Exam 2 Lagniappe Flashcards
(141 cards)
1
Q
What is the main function of the ANS?
A
Maintain homeostasis via regulating activity of internal organs and vasculature
2
Q
What are the three branches of the ANS?
A
Sympathetic Nervous System (SNS)
Parasympathetic Nervous System (PNS)
Enteric Nervous System (ENS)
3
Q
How does the ANS affect thermoregulation?
A
It regulates sweating and blood flow to the skin to maintain body temperature
4
Q
What are the main transmitters for the SNS, and what are their effects?
A
Epinephrine and norepinephrine
Effects: raise HR and BP, vasoconstrict, bronchodilate, pupil dilation.
5
Q
What do epinephrine and norepinephrine inhibit?
A
Digestion and bowel + bladder
6
Q
What is the primary neurotransmitter of the parasympathetic nervous system, and what effects does it have?
A
Acetylcholine
Effects: decrease HR and BP, vasodilation, bronchoconstriction, pupil constriction (AKA Miosis), and stimulates digestion via peristalsis
7
Q
Both the SNS and PNS use a _______ pathway to regulate involuntary bodily functions.
A
Two-neuron pathway
(Consists of a preganglionic and postganglionic neuron)
8
Q
Attributes of preganglionic neurons:
A
-originates in CNS and synapses at a ganglion outside of the CNS
-myelinated
-SNS has SHORT axons
-PNS has LONG axons
-ALWAYS USES ACETYLCHOLINE
9
Q
Attributes of postganglionic neurons:
A
-originates in ganglion, synapses in the target organ (heart, GI tract, blood vessel, etc.)
-Unmyelinated
-SNS has LONG axons
-PNS has SHORT axons
10
Q
What is the central control center of the ANS?
A
The hypothalamus, with complex circuits projecting to the brainstem, reticular formation, and spinal cord
11
Q
Where do thermoreceptors respond to changes in circulating blood temperature?
A
In the hypothalamus
12
Q
What does the solitary nucleus consist of?
A
Cranial Nerves 7, 9, and 10
These provide visceral information to the brainstem!
13
Q
Where is afferent autonomic information processed in the brain?
A
-Solitary nucleus
-Spinal cord
-Brain stem
-Hypothalamus
-Thalamus
14
Q
What is the reticular formation?
A
A neural network of brainstem nuclei and neurons
15
Q
What is the function of the reticular formation?
A
Adjusts the general level of activity throughout the nervous system
Specifically:
-motor and autonomic function
-nociceptive info
-consciousness
-regulates vital autonomic functions (HR, breathing, vasoconstriction/dilation)
16
Q
Where can the reticular formation be found?
A
Runs vertically in the brainstem from the medulla oblongata to the upper portion of the midbrain
17
Q
Visceral information reaching the thalamus is mainly projected by the ________.
A
Limbic system (Emotion/motivational system)
This is why when we get anxious or embarrassed certain autonomic responses like increased HR happens
18
Q
Neurons that secrete acetylcholine are called _____.
Neurons that secrete norepinephrine or epinephrine are called _______.
A
Cholinergic; adrenergic
19
Q
What type of ACH receptors are on the post-ganglionic neuron? What about on the target tissues?
A
Post-ganglionic receptors = nicotinic
Target tissue receptors = muscarininc
20
Q
What are the motor symptoms of Parkinson’s Disease?
A
T: Tremor
R: Rigidity
A: Akinesia (bradykinesia)
P: Postural instability
21
Q
Apart from motor symptoms, what else do you see in patients with too little dopamine?
A
-Cognitive impairments (dementia, etc.)
-Mood and emotional symptoms (depression, anxiety, apathy)
-Sleep disturbances
-Autonomic dysfunctions (orthostatic hypertension, excessive sweating)
-Sensory symptoms
-Hyposmia
22
Q
True or false. Many internal organs cannot function independently of CNS input.
A
False! They sure can. How neat is that?
