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Gangguan motorik, appetizer ;)
 

Gangguan motorik, appetizer ;)

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Banyak pasien neuro dengan keluhan gangguan motorik, terutama kelemahan anggota badan. Tapi ternyata gangguan motorik tu nggak cuma "parese" aja.. ada banyak macemnya! (Ada yg pernah bikin ...

Banyak pasien neuro dengan keluhan gangguan motorik, terutama kelemahan anggota badan. Tapi ternyata gangguan motorik tu nggak cuma "parese" aja.. ada banyak macemnya! (Ada yg pernah bikin stats-nya??)
File ini cuma menceritakan sekelumit tentang gangguan motorik, dan si desainer ppt ini pun cuma sempet baca sedikit. Tapi dari yang sedikit ini, rasanya bikin pengen belajar lebih banyak lagi! (karena itu dikasi subtitle "Appetizer"..)
Menarik banget cerita tentang jenis2 gangguan motorik ini, lokasi lesi-nya, ciri2 khususnya, n penyebabnya..
Oia, insyaAllah ppt ini akan selalu dilengkapi & diupdate sesuai referensi yg sanggup dibaca si desainer^^v
(Tugas modul ini pun digarap dengan sangat senang hati, hehehehe..)

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  • Control of movement in humanMovement is organized in increasingly complex and hierarchical levels. Reflexes are controlled at the spinal or higher levelsStereotypic repetitious movements, walking/swimming, are governed by neural networks that include the spinal cord, brain stem, and cerebellum… + central pattern generators, or local circuits of neurons that can trigger simple repetitive motor activities, in the lower brain stem or spinal cord. Specific, goal-directed movements are initiated at the level of the cerebral cortexA concept from Hughlings Jackson, 1858, purely onthe basis of clinical observations: Motor system is organized hierarchically in threelevels, each higher level controlling the one below.- The spinaland brain stem neurons represent the lowest, simplest, and most closely organized motorcenters;- The motor neurons of the posterior frontal region [motor cortex] represent a more complexand less closely organized second motor center;- The prefrontal parts of the cerebrum [premotor] are the third and highest motor center.Essentially correct, but Jackson failed to recognize the importance of the parietal lobe and basal ganglia in motor control.Without sensory feedback, motor control is ineffective.And at the higher cortical levels of motor control, motivation, planning, and other frontallobe activities that subserve volitional movement are always preceded and modulated by activity in the parietal sensory cortex.
  • The psychomotor, or cortical associative, level has to do with memory, initiative, andconscious and unconscious control of motor activity that arises primarily from the motor association cortex anterior to the motor strip.
  • Pure unilateral lesions of the corticospinal tract (ie, lesions that spare the other descending pathways) may result in relatively minor weakness, although precise movements of distal musculature (eg, movements of the individual fingers) are usually impaired. It is likely that, in these cases, descending control of motor neurons innervating proximal parts of the limbs and the trunk is mediated by the reticulospinal, vestibulospinal, and tectospinal pathways and by uncrossed axons in the anterior and lateral corticospinal tract.
