Neuroscience Post-Midterm Flashcards

1
Q

Lower motor neuron

A

Motor neuron that communicates directly with somatic muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Upper motor neuron

A

Motor neuron that arises from motor centers in the brain that communicate with lower motor neurons directly or through local interneurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Pyramidal motor system

A

Corticolspinal tract (ventral medulla)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Paralysis

A

Complete loss of motor function due to lesion of neurons or muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Plegia

A

Paralysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Paresis

A

Subparalytic muscle weakness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Hemiparesis

A

Partial paralysis on one side of the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

ALS

A

Amyotrophic lateral sclerosis is a progressive NM disease that initially affects and later destroys lower motor neurons and eventually parts of the corticospinal/bulbar tracts and primary motor area

Classic presentation: 50% cases begin in hand; loss of muscle bulk thenar, hypothenar, interossei, arm/shoulder
Symptoms: Weakness and difficulty speaking/swallowing
Pts. require ventilation/gastronomy; reduction cough reflex (aspiration pneumonia), fasiculations/weakness tongue
Unaffected: sphincter control, sensory function, intellect
Prognosis: death 3-5 years after diagnosis; death from respiratory insufficiency and aspiration pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

ASA syndrome

A

Cause: ASA infarction, less commonly: tumor, epidural abscess
Symptoms: Spastic paraparesis, bilateral extensor plantar response, bilateral loss pain, temp below, touch/vib/prop in tact, retention of urine, sexual functions imparied
* ASA supplies anterior 2/3 spinal cord
Lesion: 2nd order motor neurons in anterior horn, ALS, Corticospinal tracts (lateral and anterior)
* Rare, can cause paraplegia (damage of LMN in anterior horn) and lateral Corticospinal tract (UMNS’s)
* Bladder, lung infections, PE, pressure sores

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Central medullary syndrome

A

Cause: Syringomyelia, tumor, hemorrhage
Pathological cyst in central canal; cervical involvement
* Develops anterior; pressure to anterior horns and anterior white commissure
* Segmental muscle atrophy (muscles of hand/fingers); loss of pain/temperature due to destruction of anterior white commissure
*Other symptoms: pain/weakness, stiffness in back, arms, shoulders, legs; disturb sweating, sexual function and bladder/bowel control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Which descending tracts are concerned with flexion vs. extension?

A

Flexion: Doral/Lateral; lateral corticospinal, rubrospinal, medullary lateral reticulospinal
Extension: Anterior/Medial; (lat+medial) vestibulospinal, pontine medial reticulospinal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Where is the lateral corticospinal tract located in the spinal cord?

A

Lateral horn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

All motor pathways, except the _________________ tract ends at synapses on LMN in the spinal cord or on interneurons

A

Corticobulbar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Name the descending motor pathways

A

Cortical – CS, CB

Subcortical – Rubrospinal, reticulospinal, vestibulospinal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Where are the descending motor fibers for the proximal vs. distal muscles?

A

Proximal: medial
Distal: lateral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Which of the motor pathways is involuntary?

A

Vestibulospinal (medial-medulla+pons and lateral-pons)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Damage to corticobulbar fibers innervating the facial nucleus results in…

A

Contralateral lower facial paralysis (upper facial nucleus is innervated by both ipsi/contra-lat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Damage to corticobulbar fibers to the hypoglossal nucleus results in…

A

Contralateral deviation of the tongue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

A central lesion of PPRF results in…

A

Deviation of eyes towards the side of the lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

A unilateral internal capsule infarction results in…

A

Contralateral UMN syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Differentiate between the pre-frontal, pre-motor and primary motor cortices

A

Pre-frontal: planning, social restraint
Pre-motor: motor programs
Primary motor: Strong excitation LMN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Differentiate between simple, complex and imagined motor tasks

A

Simple: Primary motor, primary sensory
Complex: Pre-motor (supplementary-medial) & primary motor
Imagined: Supplementary-medial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

> 90% of ______________________ fibers decussate in the ventral medulla

A

Corticospinal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

> 90% of ______________________ fibers decussate in the ventral medulla

A

Corticospinal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Spinal shock

A

Flacidity, areflexia several weeks following a lesion to a motor tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Spinal shock

A

Flacidity, areflexia several weeks following a lesion to a motor tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Paraplegia

A

Bilateral s/c lesion; UMN below the lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

UMN’s release _________________ onto ____________ receptors of LMN’s or interneurons

A

Glutamate; AMPA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Brown-Sequard Syndrome

A

Ipsilateral UMN, DC/ML below
Contralateral: ALS below
Segmental LMN @ level lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Brown-Sequard Syndrome

A

Ipsilateral UMN, DC/ML below
Contralateral: ALS below
Segmental LMN @ level lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Paraplegia

A

Bilateral s/c lesion; UMN below the lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

UMN’s release _________________ onto ____________ receptors of LMN’s or interneurons

A

Glutamate; AMPA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

From where does input come for the motor cortex?

