פרק 2 Chapter 2 Diagnostic Testing in Neurologic Disease Flashcards
למה נגרמת רסטרקציה ברצף דיפוזיה?
א. הגדלת הרווח הבין תאי
ב. בצקת תאית
ג. הגדלה של תנועת מים במוח
ד. עליהבגלוטמט
תשובה ב
Magnetic Resonance Imaging:
hydrogen atoms ‘The image is essentially a map of the hydrogen content of tissue, therefore reflecting largely the water concentration.
** The terms T1- and T2-weighting refer to the time constants for proton relaxation; In T1-weighted images, CSF appears dark and gray matter is hypointense to white matter. In T2-weighted images, CSF appears bright, and gray matter is hyperintense to white matter.
Lesions within the white matter, such as the demyelination of multiple sclerosis, are more easily seen on T2-weighted images, appearing hyperintense against normal white matter (Table 2-3).
Lesions near the skull base and within the posterior fossa, in particular, are seen with greater clarity on MRI
products of disintegrated RBCs—oxyhemoglobin, deoxyhemoglobin, methemoglobin, and hemosiderin—can be recognized, enabling one to approximate the age of hemorrhages and to follow their resolution.
** Gradient-echo (GRE), or susceptibility weighted imaging (SWI), is especially sensitive to blood and its breakdown products that appear hypointense.
** FLAIR (bright signal of fluid that is not contained within tissues is suppressed. useful for lesions located near CSF compartments.
Fat suppression, demonstration of inflammation of the optic nerve, visualize pathologic inflammation within the vertebral bodies, and show thrombus within the false lumen of a cervical dissection.
** Diffusion-weighted imaging (DWI) is a technique that measures the free diffusion of water molecules within tissue. movement of water molecules along a particular direction, In acute ischemic stroke, failure of the sodium-potassium ATPase pump leads to cellular swelling and reduced intercellular space, thus limiting the free movement of water and producing hyperintensity on DWI. This imaging technique reveals the abnormalities of ischemic stroke earlier than standard T1- or T2-weighted MRI.
Pus-filled abscesses and hypercellular tumors can also show DWI hyperintensity, reflecting the limitation of free diffusion of water in these lesions.
True restricted diffusion, appearing hyperintense on the DWI sequence in acute infarction, is hypointense on a related sequence termed apparent diffusion coefficient (ADC).
** If the hyperintense DWI signal is also hyperintense on ADC, then diffusion is termed facilitated rather than restricted.
מטופלת לאחר לידה עם כאב ראש מבצעת הדמיות.
בהדמיית CT- ממצא היפודנסי בקרן קדמית של חדר לטרלי.
MRI- T1 ממצא היפודנסי שאינו עובר האדרה עם גדוליניום
MRI-T2 ממצא היפודנסי
מה הממצא?
אוויר
MRS
ד. decreased NAA increased Choline
The tissue concentrations of a variety of cellular metabolites
can be determined with the technique of magnetic
resonance spectroscopy (MRS). Among these substances,
N-acetyl aspartate (NAA) is a marker of neuronal integrity;
and is decreased in both destructive lesions and in
circumstances in which there is a reduction in the density
of neurons (e.g., edema or glioma that increases the
distance between neurons).
Choline (Cho), a marker of
membrane turnover, is elevated in some rapidly dividing
tumors.
Therefore, compared to normal white matter, the
spectrogram of a glioma characteristically shows decreased
NAA and increased Cho.
אישה לאחר תאונת דרכים מתלוננת שאינה שומעת בשתי האוזניים, איזו בדיקה תסייע להראות שמדובר במצב לא אורגני?
א. אודימטריה
ב. BERA
ג. ENG
תשובה ב. BERA
מה משמעות הגלים השונים בBERA/BEAP
מהו הכלי השימושי לזיהוי פגיעה במסלולי המערכת האודיטורית
EMG
עוזרת באבחון מיופתיה ע”י
א. מאמתת את ההשערה הקלינית
ב. ממקדת את המיקום האופטימלי לביופסיית שריר
ג. מבדילה בין מחלה נוירוגנית למיופתית
ד. מעידה על חומרת המחלה
ה. כל הנ”ל
תשובה ה
תשובה ד.
