Neuro 6.07 - Parkinson Disease

Front 1

What clinical issues arise from lesions to the basal ganglia?

Back 1

Abnormal voluntary movements

Front 2

What makes up the Basal Ganglia?

Back 2

6 masses of grey matter:
- caudate, putamen, globus pallidus (GP), subthalamus (Sub)
- substantia nigra (SN), pedunculopontine tegmental nucleus (PpT)

Front 3

What separates the caudate from the putamen?

Back 3

The internal capsule

Front 4

What are the afferent and efferent connections to the caudate and putamen?

Back 4

afferents: cortex, SNc
efferents: GP

Front 5

What are the afferent and efferent connections to the globus pallidus?

Back 5

afferents: CPu, Sub
efferents: thalamus, PpT, Sub

Front 6

What cell types are in the caudate and putamen?

Back 6

Spiny cels (projection cells)
- GABA-SP (substance P)
- GABA-Enk (Enkephalin)
Aspiny cells (interneurones)
- GABA
- ACh

Front 7

What cell type is in the globus pallidus?

Back 7

GABA

Front 8

What are the afferent and efferent connections to the subthalamus?

Back 8

Afferent and efferent: GP

Front 9

What cell types are in the subthalamus?

Back 9

Glutamate

Front 10

What cell types are in the substantia nigra?

Back 10

SNr (pars reticulata) - GABA
SNc (pars compacta) - Dopamine

Front 11

What are the afferent and efferent connections of the substantia nigra?

Back 11

SNr
- afferents: CPu, Sub
- efferents: thalamus, PpT, Sub
SNc:
- afferents: cortex
- efferents: CPu

Front 12

What cell types are in the pedunculopontine area?

Back 12

Ach, Glu

Front 13

What are the afferent and efferent connections of the pedunculopontine area?

Back 13

Afferents: GP
efferents: SpC

Front 14

What is the DIRECT pathway?

Back 14

Front 15

What is the INDIRECT pathway?

Back 15

Front 16

What function does the SNc (substantia nigra pars compacta) have on the direct and indirect pathways?

Back 16

Front 17

What effect does Parkinson Disease have on the SNc?

Back 17

SNc gets switched off
DIRECT pathway:
- Inhibition from CPu to GPi stopped
- Inhibition to thalamus and PpT increases
- Stimulation of cortex (skilled)/ PpT (global)/SC/motor decreased
INDIRECT pathway:
- Inhibition from CPu to GPe increased
- Inhibition from GPe to subthalamus decreased
- Subthalamus goes off tap stimulating GPi all the time
- GPi inhibits the thalamus and PpT all the time
- Skilled (cortex) and global (PpT) movements suppressed

Front 18

What are 9 key signs in Parkinson disease?

Back 18

1. lead-pipe rigidity* (hypertonia)
2. akinesia* (no spontaneous movements)
3. bradykinesia* (slow walking)
4. expressionless face
5. shuffling gait
6. cog-wheel rigidity
7. flexed posture (reflex)
8. speech
9. micrographia

Front 19

Which parts of the brain are involved in the tremor and postural/gait aspects of Parkinson Disease?

Back 19

Tremor - thalamus
Posture/gait - PpT

Front 20

What drugs are first line treatment for Parkinson Disease?

Back 20

- Levodopa (converted to dopamine)
- Da agonist (eg bromocriptine)
- MaOI (monoamine oxidase inhibitors - eg selegiline, COM-T inhibitors)

Front 21

What are the aims of surgical/deep brain stimulation treatments for Parkinson Disease?

Back 21

Disrupt the abnormal circuit
Target Subthalamus, thalamus, GP

Front 22

What is the cellular pathology associated with chorea?

Back 22

Decreased GABA-Enk cells (genetic mutation)
--> decreased CPu volume - leads to decreased Indirect pathway

Front 23

What is the blood supply of the cerebellum?

Back 23

PICA (Posterior inferior cerebellar artery)
AICA (Anterior inferior cerebellar artery)
SCA (Superior cerebellar artery)

Front 24

Back 24

1. Superior cerebellar peduncle
2. Lingula
3. Vermis
4. Emboliform nucleus
5. Dentate nucleus
6. Globose nucleus
7. Fastigial nucleus
8. Fourth ventricle
9. Decussation of the superior cerebellar peduncles

Comment: The cerebellum helps to smooth and coordinate movements as its most conspicuous function, and it also coordinates neural activities associated with nonmotor functions.

