Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Year 2 - Theme 2 > Parkinson's disease and drug therapy of basal ganglia disorders > Flashcards

Parkinson's disease and drug therapy of basal ganglia disorders Flashcards

(95 cards)

Start Studying
1
Q

Condition with hyperkinetic movements

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

Conditions with jerky movements

A
  • Hemiballismus
  • Tics
  • Chorea
  • Myoclonus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Conditions with non-jerky movements

A
  • Dystonia

- Tremor

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

Conditions with hypokinetic movements

A
  • Hypokinesis

- Parkinsonian conditions

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

What is ataxia

A
  • Disturbance of co-ordination
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is apraxia

A
  • Disturbance of planning
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is ballismus

A
  • A high amplitude flailing of the limbs on one side of the body
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Pathophysiology of hemiballismus

A
  • Inhibition of STN

- Therefore prevents hyperdirect and indirect pathways from functioning properly

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

Most common cause of hemiballismus

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

What are tic disorders

A
  • Brief repetitive stereotypes movements with a premonitory urge
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Types of tic disorders

A
  • Simple - like blinking, coughing
  • Complex - jumping or twirling
  • Plus - motor disorder
  • Coprolalia - Swearing - rare
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are tic disorders reduced by

A
  • Distraction and concentration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What worsens tic disorders

A
  • Anxiety

- Fatigue

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

Most severe expression of a spectrum of tic disorders

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

Causes of tic disorders

A
  • Often associated with other co-morbid conditions
  • Complex genetic inheritance
  • Post infectious immune
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What percentage of tic disorder patients have ADHD

A
  • 50%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What percentage of tic disorder patients have OCD

A
  • 33.3%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What percentage of tic disorder patients have anxiety

A
  • up to 50%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is chorea

A
  • Jerky, brief, irregular contractions that are not repetitive or rhythmic, but appear to flow from one muscle to the next
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How does a patient with chorea appear

A
  • Fidgety, restless
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Pathophysiology of chorea

A
  • STN is disturbed in hyperdirect and indirect pathway
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Causes of chorea