23
Q
Parasympathetic efferents arise from the _____
A
Sacral parasympathetic nuclei (S2-4)
24
Q
General neuron pathway of the sympathetic nervous system
A
Cell body in lateral horn of spinal cord -> preganglionic neuron exits through the ventral root and enter sympathetic trunk -> synapse with postganglionic neuron in paravertebral ganglia -> post ganglionic neuron travels to either the same, higher, or lower spinal level and synapses there
25
Where are the cell bodies of the postganglionic neurons found?
In the paravertebral ganglia (sympathetic trunk)
26
Preganglionic axons travel into the sympathetic trunk through the ______, whereas postganglionic axons leave the sympathetic trunk through the _______.
White communicating ramus; gray communicating ramus
27
Two-neuron tracts to the periphery and thoracic viscera synapse where?
In the paravertebral ganglia (sympathetic trunk)
28
Two-neuron tracts to the abdominal and pelvic organs synapse where?
In the prevertebral ganglia which are close to the organs
29
Where does the parasympathetic nervous system arise from?
The cranial nerve nuclei all the way to S2-4
30
What is the name of the system the PNS uses as a two-neuron pathway from the brainstem and sacral cord to the end organs?
The cranial sacral outflow
31
All parasympathetic preganglionic neurons originate where?
In the brainstem or the sacral spinal cord
32
Which brainstem nuclei have parasympathetic preganglionic neuron cell bodies?
CN III - Edinger-Westphal (oculomotor) nucleus
CN VII - Superior salivatory nucleus
CN IX - Inferior salivatory nuclei
CN IX,X - nucleus ambiguus
CN X - dorsal motor nucleus of vagus
33
What are the parasympathetic functions of the cranial nerves?
CN III - Constricts pupils and increases convexity of pupils to improve focus on nearby objects
CN VII - innervates lacrimal gland
CN VII and IX - innervate salivary glands
CN X - innervates heart, smooth muscle of lungs, and digestive system
34
What are some causes of Horner's Syndrome?
-Ischemia
-Trauma
-Tumor
-Cluster headache
-Stellate ganglion block
35
What is Autonomic Dysreflexia (AD) in a nutshell?
Basically, in a SCI above T5/T6 you cannot regulate your ANS. This causes your SNS to become hyperactive when you have a noxious stimulus BELOW THE LEVEL OF THE LESION and leads to deadly symptoms like rapid increase of BP. The descending inhibition from your brain does not kick in and can't calm your sympathetic responses down.
36
What are the three types of syncope?
-Neural reflexive
-Orthostatic
-Cardiac
37
What are the three types of neural reflexive syncope?
-Neurocardiogenic
-Situational
-Hypersensitive carotid sinus syndrome
38
What are common symptoms of a brainstem injury?
-Impairments with controlling BP, HR, and RR
-Dysfunction of CN nuclei. Issues with pupil constriction, tear and saliva production, and control of the thoracic/abdominal viscera
39
What is the continuum of muscle tone?
-Flaccidity (complete lack of resistance to stretch)
-Hypotonia (Abnormally low resistance to stretch)
-Normal
-Hypertonia (Breaks into spasticity and rigidity)
40
What is the difference between spasticity and rigidity?
Spasticity = velocity dependent resistance to stretch. More speed = more resistance
Rigidity = non-velocity dependent increase in resistance. Speed doesn't matter!
41
What are common causes of flaccidity/hypotonia?
-LMN Lesions
-Genetic disorders (Prader-Willi or Down Syndrome)
-Metabolic disorders ( hypothyroidism)
-Immune disorders (Myasthenia gravis)
-Brain injury, CP, or intracranial hemorrage
42
What is spinal shock?
A response after acute trauma to the CNS where you have temporary hypotonia because the descending tracts are interrupted by swelling
DTR's go away and muscles are hypotonic
Eventually though once the swelling subsides you develop HYPERTONIA
43
Hypertonia is caused by a(n) __________ lesion
Upper motor neuron
Happens after spinal shock has been resolved!
44
What are the two mechanisms behind upper motor neuron overactivity (hypertonia)?
