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Neurology > Neurology- Embryology and Physiology- FA > Flashcards

Neurology- Embryology and Physiology- FA Flashcards

1
Q

Notochord induces

A

Ectoderm –> neuroectoderm and neural plate

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2
Q

Neural plate becomes

A

neural tube and neural crest cells

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3
Q

Notocord becomes

A

nucleus pulpous of intervertebral disc in adult

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4
Q

Alar plate (dorsal)

A

sensory

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5
Q

Basal plate (ventral)

A

motor

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6
Q

Forebrain (prosencephalon)

A

Telencephalon –> cerebral hemispheres & lateral ventricles

Diencephalon –> Thalamus and hypothalamus & third ventricle

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7
Q

Midbrain (mesencephalon)

A

Mesencephalon –> Midbrain & aqueduct

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8
Q

Hindbrain (rhombencephalon)

A

Metencephalon –> Pons and cerebellum & upper part of 4th ventricle

Myelencephalon –> Medulla & lower part of 4th ventricle

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9
Q

Neuroectoderm becomes

A

CNS neurons, ependymal cell (make CSF), oligodendroglia, astrocytes

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10
Q

Neural crest

A

PNS neurons and Schwann cells

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11
Q

Mesoderm

A

Microglia (macrophages of the CNS)

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12
Q

Neural tube defects

A

NEUROPORES fail to fuse (4th week); persistent connection between amniotic cavity and spinal canal

Associated with low folic acid and high alpha-fetoprotein and high acetylcholinesterase

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13
Q

Spina bifida occulta

A

Most mild; failure of bony spinal canal to close, but no herniation

Usually seen at lower vertebral levels and dural is intact

Normal AFP; hair or skin dimple may be seen above region

Folic acid helps if given before the 28th day

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14
Q

Meningocele

A

Meninges/ dura (but no neural tissue) herniate

Skin defect/ thinning seen on surface

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15
Q

Meningomyelocele

A

Meninges and neural tissue (spinal cord/ cauda equina) herniate

Skin thin or absent

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16
Q

Anencephaly

A

Malformation of anterior neural tube; no forebrain

Associated with increased AFP and polyhydramnios

Associated with Type I diabetes

Decreased risk with maternal folate supplementation

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17
Q

Holoprosencephaly

A

Failure of left and right hemispheres to separate

Usually occurs during weeks 5-6

Related to mutations in Sonic Hedgehog pathway

Ranges from cleft lip/palate –> cyclopean

Seen in Patau syndrome and fetal alcohol syndrome

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18
Q

Chiari II malformation

A

herniation of low-lying cerebellar VERMIS through foramen magnum with aqueduct stenosis –> hydrocephalus

Generally associated with meningomyelocele and paralysis/sensory loss at and below the level of the lesion

Typically presents at childhood (as opposed to Chiari I malformation- where tonsils herniate)

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19
Q

Dandy Walker

A

Agenesis of cerebellar vermis with cystic enlargement of the fourth ventricle (fills the posterior fossa)

Associated with noncommunicating hydrocephalus (obstruction) and spina bifida

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20
Q

Syringomyelia

A

Fluid filled cavity within the spinal cord (vs. syrigobulbia- medulla/ lower brainstem)

Fissures crossing in the anterior white commissure (spinothalamic tract- pain and temp) are typically damaged first

Associated with Chiari malformations, trauma, and tumors

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21
Q

Syringobulbia

A

Fluid filled cavity within the medulla or lower brainstem

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22
Q

Syringomyelia S&S

A

Cape-like loss of pain and temp (bilateral and affects upper extremities); with normal fine touch

Most commonly affects C8-T1

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23
Q

Chiari I malformation

A

Cerebellar TONSILLAR ectopia; congenital, but usually asymptomatic in children

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24
Q

Chiari I- S&S

A

Occipital headache and cerebellar dysfunction that may worsen with Valsalva

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25
Q

Tongue development- anterior

A

Anterior (arches 1 and 2)

Sensation: V3
Taste: VII
Motor: XII (protrudes tongue)

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26
Q

Tongue development- posterior

A

Posterior (arches 3 and 4)

Sensation and taste: IX (far back & uvula- X)
Motor: X (elevates posterior tongue during swallowing)

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27
Q

Tongue- Taste, Pain, and Motor (summary)

A

Taste: VII, IX, X
Pain V3, IX, X
Motor: X, XII

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28
Q

Neurons

A

Signal-transmitting cells of NS

Permanent/ do not divide

Cell bodies and dendrites IDed through Nissl staining (stains RER)

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29
Q

Wallerian degeneration

A

Injury to axon causes degeneration distal to injury and axonal retraction proximally (allows for regeneration of axon- if in PNS)

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30
Q

Astrocytes

A 
Physical support
Repair K+ metabolism
Remove excess neurotransmitter
Component of BBB
Glycogen fuel reserve buffer

Astrocyte marker: GFAP

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31
Q

Microglia

A

Phagocytic scavenger of cells of CNS (mesodermal and mononuclear origin)- activate in response to tissue damage

HIV-infected microglia fuse to form multinucleated giant cells (HIV encephalitis)

vs. JC virus- infects oligodendrocytes

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32
Q

Myelin

A

Increases conduction velocity of transmitted signals (and increases space constant)

CNS: oligodendrocytes
PNS: Schwann cells

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33
Q

Nodes of Ranvier

A

Gaps of myelin sheath where there are high concentrations of Na+ channels (where Na+ flows into neuron)- allowing for saltatory conduction of action potentials (boosters??)

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34
Q

Schwann cells

A

Each cell myelinates ONE PNS axon (vs. multiple and CNS for oligodendrocytes)

Derived from neural crest

Promotes axonal regeneration

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35
Q

Guillian Barre

A

Causes injury to Schwann cells

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36
Q

Vestibular schwannoma (aka acoustic neuroma)

A

Typically located on CN VIII in internal acoustic meatus –> may extend to cerebellopontine angle

S&S: progressive hearing loss and impaired balance

Bilateral acoustic neuroma- Seen in NF Type II (affects myelination of peripheral neurons)

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37
Q

Oligodendroglia

A

Myelinates axons of neurons in CNS (each oligo can myelinated about 30 axones)

Seen in white matter

Fried egg appearance in histology

Injured in MS and progressive multifocal leukoencephalopathy (PML), leukodystrophies (degeneration of white matter)

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38
Q

Sensory receptors: Free nerve endings- fiber type

A

C- slow unmyelinated

Adelta- fast myelinated

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39
Q

Sensory receptors: Free nerve endings- location

A

All skin, epidermis, some viscera

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40
Q

Sensory receptors: Free nerve endings- sensation

A

Pain and temp

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41
Q

Sensory receptors: Meissner corpuscles- fiber type

A

Large, myelinated fibers, adapt quickly

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42
Q

Sensory receptors: Meissner corpuscles- location

A

Glabrous skin (hairless)

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43
Q

Sensory receptors: Meissner corpuscles- sensation

A

Dynamic, fine/light touch, position sense, low-frequency vibration

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44
Q

Sensory receptors: Pacinian corpuscles- fiber type

A

Large, myelinated fibers, adapt quickly

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45
Q

Sensory receptors: Pacinian corpuscles- location

A

Deep skin layers, ligaments

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46
Q

Sensory receptors: Pacinian corpuscles- sensation

A

Deep/coarse touch, vibration, pressure

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47
Q

Sensory receptors: Merkel discs- fiber type

A

Large, myelinated fibers, adapt quickly

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48
Q

Sensory receptor: Merkel discs- location

A

Finger tips, superficial skin

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49
Q

Sensory receptor: Merkel discs- sensation

A

Sustained pressure, deep static touch (e.g. shapes, edges), position sense

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50
Q

Sensory receptor: Ruffini corpuscles- fiber type

A

Dendritic ending with capsule, adapt slowly

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51
Q

Sensory receptor: Ruffini corpuscles- location

A

Finger tip, joints

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52
Q

Sensory receptor: Ruffini corpuscles- sensation

A

Sustained pressure, slippage of objects along surface of skin, joint angle change

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53
Q

Peripheral nerve (3 layers)- endoneurium

A

Endoneurium: layer around a single nerve fiber, inner (inflamed in Guillain-Barre)

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54
Q

Peripheral nerve (3 layers)- perineurium

A

Perineurium: Permeability barrier (surrounds fascicle of nerve fibers)- must be rejoined during surgery for limb attachment

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55
Q

Peripheral nerve (3 layers)- epineurium

A

Epineurium: dense connective tissue that surrounds entire nerve (includes many fascicles and blood vessels)

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56
Q

Unmyelinated vs. myelinated

A

Unmyelinated- smaller diameters, conduct more SLOWLY

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57
Q

Examples of unmyelinated fibers

A

afferent neurons that conduct heat sensation, burning, visceral pain
efferent autonomic POST-ganglionic nuerons
first order bipolar sensory neurons of olfaction

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58
Q

NTs- ACh

A

Synthesized in basal nucleus of Meynert (superior and lateral to hypothalamus)

Decreased in Alzheimers, Huntington, and Parkinsons

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59
Q

NTs- Dopamine

A

Synthesized in ventral tegmentum, SNpc (midbrain)

Increased in Schizophrenia and Huntington

Decreased in Parkinsons and Depression

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60
Q

NTs- GABA

A

Synthesized in nucleus accumbens (basal forebrain, above hypothalamus)

Decreased in anxiety and Huntingtons

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61
Q

NTs- NE

A

Synthesized in locus ceruleus (pons)

Increased in anxiety

Decreased in depression

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62
Q

NTs- Serotonin

A

Synthesized in raphe nucleus (brainstem)

Decreased in depression and ANXIETY (which is why SSRIs are a tx for both of these condns)

Increased in Parkinsons

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63
Q

Blood brain barrier

A

Formed by three structures:
Astrocyte foot processes
Tight junctions between endothelial cells (non-fenestrated)
Basement membrane

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64
Q

BBB- transport

A

Glucose and AAs- by carrier mediated transport mechanisms

Nonpolar/ lipid-soluble: passive diffusion

Hydrophilic mcs require carrier proteins

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65
Q

Specialized regions without BBB

A

Area postrema- medulla (vomiting after chemo)