A

Premotor, somatosensory, posterior parietal, BG, cerebellum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Decerebrate posturing

A

A lesion at or caudal (below) the red nucleus impairs CS, CB, Rubrospinal
Patient extends upper and lower limbs
* 2 GCS points

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Decortiate posturing

A

A lesion rostral (above) the red nucleus that impairs CB and CS fibers

  • Flex the upper limbs and extend the lower limbs (following a noxious stimulus or spontaneously)
  • 3 GCS points
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Who is responsible for tuning of the intrafusal muscle fibers?

A

Gamma motor neuron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Specialized aggregations of _______________ fibers form muscle spindles.

A

Intrafusal fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

The pontine reticulospinal tract primarily innervates alpha/gamma motor neurons.

A

Gamma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

The ____________________ tract primarily innervates gamma motor neurons.

A

pontine reticulospinal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

The rubrospinal pathway…
Is it contralateral or ipsilateral?
From where does its input come?

A

Flexion in the upper limbs
* Excites alpha and gamma motor neurons
** Contralateral
Input: ipsilateral motor cortex, contralateral cerebellar nuclei

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

The medullary reticulospinal pathway…

Is it contralateral or ipsilateral?

A

Flexion limbs

  • Contra + Ipsilateral
  • Bilateral cortical input
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

The pontine reticulospinal tract…

Ipsilateral or contralateral?

A

Ipsilateral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

The lateral pontine vestibulospinal tract innervates which motor neurons?

A

Alpha

** Axial and limb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

The medial vestibulospinal tract innervates motor neurons in an excitatory or inhibitory manner?

A

Inhibitory (glycine)

** Cervical and upper thoracic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Differentiate between cervical/neck & axial/limb innervation among the lateral and medial vestibulospinal tracts.

A

Cervical neck: medial

Axial/limb: lateral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Intrafusal fiber

A

Specialized muscle fiber within a muscle spindle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Extrafusal fiber

A

Muscle fiber located outside of muscle spindles forming the bulk of the muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Motor neuron pool

A

All motor neurons innervating a given muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

How do you test for hypotonia?

A

Reduced muscle tone; detectable by palpation and testing resistance to passive stretch of the limb.

Damage to either the 1a afferent or alpha motor neurons will reduce muscle tone, yielding hypotonia and flaccid paralysis
Can also arise from lesion in other parts of the motor system, even when alpha motor neurons and 1a afferents have been spared

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Myotatic reflex

A

A reflex whereby stretching of a muscle provokes contraction of the same muscle. It is mediated by a monosynaptic connection between 1a afferents and alpha motor neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Inverse myotatic reflec

A

A reflex where muscle relaxation is evoked by increased tension developed in the same muscle. Mediated by 1b afferents and alpha motor neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

The conduction velocity of a nerve is dependent on…

A

Myelination (faster) and diameter (faster)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Muscles involved in fine movement have more density/less density of muscle spindles.

A

More density

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

With respect to Group 1A and 2 sensory neurons, what is the difference between the type of stretch that they sense.

A

1A: static + dynamic (rate of change of length): static nuclear bag, nuclear chain + dynamic nuclear bag
2: static (static nuclear bag, nuclear chain)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What fibers are in series with the extrafusal muscle fibers?

A

Golgi tendon organ fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What type of afferent fiber innervates the golgi tendon organ?

A

1B (unmyelinated on the inside)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Who is responsible for the “inverse myotatic” reflex and what is the reflex?

A

Golgi tendon organ; at very high levels of tension/over-active alpha-motor neurons, the golgi tendon relaxes the agonist muscle and excites the antagonist muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What are Renshaw cells?

A

Inhibitory interneurons innervated by alpha motor neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Motor neuron pools are derivatives of the alar/basal plate?

A

Basal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Where is the greatest density of lower motor neurons in the S/C? (2 locations)

A

Cervical and lumbar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Motor neurons receive input from 3 different types of neurons.

A
  1. Muscle spindle afferents
  2. Local interneurons
  3. Upper motor neurons
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What is the formal definition of a motor unit?

