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M2 Neuron Brain Behavior > 9/20 Basal Ganglia - Glendinning > Flashcards

9/20 Basal Ganglia - Glendinning Flashcards

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1
Q

what are the basal ganglia?

A

tightly woven group of nuclei in cerebrum, diencephalon, midbrain

  1. caudate nucleus
  2. putamen
  3. globus pallidus
    • external segment
    • internal segment
  4. subthalamic nucleus
  5. substantia nigra
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2
Q

functions of basal ganglia

A

regulate frontal lobe, motor, limbic fx

*involved in several neurodegen, neuropsych disorders

  • motor disorders: movement disorders or extrapyramidal disorders
  • disorders of “habit”/neuropsych disorders: addiction, OCD, tics
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3
Q

basal ganglia loop fx

A

help facilitate motor cortical areas

  1. initiating movement
  2. sequencing movement
  3. automaticity

bc they play a role in gating proper initiation of movement, lesions to this area lead to incr/decr movement

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4
Q

overview: basal ganglia regulation of motor areas

A

basal ganglia…

  • inputs: premotor cortex, primary motor cortex
  • output: VA (ventral ant) and VL (ventral lat) thalamus → projects back up to cortical areas

DO NOT get sensory feedback

  • BG are not sensory structures (as opposed to cerebellum, which gets a lot of sensory input)
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5
Q

basal ganglia anatomy

A

striatum

  • caudate: head/body/tail, wraps around lateral wall of lateral ventricle
  • putamen: lateral to caudate nucleus
  • C/P are referred to as a unit bc they come from same embryological tissue, perform the same fx. would be same structure except that they are bisected by internal capsule

globus pallidus: medial to putamen

  • comprised of internal and external segments

*together, putamen + globus pallidus = lentiform nucleus

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6
Q

basal ganglia structures outside cerebrum

A
  1. subthalamic nucleus (diencephalon)
  2. substantia nigra (mesencephalong)
  • pars compacta neurons: deep, contain dopamine, which modulates BG fx
  • pars reticulata neurons: more superficial
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7
Q

dopamine modulates basal ganglia

3 pathways

  • associated fx
  • associated diseases
A

1. mesostriatal (nigrostriatal) pathway

  • fx: movement control
  • Parkinson’s Disease

2. mesolimbic pathway

  • fx: reward pathway
  • schizophrenia
  • depression

3. mesocortical pathway

  • fx: working memory
  • schizophrenia (negative signs)
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8
Q

2 “connected” units within basal ganglia

A

even though separated somewhat in space,

  • caudate and putamen
  • globus pallidus and substantia reticulata of substantia nigra

receive same inputs, perform same fx in response to those inputs

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9
Q

general flow of info through basal ganglia loops

normal excitation in basal ganglia loops

normal inhibition in basal ganglia loops

A

cortex → caudate/putamen → VA/VL complex of thalamus → cortex

  • cortex then influences motor output

under normal circumstances,

  • thalamus is providing excitatory (Glu) stim → cortex
  • cortex is providing excitatory (Glu) stim → motor pathways
  • globus pallidus (GPi & SN reticulata) is providing tonic inhibition (GABA) stim → VA/VL thalamus
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10
Q

excitation and disinhibition

A

GPi&SN_reticulata are inhibiting the thalamus, reducing level of excitatory signal to cortex/motor pathways

implication:

stimulate the GPi&SN_ret → increase inhibition → decrease movement

INHIBIT the GPi&SN_ret → decrease inhibition → increase movement

  • state known as disinhibition
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11
Q

excitation/inhibition of GPi

players & roles

A

subthalamic nucleus: excites GPi → inhibition of cortex/movement

  • lesions produce EXTRA movement (contralat hemiballismus)

striatum: inhibits GPi → excitation of cortex/movement (disinhibition)

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12
Q

basal ganglia “direct” pathway

A

facilitates movement via disinhibition

cortex sends excitatory signal to striatum → potentiates inhibitory signal to GPi → disinhibition of thalamus leads to increased movement

