Treatment of dysphagia

1. What are techniques used for treating dysphagia and preventing aspiration?
2. When does swallowing function usually return in brainstem strokes?
3. What is the cause of nasal speech?

Answer:
1. Non-oral feeding (does not treat dysphagia), changes in posture and head position, elevation of HOB, feeding in upright position, chin tuck, turning head to paretic side, diet modifications.
2. 3 weeks.
3. Caused by failure of the soft palate to close off the nasal cavity from the oral cavity or incomplete closure of the hard palate. Uplifting of the soft palate prevents nasal speech.

Dysphagia

1. On bedside swallow, what are predictors of aspiration?
2. What are the three phases of swallowing?
3. What is a chin tuck?
4. What are predictors of aspiration on video swallow study?
5. What are the risk factors for developing aspiration pneumonia?

Answers:
1. Abnormal cough, cough after swallowing, dysphonia, dysarthria, abnormal gag reflex, voice changes after swallow.
2. Oral, pharyngeal, esophageal.
3. Protection of airway by preventing entry of liquid into larynx via facilitating forward movement of the larynx. Also decreases the space between the base of tongue and posterior pharynx.
4. Delayed initiation of swallow reflex, decreased pharyngeal peristalsis.
5. Decreased LOC, tracheostomy, emesis, reflux, NGT feeding, dysphagia, prolonged pharyngeal transit time.

Aphasia

For the following types of aphasia, what are the characteristics, location of injury, and blood vessel that results in the aphasia:
1. Wernicke's?
2. Broca's?
3. Global aphasia?
4. Anomia?
5. Conduction aphasia?
6. Transcortical motor?
7. Transcortical sensory?

Answers:
1. Fluent speech, alexia, agraphia, marked paraphasias. Located in postero-superior temporal gyrus of dominent hemisphere. Caused by lesion of inferior division of the MCA.
2. Nonfluent speech, preserved comprehension. Located in postero-inferior frontal lobe. Caused by lesion of superior division of the MCA.
3. Poor comprehension and repetition, incomprehensible speech or mutism. Located in the entire perisylvian region. Caused by MCA lesion.
4. Word-finding difficulty, alexia, agraphia. Located in angular gyrus. Caused by a lesion affecting the temporo-parietal region.
5. Impaired repetition, literal paraphasias (substituting similar sounds). Located in arcuate fasciculus, which joins Broca's and Wernicke's areas.
6. Reduced rate of speech and output, initiation, good comprehension and repetition. Located in frontal lobe, ant/sup to Broca's area. Caused by an ACA lesion.
7. Poor comprehension, fluent speech, preserved repetition. Located in watershed area isolating perisylvian speech structures from the posterior brain. Caused by PCA lesion.

Other causes of shoulder pain in CVA

1. How is brachial plexus and peripheral nerve injury usually diagnosed? How is it treated?
2. What are the symptoms of bicipital tendonitis and how is it diagnosed?
3. Where does HO usually appear in CVA patients?
4. How is dependent edema treated?

Answers:
1. Diagnosis is by physical exam showing segmental muscle atrophy, finger extensor contractures, delayed spasticity, and by EMG. Treatment is proper bed positioning to protect paretic arm, ROM, 45 degree abduction sling, sling for ambulation, WC armrest.
2. Symptoms are chronic pain in anterolateral shoulder, pain in abduction/external rotation, pain over bicipital groove. There is a positive Yergason's test. Diagnosis is confirmed with decreased pain after injection of tendon sheath with lidocaine.
3. In the extensor side of the elbow and in the shoulder.
4. Compression gloves, foam wedge, pneumatic compression, retrograde massage, arm elevation.

Shoulder subluxation in CVA

1. What is the Basmajian principle and how does it contribute to shoulder subluxation in CVA?
2. What are the pros and cons to a shoulder sling?
3. What are treatments for shoulder subluxation?
4. How can subluxation be prevented?

Answers:
1. Decreased trapezius tone causes the scapula to rotate and the humeral head to sublux from the glenoid fossa.
2. Shoulder slings are not indicated for subluxation, but may be used when patient ambulates to support extremity. Cons include the development of contractures in shoulder adduction/int rot and elbow flexion.
3. Functional e-stim, armboard, arm trough, lapboard, overhead slings (also prevents hand edema).
4. Combining the early reactivation of shoulder musculature with e-stim, passive support of the glenohumeral jt (arm trough).

CRPS, type I

1. What is the most common cause of hemiplegic shoulder pain?
2. What is Complex Regional Pain Syndrome (CRPS)? What is the most common subtype?
3. What are the stages of CRPS?
4. How is CRPS diagnosed?
5. What are the physical exam findings of Shoulder-hand syndrome?
6. What is the treatment for CRPS?

