CNS Flashcards

1
Q

What goes into midbrain?

A

Mesencephalon

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2
Q

What goes to pons and cerebellum?

A

Metencephalon

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3
Q

What goes in medulla?

A

Myelencephalon

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4
Q

What goes into Thalamus?

A

Diencephalon

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5
Q

What goes into Cerebral hemispher?

A

Telencephalon

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6
Q

What causes anecephaly?

A

Failure of anterior neural tube

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7
Q

What findings do you see in ancephaly?

A

Increased AFP

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8
Q

What labs do you see in neural tube defects?

A

Increased AFP

INcreased AChE

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9
Q

What causes holoprosenphaly?

A

SHH genes
Weeks 5-6
Associated with FAS, adn PATAU

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10
Q

What is Chiari II?

A

Herniation of cerebellar tonsils

Associated with aqueductal stenosis and HYDROCEPHALUS

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11
Q

What is DANDY Walker?

A

Agenesis of cerebelleum

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12
Q

What do you see in Syringomyleia?

A

A blanket distrubtion (cape like)
Dude to Chiari I malfornation
Trauma
Tumors

MOST Common C8-T1

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13
Q

How does the tongue 2/3 anterior develop?

A

Arch 1: Sensation V

Arch 2: Taste VII

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14
Q

How does the tongue posterior 1/3 develop?

A

Arch 3: Sensation IX

Arch 4: Taste X

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15
Q

What are the roles of astrocytes?

A
Physical support
K metabolism
Repair
Remove excess NTs
BBB
Glycogen fuel reserve

REACTIVE GLIOSIS

Derived from NEUROECTODERM

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16
Q

What do you see in HIV encephalitis?

A

Multinucleated cells (fused microglial cells)

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17
Q

How do you discern microglia?

A

Can’t see them by Nissl stain

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18
Q

What is the predominant type of glial cell in teh White matter?

A

Oligodendroglia
Myelinates CNS
Fried Egg appearnce
From NEUROECTODERM

Injured in: MS

  • PML
  • Leukodystrophies
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19
Q

What is the difference between C fibers and Adelta fibers?

A

C: slow unmyelinated
Adelta: Fast, myelinated

Both sense pain and temp (skin, epidermis, some viscer

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20
Q

What is the difference between meissner corpuscles and Merkle discs?

A

Meissern adapt quickly (HAIRLESS SKIN)
- Fine/light touch, position sense
Merkle adapt slowly (Finger tips, superficial skin)
- Pressure, deep static touch, body poisition

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21
Q

Where is NorEpi made?

A

LOCUS CERULEUS (Pons)

  • Increased in ANXIETY
  • Decreased in DEPRESSION
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22
Q

Where is DOPA made?

A
Ventral Tegmentum (midbrain)
Substantia Nigra pars compacta (midbrain)

Increased in Huntingons
Decreased in Parkinson
Decreased in Depression

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23
Q

Where is 5-HT made?

A

Raphe nuclei (pons, medulla, midbrain

Decreased in Anxiety
Decreased in Depression

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24
Q

Where is ACh Made

A

Basal nucelus of Meynert

Increased in Parkinson’s
Decreased in Alzheimer’s
Decreased in Huntingons disease

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25
Q

Where is GABA made?

A

Nucelus accumbens (reward center, pleasure, addiction, fear)

Decreased in anxiety
Decreased in Huntington’s

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26
Q

How do glucose and AA make it across the BBB?

A

They are transported by Carrier mediated transport

Area postrema: No BBB, vomiting center

OVLT: Osmotic sensing

Neurohypophysis: Allows ADH secretion

Infarction destroys tight junctions: Vasogenic edema

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27
Q

What does the Supraoptic nucleus do of the Hypothalamus?

A

Makes ADH

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28
Q

What does the paraventricular nucleus of the hypothalamus do?

A

Makes OXYTOCIN

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29
Q

What does the hypothalamus do?

A

TAN HATS

Thirst
Adenohypophysis (ant. pit)
Neurohypophysis (post pit)
Hunger
Autonomic
Temp
Sexual
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30
Q

What does the lateral area of the hypothalamus do?

