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Neuro Flashcards

1
Q

Nuero Development

A
  • Notochord causes overlying ectoderm to become neuroectoderm and neural crest cells come off.
  • Notochord becomes nucleus pulposus
  • Basal plate is motor and alar plate is sensory
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2
Q

Forebrain

A
  • Telencephalon: Hemispheres and lateral ventricle

- Diencephalon: Thal and hypothal, third ventricle

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3
Q

Midbrain

A

-Mesenencephalon: midbrain, and cerebral aqueduct

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4
Q

Hindbrain

A
  • Metencephalon: Cerebellum and pons (4th vent)

- Myelenchephalon: 4th ventricle

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5
Q

Neural Tube Defects

A
  • Elevated AFP and AchE
  • Occur before 8 weeks and are assocaited with decreased folic acid in the mother at the begning of pregnancy
  • Valproic acid, carbemazapine, phenytoin (fetal hydantoin: Microcephaly, retardation, IUGR, cleft lips)
  • Anti-epileptics are also common causes of cleft lip and palate, give phenobarbitol to pregnant women
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6
Q

SB

A

Meningomyelocele associated with chiari 2 (Paralysis below the lesion is common)

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7
Q

Anencephaly

A
  • Failure of cranial neuropore to close
  • Increased AFP and polyhydramnios
  • Associated with DM1 and decreased folate
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8
Q

Holoprosenchephaly

A
  • Failure of hemispheres to separate
  • Associated with cleft lip and palate and maybe cycloplegia
  • Patau is common cause
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9
Q

Chiari 2

A

Hernation of cerebellar tonsils and vermis

  • Aqueductal stenosis and hydrocephalus
  • Associated with syringomeyleia and meningomyelocele
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10
Q

Dandy Walker

A

Agenesis of the cerebellar vermis leading to dilation of the 4th ventricle and hydrocephalus
-Spina bifida can also commonly be seen

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11
Q

Syringomyelia

A
  • Cystic dilation of central canal leading to compression of crossing spinothalamic results in loss of pain and temp in cape like distrbution
  • May progress to involve symps (Lateral Horn) or motor
  • May cause hydrocephalus and headaches
  • Associated with chiari malformations
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12
Q

Tongue Development

A
  • Anterior 2/3 is bordered posteriorly by the foramen cecum and terminal sulcus. Senstation from arch 1 in V3 and taste from arch 2 in VII. Sends axons to solitary nucleus
  • Post 1/3 formed by 3rd and 4th arches. Glossopharyngeal is tongue tast and sensation, X is palate taste and sesnation, send axons to nucleus soliatarius
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13
Q

Arch 1

A

V2,3

-Mandilble, muscles of matication, inner ear muscles, general sensatino to face and tongue

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14
Q

Arch 2

A

Facial, PANS to facial glands, sensation around ear and motor to ear and face

  • Facial artery, hyoid, musles of inner ear
  • Taste to ant 2/3 sent to solitary
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15
Q

Arch 3

A

Sytolopharungeus, post tongue taste and sensation, solitary nucleus. Internal carotid artery from 3rd aortic arch
-Thymus, PTH, Hyoid

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16
Q

Arch 4

A
  • Aortic becomes subclavian and arch
  • Post tongue, vagus above runs with superior laryngeal
  • cricothyroid
  • taste and aortic arch to nucleus solitarius
  • Superior PTH,
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17
Q

Thyroid

A

Invagination of endodermal floor

-Foramen Cecum and cyst possible

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18
Q

Muscles of tongue

A

Derived from occipital myotomes and are innervated by 12 from

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19
Q

Narcolepsy

A
  • Genetic defect in orexin from the lateral hypothalamus

- Begins with REM sleep and causes cataplexy, associated with hallucinations leading to and coming out

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20
Q

Neronal Cell origin

A

Majortiy derived from neuroectoderm excpet Schwann and PNS from NC
-Microglia are mesodermal

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21
Q

Microglia

A

-When infected with HIV fuse to form multinucleated giant cells

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22
Q

Wallerian Degeneration

A
  • PNS, retraction proximal, disllolution dystal. Nucleus moved to periphery and dissultion of Nissl substance.
  • Recovery occurs.
  • Loss of nuclear integrity leads to death
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23
Q

Oligodendrocytes

A

These cells are destroyed in MS

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24
Q

Schwann Cells

A
  • Neural Crest
  • Destroyed by Guillan Bare (Ascending paralysis)
  • Acoustic Neuroma NF-2
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25
Q

Miessners Copuscles

A

Dyamic fine touch and position sense, glaborous skin (hairless)

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26
Q

Pacinian

A

Deep skin layers. Vibration and pressure

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27
Q

Merkels discs

A

Hair Follicles

-Pressure, static touch,

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28
Q

Peripheral Nerve

A

Endoneureum: Invests individual nerves, site of inflammation in GB

  • Perineureum: Surrounds a fascile, site of reattacment in surgery
  • Epineureum: Carries blood vessels
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29
Q

Merkels Discs

A

Slowly adapting, deep pressure

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30
Q

Meisners orpuscles

A

Smooth, glaborous hairless skin for fine touch

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31
Q

Pacinian Corpuscles

A

-Vibration and pressure

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32
Q

NE

A
  • Pons in locus ceruleus

- Increase in anxiety and decrease in dpression

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33
Q

DA

A

-SNc for nigrostriatal
-Ventral tegmental and septal (along with GABA) mediated pleasure. Midbrain
+ Psychosis
-Depression and parkinsons

