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Neurology Flashcards

0
Q

What are the primary vesicles?

A

1) Prosencephalon (forebrain)
2) Mesencephalon (midbrain)
3) Rhombencephalon (hindbrain)

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1
Q

How are the alar & basal plates organized?

A

In closed spinal cord, alar plate (sensory) is dorsal & basal plate (motor) is ventral.

In the medulla & pons, the basal plate is medial & the alar plate is lateral. Within these, the visceral nuclei are generally closest to the sulcus limitans.

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2
Q

What are the secondary vesicles?

A

1) Telencephalon
2) Diencephalon
3) Mesencephalon
4) Metencephalon
5) Myelencephalon

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3
Q

What does the telencephalon give rise to?

A

Cerebral hemispheres & lateral ventricles

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4
Q

What does the diencephalon give rise to?

A

Thalamus
Hypothalamus
Retina
Third ventricle

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5
Q

What does the mesencephalon give rise to?

A

Midbrain & cerebral aqueduct

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6
Q

What does the metencephalon give rise to?

A

Pons
Cerebellum
Top half of 4th ventricle

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7
Q

What does the myelencephalon give rise to?

A

Medulla

Bottom half of fourth ventricle

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8
Q

When does the neural tube develop?

A

Day 18-day 21

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9
Q

What is seen in the amniotic fluid with a neural tube defect?

A

^AFP

^AChE

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10
Q

What are the caudal neural tube defects?

A

Spina bifida occulta –> bony canal not closed, tuft of hair

Meningocele –> meninges herniate through spinal canal defect

Meningomyelocele –> meninges & spinal cord

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11
Q

What is seen with anencephaly

A

^AFP
Polyhydramnios (no swallowing center in brain)
No forebrain, open calvarium
“Frog-like appearance”

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12
Q

What causes anencephaly?

A

Maternal T1DM
Lack of folate

Anterior neural tube does not close

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13
Q

What causes holoprosencephaly?

A

Failure of R & L hemispheres to separate

May be due to sonic the hedgehog defect

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14
Q

What is seen with holoprosencephaly?

A

Cleft lip/palate

Severe form –> cyclopia

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15
Q

What is seen with congenital cerebral aqueduct stenosis?

A

Enlargement of lateral & third ventricles

Enlarging head circumference (sutures not yet fused)

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16
Q

What is seen with Arnold-Chiari malformation?

A

Type I - modest herniation, usually clinically silent

Type II:
Tonsillar herniation
Hydrocephalus
Meningomyelocele
Syringomelia
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17
Q

What is seen with Dandy-Walker malformation?

A

Agenesis of cerebellar vermis –> cystically enlarged 4th ventricle
The cerebellum is basically missing.
Hydrocephalus & spina bifida can be seen

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18
Q

Where is the most common site of a syringomyelia?

A

C8-T1

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19
Q

What is seen with a syringomyelia?

A

Bilateral loss of pain & temperature sensation in upper extremities
“Cape-like”
Later stages –> LMN signs of arms; Horner’s syndrome
Can extend downward
Fine touch & proprioception are spared

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20
Q

What causes syringomyelia?

A

Trauma
Chiari I malformation

Scoliosis is a hint that syringomyelia may be present

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21
Q

What is the sensory innervation of the tongue?

A

Anterior 2/3:
Sensation - V3
Taste - VII

Posteior 1/3:
Sensation & taste - IX or X (extreme posterior is X)

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22
Q

What neural cells arise from the neuroectoderm?
Neural crest?
Mesoderm?

A 
Neuroectoderm:
CNS neurons
Ependymal cells
Oligodendrocytes
Astrocytes

Neural crest:
PNS neurons
Schwann cells

Mesoderm:
Microglia

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23
Q

How can one stain for the cell bodies of neurons?

A

Stain for Nissl substance (RER). Only present in the cell body.

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24
Q

What do Meissner’s corpuscles sense?

A

Dynamic touch
Fine touch
Position sense

Found on hairless (glabrous) skin

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25
Q

What do Pacinian corpuscles sense?

A

Vibration

Pressure

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26
Q

What do Merkel’s discs sense?

A

Pressure

Deep static touch

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27
Q

What are the layers surrounding a PNS nerve?

A

Epineurium surrounds whole nerve
Perineurium surrounds fascicle of nerve fibers
Endoneurium surrounds individual fibers

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28
Q

Where is NE synthesized?

A

Locus ceruleus

pons

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29
Q

Where is dopamine produced in the brain?

A 
Ventral tegmentum (VTA)
Substantia nigra (pars compacta)
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30
Q

Where is serotonin produced in the brain?

A

Raphe nucleus (pons)

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31
Q

Where is ACh produced in the brain?

A

Basal nucleus of Meynert

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32
Q

Where is GABA produced in the brain?

A

Nucleus accumbens

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33
Q

What is the BBB composed of?

