L.2.1 Flashcards
1
Q
What is the spinal cord
A
- a column of nerve tissues that carries nerve impulses from the brain to the rest of the body
- it consists of grey matter and white matter
2
Q
What is the function of the ventral horn of spinal cord
A
houses motor neuronal cell bodies
3
Q
What is the function of the dorsal horn of spinal cord
A
houses neurons receiving sensory input
4
Q
TRUE OR FALSE: the horns are part of the grey matter in the spinal cord
A
TRUE
5
Q
What is the function of the ascending tracts in spinal cord
A
carry afferent sensory information/nerve impulses to centres within the brain
6
Q
What is the function of descending tracts in spinal cord
A
carry efferent motor information from centres within the brain
7
Q
What is the relationship between tracts and cerebral hemispheres
A
- tracts to & from cerebral hemispheres are crossed
- left hemisphere controls right side of the body
8
Q
What does the dorsal column house
A
ascending tracts
9
Q
What does the lateral column house
A
ascending & descending tracts
10
Q
What does the ventral column house
A
descending tracts
11
Q
What is another name for the corticospinal tract
A
pyramidal tract
12
Q
What is the corticospinal tract
A
motor pathway which carries motor information from the cerebral cortex to the spinal cord
13
Q
What are the 2 main types of neurons that are part of the corticospinal pathway
A
upper & lower motor neurons
14
Q
What are upper motor neurons
A
neurons located in the brain and that transmit nerve impulses from the cerebral cortex to the spinal cord (ventral horn)
15
Q
What are lower motor neurons
A
neurons located in the spinal cord (ventral horn) and that transmit nerve impulses from the spinal cord to the skeletal muscles
16
Q
Outline the main anatomical structures in the corticospinal pathway
A
- primary motor cortex (pre-central gyrus)
- Internal capsule
- Cerebral peduncle (midbrain)
- Pons
- Pyramids of medulla (80% neurons decussate to lateral cortical spinal & 20% neurons stay on same side and join anterior cortical spinal)
17
Q
Why do upper motor neurons control muscles on the contralateral side of the body
A
upper motor neurons synapse with lower motor neurons in the ventral horn (spinal cord)
18
Q
What are the main types of lower motor neurons
A
- alpha motor neurons
- gamma motor neurons
19
Q
What muscles do alpha motor neurons innervate and what is their function
A
they innervate extrafusal muscle fibres and generate contractions
20
Q
What are the features of alpha motor neurons
A
large and fast-conducting neurons
21
Q
What muscles do gamma motor neurons innervate and what is their function
A
they innervate intrafusal muscle fibres & regulate muscle spindles
22
Q
What are the features of gamma motor neurons
A
small and slower conducting neurons
23
Q
What is a motor unit
A
consists of 1 alpha motor neuron and all the muscle fibres it innervates
24
Q
How do small motor units generate movement/muscle contraction
A
- innervate few muscle fibres
- allow precise control
25
How do large motor units produce movement
- innervate many muscle fibres
- allow gross movement
26
What is a motor neuron pool
a group of lower motor neurons that innervate 1 muscle
27
What are features of motor neuron pools
- each muscle has its own motor pool
- clustered together in rod-shape in spinal cord
28
What happens if there is damage to a single ventral root or spinal nerve
muscle weakness
29
How is the force of muscle contraction regulated
- firing rate of alpha motor neurons
- recruitment of additional motor units
30
How is the firing rate of alpha motor neurons related to muscle contraction generated
- increased firing rate
- greater muscle contraction
31
How is the recruitment of additional motor units linked to muscle contraction generated
- more motor units
- more muscle force
- more contraction
