Motor Control - Disorders of Movement Flashcards
1
Q
What motor disturbances can be seen in disease?
(give 6)
A
- Weakness
- Spasticity
- Rigidity
- Ataxia
- Akinesia
- Apraxia
(usually a patient will show more than one of these symptoms)
2
Q
What is meant by ‘weakness’?
A
- This is not the same as having weak force production in muscles
- Inability to produce forceful movements under voluntary control
- It can be a weak but active muscle response
3
Q
What is meant by spasticity?
A
- Too much tonic (basal) drive to the muscles
- This causes unwanted contractions
- Therefore causing joints to be fully flexed/extended
- It can apply to both agonists & antagonists
- It causes co-contraction spasticity –> making joints very rigid –> giving spastic rigidity
4
Q
What is ataxia?
A
- Cerebellum Damage
- Loss of Coordination
- The sequence of muscle activation/contraction is messed up –> thus the cooperation between agonist & antagonist is faulty
- There is a decomposition of movement
5
Q
What is meant by akinesia?
A
- Absence of Movement
(little/no movement)
6
Q
What is bradykinesia?
A
Low Level of Movement
7
Q
What is apraxia?
A
-
Inability to produce purposeful movements (e.g. can move arms but with no purpose)
(i. e. cannot make a specific grasp)
8
Q
What is praxia?
A
Movement with purpose
9
Q
In terms of time, what effect will a vascular occlusion or haemohrrage have?
A
- Immediate Paralysis
10
Q
In terms of time, what effect will a tumour have?
A
- Slowly progressive symptoms & signs
- Tumour progresses slowly so motor deficit will be slowly progressive
11
Q
What is the confusion caused with small ministrokes?
A
- Their effects can accumulate
- They are more difficult to establish
- Usually though there is one major event which is critical that causes a major loss which is obvious
*
12
Q
In terms of time, how do neurodegenerative losses (e.g. Parkinson’s) present?
A
- Slow & progressive symptoms
13
Q
Where are flexors & extensors generally located in the spinal cord?
A
- Flexors –> near the centre (central canal)
- Extensors –> further out (edges)
14
Q
Image showing Rexed Laminas.
A
15
Q
What four tracts does the cerebellum access & influence?
A
- Corticospinal Tract
- Rubrospinal Tract
- Reticulospinal Tract
- Vestibulospinal Tract
16
Q
What does the basal ganglia mainly influence?
A
- Corticospinal / Pyramidal Tract
17
Q
What is the vestibulospinal tract important for?
A
- Balance Control
- Posture Control
(Pathologies here will cause problems with posture & balance)
18
Q
What is the reticulospinal tract important for?
A
Locomotion
19
Q
What is an important point to note in general about the signals between neurones in the NS?
A
- There is always a basal/tonic firing rate/drive
- Signals are simply modulated on top to increase/decrease activity with excitatory/inhibitory flow
20
Q
Why is it important there is always a tonic drive to the muscles?
A
- So small motor units can contract –> all the time
- Giving the muscle tone
21
Q
Why do big neurones not fire in the background at basal/tonic levels?
A
- Size Principal
- Bigger drive needed to stimulate them as they have low resistance
- Tonic levels only sufficient for small motor units which have high resistance
- More drive can cause the bigger ones to contract
22
Q
What are the two functionally distinct divisions in nervous system pathology?
A
- Lower Motoneurone (LMN)
- Upper Motoneurone (UMN)
They produce entirely different symptoms & consequences
23
Q
What is a lower motoneurone lesion usually caused by?
A
- Alpha Motor Neurone Damage
24
Q
What is an upper motoneurone lesion usually caused by?
A
- Motor Cortex
- Corticospinal Tract
25
What **damage** corresponds (can cause) a **Lower** **Motoneurone** **Lesion**?
* **Alpha** **motoneurones** (usually this)
* Muscle Spindle
* Primary Afferents (1a afferents)
* Type II Afferents (for sustained movement)
* Myelination of the Efferent/Afferent Signals
* Spinal Cord
* Alpha-Motoneurons
* Motoneuron axons
* Neuromuscular junction
* Muscle (itself)
(think of the whole reflex arc and anything involved in it)
26
What are the effects of a **lower motor neurone lesion** (LMN)?
* **Strength** of **Muscle** **Stretch** **Reflex** **Decrease** (or even absent)
* **Weak** **Voluntary** **Movements** (cannot move limbs)
* **_Muscle weakness_**
All the components of the reflex arc can cause LMNL thus can cause these symptoms
27
In terms of afferent signals, what are you testing with a muscle jerk reflex?
