what three conditions is it associated with?

A

weakness and loss of sensation, or pain, tingling, dull ache, in arms and hands > LE, also w bladder dysfunction acutely sometimes

  • hyperextension injury
    (especially older adults w arthritis, spondylosis),
  • syringomyelia
  • intramedullary tumors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are MCC intramedullary tumors of spinal cord?

A

astrocytomas, ependymomas, and hemangioblastomas.

Astrocytomas
Originate from astrocytes, which are star-shaped cells that help nerve cells function

The most common type of spinal cord tumor in children

Ependymomas
Originate from ependymal cells, which line the central canal of the spinal cord

Occur roughly twice as often as astrocytomas in adults

Hemangioblastomas
Contain many blood vessels and can occur anywhere in the spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is MCC intramedullary tumor of spinal cord in children?

A

atrocytomas

33
Q

what is MCC intramedullary tumor of spinal cord in adults?

A

ependymomas

34
Q

Syringomyelia symptoms…

associated w what conditions/events?

A

loss of pain and temperature in cape-like distribution in UEs (decussating spinothalamic fibers in anterior commissure), Horners syndrome (descending autonomic fibers), central cord syndrome

associated w: Chiari malformations, tumors or trauma

35
Q

Lamellation of CST and STT from lateral to medial?

A

legs, trunk, arms

36
Q

Benign familial infantile seizures
inheritance pattern
Chanel mutations (list 2)

A

AD
sodium channels SCN2A and SCN8A

Cat woman and Poison Ivy over a baby - catwoman is shaking salt and Ivy is holding up a hen, the baby is laughing and cooing :)

37
Q

Vascular dementia treatment

A

control risk factors: BP, LDL, DM, smoking, and taking anti-platelet agents

38
Q

Lewy body dementia has
- what deposits where?
- clinical features?

A

alpha synuclein deposits (intracellular) in cortical layers V and VI
REM sleep behavior disorder, fluctuating cognition, visual hallucinations, Parkinsonism

39
Q

REM sleep behavior disorder
- clinical features
- associated with…

A

physically act out dreams while in REM sleep

alpha synucleinopathies: PD, DLB, MSA
Progressive supranuclear palsy PSP
Narcolepsy type 1

40
Q

Frontotemporal dementia
- male vs female?
- inheritance pattern when heritable?
- associated w what other disease?
- pathologic markers?
- key clinical characteristics
- variants

A
  • mostly men
  • AD
  • 15% cases associated with ALS
  • ubiquitin, and tau (Pick bodies) inclusions (intracellular) in paralimbic region
  • variants: frontal-behavioral, semantic, progressive non-fluent aphasia
41
Q

Alzheimers Disease
- clinical characteristics
- variants
- pathologic markers extra and intra cellular

A
  • amnestic mcc (hippocampal)
  • atypical forms: posterior cortical atrophy, frontal variant, down syndrome variant

extracellular amyloid plagues
intracellular neurofibrillary tangles

42
Q

Progressive encephalomyelitis with rigidity and myoclonus (PERM)
- presentation
- associations
- rx
- associated abs

A

encephalopathy, autonomic instability, rigidity, myoclonus and other upper motor neuron findings

  • autoimmune or paraneoplastic
    Or thymomas, v rare West Nile virus or brucellosis,

rx: steroids, IVIG, PLEX AND benzodiazepines for rigidity

ABS: GAD-65, glycine, DPPX, amphiphysin

43
Q

LGI1 limbic encephalitis
- key features

A

subacute encephalopathy with disturbances in
behavior and short-term memory and with seizures and confusion.

pathognomonic faciobrachial dystonic seizures

hyponatremia or REM sleep behavior changes.

MRI may show bilateral medial temporal lobe changes, and
treatment is with immunotherapy.

44
Q

Stiff Person Syndrome
- abs?

45
Q

NMDAR-associated limbic encephalitis
- associated with…
- key features
- test serum and CSF - which is more sensitive?