32
What are muscle proprioceptors
they provide sensory feedback about muscle activity to help control movement and balance
33
What are the 2 types of muscle proprioceptors
- muscle spindles
- golgi tendon organs
34
Outline the structure of muscle spindles
- located in skeletal muscles
- have intrafusal muscle fibres
35
What is the function of muscle spindles
they detect changes in muscle length when the muscle is stretched
36
How do muscles spindle detect that a muscle has been stretched
- sensory nerve fibres (Group Ia) send signals to brain when muscle is stretched
- it increases muscle spindles firing rate
37
What is the function of golgi tendon organs
they detect muscle tension
38
Where are golgi tendon organs located
- tendon
39
How do golgi tendon organs detect muscle tension
- during muscle contraction, Group Ib fibres send signals to brain
40
What happens when gamma motor neurons are activated
- they keep muscle spindles tight (taut) even when the muscle changes length
41
What is the purpose of keeping muscle spindles taut at different muscle lengths
- muscle spindles can keep sending accurate information about muscle stretch
- no matter how long or short the muscle is
42
What are reflexes
- involuntary responses to an external stimulus mediated by the spinal cord
43
What are monosynaptic reflexes
simplest reflex and involves only 1 synapse between a sensory neuron and motor neuron
44
What is an example of a monosynaptic reflex
knee-jerk reflex
45
Outline the knee jer reflex
1. tapping the patellar ligament stretches muscle
2. Group la fibres from muscle spindles activated
3. Activates alpha motor neurons in ventral horn
4. Quadriceps muscle contracts
46
What are polysynaptic reflexes
most reflexes are polysynaptic and have multiple synapses in circuit
47
Name an example of a poly-synaptic reflex
golgi tendon reflex
48
Outline the golgi tendon reflex
1. Muscle tension increases
2. Group Ib fibres activated
3. Inhibitory interneurons activated
4. Alpha motor neurons inhibited and muscle tension reduced
5. Stops muscle from contracting for protection
49
What is reciprocal inhibition
- contraction of muscle with the relaxation of antagonist muscle
50
What is the flexion/withdrawal reflex
- a spinal reflex to protect the body from damaging stimuli
- a polysynaptic reflex, caused by nociceptor activation
51
What is the cause of an upper motor neuron disease
disruption of the corticospinal tract
52
What are the effects of upper motor neuron disease
- spastic paralysis (increased muscle tone)
- overactive tendon reflexes
- no significant muscle atrophy
53
What is an example of an upper motor neuron disease
stroke
54
Explain the reason behind the motor neuron disease effects
- disrupted control over muscle movement causes stiffness and exaggerated reflexes
- no muscle wasting (atrophy) because some nerve signals can still reach the muscles
55
What is the cause of lower motor neuron disease
degeneration of lower motor neurons
56
What is an example of a lower motor neuron disease
spinal muscular atrophy
57
What are the effects of lower motor neuron disease
- flaccid paralysis
- no tendon reflexes
- muscle atrophy (weakening/shrinking of muscles)
58
What are the causes of amyotrophic lateral sclerosis
both lower and upper motor neurons
59
What are the effects of amyotrophic lateral sclerosis
progressive muscle weakness and atrophy but mind intact
60
Explain the effects of lower motor neurons diseases
Flaccid Paralysis: LMNs degenerate, so muscles no longer receive electrical signals to contract, causing weak and floppy muscles.
No Tendon Reflexes: Reflex arcs are disrupted because LMNs are damaged, preventing the muscle from responding to stimuli.
Muscle Atrophy: Muscles shrink and weaken due to lack of stimulation (trophic support) and disuse when LMNs are lost.
