Stroke rehabilitation --------------------------------------------------	P1
Traumatic brain injury rehabilitation -------------------------------	P12
Spinal cord injury rehabilitation ------------------------------------	P28
Electrodiagnosis ------------------------------------------------------	P37
Pediatric rehabilitation -----------------------------------------------	P45
Musculoskeletal ultrasound -----------------------------------------	P59

Stroke rehabilitation

Definition

�a nontraumatic brain injury caused by occlusion or rupture of cerebral blood vessels

� results in sudden neurological deficit

�losss of motor control,

�altered sensation,

�cognitive or language impairment,

�disequilibrium,

� coma

Pathological classification of stroke

�Hemorrhagic: 15%

�Intracerebral: 10% --HTN, AVM, tumor

�Subarachnoid: 5% -- aneurysm rupture

�Ischemic: 85%

�Large vessel: 40% --artherosclerotic à large and small vessels thrombosis.

nSmall vessel: 20% -- HTN

�Cerebral embolism: 20% -- cardiac origin

�Less common cause: 5% -- vasculitis, hypoperfusion

Temporal classification of stroke

�TIA: an event in which neurological symptoms develop and disappear over several minutes and completely resolve within 24 hours

�Artherosclerotic carotid disease à urgent evaluation and preventive treatment.

�RIND: a transient neurological event that lasts longer than 24 hours

�Infrequent, unknown etiology,

�Stroke in evolution: unstable ischemic event, progressive development of more severe neurological impairment

�Complete stroke

When to start rehabilitation

When a patient’s neurological and medical status is stable.

Stroke risk factors

�Hypertension: most important----Leading risk factor of stroke and CAD

�Heart disease and chronic atrial fibrilation

�TIA, asymptomatic carotid bruit

�Smoking

�Hypercholesterolemia

�Obesity

�Stroke history

Stroke pathophysiology

�Ischemic stroke

�Thrombosis

�Embolism

�Lacunes

�Hemorrhage stroke

�Intracerebral hemorrhage

�Subarachonid hemorrhage

�hydrocephalus

Stroke related impairments

�Motor control and strengthen

�Motor coordination and balance

�Spasticity

�Sensation

�Language and communication

�Apraxia

�Neglect syndrome

�Dysphagia

�Uninhibited bladder and bowel

Motor control and strength

�Anatomy

�Primary motor area: precentral gyrus

�Topography of precentral gyrus

�Cortex—internal capsule—pyramidal tract(brain stem)—corticospinal tract(spinal cord)

�Recovery

�Weakness and poor control of voluntary movement, reduced muscle tone

�Recover: nonfunctional mass flexion and extension of the limbs(synergy, mass contraction) -> independent of synergy

Motor coordination and balance

�Extrapyramidal system..

�Anatomy:

�Premotor area, anterior to precentral gyrus: motor planningà int. capsule ant.limb àbasal ggl and cerebellum

�Input from visual, vestibular, and somatosensory

�If damageà static/dynamic balance impaired as ataxia, chorea, hemiballismus, tremor

Spasticity

�Velocity-dependent increased in resistance to muscle stretch that develops after an UMN injury within the CNS

�Loss of upper motor neuron control à disinhibited αand γmotor neuron activity and ↑sensitivity to Ia and II muscle spindle afferent fiber à hyperactive spinal reflex

�Both increase in tonic and phasic reflexes

�If voluntary motor activity returns à reduction in tone and reflex response is noted. But incomplete

Sensation

�Loss of joint and skin protection, balance, coordination and motor control

�Hypoesthesia

�Severe pain occasionally in spinothalamic tract or thalamus à TCA, anticonvulsant, ES

�Anatomy

�(pain/temperature) dorsal root ggl à spinothalamic tract à VPL n. of thalamus à primary sensory cortex

�(proprioception/stereognosis) à dorsal root ggl à dorsal column à nucleus gracilis/cuneatus à medial lemniscus à VPL n. of thalamus à primary sensory cortex(postcentral gyrus)

Language and Communication

�Testing: oral expression, verbal comprehension, naming, reading, writing and repeating

�Language: left or dominant hemisphere

�Prosody: non-dominant hemisphere

�Rhythmic pattern and vocal intonation of speech that adds emphasis and emotional content to language

Management

Acute stroke management

�Cerebral flow

�normal cerebral autoregulation: 50 mL/100g/min

�20 mL/100g/min: normal neural activity can maintain

�10-20 mL/100g/min: electrically silent(energy dependant Na-K pump fails), basilar cellular function are supported

�< 10 ml/100g/min: cellular death

�Ischemic penumbra: Surviving but inactive neural cells area located at the rim of the ischemic injury

�但時間越久越難救活

�National Stroke Association suggest acute stroke management within first 6 hrs.

The first 6 hours

�Thrombolytic agent

�rt-PA(recombinant tissue plasminogen activator: NINDS study: reduced unfavorable outcome in selected patients who present to the emergency department within the first 3 hours after acute stroke onset FDA採納此項研究

�IV 0.9 mg/kg

�IV Streptokinase: unacceptable ICH rate and mortality

�Intra-arterial infusion: Pro-urokinase: acceptable safety,

�Heparin:

�IV heparin, usually used, but little evidence of its efficacy and guidelines of use

�Cardioembolic stroke 12% recurred within 3 weeks à heparin àwarfarin

�Many clinician advocate use heparin > 48 hrs to prevent hemorrhagic transformation of infarcts.

�Calium channel blocker(Nimodipine): for SAH vasospasm --> routine for 21 days

�Not effective in ischemic stroke

�NMDA antagonist: potential protective

�During acute stroke, glutamate and aspartate are released à NMDA receptor à influx of cation à cell death

�Many study trial stopped because of safety concern and lack of effect

Emergency department evaluation and treatment

�NINDS recommended: Physical assessment, laboratory testing, cranial CT and CT interpretation within 45 minutes

�Lab: electrolyte, Bun/Cr, glucose, cholesterol, CBC with platelets count, PT, aPTT, ESR, UA

�Brain CT: to identify ischemic VS hemorrhage

�Negative for the first 24~48 hrs, in ischemic stroke except:

�Loss of definition of gray-white matter junction, sulci effacement, bright area in the MCA main stem

�ICH: hyerdensityàbecomes hypodense within 1~2 weeks,à resolution with residual small hypodense area

�ICH of basal ggl. and thalamusàhypertension related

�IVH or SAHàaneurysm and AVM related

Acute medical management

�Airway management

�IICP (cerebral edema,acute hydrocephalus) àhyperventilation or external ventriculostomy device (EVD)

�BP:

�Usually elevated for weeks

�Acute HTN should be treated only if: symptomatic, end-organ injury, DBP> 120 mmHg

�When treated, SBP maintain 150/DBP maintain 90 mmHg

�Ca-blocker not ideal because it may cause vasodilatation of cerebral vessel à further IICP and poor cerebral perfusion

�Better choice: mixed αand βblocker (labetolol), α2-receptor antagonist (clonidine)à less effect on cerebral perfusion

�Hyperglycemia, response to physiologic stress associated with ↑cortisol

�Animal study: ↑glucose as the substrate for partially perfused area cell à ↑anaerobic metabolism à ↑ lactateà cytotoxic, so use of insulin and strict glucose control are potentially neuroptrotective

�

Natural spontaneous neurological recovery

�The degree of natural recovery variable, generally, deficits decline in frequency by about 1/2-1/3

�At one year follow-up, hemiparesis(73 à37%), aphasia(36à20%), dysarthria(48à16%), dysphagia(13à4%), incontinence(29à9%)

�The time course for recovery also variable

�Most improvements in physical functioning occur within the first 3-6 months, but later recovery also is commonly seen

�Recovery (two types)

�Reduction in the extent of neurological impairment –natural spontaneous neurological recovery

�Improved ability to perform daily functions in their environment, within the limitations of their physical impairments

�Feed, dress, bathe, control elimination,, walk, ADL

�rehabilitation intervention is thought to exert the greatest effect. Even patients with no or minimal neurological recovery significantly improved in their ability to carry out day-to-day skills with rehabilitation.

�Most (but not all) stroke motor recovery follow up the pattern

�lower extremity function recovers earliest and most completely, followed by upper extremity and hand function

�return of tone precedes return of voluntary movement

�proximal precedes distal

�mass movement(synergy patterns) precis specific isolated coordinated volitional motor functions

�Lower extremity motor control recovery

�Improve of 1 Brunnstrom: 39%

�2 or more Brunnstrom: 12 %

�Upper extremity motor control

�1 Brunnstrom: 24%

�2 Brunnstrom: 8 %

Principles of stroke rehabilitation

�Holistic care

�including social, vocational and economic factors

�Team management

�interdisciplinary team: physician, nurse, PT, OT, ST, orthotist, psychologist, social worker

�Goal-directed treatment

�early step: establishing realistic, practical and feasible goals that are mutually agreed upon by the patient, family and professionals

�Focus on learning and adaptation

�Rehabilitation process consists of learning and adaptation.

�Theory of learning: reacquire old skills or develops means to compensate for new impairements in a logical, coherent manner.

� “Supervised practice” and” timely support, education, reasurance, direct assistance, immediate feedback” are two necessary component of this learning process.

�Rehabilitation is “the planned withdrawal of support”

�Therapy environment

�Beneficial greatly from practice in therapy environments that closely reflex natural home or community settings

�Timing of therapy

�Specific therapy schedules should be individualized.

