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Motor System
본 3 신경과학
신형철 교수
1. Reflex-controlled MovementsKnee Jerk, withdrawal from HOT stuff, reflex
Stimulus---> automatic, repetitive, stereotyped responses
Spinal Cord is important Ex: decerebrate frog: a) pinch to hind foot---> pulled awayb) noxious stimulation to frog's back---> response with hind foot Corneal reflex , coughing , swallowing, food propel, breathing , blood flow etc.
Stimulus-Response theory of behavior: Combinations of reflex---> complex behaviours
2. Program-controlled (automatic) movements walking (newborn baby: 12-18 month, independent), running , crawling breathing, chewing
species specific fixed action pattern (nesting, tunneling, urination, etc)
learned programs: sport, work, typing, drawing, driving enough practice--->automatic. central programs can be influenced by sensory feedback.
Program theory of behavior without any external sensory inflow (stimulus independent, innate, inherited, spontaneous, voluntary (initiation & termination), rhythmic motor pattern)
Movements
3. Voluntary & involuntary movements
Voluntary: Purposeful, goal directed, learned Learning sports skills, speech, writing, After learning---> automatic (program-controlled movements)
Involuntary: highly stereotyped reflex, learning unnecessary
4. Postural & goal-directed functions
Intrapersonal: posture (standing, sitting, lying, balance) orientation in space Extrapersonal: goal-directed
•intimate interlinkage between postural & goal-directed movements
Control: feed back: slow movement, object touch, feed forward: rapid movement, catching ball
Three levels in hierarchy of motor control
1) motor areas of cerebral cortex - top of hierarchy *3 major areas, all in frontal lobe
a) primary motor cortex - executes commands to motoneurons b) premotor cortex c) supplementary motor cortex
*all three project directly to spinal cord via corticospinal tract *premotor and supplementary motor cortex (b & c) also project to pri
mary motor cortex and are important in coordinating and planning complex sequences of movement (motor learning)
2) brain stem *important nuclei include reticular formation, vestibular nuclei and inf
erior olivary complex *axons project and regulate the segmental networks of spinal cord *brains stem integrates visual and vestibular information with somat
osensory input to modify movements initiated by cortex
3) spinal cord - neurons mediate automatic reflexes (e.g., stretch reflex)
Two important subcortical systems which act on cortex via the thalamus
1) cerebellum - receives input from spinal cord -projects to both brainstem and thalamus (and onto cort
ex) -improves accuracy of movement (by comparing descen
ding motor commands with information about resulting motor action; thus important in learning)
2) basal ganglia -receives inputs from all cortical areas (not just motor) -projects to thalamus and then to areas of cortex involv
ed in motor planning -diseases of BG produce range of motor abnormalities i
ncluding hypokinesia and hyperkinesia, Parkinson’s disease
Concept of upper and lower motor neurons (Sherrington) lower motor neurons - motoneurons of brainstem and spinal cord which directly innervate skeletal muscle ("final common pathway")
- symptoms of lesions: 1) muscle tone reduced or absent (flaccid paralysis) 2) stretch reflex weak or absent 3) muscle atrophy 4) fibrillation (observed by EMG)
- common causes: poliomyelitis ( 척수성 소아마비 ), nerve lesion - can be mimicked by systemic diseases of nerve end-plate (e.g., myasthenia gravis) or muscle (e.g., dystrophy, myopathy
upper motor neurons - all descending pathways of the brain and spinal cord involved in volitional control of the musculature
- include vestibulospinal (postural) , reticulospinal and corticospinal - unsatisfactory term for research as too inclusive but useful clinically to distinguish from lower motor neuron
- symptoms of lesions 1) voluntary movements of affected muscle absent or
weak 2) tone of muscle is increased (spasticity) 3) atrophy minimal initially 4) alteration of reflexes
common causes include infarctions of the following regions: posterior limb of internal capsule, primary motor and premotor cortex
Schematic representation of the upper motor neuron system and the muscle motor-sensory unit. 1: motor cortex; 2: basal ganglia; 3: cerebellum; 4: red nucleus; 5: reticular formation; 6: lateral vestibular nucleus; 7: axons from extrapyramidal neurons; 8: intertesial neurons; 9: alpha motor neuron; 10: gamma motor neuron; 11: dorsal ganglion cell; (A) brain; (B) cerebellum; (C) brainstem; and (D) spinal cord.