OVLT (vascular organ of lamina terminalis)- anteroventral third ventricular region (osmotic sensing)

Neurohypophysis/ posterior pituitary- secrets ADH

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66
Q

Vasogenic edema

A

Caused by destruction of endothelial cell tight junctions

Causes: infarction or neoplasm

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67
Q

Important blood/ tissue barriers

A

Blood-brain barrier
Blood-testes barrier
Maternal/ fetal blood barrier of placenta

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68
Q

Hypothalamus- TANHATS

A

Thirst and water balance
Adenohypophysis- regulates anterior pituitary
Neurohypophysis (posterior pituitary)- releases hormones produced in hypothalamus
Hunger
Autonomic regulation
Temperature regulation
Sexual urges

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69
Q

Inputs to hypothalamus (area not protected by BBB)

A

Supraoptic nucleus (makes ADH)
OVLT: regulate osmolarity
Area postrema: found in medulla, responds to emetics

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70
Q

Supraoptic nucleus (hypothalamus)

A

makes ADH

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71
Q

Paraventricular nucleus (hypothalamus)

A

makes oxytocin

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72
Q

Neurophysins

A

Carry ADH and oxytocin down axons to posterior pituitary

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73
Q

Lateral area of hypothalamus

A

Hunger

Destruction –> anorexia, failure to thrive (destruction of lateral hypothalamus makes you shrink laterally)

Stimulated by ghrelin, inhibited by leptin

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74
Q

Ventromedial area of hypothalamus

A

Satiety

Destruction (e.g. craniopharyngioma) –> hyperphagia (if you destroy the ventromedial area of the hypothalamus, it makes you shrink ventrally and medially)

Stimulated by leptin

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75
Q

Anterior hypothalamus

A

Cooling, parasympathetic

Anterior nucleus- Cooling (AC); pArasympathetic- when you rest and digest- you COOL down

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76
Q

Posterior hypothalamus

A

Heating, sympathetic

When you exercise (increase sympathetic response), you back (posterior) gets hot

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77
Q

Suprachiasmatic nucleus

A

Circadian rhythm

You need to sleep to be charismatic (schismatic)

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78
Q

Chemoreceptor Trigger Zone

A

Located within the area postrema of the medulla (floor of the 4th ventricle)

Vomiting control center

Prochlorperazine is an anti-emetic that suppresses dopamine release at the CTZ

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79
Q

Sleep physiology

A

Regulated by the circadian rhythm (suprachiasmatic nucleus)

Controls nocturnal release of ACTH, prolactin, melatonin and NE

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80
Q

Path of melatonin release

A

SCN –> NE release –> pineal gland –> melatonin

Where SCN is regulated by environment (light)

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81
Q

Two main stages of sleep

A

REM and non-REM

Eyes move in REM sleep due to activity of the PPRF (paramedic pontine reticular formation/ conjugate gaze center)

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82
Q

REM

A

occurs every 90 minutes

INCREASED ACh during REM sleep

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83
Q

Things that decreases REM sleep

A

alcohol, benzos, and barbs (also decrease delta wave sleep- Stage N3 of non-REM sleep)

NE (doesn’t have effect on N3, but decreases REM)

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84
Q

Bedwetting

A

Tends to occur during N3 Stage of sleep

Tx with desmopressin (rather than imipramine- more SEs)

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85
Q

Night terrors, sleep walking

A

Also occur during N3 stage of sleep

Tx with benzos (decreases N3 stage of sleep)

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86
Q

Awake (eyes open)

A

Alert, active; beta waves (high frequency, low amplitude)

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87
Q

Awake (eyes closed)

A

Alpha waves (lower frequency than beta, low amplitude)

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88
Q

Non -REM sleep: N1

A

Light sleep; Theta waves (hallucinations, hypnogogic)

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89
Q

Non-REM sleep: N2

A

Deeper sleep; sleep spindles and K waves (jaw-clenching/ bruxism)

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90
Q

Non-REM sleep: N3

A

Deepest non-REM sleep; delta waves (low frequency, highest amplitude)

Associated with sleep-walking, night terrors, bed wetting

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91
Q

REM sleep

A

Loss of motor tone, increased brain O2 use, variable pulse and BP

Dreaming, nightmares, and penile/clitoral tumescence

May serve memory processing function

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92
Q

Sleep cycle

A

N1 –> N2 –> N3 –> N2 –> REM –> N1 …

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93
Q

Wave mnemonic: BATS Drink Blood

A 
Awake- eyes open (beta)
Awake- eyes closed (alpha)
Sleep- N1 (theta)
Sleep- N2 (sleep spindles & K waves)
Sleep- N3 (delta)
Sleep- REM (beta)
94
Q

Thalamus

A

Major relay for all ascending sensory info (EXCEPT olfaction)

95
Q

Ventral posterolateral (VPL) thalamus

A

Spinothalamic and DCML –> primary somatosensory cortex

Senses: ST (pain and temp) & DCML (position, touch, vibration, pressure, proprioception)