A

autoimmune
ovarian teratoma
behavioral disturbances, abnormal posturing, seizures
CSF and MRI variably normal
CSF more sensitive than serum for autoantibodies

46
Q

Creutzfeldt-Jakob disease

A

rapid dementia and death w/in months

MRI: diffusion restriction in BG and or cortex (cortical ribbon sign)

47
Q

Carbon Monoxide Poisoning
- clinical features
- rx
- location affected

A

ha, nausea, vomiting, dizziness, malaise, cherry red skin/mucosa
rx: high-flow oxygen

Globus pallidus

Carbon Monoxide (CO) Poisoning: Key Features and Clinical Considerations

Pathophysiology

Carbon monoxide (CO) is a colorless, odorless, tasteless gas that exerts its toxic effects primarily by binding to hemoglobin with an affinity 200–250 times greater than oxygen. This results in carboxyhemoglobinemia (COHb), impairing oxygen delivery and utilization at the tissue level. Additionally, CO binds to myoglobin and cytochromes, further disrupting aerobic metabolism, leading to cellular hypoxia and metabolic acidosis.

Sources of Exposure
• Incomplete combustion of hydrocarbons (fires, vehicle exhaust, gas heaters, furnaces, wood stoves)
• Industrial exposure (steel production, methylene chloride inhalation)
• Indoor exposure (faulty home heating systems, charcoal grills in enclosed spaces)
• Cigarette smoking (chronic low-level COHb elevation)

Clinical Presentation

CO poisoning is often misdiagnosed due to nonspecific symptoms. The classic presentation includes:
1. Mild to Moderate Poisoning
• Flu-like symptoms (headache, dizziness, nausea, vomiting)
• Fatigue, malaise
• Confusion, impaired concentration
• Chest pain, dyspnea (especially in patients with underlying CAD)
2. Severe Poisoning
• CNS dysfunction: Confusion, ataxia, syncope, seizures, coma
• Myocardial ischemia: ST-T wave changes, arrhythmias, hypotension, cardiac arrest
• Metabolic acidosis: Due to lactate accumulation from anaerobic metabolism
• Cherry-red skin/mucosa (late finding, often unreliable)
3. Delayed Neurological Sequelae (DNS)
• Occurs in 10–40% of survivors within days to weeks
• Memory loss, cognitive impairment, mood disorders
• Parkinsonian features, white matter demyelination (MRI: globus pallidus necrosis)

Diagnosis
• Carboxyhemoglobin (COHb) levels via arterial or venous blood gas (ABG/VBG)
• Normal: <2% (non-smokers), <9% (smokers)
• Symptomatic >10–15%, severe poisoning >25%
• Levels may not correlate with symptom severity
• Pulse oximetry is unreliable (cannot distinguish oxy-Hb from COHb)
• Lactate >2.5 mmol/L correlates with severe poisoning
• EKG and troponins in high-risk patients (CO can precipitate MI)
• Neuroimaging (MRI with DWI) for suspected DNS (basal ganglia, subcortical white matter lesions)

Management
1. Immediate 100% Oxygen via Non-Rebreather Mask
• Reduces COHb half-life from ~5 hours (on room air) to ~1 hour
2. Hyperbaric Oxygen Therapy (HBOT)
• Indications:
• COHb ≥25% (>15% if pregnant)
• Neurological symptoms (confusion, LOC, seizures)
• Myocardial ischemia
• Persistent symptoms despite normoxia
• Reduces DNS risk and speeds CO clearance (COHb half-life ~20–30 min in HBOT)
3. Supportive care
• IV fluids, vasopressors for hypotension
• Anticonvulsants for seizures
• Avoid sedatives that can mask neurological deterioration

Prognosis
• Most mild cases recover fully with prompt treatment.
• Delayed Neurological Sequelae (DNS) can be debilitating, requiring cognitive rehabilitation.

48
Q

What two poisonings classically affect the Globus Pallidus?

A

CO and manganese

49
Q

Thiamine deficiency from alcohol abuse classically affects what location?

A

mammillary bodies

50
Q

Pyridoxine (B6)
toxicity affects what location?

A

Dorsal root ganglia causing neuronopathy

(Usually sensory neuronopathy in stocking glove distriubtion)

51
Q

Methanol toxicity affects what location?

