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Citow Review Book > Neurology > Flashcards

Neurology Flashcards

1
Q

Primitive reflexes should not persist beyong _______.

A

3-5 months

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2
Q

What is the Galant reflex?

A

stroking one side of the back of the infant causes lateral curvature of the

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3
Q

What is the Moro reflex?

A

when support is lost, the arms will abduct (swing out) and extend and hands will open followed by adduction and flexion

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4
Q

Stuttering affects what percent of children?

A

2%

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5
Q

What improves fluency in stuttering?

A

ethanol and singing

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6
Q

Mental retardation affects what percent of births?

A

3%

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7
Q

What generally separates delirium from other confusional states?

A

typically has autonomic symptoms (dilated pupils, tachycardia, hyperthermia, increased sweating)

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8
Q

What percent of Alzheimer’s disease is sporadic? What is the life expectancy following the diagnoses of Alzheimer/s?

A

95% usually progress to death in 7 to 10 years

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9
Q

What type of cortical atrophy is seen in Alzheimer’s?

A

general cortical atrophy, most pronounced in parietal and temporal lobes

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10
Q

What histologic features are seen in Alzheimer’s?

A
  • Neurofibrilary tangles- Senile Plaques-Hirano’s bodies
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11
Q

What are neurofibrilary tangles?

A

intraneuronal inclusion

Paired helical filaments formed by hyperphosphorylation of microtubule- associated protein tau

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12
Q

What are senile plaques?

A

extracellular accumulation

Comprised of amyloid β peptides, proteolytic product of amyloid precursor protein (APP)

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13
Q

What are two scenarios that lead to increased accumulation of amyloid?

A

Trisomy 21 (Down’s syndrome)

ApoE4 mutation

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14
Q

APP is on what chromosome?

A

Ch 21

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15
Q

What are Hirano’s bodies?

A

intraneuronal inclusion

eosinophilic intracellular aggregates of actin and associated proteins in neurons

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16
Q

What neurotransmitter changes are seen in Alzheimer’s disease?

A

decreased ACh and increased glutamate

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17
Q

Name three AChEi.

A

donepizil, galantamine, rivastigmine

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18
Q

What histologic features are seen in Pick’s disease?

A

Pick’s bodies and Pick’s cells

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19
Q

What are Pick’s bodies?

A

intracellular inclusions of tau protein

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20
Q

What are Pick’s cells?

A

swollen neurons

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21
Q

What clinical picture typifies Lewy Body Disease?

A

alzheimer like patient with early onset hallucinations and parkinsonian features

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22
Q

What neurotransmitter changes are seen in Lewy Body Disease?

A

Loss of ACh and dopamine producing neurons

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23
Q

What histologic feature is characteristic of Lewy Body Disease?

A

a-synuclein cytoplasmic inclusions (Lewy Bodies)

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24
Q

What cerebral structure is affected in Wernicke-Korsakoff Syndrome?

A

atrophy of the mammillary bodies

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25
Q

What is apraxia? What cortical lesion can cause apraxia?

A

inability to perform complex movements in the absence of paralysis

premotor lesion (lateral portion of BA 6)

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26
Q

Frontal Eye fields are located in BA ___. Stimulation causes _____ whereas lesioning causes ______.

A

BA 8

contralateral eye movement

impaired contralateral gaze

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27
Q

Broca’s speech is associated with what BA and what anatomical structures?

A

BA 44 and 45pars opercularis and pars triangularis

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28
Q

What is abulia? What cortical lesion can cause it?

A

decrease in thought, movement, speech, will, or initiative

b/l frontal lobe lesions can cause it

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29
Q

Akinetic mutism can be seen in adults with what cortical lesion?

A

b/l cingulate lesions

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30
Q

What are the symptoms of pseudobulbar palsy?

A

unable to close their eyes or move their mouth ortongue, but are able to yawn, cry, cough, etc., which are reflexes of the pons and medulla

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31
Q

What leads to pseudobulbar palsy?

A

damage to cortical motor fibers projecting to lower brainstem

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32
Q

Stimulation to supplementary motor cortex leads to _______.

A

gross b/l movements

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33
Q

What is the function of the ventromedial pathway? What composes it?

A

controls axial movements and posture

tectum, vestibular nuclei, and pontine and medullary reticular nuclei to the interneurons in the ventromedial spinal cord

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34
Q

Dominant parietal lobe is involved in ________ and non-dominant parietal lobe is involved in ________.

A

mathematical calculations and language

visuospatial relationships and geographic memory

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35
Q

The secondary somatosensory area is located on ______ and is BA ______.

A

supramarginal gyrus

area 40

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36
Q

Primary gustatory cortex is located on ______ and is BA _______.

A

anterior portion of parietal operculum

43

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37
Q

What causes Gerstmann’s syndrome?

A

dominant parietal lobe lesion at angular gyrus (area 39)

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38
Q

Gerstmann’s syndrome is characterized by what symptoms?

A

right/left dissociation, finger agnosia, acalculia, and agraphia

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39
Q

The uncinate fasciculus connects the ______ to the ______,

A

anterior temporal lobe to the orbitofrontal gyrus

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40
Q

Arcuate fasciculus connects ______ and ________.

A

Wernicke’s area and Broca’s area

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41
Q

Heschl’s gyrus is the _______, located in ______, and is BA ________.

A

primary auditory cortex

posterosuperior temporal lobe deep to Sylvian fissure

41, 42

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42
Q

Kluver Bucy syndrome results from ________.

A

b/l amygdala injuries

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43
Q

Kluver Bucy syndrome is characterized by _______.

A

Absence of emotional response, compulsion to explore all objects visually, tactilely, and orally; hypersexuality and visual agnosia

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44
Q

The Band of Gennari is located in ________.

A

the fourth layer of the occipital lobes

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45
Q

Cortical blindness is characterized by what on EEG?

A

absence of a-waves on EEG in the occipital waves

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46
Q

What is Anton’s syndrome?

A

an anosognosia; cortical blindness with an affected association area such that the patient denies that he or she is blind

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47
Q

What is Balint’s syndrome?

A

caused by a bilateral lesion in the parietooccipital cortices

Ocular ataxia and apraxia with normal extraocular function. Associated with inattention to the peripheral visual field and simultanagnosia

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48
Q

<p>What connects the receptive and expressive speech areas of the brain?</p>

A

<p>arcuate fasciculus</p>

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49
Q

What is the concept of kindling in regards to seizures?

A

seizures beget seizures

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50
Q

What is the irritative zone?

A

area of cortex that generates interictal spikes

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51
Q

What is the ictal onset zone?

A

area of cortex where seizures are generated

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52
Q

What is an epileptogenic lesion?

A

structural abnormality that is direct cause of epileptic seizures

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53
Q

What is a symptomatogenic lesion?

A

area of the brain that first manifests seizure symptoms

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54
Q

What is the functional deficit zone?

A

cortical area of nonepileptic dysfunction

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55
Q

What is the epileptogenic zone?

A

area of brain necessary and sufficient for initiating seizures; removal or disconnection required for amelioration of seizures

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56
Q

What is Todd’s paralysis? What causes it?

A

post ictal paralysis, could be due to decreased glucose or increased lactate

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57
Q

What EEG findings are seen on Absence seizures?

A

3 Hz Spike and Wave

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58
Q

What does pathology show on mesial temporal lobe sclerosis?

A

hippocampal atrophy with gliosis and neural loss in CA1, CA4, and dentate gyrus

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59
Q

What is West’s syndrome?

A

infantile spasms; repeated extension and flexion of the neck, trunk, and extremities

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60
Q

What is characterizes West’s syndrome (infantile spasms) on EEG?

A

hypsarrhythmia (chaotic background with random high voltage, slow spike and wave)

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61
Q

What is the treatment for infantile spasms (West syndrome)?

A

ACTH, vigabatrin, and ketogenic diet

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62
Q

What are Benign epilepsy of childhood with Rolandic spikes? What is the typical clinical course?

A

focal motor seizures typically of the face during sleep-wake transitions; conscious but aphasic post ictally

remits spontaneously by adolescences

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63
Q

What is Juvenile myclonic epilepsy?

A

myoclonus in the morning without loss of consciousness, affects upper > lower

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64
Q

What is the inheritance pattern of Juvenile myoclonic epilepsy?

A

Autosomal dominant

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65
Q

What is the treatment of juvenile myoclonic epilepsy?

A

valproic acid for life

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66
Q

What characterizes Lennox-Gastaut syndrome?

A

multiple seizure types with mental retardation

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67
Q

What surgical options are available for patients with Lennox Gastaut syndrome?

A

VNS and corpus callosotomy

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68
Q

What is the mechanism of action of phenytoin?

A

Na Channel blockade

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69
Q

There are many side effects to phenytoin. What are some of the most serious ones?

A

Steven Johnson syndrome, cerebellar degeneration

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70
Q

What is the mechanism of action of Carbamazepine/Oxacarbazepine?

A

Na channel blockade

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71
Q

What are the side effects of Carbemazepine/Oxacarbazepine?

