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Neurology Flashcards

1
Q

Notochord induces overlying ectoderm to

A

Notochord induces overlying ectoderm to differentiate into neuroectoderm and form neural plate

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2
Q

Neural plate gives rise to

A

Neural plate gives rise to neural tube and neural crest cells

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3
Q

Notochord becomes

A

Notochord becomes nucleus pulposus of intervetebral disc in adults

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4
Q

Prosencephalon gives rise to

A

Telencephalon and diencephalon

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5
Q

Mesencephalon (of the 3 primary vesicles) gives rise to

A

Mesencephalon

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6
Q

Rhombencephalon gives rise to

A

Metencephalon and myelencephalon

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7
Q

Telencephalon gives rise to

A

Cerebral hemispheres and lateral ventricles

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8
Q

Diencephalon gives rise to

A

Thalamus, hypothalamus, and third ventricle

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9
Q

Mesencephalon gives rise to

A

Midbrain and aqueduct

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10
Q

Metencephalon gives rise to

A

Pon, cerebellum, and upper part of 4th ventricle

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11
Q

Myelencephalon gives rise to

A

Medulla and lower part of 4th ventricle

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12
Q

Neuroectoderm

A
  • CNS neurons
  • Ependymal cells (inner lining of ventricles, make CSF)
  • Oligodendroglia
  • Astrocytes
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13
Q

Neural crest

A
  • PNS neurons

- Schwann cells

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14
Q

Mesoderm

A

Microglia

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15
Q

When do neuropores normally fuse

A

4th week

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16
Q

Confirmatory test for neural tube defect after AFP

A

↑ acetylcholinesterase (AChE) in amniotic fluid

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17
Q

Anencephaly

A
  • Malformation of anterior neural tube → no forebrain, open calvarium
  • Clinical findings: ↑ AFP, polyhydramnios (no swallowing center in brain)
  • Associated with maternal type 1 diabetes
  • Maternal folate supplementation ↓ risk
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18
Q

Holoprosencephaly

A
  • Failure of right and left hemispheres to separate
  • Usually occurs during weeks 5-6
  • May be related to mutations in sonic hedgehog signaling pathway
  • Moderate form has cleft lip/palate, most severe form results in cyclopia
  • Seen in Patau syndrome and fetal alcohol syndrome
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19
Q

Anencephaly is associated with

A

Maternal type 1 diabetes

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20
Q

Holoprosencephaly is associated with

A

Patau syndrome and fetal alcohol syndrome

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21
Q

Chiari II malformation

A
  • Herniation of low-lying cerebellar vermis through foramen magnum with aqueductal stenosis → hydrocephalus
  • Usually associated with lumbosacral meningomyelocele (paralysis/sensory loss at and below the level of the lesion)
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22
Q

Dandy-Walker syndrome

A
  • Agenesis of cerebellar vermis with cystic enlargement of 4th ventricle (fills the enlarged posterior fossa)
  • Associated with noncommunicating hydrocephalus, spina bifida
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23
Q

Chiari I malformation

A
  • Cerebellar tonsillar ectopia > 3-5 mm
  • Congenital, usually asymptomatic in childhood, manifest with headaches and cerebellar symptoms
  • Associated with syringomyelia
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24
Q

Tongue development

A
  • 1st and 2nd branchial arches form anterior 2/3 (thus sensation via CN V3, taste via CN VII)
  • 3rd and 4th branchial arches form posterior 1/3 (thus sensation and taste mainly via CN IX, extreme posterior via CN X)
  • Motor innervation is via CN XII to hyoglossus (retracts and depresses the tongue), genioglossus (protrudes tongue) and styloglossus (draws sides of tongue upward to create a trough for swallowing)
  • Motor innervation is via CN X to palatoglossus (elevates posterior tongue during swallowing)
  • TASTE → CN VII, IX, X (solitary nucleus)
  • PAIN → CN V3, IX, X
  • MOTOR → CN X, XII
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25
Q

What forms multinucleated giant cells in the CNS of HIV infected patients

A

HIV-infected microglia fuse to form multinucleated giant cells in the CNS

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26
Q

How does myelin change the space constant, conduction velocity and time constant

A
  • ↑ space constant
  • ↑ conduction velocity
  • ↓ time constant
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27
Q

What is the embryologic derivation of Schwann cells and oligodendrocytes

A

Oligodendrocytes → neuroectoderm

Schwann cells → neural crest

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28
Q

Oligodendroglia are injured in what disease processes

A
  • MS
  • Progressive multifocal leukoencephalopathy (PML)
  • Leukodystrophies
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29
Q

Free nerve endings

A
  • C → slow, unmyelinated fibers
  • A-delta → fast, myelinated fibers
  • All skin, epidermis, some viscera
  • Pain, temperature
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30
Q

Meissner corpuscles

A
  • Large, myelinated fibers; adapt quickly
  • Glabrous (hairless) skin
  • Dynamic, fine/light tough, position sense
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31
Q

Pacinian corpuscles

A
  • Large myelinated fibers; adapt quickly
  • Deep skin layers, ligaments, joints
  • Vibration, pressure
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32
Q

Merkel discs

A
  • Large, myelinated fibers; adapt slowly
  • Finger tips, superficial skin
  • Pressure, deep static touch (eg shapes, edges)
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33
Q