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13
Q

basal ganglia “indirect” pathway

A

inhibits movement

cortex sends excitatory signal to striatum →

striatum sends INHIBITORY signal to GPe →

GPe reduces its inhibitory signal to subthalamus →

  • GPe is typically inhibiting subthalamic
  • inhibition of GPe means LESS INHIBITION of subthalamic means MORE EXCITATION of GPi

subthalamic nucleus sends large excitatory signal to GPi →

GPi sends large inhibitory signal to thalamus

→ inhibits movement

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14
Q

graphic summary of direct and indirect pathways

A
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15
Q

striatal dopamine receptors

A

dopamine receptors are located on medium spiny neurons

  • dendritic spines receive cortical inputs
  • base of spines receive dopaminergic inputs

medium spiny neurons project to

  • globus pallidus
  • substantia nigra pars reticulata
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16
Q

dopamine receptors

families and characteristics

A

metabotropic receptors

D1 receptor family : EXCITATORY

  • incr cAMP
  • incr PIP2 hydrolysis
    • Ca mobilization
    • PKC activation

D2 receptor family : INHIBITORY

  • decr cAMP
  • incr K current
  • decr voltage-gated Ca current
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17
Q

role of dopamine in pathways

A

nigrostriatal dopamine facilitates “direct” pathway via D1 receptors (excitatory)

SNpc releases dopamine → hits DA1 receptor on striatum, excitation occurs

  • potentiates inhibitory signal to GPi → increases disinhibition → increases movement!

nigrostriatal dopamine inhibits “indirect” pathway via D2 receptors (inhibitory)

SNpc releases dopamine → hits DA2 receptor on striatum, inhibition occurs

  • inhibits inhibitory signal to GPe → potentiates inhibitory signal to subthalamus → dampens excitatory signal to GPi → dampened inhibitory signal from GPi → increased movement!

SUMMARY: dopamine is excitatory to direct pathway, inhibitory to indirect pathway → FACILITATES MOVEMENT in both cases!

18
Q

role of Ach interneurons in striatum

pharma link

A

20% of striatal neurons contain ACh

  • preferentially excite INDIRECT PATHWAY → increase inhibition → decrease movement

implication: anticholinergics can have tx benefit in PD

19
Q

general classification of movement disorders

3 types

A

hypokinesia

  • too little movement
  • “negative sx”

hyperkinesia

  • too much movement
  • “positive sx”

dyskinesia

  • abnormal movement
  • often drug induced by tx for psych/PD/etc

*all contralateral to lesion!

20
Q

negative sx

A

akinesia: no movement (can’t initiate)

bradykinesia: slow movements

decreased postural adjustments

hypokinesia: decr amplitude of movement

rigidity: “waxy”, “lead pipe”, “cogwheeling”

all best characterized by PD

21
Q

positive sx

A

occur at rest

hemiballismus: spontaneous, invol movements

  • usually due to lacunar infarcts in subthalamic nucleus

chorea: almost cont rapid movements of face, tongue, limbs

  • most common: Huntington’s disease

athetosis: slow, writing movements (hands, fingers)

  • can’t maintain fixed position
  • often kids with cerebral hypoxia affecting BG
22
Q

dystonia

A
  • slower, twisting postures triggered by voluntary movements
  • role of BG is unclear: could be disorder of synaptic plasticity in BG
  • botulinum tox, electrical stim of GP has shown some benefit

most common: writer’s cramp

most cases familial

23
Q

hyperkinetic sx

A

tics: sudden, brief action preceded by an urge to perform it

  • Tourette’s Syndrome is characterized by persistent motor and vocal tics

Restless Leg Syndrome (RLS): discomfort and urgent desire to move legs

  • usually during sleep, usually relieved by movement
  • familial pattern
  • might be related to DA neurotrans!
    • PET scans show decr D2 receptors
24
Q

tardive dyskinesia

A

most commonlly in schizophrenia from antipsychotic or antiemetic drugs

  • prolonged use of DA antagonists → receptor hypersensitivity
  • can persist after discont of drugs
  • less of an issue with new anti-psychs

can cause any dyskinesia or combo

25
Q

tremor

why do tremors happen?

A

cerebellum, thalamus, BG all have regular, oscillating rhythms

  • disruption in rhythm leads to tremor
  • Parkinson’s (3-5 Hz at rest)*
  • hands and arms common; can also include legs and mouth
  • begins unilaterally

essential tremor (5-8 Hz)

  • hands, arms, face, legs, trunk
  • usually bilat (cerebellar origin)
26
Q

4 parallel basal ganglia pathways

A

general loop: cortex → striatum → pallidum → thalamus → back to cortex

  1. motor → abnormal movement
  2. oculomotor → abnormal eye movements
  3. cognition (prefrontal) → poss relationship to psychosis and impaired exec fx
  4. emotions (limbic) → addictive/impulsive behaviors
27
Q

Huntington’s Chorea

what is it

symptoms

psych manifestations

tx

A

autosomal dominant neuroderen disorder with cell loss in caudate and putamen, also frontal/temporal cortex

  • progressive → leads to akinetic/rigid form of disease

major sx:

  • chorea
  • dementia

psych manifestations

  • anxiety
  • mood changes
  • OCDs
  • impulsiveness
  • cognitive impairment
  • memory loss

tx: drugs that decrease dopamine

28
Q

which pathway is affected in Huntington’s?