Answers:
1. CRPS, soft tissue lesions (including plexopathy).
2. CRPS is characterized by sympathetic mediated pain and related sensory abnormalities, abnormal blood flow, abnormalities in motor system, and changes in superficial and deep structures. Most common subtype is shoulder-hand syndrome.
3. Stage 1 (acute) lasts 3-6 months, involving burning pain, swelling.edema, exquisite tenderness, vasomotor changes. Stage 2 (dystrophic) lasts 3-6 months and involves more intense pain that spreads proximally, with skin/muscle/nail atrophy, edema, cold insensitivity. Stage 3 (atrophic) involves decreased pain with pale cyanotic skin, smooth and shiny appearance, cool and dry, with weakness/atrophy, contractures/flexion deformities.
4. X-rays may show periarticular osteopenia. Bone scan showing diffusely increased juxta-articular tracer activity on delayed images. EMG showing spontaneous activity predicts eventual development of CRPS. Stellate ganglion block that alleviates pain is the gold standard.
5. Shoulder pain with ROM, lack of elbow pain, no pain with pronation/supination, wrist dorsiflexion pain, pain with MCP/PIP flexion, PIP edema, MCP tenderness, pain out of proportion to clinical findings.
6. ROM exercises, corticosteroids, intra-articular corticosteroid injection, NSAIDs, tricyclics, diphosphonates, calcitonin, anticonvulsants, alpha-blockers, beta-blockers, Ca-blockers, topical capsaicin, TENS, contrast bath, edema control, desensitization, US, sympathetic ganglion blocks, local injections, sympathectomy.

Stroke Rehabilitation methods

1. What is proprioceptive neuromuscular facilitation?
2. What is neurodevelopmental technique (Bobath's approach)?
3. What is Movement therapy (Brunnstrom's approach)?
4. What is the sensorimotor approach (Rood's approach)?
5. What are behavioral approaches to stroke therapy?

Answers:
1. Use of spiral and diagonal components of movement with the goal of facilitating functional movement patterns rather than strengthening individual muscles.
2. This is the most common approach. The goal is to normalize tone, inhibit primitive movement patterns, and facilitate normal movement patterns.
3. Use of primitive synergistic patterns in training to improve motor control through central facilitation.
4. Modification of muscle tone and voluntary motor activity using cutaneous sensorimotor stimulation.
5. Kinesthetic or positional biofeedback and forced-use exercises.

Stroke recovery pattern

1. According to Twitchell, when do DTR return? When does clonus usually appear? When do the first intentional movements appear?
2. What is a positive predictor of return of hand movement?
3. What are predictors of poor prognosis?
4. What are Brunnstrom's 7 stages of stroke recovery?

Answers:
1. DTR return within 48 hrs. Clonus is seen at 1-38 days post-onset. Movement returns at 6-33 days post onset.
2. If there is recovery of the hand at 4 weeks, there is a good chance of recovery.
3. Complete arm paralysis at onset (only 9% have hand fxn recovery), severe proximal spasticity, prolonged flaccid period, late return of proprioceptive facilitation (tapping) response, late return of shoulder flexors/adductors (>13 days).
4. Flaccidity --> Spasticity, min voluntary movement, basic synergy --> control over synergy, increased spasticity --> break in synergy, decreased spasticity --> continued decr synergy and spasticity --> disappearance of spasticity, increased coordination --> normal function.

CEA and treatment of hemorrhage

1. Under what circumstances is carotid endarterectomy recommended by the AHA?
2. What is the treatment for subarachnoid hemorrhage?
3. What is the treatment for intracranial hemorrhage?
4. What is the treatment for AVM?

Answers:
1. Symptomatic patients with one or more TIAs (or mild stroke) within past 6 months and >70% carotid stenosis.
2. Cardiac monitoring for arrhythmias, pain control, mannitol, BP control, aneurysm clipping early, nimodipine within 96 hrs.
3. Manage increased ICP and BP, possible surgical intervention.
4. Treatment for both symptomatic and asymptomatic AVM includes: surgical excision, embolization, proton beam therapy, radiosurgery/microsurgical resection for small AVMs.

Thrombolytic/anticoagulation therapy

1. What is the effect of giving tPA within 3hrs of stroke onset?
2. What is the inclusion and exclusion criteria for tPA?
3. What are possible indications for anticoagulation?
4. How long following the CVA should anticoagulation for cardiac emboli be started?

Answers:
1. 30% reduction in disability, increased mortality.
2. Inclusion: age >18yrs, onset within 3hrs, moderate to severe symptoms, and head CT negative for blood. Exclusion: minor symptoms, CT positive for blood, BP >185/100, increased PT/PTT, decreased plt, hypoglycemia, hyperglycemia (>400), h/o CVA within 3 months, h/o ICH/AVM/aneurysm, seizures.
3. Cardiac emboli (most commonly from chronic a-fib), TIAs (especially of increasing frequency). Possibly used for a mild stroke, to prevent further progression.
4. If deficit is mild, start immediate anticoagulation. If deficit severe, wait 3-5 days.