�The stroke rehabilitation literature does not provides specific guideline about the amount of therapy for each specific problems. 不過一般認為，Reasonable participate in functional activities at least once a day

�Endurance, medical stability, mood, motivation à會影響病患的耐受度

�

Attention to psychosocial issues

�Depend largely on pre-stroke coping styles. Levels of frustration tolerance and ability and mechanism used to deal with adversity

�Family issue of emotion

�Focus of families

�Family members serve as members of the rehabilitation team

�Participate activity in the rehabilitation process

�Emphasis on community issues

�Enable smooth safe transition to community living

Rehabilitation assessment and interventions during the acute phase

�The maximum benefit of rehabilitation can be achieved when rehabilitation interventions area begun as early as possible after stroke

�Early poststroke rehabilitation is “preventive” + “therapeutic”

Levels of post-acute stroke care

�Acute inpatient rehabilitation

�Traditional interdisciplinary hospital-based coordinated program of medical, nursing and therapy.

�>= 3 hrs of therapy per day

�Need daily physician supervision and around-the-clock nursing care.

�Subacute inpatient rehabilitation

�Less intensive program is used(因為mild stroke or poor endurance tolerance), 1-3 hrs of therapy per day

�以護士為主的照顧，24 hrs nursing care, Dr查房一週1-3次

�Day rehabilitation

�3-8 hrs/day

�病人白天來作復健，晚上回家，but the program all the same with inpatient rehab.

�A comprehensive and coordinated program, rehab. team had regular scheduled conference.

�Outpatient therapy

�病人白天來作復健，晚上回家

�PT/OT/ST各做各的，for patient with focal deficit and need specific functional training.

�Home therapy

�Home is the most familiar environment, all the patient and family to learn specific functional tasks

�But may lack support of specific equipment and experienced staff

Rehabilitation outcomes

�Functional and social outcomes

�**Physical performance, functional abilities and quality of life got better after rehab.

�Greatest improved in locomotion, mobility, self-care, and sphincter control improved after rehab.

�A report: Hospitalization FIM: average from 63 on admission to 87 at discharge.

�Less improved in communication and social cognition.

�In general, 75%~85% of stroke patient are discharged to home after formal acute rehab. care.

�3/4 discharged to community

�

U.S. AHCPR(agency for health care policy and research) Post-Stroke Rehabilitation Guidelines---5 major points:

1. The importance of thorough and consistent assessment of status at each stage of The recovery process to help guide treatment decisions and to monitor patient progress

2.Early implementation of rehabilitation interventions during acute care to promote recovery and prevent complications

3.Selection of the type of rehabilitation program and services best suited to meet the patient’s needs

4.Establishment of realistic rehabilitation goals and provision of treatment in accordance with a carefully developed rehabilitation management plan

5.Combined follow-up and treatment during transition to a community residence

AHCPR guidelines

�Threshold criteria of the need for rehab.:

�Medical stability

�Presence of functional deficit

�Ability to learn

�Endurance to sit up at least for 1 hr.

�Ability to participate actively in the rehab. program.

�One criteria for admission to a comprehensive interdisciplinary program:

�有≧2 types of disabilities, need ≧2 disciplines of professionals to assist in management.

Special patient considerations

Pediatric stroke

�Incidence: 2.55 per 100,000 children per year

�Different presentation from adult

�Seizures, fever, delayed achievement of development milestones

�Cause different from adult:

� hereditary, congenital heart disease, metabolic disorders, coagulopathy, drugs, intracerebral vascular anomalies.

�Prognosis: better than adult

Stroke in young adults

�1/3 of stroke in individuals < 65 y/o

�26% in persons 45-65 y/o

�Hemorrhage stroke 1/3 of young adult, 1/5 of all stroke survivors.

�Ischemic stroke/infarction

�Atherosclerosis 20%

�Cardiogenic embolism 20%

�Collagen vascular disease 10%

�Coagulopathy 10%

�Young stroke survey: angiography, coagulation test, collagen vascular disease evaluation, cardiac work-up (e.g. TEE)

Geriatric stroke

�Young age at stroke onset has a favorable effect on long-term and short-term stroke survival, BUT THE EFFECT ON FUNCTIONAL RECOVERY IS LESS CERTAIN!

�Age may be just a marker for co-morbidities, prior stroke, limited social supports

Traumatic Brain Injury

Terminology

nGeneral term for all injuries to the brain caused by external force (泛指所有外力造成的腦傷)

nTBI is a general term that dose not imply a specific pathology

Non-traumatic brain injury

nA Specific etiology and pathology

nAnoxic brain injury(=hypoxic encephalopathy, hypoxic brain injury)

nCause: cardiac/respiratory arrest, CO poisoning

nStroke

nInfection

nToxic-metabolic brain injury

Pathophysiology – closed or open head injury

nPrimary mechanism occurs at the moment of impact, secondary mechanism are triggered by primary mechanism and cause additional damage.

nBrain injury is often the summation of effects of multiple primary and secondary mechanisms à diffuse injury, especially in closed head injury.

nThe major mechanism are caused by acceleration-deceleration à diffuse axonal injury, multiple petechial hemorrhage, contusion, and cranial nerve injury.

A. Primary injury

1.Diffuse axonal injury (DAI)

* Acceleration-deceleration and rotational force

*The distribution is centripetal model, in mild TBI, cortex(surface) is more likely injured, in severe TBI, deeper structures are injured, like cropus callosum( longer fiber tract).

* May cause loss of consciousness

2. Cerebral contusion

* Relative low velocity impact

* Inferior frontal lobes and anterior temporal lobes are most frequent due to irregular bony surface.

* Focal cognitive and sensory motor deficit, risk of

seizure

B. secondary injury

* IICP

* SDH, EDH, ICH

* Vasogenic or cytogenic brain edema

* Herniation

* Hydrocephalus

* Brain ischemia/hypoxia

* Free radical injury, excitotoxicity

One study: moderate hypothermia (32’~33’c) for 24 hrs, improve outcome

Damage is located along the track of the bullet and indriven bony fragment

Cause focal damage (e.g. hemiplegia, hemianopsia)

Anoxic brain injury

nCaused by hypoxemia or decreased cerebral perfusion.

nAlthough diffuse injury is often noted, but selective vulnerable areas are existed.

nHippocampus, most vulnerable à amnesia

nBasal ganglion, cerebellum à movement disorder

Epidemiology

nMale > female, young adult(18~25 y/o)最多

nSingle largest indirect cause: alcohol drinking

nSingle largest external cause: motor vehicle crash (young adult), followed by auto-pedestrian crashes (children), falls (children and elderly person), assaults

Assessment techniques and prognosis

Glasgow Coma Scale(GCS)

nInitial used for TBI severity classification, now also used in other brain injury resulting in conscious disturbance

nDepth and duration of unconsciousness measured by GCS is the single best predictor of outcome

Severe TBI

nGCS: ≦8, à coma, not open the eyes, no evidence of cognition(follow command, communication)

nAccounts for large majority of TBI inpatient rehabilitation.

nMajority have permanent neurologic impairement and functional disabilities.

nUsually takes one year or longer to reach maximal neurological recovery

Moderate TBI

nGCS: 9~12, combative or lethargic, possible follow command, but not answer question appropriately(V3~4)

nMajority resumes preinjury activity, despite few have mild cognitive deficit.

nRecovery, shorter than severe TBI

Mild traumatic brain injury

nDefinition:

nLowest GCS≧ 13, might be confused, but awake

nMild TBI can be defined

ndespite GCS =15 if there is lesion noted by images,

nor if the injury caused altered mental status such as loss of consciousness, a period of confusion or disorientation, or amnesia for the injury itself

nUncomplicated mild TBI à Negative CT and/or MRI

nComplicated or high- risk mild TBI. àCT and/or MRI reveals brain trauma

nLoss of consciousness, if any, <= 30 mins

nPosttraumatic amnesia <= 24 hrs

nNo focal neurological deficit

nConcussion = mild TBI

nNeuroimaging findings are the single best prognostic indicator for mild TBI.

nGenerally returns to preinjury activity without detectable cognitive deficits.

nRecovery, usually within 3 months, most case within 1 month

nCommon complains of mild TBI:

nCognitive: attention and concentration difficulties, memory impairment

nAffective: irritability, depression, anxiety

nSomatic: headache, dizziness, insomnia, fatigue, sensory impairments

Neuroimaging of brain injury

nCT is the choice of test during the acute stage:

nSensitivity to blood, bony fracture

nNot contraindicated with metallic material implant

nMRI

nMore sensitive than CT(e.g. nonhemorrhage shear injuries, some areas of contusion;)

nInferrior frontal region and brain stem contusion or other injury may be obscured by bony defect in CT

nDisadvantage: contraindicated by metallic material, needing long time for exam

nCT findings are related to later gross outcome(conscious survival VS vegetative), but some studies suggested poor correlation between it and functional outcome.

nMRI should be more useful than CT in rehab planning( helpful in explaining patients neurologic and neuropsychological deficits )

nSPECT(single proton emission CT) could have an important role in evaluating unconscious or mild TBI, may be more sensitive

nEEG

nLimited usefulness in detecting posttraumatic seizure since interictal EEG abnormalities can merely reflect the severity of TBI

nIn acute setting, EEG is a powerful predictor of survival from TBI.

nPoor outcome: abnormal sleep spindles and predominance of alpha waves

nSSEP: Studies: bilateral absence of N20 to P22 of comatose TBI patient was a strong predictor of failure to recover consciousness

nBAEP: Studies: absence of wave V or other components also predicts poor outcome

Summary of Acute Prognostic Indicators

Others:

