1. Cerebellum

2. cerebellum Massive amounts of sensory information enter the cerebellum
Cerebellar output is vital for normal movement
Severe damage to the cerebellum : not interfere with sensory perception or with muscle strength
degrade coordination of movement and postural control

3. Three layers of the cerebellar cortex
The outer and inner layers : interneuron (granule, Golgi, stellate, basket cells)
In the middle layer : purkinje cell bodies, the output neurons of the cerebellar cortex, and their projections inhibit the deep cerebellar nuclei and the vestibular nuclei

4. Deep to the cortex is white matter (deep cerebellar nuclei)
Climbing and mossy fibers are the input fibers to the cerebellar cortex
Most climbing fibers arise from the inferior olivary nucleus
Mossy fibers originate in the spinal cord (spinocerebellar tracts) and in the brain stem
Deep to the cortex is white matter (deep cerebellar nuclei)

6. Vertically, cerebellum : specific class of movements
Three lobes
Anterior
Posterior
Flocculonodular
Vertically, cerebellum : specific class of movements
Midline vermis
Paravermal hemisphere
Lateral hemisphere
Cerebellar peduncles : fibers connecting the cerebellum with the brain stem
Superior : attaches to the midbrain and contain cerebellar efferent fibers
Middle : cerebral cortex->pons-> middle peduncle
->cerebellum
Inferior : brain stem and spinal cord -> cerebellum -> vestibular nuclei and reticular nuclei in the brain stem

12. Deep cerebellar nuclei
a. Fastigial nucleus
b. Globose nucleus
c. Emboliform nucleus
d. Dentate nucleus

13. Functions of spinocerebellar tracts
not consciously perceived
unconscious adjustments to movements and posture
internal feedback tract
high-fidelity pathway
cerebellum can compare the intended motor output with the actual movement output

15. Input to the cerebellum is from
Cerebral cortex (via pontine nuclei)
The vestibular apparatus
Vestibular and auditory nuclei
Spinal cord via both high fidelity pathways and internal feedback tracks
Output of the cerebellum is via connections
Vestibulospinal
Reticulospinal
Rubrospinal
Corticobulbar
Corticospinal tracts

16. Connections via cerebellar peduncles
Neocerebellum
Anterior
lobe
Pyramid and
Uvula
MCP
SCP
ICP
D. Spinocerebellar T.
Dentate N.
Corticopontine
fibers
V. Spinocerebellar T.
Pontine N.
Vestibular N.
Inf. olivary N .
Fastigial N.
Uncinate fasciculus
SCP
ICP
To spinal cord
To thalamus
Vestibularl N.
Red N.
Reticular F.

17. Functional Regions of the Cerebellum
Equilibrium
Gross movements of the limbs
Fine, distal, voluntary movements

19. Equilibrium : vestibulocerebellum
Flocculonodular lobe
Information directly from vestibular receptors and connects reciprocally with the vestibular nuclei
Information from visual areas of the brain
Vestibulocerebellum influences eye movements and postural muscles

21. Connections of Vestibulocerebellum
Nuclei of
III, IV, VI
Fastigial
nucleus
MLF
Uncinate fasciculus RF
Vestibular nuclei
Flocculonodular lobe
Vestibular
ganglion
Accessory
olivary nuclei
Vestibular nuclei
Vestibulospinal tract
Primary affarent
Reticulospinal tract

22. Gross movements of the limbs : spinocerebellum
Vermis and paravermal region
Somatosensory information, internal feedback from spinal interneurons, sensorimotor cortex information
Vermis
projects to fastigial nucleus; adjusts in the medial activation tracts by brain stem nuclei and on the cerebral cortex via the motor thalamus
Vermis also has connections with cranial nerve nuclei that control speech muscles

23. Paravermal area
projects to the globose and emboliform nuclei; influence the lateral activation tracts by action on brain stem nuclei and by projecting to the cerebral cortex via the motor thalamus

25. Connections of Spinocerebellum
Interpositus
nucleus
Spinocerebellar tract
(Dorsal)
Accessory
Olivary nuclei
VL of
thalamus
Reticulospinal tract
Vermal and
paravermal part
Rubrospinal tract
SCP
Red nucleus
Motor area RF
(Ventral)