* **1a Afferents**
* **_NOT_** the **Type II Afferents** --\> as these **measure** **sustained** **movements**
* The tendon reflex is **_dynamic_** therefore it is testing the **1a afferents & _not_ Type II**
28
What happens if a muscle loses its innervation?
Muscle Atrophy
29
What needs to happen next after you have determined a LMNL?
* Further tests to assess which part of **reflex** **arc** has the problem
30
Give 5 causes of a LMN Lesion, which have been indicated with weak Muscle Stretch Reflex.
* **Peripheral Neuropathies**
* **Injury** in **Dorsal/Ventral Root** (e.g. herniated vertebral disc)
* **Poliomyelitis** (virus kills motoneurons)
* **Myasthenia** **Gravis** (decreased neuromuscular transmission)
* **Muscular** **Dystrophy** (primary muscle disease)
31
What is peripheral neuropathy?
* Damage to Nerve in the Periphery
32
What occurs in Myasthenia Gravis?
Decreased neuromuscular transmission (due to reduced post-synaptic AChRs)
33
What is a common cause of LMNL?
* **Injury to Dorsal/Ventral Root**
* This is usually caused by a **herniated vertebral disc**
34
What is a common phrase used by those with an **Upper Motoneurone Lesion (UMNL)**?
* 'I cannot move'
* 'I am too tired to move'
35
What occurs in an Upper Motoneurone Lesion?
* System that tries to **generate** **movements** **voluntarily** (primarily the corticospinal tract but maybe reticulospinal tract) --\> causes **_weak_** **movements** which are **tiring** to **produce**
36
What occurs when you perform a Knee Jerk Reflex on someone with an UMNL?
Unusually **brisk** **reflex** (rapid & strong)
37
Why does the reflex jerk on UMNL do what it does?
* **Voluntary** **Control** via **Corticospinal** **Tract** is **Lost**
* It **cannot** **generate** **voluntary** **movement**
* However **reflex** **system** works **_better_** (no descending inhibition)
38
Describe the pathway of the corticospinal tract.
* **Excitatory** **axons** from **Motor** **Cortex**
* Come down the **spinal** **cord** --\> **synapse** with **motor** **neurones** & **interneurones** which **control** **movements**
* These are **turned** **off** --\> so **_no_** **voluntary** **movements**
* Causes a **decrease** of **excitatory** **movements** --\> thus **_less_** **likely** to **depolarise**
39
Why does the reflex get **stronger** in UMNL?
* **Reflex** **circuits** have a **_lot_** of **inhibitory** **interneurones** which **synapse** onto it (renshaw cells 1a & 1b)
* There are **_more_** **inhibitory** **motoneurones** than **excitatory** **motoneurones**
* These **all get their drive** from the **motor** **cortex**
* Therefore, the **motor** **cortex** sends **tonic instructions** to **_excitatory_** & **_inhibitory_** **interneurones** --\> **excitation** of **motoneurones** based on **net sum balance**
* If **_both_** **stop** (due to more inhibitory stopping) --\> there is a **net** **gain** in **excitation** --\> thus **motoneurones** **_more_** **excitable** --\> **closer** to **threshold** --\> thus **brisk reflex**
40
Generally, why does UMNL cause a brisk reflex?
* Due to **overall** **disinhibitory** **effect** of **loss** the **descending** **command**
* Causing a **_net_** **loss** of **inhibitory** **commands** --\> thus **increased** **excitability**
* This **_raises excitability_** + **_changes property of some intrinsic spinal reflexes_**
41
Does muscle wasting take place in UMNL?
* **No**
* There is **no** **denervation** --\> thus **no** **atrophy**
42
What are the effects of an UMN lesion?
* **(Spastic) Weakness**
* **Voluntary** Movements are **weak** & **tiring** to **produce**
* Unusually **brisk (exaggerated) muscle** **stretch** **reflexes** - **spasticity**
* **No** **signs** of **muscle denervation (no wasting) - Normal Tone**
43
What does UMN lesions do in terms of FRA-driven reflexes?
Reverse some FRA-driven reflexes
44
**Where** can **damage** take place to cause an **Upper Motoneurone Lesion**?
Involves the:
* **Corticospinal Tract** (always)
* (with or without) the **rubrospinal** **tract**
* (with or without) the **reticulospinal** **tract**
Damage may be in:
* **Motor Cortex**
* **Any** **part** of the **descending** **corticospinal** **tract**
45
How does an UMNL affect muscle?