A

Pancytopenia and SIADH

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72
Q

What is the MOA of Lacosamide?

A

Na channel blocker

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73
Q

What is the MOA of Ethosuximide?

A

Ca Channel blocker

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74
Q

What is the MOA of acetazolamide?

A

carbonic anhydrase inhibitor

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75
Q

What is the MOA of lamotrigine?

A

inhibit presynaptic glutamate release

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76
Q

What is the MOA of Topiramate?

A

affects Na channels, GABA, and Glutamate receptors

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77
Q

What is the MOA of Valproic acid?

A

inhibits Na and Ca channels

increases GABA synthesis and activity

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78
Q

What are the side effects of Valproic acid?

A

Thrombocytopenia, hyperammonemia (hepatotoxicity in < 2 years)

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79
Q

What is the MOA of Felbamate?

A

NMDA receptor antagonist

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80
Q

What are the side effects of Felbamate?

A

aplastic anemia and hepatic failure

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81
Q

Absence seizures are thought to originate/involve what cerebral structure?

A

thalamus

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82
Q

What is the go to treatment for absence seizures?

A

Ethosuximide

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83
Q

WADA testing determines _______.

A

laterality of speech and memory

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84
Q

What is injected in a WADA test?

A

sodium amobarbital

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85
Q

Corpus callosotomy can be used for _______ and _______.

A

atonic seizures (drop attacks)

seizures with secondary generalization

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86
Q

What HLA type is associated with MS?

A

HLA-DR2

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87
Q

What causes an oligoclonal band pattern in MS?

A

elevated IgG in the CSF

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88
Q

What is Schilder’s disease?

A

massive demyelination in children and adolescents, affecting bilateral hemispheres, brainstem, and cerebellum

Malignant course

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89
Q

What is Balo’s concentric sclerosis?

A

alternating spared and damaged white matter progressing in concentric ring like fashion from the ventricles outward

typically fatal

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90
Q

What is the pathophysiology of neuromyelitis optica (Devic’s disease)?

A

IgG autoantibodies versus aquaporin 4 on astrocytes

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91
Q

What are the imaging findings for neuromyelitis optica?

A

MRI shows optic nerve/chiasm enhancement and/or spinal cord lesion affecting more than three segments in length

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92
Q

Describe the tremor seen in Parkinson’s disease.

A

resting tremor of 4-5 per second in the lips, head, and fingers (pill rolling)

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93
Q

Where is the mutation in primary dystonia?

A

DYT1 TOR1A gene

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94
Q

What is the other name for Wilson’s Disease?

A

hepatolenticular degeneration

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95
Q

What tests are indicative of Wilson’s disease?

A

LFTs, slit lampe test (Kayser-Fleischer rings), decreased ceruloplasmin, elevated urine copper

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96
Q

What defines Tourette’s syndrome?

A

multiple motor tics with at least one vocal tic

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97
Q

Name two COMT inhibitors.

A

entacapone, tolcapone

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98
Q

Name two Monoamine oxidase B inhibitors.

A

selegiline, rasagiline

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99
Q

What is olivopontocerebellar degeneration?

A

multiple system atrophy associated with ataxia

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100
Q

What is Striatonigral degneration?

A

form of MSA in which Parkinsonian features predominate although autonomic and cerebellar symptoms can be seen

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101
Q

What is Shy-Drager syndrome?

A

MSA with autonomic dysfunction predominating; Orthostatic hypotension is the key finding

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102
Q

What is Progressive Supranuclear Palsy?

A

triad of :

  • progressive supranuclear ophthalmoplegia (impaired voluntary vertical gaze, but preserved doll’s eyes)
  • pseudobulbar palsy
  • axial rigidity
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103
Q

What is the inheritance of Huntington’s disease?

A

AD

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104
Q

What is the genetic abnormality seen in Huntington’s disease?

A

great than forty tri-nucleotide CAG repeat on Ch 4

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105
Q

Where is degeneration seen in Huntington’s disease?

A

Frontal lobe and caudate

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106
Q

Autonomic dysfunction is associated with what type of headache?

A

cluster headaches

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107
Q

What procedure can be used to treat refractory cluster headaches?

A

sphenopalatine ganglion lesioning

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108
Q

What is Tolosa-Hunt syndrome?

A

nonspecific inflammation of the cavernous sinus or superior orbital fissure

ocular and retro-orbital pain, ocular motor paralysis (pupil may be involved), and possibly sensory loss over the forehead (CNs III, IV, V1, and VI, sympathetics)

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109
Q

Where is the area of compression/demyelination of the Trigeminal nerve in Trigeminal neuralgia?