  • the ventral nuclei (ventral anterior, VA; and ventral lateral, VL) of the thalamus: receives input from the basal ganglia, cerebellum). The VA and VL thalamic nuclei complete the feedback circuit by sending axons back to the cerebral cortex
  • Decerebrate rigidity occurs when the posterior part of the brain stem and spinal cord are isolated from the rest of the brain by injury at the superior border of the pons. In decere-brate rigidity, the extensor muscles in all of the limbs and those of the trunk and neck have increased tone. When the brain stem is transected, inhibitory influences from the cortex and basal ganglia can no longer reach the spinal cord, and fa-cilitator)' influences, which descend in the vestibulospinal and reticulospinal tracts, dominate. This results in increased activ-ity of alpha motor neurons innervating extensor muscles, which is due to increased gamma motor neuron discharge for these muscles
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  • Cari video-nyaCadenceThe beat or timing of a particular rhythmic activity—e.g., the rhythm of pedalling in cycling

Gangguan motorik, appetizer ;) Gangguan motorik, appetizer ;) Presentation Transcript

  • Gangguan Motorik- appetizer ^^v Ersifa fatimah PPDS Neurologi RSUD Dr Soetomo – Univ. Airlangga 2013
  • ReferensiMotor Disturbances Disorder of Motility• Muscle • Motor paralysis• LMN • Abnormal of movement &• UMN posture due to disease of• Basal Ganglia Basal Ganglia• Cerebellum • Incoordination & other disorders of Cerebellar(Waxman, 2010) function • Tremor, Myoclonus, Focal dystonias, and Tics • Disorder of Stance & Gait (Adams & Victor’s, 2005) ERS 2
  • The Motor System (DeJong, 2010)Level: Motor unit, Spinal cord, Pyramidal, ExtrapyramidalMotor strength & PowerMuscle ToneMuscle Volume & ContourAbnormality of Movement ERS 3
  • Knowing the structure and functionof the different levels of motor control, the relationships between the motor systems, and the changes in motor activity that occur in disease helps in understanding disorders of the motor system. DeJong, 2010 ERS 4
  • Sensory and motor functions are interdependent in the performance of volitional movement, and it is not possible to consider the motor system apart from the sensory system. Impairment of sensation may affect all aspects of motion— volitional, reflex, postural, tonic, and phasic.DeJong, 2010 ERS 5
  • Corticospinal & Corticobulbar Tracts, Composition 10% area 4 & 635% 55% area 3, 1, 2 Others: frontal & parietal The axons arising from the large pyramidal cells in layer V (Betzs cells) of area 4 contribute only about 5% of the fibers of the corticospinal tract and its pyramidal portion. Waxman, 2010 ERS 6
  • Disorder of Motility The following parts of the nervous system are engaged primarily in the control of movement and, in the course of disease, yield a number of characteristic derangements (Adams & Victor, 2005)Large motor neurons in the anterior horns of the Paralysis due to an interruption ofspinal cord & the motor nuclei of the brainstem  LMNs.the axons comprise the anterior spinal roots , the Complete lesions of LMN result in aspinal nerves & cranial nerves  innervate the loss of all movement—skeletal muscles. voluntary, automatic, postural, andThe LMNs are the final common path by which all reflex.neural impulses are transmitted to muscle.Motor neurons in the frontal cortex adjacent to the Paralysis due to dysfunction ofrolandic fissure connect with the spinal motor upper motor (corticospinal)neurons by a system of fibers known as the pyramidal neurons.tract.Since the motor fibers that extend from the cerebralcortex to the spinal cord are not confined to thepyramidal tract , they are more accurately designatedas the corticospinal tract, or UMNs,to distinguishthem from the LMNs. ERS 7
  • Disorder of Motility (Adams & Victor, 2005)Several brain stem nuclei that project to the spinalcord, notably the pontine and medullary reticularnuclei, vestibular nuclei, and red nuclei. + theirdescending fibers posture & movement (particularly when movement is highly automatic and repetitive)Certain of these brain stem nuclei are influenced bythe motor or premotor regions of the cortex, e.g., viacorticoreticulospinal relays.Two subcortical systems: the basal ganglia Involuntary movements &(striatum, pallidum, and related structures, including abnormalities of posture due tothe substantia nigra and subthalamic nucleus) & the disease of the basal gangliacerebellum Abnormalities of coordination Play important role in the control of muscle (ataxia) due to lesions in thetone, posture, and coordination of movement by cerebellum.virtue of its connections with the corticospinalsystem (via thalamocortical fibers) and otherdescending cortical pathways ERS 8