Ruffini corpuscles

A
  • Dendritic endings with capsule; adapt slowly
  • Fingertips, joints
  • Pressure, slippage of objects along surface of skin, joint angle change
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34
Q

What must be rejoined in microsurgery for limb reattachment

A

Perineurium

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35
Q

Epineurium

A

Dense connective tissue that surrounds entire nerve (fascicles and BLOOD VESSELS)

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36
Q

Location of acetylcholine synthesis

A

Basal nucleus of Meynert

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37
Q

Location of dopamine synthesis

A

Ventral tegmentum, SNpc

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38
Q

Location of GABA synthesis

A

Nucleus accumbens

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39
Q

Location of norepinephrine synthesis

A

Locus ceruleus

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40
Q

Location of serotonin synthesis

A

Raphe nucleus

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41
Q

Neurotransmitters in anxiety

A
  • ↓ GABA
  • ↑ norepinephrine
  • ↓ serotonin
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42
Q

Neurotransmitters in depression

A
  • ↓ dopamine
  • ↓ norepinephrine
  • ↓ serotonin
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43
Q

Neurotransmitters in schizophrenia

A

↑ dopamine

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44
Q

Neurotransmitters in Alzheimer disease

A
  • ↓ acetylcholine

- ↑ glutamate

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45
Q

Neurotransmitters in Huntington disease

A
  • ↓ acetylcholine
  • ↑ dopamine
  • ↓ GABA
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46
Q

Neurotransmitters in Parkinson disease

A
  • ↑ acetylcholine
  • ↓ dopamine
  • ↑ serotonin
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47
Q

Blood-brain barrier formed by what 3 structures

A
  • Tight junctions between nonfenestrated capillary endothelial cells
  • Basement membrane
  • Astrocyte foot processes
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48
Q

How do glucose and amino acids cross the BBB

A

Slowly by carrier mediated transport mechanisms

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49
Q

What kinds of substances cross the BBB rapidly via diffusion

A

Nonpolar/ lipid-soluble substances

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50
Q

Vasogenic edema

A

Infarction and/or neoplasm destroys endothelial cell tight junctions causing vasogenic edema

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51
Q

What is the hypothalamus responsible for

A
  • Thirst and water balance
  • Adenohypophysis control (regulates anterior pituitary)
  • Neurohypophysis releases hormones hormones produced in the hypothalamus
  • Hunger
  • Autonomic regulation
  • Temperature regulation
  • Sexual urges

“TAN HATS”

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52
Q

What are input areas of the hypothalamus

A
  • Organum vasculosum of the lamina terminalis (OVLT) → senses changes in osmolarity
  • Area postrema (found in medulla) → responds to emetics
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53
Q

Lateral area of hypothalamus

A
  • Hunger
  • Destruction → anorexia, failure to thrive (infants)
  • Stimulated by ghrelin
  • Inhibited by leptin
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54
Q

Ventromedial area of hypothalamus

A
  • Satiety
  • Destruction (eg craniopharyngioma) → hyperphagia
  • Stimulated by leptin
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55
Q

Anterior hypothalamus

A
  • Cooling

- Parasympathetic

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56
Q

Posterior hypothalamus

A
  • Heating

- Sympathetic

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57
Q

Suprachiasmatic nucleus

A

Circadian rhythm

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58
Q

Sleep physiology

A
  • Circadian rhythm controls nocturnal release of ACTH, prolactin, melatonin, norepinephrine
  • SCN → norepinephrine release → pineal gland → melatonin
  • SCN is regulated by environment
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59
Q

Extraocular movements during REM sleep are due to

A

Activity of PPRF (paramedian pontine reticular formation/ conjugate gaze center)

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60
Q

Increase in what neurotransmitter occurs during REM sleep

A

Acetylcholine

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61
Q

What drugs are associated with ↓ REM sleep

A
  • Alcohol, benzodiazepines, and barbiturates → ↓ REM sleep, ↓ delta wave sleep
  • Norepinephrine → ↓ REM sleep
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62
Q

In which stage of sleep do bruxisms occur

A

N2

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63
Q

In what stage of sleep do night terrors, sleepwalking and bedwetting occur

A

N3

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64
Q

Ventral posterolateral nucleus of thalamus

A
  • Input from spinothalamic and dorsal columns/medial lemniscus
  • Senses pain, temperature, touch, vibration and propioception
  • Destination is primary somatosensory cortex
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65
Q

Ventral posteromedial nucleus of thalamus

A
  • Input from trigeminal and gustatory pathway
  • Senses face sensation and taste
  • Destination is primary somatosensory cortex

“Makeup goes of the face”

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66
Q

Lateral geniculate nucleus of thalamus

A
  • Input from CN II
  • Vision
  • Destination is calacrine sulcus

“Lateral = light”

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67
Q

Medial geniculate nucleus of thalamus

A
  • Input from superior olive and inferior colliculus of tectum
  • Hearing
  • Destination is auditory cortex of temporal lobe

“Medial = music”

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68
Q

Ventral lateral nucleus of thalamus

A
  • Input from basal ganglia and cerebellum
  • Motor
  • Destination is motor cortex
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69
Q

