Neural Control of Movement PDF

Neural control of movement ========================== Vragen: LE Motor units, spinal reflexes : - Twitch ? Leren, gebleven bij: SSA cerebellum and movement coordination, question 9 - GA central neurological movement disorders doornemen - Ppts bij antwoorden SSA bekijken - E-learnings...

Neural control of movement ========================== Vragen: LE Motor units, spinal reflexes : - Twitch ? Leren, gebleven bij: SSA cerebellum and movement coordination, question 9 - GA central neurological movement disorders doornemen - Ppts bij antwoorden SSA bekijken - E-learnings - Leerdoelen per SSA doornemen LE module introduction ---------------------- Motor system: - Hierarchical: - Cortex brain stem spinal cord - Parallel - Cerebellum / basal ganglia **Spinal cord:** - Spinal reflexes: - Stretch reflex (muscle splindles) - Golgi reflex (tendon organs) - Withdrawal reflex (nociceptors) - Low level feedback: gives the motor system the ability to rapidly adjust **Brain stem:** - Motor commands from cerebral cortex - Modulation spinal circuits (reflex modulation) - Reflexes (e.g. visual and vestibular reflexes for maintaining balance) - Sensory feedback **Motor cortex:** - Planning coordination, and execution - Sends commands to brain stem and spinal cord - Loops via cerebellum and basal ganglia - Very precise, but slow because of long feedback loops **Sensory feedback** - Parallel systems - Spinal reflexes - Cutaneous receptors - Proprioreceptors - Fast adjustments - Cortical loop - Somatosensory tracts - Visual feedback - Takes longer **Cerebellum** - Fine tuning - Plan from motor cortex - Compare with actual movement - Corrective commands via brainstem - Also inform cortex about this - Motor learning - Right timing - Right size **Basal ganglia** - Starting, stopping - Lift suppression of commands - Suppress unwanted commands - Smooth cooperation - Input from cortex and output to cortex - Selection of certain movements - Suppression of others SSA1 motor units and spinal reflexes ------------------------------------ **Function lower motor neurons and local circuit neurons** The lower motor neurons send their axons out of the brainstem and spinal cord to innervate the skeletal muscles of the head and body and the local circuit neurons are the major source of synaptic input to the lower motor neurons. **Function central (upper) motor neurons in the brainstem and cerebral cortex** The axons of the upper motor neurons have descending pathways that send movement commands to lower motor neurons either directly or indirectly via local circuit neurons. The cell bodies of upper motor neurons are located in the brainstem and cerebral cortex. **Function of the cerebellum** Motor coordination, posture, and balance. The cerebellum acts via its efferent pathways to the upper motor neurons as a servomechanism, detecting the difference, or 'motor error', between an intended movement and the actual movement. The cerebellum uses this information to mediate real-time and long-term reductions in these motor errors. **Function of the basal ganglia** Lying deep in the subcortical white matter of the frontal lobes, organizing motor behaviour. The basal ganglia suppress unwanted movements and prepare upper motor neuron circuits for the initiation of movements. Disorders in the basal ganglia, such as Parkinson's disease and Huntington disease result in the initiation of voluntary movements. [Difference cerebellum and basal ganglia:] The basal ganglia system ensures that the correct movements are initiated and maintained, while unwanted movements are suppressed (Klaus et al., 2019). In contrast, the cerebellum guarantees that movements take place in a smooth and coordinated way. Basal ganglia and cerebellum have no direct access to the local circuit, but they control movement by regulating the activity of the upper motor neurons. The anatomical location of a motor neuron pool is discovered by retrograde tracing: a tracer is injected into a particular muscle. The tracer is transported back to the spinal cord via the innervating axons and stains the cell bodies of the motor neurons. The stained cell bodies are then visualized in anatomical cross section. Two mechanisms at motor-neuron level to regulate muscle force: - Increasing or decreasing the number of motor units active at any time (through recruitment) - Modulation of the firing rate of each recruited motor unit Order of recruitment: 1. Small motor units with slow-type muscle fibers 2. Larger motor units with fast fatigue-resistant fibers 3. Large motor units with fast fatigable fibers LE motor units, spinal reflexes and muscle coordination ------------------------------------------------------- The ability of a muscle to produce a certain amount of force is dependent of its