Lecture 19- Pathophysiology of motor control Flashcards
What regions are involved in motor control cortex
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
What are the components of descending motor pathways
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
What are the different types of lower motor neurons
A- voluntary muscle contraction, myostatic stretch reflex
Gamma- regulate muscle tone, maintain proprioception
Where are the cell bodies of lower MNs found
within anterior horn of spinal cord/ brainstem
What are the two types of descending motor pathways
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
An upper motor neuron lesion may cause what symptoms?
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)
What effect will an UMN lesion have on stretch reflex
hyperexcitability (Loss of inhibitory control)
when stretch applied quickly, contraction stronger (velocity dependent increased muscle tone ‘clasp knife’ )
Signs of UMN lesion
Increased tone/ spasticity, clonus, hyperreflexia, babinski sign (extensor plantar)
What are the signs of hemiparesis
Adducted/flexed upper limb
Extended lower limb muscle
Plantar flexed, inverted foot
Characteristics of spastic quadriplegia
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
Spastic paraparesis
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
Spinal cord lesions- what types of signs present
tract signs- UMN signs, sensory level, bladder, bowel, sex dysfunction
segmental signs- pain, dermatomal sensory disturbance, LMN signs
Conditions with UMN signs
brain tumour, ischaemic stroke, intracranial haemorrhage, post head injury/trauma, MS, spinal cord stenosis, prolapsed disc
What damage is caused by LMN lesions
Damage to peripheral nervous system- motor neuron in AH spinal cord > nerve roots > nerve plexus > peripheral nerve > NMJ > muscle
LMN signs
wasting and flaccid tone, fasciculations, waddling gait
Patterns of LMN lesions
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
LMN lesion- foot drop
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
LMN lesion- wrist drop
no wrist extension, hang hands flaccidly- wasting of triceps if chronic?
Radial nerve lesion- penetrating trauma, extrinsic compression, humeral fracture or MND
Clinical UMN signs in neurology
Spasticitity- ‘clasp knife’ increased tone
Hyperreflexia
Clonus
Positive babinski (extensor plantar response)
Clinical LMN signs in neurology
Flaccidity (reduced muscle tone)
Hyporeflexia
Fasciculations
Muscle wasting/ atrophy
UMN + LMN signs
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
Extrapyramidal system of BG- components and role
Striatum (caudate/putamen), globus pallidus, STN, SN
Sequencing and smooth control/fluidity of movement
Basal ganglia pathology- types of movements
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
Cerebellar function and ataxia
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)
Signs of cerebellar dysfunction
Nystagmus, dysarthria, intention tremor/dysmetria, dysdiadochokinesia, wide based unsteady gait
- Ipsilateral representation: L cerebellar hemisphere lesion will cause left sided ataxia
Clinical signs of extrapyramidal dysfunction- movement disorders and ataxia
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