26. Fine, distal, voluntary movements: cerebrocerebellum
lateral cerebellar hemisphere
Input to the cerebrocerebellum : from cerebral cortexpontine neuronscerebrocerebellum
Efferents from the lateral cerebellar hemisphere project to the dentate nucleus
Dentate is involved in motor planning
Dentate nucleusmotor thalamuscerebral cortex
The functions of the cerebrocerebellum and dentate ;
coordination of voluntary movements via influence on corticofugal tracts
planning of movements
ability to judge time intervals and produce accurate rhythms

28. Connections of pontocerebellum
Motor area
VL of
thalamus
Dentate
nucleus
SCP
Red nucleus
Lateral zone of
hemisphere
Pontine N.
MCP
ICP
Principal
Inferior olivary nuclei
Corticospinal tract

30. Lower Motor Neuron (LMN)
Cerebellum and Automatic Motor Control
Motor Cortex
CEREBELLUM
Red Nucleus
Vestibular
Nucleus
Reticular
Formation
Lower Motor Neuron (LMN)
Proprioceptors

31. Cerebellar Clinical Disorders
Cerebellar signs: ipsilateral
Ataxia:
a lack of coordination; movement disorder common to all lesions of the cerebellum
Cerebellar lesions
Midline : truncal ataxia
Paravermal : gait ataxia
Lateral : limb ataxia

32. Cerebellar limb ataxia:
unable to stand with their feet together, with or without vision
Normal vibratory sense, proprioception, ankle reflexes.
Sensory ataxia :
Able to stand steadily with the feet together with the eyes open
Balance is impaired with the eyes closed
Impaired conscious proprioception and vibratory sense, and ankle reflexes are decreased or absent

33. Vermal lesions Lesions involving vestibulocerebellum :
Abnormal eye movements(nystagmus)
Dysequilibrium
Difficulty maintaining sitting and standing balance (truncal ataxia)
Vermal lesions
dysarthria (slurred, poorly articulated speech)
Dysfunction of the spinocerebellum
Ataxic gait : a wide-based, staggering gait
Chronic alcoholism (ant. lobe section of the spinocerebellum is often damaged because of malnutrition, resulting in the characteristic ataxic gait)

34. Cerebrocerebellar lesions: limb ataxia
Dysdiadochokinesia: inability to rapidly alternate movement
Dysmetria : inability to accurately move an intended distance
Action tremor : shaking of the limb during voluntary movement
Deficits in the ability to perceive time intervals

36. Summary of normal motor control
Motor planning areas, control circuit, and descending tracts must act with sensory information to provide instruction to lower motor neurons
Basal ganglia receive input from cerebral cortex : their influence on movement is via cerebral cortex and pedunculopontine nucleus
Cerebellum receive information from the spinal cord, vestibular system, and brain stem; influence movement via motor areas of the cerebral cortex and extensive connections with upper motor neurons that arise in the brain stem
Lower motor neuron deliver the signals from CNS to skeletal muscles that generate movements

38. Three fundamental types of movement
Postural : brain stem mechanisms
Ambulatory : brain stem and spinal regions
Reaching/grasping : cerebral cortex

39. Assessment : EMG
1) M1 : monosynaptic stretch reflex ; msec
2) M2 : second response (long latency response);
brain stem connections ; 50~80 msec
3) voluntary response : synapses in the cerebral cortex; msec

40. Postural control
Postural control : orientation and balance(equilibrium)
Orientation: adjustment of the body and head to vertical
Balance : ability to maintain the center of mass relative to the base of support
Postural control : by central commands to lower motor neurons
tectospinal, medial reticulospinal, vestibulospinal, medial corticospinal tracts
Central output : environmental context by sensory input
Sensory input : both feedback and feed-forward mechanism
Feed-forward : prediction and anticipation to prepare for upcoming hazards to stability
Feedback : a response to disturbance

41. To orient in the world somatosensation: Vision: Vestibular:
information about weight bearing and the relative positions of body parts
Vision:
information about movement and cues for judging upright
Vestibular:
input from receptors in the inner ear information us about head position relative to gravity and about head movement

43. Vestibular gravity receptors : influence limb muscle activity
Head position in space is signaled by neck proprioception and vestibular and visual information
Activity of cervical joint receptors and neck muscle stretch receptors: elicits neck reflexes
Symmetrical tonic neck reflex
Asymmetrical tonic neck reflex
Vestibular gravity receptors : influence limb muscle activity
Tonic labyrinthine reflex

44. During stance, we sway continuously;
to prevent falling
the postural control system makes adjustments to maintain upright posture
Posturography :
to determine sensory organization and muscle coordination
Motor coordination