length. If its stretched out it cannot produce force, but if its compromised it also cannot exert any force. Three types of motor units: - Slow (S): - Small twitch response, small amount of force being generated, but you can do this endlessly, they will not fatigue - Fatigue Resistant (FR): - More force than small response, and fatigue in between slow and fast fatigable. - Fast Fatigable (FF): - Generated a lot more force, but are fast fatigue [Motor unit activation] Not fast fatigable: rely on oxygen use, so red muscle fibers. Recruitment of motor units according to the size: small motor units slow, will be recruited faster than large, fatigue motor units. [Motor unit coordination] Redundancy: muscles act across multiple joints/contribute to multiple degrees of freedom. [Reflexes]: - Stretch reflex (short loop reflex): when muscle is stretched 1a - Golgi tendon organ reflex: sense the amount of force on the tendon 1b, via interneuron inhibiting the motor neuron - Long loop reflex: ascending fibers, via the somatosensory cortex, back via the motor cortex to the descending fibers. Original signal comes from the proprioceptive sensors (both muscle and golgi tendons) LE concepts and techniques in neuromuscular disease + LE concepts and techniques in clinical EMG ------------------------------------------------------------------------------------------------ Neuromuscular disorders: disorders affecting a part of the peripheral nervous system Symptoms: - Weakness ('paresis') - Delayed motor milestones during development - Hypotonia ('floppy infant') - Low or absent muscle stretch reflexes - Muscle atrophy - Diminished cutaneous sensation ('hypesthesia')  NMD categories: - Spinal cord/anterior horn cells - Spinal muscular atrophy - Amyotrophic lateral sclerosis (ALS) - Nerve roots - Hernia nuclei pulposi - Guillan-Barré syndrome - CIPD - Brachial and lumbosacral plexus - Neuralgic amyotrophy - Peripheral nerves - Polyneuropathy - Carpal Tunnel Syndrome - Neuromuscular junction (measure with single fibre EMG (SFEMG)) - Myasthenia gravis - Lambert Eaton myasthenic syndrome - Muscle - Congenital or metabolic myopathies - Muscular dystrophies (Duchenne) Als zenuwvezels of spiervezels niet meer worden aangestuurd, worden ze spontaan actief: - Fasciculaties: motore zenuwvezel / motor unit niveau - Fibrillaties: spiervezel niveau NMD, diagnostic approach: - Clinical investigation: - History taking - Ask for symptoms of weakness and sensory abnormalities - Age of onset, rate of progression - Family history - Physical examination: - Severity and distribution of weakness - Sensory involvement and distribution - Tendon reflexes, muscle tone, contractures - Laboratory parameters : - Blood testing for : - CK level - Auto-antibodies against Ach receptors, nerves - Lactate and other metabolic enzymes - Exclusion of other internal disorders causing weakness (thyroid function, electrolytes) - Cerebrospinal fluid testing for: - Increased protein levels, increased cells - Urine testing for: - Metabolic enzymes - Muscle imaging - For charting muscle pathology distribution and selective involvement of muscle groups - Can be made with: - Ultrasound - Computed tomography (CT)p - Magnetic resonance imaging (MRI) Clinical methods for NMD - Nerve conduction studies - Needle electromyography - Stimulated single fiber EMG and repetitive nerve stimulation EMG is actually a combination of 2 techniques: - Nerve conduction studies - Needle examination of muscles - Contraindications: - Measuring nerves in open wounds - Limb not accessible - Blood coagulation disorder **Nerve conduction studies** - [Helpful for localization:] - Differentiate between pathology of nerve root vs plexus or peripheral nerve - Differentiate between mono- vs polyneuropathy or mono- vs polyradiculopathy - [Helpful to determine type of pathology:] - axonal vs demyelinisation - Surface electrodes - Unvoluntary supramaximal nerve stimulation - Measuring: - Motor nerves, with electrodes on target muscle - Sensory nerves, with electrodes on the skin - Proximal nerve segments, with H-reflexes and F-responses - Important for nerve conduction = temperature. Should be \>30 degrees. Otherwise lower NCV's (nerve conduction velocities) and higher SNAP amplitudes - Also important = sufficient current for supramaximal nerve stimulation. Otherwise too low maximum amplitudes, which gives false positive results. - Watch out for patient safety: - Ground both patient and bed make sure no leak current can go through the body - Stimulation with routine ECG = up to 100 mA for 1.0ms - 20mA through the heart can kill you Results from nerve conduction studies: - CMAP compound muscle action potential - SNAP sensory nerve action potential - Neuropathy or plexopathy: reduced/absent CMAP [and] SNAP - Radiculopathy: reduced/absent CMAP only! - Parameters: - Amplitude - Lower CMAP/SNAP amplitude in axonal injury - (distal) latency - Distal motor latency (DML) = time it takes for a nerve signal to travel from a point of stimulation to a specific muscle. - Prolonged in demyelinisation - Nerve conduction velocity - Lower in demyelinisation - Dispersion - Normal velocities: - Fasted myelinated fibers: 61 m/s - Smallest myelinated fibers: 19 m/s - Unmyelinated fibers: 1.6 m/s **Repetitive nerve stimulation (neuromuscular disease, myasthenia gravis + Lambert Eaton myasthenic syndrome)** - Extension of motor nerve conduction study - Instead of single stimuli a train of 10-20 - Tests safety threshold of neuromuscular transmission - If transmission fails (e.g. in myasthenia), the resulting CMAP will be lower with the 4^th^ stimulus than the 1^st^ (\>10%) **Needle EMG (Polyneuropathy in peripheral nerves + Congenital or metabolic myopathies in muscle)** - [Helpful for localization:] - Differentiate between neurogenic pathology or myopathic pathology - Detect which muscles or nerve roots are affected - Detect if multiple regions are affected (motor neuron disease) - [Helpful to differentiate between 'ongoing' or 'old' neurogenic pathology] - Denervation (spontaneous muscle activity) vs reinnervation (reconnection of motor units to disconnect muscle fibers) - Denervation = disconnection between motor-unit and muscle - Reinnervation (follows after denervation) = other motor units will take over function and reconnect to muscle fibers (after few weeks) - Changes in motor unit action potential (MUAP): larger amplitude, longer duration, polyphasic phase - Needle electrode - Voluntary stimulation - Measuring: - Motor neuron loss (neuropathy) or muscle fiber loss (myopathy) - Spontaneous activity in rest due to nerve denervation or muscle cel degeneration - Abnormal changes in the shape of the motor unit action potential due to a neuropathy or myopathy - Important: - Inform the patient on what's going to happen - Ensure correct relaxed posture of limb / body - Careful in case of coagulation disorder - 'listening is easier than looking' - Examine the intended muscle: know your anatomy   H-reflex : stimulation of sensory nerves, low stimulation Higher stimulation: motor fibers are also stimulated, +M response Radiculopathy: - Low CMAP - Absent H-response - Normal SNAP F-wave reflex: estimation of total time from stimulation, through spinal cord to the muscle. F estimate = 2X + Y + Z LE introduction to central movement disorders --------------------------------------------- Neurodegenerative diseases: - [Symptoms] underly the problems that the patient experiences - Stumbling / later: Loss of fine motor control - Dysarthria speech problems - [Signs] are the clinical things that the physician can recognize in the symptoms - Spasticity sign = hyperreflexia ALS = motor neuron disease Auto-immune diseases of the CNS are of scientific interest nowadays. When an ataxia is not acquired and not neurodegenerative and there is no genetic abnormality identified: ILOCA = idiopathic late onset cerebellar ataxia  The right picture was a person with parkinson's disease, because there's less substantia nigra  Movement disorders, main categories: - Too little movement - Akinesia (absence of movement) - Bradykinesia (slowness of movement) - Hypokinesia (abnormally decreased movement) - Too much movement - Chorea (involuntary movements that are abrupt, unpredictable and nonrhythmic, resulting from a continuous random flow of muscle contractions) - Myoclonus (sudden, brief, shock-like involuntary movements) - Tics - Tremor - Dystonia (abnormal characteristic postures and movements, produced by slow sustained muscle contraction) - Abnormal movement - Ataxia (poor muscle control that causes clumsy movements) - Disturbed balance - Spasticity SSA3 upper motor neuron control of the brainstem and spinal cord ---------------------------------------------------------------- Corticobulbar tract: - Descends from the lateral region of the primary motor cortex to the bulbus (= medulla oblongata in the brain stem) Corticospinal tract: - Descends from the more dorsal and medial parts of the cortex to motor neurons and interneurons in the spinal cord. - Controls movements of the limbs and trunk Both tracts originate from Betz cells, which are large pyramidal cells in the motor cortex. Advantages unilateral and bilateral innervation: - Bilateral: when 1 side of the cortex or descending nerves are damaged, there is still innervation from the contralateral side, so there is no loss of function. - Unilateral: independent control of distal muscles in our arms and legs which allows us to control left and right limbs separately. [Direct pathways] are responsible for movements in distal limbs with high degree of precision and [indirect pathways] are responsible for movements of the core body and course motor control. [Lateral system] (of the spinal cord and brainstem) controls the distal muscles of the limbs. [Ventromedial system] controls the axial muscles of the trunk and the proximal limb muscles.  **Lateral system: (fine motor tasks)** - [Corticospinal tract] fine voluntary movements of body and limbs - [(cortico)rubrospinal tract] voluntary movements, mainly in limbs (less important than corticospinal) **Ventromedial system: (stepping, posture)** - [(cortico)reticulospinal] tract movements and postural control in trunk and proximal limbs - [Vestibulospinal tract] maintain head and eye coordination, posture and balance, conscious realization of spatial orientation and motion - [Tectospinal tract] coordination hand and eye movements Conclusion experiment monkey to determine the function of a single motor neuron in the motor cortex: - A single motor neuron controls a movement, but rather imprecise - Every single motor neuron has a preferred movement direction - Multiple neurons work together, in which the average of all preferred movements determined the actual movement direction Lateral premotor cortex: movements based on [external events] Medial premotor cortex: movements based on [internal cues] Spinal shock: hypotonia after upper motor neuron injury (often spinal cord injury / dwarslaesie), because of decreased activity of spinal circuits and suddenly deprived input from motor cortex and brainstem. Symptoms in disease of the peripheral neurons and central motor neurons: - Babinski sign stroking foot sole induces extension of big toe and fanning of the other toes instead of flexion of big toe and often others - Spasticity increased muscle tone, hyperactive stretch reflexes and clonus - Hyporeflexia / superficial reflexes decreased vigor of superficial reflexes - Loss of ability to perform fine movements Muscle tone = resting level of tension in a muscle tone, depends on resting levels of discharge of alpha motor neurons. This allows a muscle to make an optimal response to voluntary/reflexive commands. LE population coding in the motor cortex ---------------------------------------- Subcortical structures: cerebellum and basal ganglia How is the primary motor cortex organized: Homunculus How is information coded by a single neuron: membrane potentials and action potentials by depolarization.  TMS/tDCS: helps localize where the lesion is. Stimulation at the brain / spinal cord for example and see when there's a reaction or not. Function of a single neuron in the motor cortex: - Neural encoding: how neurons respond selectively to stimuli. - Neural decoding: how information can be extracted from neurons. - Vector summation: intenser firing = longer vector Anatomy motor cortex: Area 4: - M1 = primary motor cortex Area 6: - PMA = premotor area - SMA = supplementary motor area PD = preferred direction of the neuron for which it fires most. The magnitude of the contribution of the cell depends on its firing rate. WG central neurological movement disorders ------------------------------------------ Video 1: grote onwillekeurige bewegingen Huntington's Video 2: tremor in de linkerhand in rust parkinson's Video 3: chorea links en rechts dyskinesia in Parkinson's Video 4: dystonie beiderzijds dystonie door kernicterus Video 5: dook ineens ineen, hoofd schudden functional movement disorder Video 6: twee kanten, kan armen niet goed omhoog houden, been ook niet (iets met spierzwakte) negative myoclonus Video 7: vingers op elkaar gaat sloom, beweging wordt kleiner bradykinesie Video 8: heel traag handen openen, maar beweging werd niet kleiner slowness not bradykinetic Video 9: voelt trilt, reflexen aanwezig bipiramidaal syndroom Video 10: vinger volgproef gaat niet goed cerebellair syndroom Video 11: spasmen, kan handen niet stil houden myoclonic (muscle spasms) ataxia (speech and eye) Video 12: hoofd trilt, kan wel handen stilhouden dystonie door tremor Een negatieve myoclonie is een schok die ontstaat doordat de spieren eerst ontspannen en daarna aanspannen. Progressieve myoclonus ataxie is een zeldzame bewegingsstoornis wat vaak al op kinderleeftijd begint, waarbij mensen last hebben van zowel spierschokken (myoclonus) als coördinatiestoornissen (ataxie). Dyskinesia is the involuntary movement of a body part or the entire body that you can\'t control. Dystonia is the involuntary stiffening or contraction of a muscle. SSA cerebellum and movement coordination ---------------------------------------- Three main subdivisions of the cerebellum: - **Vestibulocerebellum:** - Input: vestibular, visual - Output: vestibular nuclei - Function: balance control and compensatory eye movement reflexes - Signs: - Ataxia - Imbalance with eyes closed - Nystagmus - **Spinocerebellum:** - Input: somatosensory, proprioceptive, acoustic, visual - Output: lateral & medial motor system - Function: muscle tone and fine-tuning of movement execution - Signs: - Hypotonia - Dysmetria (no smoothly coordinated movements) - **Cerebrocerebellum:** - Input: cerebral cortex, copy of motor commands - Output: back to motor and premotor cortex - Function: initiation/timing of skilled movements - Signs: - Clumsiness, tremor, slow initiation - Timing problems Three fiber bundles that carry the input and output of the cerebellum: - **Inferior cerebellar peduncle:** - [Afferent] fibers from the medulla - Efferents to the vestibular nuclei - **Middle cerebellar peduncle:** - [Afferents] from the pontine nuclei - **Superior cerebellar peduncle:** - [Efferents] from the cerebellar nuclei - Afferents from the spinocerebellar tract The inputs arise from the [ipsilateral] side of the body, and the outputs also go to the [ipsilateral] side of the body. The outputs of the cereberocerebellum to the red nucleus and the thalamus need to cross on their way to the motor cortex and premotor cortex. This is because the cerebellum modulates movements on the ipsilateral side while the cortex is involved in controlling the contralateral side of the body. **Elements of the circuit**: - Mossy fibers - Granule cells - Parallel fibers - Purkinje cells - Climbing fibers Direct path: - Input via deep cerebellar nuclei directly to motor systems Indirect side-loop: - Mossy fibers input to granual cells - Via parallel fibers to Purkinje cells - And back again to deep cerebellar nuclei Climbing fiber input: - From inferior olive to Purkinje cells - Related to [reflex] adjustments Output inhibitory (GABA): - Only from Purkinje cells **Simple spike:** Can only occur when there are many [parallel fibers] inputs. Each input yields only a small EPSP. **Complex spike:** Each input from the [climbing fiber] produces a series of spikes  Supportment for hypothesis that the cerebellum is involved in motor learning: - Adaptation of the Vestibulo-ocular reflex - Adaptation of e.g. darts throwing after wearing prism glasses depend on the cerebellum Marr-Albus-Ito theory: the [flocculus] of the vestibulocerebellum is important in the plasticity of the vestibulo-ocular reflex (VOR): Granule cells receive signals from the semicircular canals about head rotation velocity. These signals are transmitted to the Purkinje cells via the parallel fibers. Climbing fibers come from the dorsal cap of the inferior olive (IO), and signal visual slip on the retina. Since this retinal slip signal is an error signal about VOR performance (it represents the difference between eye and head velocity), it is ideally suited as to alter the strength of the synaptic connections between parallel fibers and Purkinje cells, and thus alter the VOR gain to improve performance. The plastic synapses are the synapses between the parallel-fibers and Purkinje cells. Consequences of cerebellar lesions vs movement disorders in basal ganglia: - Cerebellum: - Ataxia: can initiate movements but they are not accurate - Intension tremor: when trying to move, no tremor at rest, sway while standing - Hypotonia - Symptoms improve with time - Basal ganglia syndromes (Parkinson's disease) - Akinesia: resistance when initiating voluntary movements, need an external sensory trigger to initiate movement - Bradykinesia: slow movements - Tremor at rest - Rigidity (stijfheid) - Symptoms usually get worse If symptoms of dizziness disappear after three days, is the problem that caused the dizziness really gone? - No, not necessarily. The cerebellum may have learned to cope with the problem e.g. by reweighting of the vestibular versus proprioceptive inputs. LE cerebellum dependent motor learning -------------------------------------- Subdivisions of the cerebellum: - Three major subdivisions of the cerebellum: - What movement disorders are associated with each of them: - Cerebrocerebellum: - Spinocerebellum - vestibulocerebellum Dysmetria: muscles work not proportional. Can result in hypermetria or hypometria (pointing your finger too far forward or not far enough) Right side of the vestibulocerebellum: controls movement of the right side cerebellum controls movement of the ipsilateral side of the body Medial side controls bilateral, both right and left side of the axial muscles Left motor cortex is sending signals to the right side of the cerebellum. The crossing is in the brainstem. The cerebellum only communicates to the motor cortex, not directly to the spinal. Right side of the motor cortex left side of the cerebellum right side of the motor cortex left side of the body. Mossy fibers contact to granule cells, they communicate to parallel fibers, which are parallel to the cerebral