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34
Q

5-HT

A
  • In gut and dorsal raphe (pons)

- Depression and aniety

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35
Q

Ach

A

Basal Meynert
-Alzhiemers huntingtons
+parkinsons relative, and REM

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36
Q

GABA

A

septal, nucleus acumbens for pleasure

-huntingtons and anxiety

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37
Q

BBB

A

Endothelial cells tight junctions and non fenestated

  • BM
  • Astrocyte foot processes
  • Polar solutes cannot cross, glucose and AA need carriers
  • Fenestrated at area postrema, OVLT, neuropohysis
  • Destruction by trauma, tumor, infection can lead to vasogenic edema
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38
Q

Lateral Hypothalamus

A
  • Destruction leads to anorexia and apathy
  • Leptin will inhibit and lead to similar symptoms
  • Normally mediates feelings of hunger and aggression
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39
Q

DM hypothalamus

A
  • Destruction leads to agression and hunger (Craniopharyngoma possible cause)
  • Leptin will stimulate (normaly mediates feelings of satiety)
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40
Q

Anterior

A

PANS, part of papez circuit

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41
Q

Posterior

A

SANS

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42
Q

Suprachiasmatic

A

-Circadian Ryhtms

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43
Q

Paraventricular and supraoptic

A

Neurons from the PP that secrete oxytocin and ADH. Production of hormones occurs in cell bodies in paraventricular and supraoptic hypothalamus

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44
Q

VPL

A

Input from sesnation of body, output to sensory cortex

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45
Q

VPM

A

Input from sensation of face, output to sensory cortx

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46
Q

VA/VL

A

-Input basal ganlia and cerebellum, output to motor cortex of cerebrum

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47
Q

MGN

A

-Input from superior olive and inferior colliculus, output to temporal lobe

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48
Q

LGN

A

-Input from CNII, vision. Output to calcarine sulcus of occipital lobe

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49
Q

Limbic

A

Emotions, Feelings, memory, etc

-Olfactory is part

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50
Q

Kluver Bucy

A
  • HSV encephalopathy or strokes

- Bilateral lesions lead to docility, hyperphagia, hypersexuality

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51
Q

Foster Kenedy

A

-Meningoma or other destruction of olfactory tract and associated emotional liability. Damage to frontal lobe

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52
Q

Papez Circuit

A

-Hippocampus to mamlary bodies via the fornix. To the anterior hypothalamus to the cingulate gyrus ot the entorhinal cortex

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53
Q

Cerebellum

A

Inputs via the inferior peduncle (body) and middle peducnle (contralateral cortex) all sensation is from the ipsilateral side

  • Output via the superior cerebellar peduncle. To VA/VL thalamus to contralateral motor cortex. Motion is to ipsilateral side
  • All lesions will result in ipsilateral defect
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54
Q

Localizations

A
  • Anterior is legs and posterior is upper body
  • Vermal is balance and lateral is directed purposeful movements
  • Floculonodular communicates with vestibular nuclei of CN8 and is impt for vertigo and nystagmus
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55
Q

Lesions

A
  • anterior vermal commonly seen in alcoholics causes cerebellar ataxia, intention problems
  • Posterior vemal is more commonly seen involving tumors of kids, upper body ataxia
  • Lateral is commonly involved in stroke and can be seen involving problems with purposeful movement
  • Floculonodular damage in a stroke will lead to nystagmus and vertigo
  • All lesions will be ipsilateral. More important for stroke localization
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56
Q

Basal Ganglia

A

Control and process motion and cognition from cerebellum and cortex

  • Cortical input with negative feedback on cortex
  • Output is inhibitory via the Gpi/snr
  • Input is dopaminergic from snr (parkinsons)
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57
Q

Striatum

A

Putamen (motor) and Caudate (cognition)

  • D1 Gs receptor mediates direct pathway increasing motion
  • D2 mediates inhibitory pathway (Gi)
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58
Q

Direct Pathway

A

-D1 leads to inhibition of Gpi/snr which is the inhibitory output. Net is loss of inhibition and action

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59
Q

Indirect Pathway

A

D2 leads to inhibition of STN which is normally excitatory onto snr/gpe. This leads to an increased action of inhibitory outputs and a decrease in motion
-D2 antagonist used in psychosis can cause tardive dyskinesia through this receptor

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60
Q

Parkinsons

A
  • Characterized by loss of neurons in the snc that leads to a decrease of stimulation of the putamen and caudate.
  • Dead neurons have lewy bodies composed of intracellular aggregates of alpha synuclein
  • Leads to classic quartade of Bradykinesia, resting tremor, rigidity, and gait instability
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61
Q

Huntingtons

A
  • Characterized by destruction of caudate nucleus due to AD trinucleotide repeat.
  • Loss of Ach and GABA can lead to NMDA induced excititotoxicity
  • Clinically will present as depression and choreoathetosis leading to death in midlife
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62
Q

Hemibalism

A

Infarction of STN which leads to loss of excitment to inhibitory snr/gpi leads to a net increase in motor activity

  • Clinically will present as contralateral random flinging movements
  • Infarction is due to disruption of flow in branches of posterior communicating artery
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63
Q

Wilsons Disease

A
  • Mutation in ATPB7 involved in copper loading into cerruloplasm
  • Leads to hepatoleticular degeneration
  • Commonly see deposits in lenticular nuclei (putamen and globus pallidus)
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64
Q