A

Alpha motor neuron and the extrafusal fibers that it innervates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Each alpha motor neuron controls how many extrafusal muscle fibers for: (a) postural; (b) ocular: 1, 10, 100, 1000?

A

Postural: 1000
Ocular: 10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Approximately how many motor neurons control a single muscle?

A

100

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Differentiate between types I, IIA, IIB motor units.

A

I: slow-twitch, low tension, aerobic, low number of nerves
IIa: fast twitch; 1/2 aerobic
IIb: fast twitch; anaerobic, large number of motor neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What are the two major factors that control skeletal muscle contraction?

A
  1. Firing rates

2. Motor units recruited

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What types of motor disorders can cause muscle weakness?

A

All!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What types of motor disorders can cause muscle atrophy?

A

All but NMJ disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What types of motor disorders can cause fasiculations?

A

Motor neuron damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What types of motor disorders can cause a reduction in conduction velocity?

A

Schwann cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What types of motor disorders can cause fluctuations in amplitude of EMG?

A

NMJ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

EMG consisent with denervation…

A

Motor neuron or Schwann cell disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What is Myotonia congenita?

A

Cl- channel syndrome; smaller stimulus for depolarization – prolonged repetitive firing even without stimulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What is the difference in distribution of nAChR in embryo vs adult?

A

Embryo: widely spread out
Adult: concentrated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

2 congenital myasthenias

A

Deficiency in ACh-esterase

Slow channel syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What condition is associated with a “facilitating neuromuscular block”

A

Lambert-Eaton syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Polio destroys…

A

cell body of lower motor neuron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What is a characteristic sign of cortical damage?

A

Aphasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

T/F The primary motor cortex handles movements of individual muscles.

A

False – that is the role of the lower motor neuron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Acute stage motor lesions can cause…

A

Flaccid paralysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What are the 4 types of tremor?

A
  1. Physiological
  2. Resting – BG/Parkinson’s
  3. Kinetic (intention) – cerebellum – when moving
  4. Essential/Postural – with a certain posture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What is chorea?

A

Involuntary, jerky movements (as in choreography)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What is ballismus? Where is the lesion?

A

Flinging, rotating

*Sub-thalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What is athetosis?

A

Slow writhing of fingers, toes, hands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

How do we assess gait?

A

Walk straight path (heel-to-toe) or heel or toe; turn smoothly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

How do we assess station?

A

Feet together, eyes closed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

How do we assess posture?

A

Muscle tone; decortiate/decerebrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Chorea is most associated with these 2 diseases

A

Huntington disease

* Sydenham disease (childhood rheumatic fever)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Describe the 5 stages of Parkinson’s

A
  1. Unilateral
  2. Bilateral with posture
  3. Bilateral without posture
  4. Sever disability/with falls
  5. Akinesia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Describe the features of Parkinson’s disese

A
(TRAPS)
Tremor (resting tremor)
Rigidity
Akinesia
Postural changes (stooped)
Stare (serpentine stare)
· To remember what kind of tremor and postural change, can look at letter that follows in TRAPS: Tremor is Resting, Posture is Stooped.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What is spasmodic torticollis?

A

Dystonia/muscle spasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What is tardive dyskinesia?

A

Drug induced oral movements (dopamine receptor antagonists)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What are the major hyperkinesia disorders?

A

Parkinson’s
Drug induced Parkinson’s
Vascular - Strokes interrupting the nigrostriatal pathway may cause parkinsonism,
affecting both direct and indirect pathways
Dementia pugilistica - trauma
Post-encephalitic
Neoplastic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What are the major hypokinesia disorders?

A
Huntington
Sydenham Disease (Autoimmune)

Drug-induced Chorea
Athetosis
Hemiballismus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

How is Huntington disease treated?

A

Treatment: D2 antagonists, VMAT inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Describe drug-induced Parkinsons

A

Phenothiazines, which block D2 receptors in the forebrain in the treatment
of psychosis (or hyperkinesis), may cause parkinsonism by limiting
dopamine-mediated inhibition of striatal neurons contributing to the
indirect pathway
• Drugs that deplete dopamine stores within nerve endings (e.g. reserpine)
may diminish striatal dopaminergic transmission to affect both the direct
and indirect pathways, thereby producing parkinsonism
• A metabolite of MPTP, a contaminant produced during improper
preparation of a synthetic narcotic, causes parkinsonism by damaging
nigral mitochondria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Describe several treatmens for Parkinson’s

A

Treatments
L-dopa, D2 agonist, dopamine enhancers, Anticholinergics, MAOI/COMTi, Ablative surgery (subthal or GPI), deep brain stimulation (thal, GPI)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

An infarct to the vestibulocerebellum

A

•Disturbances affect equilibrium-related motor functions
o Nystagmus (ocular ataxia)
o Tilted head
o Titubation (head-nodding)
o Truncal ataxia (imbalance) with compensatory wide-based stance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Disturbance to the spinocerebellum

A

Disturbances affect posture and movement of limbs
o Ataxias of the limbs common (ipsilateral)
•Gait ataxia accompanied by lurching to the side of the lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Disturbance to the cerebrocerebellum

A
Disturbances affect accuracy and timing of movement
o Ataxia
o Decomposition of movement
o Dysarthria (slurred monotonous speech)
o Dyssynergia (uncoordination of limbs)
Dysdiadokinesia (inability to perform rapidly alternating
movements)
Dysmetria (past-pointing)
o Hypotonia
o Intention tremor
o Rebound phenomenon
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Louis-Bar Syndrome

A
  • Autosomal recessive disorder with widespread degeneration of cerebellar Purkinje cells and compromised immune function (chromosome 11)
  • Delayed development of motor skills accompanies increased vulnerability to infection
  • Most obvious signs relate to walking, talking, facial and ocular movements
  • On the longer term, sensitivity to ionizing radiation is observed along with increased vulnerability to cancers
  • Skin and eyes tend to express small dilated blood vessels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Cerebellar cognitive affective syndrome

A

•Lesions of the posterior lobe are considered (by some) to correlate with failures of cognitive and emotional systems, leading to:
o Emotional blunting and depression, disinhibition, and psychotic features
o Executive, visual-spatial, and linguistic deterioration
•The condition is conceptualized in relation to “dysmetria of thought,” suggesting a larger role for the cerebellum in cortical control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Dementia pugilistica

A

Parkinson’s secondary to trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Define muscle tone

A

Force with which a muscle resists being lengthened

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Define spasticity

A

A hypertonic state with increased deep tendon reflexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Define falccidity

A

Weak, lax and soft muscle, without resistance to passive movement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Define clonus

A

Rhythmic palpable oscillations between flexion and extension

108
Q

When a muscle is passively stretched, it reflexively

A

contracts

109
Q

Biceps reflex

A

C5, 6, 7

110
Q

Triceps reflex

A

C6, 7, 8

111
Q

Knee-jerk reflex

A

L2, 3, 4

112
Q

Ankle-jerk reflex

A

S1, 2

113
Q

Differentiate between 0, 1+, 2+, 3+, 4+ reflex scale

A
0 - no response
1+ - weak
2+ - normal
3+ - high normal
4+ - brisk with clonus
114
Q

Anal sphincter reflex

A

S2, 3, 4

115
Q

What is the objective of the Golgi Tendon Organ relfex

A

Protection of muscle/tendon; maintenance of posture

116
Q

What is the flexion reflex?

A

Noxious stimulus (A-delta and C fibers) causes ipsilateral flexion, and contralateral extension

117
Q

Positive Babinski Sign

A

Extension of big toe (dorsiflexion) often accompanied by fanning of other toes
* Problem with lateral CS tract

118
Q

Which response is slower: myotatic or inverse myotatic?

A

Inverse myotatic

119
Q

Dysarthria

A

Slurred, monotnous speech

120
Q

Dyssynergia

A

Uncoordinated limbs

121
Q

Dysdiadokinesia

A

Inability to perform rapidly alternating movements

122
Q

Dysmetria

A

Past-pointing (Finger-to-nose)

123
Q

Alcoholics are at risk of this cerebellar dysfunction

A

Anterior cerebellar lobe; degeneration of Purkinje cells; motor signs

124
Q

Vermis/Paravermis/Lateral hemispheres of the cerebellum communicate with which deep nuclei?

