פרק 42- Chapter 42 Diseases of the Spinal Cord Flashcards
Table 42-1
MAJOR VERTEBRAL FRACTURES AND DISLOCATIONS (9)
באיזו מחלה ראומטית פחות צפוי סיבוך של מיאליטיס ?
א. Behçet’s disease
ב. Rheumatoid arthritis
ג. Sjӧgren disease
ד. Systemic Lupus Erythematosus
בrehumatoid arthritis
פחות צפוי לראות סיבוך של מיאליטיס
נרקומנית עם מחלה חריפה של חום גבוה ופאראפרזיס ובהדמיה תהליך תופס מקום לומברי או תוראקאלי
מהו התהליך בסבירות הגבוהה?
1. אבצס אפידורלי
2. בלט דיסק
3. אפנדימומה
4. גרנולומה מסויידת
אבצס אפידורלי
בת 22 . לאחר הרדמה אפידוראלית, פיתחה חום, כאבי גב עזים וחולשה ברגליים. מהו המחולל הנפוץ
ביותר לסיבוך זה?
א. Anaerobic bacteria
ב. Listeria monocytogenes
ג. Staphylococcus aureus
ד. Streptococcus agalactiae
סטאף אארוס
מטופל מבוגר עם טיפול בקומדין עקב פרפור, תיאור של פלס פתאומי בגובה T6
בניקור- קסנטוכרומיה. CT ראש תקין
- המטומיאליה
- דימום בפאלקס
- bilateral ACA
- אוטם באדמקביץ’
המטומיאליה
Hemorrhage into the spinal cord is rare compared with the frequency of cerebral hemorrhage. The apoplectic onset of symptoms that involve spinal
tracts (motor, sensory, or both), associated with blood and xanthochromia in the spinal fluid are the identifying features of hematomyelia. Aside from trauma, hematomyelia is usually traceable to a vascular malformation or a bleeding disease and particularly to the administration of anticoagulants.
Actually, most vascular malformations of the spinal cord do not cause hemorrhage, but instead produce a progressive, presumably ischemic myelopathy as described later and mentioned in the earlier section on the FoixAlajouanine type of subacute necrotic myelopathy.
The same causes (anticoagulation, blood dyscrasia with coagulopathy, and arteriovenous malformation [AVM]) may underlie bleeding into the epidural or subdural space and give rise to a rapidly evolving compressive myelopathy. In some cases, as in those of Leech and coworkers, one cannot ascertain the source of the bleeding, even at autopsy. Epidural or subdural bleeding, like epidural abscess, represents a neurologic emergency and calls for immediate localization by imaging and, in some cases, surgical evacuation.
מהו הסימפטום המכוון ל-
conus medularis
ולא ל-
cauda equina
1. חולשה סימטרית ברגליים
2. כאבים חד צדדים
3. איבוד שליטה על סוגרים
4. ארפלקסיה
התשובה היא חולשה סימטרית ברגליים- מכוון יותר לקונוס מאשר לקאודה בגלל שקאודה זו פגיעה שורשית והיא אסימטרית.
* Lesions of the cauda equina alone, always difficult to separate from those of the lumbosacral plexuses and multiple nerves, are usually attended in the early stages by sciatic and other root pain and lumbar ache, which are variously combined with a bilaterally asymmetrical, atrophic, areflexic paralysis, radicular sensory loss, and
sphincteric disorder.
- These must be distinguished from lesions of the conus medullaris (lower sacral segments of the spinal cord), in which there are early disturbances of the bladder and bowel (urinary retention and constipation- atonicity), back pain, symmetrical hypesthesia or anesthesia over the sacral dermatomes, a lax anal sphincter with loss of anal and bulbocavernosus reflexes, impotence, and sometimes weakness of leg muscles. Sensory abnormalities may precede motor and reflex changes by many months.
arterio-venous malformation
-
Intramedullary AVM The true spinal cord AVM, previously referred to as angioma racemosum venosum or dorsal extramedullary arteriovenous malformation, is typically located on the dorsal surface of the lower half of the spinal cord and occurs most often in middle- aged and elderly men. However, this lesion may occur at any age and at any location in the cord and may be quite widespread. In a few cases has there been an overlying dermatomal nevus.