Immediate management of CVA

1. What is the first step in acute CVA management?
2. What are the indications for emergent CT?
3. Why should hypotonic fluids be avoided?
4. What are the cutoffs for BP treatment in a nonthrombolytic candidate? A thrombolytic candidate? Hemorrhagic CVA?
5. How are post-CVA seizures treated?
6. How is cerebral perfusion calculated? What is the goal value?
7. What are methods used to decrease ICP?

Answers:
1. ABCs.
2. To determine if patient is candidate for emergent thrombolytic therapy, impaired consciousness, coagulopathy present, fever.
3. Possibility of worsening brain edema.
4. Treat for SBP>220, DBP>120 in nonthrombolytic candidate. Treat for SBP>185, DBP>110 in thrombolytic candidate, before giving treatment. Treat for SBP>180, DBP>105 in hemorrhagic CVA, usually with labetalol (which does not cause cerebral vasodilation).
5. Benzos. If not effective, can use phenytoin.
6. Cerebral perfusion = MAP - ICP. Goal is >60mmHg.
7. ICP is managed by correcting contributing factors (hypercarbia, hypoxia, hyperthermia, acidosis, hypotension, hypovolemia), elevating HOB, avoid jugular compression, hyperventilation, hyperosmolar therapy (mannitol), Lasix, barbiturates, fluid restriction, surgical decompression.

Diagnostic tests for CVA: other

1. How is carotid ultrasound useful for diagnosis of CVA?
2. What is angiography used for? What is the complication rate?
3. What is MRA used for?
4. What is lumbar puncture useful for/
5. What is TEE useful for?

Answers:
1. Useful as a screening tool for carotid stenosis.
2. Diagnosis of aneurysms, vascular malformations, arterial dissections, narrowed or occluded vessels, and angiitis. Complications, including aortic or carotid artery dissection, embolic stroke, vascular spasm, and occlusion occur in 2-12%.
3. Detection of extracranial carotid artery stenosis, evaluation of large cervical and basal vessels.
4. LP is used to detect blood in CSF, primarily in SAH.
5. TEE is used to detect potential cardiac sources of embolism.

Diagnosis of stroke: CT and MRI

1. Why is a CT without contrast ordered?
2. How does the appearance of an infarct evolve on CT scan?
3. How does SAH appear on CT?
4. What is the benefit of using MRI over CT?
5. What is seen on the MRI for a cerebral infaction?
6. What is seen on the MRI for intracerebral hemorrhage?
7. What is seen on the MRI for SAH or IVH?

Answers:
1. If a bleed is suspected, contrast may be confused with bleeding.
2. Initially normal for first few hours, ill-defined hypodensity (black) after 24-48 hrs, edema (hypodense) better defined after 3-4 days. Hemorrhage in infarcted area appears as hyperdense mass within hypodense edema.
3. 90% of CTs visualize hyperdense area in basal cisterns or around brainstem within 4-5 days.
4. MRI is more sensitive than CT for small infarcts and posterior fossa infarcts. Ischemic edema detected earlier with MRI (within hours).
5. Early there is increased white signal on T2 images, more pronounced at 24hrs to 7 days. Chronically (>21 days) there is decreased T1 and T2 signals.
6. With acute hemorrhage, there is decreased (black) signal on T1 and T2 image. As hemorrhage ages, it develops increased signal on T1 and T2.
7. Acute, there is low signal (black) on T1 and T2.

Arteriovenous malformations (AVMs)

1. What is the pressure in an AVM? Are larger or smaller AVMs more likely to result in hemorrhage?
2. What is the lifelong risk of hemorrhage from an existent AVM?
3. When is bleeding most likely to occur?
4. What is the presentation of an AVM rupture?

Answers:
1. Low pressure. The larger the shunt, the lower the interior pressure. Smaller AVMs are more likely to result in hemorrhage due to higher pressure.
2. 40-50%. First hemorrhage is fatal in 10%.
3. Ages 20-40 years.
4. Hemorrhage (parenchymal, subarachnoid, intraventricular), seizures, headaches.

Subarachnoid hemorrhage

1. Where are the majority of saccular (berry) aneurysms found?
2. What size aneurysms are most likely to rupture?
3. What is the peak age for rupture?
4. What are the symptoms due to aneurysm?
5. What are the symptoms of rupture?
6. What is the most common complications and how are they treated?

Answers:
1. 90-95% occur on the anterior circle of Willis.
2. If 10mm or larger, usually while active.
3. fifth and sixth decades.
4. Usually asymptomatic, may have compression of CN 3 (with posterior aneurysm).
5. Sentinel HA (50% of patients), LOC, CN 3 or 6 palsy, hemiparesis, aphasia, memory loss, seizures.
6. Risk of early rebleeding is 50-60%. Vasospasm occurs in 25%, caused by vasoactive blood breakdown products, 3-12 days after rupture. It is treated with nimodipine.