Treatment 1. Physical Therapy & Exercise 2. Medications 3. Spine Surgery 4. Is a cure possible?
Consequences of spinal cord injury
Cells from the immune system infiltrate the area of primary injury, which expands for several days as local pathological processes continue in a cascade of secondary injury.
The primary and secondary injuries cause the death of neurons and oligodendrocytes, resulting in
the disruption of synaptic connections and the demyelination of axons.
Demyelination of surviving intact axons greatly impairs action potential message conduction, and can render remaining connections useless.
By several weeks after the initial injury, the area of tissue damage has been cleared away by microglia from the CNS and macrophages from the immune system, and a fluid-filled cavity surrounded by a glial scar made up of astrocytes is left behind.
Molecules that inhibit regrowth of severed axons are expressed at this site. This fluid-filled cavity,
called a syrinx, now forms a barrier to the reconnection of the two sides of the damaged spinal cord.
a surprising amount of the basic circuitry to control movement and process somatosensory information can remain intact.
because the spinal cord is arranged in layers of circuitry. Many of the connections and neuronal cell bodies forming this circuitry above and below the site of injury survive the trauma.
The goal of spinal cord injury research is to reconnect the wiring that controls muscle movement a
nd provides sensory information to the brain.
can neurons in the spinal cord regenerate and make not only new connections, but the correct connections ?
Why doesn't the nervous system regenerate very well?Many cells of the CNS, especially neurons, are so specialized that they have lost this ability to divide and generate new cells. As a result, injury to the brain or spinal cord isn’t easily repaired by replacing the cells that have been injured or have died with new ones.
Key Intervention Strategies for the treatment of spinal cord injury
Acute intervention strategies to limit degeneration that occurs immediately after an injury. More long-term intervention strategies involve regenerative and reconstructive approaches to promote rebuilding and reconnection of the injured cord.
1) Limit initial degeneration: primary necrosis, excitotoxicity, and apoptosis.2) Treat inflammation: Swelling and inflammation may foster secondary damage to the cord after the initial injury. Enhancement of axonal regrowth, the correct targeting of axons (path finding), the formation of functional neuronal connections (synapses), and remyelination. 3) Stimulate axonal growth: Neurotrophins such as NT-3 and BDNF can both promote cell survival by blocking apoptosis and stimulate axonal growth. Each neurotrophin has very specific target cell functions. (4) Substrate or guidance molecules to promote new growth (5) Block endogenous inhibition of regeneration: (6) Supply new cells to replace lost ones: Stem cells, which are isolated from the CNS and can divide to form new cells, may make it feasible to replace lost neurons and glia. (7) Build bridges to span the lesion cavity
The motor unit = a motor neuron + the muscle fibers it innervates.
A muscle cell is innervated by only one neuron. An alpha motor neuron may innervate many muscle fibers (3-2000).
The fewer fibers involved, the finer the muscle control will be. Cell bodies for the alpha motor neurons are located in the spinal cord.
Acetylcholine is the neurotransmitter between the motor neuron and the muscle cell, and the muscle cell has nicotinic receptors.
Polysynaptic Reflexes
Most of the reflexes are polysynapticSensor is remote from effectorautonomic reflexes, polysynaptic somatic reflexes.
Characteristics of polysynaptic reflexes, ex: coughing a) presence of delay periodb) Summation of the subthreshold stimulus in central neurons & motorneurons of the reflex arc.c) Reflex time & intensity of response depend on the stimulus intensity.d) plasticity of the reflex response, habituation, dishabituation, sensitization, conditioning (long-term changes in the reflex response)
Recurrent inhibition & presynaptic inhibition in spinal motor systems
Motor neuron--->excite muscle--->excite Renshaw cells (inhibitory interneuron)---> feedback inhibition on the same Motor neuron. Function: to prevent an uncontrolled oscillation of motor neuron activity (increased muscle tone (spasticity) may be caused by Renshaw cell malfucnction)
The Propriospinal System & the Capabilities of the Isolated Spinal Cord
1) Intersegmental reflex connections by Propriospinal neurons & propriospinal tracts (fore- & hindlimbs, neck & limb movements) 2) Spinal LocomotionBasic pattern of locomotion, programmed at the level of the spinal cord.