1. Glasgow-Liege Score: GCS + brainstem reflex

2. SEP: particular sensitive and specific

3. EEG

4. Apolipoprotein E4: play a role in neural regeneration

studies: presence of the apolipoprotein e4 allele

( which produces APOE-4) increase the risk of Alzheimer’s

disease and severity in certain TBI populations

Outcomes measurements

nGlasgow Outcome Scale (GOS): used mostly, but insensitive to change

nDisability Rating Scale (DRS): from coma to community, more sensitive and comprehensive than GOS

nThe Rancho Los Amigos Levels of Cognitive Functioning Scale: cognitive recovery

nFunctional Independence Measure (FIM)

nFunctional Assessment Measures (FAM): more cognitive oriented items

nCommunity Integration Questionnaire(CIQ)

nSupervision Rating Scale(SRS)

Continuum of brain injury rehabilitaiton

Rehabilitation during critical care

nGoal: prevent complication

nMeasure:

nPROM 2 times/day: prevent contracture

nPositioning: prevent pressure ulcer, edema, contracture

nPrevent spasticity

nIncontinence

nNutrition

nEarly surgical treatment of orthopedic injury

Acute brain injury rehabilitation

nInitial rehab. Evaluation à acute/subacute/or post-acute program

nMedical stable à transfer to acute program

nThe criteria of following commands to be admitted to rehabilitation is unjustifiable.

nMajority of TBI regain consciousness(40~60% at one year, table 49-9)

nIndication for admission to brain injury rehabilitation units instead of general rehab. unit

nUnconsciousness/inconsistent consciousness, agitation, risk of complication, severe cognitive deficit

Stages of neurobehavioral recovery from brain injury– TBI patient have long course of recovery, more functional progress

nComa/Unconsciousness/Impaired consciousness

nRehab of patient with impaired consciousness

nPost-traumatic Amnesia and Agitation

nRehabilitation of the Agitated Patients

nRehabilitation During and After Posttraumatic Amnesia

nPost-acute brain injury rehabilitation

Coma and unconsciousness

nComa: not open the eyes, no evidence of cognition

nDue to disruption of ascending pathway from deep structure to surface cortex

nDAI, brain stem or diencephalic structure compression

nRecovery from coma(centripetal model)

nBegins with eye opening and sleep-awake cycles à then followed commands à speak

nStudies: 10~15% still unconscious at discharge

nAt one month, those still unconscious patients regained sleep-awake cycles, also have pupillary reactivity/oculocephalic reflex, primitive behavior(chewing, eye roving eye movement), vegetative function(respiration) àall of which reflect brain stem and hypothalamus function

Persistent vegetative state(PVS)

nWakeful unresponsiveness

nCharacterized by the presence of spontaneous sleep-wake cycles

nAbsence of cortical activity as judged behaviorally

nNo reproducible, purposeful, or voluntary behavior response to stimuli

nNo evidence of language comprehension or expression

nIt is a diagnostic term, not prognostic.

nThe Task Force defined PVS: present for one month after an acute traumatic/nontraumatic brain injury

nThe vegetative state should not be labeled permanent until high degree clinical certainty after 12 months post-TBI and 3 months after nontraumatic TBI

Prediction of regaining consciousness

nEtiology

nAge

nBest recovery: children, followed by adult< 40y/o, 但此不適用於non-traumatic

nAlso poor in severe cerebral atrophy in CT, and bilateral absence of SSEP potentials

nDuration of unconsciousness

目前 Unconsciousness duration vs 一年內醒來機率

	Regain consciousness by one year
Unconscious duration	TBI	Non-TBI
One month	40-50%
3 months	36%	7%
6 months	21%	更低

Minimally conscious state

nSome evidence of awareness

nVisual tracking and/or motor behavior that is nonreflexive and contingent on environmental events

Rehabilitation of patients of impaired consciousness

nRemove obstacles to recovery, treat medical complication, education/ counseling to the family

nR/O artifact of examination techniques, sedating drug, systemic illness, malnutrition

nDrug-induced sedation can be magnified in injured brain

nAnit-hypertensive: use clonidine, ACEI, Ca-blocker, diuretic instead of propranolol, methyldopa, metoprolol

nAmitriptyline can cause paradoxically sedation of its anticholinergic effect

Rehab. of unconscious patient remains controversial

n Sensory stimulation(coma stimulation) used multiple modalities: no evidence of effect in chronic traumatic unconsciousness

n Pharmacological treatment remains the most promising intervention

Neurostimulant medication

nMethylphenidate, Dextroamphetamine

nAntiparkinsonian agents

nAmantadine

nBromocriptine

nLevodopa/Carbidopa

nAtypical: TCAs, protriptyline, SSRI, sertraline, Bupropion, venlafaxine

Posttraumatic amnesia (PTA)

nDefinition: the period during which the patient’s ability to learn new information is minimal or nonexistent

nS/S: Confabulation

nAssessment for end of PTA:

nOrientation to time and place

nGalveston Orientation and Amnesia Tool (GOAT)

nGOAT: 0 – 100, >75 defined normal

nEnd of PTA: The date after which GOAT score > 75 consistently

nPermanent amnesic disorder: failure to clear from PTA.

nOther nontraumatic brain injury may have the same condition, and alternative term may be more suitable.

Agitation

nDuring PTA, many patients may have agitation.

nS/S: emotional lability, motor overactivity, physical or verbal aggression, poor attention

nTo date, no consensus on definition, some authors defined it a subtype of delirium.

nAssessment: ABS: Agitated Behavior scale

nEvaluate 3 realms: disinhibition, aggression, lability

nStudies: minority of TBI patient have agitation with aggression, many more: only agitation with motor restlessness, many others: no agitation

Rehabilitation of Posttraumatic Amnesia

nThe rehabilitation unit should have a system for identifying how closely each patient needs to be supervised

nAvoid overstimulating the patient with a demanding herapy schedule, unrealistic therapeutic epectations, and unpleasant emotional interactions with family or staff.

Rehabilitation agitated patient

nRule out medial and neurologic conditions ---> then dx agitation, table 49-14

nRestraints: minimal degree if necessary

nFloor bed: Craig Bed (如圖)

nEnvironment management:

nreduce the level of stimulation in the environment

nreduce the patient’s confusion

nProtect the patient from harming self or others

nTolerate restlessness as possible

nMedication: when environment management failed, no guideline exists to date

n TBI experts 較少用haloperidol, benzodiazpines

n Lorazepam(ativan) 1~2 mg IM may be needed only in uncontrolled emergent and danger violent behavior patient.

Medical complication of TBI

nSpasticity

nPosttraumatic epilepsy

nPosttraumatic hydrocephalus

nCranial nerve damage

nPosttraumatic hyperthermia

nSleep disorder

nPulmonary complications

nGI and nutritional complications

nThrombophlebitis

nGU complications

nMusculoskeletal complication— HO

nSexual and reproductive functioning

Spasticity

nCerebral origin spasticity(COS) different from that of SCI

nGreater extensor tone in extremity, less spasm

nSpasticity that interferes with functional goal warrants treatment.(table 49-18)

nRecent approach suggests concurrently employed various treatment strategies:

nPrevention of nociceptive stimuli, ROM, stretch, casting, orthosis, modality, invasive motor point block, operation

nProper positioning: ↑muscle relaxation, improve alignment, ↓primitive reflex; lying supine can increase the tonic labyrinthine supine reflex(TLSR), thereby increasing extensor tone

nAntispasticity ball splint for spastic hand

nChemoneurolysis: phenol, alcohol, anesthetic agent; side effect: swelling, pain, bleeding, dysesthesia, DVT

nChemodenervation: Botulinum toxin A, side effect: atrophy, pain, infection; 注射完不像phenol block 必須休息

nITB: intrathecal baclofen, concentration more in lumbar spine à more effective in lower limbs spasticity, 因此對上肢的spasticity較不是主要的indication

n Trial: 50, 75, 100 mg on consecutive days, if effective, then ITB pump is implanted

nOP: tendon lengthening or transfer, rhizotomy more performed in children成人較不favor

n Oral medication generally not recommended due to it might interfere cognitive function, especially diazepam and baclofen

nDantrolene sodium may be medication of choice

n It acts peripherally, at the muscle, à ↓depolarization induced Ca influx into the sarcoplasmic reticulum(SR)

n Side effect: can also be sedating, general weakness. Liver enzyme should be monitored

nTizanidine, α2 agonist, ↑presynaptic inhibition of motor neuron, ↓release of excitatory amino acids.

Posttraumatic epilepsy (PTE)

nIncidence in hospitalized TBI: 5%

nRisk factors

nPenetration injury

nseizure during the first week (early seizures)

ndepressed skull fractures

nacute intracranial hematomas

ndural tearing

npresence of foreign bodies

nfocal sign such as aphasia and hemiplegia

nago ≧ 65 y/o

nloss of consciousness > 1 days

nPTA > 24 hrs

nPrevention: no longer recommended except penetrating injury or early seizure noted, not beneficial

nDrug of choice:

n Carbamazepine: drug of choice

n Most late seizure are simple/complex partial seizure, carbamazepine as effective as phenytoin in control generalized seizure, and more effective in partial seizure

n Side effect: GI distress, headache, dizziness, diplopia, bone marrow suppression àkeep WBC > 3000 cells/mm3 其中neutrophil必須 ≧ 50%

n Initial sedative, but fewer cognitive side effect than carbamazepine Valproic acid(Depakene)

n Gabapentin(Neurontin)

n Not significant cognitive side effect, not requiring monitoring blood level

n Duration of anticonvulsant: most clinician DC medications after 1-2 yrs seizure-free years

Posttraumatic hydrocephalus

nTBI: most are NPH or communicating type

nS/S of normal pressure hydrocephalus(NPH)

nTriad: gait disturbance, mental deterioration, urinary incontinence

nVentricular enlargement and normal CSF pressure

nIn severe TBI case, more subtle change may be related to NPH: functional decline, seizure, emotional problems, abnormal posturing, increased spasticity, Newly onset of hypertension