Limbic system

A
  • Collection of neural structures involved in emotion, long-term memory, olfaction, behavior modification, ANS function
  • Structures include hippocampus, amygdala, fornix, mammillary bodies, cingulate gyrus
  • Responsible for “Feeding, Fleeing, Fighting, Feeling and Fucking”
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70
Q

Dopaminergic pathways

A
  • Mesocortical
  • Mesolimbic
  • Nigrostriatal
  • Tuberoinfundibular
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71
Q

Mesocortical dopaminergic pathway

A
  • ↓ activity → “negative” symptoms (eg flat affect, limited speech)
  • Antipsychotic drugs have limited effect
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72
Q

Mesolimbic dopaminergic pathway

A
  • ↑ activity → “positive” symptoms (eg delusions, hallucinations)
  • Primary therapeutic target of antipsychotic drugs → ↓ positive symptoms (eg schizophrenia)
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73
Q

Nigrostriatal dopaminergic pathway

A
  • ↓ activity → extrapyramidal symptoms (eg dystonia, akathisia, parkinsonism, tardive dyskinesia)
  • Major dopaminergic pathway in brain
  • Significantly affected by movement disorders
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74
Q

Tuberoinfundibular dopaminergic pathway

A
  • ↓ activity → ↑ prolacting → ↓ libido, sexual dysfunction, galactorrhea, gynecomastia (in men)
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75
Q

Input to cerebellum

A
  • Contralateral cortex via middle cerebellar peduncle

- Ipsilateral propioceptive information via inferior cerebellar peduncle from spinal cord

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76
Q

Output from cerebellum

A
  • Sends information to contralateral cortex to modulate movement
  • Output nerves: Purkinje cells → deep nuclei of cerebellum → contralateral cortex via superior cerebellar peduncle
  • Deep nuclei (lateral to medial): dentate → emboliform → globose → fastigial (“Don’t Eat Greasy Foods”)
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77
Q

Lateral lesions to cerebellum

A
  • Affect voluntary movement of extremities

- When injured, propensity to fall toward injured (ipsilateral) side

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78
Q

Medial lesions to cerebellum

A
  • Involvement of midline structures (vermal cortex, fastigial nuclei) and/or flocculonodular lobe → truncal ataxia (wide based cerebelar gait), nystagmus, head tilting
  • Generally result in bilateral motor deficits affecting axial and proximal limb musculature
79
Q

Excitatory pathway

A

Cortical inputs stimulate the striatum, stimulating the release of GABA, which inhibits GABA release from the GPi, disinhibiting the thalamus via the GPi (↑ motion)

80
Q

Inhibitory pathway

A

Cortical inputs stimulate the striatum, releasing GABA that disinhibits STN via GPe inhibition and STN stimulates GPi to inhibit the thalamus (↓ motion)

81
Q

Compare D1 and D2

A

D1 → stimulates the excitatory pathway

D2 → inhibiting the inhibitory pathway (↑ motion)

82
Q

Athetosis

A
  • Slow, writing movements; especially seen in fingers

- Lesion of basal ganglia (eg Huntington)

83
Q

Chorea

A
  • Sudden, jerky, purposeless movements

- Lesion of basal ganglia (eg Huntington)

84
Q

Dystonia

A
  • Sustained, involuntary muscle contractions

- Writer’s cramp; blepharospasm (sustained eyelid twitch)

85
Q

Essential tremor

A
  • High-frequency tremor with sustained posture (eg outstretched arms)
  • Worsened with movement or when anxious
  • Often familial
  • Patients often self-medicate with alcohol, which ↓ tremor amplitude
  • Treatment: nonselective β blockers (eg propanolol), primidone
86
Q

Hemiballismus

A
  • Sudden, wild flailing of 1 arm +/- ipsilateral leg

- Lesion to CONTRALATERAL subthalamic nucleus (eg lacunar stroke)

87
Q

Intention tremor

A
  • Slow, zigzag motion when pointing/extending toward a target
  • Cerebellar dysfunction
88
Q

Myoclonus

A
  • Sudden, brief, uncontrolled muscle contraction
  • Jerks
  • Hiccups
  • Common in metabolic abnormalities such as renal or liver failure
89
Q

Resting tremor

A
  • Uncontrolled movement of distal appendages (most noticeable in hands)
  • Tremor alleviated by intentional movement
  • Parkinson disease (“pill-rolling tremor”)
90
Q

How to treat essential tremor

A

Nonselective β blockers (eg propanolol) or primidone

91
Q

How does neuronal death occur in Huntington disease

A

Neuronal death via NMDA-R binding and glutamate excitotoxicity

92
Q

Compare aphasia and dysarthria

A

Aphasia → higher-order language deficit (inability to understand/ speak/ read/ write)

Dysarthria → motor inability to speak (movement deficit)

93
Q

Conduction apahsia

A
  • Fluent speech
  • Intact comprehension
  • Impaired repetition
  • Can be caused by damage to arcuate fasciculus
94
Q

Global aphasia

A
  • Nonfluent speech
  • Impaired comprehension
  • Impaired repetition
  • Damage to arcuate fasciculus, Broca and Wernicke area
95
Q

Transcortical motor aphasia

A
  • Nonfluent speech
  • Intact comprehension
  • Intact repetition
  • Affects frontal lobe around Broca area, but Broca area is spared
96
Q