A

Obersteiner-Redlich zone

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110
Q

Steroids help prevent what complication of temporal arteritis?

A

Blindness

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111
Q

What is Ramsay Hunt syndrome?

A

geniculate ganglion (CN VII) herpes infection with ear pain and vesicles (in the external auditory meatus), facial weakness, possible hearing deterioration, vertigo, and tinnitus

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112
Q

Climbing fibers enter via the ________ and mossy fibers enter via the _______.

A

inferior cerebellar peduncle

middle cerebellar peduncle

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113
Q

What is the main function of the flocculonodular lobe?

A

vestibular function (inputs from vestibular apparatus and nuclei)

114
Q

What is the main function/input of the anterior lobe of the cerebellum?

A

posture, muscle tone, processing information from muscle tendons

input from spinocerebellar tracts

115
Q

What does the anterior lobe of the cerebellum arise from?

A

dorsal nucleus of Clarke

116
Q

The output of the vermis is via the __________.

A

fastigial nucleus

117
Q

Output of the intermediate zone is via ______.

A

globose and emboliform nuclei

118
Q

Output of the latera zone is via ________.

A

dentate nucleus

119
Q

Anterior lobe of the cerebellum degeneration occurs from _______ or _______.

A

ethanol and malnutrition

120
Q

What is titubation? If present, where is the pathology?

A

3 Hz anterior/posterior head bob

cerebellar

121
Q

What causes slurred speech?

A

corticobulbar tract interruption

122
Q

What is the inheritance pattern of Friedrich’s ataxia?

A

AR

123
Q

What is the genetic cause of Friedrich’s ataxia?

A

GAA repeat on Frataxin gene on Ch 9

124
Q

Pathologically what occurs in Friedrich’s ataxia?

A

Demyelination of posterior columns, corticospinal, ventral, and lateral spinocerebellar tracts, leading to gait ataxia and clumsiness

125
Q

The most frequent visual disorder in children is ______. In adults, it’s ________.

A

Myopia (nearsigtedness)

Hyperopia (farsightedness)

126
Q

On CN III, why does a fixed and dilated pupil present earlier than a “down and out” motor palsy with a compressive lesion?

A

parasympathetics are located peripherally on the nerve, motor is central

127
Q

What causes pinpoint pupils?

A

pontine lesion causing loss of sympathetic input (from the hypothalamus to the superior cervical ganglion) resulting in unapposed sympathetic tone

128
Q

What defines an Argyll Robertson pupil?

A

reacts to accomodation and not light

129
Q

What is Adie’s tonic pupil? What causes it? What’s the treatment?

A

mydriasis and blurry vision that occurs at 20 to 40 years with female predominance from degeneration of the ciliary ganglion (parasympathetics)

eyes respond to accommodation and not light

no treatment needed

130
Q

What nerve brings sympathetic fibers to Muller’s muscle in the eyelid? What does this cause?

A

long ciliary nerve

ptosis (such as in Horner’s syndrome)

131
Q

What is pilocarpine? How does it affect pupils?

A

ACh agonist

should constrict any pupil unless dilated by atropine

132
Q

The region in the retina responsible for high acuity vision is called the ________ and the central portion of it is called ________.

A

macula

fovea

133
Q

The macula contains (rods/cones) while the fovea contains (rods/cones).

A

rods and cones

rods

134
Q

What is Terson’s syndrome?

A

vitreous hemorrhage associated with SAH/ICHis associated with more severe SAH/ICH

135
Q

What are Roth’s spots? What are they associated with?

A

a pale spot in the retina from the accumulation of white blood cells and fibrin

Associated with subacute bacterial endocarditis or embolic plaques

136
Q

What percent of people with optic neuritis develop MS?

A

75%

137
Q

What percent of optic neuritis cases are bilateral?

A

10%

138
Q

What percentage of optic neuritis patients completely recover their vision? What symptoms often lingers?

A

30%

color blindness (dyschromatopsia)

139
Q

What can be seen on fundoscopic exam with ischemic optic neuropathy?

A

flame hemorrhages and edema w/ disc atrophy

140
Q

Toxic and nutritional optic neuropathies cause what kind of visual loss?

A

bilateral, symmetric central, or centrocecal scotomas(unlike demyelinating disease) with normal peripheral fields

141
Q

What is the most common type of glaucoma?

A

open angle glaucoma

142
Q

What is the visual loss in gluacoma?

A

arcuate defect in the upper and lower nasal fields

143
Q

What causes floaters?

A

opacities in the vitreous humor

144
Q

A sudden increase in floaters with a bright flash of light is a concern for what?