61
What is dyskinesia
involuntary muscle movements (jerks
62
What is dystonia
involuntary muscle contractions (spasm)
63
What is the spinothalamic tract
a sensory pathway in spinal cord that carries information about pain, temperature and crude touch from the body to the thalamus
64
What are the extrapyramidal tracts
- Descending motor pathways that do not pass through the pyramids
65
What is the function of extrapyramidal tracts
Involuntary motor control, crucial for regulating reflexes and maintaining posture
66
What are the 3 structures that the extrapyramidal tract descends through
- rubrospinal
- reticulospinal
- vestibulospinal
67
What are the 4 types of movement
- passive
- stereotypes
- reflexive
- self-generated
68
Definition of passive movements
movements happen w/o voluntary muscle contractions
69
What are the types of passive movements
- hypotonia & hypertonia
- spasticity
70
What are reflexive movements
involuntary responses to external stimuli mediated by the spinal cord
71
What are the types of reflexive movements
- hyporeflexia
- hyperreflexia
72
What is the cause of hyporeflexia
lower motor neuron lesion
73
What is the effect of hyporeflexia
reduced/absent reflexes
74
What is the cause of hyperreflexia
upper motor neuron lesions
75
What is the effect of hyperreflexia
exaggerated reflexes
76
What is the cause of hypotonia
lesion in lower motor neuron or cerebellum
77
What is the effect of hypotonia
- low muscle tone
- muscles are weak
78
What is the cause of spasticity
lesion in the corticospinal tract
79
What is the effect of spasticity
- increase muscle tone
- resistance to movement
80
What is a stereotyped movement
movements that are automatic, patterned and repetitive
81
What are examples of stereotyped movements
- chewing
- walking
- talking
82
What are the two types of self-generated movements
- emotional
- voltional
83
What are emotional self-generated movements
movements driven by emotional state
84
What is an example of an emotional self-generated movement
- smiling
- frowning
85
What are volitional self-generated movements
goal-directed movements
86
What is an example of a volitional self-generated movement
reaching for an object
87
What is the main cause of loss of descending inhibition (reflexive movements)
upper motor neuron lesions
88
How do upper motor neurons lesions result in loss of descending inhibition
they disrupt inhibitory signals from brain to the spinal cord
89
What are the main consequences of loss of descending inhibition?
- increased reflex excitability
- spasticity
- Brisk reflexes
90
Explain why reflexes excitability increases during loss of descending inhibition
- upper motor neurons fail to suppress reflex actions
- the inhibitory signals have been disrupted
91
Explain why the spasticity occurs during loss of descending inhibition
- the muscle tension & contraction is not being properly inhibited by the brain, so they become stiff and difficult to move. --> increase muscle tone
92
How does lower motor neuron damage contrast with upper motor neuron damage in terms of tone and reflexes?
- LMN = reduced tone + loss reflexes
- UMN = increased tone + brisk reflexes
93
What are brisk reflexes?
they are exaggerated reflexes
94
What is spasticity
an increase in muscle resistance during passive muscle stretching
95
What is the typical reflex response in spasticity?
extensor reflexes dominate
96
Where does the tectospinal tract pathway
from the superior colliculus (midbrain) down to the spine
97
What is the function of the tectospinal tract
- associated with visual pathways
- controls head and neck movements in response to visual stimuli
98
What is the overall pathway of the vestibulospinal tract
starts from the vestibular nuclei in the brain stem down to the spinal cord
99
What is the function of the vestibulospinal tract
- ensures postural stability
- stabilises eyes and head during body movements
100
What are the 2 divisions of the vestibulospinal tract
- lateral vestibulospinal tract
- medial vestibulospinal tract
101
What is the lateral vestibulospinal tract responsible for
activates extensor muscles in arms and legs
102
What is the medial vestibulospinal tract responsible for
controls head and neck movements to stabilise eyes during movement
103
What is the function of the reticulospinal tract
- maintains posture and balance
- coordinates limb movements (ex: walking)
104
What are the 2 divisions of the reticulospinal tract
- medial reticulospinal tract
- lateral reticulospinal tract
105
What is the medial reticulospinal tract responsible for