3) Spinal Shock Reversible motor & autonomic areflexia following spinal cord section (local cooling, local anesthesia) many months in humans, few minutes in frogs, hours in carnivores, days or weeks in monkeysMechanisms responsible for the return of certain spinal function : not konwn
Types of Myasthenia GravisDrug RelatedViral/BacterialTransient NeonatalAdult-OnsetExperimental Autoimmune
Schematic diagram of an intracellular muscle fiber recording showing the generation of end-plate potentials (EPPs) and muscle fiber action potential (APs).
On the left, normal neuromuscular junction function ensures that the rise time and amplitude of successive EPPs are sufficient to generate APs. Note the fluctuating threshold for generating an AP and resultant variability of the AP latency. This is normal jitter.
On the right, in myasthenia gravis, there are insufficient acetylcholine receptors and the EPP rise times and amplitudes vary markedly. This results in increased jitter and at times failure to initiate an AP This is called blocking.
Cortex Stimulation
Wilder Penfield, a Canadian surgeon, exploratory voyage of the brain's organization starting in the 1950s.
epileptic patients (awake), electric currents to the brain's surface in order to find problem areas.
trigger whole memory sequences.
familiar song that sounded so clear
any movement of the patients' bodies. From this
information, he was able to map out the motor cortex
http://www.pbs.org/wgbh/aso/tryit/brain/#
fMRI of the motor cortex, overlaid upon a standard high resolution data set. Finger oposition task at 2Hz. p < 0.05
[Efferent connection]
1)Corticospinal tract (Pyramidal Tract), at spinal cord, cortical control of segmental reflex circuit
2)The axons from the giant Betz cells send short collaterals back to the cortex itself; inhibit adjacent regions of the cortex when the Betz cells discharge--> sharpening the boundaries of the excitatory signal
3)To Caudate nucleus and putamen
4)To Red nucleus
5)To Reticular formation and Vestibular nuclei
6)To Pontine nuclei
7)To Inferior olivary nucleus
[MI Afferent connection]
1) Subcortical fibers from adjacent regions of cortex (somatic sensory areas of the parietal cortex, frontal areas, visual cortex, auditory cortex)
2) Subcortical fibers that pass through the corpus callosum from the opposite cerebral hemisphere.
3) Somatic sensory fibers derived directly from the ventrobasal complex of the thalamus;transmit mainly cutaneous tactile signals and joint and muscle signals.
4) Tracts from the ventrolateral and ventroanterior nuclei of thalamus ;coordination between the functions of the motor cortex, basal ganglia, and the cerebellum
5) Fibers from the intralaminar nuclei of the thalamus;control the general level of excitability of the motor cortex
Rubrospinal tract
Recent evolutionary adding than medial systemOrigin: Red Nucleus (magnocellular portion) in the midbrain. Termination: propriospinal neurons, lateral motor neurons, lateral interneurons Function: fine movements, distal muscles (flexors) reaching, manipulating objects with fingers & hand
* in human, the remnant of rubrospinal tract, function carried by corticospinal system
The Supplementary Motor Area (SMA) The neural activity increase in the SMA especially in relation to complex movements.
Increased activity in the SMA is not related to the movement itself, since it is sufficient that the person imagines the goal directed performance of a fairly complex movement. In such case there is no increase of activity in M1.
Recording of single-cell activity in the SMA has shown that many cells change their activity in relation to sensory stimulus (light, passive movements, etc) that the animal knows its signal to start a certain voluntary movement.
The SMA is important for organizing and planning fairly complex movements and for mediating an appropriate motor response to sensory stimuli.
The Premotor Cortex (PM), largest part of area 6.
Sends fewer fibers to the spinal cord than SMA but has strong connections with the RF, red nucleus, basal ganglia. It has important projection to M1.
