פרק 3 Chapter 3 Paralysis and Weakness Flashcards
מה נכון לגבי נוירוטרנסמיטורים?
א. גליצין אקסיטטורי בנוירונים ספינליים
ב. גלוטמט ואספרטט העיקריים במערכת הקורטיקוספינלית היורדת.
ג. אצטיל כולין ברצפטורים מוסקריניים במערכת המוטורית
תשובה ב. גלוטמט ואספרטט העיקריים במערכת הקורטיקוספינלית.
There is considerable information concerning the
pharmacology of motor neurons.
-The large neurons of the anterior horns of the spinal cord contain high concentrations of choline acetyltransferase and use acetylcholine as their transmitter at the neuromuscular junction.
-The main neurotransmitters of the descending corticospinal tract, in so far as can be determined in humans, are aspartate and glutamate.
-Glycine is the neurotransmitter released by Renshaw cells, which are responsible for recurrent inhibition, and by interneurons that mediate reciprocal inhibition during reflex action.
-Gamma-aminobutyric acid (GABA) serves as the inhibitory neurotransmitter of interneurons in the posterior horn.
-L-glutamate and L-aspartate are released by primary afferent terminals and interneurons and act specifically on excitatory amino acid receptors.
בן 70 בעל גורמי סיכון וסקולרים מגיע למיון עם הפרעה בתפקוד של יד שמאל. בבדיקתו תנועות בלתי רצוניות מתמידות ביד שמאל: לעיתים היד למעלה, לעיתים היד מושכת את בגדיו. המטופל טוען ש”אין לו שליטה על היד” מהו המיקום האופייני לאוטם שעלול לגרום לתופעה זו
MRI- DWI-
תשובה א
alien hand. In the absence of volition, the hand and arm undertake complex and seemingly purposeful movements such as reaching into a pocket or handbag, placing the hand behind the head, tugging on the opposite hand or other body part, and rebuttoning the shirt immediately after it has been unbuttoned by the other hand.
Most instances arise as a result of infarction in the territory of the opposite anterior cerebral artery, including the corpus callosum.
Damage in the left supplementary motor area from any cause, as well as from the degenerative parietal lobe disease called corticobasal ganglionic degeneration are associated with a similar alien hand syndrome.
A third form that results from a stroke in the posterior cerebral artery territory with associated sensory loss
מהם סוגי האפרקסיות השונות?
חולה מתבקש לחקות שריקה ומתקשה. מה המיקום של הפגיעה?
א. ג’יירוס סופרה מרג’ינלי
ב. פרה מוטור קורטקס
ג. Ventrolateral nucleus of thalamus
ד. fronto orbital cortex
תשובה א- סופרא מרג’ינל ג’יירוס מקושר לאורל-בוקל-לינגוואל אפרקסיה.
Of a somewhat different nature is an oral-buccal-lingual apraxia, which is probably the most commonly observed of all apraxias in practice. It may occur with lesions that undercut the left supramarginal gyrus or the left motor association cortex and may or may not be associated with the apraxia of the limbs described above. Such patients are unable to carry out facial movements on command (lick the lips, blow out a match, etc.),
איזה מסלול קשור להתפתחות תנועות “מראה” בעיקר בתנועות עדינות ביד?
א. קורטיקוספינלי
ב. רוברוספינלי
ג. וסטיבולוספינלי
תשובה א. קורטיקוספינלי
תשובה ב- היותו אגוניסט של גאבא
-Baclofen, a derivative of GABA, is thought to act by reducing the release of excitatory transmitters from the presynaptic terminals of primary afferent terminals.
-Diazepam and other benzodiazepines have a similar effect but by a different mechanism of potentiating postsynaptic GABA receptors. Actually, none of these agents is entirely satisfactory in the treatment of spasticity when administered orally; the administration of baclofen intrathecally at times has a more beneficial effect.
-The antispasticity agent tizanidine acts by yet another mechanism as an alpha-2 adrenergic agonist, which increases presynaptic inhibition.
