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MS3 > Neuro 1 > Flashcards

Neuro 1 Flashcards

1
Q

What is dysarthria

A

Condition in which the muscles you use for speech are weak or you have difficulty controlling them

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2
Q

What is apraxia

A

Apraxia is a motor disorder caused by damage to the brain (specifically the posterior parietal cortex), in which the individual has difficulty with the motor planning to perform tasks or movements when asked, provided that the request or command is understood and he/she is willing to perform the task

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3
Q

What is aphasia

A

A language disorder that affects a person’s ability to communicate

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4
Q

What is catatonia

A

A behavioral syndrome marked by an inability to move normally

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5
Q

What is Keppra

A

Levetiracetam

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6
Q

Damage to what part of the brain causes hemispatial neglect

A

Non-dominant parietal cortex

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7
Q

Damage to dominant parietal cortex causes what?

A

Gerstmann syndrome = agraphia (inability to write), acalculia (inability to calculate), finger agnosia (inability to distinguish fingers), left-right disorientation

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8
Q

What is the reticular activating system

A

Located in the midbrain

Mediates consciousness and alertness

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9
Q

Damage to basal ganglia causes what?

A

♣ Resting tremor, chorea, athetosis

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10
Q

Damage to lateral cerebellum causes what?

A

♣ Occurs with chronic alcohol use

♣ Intention tremor, limb ataxia

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11
Q

Damage to medial cerebellum causes what?

A

♣ Truncal ataxia, dysarthria

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12
Q

Damage to PPRF causes what?

A

♣ Eyes look away from side of lesion

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13
Q

What are the 4 midline columns in the brainstem and presentation of damage to each

A
  • Motor pathway (corticospinal tract) – Contralateral weakness
  • Medial lemniscus – loss contralateral proprioception/vibration
  • Medial longitudinal fasciculus – Ipsilateral intranuclear ophthalmoplegia
  • Motor nucleus and nerve – Ipsilateral CN motor loss (3, 4, 6, 12 – midline motor divide into 12)
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14
Q

What are the 4 lateral (side) columns in the brainstem and presentation of damage to each

A
  • Spinocerebellar pathway – Ipsilateral ataxia
  • Spinothalamic – Contralateral pain/temp sensation loss
  • Sensory nucleus of CN 5 – Ipsilateral pain/temp loss in face
  • Sympathetic pathway – Ipsilateral Horner’s syndrome
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15
Q

Blood supply of medial and lateral midbrain

A

Posterior cerebral artery

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16
Q

Blood supply of medial and lateral pons

A 
Medial = basilar
Lateral = AICA
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17
Q

Blood supple of medial and lateral medulla

A 
Medial = anterior spinal
Lateral = PICA
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18
Q

Parts of brain most vulnerable to ischemic damage

A

Cerebellum
Neocortex
Hippocampus
Watershed areas (between ACA and MCA; MCA and PCA)

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19
Q

What is hydrocephalus

A

increased CSF leading to ventricular dilation (+/- increased ICP)

20
Q

What is pseudotumor cerebri

A

♣ Aka idiopathic intracranial HTN

♣ Increased intracranial pressure without hydrocephalus

21
Q

Presentation of pseudotumor cerebri

A
  • Headache, diplopia, papilledema

* Lumbar puncture shows increased opening pressure with headache relief

22
Q

Describe migraine HA

A

♣ Usually 4 – 72 hours
♣ Unilateral pulsing, throbbing headache
♣ Associated with nausea, photophobia, phonophobia, and aura

23
Q

Tx of migraine HA

A

Triptans

24
Q

Describe tension HA

A

♣ Usually 4 – 6 hours
♣ Bilateral headache with constant, steady pain (non-throbbing)
♣ Usually in frontal or occipital lobe
♣ No throbbing, no photophobia, no phonophobia, no aura

25
Q

Tx of tension HA

A

NSAIDs, Acetaminophen

26
Q

Describe cluster HA

A

♣ 15 min – 3 hours
♣ Repetitive (often occur daily at the same time)
♣ Unilateral, non-throbbing heading
♣ Excruciating pain, usually perioribital
♣ Associated with lacrimation, rhinorrhea, and Horner syndrome (ptosis and miosis, not anhidrosis)

27
Q

Tx of cluster HA

A

100% O2, sumatriptan

28
Q

Presentation of fetal hydantoin syndrome

A

o Caused by exposure to anticonvulsants (e.g. Phenytoin and Carbamazepine)
o Midfacial hypoplasia, microcephaly, cleft lip and palate, digital hypoplasia, hirsutism, and developmental delay

29
Q

Presentation of fetal alcohol syndrome

A

o Midfacial huypoplasia, microcephaly and stunted growth

o CNS damage may manifest as hyperactivity, mental retardation, or learning disability

30
Q

What will you see in motor function, pain & temp, and vibration & proprioception in Brown Sequard syndrome

A

Contralateral loss of pain and temp (beginning 2 levels below lesion)

Ipsilateral motor and vibratory/proprioception

31
Q

What are the nerve roots of the reflexes?

