Episodic Impairment Of Consciousness Flashcards
(35 cards)
Causes of temporary loss of consciousness
- Cardiovascular/syncopal transient loss of consciousness
(TLOC)
–cardiac syncope
tachyarrhythmias (supraventricular tachycardia,
ventricular arrhythmias)
bradyarrhythmias (complete atrioventricular block
(AVB), Mobitz type II block)
structural cardiac disease (myocardial infarction,
aortic stenosis)
–orthostatic/postural syncope
extrinsic causes (drugs, dehydration, volume depletion)
postural tachycardia syndrome
autonomic failure (primary, secondary)
–neurally mediated syncope
vasovagal attacks
situational syncope (exercise, micturition, pain, fear)
carotid sinus syndrome
others (breath holding spells, “fainting larks”)
–neurologic/cerebrovascular syncope
transient ischemic attacks (TIAs)
subclavian steal syndrome (SSS)
epilepsy with bradyarrythmias/asystole (ictal asystole)
cough syncope
2. Noncardiovascular/nonsyncopal TLOC**
–epileptic TLOC
grand mal epilepsy
petit mal epilepsy
temporal lobe epilepsy
Panayiotopoulos syndrome
–nonepileptic, neurologic TLOC
excessive sleepiness/“sleep attacks”
other forms of fluctuating vigilance*
increased intracranial pressure (hydrocephalus, colloid
cyst of the third ventricle)
others (basilar migraine)
–medical TLOC
metabolic disorders (hypoglycemia)
neuroendocrine disorders (mast cell activation
disorders, pheochromocytoma, carcinoid syndrome,
idiopathic flushing, medullary thyroid carcinoma)
drugs (alcohol, benzodiazepines, opioids, GHB){
–psychiatric TLOC
“psychogenic nonepileptic seizures”
“psychogenic pseudosyncope”
–traumatic TLOC
- TLOC of unknown origin
Pathophysiological basis of syncope
Gradual failure of cerebral perfusion with a reduction in cerebral oxygen availability
Which are the two groups of symptoms in syncope and which are the symptoms
A) Symptoms of cerebroretinal hypoperfusion blurred or impaired color vision hearing disturbances hallucinations near death experiences involuntary movements (automatisms, limb jerks, myoclonus, spasms, opisthotonus, head turns), ocular motility abnormalities (staring, downbeat nystagmus, upward turning of the eyes) bladder incontinence amnesia confusion “cloudy thinking"
B) Symptoms of autonomic activation facial pallor, sweating palpitations hypersalivation pupillary dilatation yawning nausea hyperventilation
Classification and etiology of syncope
A) Cardiac: 1) Arrhythmias: Bradyarrhythmias Tachyarrhythmias Reflex arrhythmias
2) Decreased cardiac output:
Outflow obstruction
Inflow obstruction
Cardiomyopathy
3) Hypovolemic
4) Hypotensive:
Vasovagal attack
Drugs
Dysautonomia
5) Cerebrovascular: Carotid disease Vertebrobasilar disease Vasospasm Takayasu disease
6) Metabolic:
Hypoglycemia
Anemia
Anoxia
7) Hyperventilation
8) Multifactorial: Vasovagal (vasodepressor) attack Cardiac syncope Situational: Cough, micturition, defecation, swallowing, diving Valsalva maneuver
Pathophysiologic mechanisms of syncope related to hypoperfusion
● insufficient venous return (decreased filling,
increased pooling) (orthostatic syncope)
● insufficient cardiac output (cardiogenic syncope)
● insufficient vascular tone/resistance (thermal stress,
drugs, autonomic neuropathy) (orthostatic syncope)
● insufficient baroreflex function (reflex syncope/
neurocardiogenic syncope)
● increased resistance to cerebral blood flow (cerebral
vasoconstriction, increased pressure in the venous or
cerebrospinal CSF compartments of the brain)
Feautures of cardiogenic syncope
● spells in the supine position ● spells during exertion or effort ● no prodrome (cardiac asystole) ● symptoms and/or signs of structural heart disease ● abnormal ECG ● family history of sudden death
At the end of a cardioarrhythmic syncope, patients
typically present a scarlet flushing discoloration of the
face, secondary to an overshoot in blood pressure
Commmon causes of cardiac syncope
A) Cardiac arrhythmias
1) Intrinsic disease of the conduction system (sinus
node dysfunction, sick sinus syndrome, AV conduction
disorders such as Mobitz type II block, and complete
AVB);
2) Structural cardiac/cardiopulmonary diseases;
channelopathies (Brugada syndrome, long QT syndrome)
3) Drug effects.
B) Structural cardiac disease such as acute coronary
syndrome, acute myocardial infarction, acute aortic dissection, valvular heart diseases (aortic stenosis, pulmonic stenosis), pulmonary embolism, hypertrophic
cardiomyopathy, atrial myxoma, pericardial tamponade.
Definition of orthostatic hypotension
Sustained reduction in systolic blood pressure of>20 mmHg or in diastolic blood pressure of>10 mmHg within 3 minutes of standing or during head-up tilt to at least 60 degrees on a tilt table
Features suggestive of orthostatic suncope
● spells upon standing up
● spells during prolonged sitting or standing
● spells in crowded or hot places
● spells after initiation or changing doses of antihypertensive medications
● spells after eating and after alcohol intake
● spells immediately following exertion
● improvement upon lying down
● lack of autonomic prodrome
● coat-hanger pain, chest pain
● presence of autonomic neuropathy or parkinsonism
Symptoms of orthostatic syncope and which are considered typical for OH
OH is seldom preceded by autonomic manifestations
Symptoms of cerebral or retinal hypoperfusion
are similar to those experienced by patients with
neurally mediated syncope
Typical for OH
1) scotomata and visual hallucinations resulting from occipital ischemia
2) neck pain radiating to the shoulders and head (“coat-hanger” pain) resulting from ischemia of postural neck muscles
3) chest pain resulting from cardiac ischemia
Which are the two pathophysiologic phenomena in OH
1) Initial hypotension
The underlying mechanism is thought to be a transient
mismatch between cardiac output and peripheral
vascular resistance that occurs with rapid postural
changes
2) Delayed hypotension (after 13-30min)
Two pathophysiologic mechanisms probably
account for the observed delayed failure. First, in healthy adults prolonged orthostatic stress leads to continuous decrease in plasma volume of approximately 20% after 10 minutes, due to transcapillary fluid filtration into the interstitial space. Second, the venous capacitance vessels show a slow relaxation leading to additional peripheral
pooling
Etiology of orthostatic syncope
A)Extrinsic causes of OH
1) Medications (most common)
vasodilators, diuretics, common antidepressants
(particularly tricyclics), antiparkinsonian agents
2) Dehydration (prolonged exposure to hot
environments, inadequate fluid intake, volume depletion
due to hemorrhage, diarrhea, or Addison’s disease)
B) Postural tachycardia syndrome
C) Autonomic failure Orthostatic hypotension (OH) may also result from autonomic diseases where adaptation to the upright posture is inadequate. This is found in central nervous system (CNS) disorders such as multiple system atrophies (MSAs) or Parkinson disease (PD), in peripheral nervous system (PNS) disorders such as pure autonomic failure, sequelae from GBS, or postganglionic autonomic polyneuropathies (ganglionopathies).
Postural tachycardia syndrome definition and symptoms
It mainly affects young women, and is characterized
by a marked rise in heart rate while standing without
OH.
PoTS is usually defined as a heart rate increase of>30 beats per minute (bpm) occurring within 10 minutes of standing (>40 bpm for individuals aged 12–19 years), or a heart rate while upright of>120 bpm without a fall in blood pressure
Patients often complain of dizziness,
palpitations, tremulousness, exercise intolerance,
hyperventilation, leg weakness, or fatigue, and some
experience occasional syncope. Symptoms can be exacerbated by exertion, food and alcohol ingestion, and heat. In some patients, onset is linked to a previous infection/ viral illness, Guillain–Barre´ syndrome (GBS),
trauma, or surgery
Primary and secondary autonomic failure
In primary autonomic failure there is primarily a structural autonomic failure typically found in neurodegenerative diseases (MSAs, PD, pure autonomic failure), while secondary autonomic failure occurs in the
context of systemic diseases, such as diabetes mellitus,
chronic renal failure, long-standing alcohol abuse, autosomal dominant familial amyloid polyneuropathy, and GBS with autonomic involvement
Can an autonomic neuropathy occur acutely or subacutely?
An autonomic neuropathy may rarely develop acutely
or subacutely. In such instances of acute pandysautonomia, there is widespread sympathetic and parasympathetic autonomic disintegration leading to severe orthostatic hypotension, anhydrosis, unreactive pupils, impaired lacrimation and salivation, gastrointestinal paresis, and impaired genitourinary function. The clinical spectrum ranges from purely autonomic dysautonomia to autonomic neuropathy with sensory or sensorimotor involvement (GBS with dysautonomia). Chronic and inherited pandysautonomia
is rare. The rare familial dysautonomia (Riley– Day syndrome) has an autosomal recessive inheritance
Which are the major subdivisions of neurally mediated (reflex) syncope
1) Vasovagal (induced by standing)
2) Situational (triggered by different stimuli)
3) Carotid sinus syndrome
4) Other:
Breath holding spells
Fainting larks
Typical presentation of neurally mediated syncope
NMS typically presents with a prodrome preceding the
loss of consciousness by approximately 30–60 seconds
(this is seldom reported by elderly subjects, probably
because of less autonomic activation and greater propensity for amnesia)
Prodrome symptoms:
Facial pallor, cold sweating, yawning, salivation, palpitations, pupillary dilatation, and increased peristalsis.
This is followed by symptoms of cerebral or retinal hypoperfusion such as:
mental changes, lightheadedness, fatigue, visual and hearing changes, hallucinations, and even near death experiences.
Typically, the duration of unconsciousness varies from 10–20 seconds to 5 minutes. This is influenced by body position.
Features characteristic of neurally mediated syncope
● spells following sudden unexpected sight, sound,
smell or pain
● spells after pressure on the carotid sinus (head rotation, shaving, tight collar)
● spells during prolonged standing in crowded and/or
hot places
● spells after eating and alcohol intake
● spells following exertion.
(The last three are also often seen in the context of syncope due to orthostatic hypotension)
Circumastances associated with situational neurally mediated syncope
● exercise
● urogenital triggers: micturition, prostatic massage,
vaginal examination
● gastrointestinal triggers: swallowing, defecation,
rectal examination
● respiratory triggers: airway instrumentation
● pain: venipuncture, trigeminal or glossopharyngeal neuralgia
● fear: sight of blood, needle phobia, blood-injury phobia, dental phobia
● increased intrathoracic pressure: sneezing, coughing,
wind instrument playing, weight lifting, stretching,
breath holding spells, “fainting lark”.
Neurologic causes of syncope (that is, loss of consciousness due to cerebral hypoperfusion)
Most TLOC due to neurologic disorders are not due to
cerebral hypoperfusion
However, the following few exceptions exist:
Transient ischemic attacks (TIAs)
Subclavian steal syndrome (SSS)
Epilepsy leading to cardiac asystole and other cardiac
arrhythmias
Cough syncope
Symptoms suggesting an epileptic transient loss of consciousness
● unusual tastes, smells, de´ja` vu or jamais vu sensations (though not specific for epilepsy; also in Psychiatric disorders), preceding the spell
● lateral tongue biting (though biting at the tip of the tongue can occur during syncope)
● head turning during the spell
● amnesia for the spell
● prolonged confusion or somnolence following the
spell.
Features against TLOC due to epilepsy
Sweating and nausea preceding the spells and their frequent association with prolonged sitting or standing
Forms of epilepsy that can lead to TLOC
● epilepsy with generalized tonic-clonic seizures
● epilepsy with absence seizures
● epilepsy with temporal lobe seizures
● miscellaneous. Syncopal-like episodes have been
described in Panayiotopoulos syndrome
Non-epileptic, non-syncopal neurologic causes of TLOC
● Excessive sleepiness/sleep attacks
(Occasionally “sleep attacks,” mainly in patients with narcolepsy, may present in association with cataplexy, thus mimicking a syncopal episode. However, excessive sleepiness and sleep attacks most commonly present with episodes of altered consciousness without associated postural failure)
● Other forms of fluctuating vigilance
● Increased ICP
(A colloid cyst of the third ventricle
can present with recurrent episodes of TLOC
with or without postural failure. This is typically
accompanied by headaches triggered by changes
in head position. Other manifestations include visual
disturbances, nausea, cognitive disturbances)
● Basilar migraine
(Typically basilar migraine is accompanied by headache and other manifestations of brainstem dysfunction)