The clinical picture- Acute cramplike, lancinating pain, sometimes in a sciatic distribution, is often a prominent early feature. It may occur in a series of episodes over a period of several days or weeks; sometimes it is worse in recumbency. Almost always there is weakness or paralysis of one or both legs and numbness and paresthesias in the same distribution with a highly variable duration of evolution; an abrupt apoplectic onset is known or the neurologic signs may appear over months. These lesions only infrequently give rise to intramedullary or subarachnoid hemorrhage. The spinal fluid shows high protein but little or no cellular reaction.
When viewed directly, the dorsal surface of the lower cord may be covered with a tangle of veins, some involving roots and penetrating the surface of
the cord. The progression of symptoms is presumably a result of chronic venous hypertension and secondary intramedullary ischemic changes, and the abrupt episodes of worsening are attributed to the thrombosis of vessels, all on uncertain grounds. -
Intradural perimedullary and subpial AVM probably of a similar nature to the dural type; tend to involve the lower thoracic and upper lumbar segments or the anterior parts of the cervical enlargement. patients are younger. The clinical syndrome slow spinal cord compression, sometimes with a sudden exacerbation, or apoplectic in nature, either because of thrombosis of a vessel or of a hemorrhage from an associated draining vein that dilates to aneurysmal size and bleeds into the subarachnoid space or cord (hematomyelia and subarachnoid hemorrhage); the latter complication occurred in 7 of 30 cases reported by Wyburn-Mason.
Diagnosis apparent on MRI or CT myelography by the presence of one or more enlarged and serpiginous draining vessels in the subarachnoid space; just as often, they are not visualized by these methods .
unexplained myelopathy with signs of congestion of the cord on MRI may be the result of a vascular malformation.
Imaging features that have been emphasized with dural fistulas include enlargement of the spinal cord at the level of the lesion and T2 bright signal of the swollen cord over several segments,
The diagnosis is usually established through selective angiography,
אנגיוגרפיה
Dural AV Fistula
The presenting clinical features in our patients have included slowly progressive bilateral but asymmetric leg weakness with variable sensory loss.
most common initial symptoms were gait imbalance, numbness, and paresthesias. As the process progressed, the majority developed urinary problems, leg weakness, and numbness in the legs and buttocks. The degree of leg weakness varied greatly and back pain in their series was infrequent and has not been a consistent feature in the patients under our care.
The myelopathy may have a subacute or saltatory evolution, presumably from fluctuating venous congestion within the cord. A claudicatory syndrome has also been reported. Characteristically, activities that increase venous pressure (Valsalva maneuver, exercise) transiently amplify the symptoms or produce irreversible, stepwise worsening. One remarkable such case involved a baritone opera singer whose legs gave way repeatedly
while singing.
The diagnosis is usually established through selective angiography, which shows the fistula in the dura overlying the cord or on the surface of the cord itself but the most conspicuous finding is often the associated early draining vein (Fig. 428B).
Demonstration of the fistula requires the injection of
feeding vessels at numerous levels above and below the suspected lesion, because the main artery of origin is often some distance away from the malformation. The small angiodysplastic vessels of the Foix-Alajouanine lesion may not be opacified with angiography. In rare instances, the fistula or highflow arteriovenous malformation lies well outside the cord, for example, in the kidney, and gives rise to a myelopathy, presumably by raising venous pressures within the cord
תיאור של כבר עם חולשת רגליים פלוקטואטיבית.
MRI עמ”ש- עיבוי ורידים
1. AV fistula
2. AVM
3. aneurysm
AV Fistula
Fistulas within the dura that overlies the spinal cord are capable of causing a myelopathy, sometimes several segments distant from the vascular lesion. Most are situated in the region of the low thoracic cord or the conus and have a limited venous draining system. Some are in a dural root sleeve and drain into the normal perimedullary coronal venous plexus. Men seem to be affected disproportionately.
he presenting clinical features in our patients have included slowly progressive bilateral but asymmetric leg weakness with variable sensory loss.
most common initial symptoms were gait imbalance, numbness, and paresthesias. As the process progressed, the majority developed urinary problems, leg weakness, and numbness in the legs and buttocks. The degree of leg weakness varied greatly and back pain in their series was infrequent and has not been a consistent feature in the patients under our care.
The myelopathy may have a subacute or saltatory evolution, presumably from fluctuating venous congestion within the cord. A claudicatory syndrome has also been reported. Characteristically, activities that increase venous pressure (Valsalva maneuver, exercise) transiently amplify the symptoms or produce irreversible, stepwise worsening. One remarkable such case involved a baritone opera singer whose legs gave way repeatedly
while singing.