1. Absence of cortisospinal/reticulospinal inhibition to the LMN's
2. Brainstem UMN overactivity
45
What are the different types of rigidity?
1. Cogwheel
2. Lead-pipe
3. Gegenhalten
4. Decerebrate rigidity/posturing
5. Decorticate rigidity/posturing
46
Cogwheel rigidity
-Jerky, catch and release movement through ROM.
-Combination of lead-pipe and tremors
-Commonly seen in Basal Ganglia disorders like Parkinson's Disease
47
Lead-pipe rigidity
-Constant resistance throughout ROM
-Commonly seen in Basal Ganglia disorders like Parkinson's Disease
48
Gegenhalten
-Involuntary resistance to passive movements, or the patient tensing up passively whenever you move their limb
-Seen in severe dyspraxia, apraxia, and dementia
49
Decerebrate rigidity/posturing
-Damage b/w midbrain and pons
-Extension of the limbs and trunk, IR of the shoulders, elbow EXTENSION, wrist and finger flexion
-SEVERE brain injury
50
Decorticate rigidity/posturing
-Damage of the superior midbrain or severe B lesions of the cerebral cortex
-Extension of neck, trunk and lower limbs, elbow FLEXION, flexion of wrists and fingers
51
What is the difference in posture presentation between decerebrate and decorticate?
In decerebrate, the elbows are EXTENDED.
In decorticate, the elbows are FLEXED.
52
Will spasticity have exaggerated or reduced DTR?
Exaggerated b/c of hyper-excitability of the stretch reflex
53
What is the SPASM consortium (UK, 2006) definition of spasticity?
Spasticity is an intermittent or sustained INVOLUNTARY HYPERACTIVITY OF A SKELETAL MUSCLE associated with an UMNL
54
After an UMNL, what are the two types of adaptations that your body can undergo?
Myoplasticity (Muscle adapation)
-response to immobility, causes muscle fiber atrophy, increased # of actin myosin bonds, and contractures
Neural overactivity (Nerve overactivity)
-response to paresis/paralysis, causes hyperreflexia for SPINAL lesions and excess reticulospinal drive in CEREBRAL lesions to increase muscle contractions
Note: Both lead to SPASTICITY!
55
What is clasp knife phenomenon?
Initial resistance to passive stretch or movement followed by a sudden decrease in resistance as the movement continues
56
What is the Supra-Segmental (Supraspinal) contribution of spasticity?
Basically this is when the descending inhibitory signals from the brain, specfically the pyramidal and extrapyramidal tracts, are impaired and lead to increased DTR and tone
57
What are the pyramidal tracts associated with the brain? What about extrapyramidal tracts?
Pyramidal = corticospinal
Extrapyramidal = reticulospinal, rubrospinal, and vestibulospinal
58
Somatosensory pathways to postcentral corticies become ______ after injury?
Hyperactive
59
For the extrapyramidal tracts, which tracts are inhibitory, and which are excitatory?
Inhibitory = Dorsal (lateral) reticulospinal tract (DRT)
Excitatory = (Ventral) medial reticulospinal tract (VMRST) and vestibulospinal tract (VST)
60
Where does the corticoreticular tract arise from?
the premotor and supplementary motor areas
61
Where does the reticulospinal tract project to?
MN's and interneurons in the spinal cord
62
What is the ventromedial reticular formation? Where can you find it? and What does it do?
It is an inhibitory area in the medulla, located behind the pyramids
It inhibits the spinal stretch reflex through the dorsal (lateral) reticulospinal tract
63
The excitatory system of the extrapyramidal tracts facilitates ______, and inhibits _____.
Facilitates spinal stretch reflexes + extensor tone (of antigravity muscles)
Inhibits flexors
64
What is the difference between paralysis and paresis?
Paralysis is found in SCI's, and leads to stretch reflex hyperreflexia
Paresis is found after a cortical stroke, and leads to decreased inhibition from corticospinal tract, which causes excess reticulospinal tract activation and muscle contraction
Both cause:
-Contractures
-Atrophy
-Weak actin-myosin bonds
65
In a nutshell, what are the mechanisms of supraspinal control in spasticity?