* Does **_not_** **affect** **individual** **muscles**
* Muscles **affected** **as** **groups**
This can **involve** _**whole** **limbs**_ or **_whole sides of the body_**
46
Which places do not produce the same pattern of deficits as an UMNL?
**Other** **parts** of the **motor** **system** that do **_not_** **produce** the **UMNL** **pattern** of **deficit**:
* Basal Ganglia
* Cerebellum
47
Why is an UMNL non-specific?
* Affecrs anywhere below the level of the lesion in the corticospinal tract (or even M1)
48
Clinical signs of an UMNL.
* **Spastic Weakness**
* **Normal Muscle Tone** (no/little atrophy)
* **Not entirely rigid**
* **Vigirous activation of 1a afferents** (very quick - part of dynamic system)
* **Exaggerated dynamic stretch reflex**
* **Joint is _not_ rigid** (weakness not co-contraction)
(If patient's arm is pulled back there is a jerk pull back reflex as arm is extended - this is an exaggerated dynamic stretch reflex - spastic weakness0
49
What is **spasticity** **of** **gait** formally called?
Scissor Walking
50
What does scissor walking involve (spasticity of gait)?
* **Flexed hips & knees** (patient leans forwards)
* **Plantar flexed ankles**
* Tone **increases** in **agonists** & **antagonists** leads to **limb** **stiffness**
* **Inward** **rotation** of **each** **lower** **limb**
* Walking by **circumduction** at the **hip** (giving swivelling movement)
51
What is important when making a **normal** **locomotory** **gait**?
* Hip flexion
* Ankle flexion
* Knee flexion
52
Why do they use scissor walking pattern?
* **Point on Point rotation** of the **legs**
* **Limitations** in **walking** **trajectory**
* Solution is to **swivel** with **trunk** **movements** with relatively **stiff** **legs**
53
What causes **scissor** **walking?**
* **Spastic Rigidity**
* Due to **Upper** **Motor** **Neurone** **Lesion** of the **_Lower_** **Limb**
54
What is the **babinski** **sign**?
* **Reflex** associated with **vigorous** **stimulation**/**irritation** of the **sole** of the **foot**
55
In which **cohort** of **patients** do we see a **positive** **babinski** **sign**?
* Babies before 6 months
* UMN Lesion Patients
56
What do babies or UMNL adults when you perform the babinski test do?
* Dorsiflex
57
What do healthy adults when you perform the babinski test do?
* Plantarflex
(stand up on their toes)
58
Why is there a positive babinski reflex for 6-12 months in babies?
* Due to **demyelination** of the **corticospinal** **tract**
* It takes around 6-12 months
59
How is the babinski reflex suppressed in healthy adults?
* Suppressed in **healthy** **adults** by **corticospinal** **tract**
* This **tract** **activated** by the **interneurone** **pool** where some are **inhibitory**
* These **inhibitory** **neurons** **_reverse_** **direction** of the **reflex**
* They cause **plantarflexion** (healthy adults)
60
Why do babies below 12 months not need to plantarflex?
* They are **_not_** **walking** **yet**
* Do **_not_** need to **step** **on** **toes** to **avoid** **irritatant**
* Replaced by **plantarflexion** **reflex** when they **begin** to **walk** (around 1)
61
What is the Bing Sign?
* **Reflex** which applies to **any** **_high_** **level** **stimulation** (not just nociception)
62
What is the **Bing** **Sign** used for?
* UMN Lesion
63
Describe the Bing Sign?
* **Repeated** **pin** **prick** which eventually causes **dorsiflexion**
* Unusual as the foot moves **towards** the **stimulus**
* Same **reflex** as **babinski** **reflex**
* It is not specific to a particular place on the foot --\> thus prick on dorsal side will cause dorsiflexion
64
What is the Babinski & Bing sign diagnostic for?
* **Upper** **Motor** **Neurone** **Lesions** in the Lower Limb
65
Why use these reflexes and why lower limb?
* These will **_always_** be **present** if there is an **UMNL** --\> as even if the **lesion** is **_lower_** **down** it should **stil** **be** **included**
(Foot etc. is a good place to start when looking for an UMNL as the insult is always above or the same level as the one you are testing - work your way up)
66
What are the symptoms of a **complete** **spinal** **cord** **lesion (UMN)**?