cortex. They send information to the dendritic tree of the Purkinje cells. These cells are the only output type neuron of the cerebellar cortex, projecting information to the CN, cerebellar nucleus. These signals are always inhibitory. On the other side, climbing fibers are communicating to the dendritic tree of the Purkinje cells. LTD: long term depression: the stronger the error of the visual learning signal, the more the synaptic path of the waiting of the input has to adjust. SSA basal ganglia and movement disorders ---------------------------------------- The corpus striatium is an input zone for the basal ganglia. The corpus contains medium spiny neurons. They get information from: - the cortical pyramidal neurons - the local circuit neurons - the dopaminergic neurons  Nucleus caudatus and the putamen are some of the regions in the corpus striatum, differences between them are: - caudate is linked to the control of orienting movements of the eye's head and body, while putamen is for the control of limb and trunk movements - caudate influences activity in the superior colliculus (SC), while putamen influences activity in the (pre)motor cortex - many caudate neurons modulate their firing rate in relation to saccadic eye movements, while the activity of neurons in the putamen are linked often to movements of the arm and other parts of the body All output of the basal ganglia is **inhibitory**. The globus pallidus externa and the nucleus subthalamicus are in the indirect pathway. The function of this pathweay is to suppress unwanted movements.  In parkinsonism, the stimulation of the glocus pallidus internal by the subthalamic nucleus (STN) is increased, which causes more tonic inhibition of the the VA/VL complex and a decreased excitation of the motor cortex. However, when lesioning the STN, the increased stimulation of the globus pallidus internal decreases which eventually results in a decrease of the hypokinesia. **Primary motor symptoms** of Parkinson's disease: - tremor - rigidity - postural instability - bradykinesia (gradual loss and slowing down of spontaneous movement) **Secondary motor symptoms:** - freezing of gait - unwanted accelerations - speech difficulty - stooped posture (body leans forward and the head may be slightly turned down) - dystonia - impaired fine motor dexterity - poverty of movment - difficulty swallowing - cramping - sexual dysfunction LE modulation of movement by the basal ganglia ----------------------------------------------  Striatum = input station GPi = output station Indirect and direct pathway between those two Dopamine has effect on direct (stimulation) and indirect (inhibition) pathways Gaiting proper initiation of movement: more of selection of the higher level of motor control. Reaction time: delay between the signal and the start of the movement. EMG provides you with a continue measure instead of a point measure with reaction time. Parkinson: deficient dopaminergic stimulation of the SP **Most important slide:** Not important:  SSA movement and cognition -------------------------- Symptoms resulting from a lesion at the border between the parietal and frontal lobe in the **right** hemisphere: - contralateral neglect syndrome. inability to perceive and attend to objects / own body in a part of space, despite the fact that visual acuity, somatic sensation, and motor ability remain intact. - Affected individuals fail to report, repond to, or even orient to stimuli present on the other side of the body. - They may also have difficulty performing complex motor tasks on the neglected side of the body Symptoms resulting from a lesion at the border between the parietal and frontal lobe in the **left** hemisphere: - Often associated with Wernicke's aphasia ability to grasp the meaning of spoken words and sentences is impaired, while the ease of producing connected speech is not very affected. Sub-types of hemi-neglect: - Allocentric spatial deficits - Egocentric spatial deficits - Object centered neglect - Representational neglect Difference neglect and agnosia: - Neglect: patients fail to be aware of items to one side of space - Agnosia: patients are able to acknowledge the presence of the stimuli, but cannot identify them. - [Apraxia]: patient has difficulty with the motor planning to perform tasks or movements when asked, although the request or command is understood and he/she is willing to perform the task. **Executive dysfunction:** cognitive, emotional and behavioural difficulties which often occur after injury to the frontal lobes of the brain. Split-brain patients: - Will be unable to [say] he sees a word presented exclusively in the left visual field, but he will be able to pick out the object corresponding to the word by touch alone with his left hand. Can be explained by: - 