Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 2 semester 2 > Parkinsons > Flashcards

Parkinsons Flashcards

1
Q

What is a gamma motor neuron?

A

They innervate intrafusal muscles fibres which together with sensory afferents compose muscle spindles. These are part of the system for proprioception

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

What is a alpha motor neuron?

A

They innervate the extrafusal muscle fibres (the ones involved in muscle contraction)

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

What is the physiology of a muscle contraction?

A

Glutamate released from upper motor neurons triggers depolarization in the lower motor neurons in the ventral horn which in turn causes an action potential to propagate the length of the axon to the neuromuscular junction where ACh is released to carry the signal across the synaptic cleft to the postsynaptic receptors of the muscle cell membrane, signaling the muscle to contract.
Nicotinic Ach receptor on muscle -> muscle contraction

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

What is the characteristic of damage to a LMN?

A

Causes decreased tone (flaccid), decreased strength and decreased reflexes in affected areas (areflexia, hyporeflexia).
Abnormal EMG potentials, fasciculations, paralysis, weakening of muscles and
neurogenic atrophy of skeletal muscle.

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

What is the pathway of the corticospinal tract?

A

From motor cortex to LMN in ventral horn of the spinal cord (anterior doesn’t decussate until end but lateral decussates in the medulla)
- Fine voluntary motor control of limbs and posture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the corticobulbar tract?

A

Motor cortex to several nuclei in the pons and medulla

- Control of facial and jaw musculature, swallowing and tongue movements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the tectospinal tract?

A

From Superior Colliculus decussates ventrally to contralateral (also have local interneurons to ipsilateral) LMN in midbrain (3,4,6)
- Voluntary adjustment of head position in response to visual information

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the rubrospinal tract

A

From (dentate nucleus of cerebellum) Red nucleus decussates to other side of midbrain and desends to LMN
- Voluntary adjustment of arm position in response to balance info (support of the body)
Fine movements

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

What is the vestibulospinal tract?

A

From vestibular nuclei which processes stimuli from semicircular canals
Adjusting posture to maintain balance

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

What is the reticulospinal tract?

A

From reticular formation.

Regulates various involuntary motor activities and assists in balance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does damage to the globus pallidus do?

A

Athetosis (continuous writhing movements of hand, arms, neck or face)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What does damage to the subthalamus do?

A

Hemiballismus (flailing movements of entire limb)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does damage to the putamen do?

A

Multiple small lesions causes chorea (flicking movements in hands, face other parts of body

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

What does damage to substantia nigra do?

A

Parkinson’s disease (rigidity, akinesia, tremors)

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

What are the deep cerebellar nuclei?

A

Dentate, Emboliform, Globose, Fastigii (don’t eat greasy food)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the functional organization of the cerebellum based on input source?

A

Cerebrocerebellum: from cortex to UMN in cortices and red nucleus controlling skilled movements (planning and execution of spatial ad temporal sequences)
Spinocerebellum: From spinal cord and projects to medial and lateral organizationlateral part controls gross movements of distal limbs and vermis/median controls proximal muscles and eye muscles
Vestibulocerebellum (flocculonodular lobe): to vestibular nucleus posture and balance

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

What is a resting/static tremor?

A

Position: At rest (supported against gravity with inactive muscles
Freqency: 3-6Hz
Amplitude: high, reducing/suppressed on voluntary movements and is enhanced by performing cognitive or motor tasks with other parts
Examples: Parkinsonian syndrome, essential tremor, atypical antipsychotic (dopamine antagonist)

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

What is a postural tremor?

A

Position: During sustained/motionless posture (maintaining position against gravity)
Frequency: 4-12 Hz
Amp: Low, may continue during movement
Examples: Essentail remor enhanced physiological tremor, familial autosomal dominant , cerebellar disorder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is an intention tremor?

A

Position: during intention or voluntary movement (eg finger to nose test)
Frequency: <5Hz
Amp: increases on voluntary movement
Examples: Cerebellar lesions, brainstem issues, drugs, alcohol

20
Q

What is an action-contraction tremor?

