NS 5: Motor disorders and patterns of sensory deficits

Question 1

In which region of the brain does degeneration of dopaminergic neurones take place in Parkinson’s disease?

Answer 1

the substantia nigra pars compacta= pars compacta is a portion of the substantia nigra which is located in the midbrain (mesencephalon)

Question 2

damage to what causes an UMNLs?

Answer 2

motor tracts of brain and SC

Question 3

damage to what causes LMNLs?

Answer 3

crainal or spinal motor nuclei, or peripheral nerves

Question 4

extrapyramidal signs are related to dysfunction of what structures?

Answer 4

non-cortical motor systems e.g. basal ganglia and cerebellum.
and extrapyramidal tracts.
Damage to extrapyramidal tracts (originate from brainstem motor nuclei) impairs way movements carried out e.g. gait abnormality.

Question 5

how does damage to corticospinal tract (pyramidal tract) impair fine movements?

Answer 5

it impairs the ability to decide on and commit to performing fine movements

Question 6

describe the features of spinal shock

Answer 6

this occurs following severe damage to descending tracts of SC. May last for wks or mnths, and charactersised by flaccid paralysis and areflexia.
Limbs eventually become spastic and show hyperactive deep reflexes typical of UMN damage.
Loss of reflex activity due to loss of motor influences exerted by descending fibres from reticular formation, allowing intact connections in reflex circuits to become dominant, producing UMN signs.
* inital loss of reflexes result of loss of basal excitatory stimulation to nuerones which become hyperpolarised and so less responsive to stimuli.

Question 7

in which 4 places might a lesion lie to result in lower motor neurone signs?

Answer 7

cell bodies of alpha motorneurones
axons of alpha motorneurones
NMJ
muscle itself

Question 8

what does muscle tone depend solely on the operation of?

Answer 8

the muscle stretch reflex

Question 9

why are UMNLs characterised by hypertonia?

Answer 9

reduced descending inhibition from extrapyramidal system to muscle stretch reflexes

Question 10

why is overall flexion of upper limb often seen with UMNLs?

Answer 10

flexors of UL usually stronger than extensors so spastic paralysis with hypertonia usually causes overall flexion.

Question 11

3 functional zones of cerebellar cortex?

Answer 11

vestibulocerebellum
spinocerebellum
cerebrocerebellum

Question 12

function of vestibulocerebellum?

Answer 12

balance and ocular reflexes
main input from vestibular system (vestibular nucleus in pons and medulla- vestibulospinal tract- extrapyramidal pathway from brainstem to SC)

Question 13

function of spinocerebellum?

Answer 13

involved in error correction

Question 14

function of cerebrocerebellum?

Answer 14

involved in movement planning and motor learning, part. in relation to visually guided movements and coordination of muscle activation

Question 15

sings of cerebellar dysfunction?

Answer 15

ataxia
past pointing (dysmetria)
'scanning' speech (dysarthria- pronunciation difficult)
dysequilibrium
hypotonia
dysdiadochokinesia
cannot learn new movements
coarse nystagmus
no muscle weakness/atrophy

Question 16

common causes of cerebellar dysfunction?

Answer 16

tumour
cerebrovascular disease
genetic e.g.friedreich’s ataxia

Question 17

how do the basal ganglia control voluntary movements?

Answer 17

balanced activity in direct and indirect pathways to the globus pallidus interna, resulting in selective disinhibition (hence stimulation) of desired movements, and inhibition of undesired movements in different neurones.

Question 18

what constitutes the striatum?

Answer 18

caudate nucleus and putamen

Question 19

how are cortical neurones activated via the direct pathway to allow desired voluntary movements to occur?

Answer 19

• cerebral cortex stimulates striatum through glutamate release.
• striatum inhibits GPi/SNr via GABA, and the GPi/SNr inhibits the thalamus via GABA, so by inhibiting an inhibitory pathway, we get disinhibition of thalamic neurones, and hence we inhibit the GPi from inhibiting the thalamus, so thalamus is stimulated, permitting activation of cortical neurones as glutamate released from thalamic neurones is excitatory to cerebral cortex.

Question 20

how are cortical neurones inhibted via the indirect pathway to inhibit particular movement programs?

Answer 20

cerebral cortex stimulates striatum.
Striatum inhibits the inhibitory pathway from the GPe, causing GPe to stimulate the subthalamic nucleus, which in turn stimulates the GPi/SNr, resulting in inhibition of thalamic neurones and so you don’t get excitation sent o cerebral cortex and movement is inhibited.

Question 21

why do symptoms of Parkinson’s occur much after disease onset?