A

1) Tight junctions between endothelial cells
2) Basement membrane
3) Astrocyte foot processes

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34
Q

What are the circumventricular organs?

A

Area postrema - chemo induced vomiting
OVLT - osmolarity sensing
Neurohypophysis
Median eminence of hypothalamus

They have fenestrated capillaries to circumvent the BBB

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35
Q

Where is ADH produced?

A

Supraoptic nucleus

Hypothalamus

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36
Q

Where is Oxytocin produced?

A

Paraventricular nucleus

Hypothalamus

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37
Q

Where does Leptin act in the brain?

A 
Acts at the hypothalamus:
Lateral area (hunger) --> inhibited by leptin --> satiety
Ventromedial area (satiety) --> stimulated by leptin --> satiety

Destruction of the Lateral area –> anorexia
Destruction of the Ventromedial area –> hyperphagia

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38
Q

What parts of the hypothalamus control body temperature?

A

Anterior hypothalamus (parasympathetic) –> cooling

Posterior hypothalamus (sympathetic) –> heating

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39
Q

What in the CNS controls sleep/wake cycles?

A

Suprachiasmatic nucleus

hypothalamus

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40
Q

What is secreted by the neurohypophysis?

A

Oxytocin & Vasopressin

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41
Q 
What are the inputs & outputs of these Thalamic nuclei?
VPL
VPM
LGN
MGN
VL
A

VPL - STT & DCP from body –> sensory cortex
VPM - Trigeminal & gustatory pathway –> sensory cortex
LGN - CNII (SLO AIM) –> calcarine sulcus
MGN - Hearing (SLO AIM) –> Auditory cortex
VL - Motor input from basal ganglia –> motor cortex

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42
Q

What structures make up the limbic system?

A 
Hippocampus
Amygdala
Fornix
Mamillary bodies
Cingulate gyrus
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43
Q

What does the cerebellum control?

A

Ipsilateral coordination of movement.

It generally makes sure that the movement you get is the one that you want.

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44
Q

What are the inputs & outputs of the cerebellum?

A

Inputs:
Contralateral cortex via middle cerebellar peduncle
Ipsilateral proprioceptive input via inferior cerebellar peduncle

Outputs:
Purkinje fibers –> deep nuclei of cerebellum –> contralateral cerebral cortex via superior cerebellar peduncle

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45
Q

What are the deep nuclei of the cerebellum?

A

Medial–>Lateral “Fat Guys Eat Donuts”

Fastigial
Globose
Emboliform
Dentate

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46
Q

What is the homunculus of the cerebellum like?

A

Medial - balance & truncal coordination
Lateral - voluntary movement of extremities (ipsilateral)
Floculus/Nodulus - Truncal balance & vestibulo-ocular reflexes

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47
Q

What are climbing & mossy fibers?

A

They are inputs to the cerebellum. Climbing fibers originate in the inferior olivary nucleus, while mossy fibers carry everything else.

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48
Q

What dopamine receptors correspond to the direct & indirect pathway of the basal ganglia?
What are the effects of each pathway?

A 
D1 = D1rect
(D2 = indirect)
INdirect = INhibitory
(Direct = excitatory)

Dopamine normally stimulates the excitatory pathway & inhibits the inhibitory pathway –> ^movement

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49
Q

What is the direct basal ganglia pathway?

A

SN activate Putamen (D1 receptor) –> Putamen inhibits Globus Pallidus interna –> releases thalamus from GPi inhibition –> ^movement

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50
Q

What is seen histologically with Parkinson’s disease?

A 
Lewy bodies (intracellular, round, pink; alpha-synuclein)
Loss of Substantia Nigra pars compacta
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51
Q

What is seen clinically with Parkinson’s disease?

A 
Your body becomes a TRAP:
Tremor (resting; pill-rolling tremor)
Rigidity (cogwheel)
Akinesia (slowed voluntary movement; expressionless face)
Postural instability --> shuffling gait

Dementia seen late in disease process.

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52
Q

What is the striatum composed of?

A

Putamen + Caudate

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53
Q

What are the lentiform nuclei?

A

Putamen + Globus pallidus

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54
Q

What causes Huntington’s disease?

A

Autosomal dominant expansion (during spermatogenesis) of CAG repeats on chrom. 4
“Hunting 4 CAGs”

Caudate loses ACh & GABA (CAG) –> Caudate atrophy
(Neuronal death occurs via glutamate toxicity)
(Direct basal ganglia pathway predominates)

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55
Q

What is seen clinically with Huntington’s disease?

A

Choreoathetosis
Aggression
Depression (suicide)
Dementia

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56
Q

What causes Hemiballismus?

A

Contralateral subthalamic nuclei lesion
(no indirect basal ganglia pathway)

Either flailing or rotatory movement of 1 arm & 1 leg (both same side)

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57
Q

What is myoclonus?

What is it seen in?

A

Jerks; hiccups

Often seen in matabolic diseases (liver failure, renal failure, etc.)

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58
Q

What is seen with essential tremor?

