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Neurology and Psychiatry > Neuro > Flashcards

Neuro Flashcards

1
Q

The forebrain (prosencephalon) develops into what?

A

Telencephalon and diencephalon

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2
Q

What are the wall and cavity derivatives of the telencephalon?

A

Walls: cerebral hemispheres, Cavities: lateral ventricles

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3
Q

What secondary vesicles does the Hindbrain (rhombencephalon) develop into?

A

Metencephalon and myelencephalon

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4
Q

What are the wall and cavity derivatives of the diencephalon?

A

Walls- thalamus, cavity- 3rd ventricle

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5
Q

What are the wall and cavity derivatives of the mesencephalon?

A

walls- midbrain, cavity- aqueduct

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6
Q

What are the wall and cavity derivatives of the metencephalon?

A

walls-> pons and cerebellum, cavity-> upper part of 4th ventricle

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7
Q

What are the wall and cavity derivatives of the myelencephalon?

A

walls-> medulla, cavity -> lower part of 4th ventricle

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8
Q

What are the characteristics of spina bifida occulta?

A

Failure of bony spinal canal to close, no structural herniation. Dura in tact

Usually seen at lower vertebral levels, associated with tuft of hair or skin dimple at level of defect

Normal AFP**

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9
Q

What are the findings in anencephaly?

A

Malformation of anterior neural tube-> no forebrain, open calvarium

Findings: increased AFP, polyhydramnios

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10
Q

What maternal conditions are associated with anencephaly?

A

Type 1 diabetes, low folate

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11
Q

Holoprosencephaly can be found in which syndromes?

A

Patau syndrome and fetal alcohol syndrome

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12
Q

What mutation can cause holoprosencephaly?

A

sonic hedgehog signaling pathway mutations

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13
Q

Chiari II

A

herniation of cerebellar tonsils and vermis through foramen magnum w/ aqueductal stenosis and hydrocephalus

Usually presents with meningomyelocele, paralysis below defect

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14
Q

Dandy-Walker

A

Agenesis of cerebellar vermis with cystic enlargement of 4th ventricle (fills enlarged posterior fossa)

Associated with spina bifida and hydrocephalus

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15
Q

What is syringomyelia associated with?

A

Chiari malformations, trauma and tumors

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16
Q

What causes syringomyelia? How does it present?

A

cystic cavity (syrinx) within spinal cord

Crossing anterior spinal commissural fibers damaged first -> “cape-like” bilateral loss of pain and temp in upper extremities (fine touch preserved)

Symptoms usually present in late adulthood

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17
Q

Where in the spinal cord is syringomyelia most common?

A

C8-T1

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18
Q

Anterior 2/3 of tongue -> what brachial arches is it derived from? CNs for taste and sensation?

A

Brachial arches 1 and 2

Taste - CN VII, Sensation - CN V3

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19
Q

Posterior 1/3 of tongue -> what brachial arches is it derived from? CNs for taste and sensation?

A

Brachial arches 3 and 4

Taste and sensation - CN IX, extreme posterior CN X

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20
Q

What muscle retracts and depresses the tongue and what CN innervates it?

A

hyoglossus, CN XII

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21
Q

What muscle protrudes the tongue and what CN innervates it?

A

genioglossus, CN XII

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22
Q

What muscle draws sides of tongue upward and what CN innervates it?

A

styloglossus, CN XII

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23
Q

What muscle elevates posterior tongue during swallowing and what innervates it?

A

palatoglossus, CN X

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24
Q

What can be seen on Nissle staining?

A

Stains RER -> can see dendrites and cell body, but NOT axons

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25
Q

What is Wallerian degeneration

A

injury to axon causes degeneration distal to injury and axonal retraction proximally

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26
Q

What is the function of astrocytes and what are they derived from?

A

Derived from neuroectoderm

Function: physical support, repair, K+ metabolism, remove excess NT, component of BBB, glycogen reserve buffer, reactive gliosis in response to neural injury

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27
Q

What is the marker for astrocytes?

A

GFAP

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28
Q

What does HIV-infected microglia cause

A

HIV infected microglia fuse to form multinucleated giant cells in CNS

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29
Q

What are microglia derived from? What is their function?