CT criteria to define hydrocephalus

n1. “Distended” appearance of the anterior horns of the lateral ventricles

n2. Enlargement of the temporal horns and third ventricle

n3. Normal or absent sulci

n4. If present, enlargement of the basal cisterns and 4^th ventricle

n* Periventricular lucency was used as an indicator of communicating hydrocephalus

SPINAL CORD INJURY (SCI)

The earliest reference to spinal cord injury (SCI) is found in the Edwin Smith Surgical Papyrus, written between 2500 and 3000 B.C., where it is described as "an ailment not to be treated". Much has changed in spinal cord care over the centuries, particularly in the last 50 years as it relates to increasing survival, life expectancy, community reintegration, and quality of life. Major advances include the specialized spinal cord centers of care, model SCI centers funded by the National Institute on Disability and Rehabilitation Research (NIDRR) in the United States Department of Education, establishment and growth of organizations and journals dedicated to SCI care, and the development of the subspecialty of SCI medicine in 1998. This subspecialty addresses the prevention, diagnosis, treatment, and management of traumatic and nontraumatic etiologies of spinal cord dysfunction. The advances of the last 20 years alone have been dramatic in terms of the understanding of the pathology of the initial and secondary aspects of the injury, and the barriers that must be overcome to enhance recovery. Newer techniques to improve function and intervene at the cellular level for possible cure are being developed. These will further allow individuals who sustain an SCI to be more independent in the future.

Selected Tracts

The majority of descending corticospinal fibers cross at the medulla to become the lateral corticospinal tract(CST). A small number of CST fibers do not decussate at the medulla and descend via the anterior CST before crossing at the level of the anterior white commissure. Although often depicted in many representations of the spinal cord, the existence of a somatotopic organization of the lateral CST has recently been challenged.

The ascending dorsal white columns cross in the medulla, via the medial lemniscus, then go on to the thalamus. The spinothalamic tracts, which carry pain, temperature, and non-discriminative tactile sensations, cross obliquely in the ventral white commissure of the spinal cord, ascending a level as they do so.

Classification of SCI

1.Perform a sensory exam in 28 dermatomes for pin prick and light touch,

including rectal sensation. The sensory level is the most caudal

level with intact (grade 2) sensation.

2. Perform a supine motor exam of 10 key muscle groups, including

voluntary anal contraction. The motor level is the most caudal

level with grade ≧3, where all muscles rostral to it are grade 5.

3. Determine the neurologic level, which is the most caudal level

at which both sensory and motor modalities are intact bilaterally

4. Classify as complete or incomplete. Completes have no motor or

sensory function, including deep anal sensation, preserved in

sacral S4-5. (Note: SSEPs may be useful in differentiating

complete versus incomplete SCI in pts who are uncooperative or

unconscious. SSEPs are also unaffected by spinal shock.)

5. Categorize by American Spinal Injury Association (ASIA)

Impairment Scale, A-E. (Determine the rone of partial preserva-

tion ifASIA A.)

ASIA key sensory points

C2 Occipital protuberance	T1 Medialantecubital fossa	L3 Medialanterior knee
C3 Supraclavicular fossa	T2 Aper of the anilla	L4 Medialmalleolur
C4 Top of the AC joint	T4 Medial to nipple	LS Medialdorsalfm
C5 Lateral antecubital fossa	T10 Lateral to umbilicus	S1 Inf lal malleolur
C6 Dorsal proximal thumb	T12 lnguinal ligament	S2 Poplitealfossa
C7 Dorsal proximal mid finger	L1 B/t T12 and L2	S3 Ischial tuberosi*
C8 Dorsal proximal 5' finger	L2 Medial anterior thigh	S4-5 Analmucocutan lu

ASIA key muscles

C5 Elbow flexon	L2 Hip flexors
C6 Wrist extensors	L3 Knee extensors
C7 Elbow extensors	L4 Ankle DF
C8 FDP of 3rd digit	L5 EHL
T1 Small finger abductors	S1 Ankle PF

Sensory are scored as O (absent). 1(impaired, including hyperaesthesia). 2 (normal), or NT When sconng pin prick inability to distinguish pin prick from LT is scored 0/2. Muscles are graded from O (total paralysis) to 5 (normal active movement with FROM against full resistance), or NT

ASIA Impairment Scale, Revised (2000)

A Complete No sensory or motor function is preserved in the sacral segments S4-5. The rone of partial preservation (only used in ASIA A) refers to the most caudal segment with some sensory or motor function.

B Incomplete - Sensory but no motor function is preserved below the neurologic level and includes sacral segments S4-5.

C Incomplete Motor function is preserved below the neurologic level, and more than half of the key muscles below the neurologic level have a muscle grade <3

D Incomplete - Motor function is preserved below the neurologic level, and at least half of key muscles below the neurologic level have a muscle grade ≧3.

E Normal - Sensory and motor function are normal.

Note: For an individual to receive a grade of ASIA C or D, there must be sensory or motor S4-S sparing In addition, theindividual must have either: )) voluntary anal sphincter contraction or 2) sparing of motor function >3 levels below the motor level.

Spinal Cord Injury Clinical Syndromes

Anterior cord - These may be due to retropulsed disks/vertebral fragments, aortic clamping during surgery, or lesions of the anterior spinal artery. Intraoperative SSEPs (which primarily monitor the posterior column pathways) may miss the development of an anterior cord syndrome. There is variable loss of motor and pinprick sensation, with relative preservation of proprioception and light touch. Prognosis for motor recovny is generally considered poor.

Brown-Sequard - Etiologies may include stab wounds or tumors. Hemisection of the cord produces ipsilateral weakness, hyperreflexia, and proprioceptive loss and contralateral loss of pinprick and temperature sense. The prognosis for ambulation is best among the incomplete SCI syndromes.

Cauda equina - Cauda equina injuries may be due to neural canal compression or fxs of the pelvis, sacrum, or spine at L2 or below. The syndrome can be described as "multiple radiculopathies" since the cauda is comprised of lumbosacral nerve roots. Sequelae depend on the roots involved and may include bowel/bladder areflexia, erectile dysfunction, saddle anesthesia, and flaccid LEx weakness that can progress to complete paraplegia. Radicular pain is common and can be severe. Anal, bulbocavemosus, plantar, and ankle deep tendon reflexes may be lost. Recovery is possible because the nerve roots can regenerate. Consultation for possible early, but not necessarily emergent, surgery is indicated.

Central cord - This syndrome is typically seen in older persons with cervical spondylosis following neck hyperextension injury, resulting in upper > lower limb involvement and sparing of the lowest sacral segments. Bowel, bladder, and sexual dysfunction is variable. The postulated mechanism of injury involves cord compression both anteriorly and posteriorly, with inward bulging of the ligamentum flavum during hyperextension in a stenotic spinal canal. Penrod retrospectively studied 51 pts with central cord syndrome and noted better overall recovery of ambulation, self-care, and bowel/bladder function in pts <50 yrs of age (n=30) than their older counterparts (n=21) at time of discharge from rehabilitation.

Conus mednllaris - A pure conus medullaris lesion (e.g.,intramedullary tumor) can result in saddle anesthesia and bladder anal sphincter/erectile dysfunction due to cord injury at S2-4. Anal (S2-4), bulbocavemosus (S2-4), and ankle deep tendon reflels (S1,S2) may be lost if there is injury to the corresponding level of the spinal cord. Prognosis for recovery is poor.

Conus medullaris lesions due to trauma (e.g, L1 vertebral body fx) are typically accompanied by injury of some of the lumbosacral nerve roots, resulting in a variable degree of LEx dysfunction.

Neurological prognosis and functional outcomes

1. 事實上所有traumatic SCI survivor都經歷某種程度的neurological recovery，對某些病人這種恢復可導致level function改善。恢復可由臨床檢查和電診斷加以監測。

2. 在靠近injury zone的segment神經學功能恢復或是“root recovery”要和在spinal cord functional global improvement區分出來，因為後者會導致ASIA Impairment Scale的改變。一般而言，病人若一開始即表現出些許運動功能的保留，而且受傷後早期即有神經學恢復的話，會有最好的預後。

3. 有幾篇paper都顯示雖然strength的恢復可達二年之久，在受傷後一個月到一年中間motor recovery的速率會在頭六個月快速下降。。Incomplete injury的P't在injury zone 恢復的速度會快於complete injury的P't，但他們恢復的程度不見得會更好。幾乎所有在受傷後一個月肌力只有1/5或2/5的muscle的一年後會恢復到3/5（antigravity）。

4. 位於有motor function最後一節之下第一節neurological level，若muscle只有0/5的肌力，病人只有1/3的機會恢復到3/5肌力。假如在有motor function最後一節下二節muscle power是0/5的話，functional recovery是極少的。

5. 在tetraplegia病人身上上肢muscle weakness似乎反映不同程度upper motor neuron和lower motor neuron的damage。在voluntary muscle作compound muscle action potential的肌電圖分析或作表面肌電圖root mean square measure（平方根測量）通常有助於分辨upper motor neuron或lower motor neuron weakness。復健計畫也可根據這結果加以修改。

6. 利用ASIA Impairment Scale和它的前身，Frankel classification可產生相當多的資料來描述受傷區域預後情形。Complete injuries (grade A) 的病人有較差的預後，在如此傷害後grade還會改變的情形估計只有0%～9%。

7. 雖然ASIA impairment grade A的case有時晚期會有所變化，究其原因，發現有許多case一開始受傷時有concurrent condition（像brain injury或sedation）而妨礙了正確的評估。從NSCISC model所提供information可知grade變化的情形（Table 55-3），一個超過5000人對於Frankle grade改變的study也顯示在incomplete injuries的病人有較佳的預後。

8. 只有Sensation的保留的人在神經學上會有中等程度的改善。Pinprick sensation的保留似乎比light tough sensation preservation有更大機會恢復ambulation能力，有人推測這可能是傳遞pinprick sensation的spinothalamic tract比較靠近corticospinal tract的緣故。

9. 在injury zone以下部位有motor function保留的人包括central cord syndrome和Brown-Sequard syndrome的病人在功能恢復上會有最好的預後。

10. Central cord syndrome的病人大部份最終都會得到hand-function和control bladder和bowel function的能力。Ambulation恢復程度和受傷時年齡有關，越年輕恢復愈多。Brown-Sequard的Pt有最好的預後，超過90%的Pt在受傷六個月後能夠恢復步行狀態。

Expected Functional Levels (I, independent: A, assist: D. dependent)

C1-3 –

{ Ventilator-dependent (or may have phrenic nerve pacing);

{ D for secretion management.