96
Q

Ventral posteromedial (VML) thalamus

A

Trigeminal and gustatory –> Primary somatosensory cortex

Senses: Face and taste

97
Q

Lateral geniculate nucleus (LGN)

A

CN II –> Calacrine sulcus

Senses: vision

98
Q

Medial geniculate nucleus (MGN)

A

Superior olive and interior colliculus of tectum –> Temporal lobe (auditory cortex)

Senses: Hearing

MGM (MGN) studios has a lot of sounds and music that we HEAR

99
Q

Ventral lateral nucleus (NOT VPL)

A

Basal ganglia, cerebellum –> Motor cortex

Senses: Motor

100
Q

Limbic system- 5 Fs

A 
Feeding
Fleeing
Fighting
Feeling
Sex

Neurons involved in emotion, long-term memory, olfaction, behavior modulation, ANS function

101
Q

Limbic system- components

A 
Hippocampus
Amygdala
Fornix
Mammillary bodies
Cingulate gyrus
102
Q

Dopaminergic pathways- MMNT

A

Mesocortical (decreased)
Mesolimbic (increased)
Nigrostriatal (decreased)
Tuberoinfundibular (decreased)

()- indicate response that causes altered activity

103
Q

Mesocortical- symptoms of alteration

A

Decreased activity –> “negative” symptoms (flat affect)

Antipsychotics not very effective; atypical better than typical antipsychotics

104
Q

Mesolimbic- alteration

A

Increased activity –> “positive” symptoms (delusions, hallucinations)

Main target of antipsychotics (spec. typical)- tx for schizophrenia

105
Q

Nigrostriatal- alteration

A

Decreased activity- extrapyramidal symptoms (dystonia (involuntary muscle contractions), akathisia (inner restlessness), parkinsonism, tardive dyskinesia)

Significantly affected by movement disorders and antipsychotics (which induce these symptoms)

106
Q

Tuberoinfundibular- alteration

A

Decreased activity- increased prolactin, decreased libido, sexual dysfunction, galactorrhea, and gynecomastia (in men)

Remember from endocrine: prolactin is inhibited by dopamine and prolactin suppresses GnRH axis

107
Q

Cerebellum- role

A

Modulates movement; aids in coordination and balance

Somatotopic distrubution

108
Q

Cerebellum- input

A 
CONTRALATERAL cortex (via middle cerebellar peduncle)
IPSILATERAL proprioception (via inferior cerebellar peduncle/ spinal cord)
109
Q

Cerebellum- output

A

Info sent to CONTRALATERAL motor cortex

(Purkinje cells –> deep nuclei of cerebellum –> contralateral cortex) via superior cerebellar peduncle

110
Q

Deep nuclei of cerebellum

A 
from lateral to medial
Dentate
Emboliform 
Globose
Fastigial

Emboliform and globose together make the interposed nucleus

111
Q

Lateral lesions

A

affect VOLUNTARY movement of extremities

causes IPSILATERAL weakness

112
Q

Medial lesions

A

involves midline structures (vermal cortex, fastigial nucleus) and flocculonodular lobe (vestibular system)

causes truncal ataxia, nystagmus, head tilting

generally results in bilateral motor deficits (affects axial and proximal limbs)

113
Q

Basal ganglia

A

Responsible for voluntary movements and postural adjustments

114
Q

Basal ganglia- input

A

from cortex

115
Q

Basal ganglia- output

A

back to cortex (negative feedback to modulate movement)

116
Q

Striatum

A

putamen (motor) and caudate (cognitive)

117
Q

Lentiform

A

putamen (motor) and globus pallidus

118
Q

Direct pathway

A

Movement is activated in the presence of dopamine (acts at D1 receptors to facilitate movement)

SN releases DA –> acts at D1 receptors –> stimulates striatum to release GABA –> inhibits GABA release from GPi –> Thalamus becomes disinhibited and movement is allowed

119
Q

Indirect pathway

A

When dopamine is not present: indirect pathway inhibits movement

Without dopamine acting on D2 receptors –> Striatum stimulated to release GABA –> inhibits GABA release from the GPe –> Causes stimulation of STN (glutaminergic) –> stimulates GABA release from the GPi –> Thalamus is inhibited and movement is halted

120
Q

Effect of Dopamine

A

Binds to D1 receptors to STIMULATE the excitatory pathway

Binds to D2 receptors to INHIBIT the inhibitory pathway

121
Q

Athetosis

A

Writhing

Lesion in basal ganglia

122
Q

Chorea

A

Sudden, jerky movements

Lesion in basal ganglia

123
Q

Dystonia

A

Involuntary muscle contractions

124
Q

Essential tremor

A

High frequency tremor with sustained posture

Worsened with movement

Tx: non-selective beta blockers, primidone

125
Q

Hemiballismus

A

Sudden, flailing arm

Lesion in CONTRALATERAL subthalamic nucleus

126
Q

Intention tremor

A

Slow, zig-zag motion when pointing/ moving toward target

Sign of cerebellar dysfunction (on ipsilateral side???)