What is the treatment?

A

Active tremor
Exacerbated by holding a position
Genetic predisposition

Pts often self medicate with EtOH. Treatment is propranolol.

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59
Q

What causes intention tremor?

A

Intention tremor is a slow zigzag movement when extending arm toward a target. Seen in cerebellar dysfunction.

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60
Q

What is the organization of the homunculus?

A

Feet are medial

Head is lateral

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61
Q

What causes Kluver-Bucy syndrome?

What is seen?

A

Bilateral amygdala destruction. Can be associated with HSV-1.

Symptoms:
Hyperorality
Hypersexuality
Disinhibition

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62
Q

What is seen with frontal lobe lesions?

A

Disinhibition
Concentration deficits
Poor judgement
Reemergence of primitive reflexes

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63
Q

What is seen with lesions in the right parietal lobe?

A

Contralateral hemineglect

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64
Q

What is seen with a lesion to the reticular activating system?

A

Reduced levels of arousal (coma)

It is located in the midbrain.

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65
Q

What side do cerebellar defects cause a fall towards?

A

Patients fall toward the side of their lesion (ipsilateral defects)

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66
Q

What is seen with a lesion to the paramedian pontine reticular formation?

A

PPRF lesion –> eyes look away from side of lesion

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67
Q

What is seen with a lesion in the frontal eye fields?

A

Eyes look toward lesion

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68
Q

Where is Broca’s area?

Wernicke’s area?

A

Broca’s - inferior frontal gyrus

Wernicke’s - Superior temporal gyrus

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69
Q

What is seen with conduction aphasia?

What causes it?

A

Fluent speech & intact comprehension but impaired repetition

Caused by a lesion to the arcuate fasciculus (connects Broca’s & Wernicke’s)

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70
Q

What is the brain autoregulatory range for CO2?

O2?

A

CO2 –> ^ in perfusion up to 90 mmHg of CO2

O2 –> ^ in perfusion if PO2 < 50 mmHg

Thus normally CO2 drives cerebral autoregulation. Hyperventilation can decrease ICP.

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71
Q

What is seen with a MCA infarction?

A

Contralateral paralysis & loss of sensation of upper limb & face
Aphasia if in left (dominant) hemisphere
Hemineglect if in right (nondominant) hemisphere

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72
Q

What is seen with an ACA infarction?

A

Contralateral paralysis & loss of sensation in leg

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73
Q

What can be caused by lacunar strokes?

What arteries are involved?

A

Lenticulostriate arteries are typically involved –> Striatum, Thalamus, or Internal capsule (deep structures)

Internal capsule –> pure motor stroke
Thalamus – pure sensory stroke

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74
Q

What causes lacunar infarcts?

A

Unmanaged HTN –> hyaline arteriolosclerosis (of lenticulostriate vessels) –> lacunar infarcts (little hollow “lakes”)

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75
Q

What can cause Medial Medullary Syndrome?

What is affected?

A

Anterior spinal artery occlusion or paramedian branches

Affected:
Lateral CST –> contralateral hemiparesis
Medial lemniscus –> contralateral proprioceptive defect
Hypoglossal nerve –> Lick your wounds

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76
Q

What can cause Lateral Medullary Syndrome?

What is affected?

A

Lateral Medullary = Wallenberg = PICA syndrome

Affects:
Nucleus ambiguus –> dysphagia & hoarseness (PICA specific)
Vestibular nuclei –> vertigo & vomiting
STT & Trigeminal nuc. –> no pain/temp to limbs/face
Sympathetic fibers –> ipsilateral Horner’s
Inferior cerebellar peduncle –> ataxia

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77
Q

What is seen with AICA occlusion?

A

Paralysis of face is specific to AICA

“Facial droop means AICA’s pooped”

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78
Q

What can PCA occlusion cause?

A

Contralateral hemianopsia with macular sparing.

If bilateral –> cortical blindness (pupillary light reflex intact)

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79
Q

What can be seen clinically with Saccular aneurysms?

A

Berry aneurysms:
Rupture –> subarachnoid hemorrhage
Bitemporal hemianopia (compression of optic chiasm)

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80
Q

What are the risk factors for saccular aneurysms?

A

Berry aneurysms:
ADPKD
Ehlers-Danlos
Marfan’s

Age
HTN
Smoking
Blacks

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81
Q

Where is the most common site of a berry aneurysm?

A

Anterior communicating artery branch points

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82
Q

Where are Charcot-Bouchard microaneurysms found?

A

The lenticulostriate arteries

They are due to HTN and can cause intracerebral hemorrhage.

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83
Q

What arteries arise from the vertebral arteries?

A

Anterior spinal artery
Posterior spinal arteries
PICA

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84
Q

What is the shape of an epidural hematoma?

Subdural hematoma?

A

Epidural - biconvex (lens) shape, crosses falx/tent but not sutures

Subdural - crescent shape, crosses sutures but not falx/tent

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85
Q

What is seen in epidural hematoma?

