-
Categories
-
Pharmaceutical Intermediates
-
Active Pharmaceutical Ingredients
-
Food Additives
- Industrial Coatings
- Agrochemicals
- Dyes and Pigments
- Surfactant
- Flavors and Fragrances
- Chemical Reagents
- Catalyst and Auxiliary
- Natural Products
- Inorganic Chemistry
-
Organic Chemistry
-
Biochemical Engineering
- Analytical Chemistry
-
Cosmetic Ingredient
- Water Treatment Chemical
-
Pharmaceutical Intermediates
Promotion
ECHEMI Mall
Wholesale
Weekly Price
Exhibition
News
-
Trade Service
How to diagnose and differentially diagnose patients with frequent transient alteration in awareness (TAA)? A recent issue of the Journal of Neurology Clinical Reasoning Series reported a 21-year-old male patient with episodic changes in consciousness every day.
Let's take a look at how foreign colleagues conduct clinical reasoning through clinical history and auxiliary examinations
.
Translation: Reflection without trace This article is published by the author authorized by Yimaitong, please do not reprint without authorization
.
Case presentation The patient is a 21-year-old male, right-handed, who presented with "episodic altered consciousness"
.
The patient's episodes began at age 15, when the patient stood up from a chair and stretched his arms up while studying, followed by a loss of consciousness of unknown duration, which was found lying on the floor by the patient's father
.
Before long, the patient started having daily attacks
.
Patients report 1-2 seconds of prodromal symptoms, described as "they're coming", followed by "passing out", "feeling like a roller coaster", "vision flashing in and out", "feeling a pulse in the brain", Feelings of "blurred brain" and/or "body numbness"; followed by "loss of consciousness for about 30 seconds" but return to normal soon after
.
Posture is usually preserved
.
However, some episodes are accompanied by non-stereotyped, brief body tremors and, rarely, falls
.
The patient denied a history of severe trauma, oral trauma, or incontinence
.
The patient did not notice an obvious trigger
.
Denial of orthostatic intolerance
.
Denied a history of migraine or migraine aura
.
Sleep disturbance, endocrine disease, or risk factors for epilepsy were denied
.
Denied neurological disease or family history of recurrent syncope
.
The patient had a history of depression, attention deficit/hyperactivity disorder, and obsessive-compulsive disorder, and had been taking fluoxetine, atomoxetine, rildimer mesylate, vortioxetine, and tetramine in the past few years spirone, but these drugs had no significant effect on episodes and affected college academic performance due to multiple episodes per day
.
Systemic and neurological examinations were normal
.
Questions to consider: 1.
What are the differential diagnoses? Differential diagnosis of TAA is usually a manifestation of transient cortical dysfunction
.
In the absence of head trauma, acute intoxication with drugs, or toxins, different epileptic and non-epileptic etiologies can lead to TAA and spontaneous recovery
.
Clinical history is critical for differential diagnosis
.
In this patient, transient cerebral hypoperfusion due to syncope/presyncope should be considered given the visual and sensory disturbances and brief duration of TAA onset, but syncope is usually accompanied by abnormal motor activity
.
The seizure event may also be a seizure
.
For example, ambiguous "head sensation", autonomic manifestations, and/or somatosensory/visceral symptoms and subsequent impairment of consciousness can occur when the frontal, insular, or cingulate cortex is involved
.
Somatosensory aura is more common in parietal lobe epilepsy
.
Visual symptoms are common in occipital lobe epilepsy
.
The patient had no migraine or migraine aura, and no sleep disturbance
.
Insufficiency of the vertebrobasilar artery is often associated with brainstem dysfunction
.
Although patient-reported symptoms fit the illusion of reality, feeling "like passing out" and paresthesias, they did not meet the criteria for a panic attack
.
Functional neurological disorders should be considered, especially in the context of psychiatric comorbidities
.
In addition, rare causes of syncope/pre-syncope, including Eagle syndrome, carotid body tumor, or pheochromocytoma, should be considered, but unlikely
.
Finally, "hypervigilance" or overinterpretation of benign, nonspecific symptoms is also possible, but unlikely
.
The patient underwent the following examinations, all of which were normal: transthoracic echocardiography, tilt table test, cranial MRI, and head and neck MRA
.
Cardiac monitoring over 30 days found "7 self-limited premature atrial beats, normal sinus rhythm and sinus tachycardia"
.