1+2
3=not unit because units aren’t rythmic
מאפייני מיופתיה בEMG הם:
א. גיוס ירוד של יחידות קטנות
ב. גיוס מופחת של יחידות קטנות
ג. גיוס מוקדם של יחידות גדולות
ד. גיוס מוקדם של יחידות קטנות
ה. פיברילציות
התשובה היא ד. גיוס מוקדם של יחידות קטנות.
פיברילציות אפשריות אך לא מאפיינות.
מופחת= נוירוגני
מוקדם= מיופתי
מה המשמעות של פיברילציות במיופתיה?
(positive sharp waves/ fibrilations)
א. דנרבציה של סיבי שריר
ב. נקרוזיס של סיבי שריר
ג. נוירופתיה בנוסף למיופתיה
ד. מחלת נוירון מוטורי עם מיופתיה
ה. א+ב
תשובה ה. א+ב
תשובה 2.
CMT1
תשובה 3.
דה מיאלינטיבי= הורדה במהירות= latency
אקסונלי =decreased CMAP
Repetitive motor nerve stimulation מה מאפיין את המבחן
א. באדם בריא קיימת ירידה באמפליטודה בשריר דיסטלי בגירויים חזקים חוזרים בקצב של 3 הרץ (CMAP)
ב. ירידה ב5 אחוזים באמפליטודה של שריר טרפזיוס בגירוי עצב אקססורי בקצב של 3 הרץ אופיינית רק למיאסטניה גרביס
ג. גירוי טטני גורם לעלייה באמפליטודה בשריר שהוזרק בו בוטוליניום טוקסין.
ד. במיאסטניה גראביס הירידה באמפליטודה גדולה יותר בשרירים דיסטאליים (CMAP)
ה. הירידה באמפליטודה פוחתת בגירוי טטני (20 הרץ) עם מתן נאוסטיגמין.
התשובה היא ג- גירוי טטני גורם לעלייה באמפליטודה בשריר שהוזרק בו בוטוליניום טוקסין.
Characteristic of myasthenia
is a rapid reduction in the amplitude CMAP during a series of repetitive stimulations of a peripheral nerve at a rate of 3 per second (decrementing response as shown in Fig. 45-4A). Reversal of this response by neostigmine or edrophonium has been
a reliable confirmatory finding in most cases.
A decremental response to stimulation can usually be obtained most often from the proximal limb muscles followed by the facial and, to a lesser extent, the hand muscles, which may or may not be clinically weak.
In certain disorders, notably myasthenia
gravis, a train of 4 to 10 stimuli at rates of 2 to 5
per second (optimally 2 to 3 per second), the amplitude of the motor potentials decreases and then, after four or five further stimuli, may increase slightly (Fig. 45-4A). A progressive reduction in amplitude is most likely to be found in proximal muscles.
The Lambert-Eaton myasthenic syndrome, often
associated with oat cell carcinoma of the lung, is characterized by a presynaptic blockage of acetylcholine release and produces the opposite defect of neuromuscular transmission to the one recorded in myasthenia gravis.
During tetanic stimulation (20- to 50-per-second repetitive stimulation of nerve), the muscle
action potentials, which are small or practically absent with the first stimulus, increase in voltage with each successive response until a more nearly normal amplitude is attained. Exercising the muscle for 10 s before stimulation will cause a similar posttetanic facilitation in patients with the Lambert-Eaton syndrome (200-fold increases are not uncommon).
A less important decremental response to slow stimulation may occur, but it is difficult to discern because of the greatly diminished amplitude of the initial responses. Neostigmine has little effect on this phenomenon, but it is reversed by guanidine and 3,4-diaminopyridine, which stimulate the presynaptic release of ACh.
The effects of botulinum toxin and of aminoglycoside antibiotics are similar, i.e.,
being active at the presynaptic membrane, they produce an incremental response at high rates of stimulation.
EMG- בנקודה המסומנת הכו על הגיד עם פטיש רפלקסים.
א. מיוטוניה
ב. מיוקימיה
ג. continuus muscle activity
ד. מנוחה
תשובה א. מיוטוניה.