A
  • Biceps and brachioradialis reflexes = C5, C6 (“pick up sticks”)
  • Triceps reflex = C7, C8 (“lay them straight”)
  • Achilles reflex = S1, S2 (“buckle my shoe”)
  • Patellar reflex = L3, L4 (“kick the door”)
  • Cremasteric reflex = L1, L2 (“testicles move”)
  • Anal wink reflex = S3, S4 (“winks galore”)
32
Q

Describe acute intermittent porphyria

A

♣ Deficiency of Porphobilinogen (PBG) deaminase
• THINK: Acute intermittent = guys hollering “damn” (deam-inase) intermittently at A CUTE pretty big girl (PBG) walking by
♣ Symptoms – 5 P’s
• Painful abdomen, Port wine colored urine (due to increase PGB), Polyneuropathy, Psychological disturbances, Precipitated by drugs (CYP450 inducers), alcohol, and starvation

33
Q

Describe disorder of the splenium of the corpus collusum in the dominant occupital lobe

A

Can write but can’t read

You read with the occipital lobe but write with broca’s area. So if dominant occipital lobe is damaged, you need to get reading info from the R side of the brain but can’t if the corpus collosum is damaged. But Broca’s is still intact so you can still write

34
Q

Tx of status epilepticus

A
  • IV Benzo (e.g. Diazepam, Lorazepam)
  • Phenytoin
  • IV Phenobarbital
35
Q

What is Keppra

A

Levetiracetam

36
Q

What is Lyrica

A

Pregabalin (anticonvulsant; GABA analog)

37
Q

What is Versed

A

Midazolam

38
Q

What is Depakote

A

Valproate

39
Q

What is Fioricet

A

Caffeine, Acetaminophen, Butalbital

Used for tension or muscle contraction HA

40
Q

What is Addison’s disease

A

♣ Primary adrenal insufficiency problem of the adrenal gland - Aka Addison disease
• Most commonly due to autoimmune destruction of adrenal gland

Presentation:
o Lack of cortisol = Weakness, fatigue, weight loss
o Lack of aldosterone = hypotension, hyponatremia, hyperkalemia
o Increased ACTH = skin hyperpigmentation (due to POMC)

41
Q

What is AED

A

Automated external defibrillator

Portable device that checks the heart rhythm and can send an electric shock to the heart to try to restore a normal rhythm

42
Q

What is a bulbar palsy

A

Refers to a range of different signs and symptoms linked to impairment of function of the cranial nerves IX, X, XI and XII, which occurs due to a lower motor neuron lesion in the medulla oblongata or from lesions of the lower cranial nerves outside the brainstem

Symptoms: dysphagia (difficulty in swallowing), difficulty in chewing,
nasal regurgitation,
slurring of speech,
difficulty in handling secretions, choking on liquids, dysphonia (defective use of the voice, inability to produce sound due to laryngeal weakness), dysarthria (difficulty in articulating words due to a CNS problem)

43
Q

Describe presentation of Myasthenia gravis

A

Autoantibody against post-synaptic ACh receptor

Clinical features:
♣ Ptosis, diplopia, weakness
♣ Worsens with muscle use

44
Q

Cause of MS

A

o Due to autoimmune demyelination of CNS

o Most often affects women in 20s-30s

45
Q

Presentation of MS

A 
♣	Charcot triad of symptoms  SIN:
•	Scanning speech
•	Intention tremor, Incontinence, Internuclear ophthalmoplegia
•	Nystagmus 
♣	Hemiparesis, hemisensory symptoms
46
Q

Diagnosis of MS

A 
o	MRI  gold standard
♣	Periventricular plaques (areas of oligodendrocyte loss and reactive gliosis)
o	Lumbar puncture
♣	Increased protein
♣	Oligoclonal IgG bands
47
Q

Describe ALS

A

o Aka Lou Gehrig disease
o Damage to anterior motor horn and lateral corticospinal tract
o Presents with both UMN and LMN deficits
o Lack of sensory impairment distinguishes from syringomyelia
o Caused by defect in superoxide dismutase (O2- H2O2)

MS3 (88 decks)

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