Kernicterus

A

-Elevated bilirubin, commonly precipitates in BG

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65
Q

Essential Tremor

A
  • Exacerbated by static posture, not intention tremor and is present at rest
  • Treat with beta blockers
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66
Q

Resting Tremor

A

-Parkinsons

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67
Q

Intention Tremor

A

Think of cerebellar injury, especially lateral cerebellum

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68
Q

MPTP

A

Street drug that can cause symptoms of parkinsons

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69
Q

VA/Premotor

A

Communication generally between VA and premotor in frontal lobe

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70
Q

VL-primary motor

A

Most outputs go to primary motor cortex

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71
Q

Brocas area

A
  • Dominant (left hemisphere in frontal lobe, supplied by MCA)
  • Speaking aphasia
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72
Q

Arcuate fasiculus

A

Connects the two

-Each work fine idependently, but can’t repeat

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73
Q

Wernickes Area

A
  • Auditory sensory and association
  • Damage, MCA leads to fluent aphasia
  • Temporal lobe posterior to sylvian fissure
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74
Q

Primar Auditory

A

Temporal lobe, receieves input from MGN

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75
Q

Fronatl Eye fields

A

Damage leads to looking towards lesion, MCA

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76
Q

PPRF

A

Midbrain, lesion leads to looking away from lesion

-Horizontal palsy with lack of saccades. Connects to superior colliculus and vestibular

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77
Q

Homunculus

A
  • Legs are aterior cerebral
  • Hand is MCA and loctate at superior frontal lobe
  • Mouth and tongue is lateral frontal lobe MCA
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78
Q

Amygdala

A
  • Damaged by HSV-1 encephalitis, leads to Kluver Bucy

- Hyperorality, phagia, sexuality

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79
Q

Frontal Lobe

A

Damage leads to loss of concentration and inhibition

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80
Q

Right, non dominant parietal

A

-Spatial neglect on the nondominant side (anosognosia)

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81
Q

RAS

A
  • Midbrain, Ach and NE with locus ceruleus and septal etc

- Coordinates arousal status

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82
Q

Mamillary Bodies

A
  • Wernicke Encephalopathy
  • Hemorrhagic necrosis leading to opthalmoplegia, ataxia, anterograde amnesia (confabulations and confusion)
  • Lack of thiamine
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83
Q

Central Pontine Myelinolysis

A
  • Too rapid of correction of Na leads to osmotic necrosis of central pons
  • Leads to paralysis, dysarthria, and loss of conciousness can lead to locked in syndrome
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84
Q

Gerstmann’s

A

-Damage to angular gyrus or superior parietal lobule leads to acalcula and agraphia on dominant side

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85
Q

Watershed Areas

A

-Upper leg and arm and higher order visual processing

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86
Q

Regulation

A
  • Relies almost exclusively on CO2

- Theraputic hyperbetalation leads to constriction and decreased cerebral blood flow and decreased cerebral edema

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87
Q

Vulnerable spots to global ischemia

A
  • Cerebral layers 3,5,6
  • Perkinje Cells of cerebellum
  • Hipocampal pyramidal cells
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88
Q

Infarcts

A

Pale: Thrmobus, atheroscleososis, most common at branch points

  • Red: Embolus, A fib
  • Lacunar: HTN and hyaline arteriosclerosis
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89
Q

Lenticulostriate artery

A
  • Branch of MCA at proximal leave of internal carotid

- internal capsule motor stroke or BG

90
Q

Anteroir Choroidal

A

-Internal Capsule stroke or pure sensory thalamus

91
Q

Internal Capsule

A

Posterior is corticospinal tract motor

  • Genu is cranial nerve motor
  • Anterior is communicating brain tracts
92
Q

Anterior Spinal in Brainstem

A
  • Medial Caudal Medulla
  • CN 12 is deviation of tongue ipsilaterally
  • Also involvment of corticospinal
93
Q

PICA

A
  • Lateral cranial medulla
  • 9,10 leading to impaired gag reflex because of loss of nucleus ambiguus
  • Also vestibular nuclei leading to nstagmus and vommiting as well as cerebellum, spinal 5, ipsilateral horners, and spinothalamic
94
Q

AICA

A
  • Lateral Pons
  • 7,8 leads to facial paralysis and ipsilateral reduction in hearing because of cochlear nuclei
  • Also vestibular and cerebellar, spinal V, spinothalamic and ipsilateral horners
95
Q

Superior Cerebellar

A
  • Can compress CN 3

- Cerebellar signs

96
Q

Posterior Cerebellar

A
  • Anyeurism can compress 3
  • Otherwise hits midbrain and posterior brain
  • homonymous Hemiaopia with macular sparing
97
Q

A comm

A
  • Generally is an anyeurism and is most common at anterior comm
  • Causes compression of optic chiasm bitemproal hemianopia
98
Q

Post Comm

A
  • Anyeurism will compress CN 3

- Branches supply STN leading to hemiballism

99
Q

Berry ANyeurism

A

-Rupture leads to SAH and worst headache of life

100
Q

Charcot Broussard

A
  • Lacunar infarcts due to HTN and arteriolosclerosis

- Lenticulostriate and anterior choroidal

101
Q

Schwannoma

A
  • Cerebellopontine angle leads to compression of CN 5,7,8

- NF-2

102
Q

Prinauds

A
  • Pinealoma which is commonly a dysgerminoma that may be calcified and oily
  • May also cause precocious puberty and lead to altered melatonin secretion and disruption of sleep patterns
  • Superior colliculus compression leading to vertical gaze palsy
103
Q