A 
Temporal bone fracture --> ruptured middle meningeal artery
Lucid interval
CNIII palsy (transtentorial herniation)
86
Q

Who is at risk for subdural hematoma?

A

Neonates (shaken-baby)
Elderly (brain atrophy)

Often caused by whiplash-like injury

87
Q

What is seen with subarachnoid hemorrhage?

A

WHOML
Xanthochromatic (yellow) spinal tap
Risk of vasospasm 2 days afterward (Tx: Nimodipine)

88
Q

What is the timeline of histology following a stroke?

A 
12h - Red neurons appear
24h - PMN's
3 days - Macs
1 week - Gliosis
2 weeks+ - Glial scar
89
Q

What is the treatment for an ischemic stroke?

A

tPA within 4.5h if no risk of hemorrhage

90
Q

What is a TIA?

A

Focal neurologic dysfunction lasting < 24h

No acute infarction seen on MRI

91
Q

What is the path of CSF?

A

Ependymal cells of lateral ventricles –> Interventricular foramina of Monroe –> 3rd ventricle –> Cerebral aqueduct –> 4th ventricle –> Foramina of Luschka & Foramen of Magendie –> subarachnoid space –> Arachnoid granulations

92
Q

What is seen with normal pressure hydrocephalus?

A 
Urinary incontinence (wet)
Ataxia (wobbly)
Cognitive dysfunction (wacky)

Results from overproduction of CSF. Treatment is a VP shunt.

93
Q

What can cause hydrocephalus ex vacuo?

A

Alzheimer’s
Advanced HIV
Pick’s disease

Any condition with brain atrophy.

94
Q

How many spinal nerves are there & from what divisions?

A 
8 cervical
12 thoracic
5 lumbar
5 sacral
1 coccygeal

31 total

95
Q

Where do spinal nerves exit?

A

C1-C7 exit above the corresponding vertebrae

All others exit below the corresponding vertebrae

96
Q

Where does disc herniation occur most commonly?

What is breached?

A

Occurs most commonly at L4-L5 or L5-S1

Nucleus pulposus herniates through anulus fibrosis

97
Q

Where does the spinal cord end?
The Subarachnoid space?
Where should LP be performed?

A

Cord ends at L2
Subarachnoid ends at S2
LP between L3-L4 or L4-L5
“L3-L5 keeps the spine alive”

98
Q

What comprises the DCP in the spinal cord?

A

Fasciculus gracilis (legs; medial)

Fasciculus cuneatus (arms; lateral)

99
Q

Describe the dorsal column pathway

A

1st order:
Cell body in DRG, enters cord & ascends in ipsilateral dorsal column, synapse in nucleus cuneatus/gracilus (medulla)

2nd order:
Decussates in medulla, ascends in contralateral medial lemniscus, synapses on VPL (thalamus)

3rd order:
Goes from VPL to sensory cortex

100
Q

Describe the spinothalamic tract

A

1st order:
Sensory nerve ending has cell body in DRG, enters cord & synapses on ipsilateral nucleus proprius

2nd order:
Decussates at anterior commissure (at level where it entered) & ascends contralaterally. Synapses on VPL

3rd order:
VPL –> sensory cortex

101
Q

What do the anterior & lateral spinothalamic tracts do?

A

Lateral - pain & temperature

Anterior - crude touch & pressure

102
Q

Describe the lateral corticospinal tract

A

1st order:
UMN cell body in primary motor cortex. Descends ipsilateral through internal capsule & decussates at pyramidal decussation (caudal medulla). Then descends contralaterally & synapses on cell body of anterior horn.

2nd order:
LMN leaves spinal cord & synapses on neuromuscular junction

103
Q

What are the classical deficits in MS?

A

SIIIN

Scanning speech
Intention tremor
Internuclear ophthalmoplegia
Incontinence
Nystagmus
104
Q

What tracts are affected by ALS?

A

Lateral CST –> UMN signs
Anterior horns –> LMN signs

Both are seen, with no sensory, cognitive, or oculomotor deficits.

105
Q

What causes familial ALS?

A

Mutation in superoxide dismutase 1 –> free radical injury of neurons

106
Q

What is seen with ALS?

A

40-70y males
Atrophy & hand weakness is often early sign (motor only)
Mixed UMN & LMN signs
No sensory, cognitive, oculomotor defects (Stephen Hawking)

107
Q

What is the treatment for ALS?

A

Riluzole –> inhibits presynaptic glutamate release

“Give Lou Riluzole”

108
Q

Where is the watershed area for the anterior spinal artery?

A

Upper thoracic area

Below T8, artery of Adamkiewicz supplies ASA

109
Q

What is seen with Anterior Spinal Artery syndrome?

A

The most common result of spinal ischemia.

Back pain at the level of the lesion
Loss of sensory motor function (LMN shock then eventual UMN)
Preservation of proprioception & vibratory sense

110
Q

What tracts are affected by Tabes dorsalis?

