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Clin. Neuro Class 5
| Question | Answer |
|---|---|
| What is a LMN lesion? | injury to peripheral nerve, affects its sensory, motor or both |
| What is the result of LMN lesion? | Diminished sensation Decreased muscle performance (weakness) Decreased DTR’s |
| What results from a loss or impairment of UMN control of LMN? | Paresis Loss of fractionated movement Abnormal reflexes Muscle hyperstiffness Maybe co-contraction and movement synergies |
| What results from paresis? | Inadequate recruitment of LMN by UMN Some evidence of denervation on EMG Adaptive muscle contracture with disuse “Learned non-use” and maladaptive sensory-motor plasticity |
| What problems with cutaneous reflexes result? | Plantar Response (Babinski) Withdrawal reflex exaggerated |
| What are the features of hyper-reflexia? | increased DTRs, velocity dependent |
| What is diaschisis? | |
| What early changes occur with LMN lesion? | upregulation of receptors |
| What are the later changes that occur? | competitive use- dependent plasticity |
| What is hyper-reflexia's relationship to motor recovery? | inversely proportional to motor recovery |
| What is the tonic stretch reflex? | Mediated by Primary and Secondary MS endings Normally absent (i.e. MS input is not enough to bring alpha motor neuron to threshold) With UMN lesion may be present |
| What is the clasped knife reflex? | Resistance suddenly drops off with sustained stretch See only in UMN lesions (difficulty for a person to flex, asyou stretch the limb initially will be difficult, and then suddenly collapse into flexion |
| What is normal muscle stiffness? | resistance to either active or passive stretch |
| What is normal muscle stiffness determined by? | Active factors Intrinsic factors Passive Factors |
| What are the active factors for normal muscle stiffness? | Active muscle contraction (may be reflex induced) Active actin-myosin cross bridging with Ach release |
| What are the intrinsic factors for normal muscle stiffness? | Weak Actin and Myosin bonds at rest |
| What is the passive factors of normal muscle stiffness? | Titin largest known protein – 34,350 amino acids |
| What causes muscle hyperstiffness= non-neural components? (with contractures) | With contractures – loss of sarcomeres Decreased titin with loss of sarcomeres So less elastic, more stiff |
| What is another non-neural component for hyperstiffness? | Increased weak actin-myosin bonds in inactive muscle |
| What happens to a muscle during immobilization? | Contracture so loss of sarcomeres, decreased titin (passive, non-neural factor) Increased actin-myosin bonds at rest (because of disuse; non-neural, intrinsic factor) |
| What is the cause of hyper-stiffness with UMN lesion? (non-neural comp) | Myoplasticity (non-neural component) Muscle contracture (secondary to disuse) Increased weak actin-myosin bonds (secondary to disuse) Prominence of Type I fibers (seen in UMN only, not normal immobilization) |
| What is the cause of hyperstiffness in UMN? (neural component) | Overactive Neural Input (neural component) Hyperreflexia Increased UMN activity (sometimes) |
| What is muscle tone? | The resistance that an examiner perceives when moving someone’s limb in a passive manner Normally resistance is minimal |
| What does normal resistance come from? | Weak actin-myosin bonds (intrinsic) Titin (passive) |
| What is hypertonia? | Increased resistance to passive stretch Either quick stretch (increased DTR’s) Or sustained stretch |
| Cause of hypertonia | Causes: Increased excitability of LMN by MS afferents Increased tonic stretch reflexes Myoplasticity |
| What is hypotonia? | Decreased resistance to passive movement |
| What is usually associated with hypotonia? | Usually associated with decreased DTR’s Usually associated with weakness and/or acute paralysis(some more chronic UMN lesions) |
| Causes of hypotonia | Always seen in peripheral n. damage Acute CNS damage (diaschisis or spinal shock) |
| What is spasticity? | “A motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting in hyperexcitability of the stretch reflex, and is one of the components of the upper motor neuron syndrome” |
| Measurement of hyperreflexia? | H reflex for laboratory measure |
| Modified Ashworth Scale | Developed as “spasticity” scale But really measures muscle stiffness |
| What pathway does the H reflex follow? | H reflex follows the same pathway at the monosynaptic stretch reflex |
| Management of excessive tone | Baclofen Pump Medications applied to motor end plate or proximal nerve Botulinum Toxin Phenol Oral agents Dorsal Rhizotomy or Phenol Block Muscle/tendon lengthening |
| What is dystonia? | Sustained muscle contractions that produce twisting repetitive |
| Where can dystonia occur? | any muscle group except extraocular |
| What are the contractions like? | Contractions can be sustained, intermittent, rhythmic or tremulous |
| What can make dystonia worse? | stress or fatigue |
| What type of mechanism is involved in dystonia? | basal ganglia mechanisms |
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