-Glycine is the transmitter released by inhibitory interneurons and is measurably reduced in quantity, uptake, and turnover in the spastic animal. There is some evidence that the oral administration of glycine reduces experimentally induced spasticity.
-Interruption of descending noradrenergic, dopaminergic, and serotonergic fibers is undoubtedly involved in the genesis of spasticity, although the exact mode of action of these neurotransmitters on the various components of spinal reflex arcs remains to be defined.
-Gabapentin is chemically similar to GABA, but its anticonvulsant mechanism is not known; it has an apparent effect on calcium channels. It is moderately effective in partial and secondary generalized seizures and has the advantage of not being metabolized by the liver.
תשובה ב. דיאזפם
-Baclofen, a derivative of GABA, is thought to act by reducing the release of excitatory transmitters from the presynaptic terminals of primary afferent terminals.
-Diazepam and other benzodiazepines have a similar effect but by a different mechanism of potentiating postsynaptic GABA receptors. Actually, none of these agents is entirely satisfactory in the treatment of spasticity when administered orally; the administration of baclofen intrathecally at times has a more beneficial effect.
-The antispasticity agent tizanidine acts by yet another mechanism as an alpha-2 adrenergic agonist, which increases presynaptic inhibition.
-Glycine is the transmitter released by inhibitory interneurons and is measurably reduced in quantity, uptake, and turnover in the spastic animal. There is some evidence that the oral administration of glycine reduces experimentally induced spasticity.
-Interruption of descending noradrenergic, dopaminergic, and serotonergic fibers is undoubtedly involved in the genesis of spasticity, although the exact mode of action of these neurotransmitters on the various components of spinal reflex arcs remains to be defined.
-Gabapentin is chemically similar to GABA, but its anticonvulsant mechanism is not known; it has an apparent effect on calcium channels. It is moderately effective in partial and secondary generalized seizures and has the advantage of not being metabolized by the liver.
תשובה 3.
trunk- thigh sign of babinski.
פגיעה באיזה מיקום תגרום לסימפטטיק אפרקסיה ביד שמאל?
sympathetic apraxia
א. פרונטלי ימני
ב. פרונטלי שמאלי
ג. פריאטלי ימני
ד. פריאטלי שמאלי
ה. פריאטלי דו”צ
תשובה ב. פרונטלי שמאלי
The term limb-kinetic apraxia has also been applied to cases of paralysis that obscures the apraxia on one side but causes a breakdown of fine finger movements on the opposite side. This is more properly termed “sympathetic apraxia”. In particular, in a right-handed person, a lesion
in the left frontal lobe that includes Broca’s area, the left motor cortex, and the deep underlying white matter may cause left-limb apraxia. Clinically, there is a non fluent aphasia, a right hemiparesis, and clumsiness of the nonparalyzed left hand.
Sympathetic apraxia in Broca’s aphasia. By destroying the origin of the fibers that connect the left and right motor association cortices, a lesion in the more anterior parts of the corpus callosum or the subcortical white matter underlying Broca area and contiguous frontal cortex causes an apraxia of commanded movements of the left hand.
מטופל עם שבץ כולל אפאזיה מוטורית, חולשה מימין, סרבול תנועות עדינות ביד שמאל. איפה הפגיעה?
א. פרונטלי שמאלי ליד אנטריור קומישור
ב. ברוקה, קורטקס מוטורי שמאלי וחומר לבן עמוק
ג. פונס
ד. פריאטלי דו”צ
תשובה ב. ברוקה, קורטקס מוטורי שמאלי וחומר לבן עמוק
The term limb-kinetic apraxia has also been applied to cases of paralysis that obscures the apraxia on one side but causes a breakdown of fine finger movements on the opposite side. This is more properly termed “sympathetic apraxia”. In particular, in a right-handed person, a lesion
in the left frontal lobe that includes Broca’s area, the left motor cortex, and the deep underlying white matter may cause left-limb apraxia. Clinically, there is a non fluent aphasia, a right hemiparesis, and clumsiness of the nonparalyzed left hand.
