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Basal ganglia and movement disorders Flashcards

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1
Q

Main functions of basal ganglia

A

modulation of voluntary motor activity
balance of inhibitory/excitatory pathways, gives input to thalamus and from there to cortex
activity encodes for:
- decision to move
- direction/amplitude of movement
- motor expression of emotions
- making movemetns and behaviour more efficient (proceduralization)

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2
Q

circuits in basal ganglia

A

motor: controls body/eye movements
associative: higher level cognitive function
limbic: emotional/motivational processing

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3
Q

Thalamus main role

A

under chronic inhibition when we are not moving

want to move –> balance of inhibitory and excitatory circuits –> measured input to motor cortex, and measured movement

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4
Q

Release-inhibition model (Direct)

A

release tonic inhibition of thalamus –> increased excitation of motor cortex –> increased motor output

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5
Q

Release-inhibition model (Indirect)

A

inhibits output from thalamus –> decreased excitation of motor cortex –> reduced motor output

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6
Q

Function of direct/indirect pathways

A

happening simultaneously –> fine balance
Target-oriented, efficient movements are facilitated (direct)
superfluos competing movements are inhibited (indirect)
streamline movement –> target-oriented, efficient

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7
Q

Lesions to the Basal Ganglia

A

Parkinson’s: inhibition of motor output

Ballism/Huntington’s: excessive motor output

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8
Q

Ballism

A

hyperkinetic
large amplitude, non-rhythmic, sudden uncontrolled flinging movements of extremities
usually only occurs on one side (hemiballism)
underlying cause –> lesion/stroke of contralateral subthalamic nucleus
LOSS of indirect pathway –> no more suppression of superfluos movement

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9
Q

Huntington’s disease

A

hyperkinetic
deficits in cognition, behaviour and a characteristic hyperkinetic disorder
Brief, irregular unpredictable movements that move randomly from one part of body to another (Chorea)
Degeneration of striatum (caudate/putamen)
- damage to striatum: effects on both direct and indirect pathways
- direct pathway: loss of target-oriented, efficient movemetns
- indirect: subthalamus remains inhibited; no control over superfluous competing movements
CAG repeats on chromosome 4 –> abnormal amount of huntingtin

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10
Q

Parkinson’s disease

A

degeneration of dopaminergic neurons of substantia nigra
Direct: less inhibition of tonic inhibition of thalamus –> target oriented and efficient movements not facilitated
Indirect: GPe is inhibited, less inhibitory input to STN, more excitatoyr input to GPi, more inhibition of thalamus
Hypo/akinesia
Loss of facial expression - hypomimia

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11
Q

PD treatment options

A

L-Dopa
deep brain stimulation of subthalamic nucleus, restores tonic firing pattern from STN to GPi –> less inhibition of the thalamus

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12
Q

Motor circuit of basal ganglia fxn

A

motor performance and regulation of eye movemetns
both direct/indirect
measured and coordinated motor performance
regulation of gaze and orientation of eyes, amplitude of saccades

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13
Q

Associative circuit of basal ganglia fxn

A

participates in planning complex motor activity
when a novel task has been practiced/well-learned, activity in associative circuit decreases and motor circuit becomes more active

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14
Q

Limbic circuit of basal ganglia fxn

A

motor expression of emotion
postures, gestures and facial expresion related to emotion
rich in dopaminergic neurons - mask face in PD

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15
Q

Classification of movement disorders

A

Pyramidal syndromes
Basal ganglia disorders
Cerebellar disorders

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16
Q

Basal ganglia disorders

A

Parnkinsonian syndromes
Dyskinesias
Stereotyped movements

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17
Q

Cerebellar disorder characteristic

A

ataxia

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18
Q

Parkinsonian syndrome characteristics

A

akinesia

rigidity

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19
Q

Dyskinesias characteristics

A 
chorea
dystonia
myoclonus
tics
tremor
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20
Q

Pyramidal symptoms

A

spasticity - velocity/direction dependent
weakness
paralysis
UMN (CST, corticobulbar)

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21
Q

extrapyramidal symptoms

A

rigidity
no overt weakness
insufficient/excessive/abnormal movements
“basal ganglia”

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22
Q

Basal ganglia lesion symptoms

A 
no weakness
no paralysis
slowed movement/involuntary movement
rigidity, not velocity dependent
constant resistance throughout range of movement
normal muscle tone
normal reflexes
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23
Q

Basal ganglia structures

A

caudate-putamen (neostriatum)
Globus pallidus (external/internal)
substantia nigra (source of dopamine), pars reticulata, pars compacta
subthalamic nucleus