How can the EMG NCS help us differentiate between a congenital type of demyelination and an acquired type of demyelination
1. distal latency
2. CMAP amplitude
3. Temporal dispersion
4. prolonged F wave
- temporal dispersion- במולדת אין בלוקים ולכן לא יהיה פיזור בזמן.
A distinctive feature of hereditary neuropathy is the uniformity of the electrophysiologic changes, e.g., a similar degree of slowing of nerve conduction velocity in all the nerves, a feature that distinguishes this group from most acquired neuropathies.
The distinction between the demyelinating and axonal types of inherited neuropathies is based on the motor nerve (typically ulnar or median nerve) conduction velocities in the arms, with slowing to velocities below 38 m/ s defining the demyelinating category.
Conduction block: A reduction of proximal CMAP area/amplitude of at least 20% (usually > 50%) compared with distal CMAP area/amplitude. The duration of the proximal CMAP should not increase by > 20% (see temporal dispersion).
Temporal dispersion: A reduction in proximal CMAP amplitude compared with distal CMAP amplitude when the proximal CMAP duration increases by > 20%.
Conduction block or temporal dispersion both result in a reduction in CMAP amplitude. The CMAP area is used to assess the contribution of these two processes. In conduction block there is complete failure of conduction in some or all of the motor axons studied. Therefore the CMAP area with stimulation proximal to site of conduction block is smaller (> 20% reduction) compared with distal stimulation (fig 4). For true conduction block to be detected, the proximal CMAP duration must not increase by > 20%. In temporal dispersion (fig 4) there is a loss of synchrony in the nerve action potentials resulting in a loss of CMAP amplitude because the positive part of one muscle fiber action potential cancels out the negative part of another.
תשובה ג. הפקה של גירוי תקין משרירים אולנריים לאחר גירוי פרוקסימלי של העצב המדיאני.
The examiner should also be aware of a normal variant, the Martin-Gruber anastomosis that exists in close to 20 percent of individuals; in this configuration, axons from the median nerve cross into the ulnar nerve in the mid-forearm to innervate normally ulnar associated muscles in the hand. Distal stimulation of the ulnar nerve then gives higher amplitude ulnar CMAP than proximal stimulation, simulating conduction block, but without weakness or atrophy. The anastomosis can be demonstrated by obtaining a normal CMAP when stimulating the proximal median nerve and recording over ulnar innervated muscles
תשובה ב. רפלקס זה הוא רפלקס סנסורי
תשובה 5. גירוי כאב.
Patients are usually examined with their eyes
closed and while relaxed in a comfortable chair or bed. Consequently, the ordinary EEG represents the electrocerebral activity that is recorded under restricted circumstances, usually during the waking or sleeping state, from
several parts of the cerebral convexities during an almost infinitesimal segment of the person’s life.
In addition to the resting record, a number of so called activating procedures are usually employed. First, the patient is asked to breathe deeply 20 times a minute for 3 min. Hyperventilation, through a mechanism yet to be determined, may activate characteristic seizure patterns or other abnormalities.
Second, a powerful strobe light is placed about 15 inches from the patient’s eyes and flashed at frequencies of 1 to 20 per second with the patient’s eyes open and closed. In a healthy subject, the
occipital EEG leads show waves corresponding to each flash of light (photic driving, Fig. 2-SB). The EEG is recorded after the patient is allowed to fall asleep naturally or occasionally, following the administration of sedative drugs. The drowsy state and the transition to and from deeper stages of sleep can reveal abnormalities.
מה יגרום לנוזל שדרה בצבע צהוב?
א. חלבון מעל 1000
ב. גלוקוז מעל 200
ג. 50 תאים אדומים
ד. 200 תאים לבנים
תשובה א. חלבון מעל 1000
Gross Appearance and Pigments:
-red blood cells imparts a hazy or ground-glass appearance; at least 200 red blood cells (RBCs) per cubic millimeter (mm3) must be present to detect this change. The presence of 1,000 to 6,000 RBCs per cubic millimeter imparts a hazy pink to red color.
-white blood cells (WBCs) in the fluid (pleocytosis) may cause a slight opaque haziness.
-In subarachnoid hemorrhage, the RBCs begin to hemolyze within a few hours, imparting a pink-red discoloration (erythrochromia) to the supernatant fluid; if the spinal fluid is sampled more than a day following the hemorrhage, the fluid will have become yellow-brown (xanthochromia).