127
Q

Myoclonus

A

Sudden, brief uncontrolled muscle contraction (e.g. jerks, hiccups)

vs. dystonia (which is sustained contractions)

128
Q

Resting tremor

A

Uncontrolled movement of distal appendages (e.g. hands)

Gets better with movement

Seen in Parkinson dz (pill-rolling)

129
Q

Parkinson dz symptoms- TRAPS

A 
Tremor (resting/ pill-rolling)
Rigidity (cogwheel)
Akinesia (or bradykinesia)
Postural instability
Shuffling gait
130
Q

Parkinson dz characteristics

A 
Lewi bodies (with alpha-synuclein deposits- eosinophilic inclusions)
Caused by neuron damage and loss of dopaminergic neurons of substantia nigra
131
Q

Huntington dz- S&S

A

choreiform movements, aggression, depression, and dementia (may be mistaken for substance abuse)

Often seen between 20 and 50

132
Q

Huntington dz characteristics

A

Expansion of CAG repeats- Caudate loses ACh and GABA (C-A-G)

Caused by atrophy of caudate and putamen (striatum)

Increased dopamine, decreased GABA and ACh

Neuronal death caused by NMDA-R binding and glutamate excitotoxicity

133
Q

Sensory vs. motor cortex

A

Sense BEFORE (somatosensory- posterior) you move (motor- anterior)

134
Q

Broca area

A

Left inferior frontal lobe (speech)

135
Q

Wernicke area

A

Left superior temporal lobe (comprehension)

136
Q

Arcuate fasciculus

A

connection between Broca and Wernicke area

137
Q

Aphasia vs. dysarthria

A

Aphasia: Higher order language (read/ speak/ write/ understand)

Dysarthria- cannot move vocal cords (motor deficit)

138
Q

Broca Aphasia

A

Cannot: speak & repeat

Can: understand

139
Q

Wernicke Aphasia

A

Cannot: Understand & repeat

Can: Speak (doesn’t make sense)- but lack insight about their problem

140
Q

Conduction Aphasia

A

Cannot: Repeat

Can: Speak, Understand

Arcuate fasiculus damage

141
Q

Global Aphasia

A

Cannot: repeat, speak, or understand

B, W, and AF damaged

142
Q

Transcortical- region near Broca/ Wernicke damaged but some of these regions are spared (repetition is not lost)

A

Motor (anterior)- near Broca –> cannot speak, but can repeat

Sensory (posterior)- near Wernicke –> cannot understand, but can repeat

Mixed- cannot speak or understand, but can repeat

143
Q

Amygdala lesion

A

Kluver-Bucy syndrome (disinhibited behavior- hyperphagia, hyper sexuality, hyperorality)

144
Q

Frontal lobe lesion

A

Disinhibition and concentration & judgement probs

May have reemergence of primitive reflexes

145
Q

Non-dominant parietal cortex lesion

A

Hemispatial neglect (ignores contralateral side)- more commonly left sided neglect (due to right parietal lobe (non-dominant) injury- because right and left parietal lobe covers right side, but only right parietal lobe covers left side)

In other words, the right parietal lobe covers both sides, and the left parietal lobe covers only the right side –> because it has a lot of other responsibilities (mathematics, writing, etc)

146
Q

Dominant parietal cortex lesion

A

Agraphia, acalculia, finger agnosia (cannot recognize things), left-right disorientation

147
Q

Reticular activating system (midbrain) lesions

A

Reduced levels of arousal/ wakefulness

148
Q

Mamillary bodies (bilateral) lesions

A

Wernicke-Korsakoff (W: confusion, ophthalmoplegia, ataxia vs. K: amnesia (anterograde&raquo_space; retrograde), confabulation, personality changes)

Associated with B1 (thiamine deficiency) and excess alcohol

149
Q

Wernicke- CAN

A

Confusion
Ataxia
Nystagmus (ophthalmoplegia)

150
Q

Thiamine deficiency

A

W-K syndrome/ mammillary body lesions can be precipitated by giving glucose before giving B1 to someone who is deficient

151
Q

Basal ganglia lesions

A

Tremor at rest, chorea, athetosis (e.g. Parkinson, Huntington)

152
Q

Cerebellar hermisphere lesion

A

Intention tremor, limb ataxia, loss of balance (limbs- lateral- hemispheres)

Damage to cerebellum –> IPSILATERAL defects (falls toward the side of the lesion)

Can be seen with chronic alcohol use

153
Q

Cerebellar vermis lesion

A

Truncal ataxia, dysarthria (trunk- central/ midline- vermis)

154
Q

Subthalamic nucleus lesion

A

CONTRALATERAL hemiballismus

155
Q

Hippocampus (bilateral) lesion

A

Anterograde amnesia (can’t make new memories)

156
Q

Paramedial pontine reticular formation (PPRF) lesion

A

Eyes look AWAY from side of lesion

157
Q

Frontal eye field lesion

A

Eyes look TOWARD the side of lesion

158
Q

Homonculus (Medial to lateral)

A

Feet –> Hands –> Face –> Mouth

More innervation means more representation (e.g. hands, lips, etc.)

159
Q

Cerebral perfusion

A

Driven by pCO2 (not pO2!!!)