Transcortical sensory aphasia

A
  • Fluent speech
  • Impaired comprehension
  • Intact repetition
  • Affects temporal lobe around Wernicke area, but Wernicke area is spared
97
Q

Transcortical aphasia, mixed

A
  • Nonfluent speech
  • Impaired comprehension
  • Intact repitition
  • Broca and Wernicke area and arcuate fasciculus remain intact
  • Surrounding watershed areas affected
98
Q

Lesion to amygdala (bilateral)

A
  • Kluver-Bucy syndrome → disinhibited behavior (eg hyperphagia, hypersexuality, hyperorality)
  • Associated with HSV1 encephalitis
99
Q

Lesion to frontal lobe

A
  • Disinhibition and deficits in concentration, orientation, judgement
  • May have reemergence of primitive reflexes
100
Q

Lesion to nondominant parietal cortex

A

Hemispatial neglect syndrome (agnosia of the contralateral side of the world)

101
Q

Lesion to dominant parietal cortex

A
  • Agraphia
  • Acalculia
  • Finger agnosia
  • Left-right disorientation
  • Gerstmann syndrome → ability to read and speak is intact, results from damage to visual association cortex (located in angular gyrus)
102
Q

Lesion to reticular activating system (midbrain)

A

Reduced levels of arousal and wakefulness (eg coma)

103
Q

Lesion to mamillary bodies (bilateral)

A
  • Werncke-Korsakoff syndrome → confusion, ophthalmoplegia, ataxia; memory loss (anterograde > retrograde amnesia), confabulation, personality changes
  • Associated with thiamine (B1) deficiency and excessive alcohol use
  • Can be precipitated by giving glucose without B1 to a B1 deficient patient
  • Wernicke problems come in a CAN of beer → confusion, ataxia, nystagmus
104
Q

Lesion to basal ganglia

A
  • May result in a tremor at rest, chorea, athetosis
  • Parkinson disease
  • Huntington disease
105
Q

Lesion to cerebellar hemisphere

A
  • Intention tremor
  • Limb ataxia
  • Loss of balance
  • Damage to cerebellum → ipsilateral deficits
  • Fall toward side of lesion
  • Degeneration associated with chronic alcohol use
106
Q

Lesion to cerebellar vermis

A
  • Truncal ataxia

- Dysarthria

107
Q

Lesion to subthalamic nucleus

A

Contralateral hemiballismus

108
Q

Lesion to hippocampus (bilateral)

A

Anterograde amnesia → inability to make new memories

109
Q

Compare lesion to paramedian pontine reticular formation and frontal eye fields

A

Paramedian pontine reticular formation → eyes look AWAY from side of lesion

Frontal eye fields → eyes look toward lesion

110
Q

Cerebral perfusion relies on

A
  • Pressure gradient between mean arterial pressure (MAP) and ICP
  • ↓ BP or ↑ ICP → ↓ cerebral perfusion pressure (CPP)
  • CPP = MAP - ICP
  • If CPP = 0, there is no cerebral perfusion → brain death
111
Q

Therapeutic hyperventilation

A

↓ pCO2 → vasoconstriction → ↓ cerebral blood flow → ↓ intracranial pressure (ICP)

May be used to treat acute cerebral edema (eg secondary to stroke) unreponsible to other interventions

112
Q

Middle cerebral artery stroke

A

Areas of lesions:

  • Motor and sensory cortices → upper limb and face
  • Temporal lobe → Wernicke area
  • Frontal lobe → Broca area

Symptoms:

  • Contralateral paralysis and sensory loss → face and upper limb
  • Aphasia if in dominant (usually left) hemisphere
  • Hemineglect if lesion affects nondominant (usually right) side
113
Q

Anterior cerebral artery stroke

A

Areas of lesions:
- Motor and sensory cortices → lower limb

Symptoms:
- Contralateral paralysis and sensory loss → lower limb

114
Q

Lenticulostriate artery stroke

A

Areas of lesions:

  • Striatum
  • Internal capsule

Symptoms:

  • Contralateral paralysis and/or sensory loss → face and body
  • Absence of cortical signs (eg neglect, aphasia, visual field loss)

Common location of lacunar infarcts, secondary to unmanaged hypertension.

115
Q

Anterior spinal artery stroke

A

Areas of lesions:

  • Lateral corticospinal tract
  • Medial lemniscus
  • Caudal medulla → hypoglossal nerve

Symptoms:

  • Contralateral paralysis → upper and lower limbs
  • ↓ contralateral propioception
  • Ipsilateral hypoglossal deviation (tongue deviates ipsilaterally)

MEDIAL MEDULLARY SYNDROME → caused by infarct of paramedian branches of ASA and/or vertebral arteries

116
Q

Posterior inferior cerebellar artery stroke

A

Areas of lesions:
- Lateral medulla → vestibular nuclei, lateral spinothalamic tract, spinal trigeminal nucleus, nucleus ambiguus, sympathetic fibers, inferior cerebellar peduncle

Symptoms:

  • Vomiting, vertigo, nystagmus
  • ↓ pain and temperature sensation from ipsilateral face and contralateral body
  • Dysphagia, hoarseness, ↓ gag reflex
  • Ipsilateral Horner syndrome
  • Ataxia, dymetria

NUCLEUS AMBIGUUS → effects are specific to PICA lesions

LATERAL MEDULLARY (WALLENBERG) SYNDROME

“Don’t pick a (PICA) horse (hoarseness) that can’t eat (dysphagia)”