SAH

A
  • Generally caused by rupture of anyeurism, lack of media at branch points predisposes to anyeurism
  • Xanthochromia or blood in CSF
  • Blood breakdown may lead to vasospasm and rebleed, treat with Ca channel blocker (nimodipine)
  • WHOML
104
Q

Intraparenchymal

A
  • Caused by HTN, Amyloid angiopathy, Cancer, AVM, DM, Vasculitis
  • Generally occur in BG and internal capsule
105
Q

Pathology of Ischemia

A
  • Irreversible damage occurs within 5 mins
  • 12-48 hours is red neurons
  • 24-72 hours is neutrophils
  • 3-5 days is macrophages
  • 1-2 weeks is BV proliferation and gliosis
  • 2 weeks is glial scar
  • Liquefactive necrosis
106
Q

Radiology of Stroke

A
  • Diffuse weighted will show a bright area at the location of ischemia
  • non contrast CT bright will be hemorrhage and dark will be ischemia
107
Q

Hemorrhage

A

-See causes above and also from reperfusion following ischemia

108
Q

Embolism

A

-Carotid disection, A fib, PFO, endocarditits

109
Q

Sinuses

A

Arachnoid granulations drain into dural sinuses which accumulate at the sigmoid into the internal jugular
-Meningitis can cause scarring and dysfnction of granulations leading to hydrocephalus

110
Q

CSF

A
  • Made in the choroid plexus by ependymal cells.
  • Contains increased Na and Cl and decreased K, Ca, Glucose, AA (Need transporter to cross BBB)
  • Lat vents to monroe to third to aqueduct to 4th to magendie and luschka to SAH (Cisterns) to granulations to superior sagital and other sinuses
111
Q

Communicating Hydrocephalus

A
  • Increased production by ependymoma or more commonly decreased resorption by granulations
  • Commonly due to scarring from menintis
  • Increasd ICP, papilledema, herniation, etc
112
Q

NPH

A
  • Normal pressure but increased ventricular size
  • Leads to stretching and dysfinction of corona radiata
  • Wacky, Wobly, Wet. More acute than dementia
113
Q

Ex Vacuo

A

No increase in pressure but due to atrophy. Huntingons, alzheiers, picks, etc

114
Q

Noncommunicating

A

-Aqueducatal stenosis, chiari 2, dandy walker (luschka and magendie), tumors

115
Q

Organization of Spinal Cord

A

Fasiculus gracilus is medial and cuneatus is lateral carry DCML

  • Lateral spinothalamic tract carries P/T. Organized with legs lateral and arms medial (oposite of DCML) Sits anteriorly to the lateral corticospinal
  • Anteroior spinothalamic is much smaller and carries cude touch and pressure. Located just anterior to the anterior horn gray matter
  • Lateral Corticospinal lies laterally and posterior to the lateral spinothalamic. Organized with legs lateral and arms medial
  • Lateral horns carry primary SANS from posterior hypothalamus
116
Q

DCML

A
  • Gracilus is medial and cuneatus is lateral
  • Primary have cell bodies in DRG and ascend ipsilaterally to synapse in the caudal medulla in the gracile, cuneiform nucleus.
  • Second order neurons cross over at medial lemniscus (central to posterior medulla) (basilar) and head to VPL
  • VPL to primary sensory
117
Q

ALS

A
  • Lateral spinothalamic first order neurons synapse in the chord in substantia gelatinosa and cross over in lissears tract
  • Ascend contralaterally and ascend medulla in the lateral protion (AICA, PICA) SANS run with in pons and medulla
  • Second synapse in the VPL thalamus
  • 3rd go to cortex
  • ANterior is same, but runs anteriorly to the ventral horn in the spinal cord
118
Q

Corticospinal tract

A

Primary neurons are in the motor cortex and descend in posterior limb of internal capsule

  • cross over in caudal medulla (ASA)
  • Synapse in dorsal horn and then to NMJ
119
Q

Polio

A
  • SS + picorovirus fecal oral to gut. Normal illness with few progressing to poliomyelitis
  • Death of anterior horn cells leading to LMN signs. Fasiculations and hypotonia
120
Q

Werdnig Hoffman

A
  • Congential Defect leading to death of LMN

- Floppy baby with hypotonia and fasiculations. Death at young age.

121
Q

Tabes Dorsalis

A
  • teritery syphilis leads to death of posterior columns and lower sensory neurons.
  • Demlination
  • Sensory ataxia with charcot joint. Commonly painful
  • Will have no proprioception, vibration etc leads to positive rhomberg
  • Also loss of DTRs because of death of afferent proprioceptive neurons
122
Q

Subacute COmbined Degeneration

A

B12 or E deficency leads to vaculozation and demylination and dysfunction of corticospinal , spinocerebellar, and DMCL
-Leads to ataxia, paresthsia, impiared vibration and proprioception

123
Q

ASA infarcction

A
  • Watershed zone above the level of T8 is common due to adamkewitz artery entering at that area
  • Loss of everything except for Dorsal Columns.
  • Will present with loss of pain and temperature bilaterally and lower motor neuron signs at the site of the injury, and UMN signs below injury
124
Q

MS

A

-Multiple scattered lesions that can repair and remit, commonly involves urinary incontnence

125
Q

ALS

A
  • Loss of upper and lower motor neuron signs, believed to be due to SOD1 mutation
  • Can be treated with rislovin that can decrease glutamate induced excitotoxicity
  • Lower motor neuron sign predominate with early hypotonia and fasiculations in hand and mouth
126
Q

Syrinngomeyleia

A
  • Increase in size of central canal
  • Associated with Chiari 1 and 2 and also anatomical probles like scoliosis. Also seen post meningitis sometimes
  • Causes early loss of P/T most likely in cervicothoracic area in cape like distribution
  • Later may involve lateral horns and horners and motor LMN signs
127
Q

Freidrichs ataxia

A
  • trinucleotide repeat in protien that regulates Fe-S complexes in the mitochondria.
  • Leads to cell death especially of cerebellar tracts
  • Ataxia, pez kavus, kyphoscoliosis,
  • Hypertrophic cardiomyopathy is cause of death
128
Q

Brown Sequard

A
  • Think about lesions.

