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E3: everything else Flashcards

1
Q

What is the most common motor disorder and how do you treat it?

A

Essential tremor

Treat w/ Propanolol or Primidone

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2
Q

What is the MOA of botulinum toxin?

A

Interferes with SNARE proteins in presynaptic cell –> inhibition of Ach release

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3
Q

What are the limbs of the corneal reflex?

A

Afferent: V1
Efferent: VII

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4
Q

Where is the lesion in right hemianopia of the left eye?

A

Right optic tract

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5
Q

Where is the lesion in right superior homonymous quadrantopia of the left eye?

A

Meyer’s loop (temporal lobe infarct) –> post-chiasmal

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6
Q

What is papilledema?

A

Optic disc swelling due to increased intracranial pressure

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7
Q

CN XI lesion results in loss of function on which side?

A

Ipsilateral

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8
Q

What are the abnormal results of a Weber’s test?

A

Conductive –> Affected Ear

Sensorineural –> Unaffected ear

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9
Q

What are the limbs of the gag reflex?

A

Afferent: IX
Efferent: X

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10
Q

Patient presents with dysphagia, dysarthria, and difficulty gagging. Where is the lesion?

A

Efferent limb –> CN X

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11
Q

Which nerve is tested in Hoffmann’s reflex?

A

Median nerve - C5-7

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12
Q

Which muscles are involved in Hoffmann’s reflex?

A

Stretched: lumbricals 1 and 2, flexor pollicis brevis
Contracted: abductor pollicis or opponens pollicis

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13
Q

What is the abnormal result in testing Hoffmann’s reflex?

A

Thumb flexion

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14
Q

Abnormal Hoffmann’s reflex indicates what kind of lesion?

A

UMN lesion (corticospinal tract)

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15
Q

Which nerve is tested in the jaw jerk reflex?

A

CN V3

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16
Q

What are the limbs of the biceps reflex?

A

Musculocutaneous nerve - C5,6

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17
Q

What are the limbs of the Achilles reflex?

A

Tibial nerve - S1-2

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18
Q

Absent direct response, present consensual response. Where is the lesion?

A

Ipsilateral damage to CN III or Edinger-Westphal nucleus

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19
Q

Present direct response, absent consensual response. Where is the lesion?

A

Contralateral damage to CN III or Edinger-Westphal nucleus

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20
Q

What are the limbs of the pupillary light reflex?

A

Afferent: CN II
Efferent: CN III

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21
Q

What is the chemical formula for extraocular muscles?

A

LR6SO4R3

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22
Q

Nystagmus on abduction. Where is the lesion?

A

Contralateral MLF

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23
Q

Inability of the eye to abduct. Where is the lesion?

A

CN VI

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24
Q

What nerves are tested in the Glabellar reflex?

A

Afferent: CN V
Efferent: CN VII

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25
Q

Parkinson’s patients often present with what abnormal reflex response?

A

Glabellar –> persistent blinking

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26
Q

What are the limbs of the anal sphinchter reflex?

A

Afferent: Pudendal
Efferent: S2-4

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27
Q

What are the limbs of the plantar reflex?

A

Tibial nerve - L5-S1

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28
Q

Muscles involved in plantar reflex

A

Normal: flexor hallucis longus, flexor digitorum longus
Abnormal: extensor hallucis longus, extensor digitorum longus

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29
Q

What are the limbs of the triceps reflex?

A

Radial nerve - C7-8

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30
Q

What are the limbs of the patellar reflex?

A

Femoral nerve - L2-4

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31
Q

UMN or LMN lesion will present with positive Babinski?

A

UMN

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32
Q

How does fat appear on MRIs?

A

T1: bright
T2: dark

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33
Q

How does water appear on MRIs?

A

T1: dark
T2: bright

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34
Q

What is dark on T1 and T2?

A

Air
Calcium – bone also tendons & ligaments
Rapidly flowing blood
Hyper acute hemorrhage

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35
Q

What kind of imaging can detect active MS lesions?

A

Gadolinium-enhanced T1-weighted MRIs

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36
Q

Why is MR preferred for Alzheimer’s imaging?

A

It allows for accurate measurement of the 3-dimensional (3D) volume of brain structures, especially the size of the hippocampus and related regions.