A

Degenerative - huntington’s disease

Drugs - neuroleptics

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

Genetic abnormality in huntington’s chorea

A
  • Trinucleotide repeat on Chr 4

- Autosomal dominant with complete penetrance

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

What does a longer trinucleotide repeat on chr 4 cause in huntington’s chorea

A
  • Causes the disease to present earlier
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Normal and abnormal numbers of repeats in huntington's chorea
- Normal - 10-28 repeats | - Disease - 36-121 repeats
26
How does huntington's present clinically (cognitive)
Cognitive - inability to make decisions, multitasking. Slowness of thought
27
What is myoclonus
- Brief movement - Rapid onset and offset - Positive(muscular contractions) or negative(muscular inhibitions)
28
Pathophysiology of myoclonus
- Unknown - Possibly an imbalance between excitatory and inhibitory neurotransmitters - Perturbations of the motor control system leading to a brief disequilibrium
29
Common causes of myoclonus
- Juvenile myoclonic epilepsy - Brain hypoxia - Prion disease
30
What is dystonia
- Abnormal twisting posture - often axial/facial/truncal, may be associated with jerky tremor
31
Pathophysiology of dystonia
- Not fully understood - Functional PET studies suggest abnormal activity in the motor cortex, supplementary motor areas, cerebellum and basal ganglia - Abnormal dopaminergic activity in basal ganglia
32
What suggests abnormal dopaminergic activity in basal ganglia in dystonia
- Dystonia being caused by blocking dopamine receptors | - Some dystonias being L-dopa responsive
33
Causes of dystonia
- Stroke - Brain injury - Encephalitis - Parkinson's disease - Huntington's disease
34
What is a tremor
- Involuntary, rhythmic, sinusoidal alternating movements of parts of the body - Affect different parts of the body such as limbs, head, chin and soft palate
35
Moment of tremor occurrence
- Rest, postural, kinetic
36
Most common type of tremor
- Essential tremor(simple kinetic tremor)
37
Pathophysiology of tremors
Postulated theory - Increased activity in the cerebellothalamocortical circuit
38
Pathophys of tremors in PD
- Dopamine dysfunction in the pallidum results in this
39
Pathophys of tremors in ET
- GABAergic dysfunction in the cerebellum causes this
40
What type of radiotherapy can be used for treatment of essential tremors
- Unilateral MRI-guided focused ultrasound thalamotomy for treatment-resistant essential tremor
41
Examples of dopamine(D2) receptor blocking agents used for treatment of hyperkinetic movement disorders
- Haloperidol - Chlorpromazine - Pimozide - Risperidone
42
Examples of dopamine depleting agents used for the treatment of hyperkinetic movement disorders
- Tetrabenazine | - Reserpine
43
Examples of atypical anti-psychotics used to treat hyperkinetic movement disorders
- Clozapine - Olanzapine - Aripiprazole
44
Acute problems(over days/weeks) caused by neuroleptics and other D2 blockers
- Oculogyric crisis | - Neuroleptic malignant syndrome
45
Subacute problems(over weeks/months) caused by neuroleptics and other D2 blockers
- Drug induced parkinsonism | - or long term(tardive) dyskinesias(over months/years)
46
What is oculogyric crisis
- Very characteristic acute response to certain drugs - Fixed stare, upward deviation of eyes - Neck extension - Trunk extension - Jaw spasms +/- tongue protrusion - ‘Acute dystonic’ reaction
47
What is neuroleptic malignant syndrome
- Acute medical emergency developing over hours/ days in response to D2 blocking drugs
48
Tetrad of features indicative of neuroleptic malignant syndrome
- Fever - Rigidity(raised CPK) - Autonomic instability(volatile BP/PR) - Confusion
49
How can serotonin syndrome be distinguished from NMS
- SS occurs within 24 hours(days to weeks) - SS: hyperreactivity - NMS: hyporeflexia, severe muscular rigidity
50
What is tardive dyskinesia
- Choreic oral-facial movements (video), dystonic trunk posturing
51
Mechanism of tardive dyskinesia
- Exact mechanism unclear – likely dopamine supersensitvity of basal ganglia –ie secondary receptor/ plastic changes
52
Treatment for tardive dyskinesia
Treatment -gradual withdrawal of offending agent, substitution with an atypical anti-psychotic ; use of a dopamine depleting agent (tetrabenazine); use of a benzodiazepine (clonazepam) if distressing
53
Switching to what drugs in hyperkinetic movement disorder management can cause tardive dyskinesia
- Atypical neuroleptics
54
What are some clinical manifestations of tardive dyskinesia
- chorea - athetosis - dystonia - akathisia - stereotyed behaviours - rarely tremor.
55
What group of patients have a greater incidence of oral, facial and lingual dyskinesia
- Older adult patients
56
Clinical manifestations of tardive dyskinesia in older adult patients
- Protruding and twisting movements of the tongue - Pouting, puckering, or smacking movements of the lips - Retraction of the corners of the mouth - Bulging of the cheeks - Chewing movements - Blepharospasm
57
Another name for parkinsonism
- Akinetic-rigid syndrome
58
Symptoms of parkinsonism
* Slowness of movement (also thought/ psychomotor retardation) * Stiffness * Shaking
59
Physical signs of parkinsonism
- Slowness and poverty of movement (bradykinesia) e.g. loss of facial expression and arm swing, difficulty with fine movements - Rigidity - Rest tremor.
60
Non-motor symptoms of parkinsonism
