Evaluation of autonomic nervous system
- 1. Presenter: Dr.Nikhil Panpalia Guide: Dr.K.R.Naik 16/2/2016Evaluation of autonomic functions 1
- 2. Central control of autonomic functions Overview of peripheral autonomic system Classification of dysautonomia Clinical features of autonomic involvement Clinical approach and Assessment of autonomic functions. Disorders of autonomic system 2/20/2016Evaluation of autonomic functions 2
- 3. The central autonomic network is composed of both hypothalamic and extra-hypothalamic nuclei. Hierarchy in the autonomic network results in the loops from 1. the brainstem to spinal cord being responsible for rapid short-term regulation of the autonomic nervous system, 2. hypothalamic-brainstem-spinal cord pathways serving longer-term, metabolic and reproductive regulation, 3. Finally limbic system-hypothalamic-brainstem-spinal cord loops serving anticipatory autonomic regulation 2/20/2016Evaluation of autonomic functions 3
- 4. The single most important hypothalamic nucleus of the central autonomic network is the paraventricular nucleus (PVN). The PVN has two morphological classes of neurons that fall into three functional categories. The first morphological class magnacellular (big) neuronsvasopressin and oxytocin posterior pituitary where these hormones are released directly into the blood stream. The second morphological class parvocellular (small) neurons releasing hormones into the hypophyseal portal blood stream for control of anterior pituitary hormone secretion. Stimulation of posterolateral hypothalmus results in sympathetic and anterior results in parasympathetic 2/20/2016Evaluation of autonomic functions 4
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- 6. These extra-hypothalamic sites can be roughly divided into those associated with control of the two components of the autonomic nervous system. The sites associated with control of sympathetic outflow include the norepinephrine-containing neurons of the dorsal mesencephalon (locus ceruleus) and the rostral and caudal ventrolateral medulla (the A5 and A1 regions) and the serotonin- containing neurons of the pontine and medullary raphe nuclei. The extra-hypothalamic sites associated with control of parasympathetic outflow include the central nucleus of the amygdala, the dorsal motor nucleus of the vagus, the nucleus ambiguus, the raphe nuclei, the periaqueductal gray, and the parabrachial nucleus. Finally, limbic cortices, including the cingulate, orbitofrontal, insular and rhinal cortices, and the hippocampus influence both sets of autonomic outflow. 2/20/2016Evaluation of autonomic functions 6
- 7. The insular cortex and amygdala mediate high-order autonomic control, and their involvement in seizures or stroke may produce severe cardiac arrhythmias and other autonomic manifestations. Hypothalamic autonomic disorders commonly produce hypothermia or hyperthermia. Hyperthermia and autonomic hyperactivity occur in patients with head trauma, hydrocephalus, neuroleptic malignant syndrome, and fatal familial insomnia. In the medulla, the nucleus of the tractus solitarius and ventrolateral medulla contain a network of respiratory, cardiovagal, and vasomotor neurons. Medullary autonomic disorders may cause orthostatic hypotension, paroxysmal hypertension, and sleep apnea. Neurologic catastrophes, such as subarachnoid hemorrhage, may produce cardiac arrhythmias, myocardial injury, hypertension, and pulmonary edema. Multiple system atrophy affects preganglionic autonomic, respiratory, and neuroendocrine outputs. The CAN may be critically involved in panic disorders, essential hypertension, obesity, and other medical conditions. 2/20/2016Evaluation of autonomic functions 7
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- 9. Associated with multisystem degeneration 1. Multisystem degeneration: autonomic failure clinically prominent 2. Multisystem degeneration: autonomic failure clinically not usually prominent Unassociated with multisystem degeneration 1. Disorders mainly due to cerebral cortex involvement 2. Disorders of the limbic and paralimbic circuits 3. Disorders of the hypothalamus 4. Disorders of the brainstem and cerebellum 2/20/2016Evaluation of autonomic functions 9
- 10. Autonomic disorders with spinal cord involvement A. Traumatic quadriplegia B. Syringomyelia C. Subacute combined degeneration D. Multiple sclerosis and Devic’s disease E. Amyotrophic lateral sclerosis F. Tetanus G. Stiff-man syndrome H. Spinal cord tumors Autonomic neuropathies Acute Guillain-Barre syndrome, Botulism ,Porphyria, Drug-induced Chronic Amyloid, Diabetic Autoimmune , Familial dysautonomia (Riley-Day syndrome), uremic, or nutritional deficiency, Dysautonomia of old age 2/20/2016Evaluation of autonomic functions 10