- Will show complete loss at level of lesion and LMN signs will dominate UMN

129
Q

Horners

A

-Post hypothal to lateral horns to prevertebral ganglia to stellate ganglia 3rd order to eye along internal carotid and to eye via the long cilliary (B2 leads to production of aqueos humor and dilation of eye)

130
Q

Reflexes

A
  • S1 achiles
  • L4 Patellar
  • C5,6 is biceps
  • C7,8 is triceps
131
Q

Babinski

A

-Dorsiflexion is babinski, is pathalogic and a sign of upper motor neuron injury

132
Q

0-6 months

A
  • Loss of primative moro reflex etc

- Social smile, orients to sound

133
Q

7-9 months

A

-Stranger anxiety, sits, transfers toys

134
Q

12-15 months

A

-Loss babinski, separation anxiety, begins to walk

135
Q

2 years

A

Climbs stairs and stacks blocks. 200 words

136
Q

3 years

A

-Rides tricycle, learns to pee, copies line and circle, paralleel play, core gender identitiy. 900 words

137
Q

4 years

A

-Cooperative play, tells stories, can groom himself

138
Q

Pineal gland

A
  • normally secretes melatonin
  • Tumor can be dygerminomat that can compress superior colliculus and lead to impaired vertical gaze
  • May cause precocious puberty
139
Q

Superior Colliculus

A

-Vertical gaze conjugate

140
Q

Inferior colliculus

A

-Auditory relay

141
Q

Nucleus Solitarius

A
  • Visceral sensory information

- Taste, GI, carotid receptors

142
Q

Ambiggus

A
  • Somatic Motor
  • Muscles to larynx and palate (superior and recurrent laryngeal nerves)
  • Lesion leads to uvula pointing away from lesion. Normally contract to pull uvula towards
143
Q

Dorsal Motor

A
  • PANS output to 10

- Heart, lungs, upper GI

144
Q

Cribiform Plate

A

CN1

-Entry for naigei fowleri and rhizopus

145
Q

Middle Cranial Fossa

A

CN2 through orbital canal with retinal vein and artery and opthalmic artery
-CN 3, 4, V1, V2, 6, SANS run through the cavernous sinus
-CN 3, 4, V1, 6 and opthalmic vein run through superior orbital fissure
-CN V2 branches, pterygoid ganglion, and branches of maxillary run through inferior orbital fissure
-V2 runs through rotindum
-V3 runs through ovale
-Spinosum (Maxillary and middle meningeal)
Posterior Cranial Foss
-7,8: through internal acoustic meatus with 7 exiting in styloid foramen
-9,10,11 run out jugular foramen
-12 runs out hypoglossal canal
-Foramen magum also carries parts of 11

146
Q

Cavernous Sinus

A

Carries internal carotid and SANS to long cilliary

  • Also carries 3, 4, V1, V2, 6
  • Thrombosis can occur because of internal carotid anyeurism. Also a common site of infection with cutaneous bugs (Staph and strep)
  • Syndrome is characterized by opthalmoplegia with fixed dilated pupil with normal vision because 2 does not pass through canal
  • Borders the pituitary on both sides
147
Q

CN 5 lesion

A

Jaw points towards the side of the lesion
-Unopposed action of the lateral pterygoid whih pushes out.
All other muscles of mastication close the mouth

148
Q

CN10

A
  • Uvula points away from the lesion

- Normal function is to contact and pull towards, loss leaves other side unopposed

149
Q

CN11

A
  • Paralysis of SCM which normally functions to turn the head to the contralateral side
  • Lesion leads to inability to turn contralaterally, and head will tend to look towards side of lesion
150
Q

CN12

A
  • Tongue will deviate towards the lesion
  • Action of tongue muscles is to stick tongue out. Lesion leads to unopposed action and sticking out towards lesioned side
151
Q

CN 7 lesions

A
  • Forehead recieves bilateral innervation. Therefore a lesion to the UMN will leave motor to the forehead intact. Occurs with damage to cortex or to genu of internal capsule. Damage will be contralateral to the lesion
  • Lesion at LMN or nucleus leads to loss of complete function ipsilaterally.
  • If the lesion is distal in neuron there can be maintained special senses due to travel along other neurons. Don’t count on it though
  • Can occur idiopathically, with Lyme, DM, AIDS, Infection, Tumor (Parotid especially), HSV
152
Q

Hyperopia

A
  • Farsighted ness

- Can’t see close objects but can see far. Focus occurs behind the retina

153
Q

Myopia

A
  • Nearsightedness

- Can’t see far but can see close. Focus occurs in front of retina

154
Q

Astigmatism

A

-Odd shape of lens leads to different refractive powers at different distances

155
Q

Accomidation

A
  • Controlled by PANS of CN 3 originating in Ed West nucleus.
  • Ciliary muscle (M3) contraction leads to relaxation of zonular fibers and the elasticity of the lens is allowed to cause it to round and recoil, allowing for focus on close objects
  • This will also decrease the tension between the lens and the iris, opens angle.
  • Anticholinergics block M3 and can lead to loss of contriction and acute angle closure.
  • Angle closure can be treated with pilocarpine or other cholinergic agonists
156
Q