Front 25

Back 25

1. Habenular commissure
2. Cerebral aqueduct
3. Superior medullary velum
4. Inferior medullary velum
5. Choroid plexus of fourth ventricle
6. Central canal of spinal cord
7. Median aperture (foramen of Magendie)
8. Fourth ventricle
9. Posterior commissure
10. Interventricular foramen of Monro
11. Choroid plexus of third ventricle

Front 26

Back 26

Cerebellum
1. Molecular layer
2. Purkinje layer
3. Granule layer
4. White matter of folium

Front 27

Back 27

Flocculus

Front 28

Back 28

A. Anterior Lobe
B. Posterior lobe
C. Primary fissure
D. Vermis
E. Paravermis
F. Lateral hemisphere

Front 29

Back 29

1. Lateral hemisphere
2. Paravermis
3. Vermis
4. Tonsil

Front 30

What information does the spinocerebellum (vermis and paravermis) receive?

Back 30

the vermis receives information from the trunk and controls the trunk muscles whereas the paravermal region receives information from the limbs and controls limb muscles

Front 31

Locate the lesion:
Unsteadiness, swaying, falling. Tendency to fall backwards when walking. Spontaneous nystagmus. Signs are usually bilateral.

Back 31

Vestibulocerebellum (Archicerebellum)

Front 32

Locate the lesion:
loss of muscle tone and fatigue, asynergia, dysmetria (hypermetria, pastpointing), intention tremor, dysdiadochokinesia (inability to perform rapid successive movements), nystagmus, speech disturbances (slurred speech, separating of syllables).

Back 32

Cerebrocerebellum (Neocerebellum)

Front 33

Which lesions can typically produce four types of disturbances:
i) delays in initiating and terminating movement,
ii) intention tremor at the end of the movement,
iii) disorders in the temporal coordination of movements involving multiple joints, and
iv) disorders in the spatial coordination of hand and finger muscles.

Back 33

Cerebrocerebellar

Front 34

What do the putamen and GPe and GPi form?

Back 34

The lentiform nucleus

Front 35

Which part of the substantia nigra makes it appear black?

Back 35

SNc (pars compacta)

Front 36

Functionally the basal ganglia can be divided into input nuclei, output nuclei and intrinsic nuclei. Which nuclei are in each group?

Back 36

Input: Caudate and putamen (striatum)
Output: GPi and SNr
Intrinsic: GPe, subthalamic nucleus and SNc

Front 37

What is the disorder:
Rapid involuntary movements of the face, tongue and limbs. It is associated with neuronal degeneration of the striatum, especially the caudate and to a lesser extent the cerebral cortex. Dementia appears in the later stages. It is due to an autosomal dominant gene.

Back 37

Huntington't Chorea

Front 38

What is the disorder:
"Continuous, violent, coordinated involuntary activity involving the axial and proximal appendicular musculature such that the limbs are flung about". Ballistic movements are large, proximal, rotatory throwing or kicking movements. The violence of the movements may injure skin, tissues, and joints and, if severe, bones. The ceaseless vigorous activity of hemiballismus may result in malnutrition and emaciation in untreated individuals. The movements, although sometimes briefly suppressed volitionally, are usually continuous during the waking hours and are enhanced by voluntary movement of the involved limb, stress, and anxiety. The movements are reduced or absent during sleep

Back 38

Hemiballismus

Front 39

What is the disorder:
Involuntary slow writhing movements of the hands and fingers, seems to involve damage to the striatum.

Back 39

Athetosis

Front 40

What is the gold standard of pharmacological treatment for Parkinson Disease?

Back 40

Levodopa/ Carbidopa
(Levodopa converted to dopamine, Carbidopa inhibits the peripheral conversion of levodopa to dopamine and the decarboxylation of oxitriptan to serotonin by aromatic L-amino acid decarboxylase. This results in increased amount of levodopa and oxitriptan available for transport to the CNS)