``` Mood: Depression, anxiety Dementia: slowed thought, mental inflexibiity, Autonomic involvement Postural hypotension, Hypersalivation Sleep disturbance Restless legs, REM parasomnia Reduced sense of smell ```
61
Pathophys of PD
- Decreased dopamine input from SN to striatum leads to reduced activation of direct pathway and reduced inhibition (higher activity) of indirect pathway - This leads to reduced movements
62
What is PD
- A neurodegenerative condition, primarily affecting dopaminergic cells of the substantia nigra
63
What is a histopathological hallmark of PD
- Lewy bodies - intraneuronal protein inclusion
64
Neurodegenerative causes of parkinsonism
- (Idiopathic) Parkinson’s disease >80% - Diffuse Lewy body disease - Atypical Parkinsonism (MSA, PSP, CBD) - Multiple system atrophy, Progressive supranuclear palsy, Corticobasal degeneration
65
Secondary causes of parkinsonism
Drugs (eg haloperidol, MPTP) Cerebrovascular disease Hydrocephalus Toxicity/ metal deposition disoders
66
Genetic causes of parkinsonism
``` Metabolic - Wilson’s disease (copper deposition) Rare familial (dominant/ recessive) causes ```
67
What is amantadine
- Initially anti-flu agent | - NMDA antagonist
68
What is amantadine used to treat
- Is an antiviral agent to treat influenza A
69
Examples of anti-cholinergics
- Procyclidine, benzhexol - May help with tremor - Limited by side effects(confusion, urinary retention, dry mouth...)
70
Why are anticholinergics effective in parkinson's patients
- Dopamine and acetylcholine are normally in a state of electrochemical balance in the basal ganglia. In PD, dopamine depletion produces a state of cholinergic sensitivity so that cholinergic drugs exacerbate and anticholinergic drugs improve parkinsonian symptoms
71
Other drugs used as treatment in parkinson's disease
Mono-amine oxidase inhibitors
72
How do monoamine oxidase inhibitors work
- Prevent breakdown of monoamine chemical neurotransmitters
73
Types of monoamine oxidase neurotransmitters
- MAO-type A | - MAO-type B
74
Examples of MAO-type A neurotransmitters
- Serotonin, adrenaline, noradrenaline, dopamine
75
Example of MAO-type B neurotransmitter
- Dopamine
76
Example of a non-selective MAO-I
- Moclobemide | - For depression
77
Why is moclobemide rarely used now
- Due to problems with metabolising dietary amines/tryptophans - risk of hypertensive crisis - cheese, red wine, marmite
78
Examples of more selective MAO-IB for PD
- Selegiline | - Rasagiline
79
In what situation can an unselective MAOI precipitate a hypertensive crisis
- MAOIs inhibit the catabolism of dietary amines. Therefore tyramine containing foods with unselective MAOI can precipitate a hypertensive crisis
80
What is L-dopa always combined with
- Dopa decarboxylase inhibitor(to prevent peripheral conversion to dopamine
81
Commercial preparations of L-dopa
- Madopar, sinemet | - Immediate and controlled release
82
Side effect of l-dopa
- Dyskinesias
83
Benefit of L-dopa over disease progression
Early disease - long duration of clinical benefit. Low incidence of dyskinesias Mid-stage disease - diminshed duration of clinical benefit. Increased incidence of dyskinesias Advanced disease - Clinical response mirrors levodopa plasma pharmacokinetic profile. On time is associated with dyskinesias
84
What is entacapone/tolcapone
- Reduces peripheral(to a lesser extent central) metabolism of L-dopa
85
Pros and cons of entacapone/tolcapone
Pros - increases duration of action of L-dopa, increases efficacy of L-dopa, good for 'wearing off' with L-dopa between doses Cons - Makes dyskinesia worse, diarrohea(both) liver disease(tolcapone)
86
What is duodopa for advanced PD
L-dopa is absorbed in duodenum Absorption affected by poor gastric motility/ constipation and diet / protein load Unpredictable bioavailability makes it very difficult to hit narrow therapeutic window in advanced PD (for ON without dyskinesia) Direct delivery of L-dopa to duodenum via infusion pump potentially very useful strategy to manage motor fluctuations. But very expensive Does not affect disease progression
87
Advantages of dopamine agonists
- Bypass degenerating nigrostriatal neurons - Directly activate dopamine receptors. - No need for enzymatic conversion. - More stable and longer-acting.
88
Action of all dopamine agonists in PD patients and also cons
- All reduce frequency of motor complications cons - dopamine dysregulation syndrome
89
What is apomorphine s/c infusion
- Dopamine agonist | - Given by subcutaneous(s/c) infusion
90
Pros of apomorphine s/c infusion
Very effective Instant effect. Reduces dyskinesia by allowing continuous dopaminergic stimulation (pulsatile dopaminergic stimulation thought to prime basal ganglia for motor complications)
91
Cons of apomorphine s/c infusion
- Only for the right patients | - Skin nodules
92
Example of non-drug therapy for PD
- Deep brain stimulation
93
Features of DBS
Probably high freq stimulation causing ‘jamming’(inhibition of neurons by depolarising block) Also disrupts abnormally synchronous basal ganglia rhythms ``` Favoured target subthalamic nucleus (STN) for PD Also pallidum (for dystonia) and thalamus (for tremor) ``` ``` Disease will still progress and no effect on non-motor dementia, dysautonomia, postural instability….. ```
94
How does huntington's present clinically? (behavioural)
Behavioural - irritability, depression, apathy, anxiety, delusions
95
how does huntington's present clinically? (Physical)
Physical - chorea, motor persistence, dystonia, eye movements

Year 2 - Theme 2 (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions