The document discusses autonomic function testing which involves various tests to evaluate the autonomic nervous system. It describes tests such as heart rate response to deep breathing, Valsalva maneuver, tilt table testing, and blood pressure responses to assess cardiovagal and adrenergic functions. The tests provide information about parasympathetic and sympathetic integrity and are used to diagnose and monitor autonomic disorders.
this presentation overviews about heart rate variability and its uses as a biofeedback mechanism in varying the heart rate and thus releaving stress and other applications of it
Basic MEP techniques and understanding for Intraoperative neuromonitoring of the motors tracts during Brain and Spinal surgeries to prevent postoperative complications.
AV nodal reentrant tachycardia (AVNRT), or atrioventricular nodal reentrant tachycardia, is a type of tachycardia (fast rhythm) of the heart. It is a type of supraventricular tachycardia (SVT), meaning that it originates from a location within the heart above the bundle of His. AV nodal reentrant tachycardia is the most common regular supraventricular tachycardia. It is more common in women than men (approximately 75% of cases occur in females). The main symptom is palpitations. Treatment may be with specific physical maneuvers, medication, or, rarely, synchronized cardioversion. Frequent attacks may require radiofrequency ablation, in which the abnormally conducting tissue in the heart is destroyed.
AVNRT occurs when a reentry circuit forms within or just next to the atrioventricular node. The circuit usually involves two anatomical pathways: the fast pathway and the slow pathway, which are both in the right atrium. The slow pathway (which is usually targeted for ablation) is located inferior and slightly posterior to the AV node, often following the anterior margin of the coronary sinus. The fast pathway is usually located just superior and posterior to the AV node. These pathways are formed from tissue that behaves very much like the AV node, and some authors regard them as part of the AV node.
The fast and slow pathways should not be confused with the accessory pathways that give rise to Wolff-Parkinson-White syndrome (WPW syndrome) or atrioventricular reciprocating tachycardia (AVRT). In AVNRT, the fast and slow pathways are located within the right atrium close to or within the AV node and exhibit electrophysiologic properties similar to AV nodal tissue. Accessory pathways that give rise to WPW syndrome and AVRT are located in the atrioventricular valvular rings. They provide a direct connection between the atria and ventricles, and have electrophysiologic properties similar to ventricular myocardium.
ventricular premature complexes and idioventricular rhythm identification is important in the ICU ..they may run into arryhthmias..look over my seminar...
any queries...
here i am to explain the Anatomy and physiology of part of the Pyramidal tract, that is the corticospinal tract. I also added the clinical significance of corticospinal tract. The course of the corticospinal tract are well explained.
this presentation overviews about heart rate variability and its uses as a biofeedback mechanism in varying the heart rate and thus releaving stress and other applications of it
Basic MEP techniques and understanding for Intraoperative neuromonitoring of the motors tracts during Brain and Spinal surgeries to prevent postoperative complications.
AV nodal reentrant tachycardia (AVNRT), or atrioventricular nodal reentrant tachycardia, is a type of tachycardia (fast rhythm) of the heart. It is a type of supraventricular tachycardia (SVT), meaning that it originates from a location within the heart above the bundle of His. AV nodal reentrant tachycardia is the most common regular supraventricular tachycardia. It is more common in women than men (approximately 75% of cases occur in females). The main symptom is palpitations. Treatment may be with specific physical maneuvers, medication, or, rarely, synchronized cardioversion. Frequent attacks may require radiofrequency ablation, in which the abnormally conducting tissue in the heart is destroyed.
AVNRT occurs when a reentry circuit forms within or just next to the atrioventricular node. The circuit usually involves two anatomical pathways: the fast pathway and the slow pathway, which are both in the right atrium. The slow pathway (which is usually targeted for ablation) is located inferior and slightly posterior to the AV node, often following the anterior margin of the coronary sinus. The fast pathway is usually located just superior and posterior to the AV node. These pathways are formed from tissue that behaves very much like the AV node, and some authors regard them as part of the AV node.
The fast and slow pathways should not be confused with the accessory pathways that give rise to Wolff-Parkinson-White syndrome (WPW syndrome) or atrioventricular reciprocating tachycardia (AVRT). In AVNRT, the fast and slow pathways are located within the right atrium close to or within the AV node and exhibit electrophysiologic properties similar to AV nodal tissue. Accessory pathways that give rise to WPW syndrome and AVRT are located in the atrioventricular valvular rings. They provide a direct connection between the atria and ventricles, and have electrophysiologic properties similar to ventricular myocardium.
ventricular premature complexes and idioventricular rhythm identification is important in the ICU ..they may run into arryhthmias..look over my seminar...
any queries...
here i am to explain the Anatomy and physiology of part of the Pyramidal tract, that is the corticospinal tract. I also added the clinical significance of corticospinal tract. The course of the corticospinal tract are well explained.
