Introduction to Biological Psychology
Central Control
of Movement
Classification of movement
1 – Simple reflex
- stretch reflex, knee jerk
- mediated at the level of the spinal cord
2 – Posture and postural change
- standing, balancing
3 – Locomotion
- walking, running
4 – Sensory orientation
- head turning, eye fixation
5 – Species specific action patterns
- ingestion, courtship, escape/defence, grooming, gestures
6 – Acquired skills
- speech dressing, painting, driving, sports, etc
Control of movement
Motor output comes from the motor cortex
Projects through pyramidal tracts to spinal cord, where it
synapses with peripheral motor neurones
Other pathways run parallel from cortex, basal ganglia and
cerebellum via brainstem and spinal cord
- these run outside the pyramidal tract and are called the
extrapyramidal system
Motor control systems in the cortex
Primary motor cortex
– source of pyramidal tract neurones
Supplementary motor cortex
- conception and initiation of movement.
- lesions cause deficits in voluntary
movement or speech
Premotor cortex
- important in motor coordination.
- lesions cause impairments in stability
of stance, gait and hand coordination
From:
Biopsychology, JPJ Pinel
Primary motor cortex
From:
Biopsychology, JPJ Pinel
Motor control systems outside the cortex
Cerebellum
-controls neural ‘programs’ for the
executionl of skilled movements
Basal ganglia
- a group of subcortical forebrain nuclei
(caudate nucleus, putamen (= striatum),
globus palludus, subthalamic nucleus)
- modulate patterns of motor activity
Organisation of the motor system
Visual cortex
Cerebellum
Somatosensory
cortex
Prefrontal cortex
Supplementary
motor cortex
Premotor
cortex
Motor nuclei
of the thalamus
Basal
ganglia
Brainstem
Extrapyramidal
Motor pathways
Primary
motor cortex
Pyramidal
tract
Spinal motor pathways
Pyramidal tract
- control most of our fine movements
Tectospinal tract
- coordinating head and eye movements
as part of the optic reflexes
Vestibulospinal tract
- influences postural muscles
Reticulospinal tract
- projects from the reticular formation
- inhibition or facilitation of movement
From : The Central Nervous System, P. Brodal
Spinal reflexes
• Mediated at the level of the
spinal cord
• Do not require any cortical input
e.g. Knee jerk reflex
• Tapping the knee tendon stimulated
tendon stretch receptors
• Sensory neurone synapses directly
to motor neurone
• Muscle contracts to cause limb
extension
From:
Biopsychology, JPJ Pinel
Neurological diseases of the motor system
Dysfunctions of the Motor System
• Paralysis
• Apraxia
• Decomposition of movement
• Parkinson’s disease
• Huntington’s disease
• Duchenne’s muscular dystrophy
• Myesthenia gravis
Diseases of peripheral rather than central origin:
more information is available on the web slides
Paralysis
Damage to motor neurones
• viral (e.g. poliomyelinitis – leads to destruction of spinal
motorneurones)
• toxins and/or hereditary (e.g. amyotrophic lateral sclerosis –
degeneration of motoneurones in the brainstem and spinal cord)
• injury
• severing of spinal cord – permanent
• bruising or compression of spinal cord – transient
Damage to primary motor cortex
• paralysis or partial paralysis of voluntary movement on one
side of the body (contralateral to damage)
• extent of paralysis depends on extent of damage
• often accompanied by spasticity and abnormal reflexes
Apraxia
Inability to carry out movements in response to commands
• no paralysis
• no loss of comprehension
• no loss of motivation
May be due to disconnection of
primary motor cortex from
supplementary motor areas and
motor association cortex
From:
Biopsychology, JPJ Pinel
Decomposition of movement
Inability to perform “motor patterns” (e.g. walking)
• motor patterns are broken up into individual segments
instead of being executed smoothly
• movements require thought for execution, rather than
being “automatic”
Due to cerebellar damage
Influence of the cerebellum
Visual cortex
Cerebellum
Somatosensory
cortex
Prefrontal cortex
Supplementary
motor cortex
Premotor
cortex
Motor nuclei
of the thalamus
Basal
ganglia
Brainstem
Extrapyramidal
tract
Primary
motor cortex
Pyramidal
tract
Symptoms of Parkinson’s Disease
• Resting tremor in limbs – disappears on movement or
during sleep
• Muscle rigidity – resistance to passive movement: jerky
(cogwheel) movement
• Akinesia – general paucity of involuntary movement
• Stooped posture
• Shuffling gait
• Excessive sweating and salivation
• Micrographia
• Altered cognitive function, depression and/or dementia
• Deficits in movement controlled by extra-pyramidal
motor pathways
Neuropathology of Parkinson’s disease
• nigro-striatal pathway degeneration
• leading to a depletion of striatal dopamine
• some degeneration of other dopamine pathways too
Dopamine
Glutamate
X
Striatum
GABA
Treatment of Parkinson’s disease
• prior to 1960s there were no effective treatments
• realisation of dopamine’s involvement led to use of drugs
which increase brain dopamine
• dopamine itself cannot cross from the blood to the brain
• use precursor, L-DOPA, which enters the brain and is
converted there into dopamine
• can cause severe side effects (dyskinetic movements,
psychotisism)
• surgical interventions and neural transplantation are under
investigation as alternative therapies
Huntington’s disease
• Progressive disease causing involuntary muscle jerks
• Ultimately affect the whole body
• Also intellectual deterioration, depression and
occasionally psychotisism
• Onset of symptoms usually at 30 to 45 years
• Genetically determined (single dominant gene)
• Causes degeneration of the output
neurones from the striatum, reducing
inhibitory modulation of motor function
Dopamine
Glutamate
Striatum
X
GABA
Treatment of Huntington’s disease
• no effective treatment
• GABA replacement or dopamine antagonists provide
some relief
• no means of halting the progression of the disease
Influence of the basal ganglia
Visual cortex
Cerebellum
Somatosensory
cortex
Prefrontal cortex
Supplementary
motor cortex
Premotor
cortex
Motor nuclei
of the thalamus
Basal
ganglia
Brainstem
Extrapyramidal
tract
Primary
motor cortex
Pyramidal
tract
Additional slides
• Muscular dystrophy
• Myesthenia gravis
Muscular dystrophy
A group of diseases characterised by a generalised wasting of muscles
Appears to involve biochemical abnormalities leading to structural
changes in muscle cells
Duchenne’s muscular dystrophy
• wasting of muscles caused by a single gene on the x-chromasome
(effects only males)
• the gene is responsible for the protein product, dystrophin, which
may be involved in regulating intracellular calcium
• onset of symptoms around 6years old, with death resulting within
about 10 years
• may respond to gene therapy
X-Linkage in Duchenne’s muscular dystrophy
• The gene responsible is recessive
• Therefore for a female to be affected they would have to have
two copies of the DMD gene, one derived from each parent
• If a female has one DMD gene (i.e. heterozygous) she would
be a carrier, but would not express the disease
• For a male to be affected they only need one copy of the DMD
gene, which must come from his mother
• Since affected individuals die before reaching reproductive age,
it is impossible for a male to pass on the DMD gene
• Therefore it is impossible for a female to be homozygous for
the DMD gene
• Therefore a female cannot express the disease.
Myesthenia gravis
• profound weakening of sketetal muscles
• due to reduced numbers of acetylcholine receptors at the
neuromuscular junction
(c.f. snake venom toxins such as bungarotoxin)
• this leads to reduced transmission of neuronal signals
activating muscles
• caused by autoimmune destruction of the neuromuscular
junction
• removal of the thymus gland (where immune cells are made)
has some beneficial effects