A

Postion: Happens during contraction (eg tight fist while arm is resting and supported)
Examples: essential tremor

21
Q

What are the main types of tremor?

A

Physiological (8-12Hz, normal)
Essential/familial (4-6hz, gradually progressive)
Dystonic (jerky, irregular)
Orthostatic (unstreadiness during standing)
Parkinsonian tremor (4-6hz, pill rolling)
Cerebellar tremor (intention, postural or action, s disease remor: age 4-25, intention tremor with flapping

22
Q

What are some mechanisms of tremors?

A

Mechanical oscillations of the limb
Reflex oscillations is elicited by afferent muscle spindle pathways and is responsible for stronger tremors by synchronisation
Central oscillators are groups of cells in CNS (thalamus, BG, inf olive) and have capacity to fire repetively and produce tremor (parkinsonian- in BG, essential tremor in olive and thalamus)
Abnormal functioning of the cerebellum
Ataxic: complex influence of the deep cerebellar nuclei by sectioning the sup peduncle below decussation

23
Q

How will a midline cerebellar lesion present?

A

Assumes a broad/wide based stance when walking (same whether eyes opened or closed)

24
Q

How will a cerebellar hemisphere lesion present?

A

Tendency to veer to affected side (esp when eyes closed)

25
Q

How will damage to vestibulocerebellum present?

A

ataxia, dysequilibrium, nystagmus

26
Q

How will damage to vermis and fastigial nuclues (spinocerebellum) present?

A

distrubances in control of axial and trunk muscles during attempted antigravity postures and scanning speech

27
Q

How will damage to cerebrocerebellum present?

A

delay in inititating movements and decomposition of movements

28
Q

What are the signs and sx of a cerebellum lesion?

A

DR PANISH D
D- dysdiadachokinesia (rapidly alternating)
R- Romberg’s sign (need 2/3 of proprioception, vestibular function and vision)- ataxia and -ve
P- past pointing
A-Ataxia (lack of volunatry coordination)
N- Cerebellar nystagmus
I- Intention/action tremor
S-Slurred/scanning speech (dysarthria)
H-Hypotonia- knee jerk keeps swinging
D- Decomposition of movement (difficultly performing actions that involve simultaneous motion at >1 joint)

29
Q

What is one supposed mechanism for death of substantia nigra par compacta dopaminergic cells?

A

Abnormal accumulation of presynaptic protein alpha synuclein bound to ubiquitin in the damaged cells- Lewy bodies which displace other cell components

30
Q

What are the stages of parkinsons?

A

1) Predisposed inductions sites
2) Inclusion bodies begin to appear in portions of the medulla and the pontine tegmentum (raphe nuclei, reticular nucleus and coeruleus complex)
3) midbrain (SNc, amygdala, subnuclei)
4) Cerebral cortex (deficits in responses to emotional stimuli)
5 and 6) extensive stretches of the neocortex

31
Q

What are the genes involved in parkinsons?

A

Parkin (ch6, PARK2)
alpha synuclein (4, PARK1/4)
NURR1 (nuclear receptor related protein (chromosome 2)
Leucine-rich repeat kinase 2 (Lrrk2) (12, PARK 8)
PINK1

32
Q

What are the cardinal features of Parkinsonism?

A 
Resting tremor
Bradykinesia
Rigidity
Gait disturbance
Postural instability
Abnormal fixation fo posture (stooping)
33
Q

What are some other features of Parkinsons

A 
Micrographia
Masked facies
Reduced eye blink
soft voice
dyphagia
freezing
34
Q

What are the diagnostic tests for Parkinson’s

A

1) Dopaminergic agent trial

2) MRI, functional neuroimagin, genetic testing,

35
Q

What is the aims of tx in the various stages of Parkinsons?

A

Goals of treating the mildly symptomatic patient:
o Delay disease progression. No medication has been shown to alter disease course.
o Refrain from impairing benefit of future therapies.
Nonpharmacologic therapy can be the most beneficial measures at the early stage:
o Exercise – emphasizing flexibility, balance and mobility.
o Cognitive stimulation.
o No proven dietary modulators.