A

Regulates hunger

Inhibited by LEPTIN

Destruction: Anorexia

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31
Q

What does the VM area of the hypothalamus do?

A

Senses when you are full
Stimulated by Leptin

Destruction (craniopharyngioma): Eat too much (get fat)

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32
Q

What does the anterio hypo do?

A

Temp reg, COOLING

Parasympathetic

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33
Q

What does you posterior hypo do?

A

It heats you up
Sympathetic
Become cold blooded if this is knocked out

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34
Q

What does the Suprachiasmatic nucleus do?

A

It regulates circadian rhythm

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35
Q

Circadian rhytm works how?

A

It regulates the release of ACTH, Prolactin, melatonin, norepi

SCN-NE-Pineal-Melatonin
Regulated by light

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36
Q

What happens during REM sleep?

A

EOM activated by PPRF (paramedian pontine reticular formation

Every 90minutes

Duration increases through night

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37
Q

What does alch, BZ, and Barbs do to sleep?

A

Decrease REM and Delta wave sleep (more tired feeling)

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38
Q

How do you treat bedwetting?

A

ADH (desmopressin)

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39
Q

What stage do night terrors, sleep walking and bedwetting occur?

A

Stage N3: delta wave

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40
Q

When does bruxism occur (grinding teeth)?

A

Stage N2: S wave

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41
Q

What is responsible for the 5 Fs?

A

Feeding, Fleeing, Fighting, Feeling, Sex

Limbic System (hippocampus, amygdala, fornix, mamm bodies, cingulate gyrus)

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42
Q

How does the cerebellum function?

A

Modulates movements

Input: contralateral cortex (middle peduncle)
- Ipsilateral proprioceptive from DCML through inferior peduncle

Output: Contralateral cortex
- Purkinje cells-Deep nuclei-contralat cortex via SUPERIOR PEDUNCLE

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43
Q

What is the order of deep nuclei lateral to medial?

A

Dentate, emboliform, globose, fastigial (DONT EAT GREASY FOOD)

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44
Q

What happens in a ipsilateral lesion of cerebellum?

A

Ipsilateral falls

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45
Q

What happens in medial lesions?

A

Truncal ataxia (wide based gait), nystagmus, head tilting,

bilateral motor deficits

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46
Q

How does D act on the basal ganglia?

A

Inhibitor has D2 receptor: Inhibits activation when DA comes

Stimulator has D1 which activate it that causes movement

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47
Q

What is athetosis?

A

Slow writhing movements

Lesion in Basal ganglia

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48
Q

What is chorea?

A

Sudden jerky movements

Lesion is Basal ganglia (huntingtons)

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49
Q

What is essential tremor?

A

High frequency tremor (sustained posture)
Worsened with movement
- Treatment: B blockers, primidone

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50
Q

What is dystonia?

A

Sustained involuntary contractions

Writer’s crap
- Blepharospasm (eyelid twitch)

51
Q

What is hemibasllismus?

A

Sudden wild flailing

Contralater subthalamic nucleus (LACUNAR STROKE)

Contralateral lesion

52
Q

What is intention tremor?

A

Slow zigzag motion with extension or pointing

Cerebellar dysfunction

53
Q

What is myoclonus/

A

Sudden brief uncontrolled contraction

Hiccups: Renal liver failure, or metabolic disturbance

54
Q

What is resting tremor?

A

Uncontrolled movement of distal appendage, alleviated by intentional movement

Seen in Parkinson’s disease

occurs as pill rolling tremor

55
Q

What are characteristics of Huntington’s disease?

A

Chorea,
Depresion
Agitation
Dementia

Increased DA
Decreased GABA
Decreased ACh

Atrophy of caudate nucleus (ex vacuo dilation)

CAG repeats (Chromosome 4)

56
Q

What is Kluver Bucy Syndrome?

A

Lesion of AMYGDALA

HSV-1 encephaltis

HYPERPHAGIA, Hypersexual, Hyperorality

57
Q

What happens in frontal lobe lesion?

A

Deficit in concentration, orientation, judgment,

reemergence of primitive reflexes

58
Q

What happens if non dominant parietal temporal complex hurt?

