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09f CLINICAL APPLICATIONS OF YOUR KNOWLEDGE OF THE MOTOR SYSTEMS.

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Presentation on theme: "09f CLINICAL APPLICATIONS OF YOUR KNOWLEDGE OF THE MOTOR SYSTEMS."— Presentation transcript:

1 09f CLINICAL APPLICATIONS OF YOUR KNOWLEDGE OF THE MOTOR SYSTEMS

2 Think: Unilateral damage to upper motor neuron… and reasons for associated spastic hemiplegia At first: At first: –Flaccidity of distal muscles –Loss of precise control –Positive Babinski 1 to 4 weeks later 1 to 4 weeks later –Spasticity of distal muscles, esp. for cortico- spinal system –Hyperreflexia –Clasp-knife rigidity Signs present ____________ to site of lesion See pp. 352-357 in book

3 Spastic hemiplegia, spastic monoplegia Which UMNs have been affected?

4 Think: Bilateral damage to upper motor neuron… and reasons for associated pseudobulbar palsy Signs Signs –Flaccidity of facial muscles –Loss of precise control of facial muscles –hyperreflexia –Strain-strangled spasticity of voice –Voluntary mvmnt of face poor, but emotional mvmnt of face (via limbic system) present Little spasticity in face, but voice strained (spastic) See p. 353-357 in book

5 Pseudobulbar palsy Examples of hyper-reflexia, as well as preservations of normal reflexes, in cases of severe TBI with associated pseudobulbar palsy Examples of hyper-reflexia, as well as preservations of normal reflexes, in cases of severe TBI with associated pseudobulbar palsy Strained-hoarse voice, slow rate, imprecision of articulation and hypernasality in Case 13 (pseudobulbar palsy) Strained-hoarse voice, slow rate, imprecision of articulation and hypernasality in Case 13 (pseudobulbar palsy)

6 Think: Brainstem stroke, and how it may result in alternating or “crossed” hemiplegia Simultaneous lesion of Simultaneous lesion of –Cranial nerve motor nuclei and/or nerves, LMN (motor unit) –UMN LMN signs ipsilateral to lesion LMN signs ipsilateral to lesion UMN signs contralateral to lesion UMN signs contralateral to lesion See p. 353-354 in book

7 Think: Damage to LMN and its clinical presentation. Why this association? Includes bulbar palsy, damage to nerves, or poor neuro-muscular communication Includes bulbar palsy, damage to nerves, or poor neuro-muscular communication Signs Signs –Absent reflexes –Flaccid tone –Muscle wasting/atrophy –Fasciculations and fibrilations (activity of denervated muscle) See p. 353-357 in book

8 Example of fasciculations and atrophy with LMN involvement Case 14—Fasciculations of tongue Case 14—Fasciculations of tongue Case 15---Flaccidity of face and soft palate Case 15---Flaccidity of face and soft palate

9 Speech motor system complex and neurologically sensitive Over 100 muscles must be controlled and coordinated Over 100 muscles must be controlled and coordinated Approximately 14 recognizable speech sounds are uttered per second Approximately 14 recognizable speech sounds are uttered per second “Normal speech production requires the finest motor control in the body” (W&A, p. 125) Speech motor system highly sensitive to even small neurological changes/damage, at any point in the motor neural pathways

10 SLP / A----Our role in diagnosis “Motor speech disorders (and other communication disorders) often can be linked to disease location and sometimes to specific diseases, even when localization and diagnosis have not yet otherwise been established.” “Motor speech disorders (and other communication disorders) often can be linked to disease location and sometimes to specific diseases, even when localization and diagnosis have not yet otherwise been established.” (Joseph Duffy, Mayo Clinic, The ASHA Leader, November 25, 2008) (Joseph Duffy, Mayo Clinic, The ASHA Leader, November 25, 2008)

11 Dysarthrias (speech motor disorders) Dysarthria associated with bilateral upper motor neuron damage: Spastic dysarthria (muscles are overly tight, because inhibition of LMN which would normally be supplied from cortex through UMN cannot reach the LMN; hyper-reflexia makes muscles extra tight) Dysarthria associated with bilateral upper motor neuron damage: Spastic dysarthria (muscles are overly tight, because inhibition of LMN which would normally be supplied from cortex through UMN cannot reach the LMN; hyper-reflexia makes muscles extra tight) Dysarthria associated with lower motor neuron damage: Flaccid dysarthria (muscles are floppy because they are not receiving activation through LMN) Dysarthria associated with lower motor neuron damage: Flaccid dysarthria (muscles are floppy because they are not receiving activation through LMN)

12 Dysarthrias (speech motor disorders), cont. Dysarthrias associated with basal ganglia involvement Dysarthrias associated with basal ganglia involvement –Hypokinetic dysarthria (prob. w/ movement inititation) Dysarthria associated with Parkinson’s disease (not enough dopamine in substantia nigra) Dysarthria associated with Parkinson’s disease (not enough dopamine in substantia nigra) –Hyperkinetic dysarthria (prob. w/ movement inhibition) E.g. Huntington’s chorea E.g. Huntington’s chorea E.g. myoclonus E.g. myoclonus Dysarthria associated with cerebellar involvement: Ataxic dysarthria Dysarthria associated with cerebellar involvement: Ataxic dysarthria

13 IF DAMAGE/LESION IS IN…. …THE SPEECH/VOICE/ RESPIRATORY MUSCLES… …AND THIS IS CALLED lower motor neuron are weak and lacking in muscle tone flaccid dysarthria upper motor neuron (bilaterally) have too much muscle tone (a “tight feeling”) and move slowly and with difficulty spastic dysarthria cerebellum or cerebellar pathways are uncoordinated in their movements ataxic dysarthria basal ganglia circuits, for: --movement initiation --movement inhibition --display excessive, small movements, not fully movements, not fully initiated initiated --display extraneous, involuntary movement involuntary movement dyskinetic dysarthria --hypokinetic dysarthria --hyperkinetic dysarthria language dominant hemisphere, especially frontal lobe motor planning areas …are NOT weak, tight, uncoordinated, or dyskinetic, BUT the planning for the correct movements is poor apraxia of speech Note: Mixed dysarthria also possible

14 Additional examples of dysarthria Case 16—Cerebellar degenerative disease Case 16—Cerebellar degenerative disease –_______________ articulatory breakdown Case 17—Hypokinetic dysarthria of Parkinson’s disease Case 17—Hypokinetic dysarthria of Parkinson’s disease Cases 18, 19, 20—Focal hyperkinetic dyskinesias affecting speech (facial and fasciaolingual dyskinesias) Cases 18, 19, 20—Focal hyperkinetic dyskinesias affecting speech (facial and fasciaolingual dyskinesias)


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