The PM is important for the control of visually guided movements, such as the proper orientation of the hand and fingers when they approach an object to be grasped.
After damage to the M1, the handling of an object is clumsy and insecure, but the ability to avoid an obstacle is not lost. Connections from the extrastriate areas in the occipital lobe to the PM are necessary for the ability to perform such goal directed movements.
In agreement with the above observations, single-cell recordings show that many cells in the PM change their activity about 60 msec after a light signal that the monkey is trained to respond to with a certain movement.
In the acute stage after a stroke, patients with lesions of the SMA reach out and grasp objects with the affected arm, even when they have been told to refrain from moving.
This alien hand syndrome reflects a dominance of externally guided lateral PM pathways. The sight of an object within reaching distance evokes a motor plan to grasp an object. We usually can inhibit movement if we are instructed to do so or if the movement is inappropriate. But when internal control sources are removed, the movement can be triggered by appropriate external stimulus.
Posterior Parietal Cortex
Many neurons are active in relation to movements in the posterior parietal cortex (area 5, 7).
One kind of neuron is active before goal-directed, reaching movements, such as when a monkey stretches its hand toward a banana. Such neurons do not become active, however, in relation to movement in the same direction but without a specific aim, or in relation to a passive movement.
Other kinds of neurons increase their activity in relation to exploratory hand movements, such as when a monkey studies a foreign object.
In area 7, some neurons increase their activity only when the monkey stretches the hand toward an object that it also looks at.
In humans, lesions of the posterior parietal cortex may, for example, make them unable to open a door or to handle previously familiar tools. Such persons also have difficulties with proper orientation of the hand with relation to an object, and they easily miss an object even though they see it clearly. This kind of symptom is called apraxia.
Recent studies, using both single-cell recordings with primates and brain imaging techniques suggest that parallel circuits may be involved in motor planning. One circuit, including the parietal lobe, lateral premotor and cerebellar pathways is essential for producing spatially directed or guided movements. These regions are active during the early stages of skill acquisition. A second circuit, associated with the SMA, basal ganglia and perhaps the temporal lobe, becomes more dominant as the skill is well learned and driven by the internal representation of the desired action. Both circuits converge on the motor cortex, the primary link between the cortex and limbs for voluntary movements.
Vestibular reflex: evoked by changes in the position of the head: evoked by otolith organs
a) Vestibulocollic reflexes (act on the neck), counteract head movements, keeping the head stable
b) Vestibulospinal reflexes (act on the limbs): extension of arms, flexion of the lower limbs
c) Vestibulo-occular reflexes: stabilize images on the retina.
Neck Reflexes: triggered by tilting (bending) or turning the neck
a) Cervicocollic reflexes: if neck pushed to one side, opposite neck muscle contracts, to restore normal neck postition, synergistic with vestibulocollic reflexes b) Cervicospinal reflexes*bending the neck forward==> flexion of the upper & lower extremities *tilting the neck backward==> extension of the upper & lower extremities *turning to right==> extension of right arm & leg (flexion of left limb) *** Vestibular and neck afferents converge on the Vestibular Nuclei & Propriospinal Neurons
Asymmetrical Tonic Neck Reflex
Balance between basal ganglia and cerebellum The balance between these two systems allows for smooth, coordinated movement, and a disturbance in either system will show up as movement disorders
Damage to the basal ganglia results in: Abnormal body movements:
-Tremor (uncontrollable shaking) -Involuntary movements of the skeletal muscles -Paralysis – Akinesis: (destruction of the caudate (most affected site in stokes) results in paralysis in the opposite side of the body). -Globus pallidus: mostly concerned with muscle tone for specific body movements. -Lesion in the subthalamic nucleus – hemiballisms, jerky movements, spontaneous movements of the arms (affects the extremities – legs and arms)
movement, motivation, reward, and addiction
most symptoms do not appear until striata DA levels decline by at least 70-80%. Imbalance primarily between the excitatory neurotransmitter Acetylcholine and inhibitory neurotransmitter Dopamine in the Basal Ganglia
-tremor is most apparent at rest.