* **Loss of Voluntary Movements** (reported weakness - cannot move)
* **Total Anaesthesia**
* **_Temporary_** **Loss** of **Reflexes** (spinal shock)
* **Followed** by **Hyper-Reflexia**
67
What does a **cervical** **transection** cause?
* Quadriplegia
68
What is quadriplegia?
**Paralysis** of **all** **four** **limbs**
69
What effect does a **transection** **_below_** the **cervical** **enlargement** produce?
* Paraplegia
70
What is **paraplegia**?
Paralysis of the **_legs_** and **_lower body_**
71
Why cant you make a diagnosis shortly after an UMNL onset?
* **Spinal Shock**
* May **_not_** see **exaggerated** **reflex** (may see no reflex at all)
* Need a **period** of **hours**/**days**/**weeks** for **system** to **rebalance** itself for **excitability**
* Then **hyperreflexia** takes place (variable)
72
What does a brainstem lesion produce?
* **UMN deficits** on the **contralateral** **side** of the **body**
* Often **LMN** **deficits** for **cranial** **nerve** **nuclei**
(depends if above or below decussation of course)
73
Why does a lesion in the brainstem cause a LMN deficits for cranial nerve nuclei?
* **Corticospinal** **tract** in **_pons_** & **_midbrain_** sections
* These are **very** **close (proximal)** to **cranial** **motor** **neurones** (e.g. facial nucleus which controls facial muscles + oculomotor neurons which control eye movements)
* Therefore a **lesion** in **corticospinal** **tract** --\> will often **also** **_directly_ damage** **motor** **neurones**
(due to cut/damaged fibres which will do local damage at the levels of the motoneurones themselves of the cranial nuclei + combined effect for motoneurones down the body)
74
If there is a lesion in the brainstem, what are the general signs?
* **LMN** **Lesion** on **Ipsilateral Side** of **Face** & **Neck** (e.g. facial/trigeminal/oculomotor nuclei)
* **UMN** **Lesion** on the **Contralateral** **Side** of the **Body**
75
Damage to the internal capsule & cerebral cortex is often due to cerebrovascular disease (i.e. stroke). What are the **3 main causes**?
* **Thrombosis** (clot)
* **Embolism** (bubble)
* **Haemorrhage** (bleed)
76
What **arteries** **supply** the **internal** **capsule**?
* Lateral Striate Arteries
77
What is important to note about the Lateral Striate Arteries?
* Supply Internal Capsule
* Very fine & vulnerable
* Sensory & motor fibres are separated at internal capsule
78
How can capsular strokes be presented?
**Sensory** & **motor** **fibres** are **separated** at **internal** **capsule** (blood supply can be blocked to parts or all)
Therefore lesion can be:
* Motor
* Sensory Mixed
79
What happens if there is a full stroke of one-side of the internal capsule?
* Hemiplegia
80
What is a hemiplegia?
* **Analgesia** on **whole contralateral side** of the **body**
81
What are the possible effects of a **cerebral** **cortex** **lesion?**
* **Apraxia**
Therefore:
* **Inability** to **conceptualise**
* **Inability** to **plan** **movement**
(you cannot execute movements)
82
What is apraxia?
* Ability to make purposeful movement
83
How are diseases of the basal ganglia & cerebellum presented?
* **Unique** & **Particular** **Symptoms**
* They cannot be characterised using the LMN & UMN concepts
84
What do **basal** **ganglia** diseases cause generally?
* **Dyskinesia** (bad movement)
* **No Weakness**
* **No Apraxia** (movements can be conceptualised)
85
What are the **two sub-divisions** of **dyskinesia**?
* Hyperkinesia
* Hypokinesia
86
What is **hyperkinesia**?
* **Excess** & **involuntary** **spontaneous** movement
87
What is **hypokinesia**?
* **Lack** of **spontaneous** movement
* **Slowing** of **voluntary** movement
88
Name 3 types of basal ganglia diseases.
1. Parkinson's disease
2. Huntington's disease
3. Ballism (hemiballism)
They are characterised by dyskinesia (i.e. hyperkinesia or hypokinesia)
89
What do **basal** **ganglia** diseases **_not_** **present**?
* **Weakness** (there is no weakness)
* **Apraxia** (they show clear intent & motor plan & conceptualise movements)
(problem lies with executing the motor plan)
90
What are the different **_hyperkinetic_** **movements**?