A

Get hemispatial neglect (agnosia of contralateral side of the world

59
Q

What happens if dominant parietal temporal complex hurt?

A

Agraphia, Acalculia, Finger agnosia, Left-right disorietnation

GERSTMANN SYNDROME

60
Q

What is RAS hurt?

A

Midbrain

Reduced levels of arousal/wakefulness

61
Q

What happens in Wernicke Korsakoff syndrome?

A

Due to thiamine deficiency (B1)

Confusion
Opthalomplegia
Ataxia
Memory loss
Confabulation
Personality chagnes
62
Q

What happens if subthalamic nucleus hurt?

A

Contralateral hemiballism

63
Q

What is paramedian pontine reticular formation hurt?

A

Eyes look away from lesion

64
Q

What is Frontal eye fields are hurt?

A

Look towards the lesion

65
Q

What ventilation intervention helps in Increased ICP situations?

A

Hyperventilation, decreased pCO2 helps lower ICP
- What causes fainting in Hyperventilation attacks (anxiety)

Brain perfusion most regulated by pCO2
- Lower the CO2 the lower the CBF

66
Q

How do you calculate Cerebral perfusion pressure (CPP)?

A

CPP= MAP-ICP
If CPP=0 then there is no perfusion, equals death

MAP: 2/3 diastolic+1/3 systolic

67
Q

What is the most common cause of stroke in the lenticul striate artery?

A

Hit the midbrain (contralaeral hemiparesis and hemiplegia)

Due to HTN mostly

68
Q

What does a stroke in the ASA produce?

A

Medial Meullary Syndrome (contralateral hemiparesis and contralateral proprioception

Ipsilateral hypoglossal dysfunction (lick your wounds)

69
Q

What happens if PICA hit by stroke?

A

Lateral medullary syndrome (wallenburg)

Don’t PICK a HORSE (hoarseness) that can’t eat (dysphagia)

Vomiting, vertigo, nystagmus, decreased pain and temp (ipsilateral face, contralateral body, dysphagia, hoarseness, decreased gag reflex, ipsilateral HORNER’s, ataxia, dysmetria

Lateral medulla
Inferior Cerebellar peduncle

70
Q

What if AICA hit by stroke?

A

Lateral Pontine Sydrome

Hits the lateral pons (CN nuclei, vestiulbar nuclei, facial nucleus, ST nucleus, cochlear nuclei, sympathetic fibers)

Vomiting, vertigo, nystagmus

paralysis of face

71
Q

What if PCA hit?

A

OCcipital cortex
Visual cortex
Contralateral hemianopia with macular sparing

72
Q

What happens if basilar artery is hit?

A

Pons, medulla, lower midbrain, Corticospinal/bulbar hit, ocular crainial nerves, paramedian pontine reticular formation

Preserved conciousness but LOCKED IN

73
Q

What is ACom hit?

A

Most common site of aneurysm

Saccular berry aneursm (visual field defect)

74
Q

What is PCom hit?

A

Common site of saccular aneurysm

CNIII palsy, down and out with ptosis and mydriasis

75
Q

What is the disease associated with saccular aneurysms?

A

Ehlers’Danlos syndrome
ADPKD

RF: advanced age
HTN
Smoking
Black

76
Q

What causes central post stroke pain?

A

Neuropathic pain due to thalamic lesions
Initial paresthesias followed by ALLODYNIA (pain at non painful stimulus) dysesthesia (abn sensation)

10% stroke

77
Q

How long until irrevesrible damage seen in brain?

A

5 minutes of hypoxia

78
Q

What are the most vunerable spots to ischemia?

A

Hippocampus
Neocortex
Cerebellum
Watershed zones

Must do non contrast CT to make sure it’s not hemorrhagic before giving thrombolytics

79
Q

What do you see in 12-48 hours of infarct?

A

Red Neurons

80
Q

What do you seen in 24-72 hours post infarct?

A

Necrosis, PMNs

81
Q

What do you see in 3-5 days?

A

Macrophages (microglia

82
Q

What do you see in 1-2 weeks?

A

Reactive gliosis, vascular proliferation

83
Q

What do you see in greather than 2 weeks?

A

Glial Scar (looks like empty portion)

84
Q

When do you give tPA in ischemic stroke?