What is seen?

A

Demyelination of dorsal roots & DCP

Symptoms:
Impaired sensation & proprioception
Progressive sensory ataxia
Charcot's joints (injuries go unnoticed --> ulcers)
Radicular pain
Argyll-Robertson pupils (accommodation but no light reflex)
Absent DTR's
Positive Romberg
111
Q

What tracts are affected by B12 deficiency?

A

Subacute combined degeneration = demyelination of:
Dorsal columns
Laeral CST
Spinocerebellar tracts

Combined = ascending & descending tracts affected

112
Q

What is seen in subacute combined degeneration?

A 
Poor proprioception (DCP)
Spastic paresis (CST)
Gait ataxia (spinocerebellar)
113
Q

How is Werdnig-Hoffman disease inherited?

What is seen?

A

Autosomal recessive

Congenital degeneration of anterior horn cells
Hypotonia (floppy baby)
Tongue fasciculations
Prognosis = 7mo

114
Q

What causes Friedreich’s Ataxia?

A

Autosomal recessive expansion of GAA in frataxin gene –> impaired mitochondrial iron regulation –> free radical damage

115
Q

What is seen in Friedreich’s Ataxia?

A 
Degeneration of cerebellum & multiple cord tracts
Death by hypertrophic cardiomyopathy
Childhood kyphoscoliosis (both coronal & saggital plane)
Ataxia
Frequent falls
Nystagmus
Dysarthria
Pes cavus
Hammer toes

“Friedreich is fratastic, slurring & falling, but he’s got a big heart.

116
Q

What causes Brown-Sequard syndrome?

What is seen?

A

Hemisection of the spinal cord

At level of lesion - Ipsilateral LMN signs & loss of all sensation

Below lesion:
Ipsilateral UMN signs (CST) & loss of proprioception & vibration sense (DCP)
Contralateral loss of pain & temperature (STT)

117
Q

What level must a spinal cord lesion be to cause Horner’s syndrome?

A

Above T1

118
Q 
What do are the dermatomes of these structures?
Kneecaps
Penis
Umbilicus
Nipples
Arms
Posterior head
A 
Kneecaps - L4
Penis - S2,3,4 keeps the penis off the floow
Umbilicus - T10 at the belly butTEN
Nipples - T4 (teat pore)
Arms - C5,6,7,8,T1
Posterior head - C2
119
Q

What are the clinical DTR’s & their nerve roots?

A

S1,2 - achilles
L3,4 - patella
C5,6 - biceps
C7,8 - triceps

120
Q

What are the primitive reflexes?

A

Moro reflex - flail out limbs when scared (hold on for dear life)
Rooting - turn when stroke cheek
Sucking - suckling when roof of mouth is touched
Palmar - fingers curl when palm is touched
Plantar - Babinsky sign (not considered as such when infant)
Galant - lying face down, stroke one side of spine, flexes toward

121
Q

What is Parinaud syndrome?

What causes it?

A

Parinaud syndrome is paralysis of conjugate upward vertical gaze due to a lesion in the superior colliculi (often pinealoma, MS, stroke). Downward gaze is normally preserved.

122
Q

What nucleus controls the pupillary sphincter & ciliary muscle?

A

Edinger-Westphal nucleus

123
Q

What is mediated by the trigeminal nerve?

A

Muscles of mastication

Sensation of the face & anterior 2/3 of tongue

124
Q

What is mediated by the facial nerve (CNVII)?

A 
Facial movement
Taste from anterior 2/3 of tongue
Lacrimation
Salivation (sublingual & submandibular)
Stapedius muscle in ear
Orbicularis oculi
125
Q

What is mediated by the glossopharyngeal nerve (CNIX)?

A 
Taste & sensation from posterior 1/3 of tongue
Swallowing
Salivation (parotid)
Carotid body & sinus
Stylopharyngeus
126
Q

Where are the CN nuclei located?

A

Midbrain = 3-4
Pons = 5-8
Medulla = 9,10,12
Spinal cord = 11

127
Q

What cranial nerves facilitate the gag reflex?

A

In on IX

Out on X

128
Q

Describe the path of the carotid sinus & aortic arch baroreceptors

A

Carotid sinus –> Hering’s nerve –> CNIX –> Nucleus solitarius

Aortic arch baroreceptors –> CNX –> Nucleus solitarious

129
Q

What is nucleus solitarius for?

What are its cranial nerves?

A

Visceral sensory information

CNVII, CNIX, CNX

130
Q

What is nucleus ambiguus for?

What are its cranial nerves?

A

Motor innervation of pharynx, larynx, upper esophagus

CNIX, CNX

131
Q

What is the dorsal motor nucleus for?

What are its cranial nerves?

A

Parasympathetics to heart, lungs, upper GI

CNX

132
Q

What passes through the cavernous sinus?

A 
EOM nerves (III, IV, VI) and V1, V2
Portion of internal carotid
133
Q

What is seen in cavernous sinus syndrome?