Sympathetic apraxia in Broca’s aphasia. By destroying the origin of the fibers that connect the left and right motor association cortices, a lesion in the more anterior parts of the corpus callosum or the subcortical white matter underlying Broca area and contiguous frontal cortex causes an apraxia of commanded movements of the left hand.
מטופל עם הופעה אקוטית של פציאליס במתווה מרכזי בלבד. איפה תהיה הלזיה?
א. גפה קדמית של קפלסולה אינטרנה
ב. קורטקס פרה-סנטרל שמאלי לטראלי
ג. צרברל פידנקל מדיאלי cerebral peduncle
תשובה ג. צרברל פידנקל
This topographic distribution is maintained in the cerebral peduncle, where the corticospinal fibers occupy approximately the middle of the peduncle, the fibers destined to innervate the facial nuclei lying most medially
Table 3-1DIFFERENCES BETWEEN UPPER AND LOWER MOTOR NEURON PARALYSIS
Figure 3-1.
A. Patellar tendon reflex. Sensory fibers of the femoral nerve (spinal segments L2 and L3) mediate this myotatic reflex. The principal receptors are the muscle spindles, which respond to brisk stretching of the muscle affected by tapping the patellar tendon. Afferent fibers from muscle spindles are shown entering only the L3 spinal segment, while afferent fibers from the Golgi tendon organ are shown entering only the L2 spinal segment. In this monosynaptic reflex, afferent fibers entering spinal segments L2 and L3 and efferent fibers issuing from the anterior horn cells of these and lower levels complete the reflex arc. Motor fibers show leaving the S2 spinal segment and passing to the hamstring muscles demonstrate the disynaptic pathway by which inhibitory influences are exerted upon an antagonistic muscle group during the reflex.
B. The gamma loop is illustrated. Gamma efferent fibers (γ) pass to the polar portions of the muscle spindle. Contractions of the intrafusal fibers in the polar parts of the spindle stretch the nuclear bag region and thus cause an afferent impulse to be conducted centrally. The afferent fibers from the spindle synapse with many alpha motor neurons. Because the alpha motor neurons innervate extrafusal muscle fibers, excitation of the alpha motor neurons by spindle afferents causes a cocontraction of the muscle. In this way, both gamma and alpha fibers can simultaneously activate muscle contraction. Both alpha and gamma motor neurons are influenced by descending fiber systems from supraspinal levels. (Adapted by permission from Carpenter MB, Sutin J: Human Neuroanatomy, 8th ed. Baltimore, Williams & Wilkins, 1983.)
Figure 3-2. Corticospinal and corticobulbar tracts. The various lines indicate the trajectories of these pathways, from their origin in particular parts of the cerebral cortex to their nuclei of termination.
Figure 3-3. Lateral (A) and medial (B) surfaces of the human cerebral hemispheres, showing the areas of excitable cortex, numbered according to the scheme of Brodmann. (Reprinted with permission from House EL, Pansky B: A Functional Approach to Neuroanatomy, 2nd ed. New York, McGraw-Hill, 1967.) See also Fig. 22-1.
Figure 3-4. The representation of body parts in the motor cortex, commonly called the motor homunculus. The large area of cortex devoted to motor control of the hand, lips, and face is evident. A in the smaller diagram represents the motor cortex; B is the sensory cortex.
Figure 3-5.
A. Supranuclear facial palsy. There is lower facial weakness contralateral to the lesion, but the upper face is spared due to its bilateral cortical innervation.
B. Nuclear and infranuclear facial palsy. Both upper and lower portions of the face are weak.
Figure 3-6.
A. The plantar response is elicited by stroking from the heel to the ball of the foot.
B. The normal plantar response consists of flexion of the toes.
C. The extensor plantar response (Babinski sign) consists of extension of the great toe coupled with fanning of the remaining digits.