-Rigidity is a result of simultaneous contraction of flexors and extensors, which tends to lock up the limbs.
-Bradykinesia, or "slow movement", is a difficulty initiating voluntary movement, as though the brake cannot be released.
Postural Instability - abnormal fixation of posture (stoop when standing), equilibrium, and righting reflex
• Hypotension• Dementia• Dystonia• Ophthalmoplegia• Affective Disorders
Other Accompanied Autonomic Deficits Seen Later in Disease Process
Major Symptoms Involve
Etiology• Cerebral atherosclerosis• Viral encephalitis• Side effects of several antipsychotic dru
gs (i.e., phenothiazides, butyrophenones, reserpine)
• Pesticides, herbicides, industrial chemicals - contain substances that inhibit complex I in the mitochondria
Putative Functions of the Basal Ganglia
Motor Functions initiates motor patterns of cognitive or motivational significance (Heimer et al. 1982) motor sequence planning, coordination (Graybiel 1995) inhibition of competing motor programs (Mink 1996)
Sensory functions somatosensory motor control (Schneider & Lidsky 1981, Brown et al. 1997) somatosensory discrimination; pain (Brown et al. 1997); visual discrimination (Pribram 1977) including facial expression and hallucinations (Middleton and Strick 1996, Brown et al. 1997) auditory (Brown et al. 1997)
Cognitive functions cognitive sequence planning ("acquisition, retention, and expression of cognitive patterns" Graybiel 1997) expectations, prediction (ventral striatum, Schultz 1998) attention (Hayes et al. 1998) categorizing (tactile stimuli, Merchant et al. 1997) learning (Jueptner et al 1997); procedural memory (for habits and skills: Jog et al. 1999) habit learning & acquisition of "non-motor dispositions and tendencies (Knowlton et al. 1996) classify spatial patterns and serial ordering of sensory events (Beiser & Houk 1998) executive function (". . . focused and sustained attention in concert with flexibility of thought . . . planning and regulation of adaptive and goal directed behavior . . . [utilizing] working memory . . ." Peigneux 2000) creativity (ventral striatum becomes activated when predictions are violated by stimuli that appear in an unexpected context: references in Cotterill 2001)
SerotoninAcetylcholineGABAEnkephalinSubstance PGlutamateDopamine
Neurotransmitters
Parkinson's disease: Treatment
Its symptoms and potential therapies were mentioned in the Ayurveda, the system of medicine practiced in India as early as 5000 BC
in the first Chinese medical text, Nei Jing, which appeared 2500 years ago.
Drug Therapy Against Parkinson Disease Is Aimed at Bringing theBasal Ganglia Back to BalanceDecrease Cholinergic Activity Within Basal Ganglia and this Can Be Done Two Ways: Activating Dopamine receptors in Substantia Nigra feeding back to Cholinergic Cells in the striatum
-Turn off the Cholinergic Cells, Then Things Are Brought Back to Balance
Antagonize Acetylcholine receptors
Agents that Increase Dopamine
functions• Increasing the synthesis of dopamine - l-Dopa• Inhibiting the catabolism of dopamine - selegiline• Stimulating the release of dopamine - amphetamine• Stimulating the dopamine receptor sites directly - bromocript
ine & pramipexole• Blocking the uptake and enhancing the release of dopamine
- amantadine
Parkinson's disease: Treatment
Treatment for akinesia: L-Dopa
*decarboxylase inhibitor*Ach antagonist (atropine)
1. Replacement 2. Substitution, 3. Relase helper 4. Conservation
Increasing the synthesis of dopamine - l-DopaInhibiting the catabolism of dopamine - selegilineStimulating the release of dopamine - amphetamineStimulating the dopamine receptor sites directly - bromocriptine & pramipexoleBlocking the uptake and enhancing the release of dopamine - amantadine
*fetal dopamine cell transplantation * destruction of feed-back circuit: ventrolateral, ventroanterior nuclei
Effects of L Dopa on the Symptoms of Parkinson Disease
• L Dopa Fairly Effective in Eliminating Most of the Symptoms of Parkinson Disease
• Bradykinesia and Rigidity Quickly Respond to L Dopa
• Reduction in Tremor Effect with Continued Therapy
• L Dopa less Effective in Eliminating Postural Instability and Shuffling Gait Meaning Other Neurotransmitters Are Involved in Parkinson Disease
• Many side effects
Glial Cell Line Derived Neurotrophic Factor (GDNF) is Potent Promoting Survival for Dopaminergic Neurons in Parkinson’s Disease
Neurotrophic proteins--These appear to protect nerve cells from the premature death that prompts Parkinson's. One hurdle is getting the proteins past the blood-brain barrier.