If the premotor and supplementary motor areas, brainstem inhibitory center, and/or the dorsal lateral reticulospinal tract get injured there are not enough DESCENDING INHIBITORY signals telling the excitatory pathways (vestibulospinal and ventromedial reticulospinal tracts) to shut up, and so you get increased excitation of spinal MN's and interneurons leading to the bad stuff like spasticity and contracture
66
What happens at the level of the spinal cord with spasticity?
1. The spinal reflexes become exaggerated (hyperreflexia)
2. The fusiform drive (gamma motor neurons + muscle spindles) becomes overactive, which makes muscles respond excessively to stimuli (contract in response to small stretches)
3. Dysfunction of the spinal inhibitory mechanisms (1a, 1b, and Renshaw)
4. Reorganization of the spinal circuits / Neuroplasticity
67
Long term neuromuscular adaptions such as changes in muscle length and receptor sensitivity are a result of what? How does this affect DTR's?
Myoplasticity! It is how the body compensates after spinal shock.
DTR's will disappear at first then return once the shock has subsided
68
Ia presynaptic inhibition related to spasticity
In spasticity the Ia presynaptic inhibition is impaired, meaning that muscles spindles are INHIBITED LESS, so they are more excitable and more likely to have hyperreflexia and/or hypertonia
69
How is Ia reciprocal inhibition affected with spasticity?
Normally, Ia reciprocal inhibition allows for smooth movement by inhibiting the antagonist while the agonist is contracting.
In spasticity this is impaired, meaning that the antagonist will keep contracting while the agonist is contracting, leading to excessive co-contraction and stiff movement.
70
How is Ib non-reciprocal inhibition (autogenic inhibition) affected in spasticity?
The normal function of Ib non-reciprocal inhibition is to fine tune movements and make movements more smooth by somewhat inhibiting the homonymous muscle.
In spasticity this is reduced, meaning that there will be excessive muscle tone + stretch reflexes
71
How is Renshaw cell (interneuron) inhibition affected during spasticity?
Similar to Ib non-reciprocal inhibition, the purpose of Renshaw cell is to inhibit the homonymous and synergist muscles.
In spasticity this is reduced, and so will lead to excessive muscle tone and hyperreflexia.
72
How do the spinal cord circuits reorganize (neuroplasticity) after an UMN injury?
Abnormal motor control and reflex pathways may be strengthened, which leads to spasticity
Basically your body is trying to help and repair itself but it ends up becoming over-sensitized
73
What can happen when the spinal cord is deprived of supraspinal (brain) influences?
-Collateral sprouting of axons
-Unmasking previously silent synapses
-Heightened sensitivity of sensory receptors
-Enhanced cutaneous reflexes (Babinksi and Flexor withdrawal reflex)
74
Changes in ______ due to constant muscle activity result in _____ and altered muscle function, which can worsen ______.
Soft tissue; contractures; spasticity
75
What are some common stimuli that trigger spasticity?
-Rapid stretching (ex. clonus)
-Nociceptive stimuli (pain, infections, pressure ulcers)
-Non-nociceptive stimuli (cutaneous and visceral stimuli)
Note: stress/anxiety or excitement can increase muscle tone and put a person at greater risk of spasticity
76
What is the most common outcome measure for spasticity?
The modified Ashworth Scale (MAS)
-put patient in relaxed position (normally supine)
-passively move joint rapidly through available PROM
77
How will spasticity present in an EMG?
EMG will not specifically detail spasticity but can help identify whether the patient has a nerve or muscle issue.
For contractures and hyperreflexia, EMG readings will be normal or higher.
If muscles are firing out of sequence with each other, this will present as atypical EMG patterns
78
What are the treatment options for spasticity?
-Pharmacologic management
-PT and OT
-Surgery
79
What is festinating gait?
A gait pattern common to Parkinson's Disease where the person has a hard time initiation gait, and thus their trunk moves forward and the weight shifts to their toes and the anterior parts of their feet. It resembles a running posture and progresses in speed over time.