A

Fastigial/Interposed/Dentate

125
Q

HTLV infection can causes (in addition to leukemia)

A

Tropical spastic paresis (demyelination of S/C)

126
Q

Paresthesia

A

Morbid/abnormal sensation (burning, prickling, pins/needles, numbness)

127
Q

Ephapse

A

Pathological contact between parallel nerve fibers where electrical nerve impulses can leak from one fiber to the other

128
Q

Guillan Barre

A

Acute inflammatory polyneuropathy (begins distal) following an infection

129
Q

Leprosy

A

Profound sensory loss (pain/temperature)

Preferentially unmyelinated axons

130
Q

Hansen disease

A

Profound sensory loss (pain/temperature)

Preferentially unmyelinated axons

131
Q

Lead poisioning

A

Motor loss in fingers/arms
Encephalopathy/Memory loss
No sensory loss

132
Q

Alcoholic polyneuropathy

A

Symmetrical motor and sensory loss

* Numbness, tingling, burning in feet

133
Q

Diabetic neuropathy

A
Symmetric sensory (starts), asymmetric motor loss
*Stocking distribution
134
Q

Differentiate between negative loss and positive gain (with respect to neuropathy)

A

Loss: weakness, tendon reflexes, ANS, impaired sensory
Gain: Paresthesia, pain

135
Q

Motor neuron soma, peripheral nerve, demyelination, axonal degradation, NMJ
* Any sensory/motor NCV damage?

A

Peripheral nerve & Demyelination

136
Q

3 major type of nerve trauma

A
  1. Compression
  2. Crush
  3. Axotomy
137
Q

Describe axotomy

A
  1. Wallerian degradation – distal axon
  2. Anterograde degredation – distal n. cell
  3. Retrograde degradation – proximal n. cell
138
Q

Describe regeneration of nerves in the PNS

A

Axonal sprouting, lingering Schwann cells

  • NGF, laminin, adhesion molecules
  • 1mm/day
139
Q

Describe regeneration of nerves in the CNS

A

Not possible; oligodendrocytes do not secrete NGF

140
Q

What is gliosis?

A

A scar formed by astrocytes; a mechanical barrier to sprouting axons

141
Q

Axons differentiate into nerve terminals when they contact…

A

The basal lamina

142
Q

T/F Inner parts of the nerve are more vulnerable to damage compared to outer parts, i.e. the epinerieum

A

True

143
Q

Complex regional pain syndrome

A

Neuropathic pain secondary to resolved injury of bone, soft tissue, nervous tissue
*Increased sympathetic output; hyperhidrosis, sensitization to NE

144
Q

Hirschsprung disease

A

Congenital decrease in motility/peristalsis of the distal colon
Lack of Mesiner’s and Auerbach’s plexuses
-Trapped feces  dilation

145
Q

Sympathetic T1-T2

A

Superior cervical ganglion (face, eyes)

146
Q

Sympathetic T2-T6

A

Inferior cervical ganglion/upper thoracic (upper extremity, heart, bronchi)

147
Q

Sympathetic T6-L1

A

Celiac ganglion (liver/GI)

148
Q

Sympathetic T9-L1

A

LS plexus; lower extremeity

149
Q

Sympathetic T10-L1

A

Adrenal gland

150
Q

Sympathetic T11-L1

A

SMG

151
Q

Sympathetic L1-L2

A

IMG

152
Q

Parasympathetic: CN 3, 7, 7, 9, 10, S2-4

A
CN3: EW nucleus -- ciliary
CN7 SS nucleus -- PT/SM
CN9 IS nucleus --  Otic
CN10 Dorsal motor nucleus (bronchial tree, heart, GIT)
S2-4: rectum, bladder, repro
153
Q

Differentiate between pathological hypothermia/hyperthermia

A

Hypothermia: damage to posterior
Hyperthermia: damage to anterior

154
Q

Diabetes insipidus

A

Damage to supraoptic/paraventricular nuclei, no ADH, excessive thirst
* Treatment: ADH agonist

155
Q

Frolich syndrome

A

Lesion to medial thalamus (unopposed lateral hunger stimulation)

156
Q

Hypothalamus: feeding

A

Medial: satiety
Lateral: hunger

157
Q

Hypothalamus: h2o balance

A

ADH, angiotensin receptors, vagal afferents

158
Q

Name the 6 anterior pituitary hormones and their hypothalamic control hormones

A
DA -inhib-> Prolactin
GHRH --> Growth hormone
GnRH --> FSH/LH
CRH --> ACTH
TRH --> TSH
159
Q

Parvo/magnocellular with respect to hypothalamus (anterior vs. posterior)

A

Parvo: anterior
Magno: posterior

160
Q

Milk ejection: prolactin or oxytocin?