A

retinal detachment

145
Q

Uveitis accounts for what percent of blindness in the US?

A

10%

146
Q

What is the inheritance of Leber’s hereditary optic neuropathy?

A

mitochondrial

147
Q

What is the clinical picture of Lever’s hereditary optic neuropathy?

A

optic atrophy with painless vision loss in one eye before the other

148
Q

What is the affected chromosome in Retinitis pigmentosa?

A

Ch 3

149
Q

What occurs in Retinitis pigmentosa?

A

b/l degeneration of all layers of the retina with foveal sparing

150
Q

What occurs in Stargardst disease?

A

b/l degneration of the macula and fovea (opposite of retinitis pigmentosa)

151
Q

What is a junctional scotoma? What causes it?

A

ipsilateral monocular blindness and contralateral superotemporal quadrantanopia

optic nerve/chiasm junction (think von Willebrand’s knee)

152
Q

What ischemic stroke causes macular sparing? Why?

A

PCA strokes

macula represented by occipital poles which is supplied by MCA collaterals

153
Q

What and where is the vertical gaze center?

A

rostral interstitial nucleus of the medial longitudinal fasciculas (riMLF) located at the junction of the midbrain and thalamus

154
Q

What nucleus assists in maintaining vertical gaze?

A

interstitial nucleus of Cajal

155
Q

What comprises the horizontal gaze center?

A

paramedian pontine reticular formation (PPRF) and CN VI nuclei

156
Q

Damage to one CN VI nucleus causes what clinical findings? Why?

A

failure of abduction of the ipsilateral eye and adduction (medial rectus) of the contralateral eye

CN VI nerve fibers cross to the contralateral CN III to innervate the medial rectus

157
Q

What midbrain nucleus is responsible for the accommodation reflex?

A

Perlia’s nucleus

158
Q

Superior colliculus is responsible for coordinating what eye movement?

A

contralateral horizontal

159
Q

What composes Parinaud’s syndrome?

A
  • impaired gaze
  • impaired convergence
  • mydriasis
  • convergence nystagmus
  • lid retraction (Collier’s sign)
160
Q

Decreased downgaze is seen in what pathology?

A

progressive supranuclear palsy

161
Q

Downward eye deviation can by caused by what hemorrhage location?

A

thalamic hemorrhages

162
Q

What causes intranuclear opthalmoplegia?

A

lesion of the ipsilateral MLF rostral to the abducens nerve

163
Q

What is the clinical picture of patients with INO?

A

ipsilateral eye cannot adduct completely while contralateral eye has nystagmus as it abducts

164
Q

What is the most common cause of INO in the young?

A

MS

165
Q

Neurons in what CNS structures undergo turnover?

A

Olfactory receptor cells, subventricular zone, dentate gyrus

166
Q

What symptoms characterize Kallman’s syndrome? What causes it?

A

absent or delayed puberty with impaired smell due to hypothalamic hypogonadism and failure of olfactory bulbs to form

167
Q

Seizures in what location cause olfactory hallucinations?

A

temporal

168
Q

Conductive hearing loss is ______ hearing loss while sensorineural hearing loss is ______ hearing loss.

A

uniform

high frequency

169
Q

Vestibular schwannomas cause ________ hearing loss.

A

high tone

170
Q

What is the symptomatology of Meniere’s disease?

A

recurrent vertigo with fluctuating unilateral tinnitus and low tone sensironeural hearing loss

171
Q

On which side is the nystagmus in Meniere’s disease?

A

contralateral to the affected side

172
Q

On to which side do patient’s generally fall in Meniere’s disease?

A

ipsilateral to the affected side

173
Q

What is the physiologic cause of Meniere’s disease?

A

distention of the endolymphatic duct with rupture into the perilymph

174
Q

What medications can be used for prophylaxis in Meniere’s disease?

A

diuretics

175
Q

What are Kussmaul respirations associated with?

A

rapid breathing associated with acidosis

176
Q

MIdbrain lesions cause ______ pupils.

A

fixed and dilated

177
Q

Pontine lesions cause _______ pupils.

A

pinpoint

178
Q

Opiates cause ______ pupils.

A

pinpoint

179
Q

Anesthesia generally causes _______ pupils.

A

mid sized fixed

180
Q

Atropine toxicity causes ______ pupils.

A

dilated

181
Q

What is decorticate posturing?

A

upper extremity flexion and adduction with lower extremity posturing

182
Q

What are Lundberg A waves?

A

plateau waves that cover every `15-30 minutes

sustained, reach levels around 50 mm Hg, may cause death

183
Q

What are Lunderg B waves?