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
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Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
MIP 201T & MPH 202T
ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
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These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Basavarajeeyam - Ayurvedic heritage book of Andhra pradesh
Autonomic testing
1.
2. Autonomic dysfunction can occur as a result of many
diseases that affect autonomic pathways.
The clinician’s role is to seek out symptoms of
dysautonomia
Necessary to determine if these symptoms are really
due to involvement of autonomic systems.
3. The conceptual framework began 19th century .
These original tests were developed over time .
Widely used in clinical practice for 50 years
Decades of extensive experience and thousands of
studies published on its use.
4. 1. To evaluate the severity and distribution of autonomic
function
2. To diagnose limited autonomic neuropathy
3. To diagnose and evaluate orthostatic intolerance
4. To monitor the course of dysautonomia
5. To monitor response to treatment
6. As an instrument in research studies
5. 1. Cardiovagal innervation (parasympathetic innervation):
heart rate (HR) response to deep breathing, Valsalva ratio,
and HR response to standing (30:15 ratio)
2. Adrenergic: beat-to-beat blood pressure (BP) responses to
the Valsalva maneuver, sustained hand grip, and BP and HR
responses to tilt-up or active standing
3. Sudomotor: quantitative sudomotor axon reflex test
(QSART), thermoregulatory sweat test (TST), sympathetic
skin response (SSR).
6. Beat to beat heart rate analysis
Heart rate documented on ECG or on EMG equipment
For ECG in EMG
Low filter 1-5 Hz; High filter 500Hz
Slow oscilloscope sweep time(0.2-1 secs)
Sensitivity- 0.5 mv
Active electrode midline posteriorly between inferior
angle of scapula; reference mid axillary line
7. Heart rate is inversely related to RR interval
Heart rate(R-R/min)=
sweep speed(mm/s)÷RR interval x60
BP sphygmomanometer
Beat to beat BP measurement formerly required
invasive intra arterial measurement; but
plethysmography
8. 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
9.
10. 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
11. Connect the ECG electrodes for recording lead II
Ask the subject to breath deeply at a rate of six
breaths per minute for 3 cycles
(allowing 5 seconds each for inspiration and
expiration)
12.
13. 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
14. 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
16. 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,
a response to prolonged orthostasis lasting for more
than 5 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
17.
18. 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)
19.
20. 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
21. RR interval at 30th beat
30:15 ratio = ------------------------------
RR interval at 15th beat
Normal > 1.04
Borderline = 1.01-1.04
Abnormal =<1.00
22. Fluctuations of blood pressure are assessed based on
somewhat later responses to standing (first 4 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
23. 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.
24. Assesses integrity of the baroreceptor reflex
Measure of parasympathetic and sympathetic function
It is “forced expiration against a closed glottis”
25. 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
26. Perform the Valsalva manoeuvre (forced expiration
against a closed glottis) by asking the subject to
breathe forcefully into a mercury manometer and
maintain a pressure of 40 mmHg for 15 seconds
Record the ECG throughout and for 30 seconds
after the procedure
27. 4 phases
Phase I
Phase II
Phase III
Phase IV
28.
29. 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
30. Early part – drop in BP lasting for about 4 seconds
Latter part – BP returns to normal
Heart rate rises steadily
31. 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
32. Transient decrease in BP lasting for a few seconds
Little change in heart rate
33. Mechanical displacement of blood into
pulmonary vascular bed, which was
under increased intrathoracic pressure
BP decreases
34. 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
35. Due to increase in venous return, stroke volume and
cardiac output
36. Phase I Increase in BP
Phase II Decrease in BP, Tachycardia
Phase III Decrease in BP
Phase IV Overshoot of BP, Bradycardia
37. 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
38. Longest RR
Valsalva Ratio = -----------------------------
Shortest RR
Values :> 1.4
more than 1.21 normal
less than 1.20 abnormal
39. Valsalva maneuver evaluates
1. sympathetic adrenergic functions using the blood
pressure responses
2. cardiovagal (parasympathetic) functions using the heart
rate responses
40. 4. Cold pressor test
Submerge the hand in ice cold water(1 minute)
diastolic pressure by >15 mmHg
HR>10/min
5. Isometric handgrip test
isometric pressing of a handgrip dynamometer at
approximately one third of the maximum contraction
strength for 3-5 min.
Blood pressure measurements are taken at the other
arm at 1 min interval
Rise of DBP>15/min
41.
42.
43. • 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)
44. 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
45. 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.
46. 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.
47. 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
48.
49. From studies HUT testing (2 occasions), with a known
time interval,an average reproducibility of 81%
However, as Behzad and collaborators and other
authors
highlighted, negative results are much more
reproducible than positive ones (about 95% and 50%
respectively).
depends strongly on population selection as it is
increased in patients with severe and frequent
orthostatic symptoms.
