Horner's syndrome is characterized by the classic triad of ptosis, miosis, and anhidrosis. It is caused by a lesion anywhere along the three-neuron sympathetic pathway supplying the eye. The etiology can be categorized based on which neuron is affected, as first-order lesions involve the brainstem or cervical cord, second-order lesions the chest or neck, and third-order lesions above the superior cervical ganglion. Pharmacological tests with cocaine, apraclonidine, or hydroxyamphetamine drops can help confirm and localize the lesion.
Cerebellum is the organ that controls tone of muscle and maintains balance of body. It is also responsible for co-ordination of the movements. There are some signs which suggest the abnormalities in Cerebellar functioning.
Cerebellum is the organ that controls tone of muscle and maintains balance of body. It is also responsible for co-ordination of the movements. There are some signs which suggest the abnormalities in Cerebellar functioning.
Horner’s syndrome (also called oculosympathetic paresis, or Horner syndrome) comprises of the classic triad of ptosis, miosis and anhidrosis.
It results from a lesion to the sympathetic pathway that supply the head and neck region.
The causes of Horner’s syndrome varies with the age of the patient and site of the lesion.
Prompt evaluation is necessary to detect and treat life-threatening conditions.
Please find the power point on Brain tumors (Acoustic Neuroma). I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
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 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 leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
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. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Title: Sense of Taste
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 structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
16. Ptosis
• Ptosis is minor, usually less than 2 mm
• Paralysis of the Müller's muscle, which is
innervated by the sympathetic pathway
• "upside-down ptosis"
17. Anhidrosis
• Anhidrosis is present in central or preganglionic
(first or second-order) lesions
• This sign is frequently not apparent to patients or
clinicians
19. Horner’s in Children
• Impaired facial flushing (Harlequin sign) is often
more apparent than anhidrosis
• Acute features of sympathetic disruption can
also include ipsilateral conjunctival injection,
nasal stuffiness, and increased near point of
accommodation
23. Localizing/Associated
Symptoms
• Diplopia, vertigo, ataxia, lateralized weakness
suggest a brainstem localization
• Bilateral or ipsilateral weakness, long tract signs,
sensory level, bowel and bladder impairment
suggest involvement of the cervicothoracic cord
• Arm pain and/or hand weakness typical of brachial
plexus lesions suggest a lesion in the lung apex
24. • Ipsilateral extraocular pareses, particularly a sixth
nerve palsy, in the absence of other brainstem signs
localize the lesion to the cavernous sinus
• An isolated Horner's syndrome accompanied by
neck or head pain suggests an internal carotid
dissection
26. First-order syndrome
Lesions of the sympathetic
tracts in the brainstem or
cervicothoracic spinal cord
can produce a first-order
Horner's syndrome.
28. • Strokes, tumors, and demyelinating lesions affecting
the sympathetic tracts in the hypothalamus,
midbrain, pons, medulla, or cervicothoracic spinal
cord are other potential causes of a central Horner's
syndrome.
• Syringomyelia and cervical cord trauma can also
produce a Horner's syndrome.
29. Second-order syndrome
Second-order or
preganglionic Horner's
syndromes can occur with
trauma or surgery involving
the spinal cord, thoracic
outlet, or lung apex
30.
31. • Lumbar epidural anesthesia can also produce a
Horner's syndrome. This is most often described in
association with obstetrical procedure.
32. Third-order syndrome
Third-order Horner's
syndromes often indicate
lesions of the internal
carotid artery such as an
arterial dissection,
thrombosis, or cavernous
sinus aneurysm.
33. Carotid Dissection
An acute Horner's syndrome with neck or facial
pain should be presumed to be caused by carotid
dissection until proven otherwise.
Between 40 and 60 percent of patients present
with an isolated painful third-order Horner's
syndrome.
Emergent diagnostic tests should be obtained
37. Pharmacologic Testing
• Pharmacologic tests can be useful to confirm the
diagnosis and to localize the lesion
• Two agents are used: cocaine
or apraclonidine drops and hydroxyamphetamine
drops
38. Confirmation of Horner’s
Syndrome
• Pharmacological testing with cocaine
or apraclonidine drops can confirm the diagnosis of
Horner's syndrome in subtle cases
• If the diagnosis of Horner's syndrome is clear
clinically, then use of cocaine or apraclonidine can
be avoided
39. Cocaine
• Blocks the reuptake of norepinephrine at the
sympathetic nerve synapse
• Intact pathway – dilates pupil. No effect on
impaired sympathetic pathway
40. Apraclonidine
• Alternative to cocaine
• Direct alpha-adrenergic receptor agonist.
Apraclonidine has weak alpha-1 and strong alpha-2
activity
• Alpha-1 mediates pupillary dilation, while alpha-2
downregulates norepinephrine release at the
neuromuscular junction
42. Localization of the Lesion
• First-order neuron
(brainstem or cervical cord)
• Second-order neuron
(chest or neck)
• Third-order or
postganglionic neuron
(above the superior cervical
ganglion at the carotid
bifurcation).