A

pressure pulses that last 30 seconds to 2 minutes, 10-20 mmHg less than A waves

184
Q

What are Lunberg C waves?

A

low amplitude waves that occur every 4-8 minutes, can occur on top of A waves

185
Q

In what percent of pseudotumor patient’s dose unilateral optic nerve sheath fenestration cause bilateral vision improvement?

A

66%

186
Q

In a normal ICP waveform, what do P1, P2, and P3 correlate with? What are their typical relative amplitudes?

A

P1 > P2 > P3

P1: percussion wave - arterial pulsation

P2: tidal wave - compliance

P3: dicrotic wave - closure of aortic valve

187
Q

Hemorrhage accounts for what percent of stroke?

A

10%

188
Q

What is the stroke mortality at 1 month? 1 year? 3 years? 7 years?

A

19%, 23%, 46%, 60%

189
Q

What is the angiogram risk of stroke in the general population? In patient’s with atherosclerosis?

A

1-3%up to 5%

190
Q

How common do seizures occur in cortical embolic strokes?

A

20%

191
Q

What is the risk of stroke following TIA? What is the risk of MI?

A

10% at 3 months, 26% over 2 years

21% over 5 years

192
Q

When is the highest stroke risk following TIA?

A

first 48 hours

193
Q

What is the risk of ICH with tPA?

A

6%

194
Q

Endovascular clot retrieval, angioplasty, or intra-arterial tPA may be performed up to ________ after onset of stroke deficit.

A

4.5 to 6 hours

195
Q

Decompressive hemicraniectomy in stroke has been show to _______ and ________.

A

decrease ICP, increase survival

196
Q

Why are thrombotic strokes generally slower onset than embolic strokes?

A

more time for collaterals to form in thrombotic strokes

197
Q

tPA can be given to patients when stroke deficit symptoms onset within _______.

A

3 hours

198
Q

What histologic finding is seen with lacunar strokes?

A

lipohyalin degeneration of small vessels (lipohyalinosis)

199
Q

What were the conclusions of the NASCET trial?

A

North American Symptomatic Endarterectomy Trial

  • CEA in symptomatic patients w/ >70% stenosis
  • reduces stroke risk from 26% to 9% over 2 years
200
Q

What were the conclusions of the ACAS trial?

A

Asymptomatic Carotid Atherosclerosis Study

  • CEA in asymptomatic patients w/ >60% stenosis
  • reduces stroke risk from 11% to 5% over 5 years
201
Q

Stroke of the anterior choroidal artery territory results in what sympotmology?

A

Contralateral hemiplegia, hemianesthesia, and homonymous hemianopsia

202
Q

What is Weber’s syndrome?

A

midbrain stroke syndrome from occlusion of interpeduncular branches to the midbrain

ipsilateral CN III palsy w/ contralateral hemiplegia

203
Q

Occlusion of what posterior circulation artery can cause horner’s syndrome?

A

AICA

204
Q

Ventral pontine syndrome is caused by occlusion of what vessel?

A

basilar artery brances (circumfrential/paramedian arteries)

205
Q

What’s another name for ventral pontine syndrome?

A

Millard-Gubler syndrome

206
Q

What are the symptoms in Ventral pontine syndrome?

A

Ipsilateral facial weakness
Contralateral hemiplegia
Horizontal diplopia

207
Q

What is another name for lateral pontine syndrome?

A

Marie-Foix syndrome

208
Q

What vessel is occluded in lateral pontine syndrome?

A

basilar artery circumferential brance or AICA

209
Q

What are the symptoms in lateral pontine syndrome?

A

Contralateral hemiplegia
Contralateral decreased pain and temperature
Ipsilateral ataxia

210
Q

What is another name for medial medullary syndrome?

A

Dejerine’s syndrome

211
Q

What vessel is occluded in medial medullary syndrome?

A

Vertebral artery

212
Q

What are the symptoms in medial medullary syndrome?

A

Contralateral hemiplegia
Contralateral impaired posterior column function
Ipsilateral tongue weakness

213
Q

What is another name for lateral medullary syndrome?

A

Wallenberg’s syndrome

214
Q

What vessel is occluded in lateral medullary syndrome?

A

PICA

215
Q

What are the symptoms in lateral medullary syndrome?

A

Decreased contralateral pain and temperature
Ipsilateral Horner’s syndrome
Ipsilateral decreased facial pain and temperature(descending fibers and spinal nucleus of V)
NystagmusNauseaVertigo (vestibular nuclei)
Decreased gag
HoarsenessDysphagiaCord paralysis (IX and X)
Decreased taste (solitary tract)
Ipsilateral falling
Ataxia (restiform body)
Hiccups

216
Q

What nerve innervates the ligaments, periosteum, outer annulus, and facet capsule of the spine?