50. Studies assessing the ability of the HUT test to diagnose
neurocardiogenic syncope averaged a sensitivity of 35%
without pharmacologic stimulation
57% with pharmacologic stimulation
Studies using HUT testing within the boundaries set by
the American College of Cardiology guidelines averaged
a sensitivity of 65%
51. The specificity of the HUT test for neurocardiogenic
syncope 92% on average without pharmacologic
stimulation
81% with pharmacologic stimulation
Two investigator-HUT test-American College of
Cardiology guidelines-both yielded a specificity of
100%.
54. 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%.
55.
56. 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.
57. 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 measured area
of anhidrosis divided by the area of the anatomic figure,
multiplied by 100
58. 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
59.
60. Limitations
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:
preganglionic lesions show an abnormal TST, while the
QSART, or silicone imprints are normal.
A postganglionic lesion will be abnormal in all tests
61. 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.
62.
63. 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.
64.
65.
66. Wait until the baseline sweat is flat, below 100
nanoliters/minute and all channels give similar baseline
sweat output (difference < 15 %,)
Start stimulation at current 2 mA for 5 minutes, turn on
the marker.
Record another 5 minute of the sweat (total 10
minutes), turn on the marker.
Obtain the latencies and volumes at each site
72. 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.
73. 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
74.
75. 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
76. 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.
77. Historical aspects
(SSR) is a change in skin potential following arousal
stimulation, described by Tarchanoff (1890).
Method introduced by Sahani in 1984 and later by
Knezevic and Bjada
78. SSR is a change in potential recorded from surface of
skin, representing sudomotor activity
Can be evoked by different stimuli
Acoustic; TMS C7, brain; 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
79. 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
80. originate from the
hypothalamus and
descend uncrossed
along the lateral
column of the
spinal cord to form
a small bundle
between the
pyramidal tract and
the anterior-lateral
tract. 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
81. Room temperature should be comfortable and the skin
surface temperature 32@C.
potentials are increased during psychological stress and
may contaminate the evoked SSR.
situation during recording has to be relaxed, without
acoustic disturbances
82. Recording is done from glabrous skin and is referenced
against hairy skin whose sweat glands are not typically
active at normal ambient temperatures.
The surface Ag-AgCl electrodes are placed on the palm
(active) and referenced against the volar forearm or
dorsum of the hand (indifferent);
and on the sole of the foot (active) and referenced
against the shin or dorsum of the foot (indifferent)
83. 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.
84. 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.
it is applied at irregular time intervals and at a
frequency of approximately 1/min to avoid habituation.
85. If electrical stimulation at one site does not evoke an
SSR, other sites of stimulation should be tried
If the response to electrical stimulation is absent
response to acoustic stimuli or to an inspiratory gasp
should be tried (Shahani et al. 1984).
86. In normal subjects, transcranial magnetic stimulation
of the motor strip
elicited palmar and plantar SSRs similar
both in latency and amplitude to those evoked by
median nerve stimulation.
Normal results
The shape of the SSR is variable.
The shortest latency to onset and the maximum peak
to trough amplitude of at least 5 recordings is used.
87.
88. Latency
The latency of the SSR includes
1. afferent conduction (about 20 ms), 2.central
processing time (a few milliseconds),
3.and efferent conduction in pre- and
slow conducting postganglionic autonomic nerve.
89. 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.
differences in fast afferent conduction are not relevant
for the SSR latency and the site of stimulation is also
not significant
90. Amplitude Measurements in theory should reflect the
density of spontaneously activable sweat glands.
interaction of the two components, sweat gland and
epidermal, makes the absolute amplitude of the
evoked EDA difficult to interpret.
the reproducibility of the electri-cally evoked SSR is
poor.
Age- latency; amplitude
SSR evoked by an auditory stimulus has less inter and
intrasubject latency and waveform variability than the
inspiratory gasp induced response.
91. Still no consensus about the evaluation and processing
Qualitative evaluation accepts only the absence of SSR
as a pathological sign
Quantitative evaluation- different opinion
92. SSR is a poor test of sympathetic sudomotor function.
No close correlation between presence or absence of
SSR and the severity of autonomic dysfunction.
polyneuropathy, erectile dysfunction, central
degenerative diseases, multiple sclerosis(50%), brain
infarction, reflex sympathetic dystrophies, spinal and
peripheral nerve lesions.
94. Distal small fiber neuropathy
Sympathetic sudomotor fibers are affected, so that
QSART will show abnormalities at the feet and normal
sweating more proximally
thermoregulatory sweat test shows anhidrosis that is
confined to the distal feet
confined or becomes generalized.
diabetes or amyloidosis can start with DSFN and
progress, while others do not
95. e.g: Autonomic neuropathies and multiple system
atrophy.
widespread loss of sweating, cardiovagal failure is
present, and OH with impaired baroreflexes is seen
97. 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
98. 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.
99. 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
100. 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