80
What are choreiform movements?
Ballistic involuntary movements of the limbs
81
What is the function of the epithalamus?
Regulates:
-circadian rhythms
-emotional responses
-endocrine system functions
82
What is the diencephalon composed of?
1. Thalamus
2. Hypothalamus
3. Epithalamus
4. Subthalamic Nuclei
83
The thalamus and hypothalamus are important for _______ and _______.
Sleep regulation; alertness.
84
What is the function of the anterior lobe of the cerebellum?
Motor coordination for trunk and proximal limbs
85
What is the function of the posterior lobe of the cerebellum?
Fine motor coordination for distal limbs
86
What is the function of the flocculonodular lobe?
Balance and eye movements
87
What separates the anterior and posterior lobe of the cerebellum?
Primary fissure
88
What separates the posterior and flocculonodular lobe of the cerebellum?
Posterolateral Fissure
89
What are the anatomical zones of the cerebellum?
-Lateral hemispheres
-Flocculonodular lobe
-Intermediate Hemispheres / Paravermis
-Vermis
90
What is the function of the cerebrocerebellum?
-Regulates highly skilled movements
-Motor planning and complex movements with sequences
91
What is the function of the spinocerebellum?
-Receives sensory input from spinal cord to help w/ position sense of body and limbs
-Helps maintain posture + balance by integrating proprioceptive feedback
92
What cerebellar nuclei is found in the vestibulocerebellum?
The vestibular nuclei
93
Pathology of the vermis leads to _____
Truncal and gait instability
94
Intermediate hemispheres of the cerebellum control _____.
Appendicular muscles (UE and LE)
95
Pathology of the intermediate hemispheres of the cerebellum can lead to ______.
Limb ataxia
96
Describe the homunculus of the cerebellum.
Its like two stick figures with oriented in opposite directions. The midline of the vermis is head region and as you go further distal it progresses to the UE and LE respectively
Its best to see the picture from the slide show. I am poor and can't afford to put pictures on brain scape :(
97
What interneurons are found in the molecular layer of the cerebellum?
Stellate and basket cells
-both release GABA
-Stellate cells also release Taurine
98
What interneurons are found in the purkinje cell layer?
Purkinje cells
-releases GABA
99
Granular layer
Golgi cells
-releases GABA
Granular cells
-releases GLUTAMATE
100
What is neural sharpening?
Synaptic connections are strengthened or refined. Helps to fine tune movements and respond effectively
101
Where does the spinocerebellum collect information from?
Golgi tendons (Ib) and muscle spindles (Ia)
102
Which spinocerebellar tracts travel through the superior cerebellar peduncle?
Ventral spinocerebellar and rostral spinocerebellar
Note: the rostral spinocerebellar tract travels through both the superior and inferior cerebellar peduncle
103
Which spinocerebellar tracts travel through the inferior cerebellar peduncle?
Dorsal spinocerebellar, cuneocerebellar, and rostral spinocerebellar
Note: the rostral spinocerebellar tract travels through both the superior and inferior cerebellar peduncle
104
Which spinocerebellar tracts receive information from the LE?
Dorsal spinocerebellar - Leg proprioceptors (Ia)
Ventral spinocerebellar - Leg interneurons (Ib)
105
Which spinocerebellar tracts receive information from the UE?
Cuneocerebellar - Arm proprioceptors (Type Ia)
Rostral spinocerebellar - Arm interneurons (Type Ib)
106
The dorsal spinocerebellar tract turns into _____ then travel to the ipsilateral cerebellar cortex
Mossy fibers
107
Lesions to the ventral spinocerebellar tract will present ______.
Ipsilaterally because this tract crosses twice!
108
What are the function of high fidelity pathways?
Transmit proprioception information with high accuracy to be arranged somatotopically in the cerebellar cortex
109
Where is serotonin produced?
The Raphe Nucleus
110
Where is acetylcholine produced?
The pedunculopontine nucleus
111
What are common attentional disorders?