With subarachnoid hemorrhage, the proportion of WBCs rises as RBCs hemolyze, sometimes reaching a level of several hundred per cubic millimeter;
The pigments that discolor the CSF following subarachnoid hemorrhage are oxyhemoglobin, bilirubin, and methemoglobin
Not all xanthochromia of the CSF is caused by hemolysis of RBCs. With severe jaundice, both conjugated and unconjugated bilirubin diffuses into the CSF. The quantity of bilirubin in the CSF ranges from one-tenth to one-hundredth that in the serum. –Elevation of CSF protein from any cause results in a faint opacity and xanthochromia. Only at protein levels greater than 150 mg/100 mL does the coloration become visible to the naked eye.
-Hypercarotenemia and hemoglobinemia (through hemoglobin breakdown products, particularly oxyhemoglobin) also impart a yellow tint to the CSF, as do blood clots in the subdural or epidural space of the cranium or spinal column. Myoglobin does not appear in the CSF because a low renal threshold for this pigment permits rapid clearing from the blood.
תשובה ב.
The fluid from a traumatic tap should contain approximately one or two WBCs per 1,000 RBCs assuming that the hematocrit and white blood cell count are normal, but in reality this ratio varies. With subarachnoid hemorrhage, the proportion of WBCs rises as RBCs hemolyze, sometimes reaching a level of several hundred per cubic millimeter;
Table 2-1CHARACTERISTIC CSF FORMULAS
Table 2-2AVERAGE VALUES OF CONSTITUENTS OF NORMAL CSF AND SERUM
Table 2-3CT AND MRI IMAGING CHARACTERISTICS OF VARIOUS TISSUES
Table 2-4MAIN SENSORY EVOKED POTENTIAL LATENCIES FROM STIMULUS (MILLISECONDS)a
Table 2-5NORMAL VALUES FOR REPRESENTATIVE NERVE CONDUCTION VALUES AT VARIOUS SITES OF STIMULATION (MEAN VALUES ± 2 SD FOR ADULTS 16 TO 65 YEARS OF AGE)
what are the different waves of a normal EEG
Figure 2-1. Normal CT in the axial plane of the brain, orbits, and skull base.
A. Image through the cerebral hemispheres at the level of the corona radiata. The dense bone of the calvarium is white, and fat-containing subcutaneous tissue is dark. Gray matter appears denser than white matter due to its lower lipid content.
B. Image at the level of the lenticular nuclei. The caudate and lenticular nuclei are denser than the adjacent internal capsule. CSF within the frontal horns of the lateral ventricles as well as surrounding the slightly calcified pineal body appears dark.
C. Image through the mid-orbits. The sclera appears as a dense band surrounding the globe. The optic nerves are surrounded by dark orbital fat. The medial and lateral rectus muscles lie along the orbital walls and have a fusiform shape. Air within the nasopharynx and paranasal sinuses appears dark.
D. Image at the base of the skull, digitally adjusted to visualize bone (“bone window”), showing the basal occipital and temporal
bones, clivus, the bony structures of the posterior nasopharynx, aerated mastoid air cells, internal auditory canals and inner ear structures, as well as the sutures in the occipital bone.
Figure 2-2. CT myelogram and MRI of the lumbosacral spine. Sagittal (A) and axial (B–C) CT images of the lumbosacral spine obtained after the intrathecal administration of radiopaque contrast material. The vertebral bodies are separated by intervertebral discs and the spinous processes are seen posteriorly. Contrast contained within the thecal sac appears white. The conus medullaris terminates at the L2 vertebral level (A–B) and the nerve roots of the cauda equina are clearly seen within the posterior thecal sac (A–C). Sagittal (D) and axial (E–F) T2-weighted MRI of the lumbosacral spine shows hyperintense CSF surrounding the conus medullaris, which terminates at the L1 vertebral level (A–B). The nerve roots of the cauda equina are seen within the posterior thecal sac (A–C). In C and F, traversing nerve roots within the lateral recess of the spinal canal are seen.
Figure 2-3. Normal brain MRI.