{ I with power WC mobility and pressure relief with equipment. otherwise essentially D for all care (but I for directing care).

C4 –

{ May be able to breathe w/o a ventilator.

{ May use a mobile arm support for limited ADLs if there is some elbow flexion and deltoid strength.

C5 –

{ May require A to clear secretions.

{ May be I for feeding after setup and with adaptive equipment,

n e.g., a long opponens orthosis with utensil slots and mobile arm support.

{ Requires A for most upper body ADLs.

{ Most pts will be unable to do self clean intermittent catheteriration (CIC).

{ I with power WC; some users may be I with manual WC on non-carpeted, level, indoor surfaces.

{ Some may drive specially adapted vans.

C6 –

{ May use a tenodesis orthosis and short oaponens orthosis with utensil slots.

{ I with feeding except for cutting food.

{ I for most upper body ADLs after setup and with modifications

n (e.g., velcro straps on clothing);

{ A to D for most lower body ADLs, Including bowel care.

{ Some males may be I with CIC after setup; females are usually D.

{ Some pts may be I for transfers using a sliding board and heel loops, but many will require A.

{ May be I with manual WC; but power WCs are also often used, especially for longer distances.

{ May drive a specially adapted van.

C7 –

{ Essentially I for most ADLs, often using a short opponens splint and universal cuff.

{ May require A for some lower body ADLs.

{ Women may have difficulty with CIC.

{ Bowel care may be I with adaptive eguipment, but suppository insertion may still be difficult.

{ I for mobility at a manual WC level, except for uneven transfers.

{ Pt mav be I with a non-van automobile if the pt can transfer and load/unload the WC.

C8 - Completely I with ADLs and mobility using manual WC and car.

Paraplegia - Trunk stability improves with lower lesions.

Upper and mid thoracics may stand and ambulate with b/l KAFOs and Lofstrand crutches (i.e., swing-through or swing-to gait), but the intent is usually exercise, not mobility.

Using orthotics and gait assistive devices, lower thoracics and L1 SCI pts can do household ambulation and may be I community ambulators.

L2-S5 SCI pts may be community ambulators with or w/o orthotics (i.e., KAFOs or AFOs) and/or gait assistive devices. (AFOs generally compensate for the ankle weakness, while canes and crutches primarily compensate for hip abduction and extension weakness.)

Selected Issues in SCI

Autonomic dysrenexia (AD) –

It can occur in 48-85% of pts with SCI at T6 or above'. (Since resting SBPs can be 90-110mm Hg in this population, SBPs of 20-40mm Hg >baseline may signify AD'.) A strong sensory impulse below the injury causes reflex sympathetic vasoconstriction (BP elevation). Due to the SCI, higher CNS centers cannot directly inhibite the sympathetic response. The body attempts to suppress BP by carotid and aortic baroreceptorivagal-mediated bradycardia, but this is usually ineffective.

Long-term routine urinary tract surveillance after SCI –

Upper tract f/u can include renal scan with GFR or renal scan with 24hr Cr clearance qyr to follow renal function. US can be done qyr to detect hydronephrosis and nephrolithiasis. Lower tract f/u can include urodynamics (UDS) once the bladder starts exhibiting uninhibited contractions (or at around 3-6mos post-injury), then as determined by the clinician (often done qyr or q2yr). Routine cystoscopy to potentially diagnose neoplasm at an earlier rather than later stage should be performed qyr after l0yrs of chronic indwelling (urethral or suprapubic) catheter use or sooner (atier 5yrs) if there are additional risk factors (heavy smoker, age>40, h/o many UTls).

Posttraumatic syringomyelia –

It is seen in -3-8% of posttraumatic SCI pts as neurologic decline, or up to 20% on autopsy. It can develop as early as 2mos to yrs post-SCl. Pain is often worsened by coughing or straining, but not by lying supine. Ascending sensory loss, progressive weakness (including bulbar muscles), ↑ sweating, orthostasis, and Homer's syndrome may also be seen. Dx is by MRI. Tx is usually observational and symptomatic. Surgical interventions are available for large, progressive lesions.

Sexual function, fertility –

Females: 44-55% of women with SCI can achieve orgasm. Menses typically returns w/in 6mos post-SCI, and reproductive function is preserved. Incidence of prematurity and small-for-date infants is high, but there is no increase in spontaneous abortions. Spinal anesthesia is recommended during delivery for pts with SCI at T6 or above.

Males: With complete SCI, reflexogenic erections can usually be achieved, although ejaculation is rare. With incomplete SCI, reflexogenic erections are usually attainable; ejaculation is less rare than for completes; and some pts can achieve psychogenic erections. Complete or incomplete injuries below T11 may result in erections of poor quality and duration. Infertility is common after SCI, due to factors including retrograde ejaculation and poor sperm quantity and motility. E[ectrovibration for ejaculation (the ventral penile shaft is stimulated) requires that the pt be >6mos post-injury and have L2-S1 intact. aecrroejaculation (seminal vesicle and prostatic stimulation through the rectum) is another option.

Tendon transfer surgery –

Triceps fUnction can be restored in the C5,6 SCI pt with a posterior deltoid-to-triceps or a biceps-to-triceps transfer. Lateral key grip can be restored in a C6 SCI pt via the modified Moberg procedure, which involves attachment of the brachioradialis (C5,6) to the flexor pollicis longus (C8,T1) and stabilization of the thumb CMC and IP joints.

Electrodiagnosis

Purposes of Electrodiagnosis

• Localization

• Guidance for disease severity

• Characterizing of disease evolution and estimate of prognosis

• D/D neuropathy and myopathy

• General evaluation in diseases of neurons, roots, plexus, peripheral nerves, NM junctions, and muscles

Possible complication and side effect

• May interfere normal pacemaker function

• May cause infection when patient with lymph edema

• May cause continuous bleeding if patient with hemophilia or under heparin/warfarin treatment

• May cause arrhythmia with artery or central venous line

• May cause pneumothorax

Clinical Assessment

• History

• Physical examination

• Differential diagnosis

• Initial plan

History

• Time course

• Quality

• Distribution

• Medical history

Systemic disease：DM, alcohol consumption, rheumatic disease

Medication：disease, toxic exposure, anticoagulant

• Family history

Physical examination

• Muscle strength

• Sensation

Pinprick, light touch

Two-point discrimination

Vibration

• Muscle stretch reflex

Biceps(C5), brachioradialis(C6), triceps and pronator teres(C6, C7)

Knee(L4), ankle(S1), medial hamstring or tibialis posterior(L5)

Hoffmann’s sign and Babinski’s sign

• Provocative test

Phalen’s test：median nerve entrapment at the wrist

Tinel’s sign：non specific

Spurling’s sign：cervical radiculopathy

Straight leg raising test or other sciatic nerve stretch maneuver：lumbosacral

radiculopathy

Differential iagnosis and initial plan

• For focal or distal problems, like entrapment neuropathy, NCS first.

• For proximal lesion, or diffuse/multifocal process, (like radiculopathy), EMG first.

Needle Electomyography

• Preparing the patient

• Deciding on an electrode to use

• Steps of the needle EMG examination

• False-positive and false negative findings on needle EMG

Preparing the patient

• Explanation:

Experience

Risk and benefits

• Consent for high-risk procedure，e.g. intercostal muscle EMG

• Positioning

• Room temperature

Deciding on an electrode to use

¬ Surface electrode:

Disposable, self adherence, size

¬ Needle electrode

Monopolar

• Stainless steel coated with Teflon with bare metal tip

• Separate reference and grounding

Concentric

• Hollow stainless steel with a central platinum or nichrome-silver wire

surrounded by epoxy resin

• Cannula serves as reference, only separate grounding needed

Single-fiber electrode

Monopolar vs. Concentric electrode

	Monopolar	Concentric
Recording territory	wider	smaller
Reference	distant: noiser	closer: quieter
Discomfort	fewer (Teflon coating)	more
Recording potential	larger	smaller, with possibly fewer phases
Duration	Same	same
Clinical use	broad area recording, e.g. finding the FP or PSW	restricted area recording, e.g. quantitative motor unit analysis
Cost	cheaper	expensive

Steps of the needle EMG examination

• Insertional activity

• Spontaneous activity

• Motor unit analysis

• Recruitment

False-positive and negative findings on needle EMG

• False-positive：overreading of subtle changes:

as insertional activity,

polyphasic waves,

recruitment,

end-plate potential ＆ fibrillation potential

• False-negative

Too short temporal course ( < 2~3 weeks)

Too few muscles examined or each muscle insufficient examined

Nerve Conduction Studies

• Measurement of compound or sensory nerve action potentials

• Measurement of compound muscle action potentials

• Late responses

Measurement of compound or sensory nerve action potential：conduction velocity

• Speed (conduction velocity or latency)：

Traditionally use peak latency

Onset latency

CV = d/t or d/(t – activation time);

CV = distance difference/onset latency difference; with two point

stimulation

• Factors affecting CV

Physiological：cold limbs, aging, increased height

Pathological：demyelination or loss of the fasting conducting fiber

Measurement of compound or sensory nerve action potential：amplitude

• Measurement：

Baseline to peak

Peak to peak

• Factors affecting amplitude：

Physiological：distance between nerve and electrode, aging, cold (increase

amplitude)

Pathological：any axonal loss lesion distal to dorsal root ganglion

Measurement of compound muscle action potentials

• Recording over muscle：

N-M junction：~1 msec

Conduction along muscle fiber：~ 3-5 m/sec

Use onset latency

• Amplitude：peak to peak, baseline to peak

• Intact SNAP amplitude with ↓CMAP amplitude

Motor neuron disease or other intraspinal process

Severe radiculopathy

Selective motor axonopathies（heavy-metal neuropathy, porphyria, some

demyelinating neuropathy）

N-M junction disease

Primary myopathy

Late response：

Late response：F-wave

• Occurs when a small percentage (3-5%) of antidromically activated motor cell discharges.