A

Basal Ganglia

bilateral putamen nuclei (black arrows) and can extend to other BG (white arrows)

52
Q

What commonly causes copper deficiency?

A

excess zinc consumption

53
Q

what locations are affected by B12 and copper deficiency?

A

Dorsal columns and lateral CST, and spinocerebellar tract

54
Q

Carpal Tunnel Syndrome
- KNOW details of it WELL

A

NCS gold standard

55
Q

Meige Syndrome
- clinical features
- associations
- rx

A

a craniocervical dystonia

blepharospasm (forced eye closure), oromandibular dystonia (lower face and jaw)

sporadic or w Parkinsonism syndromes, other dystonias, essential tremor

rx botox

56
Q

Pramipexole
MOA
RX

A

dopamine receptor agonist
rx PD, restless leg syndrome

57
Q

Trihexyphenidyl
MOA
RX

A

MOA: anticholinergic

RX: PD and anti-psychotic associated extra pyramidal sxs (tremors, rigidity, akathisia, dyskinesia, dystonia, bradykinesia)

58
Q

Extrapyramidal symptoms w anti-psychotics
and the RX for them

List 3

A

tremors, rigidity, and muscle contractions

rx: trihexyphenidyl (anti-cholinergic)

59
Q

Gelastic seizures
- clinical presentation, age of onset
- associated w…
- rx:

A

uncontrolled laughing, approx 10 months old
hypothalamic hemartoma (HH) (devleop in-utero)
surgery

MRI: HH near mammillary body

60
Q

Rivastigmine
MOA
RX
SE

A

AChE inhibitor
Dementia w AD or PD
SE: nausea and vomiting, decreased appetite and weight loss
(more nausea and vomiting during the titration phase of oral rivastigmine treatment)

61
Q

Galantamine
MOA
RX
SE

A

AChE inhibitor and nicotinic receptor modulator
Dementia w AD or PD
SE: nausea and vomiting, decreased appetite and weight loss

62
Q

Donepazil
MOA
RX
SE

A

AChE inhibitor
Dementia w AD or PD, all stages of AD
SE: nausea and vomiting, decreased appetite and weight loss

63
Q

Three AChE inhibitors rx for dementia (AD and PD)

we need Really Good Drugs for dementia

A

rivastigmine, galantamine, donepazil

64
Q

Torticollis rx

A

botox

it is a form of cervical dystonia

65
Q

Topiramate
MOA
RX
SE

A

inhibition of AMPA (glutamate) receptors and VG sodium channels, and weak inhibition of carbonic anhydrase

FDA-Approved
- Monotherapy or adjunct therapy for partial-onset seizures in adults and children (2 years and older).
- Adjunct therapy for primary generalized tonic-clonic seizures.
- Adjunct therapy Lennox-Gastaut syndrome.
- Migraine Prophylaxis adults and adolescents

OFF LABEL:
Weight Management / Weight Loss
Bipolar Disorder (Mood Stabilization)
Alcohol Use Disorder (Alcohol Dependence)
Binge Eating Disorder & Bulimia Nervosa
PTSD (Post-Traumatic Stress Disorder) w Nightmares

SE:
brain fog
nausea, decreased appetite
kidney stones
Metabolic and Electrolyte Issues
Metabolic acidosis (low bicarbonate levels in the blood)
Hyperammonemia (elevated ammonia levels in the blood),
Vision and Eye Problems
Acute myopia (sudden nearsightedness)
Secondary angle-closure glaucoma (rare but serious; presents with eye pain and vision changes)
Possible blurred vision or difficulty focusing
Decreased sweating (hypohidrosis), especially in children, heat intolerance
Birth Defects: cleft lip and/or cleft palate
Skin rash, itching, or hives
Rare severe reactions (e.g., Stevens-Johnson syndrome)
suicidality

66
Q

Zonisamide
MOA
RX
SE

A

inhibits voltage dependent sodium and T-type calcium channels, weak carbonic anhydrase inhibitor (topiramate does not inhibit T type calcium channels)