1\) the image seen in the left visual field is sent only to the right side of the brain - 2\) for most people, the speech-control center is on the left side of the brain - 3\) communication between the two sides of the brain is inhibited. - Thus the patient cannot say out loud the name of the object, but the visual information does reach the right cortex, and the right motor cortex is controlling the left hand. Mirror neurons: Neurons that discharge when a subject performs a goal-related action himself AND when the subject observes another individual performing a similar kind of action. Theories for the role of mirror neurons: - Understanding goals and intentions - Facilitation of learning - Involved in empathy - Human self-awareness - Problems with the mirror neurons system may underlie cognitive disorders, particularly autism LE movement and cognition ------------------------- What is cognition: - ability to: - attend to external stimuli and internal motivation - identify the significance of stimuli - make meaningful responses - the 5 association cortices are responsible for this complex processing - **occipito-temporal network for object/face recognition** - retino-cortical pathway: path from eye to brain, important for perception - left visual field is projected to the right primary visual cortex - from the primary visual cortex are two cortical pathways: spatial vision pathway & object recognition pathway - ventral pathway = [WHAT-pathway] - Lesions of temporal association cortices: - Agnosia: - Patients are able to acknowledge the presence of the stimuli, but cannot identify it - Prosopagnosia - Inability to recognize faces - Ability to identify other objects and subtle shapes differences might be unaffected. Also persons might still be recognized by voice, body shape and gait - **Parieto-frontal network for spatial attention** - The [WHERE-pathway] - the parietal lobe is specialized in processing of information about locations (locations relative to my body) - categorical relations (mouse is right from the keyboard) - metric or coordinate relations (in cm etc.) - hemi neglect syndrome: failure to respond or orient to novel or meaningful stimuli presented to the side opposite a brain lesion, when this failure cannot be attributed to either primary sensory or motor deficits. Neglect can be spatial or personal - doesn't matter if patients look with one or two eyes, because both the left and right eye have a left visual field and a right visual field. - Mainly the right hemisphere that has a lesion. Because the right parietal lobe is paying attention to both left and right visual field, but left parietal lobe only focuses on the left visual field, so a lesion in the left hemisphere is not as severe as in the right parietal lobe. - **Medial temporal/limbic network for learning and memory (skip in this module)** - **Left perisylvian language network** - Broca's area. Broca's aphasia is usually associated with lesion to the left frontal cortex problems with motor side of speech and writing - Wernicke's area. Wernicke's aphasia is often associated with lesions at the boundary of the superior temporal and parietal lobes on the left hemisphere. Sensory lesion, you are able to write and talk, but it doesn't make sense. - **Prefrontal network for attention and comportment** Primary motor cortex: - Executes motor movements - Damaged motor cortex results in weakness and imprecise fine motor movements Supplementary motor area :BA6 Libet experiment: - Premotor areas is measured - Person voluntary, at his own pace, presses the button - Additional trick: ask the participant to recognize at which time he decides to press the button **Apraxia**: - Inability to perform skilled, sequential, purposeful movements - This inability cannot be accounted for by disruptions in more basic motor processes such as muscle weakness, abnormal posture or tone, or a movement disorder. - Two pieces of evidence that apraxia is a higher order disorder: - It occurs bilaterally - Individuals can perform behaviors spontaneously but not when imitating someone or on verbal command - Ideational apraxia: difficulty in performing a movement when the idea of the movement is lost - Occurs when individuals can perform simple one-step movement but not multistep movement - Individual is unable to plan movements related to interaction with objects, because they have lost the perception of the object's purpose - iemand kan aansteker aanmaken, maar niet bedenken om dan de kaars aan te steken - Ideomotor apraxia: difficulty in performing a movement when a disconnection occurs between the idea of movement and its execution - Simple movements of an abstract nature are most affected **Mirror neurons** The cell doesn't care about the effector, but about the purpose of the movement.