In contrast to the
larger parenchymal arteriovenous lesions, these bleed only rarely. The spinal fluid is normal or shows a slight elevation of protein.
The disease can be inferred from the MRI appearance of a characteristic swelling of one or a few adjacent segments of the cord that represents venous congestion and edema
פריצת דיסק מרכזית גדולה בגובה
L4 L5
עלולה לגרום ללחץ גם על שורש
L5
וגם שורש
S1
-
L5 to S1 most frequently involved (after that L4-L5, L3-L4, L2-L3, L1-L2, C5-6, C6-7
S&S: - Pain – if lumbar – radiating to thigh, buttock, calf (sciatica), stiff spinal posture, paraesthesia, weakness, reflex impairement.
- Radiation to: Medial malleolus (L4), Lateral Malleolus (L5), Heel (S1)
- Generally, disc herniation compresses the root on one side, at the level just below the herniation
- The cerebrospinal fluid (CSF) protein is often elevated with disc rupture, more predictably with central rupture.
- Herniations of the intervertebral lumbar discs occur most often between the fifth lumbar and first sacral vertebrae (compressing the traversing S1 or exiting L5 root) and between the fourth and fifth lumbar vertebrae ** (compressing the traversing L5 or exiting L4 root**).
Mechanisms of compression of the fifth lumbar and first sacral roots. A lateral disc protrusion at the L4-L5 level usually involves the fifth lumbar root and spares the fourth; a protrusion at L5-S1 involves the first sacral root and spares the fifth lumbar root. Note that a more medially placed disc protrusion at the L4-L5 level (cross-hatched) may involve the fifth lumbar root as well as the first (or second and third) sacral root.
תיאור של חולשה באדוקציה ברגל, אקסטנציה של הברך, ירידה בהחזר פיקה.
בEMG
עדות לדנרבציה
SNAP שמור
איפה הפגיעה?
1. lumbosacral plexus
2. nerve roots L2-L3-L4
3. nerve roots L3-L4-L5
4. Femoral nerve
5. Obturatior nerve
nerve roots L2-L3-L4
ברכיורדיאליס-
עצב רדיאלי בגובה
C6
מדובר ברדיקולופתיה של C6
מוסקולוקואנאוס מעצבב את הבייספס סי5-סי 6
אקסטנסור קרפי רדיאליס זה C6
————
Infraspinatus C5
Pectoralis C5
פגיעה ב
INVERSION
Tibial nerve – extension of sciatic – if proximal invovlement radiculaopathy of L4,L5
Inversion of foot L4, L5
Flexion of toe L5
Straight leg raise L4,L5
(eversion –peroneal neuropathy)
פריצת דיסק בגובה בין חולייתי של
C6-7
תגרום לחולשת:
1.brachioradialis
2. Deltoid
3. Trapezius
4. Triceps
Triceps
פריצת דיסק בגובה בינחולייתי
L5-S1
תגרום ל:
1. היעלמות החזר אכילס
2. חולשת EHL
חולשת טיביאליס אנטריור .3
4. הפרעה תחושתית בשוק המדיאלית
העלמות החזר אכילס
מגיע מטופל עם בלט דיסק
C7-T1
מהתמצאבבדיקה?
א. ירידה החזרבייספס
ב.חולשהדיסטליתבכף יד- בלחיצת יד
ג. הפרעה תחושתית באצבעות 1-2
ד. הפרעת תחושה בכתף
חולשה דיסטלית בכף יד בלחיצת יד
בחור לאחר תאונה קשה מתייצג עם פלגיה ברגליים וחולשה דיסטלית בלבד בידיים, מה ימצא בהדמיית עמ”ש צווארי?
1. Atlanto-occipital dislcation
2. Fracture/dislocation C2-C3
3. Fracture/dislocation C4-C5
4. Fracture/dislocation C5-C6
5. Fracture/dislocation C6-C7
- Fracture/dislocation C6-C7
Syrinx+ syringobulbia
-
Syringomyelia (from the Greek syrinx, “pipe” or “tube”) is defined as a chronic progressive degenerative or Developmental disorder of the spinal cord, characterized clinically by painless weakness and wasting of the hands and arms (brachial amyotrophy) and segmental sensory loss of dissociated type (loss of thermal and painful sensation with sparing of tactile, joint position, and vibratory Sense). The cause is a cavitation of the central parts of the spinal cord, usually in the cervical region, but extending upward in some cases into the medulla and pons (syringobulbia) or downward into the thoracic and even into the lumbar segments.