117
Q

Anterior inferior cerebellar artery stroke

A

Areas of lesions:

  • Lateral pons → cranial nerve nuclei (vestibular nuclei, facial nerve nucleus, spinal trigeminal nucleus, cochlear nuclei), spinothalamic tract, corticospinal tract, sympathetic fibers
  • Middle and inferior cerebellar peduncles

Symptoms:

  • Vomiting, vertigo, nystagmus
  • Paralysis of face, ↓ lacrimation, salivation, ↓ taste from anterior 2/3 of tongue
  • Ipsilateral ↓ pain and temperature of face
  • Contralateral ↓ pain and temperature of the body
  • Ataxia, dysmetria

LATERAL PONTINE SYNDROME → facial nucleus effects are specific to AICA lesions

“Facial droop means AICA’s pooped”

118
Q

Basilar artery stroke

A

Areas of lesions:
- Pons, medulla, lower midbrain, corticospinal and corticobulbar tracts, ocular cranial nerve nuclei, paramedian pointine reticular formation

Symptoms:

  • Preserved consciousness, eye movement, blinking
  • Quadriplegia, loss of voluntary facial, mouth, and tongue movements

“LOCKED-IN SYNDROME”

119
Q

Posterior cerebral artery stroke

A

Areas of lesions:

  • Occipital cortex
  • Visual cortex

Symptoms:
- Contralateral hemianopia with macular sparing

120
Q

Charcot-Bouchard microaneurysm

A
  • Common
  • Associated with chronic hypertension
  • Affects small vessels (eg in basal ganglia, thalamus)
  • Not seen on angiogram
121
Q

Posterior communicating artery saccular aneurysm

A
  • Compression may cause ipsilateral CN III palsy → mydriasis (“blown pupil”)
  • May also see ptosis, “down and out” eye
122
Q

Central post-stroke pain syndrome

A
  • Neuropathic pain due to thalamic lesions
  • Initial parasthesias followed in weeks to months by allodynia (ordinarily painless stimuli cause pain) and dysesthesia
  • Occurs in 10% of stroke patients
123
Q

Intraparenchymal hemorrhage

A
  • Most commonly caused by systemic hypertension
  • Also seen with amyloid angiopathy (recurrent lobar hemorrhagic stroke in elderly), vasculitis, neoplasm
  • May be secondary to reperfusion injury in ischemic stroke
  • Typically occurs in basal ganglia and internal capsule (Charcot-Bouchard aneurysm of lenticulostriate vessels), but can be lobar
124
Q

Areas most vulnerable to ischemia

A
  • Hippocampus
  • Neocortex
  • Cerebellum
  • Watershed areas
125
Q

Dural venous sinuses

A
  • Large venous channels that run through the dura
  • Drain blood from cerebral veins and receive CSF from arachnoid granulations
  • Empty into internal jugular vein
126
Q

Venous sinus thrombosis

A
  • Presents with sign/symptoms of ↑ ICP (eg headache, seizures, focal neurologic deficits)
  • May lead to venous hemorrhage
  • Associated with hypercoaguable states (eg pregnancy, OCP use, factor V Leiden)
127
Q

Most common locations of vertebral disc herniation

A

L4-L5 or L5-S1

128
Q

Where does the spinal cord end

A

Lower border of L1-L2 vertebrae

129
Q

Where are lumbar punctures performed

A

Between L3-L4 or L4-L5

130
Q

Where does the subarachnoid space end

A

S2

131
Q

Dorsal column

A
  • Ascending
  • Pressure, vibration, fine touch, and propioception
  • 1st order neuron: sensory nerve ending → cell body in DRG → enters spinal cord, ascends ipsilaterally in dorsal column
  • Synapse 1: ipsilateral nucleus cuneatus or gracilis (medulla)
  • 2nd order neuron: decussates in medulla → ascends contralaterally in medial lemniscus
  • Synapse 2: VPL (thalamus)
  • 3rd order neuron: sensory cortex
132
Q

Spinothalamic tract

A
  • Ascending
  • Lateral: pain, temperature
  • Anterior: crude touch, pressure
  • 1st order neuron: sensory nerve ending (A-delta and C fibers) → cell body in DRG → enters spinal cord
  • Synapse 1: ipsilateral gray matter (spinal cord)
  • 2nd order neuron: decussates at anterior white commissure → ascends contralaterally
  • Synapse 2: VPL (thalamus)
  • 3rd order neuron: sensory cortex
133
Q

Lateral corticospinal tract

A
  • Descending
  • Voluntary movement of contralateral limbs
  • 1st order neuron: UMN: cell body in primary motor cortex → descends ipsilaterally (through internal capsule), most fibers decussate at caudal medulla (pyramidal decussation) → descends contralaterally
  • Synapse 1: cell body of anterior horn (spinal cord)
  • 2nd order neuron: LMN: leaves spinal cord
  • Synapse 2: NMJ
134
Q

Poliomyelitis and Werdnig-Hoffmann disease

A
  • Congenital degeneration of anterior horns of spinal cord
  • LMN lesions only
  • “Floppy baby” with marked hypotonia and tongue fasciculation
  • Infantile type has median age of death of 7 months
  • AR
  • Poliomyelitis → asymmetric weakness
  • Werdnig-Hoffmann disease → symmetric weakness
135
Q