Hypertensive intracerebral hemorrhage

1. What percentage of strokes are hemorrhagic?
2. What is the usual underlying cause of intracerebral hemorrhage?
3. What are the symptoms of new hemorrhage?
4. What are the common sites of hemorrhage? What is the most common?
5. What are the symptoms of hemorrhage into the putamen?

Answers:
1. 15%
2. Chronic HTN.
3. Sudden onset HA, LOC, vomiting, seizures (10%), nuchal rigidity. Preceded by "false aneurysms" that are arterial wall dilations 2/2 HTN.
4. Putamen (most common), thalamus, pons, cerebellum, lobar.
5. Hemiplegia (2/2 compression of adjacent internal capsule), vomiting, HA, eyes deviating away from paretic limbs. May progress to coma in hours.

Basilar artery stroke

1. How does occlusion of the basilar artery usually occur?
2. What symptoms usually occur when a branch of the basilar artery is occluded?
3. What is locked-in syndrome?
4. What sort of lesion results in clumsy hand syndrome?

Answers:
1. Occlusion results from atherosclerotic plaque in the basilar artery, occlusion of both vertebral arteries, or occlusion of one vertebral artery when the other is inadequate size.
2. Internuclear ophthalmoplegia, conjugate horizontal gaze palsy, ocular bobbing.
3. Tetraparesis with only vertical eye movement intact, but patient is fully conscious due to sparing of reticular activating system. Caused by bilateral lesions of ventral pons.
4. Basis pontis, internal capsule (anterior limb).

Syndromes of the vertebrobasilar syndrome

1. Occlusion of what blood vessels results in Wallenberg's (lateral medullary) syndrome?
2. What are the symptoms of Wallenberg's syndrome?
3. Occlusion of what blood vessels results in Benedikt's syndrome?
4. What are the symptoms of Benedikt's syndrome?
5. What are the symptoms of medial brainstem syndrome?
6. What is medial medullary syndrome?

Answers:
1. Vertebral arteries, posterior inf cerebellar artery, superior/middle/inferior lateral medullary artery.
2. Ipsilateral Horner's syndrome (ptosis, anhydrosis, miosis), decreased pain and temp in ipsilateral face, ipsilateral ataxia, contralateral decreased pain and temp in body, dysphagia, dysarthria, hoarseness, vertigo, hiccups, nystagmus, diplopia.
3. Interpeduncular branches of the basilar or posterior cerebral artery, affecting the red nucleus/tegmentum of midbrain.
4. Ipsilateral CN III paralysis, contralateral hyperesthesia and hyperkinesia (ataxia, tremor, chorea, athetosis).
5. Contralateral hemiparesis, ipsilateral CN paralysis.
6. This is a type of medial brainstem stroke, caused by infarcion of the medial medulla due to occlusion of vertebral arteries or anterior spinal artery. Symptoms include ipsilateral hypoglossal palsy, contralateral hemiparesis, and contralateral lemniscal sensory loss.

Posterior circulation CVAs

1. What are areas of the brain that are supplied by the PCA? Nerves supplied by PCA?
2. What is the clinical presentation of a PCA stroke?
3. What clinical syndrome is caused by occlusion of the CNs supplied by the PCA?
4. What parts of the brain are supplied by the vertebral and basilar arteries?
5. What are symptoms of vertebrobasilar strokes?

Answers:
1. Upper brainstem, inferior temporal lobe, medial occipital lobe, CN 3, CN 4.
2. Visual field cuts, prosopagnosia (can't read faces), palinopsea (abnormal visual images), alexia, transcortical sensory aphasia.
3. Weber's syndrome: oculomotor palsy with contralateral hemiplegia.
4. Midbrain, pons, medulla, cerebellum, posterior and ventral cerebral hemispheres.
5. Vertigo, nystagmus, bilateral abnormalities of motor function, absence of cortical signs, crossed signs (deficit on ipsilateral face, contralateral body).

Anterior cerebral artery (ACA) stroke

1. Where can the ACA be occluded without having any deficits?
2. What occurs when both ACAs arise from one stem and there is an occlusion?
3. What symptoms occur when there is occlusion of one ACA, distal to the anterior comm artery?
4. If the dominant side is affected, what sort of aphasia results?

Answers:
1. At the stem of the ACA, just proximal to its connection with the anterior communicating artery, due to collateral circulation.
2. Major disturbances in both hemispheres --> aphasia, paraplegia, incontinence, frontal lobe dysfunction.
3. Contralateral weakness and sensory loss, affecting mainly distal leg, little UE involvement, head and eyes deviating toward side of lesion, urinary incontinence, gait apraxia.
4. Transcortical motor aphasia.

Internal carotid artery (ICA) stroke

1. Where does occlusion most frequently occur?
2. What are the most common symptoms of ICA occlusion?
3. What is amaurosis fugax?
4. Why is central retinal artery ischemia rare?