responsible for extensor motor neurons
106
What is the lateral reticulospinal tract responsible for
responsible for flexor motor neurons
107
Which 2 descending pathways are responsible for control of head and neck movements
- tectospinal tract
- medial vestibulospinal tract
108
Which 2 descending pathways are responsible for activating extensor muscles in arms and legs
- reticulospinal tract
- lateral vestibulospinal tract
109
What are locomotive movements caused by
controlled pattern generators (CPGs) in spinal cord
110
What are the features of locomotive movements
- not consciously controlled
- rhythmic and repetitive movements
111
How do locomotive movements work
- pacemaker cells start rhythmic activity
- reciprocal inhibition (one group of muscle is activated, opposing muscle is inhibited)
112
Why is it that during facial palsy damage to the upper motor neuron and emotional movement can occur
a genuine smile can elicited by emotion because the emotional pathway bypasses the corticobulbar pathway
113
Which pathway mediates volitional movement
mediated by corticospinal tract
114
What is the function of the rubrospinal tract
involved in flexion of upper limbs
115
What is posturing in coma
- provides an idea about the location of lesions in brainstem
116
What is posturing
abnormal body positions that occur due to severe brain injury
117
Where does the lesion occur in decorticate posturing
lesion above the red nucleus
118
What are the effects of decorticate posturing
- rubrospinal tract is disinhibited
- extensor pathways dominate in lower limbs
- lower limbs extension & upper limb flexion
119
TRUE OR FALSE: Decerebrate posturing is the MORE severe than decorticate posturing
TRUE
120
Where does the lesion occur in decerebrate posturing
below the red nucleus
121
What are the effects of decerebrate posturing
- rubrospinal tract is disrupted
- upper and lower limb extension
- flexor facilitation in upper limb is lost
122
Which 2 pathways provide extensor dominance
- vestibulospinal tract
- reticulospinal tract
123
What pathway provides flexor dominance
rubrospinal tract
124
What are the features of corticospinal tract damage
- spasticity
- brisk reflexes
125
What is Parasagittal Meningioma
- tumour which compresses the medial parts of motor corticies
- causes bilateral leg weakness
126
Where does the middle cerebral artery supply to
lateral aspects of the motor cortex
127
What do the lateral aspects of the motor cortex control
face and hand
128
What does a proximal lesion to middle cerebral artery
causes complete one-sided body paralysis
129
Where does the anterior cerebral artery supply to
medial part of frontal lobes
130
What is the main function of the Posterior Parietal Cortex?
- Integrates sensory information to create mental images of body and environment
- Controls exploratory movements like manipulating objects
131
What are the symptoms of Posterior Parietal Cortex damage?
- Neglect syndrome (patient is aware but ignores stimuli)
- Impaired exploratory movements
132
What are the three motor planning areas?
- prefrontal cortex
- premotor area
- supplementary motor area
133
What is the function of the premotor area
Coordinates sensory-guided movements and facilitates imitation
134
What is the Bereitschaftspotential?
- Brain activity that precedes voluntary movements by 500-1000 milliseconds
* Generated by the supplementary motor area
135
What is the role of the supplementary motor area
Controls complex motor sequences
136
Compare Ideational and Ideomotor Apraxia
Ideational Apraxia:
* Caused by parietal lobe damage
* Cannot plan/execute action sequences
Ideomotor Apraxia:
* Caused by SMA damage
* Cannot use tools properly despite understanding their purpose
137
What is dystonia and its effect
- Sustained involuntary muscle contractions
- Causes abnormal postures or repetitive movements
138
What is demyelination
damage or loss of the myelin sheath
139
Why is demyelination an issue
if nerve signals slow down/disrupted it can cause neurological issues
140
Where does multiple sclerosis occur
in the CNS
141
What happens in multiple sclerosis
the inflammation and destruction of myelin which slows/blocks signals between the brain and the body
142
What are the symptoms of multiple sclerosis
- fatigue
- muscle weakness
- coordination issues
143
Define multiple sclerosis
autoimmune disease where the body attacks myelin in the CNS
144
What areas are affected by multiple sclerosis
- cerebellum
- brainstem
- spinal cord
- optic nerve
145
How does multiple sclerosis affect the cerebellum
it causes balance and coordination problems