A

Derived from mesoderm, mononuclear origin

Function: phagocytes of CNS, activated in response to tissue damage

*Not readily discernible by Nissl

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30
Q

What is the myelin of CNS and PNS?

A

CNS- oligodendrocytes, PNS- Schwann cells

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31
Q

Acoustic neuroma - what is it and what can it be associated with?

A

Type of schwannoma, usually in internal acoustic meatus (CN VIII)

If bilateral, strong associate with neruofibromatosis type 2 (autosomal dominant)

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32
Q

How many axons do schwann cells myelinate?

A

each schwann cell myelinates 1 PNS axon

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33
Q

What are Schwann cells derived from?

A

Neural crest

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34
Q

How many axons do oligodendrocytes myelinate?

A

Many axons (~30)

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35
Q

What are oligodendrocytes derived from? How do they appear histologically?

A

Derived from neuroectoderm

“Fried egg” appearance on histology

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36
Q

Which diseases injure oligodendrocytes?

A

MS, PML, leukodystrophies

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37
Q

What type of fibers use free nerve endings? Where are free nerve ending receptors located and what do they sense?

A

Fibers: C- slow, unmyelinated and A delta - fast, myelinated

Location: all skin, epidermis, some viscera

Senses: pain and temperature

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38
Q

What type of fibers have Meissner corpuscles? Where are Meissner corpuscles located and what do they sense?

A

Fibers: large, myelinated; adapt quickly

Location: Glabrous (hairless) skin

Senses: dynamic fine/light touch, position sense

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39
Q

What type of fibers have Pacinian corpuscles? Where are Pacinian corpuscles located and what do they sense?

A

Fibers: large, myelinated; adapt quickly

Location: Deep skin layers, ligaments, joints

Senses: Vibration and pressure

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40
Q

Merkel discs are associated with what kinds of fibers? Where are Merkel discs located and what do they sense?

A

Fibers: large, myelinated; *adapt slowly

Location: finger tips, superficial skin

Senses: pressure, deep static touch (shapes, edges, etc), position sense

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41
Q

Ruffini corpuscles are associated with what kinds of fibers? Where are Ruffini corpuscles located and what do they sense?

A

Fibers: dendritic endings with capsule, adapt slowly

Location: finger tips, joints

Senses: (sensitive of skin stretch and kinesthetic sense) pressure, slippage of objects along surface of skin, joint angle change

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42
Q

What part of peripheral nerves invests single nerve fiber layers?

A

Endoneurium, connective tissue that invests myelin sheath of nerve fibers

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43
Q

What surrounds a fascicle of nerve fibers?

A

Perineurium, note: must be rejoined in microsurgery for limb reattachment

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44
Q

What is the epineurium?

A

Dense connective tissue that surrounds entire nerve, contains the nerve fascicles and blood vessels that supply nerve

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45
Q

Where is Norepinephrine synthesized?

A

Locus ceruleus (pons)

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46
Q

How does NE change in disease?

A

increases in anxiety and decreases in depression

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47
Q

Where is dopamine synthesized?

A

ventral tegmentum and substantia nigra pars compacta (midbrain)

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48
Q

How does dopamine change in disease?

A

increases in Huntington disease

decreases in Parkinson disease, depression

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49
Q

Where is serotonin (5-HT) synthesized?

A

Raphe nuclei (pons, medulla, midbrain)

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50
Q

How does serotonin (5-HT) change in disease?

A

decreases in anxiety and depression

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51
Q

Where is ACh synthesized?

A

Basal nucleus of Meynert

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52
Q

How does ACh change in disease?

A

increases in Parkinson disease

decreases in Alzheimer disease and Huntington disease

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53
Q

Where is GABA synthesized?

A

Nucleus accumbens

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54
Q

How does GABA change in disease?

A

decreases in anxiety and Huntington disease

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55
Q

What forms the BBB?

A

Tight jxns between nonfenestrated capillary endothelial cells, basement membrane, astrocyte foot processes

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56
Q

How do glucose and amino acids cross BBB?

A

slowly via carrier-mediated transport

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57
Q

What is the nucleus related to “stress and panic”

A

locus ceruleus

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58
Q

what are the nuclei associated with “reward center, pleasure, addiction and fear”?