A

sinuvertebral nerve

217
Q

As we age, glycosaminoglycans in the nucleus pulposes is replaced by ___________.

A

collagen and elastin

218
Q

Lumbar disc disease is exacerbated by what movement?

A

flexion (increasing disc protrusion)

219
Q

Spondylosis and lumbar stenosis are exacerbated by what movement?

A

Extension (buckling of the ligamentum flavum)

220
Q

Where are the most common sites for disc disease in the lumbar spine?

A

L5-S1 (45-50%)L4-L5 (40-45%)

221
Q

Where are the most common sites for disc disease in the cervical spine?

A

C6-C7 (70%)C5-C6 (20%)

222
Q

Ankylosing is associated with HLA ____?

A

HLA B27

223
Q

Ankylosing spondylitis is associated with what other conditions?

A

Reiter’s syndrome, psoriasis, iritis, and inflammation of the intestines

224
Q

Ankylosing spondylitis leads to ______ deformity of the spine.

A

kyphotic

225
Q

What are the most common origins of spinal metastases?

A

breast, lung, thyroid, prostate, kidney, and multiple myeloma

226
Q

<p>What is the genetic cause of Charcot-Marie-Tooth syndrome?</p>

A

<p>mutation of peripheral myelin protein 22</p>

227
Q

<p>What is seen histologically with Charcot-Marie-Tooth syndrome?</p>

A

<p>onion bulb appearance of nerves</p>

228
Q

<p>What is the symptomolgy progression of Charcot-Marie-Tooth syndrome?</p>

A

<p>Distal muscle weakness with atrophy starting in the legs and often develop lower extremity deformities<br></br>(toe walking, foot eversion, hammertoes)</p>

229
Q

<p>What is Guillain-Barre syndrome?</p>

A

<p>acute inflammatory demyelinating polyneuropathy. that results in ascending weakness, paralysis, and hyporeflexia ± sensory or autonomic involvement</p>

230
Q

<p>Forty percent of GBS patients are seropositive for \_\_\_\_\_\_\_\_\_\_.</p>

A

<p>Campylobacter Jejuni</p>

231
Q

<p>How long does it take to recover from GBS?</p>

A

<p>1-3 months (depends on remyelination)</p>

232
Q

<p>What is seen in nerve conduction studies in GBS?</p>

A

<p>delay of F waves</p>

233
Q

<p>What is seen in CSF in GBS?</p>

A

<p>elevated protein without pleocytosis</p>

234
Q

<p>What is the treatment of GBS?</p>

A

<p>plasma exchange; no role for steroids</p>

235
Q

<p>What is Chonic Inflammatory Demyelinating Polyneuropathy?</p>

A

<p>chronic form of GBS</p>

236
Q

<p>What is ALS?</p>

A

<p>Degeneration of anterior horn motor neurons resulting in a mixed upper and lower motor neuron disease:</p>

<p>- Affects motor system (extremity weakness, bulbar symptoms, diaphragm, etc.) with ocular and<br></br>bladder sparing. There are no sensory symptoms.</p>

<p>- Tongue atrophy and fasciculations are classic</p>

237
Q

<p>What is Martin-Gruber anastamosis?</p>

A

<p>median to ulnar nerve crossover in the forearm; important to identify to prevent confusion with NCV</p>

238
Q

<p>What causes the compression in thoracic outlet syndrome?</p>

A

anterior and medial scalene muscles

239
Q

<p>What part of the brachial plexus is affected in neurogenic thoracic outlet syndrome?</p>

A

lower trunk

240
Q

<p>What are visual evoked potentials?</p>

A

<p>potentials evoked from the occipital lobe from retinal stimulation</p>

241
Q

<p>What are SSEPs?</p>

A

<p>somatosensory evoked potentials</p>

<p></p>

<p>monitor the posterior columb pathway of the sensory system</p>

242
Q

<p>Axonal disease causes \_\_\_\_\_\_ on NCV.</p>

A

<p>decreases wave amplitude</p>

243
Q

<p>Myelin disease causes \_\_\_\_\_\_\_ on NCV.</p>

A

<p>increases latency and decreases velocity.</p>

244
Q

<p>What is an H reflex on NCV?</p>

A

<p>submaximal stimulation of a mixed somatosensory nerve that is not strong enough to obtain a direct motor response</p>

245
Q

<p>What is an M wave on NCV?</p>

A

<p>direct motor response caused by stimulation of a motor nerve</p>

246
Q

What is myokymia?