Supramaximal stimulation

• Assessment of multifocal or diffuse processes, especially affecting proximal area.

Demyelinating polyneuropathy

Late response：H-reflex

• Most easily elicited in soleus, with submaximal stimulation

Flexor carpi radialis, foot intrinsic, quadriceps

Children < 3 y/o

• Stimulation

Long-duration pulses

Relaxation or minimal plantar flexion

Stimulation rate 0.2 Hz

Clinical use of H-reflex

• Latency depends on age and leg length

• Abnormal finding：

Side to side difference of latency: 1.2 msec

Side to side difference of amplitude: 40%

F-wave V.S. H-reflex:

	F-wave	H-reflex
Stimulation	Supramaximal	Submaximal
Amplitude	Small, (3-5% of M-wave)	Large
Consistency	Unstable	Stable
Mechanism	Antidromic activation	Monosynaptic reflex

Interpretation

• Normal verse abnormal

• Principle of localization

• Deducing the pathophysiology from the electrophysiological results

• Timing of electrophysiological changes

• Estimating prognosis

Normal versus abnormal

• Nerve conduction study and quantitative EMG results are not always conclusive normal or abnormal

• Reference value: Mean with 2-SD, one-sided, based on normal Gaussian distribution

• Diagnosis are best made when multiple “abnormalities” are demonstrated in a pattern consistent with clinical presentation.

Principles of localization

• EMG

For the very proximal lesion

Based on finding abnormalities distal to a branch point, with normal findings proximal to that point

Intraneural topography makes some trouble：

• Ulnar nerve lesion over elbow

• Sciatic nerve lesion over hip

• Common peroneal nerve lesion

• Nerve conduction study

Based on demyelination

• Focal slowing

• Conduction block: focal drop of amplitude

Difficulty when axon loss with little demyelination

Deducing the pathophysiology from the electrophysiological results

• Neuropraxia or focal conduction block

Large amplitude drop when stimulation proximal to the lesion compared to distal stimulation

• Demyelination

Slowing of conduction

• Axon loss

EMG：more sensitive

NCS：small amplitude of CMAP and SNAP; quantify the degree of axon

loss and prognosis

Timing of electrophysiological changes

• Day 1 after an axon loss lesion：

EMG：reduced recruitment

NCS：drop amplitude when stimulation proximal to the lesion site

• Day 7 to 10 (CMAP: 7 day, SNAP 10 or 11 day)：

NCS：a conduction block lesion can be distinguished from axon loss

• Days 14 to 21：

EMG：starts to show Fib/PSW

• Fib/PSW means denervation, not mean whether it is “active” or

“ongoing” axonal loss

• Radiculopathy：paraspinal muscle: 10~14 day, distal muscle 3~4 weeks

• Fibrillation amplitude：2 months：600 uV，6 months：300 uV，one year：

100 uV

Estimating prognosis

• EMG and CMAP amplitude

• Factors：

Pathophysiology problems：

• Focal slowing

• Conduction block: recovery in weeks to months

• Axontemesis

• Neurotemesis：EDX can’t find out the supporting tissue injury

Time since onset

Distance between lesion and target muscle

• Critical window for target muscle：18~24 months

Pediatric rehabilitation

Primary reflex

Reflex	Stimulus	Response	Age of Suppression
Moro Startle	Sudden neck extension Sudden noise, clapping	Shoulder abduction, shoulder, elbow, and finger extension, followed by arm flexion adduction	4-6 months
Rooting	Stroking limbs or around mouth	Moving mouth, head toward stimulus, in search of nipple	4 months
Positive supporting	Light pressure or weight bearing on plantar surface	Legs extend for partial support of body weight	3-5 months Replaced by volitional weight bearing with support
Palmar grasp	Touch or pressure on palm or stretching finger flexors	Flexion of all fingers, hand fisting	5-6 months
Asymmetric tonic neck	Head turning to side	Extremities extend on face side, flex on occiput side	6-7 months
Symmetric tonic neck	Neck flexion Neck extension	Arms flex, legs extend Arms extend, legs flex	6-7 months
Reflex	Stimulus	Response	Age of Suppression
Plantar grasp	Pressure on sole distal to metatarsal heads	Flexion of all toes	12-24 months when walking is achieved
Autonomic neonatal walking	On vertical support plantar contact and passive tilting of body forward and side to side	Alternating autonomic steps with support	3-4 months
Placement or placing	Tactile contact on dorsum of foot or hand	Extremity flexion to place hand or foot over an obstacle	Before end of 1st year
Neck righting or body derotational	Neck rotation in supine	Sequential body rotation from shoulder to pelvis toward direction of face	4 months Replaced by volitional rolling
Tonic labyrinthine	Head position in space, strongest at 45 degree from horizontal Supine Prone	Predominant extensor tone Predominant flexor tone	4-6 months

Some critical milestones to remember by age:

Age (mo)	Milestones
1	Lift head (prone), vocalizes
3	Follows, laughs, smiles, has good head control
5	Plays with feet, reaches for and grasps objects
6	Sits with support
8	Sits without support
9	Plays peekaboo (躲貓貓), gets to sitting position; parachute reflex present; stranger anxiety
10	Pulls to stand, cruises, babbles(牙牙學語)
12-14	First words; walks
18	Multiple single words; uses spoon, removes clothes
24	Uses two-word phrases, throws overhead; ‘terrible twos’
30	Knows full name, puts on clothing
36	Jumps, pedals tricycle, learns nursery rhythms
48	Hops, plays with others
Mobility		Fine motor	Language	Social skill
Rolling (first prone to supine, then reversed)—4-5 months Sitting independently—6-7 months Walking—1 year Runs—2 years Stairs (adult style)—4 years Skips—5 years (boys later than girls)		Grasping items—4-5 months Hand-to-hand transfer—6 months Pincer—10-11 months Feed with spoon—18 months Scribble(亂畫)—18 months Copies circle—3 years Copies cross—4 years Copies triangle—5 years	Babbling—7-8 months Single words—1 year Body parts—18 months Short sentences—2 years Full sentences—3 years Paragraphs—4 years Knows color—5 years	Interactive game (pat-a-cake)—9months Take off clothes—15 months Copies housekeeping—18 months Parallel play—3 years Social interaction—4 years

Glasgow Coma Scale for young children

Verbal score	Adult and Older Child	Young Child
5	Oriented	Smiles, oriented to sound, follows objects, interacts
4	Confused, disordered	Cries but consolable, interacts inappropriately
3	Inappropriate words	Cries but is inconsistently consolable, moaning (嗚咽)
2	Incomprehensive sounds	Inconsolable crying, irritable
1	No response	No response

Scoring of eye opening and motor responses same as for adults

The characteristics and clinical associations of the following gaits:
Spastic, crouched, hemiparetic, waddling, and ataxic gaits

Gait	Characteristics	Clinical Association
Spastic	Adducted hips Internal rotation of hips Toe walking	Cerebral palsy
Crouched	Weak quadriceps Weak hip extensors Excessive dorsiflexion Hip or knee contractures	Neuromuscular disease Cerebral palsy
Hemiparetic	Circumduction of hip Posturing of upper extremity Inversion of foot	Cerebral palsy Cerebral vascular accident
Waddling (Trendelenburg)	Weakness of hip girdle	Neuromuscular disease
Ataxic	Wide-based gait Coordination problems Poor tandem walking	Cerebellar ataxia Friedreich’s ataxia

The definition, risk factors and clinical effects for cerebral palsy.

Definition:

Collection of diverse syndromes characterized by disorders of movement and posture
Cause by a non-progressive injury to the immature brain.

Diplegia: refers to spastic paresis in the lower extremities more than in the upper extremities
Quadriplegia: involves abnormalities of both upper and lower extremities (typically worse in legs).
Hemiplegia: abnormalities that involve an arm more than the ipsilateral leg
Triplegia: abnormalities that involve both legs and one arm.

Risk Factors for Cerebral Palsy

Prenatal

Perinatal

Postnatal

Congenital malformations

Socioeconomic factors

Intrauterine infections

Teratogenic agents

Maternal mental retardation

Maternal seizures

Maternal hyperthyroidism

Placental complications

Additional trauma

Multiple gestation

Prematurity (<32wk)

Birth weight <2500gm

Growth retardation

Abnormal presentations

Intracranial hemorrhage

Trauma

Infection

Bradycardia and hypoxia

Seizures

Hyperbilirubinemia

Trauma

Infection

Intracranial hemorrhage

Coagulopathies

Clinical Effects of Cerebral Palsy

1. Disorder of neuromuscular control
2. Abnormalities of muscle tone
3. Persistent primitive reflexes
4. Weakness in individual muscles
5. Disordered kinesthetic (動覺的) sense
6. Changes in joint alignment
7. Bony deformity: hip, spine and feet

The antispastic medications used in children

What are the indications for Phenol or Botulinum toxin therapy in cerebral palsy children? What are the advantages and disadvantages of these two blocking agents.