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37
Q

What is the hallmark of MS on MR?

A

HYPERINTENSE OVOID PERPENDICULAR LESIONS TO

VENTRICLES—IF MS ACTIVE, then will ENHANCE WITH GADOLINIUM

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38
Q

What are the pathologic hallmarks of Alzheimer’s?

A

Betaamyloid (Aß) plaques, neurofibrillary tangles

(NFTs), and reactive gliosis

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39
Q

What has been used to detect persons at risk for Alzheimer disease even before the onset of symptoms?

A

FDG-PET

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40
Q

_______ _______ _______ has been noted in Alzheimer’s and the degree is associated with the severity of the disease.

A

Temporoparietal glucose hypometabolism

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41
Q

Most common sites of lesions in MS patients

A

Periventricular spaces

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42
Q

Blood supply for optic nerve?

A

Central retinal artery

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43
Q

Pituitary adenoma would cause what visual deficits?

A

Bitemporal hemianopia (chiasmal)

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44
Q

What is glaucoma?

A

Increased fluid pressure in the eye leading to optic nerve damage

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45
Q

Papilledema is always ______.

A

bilateral

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46
Q

Possible cause of papilledema

A

Intracranial hypertension

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47
Q

Where is the vascular occlusion for an right eye that is down and out?

A

Right PCA

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48
Q

Dilated pupil indicates what sort of vascular occlusion?

A

PCA aneurysm

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49
Q

Ptosis and diplopia indicates palsy of which nerve?

A

CN III

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50
Q

Diplopia
Eye down and out
Dilated pupil

A

3rd nerve palsy

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51
Q

What type of strabismus is equal in all directions of gaze?

A

Concomitant

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52
Q

Damage to rostral pontomesencephalic RF causes…

A

Coma

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53
Q

Damage to caudal pontomedullary RF causes….

A

Respiratory failure

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54
Q

T/F: The Medial Forebrain bundle caries NE, DA, and Serotinergic projections from the RF nuclei.

A

True

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55
Q

Where are motor neurons located in the motor cortex?

A

Layer V

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56
Q

Where are motor nuclei in the thalamus?

A

VA, VL

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57
Q

What two areas are important in planning movement?

A

Lateral premotor area

Supplementary motor area

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58
Q

What are the symptoms of a posterior parietal cortex lesion?

A

Apraxia, sensory neglect, or hemispatial neglect on the side contralateral to the lesion. Patient denies the condition or is unaware of it. If this patient is asked to draw something, they will draw only half of it.

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59
Q

What is apraxia?

A

Loss of the ability to execute or carry out learned purposeful movements. A person may not be able to pick up a phone when asked to do so, but can perform the action without thinking when the phone rings.

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60
Q

Where do UMNs arise?

A

May arise from the cerebral cortex or the brainstem

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61
Q

Where are the cell bodies of LMNs?

A

Gray matter of spinal cord and brainstem

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62
Q

MCA stroke often leads to what key symptom?

A

Apraxia

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63
Q

What plays a role in the inhibition of muscles during active movement, and in the execution of subconscious “motor programs” (e.g. swinging the arms while walking)?

A

Basal ganglia

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64
Q

What plays a role in the execution of learned, skilled motor movement?

A

Cerebellum. Critical for the proper timing of movement and correction of movement errors during active voluntary movement.

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65
Q

What are the symptoms of a UMN lesion?

A

1) Weakness or paralysis of specific movements
- extension of the upper limbs and flexion of the lower limbs, termed pyramidal weakness
2) No wasting of muscle
3) Spasticity: increased resistance to passive stretching of muscles
4) Clasp knife response: initial response to muscular stretching followed by relaxation
5) Hyperreflexia: Hyperactivity of deep tendons reflexes
6) Positive Babinski Reflex: Emergence of the extensor plantar response leading to dorsiflexion of the great toe after stimulation of the sole of the foot

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66
Q

What are the symptoms of a LMN lesion?

A

1) Weakness (paresis) or Paralysis (plegia) of individual muscles
2) Wasting of muscles
3) Fasciculation: visible spontaneous contractions of motor units
4) Hypotonia: Reduced resistance to passive stretching
5) Hyporeflexia or Areflexia: Diminution or loss of deep tendon reflexes

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67
Q

Lesions in the cerebral hemispheres and upper brainstem produce what symptoms?