Uveitis

A
  • Inflammation of the choiroid, cilliar body, iris
  • Most associated with systemic inflammatory conditions
  • Seen in B27, Rheumatoid Arthritis (especially juvenile), Sarcoidosis, TB, etc
157
Q

Presbyopia

A

-Occurs because of sclerosis and loss of elastic recoil of lens. Leads to inability of lens to “cinkle” in response to reduced zonular tension. Can’t focus on near objects

158
Q

Retinitis

A
  • Usually caused by a herepes familiy virus or toxo in immunosupressed state (HSV, CMV, VZV)
  • Also common with TORCH syndromes
159
Q

Central Retinal Artery Occlusion

A

Artery is a direct branch of opthalmic off internal carotid, accompanies CN2 through orbital canal

  • Leads to acute, painless blindness with retinal palor and a cherry red macula (Thrombosis or blockage of macula leads to decreased perfsion peripherally and red at artery)
  • Complication of Temporal arteritis
160
Q

Aqueous Humor

A

-Produced by ciliary epithelium in response to beta 2 stimulation, flows through Iris/Lens interface into canals of schlemm

161
Q

Open angle glaucoma

A

Flow is reduced leading to increaed ICP and progressive ischemic death to peripheral ganglion cells leading to tunnel vision

  • On exam there will be an increased cup to disc ratio
  • Causes: Steroids, trauma, AA race, vasoproliferative diseases, uveitis
162
Q

Closed angle glaucoma

A
  • Increased fluid pushes lens against Iris which is pressed against cornea and obstructs outflow to the canal of schlemm
  • Emergency, painful loss of vision and headache with rock hard eyes
  • Can be precipitated by anticholinergics (Cause loss of constrition of ciliary muscle), or epinephrine, causing increase production and dilation
  • Treat with pilocarpine to open angle
163
Q

Cataract

A
  • Accumulation and opacification of lens
  • Most commonly related to age, sun exposure, DM2 (Soribitol), galactosemia (galacticol), steroid use, smoking, infection
164
Q

Papilledema

A
  • Increased ICP leads to bulging of disk and blurring of borders, patients will complain of an enlarging blind spot
  • Tumor, hydrocephalus, malignant HTN
165
Q

Miosis

A
  • CN 3 PANS
  • First order neurons originate in Ed West nucleus in pre tectal are, send axons along CN 3 to ciliary ganglion
  • second order neurons are short ciliary ganglion to sphincter pupillae and ciliary body
166
Q

Mydriasis

A
  • SANS start in post hypothalamus and travel to cililary center of budge in C8-T1 IML
  • Second order neurons from Spinoceiliary center of budge to superior cervical ganglion
  • 3rd order travel with internal carotid through cavernous sinus to long ciliary and dilator pupillae and ciliary epithelila cells
167
Q

Pupillary Light Reflex

A
  • Afferent via CN2 to pretectal ed west nucleus
  • Ed west communicate with each other then out
  • Efferent CN3
168
Q

Afferent Pupullary Defect

A

Marcus Gunn pupil is from problem with afferent portion

-Retinal detachment or optic nerve damage

169
Q

CN3 functional units

A
  • Outer part is PANS and inner part is motor
  • Inner part more effected by DM and vascular issues. longterm DM can cause death and lead to proptosis and down and out pupil
  • Outer part PANS is vulnerable to compression from herniation of anyeurism of posterior Comm artery, and will result in a blown pupil (doesn’t respond to light)
170
Q

Retinal Structure

A

Choroid feeds deeped layer igmented epithelium which is maintained by vitamin A and is crucial for proper functioning of retina. Next layer is the Receptors (rods and cones) then the bipolar cells and the retinal ganglion cells that form to make the optic nerve

171
Q

Retinal Detachment

A

Retina is pulled away from pigmented epithelium and dies

  • Increaed risk in diabetics and patients with severe myopia
  • Leads to blindness and afferent pupullary defect
  • May be preceeded by floaters and curtains drawing down vision
172
Q

Macular Degeneration

A
  • Clinically will present as loss of central vision (scomatas)
  • Dry or exudative, from drussen or yellowish material that gets laid between the choroid and pigmented epithelium, results in progressive scomatas
  • Wet, can have a more rapid onset and is caused by neovascularization that occurs over the retina leading to scomata
  • Can be treated with lasers or anti-VEGF (BEvacizumab)
173
Q

Diabetic Retinopathy

A
  • Microvascular damage from sorbitol and glucose leads to death of pericytes and vascular dysfunction.
  • Then causes neovascularization of the retina that can be directly occluded or can bleed and cause a sudden rapid scomata appearance
  • On exam will show massive arterial proliferation in the retina
174
Q

Meyers Loop

A

Goes in the temporal lobe and takes the long way around the lateral ventricle.