43. Hydroxyamphetamine
• It releases stored norepinephrine from the
postganglionic adrenergic nerve endings
• A normal pupil and a first or second-order Horner's
pupil will dilate, whereas a third-order Horner's pupil
will not dilate as well as the normal pupil.
46. • Classic signs of a Horner's syndrome include
miosis, ptosis, and anhidrosis.
• The miosis is typically mild, associated with a
dilation lag and most prominent in dim light.
• The ptosis is also mild and also involves the lower
lid.
• Anhidrosis occurs with first or second-order lesions
only
47.
48. • The common etiologies of Horner's syndrome are
categorized by which of the three neurons is affected.
• The differential diagnosis is also distinct in children
versus adults26
49. • The presence of a Horner's syndrome can be confirmed
pharmacologically with either cocaine or apraclonidine
eye drops
• Hydroxyamphetamine eye drops can help distinguish a
third-order (postganglionic) Horner's syndrome from
either a first or second-order syndrome.
50. • In the absence of a clear history of trauma as the
cause of Horner's syndrome, imaging studies will be
required.
Editor's Notes
Horner's syndrome can result from a lesion anywhere along a three-neuron sympathetic (adrenergic) pathway that originates in the hypothalamus
The first-order neuron descends caudally from the hypothalamus to the first synapse, which is located in the cervical spinal cord (levels C8-T2, also called ciliospinal center of Budge).
The second-order neuron travels from the sympathetic trunk, through the brachial plexus, over the lung apex. It then ascends to the superior cervical ganglion, located near the angle of the mandible and the bifurcation of the common carotid artery
The third-order neuron then ascends within the adventitia of the internal carotid artery, through the cavernous sinus, where it is in close relation to the sixth cranial nerve [1]. The oculosympathetic pathway then joins the ophthalmic (V1) division of the fifth cranial nerve (trigeminal nerve). In the orbit and the eye, the oculosympathetic fibers innervate the iris dilator muscle as well as Müller's muscle, a small smooth muscle in the eyelids responsible for a minor portion of the upper lid elevation and lower lid retraction.
The third-order neuron then ascends within the adventitia of the internal carotid artery, through the cavernous sinus, where it is in close relation to the sixth cranial nerve [1]. The oculosympathetic pathway then joins the ophthalmic (V1) division of the fifth cranial nerve (trigeminal nerve). In the orbit and the eye, the oculosympathetic fibers innervate the iris dilator muscle as well as Müller's muscle, a small smooth muscle in the eyelids responsible for a minor portion of the upper lid elevation and lower lid retraction.
The degree of anisocoria is more marked in the dark than in light. There is associated dilation lag, an asymmetry in pupillary redilation between the two eyes when the light source is moved away from the eye [2]. The Horner's pupil will redilate more slowly (by 15 to 20 seconds) than the normal pupil.
A) In the light, there is mild anisocoria, with the right pupil being smaller than the left pupil. There is also decreased palpebral fissure on the right.
B) In the dark, the right pupil does not dilate well.
C) After instillation of 1 percent hydroxyamphetamine in both eyes, only the left pupil dilates, suggesting a lesion involving the postganglionic oculosympathic pathways (third order Horner's syndrome).
The ptosis is minor (less than 2 mm) and occurs as a result of paralysis of the Müller's muscle, which is innervated by the sympathetic pathway. The lower as well as the upper lid is affected, producing the so-called "upside-down ptosis." This further narrows the palpebral fissure. The levator palpebrae superioris is unaffected; weakness of this muscle produces the more profound upper lid ptosis seen in third cranial nerve palsies.
The sympathetic fibers responsible for facial sweating and vasodilation branch off at the superior cervical ganglion from the remainder of the oculosympathetic pathway; thus, anhidrosis is not a feature of postganglionic or third-order lesions [3]. This sign is frequently not apparent to patients or clinicians.
The sympathetic fibers responsible for facial sweating and vasodilation branch off at the superior cervical ganglion from the remainder of the oculosympathetic pathway; thus, anhidrosis is not a feature of postganglionic or third-order lesions
One possible cause of Harlequin syndrome is a lesion to the preganglionic or postganglionic cervical sympathetic fibers and parasympathetic neurons of the ciliary ganglion
Congenital Horner syndrome. Ptosis, miosis, and heterochromia. Lighter colored iris is on the affected left side
A congenital Horner's syndrome should be suspected when anisocoria is associated with heterochromia (unequal iris color, with the affected iris being lighter). This occurs because formation of iris pigment in the first several months of age is under sympathetic control. This may only be apparent if the natural color is relatively dark
The most common cause is delivery-related trauma to the neck and shoulder, damaging the sympathetic pathway. Associated injury to the lower brachial plexus can produce weakness in the ipsilateral forearm and hand (Klumpke's paralysis).
.
Congenital ptosis of severe degree, left upper lid.
The most common cause is a lateral medullary infarction, which produces a Horner's syndrome as part of the Wallenberg syndrome.
Typically the patient presents with vertigo and ataxia, which overshadow the Horner's syndrome. Other neurologic symptoms and signs include abnormal eye movements, ipsilateral limb ataxia, and a dissociated sensory loss (loss of pain and temperature sensation on the ipsilateral face and contralateral trunk). Hoarseness and dysphagia are also often present.
when the intermediolateral columns are affected.
Pancoast tumor
due to pharmacologic disruption of the preganglionic neuron as it exits the spinal cord. This is most often described in association with obstetrical procedures; in such cases, a Horner’s syndrome may indicate high sympathetic blockade.
Carotid endarterectomy and carotid artery stenting can also produce a Horner's syndrome
Patients with acute carotid dissection are at a high risk for cerebral infarction, which usually occurs within the first few weeks, often within days, after onset of the Horner's syndrome.
Other causes of postganglionic Horner's syndrome include neck masses, otitis media, and pathology involving the cavernous sinus. Abnormalities of eye movements, particularly a sixth nerve palsy, commonly occur when the cavernous sinus is involved
A Horner's syndrome is a common feature of cluster headache, occurring with unilateral eye or temple pain and lacrimation, generally lasting no more than an hour or two
Whether to take the time to test the pupils pharmacologically or not to confirm a Horner syndrome mostly depends on the duration of the anisocoria and the location of the consultation:
●When a patient is seen in an emergency department with acute painful anisocoria highly suggestive of Horner syndrome, it is essential to immediately obtain appropriate investigations to look for a cervical artery dissection, or a cavernous sinus lesion. In this setting, pharmacologic testing would only delay appropriate testing and management.
●When a patient presents to an outpatient clinic with incidentally found isolated anisocoria, confirming the Horner syndrome before obtaining potentially costly and unnecessary tests is helpful. Unlike cocaine drops, apraclonidine drops are readily available, and are a very reliable way to confirm (or to rule-out) a Horner syndrome in adults or even older children.
s their administration will interfere with the hydroxyamphetamine test for localization.
Cocaine blocks the reuptake of norepinephrine at the sympathetic nerve synapse and causes pupillary dilation in eyes with intact sympathetic innervation. Cocaine has no effect in eyes with impaired sympathetic innervation, regardless of the lesion location. One hour after instillation of two drops of cocaine (4 or 10 percent), a normal pupil dilates more than the Horner's pupil, increasing the degree of anisocoria; anisocoria of 1 mm or more after cocaine administration is considered a positive result
In a Horner's pupil, denervation supersensitivity to the alpha-1 receptor will cause that pupil to dilate (usually by about 2 mm), while alpha-2 stimulation in the normal eye will cause that pupil to constrict slightly (usually by <1 mm). Thus, one to two drops of 0.5 percent apraclonidine instilled in both eyes causes a reversal of anisocoria in patients with Horner's syndrome. Comparison testing in small series of patients suggests that this test compares favorably with cocaine in the diagnosis of Horner's syndrome
All photographs were taken with room lights on. A, The patient at baseline, showing left ptosis and miosis; note the incidental elevated left upper eyelid fold consistent with levator aponeurosis dehiscence. B, Forty-five minutes after instillation of 10% cocaine to each eye. Failure of the left pupil to dilate indicates Horner syndrome. C, Several weeks later, appearance 1 hour after instillation of 1 drop of 1% apraclonidine to the left eye. Note reversal of baseline anisocoria.
There is no pharmacologic test to distinguish between first and second-order lesions.
Hydroxyamphetamine eye drops will differentiate between a lesion affecting the first (brainstem or cervical cord) or second-order (chest or neck) neuron and one affecting the third-order or postganglionic neuron (above the superior cervical ganglion at the carotid bifurcation). There is no pharmacologic test to distinguish between first and second-order lesions. Because cocaine may interfere with the uptake and efficacy of hydroxyamphetamine drops, it is recommended that 24 to 72 hours elapse between the two tests.
One hour after instillation of 1 percent hydroxyamphetamine,
In the light, there is mild anisocoria, with the right pupil being smaller than the left pupil. There is also decreased palpebral fissure on the right. B) In the dark, the right pupil does not dilate well. C) After instillation of 1 percent hydroxyamphetamine in both eyes, only the left pupil dilates, suggesting a lesion involving the postganglionic oculosympathic pathways (third order Horner's syndrome).
The test is positive for postganglionic Horner's lesions when the anisocoria increases by at least 1 mm. This test has a sensitivity of 93 to 96 percent and a specificity of 84 percent for detecting postganglionic lesions. This test is not reliable in children in whom transynaptic degeneration occurs
A Horner's syndrome can be caused by a lesion anywhere along the three-neuron sympathetic (adrenergic) pathway that originates in the hypothalamus
High-yield sites of imaging can be identified based on accompanying signs and symptoms and/or the hydroxyamphetamine test