A

Paralysis of the limb opposite (contralateral) to the side of the lesion - this is because of the decussation of the principal motor pathways in the lower brain stem

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68
Q

Even though it is often difficult to attribute clinical deficits to involvement of particular pathways damage to the pyramidal tract causes what sxs? and what sxs are due to the involvement of other pathways?

A

1) Damage to the pyramidal tract itself probably accounts for the loss of discrete movements and the appearance of the Babinski reflex
2) Hyperreflexia and spasticity are due to the involvement of other pathways

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69
Q

What is decorticate posturing? What lesions would cause this?

A

Flexor posturing –> arms flex and point upward
Lesion is rostral to red nucleus, so rubrospinal tract is SPARED. Corticospinal, corticorubral, and corticoreticular tracts are interrupted.

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70
Q

What is decerebrate posturing? What lesions would cause this?

A

Extensor posturing –> arms extend and point down, rotated inward
Corticospinal, corticorubral, corticoreticular, AND rubrospinal tracts are interrupted.

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71
Q

What is pyramidal weakness?

A

Spasticity (increased tone)

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72
Q

What are the cardinal signs of UMN damage?

A

Spastic paralysis and positive Babinski

73
Q

What is the cardinal sign of LMN damage?

A

Flaccid paralysis

74
Q

Which cells are often affected in polio?

A

Anterior horn cells

75
Q

Initial signs: fever, headache, muscle pain and weakness

Later signs: LMN damage

76
Q

What is the cardinal sign of ALS?

A

Spastic reflexes in a wasted limb

77
Q

What is the most common pyramidal system disorder?

A

CVA to the internal capsule

78
Q

Interruption of the corticospinal/bulbar tracts in the internal capsule leads to….

A

paralysis of the contralateral upper and lower limbs and the contralateral lower facial muscles, as well as hypertonia.

79
Q

Corticobulbar tract lesion in genu leads to….

A

Contralateral paralysis of tongue and lower face

80
Q

Corticospinal tract lesion in genu leads to…

A

Contralateral hemiplegia

81
Q 
Head tilted
Paresis of lower facial muscles
Elbow flexed
Forearm pronated
Fingers flexed
Hip circumducted
Knee extended
Foot plantar flexed
A

Capsular stroke

82
Q

Which descending tract is critical in making postural adjustments to changes in head position?

A

Medial vestibulospinal

83
Q

Excess dopamine leads to what symptoms?

A

Hyperkinesis, mania, schizophrenia

84
Q

Neostriatal damage leads to what symptoms?

A

Involuntary motion (chorea) or dystonia (rigidity)

85
Q

Reduced dopamine leads to what symptoms?

A

Hypokinesis (reduced motor)

86
Q

Subthalamic nucleus lesion leads to what symptoms?

A

Hemiballismus aka hyperkinesis (random flailing of limbs)

87
Q

Dyskinesias are usually associated with _______ lesions.

A

cerebellar

88
Q

What structures comprise the paleostriatum?

A

GPL and GPM

89
Q

What structures comprise the striatum?

A

Caudate and putamen

90
Q

What structures comprise the corpus striatum?

A

Caudate, putamen, GP

91
Q

What structures comprise the lenticular nuclei?

A

GP and putamen

92
Q

What are the main inputs to the basal ganglia?

A

Putamen: primary motor and sensory cortices, centromedian nucleus of the thalamus
Caudate: association cortex, limbic system, frontal eye fields

93
Q

The putamen receives which neurotransmitters?

A

Glutamate, Ach

94
Q

The caudate receives which neurotransmitters?

A

Somatostatin, substance P, enkephalin

95
Q

Generally, the basal ganglia has what effect on the thalamus?

A

Inhibitory

96
Q

Preoptic hypothalamus function

A

Temperature (heat loss) and endocrine (sex)

97
Q

Suprachiasmatic hypothalamus function

A

Circadian rhythm

98
Q

Supraoptic/paraventricular hypothalamus function

A

Vasopressin (ADH) and oxytocin released in posterior pituitary

99
Q

Anterior hypothalamus function

A

Temperature, parasympathetic, sex

100
Q

Ventromedial hypothalamus function

A

Inhibition of feeding (satiety), rage, sex, endocrine

101
Q

Posterior hypothalamus function

A

Sympathetic, sleep duration

102
Q

What is the vascular supply of the hypothalamus?