(name 5)
1. Chorea
2. Athetosis
3. Dystonia
4. Ballismus
5. Tics
91
What is **chorea**?
* Continuing **series** of **_rapid_**, **_jerky_** **movements**
* They are **fragments** of **purposeful** **movements**
92
What is **athetosis**?
* Continual **uncontrolled** **writing**
(takes place especially after drug treatment)
93
What is **dystonia**?
* **Extreme contractions** forcing **unusual** **movements**
(extreme forceful co-contractions can cause strong postural problems)
94
What is **ballismus**?
* Jumping about
95
What are **tics**?
* **Repeats**, **stereotyped** **fragments** of **movement**
(segments of movements that have been fractionated out --\> usually stereotypical movements which are difficult to control)
96
What does **huntington's** **disease** exhibit in terms of **hyperkinetic** **movements**?
* Chorea
97
What can basal ganglia diseases affect?
**_Direct_** **Pathways** and/or **_Indirect_** **Pathway**
98
What is dopamine overall?
* **Pro-Movement**
Inhibits indirect pathway
Excites direct pathway
99
What is the striatum made up of?
* Putamen
* Caudate
100
What are the 2 receptors found on the striatum?
* D1 Receptors
* D2 Receptors
101
What do the **D1** **receptors** on the striatum do?
* When **dopamine** **binds** --\> they cause **stimulation** of **movement** --\> via the **direct** **pathway**
102
What do the **D2** **receptors** on the striatum do?
* When **dopamine** **binds** --\> they cause **stimulation** of **movement** --\> via the **inhibiting** the **indirect** **pathway**
103
Name **two** **basal** **ganglia** **diseases** with **hyperkinetic** **symptoms?**
* Ballismus
* Huntington's Disease
104
Why do these problems occur in basal ganglia diseases?
* System is **finely** **balanced** between **_excitation_** & **_inhibition_**
* **Disturbance of balance** --\> causes either **hyperkinesia** or **hypokinesia**
105
What is **ballism**?
* **Degeneration** of the **_Subthalamic Nucleus_**
* Leads to **disinhibition** of **movement** via the **indirect** **pathway**
106
What is **huntington's** **disease**?
* **Degeneration** of the **_caudate/putamen (striatum)_**
* Causes **choreiform** **movements**
* **Striatal** **spiny** **neurones** that **_inhibit_** the **indirect** **pathway** are the **most** **affected** **initially**
107
What is **hemiballism**?
* **Degeneration** of the **Subthalamic** **Nucleus** on **only (1) Side**
108
What does the **subthalamic** **nucleus** do?
* Involved in **Indirect Pathway**
* It excites the **Globus** **Pallidus** **Internal** **Segment** --\> which **increases inhibition** of the **Thalamus**
* This causes a **broken indirect pathway**
* **Disinhibition of GPi** --\> means **decreased** **inhibition** of **thalamus** --\> increasing **thalamic** **activity** --\> _**large** **amplitude** **involuntary** **limb** **movements**_
109
What are the symptoms of **ballism** & **hemiballism**?
* **Large Amplitude** & **Involuntary** limb movements
110
What is **Huntington's** **Disease**?
* **Progressive degenerative condition**
* **Initial** **Loss** --\> are the **D2 expressing neurones** in the **striatum** which go to the **GP external segment** (involved in **indirect** **pathway**)
* Therefore it is **_GPe is disinhibited_**
* Movement is **_not_** **supressed** as much
* **_Increased_** **inhibition** of the **subthalamic** **nucleus**
* Therefore **less** **excitation** of the **GPi** by the **subthalamic** **nucleus**
* **Less** **inhibition** of the **thalamus**
This causes increased movements --\> thus brief involuntary movements
111
What happens in a **lost**/**broken** **_indirect_** **pathway**?
* Too much movement
112
What are the signs of Huntington's disease?
* **Sudden** and **brief** **involuntary** **twitches**
* Occurs to **_all_** **parts** of the **body**
* **Voluntary** **movements** are **slowed**
113
Name a **basal** **ganglia** **disease** with **hypokinetic** **symptoms**?
* Parkinson's Disease
114
What is **Parkinson's** **disease**?
* **Degeneration** of **dopamine** **producing neurons** in the **_Substantia Nigra pars compacta_**
* **Low** **dopamine** **input** to the **striatum**
* Therefore **_cannot_** **energise movements** through the **_direct_** & **_indirect_** **pathways**
(not enough dopamine drive on D1 & D2 receptors thus decreased effect on direct & indirect pathways --\> thus hypokinesia)
115
What are the three symptoms of Parkinson's Disease?