Intermediate PD – early treatment when QoL begins to be impaired:
o Treat symptoms.
o Delay disease progression, and refrain from impairing benefit of future therapies.

Advanced disease:
o Treat symptoms.
o Minimize/treat medication side effects.
o Delay disease progression.

36
Q

What is the pharmacological tx of Parkinsons?

A

Levodopa and carbidopa first line, then combine with dopamine agonists, MAO-B
inhibitors, COMT inhibitors etc..
o Amantadine = antiviral (interfere with M2 ion channel required for viral particle to
become “uncoated” after endocytosis), antiparkinsonian (induce release of DA, NE,
weak NMDA receptor antagonist, anticholinergic on nACh R)
o Apomorphine = non-selective dopamine agonist (D1-like & D2-like receptors)

If that fails then consider surgery and deep brain stimulation

37
Q

What is the pathophysiology of Huntingtons?

A

Increase in the number of polyglutamine (CAG) repeats (over 40) in the coding sequence of the huntingtin gene located on the short arm of chromosome 4.
Unsure what protein does but fragments of the mutant protein can be toxic (possibly translocating into the nucleus and interfering with transcriptional upregulation of regulatory proteins). Neuronal inclusions may be a protective mechanism

38
Q

What are some symptoms of Huntington’s Disease?

A

Motor sx: Chorea (brief, semi-directed, irregular movements that are not repetitive or rhythmic) with Parkinsonism and dystonia developing later
Psychiatric symptoms: change in behaviour and personality, impulsiveness, aggressive behaviour, depression and paranoid psychosis
Cognitive sympotms: Progressive subcortical demential, with disturbed attention, concentration, depression and irrtability

39
Q

How do you diagnose Huntington’s?

A

Family history and genetic testing (positive is >40 CAG repeats)
MRI and CT only shows visible cerebral atrophy in the advanced stages of the disease- fMRI and PET can show changes in brain activity before onset of physical sx

40
Q

What is the treatment of Huntingtons?

A

1) Patient education
2) Symptom management
Treatment for chorea: tetrabenazine
clonazepam (benzo site on GABA- anticonvulsant and muscle relaxant), Haloperidol (Dopamine D2 receptor antagonist, strong alpha adrenergic blocking effects), reserpine (atypical, highly potent serotonin and dopamine receptor)
Rehabilitation therapy

41
Q

What is the prognosis of Huntington’s disease?

A

average duration of illness is approx 19 years (mean death ranging from 51-57 years) with most becoming bedridden- death caused by concurrent infection and high suicide rates

42
Q

What is the mechanism of action of Levodopa?

A

Increased release of dopamine from the few surviving dopaminergic neurons or a floddin gof the synapse with dopamine formed elsewhere
SE: dyskinesia, On/off effect as well as nausea, anorexia, postural hypotension, psychological effcts

43
Q

What are the dopamine agonists in Parkinsons?

A

Act directly on dopamine receptors and their use is associated with a lower incidence of the response fluctuation and dyskinesias that occur with LT levodopa therapy.
Ergot or non ergot
SE: fatigue, somnolence, peripheral oedma, dyskinesias, confusion, impulse control disorders

44
Q

What are monoamine oxidase inhibitors?

A

Inhibition of MAO-B protects dopamine from extraneural degradation, used with levodopa.
• Two different MAO-B inhibitors – Selegiline (which is metabolized to amphetamine, causing
excitement, anxiety and insomnia) and Rasagiline, which lacks the unwanted effects of
Selegiline.

45
Q

What are COMT inhibitors?

A

Catecholamine-O-methyltransferase (COMT) inhibitors:
Reduce the metabolism of levodopa to 3-O-methyldopa, thereby altering plasma
pharmacokinetics of levodopa, leading to more sustained plasma levels and more constant
dopaminergic stimulation of the brain.
Given in conjunction with levodopa and a decarboxylase inhibitor. Stalevo is the
commercial preparation available that combines levodopa, carbidopa and entacapone.
Unwanted effects:
Dyskinesias, confusion, hypotension, syncope, diarrhoea, hepatotoxicity (with
entacapone).

Year 2 semester 2 (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions