Functional neuroanatomy of movement disorders Flashcards

1
Q

features of UMN lesion

A

weakness, spasticity, clonus, and hyperreflexia, hypotonia

babies have low muscle tone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is a monosynaptic reflex

A

The monosynaptic stretch reflex, or sometimes also referred to as the muscle stretch reflex, deep tendon reflex, is a reflex arc that provides direct communication between sensory and motor neurons innervating the muscle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

LCST decussation

A

medulla

fibres from motor cortex, motor area, premotor cortex, somatosensory cortex, parietal lobe and cingulate gyrus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

where is the primary motor cortex found

A

precentral gyrus of the frontal lobe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what does the primary motor cortex do

A

Generates signals execute movement opposite side of body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what does the secondary motor area include

A

posterior parietal cortex

premotor cortex ( anterior to primary MC)

supplementary motor area SMA above and medial to premotor area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

the secondary motor area includes is involved in motor planning
the posterior parietal Cortex is involved in the secondary motor area what does it do

A
  • transforms visual info into motor commands eg steering hand to glass in space. It sends signals to premotor cortex and SMA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what does the premotor cortex do

A

sensory guidance of movement controlling proximal and trunk muscles (orientation of body before reaching for the glass)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what does the supplementary motor area SMA do

A

planning complex movements and coordinates two handed movements - tai chi, double handed tennis stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

the supplementary motor areas sequences of movement form memory. how does normal movement occur

A

start in premotor cortex and SMA goes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

BG receive input from …….. …….. …….. e.g. premotor cortex & supplementary motor areas (SMAs - sequences of movements from memory)
Integrates these signals & feeds back to pre-motor cortex via …………
Pre-motor cortex then activates the primary motor cortex (to execute movement) & the cerebellum (to coordinate & fine-tune the movement)
BG also have access to descending pathways for axial & proximal limb muscle control

A

BG receive input from cortical motor areas, e.g. premotor cortex & supplementary motor areas (SMAs - sequences of movements from memory)
Integrates these signals & feeds back to pre-motor cortex via thalamus
Pre-motor cortex then activates the primary motor cortex (to execute movement) & the cerebellum (to coordinate & fine-tune the movement)
BG also have access to descending pathways for axial & proximal limb muscle control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

wha is BSS

A

Brown-Sequard syndrome (BSS) is a rare neurological condition characterized by a lesion in the spinal cord which results in weakness or paralysis (hemiparaplegia) on one side of the body and a loss of sensation (hemianesthesia) on the opposite side.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

UMN
cortical grey matter - cell bodies
white matter tracts - myelin
spinal tracts

A
LMN 
ventral horn of spinal cord 
cauda equina 
peripheral nerve ( spinal and cranial) 
neuromuscular junction alpha * muscle fibres force) and gamma motor neurones ( innervate fibres in muscle spindles - measuring length and stretch of the muscle)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

UMN lesion

A

Paralysis of movement rather than individual muscles
Hypertonic muscles (spasticity) after a couple of days
‘Hopping rabbit’ posture
Moderate muscles wasting
Tendon reflexes increased & modified
Babinski sign
clonus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

LMN lesion

A

Paralysis of individual muscles
Hypotonic muscles (flaccidity)
Pronounced muscle wasting
Tendon reflexes absent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the SMA

A

sequences of movements from memory – choreography like martial arts forms/kata, dance like Strictly (GABA)

BG & Cerebellum integrates these signals & feeds back to pre-motor cortex via thalamus

BG also have access to descending pathways for axial & proximal limb muscle control

Damage leads to spontaneous & inappropriate movement

17
Q

putamen and the caudate

A

striatus ( corpus striatum)

18
Q

putamen and the globus pallidus

A

lentiform nucleus

19
Q

caudate nucleus runs in the wall of what ventricle

A

lateral ventricle

20
Q

major role of the basal ganglia

A

imitation and termination of movement

neuronal activity in putamen seen before body movements
neuronal activity in caudate seen before eye movements

also involved in initiation and termination of some cognitive functions

21
Q

the basal ganglia is a collection of nuclear masses in the forebrain what is contained in the basal ganglia

A

caudate nucleus
putamen
globus pallidus

amygdala is anatomically and embryonically similar but functionally part of the limbic system

