Cole 14

Front 1

basal ganglia

Back 1

-caudate, putamen, globus pallidus

-subthalamic nucleus

-substania nigra

Front 2

movement disorders: basal ganglia

Back 2

not weak, just hard to control

Front 3

how does the cortex communicate with the basal gang?

Back 3

via the striatum (caudate putamen), then this info is processed and output goes back to MOTOR CORTEX via thalamus

Front 4

interneurons WITHIN the striatum use what as their neurotransmitter?

Back 4

Ach

Front 5

inputs to the striatum form the globus pallidus use what as the NTS?

Back 5

Dopamine

Front 6

D1 receptor: stimulated by dopamine (increasing cAMP)

Back 6

D2 receptor: inhibited by dopamine

Front 7

subthalamic nucleus

Back 7

relay between the external segment of the globus pallidus (GABA) and the internal segment of the globus pallidus (glutamate).

Front 8

less DOPA by substantia nigra leads to less GLUTAMATE stimulation of cerebral cortex

Back 8

leads to poverty of movement (bradykinesia)

Front 9

PK

Back 9

-Tremor

-Rigidity

-Akinesia

-Postural Instability

Front 10

asymmetrical tremor, worse during stress and walking

Back 10

PK

Front 11

cogwheel rigidity

Back 11

rigidity in PK is the same, no matter the velocity (how fast you move muscle)

Front 12

softern voice, drooling, smaller handwriting

Back 12

akinesia in PK

Front 13

REM sleep behavior disorder: acting out dreams

Back 13

PK

Front 14

alpha synuclein makes up Lewy Bodies

Back 14

replace dopa in S.N.

Front 15

3 drugs for EARLY Parkinsons

Back 15

1. Rasagilin: MAO-B inhibitor (slows down DOPA breakdwon in striatum)

2. Amantadine:

3. Anticholinergics (trihex/benztropine): best for tremor

Front 16

SE of anticholinergics

Back 16

constipation, dry mouth, blurry vision, retention (muscarinic)

Front 17

Tx for MILD PK when symptoms start interfering with life

Back 17

DOPA receptor agonists: Bromocriptine, Pramipexolem, Ropinirole

Front 18

if patient is less than 60: use dopa agonists

Back 18

if patient is over 70 or has severe dz, go straight to Levodopa

Front 19

Why is Bromocriptine used less frequently?

Back 19

MORE SE!!! (also used to treat prolactinomas)

Front 20

Common SE of pramipexole & ropinorole

Back 20

- Nausea

- Hallucinations

- Sudden attacks of sleep – this requires discontinuation of the medications

- Gambling and other obsessive behaviors

- Confusion

Front 21

Tx for moderate to severe PK

Back 21

1. Levodopa

2. COMT inhibitors

3. DOPA agonists

4. low protein diet

5. surgery

Front 22

how is levodopa different from dopamine?

Back 22

precursor of dopamine and actually crosses the BBB (converted in the striatum)

Front 23

how does carbidopa help?

Back 23

inhibits peripheral conversion of Levodopa, leading to less SE like naseau/hypotension

Front 24

SE of levodopa

Back 24

- Nausea

- Hallucinations

- DYSKINESIAS*** (more common than with dopamine agonists)

- Vivid dreams

- Hypotension

- Confusion (less common than dopamine agonists)

Front 25

how do COMT inhibitors work (Tolcapone & Entacapone)?

Back 25

inhibit destruction of dopa in the periphery, prolonging effect of levodopa

Front 26

SE of Tolcapone

Back 26

liver failure: check liver enzymes every 2 weeks

Front 27

Entacapone is short!

Back 27

Entacapone is usually given with levodopa since its duration of action is only 2 hours. It is used primarily in patients that have the wearing off phenomenon.

Front 28

Surgical options for PK

Back 28

-pallitodomy

-thalotomy

-deep brain stimulation of globus pallidus

Front 29

3 types of Multisystem Degeneration

Back 29

1. progressive supranuclear palsy

2. multisystem atrophy

3. corticobasal degeneration

Front 30

looks like PK but EARLY FALLING*****

Back 30

PSP

Front 31

special parts of PSP

Back 31

-bulbar (dysarhria/dysphagia/EMO****)

-vertical gaze palsy

-FRONTAL SUBCORTICAL DEMENTIA (withdrawn apathy**)

-poor response to medication

Front 32

MRI for PSP

Back 32

-midbrain atrophy**** (hummingbird) without pontine atrophy

-Tau proteins on pathology

Front 33

looks like PK, but RAPID PROGRESSION

Back 33

· Early falling

· Craniocervical dystonia (especially anterocollis where the head is pulled forward)

· Poor response to therapy

· Minipolymyoclonus tremor (more prominent with hands outstretched and during action****)

· Autonomic instability (orthostatic hypotension, erectile dysfunction)

· Pseudobulbar palsy (dysarthria, dysphagia, emotional incontinence)

· Sometimes a high-pitched dysarthria

· REM sleep disorder

-> 50% also have an obstructive sleep apnea

Front 34

MRI of MSA

Back 34

putaminal atrophy and with a hyperintense rim around the putamen on T2 weighted images.

-signal changes in the pons and middle cerebellar peduncle: “hot cross bun” sign.

Front 35

Antipsychotics & Dopamine blockers can cause PK!!!!!

Back 35

-Metoclopromide & prochlorperazine

-first generation antipsychotics (neuroleptics): Haldol (blocks dopa)

- Quietapine & Clozapine DO NOT CAUSE PK!!!

Front 36

sustained muscle contractions that are twisting in nature

Back 36

DYSTONIA (Tx: botox)

Front 37

too much copper in liver and BASAL GANGLIA

Back 37

Wilsons

Front 38

low ceruloplasmin, high urine copper

Back 38

wilsons

Front 39

GABA deficit (atrophy in caudate)

Back 39

huntingtons

Front 40

3 main features of Huntingtons

Back 40

1. dementia/irritability

2. chorea

3. FHx

Front 41

CAG

Back 41

huntingtons

Front 42

stroke in CONTRA subthalamic*** nucleus

Back 42

hemiballismus

Front 43

multiple*** motor tics, one or more vocal tics, onset before age 21

Back 43

touretes

Front 44

neuroleptics (antipsychotics) and anti-emtics block dopamine and lead to PK, what else can they do

Back 44

TARDIVE DYSKINESIA!!! permanent!