Frequently, there are associated developmental abnormalities of the
vertebral column (thoracic scoliosis, fusion of vertebrae, or Klippel-Feil anomaly), of the base of the skull (platybasia and basilar invagination), and there is a special relationship to developmental deformations of the cerebellum and brainstem particularly type I Chiari malformation) - Syringobulbia is the lower brainstem equivalent of syringomyelia. Usually the two coexist and the brainstem cavity is simply an extension of one in the upper cord, but occasionally the bulbar manifestations precede the spinal ones or, rarely, occur independently. The glial cleft or cavity is located most often in the lateral tegmentum of the medulla, but it may extend into the pons and, rarely, even higher. The symptoms and signs are characteristically unilateral and consist of nystagmus, analgesia, and thermoanesthesia of the face (numbness); wasting and weakness of the tongue (dysarthria); and palatal and vocal cord paralysis (dysphagia and hoarseness). Diplopia, episodic vertigo, trigeminal pain or facial sensory loss, and persistent hiccough are less common symptoms.
- When a Chiari malformation is associated with syringomyelia and syringobulbia, it may be difficult to separate the effects of the two disorders. Clinical features that favor the predominance of Chiari malformation are nystagmus, cerebellar ataxia, exertional head and neck pain, prominent corticospinal and sensory tract involvement in the lower extremities, hydrocephalus, and craniocervical malformations. In syringomyelia the clinical picture is much the same, and the nature of the foramen magnum lesion can be determined only by MRI or surgical exploration.
(1) segmental weakness and atrophy of the hands and arms,
(2) loss of some or all tendon reflexes in the arms, and
(3) segmental anesthesia of a dissociated type (loss of pain and thermal sense and preservation of the sense of touch)over the neck, shoulders, and arms.
מה לא אופייני ב-
syringomyelia
1. חולשה בידיים
2. אטרוםיה דיסטלית בידיים
3. החזרים ירודים בידיים
4. הפרעה בתחושת כאב בידיים
5. הפרעה בתחושת מגע עדין
הפרעה בתחושת מגע עדין לא אופיינית בסירינגומיאליה
Syrinx+ syringobulbia
-
Syringomyelia (from the Greek syrinx, “pipe” or “tube”) is defined as a chronic progressive degenerative or Developmental disorder of the spinal cord, characterized clinically by painless weakness and wasting of the hands and arms (brachial amyotrophy) and segmental sensory loss of dissociated type (loss of thermal and painful sensation with sparing of tactile, joint position, and vibratory Sense). The cause is a cavitation of the central parts of the spinal cord, usually in the cervical region, but extending upward in some cases into the medulla and pons (syringobulbia) or downward into the thoracic and even into the lumbar segments.
Frequently, there are associated developmental abnormalities of the
vertebral column (thoracic scoliosis, fusion of vertebrae, or Klippel-Feil anomaly), of the base of the skull (platybasia and basilar invagination), and there is a special relationship to developmental deformations of the cerebellum and brainstem particularly type I Chiari malformation).
There is also a group of less frequent but well described syringomyelias that derives from the acquired processes mentioned earlier such as intramedullary tumor (astrocytoma, hemangioblastoma, ependymoma) and from preceding traumatic or hemorrhagic necrosis of the spinal cord. - Syringobulbia is the lower brainstem equivalent of syringomyelia. Usually the two coexist and the brainstem cavity is simply an extension of one in the upper cord, but occasionally the bulbar manifestations precede the spinal ones or, rarely, occur independently. The glial cleft or cavity is located most often in the lateral tegmentum of the medulla, but it may extend into the pons and, rarely, even higher. The symptoms and signs are characteristically unilateral and consist of nystagmus, analgesia, and thermoanesthesia of the face (numbness); wasting and weakness of the tongue (dysarthria); and palatal and vocal cord paralysis (dysphagia and hoarseness). Diplopia, episodic vertigo, trigeminal pain or facial sensory loss, and persistent hiccough are less common symptoms.
- When a Chiari malformation is associated with syringomyelia and syringobulbia, it may be difficult to separate the effects of the two disorders. Clinical features that favor the predominance of Chiari malformation are nystagmus, cerebellar ataxia, exertional head and neck pain, prominent corticospinal and sensory tract involvement in the lower extremities, hydrocephalus, and craniocervical malformations. In syringomyelia the clinical picture is much the same, and the nature of the foramen magnum lesion can be determined only by MRI or surgical exploration.
