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Motor pathways Flashcards

1
Q

Primary motor cortex

A

Location: precentral gyrus, anterior to the central sulcus
Function: controls fine, discrete, precise voluntary movement with input from cerebellum
-Provides descending signals to execute movement

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2
Q

Premotor cortex

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Location: frontal lobe, anterior to primary motor cortex
Function: planning of movements
-regulates externally cued movements
-intra-personal space: moving a body part relative to another body part
-extra-personal space: movement of the body in the environment

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3
Q

Supplementary motor area

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Location: in frontal lobe. anterior to primary motor cortex, medially
Function: planning complex movements, programming sequencing of movements
-regulates internally driven movements (eg: speech=regulates complex movements of larynx)
-the supplementary motor area becomes active (as seen on a brain MRI) when thinking about a movement before executing that movement (pre-movement in planning phase)

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4
Q

Association cortex

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NOT MOTOR AREAS BY DEFINITION AS THEIR ACTIVITY DOES NOT CORRELATE WITH MOTOR OUTPUT/ACTION

  • composed of the posterior parietal cortex and the prefrontal cortex
  • Posterior parietal cortex: ensures movements are targeted accurately to objects in external space (link to apraxia), borders the occipital cortex
  • Prefrontal cortex: selection of appropriate movements for a particular course of action (activity based on previous experience, works closely with the temporal cortex)
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5
Q

Lower motor neuron

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Motor neurons in the ventral horn of the spinal cord and bulbar region of the brainstem

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6
Q

Upper motor neuron problem

A

Betz cells and their projections to the spinal cord/brainstem
-related to the corticospinal tract and corticobulbar tract

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7
Q

Pyramidal problem

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Relates to the lateral corticospinal tract

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8
Q

Extrapyramidal problem

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Relates to the basal ganglia and cerebellum

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9
Q

Upper motor neuron lesion negative signs

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LOSS OF FUNCTION

  • Paresis: graded weakness of movements
  • Paralysis (plegia): complete loss of muscle activity
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10
Q

Upper motor neuron lesion positive signs

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INCREASED ABNORMAL MOTOR FUNCTION DUE TO LOSS OF INHIBITORY DESCENDING INPUTS

  • Spasticity: increased muscle tone
  • Hyperreflexia (exaggerated reflexes)
  • Clonus: abnormal oscillatory muscle contraction
  • Babinski’s sign (stimulation results in upward movement of the big toe alongside fanning out of the toes, distinctive difference with normal reflex)
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11
Q

Apraxia

A
  • Disorder of skilled movement
  • Patient not paretic (partial paralysis) but has lost information about how to perform skilled movements (putting muscle actions together properly)
  • due to lesion of the inferior parietal lobe or of the frontal lobe (premotor cortex, supplementary motor area)
  • most common causes of apraxia are stroke and dementia but any disease of these areas can cause this
  • In Alzheimers, patients can develop apraxia as he disease spreads and damages the parietal lobe (damages ability to perform actions they were able to do beforehand without thinking)
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12
Q

Lower motor neuron lesion signs

A
  • Weakness (reduced muscle strength)
  • Hypotonia (reduced muscle tone)
  • Hyporeflexia (reduced reflexes)
  • Muscle atrophy (reduced muscle mass due to loss of muscle innervation)
  • Fasciculations: damaged motor units produce spontaneous action potentials (not planned or driven by the brain), resulting in a visible twitch
  • Fibrillations: spontaneous twitching of individual muscle fibres, recorded during needle electromyography examination
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13
Q

Motor neuron disease

A
  • Progressive neurodegenerative disorder of the motor system
  • relatively rare
  • Spectrum of disorders (eg: ALS) with various presentations (diverse clinical phenotype)
  • Can affect only upper motor neurons, only lower motor neurons or both
  • research shows lots of genetic causes for motor neuron disease
  • Motor neuron disease affecting both upper motor neurons (in brain) and lower motor neurons (in spinal cord and brainstem) is Amyotrophic Lateral Sclerosis
  • Motor neuron disease tends to progress distal to proximal
  • Mortality from motor neuron disease typically occurs when respiratory musculature is no longer functional
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14
Q

Motor neuron disease signs

A 
UPPER MOTOR NEURON SIGNS:
-Increased muscle tone (spasticity of limbs and tongue=become more rigid as continuously contracted)
-Brisk limbs and jaw reflexes
-Babinski's sign
-Loss of dexterity (slight type of dyspraxia)
-Dysarthria (problems speaking)
-Dysphagia (problems eating)
LOWER MOTOR NEURON SIGNS:
-Weakness
-Muscle wasting
-Tongue fasciculations and wasting
-Nasal speech
-Dysphagia
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15
Q