Indications for Phenol or Botulinum Toxin Therapy

Spasticity interfering with activities of daily living and functional activities.
Spasticity unresponsive to conservative measures
Spasticity requiring impractical or impossible frequency and duration of adjunctive measures such as ROM therapy
Spasticity involving antagonist musculature that interferes with agonist function
Spasticity that may compromise the success of planned surgery. Some patients have undergone more than one surgical procedure at a given joint because the underlying problem of spasticity was inadequately managed.

Botox

Blocking agent	Botulinum type A toxin	Phenol block
Administered	Injected into muscle	Injected into motor points of involved muscle
Effectiveness	Lasts 12 to 30 weeks	Lasts 4 to 12 months
Advantages	Easy to administer Diffuses readily into muscle Painless Can be administered without anesthesia	Use is widely approved Lasts longer than botulinum toxin Cumulative effects often occur
Drawbacks	Effects are always transient Lasts only 12 to 30 weeks Limited approval	Can be painful May require general anesthesia during administration Takes more skill to administer
Complications	No significant complications reported	Transient dysesthesias and numbness Hematomas may occur, which negate the effects of treatment If a large intravascular injection occurs, phenol can cause systemic effects such as muscle tremors and convulsions, as well as depressed cardiac activity, blood pressure, and respiration

SDR(SPR): Selective Dorsal (Posterior) Rhizotomy

Selective dorsal rhizotomy is a surgical procedure performed to reduce leg joints stiffness and spasticity in children who have cerebral palsy.
SPR involves selecting a variable percentage of sensory nerve rootlets after L2-S1 laminectomy.
Each sensory nerve root is divided into 3-5 rootlets. Each rootlet is tested with EMG, which records electrical patterns in muscles. The severely abnormal rootlets are cut.
This results in a decrease in peripheral excitatory influences on the anterior horn cell in patient with spastic cerebral palsy.
L5 and S1 are the most frequently abnormal roots.
The most common unwanted post-surgical effects: hypotonia (usually transitory) , weakness, sensory changes, bladder dysfunction, and hip subluxation/dislocation have also been reported.

SDR(SPR): Selective Dorsal (Posterior) Rhizotomy: Favorable Selection Criteria

§Pure spasticity (limited dystonia/athetosis)

§Function limited primarily by spasticity

§Not significantly affected by primitive reflexes/movement patterns

§Absence of profound underlying weakness

§Selective motor control

§Some degree of spontaneous forward locomotion

§Adequate truncal balance/righting response

§Spastic diplegia

§History of prematurity

§Age 3-8 years

§Minimal joint contractures or spine deformity

§Adequate cognitive ability to participate in therapy

§No significant motivational/behavioral problems

§Supportive and interactive family

Describe the classification of Congenital BPI

Congenital Brachial Plexopathy(1)

Plexopathy	Level (Nerve Roots/Trunk)	Clinical Findings (Related Weakness)
Duchenne-Erb’s palsy (most common)	C5-C6±C7 Upper trunk	Weakness of shoulder abduction, external rotation, elbow flexion, supination, wrist extension, finger extension, waiters tip posture.
Klumpke’s plexopathy	C8-T1 Lower trunk	Weakness of elbow extesion, pronation, wrist flexion, hand weakness, associated with Horner’s syndrome
Pan plexopathy	C5-T1 Arm, entire plexus	Weakness of all motions listed above, flail chest

Usually unilateral, can be bilateral.
Most common etiologies: large baby and shoulder dystocia.
Caused by injury to brachial plexus by excessive lateral traction to fetal head or neck and/or intrauterine propulsion due to force of contraction.
Treatment: ROM exercise, strengthening, splinting, encourage use of affected arm.
Complete recovery occurs in more than 65%. Mild and moderate deficits are seen in 10% each. 15% will have severe residual deficits.
The optimum age for surgery is younger than 9 months because nerve growth factor is at a maximum before 1 year of age, and there is less nerve scarring and distal muscle atrophy at that age.
Surgical procedures: neurolysis of scars, end to end anastomosis with microsurgical fascicular repair and cable graft of nerve rupture.

1. 發展遲緩(developmental delay)兒童的定義?

§兒童因為各種不同的原因，在功能發展趕不上該年齡所應有的程度，例如運動、感官知覺、語言、認知、社會適應、情緒及行為各方面的能力，使其在發展上造成各種程度不同的落後現象(未達正常孩子80%) ，稱之為發展遲緩兒童。

§1992 Colorado Interagency Coordination Council defines that the child exhibit a 20 % delay in functioning when compared to his or her same age peers.功能低於同年齡兒童之百分之二十

§1987 Peterson defines criterion that a score 2 or more standard deviation below the mean of a reference group.低於平均值兩個或兩個以上之標準差

發展遲緩等級判定

§顯著極重度遲緩：量表指標未達平均值下5標準差

§顯著重度遲緩：量表指標未達平均值下4~5標準差

§顯著中度遲緩：量表指標未達平均值下3~4標準差

§顯著輕度遲緩：量表指標未達平均值下2~3標準差

§輕微遲緩：量表指標未達平均值下1~2標準差

衛生署發展遲緩兒童功能性診斷分類

§認知發展遲緩

§語言發展遲緩

§動作發展遲緩

§社會情緒發展遲緩

§全面性發展遲緩

§非特定性發展遲緩

Prevalence of Developmental Delay

6-8 % by WHO study

發展遲緩兒之發展評估測驗

w簡易兒童發展量表（衛生署）

w中國兒童行為發展量表（CCDI）

w嬰幼兒綜合發展測驗（教育部）

wBayley Scales of Infant Development (Bayley II)

wDenver Development Screening Test (Denver II)

wPeabody Development Scale

wAlberta Infant Scales

wStanford-Binet Intelligence Scale (IV)

wWechsler Intelligence Scale

a. Preschool and Primary Scale (WPPSI-R)

b. Children (WISC-III)

wVisual Motor Integration (VMI)

wStycar Test (Visual Acuity)

wSensory Integration Evaluation

發展評估

§A.新生兒類別(Neonatal Assessment)

§B.篩檢類別(Screening Test)

§C.診斷類別(Diagnostic tool)

§D. 介入類別 (Early Intervention)

A 新生兒類評估(Neonatal Assessment)

§Apgar Score

§Clinical Assessment of Gestational Age in the Newborn Infant

§Neonatal Behavioral Assessment Scale

§Assessment of Preterm Infant's Behavior

§Neurological Assessment of the Fullterm & Preterm Newborn Infant

§Morgan Neonatal Neurobehavioral exam.

§Movement Assessment of Infants

§Milani-Comparetti Motor Development Screening Test

B 篩檢類評估 (Screening Test)

丹佛發展篩檢量表II

(Revised Denver Developmental Screening Test, Denver II)

中國學齡前兒童發展量表

(Chinese Child Developmental Inventory, CCDI)

簡易兒童發展量表

(Simple and Accurate Child Development Screening Test)

米勒學齡前評量

(Miller Assessment for Preschooler, MAP)

嬰幼兒綜合發展測驗篩選題本

(Infant and Child Comprehensive Developmental Battery, screening test )

Chinese Child Developmental Inventory( CCDI)
學齡前中華兒童發展量表

§Gross Motor 粗動作

§Fine Motor 精細動作

§Expressive Language 語言表達

§Comprehension Conceptual 語言了解

§Situation Comprehension 環境理解

§Self Help 自我照顧

§Personal Social 社會互動

簡易兒童發展量表

§精細動作

§粗動作

§語言溝通

§身邊處理及社會性

D 診斷類發展評估 (Diagnostic tool)

§貝萊氏嬰兒發展量表

(Bayley Scale of Infant Development, BSID)

§粗動作功能評量表

(Gross Motor Function Measure, GMFM)

§布巴斯歐斯索動作量表

(Bruininks-Oseretsky Test of Motor Proficiency, BOTMP)

§嬰幼兒綜合發展測驗診斷題本

(Infant and Child Comprehensive Developmental Battery, Diagnosis)

§兒童身心障礙評估量表

(Pediatric Evaluation of Disability Inventory, PEDI)

§皮巴迪動作發展量表

(Peabody Developmental Motor Scale, PDMS)

E 介入類發展評估工具

§早期介入量表

(Early Intervention Developmental Profile, EIDP)

§Portage 早期教育指導手冊

(Portage Guide to Early Education )

§兒童訓練指南

§生活適應能力檢核手冊

§中重度智障者功能性教學綱要

何謂早療及早療對象?