Amyotrophic lateral sclerosis

A
  • Combined UMN and LMN deficits with no sensory or bowel/bladder deficits (due to loss of cortical and spinal cord motor neurons, respectively)
  • Can be caused by defect in superoxide dismutase 1
  • Commonly presents with asymmetric limb weakness (hands/feet), fasciculations, and eventual atrophy
  • Treatment: riluzole
136
Q

Complete occlusion of anterior spinal artery

A
  • Spares dorsal columns and Lissauer tract
  • Upper thoracic ASA territory is watershed area, as artery of Adamkiewicz supplies ASA below T8
  • Obstruction of artery of Adamkiewicz can also result in an ASA syndrome with urinary and fecal incontinence and impaired motor function of the legs; sensory is often preserved
137
Q

Tabes dorsalis

A
  • Caused by tertiary syphilis
  • Results from degeneration (demyelination) of dorsal columns and roots → progressive sensory ataxia (impaired propioception → poor coordination)
  • Associated with Charcot joints, shooting pain, Argyll Robertson pupils
  • Exam will demonstrate absence of DTRs and + Rhomberg sign
138
Q

Syringomyelia

A
  • Syrinx expands and damages anterior white commissure of spinothalamic tract (2nd order neurons) → bilateral loss of pain and temperature sensation in cape like distribution
  • Seen with Chiari I malformation
  • Can expand and affect other tracts
139
Q

Vitamin B12 deficiency

A
  • Subacute combined degeneration (SCD) → demyelination of Spinocerebellar tracts, lateral Corticospinal tracts and Dorsal columns
  • Ataxic gait, paresthesia, impaired position/vibration sense
140
Q

Where does poliovirus first replicate

A

Oropharynx and small intestine before spreading via bloodstream to CNS

141
Q

Where is poliovirus recovered from

A

Stool or throat

142
Q

Friedreich ataxia

A
  • AR trinucleotide repeat (GAA) on chromosome 9 in gene that encodes frataxin (iron binding protein)
  • Leads to impairement in mitochondrial functioning
  • Degeneration of multiple spinal cord tracts → muscle weakness and loss of DTRs, vibratory sense, propioception
  • Staggering gait, frequent falling, nystagmus, dysarthria, pes cavus, hammer toes, diabetes mellitus, hypertrophic cardiomyopathy (cause of death)
  • Presents in childhood with kyphoscoliosis

“Friedreich is a fratastic brother: he’s your favorite frat brother, always staggering and falling but has a sweet, big heart”

143
Q

What is the most common cause of death in patients with Frederich ataxia

A

Hypertrophic cardiomyopathy

144
Q

Brown-Sequard syndrome

A
  • Hemisection of spinal cord
  • Ipsilateral UMN lesions below the level of lesion (due to corticospinal tract damage)
  • Ipsilateral loss of tactile, vibration, propioception sense below level of lesion (due to dorsal column damage → this is because decussation occurs at medulla)
  • Contralateral pain and temperature loss below level of lesion (due to spinothalamic tract damage)
  • Ipsilateral loss of all sensation at level of lesion
  • Ipsilateral LMN signs at level of lesion
  • If lesion occurs above T1, patient may present with ipsilateral Horner syndrome due to damage of oculosympathetic pathway
145
Q

Galant reflex

A

Stroking along one side of the spine while the newborn is in ventral suspension (face down) causes lateral flexion of lower body toward stimulated side

146
Q

Parinaud syndrome

A

Paralysis of conjugate vertical gaze due to lesion in superior colliculi (eg stroke, hydrocephalus, pinealoma)

147
Q

Nucleus solitarius

A
  • Visceral sensory information (eg taste, baroreceptors, gut distension)
  • CN VII, IX, X
148
Q

Nucleus ambiguus

A
  • Motor innervation of pharynx, larynx, upper esophagus (eg swallowing, elevation)
  • CN IX, X, XI (cranial portion)
149
Q

Dorsal motor nucleus

A
  • Sends autonomic (parasympathetic) fibers to heart, lungs, upper GI
  • CN X
150
Q

CN VII UMN lesion

A
  • Destruction of motor cortex or connection between motor cortex and facial nucleus in pons → contralateral paralysis of lower muscles of facial expression
  • Forehead is spared due to its bilateral UMN innervation
151
Q

CN VII LMN lesion

A

Destruction of facial nucleus or CN VII anywhere along its course → ipsilateral paralysis of upper and lower muscles of facial expression, hyperacusis, loss of taste sensation to anterior tongue

152
Q

Facial nerve palsy

A
  • Clinical syndrome of peripheral CN VII (LMN) lesion
  • Depending on lesion location and severity, may cause partial or complete loss of function
  • When idiopathic (most common), called BELL PALSY
  • May also be caused by: Lyme disease, herpes simplex, herpes zoster (Ramsay Hunt syndrome), sarcoidois, tumors, diabetes mellitus
  • Treatment is corticosteroids, acyclovir
  • Most patients have gradual recovery of function
153
Q

Cavernous sinus syndrome

A
  • Presents with variable opthalmoplegia, ↓ corneal sensation, Horner syndrome and occasional decreased maxillary sensation
  • Secondary to pituitary tumor mass effect, carotid-cavernous fistula, or cavernous sinus thrombosis related to infection
  • CN VI is most susceptible to injury
154
Q