46. 조건 1: 눈을 뜨고 서 있게 한다. 시각, 전정, 체성감각 기능을 알 수 있다.
조건 2 : 눈을 감고 서 있게 한다. 전정과 체성감각 기능을 알 수 있다.
조건 3 : 눈을 뜨고 서 있게 하고, visual surround를 움직인다.
부적절한 시각(sway referenced vision)시 전정과 체성감각 기능을 알 수 있다.
조건 4 : 눈을 뜨고 서 있게 하고, 발판을 상하로 비스듬히 기울인다.
부적절한 체성감각(sway referenced somatosensation)시 시각과 전정 기능을 알 수 있다.
조건 5 : 눈을 감고 서 있게 하고, 발판을 상하로 비스듬히 기울인다.
시각 기능이 없고 부적절한 체성감각 상태에서 전정 기능을 알 수 있다.
조건 6 : 눈을 뜨고 서 있게 하고, visual surround를 움직이고, 발판을 상하로 비스듬히 기울인다.
부적절한 시각 및 체성감각 상태에서 전정 기능을 알 수 있다.

47. Postural abnormalities
CNS dysfunction : postural abnormality
Spinocerebellar lesions : gait and stance ataxia
Muscle activation patterns are normal in people with spinocerebellar lesions, but the duration and amplitude of postural adjustments are larger than normal, and anticipatory adjustments for predictable conditioning are lacking
Vestibulocerebellar lesion : truncal ataxia

48. Ambulation Cerebral cortex provides:
goal orientation & control of ankle move…
Basal ganglia: generation of force
Cerebellum : timing, interlimb coordination, error correction
Brain stem descending tracts : adjust the strength of muscle contraction
direct connection
adjusting transmission in spinal reflex pathways

49. Ambulation
During normal gait initiation, the swing limb first pushes downward and backward against the support surfacebeing moved forward and onto the stance leg in preparation for foot-off and increases the magnitude of the subsequent movement
Hemiplegia : the contribution of the paretic leg to weight transfer is much less than normal
Parkinson’s disease : fail to adequately move the center of mass prior to attempting stepping, causing inability to initiate gait

50. Reaching and grasping Vision and somatosensation: Vision
essential for normal reaching and grasping
Vision
information for locating the object in space, shape and size of the object
Feed-forward : primary role of visual information
Feedback : if the movement is inaccurate, vision also guides corrections

51. Stream of vision : visual cortexposterior parietal cortex (sensation and movement) premotor cortical area (controlling reaching, grasping, eye movement)
Cerebral cortex (sensory and planning) basal ganglia and cerebellum  sensorimotor cortex via thalamus
Proprioception : to prepare for movement and to provide information regarding movement errors

52. First phase of reaching:
before one can reach accurately, visual grasp(fixing the object in central vision) and proprioceptive information about upper limb position are required
Second phase of reaching:
slower, corrective adjustment to achieve contact with the target
Grasping:
coordinated with activity of the eyes, head, proximal upper limb, and trunk; orientation and postural preparation are integral to the movement

53. Motor circuit for fractionated finger movements

54. Adults with parietal lobe damage:
abnormal timing of reaching and grasp
Lack anticipatory adjustments of the fingers, and use a palmar, rather than pincer, grasp.
In normal actions:
feed-forward and feedback interact to create movement

55. Integration of feedforward and feedback in determing movements

56. Testing motor system Strength Muscle bulk Muscle tone Reflexes
Movement efficiency
Speed
Postural control
Abnormal movement

57. Peripheral nervous system

58. Dysfunction of peripheral nerves
Sensory changes
Autonomic changes
Motor changes
Denervation : trophic changes

59. Sensory changes Decreased or lost sensation Abnormal sensations
hyperalgesia: decreased pain threshold, increased pain to suprathresold stimuli and spontaneous pain
dysesthesia : unpleasant abnormal sensation
paresthesia : abnormal sensation in the absence of nociceptor stimulation

60. Autonomic changes
Autonomic signs depend on the pattern of axonal dysfunction
If a single nerve is damaged, autonomic signs are usually only observed if the nerve is completely severed
Lack of sweating and loss of sympathetic control of smooth muscle fibers in arterial walls
The latter may contribute to edema in an affected limb.
If many nerves are involved, autonomic problems may include…
Difficulty regulating blood pressure
Heart rate
Sweating
Bowel and bladder functions
impotence