Answer 21

upregulation of dopamine receptors in striatum allow selective disinhibition of thalamic neurones via direct pathway and inhibition of GPi/SNr via indirect pathway which allows stimulation of thalamic neurones as inhibiting the inhibitory pathway from GPi to thalamus.

Question 22

why do fasciculations (muscle twitching*) occur with LMNLs?

Answer 22

increased sensitivity of ACh receptors to ACh following dennervation of a muscle- fibres degenerate, so any very small amount of ACh will lead to muscle contraction- spontaneous.

Question 23

name given to unilateral large-amplitude, proximal, flinging movements?

Answer 23

hemiballismus
this is associated with abnormalities, usually vascular, of the subthalamic nucleus= indirect pathway of basal ganglia passes through this structure, this pathway normally allowing inhibition of particular movements through stimulation of the GPi/SNr, which inhibits thalamic neurones.

Question 24

why might cog wheel rigidity be seen following an UMNL?

Answer 24

Cogwheel rigidity is resistance to a passive range of movement of a joint, which intermittently gives way like a lever pulling over a rachet. Rigidity is a sign of extrapyramidal dysfunction.
Rigidity has three characteristics:
Resistance is velocity-independent (i.e., the degree of resistance to passive movement is constant with slow or fast movement- different from clasp knife).
Flexor and extensor tone are equal.
There is no associated weakness.

Question 25

why is hypereflexia seen with UMNLs (pyramidal)?

Answer 25

“damping” effect of descending tracts upon reflex activity in cord removed. loss of inhibition to disynaptic and oligosynaptic pathways of muscle stretch reflex?

Question 26

why is hyporeflexia/areflexia seen with LMNLs?

Answer 26

loss of efferent part of muscle stretch reflex

Question 27

why does Babinski sign occur with UMNLs (pyramidal)?

Answer 27

hypereflexia following loss of descending tract inhibition: extensor responses exaggerated in legs as extensor muscles stronger, so normal flexor response of foot becomes extensor, so normal plantarflexion replaced by dorsiflexion and a fanning of the toes.

Question 28

why might muscle contractures be seen with end stage LMNLs?

Answer 28

muscle fibres dennervated replaced with fibrous tissue

Question 29

contrast sensory patterns of loss in UMNLs and LMNLs?

Answer 29

upper= tends to be quadrants or halves e.g. hemiparesis
lower= tends to be peripheral nerve pattern of sensory defecit.

Question 30

what do the basal ganglia regulate in relation to voluntary movements?

Answer 30

amplitude and velocity of planned movements part. in relation to processing of proprioceptive information

Question 31

why do we not move when at rest?

Answer 31

movements actively inhibited as GPi stimulating inhibition of thalamic neurones.
movement amplitude increased with upregulation of direct pathway, and downregulation of indirect pathway.

Question 32

types of disorders generated by basal ganglia dysfunction?

Answer 32

hyper and hypo kinetic
(hyper- Huntington’s chorea)
(hypo- Parkinson’s)
movement coordination normal as generated by cerebellum

Question 33

signs of extrapyramidal lesions (EP tracts, cerebellum, basal ganglia)?

Answer 33

dysdiadochokinesis
festering gait
pill rolling tremor
paucity of facial expression e.g.  as smile normally associated with walking- don't really think about it, but gait altered.
cog wheel rigidity
choreiform movements
intention tremor

Question 34

describe the process of motor planning that allows movement

Answer 34

SMA and pre-motor cortex talk to cerebellum, does it have a motor plan used before?, determine sequence of activation of muscles, and mment coordination.
talk to basal ganglia, use proprioceptive info, to set speed and amplitude of movement.
both taken through thalamus back to cerebral cortex- M1, to result in output driving movement.
sensory feedback during completion of movement used to modulate cerebellum and basal ganglia function.

Question 35

example of a disease that selectively destroys alpha motorneurone cell bodies?

Answer 35

polio myelitis

Question 36

example of a cause of a pure lesion to an alpha motorneurone axon?

Answer 36

complete transection of a peripheral nerve due to trauma

Question 37

how can alpha and gamma motorneurones be distinguished between in the grey matter of the SC, lamina IX?

Answer 37

alpha= large cell body diameters
gamma= smaller cell body diameters

Question 38

how does impairment of movement differ between parkinson’s disease and cerebellar ataxia?

Answer 38

parkinson: disorder of motor planning and initiation. Patient may allow themselves to fall to elicit protective reflex that then allows them to carry on with movement. Hypertonicity and resting tremor- both go away when movement initiated.
cerebellar ataxia: problem with movement execution. tremor= intentional, seen only during movement.