Neuromus Disorders 3 Flashcards
Peripheral Neuropathies Causes
Single: trauma, pressure paralysis, forcible overexten of joint, hemorrhage into nerve, exposure to cold/radiation or ischemic (restriction of blood flow) paralysis. Multiple: collagen vascular disease, metabolic diseases (DM) or infectious agents (Lyme). Other: alcohol, nutritional deficiencies, malignancy, toxic agents/microorganism
Peripheral Neuropathies Symptoms
A syndrome of sensory/motor/reflex/vasomotor symptoms. Pain, weakness, parasthesis (pins/needles) in distribution of affected nerve
Guillan-Barre Syndrome
Unknown etiology but may occur after infectious d/o, surgery or immunization. Affects both sexes/any age. Onset of recovery is 2-5wks after inital symptoms
Long term prognosis of Guillan-Barre Syndrome
50% exhibit mild neurolog deficits, 15% exhibit residual fx’al deficits, 80% are ambulatory after 6mo and only 5% die of complications
Guillan-Barre Syndrome Symptoms
Acute, rapidly progressive form of polyneuropathy characterized by symmeteric muscular weakness and mild distal sensory loss/parasthesias. Weakness always most predominant. Sensory symptoms are relatively mild. Deep tendon reflexes are lost/sphincter control spared.
Myasthenia Gravis
Diseased caused by autoimmune attack on ACT receptor of postsynaptic neuromus junction; considered disorder of neuromus transmission. Onset at any age: most often older men/younger women. Usually progressive & death may occur from respiratory comps.
Myasthenia Gravis Symptoms
Characterized by episodic mus weakness - chiefly mus innervated by CNs. Ptosis, diplopia, muscle fatigue after exercise, dysarthria, dysphagia, prox limb weakness. Symptoms fluctuate over the day. Deep tendon reflexes/sensation in tact. Ability to relapse w quadriparesis
Post-Polio Syndrome
Some MN infected w Polio virus die, others survive. Recovered develop new terminal axon sprouts that reinnervate muscle cells. After years of stability, motor units breakdown cause muscle weakness. Typ occurs 15yrs after Polio recovery. Slow to progress and good prognosis.
Post-Polio Syndrome Symptoms & Tx
New onset of weakness, easily fatigued, muscle pain, joint pain, cold intol, atrophy, loss of fx’al skills > Bracing, stretching/exercise programs
Multiple Sclerosis (MS)
Slowly progressive CNS disease characterized by patches of demyelination of brain and SC. Occurs most often between 20-50yrs. Overall prognosis is variable w unpredictable disease course > multiple CNS lesions & at least 2 episodes of neurolog disturbance. remissions and exacerbation
MS Symptoms
Onset usually insidious (gradual but harmful). Parasthesias in one+ extremities/trunk/face. Weakness of hands/legs. Visual/emotional/cog disturbances. Balance loss/vertigo. Bladder dysfunction. Sensorimotor findings.
MS Patterns
Relapsing remitting, secondary progressive, primary progressive, progressive relapsing
Eval for Neurolog D/o
Determine sensory/motor dysfunction strengths: paralysis/weakness, GM/FM, spasticity, sensory, postural control, ROM, MMT, skin integrity, foundation visual skills, pervasive impairments, psychosoc. Impact of deficits on ADLs/occs
General Intervention/Tx for Neurolog D/o
Positioning, pressure reduction, postural control, motor learning approaches, motor control retraining/relearning, specific ADL training/retraining/adaptations, AT, splinting for contractures, fam/caregiver edu, cog retraining, visual skills retraining, sexual dysfunction help, B&B training, skin care edu, DME, sensory re-edu, community re-integration, return to work/work hardening
Work Hardening Program
Highly structured, goal oriented, individualized treatment program designed to maximize the indiviual’s ability to return-to-work.
Fast Pain
Transmitted over A Delta fibers. Processed in SC dorsal horn lamina. Crosses to excite lat spinothalamic tract & terminates in BS reticular formation. Functions for discrimination of pain/localization
Slow Pain
Transmitted over C fibers. Processed in SC lamina. Crossed to excite ant spinothalamic tract. Terms in BS reticular formation > excites Reticular Activating System (RAS)/ Functions for diffuse arousal, affective & motivational aspects of pain
Acute Pain
Sharp pain, sympathetic changes (increased HR, BP, pup dilation, sweating, hyperventilation, anx, escape/protective behaviors
Chronic Pain
Pain that persists beyond usual healing course. Symptoms present for longer than 6mo for which underlying pathology is no longer identifiable or may never have been present
Neuropathic Pain
Pain as result of lesions in some part of nervous system; usually accompanied by some degree of sensory deficit.
Thalamic Pain
Continuous, intense, occurring on contralat hemiplegic side > result of stroke involving vent postlat thalamus; poor rehab potential
Complex Regional Pain Syndrome Type I
Formerly known as Reflex Sympathetic Dystrophy (RSD).; pain maintained by efferent activity of sympathetic nervous system. Characterized by abnorm burning pain, hypersensitivity to light touch & sympathetic hyperfunction (sweating/coldness) > usually associated w traumatic injury
Complex Regional Pain Syndrome Type II
Formerly known as Neuralgia. Pain occurring along branches of a nerve.
Herpes Zoster (Shingles)
Acute, painful mononeuropathy caused by varicella virus. Vesicular eruption and marked inflam of post root gang if affected SN or sensory gang of CN - vent root involvement (motor weakness). Can last 10days- 5wk > pain may persist for months
Psychosomatic Pain
origin of pain experience is d/t mental/emo disorder
Referred Pain
Pain arising from deep visceral tissues that is felt in body region remote from the site of pathology resulting in tenderness & cutaneous hyperalgesia (abnorm heightened pain sensitivity)
Postural Stress Syndrome (PSS)
Chronic mus lengthening/shortening that causes postural malalignment and stress to soft tissue > check for during pain eval
Eval for Chronic Pain
Hx, localization, nature of pain (constant/intermittent), subject pain intensity scale, physical assessment, PSS, autonomic changes (sympathetic activity), abnorm mvmts, degree of suffering, fx’al changes, emo changes, precrip drug misuse, dependence on health care system, responsiveness to pain, motivation/affective components
Chronic Pain Tx
Edu on contributing factors, edu on responding adaptively to pain behaviors, develop strategies/techniques to manage pain (relaxation training), refer to other professionals, estab realistic daily activity program, improve overall fx’al capacity, fam edu
Sensory Processing D/o
Subtle, prim subcorticala, neural dysfun w impaired processing of sensory info and modulation of multisensory systems
Dunn’s Model of Sensory Processing Symptom Classification
classified according to interaction of sensory stim that are needed to stim behavioral response. High/low threshold & passive/active response
Sensory Modulation D/o
Sensory Overresponsitivity, Sensory Underresponsitivity or Sensory Seeking/Craving
Sensory Based Motor D/o
Includes underlying sensory discrim d/o as well as possible sensory mod d/o: dyspraxia (developmental coordination disorder variation) or sensory-based postural disorders
Eval for Sensory Processing D/o
Hx, fam/teacher interview, informal observation followed by formal assessment of clinical observations, standardized testing
Seizure D/o vs Epilespy
Epi= chronic state of recurrent seizures. Seizure D/o= temp disturbance in brain activity causing a group of nerve cells to fire excessively, interfering with norm brain fx
Seizures are often associated w these other conditions
O deprivation, severe head injury or brain hemorrhage, CP, stroke, brain tumor, other neurolog d/o, hydrocephalus, metabolic d/o, infections, meningitis, encephalitis, rubella
Prim Gen Seizures]
Begin w widespread involv of both sides of brain
Partial Seizures
Involv of smaller/localized area > can still spread within seconds/mins to gen (secondary gen seizure)
Tonic-Clonic Seizures (grand-mal)
Most common type of seizure d/o in children. Brief warning/aura (numbness, taste, smell). Tonic phase includes LOC, stiff of bod, heavy/irreg breathing, drooling, skin pallor, occasional incontinence. Clonic phase includes alternating rigidity/relax of muscles. Following= Postictal State which includes drowsiness, disorientation or fatigue
Myoclonic-Akinetic Seizures
*Not the same as infantile. Brief, invol jerking of extem w or w/o LOC, include loss of tone - difficult to control.
Petit-Mal Seizures
Absent seizures. Typically between 4-12y/o, LOC w/o loss of mus tone. Rapid blinking or staring into space - does not fall but does not recall episode
First Aid Seizure Procedures
Remain calm and if status elepticus call for immediate med attn, remove all dangerous objects from area, do not interfere w mvmts, raise bed rails, make sure nothing is in the mouth, turn to side if aspiration risk (recovery position), allow seizure to happen while protecting head, monitor for improved mental state
Call for med attn during seizure if
Individual’s first, in H2O, if has second seizure, if consciousness is not regained after 5-10min, if seizure last 5min or more, if individual is diabetic or pregs
Post Seizure Care
Allow individual to rest/sleep, inform parents/caregiver, observe safety precautions
Seizure Eval and Intervention
Assess/intervene for DD as necessary. Observe all med/safety precautions. Doc/report any seizure activity, med side effects or behavioral changes.