61. Motor changes Motor signs of peripheral nerve demage
Paresis(weakness) or paralysis
If muscle is denervated, EMG recording show no activity for about 1 week following injury
Muscle atrophy progresses rapidly
Then muscle fibers begin to develop generalized sensitivity to acetylcholine along the entire muscle membrane, and fibrillation ensues.
Fibrillation: diagnostic of muscle denervation

62. Denervation: trophic changes
When nerve supply is interrupted, trophic changes begin in the denervated tissues
Muscle atrophy
Skin shiny
Nails brittle
Subcutaneous tissues thicken
Ulceration of cutaneous and subcutaneous tissues
Poor healing of wounds and infections
Neurologic joint damage
Secondary to blood supply changes, loss of sensation, lack of movement

63. Classification of neuropathies
Mononeuropathy: (single nerve) focal dysfunction
Multiple mononeuropathy: (several nerves or many nerves) multifocal, asymmetrical involvement of individual nerves
Poly neuropathy : generalized disorder that typically presents distally and symmetrically
**dysfunction : damage to the axon, myelin sheath, or both

64. Mononeuropathies (depending on the severity of damage, traumatic injury)
Class I :
- focal compression due to entrapment or pressure : median(carpal tunnel), ulnar(ulnar groove), radial(spiral groove), peroneal(fibular head)
- prolonged pressure from casts, crutches, or sustained positions
- compression: interfere with blood supply :
prolonged compression : local demyelination -> slows or prevents nerve conduction at the demyelinated site
- class I injury : decreased or lost function of large-diameter axons(motor, touch and proprioceptive, lost phasic stretch reflex), intact autonomic function, lack of damage to the axon

65. Recovery : complete (remyelination)
Carpal tunnel syndrome : compression injury of the median nerve in the space between the carpal bones and the flexor retinaculum
Pain and numbness at night
Later, persist throughout the day
Decreased or lost in the lateral three and one-half digits and adjacent palm of the hand
Dorsum of the hand, the distal half of the same digits are involved
Paresis and atrophy of the thumb intrinsic muscles
Pain from carpal tunnel syndrome radiate into the forearm and to the shoulder
Repetitive hand movements or the gripping of vibrating tools than in the general population
1 month of rest, splinting and anti-inflammatory medication followed by exercise designed to promote gliding of the tendon

67. Class II : arise from crushing the nerve
connective tissue sheaths and myelin sheaths remain uninterrupted, but the axons are disrupted, and wallerian degeneration occurs distal to the lesion
axon regrowth : 1 mm/day
return of nerve conduction in the regenerating axon
Class III : occur when nerves are physically severed, by excessive stretch or laceration
Axons and connective tissue are completely interrupted, causing immediate loss of sensation and muscle paralysis in the area supplied
Wallerian degeneration : distal to the lesion 3 to 5 days later
Nerve conduction distal to the injury may never return because of poor regeneration

68. Multiple mononeuropathy
Involvement of two or more nerves in different parts of the body :
Occur most commonly from
ischemia of the nerves
either from diabetes or inflammation of the blood vessels
In multiple mononeuropathy
Individual nerves are affected,
producing a random,
asymmetrical presentation of signs

69. Polyneuropathy
Symmetrical involvement of sensory, motor, and autonomic fibers
Progressing from distal to proximal (hallmark)
Typically begin in the feet and then appear in the hands, areas of the body supplied by the longest axons
Etiology : toxic, metabolic, or autoimmune
Common causes : diabetes, nutritional deficiencies secondary to alcoholism, and autoimmune disease

70. In severe polyneuropathy, trophic changes (poor healing, ulceration of skin, neurologic joint damage) occur; these changes probably occur because the person is unaware of injuries to the part, owing to lack of sensation
Education regarding monitoring and care of intensive areas is vital
Therapists are likely to treat people with diabetic (metabolic) and Guilliain-Barre (autoimmune) poly neuropathies
In diabetic poly neuropathy, axons and myelin are damaged; stocking / glove distribution (fig 11-6)

71. Diabetic polyneuropathy
Damaged all sizes of sensory axons resulting in decreased sensations and pain, paresthesia, dysesthesia
Charcot’s joints : a progressive degenerative disease of the joints caused by nerve damage resulting in the loss of ability to feel pain in the joint and instability of the joint.
Proper diabetic foot care, Wearing of appropriate shoes, Regular self-inspection of the feet, Proper care of the skin and toenails
May prevent amputation
Later in the disease process muscle weakness and atrophy also tend to occur distally

72. Autonomic functions are susceptible;
cardiovascular, gastrointestinal, genitourinary, sweating dysfunction (lack of sweating distally, excessive compensatory sweating proximally)
Polyneuropathy in Guillain-Barre syndrome:
more severe effects on the motor than sensory system
Contrary to the pattern in most polyneuropathies, paresis may be worse proximally.