Neuroprotective agents--Researchers are examining naturally occurring enzymes that appear to deactivate "free radicals," chemicals some scientists think may be linked to the damage done to nerve cells in Parkinson's and other neurological disorders.
Risk of Parkinsonism in smokers is 20-70% less than non-smokers; nicotine may increase firing rate of dopaminergic neurons
Neural tissue transplants--Researchers are studying ways to implant neural tissues from fetal pigs into the brain to restore the degenerate area. In a clinical trial conducted in part at Boston University School of Medicine, three patients out of 12 implanted with the pig tissues showed significant reduction in symptoms.
Genetic engineering--Scientists are modifying the genetic code of individual cells to create dopamine-producing cells from other cells, such as those from the skin.
The Cause of Huntington's Disease
inherited as an autosomal dominant disorderresulting from a mutation on chromosome 4. expansion of CAG repeats at the end of the gene. the gene product (the protein huntintin) is not fully understood. it is known to be expressed ubiquitously and needed for normal cell survival. huntinin mutation leads to inappropriate apoptosis, and destruction of cells. ACh neuron death at cerebral cortex Why this cell destruction is differentially targeted to the basal ganglia and cerebral cortex is not understood.
Early symptoms of HD mood swings, depression, irritability or trouble driving, learning new things, remembering a fact, or making a decision.
As the disease progresses, concentration on intellectual tasks becomes increasingly difficult
difficulty feeding himself or herself and swallowing.
Cerebellum
Involved in the coordination of movement
Compares what you thought you were going to do (according to motor cortex) with what is actually happening down in the limbs (according to proprioceptive feedback), and corrects the movement if there is a problem.
-partly responsible for motor learning, such as riding a bicycle. -the cerebellum works ipsilaterally. -now the cerebellum is regarded as a structure that can help not only motor but also non-motor regions to do their work effectively.
-compared to a powerful computer, capable of making contributions both to the motor dexterity and to the mental dexterity of humans.
-immature at birth but develops through childhood and adolescence, reaching its full structural growth by the 15th to 20th year of life.
ANATOMY OF THE CEREBELLUM
Floculonodular Lobe
Lateral
Zone
Intermediate
Zone
[Characteristics] 1) contains more neurons than all the rest of the brain combined. 2) a more rapidly acting mechanism than any other part of the brain 3) it receives an enormous amount of information from the highest level of the human brain (40 million fibers).
Divisions of the cerebellum VestibulocerebellumInput from vestibular nuclei in medulla; output back to medulla, Maintains posture and balance
SpinocerebellumSensory input from periphery; output to descending motor tracts Compares intended and actual movement and corrects for differences
CerebrocerebellumInput from pontine nuclei in pons relayed from cortex; output through thalamus to cortex Involved in planning and initiation of movement
Cat cerebellum, sagittal section
Single folium, enlarged
The cerebellum ("little brain") has convolutions similar to those of cerebral cortex, only the folds are much smaller.
Like the cerebrum, the cerebellum has an outer cortex, an inner white matter, and deep nuclei below the white matter.
Inputs and outputs of the cerebellum 3 main inputs, 3 main outputs from 3 deep nuclei. They are:
peduncles, or "stalks". There are 3 pairs: the inferior, middle, and superior peduncles.
3 inputs are: 1) Mossy fibers from the spinocerebellar pathways, 2) climbing fibers from the inferior olive, and 3) more mossy fibers from the pons, which are carrying information from cerebral cortex.
The mossy fibers from the spinal cord have come up ipsilaterally.