FDA: adjunctive partial onset seizures in adults

brain fog
nausea, decreased appetite
kidney stones
Metabolic and Electrolyte Issues
Metabolic acidosis (low bicarbonate levels in the blood)
Hyperammonemia (elevated ammonia levels in the blood),
Vision and Eye Problems
Acute myopia (sudden nearsightedness)
Secondary angle-closure glaucoma (rare but serious; presents with eye pain and vision changes)
Possible blurred vision or difficulty focusing
Decreased sweating (hypohidrosis), especially in children, heat intolerance
Birth Defects: cleft lip and/or cleft palate
Skin rash, itching, or hives
Rare severe reactions (e.g., Stevens-Johnson syndrome)
suicidality
blood dyscrasia

67
Q

Lacosamide
MOA
RX
SE

A

MOA: enhancing the slow inactivation of voltage-gated sodium channels

FDA:Monotherapy or adjunctive therapy in patients aged 4 years and older for the treatment of partial-onset (focal) seizures, adjunctive Primary Generalized Tonic-Clonic Seizures

Common Off-Label Uses: status epilepticus, neuropathic pain (incl diabetic neuropathy)

Warnings: cardiac: PR prolongation, AV block; CNS: depression and dizziness; suicidality, DRESS, schedule V controlled substance, renal and hepatic, headache, n/v, diplopia or blurred vision, mood (euphoria), tremor, abrupt stop increases seizure risk
Regular labs

68
Q

Levetiracetam
MOA
RX
SE

A

binds to synaptic vesicle protein 2A (SV2A)
broad spectrum uses
SE: agitation and aggression

69
Q

sleep apnea is associated with what cardiac condition?

A

heart failure associated with central sleep apnea, especially w cheyne-stokes breathing pattern (crescendo-decrescendo)

70
Q

Diagnosis of sleep apnea should prompt search for underlying causes, especially ….(3)

A

heart failure, stroke, opioid use

71
Q

EMG distinguishing between myopathies and motor neuropathies

A

myopathies: fibrillations, small complex MUP
motor neuropathies: fibrillations, fasciculations, large varying MUPs with reduced recruitment

72
Q

Recurrent thunderclap headache, consider

A

reversible cerebral vasoconstriction syndrome RCVS

73
Q

Reversible cerebral vasoconstriction syndrome (RCVS)
key features
triggers

A

Thunderclap headaches

multifocal narrowing of the cerebral arteries followed by dilatation, resolve 1-3 months

triggers:

Postpartum, Vasoactive Substances:
Illicit drugs (cocaine, marijuana)

Certain prescription medications (e.g., triptans, SSRIs, pseudoephedrine)

Over-the-counter decongestants

Stress/Emotional Factors: High catecholamine states (though less well-defined as a trigger).

74
Q

Posterior Reversible Encephalopathy Syndrome (PRES)
presentation
causes
diagnosis

A

Headache, visual changes (blurred vision, visual field defects), confusion, altered mental status, seizures, nausea, vomiting, focal neurological deficits.

Causes:
uncontrolled high blood pressure
Eclampsia (pregnancy complication)
Severe infections
Kidney disease
Autoimmune diseases
Certain medications (chemotherapy drugs, immunosuppressants)

Diagnosis:
Based on clinical presentation, neurological examination, and brain imaging (MRI) showing characteristic pattern of white matter edema in the posterior brain regions.
Treatment:
Primarily focuses on managing the underlying cause, usually by rapidly lowering blood pressure with appropriate medications.

75
Q

What cranial nerves are in the ambient cistern?

A

Located lateral to the midbrain and medial to the temporal lobe.

CN 3,4,5
PCA
SCA
Choroidal arteries

76
Q

5 AEDs that cause DRESS

A

• Carbamazepine
• Phenytoin
• Lamotrigine
- lamictal
• Phenobarbital

77
Q

Transcortical motor aphasia definition

A

Transcortical Motor Aphasia
Transcortical motor aphasia is a rare syndrome that is due to a small subcortical lesion superior to Broca’s area or to a lesion outside of the anterior language areas of the left hemisphere.19,32 Because of the location of the lesion in the frontal lobe, transcortical motor aphasia includes both language and cognitive components. The cognitive failures that result in limited and disorganized output are most evident in the patient’s failure to initiate speech.76 In contrast, effortless and accurate repetition of even long sentences is preserved