A

3-4.5 hours post onset

Reduce risk with medical therapy: aspirin, clopidogrel
- Optimum control of BP, blood sugars, lipids,
Treat conditions that increase risk (afib)

85
Q

What is the order of CSF in brain?

A

Lateral ventricles– Foramen of Monro– 3rd ventricle–cerebral aqueduct–4th ventricle – Subarachnoid via (lateral is lushka, media is magendie)

86
Q

What lesion in the spinal cord is caused by 3 syphilis?

A

Tabes dorsalis

Degeneration of DCML

Charcot joints, shooting pain, argyll roberston pupils (reduce to accomodation but NOT light)

Exam: Positive romberg test but no DTRs

87
Q

What causes Friedreich ataxia?

A
GAA repeat (chromosome 9)
Frataxin (iron binding protein)_
Impaired mitochondria
Degenration of spinal tracts
Staggering gait
Frequent Falls
DM
Hypertrophic CARDIOMYOPATHY

kyphoscoliosis

88
Q

What is Spinal Muscular Atrophy (Werdnig-Hoffman disease)?

A

Congenital degeneration of AH of spinal cords- LMN lesion

FLOPPY BABY

Marked hypotonia with tongue fasciulations

Autosomal recessive

Age of death 7 months

89
Q

Which nuclei are medial?

A

III, IV, VI, XII (purely motor)

90
Q

What do the superior colliculi do?

A

Vertical Conjugate gaze

91
Q

What do inferior colliculi do?

A

Auditory

92
Q

What is parinaud syndrome?

A

Paralysis of Vertical conjugate gaze due to lesion of superior colliculi

(stroke, pinealoma, hydrocephalus)

93
Q

What goes through the foramen rotundum?

A

V2

94
Q

What goes through the foramen ovale?

A

V3

95
Q

What goes through the superior orbital fissure?

A

CN III, IV, VI, V1, opthalmic vein, sympathetics

96
Q

What goes through the optic canal?

A

CNII, Opthal artery, central retinal vein

97
Q

What are the vagal nuclei?

A

Nucleus solitarius (Visceral Sensory, inormation (taste), baroreceptors, gut distension) VII, IX, X

Nucleus aMbiguus (motor innervation of pharynx, larynx, upper esophagus (IX, X, XI)

Dorsal motor nucleus: Parasympathetics to heart, lungs, upper GI X

98
Q

What nerves sit inside the Cavernous sinus?

A

III, IV, VI, V1, V2

Internal carotid artery

Postganglionic sympathetic fibers pass through also

99
Q

What is Cavernous sinus syndrome?

A

Opthalomoplegia
Decreased Corneal sensation (V1 missing)
Horner Syndrome (sympathetic go through)
Decreased Maxillary sensation

Due to pituitary tumor that has grown too big
Carotid cavnerous fistula

Or Cavernous sinus thrombosis due to Infection

CN VI is most susceptible to injury ( lateral rectus)

100
Q

Which sounds hit the base of the cochlea?

A

High Frequency sounds Thin and Rigid

Low frequency hit the apex (near helicotrema) becuase they hair are wide and flexible

101
Q

What are the test results for Conductive hearing loss?

A

Rhinne: Abnormal (bone >air)
Weber: Localizes to affected ear

102
Q

What are the test results of sensoneural hearing loss?

A

Rinne test: Normal (air>bone)

Weber: Localizes to unaffected ear

103
Q

What diseases are associated with bell’s palsy/

A
Lyme
Herpes
Herpes zoster (Ramsay hunt syndrome)
sarcoidosis
Tumors
Diabetes

Treatment: Corticosteroids

104
Q

What are associated with uveitis?

A

Inflammatory conditions (IBD)

HLA-B27 stuff
Sarcoidosis
Rheumatoid arthritis
Juvenile idiopathic arthritis

105
Q

What is seen in dry Macular degeneration?

A

Deposits of yellow extracellular material
Retinal Pigment epi (drusen)
Prevent: MULITVITAMIN

106
Q

What is seen in wet macular degeneration?

A

Choroiddal neovascularization

Treat: anti-VEGF (ranibizumab) or laser

107
Q

What are the types of Diabetic retinopathy?

