פרק 25 Chapter 25 Disorders of the Autonomic Nervous System, Respiration, and Swallowing Flashcards
Table 25-1
CLINICAL TESTS OF AUTONOMIC FUNCTION
part 1- non invasive bedside tests
Table 25-1
CLINICAL TESTS OF AUTONOMIC FUNCTION
part 2 invasive tests
Table 25-1
CLINICAL TESTS OF AUTONOMIC FUNCTION
part 3 other tests of vasomotor control
Table 25-1
CLINICAL TESTS OF AUTONOMIC FUNCTION
part 4 pupillary function tests
איפה אין מעורבות של אצטיל כולין?
1. נוירון פרה סינפטי סימפטטי
2. נוירון פוסט סינפטי פאראסימפטטי
3. בלוטות זיעה
4. כלי דם
כלי דם
Ach is released at the terminals of all preganglionic fibers (in both the sympathetic and parasympathetic ganglia), as well as at
the terminals of all postganglionic parasympathetic and a few special postganglionic sympathetic fibers, mainly
those subserving sweat glands. Of course, ACh is also the chemical transmitter of nerve impulses to the skeletal muscle fibers. Parasympathetic postganglionic function
is mediated by two distinct types of ACh receptors:
nicotinic and muscarinic
* The postganglionic parasympathetic receptors are located within the innervated organ and are muscarinic; i.e., they are antagonized by atropinic drugs.
* As already mentioned the receptors in ganglia, like those of skeletal muscle, are nicotinic; they are not blocked by atropine but are counteracted by other agents (e.g., tubocurarine).
* With two exceptions, postganglionic sympathetic fibers release only NE at their terminals. The sweat glands and some blood vessels in muscle are innervated
by postganglionic sympathetic fibers, but their terminals, as mentioned, release ACh.
אישה בת 60 עם חולשה מתקדמת ברגליים במשך חמישה חודשים. בבדיקה, נמצאו פרפרזיס ספסטי,
סימן בבינסקי דו צדדי ופלס תחושתי בגובה T6 .
מאילו תסמינים אורינריים סביר שתסבול?
א. דליפת שתן ב Valsalva
ב. כאבים וצריבה בעת הטלת שתן.
ג. דחיפות ותכיפות במתן שתן .
ד. זרימת שתן חלשה
דחיפות ותכיפות בעת הטלת שתן
* Upper spinal cord lesions, above T12 Such lesions result in a reflex neurogenic (spastic) bladder. In addition to multiple sclerosis and traumatic and compressive myelopathies, which are the most common causes, myelitis, neuromyelitis optica, spondylosis, dural arteriovenous fistula, syringomyelia, and tropical spastic paraparesis may cause a bladder disturbance of this type. If the cord lesion is of sudden onset, the detrusor muscle suffers the effects of spinal shock. At this stage, urine accumulates and distends the bladder to the point of overflow. This overflow incontinence is the result of vesicular pressure exceeding the opening pressure of the sphincter in an areflexic bladder. As the effects of spinal shock subside, the detrusor usually becomes reflexively overactive, and because the patient is unable to inhibit the detrusor and control the external sphincter, urgency, precipitant micturition, and incontinence result. Bulbocavernosus and anal reflexes are preserved. The cystometrogram shows uninhibited contractions of the detrusor muscle in response to small volumes of fluid. Most puzzling to the authors have been cases of cervical cord injury in which reflex activity of the sacral mechanism does not return; the bladder remains hypotonic.
* Complete destruction of the cord below T12 This occurs with lesions of the conus, as from trauma, myelodysplasias, tumor, venous angioma, and necrotizing myelitis. The bladder is paralyzed for voluntary and reflex activity and there is no awareness of the state of fullness; voluntary initiation of micturition is impossible; the tonus of the detrusor muscle is abolished and the bladder distends as urine accumulates until there is overflow incontinence; voiding is possible only by the Credé maneuver, that is, lower abdominal compression and abdominal straining. Usually the anal sphincter and colon are similarly affected, and there is “saddle” anesthesia and abolition of the bulbocavernosus and anal reflexes as well as the tendon reflexes in the legs. The cystometrogram shows low pressure and no emptying contractions.
* Disease of the sacral motor neurons in the spinal gray matter, the anterior sacral roots, or peripheral nerves innervating the bladder lumbosacral meningomyelocele and the tethered cord syndrome-lower motor neuron paralysis of the bladder. The disturbance is the same as Complete destruction of the cord below T12 except that sacral and bladder sensation are intact.
Interruption of sensory afferent fibers from the bladder Diabetes and tabes dorsalis are typical causes, motor nerve fibers unaffected. This is a primary sensory bladder paralysis. The disturbance in function is the same as in the two processes earlier Neuropathies affecting mainly the small fibers are the ones usually implicated (diabetes, amyloid, etc.), but urinary retention also occurs in certain acute neuropathies such as Guillain-Barré syndrome.
* Frontal lobe incontinence hyperactivity of the detrusor that results in precipitant voiding. unconcerned by the subsequent incontinence. The bladder itself and the associated sphincter functions are normal as would be seen in a precontinent child.
* Brainstem lesions influencing bladder function isolated pontine lesions as a cause of several different types of micturition difficulties.
* Stretch injury of the bladder wall Repeated overdistention of the bladder wall often results in varying degrees of decompensation of the detrusor muscle and permanent atonia or hypotonia.
הפרעה בתחילת הבליעה
initation of swallowing
אופיינית לכל הבאים פרט ל-
1. מיאסטניה גראביס
2. מחלת נוירון מוטורי
3. מחלת פרקינסון
4. פגיעה בעצב 12
5. פולימיוזיטיס
מחלת פרקינסון לא גורמת לפגיעה בתחילת הבליעה.
A defect in the initiation of swallowing is usually attributable to weakness of the tongue and may be a feature of myasthenia gravis, motor neuron disease or rarely, inflammatory disease of the muscle; it may be caused by palsies of the twelfth cranial nerve (metastases at the base of the skull or meningoradiculitis, carotid dissection), or
to a number of other causes.
Extrapyramidal diseases, notably Parkinson disease, reduce the frequency of swallowing and cause an incoordination of breathing and swallowing
מה לא נכון לגבי ה-
area postrema
1. נמצא אנטומית בבסיס החדר ה-4
2. קשור להקאות
3. איזור שיש בו מחסום דם מוח (BBB)
4. איזור הקשור לתעלות אקוואפורין
אין ב
area postrema
BBB מחסום דם מוח
The main central nervous system structure of
interest in eliciting the vomiting reflex is the area postrema, which is located at the base of the fourth ventricle. The neurons within the area postrema are chemosensitive and are activated by circulating toxins, which have direct access to these neurons because of the absence of a blood brain Barrier.
The vagus carries afferent information from the
enteric system as well as conducting efferent signals from the NTS to the gastrointestinal structures. The neurons in the area postrema contain D2 dopamine, 5-HT3 serotonin, opioids, substance P, and acetylcholine receptors, as well as the aquaporin channel. This affords an explanation for the emetic properties of doparninergic agents and the antiemetic activity of dopamine and serotonin antagonists. However, other potent antiemetics such as ondansetron, a 5-HT3 receptor antagonist, have their effect on vagal afferents.
אפינפין תקין בשכיבה ולא עולה בעמידה
In **the central preganglionic MSA type, the resting NE levels in the plasma are normal but again, on standing, there is no rise, and the response to exogenously administered NE
is normal. **
—-
Autonominc Failure:
This clinical state is now known to be caused by at least two Conditions:
* One is a degenerative disease of middle and late adult life - idiopathic orthostatic hypotension /primary autonomic Failure. In this disorder, the lesions involve mainly the
postganglionic sympathetic neurons; the parasympathetic system is relatively spared and the CNS is uninvolved.
* In the second more common disorder multiple system atrophy, the preganglionic lateral horn neurons of the thoracic spinal segments degenerate; these changes are responsible for the orthostatic hypotension. Later, signs of basal ganglionic or cerebellar disease or both are added.
In both types of orthostatic hypotension, anhidrosis, erectile dysfunction and atonicity of the bladder may be conjoined, but orthostatic fainting is the main problem.
- Primary Orthostatic Hypotension: In the postganglionic type of autonomic failure, plasma levels of NE are subnormal while the patient is recumbent because of failure of the damaged nerve terminals to synthesize or release catecholamines. When the patient stands, the NE levels do not rise, as they do in
a normal person. Also, in this type, there is denervation hypersensitivity to infused NE. - In the central preganglionic MSA type, the resting NE levels in the plasma are normal but again, on standing, there is no
Rise, and the response to exogenously administered NE is normal.
In both types, the plasma levels of dopamine
f3-hydroxylase, the enzyme that converts dopamine to NE, are subnormal
-
Treatment of orthostatic hypotension consists of having the patient sleep with the head of the bed elevated, administering the peripherally acting alpha agonist, midodrine starting at 2.5 mg q4h, slowly raising the dose to 5 mg q4h, taking the last dose before about 7 P.M. to avoid supine hypertension while asleep, and if that is not successful, the mineralocorticoid fludrocortisone acetate
(Florinef) 0.1 mg twice daily.
Upright tilting on a tilt table may cause, within seconds, up to 20 or 25 mm Hg drop in systolic blood pressure and 5 to 10 mm Hg in diastolic pressure in normal individuals, usually with only minor symptoms. In response, the heart rate rises 5 to 15 beats per minute.
There are 2 types of abnormal response to upright tilting:
(1)** early hypotension** (occurring within moments of tilting) that slowly progresses with continued upright posture; this signifies inadequate sympathetic tone and
baroreceptor function;
(2) a delayed (up to several minutes) hypotension that appears abruptly at the end of that period and indicates a neurocardiogenic mechanism.
The normal response to a 60- to 80-degree head-up tilt after approximately 10 min is a transient drop in systolic blood pressure (5 to 15 mm Hg), a rise in diastolic pressure (5 to 10 mm Hg), and a rise in heart rate (10 to 15 beats per minute). Hypotension and fainting after tilting for this duration, a positive test, as already emphasized,
is taken as a proclivity to neurocardiogenic fainting
and at least an ostensible explanation for the problem. However, because it occurs in a proportion of individuals who have never fainted; it is not to be taken as incontrovertible
evidence that a recent spell is explained by this
mechanism.
באיזה מהמחלות הבאות ניתן למצוא שקיעה של
alpha synuclein
1. PSP
2. MSA
3. FTD
4. CBD
5. AD
MSA
איך לזכור-
סינוקלאופתיות= PML
PD, MSA, LBD
הנוירוטרנסמיטר בשרשרת הגנגליונית הפאראוורטברלית הוא אצטיל כולין
The preganglionic neurons of the sympathetic division* originate in the intermediolateral cell column of the spinal gray matter, from the *eighth cervical to the second lumbar segments. The axons of the nerve fibers originating in the intermediolateral column are of small caliber and are myelinated; when grouped, they form the white communicating rami These preganglionic fibers synapse with the cell bodies of the postganglionic neurons, which are collected into two large ganglionated chains or cords, one on each side of the vertebral column (paravertebral ganglia), and several single prevertebral ganglia. These constitute the sympathetic ganglia. and they communicate using ACH!
Axons of the sympathetic ganglion cells are also of small caliber but are unmyelinated. Most of the postganglionic fibers pass via gray communicating rami to their adjacent spinal nerves of T5 to L3; they supply blood vessels
בן 28 , ברקע סכרת נעורים מגיל 8, סובל מאין-אונות (אימפוטנציה). בתשאול, הוא מוסר כי אין לו
יכולת לקבל זקפה כבר שנה, וגם איבד את זקפת הבוקר. פגיעה באיזה גובה של חוט השדרה עשויה
להסביר את תלונותיו?
א. L5-S1 .
ב. S1-S2
ג. S2-S3 .
ד. S3-S4 .
S3- S4
Disturbances of Sexual Function
(1) sexual impulse, drive, or desire, referred to as libido (2) penile erection, (3) ejaculation of semen by the prostate through the urethra.
(1) The arousal of libido involve the limbic system ,the hypothalamus and spinal centers.
(2) Penile erection is effected through sacral parasympathetic motor neurons (S3 and S4), the nervi erigentes, and pudendal nerves.
sympathetic outflow from thoracolumbar segments (originating in T12-L1) via the inferior mesenteric and hypogastric plexuses can mediate psychogenic erections in patients with complete sacral cord destruction.
(3) Ejaculation involves rhythmic under the control of both the sympathetic and parasympathetic centers. parasympathetic centers at S3 and S4 (reflexogenic erections).
Figure 25-1. Sympathetic outflow from the spinal cord and the course and distribution of sympathetic fibers. The preganglionic fibers are in blue; postganglionic fibers are red and purple. (From Pick.)
Figure 25-2. The parasympathetic (craniosacral) division of the autonomic nervous system. Preganglionic fibers extend from nuclei of the brainstem and sacral segments of the spinal cord to peripheral ganglia. Short postganglionic fibers extend from the ganglia to the effector organs. The lateral-posterior hypothalamus is part of the supranuclear mechanism for the regulation of parasympathetic activities. The frontal and limbic parts of the supranuclear regulatory apparatus are not indicated in the diagram (see text). (Reproduced by permission from Noback CL, Demarest R: The Human Nervous System, 3rd ed. New York, McGraw-Hill, 1981.)
Figure 25-3. The sympathetic (thoracolumbar) division of the autonomic nervous system. Preganglionic fibers extend from the intermediolateralnucleus of the spinal cord to the peripheral autonomic ganglia, and postganglionic fibers extend from the peripheral ganglia to the effector organs, according to the scheme in Fig. 25-1. (Reproduced by permission from Noback CL, Demarest R: The Human Nervous System, 3rd ed. New York, McGraw-Hill, 1981.)
Figure 25-4. Innervation of the urinary bladder and its sphincters.
Table 25-1
CLINICAL TESTS OF AUTONOMIC FUNCTION
Figure 25-5. Comparisons of normal responses to the tilt (Control) with orthostatic hypotension (OH). Normal heart rate (HR) increment (>10 BPM and < 30 BPM) is seen in both examples. Blood pressure is stable in a healthy control subject. The right panel shows supine hypertension and marked OH during the tilt. Cerebral blood flow velocity (CBFv) is stable in a control subject and reduced in OH. (Modified and with permission from Novak P: Cerebral blood flow, heart rate, and blood pressure patterns during the tilt test in common orthostatic syndromes. Neurosci J 2016:6127340, 2016 (epub).)
Figure 25-6. Comparisons of three main types of neurally mediated syncope. Syncope is associated with profound decline in blood pressure and in diastolic cerebral blood flow velocity (CBFv). The heart rate and blood pressure responses differentiate each type of syncope while CBFv responses are similar among all syncope types. Heart rate declines before blood pressure in cardiovagal syncope, the heart rate decline is absent in the vasodepressor syncope and heart rate and blood pressure decline simultaneously in mixed syncope. CBFv shows typical vasodilation pattern in all types of syncope that is characterized by decline in diastolic and increase in systolic CBFv. The diastolic CBFv is equal or close to zero during syncope. (Modified and with permission from Novak P: Cerebral blood flow, heart rate, and blood pressure patterns during the tilt test in common orthostatic syndromes. Neurosci J 2016:6127340, 2016 (epub).)
Figure 25-7. The pathways involved in human penile erection. See text for details. (Reproduced by permission from Weiss.)
Figure 25-8. The location of the main centers of respiratory control in the brainstem as currently envisioned from animal experiments and limited human pathology. There are three paired groups of nuclei: (1) The dorsal respiratory group (DRG), containing mainly inspiratory neurons, located in a subnucleus of the nucleus of the tractus solitarius; (2) a ventral respiratory group (VRG), situated near the nucleus ambiguus and containing in its caudal part neurons that fire predominantly during expiration and in its rostral part neurons that are synchronous with inspiration—the latter structure merges rostrally with the Botzinger complex, which is located just behind the facial nucleus and contains neurons that are active mostly during expiration; and (3) a pontine pair of nuclei (PRG), one of which fires in the transition between inspiration and expiration and the other between expiration and inspiration. The intrinsic rhythmicity of the entire system probably depends on interactions between all these regions, but the “pre-Botzinger” area in the rostral ventromedial medulla may play a special role in generating the respiratory rhythm. (Adapted by permission from Duffin et al.)