  • Disorder of Motility (Adams & Victor, 2005)Several other parts of the cerebral cortex, particularly Apraxic or nonparalytic disturbancesthe premotor & supplementary motor cortices. of purposive movement due toThese structures are involved in the programming involvement of association(i.e., the sequencing and modulation) of voluntary pathways in the cerebrummovement.The prefrontal cortex  planning & initiation ofwilled movement.Fibers from the prefrontal cortex project to thesupplementary & premotor cortex and provide theinput to the some restrictly motor areas.Similarly, certain parietal cortical areas (superiorparietal lobule) supply the somatic sensoryinformation that activates the premotor andsupplementary motor cortices and leads to directedmovement. In addition, other parts of the nervoussystem concerned with tactile, visual, and auditorysensation are connected by fiber tracts with themotor cortex. These association pathways providetheir own sensory regulation of motor function ERS 9
  • Levels: • Motor Unit (LMN) • Segmental/spinal cord • Suprasegmental – Various descending systems modulate activity in segmental level – Brainstem, cerebellar, extrapyramidal, pyramidal – Psychomotor/ cortical associative Fig: The most important descending pathways that act upon the anterior horn cell of the spinal cord (deJongERS 2010) 10
  • (DeJong, 2010) • Lat ReticuloSpinal: – influence the musculature of the trunk. • Med TectoSpinal: – reflex movement – Trunk, neck, eyes ~ visual stimuli • Lat CorticoSpinal: – Hand, finger movement • RubroSpinal: – Hand, finger movement – Flexor muscle tone – Postural mechanism, standing/righting reflex • Lat VestibuloSpinal: – Postural mechanism, standing/righting reflex Mainly control trunk & proximal extremityERS 11
  • DeJong, 2010ERS 12
  • Waxman, 2010ERS 13
  • Motor ParalysisTerminologyParalysis Loss of involuntary movement due to interruption of motor pathway (cerebrum – muscle fiber)Paresis A lesser degree of paralysis / partial lossPlegia Severe / complete loss of motor functionFocal ~ asymmetry Ex: hemi-Generalized ~ symmetry (although the weakness not truly general, ex.: scapuloperoneal syndrome) Truly generalized  bulbar is impairedMultifocal Ex.: bilateral CTSNon-focal Generalized, predominantly proximal, predominanly distalThese various patterns have differential diagnostic and localizing significance.Identification of the process causing weakness is further aided by accompanying signs,such as reflex alterations and sensory loss. (DeJong, 2010) ERS 14
  • Pattern of Paralysis & Their Diagnosis Adams & Victor, 2005 Apraxia: a state in which a clear- minded patient with no weakness, ataxia, or other extrapyramidal derangement, and no defect of the primary modes of sensation, loses the ability to execute highly complex and previously learned skills and gestures. NMJERS 15
  • Mumenthaler, 2004ERS 16
  • Bradley, 2010ERS 17
  • Bradley, 2010ERS 18
  • Mumenthaler, 2004ERS 19
  • Bradley, 2010ERS 20
  • Bradley, 2010ERS 21
  • ERS 22
  • Bradley, 2010ERS 23
  • ERS 24
  • ERS 25
  • ERS Bradley, 2010 26
  • ERS 27
  • Mumenthaler, 2004ERS 28
  • Bradley, 2010ERS 29
  • Bradley, 2010ERS 30
  • Proximal, Distal & General Weakness Bradley, 2010 ERS 31
  • Adams & Victor’s, 2005ERS 32
  • Features of UMN vs LMN Weakness (DeJong, 2005) + UMN LMNWeakness Corticospinal Generalized, focal, predominantlydistribution distribution, hemi-, distal, predominantly proximal, para-, quadri-, mono-, No preferential involvement of faciobrachial corticopsinal innervated muscleSensory loss Central pattern None, stocking glove, peropheral / rootdistribution distributionSphincter function Sometimes impaired Normal (except for cauda equina lesion)Pain No SometimesOther CNS sign Possibly NoCorticospinal distribution:• Distal muscle• Upper ext: esp hand; wrist, finger & elbow extnsor, supinator, external rotator, abductor shoulder• Lower ext: foot & toe dorsiflexor, knee flexor, hip flexor & internal rotator, ERS 33