A

cells in INDIRECT pathway affected

  • caudate and putamen die, which means…

inhibitory signal to GPe is dampened

→ inhibitory signal from GPe to subthalamus is amplified

→ excitatory signal from subthal to GPi is dampened

→ inhibitory signal from GPi to thalamus is dampened

→ movement is increased!

29
Q

Parkinson Disease

basics

risks/decr risk

A

neurodegen disease

progressive and chronic

risk factors

  • family history
  • older age
  • exposure to pesticides
  • migraine

risk diminishers

  • coffee
  • cig smoking
30
Q

PD cardinal symptoms

A

begin unilaterally

1. bradykinesia: slowed movement

2. resting tremor: “pill rolling”

3. rigidity: lead pipe (through range of motion) OR cogwheeling (w reg jerking)

4. postural instability

31
Q

other PD motor symptoms

A

MOTOR

  • masked facies (hypomimia)
  • Parkinson’s gait: festinating
  • loss of automaticity (can’t do two things at once, ex. stand, shake hands)
  • stooped posture
  • difficulty moving

NON-MOTOR

lots of signs incl personality changes, psych sx

32
Q

dx for Parkinson’s disease

A

1. look at symptoms and history

  • bradykinesia + one other sx
    • resting tremor (pill rolling)
    • rigidity: lead pipe
  • postural instability is a later syndrome

2. rule out other causes

  • repeated stroke, multiple head injury, encephalitis, neuroleptic tx, exposure to toxins (Mn, CO, MPTP), cerebral tumor, hydroceph

3. look for supportive evidence

  • responsiveness to Levodopa
  • unilateral onset
  • other typical motor/non-motor signs
33
Q

neuropatho of PD

A

death of cells in substantia nigra

  • degree of cell death correlated to severity of sx

neurons that do exist in substantia nigra have abnormal aggregations of proteins: Lewy bodies

34
Q

Lewy bodies

A

spherical masses within cell body of PD substantia nigra cells containing abnormal aggregations of proteins

  • primarily alpha-synuclein: cytosol protein in many regions of brain, normal involved in vesicular transport
35
Q

treatments for PD

what are they? problems?

A

pharmaceutical

  • dopamine agonists: L-DOPA (dopamine precursor, crosses bbb)
  • MAO inhibitors
  • anti-cholinergics

*problem with dopamine: “honeymoon period” at first, then on/off phenomena (dyskinesia, patho gambling - risk taking)

surgical lesions

  • thalamus: for young pt with unilat tremor, no rigidity/bradykinesia
  • globus pallidus (GPi): for tremor, rigidity

deep-brain stim

  • globus pallidus internus
  • subthalamic nucleus
  • thalamus
36
Q

deep brain stimulation

sites

theoretical goals

risks

A

GPi or subthalamic nucleus

theoretically,

  1. normalizes outputs
  2. blocks APs

serious risks/adv effects as well: headache/pain, infection (10%), death

37
Q

neuroprotective tx

A

lots of compounds for various reasons (pramipexole, CoQ10, creatine, green tea polyphenol, inosine, isradipine, cogane)

exercise is both neuroprotective and neurorestorative (after lesions)

*

38
Q

“Parkinsonism Plus” syndromes

A

diseases that share characteristics of PD

characterized by:

  • lack of resting tremor
  • symmetrical sx
  • early postural instability
  • lack of response to dopamine

PD clinical diagnosis accuracy is approx 80%

39
Q

progressive supranuclear palso

A

most common form of atypical Parkinsonism

pathophysiology

  • neurodegenerative, affects multiple regions of rostral midbrain
    • red nucleus
    • superior colliculus
    • subthalamic nucleus
    • globus palliduson

onset/progression:

sx begin after 50, progress more rapidly than PD

symptoms

  • imbalance/falling/trunk rigidity
    • compare to PD: limb rigidity
  • swallowing changes
  • decr range of vertical eye movement (often first sign)
  • dementia

tx: SOME relief from dopaminergic tx

40
Q

secondary Parkinsonism

A

caused by: stroke, tumor, infection, exposure to toxins (CO, Mn), drug exposure

ex. MPTP → frozen addicts

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