A

Oxytocin

161
Q

Functions of hypothalmus

A
Temperature/Thirst
Apetite
Libido
Emotion/Emergency
BP/Electrolytes
162
Q

Horner’s syndrome

A

Loss of sympathetic input to the head (unilateral ptosis, miosis, anhydrosis, facial flushing)
*Pre-ganglionic/Post-ganglionic; hypo-spinal (entire 1/2 of body)

163
Q

Atonic bladder

A

Interruption of urinary reflex arc; sensation of fullness is lost; dribbling and loss of reflexive emptying

164
Q

Automatic bladder

A

Supra-sacral spinal cord lesion

*Bladder fills until a threshold and then spontaneously, reflexively empties

165
Q

Sleep-wake cycles in blind people

A

Lack of visual input (zeitgeber); mismatch in circadian rhythm

166
Q

Suprachiasmatic nucleus

A

Light-sensitive retinal cells (optic nerve/chiasm)

* Also reaches pineal gland

167
Q

T/F Humans have a free-running biological clock which nearly lines up with a 24 hour day

A

True (approximately 25 hours)

168
Q

T/F Hypothalamo-spinal fibers can contribute pupillary dilation

A

True

169
Q

Describe the 3 levels of innervation of the bladder. Which is most important clinically?

A

Parasympathetic

  1. Supratentorial (frontal lobe, hypothal)
  2. Subtentorial (pontine micturition center)
  3. Spinal (T/L sympa – S2-4 para)
170
Q

Stretch receptors in the bladder can influence neurons in 3 different places

A
  1. DRG –> Sympa/Para
  2. Pons
  3. Cortex
171
Q

Androgen insensitivity syndrome

A

Mutated androgen receptor
Testicular feminization; act like XX’s
Primary amenorrhea, female distribution of fat

172
Q

Fetal exposure to DES

A
Synthetic estrogen (++ homosexuality "DES daughters") in the 50's
Enlarged SDN in females
173
Q

When is the sexual “critical period” during development

A

Weeks 12-20

174
Q

Are testosterone and estradiol required for male sexual development?

A

Yes

175
Q

Homosexuals have a larger _______________ and smaller _____________.

A

Larger: Suprachiasmatic
Smaller: INAH3 (interstitial nucleus of the anteror hypothalamus)

176
Q

Differentiate between the James-Lange and Cannon-Bard theories of emotion

A

Lange: express then feel
Cannon: feel than express

177
Q

Describe the modern concept of the limbic system

A

Cortex, cigulate, hippocampus, hypothalamus, anterior thalamus

178
Q

Kluver-Bucy

A

Bilateral removal of the amygdala; flat emotions, hyper-orality, hypersexual (temporal lobe lesion)

179
Q

Describe the fear conditioning experiment

A

Remove amygdala –> no fear

180
Q

Describe the different roles of the amygdala and the hippocampus in regulating a physiological stress response

A

Amygdala: enhanced response
Hippocampus: dampened response

181
Q

A tumor in this location can induce olfactory and gustatory hallucinations

A

Temporal lobe

182
Q

T/F Direct input to the amygdala can lead to immediate defensive behavior

A

True

183
Q

The motor pathway that is required for fine control of digits of the hand is the:

A

Lateral corticospinal

184
Q

Identify the cortical region involved in the planning of a complex sequence of movements that will cluminate in rising from a seated position, wlking across the room, opening and exiting a door, walking down a hall, turning left, and opening a refrigerator.

A

Prefrontal

185
Q

The chart of a patient states that he has a right uncal herniation due to a right intracerebral hypertensive hemorrhage. Which of the following neurological deficits would you find upon examination?

A

Left extensor plantar response

186
Q

Sympathetic sweat gland receptors: Muscarinic or Nicotinic?

A

Muscarinic

187
Q

Treatment Schizophrenia

A

Typical: Haldol, D2 antagonist
Atypical: D3, D4 antagonist (less Parkinson-like motor side effects)

188
Q

Describe the relationship between schizophrenia and Parkinsons

A

Inverse; hence treatment for one can induce the other

189
Q

Define dysthymia

A

Less severe form of depression

190
Q

Treatments for depression

A

MAOI, 3cyclic, SSRI

191
Q

Functional imaging of mania

A

Pre-frontal cortex below the genu of the corpus callosum (increased activity with mania; decreased activity with depression)

192
Q

Dyslexia

A

Developmental or secondary; read words backwards

193
Q

Alexia

A

Word blindness, can’t read L visual field; disruption of transfer to the left hemisphere; damage to splenium corpus callosum

194
Q

Aphasias

A
Fluent	
Wernicke's
Transcortical sensory
Gerstmann (written)
Conduction (can understand, can't repeat -- L superior temporal)	

Nonfluent
Broca’s
Transcortical motor
Global (B+W+Conduction)

195
Q

What is prosody?