Relies on pressure gradient between MAP and ICP (if MAP is low, or ICP is high –> perfusion (pressure) decreases)

160
Q

Therapeutic hyperventilation

A

Hyperventilation –> Decreased pCO2 –> Vasoconstriction –> decrease cerebral blood flow and ICP

Used to treat cerebral edema

161
Q

Uncal herniation- classic signs

A

Single, fixed dilated pupil

162
Q

Classic signs of increased ICP

A

Coma, bradycardia, HTN (vasoconstriction to decrease ICP), hyperventilation (to decrease ICP), papilledema

163
Q

CPP (cerebral perfusion pressure)

A

CPP = MAP-ICP if CPP = 0; indicates there is no cerebral perfusion (can cause death)

164
Q

Watershed zones

A

Between anterior and middle cerebral

Between posterior and middle cerebral

165
Q

Anterior cerebral supplies

A

Legs (sensory and motor)

Injury causes CONTRALATERAL probs

166
Q

Middle cerebral supplies

A

Arms and face (sensory and motor)
Broca (frontal) and Wernicke (temporal) area

Injury causes CONTRALATERAL probs + aphasia (if dominant side injured) or hemineglect (if non-dominant side injured)

167
Q

Posterior cerebral supplies

A

Occipital cortex

Injury causes CONTRALATERAL hemianopia with macular sparing

168
Q

Lenticulostriate artery supplies

A

Striatum and internal capsule

Injury causes CONTRALATERAL motor and sensory probs to face and body

NO CORTICAL/CORTEX probs- like hemineglect, aphasia, visual field probs- as opposed to middle cerebral infarcts

Associated with lacunar infarcts (unmanaged HTN, smoking)

169
Q

Rule of 12’s

A

Ignore CN 1 and 2…

Medial- if it can divide into 12
Midbrain (3, 4); Pons (6); Medulla (12- tongue deviates ipsilaterally)

Lateral- all others

170
Q

Medial tract syndromes

A

Medial/ midline- motor syndromes (except for medial lemniscus)

  1. Medial lemniscus (vibration/ proprioception)
  2. MLF
  3. Motor tract of UMN (corticospinal tract)
  4. Motor nuclei of CN
171
Q

Lateral tract syndromes

A

Lateral- sensory syndromes (side)

  1. Spinothalamic tract (aka anterolateral, pain and temp); IPSILATERAL face and CONTRALATERAL body
  2. Spinocerebellar tract (RAM)
  3. Sympathetic chain (Dilation, sweating, etc.); IPSILATERAL to lesion
  4. Sensory nuclei of CN
172
Q

Basilar artery

A

Supplies brainstem

Lesion causes preserved consciousness, vertical eye movement, blinking; quadriplegia, loss of voluntary facial, mouth and tongue movements

173
Q

Aneurysms

A

Dilation of all layers of an artery due to vessel wall weakening

174
Q

Saccular (berry) aneurysm

A

Occurs at bifurcation of Circle of Willis (commonly between anterior communicating and anterior cerebral a.)

Causes subarachnoid hemorrhage (worst headache of my life)

175
Q

Berry aneurysm RFs

A

ADPKD, Ehlers-Danlos, advanced age, HTN, smoking, race (increased in AA), coarctation of aorta

176
Q

Charcot-Bouchard microaneurysm

A

Associated with HTN

Affects small vessels (e.g. lenticulostriate vessel in basal ganglia and thalamus)

Results in paralysis/ sensory loss of face and body but no cortical/ cortex symptoms (neglect, aphasia, visual field probs)

177
Q

Anterior communicating artery- aneurysm and rupture

A

Aneurysm/ compression: bitemporal hemianopia (due to compression of optic chiasm)

Rupture: ischemia in ACA (anterior cerebral) distribution- lower limbs motor and sensory probs

178
Q

Posterior communicating artery- aneurysm and rupture

A

Compression: ipsilateral CN III palsy (mydriasis- dilated/ blown pupil); may also see ptosis (down and out eye)

179
Q

Central post-stroke pain syndrome

A

Neuropathic pain due to thalamic lesions (10% of stroke patients)

Paresthesias filled by allodynia (pain with normally-painless stimuli)

180
Q

Epidural hematoma- common vessel affected

A

Middle meningeal a. (branch of maxillary a.)

181
Q

Epidural hematoma- cause

A

Skull fracture

vs. pterion fracture also causes middle meningeal a. but not an epidural hematoma because it is lower in the face

182
Q

Epidural hematoma- S&S

A

Lucid interval, transtentorial herniation CN III palsy

183
Q

Epidural hematoma- CT

A

Biconvex, does NOT cross suture lines

184
Q

Subdural hematoma- vessel

A

Bridging veins

185
Q

Subdural hematoma- cause

A

Acute: trauma
Chronic: alcohol, age, mild trauma, cerebral atrophy

Seen in shaken babies :(

186
Q

Subdural hematoma- CT

A

Crescent shaped hemorrhage that CROSSES suture lines

187
Q

Subarachnoid hemorrhage- vessel

A

Aneurysm rupture (e.g. saccular/ berry) or AVM (arteriovenous malformation)

188
Q

Subarachnoid hemorrhage- S&S

A

“Worst headache of my life”
Bloody or yellow spinal tap

Increased risk of developing communicating and/ or obstructive hydrocephalus

189
Q

Intraparenchymal hemorrhage- vessel

A

Lenticulostriate vessel (Charcot-Bouchard aneurysm)/ other small vessels

190
Q

Intraparenchymal hemorrhage- cause

A

Systemic HTN, amyloid angiopathy, vasculitis, neoplasm

191
Q

Ischemia/ stroke- timeline for irreversibility

A

Begins after 5 minutes of hypoxia

Most vulnerable areas: hippocampus (“HYPOcampus”), neocortex, cerebellum, and watershed areas

192
Q

Stroke- Identification process

A

IMAGE (non contrast CT) before tPA to ensure that there is no hemorrhage

CT: detects ischemia in 6-24 hrs
Diffusion-weighted MRI: detects ischemia within 3-30 min

193
Q

Histologic features of stroke

A 
12-48 hrs: red neurons
24-72 hrs: necrosis and neutrophils
3-5 days: macrophages (microglia)
1-2 wks: reactive gliosis and vascular proliferation
>2 wks: glial scar
194
Q

Contraindications for tPA

A
  1. Subarachnoid hemorrhage
  2. Uncontrolled HTN > 185 systolic; >110 diastolic
  3. AVM
  4. Endocarditis
  5. Prior surgery (recent)
  6. Stroke in past 3 months
195
Q

Ischemic stroke- defn

A

Blockage of vessel causes disruption of flow and ischemia –> leads to liquefactive necrosis

196
Q

Type of ischemic stroke (3)

A
  1. Thrombotic: clot forms DIRECTLY at site of infarction (most commonly MCA)- usually over atherosclerotic plaque
  2. Embolic- embolus from another part of the body obstructs vessel (often affects multiple places and is the result of a-fib, DVT, PFO, etc.)
  3. Hypoxic- due to hypoperfusion or hypoxemia (generally affects watershed areas between ACA and MCA & MCA and PCA)
197
Q

Tx for stroke

A

tPA within 3-4/5 hrs of onset

Reduce recurrence/ risk: medical therapy (e.g. aspirin, clopidogrel); optimum control of BP, blood sugars, lipids, and treat condns that increase risk (e.g. a-fib)

198
Q

Transient ischemic attack

A

Brief, reversible episode of focal neurologic dysfunction without acute infarction

Generally resolves in <15min

199
Q

TIA-tx

A

Low dose aspirin to prevent stroke

SE: GI bleeding due to inhibition of COX-1

200
Q

Dura venous sinuses

A

Large venous sinuses that run through dura and drain blood into internal jugular vein

Also drains CSF from arachnoid granulations

201
Q

Venous sinus thrombosis

A

presents with signs/ symptoms of increased ICP (headache, seizure, focal neurologic deficits)

can lead to venous hemorrhage

associated with hyper coagulable states (pregnancy, OCP use, Factor V Leiden)

202
Q

Ventricular system pathway

A

Lateral ventricle –> Interventricular foramen (of Monro) –> 3rd ventricle –> cerebral aqueduct (Sylvian) –> 4th ventricle –> foramens of Luschka (lateral) and Magendie (medial) –> subarachnoid space

203
Q

CSF synthesis

A

Made by ependymal cells of choroid plexus

Reabsorbed by arachnoid granulations and then drains into dural venous sinuses

204
Q

CSF- purpose

A

Bathes the brain and spinal cord with nutrients and removes waste products

205
Q

Idiopathic intercranial HTN (aka pseudotumor cerebri)

A

Increased ICP with no apparent cause via imaging (like hydrocephalus or obstruction)

206
Q

Pseudotumor cerebri RFs

A

Woman of childbearing age, vitamin A excess, dans, TCNS

207
Q

Pseudotumor cerebri- S&S

A

headache, diplopia (CN VI palsy) without change in mental status, papilledema

LP: increased opening pressure and headache relief

208
Q

Pseudotumor cerebri- tx

A

weight loss, acetazolamide, topiramate (anti-epileptic), LPs, CSF shunt placement, optic nerve fenestration surgery

209
Q

Hydrocephalus- defn

A

increased CSF volume –> ventricular dilation (+/- increased ICP)

210
Q

Communicating hydrocephalus

A

Decreased CSF absorption by arachnoid granulations
RF: meningitis (inflammation/ scarring)
S&S: increased ICP, papilledema, herniation

211
Q

Normal pressure hydrocephalus

A

Affects the elderly and is idiopathic
Ventricles expand, but ICP does not increase

S&S: Triad of- urinary incontinence, ataxia, and cognitive dysfunction (wet, wobbly, and wacky) + wide-based/ magnetic gait

212
Q

Non-communicating hydrocephalus

A

Caused structural blockage of CSF circulation (e.g. stenosis, colloid cyst)

213
Q

Ex vacuo ventriculomegaly

A

Increased CSF because of tissue/ neuronal atrophy- ICP is normal and triad of symptoms (wet, wobbly, wacky) not seen