A

nucleus accumbens and septal nucleus

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59
Q

how do nonpolar/lipid-soluble substances cross the BBB?

A

rapidly via diffusion

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60
Q

which areas of the brain have fenestrated capillaries and allow molecules in blood to affect brain function (circumventricular organs)?

A

Area postrema - vomiting after chemo

OVLT - osmotic sensing

neurohypophysis (posterior pituitary) - ADH release

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61
Q

Which nucleus makes ADH?

A

supraoptic nucleus of hypothalamus

62
Q

Which nucleus makes oxytocin?

A

paraventricular nucleus of hypothalamus

63
Q

What is the function of the lateral area of the hypothalamus?

A

Stimulates hunger. Inhibited by leptin

Destruction -> anorexia, failure to thrive in infants

64
Q

What is the function of the ventromedial area of the hypothalamus?

A

Satiety, Stimulated by leptin

Destruction (ex craniopharyngioma) –> hyperphagia

65
Q

What is the function of the anterior hypothalamus?

A

cooling, parasympathetic “cool off”

66
Q

What is the function of the posterior hypothalamus?

A

heating, sympathetic “get fired up”

67
Q

what is the function of the suprachiasmatic nucleus (SCN) of the hypothalamus?

A

circadian rhythm

68
Q

What releases melatonin?

A

pineal gland, stimulated by NE from SCN

69
Q

What causes EOM during REM sleep?

A

activity of PPRF

70
Q

What is associated with decreased REM sleep?

A

Alcohol, benzodiazepines, barbituates and NE

71
Q

What is the EEG waveform when awake with eyes open?

A

Beta (highest frequency, lowest amplitude), alert active mental concentration

72
Q

What is the EEG waveform when awake with eyes closed?

A

alpha

73
Q

What are the features and the EEG waveform of Non-REM sleep stage N1?

A

5% of sleep; light sleep, theta waveform

74
Q

What are the features and the EEG waveform of Non-REM sleep stage N2?

A

45% of sleep, deeper sleep, bruxism (teeth grinding) occurs; waveform: sleep spindles and K complexes

75
Q

What are the features and the EEG waveform of Non-REM sleep stage N3?

A

25% of sleep, Deepest non-REM sleep (slow-wave sleep); sleepwalking, night terrors and bedwetting occur

Delta waveform (lowest frequency, highest amplitude)

76
Q

What are the features and the EEG waveform of REM sleep?

A

25% of sleep; Loss of motor tone, increase O2 use, increase variable pulse and blood pressure (dreaming and penile/clitoral tumescence occurs)

beta waveform (highest frequency, lowest amplitude)

77
Q

VPL nucleus of thalamus - what is the input? what info is carried? and what is the final destination?

A

input: spinothalamic and dorsal columns/medial lemniscus
info: pain, temp (spinothalamic tract); pressure, touch vibration and proprioception (dorsal columns/ medial lemniscus)
destination: primary somatosensory cortex

78
Q

VPM nucleus of thalamus - what is the input? what info is carried? and what is the final destination?

A

input: Trigeminal and gustatory pathway
info: face sensation and taste
destination: primary somatosensory cortex

79
Q

LGN of thalamus - what is the input? what info is carried? and what is the final destination?

A

input: CN II
info: vision
destination: calcarine sulcus

80
Q

MGN of thalamus - what is the input? what info is carried? and what is the final destination?

A

input: Superior olive and inferior colliculus of tectum
info: hearing
destination: auditory cortex of temporal lobe

81
Q

VL nucleus of thalamus - what is the input? what info is carried? and what is the final destination?

A

input: basal ganglia, cerebellum
info: motor
destination: motor cortex

82
Q

Overly rapid correction of hyponatremia can cause what?

A

Osmotic demyelination syndrome aka central pontine myelinolysis

83
Q

Overly rapid correction of hypernatremia can cause what?

A

cerebral edema and herniation

84
Q

What do lateral lesions of the cerebellum cause?

A

propensity to fall toward ipsilateral side of lesion

85
Q

what do medial lesions of the cerebellum cause?

A

midline structures like vermal cortex, fastigial nuclie and/or flocculonodular lobe

causes truncal ataxia (wide-based gait), nystagmus, head tilting

86
Q

Athetosis is caused by a lesion where?

A

Slow writing movement. Lesion in basal ganglia (ex Huntington)

87
Q

What is an essential tremor?

A

High-frequency tremor with sustained posture, worsens with movement or anxiety; often familial and patients often self-medicate with alcohol which decreases tremor amplitude

88
Q

What is used to treat essential tremors?

A

beta-blockers, primidone

89
Q

What is hemiballismus and where is the characteristic lesion that causes it?

A

Sudden wild flailing of 1 arm +/- ipsilateral leg

Characteristic lesion is in CONTRALATERAL subthalamic nucleus (ex lacunar stroke)

90
Q

What is the characteristic lesion that causes intention tremor?

A

cerebellar dysfunction

91
Q

What symptoms are associated with Parkinson disease?

A 
Tremor (pill-rolling tremor at rest)
Rigidity
Akinesia (or bradykinesia)
Postural instability
Shuffling gait
92
Q

What are the histological features of Parkinson disease?

A

Lewy bodies (alpha-synuclein, intracellular eosionohilic inclusions) and loss of dopaminergic neurons (depigmentation) of substantia nigra pars compacta

93
Q

What is the pathophysiology of Huntington disease?

A

AD trinuclotide repeat of CAG on chromosome 4 “CAG: Caudate loses ACh and GABA”

Causes increased dopamine, decreased GABA and decreased ACh in brain -> neuronal death via NMDA-R binding and glutamate toxicity

94
Q

What are the imaging findings for Huntington disease?

A

atrophy of caudate nuclei with dilation of frontal horns on MRI

95
Q

What is broca aphasia?

A

Non-fluent aphasia, intact comprehension and impaired repetition ‘Broken boca’

96
Q

Where is Broca area?

A

inferior frontal gyrus of frontal lobe

97
Q

Where is Wernicke area?

A

superior temporal gyrus of temporal lobe

98
Q

What is Wernicke aphasia?

A

Fluent aphasia with impaired comprehension and repetition “wordy but makes no sense”

99
Q

What is conduction aphasia?

A

poor repetition but fluent speech and intact comprehension. Can be caused by damage to arcuate fasciculus

100
Q

What is global aphasia?

A

Nonfluent aphasia with impaired comprehension -> damage to Broca, Wernicke and arcuate fasciculus

101
Q

What is transcortical motor aphasia?

A

Nonfluent aphasia with good comprehension and intact repetition -> understands and can only get repeated words out

102
Q

What is transcortical sensory aphasia?

A

poor comprehension with fluent speech and intact repetition

103
Q

What is mixed transcortical aphasia?

A

Nonfluent speech, poor comprehension, intact repetition -> parrot

Broca and Wernicke areas involved; arcuate fasciculus NOT involved

104
Q

amygdala lesion causes what? and what microbe is it associated with?

A

Kluver-Bucy syndrome - disinhibited behavior (hyperphagia, hypersexuality, hyperorality)

Associated with HSV-1

105
Q

What does a frontal lobe lesion cause?

A

Disinhibition and deficits in concentration, orientation and judgement

106
Q

What does a lesion in the non-dominant parietal-temporal cortex cause?

A

hemispatial neglect syndrome (agnosia of contralateral side of world)

107
Q

What does a lesion in the dominant parietal-temporal cortex cause?

A

Agraphia (inability to write), acalculia (inability to calculate), finger agnosia (inability to distinguish fingers), L-R disorientation

(Gerstmann syndrome)

108
Q

What is caused by lesions to the mammillary bodies?

A

Wernicke-Korsakoff syndrome - confusion, ophthalmoplegia, ataxia; memory loss (anterograde and retrograde), confabulation, personality changes

109
Q

What are mammillary body lesions associated with?

A

Wernicke-Korsakoff syndrome is associated with thiamine deficiency and excessive alcohol use; can precipitate from giving glucose without thiamine to a thiamine deficient patient

110
Q

Will cerebellar hemisphere lesions cause ipsilateral or contralateral deficits?

A

ipsilateral deficits -> intention tremor, limb ataxia, loss of balance, fall toward side of lesion

111
Q

What will a bilateral hippocampus lesion cause?