146
How does multiple sclerosis affect the brainstem
speech and swallowing issues
147
How does multiple sclerosis affect the spinal cord
muscle weaknesses, sensory changes and bladder/bowel issues
148
How does multiple sclerosis affect the optic nerve
visual problems
149
What are the 2 factors needed for multiple sclerosis diagnosis
- space = plaques must be found in at least 2 different regions of the CNS
- time = evidence that lesions occurred at different points in time
150
What procedure is used to detect MS
lumbar puncture (collects CSF)
151
What elements indicate MS diagnosis
- normal glucose and protein levels
- an increase in white blood cells
- oligoclonal bands present
152
What are some treatments for MS
- steroids help reduce inflammation
- physiotherapy to help improve movement & strength
153
What is the function of the basal ganglia
- helps control muscle movements
- selects an action plan that is most appropriate and relevant to the goal
154
What are the subcortical structures that are part of the basal ganglia
- corpus striatum
- globus pallidus
- substantial nigra
- thalamus
155
What is the main purpose of the direct pathway in the basal ganglia
produce movement
156
What is the main purpose of the indirect pathway
stop unwanted movements
157
What is the main purpose of the hyperdirect pathway
stops movement quickly before it even starts
158
What are the first 2 steps in the direct pathway of the basal ganglia
1. motor cortex sends excitatory signal (GLU) to corpus striatum
2. striatum inhibits (GABA) internal globus pallidus & substantia nigra
159
What are the last 2 steps in the direct pathway of the basal ganglia
3. since SN and Gi are inhibted, it stops suppressing the thalamus (can't send GABA onwards)
4. thalamus is excited and sends excitatory signals (GLU) to motor cortex
5. movement produced
160
What are the 3 first steps in the indirect pathway in the basal ganglia
1. motor cortex sends excitatory signals (GLU) to corpus striatum
2. corpus striatum inhibits (GABA) the external globus pallidus
3. GABA signals are passed onwards, disinhibiting subthalamic nucleus
161
What are the last 2 steps in the indirect pathway of basal ganglia
4. subthalamic nucleus sends excitatory signals (GLU) to internal Gi & substantia nigra
5. they are activated and can inhibit the thalamus
6. the thalamus can't excite the motor cortex so no movement is produced
162
Outline the hyperdirect pathway in the basal ganglia
1. motor cortex sends excitatory signals to subthalamic nucleus
2. it activates the internal globus pallidus --> inhibiting thalamus
3. thalamus can't send signals to motor cortex and movement is stopped
163
Which 2 beurotransmitters does the balance of the direct & indirect pathway depend on
- acetylcholine
- dopamine
164
What are medium spiny neurons
- neurons are responsible for deciding whether movement will happen
- influenced by dopamine
165
How does dopamine affect the direct pathway
- dopamine binds to D1 receptors
- excites medium spiny neurons
- direct pathway is more active and movement is produced
166
What effect does dopamine have on D1 receptors
- excitatory effect
- encourages movement
167
What effect does dopamine have on D2 receptors
- inhibitory effect
- facilitates movement
168
How does dopamine affect the indirect pathway
- dopamine binds to D2 receptors
- inhibits medium spiny neurons
- dampens the inhibitory effect of the indirect pathway
- facilitates movement
169
What is the effect of acetylcholine in the direct pathway
- Ach decreases the activity direct pathway
- making movement less likely
170
What is the effect of acetylcholine in the indirect pathway
- Ach increases the activity of indirect pathway
- making it harder to move
171
What are the overall effects of dopamine and acetylcholine on the basal ganglia
- dopamine = promotes movement
- acetylcholine = inhibits movement
172
What is hypokinetic movement?
Moving too little
173
What are examples of hypokinetic movement
- akinesia (no movement)
- bradykinesia (slowed movement)
174
What is hyperkinetic movement?
Moving too much, such as tics
175
Define ataxia
disturbance of coordination, resulting in clumsy or uncoordinated movements.
176
Define apraxia
A disturbance of planning movements, leading to difficulty planning and performing movements.
177
What is parkinsonism?
A group of movement problems characterized by slow or reduced movement, including rigidity, tremor, and bradykinesia.
178
What are the clinical features of parkinsonism?
- rigidity
- tremor
- bradykinesia
179
What is genetic parkinsonism?