What causes it?

A

Ophthalmoplegia (CNIII,IV,VI run through it)
Impaired corneal (V1) & maxillary sensation (V2)
Normal vision

It can be caused by:
Neoplasm
Internal carotid aneurysm or fistula

134
Q

Which way will the jaw deviate from a CNV lesion?

A

Toward the defect, due to unopposed pterygoids

135
Q

Which way does the uvula deviate with a CNX lesion?

A

Away from the side of the lesion

136
Q

Which way will there be weakness in head turning with a CNXI lesion?

A

Contralateral head turn will be weak (SCM aids in opposite head turn). Trapezius will droop on same side of lesion.

137
Q

What is damaged in noise-induced hearing loss?

A

Stereociliated cells within the organ of corti are damaged. High frequencies are lost first.

138
Q

What is seen with an UMN facial lesion?

LMN facial lesion?

A

UMN (cortex-facial nucleus) –> contralateral lower face paralysis

LMN (facial nucleus-muscle) –> ipsilateral whole face paralysis

139
Q

What is Bell’s Palsy seen in?

A 
AIDS
Lyme disease
HSV
Sarcoisosis
Tumors
Diabetes
140
Q

What muscles open the mouth?

Close it?

A

Open - Lateral pterygoid (“Lateral lowers”)

Close - Masseter, temporalis, medial pterygoid

141
Q

What is the clinical term for nearsighted?

Farsighted?

A

Nearsighted = you can see near only = myopia

Farsighted = you can only see far = hyperopia

142
Q

What occurs within the eyeball during accomodation?

A

Ciliary muscles contract –> zonular fibers relax –> lens becomes fatter –> you can see close

143
Q

What is uveitis?

What conditions is it seen with?

A

Inflammation of iris, ciliary body, & choroid (all anterior chamber)

Associated with chronic inflammatory conditions:
Sarcoidosis
RA
HLA-B27 conditions

144
Q

What causes retinitis?

A

Usually viral (CMV, HSV, HZV)

Associated with immunosuppression

145
Q

What is the pathway of aqueous humor in the eye?

A

Produced by ciliary epithelium (ciliary body) –> around lens –> through pupil into anterior chamber –> trabecular meshwork –> Canal of Schlemm

146
Q

What type of receptor dilates the pupil?

Constricts?

A

A1 dilates

M3 constricts

147
Q

What are the causes of open angle glaucoma?

What are the risk factors?

A

Caused by blockage of trabecular meshwork:
WBC’s (uveitis)
RBC’s (hemorrhage/trauma)
Retinopathy

Risk factors: Age, Black race, family history

148
Q

What are the symptoms of chronic glaucoma?

A

Painless
Loss of peripheral vision
Cupping on optic exam

149
Q

What causes closed angle glaucoma?

What is seen?

A

Lens moves forward & blocks pupil –> aqueous humor builds up behind iris –> pushes iris forward which blocks trabecular meshwork

Symptoms:
Ophthalmic emergency
Pain
Rock hard eye
Sudden vision loss
Halos
Frontal headach
150
Q

What type of drugs are used to treat glaucoma?

A

Cholinomimetics

You want to contract the pupil (closed angle) & contract the ciliary muscle (open angle).

151
Q

What are the risk factors for cataracts?

A 
Age
Galactokinase deficiency or classic galactosemia
Diabetes
Corticosteroid use
Smoking
EtOH
Excessive sunlight
Trauma
Infection
152
Q

What is seen with CNIII damage?

A

Eye looks down & out
Ptosis
Dilated pupil

153
Q

What is seen with CNIV damage?

A

Eye moves upward (especially w/ contralateral gaze)

Problems while walking down the stairs

154
Q

What is the pathway to cause mydriasis?

A

1) Hypothalamus –> Ciliospinal center of Budge (C8-T1)
2) Exit at T1 –> Superior cervical ganglion
3) Plexus along internal carotid –> through cavernous sinus (with V1) –> long ciliary nerve in the orbit –> pupillary dilator muscles

155
Q

What is the pathway to cause miosis?

A

Edinger-Westphal nucleus –> Ciliary ganglion (via CNIII) –> Short ciliary nerves –> pupillary sphincter muscles

156
Q

What is the pathway for the pupillary light reflex?

A

CNII –> Pretectal nucleus –> Bilateral Edinger-Westphal nuclei –> CNII –> constriction

157
Q

What is a Marcus Gunn pupil?

A

Relative Afferent Pupillary Defect

By using the swinging light test, you will see that when the light is moved to the impaired eye, it will dilate some rather than re-constrict as is seen in a normal eye. Caused by damage to the retina or early optic tract.

158
Q

What is seen with vascular vs compression damage to CNIII?

A

Vascular impairment –> O2 can’t diffuse to inner motor components –> Ptosis, down & out gaze

Compression –> peripheral parasympathetic fibers affected first –> blown pupil

159
Q

What is seen with retinal detachment?