-Dual task deficit
-Neglect
-ADD/ADHD
-Motor impersistence
112
Logorrhea
Excess and incoherent talkativeness
113
Verbal perseveration
Repeating something over and over again. Seen with aphasia b/c its the word the person can cling to
114
Confabulation
Lying without intention to deceive. The person truly thinks it happens. Could be caused by gaps in memories
115
Dyslexia
Disorder of written language
116
Oral motor dyspraxia
Issues with motor planning pertaining to speech
117
Dysarthria
Difficult or unclear articulation of speech.
118
What is the difference between a communication disorder and a language disorder?
A language disorder means that cognitively you cannot understand or express words, writing, etc.
A communication disorder is a broader term, and may involve disorders where you can comprehend and produce language just fine, but the motor planning or muscle strength/coordination are adversely affected.
119
What are the different types of sensory input to the sensory areas of the cerebral cortex?
-somatosensory
-auditory
-visual
-vestibular
120
Prosopagnosia is associated with _______ damage to the inferior secondary visual areas (part of the ventral stream)
bilateral
121
If a lesion affects the LEFT secondary auditory cortex, the person is unable to understand _______.
Speech
122
If a lesion affects the RIGHT secondary auditory cortex, it interferes with interpretation of ___________.
Environment sounds
ex. inability to differentiate b/w sound of footsteps and a doorbell
123
Anosagnosia is associated with lesion to where?
The right anterior insula
124
What are some risks if a patient has anosagnosia?
-forgetting they need to use assistive devices and falling
-forgetting they are on a special diet and aspirating on drinks or food
There are tons of examples for this but these are just a few mentioned in class ¯\_(ツ)_/¯
125
For a person with hemineglect, will their midline shift towards the affected side or the unaffected side?
The unaffected side, because with hemineglect everything on the affected side does not exist anymore!
126
Lesions to _________ can lead to hemineglect.
Any part of the awareness network.
However, the MOST COMMON area damaged is the right posterior parietal cortex or right frontal lobes
127
What are the two types of hemineglect?
-Personal neglect
-Spatial neglect
128
Lesions to inferior frontal gyrus affect _______.
Nonverbal communication
129
_____ can be considered a motor agnosia.
Apraxia
130
Constructional Apraxia
Inability to comprehend the relationship of parts to the whole
ex. difficulty with drawing, building, or assembling objects
131
Gait apraxia
AKA "magnetic gait," slow shuffling steps where feet barely lift from the ground
132
Epilepsy is characterized by _________.
Sudden burst of excessive cortical neuronal discharge that interferes with brain function
133
What are some symptoms of epilepsy?
-Involuntary movements
-Disruptions of autonomic regulation
-Illusions and hallucinations
134
What area of the brain do general seizures affect, and what are the two types?
They affect the entire cortex.
1. Absence seizures
2. Tonic-clonic seizures
135
Abscence seizures
Brief loss of consciousness without motor manifestations
136
Tonic-clonic seizures
Starts with a tonic contraction of skeletal muscles followed by alternating contraction and relaxation of muscles
137
Partial seizures affect the ________ of the cortex
Restricted area
138
What are some treatment options for epilepsy?
-Anti-epileptic drug therapy (primary treatment)
-Ketogenic diet
-Lifestyle modifications / behavior changes to avoid triggers
-Surgery (callostomy or hemispherectomy for severe cases)
139
When is a seizure a medical emergency?
-cause of seizure is unknown (no previous history of seizure disorder)
-injured
-diabetic
-pregnant
-seizure lasting longer than 5 minutes, or another seizure begins shortly after the first
-consciousness does not return
-happens in water
140
True or false. Functional Neurologic Disorders (FND) are a rule-out diagnosis.
False! They are rule-in, meaning that THERE ARE NO SPECIFIC SIGNS AND/OR SYMPTOMS FOR IT.
141
What is the cause for functional movement disorders?
Multi-network brain dysfunction
-the supplemental motor area is less active than normal
-connection b/w supplemental motor area and emotion/motivation is abnormal
-when weakness is present, the primary motor cortex is inhibited (this would not happen if the person was faking the weakness)