Parkinsonism caused by specific gene mutations, often with a family history of the condition
180
What is atypical parkinsonism?
Parkinsonism with initial symptoms that differ from typical Parkinson’s disease, such as Lewy body dementia or supranuclear palsy.
181
What is secondary parkinsonism?
Parkinsonism caused by external factors like brain injury, stroke, or medication.
182
What is genetic parkinsonism?
It is caused by specific gene mutations, often with a family history of the disease.
183
What is akinesia?
Decreased overall movement, such as reduced blinking, lack of facial expression, and sitting very still
184
What is bradykinesia?
Slowness of movement, worsening as the condition progresses.
185
What is apraxia in Parkinson’s disease?
Difficulty initiating voluntary movements.
186
What is rigidity in Parkinson’s disease?
Stiffness throughout movement.
187
What are three important negatives in Parkinson’s disease?
- Normal reflexes
- no ataxia (coordination is unaffected)
- normal eye movements
188
What is idiopathic Parkinson’s disease (IPD)?
A neurodegenerative condition affecting dopaminergic cells of the substantia nigra
189
What happens when dopamine-producing cells in the substantia nigra die?
Lewy bodies build up, worsening neuronal function.
190
What happens to movement pathways when dopamine levels are low?
- Direct pathway activation decreases, reducing movement promotion.
- Indirect pathway inhibition decreases, overly suppressing movement.
191
What is the overall result of dopamine deficiency in Parkinson's on movement ?
Movements slow down, causing stiffness and tremors
192
What are the goals of Parkinson's disease treatment?
- Manage symptoms through lifestyle changes, medications, and brain stimulation
- slow down progression
193
What enzymes reduce dopamine availability in Parkinson’s disease?
Dopamine is broken down by COMT and MAOB enzymes
194
How is L-DOPA used in Parkinson’s treatment?
It is combined with a Dopa decarboxylase inhibitor to prevent dopamine conversion in the bloodstream before reaching the brain
195
What are the benefits of Levodopa treatment for Parkinson’s disease?
Improves motor symptoms
196
What are the side effects of Levodopa treatment?
- Low blood pressure.
- Dyskinesias (uncontrolled movement).
- Dopamine dysregulation syndrome (addiction-like behavior).
- Excessive daytime sleepiness (e.g., falling asleep during activities).
197
How can continuous dopamine intake affect the brain?
dopamine dysregulation syndrome (addiction-like behavior)
198
What do dopamine agonists do in Parkinson's treatment?
Mimic dopamine and stimulate dopamine receptors.
199
What are dopamine agonist benefits in treatment
- Work even if dopamine-producing neurons are damaged.
- Don’t need enzymatic conversion, making them stable and long-acting.
200
What are the two types of dopamine agonists?
- Ergot-based Agonists: Rarely used due to serious side effects
- Non-Ergot Agonists: Commonly used
201
What are the side effects of dopamine agonists?
Can cause impulse control issues, such as gambling
202
How do monoamine oxidase inhibitors (MAOIs) work in Parkinson’s treatment?
Prevent the breakdown of dopamine in the brain, increasing its levels.
203
What are the two types of monoamine oxidase inhibitors?
- MAO-A: Affects serotonin, adrenaline, and dopamine
- MAO-B: Targets dopamine and is used for Parkinson’s disease
204
What is a key benefit of MAO-B inhibitors in Parkinson’s treatment?
Slight improvement in motor symptoms.
205
How do anticholinergics help in Parkinson’s treatment?
- Reduce tremors by balancing the effects of acetylcholine.
- Excess acetylcholine occurs due to low dopamine levels.
206
What does Amantadine do in Parkinson’s treatment?
Functions as a glutamate agonist, increases dopamine activity, and reduces involuntary movements.
207
How do COMT inhibitors work in Parkinson’s treatment?
- Block COMT enzymes that break down dopamine in the brain.
- Reduce L-dopa metabolism, enhancing its effectiveness.
208
What are the benefits of COMT inhibitors?
- increase the duration of L-dopa’s effects.
209
What are the side effects of COMT inhibitors?