Answers:
1. First part of ICA immediately beyond the carotid bifurcation.
2. Symptoms vary from no symptoms to severe massive ACA/MCA distribution infarction, resulting in contralateral motor and/or sensory symptoms.
3. Amaurosis fugax is transient monocular blindness occurring prior to ICA stroke in 25% of cases, resulting from embolic occlusion of either retinal branch or the central retinal artery.
4. Collateral supply.

Types of ischemic stroke

1. When during the day do thrombotic strokes usually occur? How do they usually progress? What percentage are preceded by TIA?
2. When do embolic strokes usually occur? What artery is usually affected? What percentage are preceded by TIA?
3. What is the most common cause of an embolic stroke? What are other common causes?
4. What are lacunar infarcts? What is the usual cause?
5. What are the symptoms of lacunar infarct? What percentage are preceded by TIA?

Answers:
1. Thrombotic strokes usually occur during sleep and have slow progression of deficits over 24-48 hrs. 50% are preceded by a TIA.
2. Embolic strokes occur during the day. Deficit is immediate and seizures may occur. The MCA is most often affected. 11% are preceded by TIA.
3. Chronic a-fib is the most common cause. Other causes include MI, cardiac aneurysm, CM, atrial myxoma, valvular heart disease, sick sinus syndrome.
4. Lacunar infarcts are small (<15mm) infarcts seen in the putamen, pons, thalamus, caudate, and internal capsule, due to occlusive arteriolar or small artery disease. They are usually associated with hypertension.
5. Symptoms include relatively pure syndromes (motor, sensory). There is an absence of higher cortical function involvement (language, praxis, non-dom hemisphere syndrome, vision). Onsent may be abrupt or gradual. 23% are preceded by a TIA.

Stroke risk factors

1. How is a stroke differentiated from a TIA?
2. What are nonmodifiable risk factors for CVA?
3. Is obesity correlated to CVA?
4. What are modifiable risk factors for CVA?

Answer:
1. TIA lasts less than 24hrs, stroke lasts more than 24 hrs.
2. Age (more important risk factor), sex (M>F), race (black > white > Asian), family history.
3. No.
4. HTN, history of CVA/TIA, heart disease (CHF, CAD, a fib, valvular disease), diabetes (good BS control does not alter risk), smoking, carotid stenosis, EtOH, cocaine, high-dose estrogens, hypercoagulable states, hyperlipidemia, migraines, OSA, PFO.

Middle Cerebral Artery CVA

1. What is the most common cause of occlusion of the superior division of the MCA?
2. What is the typical presentation of a superior MCA CVA? What sort of aphasia is seen if the dominant hemisphere is affected?
3. What is seen in a nondominant lesion of the superior MCA?
4. What is the typical presentation of an inferior MCA CVA?
5. What is seen with a dominant vs. nondominant hemisphere inferior MCA CVA?

Answers:
1. Embolus.
2. Sensory and motor deficits in the contralateral face and arm>leg, head and eyes deviated toward side of infarct. Initially there is decreased muscle tone that gradually increases over days or weeks. With dominant hemisphere involvement, initially global aphasia is seen, then Broca's.
3. Deficits in spacial perception, hemineglect, constructional apraxia, dressing apraxia.
4. Superior quadrantanopia or homonymous hemianopsia.
5. Dominant results in Wernicke's aphasia. Nondominant results in left visual neglect.

Traction

1. What are the physiological effects of traction?
2. What are contraindications to traction in general? For the cervical spine?
3. What are contraindications to traction for the lumbar spine?
4. How is traction generally prescribed in terms of positioning?
5. How is traction generally prescribed in terms of amount of pull?

Answers:
1. Effects are vertebral joint distraction (elongation of C-spine), reduction of compression and nerve root/disc irritation, reduction in pain, muscle spasm, and inflammation, loosening of adhesions in dural sleeves.
2. General contraindications are spine malignancy, osteopenia, infection, congenital spinal deformity. C-spine contraindications are cervical ligamentous instability (RA, Down's, Marfan, dwarfism), infection, atlanto-axial subluxation, vertebrobasilar insufficiency.
3. L-spine contraindications are pregnancy, cauda equina compression, aortic aneurysm, restrictive lung disease, active PUD, hiatal hernia.
4. 20-30 degrees of flexion optimally opens intervertebral foramina for cervical traction. For lumbar traction, keep patient supine with 90 degrees of hip and knee flexion.
5. For C-spine, use greater than 25 pounds. For L-spine, use 50 pounds for posterior vertebral separation, 100 pounds for anterior separation. Treat for 20 minutes.

Massage therapy

1. What are the reflexive effects of massage therapy?
2. What are the mechanical effects of massage therapy?
3. What are contraindications to massage?
4. How do the common techniques of massage differ?