(1) segmental weakness and atrophy of the hands and arms,
(2) loss of some or all tendon reflexes in the arms, and
(3) segmental anesthesia of a dissociated type (loss of pain and thermal sense and preservation of the sense of touch)over the neck, shoulders, and arms.
מה הם הסוגים השונים של
chiari malformations
Chiari’s types I and II: cerebellomedullary descent without and with a meningomyelocele, respectively
Several other morphologic features are characteristic of the true Chiari
anomaly. The medulla and pons are elongated and the aqueduct is narrowed. The displaced tissue (medulla and cerebellum) occludes the foramen magnum; the remainder of the cerebellum, which is small, is also displaced so as to obliterate the cisterna magna. The foramina of Luschka and Magendie often open into the cervical canal, and the arachnoidal tissue around the herniated brainstem and cerebellum is fibrotic. All these factors are probably operative in the production of hydrocephalus, which is always associated. Just below the
herniated tail of cerebellar tissue there is a kink or spur in the spinal cord, which is pushed posteriorly by the lower end of the fourth ventricle. In this fully expressed form of the
malformation, a meningomyelocele is nearly always found (type 2).
* In type II Chiari malformation (with meningomyelocele), the problem becomes one of progressive hydrocephalus. Cerebellar signs cannot be discerned in the first few months of life. However, lower cranial-nerve abnormalities-laryngeal stridor, fasciculations of the tongue, sternomastoid paralysis (causing head lag when the child is pulled from lying to sitting), facial weakness, deafness, bilateral abducens palsies-may be present in varying combinations. If the patient survives to later childhood or adolescence, one of the syndromes that are more typical of the type I malformation may become manifest.
* In the more common type I Chiari malformation (without meningocele or other signs of spinal dysraphism), neurologic symptoms may not develop until adolescence or adult life. The symptoms are those of
(1) increased intracranial pressure, mainly headache,
(2) progressive cerebellar ataxia,
(3) progressive spastic quadriparesis,
(4) downbeating nystagmus, or
(5) the syndrome of cervical syringomyelia (segmental amyotrophy and sensory loss in the hands and arms, with or without pain).
Or the patient may show a combination of disorders of the lower cranial nerves, cerebellum, medulla, and spinal cord (sensory and motor tract disorders), usually in conjunction with headache that is mainly occipital.
chiari type 2
סירינגומיאליה מקושרת עם סוג 1 ולא עם סוג 2
Frequently, syringomyelia is associated with developmental abnormalities of the vertebral column (thoracic scoliosis, fusion of vertebrae, or Klippel-Feil anomaly), of the base of the skull (platybasia and basilar invagination), and there is a special relationship to developmental deformations of the cerebellum and brainstem (particularly type I Chiari malformation).
איזה גידול גורם ל
Syringomyelia
בסבירות הגבוהה יותר?
1.Neurinoma
2. Chordoma
3. Ependymoma
4. Hemangioblastoma
5. Lymphoma
6. Myeloma
Hemangioblastoma (highest frequency)
afterwhich ependymoma and astrocytome
-
Syringomyelia (from the Greek syrinx, “pipe” or “tube”) is defined as a chronic progressive degenerative or Developmental disorder of the spinal cord, characterized clinically by painless weakness and wasting of the hands and arms (brachial amyotrophy) and segmental sensory loss of dissociated type (loss of thermal and painful sensation with sparing of tactile, joint position, and vibratory Sense). The cause is a cavitation of the central parts of the spinal cord, usually in the cervical region, but extending upward in some cases into the medulla and pons (syringobulbia) or downward into the thoracic and even into the lumbar segments.
Frequently, there are associated developmental abnormalities of the
vertebral column (thoracic scoliosis, fusion of vertebrae, or Klippel-Feil anomaly), of the base of the skull (platybasia and basilar invagination), and there is a special relationship to developmental deformations of the cerebellum and brainstem particularly type I Chiari malformation).