- 11. Reflex syncope POTS associated with prolonged bed rest associated with space flight chronic fatigue 2/20/2016Evaluation of autonomic functions 11
- 12. Vision CVS GIT Pulmonary Urinary tract Sexual functions Blood Sweating abnormalities 2/20/2016Evaluation of autonomic functions 12
- 13. Vision is greatly preserved Usually episodic tunneling of vision mainly on upright posture mainly attributed to changes in retinal vasculture IOP increases with supine posture and hypertension and decreases with upright posture and hypotension. Pupillary functions may be altered rare. 2/20/2016Evaluation of autonomic functions 13
- 14. Lung functions are greatly preserved MSA pts may have sleep apnea and major changes in BP It is dependent on role of CO2 in determining BP levels Hypoventilation increases BP and hyperventilation decreases BP. 2/20/2016Evaluation of autonomic functions 14
- 15. Orthostatic hypotension fall in BP by >20/10 mm hg after 3 minutes of standing. Symtoms include dizziness, dimming of vision and discomfort in neck and head. Chronic orthostatic hypotension Clear drop in diasytolic BP with no apparent symtoms. Indiactes underlying structural disorders. Heart rate increases by 5-20 beats/min after standing in 30 seconds POTS On standing no fall in BP but increase in HR >30 /min after 10 minutes of standing 2/20/2016Evaluation of autonomic functions 15
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- 17. Constipation is common Diabetic gastropathy: Severe diarrhoea with significant gastroparesis. Apoptosis of enteric neurons with imbalance of inhibitory and excitatory neuropeptides Sjogrens syndrome: GERD with risk of esophageal Ca Chagas disease: Achalasia with enlargement of esopahagus and vomiiting Allgrove syndrome: 4A Achalasia, autonomic neuropathy, Alacrima and ACTH insuffiency Genetic autonomic failure: Severe fluid loss with bowel movement of >10 times a day. Also have postprandial angina without ST-T changes. PD: Mainly constipation secondary to degeneration of central and peripheral parasympathetic nuclei POTS: Bloating, early satiety and alternating diarrhoea and constipations. 2/20/2016Evaluation of autonomic functions 17
- 18. Nocturia occurs when patients lies supine secondary to hypertension. Bladder involvement results in urgency, retention, incontinence and frequency Renin levels may be quite low due to autonomic failure because sympathetic regulation of kidney impaired. Functional disorders: Urgency and frequency 2/20/2016Evaluation of autonomic functions 18
- 19. Erectile dysfunction is most commonly affected in males. Indicates parasympathetic dysfunctions. Retrograde ejaculation in sympathetic dysfunction ( dopamine hydoxylase deficiency). Little information in females exist. Blood Mild anemia due to erythropoietin deficiency. 2/20/2016Evaluation of autonomic functions 19
- 20. Generalized hyperhydrosis 1. Episodic hypothermia 2. Pheochromocytoma 3. Shapiro syndrome 4. Tumours producing cytokinins 5. Baroreflex failure 6. Delirium tremens Localized hyperhydrosis 1. Essential hyperhydrosis( hands, feet and axilla) 2. Compensatory hyperhydrosis 3. Post cerebral infarct 4. Autonomic dysreflexia 5. CPS 2/20/2016Evaluation of autonomic functions 20
- 21. Evaluation of treatable cause Detailed history regarding symtoms and medications use The relationship of symptoms to meals (splanchnic pooling), standing on awakening in the morning (intravascular volume depletion), ambient warming (vasodilatation), or exercise (muscle arteriolar vasodilatation) should be sought. Neurologic examination should include mental status (neurodegenerative disorders), cranial nerves (impaired downgaze with progressive supranuclear palsy; abnormal pupils with Horner’s or Adie’s syndrome), motor tone (Parkinson’s disease and parkinsonian syndromes), and reflexes and sensation (polyneuropathies) Detailed evaluation for GIT and GUT symptoms. 2/20/2016Evaluation of autonomic functions 21
- 22. Heart rate variation with deep breathing Valsalva Thermoregulatory skin test Quantitative Sudomotor axon reflex test functions Sympathetic skin response test Orthostatic BP recordings Tilt table test Testing for baroreflex failure Test for neurotransmitter receptor responsiveness Other autonomic tests 2/20/2016Evaluation of autonomic functions 22
- 23. The variation of heart rate with respiration is known as sinus arrhythmia Inspiration increases the heart rate Expiration decreases the heart rate This is also called Respiratory Sinus Arrhythmia (RSA) This is an index of vagal control of heart rate
- 25. Due to changes in vagal control of heart rate during respiration Probably due to following mechanisms ◦ Influence of respiratory centre on the vagal control of heart rate ◦ Influence of pulmonary stretch receptors on the vagal control of heart rate
- 27. Record maximum and minimum heart rate with each respiratory cycle Average the 3 differences ◦ Normal > 15 beats/min ◦ Borderline = 11-14 beats/min ◦ Abnormal < 10 beats/min