  • Leads to pie in the sky superior quadrant contralateral hemianopia
  • MCA, lesions in temporal lobe such as tumor
175
Q

Dorsal Optic Radiatino

A

Runs in parietal lobe within the internal capsule to reach the occipital cortex

  • Lesions lead to inferior quadrant hemianopia
  • MCA is vascular supply
176
Q

INO

A

Connections with MLF between CN 3 and 6 to allow for smooth coordinated horizontal gaze. Lesioned in MS and demylinating diseases

  • Signal from cortex to gaze to the left leads to abducens activation on the left, but lesion to the right MLF prevents CN 3 and adductor to respond and leads to nystagmus of left eye
  • Named for the adductor that is dysfunctional. Left lateral gaze leads to left nystagmus is caused by right INO
177
Q

Alzhiemers

A
  • Accumulation of AB amyloid leads to neuronal cell death and widespread cortical atrophy
  • Generally occurs first in the hippocampus
  • APP is on chromosome 21, presenilin 1/2 are also hereditery forms. ApoE4 has increased liklihood and ApoE2 is protective
  • Extracellular neuritic plaques composed of amyloid and inflammatory cells
  • Intracellular NF tangles composed of hypophosphorylated Tau that stains with silver stain. Highly correlated with diease severity.
  • Begins with loss of memory and progresses to cognition, personality and motor problems and is eventially fatal
  • AB amyloid can accumulate in vasculature and leads to increased risk of hemorrhage.
  • Decreased Ach from meynert. Treatment is donepazil which is a centerally acting AchE inhibitor
178
Q

Picks Dementia

A
  • Frontotemporal dementia characterized by spherical intracellular tau aggregates that stain with silver stain.
  • Preferentailly effects frontal lobe and temporal lobe with sparing of parietal
  • Leads to early personality changes with memory coming later
  • Often also associated with parkinson like signs.
  • generally spares layers 3,5,6 and hits layers 2 and 4
179
Q

Lewy Body Dementia

A
  • Diffuse cortical lewy bodies composed of intacellular alpha synuclein and ubiquitin
  • Weird presentation with characteristic sign of hallucinations. There will also be high variablity between days
  • Also associated with parkinson like symptoms although lewy bodies occur in the cortex and spare the BG
180
Q

Crutzfeld Jacob

A

Caused by accumulaion og PrPsc (c) is normal. Beta pleated sheets induce other PrP to form aggregates

  • Rapid progression in weeks to months that is characterized by startle myoclonus and rapid cognitive and personality changes
  • Marked spongiform degeneration in gray matter
181
Q

Multi Infarct Dementia

A
  • Second most common to alzhiemers.

- Occurs in a step wise fashion in the context of clinical history

182
Q

HIV

A

Microglial cells are the host in the brain. Form large multinucleated giant cell aggregates
-Separate form infections an lymphomas that can occur in the brain.

183
Q

Wilsons Disease

A

Look for young age, liver damage and cerruloplasm levels

184
Q

B1, B3, B12

A

All can cause dementia, look for the proper clincal picture

185
Q

NPH

A
  • Rapid onset, in months or less
  • Urinary incontinence is hallmark
  • Wacky, Wobly, and Wet
186
Q

MS

A
  • Autoimmune, TH1 mediated destruction of oligodendrocytes and demylination of the central nervous system
  • Pateitns are usually child bearing white women and present with symptoms that are disseminated in time and space. Urinary incontinence and INO are classic
  • Lesions will show macrophages and lymphocytes with reactive gliosis. There will be oligoclonal IgG banding in CSF
  • Lesions tend to occur periventricularly
  • Tx: IFN Beta, Nafalizumab (alpha 1 integrin inhibitor prevents lymphocytes from infiltrating BBB), steroids during acute attack, symptomatic treatment (Catheterization, baclofen, opiods, etc)
  • HLA DR2
187
Q

Acute Inflammatory Demylinating Polyradiculopathy

Guillan Bare

A
  • Post infectous (Campylobacter/CMV) leading to endonerial lymphocytic infiltaration and demylinatin
  • Caused by molecular mimicry of schwann cell antigens
  • PAtients will present with ascending paralysis and weakness that is symmetric and often involves the autonomics and facial nerves (Which can lead to facial palsies and hypo/hypertension and arrythmias)
  • CSF will show elevated protein without an increase in cell number
  • Increased protein can lead to papilledema
  • Treatment is supoortive, especially with ventilation and potentially autonomics
  • Plasmaphoresis and IVIG if patient is especially severe
188
Q

PML

A
  • Reactivatoin of JC virus (Polyoma) leads to destruction of oligodendrocytes and disseminated white matter demylination
  • Occurs in the context of severe immunosupression (HIV)
189
Q

Acute Disseminated Postinfectous Encephalitis

A
  • Post infection (Commonly VZV or measles) leads to perivenular demylination
  • Can also occur following vaccinations
190
Q

Metachromatic Leukodystrophy

A
  • AR defect in arylsulfatase leads to accumulation of myelin and destruction of function (Can’t degrade and recycle)
  • Normal development for 6 months to 2 years and then progessive decline until death
191
Q

CMT

A
  • Hereditary Sensory and Motor Ataxia
  • Group of disorders that primarily effects myline and nerve conduction in the peripheral nerves
  • Most common symptoms are foot drop due to involvment of deep peroneal
192
Q

Krabbes Disease

A
  • AR defect in galactocerebrosidase
  • PAS positive macrophages
  • Symptoms are dominated by peipheral neuropathy that may progress to decerebate posturing and death usually by 2 years
  • Optic nerve atrophy is also commonly seen
  • Can be treated with BM transplant
193
Q

Siezures

A
  • Characterized by synchronus high frequency firing, generally originating in the temporal lobe
  • Partial: Firing located in a single area. Simple there will be no loss of conciousness and complex there will be loss of conciousness
  • Overall Causes. In young think congential malformation, febrile(doesn’t count towards epilepsy). Elderly think stroke, tumor, trauma, and metabolic in the context of other clinical findings.
194
Q

