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peripheral nn disord
peripheral nervous disorders
| Question | Answer |
|---|---|
| are the vental or dorsal root fibers more affected in an aging persons PNS? | ventral root |
| T/F Neuropathy is always indicative of a disease process. | FALSE it can be a part of normal aging |
| What vascular events occur with aging and what is the result? | athlerosclerosis of blood vessels to nerve resulting in the loss of nerve fibers and peripheral neuropathies. |
| myelin deterioration occurs with aging secondary due to what and results in what? | secondary to decreased protein production and results in diminshed vibratory sense |
| Why is there ANS dysfunction doe to aging (3 reasons) | 1) loss of cell bodies in sympathetic ganglia, 2) loss of unmyelinated fibers in peripheral nerves, 3) decrease of sympathetic control of dermal vasculature |
| How soon are age related changes seen in the motor endplate (i.e. decade of life)? | 3rd decade |
| What is altered within the motor endplate due to age? | sensory receptors, axonal myelination, loss of motor units |
| What is "aging neuropathy?" | the clinical signs of peripheral neuropathy are present but there is no evidence of a neurological disease or disease process |
| What are some causes of aging neuropathy? | loss of motor and sensory cell bodies. dying back condition, comorbidities, nutritional deficiencies, fx, and swelling |
| How is recovery affected in the aging system? | Wallarian degeneration is delayed, reduced density of regenerating axons, and reduced collateral sprouting |
| What is the response of the peripheral nerve secondary to compression or disease? | segmental demyelination |
| What is the response of the peripheral nerve secondary to physical injury and disease/ directly affects the axon? | degeneration (anterograde or Wallarian degeneration) |
| What are the 3 Seddon Classifications of nerve injury? | neuropraxia, axonotmesis, neurotmesis |
| Neuropraxia results in ___ (axon and/or myelin) which causes ___ speed of an action potential at the point of the lesion. | segmental demyelination/ slow or block |
| Is there atrophy of the nerve in a neurapraxia? | no |
| What could cause neuropraxia? | mild ischemia |
| Axonotmesis is the result of of what (axon and/or myelin)? | axon damage but the myelin is still intact |
| What could cause axonotmesis? | infarction and necrosis |
| Axonotmesis can have regeneration as long as ___. | the cell body remains intact if compression is relieved |
| Neurotmesis is the result of of what (axon and/or myelin)? | complete severance of axon and disruption of connective tissue |
| How fast does a nerve reginerate? | 1mm/day |
| What is mononeurpathy vs. polyneuropathy? | mono: one nerve affected, poly: multiple nerves affected |
| What is radiculopathy vs. polyradiculitis? | rad: nerve root affected, polyrad: multiple roots inflamed |
| T/F A peripheral nerve lesion is when the peripheral nerve is affected and everything above the lesion innervated reamins intact. | TRUE |
| What is affected in a dermatomal pattern? | nerve roots or cell bodies |
| T/F a peripheral nerve degeneration typically affects the shorter nerves nefore the longer nerves | FALSE it affects the longest fibers first (LE before UE) |
| What is paresis vs paralysis? | paresis: severe weakness, paralysis: no motor function |
| What is the most common hereditary neuropathy? | Charcot-Marie-Tooth |
| What systems does CMT affect? | sensory and motor |
| Is CMT usually symmetrical or asymmetrical? | symmetrical |
| What are some clinical signs of CMT? | distal symmetrical muscle weakness, atrophy, diminished DTRs (LEs), oes cavus, hammer toes, weak DF and evertors, later involvement of hand intrinsics/ forearm muscles. |
| What is a clinical difference in CMT1 but minimal in CMT2? | sensory signs will be present in both but sensory loss is generally only in type1 |
| T/F Diabetic neuropathy occus in setting of diabetes mellitus with other causes for peripheral neuropathy | FALSE without other causes for peripheral neuropahy |
| How does diabetic polyneuropathy present? | distally and symmetrical |
| What is the cause of diabetic polyneuropathy? | chronic metabolic imbalances that affect nerve and schwann cells (high sugar levels are toxic to vascular supply and toxic to the nerve) |
| What are the classificaiton of a diabetic neuropathy? (5) | rapidly reversible, generalized symmetric polyneuropathy, chronic sensorimotor, autonomic neuropathy, focal |
| What is problematic in rapid reversible diabetic neuropathy? What population does this normally involve? | blood sugar needs to be controlled, seen in newly diagnosed diabetics or individuals with poorly controlled diabetes |
| What are the acute sensory signs of generalized symmetric polyneuropathies? | rapid onset of severe burning, sudden deep and sharp pain, "eletric shock" and hypersensitivety of the feet |