The fibers coming down from cerebral cortex, however, DO need to cross.
The 3 deep nuclei are the fastigial, interposed, and dentate nuclei. The fastigial nucleus: balance, and sends information mainly to vestibular and reticular nuclei.
The dentate and interposed nuclei: voluntary movement, and send axons mainly to thalamus and the red nucleus.
The cerebellar cortex has five kinds of cells. Basket cell, stellate cell, granule cell, Purkinje cell, Golgi cell
The cerebellar cortex is arranged in three layers:
The granular layer (Golgi and granule cells) the Purkinje cell layer (Purkinje cells) the molecular layer (stellate and basket cells)
The cerebellar cortex receives excitatory input through the mossy fibers and sends inhibitory output from the Purkinje cells to the deep nuclei of the cerebellum and the brainstem.
On-beam excitation and off-beam inhibition occurs because the parallel fibers of the granule cells stimulate on-beam Purkinje cells but cause the basket cells to inhibit off-beam Purkinje cells.
Microcircuits in a folium
molecular layer is nearly cell-free. Instead it is occupied mostly by axons and dendrites.
Purkinje cells, central players in the circuitry of the cerebellum.
Below the Purkinje cells is a dense layer of tiny neurons called granule cells.
Finally, in the center of each folium is the white matter, all of the axons traveling into and out of the folia.
These cell types are hooked together in stereotypical ways throughout the cerebellum.
SOMATIC SENSORY PROJECTIONS ONTO THE CEREBELLAR CORTEX
CEREBELLAR DYSFUNCTION
1. General a. Disequilibrium - Falling: forward, backward, laterally when standing; unsteady, staggering
gait; sensations of spinning and nausea.
b. Muscle tone disturbance - Softness of muscle bellies on palpation; decreased tendon reflexes; asthenia (muscles tire easily). Pendular swinging of dependent limb segment after displacement.
c. Movement disorders 1) Incoordination of movements - Ataxia, asynergia - decreased capability for smooth,
cooperative, segmental action between a series of muscle groups. 2) Decomposition of movements - Complex movement performed as a sequence of irr
egular disjointed episodes. 3) Adiadochokinesis - Inability to rapidly pronate and supinate. 4) Dysmetria - Inability to correctly judge distances. Tested by reaching out and touchin
g an object ("prepointing; pastpointing"). 5) Inability to trace a specific course with finger or heel (e.g., right heel to left knee). 6) Staggering gait - Tendency to fall, particularly with closed eyes. 7) Intention tremor - Tremor when voluntary movement is attempted. http://video.search.yahoo.com/search/video?p=CEREBELLAR%20DYSFUNCTION%20&ei=UTF-8&fr=yfp-t-452&fr2=tab-im
g
d. Speech deficits - Slow onset, slurring, jerky, intermittent sound productions with explosive nature: "scanning speech".
e. Cerebellar nystagmus - Inability to fixate on object. Conjugate drift of eyes away from it, with rapid return. May be positional (more pronounced when body adopts a particular posture), or directional (increasing when subject attempts to gaze in particular direction).
CEREBELLAR DYSFUNCTION
2. Specific Syndromes a. Flocculonodular syndrome: Loss of whole body equilibrium. Swaying when standing, staggering whe
n walking, tendency to fall (usually backwards), positional nystagmus. http://www.dizzyfix.com/selftest.html#nystagmus
b. Neocerebellar syndrome: Cerebellar hemisphere (lateral zone) or efferent pathways. In unilateral
disease, manifestations occur on same side as lesion. Gross intention tremor and staggering gait only supervene if dentate nucleus or brachium conjunctivum are involved. This syndrome may include dysmetria, unilateral limb weakness, adiadochokinesis, intention tremor and speech defects.
The cerebellum was strongly activated in a task involving ocular pursuit of a target with simultaneous joystick control of a cursor.
Time offsets between eye and hand motion allowed control of the degree of eye-hand coordination. Only the cerebellum showed activity changes which co-varied with time offset.
The cerebellum coordinates eye and hand tracking movements. Nature Neuroscience, 4:638-644.