Answers:
1. Reflexive effects include reflex vasodilation with improved circulation, decreased pain through opiate release, relaxation, perspiration.
2. Mechanical effects include assisting venous blood return from periphery to CNS, increase lympathic drainage, decrease muscle tightness, prevents or breaks adhesions, softens scars, loosens secretions.
3. Contraindications include massage over malignancy, open wounds, infection, burns, nerve entrapment, acute inflammatory conditions (gout, RA, cellulits, DVT), severe varicose veins, severe clotting disorder.
4. Effleurage is a gliding movement of the skin w/o deep muscle movement, for muscle relaxation. Petrissage is kneading, which increases circulation and reduces edema. Tapotement is percussion, which helps with desensitization and improves circulation and clearing of secretions. Friction massage breaks adheasion and reduces local muscle spasm. Soft tissue mobilization is forceful massage of the fascia-muscle system for reduction in contractures. Myofascial release is prolonged light pressure in specific directions to stretch focal areas of muscle or fascial tightness. Accupressure is finger pressure applied over trigger points or acupuncture points.

Neuromuscular electrical stimulation

1. What are common uses of neuromuscular e-stim?
2. How does the open-loop system work?
3. How does the closed-loop system work? What are the advantages over open-loop?

Answers:
1. Maintains muscle mass after immobilization, prevents DVT, prevents osteoporosis, strengthens muscles, increases ROM, provides feedback to enhance voluntary muscle control.
2. An open-loop system is when the user observes the results of stimulation and adjusts the stimulation based on the results.
3. A closed-loop system involves movement sensors that send signals from patient's body as results are obtained. Advantages are that it corrects unexpected problems like muscle spasms and fatigue.

Types of electrical stimulation

1. What sort of frequency and intensity stimulation does a conventional stimulator deliver? How soon is it effective? What sort of pain it is used to treat?
2. What sort of stimulation is used during acupuncture?
3. How does the pulse mode work?
4. How does modulated stimulation work?
5. How does hyperstimulation work? What is the mechanism?

Answers:
1. High frequency, low intensity stimulation. Pain relief begins after 10-15 minutes of stimulation and ends when stimulation is removed; stimulation can last for hours. It is used for neuropathic pain.
2. Acupuncture usees low frequency, high intensity stimulation, lasting 30-60 mins. 3. Pulse mode involves high frequency stimulation bursts at low frequency intervals.
4. Modulated stimulation involves pulses varying in intensity and frquency.
5. Hyperstimulation involves high frequency high intensity stimulation. It is rarely tolerated more than 15-30 mins. Mechanism is possibly via stimulation of C-fibers, causing counter-irritation.

Electrotherapy

1. What are the physiologic effects of electrotherapy?
2. What are indications to electrotherapy?
3. What are contraindications to electrotherapy?
4. What is transcutaneous nerve stimulation (TENS)? Where are electrodes usually placed?
5. What are the proposed mechanisms of pain control via electrotherapy?
6. What is the gate-control theory?

Answers:
1. Increase in joint ROM, muscle group contraction, retards muscle atrophy, increases muscle strength, increases circulation, decreases muscles spasm, releases polypeptides and neurotransmitters, decreases spasticity, promotes wound healing, induces osteogenesis, inhibits pain fibers, drives medicated ions across skin.
2. Indications are pain management (msk pain, neurogenic pain, systemic pain), joint effusion, interstitial edema, muscle disuse atrophy, dermal ulcers and wounds, circulatory disorders, postherpetic neuralgia, arthritis, ROM.
3. Contraindications are circulatory impairment, stimulation over carotid sinus or heart, pregnancy, seizure disorder, fresh fracture, active hemorrhage, malignancy, decreased sensation, atrophic skin, inability to report pain, allergy to gel or pads.
4. TENS stimulates nerve fibers through a programmable device to apply an electrical signal through lead wires and electrodes on the skin. Electrodes are usually place over peripheral nerve distribution.
5. Placebo, gate-control theory, release of endogenous opioids.
6. The gate-control theory involves blocking pain signals at the spinal cord before they are transmitted to the thalamus. For example, a TENS stimulates large Ia afferent nerve fibers that stimulate the substantia gelatinosa in the dorsal horn of the spinal cord, that closes the gate on pain transmission to the thalamus.

Light therapy: Ultraviolet

1. What is the wavelength of UV light? What are its physiological effects?
2. What are indications for using UV light?
3. What are contraindications to using UV light?
4. What is the MED? What dosage of MED is usually given and what is the maximum?
5. How often can treatments be given?

Answers:
1. Wavelength is 2000-4000A. It is bactericidal on motile bacteria, provides increased vascularization of wound margins, produces hyperplasia and exfoliation, increased Vit D production, excites Ca metabolism, and results in tanning.
2. Indications include treatment of wounds, psoriasis, acne, and folliculitis.
3. Contraindications include pellagra, porphyria, sarcoidosis, acute psoriasis, lupus, eczema, herpes simplex, xeroderma pigmentosum. Use with precaution on fair skin, scars, atrophic skin, acute renal and hepatic failure, severe DM, hyperthyroidism, generalized dermatitis, advanced arteriosclerosis, active TB. Eyes should be protected with goggles.
4. MED is the Minimal Erythema Dosage, which is the minimal exposure time required to cause erythema on the volar surface of the forearm. It subsides in 24 hours. MED dosage is usually 1-2 MEDS and is kept to less than 5.
5. 2-3 times per week.