A 72-hour ambulatory EEG at another institution reported normal
.
Given the patient's psychiatric comorbidities and normal examination, it was speculated that a functional neurological disorder was likely, but her psychiatrist was skeptical and referred the patient to a comprehensive epilepsy center for evaluation
.
Questions to consider: 1.
What further inspections should be performed? What are the further checks? The patient has undergone initial evaluation for cardiovascular and autonomic causes of syncope/pre-syncope
.
Given the normal results, syncope/presyncope is less supportive
.
Ambulatory EEG did not reveal seizures, but focal seizures due to deep lesions could not be ruled out, which may not be obvious or subtle on scalp EEG
.
The patient was admitted to the Epilepsy Monitoring Unit (EMU) for continuous video EEG monitoring for this purpose
.
Results showed dozens of typical events, clinically characterized by back and shoulder extension, neck hyperextension, and accompanying lateral and upward rotation of the head, followed by TAA
.
Interictal EEG shows mixed theta-delta activity of bihemispheric polymorphisms
.
Interictal EEG was normal
.
Although no definite EEG seizures were found, the patient's fairly stereotyped symptoms and consistent EEG pattern made it necessary to consider seizures due to deep lesions (eg, insula/cingulate gyrus)
.
Cranial PET and 7T MRI were normal, 2 magnetoencephalograms were unremarkable, and single-photon emission computed tomography showed "multiple cortical foci with increased radiotracer activity in bilateral temporoparietal regions" (in "Presumptive epilepsy").
radiotracer injection within 10 seconds of onset)
.
The patients tried 7 different antiepileptic drugs (ASMs), but there was no significant change in seizure frequency
.
Questions to consider: 1.
Are there features for or against a diagnosis of epilepsy? 2.
What additional assessments should be considered? What are the additional assessments? Very frequent events with little response to ASM suggest non-epileptic events
.
One year after the patient's initial admission, the patient was re-admitted to the EMU and captured approximately 100 episodes of symptoms that were the same as previously described
.
Attacks only occur during wakefulness
.
On the video EEG, the background was normal prior to the onset of the event
.
The patient then exhibited the same motor behavior described in Part 3, accompanied by a transient decrease in the QRS complex amplitude on the ECG, followed by a very transient, diffuse, polymorphic, mixed theta-delta brain electrical activity
.
The patient subsequently experienced typical TAA
.
A seizure was followed by several clonic movements of the right upper extremity
.
A few seconds after the end of each episode, the patient presses the event button
.
The patient's medical record was reviewed again, and during the first EMU admission, the electrocardiogram had changed
.
Interictal EEG was normal
.
At this time, it is considered as a stretch syncope (Stretch syncope, SS)
.
Patients were referred to a cardiovascular research laboratory, and an experimental protocol was devised to test for potential deficits in arterial pressure and cerebrovascular regulation
.
Focus on the beat-by-beat cardiovascular response of the Valsalva maneuver
.
The Valsalva maneuver induced characteristic 4-phase changes and adequate arterial pressure and cerebrovascular modulation
.
The patient had no typical episodes during breath-holding in the supine, supine, or sitting positions
.
However, during the quiet rest in the seated position, he exhibited frequent motor behavior consistent with his typical events
.
Immediately following these motor behaviors, the patient reported symptoms consistent with his usual episodes
.
Monitoring during these events showed that he performed Valsalva-like movements while stretching, which triggered typical symptoms
.
Arterial pressure and cerebral blood flow decreased more rapidly during stretching events compared with Valsalva maneuvers (Fig.
)
.
The diagnosis of SS was confirmed, and subsequent perspiration evaluation and skin biopsy were consistent with idiopathic small fiber cholinergic neuropathy
.
Figure Cardiovascular and Autonomic Assays
.
Patients who performed the Valsalva maneuver followed by stretching reported typical symptoms
.
Both behaviors included deep breathing (A), decreased ECG amplitude (B), shortened RR interval (C), decreased blood pressure (D), and decreased cerebral blood flow (E)
.
However, the stretch event was shorter in duration than Valsalva, but resulted in a greater drop in blood pressure and cerebral blood flow
.
Discussion Distraction syncope (SS) is a rare, unique entity characterized by TAA caused by neck hyperextension during extension
.
The few published cases occurred between the ages of 7-26, male > female
.
Patients with SS usually have no history of syncope, except as a result of stretching and neck hyperextension
.
Previous studies have reported significant compulsive self-induced seizure episodes in individual patients, but this patient did not have the urge to perform these movements
.
The patient's motor behavior lasts longer than usual tics and is therefore an atypical tic disorder
.
In addition, the patient was treated with a variety of psychotropic medications, some of which were available for obsessive-compulsive disorder and/or tic disorder, with no apparent benefit
.
Although rare, SS can easily be misdiagnosed as epilepsy
.
Causes include: event-related stereotyped motor activity; development of episodic tachycardia; rhythmic/semi-rhythmic slowing on EEG in the presence of transient cerebral hypoperfusion
.
Furthermore, typical presyncope symptoms are not always seen in SS
.
Although the pathophysiology of SS has not been fully elucidated, it is clear that Valsalva maneuvers alone are not sufficient to contribute to SS
.
Earlier reports suggested that SS may be a form of vertebrobasilar insufficiency, possibly related to mechanical compression of the vertebral artery during neck rotation, i.
e.
, SS may be a form of vascular compression syncope, as suggested by other authors.
"Given the delay between stretching and hypotension and the presence of slow-wave EEG abnormalities, a reflex mechanism is likely"
.
Therefore, it can be hypothesized that in SS, when stimuli are superimposed (hyperextension of the neck during stretching), cerebral blood flow is restricted and induces a reverse stretch input to carotid baroreceptors, thereby affecting adequate pressure regulation
.
Thus, despite the decrease in arterial pressure, the stretch of carotid baroreceptors increases and does not provide an adequate sympathetic excitatory response
.
In this patient, small fibercholinergic neuropathy may have contributed to the inability to maintain blood flow through vasodilation when pressure is reduced
.
The decrease in QRS amplitude during SS stretch may be due to the increased distance between the chest wall and the heart during Valsalva/stretch
.
Prompt diagnosis of SS can avoid excessive diagnostic workup and unnecessary use of ASM
.
Furthermore, 'undoing' an epilepsy diagnosis that has been previously made by different specialists can be challenging and requires a strong doctor-patient relationship
.
Avoiding neck hyperextension while stretching effectively eliminates SS
.
The patient was referred for cognitive-behavioral and yogic breathing therapy to facilitate the management of his motor performance, and there was a subsequent decrease in the frequency of seizures
.
Original Index: Mauricio F.
Villamar, J.
Andrew Taylor, JW Hamner, et al.
Clinical Reasoning: A Young Man With Daily Episodes of Altered Awareness.
Neurology published online January 20, 2022.
DOI 10.
1212/WNL.
0000000000200049
Let's take a look at how foreign colleagues conduct clinical reasoning through clinical history and auxiliary examinations
.
Translation: Reflection without trace This article is published by the author authorized by Yimaitong, please do not reprint without authorization
.
Case presentation The patient is a 21-year-old male, right-handed, who presented with "episodic altered consciousness"
.
The patient's episodes began at age 15, when the patient stood up from a chair and stretched his arms up while studying, followed by a loss of consciousness of unknown duration, which was found lying on the floor by the patient's father
.
Before long, the patient started having daily attacks
.
Patients report 1-2 seconds of prodromal symptoms, described as "they're coming", followed by "passing out", "feeling like a roller coaster", "vision flashing in and out", "feeling a pulse in the brain", Feelings of "blurred brain" and/or "body numbness"; followed by "loss of consciousness for about 30 seconds" but return to normal soon after
.
Posture is usually preserved
.
However, some episodes are accompanied by non-stereotyped, brief body tremors and, rarely, falls
.
The patient denied a history of severe trauma, oral trauma, or incontinence
.
The patient did not notice an obvious trigger
.
Denial of orthostatic intolerance
.
Denied a history of migraine or migraine aura
.
Sleep disturbance, endocrine disease, or risk factors for epilepsy were denied
.
Denied neurological disease or family history of recurrent syncope
.
The patient had a history of depression, attention deficit/hyperactivity disorder, and obsessive-compulsive disorder, and had been taking fluoxetine, atomoxetine, rildimer mesylate, vortioxetine, and tetramine in the past few years spirone, but these drugs had no significant effect on episodes and affected college academic performance due to multiple episodes per day
.
Systemic and neurological examinations were normal
.
Questions to consider: 1.
What are the differential diagnoses? Differential diagnosis of TAA is usually a manifestation of transient cortical dysfunction
.
In the absence of head trauma, acute intoxication with drugs, or toxins, different epileptic and non-epileptic etiologies can lead to TAA and spontaneous recovery
.
Clinical history is critical for differential diagnosis
.
In this patient, transient cerebral hypoperfusion due to syncope/presyncope should be considered given the visual and sensory disturbances and brief duration of TAA onset, but syncope is usually accompanied by abnormal motor activity
.
The seizure event may also be a seizure
.
For example, ambiguous "head sensation", autonomic manifestations, and/or somatosensory/visceral symptoms and subsequent impairment of consciousness can occur when the frontal, insular, or cingulate cortex is involved
.
Somatosensory aura is more common in parietal lobe epilepsy
.
Visual symptoms are common in occipital lobe epilepsy
.
The patient had no migraine or migraine aura, and no sleep disturbance
.
Insufficiency of the vertebrobasilar artery is often associated with brainstem dysfunction
.
Although patient-reported symptoms fit the illusion of reality, feeling "like passing out" and paresthesias, they did not meet the criteria for a panic attack
.
Functional neurological disorders should be considered, especially in the context of psychiatric comorbidities
.
In addition, rare causes of syncope/pre-syncope, including Eagle syndrome, carotid body tumor, or pheochromocytoma, should be considered, but unlikely
.
Finally, "hypervigilance" or overinterpretation of benign, nonspecific symptoms is also possible, but unlikely
.
The patient underwent the following examinations, all of which were normal: transthoracic echocardiography, tilt table test, cranial MRI, and head and neck MRA
.
Cardiac monitoring over 30 days found "7 self-limited premature atrial beats, normal sinus rhythm and sinus tachycardia"
.
A 72-hour ambulatory EEG at another institution reported normal
.
Given the patient's psychiatric comorbidities and normal examination, it was speculated that a functional neurological disorder was likely, but her psychiatrist was skeptical and referred the patient to a comprehensive epilepsy center for evaluation
.
Questions to consider: 1.
What further inspections should be performed? What are the further checks? The patient has undergone initial evaluation for cardiovascular and autonomic causes of syncope/pre-syncope
.
Given the normal results, syncope/presyncope is less supportive
.
Ambulatory EEG did not reveal seizures, but focal seizures due to deep lesions could not be ruled out, which may not be obvious or subtle on scalp EEG
.
The patient was admitted to the Epilepsy Monitoring Unit (EMU) for continuous video EEG monitoring for this purpose
.
Results showed dozens of typical events, clinically characterized by back and shoulder extension, neck hyperextension, and accompanying lateral and upward rotation of the head, followed by TAA
.
Interictal EEG shows mixed theta-delta activity of bihemispheric polymorphisms
.
Interictal EEG was normal
.
Although no definite EEG seizures were found, the patient's fairly stereotyped symptoms and consistent EEG pattern made it necessary to consider seizures due to deep lesions (eg, insula/cingulate gyrus)
.
Cranial PET and 7T MRI were normal, 2 magnetoencephalograms were unremarkable, and single-photon emission computed tomography showed "multiple cortical foci with increased radiotracer activity in bilateral temporoparietal regions" (in "Presumptive epilepsy").
radiotracer injection within 10 seconds of onset)
.
The patients tried 7 different antiepileptic drugs (ASMs), but there was no significant change in seizure frequency
.
Questions to consider: 1.
Are there features for or against a diagnosis of epilepsy? 2.
What additional assessments should be considered? What are the additional assessments? Very frequent events with little response to ASM suggest non-epileptic events
.
One year after the patient's initial admission, the patient was re-admitted to the EMU and captured approximately 100 episodes of symptoms that were the same as previously described
.
Attacks only occur during wakefulness
.
On the video EEG, the background was normal prior to the onset of the event
.
The patient then exhibited the same motor behavior described in Part 3, accompanied by a transient decrease in the QRS complex amplitude on the ECG, followed by a very transient, diffuse, polymorphic, mixed theta-delta brain electrical activity
.
The patient subsequently experienced typical TAA
.
A seizure was followed by several clonic movements of the right upper extremity
.
A few seconds after the end of each episode, the patient presses the event button
.
The patient's medical record was reviewed again, and during the first EMU admission, the electrocardiogram had changed
.
Interictal EEG was normal
.
At this time, it is considered as a stretch syncope (Stretch syncope, SS)
.
Patients were referred to a cardiovascular research laboratory, and an experimental protocol was devised to test for potential deficits in arterial pressure and cerebrovascular regulation
.
Focus on the beat-by-beat cardiovascular response of the Valsalva maneuver
.
The Valsalva maneuver induced characteristic 4-phase changes and adequate arterial pressure and cerebrovascular modulation
.
The patient had no typical episodes during breath-holding in the supine, supine, or sitting positions
.
However, during the quiet rest in the seated position, he exhibited frequent motor behavior consistent with his typical events
.
Immediately following these motor behaviors, the patient reported symptoms consistent with his usual episodes
.
Monitoring during these events showed that he performed Valsalva-like movements while stretching, which triggered typical symptoms
.
Arterial pressure and cerebral blood flow decreased more rapidly during stretching events compared with Valsalva maneuvers (Fig.
)
.
The diagnosis of SS was confirmed, and subsequent perspiration evaluation and skin biopsy were consistent with idiopathic small fiber cholinergic neuropathy
.
Figure Cardiovascular and Autonomic Assays
.
Patients who performed the Valsalva maneuver followed by stretching reported typical symptoms
.
Both behaviors included deep breathing (A), decreased ECG amplitude (B), shortened RR interval (C), decreased blood pressure (D), and decreased cerebral blood flow (E)
.
However, the stretch event was shorter in duration than Valsalva, but resulted in a greater drop in blood pressure and cerebral blood flow
.
Discussion Distraction syncope (SS) is a rare, unique entity characterized by TAA caused by neck hyperextension during extension
.
The few published cases occurred between the ages of 7-26, male > female
.
Patients with SS usually have no history of syncope, except as a result of stretching and neck hyperextension
.
Previous studies have reported significant compulsive self-induced seizure episodes in individual patients, but this patient did not have the urge to perform these movements
.
The patient's motor behavior lasts longer than usual tics and is therefore an atypical tic disorder
.
In addition, the patient was treated with a variety of psychotropic medications, some of which were available for obsessive-compulsive disorder and/or tic disorder, with no apparent benefit
.
Although rare, SS can easily be misdiagnosed as epilepsy
.
Causes include: event-related stereotyped motor activity; development of episodic tachycardia; rhythmic/semi-rhythmic slowing on EEG in the presence of transient cerebral hypoperfusion
.
Furthermore, typical presyncope symptoms are not always seen in SS
.
Although the pathophysiology of SS has not been fully elucidated, it is clear that Valsalva maneuvers alone are not sufficient to contribute to SS
.
Earlier reports suggested that SS may be a form of vertebrobasilar insufficiency, possibly related to mechanical compression of the vertebral artery during neck rotation, i.
e.
, SS may be a form of vascular compression syncope, as suggested by other authors.
"Given the delay between stretching and hypotension and the presence of slow-wave EEG abnormalities, a reflex mechanism is likely"
.
Therefore, it can be hypothesized that in SS, when stimuli are superimposed (hyperextension of the neck during stretching), cerebral blood flow is restricted and induces a reverse stretch input to carotid baroreceptors, thereby affecting adequate pressure regulation
.
Thus, despite the decrease in arterial pressure, the stretch of carotid baroreceptors increases and does not provide an adequate sympathetic excitatory response
.
In this patient, small fibercholinergic neuropathy may have contributed to the inability to maintain blood flow through vasodilation when pressure is reduced
.
The decrease in QRS amplitude during SS stretch may be due to the increased distance between the chest wall and the heart during Valsalva/stretch
.
Prompt diagnosis of SS can avoid excessive diagnostic workup and unnecessary use of ASM
.
Furthermore, 'undoing' an epilepsy diagnosis that has been previously made by different specialists can be challenging and requires a strong doctor-patient relationship
.
Avoiding neck hyperextension while stretching effectively eliminates SS
.
The patient was referred for cognitive-behavioral and yogic breathing therapy to facilitate the management of his motor performance, and there was a subsequent decrease in the frequency of seizures
.
Original Index: Mauricio F.
Villamar, J.
Andrew Taylor, JW Hamner, et al.
Clinical Reasoning: A Young Man With Daily Episodes of Altered Awareness.
Neurology published online January 20, 2022.
DOI 10.
1212/WNL.
0000000000200049