- 28. Determine the expiration to inspiration ratio (E:I ratio) Mean of the maximum R-R intervals during deep expiration to the mean of minimum R-R intervals during deep inspiration longest RR interval (expiration) Ratio = ---------------------------------- --- shortest RR interval (inspiration) E:I = 1.2
- 29. An immediate response with an abrupt fall in systolic and diastolic blood pressure and a visible acceleration of heart rate (first 30 s), a phase of early stabilization, which occurs after approximately 1-2 min, during the phase of stabilization , acceleration of heart rate by about 10-15 beats per minute and a slight decrease in systolic blood pressure, while diastolic pressure increases by approximately 10 mmHg
- 31. Evaluation of changes in heart rate (30/15 ratio) is performed during the initial phase of adaptation to orthostasis . On standing the heart rate increases until it reaches a maximum at about ◦ 15th beat (shortest R-R interval after standing) ◦ after which it slows down to a stable state at about 30th beat (longest R-R interval after standing)
- 32. The ratio of R-R intervals corresponding to the 30th and 15th heart beat 30:15 ratio RR interval at 30th beat 30:15 ratio = ----------------------- ------- RR interval at 15th beat This ratio is a measure of parasympathetic response
- 33. RR interval at 30th beat 30:15 ratio = ----------------- ------------- RR interval at 15th beat Normal > 1.04 Borderline = 1.01-1.04 Abnormal =<1.00
- 34. Fluctuations of blood pressure are assessed based on somewhat later responses to standing (first 3 min) they are expressed as the difference between the baseline supine and the minimal blood pressure after standing up. A decline in systolic blood pressure by more than 20 mmHg and by more than 10 mmHg for diastolic blood pressure is considered abnormal
- 35. OH- fall of 20 mm Hg systolic or 10 mm Hg diastolic BP on standing- AAS ;AAN 1996 30mmHg systolic; 20 mmHg diastolic BP- McLeod and Tuck, 1987 Diagnostic criteria of POTS include a) a sustained increase in heart rate (HR) of 30 beats per minute (bpm) or greater during 10 minutes of assuming an upright position, b) no associated hypotension, and c) symptoms of orthostatic intolerance, which must be present for at least three months. In severe forms of the disease, HR may increase to more than 120 bpm on standing.
- 36. Assesses integrity of the baroreceptor reflex Measure of parasympathetic and sympathetic function It is “forced expiration against a closed glottis”
- 37. The Valsalva maneuver is performed by attempting to forcibly exhale while keeping the mouth and nose closed It increases intrathoracic pressure to as much as 80 mmHg
- 39. ◦ Transient increase in BP which lasts for a few seconds ◦ HR does not change much ◦ Mechanism: increased intrathoracic pressure and mechanical compression of great vessels due to the act of blowing
- 40. Early part – drop in BP lasting for about 4 seconds Latter part – BP returns to normal Heart rate rises steadily
- 41. Mechanism Early part ◦ venous return decreases with compression of veins by increased intrathoracic pressure central venous pressure decreases BP decreases Latter part ◦ drop in BP in early part will stimulate baroreceptor reflex increased sympathetic activity increased peripheral resistance increased BP ( returns to normal ) Heart rate increase steadily throughout this phase due to vagal withdrawal in early part & sympathetic activation in latter part
- 42. Transient decrease in BP lasting for a few seconds Little change in heart rate
- 43. Mechanical displacement of blood into pulmonary vascular bed, which was under increased intrathoracic pressure BP decreases
- 44. BP slowly increases and heart rate proportionally decreases BP overshoots Occurs 15-20 s after release of strain and lasts for about a minute or more Due to increase in venous return, stroke volume and cardiac output
- 46. Measure of the change of heart rate that takes place during a brief period of forced expiration against a closed glottis Ratio of longest R-R interval during phase IV (within 20 beats of ending maneuver) to the shortest R-R interval during phase II Average the ratio from 3 attempts
- 47. Longest RR Valsalva Ratio ----------------------------- Shortest RR Values :> 1.4 more than 1.21 normal less than 1.20 abnormal
- 48. Valsalva maneuver evaluates ◦ 1. sympathetic adrenergic functions using the blood pressure responses ◦ 2. cardiovagal (parasympathetic) functions using the heart rate responses
- 49. Thermoregulatory sweat testing (TST) is used evaluate the integrity of central and peripheral sympathetic sudomotor pathways from the CNS to the cutaneous sweat glands The temperature is adjusted to 45–50 °C with a relative humidity of 35–40%.