Cold therapy

1. What causes the therapeutic effects of cold therapy?
2. What are indications and precautions for cold therapy?
3. How is cold transferred via conduction?
4. How is cold transferred via convection?
5. What are other techniques of cold transfer?

Answers:
1. Cold results in local vasoconstriction, local metabolism decrease, decreased inflammation, slowed NCV, decreased muscle spindle activity, decreased pain/muscle spasm, decreased spasticity, increased tissue viscosity, transient increase in BP, release of vasoactive agents (histamine).
2. Cold therapy is used for acute processes such as trauma (first 24-48hrs), arthritis, bursitis, acute and chronic pain, spasticity management, and treatment of minor burns. Precautions and contraindications include cold intolerance (Raynaud's), arterial insufficiency, impaired sensation, communication deficits, cardiac or respiratory involvement, cryotherapy induced nerve injury, cryopathies, open wounds after 48 hrs.
3. Methods of conduction include cold packs wrapped in moist towels and ice massage, which is use to cool small areas before deep massage.
4. Methods of convection include a cold bath, which is used for treatment of localized burns, and evaporation such as a vapo-coolant spray, used to treat myofascial pain or local anesthesia.
5. Other techniques of cooling include cryotherapy compression units, which uses sleeves with circulating cold water, used to treat acute msk injury.

Deep heat: shortwave and microwave diathermy

1. How does shortwave diathermy work? What is the most common frequency and to what depth is heating provided?
2. What is the difference between the induction and conduction method of shortwave diathermy? What are indications for each?
3. What are indications and contraindications for shortwave diathermy?
4. What is microwave diathermy?
5. What are indications and contraindications for microwave diathermy?

Answers:
1. SWD produces deep heating through conversion of electromagnetic energy to thermal energy. The most common frequency is 27.12 MHz and it heats to a deapth of 4-5cm.
2. Induction method produces high temperatures in water-rich tissues via a coiled magnetic field and is indicated when heat to more superficial muscles or joints is desired. Conduction method produces high temperatures in water-poor tissues with low conductiveity via rapid oscillation in an electric field, and is more effective for deeper joints. Precise dosing is difficult and is monitored via patient's pain perception.
3. Indications for SWD include chronic prostatitis, refractory PID, myalgia, back spasms. Contraindications include general heat precautions, metal, contact lenses, gravid or menstruating uterus, or skeletal immaturity.
4. Microwave disthermy is conversion of microwaves to thermal energy. It does not penetrate as deeply as US or SWD and is better for muscle heating.
5. Indications include heating superficial muscles and joints, to speed hematoma resolution, and for local hyperthermia in cancer patients. Contraindications include general heat precautions, skeletal immaturity. It should be avoided in edematous tissue, moist skin, eyes, blisters, and fluid-filled cavities due to selective heating of fluid-filled cavities. Eye protection should be worn due to cataract risk.

Deep heat: Ultrasound

1. What is ultrasound?
2. What are the thermal and nonthermal effects of ultrasound?
3. What are the indications for ultrasound?
4. What are contraindications and precautions to using ultrasound?
5. How is ultrasound usually administered? What are the direct and indirect techniques?
6. What is phonophoresis?

Answers:
1. Ultrasound is acoustic vibrations with frequencies above the audible range, which can produce thermal and nonthermal effects.
2. Thermal effects include heating of skin, fat, and muscle, increased distensibility of collagen fibers, and absorption by bone and tendon. The highest temperture is produce in cancellous bone and absorption is greatest at the bone-muscle soft tissue interface. Nonthermal effects include cavitation (gas bubbles in a sound field) and acoustic streaming, both of which are associated with wound contraction and protein synthesis.
3. Indications include bursitis, tendinitis, msk pain, degenerative arthritis and contracture (helps to maintain stretch and increases ROM), and subacute trauma. There is less evidence to show efficacy in scar tissue, postherpetic neuralgia pain, and plantar warts.
4. Contraindications include general heat contraindications, near brain, cervical ganglia, spine, and laminectomy sites, near heart or reproductive organs, near pacemakers, near tumors, gravid or menstruating uterus, infection site, skeletal immaturity, THA with methylmethacrylate or high density polyethylene. Precautions include avoiding intensities over 3W/cm2, use stroking technique, use multiple ports over large joints, and only use over water if water is degassed (allowed to sit overnight).
5. Ultrasound is given at a frequency of 0.8-1.1 MHz with intensity of 0.5-2 W/cm2 for 5-10 mins per site, delivered either continuous (greater thermal effects) or pulsed. The direct technique is most common, in which the applicator is moved slowly over an area of 4 sq in in a circular pattern with gel. The indirect technique is for uneven surfaces and involves immersing applicator and body part in degassed water.
6. Phonophoresis is a technique that utilizes US to drive medications through the skin, but increasing cell permeability.