1. **Bradykinesia** (slow movement)
* *Resting Tremor**
2. **Rigidity** (including cog-wheel rigidity)
3. **Postural Instability**
116
What are the **different** **drug** **therapies** available?
* Levadopa (L-DOPA)
* Dopamine Agonists
* Monoamine Oxidase-B Inhibitors
117
What surgical treatments are available for Parkinson's Disease?
* Deep Brain Stimulation (DBS)
* **Electrodes** **implanted** **close** to **basal** **ganglia** **circuitry** --\> can **restore** **thalamic** **excitability** & **restore** **movements**
Placed in the **thalamic / subthalamic nucleus area** --\> to **increase** **excitability** (or **turn down activation from GPi**) --\> thus to **boost** activity
(complex treatment & may not be available to all)
118
When can L-DOPA be administered?
* When the **substantia nigra pars compacta** is **_not_** **all** **lost**
* **L-DOPA** is fed into the **system**
* **Increases** the **amount of DOPA released** by the **existing** **substantia** **nigra** that **remains**
* **Best drive** out of **remaining** **neurones**
119
When do you stop using **L-DOPA** and start using **dopamine** **agonist**?
* Neurons in **existing SNpc** are so **low** (or gone)
* **L-DOPA** is **no longer helpful**
Need to give **Dopamine** **Agonist** + **MOB** --\> to **drive** **movement** **up**
120
What is the cerebellar control of movement like?
Where does it control?
* **Ipsilateral**
Damage to the right side impaired movements on the same side
(usually damaged by infarcts to arteries to cerebellum)
It controls the contralateral side of the cerebral cortex which controls the contralateral side of it (thus cancel out --\> ispilateral)
121
What does the **flocculo-nodular lobe** control?
* Balance
* Eye Movements
122
What does the **vermis** & **pars intermedia** adjust?
* **Ongoing** **movement** of the **whole** **body**
123
What does the **cerebellar** **hemispheres** help coordinate?
Where do they project to?
* **Planning** of **movement (especially _limbs_)**
(they project to PM cortex in particular)
124
How does the **cerebellum** **exert** its **influence**?
* **_No_ private output pathways**
Acceses the:
* **Corticospinal** Tract
* **Rubrospinal** Tract
* **Vestibulospinal** Tract
125
Where does a **major** **output** from the **lateral** **parts** of the **cerebellum** go to?
* Thalamus
* Motor Cortex
126
Where does an **important** **output** from the **medial** **parts** of the **cerebellum** go to?
* Vestibular Nuclei
127
Where does a **smaller** **output** from the **intermediate** **parts** of the **cerebellum** go to?
* Red Nucleus
128
What are the different effects of cerebellar lesion? (ranked by importance)
1. **Ataxia** (loss of co-ordination)
2. **Dysmetria** (movement distance deficiency)
3. **Asynergia** (loss of co-ordination between muscle groups)
4. **Postural Abnormalities**
5. **Gait** **Ataxia** (trunk and legs)
6. **Intention** **Tremor** (loss of smooth muscle movement)
7. **Hypotonus** (loss of muscle tone - spindles?)
8. **Dydiadochokinesia** (loss of force & rhythm)
129
What effect does a cerebellar lesion potentially have on walking?
* Ataxia of Gait
(uncoordinated walking)
(Not because of problem flexing or extending joints but due to agonist-antagonist relationship breakdown)
Movement has to be done entirely consciously (rather than automatically)
130
Why does ataxia of gait occur in cerebellum patients?
* **Propioceptive** **information** **_cannot_** be **coordinated** with **vestibular** **information**
* **Agonist-Antagonist relationship breaks down**
* **Balance** is **_impaired_**
* Patient **adopts** a **wide** **stance** --\> to i**ncrease stability**
131
Which part of the cerebellum usually leads to gait ataxia?
Anterior Lobe
132
Why is someone with **anterior** **lobe** **cerebellum** **lesion** very wobbly?
* **Vestibular Loss** + **Poor Balance Control**
* Controls **vestibular** **aspects** --\> meaning **problems** with **good** **sequence** of **flexor-extensor activation** at the **knee** & **ankle** --\> which are **key** during **walking**
Need to make movements entirely conscious as there is a breakdown of communication between agonist & antagonist pairs