103
Q

Pars distalis stimulatory hormones

A 
GHRH
TRH
CRH
GnRH
Prolacting releasing factor
104
Q

Pars distalis inhibitory hormones

A

Somatostatin

105
Q

Anterior pituitary is derived from…

A

Rathke’s pouch

106
Q

Posterior pituitary is derived from…

A

Neuroectoderm

107
Q

What is the most prevalent cell type in the pituitary?

A

Growth hormone

108
Q

Which cells produce growth hormone?

A

Somatotropes (GH cells)

109
Q

What is pars tuberalis?

A

Highly vascular region of hypothalamus. Involved in ACTH, FSH, LH

110
Q

What are the parasympathetic regions of the hypothalamus?

A

Anterior and preoptic

111
Q

What are the sympathetic regions of the hypothalamus?

A

Posterior medial and lateral

112
Q

Which part of the hypothalamus suppresses feeding?

A

Medial –> Satiety Center

113
Q

Which part of the hypothalamus induces feeding?

A

Lateral –> Feeding Center

114
Q

Diabetes insipidus can result from what hypothalamic lesion?

A

Supraoptic and/or paraventricular: decreased ADH release –> increased H2O intake, increased urine volume

115
Q

Predatory and defensive behavior are controlled by which hypothalamic regions?

A

Predatory –> lateral

Defensive –> medial

116
Q

Which neurons attenuate pain sensation and what do they release?

A

Serotonergic neurons in raphe nuclei in medulla release enkephalin.

117
Q

What divides the hypothalamus into medial and lateral regions?

118
Q

Where do afferents of the hypothalamus primarily originate?

A

Limbic system and reticular formation

119
Q

What is the stria terminalis?

A

Important path arising from the medial amygdala, projecting to the bed nucleus of the stria terminalis and medial hypothalamus. Controls emotional behavior.

120
Q

What do zona glomerulosa cells secrete?

A

Aldosterone

121
Q

What do zona fasciculata cells secrete?

A

Glucocorticoids (cortisol and corticosterone)

122
Q

What do zona reticularis cells secrete?

A

DHEA, estrogens

123
Q

What is the deepest layer of the adrenal medulla?

A

Zona reticularis

124
Q

A tumor of chromaffin tissue that produces excessive quantities of catecholamines

A

Pheochromocytoma

125
Q

Which catecholamine is most frequently elevated?

A

Norepinephrine

126
Q

Hunger and satiety are regulated by which hormone?

127
Q

Pain from noninjurious stimuli to the skin

128
Q

Extreme sensitivity to pain

A

Hyperalgesia

129
Q

The absence of pain from stimuli that normally would be painful

130
Q

Nociceptive action potentials are transmitted through what types of afferent fibers?

A

Myelinated A-delta and unmyelinated C

131
Q

Which chemical mediators activate and sensitize nociceptors?

A

Bradykinin, histamine, serotonin, and potassium

132
Q

Which mediator prolongs and enhances the action of glutamate?

A

Substance P

133
Q

What is the central pathway of pain modulation?

A
  1. PAG (in midbrain) projects to nucleus rahe magnus
  2. NRM (serotoninergic) neurons project to the spinal cord and synapse on enkephalin-containing interneurons
  3. Noradrenergic pathway from locus ceruleus (upper pons) synapses with spinal cord interneurons like NRM
134
Q

What releases CGRP?

A

Dorsal horn neurons

135
Q

How does enkephalin modulate pain in vesicles?

A

Presynaptic – reduces calcium entry

Postsynaptic – hyperrepolarization (potassium increase)

136
Q

Syndrome in which the sensory threshold is raised, but when it is reached, continued stimulation (especially if repetitive), results in a prolonged and unpleasant experience

A

Hyperpathia

137
Q

Unpleasant distortions of somesthetic sensation that typically accompany partial loss of sensory innervation (burning, wetness, itching, electric shock)

A

Dysesthesia

138
Q

What are the cerebral layer projections to/from the thalamus?