A. Axial T2-weighted MRI at the level of the lenticular nuclei. Gray matter appears brighter than white matter. CSF within the ventricles and cortical sulci is very bright. The caudate nuclei, putamen, and thalamus appear brighter than the internal capsule.
B. Axial T2-weighted MRI at the level of the pons. Subcutaneous fat and calvarial marrow appear relatively bright. CSF within the fourth ventricle and prepontine cistern, endolymph within the cochlea and semicircular canals, and ocular vitreous fluid appears very bright. Signal is absent (i.e., a “flow void”) within the basilar artery.
C. Midline sagittal T1-weighted MRI of the brain. Note that white matter appears brighter than gray matter and the corpus callosum is well defined. The pons, medulla, and cervicomedullary junction are well delineated, and the pituitary gland is demonstrated with a normal posterior pituitary bright spot. The cerebral aqueduct is seen between the ventral midbrain and the tectum. The clivus and upper cervical vertebrae are noted as well.
D. Axial T2-weighted fluid-attenuated inversion recovery (FLAIR) MRI of the brain at the
same level as in A. Note that the hyperintense fluid signal from CSF is now suppressed, and the differentiation between brighter gray matter and darker white matter is accentuated.
Figure 2-4. Intracranial and cervical angiography.
A. Oblique CT angiogram of the neck showing the carotid bifurcation and the cervical segments of the internal and external carotid arteries. Note the slightly dilated carotid bulb at the initial segment of the internal carotid artery. A small focus of calcified atherosclerosis is noted near the origin of the external carotid artery. Note that the external carotid artery has multiple branches within the neck.
B. Coronal MR angiogram of the neck showing the aortic arch, the origins and cervical courses of the carotid and vertebral arteries, and the vertebrobasilar junction. The sigmoid sinuses and internal jugular veins are faintly visible.
C–D. Sagittal dynamic CT angiography of the head. Bony and soft tissue structures as well as brain parenchyma have been digitally subtracted. The image C was acquired during the arterial phase; the carotid and basilar termini and the anterior cerebral arteries are enhanced. Venous phase imaging (D) shows
enhancement of the superior and inferior sagittal sinuses, straight sinus, vein of Galen, internal cerebral veins, basal veins of Rosenthal, and the transverse and sigmoid sinuses.
Figure 2-5. Blood oxygen level-dependent (BOLD) functional MRI. The image shown is from a subject performing repetitive motor functions (tapping a button) with his right finger. Superimposed upon the grayscale structural MRI image are areas of altered BOLD signal, in color, associated with the task. The most prominent signal (yellow) is in the left lateral cerebral cortex, corresponding to the right hand area of the precentral and postcentral gyri. Other sites of lesser signal (red, orange) include the supplementary motor area, which is near the midline anteriorly. (Image courtesy of Dr. Michael D. Fox. From Fox MD, Snyder AZ, Zacks JM, Raichle ME: Coherent spontaneous activity accounts for trial-to-trial variability in human evoked brain responses. Nat Neurosci 9:23, 2006. Reproduced with permission.)
Figure 2-6. Axial 18FDG-PET of a normal brain. The PET data is colorized and overlaid on a CT image. Brain areas with higher metabolic activity such as cortex and deep gray nuclei appear bright, and areas with lower metabolic activity such as white matter appear purple.
Figure 2-7
A. “10-20” is a measurement system designed to reliably reproduce electrode positions on different patients, regardless of head size.
Electrodes are placed at intervals of either 10 or 20 percent of the hemi-circumference of the head. (Courtesy of Dr. Jay S. Pathmanathan.)
B. Each channel represents the amplified recording of voltage changes over time between two electrodes. Normal alpha (8 to 12 per second) activity is present posteriorly (bottom channel). The top channel contains a large blink artifact. Note the striking reduction of the alpha rhythm with eye opening (arrow). C. Photic driving. During stroboscopic stimulation of a normal subject, a visually evoked response is seen posteriorly after each
flash of light (signaled on the bottom channel).
Figure 2-7
D. Stroboscopic stimulation at 14 flashes per second (bottom channel) has produced a photoparoxysmal response in this epileptic patient, evidenced by the abnormal spike and slow-wave activity toward the end of the period of stimulation.