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24
Q

General approach to movement disorders

A

Identify pattern of abnormal movement
find out underlying cause, if any
treat underlying cause/give symptomatic therapy

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25
Tremor
regular repetitive sinusoidal cycles alternating contractions of antagonistic pairs of muscles
26
Clinical assessment of tremor
Topography - place Activation condition (rest, posture, non-goal/goal-directed movements) Frequency of tremor (Low 7)
27
Common causes of tremor
Enhanced physiological tremor - drugs, anxiety, hyperthyroidism Essential tremor Parkinson's disease Cerebellar disease
28
Anxiety and tremor
movement stretches agonist and causes an afferent volley eliciting reflexes in antagonistic extensors when reflex gains and conduction times are appropriate, an oscillation will result Adrenaline/thyroid hormoens sensitize muscle spindles --> stronger afferent volley, increases tremor amplitude
29
Activation condition of tremor
Intention - cerebellar Postural - essential Rest - Parkinson's disease
30
Essential tremor core criteria
Bilateral action tremor of hands and forearms (but no rest tremor) absence of other neurological signs except cogwheeling ma have isolated head tremor with no abnormal posture shouldn't have slow movements most common movement disorder
31
Essential tremor red flags
``` unilateral/focal/leg tremor gait disturbance rigidity bradykinesia rest tremor sudden/rapid onset current drug treatment that might cause/worsen tremor isolated head tremor with abnormal posture (head tilt/turning) ```
32
Essential tremor treatment first line
Propranolol CI: cardiac, pulmonary, DM Primidone: preferentially for patients >60
33
2nd line treatments for essential tremor
Gabapentin - conflicting results Clonazepam - for predominant kinetic tremor Topiramate - may work with as little as 50 mg/day
34
3rd line treatments for essential tremor
Clozapine - usually better for PD | Olanzapine - single open label trial
35
Last resort treatment for essential tremor
surgery | VIM thalamus stimulation
36
Essential tremor vs Parkinson's disease
Tremor: - Archimides' spiral poor - cogwheeling - head/voice may be affected - relatively symmetric - writing large, tremulous - typically better while walking - often improves with alcohol
37
Parkinson's disease features
``` TRAP Tremor: resting Rigidity Akinesia/bradykinesia Postural instability: relatively late presentation Masked face Micrographia ```
38
Pathology of Parkinson's disease
loss of dopaminergic cells in substantia nigra (PET scan) | causes: genetics? toxins?
39
Genetic factors of Parkinson's disease
``` increased risk in primary relatives twin studies - low concordance Recently many genes implicated in rare cases of PD that are strongly familial - alpha-synuclein - Parkin - LRRK2 ```
40
Environmental factors of Parkinson's disease
``` increased risk in people growing up in rural areas Toxins: - MPTP - Hydrocarbons - Manganese - methanol -cyanide - carbon disulfide - lacquer thinner - thiocarbamate - N-hexane - organochloride ```
41
Parkinson's disease protective agents
Coffee | smoking
42
Early signs of PD
``` Anosmia Depression, anxiety REM sleep disorder masked faces micrographia stiffness, neck pain constipation - risk increased if ```
43
Early motor symptoms of PD
symptoms most predictive of PD (rather than atypical Parkinsonism) Asymmetric onset of tremor/rigidity/bradykinesia L-dopa responsiveness note: 30% of PD patients do not have tremor
44
Parkinson's plus/Parkinsonism
``` doesn't respond significantly to medications symptomatic treatment only Multiple infarcts --> vascular Parkinsonism Progressive supranuclear palsy (PSP) Multisystem atrophy: - striatonigral degeneration - shy-Drager - Olivopontocerebellar atrophy ```
45
Impulse control disorders in Parkinson's
6-18% of PD subjects on dopamine agonists develop ICD Pathological gambling hypersexuality compulsive shopping, eating
46
Levodopa
Levodopa therapy prolongs survival BUT problems of long-term complications, e.g. dyskinesia disease progression and levodopa effectiveness - symptoms and side effects occur as levodopa therapeutic window diminishes GI problems: use carbidopa - prevents levodopa conversion to dopamine in gut to reduce GI symptoms; also doesn't cross BBB, so only acts on gut
47
Surgical treatment of PD
Stereotaxic surgery: DBS, pallidotomy | Repalcement: fetal cell transplant, genetic engineered cell lines, human retinal cells
48
Supportive treatment of PD
physio rehab occupational modification support groups