What are the risk factors?

A

Retina detaches from choroid –> retinal ischemia –> sudden monocular loss of vision (“like a curtain drawn down”)

Risk factors:
Diabetes
Myopia
Inflammation

160
Q

What causes age-related macular degeneration?

A

Dry (nonexudative; 85%) - deposition of yellow material beneath pigmented epithelium –> gradual loss in central vision (scotoma)

Wet (exudative; 15%) - choroidal neovascularization –> bleeding –> rapid loss of vision

161
Q

How is age-related macular degeneration treated?

A

Nonexudative - multivitamin & antioxidants

Exudative - anti-VEGF injections or laser

162
Q

What genes are associated with Alzheimer’s?

A

Early onset:
Amyloid precursor protein (APP; chrom 21)
Presenilin-1, Presenilin-2

Late onset:
ApoE4

Protective:
ApoE2

163
Q

What is seen histologically with Alzheimer’s?

Grossly?

A

Senile/Neuritic plaques - Extracellular beta-amyloid core with surrounding neuritic processes

Neurofibrillary tangles - Intracellular aggregations of hyperphosphorylated Tau protein (MT-associated protein)

Amyloid angiopathy may be present

Gross:
Widespread cortical atrophy (narrow gyri, wide sulci)
Hydrocephalus ex vacuo

164
Q

What is seen clinically in Pick’s disease?

A

Change in personality
Aphasia
Parkinsonian aspects
Dementia

165
Q

What is seen histologically with Pick’s disease?

Grossly?

A

Intracellular Pick bodies - ROUND aggregates of tau protein

Grossly:
Frontotemporal atrophy
Spares parietal lobe & posterior 2/3 of superior temporal gyrus

166
Q

What causes Lewy body dementia?

What is seen clinically with Lewy body dementia?

A

Defect in alpha-synuclein –> Lewy body deposition

Parkinsonism
Dementia
Hallucinations

167
Q

What causes Creutzfeld-Jakob disease?

A

Sporadic, inherited, or transmitted misfolding of PrPc –> PrPsc
Assumes a beta-pleated sheet form –> converts more copies of itself to altered form –> vacuole formation

168
Q

What is seen clinically with CJD?

A

Creutzfeldt-Jakob disease

Rapidly progressive dementia
Startle myoclonus
Ataxia
Spike wave complexes on EEG
Death in <1y
169
Q

What is seen with familial fatal insomnia?

A

A type of inherited spongiform encephalopathy

Insomnia
Startle myoclonus

170
Q

Neck flexion –> shocklike sensation down spine & into extremities

What is it called?
What can cause it?

A

Lhermitte’s sign

Caused by MS

171
Q

What are the findings on labs with MS?

A

Oligoclonal IgG bands in the CSF

Periventricular plaques on MRI (gold standard)

172
Q

Who is affected by MS?

A

White women in their 20’s-30’s with HLA-DR2 far from the equator

173
Q

What is the treatment for MS?

A

Long term:
IFN-beta
Natalizumab (prevents immune cells from penetrating the CNS)

Acute –> Corticosteroids

174
Q

What infections are associated with Guillan-Barre syndrome?

A

Campylobacter jejuni
CMV

Leads to autoimmune attack on Schwann cells due to molecular mimicry.

175
Q

What is seen in Guillan-Barre syndrome?

A

Ascending paralysis
Facial paralysis in 50%
Autonomic dysfunction

176
Q

What is the treatment for Guillan-Barre?

A

Respiratory support
Plasmapheresis
IVIg

177
Q

What is the gold standard in diagnosing Guillan-Barre?

A

Increased CSF protein with normal cell count

albuminocytologic dissociation

178
Q

What causes Progressive Multifocal Leukoencephalopathy?

A

AIDS –> Reactivation of JC virus in oligodendrocytes –> central demyelination –> rapid progression & death

179
Q

What is the cause of Charcot-Marie-Tooth disease?

What is seen?

A

aka Hereditary Motor & Sensory Neuropathy
Various inherited etiologies affecting peripheral nerves or Schwann cells

Symptoms:
Leg weakness/atrophy
High arches & hammertoes

180
Q

What is seen with partial temporal seizures?

A

Most common point of origination:
Funny feeling in stomach rising up
Weird smells

181
Q

What is seen with frontal partial seizures?

A

They occur at night

182
Q

What is the difference between simple partial & complex partial seizures?

A

Complex = loss of consciousness

183
Q

What is seen with juvenile myoclonic epilepsy?

A

Myoclonic seizures shortly after arising in the morning
Seen in teens
Precipitates by lack of sleep & EtOH (college lyfeee)

184
Q

What is seen with absence seizures?

What is the treatment?

A

EEG = 3 Hz
Ages 4-10
No postictal state

Tx: Ethosuximide

185
Q

What are the types of generalized seizures?

A

Absence (petit mal)
Myclonic - quick, repetitive jerks
Tonic-clonic (grand mal) - alternating stiffening & movement
Tonic - stiffening
Atonic - “drop seizures” often mistaken for fainting

186
Q

What is the treatment for myoclonic seizures?

A

Valproic acid

187
Q

What is status epilepticus?

A

Continuous seizure for >30 mins or recurrent seizures for >30 mins without regaining consciousness

188
Q

What is seen with a patient’s eyes in a seizure?

A

Patients look away from a seizure & into a stroke

189
Q

What causes peripheral vertigo?

A

Inner ear pathology:
Semicircular canal debris (BPPV)
Vestibular nerve infection
Ménière’s disease

Positional testing –> delayed horizontal nystagmus

190
Q

What causes central vertigo?

What is seen?

A

Brainstem or cerebellar lesion –> central vertigo

Findings:
Position testing –> immediate nystagmus in any direction

191
Q

What is seen in Tuberous Sclerosis?

A 
HAMARTOMAS:
Hamartomas in CNS & skin
Adenoma sebaceum
Mitral regurgitation
Ash-leaf spots
Rhabdomyoma in heart
Tuberous sclerosis
aut. dOminant
Mental retardation
Angiomyolipoma in kidney
Seizures
192
Q

What is seen in Neurofibromatosis Type I?

A 
Cafe-au-lait spots
Lisch nodules
Neurofibromas in skin
Optic gliomas
Pheochromocytomas
193
Q

What is seen in Neurofibromatosis Type 2?

A

Bilateral Schwannomas

Meningiomas

194
Q

What is seen in von Hippel-Lindau disease?

A

Bilateral renal cell carcinoma
Cavernous hemangiomas in skin & organs
Hemangioblastoma
Pheochromocytomas

Autosomal dominant mutation of VHL on Chromosome 3

195
Q

What is seen grossly with glioblastoma?
Histologically?
What should be stained for?

A

“Butterfly glioma” with necrosis

Histology:
Pseudopalisading cells surrounding necrotic area

Stain for GFAP

196
Q

What is seen on histology in meningioma?

A

Psammomas and whorls in middle-aged girls

often calcified, estrogen receptor positive

197
Q

What stain should be used for Schwannoma?

A

S-100

198
Q

What is seen histologically with oligodendroglioma?

A

OligoHENdroglioma:
Chicken wire capillary pattern
Fried egg cells
Often calcified

199
Q

What is seen grossly with Pilocytic astrocytoma?
Histologically?
What stain should be used?

A

Grossly - cystic portion & solid portion (piloCYSTic astrocytoma)

Histology - Rosenthal fibers (eosinophilic corkscrews)

GFAP+

200
Q

What is seen on histology of medulloblastoma?

A

Small blue cells (primitive neuroectodermal)

Homer-Wright rosettes

201
Q

What are drop metastases?

What are they seen in?

A

Medulloblastoma can send drop metastases down to the spinal cord through CSF.

202
Q

What is seen histologically with an ependymoma?

A

Perivascular rosettes

Rod-shaped blepharoplasts found near the nucleus

203
Q

Where is the most common site for an Ependymoma?

A

4th ventricle. Can cause hydrocephalus

204
Q

What are the tumors found in adults?

A

GBM = Metastasis > Meningioma > Schwannoma > Pituitary adenoma > Oligodendroglioma

205
Q

What are the primary CNS tumors found in children?

A

Pilocytic astrocytoma = Medulloblastoma > Craniopharyngioma = Ependymoma = Hemangioblastoma

206
Q

What is seen with Hemangioblastoma?

A

Arise during middle age
Associated with von Hippel-Lindau syndrome
Can produce EPO –> polycythemia

207
Q

What toxicities are seen with opioid analgesics?

A 
Addiction
Respiratory depression
Constipation
Biliary colic (sphincter of Oddi constriction)
Miosis
Additive CNS depression
208
Q

What changes are seen on CBC following glucocorticoid administration?

A

Increased serum neutrophil count
All other WBC’s are diminished

This is due to demargination of PMN’s that were previously attached to a vessel wall (in the lung).

209
Q

Why does aspirin use decrease the incidence of CRC?

A

COX-2 activity is seen to be high in som adenomatous polyps.

210
Q

What chemical exposure is a cause of Parkinson’s disease?

A

MPTP

MPPP is a synthetic opioid used in a prior time. One of the byproducts of its production was MPTP. In the body, MPTP is converted to MPP+ by MAO. This substance is toxic to dopaminergic neurons.

211
Q

What composition of bile is pro-gallstone?

A

High cholesterol
Low phosphatidylcholine
Low bile salts

212
Q

What causes pituitary apoplexy?

A

Hemorrhage into a preexisting pituitary adenoma. Presents much like a subarachnoid hemorrhage but has a history of pituitary adenoma symptoms.

Cardiovascular collapse can occur secondary to ACTH deficiency –> acute adrenal insufficiency.

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