E. Large, slow, irregular delta waves are seen in the right frontal region (channels 1 and 2). In this case a glioblastoma was found in the right cerebral hemisphere, but the EEG does not differ basically from that produced by a stroke, abscess, or contusion.
F. An EEG showing focal spike-and-wave discharges over the right frontal region (channels 1 to 3). The box isolates a single spike–wave transient.
Figure 2-7
G. Phase reversal is shown between electrode pairs, F7-T3 and T3-T5, implying that the site of the spike generator is under the T3 electrode. (Courtesy of Dr. Jay S. Pathmanathan.)
H. Localization of a spike in a montage that utilizes the right ear (A2) as a reference electrode. The amplitude of the transient at T3 is greater than at other locations, implying that the source of the spike is closest to the T3 electrode. (Courtesy of Dr. Jay S. Pathmanathan.)
I. Absence seizures, showing generalized 3-per-second spike-and-wave discharge. The abnormal activity ends abruptly and normal background activity appears.
Figure 2-7
J. Deep coma following cardiac arrest, showing electrocerebral silence. With the highest amplification, electrocardiogram (ECG) and other artifacts may be seen, so that the record is not truly “flat” or isoelectric. However, no cerebral rhythms are visible. Note the ECG (lower channel).
K. Grossly disorganized background activity interrupted by repetitive “pseudoperiodic” discharges consisting of large, sharp waves from all leads about once per second. This pattern is characteristic of Creutzfeldt-Jakob disease.
L. Advanced hepatic coma. Slow (about 2 per second) waves have replaced the normal activity in all leads. This record demonstrates the triphasic waves often seen in this disorder.
Figure 2-8. Pattern-shift visual evoked responses (PSVERs). Latency measured to first major positive peak (termed P100 because of its latency from the stimulus of approximate 100 ms) and marked by “o.” Upper two tracings: These, from the right and left eyes, are normal. Middle tracings: PSVER from the right eye is normal but the latency of the response from the left eye is prolonged and its duration is increased. Lower tracings: PSVER from both eyes show abnormally prolonged latencies, somewhat greater on the left than on the right. Calibration: 50 ms, 2.5 mV.
Figure 2-9. Short-latency brainstem auditory evoked responses (BAERs). Diagram of the proposed electrophysiologic–anatomic correlations in human subjects. Waves I through V are the ones measured in clinical practice.
Figure 2-10. Short-latency SEPs produced by stimulation of the median nerve at the wrist. The set of responses shown at left is from a normal subject; the set at right is from a patient with multiple sclerosis who had no sensory symptoms or signs. In the patient tracing, note the preservation of the brachial–plexus component (EP), the absence of the cervical cord (N11) and lower-medullary components (N/P13), and the latency of the thalamocortical components (N19 and P22), prolonged above the normal mean +3 SD for the interval from the brachial plexus potential. Unilateral stimulation occurred at a frequency of 5 per second. Recording electrode locations are as follows: FZ, midfrontal; EP, the Erb point (the shoulder); C2, the middle back of the neck over the C2 cervical vertebra; and Cc, the scalp overlying the sensoriparietal cortex contralateral to the stimulated limb. Relative negativity at the second electrode caused an upward trace deflection. Amplitude calibration marks denote 2 mV. (Reproduced by permission from Chiappa and Ropper.)
Figure 2-11. The median nerve is stimulated percutaneously (1) at the wrist and (2) in the antecubital fossa with the resultant compound muscle action potential recorded over the abductor pollicis brevis (arrow).The motor waveform is recorded as the voltage between the surface electrode and a reference electrode (Ref.) more distally. Sweep 1′ on the display depicts the stimulus artifact followed by the compound muscle action potential. The distal latency, A′, is the time from the stimulus artifact to the onset of the compound muscle action potential and corresponds to conduction over distance A. The same is true for sweep 2′, where stimulation is at site 2 and the time from the artifact to the response is B′. The maximum motor conduction velocity over segment C is calculated by dividing the distance between the two stimulating electrodes, C, by the time C′.
Figure 2-12. The principal pathologic alterations of CMAP.
A. The normal CMAP, representing the summed discharges from a group of motor units activated by a supramaximal stimulus, measured over the muscle.
