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Parkinson Epilepsy > Parkinson Epilepsy > Flashcards

Parkinson Epilepsy Flashcards

1
Q

characterized by
progressive and irreversible loss of neurons from
specific regions of the brain

A

Neurodegenerative disorders

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2
Q

Examples of prototypical neurodegenerative

disorders: (4)

A

Parkinson disease
Huntington’s disease
Alzheimer’s disease (AD)
Amyotrophic lateral sclerosis (ALS)

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3
Q

loss of neurons from structures of the basal ganglia

results in abnormalities in the control of movement

A

Parkinson disease and Huntington’s disease

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4
Q

where the loss of
hippocampal and cortical neurons leads to
impairment of memory and cognitive ability

A

-Alzheimer’s disease (AD)

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5
Q

where muscular weakness results from the degeneration of spinal, bulbar, and cortical motor neurons

A

Amyotrophic lateral sclerosis (ALS)

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6
Q 
2nd most common neurodegenerative
disease (after Alzheimer’s disease)
– Mean onset = 57 years of age
– Affects 1-2% of population over 60
years of age 
• Disease progression is highly variable
• Can be early onset in some cases
A

Parkinson Disease

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7
Q

Epidemiologic studies suggest increased risk of Parkinsons with
exposure to

A

pesticides, rural living, and drinking

well water

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8
Q

what can reduce risk of PD

A

reduced risk with cigarette smoking

and caffeine.

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9
Q

Four cardinal features of PD (4)

A

bradykinesia
muscular rigidity
resting tremor
impairment of postural balance

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10
Q

slowness and

poverty of movement

A

bradykinesia

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11
Q

stiffness and
resistance to limb movement
caused by increased muscle
tone

A

muscular rigidity

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12
Q

usually abates during voluntary movement

A

resting tremor

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13
Q

leads to disturbances of gait

and falling

A

impairment of postural balance

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14
Q 
-characterized by severe loss of
substantia nigra (SN)
dopaminergic neurons
-visible in
brain sections as depigmentation
of the SN in the midbrain.
A

Parkinson

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15
Q 
It is estimated that approximately
\_\_\_% to \_\_\_% of the SN dopamine
cells are lost by the time a patient
first presents for clinical
evaluation, diagnosis, and
treatment.
A

60

70

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16
Q

substantia nigra projects to two pathways

A

direct and indirect

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17
Q

the net effect of the ______ pathway is to excite motor cortex, and the net
effect of the _______ pathway is to
inhibit motor cortex.

A

direct

indirect

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18
Q

SN activity excites the direct pathway
(____ receptors) and inhibits the indirect
pathway (___ receptors)

A

D1

D2

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19
Q 
reduces the excitation of
motor cortex and its ability to generate
commands for voluntary movement,
resulting in the poverty of movement
of Parkinsonian patients.
A

Loss of the nigrostriatal dopaminergic pathway

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20
Q

The loss of SN neurons puts a brake on the output of motor cortex, inhibiting
_______ motor commands from descending to the brain stem and spinal cord
As a result patients have difficulty initiating voluntary movements although involuntary, reflexive movements can be normal

A

voluntary

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21
Q

Neurons in CNS of PD patients have

abnormal accumulation of the protein called

A

α-synuclein

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22
Q

_______ protein accumulates inside

neurones forming inclusions called _________

A

α-synuclein

Lewy bodies

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23
Q

the unwanted product resulting from the planned synthesis of synthetic heroin.

A

MPTP (1-methyl-4-phenyl-1,2,3,6-

tetrahydropyridine)

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24
Q

Victims became almost completely immobile
(“frozen”), unable to blink and mute only
hours after injecting this drug.

A

MPTP (1-methyl-4-phenyl-1,2,3,6-

tetrahydropyridine)

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25
Q

produce Parkinson-like
symptoms in monkeys and has been used to
develop animal models for testing new
therapies for PD

A

MPTP

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26
Q

Dopamine receptors

A

G proteincoupled receptors (GPCRs)

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27
Q

The D1 and D5 receptors are members of the

A

D2-like family

28
Q

activates adenylyl cyclase, increasing the intracellular concentration of the second
messenger cyclic adenosine monophosphate (cAMP)

A

Activation of D1-like family receptors coupled to the G protein Gαs

29
Q

directly inhibits

the formation of cAMP by inhibiting the enzyme adenylate cyclase

A

D2-like family receptors coupled to the Gαi

30
Q

Pharmacological Treatment of PD

• Goal =

A

Restore dopamine receptor function

31
Q 
Prodrug – immediate metabolic
precursor of dopamine (DA)
can cross the BBB while DA can
not; 1-3% enters the
brain
A

Levodopa

32
Q

increase amount of

L-DOPA that reaches CNS

A

COMT inhibitors

33
Q

may be given to patients who are taking levodopa
and are becoming resistant or having
fluctuations in levodopa effect

A

Dopamine receptor agonists

34
Q

each dose of ________
effectively improves mobility for a period of time, but rigidity and akinesia
return rapidly at the end of the dosing interval.