A

anterograde amnesia

112
Q

What will a paramedian pontine reticular formation (PPRF) lesion cause?

A

eyes will look away from side of lesion

113
Q

What will frontal eye fields lesions cause?

A

eyes look toward lesion

114
Q

Due to watershed zones, what are the consequences of severe hypotension?

A

upper leg/upper arm weakness (between ACA and MCA) and defects in higher-order visual processing (between MCA and PCA)

115
Q

What is the primary regulator of cerebral perfusion?

A

PCO2 –> hyperventilation (decreased PCO2) can help decrease ICP in cases of cerebral edema from vasoconstriction

116
Q

How are cerebral perfusion and BP related?

A

cerebral perfusion pressure (CPP) = mean arterial pressure (MAP) - ICP –> decreases in BP or increases in ICP decrease CPP

117
Q

What causes medial medullary syndrome?

A

infarct of paramedian branches of Anterior spinal artery (ASA) and vertebral arteries

118
Q

How does Medial medullary syndrome present?

A

Pyramid (lateral corticospinal tract) - contralateral hemiparesis of upper and lower limbs
Medial lemniscus - decreased contralateral proprioception
Caudal medulla (CN XII) - ipsilateral hypogolssal dysfunction (tongue deviates ipsilaterally)

119
Q

What vessel lesion causes lateral medullary (Wallenberg) syndrome?

A

Lesion to PICA (posterior inferior cerebellar artery)

120
Q

What are the clinical features of lateral medullary (Wallenberg) syndrome?

A
  • Dysphagia, hoarseness, decrease gag reflex
  • vomiting, vertigo, nystagmus
  • Decreased pain and temp in ipsilateral face and contralateral body
  • ipsilateral Horner syndrome (ptosis, miosis and enophthalmus)
  • ataxia and dysmetria
121
Q

What vessel lesion causes lateral pontine syndrome?

A

AICA (anterior inferior cerebellar artery)

122
Q

What are the clinical features of lateral pontine syndrome?

A

Paralysis of face, decreased lacrimation, salivation decreased taste from anterior 2/3 of tongue

  • vomiting, vertigo, nystagmus
  • Decreased pain and temp in ipsilateral face and CONTRALATERAL body
  • ataxia and dysmetria

“Facial droop means AICA’s pooped”

123
Q

Where would a stroke cause contralateral hemianopia with macular sparing?

A

PCA - impaired occipital and visual cortex

124
Q

Where would a stroke cause “locked-in syndrome?”

A

Basilar artery, preserved consciousness and blinking, quadriplegia, loss of voluntary facial and mouth movements

125
Q

What would a lesion in ACom cause?

A

visual field defects, lesions are typically aneurysms not stroke

126
Q

Where do saccular (berry) aneurysms typically occur?

A

Most common site is junction of ACom and ACA

127
Q

What is caused by a PCom lesion?

A

CN III palsy - eye is “down and out” with ptosis and mydriasis. Lesions typically aneurysms, not strokes

128
Q

What is are common complications of saccular (berry) aneurysms?

A

rupture -> subarachnoid hemorrhage or hemorrhagic stroke

Can cause bitemporal hemianopia via optic chiasm compression

129
Q

What diseases are associated with saccular (berry) aneurysms?

A

ADPKD, Ehlers-Danlos syndrome

130
Q

What are risk factors for berry aneurysms?

A

increased age, HTN, smoking, African americans

131
Q

What are Charcot-Bouchard microaneurysms of lenticulostriate vessels associated with?

A

chronic HTN, affects small vessels - basal ganglia, thalamus

132
Q

What are risk factors for idiopathic intracranial hypertension (pseudotumor cerebri)

A

woman of childbearing age, excess vitamin A, danazol (hypoestrogenic, hyperandrogenic effects that cause atrophy of the endometrium, which can alleviate the symptoms of endometriosis)

133
Q

How is idiopathic intracranial hypertension (pseudotumor cerebri) treated?

A

weight loss, acetazolamide (carbonic anhydrase inhibitor), topiramate (antiepileptic), invasive procedures if refractory to treatment

134
Q

What is the difference between communicating and noncommunicating hydrocephalus?