2 functionally related midbrain structures - substantia nigra and sub thalamus

22
Q

caudate nucleus it tadpole shaped - where is it found in comparison to the BG

A

most superior to BG
above and lateral to the thalamus and medial to internal capsule
enlarged head at the front which is continuous with the putamen

23
Q

what is the limbic system mad of

A

hippocampus, amygdala and hypothalamus

motivation dn mood

24
Q

what “loops does the limbic system have”

A

Motor loop
Oculomotor loop
Prefrontal loop – attention, planning, focus concentration
Limbic loop – emotional function – link between movement and emotion

25
Q

what is Korsakoff syndrome and what causes it

A

Korsakoff Syndrome. Korsakoff syndrome is a chronic memory disorder caused by severe deficiency of thiamine (vitamin B-1). Korsakoff syndrome is most commonly caused by alcohol misuse, but certain other conditions also can cause the syndrome.

high dose of thiamine

26
Q

substantia nigra does what

A

send dopaminergic neurones to basal nuclei

black substance due to melanin projecting to corpus striatum of BG - largest nucleus of the midbrain

27
Q

what is the subthalmus

A

The subthalamus is the most ventral part of the diencephalon.

28
Q

two problems causes by BG dysfunction

A

either hyperkinetic e.g. Parkinson’s - reduced or slow movement

hyperkinetic disorder - excessive abnormal spontaneous movement

Chorea
rapid, involuntary dancing movements eg Huntington’s disease
Ballismus
severe chorea with thrashing motions
Athetosis
Involuntary writhing (twisting & turning) movements of limbs & neck

29
Q

symptoms of Parkinsons

A
Tremor
Slow, pill-rolling
Asymmetrical
Worse at rest
Reduced on movement/distraction
Bradykinesia (slowness of movement)
Slow shuffling gate
Expressionless face with reduced blinking
Quiet monotonous speech
Micrographia (spidery writing)

Rigidity
lead-pipe rigidity in limbs, trunk & neck
cogwheel rigidity = rigidity + tremor

falls and dementia

30
Q

BG goes light what has happened

A

Degeneration of dopamine producing neurons (neuropigmented cells) in the pars compacta region of substantia nigra
- loss of melanin

31
Q

an example of a hyperkinetic disorder is Huntington’s disease - autosomal domino so 50%
caused by what

A

loss of GABA releasing neurone of the corpus striatum

chorea is primary feature
dementia, unsteadiness and speech problems
no effective treatment

32
Q

what is Wilsons disease

A

Wilson disease is a rare genetic disorder characterized by excess copper stored in various body tissues, particularly the liver, brain, and corneas of the eyes. The disease is progressive and, if left untreated, it may cause liver (hepatic) disease, central nervous system dysfunction, and death.

Researchers have determined that Wilson disease is caused by disruption or changes (mutations) of the ATP7B gene, which plays an important role in the movement of excess copper from the liver to the bile to eventually be excreted from the body through the intestines.

liver transplant

33
Q

what separates the cerebellum from the cerebrum

A

transverse fissure and tentorium cerebelli

median region separated from pons and medulla by 4th ventricle

34
Q

what does each cerebellar lobe do

A
Anterior lobe & posterior lobe = subconscious skeletal muscle movement
Flocculonodular lobe (inferior surface) = equilibrium & balance
35
Q

what is a cerebellar peduncle

A

A cerebellar peduncle is a nerve tract that permits communication between the cerebellum and the other parts of the central nervous system.

sup - efferent outpoin t
mid and inf afferent input from eyes , limbs etc

36
Q

sup cerebellar peduncles goes to where

A

midbrain

37
Q

mid c peduncles comes from voluntary motor signals from pons but where does inf c peduncles come from bringing vestibular apparatus of inner ear and body proprioceptors
and axons from medulla and spinocerebellar tracts of spinal cord to cerebellum

A

medulla

38
Q

DANISH

A
D ysdiadokokinesis
A taxia
Uncoordinated, staggering, broad-based gait 
Finger-nose ataxia (past-pointing)
Heel-knee-shin ataxia
Falls

N ystagmus
	(Involuntary, rapid, rhythmic eye   			movement)

I ntention tremor

S peech disturbance (dysarthria)

H ypotonia