Lecture 19- Pathophysiology of motor control

Question 1

What regions are involved in motor control cortex

Answer 1

Frontal lobe- executes movement
Primary motor cortex- large pyramidal neurons down spinal cord and synapse with motor neurons
Premotor cortex- organises and sequences movements
Prefrontal/orbitofrontal- abstract planning, select goal (w/ b.g), tells premotor steps to reach it

Question 2

What are the components of descending motor pathways

Answer 2

Primary motor cortex, internal capsule, cerebellar peduncles in pons (cross at medulla level, form lat. corticospinal tracts)- synapse w/ lower motor neurons (spine) or cranial nerves (brainstem)
NMJ, Muscle

Question 3

What are the different types of lower motor neurons

Answer 3

A- voluntary muscle contraction, myostatic stretch reflex

Gamma- regulate muscle tone, maintain proprioception

Question 4

Where are the cell bodies of lower MNs found

Answer 4

within anterior horn of spinal cord/ brainstem

Question 5

What are the two types of descending motor pathways

Answer 5

Direct- corticospinal (pyramidal) tracts, cross medulla level
Indirect- Rubrospinal, vestibulospinal, reticulospinal
Spinal neurons/ brainstem motor areas set baseline muscle tone, cortex exerts inhibitor signals over both

Question 6

An upper motor neuron lesion may cause what symptoms?

Answer 6

Above medulla- contralateral hemiplegia, pattern of flexed ULs, extended LLs
Below- spinal cord syndrome
Cervical sc- quadriplegia
Thoracic/ lumbar- paraplegia
Hemisection of cord- brown- sequard syndrome
UMN- cortex, brainstem, spinal cord (corticospinal tracts)

Question 7

What effect will an UMN lesion have on stretch reflex

Answer 7

hyperexcitability (Loss of inhibitory control)

when stretch applied quickly, contraction stronger (velocity dependent increased muscle tone ‘clasp knife’ )

Question 8

Signs of UMN lesion

Answer 8

Increased tone/ spasticity, clonus, hyperreflexia, babinski sign (extensor plantar)

Question 9

What are the signs of hemiparesis

Answer 9

Adducted/flexed upper limb
Extended lower limb muscle
Plantar flexed, inverted foot

Question 10

Characteristics of spastic quadriplegia

Answer 10

Cervical spinal cord-only all 4 limbs if lesion above c5
if lesion ‘complete’- complete paralysis below legion, loss of all sensory modalities below lesion, loss of all bowel, bladder, sexual functions

Question 11

Spastic paraparesis

Answer 11

Thoracic/lumbar spinal cord- spastic paraparesis in legs with normal arms
Lesions must be below t1, and often incomplete
- bilateral leg weakness, not complete paralysis
- impaired sensory function
- defective bowel, bladder, sexual function

Question 12

Spinal cord lesions- what types of signs present

Answer 12

tract signs- UMN signs, sensory level, bladder, bowel, sex dysfunction
segmental signs- pain, dermatomal sensory disturbance, LMN signs

Question 13

Conditions with UMN signs

Answer 13

brain tumour, ischaemic stroke, intracranial haemorrhage, post head injury/trauma, MS, spinal cord stenosis, prolapsed disc

Question 14

What damage is caused by LMN lesions

Answer 14

Damage to peripheral nervous system- motor neuron in AH spinal cord > nerve roots > nerve plexus > peripheral nerve > NMJ > muscle

Question 15

LMN signs

Answer 15

wasting and flaccid tone, fasciculations, waddling gait

Question 16

Patterns of LMN lesions

Answer 16

distal and ascending- flaccid areflexic paraplegia (GBS)
proximal weakness- rising, stairs, hair washing: plexopathy, radiculopathy, MD’S
Distal weakness- fine tasks (writing/phone): focal e.g radial/ulnar neuropathy/ widespread- peripheral neuropathy
Fatiguable weakness- repeated effort/ end of day
Ocular + bulbar > trunks and limbs, e.g MG

Question 17

LMN lesion- foot drop

Answer 17

Unable to dorsiflex foot, floppy at ankle
Wasting of tibialis ant if long standing?
Lesions- deep/common peroneal nerve, sciatic n, lumbosarcal plexus or L5 root

Question 18

LMN lesion- wrist drop

Answer 18

no wrist extension, hang hands flaccidly- wasting of triceps if chronic?
Radial nerve lesion- penetrating trauma, extrinsic compression, humeral fracture or MND

Question 19

Clinical UMN signs in neurology

Answer 19

Spasticitity- ‘clasp knife’ increased tone
Hyperreflexia
Clonus
Positive babinski (extensor plantar response)

Question 20

Clinical LMN signs in neurology

Answer 20

Flaccidity (reduced muscle tone)
Hyporeflexia
Fasciculations
Muscle wasting/ atrophy

Question 21

UMN + LMN signs

Answer 21

fasciculations and atrophy
brisk reflexes and extensor plantar response- dual pathology? one location?
Damage to ant. horn in spinal cord, tract and segmental signs due to spinal cord lesion- if pattern fits
MND

Question 22

Extrapyramidal system of BG- components and role

Answer 22

Striatum (caudate/putamen), globus pallidus, STN, SN

Sequencing and smooth control/fluidity of movement

Question 23

Basal ganglia pathology- types of movements

Answer 23

Movements are staccato, fragmentary, incomplete
Hypokinesis (parkinsonism)- bradykinesia, rigidity (lead pipe, stiff throughout range of movement), resting tremor
Hyperkinesis- essential tremor, chorea, ballism, myoclonus, dystonia

Question 24

Cerebellar function and ataxia

Answer 24

Coordinates agonist, antagonist and synergist muscle activity during learned movements- input from proprioceptors, inner ear and cortex
Dysfunction due to lesions in cerebellum, cerebellar peduncles or brainstem ( stroke, MS, tumour) or drug/alcohol intoxication/ loss of proprioceptive input (sensory ataxia)

Question 25

Signs of cerebellar dysfunction

Answer 25

Nystagmus, dysarthria, intention tremor/dysmetria, dysdiadochokinesia, wide based unsteady gait
- Ipsilateral representation: L cerebellar hemisphere lesion will cause left sided ataxia

Question 26

Clinical signs of extrapyramidal dysfunction- movement disorders and ataxia

Answer 26

Parkinsonism- resting tremor, bradykinesia, rigidity, postural instability
Tremor, chorea (dancing), ballism (movement prox limbs), myoclonus, dystonia
Cerebellar dysfunction ‘ataxia’- nystagmus, dysarthria (scanning/slurring), tremor, rebound phenomenon, dysmetria (past pointing), dysdiadochokinesia, truncal sway, wide based gait