- 51. Sweat produces a change in local pH resulting in the indicator dye changing color marking the location of sweat production (sweat has a pH of 4.5–5.5 at low sweat rates of 15– 100nL/gland per hour). Two common indicators include alizarin red powder (alizarin red, corn starch, sodium carbonate, 1:2:1) and iodine corn starch.
- 52. Maximal sweating is achieved within 30–65 minutes. Heating time should not exceed 70 minutes to avoid hyperthermia Sweating causes the indicator to change its color (from yellow to dark red for alizarin red and from brown to purple with iodine). Digital photographs are taken and a sweat density map is generated on standard anatomical drawings Data are expressed as TST% which is the area of anhydrosis/ total body area X 100
- 53. Normal sweating patterns are generally symmetric but vary in quantity Asymmetric sweat patterns and anhidrotic areas (focal, segmental, regional, length dependent) are noted. The TST% can provide a general index of severity of the autonomic failure
- 55. TST can localize specific areas of sudomotor dysfunction but can not differentiate preganglionic from postganglionic lesions In combination with a test measuring postganglionic sudomotor function (QSART, silicone impression) the site of a lesion can be separated: A postganglionic lesion will be abnormal in all tests
- 56. Quantitative sudomotor axon reflex test (QSART) is used to evaluate postganglionic sympathetic cholinergic sudomotor function Axon-reflex mediated sweat response over time and has achieved widespread clinical use.
- 58. Clean the recording sites vigorously with the alcohol. Recording sites are:1) the medial forearm (75 % distance from the ulnar epicondyle to the pisiform bone); 2) the proximal leg (5 cm distal to the fibular head laterally); 3) the distal leg (5 cm proximal to the medial malleolus medially 4) proximal foot over the extensor digitorum brevis muscle. Place the ground for stimulation about 5 cm next to the capsule.
- 60. Stable baseline of spontaneous sweating
- 64. In normal individuals, the sweat output starts with a delay of 1–2 minutes. The sweat output increases for up to 5 minutes after stimulation until it reaches the inflection point and decreases slowly. While males and females have similar latency the sweat output differs. Mean sweat output for males is 2–3 μl/cm2 (approximate range 0.7–5.4 μl/cm2) and females 0.25–1.2 μl/cm2 (approximate range 0.2–3 μl/cm2) with some variation depending on the site of stimulation Sweat response can be absent, decreased or increased.
- 65. Longer latency of the sweat onset can be seen as well as a lack of recovery, the “hung up” response Increased sweat production is often a sign of axonal excitability, seen in conditions such as diabetic neuropathy, reflex sympathetic dystrophy and other small fiber neuropathies. In diabetic neuropathy, especially during early stages, a length-dependent pattern of sweat reduction can be seen
- 67. QSART measures the postganglionic sudomotor response and will be unable to detect preganglionic lesions. QSART is also time-consuming, requires special equipment and is not widely available
- 68. SSR, also referred to as galvanic skin response is a measure of electrodermal activity Generated in deep layer of skin Reflex activation of sweat glands via cholinergic sudomotor sympathetic efferent fibres. Provides a surrogate measure of sympathetic cholinergic sudomotor function.