A

communicating is nonobstructive -> decreased CSF absorption by arachnoid granulations -> increased ICP

Noncommunicating is obstructive -> block of CSF circulation within ventricular system (stenosis of aqueduct for example)

135
Q

What are the symptoms and findings of normal pressure hydrocephalus?

A

Expansion of ventricles (seen on imaging) distorts fibers of corona radiata -> triad of urinary incontinence (wet), ataxia (wobbly) and cognitive dysfunction (wacky)

136
Q

What is ex vacuo ventromegaly?

A

Mimics hydrocephalus. Appears to be increase CSF on imaging but due to decreased brain tissue and ICP is normal. Seen in Alzheimer’s, advanced HIV, Pick disease..

137
Q

What causes LMN lesions only, due to anterior horn destruction? What are the resulting symptoms?

A

Poliomyelitis and spinal muscular atrophy (Werdnig-Hoffmann disease). Causes flaccid paralysis

138
Q

What are the spinal cord lesions in MS?

A

Demeylination mostly in white matter of cervial region; random and asymmetric lesions -> scanning speech, intention tremor, nystagmus

139
Q

What causes amyotrophic lateral sclerosis (ALS)?

A

Defect in superoxide dismutase 1

140
Q

What are the clinical features of ALS?

A

combined UMN and LMN deficits with NO sensory or oculomotor deficits

Presents as fasciculations with eventual atrophy and weakness of hands

141
Q

What are the spinal cord lesions that can be caused by tertiary syphilis?

A

Tabes dorsalis -> from demyelination of dorsal columns and roots -> impaired sensation and proprioception, progressive sensory ataxia (decreased sensation leads to poor coordination)

142
Q

What is Werdnig-Hoffmann disease?

A

spinal muscular atrophy- Autosomal recessive congenital degeneration of anterior horns of spinal cord -> LMN lesion

“Floppy baby” with hypotonia and tongue fasciculations

143
Q

What is Parinaud syndrome?

A

paralysis of conjugate vertical gaze due to lesion in superior colliculi damaging MLF

Causes: pineal tumor, MS, stroke

Symptoms:

  • vertical gaze palsy
  • absent pupillary reflex
  • failure of convergence
  • wide based gait
144
Q

What things pass through the cavernous sinus?

A

CN III, IV, V1, VI, sometimes V2, postganglionic sympathetic pupillary fibers, part of internal carotid artery

145
Q

How does cavernous sinus syndrome present and what are possible causes?

A

Variable ophthalmoplegia (CN III, IV, VI), decreased corneal sensation (V1), Horner syndrome and occasionally decreased maxillary sensation (V2) [Note CN VI most susceptible to damage]

Causes: pituitary tumor mass effect, carotid-cavernous fistula, or cavernous sinus thrombosis from infection

146
Q

What are the findings for the rinne and weber tests with conductive hearing loss?

A

Rinne test: abnormal (bone>air), Weber test- sounds louder in affected ear

147
Q

What are the findings for the Rinne and Weber tests with sensiorineural hearing loss?

A

Rinne test: normal (air>bone) but sound diminished in both, just proportionally

Weber test: sounds louder in unaffected ear

148
Q

Lesion of face area of motor cortex or lesion in connection between cortex and facial nucleus causes what symptoms?

A

UMN lesion - contralateral paralysis of lower face; forehead spared (bilateral UMN innervation)

149
Q

Lesion of CNVII after facial nucleus causes what symptoms?

A

LMN lesion -> ipsilateral paralysis of upper AND lower face

150
Q

What causes facial nerve palsy?

A

complete destruction of facial nucleus or efferent fibers (CN VII)

Can occur idiopathically (Bell palsy). Associated with Lyme disease, herpes simplex and less commonly: herpes zoster (Ramsay Hunt syndrome), sarcoidosis, tumors, diabetes

151
Q

What are the symptoms of facial nerve palsy

A

peripheral ipsilateral facial paralysis with inability to close eye on involved side

152
Q

Which muscles open and close the jaw?

A

Open jaw: masseter, temporalis, medial pterygoid

Close jaw: later pterygoid

Neurology and Psychiatry (4 decks)

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