Busy. Please wait.

show password
Forgot Password?

Don't have an account?  Sign up 

Username is available taken
show password


Make sure to remember your password. If you forget it there is no way for StudyStack to send you a reset link. You would need to create a new account.
We do not share your email address with others. It is only used to allow you to reset your password. For details read our Privacy Policy and Terms of Service.

Already a StudyStack user? Log In

Reset Password
Enter the associated with your account, and we'll email you a link to reset your password.
Don't know
remaining cards
To flip the current card, click it or press the Spacebar key.  To move the current card to one of the three colored boxes, click on the box.  You may also press the UP ARROW key to move the card to the "Know" box, the DOWN ARROW key to move the card to the "Don't know" box, or the RIGHT ARROW key to move the card to the Remaining box.  You may also click on the card displayed in any of the three boxes to bring that card back to the center.

Pass complete!

"Know" box contains:
Time elapsed:
restart all cards
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.

  Normal Size     Small Size show me how

Clin. Neuro Class 5

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
Created by: 696592119