Basal ganglia

A

-extrapyramidal (not part of corticospinal tract)
Includes:
-Caudate nucleus (most anterior structure, large tadpole shape in anterior-posterior plane with head anteriorly and tail emerging as you move posteriorly in the coronal plane,composes lateral wall of lateral ventricle, functionally grouped with putamen)
Lentiform nucleus (putamen and external globus pallidus)=separated from caudate nucleus by internal capsule
-Subthalamic nucleus (beneath the thalamus)
-Substantia nigra (in midbrain but projects to the basal ganglia)
-Ventral pallidum (dopaminergic neurones projecting to various brain parts), claustrum (thin layer of grey matter), nucleus accumbens (reward centre of the brain=receives dopaminergic inputs via the mesolimbic pathway) and nucleus basalis of Meynert (cholinergic neurones projecting to the cortex, important in memory function)

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16
Q

Functions of the basal ganglia

A
  • Elaborating associated movements (eg: changing facial expression to match emotions=coordination of emotional input with motor output, swinging arms whilst walking to keep balance and gait etc)
  • Moderating and coordinating movements (suppressing unwanted movements)
  • Performing movements in order
17
Q

Parkinson’s disease

A

MOST COMMON MOTOR DISORDER
Primary pathology involves the neurodegeneration of the dopaminergic neurons that originate in the substantia nigra in the midbrain and project to the striatum (degeneration of the nigro-striatal pathway)

  • histologically see Lewy bodies (abnormal accumulation of alpha-synuclein)
  • dopaminergic neurons contain neuromelanin (from dopamine oxidation=normal metabolic product) which are responsible for the dark, heavily pigmented region of the brain (substantia nigra)->in Parkinson’s Disease this pigment is gone as neurones undergo degeneration
  • > 60% loss of dopaminergic neurons in the substantia nigra required before symptom presentation
  • early symptoms are typically motor due to dopaminergic neuron loss
  • often develop cognitive decline after having Parkinson’s Disease for a long time->due to alpha synuclein pathology spreading throughout the body

Patients with Parkinson’s Disease tend to present in one of two ways:

  • distinct tremor
  • problems initiating movements (compromised basal ganglia input)
18
Q

Main motor signs of Parkinson’s disease (initial presentation)

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  • Bradykinesia: slowness of small movements (eg: doing up buttons, handling a knife)
  • Hypomimic face: expressionless, mask-like (absence of movements that normally animate the face)
  • Akinesia: difficulty in the initiation of movements
  • Rigidity: muscle tone increase, causing resistance to externally imposed joint movements
  • Tremor at rest: 4-7Hz, starts unilaterally (one hand) but tends to spread to bilateral and other parts of the body as time progresses (‘pill-rolling tremor’)
19
Q

Huntington’s disease

A

CLEAR GENETIC COMPONENT

  • Genetic neurodegenerative disorder
  • rarer than Parkinson’s disease
  • in huntingtin gene located on chromosome 4
  • autosomal dominant inheritance
  • triplet repeat disorder (CAG) with 35 repeat cut off for Huntington’s disease (predictable genetic disease from cut off value)
  • Degeneration of spiny GABAergic neurons in the striatum, caudate and then putamen
20
Q

Motor signs of Huntington’s disease

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  • Choreic movements (Chorea): rapid,jerky, involuntary movements of the body (hands and face affected first, then legs and rest of the body=begins more proximal and then moves distally)
  • speech impairment
  • dysphagia (difficulty swallowing)
  • unsteady gait from involuntary activity
  • in the later stages, the patient will develop cognitive decline and dementia (do not treat degeneration->treatment aimed at treating motor symptoms and maintaining the patient’s quality of life)
21
Q

Vestibulocerebellum functions

A

DIVISION OF THE CEREBELLUM

  • regulation of gait, posture and equilibrium
  • coordination of head movements with eye movements (receives visual input from the superior colliculi in midbrain)
22
Q

Spinocerebellum function

A

DIVISION OF THE CEREBELLUM (receives input from the spinal cord)

  • coordination of speech
  • adjustment of muscle tone
  • coordination of limb movements
23
Q

Cerebrocerebellum functions

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DIVISION OF THE CEREBELLUM

  • coordination of skilled movements
  • cognitive function
  • attention
  • processing of language
  • emotional control
24
Q