A

Pattern intonation – grammatical role, sarcasm, emotion

196
Q

Where is emotion (L or R)

A

R

197
Q

Where is language center (L or R)

A

L

198
Q

Incoming spoken word is processed

A

Wernicke

199
Q

Outgoing spoken word

A

W, B

200
Q

Reading

A

W

201
Q

Writing

A

W, B

202
Q

When does language develop?

A
5-7 months: language like sounds
7-8 months: syllables
1-2 year: first word
2 year: rich phrases
3 year: correct words and grammar
203
Q

Agraphia

A

Writing

204
Q

A lesion to the angular gyrus

A

Gerstmann Syndrome (can’t comprehend written)

205
Q

Lesion to secondary association cortex

A

transcortical sensory aphasia

206
Q

Lesion to arcuate fasiculus

A

Conduction aphasia

207
Q

Lesion to left dorsolateral frontal

A

Transcortical motor aphasia

208
Q

A 17 year old female patient of yours has never had a period. That is odd because she has developed all of the other secondary sex characteristics. During examination you notice the absence of axillary & pubic hair.

A

Androgen insensitivity syndrome

X-recessive; mutation in testosterone receptor

209
Q
  1. What enzyme is responsible for converting testosterone into estrogen?
A

Aromatase

210
Q

Where is the estradiol receptor located?

A

Cytosol

211
Q

What region of the brain has the highest number of estradiol receptors?

A

Hypothalamus

212
Q

The use of what synthetic estrogen in the 1940s-1970s to prevent spontaneous abortion led to a higher incidence of bisexual & homosexuality in girls?

A

DES [Diethylstilbestrol]

213
Q

When is the critical period of sexual differentiation

A

12-20 weeks gestation

214
Q

Testosterone producing cells

A

Leydig cells

215
Q

On what chromosome is the gene for testis determining factor?

A

Y

216
Q

3 brain regions that exhibit sexual dimorphism

A
  1. Corpus callosum
  2. Anterior commussure
  3. Hypothalamus
217
Q

Which hypothalamic nucleus is not sexually dimorphic?

A

Arcuate

218
Q

Which thalamic nucleus is 1/2 the size in homosexual men vs. heterosexual men? INAH 1, 2, 3, 4

A

INAH 3

219
Q

Which hypothalamic nucleus is responsible for reducing feeding behavior? Paraventricular or Ventromedial

A

Ventromedial

220
Q

Which hypothalamic nucleus is 2x as large in males vs. females?

A

INAH1, SDN

221
Q

Which hypothalamic nucleus is 2x as large in homosexual men vs. heterosexual men?

A

Suprachiasmatic nucleus

222
Q

Anatomical changes during a manic/depressive episode

A

Depressive phase: Reduced activity in area of prefrontal cortex below the genu of the corpus callosum
Manic phase: Increased activity in area of prefrontal cortex below the genu of the corpus callosum
This subgenul region is important for mood states & has connections w/ other regions involved in emotion [amygdala, lateral hypothalamus, nucleus accumbens, NorE, serotnergic, dopaminergic systems of the brain]

223
Q

Dysthmia

A

Less severe form of depression

224
Q

How long does it generally take before anti-depressive medications show their effects?

A

3-4 (sometimes 8 weeks)

225
Q

Antipsychotics that have almost no side effects on the extrapyramidal system?

A

Clozapine, olazapine

226
Q

D3/4 receptor antagonists

A

Clozapine, olazapine

227
Q

Mood stabalizers

A

Carbamacepine, Lamotrigine, Lithium, Valproate

228
Q

Typical anti-psychotic drugs

A

Haldol, perphenazine

229
Q

These drugs can have tardive dyskinesia as side effect

A

Haldol, perphenazine

230
Q

Anatomical anomolies seen in schizophrenics

A

*Reduced blood flow to left globus pallidus
(Disturbance is system connecting basal ganglia to frontal lobes)
*Blood flow does not increase in frontal lobes during tests of working memory:
*Cortex of medial temporal lobe is thinner & the anterior portion of the hippocampus is smaller than in normal people: memory defects
*Lateral & 3rd Ventricles are enlarged & reduced volume of temporal & frontal lobes:

231
Q

Individuals with these types of schizophrenic symptoms have the worst prognosis

A

Negative

232
Q

Would you characterize a schizophrenic w/ grossly disorganized or catatonic behavior as having positive, negative, or disorganized symptoms?

A

Negative

233
Q

What are the prodromal signs of a psychotic episode?