| How will a pt with generalized symmetric polyneuropathies motor and sensory signs present? | motor is normal and sensory could have a mild loss of with allodynia (pt has painful response to non-painful stimulus) |
| Can a person with generalized symmetric polyneuropathy recover? | if achieves a stable blood glucose the recovery can occur within a year |
| What is the most common type of diabetes neuropathy? | chronic sensorimotor |
| What is problematic in chronic sensorimotor DM? | blood supply |
| What are the clinical features (motor and sensory) of chronic sensorimotor DM? | sensory loss, small fiber involvement (burning, paresthesia), and large fiber involvement (painless paresthesia, imapired proprioception, touch and pressure, loss of ankle DTRs), mild motor |
| The pt may be experiencing sweating, orthostatic hypotension, and resting tachycardia in which classification of DM? | chronic sensorimotor |
| How does alcoholic neuropathy present? | typically peripheral involvement with distal, symmetrical distribution loss. |
| What are possible causes of alcoholic neuropathy? | toxic effects of alcohol, nutritional deficiencies (thiamine, B vitamins, etc.), accumulation of ethanol |
| T/F In alcoholic neuropathy all 4 extremities are involved and the UE and more effected than the LE. | FALSE the LE> UE |
| T/F a pt experiencing chronic renal failure will commonly complain a lot of restless leg and in general the LE are mor affected than the UE. | TRUE |
| The pain present in chronic renal failure is due to what? | excess nitrogen and waste product |
| Does chronic renal failure more commonly affect the CNS and/or PNS? | both |
| What disease is the most common to cause acute motor and sensory deficits? | Guillain-Barre |
| What are possible triggers of Guillain-Barre? | virus, bacterial, surgery, vaccinations (2/3 report recent infection) |
| What are the peaks in frequency of GBS? | teens to 20s and 50-80s |
| Are there variants of GBS? | yes |
| How is the progression of GBS and how does recovery occur in GBS? | after progession stops there is a static phase (2-4 wks) and then recovery occurs proximal to distal in fashion (months - yrs) |
| What are possible treatment options for GBS? | plasmapheresis and high-does IV immunoglobulins (corticosteroids have not been effective) |
| What can the PT do for a pt in the initial and early treatment stages of GBS? | prevent secondary complications, monitor exercise, positioning, splinting, and muscle pain relief, head-hips realtionship |
| What percent of polio survivors develop postpolio syndrome? | 25-50% |
| What does polio attack in the body? | anterior horn cells of the spinal cord (motor neuron dysfunction) |
| What are symptoms of polio? | muscle strength decline, myalgia, joint pain, muscle atrophy, excessive fatigue, decreased indurance, night pain |
| What is the prognosis of postpolio syndrome? | it is a slowly preogressive disorder with stable periods for 3-10 yrs. |
| What are PT interventions and are the well tolerated by the pt? | pt education for joint integrity, maneuvers, and orthotic prescription (not well tolerated) |
| What autoimmune disorder effects the NMJ and motor end plate? | Myasthenia Gravis |
| What age and gender is typically more affected by MG? | females 20-30s and males 50-60s, females > males |
| What are additional risk factors of MG? | thymic disorders (tumor), throid disorders (hyper, thyrotoxicosis), diabetes, RA, lupus, hormone flucturations |
| What occurs at the cellular level in MG? | decreasde number of ACh receptors and the receptors present are not enough |
| What are the cardinal features of MG? | skeletal muscle weakness and fatigability |
| T/F MG presents as motor weakness and a change in DTRs | FALSE MG only presents as muscle weakness |
| T/F MG is more notable in dital muscles | FALSE proximal |
| T/F cranial muscles are commonly affected first in MG | TRUE (ptosis, diplopia, facial expression and mastication) |
| What are the three ways to diagnose MG? | immunology, phamacological, and electrophysical testing |
| What are treatments to MG? | AChE inhibitor, immunosuppressive drugs, thymectomy, plasmapheresis/IV globulin therapy |
| What are PT considerations for pts with MG? | proximal stabilization for distal use, avoid secondary complications, respiration, energy conservation, strength training |
| What can cause paraneoplastic neuropathies? | cancer treatments and neoplasms |
| What are 3 changes to the PNS with aging? | 1) thicking of perineurium and epineurium 2) fibrous and inc collagen of endoneurium 3) decreased cross sectional area |
| Why is there a decreased cross sectional area of an aging person's nerves? (hint what is reduced in number) | reduced myelinated and unmyelinated fibers |
Created by:
Leeli.PT
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