A

spontaneous firing of a motor unit

247
Q

What causes myesthenia gravis syndrome?

A

antibodies to post synaptic ACh receptors on striated muscle

autoimmune or paraneoplastic (thymoma)

248
Q

What is the treatment for myesthenia gravis?

A

AChE inhibitor (pyridostigmine), immunosuppresion, thymus removal

249
Q

What causes Lambert Eaton syndrome?

A

paraneoplastic syndrome to presynaptic Ca channels, thus reducing ACh release

250
Q

Fasciculations are associated with (UMN/LMN) injury.

A

LMN

251
Q

What causes Clasp Knight phenomenom?

A

reticulospinal lesions

252
Q

Spasmodic toticollis predominantly affects what muscle groups?

A

sternocleidomastoid, trapezius, posterior cervical muscles

253
Q

What surgical treatment can be done for spasmodic torticollis?

A

sectioning of the ipsilateral CN XI and bilateral cervical roots C1-C3

254
Q

What causes tactile agnosias?

A

dominant parietal lesions (affects both hands)

255
Q

What is allochiria?

A

perceiving a stimulus that is on one side of the body that is thought to be on the other side

256
Q

What is tabes dorsalis?

A

involves posterior column and roots

Lower extremity numbness, pain, decreased vibration, proprioception, reflexes and tone, abnormal gait, atonic bladder, and NORMAL STRENGTH

257
Q

What are the classic sensory findings with syringomyelia?

A

sensory loss of pain and temperature with preservation of proprioception and touch

258
Q

A festinating gait is associated with what disease?

A

Parkinons’s disease

259
Q

What regulates the circadian rhythm?

A

suprachiasmatic nucleus

260
Q

K complexes and sleep spindles are seen in what stage of sleep?

A

Stage II

261
Q

What medication can suppress REM sleep?

A

Monoamine oxidase inhibitors

262
Q

Narcolepsy is associate with HLA ______.

A

DR2

263
Q

What is the classic tetrad of narcolepsy?

A

Excessive daytime sleepiness, hallucinations on going to sleep or waking up, cataplexy, sleep paralysis

264
Q

What is the cause of narcolepsy?

A

destruction of the hypothalamic hypocretin/orexin neurons which stimulates ARAS

265
Q

All patients with ________ have narcolepsy.

A

cataplexy

266
Q

There are ______ cervical, ______ thoracic, and ______ lumbar sympathetic ganglia.

A

3 cervical

11 thoracic

4-6 lumbar

267
Q

What is the stellate ganglion?

A

sympathetic ganglion formed from fusion of inferior cervical and upper thoracic ganglia

supplies UE

268
Q

Postganglionic fibers are (myelinated/unmyelinated).

A

unmyelinated

269
Q

What is atropine’s MoA?

A

muscarinic receptor blocker (parasympathetic post ganglionic synapses are affected)

270
Q

What is the MoA of curare?

A

blocks nicotinic receptors (affects autonomic ganglia and NMJ)

271
Q

Which andrenergic alpha receptors are presynatpic and which ones are post synatpic?

A

a-1 are postsynaptic

a-2 are presynaptic

272
Q

What are crocodile tears? What causes it?

A

lacrimation from gustatory stimulation

if the CN VII parasympathetic fibers are injured, they may undergo aberrant regeneration with connections of the fibers of the chorda tympani reaching the sphenopalatine ganglion

273
Q

What is the treatment for hyperhydrosis?

A

ablating T2-T3 symapthetic ganglia (leave T1 to prevent Horner’s)

274
Q

Sympathetic output to the bladder is through the _______ ganglion and ______ nerve.

A

inferior mesenteric ganglion and hypogastric nerve

275
Q

The external sphincter of the bladder and the anus is innervated by _________.

A

pudendal nerve

276
Q

The mictruition center is located in ________.

A

locus ceruleus

277
Q

LMN lesions to the bladder cause _______ and can be treated with _______.

A

atonic bladder, urinary retention, poor bladder contraction

bethanechol

278
Q

UMN lesions to the bladder cause _____ and can be treated with _______.

A

spastic bladder

ACh antagonists, propantheline, oxybutynin

279
Q

Rapid correction of hyponatremia can cause _____.

A

central pontine myelinolysis

280
Q

Pituitary adenomas causing Cushing’s have a ________ dexamethasone suppression test.

A

positive

281
Q

Ectopic ACTH secretion leading to Cushing’s has a _________ dexamethasone suppression test.

A

negative

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