A

levodopa

35
Q

Increasing the dose of levodopa and frequency of administration can improve adverse effects, but this often is limited by the development of

A

dyskinesias, excessive

and abnormal involuntary movements.

36
Q

•“On-off” Effect – fluctuations in clinical response to levodopa:

A
  • “Off” = marked akinesia

- “On” = improved mobility but marked dyskinesia.

37
Q

Conditions with PD-like symptoms
that result from other causes are
referred to as

A

parkinsonism

38
Q

a natural alkaloid that
blocks vesicular transport of
monoamines, depletes stored
monoamines, including DA

A

Reserpine

39
Q

drugs used in the treatment of schizophrenia

block the action of DA on its receptors

A

Antipsychotic drugs (neuroleptics)

40
Q

•Patients who have received
neuroleptics for long periods of time
may develop

A

hyperkinetic disorder,

known as tardive dyskinesia

41
Q 
characterized by involuntary, purposeless
movements affecting many parts of the
body (abnormal movements of the
tongue, mouth and masticatory
muscles, choreoathetoid movements of
the extremities)
A

Tardive dyskinesia

42
Q 
Drugs used in the treatment of nausea or vomiting (e.g., Compazine) or
gastroesophageal disorders (e.g., metoclopramide) are also \_\_\_\_\_\_\_\_\_ agents
A

neuroleptic

43
Q

the clinical manifestation of an abnormal and

excessive synchronization of a population of cortical neurons

A

Seizure

44
Q

a tendency toward recurrent seizures unprovoked by any systemic or acute neurologic insult

A

Epilepsy

45
Q

two or more unprovoked

seizures

A

Epilepsy

46
Q

Epilepsy etiologies of seizures can be grouped into three categories

A

genetics
structural/metabolic
unknown course

47
Q

Genetic etiology of epilepsy

A

Mutations in gene encoding a neuronal ion channel

48
Q

Structural/Metabolic effects that may cause epilepsy

A
  • trauma, tumors and other
  • space-occupying lesions
  • Certain drugs, withdrawal from alcohol or drugs, —metabolic disorders
  • Vascular diseases
49
Q

originate within networks limited to one cerebral hemisphere

and are usually associated with structural abnormalities of the brain.

A

•Focal seizures

50
Q

arise within and rapidly engage networks distributed across both cerebral hemispheres and may result from cellular, biochemical, or
structural abnormalities that have a more widespread distribution

A

•Generalized seizures

51
Q

disorders of neuronal excitability

A

epilepsies

52
Q

occur when a large collection of neurons abnormally undergo
synchronous APs that produce stereotypical, involuntary spasms and alterations
in behavior

A

Seizures

53
Q

Which factors can contribute to hyperexcitability of neurons?

A
  • Increase excitatory post synaptic potentials (EPSPs)
  • Decrease Inhibitory post synaptic potentials (IPSPs)
  • Changes in voltage gated ion channels
  • Alteration of local ion concentrations that favor depolarization
54
Q

the principal fast (“classical”)
excitatory transmitters throughout
the CNS

A

Glutamate and possibly aspartate

55
Q

the major inhibitory mediator in the brain, including being responsible
for presynaptic inhibition.

A

GABA

56
Q

The mechanisms of action of anti-seizure drugs fall into three major categories:

A
  1. promoting the inactivated state of voltage-gated Na+ channels
  2. enhanced GABA–
    mediated synaptic inhibition
    3.inhibition of voltage-activated Ca2+ channels
57
Q

Anti-seizure drugs

A

enhance Na+ channel inactivation thereby reducing the ability of neurons to fire AP at high frequencies

58
Q

Several drugs inhibit seizures by enchansing
____-mediated synaptic inhibition through
an action at distinct sites of the synapse

A

GABA

59
Q

Some _________ drugs act by reducing the
metabolism of GABA, resulting in increased
GABA concentration available for release

A

anti-seizure

60
Q

inhibits the GABA reuptake
transporter, GAT-1, and reduces neuronal
and glial uptake of GABA

A

Tiagabine

61
Q

activated at a much
more negative membrane potential (hence “low
threshold”) than most other voltage-gated Ca2+
channels expressed in the brain

A

T-type Ca2+ channels

62
Q

The principal mechanism by which anti–

absence-seizure drugs act is by

A

inhibition of the

T-type Ca2+ channels

63
Q

a common mechanism of action
among anti-seizure drugs, with anti-partial-seizure drugs inhibiting voltage-gated
Na+ channels and anti-absence-seizure drugs inhibiting voltage-gated Ca2+ channels

A

Inhibiting voltage-gated ion channels

64
Q

Seizures can occur as an adverse effect of a large
number of drugs from different pharmacological
categories: (6)

A 
antibiotics e.g. penicillins
Immunosuppressant cyclosporine
Overdose with tricyclic antidepressants
Anesthetics e.g.  propofol
antineoplastic agents
Abrupt withdrawal of therapy
65
Q

recommended in protocols for bone

marrow transplantation

A

antineoplastic agents

Parkinson Epilepsy (1 decks)

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