A

Chronic hyperglycemia
Nonproliferative: Damaged capillaires leak blood
- Treat: Control blood sugar, macular laser

Proliferative: Chronic hypoxia results in NEW BVs
- Treat: photocoag, anti-VEGF

108
Q

What do you see in Central retinal artery occlusion?

A

Painless monocular vision loss

Retinal cloudy with CHERry RED SPOT

109
Q

What happens in retinitis pigmentosa?

A

Starts with Night Blindness
(Rods affected first)
Bone spicule-shaped deposits

110
Q

What causes retinitis?

A

CMV, HSV, HZV

Associated with immunosuppression (AIDS, corticosteroids)

111
Q

What nucleus is associated with miosis/

A

Edigner westphal nucleus to short ciliary nerves to sphincter muscles

112
Q

How does mydriasis work?

A

1rst neuron: Hypothalamus to ciliospinal C8-T2
2nd Neuron: Exit at T1 to superior cervical ganglion (travels near apex of lung)
3rd Neuron: Plexus along internal carotid, through cavernous sinus, enters orbit as long ciliary nerve to pupillary dilator muscles
- Innervated smooth muscle of eyelids as well and sweat glands of forehead and face

113
Q

What is a Marcus Gann Pupil?

A

Afferent pupilary defect

Optic nerve damage or severe retinal injury

Decrease in bilateral pupillary constriction when light is shone in affected eye (test with swinging light test)

114
Q

What causes CNIII damage?

A

Both Motor and Parasympathetic components

Motor: Affected by vascular disease (DM: glucose-sorbitol) due to difficusion of inferior fibers

Parasympathetic: PCA aneurysm, uncal herniation
-Diminished or absent pupillary light reflex, blown pupil (down and out gaze)

115
Q

What happens in CN IV damage?

A

Eyes upward (contralateral gaze) head tilt towards side of lesion Cant go down stairs)

116
Q

What happens in CN VI damage?

A

Medialy directed eye that can’t abduct

117
Q

What are disease modifying drugs in MS?

A

B-interferon, natalizumab

Treat acute flares with IV steroids

Symptomatic treatment: Neurogenic bladder (catheter, muscarinic antagonist

  • Spasticity: Baclofen, GABAb receptor agonist
  • Pain: Opioids
118
Q

What happens in Krabbe Disease?

A

Lysosomal storage disease

Deficiency in galactocerebrosidase, buildup of galactocerebroside that destroys myelin sheath

Periphearl neuropathy, developmental delay, optic atrophy, globoid cells

119
Q

What happens in metachromatic leukodystrophy?

A

Lysosomal storage disease
AR

Most commonly due to arylsulfatase A deficiency

Buildup of sulfatides- impaired production and destruction of myelin sheath

Central and peripheral demyelination with ATAXIA, DEMENTIA

120
Q

What is Charcot-Marie-TOOTH disease?

A

Autosomal Dominant

Defective production of proteins involved in structure of peripheral nerves or myelin sheath

Scoliosis and Foot deformities (HIGH/FLAT arches)

121
Q

What is adrenoleukodystophry?

A

X linked genetic

Disrupts metabolism of VLC fatty acids
Excessive buildup in nervous system, adrenal glands

Progressive disease that leads to long-term coma/death with adrenal gland crisis

122
Q

Sturge Weber syndrome

A

Congenital disorder (non inherited)
Neural crest derivative anomaly
Activating mutaiton of GNAQ

Port wine stain on face
Ipsilateal leptomeningeal angioma
Seizures/epilepsy, intellectual disability, episcleral hemangioma
Increased IOP
Early onset glaucoma
123
Q

Tuberous sclerosis

A
HAMARTOMAS 
Hamartomas of CNS, skin
Angiofibromas
Mitral regurg
Ash-leaf spots
Cardiac Rhabomyoma
AUTOSOMAL DOMINANT
Mental retardation
124
Q

NF1

A
Cafe au lait spots
Lisch nodules
Cutaneous neurofibromas
Optic gliomas
Pheochromocytomas

Mutated NF1
AD
Chromosome 17, neurofibromin reg of RAS