B. With loss of motor axons, fewer motor units are activated and the CMAP has reduced amplitude.
C. With demyelination of motor axons, the same number of motor units activate, but over a prolonged duration; thus the CMAP has reduced amplitude because there is temporal dispersion of the waveform.
Figure 2-13. SNAP recording.
A. Electrical stimulation of the median nerve at the wrist with recording of sensory action potentials at two sites in the second digit. The responses are generated by antidromic propagation of action potentials from the site of stimulation.
B. A SNAP recorded from G1. Sensory nerve conduction velocity can be calculated by dividing the distance between G1 and G2 by the difference in onset latencies from these two sites.
Figure 2-14. Late responses.
A. The H reflex is elicited by stimulating a sensory nerve. The action potentials travel in an orthodromic fashion through the dorsal root into the spinal cord, where synapses occur with motor neurons. The motor axons innervate a muscle (the gastrocnemius) from which the late CMAP response is recorded.
B. The F response is elicited by stimulating a motor nerve. Some of the action potentials that have traveled in an antidromic fashion though the anterior horn are volleyed back in an orthodromic fashion along the same motor neurons. The late CMAP response is recorded from the muscle innervated by these axons.
Figure 2-15. Repetitive stimulation of the hypothenar muscles.
A. Patient with myasthenia gravis—typical pattern of decrement in first four responses followed by slight increment. At this rate of stimulation (3 per second), the decrement in response does not continue to zero.
B. Patient with Lambert-Eaton syndrome and oat cell carcinoma— marked increase from low toward normal amplitude with rapid repetitive stimulation (20 per second). Horizontal calibration: 250 ms.
Figure 2-16. The shaded areas on the muscle (A, B, and C) represent zones of the propagating action potential depicted by the dashed arrow. The correspondingly lettered portions of the triphasic muscle action potential displayed on the screen reflect the potential difference between the active (vertical arrow) and reference (Ref.) electrodes. Polarity in this and subsequent figures is negative upward as depicted.
Figure 2-17. Patterns of motor unit recruitment.
A. Normal. With each increment of voluntary effort, more and larger units are brought into play until, with full effort at the extreme right, a complete “interference pattern” is seen in which single units are no longer recognizable.
B. After denervation, only a single motor unit is recorded despite maximal effort. It is seen to fire repetitively.
C. With myopathic diseases, a normal number of units are recruited on minimal effort, though the amplitude of the pattern is reduced. Calibration: 50 ms (horizontal) and 1 mV (vertical).
Figure 2-18. Abnormal spontaneous activity.
A. Positive sharp waves and fibrillations recorded from a paralyzed, denervated muscle. A typical positive sharp wave is seen above the star. The fibrillations (arrow) are 1 to 2 ms in duration, 100 to 300 mV in amplitude, and largely negative (upward) in polarity following an initial positive deflection.
B. Fasciculation. This spontaneous motor unit potential was recorded from a patient with amyotrophic lateral sclerosis. It has a serrated configuration and it fired once every second or two. Calibrations: 5 ms (horizontal) and 200 μV in A; 1 mV in B (vertical).
Figure 2-19. A. Myotonia congenita (Thomsen disease). The five lines are a continuous record of activity in the biceps brachii following a tap on the tendon. The initial response is within normal limits, but it is followed by a prolonged burst of rapid activity, gradually subsiding over a period of many seconds or minutes.
B. Same electrode placement as in A. Response to the fifth of a series of tendon taps. “Warmup” has occurred, and the characteristic prolonged myotonic activity is no longer evident.
Figure 2-20. Normal, myopathic, and reinnervated motor units. The colored muscle fibers are functional members of one motor unit, whose axon enters from the upper left and branches terminally to innervate the appropriate muscle fibers. The action potential produced by each motor unit is seen to the right: its duration is measured between the two vertical lines. The normal-appearing but uncolored fibers belong to other motor units.
A. There are five muscle fibers illustrated in the active unit.
B. In this myopathic unit, only two fibers remain active; the other three (shrunken) were affected by one of the primary muscle diseases.
C. Four fibers that originally belonged to other motor units and had been denervated are now reinnervated by terminal sprouting from an undamaged axon. Both the motor unit and its action potential are now larger than normal. Note that only under these abnormal circumstances do fibers in the same unit lie next to one another.