Diffuse Siezures

A
  • Involve the entire cortex
  • Absence: No motion and there is no post-ictal state
  • Tonic Clonic: Motion and post ictal state
195
Q

Epilepsy

A

Multiple siezures disorder, febrile siezures don’t count

196
Q

Status epilepticus

A
  • Siezure activity for greater than 30 mins

- Tx with benzos and phenytoin

197
Q

Cluster Headache

A
  • Begins with periorbital pain that is associated with lacrimation or rhinirrhea
  • Occurs in repetive waves for 15 mins to 4 hours. Use time to distinguish between trigeminal neuralgia
  • Abortive treatment is tryptans and oxygen
198
Q

Tension Headache

A

Repetetive stable pain without aura etc that lasts form 30 mins to 4 hours

199
Q

Migrane

A

Vasodilation and contriction leads to irritation of meninges and CN5 innervation

  • Release of vasoactive substances (substance P and CGRP)
  • Preceded by aura and associated with photophobia and N/V
  • Can last from 4 hours to 3 days
  • Abortive therapy is triptans or egtamines and prophylaxis is beta blockers and topirimate
200
Q

Peripheral Vertigo

A
  • Caused by pathology in inner ear

- Will lead to mild nystagmus that is delayed on position testing

201
Q

Central Vertigo

A
  • Caused by lesion to vestibular nuclei or cerebellum (AICA, PICA, Tumor)
  • Pronounced diplopia and nystagmus at rest and that may change direction during positional testing
202
Q

Menieres Dease

A

Endolymphatic hydrops leads to vertigo, tinnitus, hearing loss
-Most commonly occurs post viral

203
Q

Sturge Webber

A
  • Postzygotic activating mutation in GNAC leading to vascular proliferation subcutaneously leading to nevusflammeus along the path of V1. Unilateral
  • Associated with leptomeningeal angiomas, pheochromocytomas,
  • May show with siezures, glaucoma, retardation, hemiparesis
204
Q

Tuberous Sclerosis

A
  • TSG mutation leading to hamartomas throughout body
  • Giant Cell astrocytomas, Cardiac Rhabdomyomas, Renal angiolipomas, Cutaneous sebacous adenomas, Ash leaf spots of hypopigmentation (loss melanin, woods lamp)
  • Mitral Regurg AD, Siezures and mental retardation possible
205
Q

NF-1

A
  • MUtatino in TSG on chrom 17 leads to activation of RAS
  • Cutanseous neurofibromas, Pheo, Lisch Nodules, cafe au lait spots, otic gliomas
  • 100 % penetrane with variable expresivity
206
Q

NF-2

A

Merlin on Chrom 22

207
Q

VHL

A
  • Chrom 3 leads to dysfunction of ubiquitin ligase and increased HIF
  • Bilateral renal cell carcinomas leading to EPO and polycythemia
  • Cerebral hemangiomas
  • Pheochromocytomas
208
Q

GBM

A

Cerebral hemisphere, Necrosis with odd cells, GFAP. Poor prognosis, proliferation of blood vessels (PDGF)

209
Q

Meningioma

A

Arachnoid cells, focal symptoms from dura

  • ER more common in women
  • Spindle cells with psammoma bodies
210
Q

Schwannoma

A
  • NC derived leads to S-100 positivity

- Cerebellopontnie angle leasd to 5,7,8 compression

211
Q

Oligodendrogliom

A

-Occur more commonly in frotal lobe, siezures are common presentation
-Calcifications are also commonly seen
Fried egg

212
Q

Pitutary adenoma

A

Most are nonsecreting can be PRL

213
Q

Metastasis

A

-Gray white boundary and multiple

Most common from lung, breast, kidney

214
Q

Pilocytic Astrocytoma

A

-Eosinophilic processes (rosenthal fibers)
-POsterio fossa in kids, GFAP positive
-Fibrillary Astrocytoma is between pilocytic and GBM
-Can cause hyddrpcephalus
-Cyst and nodule
Increased risk in NF-1, benign in comparison

215
Q

MEdulloblastoma

A

Primative neuroectodermal tumor

  • Small blue cells that form pseudorosettes around neuritic processes. Makes sense because primative cells are congregated around mature neural cells
  • Malignant and grows rapidly
  • May have drop metastasis and often compresses 4th vent leading to hydrocephalus
  • granular cells
216
Q

Ependymoma

A
  • Increased risk with NF-2
  • Ependmal cells, poor prognosis that often present with hydrocephalus
  • Pseudorosettes that occur perivasculararly (Makes sense in comparison to medulloblastoma because that is th normal funcion.)
217
Q

Hemangioblastoma

A
  • Associated with VHL
  • Causes siezures and may bleed, highly associated with retinal artery angioma
  • EPO can cause secondary PV
218
Q

Craniopharyngoma

A

Most common supratentorial in kids

  • Calcifications common (Enamal)
  • Often recurs after resection, cause of bitemporal hemianopia
219
Q

Subfalcine herniation

A
  • Cingulate gyrus

- Anterior cerebral artery compression

220
Q

UNcal and transtentorial

A

-Uncus is medal temporal lobe
compress CN3
And PCA

221
Q

Cereballar tonsilar hernation

A

Duret hemorrhages leads to coma and death becaues of compression of the brain stem
-Laceration of pontine peforating branches

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