214
Q

Nerves-vertebrae relationship

A

C1-C7 exit above respective vertebrae
C8 exits below C7
All others (T1-S5) exit below respective vertebrae

215
Q

Sinal cord in adulthood

A

Ends around L1-L2 vertebrae

Subarachnoid space extends to lower border of S2 vertebrae

Lumbar puncture performed at L3-L5 (level of caudal equina to prevent injury to spinal cord); keep spinal cord ALIVE, by puncturing between L3 and L5

216
Q

Tracts- ascending characteristics

A

SYNAPSE and then cross

217
Q

Dorsal column

A

Moves up spinal cord IPSILATERALLY, synapses at IPSILATERAL nucleus cuneatus in medulla and then crosses –> continues ascending (now CONTRALATERALLY) in medial lemniscus –> synapses at VPL thalamus –> Sensory cortex (contralateral to sensation)

218
Q

Spinothalamic tract

A

Enters spinal cord and synapses in gray matter in posterior & ipsilateral spinal cord –> crosses (within this level of spinal cord) at anterior commissure –> ascends up CONTRALATERALLY –> synapses at VPL thalamus –> Sensory cortex (contralateral to sensation)

219
Q

Lateral corticospinal tract

A

From motor cortex –> travels through internal capsule –> decussates in medulla (pyramids) –> descends CONTRALATERALLY –> synapses at cell bodies in the anterior horn (contralateral to the motor cortex site of signal origin) –> (now LMN) leaves spinal cord and travels to the neuromuscular junction (NMJ)

220
Q

White vs. gray matter

A

White matter: axons, nerve fibers (on the periphery of the spinal cord)

Gray matter: cell bodies, nuclei, synapses (looks like an H/ butterfly in the spinal cord)

221
Q

+ Romberg sign: decoding

A

Indicates loss of proprioceptive abilities

DCML origin: if paired with sensory defects
Cerebellar origin: if not paired with sensory defects

222
Q

Motor neuron signs- UMN vs. LMN

A

Upper: Weakness, Hyperreflexia, Increased tone, Positive Babinski, Spastic paralysis (everything going up)

Lower: Weakness, hyporeflexia, faciculations (muscle twtiching), decreased tone, flaccid paralysis (everything is lowered)

223
Q

Poliomyelitis (asymmetric) and Werdnig-Hoffmann dz (symmetric)

A

Affects anterior horn (causes LMN lesions)

S&S: LMN lesion- weakness, hypotonia, flaccid paralysis, facciculations, hyporeflexia, muscle atrophy (+ malaise, headache, fever, nausea)

Virus discovered in stool or throat

224
Q

Amyotropic lateral sclerosis

A

Affects anterior horns and CS tract (UMNs and LMNs are affected)

Tx: riluzole (blocks Na+ channels of damaged neurons)

225
Q

Anterior spinal artery damage

A

Damages everything (bilaterally) except for the DCML (which are supplied by the posterior spinal arteries)

primarily upper thoracic region (is watershed area), because lower thoracic- below T8- has arterial supply from a. of Adamkiewicz

226
Q

Tabes dorsalis

A

Damages/ demyelination of DCML

Caused by tertiary (neuro) syphillis (impairs proprioception- causes poor coordination, impairs light touch, impairs vibration)

S&S: + Romberg, DECREASED/ absent DTRs- due to lost sensation?, Argyll pupil (does not react/constrict to light, but can accommodate to objects near and far)

227
Q

Syringomyelia

A

Causes damage to anterior white commissure (carries fibers of ST/AL tract, therefore bilateral loss of pain and temp sensation in upper extremities)- cape-like distribution

228
Q

Vitamin B12 deficiency

A

Causes subacute combined degeneration: demyelination of the spinocerebellar tract, corticospinal tract, and DCML

S&S: ataxic gait, paresthesia, and impaired position/ vibration sense

229
Q

Friedrich ataxia- cause

“Ataxic GAAit”

A

Autosomal recessive
Trinucleotide repeat disorder (GAA)n on chr 9 (encodes frataxin)
GAA repeats frataxin gene impede transcription and therefore reduce translation of this protein

Ataxic GAAit: Causes degeneration of multiple spinal cord tracts

230
Q

Freidrich ataxia- S&S

A

“Friedrich is Fratastic- he staggers and falls, but has a sweet, big heart”

Staggering gait, frequent falling, nystagmus, dysarthria, hammer toes, high arch (pes cavus), diabetes mellitus, and hypertrophic cardiomyopathy (cause of death)

Presents in childhood as kyphoscoliosis

231
Q

Brown-Sequard syndrome

A

Hemisection of spinal cord: think of where things cross

Below lesion:
(AL/ ST tract) Pain and temp: contralateral loss
(DCML tract) Light touch, vibration, proprioception: ipsilateral loss
(CS tract) UMN motor symptoms: ipsilateral side of spinal cord damage/ (contralateral motor cortex- because decussates in medulla)

At level of lesion:
LMN signs (hyporeflexia, faciculations, etc.)
Loss of all sensation (AL/ ST and DCML)

232
Q

Frontal lobe damage

A

Right side- associated with hyper sexuality/ disinhibition

Left side- associated with apathy

Neurology (5 decks)

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