Superficial heat: Conductive and Conversive agents

1. How do hot packs work? How long should they be applied for? What are the advantages and disadvantages?
2. What is a Kenny pack?
3. What is the peak temperature for a heating pad? What is the risk when used with moist towels?
4. What is a paraffin bath? What is it used for?
5. What are three methods for using paraffin baths?
6. What is radiant heat? Who is it most useful in? What are precautions to radiant heat?

Answers:
1. A hot pack such as a hydrocollator is a canvas bag filled with silicon dioxide immersed in tanks of heated water. It is a conductive agent. It is applied for 30 min, over several layers of insulated towels. Advantages are that it's low cost, requires minimal maintenance, and ease of use. Disadvantages include skin mottling with prolonged use (erythema abigne), characterized by reticular pigment and telangiectasia.
2. A Kenny pack is a wool cloth soaked in 60C water, then spun dried.
3. A heating pad is a conductive agent with circulating heated fluid such as water. Peak temperature is 52C. If used with most towels, there can be an electric shock.
4. A paraffin bath is a conductive agent, using paraffin wax and mineral oil in a 6-7:1 ratio. It is common used in irregular surfaces such as distal extremities and have been helpful with contractures, RA, and scleroderma.
5. Dipping is most common and involves placing body part in paraffin bath, then remove and allow wax to harden, then insulate wax for 20-30 mins. Immersion involves serial dips done to form a thin glove, followed by immersion in bath for 30 mins. Brushing involves using a brush to apply paraffin to larger body parts.
6. Radiant heat such as infrared lamps is a conversive agent in which energy is absorbed through the skin and converted to superficial heat. It is used in patients who can't tolerate heat packs. Precautions include general heat precautions, light sensitivity, skin drying, and photosensitive medications.

Superficial heat:Convective Agents

1. How does fluidotherapy work? On what body parts is it most useful? When should it be avoided?
2. What is hydrotherapy? How long should it be given for?
3. What is the difference between a Whirlpool bath and a Hubbard tank?
4. What are contraindications to a Hubbard tank?
5. What is a contrast bath? What are its uses?
6. What are contraindications to a contrast bath?

Answers:
1. Fluidotherapy is a convective agent by which hot air is blown through a container holding fine cellulose particles, producing a warm air-fluid mixture with properties similar to a liquid. It works best on the hands and feet. It should be avoided in infected wounds. Burn precautions should be maintained.
2. Hydrotherapy involves external use of water to treat a physical condition, which produces convective heating and cooling, massage, and gentle debridement. Treatment should be given for approximately 10-20 minutes, depending on cardiopulmonary tolerance.
3. A whirlpool bath is used for partial body immersion. A Hubbard tank provides total body immersion. A lower temperature is used for a Hubbard tank (<39C) to avoid changing core temperature.
4. Incontinence, skin infections, unstable BP, uncontrolled epilepsy, acute febrile episodes, URI, tuberculosis, and multiple sclerosis. Caution should be taken in patients with VC < 1L.
5. A contrast bath involves distal limbs receiving alternating heat and cold in a whirlpool tank to produce reflex hyperemia. Alternate 1-4min cold soak with 4-6 min warm soaks. It is used for RA, reflex sympathetic dystrophy, to toughen residual limbs, muscular strains, and joint sprains.
6. Small vessel disease (diabetes), arteriosclerotic endarteritis, Burger's disease.

Thermotherapy

1. What are the maximum and minimum temperatures that can be used without injury to tissue?
2. What are applications for heat therapy?
3. What are contraindications to using heat therapy?
4. What is heat therapy contraindicated with scar tissue?
5. What is convection and what are some examples of heating by convection?
6. What is conduction and what are ways you can heat by conduction?
7. What is conversive heating and what are examples?

Answers:
1. T>45-50C or T<0C
2. Decrease muscle spasms, decrease pain, reduction in joint stiffness, decrease contractures, arthritis, collagen vascular diseases, chronic inflammation, superficial thrombophlebitis.
3. Ischemia (arterial insufficiency), bleeding disorders, hemorrhage (due to incr blood flow), impaired sensation (risk of burn), inability to communicate, malignancy, acute trauma or inflammation, scar tissue, edema (due to increased diffusion across membranes), atrophic skin, poor thermal regulation.
4. Scar tissue has inadequate vascular supply and heat increases its metabolic demand, this causing ischemic necrosis.
5. Convection is contact between two surfaces at different temperatures with flow of one liquid or gas past the other. The resulting flow causes transfer of heat energy. Examples include fluidotherapy, hydrotherapy (whirlpool), and contrast baths.
6. Conduction is the transfer of heat between two bodies at different temperatures without movement. Examples include hot water, paraffin, hot packs.
7. Conversive heating in when nonthermal energy converts to heat in tissues Examples include radiant heat (heat lamps), shortwave diathermy, ultrasound, and microwave.