- May increase involuntary movements (dyskinesia)
- diarrhoea
210
What are the infusion therapies for Parkinson’s?
- Apomorphine: Provides rapid relief from OFF periods.
- Levodopa-Carbidopa Intestinal Gel: Maintains steady L-dopa levels.
- Foslevodopa: New formulation for improved levodopa delivery
211
Where is L-dopa absorbed
Duodenum
212
what factors can impact L-Dopa absorption in Parkinson's disease?
- Gastric motility issues.
- Constipation.
- High-protein meals (compete with L-dopa for absorption)
213
How does Duodopa infusion help in advanced PD
Delivers L-dopa directly to the duodenum, stabilizing levels and reducing motor fluctuations.
214
what are Duodopa limitations?
Costly
215
What is Apomorphine, and how is it delivered in PD treatment?
- Dopamine agonist mimicking dopamine’s effects.
- injection under the skin
216
How does Deep Brain Stimulation work in treating Parkinson’s disease?
Disrupts abnormal activity in the basal ganglia causing motor symptoms
217
What are the limitations of DBS in Parkinson’s treatment?
Does not improve non-motor symptoms, such as dementia
218
What is Hemiballismus
Hyperkinetic movement disorder with violent limb movements, typically on one side of the body
219
what causes Hemiballismus
Cerebrovascular event, such as a stroke.
220
What are the types of tic disorders?
- Simple Tics: Blinking, coughing.
- Complex Tics: Jumping, twirling
221
What are key features of tic disorders?
- Preceded by urgency, relieved by performing the tic.
- Reduced by distraction and concentration
- Worsen with anxiety or fatigue
222
What are the main causes of chorea?
Huntington’s disease.
- drugs
223
What are the characteristics of chorea?
- Jerky, brief, irregular contractions.
- Not repetitive or rhythmic but flow between muscles.
- Appears as fidgetiness or restlessness.
224
What are the cognitive symptoms of Huntington's Disease?
Inability to make decisions.
Difficulty multitasking.
Slowness of thought.
225
What are the behavioral symptoms of Huntington's Disease?
- depression
- anxiety
226
What is myoclonus
Brief, involuntary muscle contractions.
227
What is dystonia?
An abnormal twisting posture
228
How is dystonia influenced by dopamine?
blocking dopamine receptors can cause dystonic symptoms.
229
What is long-term depression (LTD) in the context of Purkinje cells?
LTD is the weakening of synaptic connections between parallel fibers and Purkinje cells, making specific synapses less effective over time
230
What are the two key input pathways to Purkinje cells?
- Parallel Fibers:
- Climbing Fibers
231
What is required for LTD to occur in Purkinje cells?
The Purkinje cell must be simultaneously stimulated by climbing fibers and parallel fibers.
232
What happens intracellularly during simultaneous activation of climbing and parallel fibers?
A large influx of calcium occurs in the Purkinje cell.
233
How does the calcium surge affect synaptic transmission in LTD?
1. Calcium activates protein kinases.
2. These kinases phosphorylate proteins involved in receptor trafficking.
3. AMPA receptors are removed (internalized) from the postsynaptic membrane of the Purkinje cell.
234
What is the consequence of AMPA receptor internalization during LTD?
Synaptic transmission is weakened, reducing the effectiveness of the synapse
235
How does the weakening of the synapse between the parallel fiber and the Purkinje cell help with motor control?
The weakening prevents excessive or incorrect motor commands, aiding the cerebellum in refining movements
236
Why is long-term depression (LTD) important for motor control?
- Error Detection and Correction
- Refinement of Movements:
- Adaptive Motor Skills:
237
What happens during error detection and correction
LTD weakens ineffective synapses when movements are incorrect, enabling better future motor adjustments
238
What happens during refinement of movements
Over time, LTD helps optimize motor responses by reducing unnecessary or incorrect pathways
239
What happens during adaptive motor skills
LTD allows long-term changes in motor behavior, which is essential for learning new skills and adapting to new environments