早期療育

§對於特殊需求的兒童提供早期發現、早期診斷及早期治療，立即給予專業性的醫療、復健、教育、轉介及福利等協助，以有效降低其障礙程度，充分開拓其發展潛力。

§兒童早期(0-6 歲)

§利用多專業整合性服務

§協助醫療、家庭及社會相關的問題

§減少併發症，開發孩子的潛力

§整合入社會團隊中，有效的減少長期社會成本

肌肉軟組織超音波簡介

醫用超音波診斷系統，基本上是利用超音波本身能量的特性，在傳播的路徑中，藉由波和人體組織的交互作用，如肌肉和脂肪間聲阻的差異，能量發生反射、散射及吸收等物理現像，因而反應出身體組織的內部情形，提供診斷上的情報。超音波由於具有real time特性，可使檢查者在做檢查的時候，做動態檢查，同時加上最近高頻率(7.5 MHz以上)的探頭的出現和彩色Doppler影像的發展，更使得超音波的應用在診斷軟組織的病變方面成為一項利器。我們對於軟組織，從皮膚到骨骼的表面，都可以使用超音波來作診斷。骨骼肌肉超音波，過去在美國和亞洲地區使用得比較少，主要原因是大家習慣利用MRI來作診斷。其實對軟組織構造，超音波可以提供類似MRI的診斷功能，但是它的價錢卻遠比MRI低，而且操作方便迅速。因而，我們相信對於軟組織的病變，超音波的使用實在值得推廣。

在醫學診斷上，使用探頭發射一低能量超音波聲束進入人體組織時，因為身體組織之聲阻抗差異，造成聲能量部分反射及散射，形成不同的回波訊號(echo)，這些回波訊號由接收系統接收放大、調置，再利用不同的顯示方式表現出來。醫學上常用的顯示方式有：A模式（振幅模式，Amplitude Mode），B模式（亮度模式，Brightness Mode），M模式（運動模式，Motion Mode）與D模式（都卜勒模式，Doppler Mode），在骨骼肌肉系統最常使用的則是B模式與D模式。以下簡介超音波檢查在骨肌肉系統發展之現狀：

1. 肌肉外傷：肌肉最常見的病變就是外傷，由其是的四肢的肌肉。隨著時代的進步，人類對於運動的喜好增加，使得運動傷害變成醫師們日常所經常要處理的問題。當我們在處理這一類的病人的時候，若能夠得到一個肌肉的切片影像，對於我們診斷的確定是相當有幫助的。如果我們要檢查的肌肉是屬於比較淺層的肌肉，使用高頻率 (10 MHz) linear array的超音波探頭可以得到較佳的解像度。而如果要檢查的肌肉是屬於比較深層的，那麼就要使用5 MHz，或者是3.5 MHz的探頭才有足夠的穿透力。肌肉的檢查必須包括休息和收縮的肌肉狀態，而且必需同時檢查肌肉的縱向與橫向的切面圖。如果病人必須接受手術，我們也可以在皮膚的表面做上記號，當做手術時定位之用。最近由於彩色超音波的發達，對於肌肉裏的血流情形我們可以加以精確的評估，對於肌肉傷害的診斷更是多了一項武器。在一個急性期肌肉內出血的病人，一般的B-mode超音波並不太容易從超音波的回音本身 (echogenicity) 來做診斷，但是受傷的肌肉與正常的肌肉比較，會有體積增加的情形，對於這類的病人幾天之後再重覆的檢查，可以發現它的echogenicity會有變化。一個凝固的血塊 (clotted hematoma)，在超音波檢查呈現的是一個低迴音的顯像(hypoechoic)，看起來有時候像是液體的樣子，但是此時若去針刺抽取往往會失敗。

2. 軟組織的腫瘤：對於軟組織的腫瘤的診斷，普通的ｘ光xeroradiography與CT的顯像力較差，一般大家都是喜歡使用MRI。可是MRI的成本較貴，有時候還會被健保局核減費用，因而超音波在對於軟組織腫瘤的診斷上就佔有一個相當重要的地位。在做軟組織腫瘤的超音波檢查時，當然我們是根據腫瘤的部位來選取我們所使用探頭的頻率的高低。腫瘤的診斷至少要做兩個以上的切面，有時候腫瘤太大兩端會超過你所使用的探頭。然而目前已有新的機種問世，可以將探頭移動時的影像連接在一起，做成較探頭長度更長的topography。而且利用彩色超音波，我們也可以來研究腫瘤內血管的特性，比如利用spectrum analysis可以做PI(Pulsative index)與RI(Resistive index)的測定。目前已有許多的報告指出，如果軟組織腫瘤裏面的血管比較豐富，尤其在靠近中間的地方，那麼惡性變的機會就比較高，如果RI低於0.6也是代表惡性變的機會比較高。當然如果是發現一個囊腫(cyst)，那麼我們也可以在超音波的指引之下直接抽取；甚至是實心的腫瘤也可以在超音波的指引之下，用針頭抽取細胞做細胞學(cytology)的診斷，可以免去開刀做切片(biopsy)的步驟，此不僅比較便宜，病人所受的苦痛也比較少。我們不僅可以從超音波的echogenicity來診斷細胞的種類，而且也可以判斷腫瘤裏頭是否有鈣化或是血塊，或是膿瘍的發生，另外也可以查看骨骼的皮質層(cortex)是否有受到波及。通常我們在做軟組織細胞檢查的時候要注意回答下列幾個問題：1.是否真的有一個腫瘤？2.腫瘤的形態是什麼？3.腫瘤的位置在那裡？4.腫瘤的體積有多大？5.附近的組織是否有所波及？當然如果軟組織腫瘤是一個囊腫，或是血塊，或是水瘤，或是周圍比較清楚(well-marginated)，血流比較低的瘤，我們較有把握去判斷它是良性性質的時候，就可以直接做介入性的手術治療。如果還是有惡性變的可能，那麼MRI還是必須的，MRI對於惡性腫瘤的分期(staging)是值得參考的。

3. 肩關節：對於肩關節軟組織的病變，尤其是rotator cuff破裂的診斷，過去常使用contrast arthrography，但是它並沒有辦法來區分全部或部分的破裂。MRI最近也被大量使用來診斷rotator cuff的病變，但是同樣對於全部或局部破裂的病患並沒有辦法有效的來加以判別。肩關節使用超音波來診斷，可能是骨肌肉系統中使用最早的一個部位。在7.5-mhz以上的高頻率探頭使用之下，我們對於每條rotator cuff都可以清楚地看到，包括脊上肌(supraspinatus)、脊下肌(infraspinatus)，肩下肌(subscapularis)，肱二頭肌的長頭(long head of biceps)等等。如果對於一個有經驗的檢查者來說，對於rotator cuff傷害的診斷，超音波的診斷率已經可以達到百分之九十以上，國內在這方面的起步也是最早，許多醫學中心的醫師已經累積了相當的經驗。

4. 髖關節：超音波在髖關節疾病的診斷，主要是用在嬰兒期，尤其在嬰兒六個月以前，由於股骨頭部尚未鈣化，普通的X光無法顯示，對於一些先天性髖關節脫臼的病患，以往診斷上往往要做arthrography或者是MRI，前者具有侵入性而且必需接受輻射線的照射，而MRI的診斷則相當費時、費錢而且也不切實際。超音波在這方面的診斷提供了一個安全沒有輻射線，不痛迅速又正確的診斷。目前隨著診斷技術的進步，用power Doppler更可以正確的診斷出股骨頭部裏面血流的情形，可以幫助骨科醫師決定在做先天性髖關節脫臼(CDH or DDH)復位以後包石膏的角度，以免因為角度過大影響股骨頭部缺血性壞死(avascular necrosis)的產生。另外對於小孩子常見的髖關節積水症或是化膿症，也可以很正確的利用超音波來做一診斷的基礎，再加上超音波檢查的指引之下，可以簡單、迅速、正確的抽取到髖關節裏面的積水或化膿來做為診斷或治療的依據。

5. 膝關節：超音波用於膝關節的診斷，目前較確定的是關於滑膜囊炎(synovitis)，側韌帶(collateral ligament)的外傷和patellar tendon的診斷。目前也有人報告對於後十字韌帶的病變，超音波已經可以正確的診斷出來。而對於前十字韌帶或半月軟骨，目前還在發展的階段。

6. 足踝部：足踝部的超音波診斷，目前成績最好的是有關於脛後肌肌腱(posterior tibial tendon)方面的診斷。過去對於脛後肌肌腱時常除了臨床檢查斷之外，在影像學的檢查要靠tenography或者MRI。其實如果使用超音波來檢查，不僅迅速、便宜簡單，而且正確。肌腱的變化包括tenosyonvitis和完全斷裂，超音波都可以相當正確的診斷出來；另外，對於足踝扭傷，利用超音波我們也可以很直接的觀察到外側韌帶，包括anterior talofibular ligament和calcaneofibular ligament等的正確影像，作為直接診斷的基礎。

7. 其他：對於血管或神經的病變，目前超音波也有不錯的成績。比如carpal tunnel syndrome的診斷，利用超音波也可以相當正確的診斷出來。血管方面的檢查，尤其在color Doppler的問世以來，幾乎可以做得跟angiography一樣，而且它不俱有侵入性。目前由於power Doppler image的發展，使得低流速的血管亦具良好的顯像，在軟組織有關perfusion方面的量測變得更為精準與明確。

總結來說，超音波具有相當多的好處：1.它不具有輻射性，不必擔心病人重覆檢查會受到輻射性的傷害。2.它不具有侵入性，檢查的時候病人不會痛苦。3.它比較迅速、方便，不必等候時間。4.它比較便宜，不像MRI那麼昂貴。5.它可以幫助我們在超音波探頭的指引之下，受一些液體的抽取或是細胞學方面的抽取，以供診斷之用。6.可以隨著操作者的操作，可以將神經、血管、肌腱等，長形構造的組織做一縱向的影像追蹤，不像MRI通常只是片斷的切出我們所要看到的影像。綜合以上這些好處，超音波在骨骼肌肉系統的應用，對於骨科、復健科或是神經科醫師來說，都很有診斷上幫忙的價值。尤其隨著時代的進步，硬體不斷的改良，我們也相信在不久的將來，超音波一定會有更好的貢獻提供大家診影像上一個相當好的診斷幫忙。