Cholesteatoma

A
  • Overgrowth of desquamated keratin debris within the middle ear space
  • May erode ossicles, mastoid air cells → conductive hearing loss
155
Q

What produces aqueous humor

A

Produced by nonpigmented epithelium of ciliary body (↓ by β-blockers, α2-agonists, and carbonic anhydrase inhibitors)

156
Q

Aqueous humor outflow

A

Trabecular outflow (90%): drainage through trabecular meshwork → canal of Schlemm → episcleral vasculature (↑ with M3 agonist)

Uveoscleral outflow (10%): drainage into uvea and sclera (↑ with prostaglandin agonists)

157
Q

Open angle glaucoma

A
  • Associated with ↑ age, African-American race, family history
  • Painless, more common in US
  • PRIMARY → cause unclear
  • SECONDARY → blocked trabecular meshwork from WBCs (eg uveitis), RBCs (eg vitreous hemorrhage), retinal elements (eg retinal detachment)
158
Q

Closed or narrow-angle glaucoma

A
  • PRIMARY → enlargement or forward movement of lens against central iris (pupil margin) → obstruction of normal aqueous flow through pupil → fluid builds up behind iris, pushing peripheral iris against cornea and impeding flow through trabecular meshwork
  • SECONDARY → hypoxia from retinal disease (eg diabetes mellitus, vein occlusion) induces vasoproliferation in iris that contracts angle
  • CHRONIC CLOSURE → often asymptomatic with damage to optic nerve and peripheral vision
  • ACUTE CLOSURE → true emergency; ↑ IOP pushes iris forward → angle closes abruptly; very painful red eye with vision loss, halos around lights, rock-hard eye, frontal headache → DO NOT GIVE EPINEPHRINE B/C OF MYDRIATIC EFFECT
159
Q

Uveitis

A
  • Inflammation of uvea, specific name based on location within affected eye
  • Anterior uveitis → iritis
  • Intermediated uveitis → pars planitis (part of ciliary body)
  • Posterior uveitis → choriditis and/or retinitis
  • May have hypopyon (accumulation of pus in anterior chamber) or conjunctival redness
  • Associated with systemic inflammatory disorders (eg sarcoidosis, rheumatoid arthritis, juvenile idiopathic arthritis, HLA-B27 associated conditions)
160
Q

Age related macular degeneration

A
  • Degeneration of macula (central area of retina)
  • Causes distortion (metamorphopsia) and eventual loss of central vision (scotomas)
  • DRY (NONEXUDATIVE, > 80%) → deposition of yellowish extracellular material in and between Bruch membrane and retinal pigment epithelium (“drusen”) with gradual ↓ in vision; prevent progression with multivitamin and antioxidant supplements
  • WET (EXUDATIVE, 10-15%) → rapid loss of vision due to bleeding secondary to choroidal neovascularization; treat with anti-VEGF (eg ranibizumab)
  • Bruch membrane is the innermost layer of the choroid
161
Q

Diabetic retinopathy

A
  • Retinal damage due to chronic hyperglycemia
  • NONPROLIFERATIVE → damaged capillaries leak blood → lipids and fluid seep into retina → hemorrhages and macular edema; treat with blood sugar control
  • PROLIFERATIVE → chronic hypoxia results in new blood vessel formation with resultant traction on retina; treat with peripheral retinal photocoagulation, surgery, anti-VEGF
162
Q

Retinal vein occlusion

A
  • Blockage of central or branch retinal vein due to compression from nearby arterial atherosclerosis
  • Retinal hemorrhage and venous engorgement, edema in affected areas
163
Q

Retinal detachment

A
  • Separation of neurosensory layer of retina (photoreceptor layer with rods and cones) from outermost pigmented epithelium (normally shields excess light, supports retina) → degeneration of photoreceptors → vision loss
  • May be secondary to retinal breaks, diabetic traction, inflammatory effusions
  • Visualized on fundoscopy as crinkling retinal tissue and changes in vessel direction
  • Breaks more common in patients with myopia and/or history of head trauma
  • Often preceded by posterior vitreous detachment (flashes and floaters) and eventual monocular loss of vision
164
Q

Retinitis pigmentosa

A
  • Inherited retinal degeneration
  • Painless, progressive vision loss beginning with night blindness (rods affected first)
  • Bone spicule shaped deposits around macula
165
Q

Retinitis

A
  • Retinal edema and necrosis leading to scar
  • Often viral (CMV, HSV, VZV) but can be bacterial or parasitic
  • May be associated with immunosuppression
166
Q

Meyer loop

A
  • Inferior retina

- Loops around interior horn of lateral ventricle in the temporal lobe

167
Q

Dorsal optic radiation

A
  • Superior retina

- Takes the shortest path via internal capsule in the parietal lobe

168
Q

Charcot triad of MS

A
  • Scanning speech
  • Intention tremor (also Incontinence and Internuclear ophthalmoplegia)
  • Nystagmus

“SIN”

169
Q

Treatment for acute inflammatory demyelinating polyradiculopathy

A
  • Respiratory support is critical until recovery
  • Plasmapheresis, IV immunoglobulins
  • No role for steroids
170
Q