A

Social isolation & withdrawal, Impairment in normal fulfillment of expected roles, Odd behavior & ideas, Neglect of personal hygiene, Flat affect

234
Q

What types of hallucinations are most common in schizophrenics?

A

Auditory

235
Q

3 major classes of symptoms in schizophrenics

A

Positive symptoms: Additional pathological symptoms
Negative symptoms: Loss of function [presence indicates poorer prognosis]
Disorganized symptoms: Disorder of thought & memory dysfunction & confusion

236
Q

The ventral tegmentum releases…. onto the ___________________.

A

Dopamine; nucleus accumbens

237
Q

People that are genetically prone to addiction have what difference in NT activity compared w/ people that don’t?

A

Seem to have a general reduction in serotonin [5-HT]

238
Q

How did Cloniger describe his two “types” of addiction?

A

Type 1: Low novelty seeking, High harm avoidance, High reward dependence
Type 2: High novelty seeking, Low harm avoidance, Low reward dependence

239
Q

Ketamine is a stimulant/sedative/hallucinogen

A

Hallucinogen

240
Q

Out of hallucinogens, sedatives & stimulants, which drugs cause psychological dependence?

A

All

241
Q

Out of hallucinogens, sedatives & stimulants, which drugs cause physical dependence?

A

Sedatives

242
Q

What change in what NT results in psychotic symptoms in alcohol withdrawal?

A

Dopamine

243
Q

What change in what NT results in epileptic seizures in alcohol withdrawal?

A

Glutamate

244
Q

What drug is used most often in the treatment of alcohol withdrawal?

A

Benzodiazapenes

245
Q

What are more serious symptoms of alcohol withdrawal?

A

Marked tremor [the shakes], Delirium [psychomotor agitation, confusion, optic hallucinations], Seizures, Hallucinations  May result in death

246
Q

Can opiate withdrawal cause death?

A

No

247
Q

What are the symptoms of opiod detox?

A
GI flu (nausea, tachy)
* Warm or Cold (methadone)
248
Q

EEG is used to assess:

A

Brain death, Brain damage, epilepsy, sleep

249
Q

Awake, active & thinking individuals w/ open eyes

Background frequency of awake person or closed eyes

  • Alpha/Beta; Frontal/Posterior
A

Awake, open eyes: beta, frontal

Awake, closed eyes: alpha, posterior

250
Q

When your waves have a lower frequency than they should they are known as?

A

Slow waves [the slower the wave the more severe the abnormality]

251
Q

Epilepsy is a chronic condition of…

A

Repetitive seizures

252
Q

What are some drugs that enhance the activity of GABAergic receptors & are used in the treatment of epilepsy?

A

Barbs & Benzos

253
Q

An aura precedes a partial or generalized seizure?

A

Partial

254
Q

A seizure that has a focus in one part of the brain and remains in a localized region is known as a…

A

Partial epileptic seizure

- Negative LOC

255
Q

What are two drugs used in the treatment of epilepsy that work by REDUCING the # of Na+ channels? Phenytoin, Carbamazepine

A

Phenytoin, Carbamazepine

256
Q

Todd’s paralysis

A

Brief period of transient (temporary) paralysis following a seizure

257
Q

Which of the seizures are also known as Petit-Mal seizures? Absence typical or absence atypical

A

Absence typical

258
Q

Absence typical or atypical

Gradual/sudden

A

Typical: sudden
Atypical: gradual

259
Q

Grand mal seizure characteristics

A

Tonic-Clonic-Post-tictal

260
Q

Seizures can be classified into 2 general categories. What are they?

A

Primary
Secondary (Focal or generalized)
* Localized = partial; start local, then spreads = 2econdary generalized and LOC

261
Q

What is the difference between a simple partial and complex partial seizure?

A

Simple: No LOC

Complex partial: Aura

262
Q

A petit mal, or absence seizure…

A

specific pattern of generalized convulsion - brief (usually seconds); no movement (except maybe eye blink or lip movement), no loss of tone; no memory for time; no postictal period; it is most common in children and may be “outgrown.

263
Q

Ampa receptors, phosphorylation
GluR1, GluR2
Hippocampus, cerebellum
LTP, LTD

A

Hippocampus: GluR1, phosphorylation, LTP

264
Q

How are NMDA receptors activated in the brain with respect to memory?

A

Increased AMPA conductance, receptors, synapses

265
Q

Alzheimers brains can show…

A

Senile amyloid plaques (ECF)

ICF – tangles/tau proteins, granulovascular degeneration