PSYC30020 Lecture Notes - Lecture 7: Parietal Lobe, Postcentral Gyrus, Agraphia
10 May 2018
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Lecture 7
- Possible locations of dysfunction: muscle, alpha motor neuron, spinal cord, cortex
(PPC, PFC, PMC), basal ganglia, cerebellum
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- Posterior parietal cortex receives information from our visual, auditory, vestibular
systems about where things in our environment and body are located → information
is passed to prefrontal cortex where most of the plan is generated → then goes to
premotor cortex and supplementary motor cortex for fine tuning of plans → then sent
to primary motor cortex and one of the loops to basal ganglia and cerebellum for
modifications of movement → final output from brain mostly comes from primary
motor cortex down lateral and ventromedial tracts down spinal cord → signal then
comes out the alpha motor neuron to muscles [when alpha motor neuron has AP
come down it → acetylcholine is released → binds on muscle fibre cell → results in
sodium voltage-gated channels opening and AP on muscle fibre cell itself → causes
calcium release → muscle filaments to slide over one another]
- Apraxia [a = no, praxia = movement/action]:
- ⇒ Symptoms - without action but not paralysed, can’t imitate or perform actions in
response to vocal instruction
find more resources at oneclass.com
find more resources at oneclass.com
- ⇒ 4 types - limb, oral, constructional and apraxic agraphia; limb → give a pen and
write name is fine, but pretend finger is pen and write name is not fine, can’t do
imaginary activities; oral → problem moving facial muscles [e.g. show me how you
would move mouth to brush teeth], can also be for speech [can occur in childhood
and be treated with speech therapy, can be later in life in response to strokes etc];
constructional → give box of lego and say build a house but struggle to build a house
even though knows how a house looks like, recognises picture of house, but when
comes to physically putting blocks together to build house → have difficulty, can’t
draw house as well; apraxic agraphia → specific kind of writing deficit, can speak and
spell fine but when comes to writing [even if they know the letters and can spell word
out] → have difficulty writing; very discrete certain movements that people have
trouble with
- ⇒ Cause: parietal lobe lesions: limb - left frontal and parietal lesions, constructional -
right parietal lobe lesions
- ⇒ Treatment: physical/occupational/speech therapy
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- Ataxia (taxia = coordination):
- ⇒ symptoms: without coordination; poor coordination, speech changes, unsteady
walking/stumbling, swallowing difficulty; not paralysed; seems like drunk movement
- ⇒ causes: cerebellar damage due to: alcohol abuse, strokes, tumours, multiple
sclerosis, hereditary forms (e.g. Fredericks’s), viruses (e.g. chickenpox, shingles)
- ⇒ treatment/management: treating underlying cause where possible; viral may
reverse spontaneously; physical, speech, occupational therapy; devices to aid
mobility etc when untreatable
- Parkinson’s Disease: involves dysfunction in basal ganglia
- ⇒ symptoms: muscle tremors, slow movements, rigidity; cognitive difficulties, memory
loss, depression; loss of olfaction (early)
find more resources at oneclass.com
find more resources at oneclass.com
- ⇒ causes: neuronal death in substantia nigra which have dopamine releasing axons
to the basal ganglia; genetic and environmental contributors [smokers have greater
risk and farmers who use certain pesticides even in youth]
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- Dopamine effect on motor control
- GP: globus pallidus
- Direct pathway: overall positive, exciting or enhancing pathway
- Indirect pathway: overall inhibitory, putting brake on movement
- Substantia nigra neurons: dopamine releasing neurons on both sides of pathway
- Receptors that dopamine binds to on each pathway has different effects
- Inhibitory receptors on indirect pathway → if dopamine released there, inhibits path
- Dopamine normally results in excitation and enhancement of movement regardless
of which side dopamine is released at
- When dopamine releasing neurons die → lose the stimulation → overall inhibitory on
movement
- Freezing gait: involuntary inability to move at unpredictable times
- Tricks to avoid it include: marching, stepping with rhythmical music, stepping over an
imaginary line in front of them
- ⇒ Treatment/Management: behavioural (exercise); carbidopa-levodopa/Dopamine
agonists; MAO-B inhibitors (inhibit breakdown of dopamine) [drugs do lose
find more resources at oneclass.com
find more resources at oneclass.com
Document Summary
Possible locations of dysfunction: muscle, alpha motor neuron, spinal cord, cortex (ppc, pfc, pmc), basal ganglia, cerebellum. Apraxia [a = no, praxia = movement/action]: Symptoms - (cid:3247)without action(cid:3248) but not paralysed, can"t imitate or perform actions in response to vocal instruction. Cause: parietal lobe lesions: limb - left frontal and parietal lesions, constructional - right parietal lobe lesions. Symptoms: (cid:3247)without coordination(cid:3248); poor coordination, speech changes, unsteady walking/stumbling, swallowing difficulty; not paralysed; seems like drunk movement. Causes: cerebellar damage due to: alcohol abuse, strokes, tumours, multiple sclerosis, hereditary forms (e. g. fredericks"s), viruses (e. g. sclerosis, hereditary forms (e. g. fredericks"s), viruses (e. g. chickenpox, shingles) Treatment/management: treating underlying cause where possible; viral may reverse spontaneously; physical, speech, occupational therapy; devices to aid mobility etc when untreatable. Parkinson"s disease: involves dysfunction in basal ganglia. Symptoms: muscle tremors, slow movements, rigidity; cognitive difficulties, memory loss, depression; loss of olfaction (early)