A

Input: Layer VI pyramidal
Output: Layer III Pyramidal, Layer IV Interneurons

139
Q

Where does the cerebellar vermis project to?

A

Fastigial nucleus

140
Q

What are the interposed nuclei?

A

Emboliform and globose

141
Q

Where does the paravermal zone project to?

A

Interposed nuclei

142
Q

Where does the lateral zone of the cerebellum project to?

A

Dentate nucleus

143
Q

What is the largest contributor of fibers to the deep pontine nuclei?

A

Frontal lobe

144
Q

Mossy fibers release what neurotransmitter?

145
Q

What do mossy fibers synapse on?

A

Granule cell dendrites, Golgi cell axons

146
Q

What do climbing fibers synapse on?

A

Purkinje cell dendrites

147
Q

What neurotransmitter do climbing fibers release?

A

Aspartic acid

148
Q

What neurotransmitter do climbing fibers release?

A

Aspartic acid

149
Q

Output from the cerebellum occurs through what cell?

A

Purkinje cell

150
Q

Basket cells are similar to ____ cells

151
Q

What inhibits Purkinje cells?

A

GABA from basket and stellate cells

152
Q

What do Purkinje cells project to cerebellar and vestibular nuclei?

A

GABA / inhibitory output

153
Q

What excites Purkinje cells?

A

Parallel and climbing fibers

154
Q

Which cells do granule cells excite?

A

Purkinje, basket, stellate, and Golgi

155
Q

What inhibits granule cells?

A

Golgi cells

156
Q

What excites granule cells?

A

Mossy fibers

157
Q

Where do climbing fibers terminate?

A

On cerebellar nuclei and dendrites of Purkinje cells

158
Q

What is the triad of cerebellar dysfunction?

A

Hypotonia, disequilibrium, dyssynergia

159
Q

What is dyssynergia?

A

Loss of coordinated muscle activity

160
Q

What is intention tremor?

A

Type of dysmetria that occurs during a voluntary movement

161
Q

What is dysdiadochokinesia?

A

Inability to perform rapid alternating movements

162
Q

Anterior vermis syndrome is commonly caused by _____ and results in _______.

A

Alcoholism / gait, trunk, and leg dystaxia

163
Q

Posterior vermis syndrome is commonly caused by _____ and results in ______.

A

Brain tumors in children (esp. medulloblastomas, ependymomas) / truncal dystaxia

164
Q

Polio and ALS affect which cells?

A

Anterior horn cells

165
Q

Flocculonodular lobe projects to vestibular nuclei to regulate activity of which muscles?

166
Q

Cerebellar nystagmus is caused by…

A

Lesions of the vermal region or fastigial nucleus –> MLF interruption

167
Q

What do you treat Hungtington’s with?

A

Chlorpromazine (dopamine antagonist)

Baclofen (GABA-B agonist)

168
Q

What do you treat chorea with?

A

Tetrabenazine/Reserpine (blocks reuptake of dopamine)

169
Q

What do you treat ALS with?

A

Riluzole (enhances reuptake of glutamate by astrocytes and neurons)

170
Q

What do you treat RLS with?

A

Ropinirole (dopamine agonist)

171
Q

What is Rasagiline used for and why?

A

Mildly affected Parkinson’s patients. Does not convert to amphetamine.

172
Q

How would you increase the benefits of Levodopa?

A

add dopamine agonist
add MAO-B inhibitor
add Carbidopa

173
Q

Which receptors play a major role in PD therapy?

174
Q

Represents the existence of neural gating mechanisms at the segmental spinal cord level to account for interactions between pain and other sensory modalities

A

Gate control theory

175
Q

The perception of pain does not result from the brain’s passive registration of tissue trauma, but from its active generation of subjective experiences through a network of neurons known as __________.

A

the neuromatrix

176
Q

What are wide-dynamic range neurons?

A

Subset of dorsal horn (second order) neurons that respond to low-intensity stimuli

177
Q

What happens when C pain fibers are repetitively stimulated?

A

Each stimulus produces a progressively increasing response from WDR neurons

178
Q

What is the lesion associated with Chiari I malformation?

A

Cerebellar tonsil herniation into foramen magnum

BCN (6 decks)

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