49
Chorea
``` irregular non-repetitive non-purposeful unpredictable smooth, flowing, fast/slow not suppressible ```
50
Causes of chorea
``` Huntington's disease Drugs - levodopa, neuroleptic drugs Infections Thyrotoxicosis Pregnancy ```
51
Huntington's disease treatment
Chorea: anti-dopaminergic drugs - dopamine depleting agents preferred over dopamine receptor blockers Dementia: no treatment Counselling
52
Tic
``` irregular non-purposeful predictable in pattern but not in time stereotypic suppressible ```
53
Tourette's syndrome
multiple tics childhood onset persistent for > 1 year Coprolalia (involuntary swearing)
54
Tourette's treatment
Anti-dopaminergic drugs | Dopamine depleting agents preferred > dopamine receptor blockers
55
Ballism
``` irregular non-repetitive non-purposeful unpredictable violent, proximal not suppressible Normally associated with damage to subthalamic nucleus ```
56
Causes/treatment for ballism
``` cerebrovascular (hemiballismus) infections tumors sedation develops into chorea - treatment with dopamine blocking agents ```
57
Dystonia
``` involuntary msucle contractions co-contraction of antagonists abnormal postures may be worse with specific actions disappears during sleep Classified by etiology, age of onset, anatomical ```
58
Dystonia - rule out
``` drug DOPA-responsive WIlson's Huntington's Structural lesions of the basal ganglia ```
59
Generalized dystonia
``` normal birth history, milestones autosomal dominant childhood onset starts in lower limbs, spread upwards also know as idiopathic torsion dystonia ```
60
Focal dystonia
``` eyelids face jaws neck voice upper limbs task-specific dystonia lower limb dystonia truncal dystonia ```
61
Task-specific dystonia
writer's, musician's, painter's, golfer's, dartsman's, trapshooter's cramps
62
Dystonia treatment of primary cause
treat primary cause if any discontinue drugs if possible DOPA for DOPA-responsive dystonia Reduce copper if WIlson's disease
63
Dystonia symptomatic treatment
Medications - usually don't work very well - anticholinergic, dopaminergic, anti-dopaminergic - GAGA-ergic - anticonvulsants -baclofen Botox: mainly focal - blepharospasm, oromandibular, cervical, others
64
Surgical treatment of dystonia
myectomy tenotomy thalamotomy ?? DBS
65
Myoclonus
shock-like movements caused by sudden muscle contraction (positive myoclonus) or by muscle relaxation (negative myoclonus) Asterexis is a type of negative myoclonus
66
Drug-induced movement disorders
``` Acute dystonic reactions Parkinsonism Akathisia Neuroleptic malignant syndrome Tardive dyskinesias ```
67
Acute dystonic reactions
within 96 hours of therapy oculogyric crisis seen in 2.3-21%, usually young males mechanism unknown - related to greater activation of unblocked D1 receptors?? Effectively controlled by anticholinergics
68
Drug-induced Parkinsonism
``` Dopamine receptor blocking agents neuroleptics antiemetics (metoclopramide) Ca channel blockers (flunarizine) antihypertensives ```
69
Drug-induced akathisia
inability to remain seated often seen with neuroleptic use sensation of inner restlessness, dysphoria, anxiety compulsion to move legs - walking on spot may be associated with Parkinson's disease usually 1 hour after administration, but may be several weeks later
70
Neuroleptic malignant syndrome
uncommon, but canbe fatal agitation, lethargy, confusion, delirium, stupor, coma hyperthermia, tachypnea, BP changes rigidity, akinesia, tremor, dystonia, chorea seizures elevated CK myoglobinuria may occur with first exposure to neuroleptics, or when re-instituting therapy after a long period of time acute withdrawal of dopaminergic drugs general supportive measures - management of hyperthermia, adequate hydration, dopamine agonists
71
Tardive syndrome
abnormal involuntary movement exposure to causative agent within 6 mo of onset persistence for at least 1 mo after stopping minimum 3 mo exposure Tardive dyskinesia: can get almost any movemetn disorder as a tardive phenomenom: - dyskinesia - dystonia - tic - akathisia - tremor - myoclonus
72
Treatment summary of movement disorders
tremor - PD: levodopa, dopamine agonists Essential tremor - beta blockers, anticonvulsants Chorea, tics, ballism: tetrabenazine (dopamine depleting agent) dystonia: anticholinergics, botox
73
Braak hypothesis
``` Parkinson's disease selective neuronal death in brainstem caudo-rostrally progressive pattern 1, 2) autonomic/olfactory disturbances 3,4) sleep and motor 5, 6)emotional and cognitive disturbances ```

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