  • Muscle Tone (DeJong, 2010) Hypotonia HypertoniaMyopathy Cerebellar Spasticity Rigidity Dystonia: disease most marked the increased tone occurs to transient or near the more or less the same degree sustained middle of the throughout the range of hypertonic range of passive motion of a limb, and is conditions that motion, more independent do not fit into apparent with of the speed of the movement the other fast than with categories slow passive Lead pipe Cogwheel Paratonia: movement smooth ratchety, jerky, increase in tone resistance tremulous in a limb throughout variation in the more or less the range hypertonia, proportional to independent due primarily the examiners of the rate of to attempt to move. superimposed move it. tremor (Gegenhalten) ERS 35
  • Muscle Volume & Contour (DeJong, 2010) Atrophy Hypertrophy Neurogenic Myogenic Disuse True PseudoWeakness // Weakness >> Immobilization: Physiologic apparent musclewasting wasting Wasting >> enlargement due toMay be Mild-moderate weakness replacement ofsevere Mild-moderate diseased muscle by Recovers quickly fat and fibrousAnterior horn with resumption tissuecell  of uses Ex: DuchenneperipheralnerveUMN:Usually notfollowed byatrophy ERS 36
  • Abnormal of movement & posture due to disease of Basal Ganglia• Akinesia: absence of • Tremor movement • Athetosis: slow, writhing• Bradykinesia: abnormally movements of the slow movement extremities & neck• Hypokinesia: a decreased musculature amount or amplitude of • Chorea: movement. quick, repeated, involunta• Dyskinesia: ry movements of distal involuntary, abnormal extremity movement muscle, face, tongue, ~Waxman, 2010 corpus striatum ERS 37
  • Extrapyramidal System A: Basal ganglia: major Extrapyramidal motor structures. system: MD, medial dorsal; VA, ventral anterior; VL, – Corpus striatum ventral lateral nuclei of – Subthalamic nucleus thalamus – Substansia nigra – Red nucleus – Brain stem reticular formation – Descending spinal cord tract other than corticospinal tract (Waxman, 2010) ERS 38
  • Waxman, 2010ERS 39
  • Adams & Victor, 2005 Waxman, 2010ERS 40
  • Adams & Victor, 2005ERS 41
  • Adams & Victor’s, 2005 ERS 42
  • Adams & Victor’s, 2005ERS 43
  • Adams & Victor’s, 2005ERS 44
  • Incoordination & other disorders of Cerebellar function Truncal ataxia, drunken gait Ataxia, asynergy, dysmetria, dysdia docho- kinesia, intention tremor, rebound phen.Loss of equilibrium,nystagmus Adams & Victor’s, 2005 | Waxman, 2010 ERS 45
  • There is a somatotopicorganization of body partswithin the cerebellar cortex.In addition, the cerebellumreceives collateral input fromthe sensory and specialsensory systems.Waxman, 2010 ERS 46
  • Waxman, 2010ERS 47
  • Efferents from Cerebellum:the dentatorubrothalamocortical pathway Via this pathway, activity in the dentate nucleus & other deep cerebellar nuclei modulates activity in the contralateral motor cortex. This crossed connection, to the contralateral motor cortex, helps to explain why each cerebellar hemisphere regulates coordination and muscle tone on the ipsilateral side of the body. Waxman, 2010 ERS 48
  • Waxman, 2010TerminologyDysmetria Past-pointing phenomenon, unable to estimate the distance involved in muscular acts  their attempt to touch the object will overshoot the targetDysdiadochokinesia Inability to perform rapidly alternating movementsRebound phenomenon Loss of interaction between agonist & antagonist smooth muscle ERS 49
  • Signs of Various Lesions of Human Motor system (Waxman, 2010) * Fasciculations are spontaneous, grossly visible contractions (twitches) of entire motor units ERS 50
  • Abnormality of movement (DeJong, 2005)Hypokinetic Hyperkinetic• Parkinsons disease • Regular/predictable• Parkinsonian syndromes – Progressive supranuclear palsy – Tremor – Multisystem atrophy – Hemiballism – Olivopontocerebellar degeneration (sporadic form) – Palatal myoclonus – Striatonigral degeneration • Intermediate – Shy-Drager syndrome – Dystonia – Diffuse Lewy body disease – Corticobasal degeneration – Myokymia – Drug-induced parkinsonism – Athethosis – Dopa responsive dystonia – Tic• Other non-Parkinsons akinetic-rigid syndromes – Stereotypy• Huntingtons disease (rigid or juvenile – Myorythmia form) • Fleeting/unpredictable• Wilsons disease – Fasciculations• Essential tremor• Depression – Myoclonus• Arthritis, polymyalgia, fibromyalgia – Chorea ERS – Dyskinesias 53
  • 54Bradley, 2010 ERS
  • 55Bradley, 2010 ERS
  • Adams & Victor’s, 2005ERS 56
  • 57Bradley, 2010 ERS
  • Disorder of Stance & Gait Adams & Victor’s, 2005 ERS 58
  • Disorder of Stance & Gait Adams & Victor’s, 2005 ERS 59
  • Bradley, 2010ERS 60
  • Apraxiahttp://thebrain.mcgill.ca Bradley, 2010 ERS 61
  • Bradley, 2010ERS 62
  • Bradley, 2010ERS 63
  • Finally, it should be remarked once again that the complexity of motor activity is almost beyond imagination. Adam & Victor, 2005 ERS 64