Acute disseminated (postinfectious) encephalomyelitis

A
  • Mutlifocal periventricular inflammation and demyelination after infection or vaccination
  • Presents with rapidly progressive multifocal neurologic symptoms, altered mental status
  • Autoimmune disease marked by sudden widespread inflammation of brain and spinal cord, destruction of white matter
171
Q

Charcot-Marie-Tooth disease

A
  • AKA hereditary motor and sensory neuropathy (HMSN)
  • Group of progressive hereditary nerve disorders related to the defective production of protein involved in the structure and function of peripheral nerves or the myelin sheath
  • AD
  • Assoicated with foot deformities (pes cavus), lower extremity weakness and sensory deficits
172
Q

Adrenoleukodystrophy

A
  • X linked disorder typically affecting males
  • Disrupts metabolism of very-long-chain-fatty acids → excessive buildup in nervous system, adrenal glands, testes
  • Progressive disease that can lead to long-term coma/death and adrenal gland crisis
173
Q

Partial (focal) seizures

A
  • Affect single area of the brain
  • Most commonly originate in medial temporal lobe
  • Often preceded by seizure aura
  • Can secondarily generalize
  • TYPES → simple partial, complex partial
  • SIMPLE PARTIAL → consciousness intact; motor, sensory, autonomic, psychic
  • COMPLEX PARTIAL → impaired consciousness
174
Q

Generalized seizures

A
  • ABSENCE → petit mal, 3 Hz, no postictal confusion, blank stare
  • MYOCLONIC → quick, repetitive jerks
  • TONIC-CLONIC → grand mal, alternating stiffening and movement
  • TONIC → stiffening
  • ATONIC → “drop” seizures (falls to floor); commonly mistaken for fainting
175
Q

Excruciating periorbital pain with lacrimation and rhinorrhea

A

Cluster headache

176
Q

Cluster, tension and migraine localization

A
  • Cluster → unilateral
  • Tension → bilateral
  • Migraine → unilateral
177
Q

Peripheral vertigo

A
  • More common
  • Inner ear etiology (eg semicircular canal debris, vestibular nerve infection, Meniere disease [low frequency hearing loss])
  • Positional testing → DELAYED horizontal nystagmus
178
Q

Central vertigo

A
  • Brain stem or cerebellar lesion (eg stroke affecting vestibular nuclei or posterior fossa tumor)
  • Findings: directional change of nystagmus, skew deviation, diplopia, dysmetria
  • Positional testing → IMMEDIATE nystagmus in any direction (may change directions)
  • Focal neurologic findings
179
Q

Encephalotrigeminal angiomatosis

A
  • Sturge-Weber syndrome
  • Congenital, non-inherited (somatic) developmental anomaly of neural crest derivatives due to activating mutation of GNAQ gene
  • Affects small (capillary-sized) blood vessels → port-wine stain of the face (nevus flammeus, a non-neoplastic “birth mark” in CN V1/V2 distribution)
  • Ipsilateral leptomeningeal angioma → seizures/epilepsy
  • Intellectual disability
  • Episcleral hemangioma → ↑ IOP → early-onset glaucoma
  • STURGE-Weber → Sporadic, port-wine Stain, Tram track calcifications (opposing gyri), Unilateral, Retardation, Glaucoma, GNAQ gene, Epilepsy
180
Q

“Pseudopalisading” pleomorphic tumor cells that border central areas of necrosis and hemorrhage

A

Glioblastoma multiforme (grade IV astrocytoma)

181
Q

Can produce EPO and cause secondary polycythemia

A

Hemangioblastoma → most often cerebellar

182
Q

Chicken-wire capillary pattern

A

Oligodendroglioma

183
Q

Cystic + solid gross appearance

A

Pilocytic astrocytoma

184
Q

Can compress 4th ventricle and cause noncommunicating hydrocephalus

A

Medulloblastoma

185
Q

Drop metastases to spinal cord

A

Medulloblastoma

186
Q

Rod shaped blepharoplasts (basal ciliary bodies) found near nucleus

A

Ependymoma

187
Q

Cholesterol crystals found in “motor oil” like fluid within tumor

A

Craniopharyngioma

188
Q

β-hCG production

A

Pinealoma

189
Q

Pinealoma

A
  • Tumor of pineal gland
  • Can cause Parinaud gland (compression of tectum → vertical gaze palsy)
  • Obstructive hydrocephalus (compression of cerebral aqueduct)
  • Precocious puberty in males (β-hCG production)
  • Histologically similar to germ cell tumors (eg testicular seminoma)
190
Q

Cingulate (subfalcine) herniation under falx cerebri

A

Can compress anterior cerebral artery

191
Q

Downward transtentorial (central) herniation

A
  • Caudal displacement of brain stem → rupture of paramedian basilar artery branches → Duret hemorrhages
  • Usually fatal
192
Q

Uncal herniation

A
  • Uncus = medial temporal lobe
  • Compresses ipsilateral CN III (blow pupil, “down and out” gaze, ipsilateral PCA (contralateral homonymous hemianopiawith macular sparing), contralateral crus cerebri at the Kernohan notch (ipsilateral paresis; a “false localization sign”)
193
Q

Cerebellar tonsillar herniation into the foramen magnum

A

Coma and death results when these herniations compress the brain stem

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