Vestibulocerebellar (Flocculonodular Lobe) Syndrome

A
  • Damage (tumour) causes syndrome similar to vestibular disease
  • patients have gait ataxia and a tendency to fall (even when patient is sitting and has their eyes open=unsteady))
25
Spinocerebellar Syndrome
- Damage to tracts (degeneration and atrophy associated with chronic alcoholism) - mainly affects the legs - causes abnormal gait and wide-based stance
26
Cerebrocerebellar (Lateral Cerebellar) Syndrome
- Damage mainly affects arms | - affects skilled coordinated movements and speech (staccato speech)
27
Main signs of cerebellar dysfunction
DEFICITS APPARENT ONLY UPON MOVEMENT (UNTIL MOTOR FUNCTION CARRIED OUT) - Ataxia: general impairments in movement coordination and accuracy. Disturbances of posture or gait (wide-based and staggering='drunken' gait) - Dysmetria: inappropriate force and distance for target-directed movements (loss of ability to gauge distance and force required to carry out action) - Intention tremor: increasingly oscillatory trajectory of a limb in a target-directed movement (nose-finger tracking)=initiated by thinking about carrying out action - Dysdiadochokinesia: inability to perform rapidly alternating movements (rapidly pronating and supinating hands and forearms to test) - Scanning speech: otherwise known as staccato speech, due to impaired coordination of speech muscles
28
Motor system heirarchy
- Primary motor cortex at the top in the precentral gyrus, then various associated non-primary motor areas - The motor cortex receives information from various other cortical areas and sends commands to the thalamus and brainstem (all info rooted to primary motor cortex to react to the outside world) - output from primary and non-primary motor cortex to the basal ganglia - output from primary and non-primary motor cortex to cerebellum (modifies motor cortex output on its way down the corticospinal tract, refining the signal to carry out fine motor activity) - The cerebellum and basal ganglia adjust commands received from other parts of the motor control system - The brainstem passes commands from the cortex to the spinal cord - Spinal cord innervates muscles of the body at the bottom of the heirarchy - Brainstem directly innervates muscles of the face, head and neck at the bottom of the heirarchy also
29
Basal ganglia circuitry
- cortex inputs to striatum (caudate nucleus, external globus pallidus and putamen) - striatum links with the subthalamic nucleus, the internal globus pallidus and the substantia nigra - the thalamus and the supplementary motor area are also involved in the circuitry (internal globus pallidus links to thalamus, thalamus links to SMA and SMA links to substantia nigra) - Parkinson's disease when problem with links from substantia nigra to striatum (nigrostriatal system)
30
Broad principles of motor control
FUNCTIONAL SEGREGATION -the motor system is organised in a number of different areas which all control different aspects of movement HEIRARCHICAL ORGANISATION -some areas coordinate more complex tasks than others -high order areas of heirarchy->more complex task involvement (programme and decide on movements, coordinate muscle activity from muscular systems etc) -low level areas of heirarchy->low level tasks (execution of movement)
31
Cerebellum
- sits in posterior cranial fossa with tentorium cerebelli separating the cerebellum from the occipital lobe (folded extension of the dura mater) - transverse fibres connect the pons to the cerebellum - posterior aspect of the pons
32
Layers of the cerebellum
Outermost to innermost: - Molecular layer (does not contain many neurons) - Piriform layer (contains purkinje cells=main processing cells of cerebellum with huge dendritic trees to receive lots of input for coordination of activity and projections to nuclei in the white matter of the cerebellum) - granular layer (contains lots of small neurons involved in processing)
33
Cerebellum circuitry
- Inferior olivary nucleus in the medulla oblongata projects to Purkinje cells via climbing fibres (climbing fibres synapse with Purkinje cell dendritic trees) - All other input to occurs to granule cells in the cerebellum via mossy fibres and then onwards via parallel fibres - All output from Purkinje cells in cerebellum via deep nuclei in white matter
34
Corticobulbar pathway
DESCENDING MOTOR PATHWAY -Fibres from the primary motor cortex (in the cerebral cortex) descend through the internal capsule and synapse in the bulbar region of the brainstem (at the motor nuclei of the cranial nerves)
35
Lateral corticospinal pathway
DESCENDING MOTOR PATHWAY (VOLUNTARY) - biggest of the motor pathways - starts in the primary motor cortex (of the cerebral cortex), with upper motor fibres (upper motor neuron) descending through internal capsule on the same side to the cerebral peduncle of the midbrain (fibres visible externally) where they then pass through the pons (fibres not visible externally as covered by transverse fibres linking the two halves of the cerebellum) and re-emerge at the medullary pyramids of the medulla oblongata - decussation of most fibres in the lateral corticospinal tract occur at the base of the medulla (pyramids of the lower medulla=pyramidal decussation) - upper motor fibres descend in the lateral corticospinal tract until they reach the appropriate level of the spinal cord - fibres project to the ventral horn at the appropriate spinal cord level and project outwards to the skeletal muscles in the distal limb parts through the ventral root - right side of body controlled by left side of brain in terms of motor function here
36
Anterior corticospinal pathway
DESCENDING MOTOR PATHWAY (VOLUNTARY) - starts in the primary motor cortex (of the cerebral cortex), with upper motor fibres (upper motor neuron) descending through internal capsule on the same side to the cerebral peduncle of the midbrain (fibres visible externally) where they then pass through the pons (fibres not visible externally as covered by transverse fibres linking the two halves of the cerebellum) and re-emerge at the medullary pyramids of the medulla oblongata - remaining 5-10% of fibres which do not cross over in the medulla stay ipsilateral and descend in anterior corticospinal tract to the spinal cord - decussation happens at the level of the spinal cord - fibres project to the ventral horn at the appropriate spinal cord level and project outwards to innervate the skeletal muscles in the trunk and proximal limb parts (largely muscles of the thorax and axial musculature) - not a huge motor neuron component at this level as not many muscles innervated
37
Somatotopic organisation of the primary motor cortex
SOMATOTOPIC MAPPING OF MOTOR FUNCTION - Inverted motor homunculus (little person) derived by Penfield - lower limbs supplied by the motor cortex which itself is supplied by the anterior cerebral artery - not proportional mapping (some body areas are overrepresented in the homunculus=fine movements of the hands, lips in terms of speech etc)

Neuroscience and Mental Health (18 decks)

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