73. Dysfunctions of the neuromuscular junction
Myasthenia gravis : an autoimmune disease that damages acetylcholine receptors at the neuromuscular junction (muscle weakness)
Botulism : ingesting the botulinum toxin from improperly stored foods causes interfere with the release of acetylcholine from the motor axon
Acute, progressive weakness, with loss of stretch reflex
Sensation remains intact.
**Botox therapy(?)

74. Myopathy Disorders intrinsic to muscle (muscular dystrophy)
Random muscle fibers degenerate
Leaving motor units with fewer muscle fiber than normal
Activating such a motor unit produces less force than a healthy motor unit
Because the nervous system is not affected by myopathy, sensation and autonomic function remain intact.
Coordination, muscle tone, and reflexes are unaffected until muscle atrophy becomes so severe that muscle activity cannot be elicited

75. Electrodiagnostic studies
Dysfunction of peripheral nerves and the muscles : evaluate by EMG
nerve conduction study(NCS) and EMG studies
- processes that are primarily demyelinating (myelinopathy) and those that primarily damage axons (axonopathy).
Myelinopathies produce marked slowing of velocity.
Axonopathies produce decrease in the amplitude of recorded potentials and may produce slowing of conduction velocity
- upper motor neuron and lower motor neuron paresis.
upper motor neuron lesions have no effect on NCS, so NCS is normal. Lower motor neuron lesions produce abnormal NCS.
- local conduction block and wallerian degeneration. Local conduction block interfere with nerve conduction only at one site, whereas wallerian degeneration affects the entire axon distal to the lesion

76. Class I injury on nerve conduction : slow or stop conduction across the site of damage, with normal conduction in the axon segments proximal to and distal to the injury
Class II injury : axons lose their ability to conduct action potential across the damaged site at the time of injury. The amplitude of the evoked potential is decreased

77. Generalized neuropathies(polyneuropatheies) :
- slowed nerve conduction throughout the affected nerve
- decreased amplitude
- increased distance between stimulation and recording sites
Myopathy
Nerve conduction : normal
Amplitude of the potential recorded from muscle : decreased

78. Myopathy Myopathy : disorders intrinsic to muscle
Muscular dystrophy: random muscle fibers degenerative, leaving motor units with fewer muscle fibers than normal
Activating such a motor unit produces less force than a healthy motor unit

79. Electrodiagnostic studies
Dysfunction of peripheral nerve and the muscles they innervate : EMG, NCS
Myelinopathies : marked slowing of velocity, axonopathies : decrease in the amplitude of recorded potentials and slowing of conduction velocity
Upper motor neuron lesions : no effect on NCS, so NCS is normal, Lower motor neuron lesion : abnormal NCS
Local conduction block : interfere with nerve conduction only at one site, whereas wallerian degeneration : entire axon distal to the lesion

80. Clinical application
Signs of peripheral nervous system damage : hypoactivity or hyperactivity of neurons
Neuronal hypoactivity : decrease or loss of neuronal activity (loss of proprioception)
Neuronal hyperactivity : light touch to elicit a painful sensation
Signs and symptoms of mononeuropathy (table 11-3)
Polyneuropathy : symmetrical distribution, postural hypotension, bowel or bladder incontinence, and disability to have a sexual erection

82. Distinction between peripheral neuropathy and central nervous system dysfunction

83. treatment
Treatment of sensory, manual muscle, EMG – treatment decisions
Education : lack of sensation, disuse, or overuse
The person with peripheral neuropathy that affects sensation : taught to visually inspect the involved areas daily, using mirrors if necessary, to monitor for wounds and for reddening of the skin that persists more than a few minutes
Edema : elevation of limb, compression bandaging with an elastic wrap, electrical stimulation
Contractures : prolonged stretching or by daily activities
Exercise beginning : enhance both sensory and motor recovery
Orthosis : stabilize weight-bearing joints, preventing sprains and strains, prevent dropping of the forefoot during gait in cases of paresis or paralysis of tibialis anterior muscle, prevent deformity
Electrical stimulation : prevent atrophy of denervated muscles