- 69. SSR is a change in potential recorded from surface of skin, representing sudomotor activity Can be evoked by different stimuli Acoustic;TCM, startle; laser skin; reflex hammer percussion on sternum Resende et al deglutition; blinking; skeletal movements; biting; light stimuli; vocalization; sphincteric contraction Stimulus modality determine the afferent tract
- 70. Electrical stimulation of peripheral nerve activates afferent part of reflex consisting thick myelinated sensory fibres(typeII) sensory spinal cord tract brain stem(influenced by hypothalamus, medial and basal part of frontal lobe and medial part of temporal lobe
- 71. originate from the hypothalamus send descend uncrossed along the lateral column of the spinal cord Terminates on sympathetic preganglionic neurons in the intermediolateral cell column. Myelinated sympathetic fibres from intermediolateral nucleus in T1- L2 of spinal cord Paravertebral sympathetic ganglia Post ganglionic by non myelinated( type c); innervating sweat gland
- 72. Room temperature should be comfortable and the skin surface temperature 32@C. Potentials are increased during psychological stress and may contaminate the evoked SSR. Patients during recording has to be relaxed, without acoustic disturbances
- 73. The surface Ag-AgCl electrodes are placed on the palm (active) and referenced against the volar forearm or dorsum of the hand (indifferent); On the sole of the foot (active) and referenced against the shin or dorsum of the foot (indifferent)
- 74. The recording time should be 5±10 s, The lower frequency limit 0.1±2 Hz (better,1 Hz), and the upper limit 100±2000 Hz (not critical). Amplification should be 0.05±3 mV/division.
- 75. Electrical stimulation is carried out with a constant current stimulus (0.2 ms, supramaximal, 10±30 mA). Typically the median, posterior tibial, peroneal, sural or supraorbital nerves are stimulated at a strength at least three times the sensory threshold. In normal subjects, transcranial magnetic stimulation of the motor strip elicited palmar and plantar SSRs similar
- 77. The latency of the SSR includes 1. afferent conduction (about 20 ms), 2.central processing time (a few milliseconds), 3. efferent conduction in pre- and slow conducting postganglionic autonomic nerve.
- 78. The mean conduction velocity of sudomotor nerve fibers is about 1±2 m/s. Conduction in post- ganglionic C fibers as well as activation time of sweat glands include about 95% of the SSR latency of around 1.5 s at the hands and 2 s at the feet
- 79. Amplitude Measurements in theory should reflect the density of spontaneously activable sweat glands. Qualitative evaluation accepts only the absence of SSR as a pathological sign
- 82. • Patient refusal • Morbid obesity (technicians cannot tilt safely) • Unable to stand for long periods due to pain • Pregnancy • Recent (within 6 months) myocardial infarction or stroke/TIA • A known tight stenosis anywhere (eg heart valve, LV outflow obstruction, coronary or carotid/cerebrovascular artery)
- 83. Fast 2 or more hrs Rest supine 20-45 minutes Stop drugs affecting cvs or autonomic function; minimum of 5 half life pretest Minimize lower limb movements Get the baseline blood pressure from the brachial artery. Acquire the 5-10 minutes baseline Tilt angle and duration
- 84. Tilt patient up. The tilt should be done at 70 degree. The transition from supine to tilt position should smooth and of duration 5-10 seconds. Obtain the blood pressure from a brachial artery every minute. Observe subject for the presence of any discomfort, chest pain, shortness of breath, dizziness, lightheadedness, syncope Be prepared to terminate the tilt of any serious event occurs during the tilt based on clinical judgment. The tilt can be continued if no obvious abnormalities are detected but a clinical history is strongly suggestive of dysautonomia or blood pressure instability. Tilt the patient back.
- 85. The normal responses in heart rate during the tilt is heart rate increment within 10 - 15 beats per minute. At the same time the maximal heart rate should be less than 120 beats per minute. Normal responses in the blood pressure during the tilt modest rise of diastolic blood pressure ; slight fall of <10 mm Hg in SBP.
- 86. Through vasoconstriction of capacitance and arteriolar vessels and through increased heart output, a healthy subject is able to reach orthostatic stabilization in 60 seconds or less. Within seconds of this sudden decrease in venous return, pressure receptors in the heart, lungs, carotid sinus and aortic arch are activated and mediate an increase in sympathetic outflow about 300 to 800 mL of blood is forced downward to the abdominal area and lower extremities
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- 90. Functional disorders Disorders of excessive autonomic outflow Peripheral afferent autonomic disorder Peripheral Efferent autonomic disorder Central structural autonomic disorder 2/20/2016Evaluation of autonomic functions 90
- 91. Reflex syncope: It is a transitory loss of consiousness due to loss of brain perfusion resulting in loss of postural disease. Usually associated with stimulus with no underlying heart disease. Syncopal migraine: Headache with migranous feature immediately prior to syncopal spell Carotid sinus hypersentivity:Defined as BP fall of >50 mmhg or asystole >3 seconds after carotid artery massage in pt with otherwise unexplained dizziness or syncope. POTS: HR of >30 on standing with symptoamtic sympathetic symtoms. Plasma norepinehrine is 600pg/ml. Fundamental deficits is reduced venous return. It can be neuropathic and central. 2/20/2016Evaluation of autonomic functions 91
- 92. Autonomic storm: Seen cerebral catastrophe. There is a acute alteration HR, RR, temperature, sweating and muscle tone. There is heightened activity of brainstem sympathoexcitatory pathway. Takotsubo Heart syndrome: Mimics MI with chest pain and shortness of breath. Non specific EKG changes in a pateint with acute emotional stress. 2dEcho shows venticular dilation with reduced EF. 2/20/2016Evaluation of autonomic functions 92
- 93. Familial Dysautonomia: Mutation in IB kinase protein gene. Part HSAN mainly HSAN 3. Impaired peripheral and central myelination. Features include labile autonomic response, poor oropharyngeal co- ordination, absence of lingual fungiform papillae, alacrima and hypolreflexia. Baroreflex failure: Stress induced systolic surge >300 mmhg. Resembles pheocromocytoma. Afferent in put from vagus or glossopharngeal becomes impaired. Jordans syndrome: Malignant vagotonia from selective baroreflex failure presenting with bradycardia and asystole. 2/20/2016Evaluation of autonomic functions 93
- 94. Pure autonomic failure: Synucleinopathy deposition of synnucuclein in autonomic ganglia. Common manisfestation is orthostatic hypotension, postprandial angina. Autoimmune pandysautonomia: Autonomic symptoms with raised AcHR antibodies nad response to IVIg. Autonomic neuropathy: Distal vasomotor involvement of hands and feet. Drug induced autonomic dysfunction. Dopamine hydroxylase deficiency: Absent sympathetic function with no noradrenergic functions. OA, intact sweating and ptosis with a rche palate. Undetectable urinary, plasma and CSF norepinephrine levels. 2/20/2016Evaluation of autonomic functions 94
- 95. Recent studies indicate that MSA is distinguishable from PD using autonomic tests. PD is characterized by a length-dependent involvement of postganglionic sudomotor fibers MSA is characterized by widespread, early and preganglionic autonomic failure. MIBG or fluorodopa scan of the heart, which images postganglionic adrenergic innervation, is typically defective in PD and normal in MSA
- 96. PD case showed very distal anhidrosis, affecting only parts of the toes, and did not progress over time. In contrast, MSA causes widespread anhidrosis. If both QSART and TST are performed, normal QSART volume in an anhidrotic region indicates that the lesion is preganglionic in site.
- 97. Plasma norepinephrine measured with the subject supine and after a period of standing provides another method of studying adrenergic function. A normal response consists of doubling of NE on standing. The patient with generalized postganglionic adrenergic failure, as in pure autonomic failure (PAF), will have low supine NE. The patient with preganglionic lesion, as in MSA, will typically have normal supine values (since the postganglionic fibers are intact) but a failure to increment on standing
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- 99. Bradley book of neurology Harrisons book of neurology Mishra and kalita: clinical neurophysiology D. Clausa,* and R. Schondorf: Sympathetic skin response; 1999 International Federation of Clinical Neurophysiology. Kucera p, Goldenberg Z, Kurca E: SSR: Review of method and its clinical use;Bratis1 Lek Listy 2004 Ben M.W. Illigens, MD and Christopher H. Gibbons, MD MMSc:Sweat testing to evaluate autonomic function; Clin Auton Res. 2009 April Peter Novak:Video Article Quantitative Autonomic Testing; 2011 Journal of Visualized Experiments
Editor's Notes
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