There is also a group of less frequent but well described syringomyelias that derives from the acquired processes mentioned earlier such as intramedullary tumor (astrocytoma, hemangioblastoma, ependymoma) and from preceding traumatic or hemorrhagic necrosis of the spinal cord. -
Hemangioblastoma This tumor is referred to most often in connection with von Hippel-Lindau disease. dizziness, ataxia of gait or of the limbs on one side, symptoms and signs of increased ICP from compression of the fourth ventricle, and in some instances an associated retinal angioma or hepatic and pancreatic cysts (disclosed by CT or MRI) constitute the syndrome. There is a tendency later for the development of malignant renal or adrenal tumors. Many patients have polycythemia as a result of elaboration of an erythropoietic factor by the tumor.
The diagnosis can be deduced from the appearance on CT or MRI of a cerebellar cyst containing an enhancing nodular lesion on its wall. Often the associated retinal hemangioma will be disclosed by the same imaging procedure. The angiographic picture is also characteristic: a cluster of small vessels forming a mass 1 .0 to 2.0 mm in diameter.
*Hemangioblastomas of the spinal cord are frequently associated with a syringomyelic lesion (greater than 70 percent of cases); such lesions may be multiple and are located mainly in the posterior columns.
סירינקס
מדובר בקיארי מלפורמיישן
בקשר לשאר המסיחים-
אגנזיס של הקורפוס קלוסום מאפיין ציסטרנה מגנום
אקוודוקט צר זה חלק מהאבחנה של מלפורמציית קיארי.
צרבלום אטרופי לא בהכרח הוורמיס (
Chiari’s types I and II: cerebellomedullary descent without and with a meningomyelocele, respectively
Several other morphologic features are characteristic of the true Chiari
anomaly. The medulla and pons are elongated and the aqueduct is narrowed. The displaced tissue (medulla and cerebellum) occludes the foramen magnum; the remainder of the cerebellum, which is small, is also displaced so as to obliterate the cisterna magna. The foramina of Luschka and Magendie often open into the cervical canal, and the arachnoidal tissue around the herniated brainstem and cerebellum is fibrotic. All these factors are probably operative in the production of hydrocephalus, which is always associated. Just below the
herniated tail of cerebellar tissue there is a kink or spur in the spinal cord, which is pushed posteriorly by the lower end of the fourth ventricle. In this fully expressed form of the
malformation, a meningomyelocele is nearly always found (type 2).
* In type II Chiari malformation (with meningomyelocele), the problem becomes one of progressive hydrocephalus. Cerebellar signs cannot be discerned in the first few months of life. However, lower cranial-nerve abnormalities-laryngeal stridor, fasciculations of the tongue, sternomastoid paralysis (causing head lag when the child is pulled from lying to sitting), facial weakness, deafness, bilateral abducens palsies-may be present in varying combinations. If the patient survives to later childhood or adolescence, one of the syndromes that are more typical of the type I malformation may become manifest.
* In the more common type I Chiari malformation (without meningocele or other signs of spinal dysraphism), neurologic symptoms may not develop until adolescence or adult life. The symptoms are those of
(1) increased intracranial pressure, mainly headache,
(2) progressive cerebellar ataxia,
(3) progressive spastic quadriparesis,
(4) downbeating nystagmus, or
(5) the syndrome of cervical syringomyelia (segmental amyotrophy and sensory loss in the hands and arms, with or without pain).
Or the patient may show a combination of disorders of the lower cranial nerves, cerebellum, medulla, and spinal cord (sensory and motor tract disorders), usually in conjunction with headache that is mainly occipital.
גבר לאחר ניתוח מעקפים עם חולשה בשתי הרגליים, ירידה בתחושה עם פלס תחושתי ב
D10,
פרופריוצפציה שמורה. מה מקור הבעיה?
1. anterior spinal artery
2. posterior spinal artery
3. left MCA
4. posterior cerebral artery
anterior spinal artery
The most common cause of acute paraplegia (or quadriplegia if the cervical cord is involved) is spinal cord trauma, usually associated with fracture-dislocation of the spine. **Less-common causes are hematomyelia because of a vascular malformation, or a malformation that causes ischemia by an obscure mechanism, and infarction of the cord as a result of occlusion of the anterior spinal artery or, more often, to occlusion of segmental branches of the aorta because of dissecting aneurysm or atheroma, vasculitis, or nucleus pulposus embolism. Epidural or subdural hemorrhage from a hemorrhagic diathesis or warfarin therapy cause an acute or subacute paraplegia; in a few instances the bleeding follows a lumbar puncture. A special syndrome occurs in older men where chronic lumbar pain is followed after some months or years by the rapid development of paraplegia. This is caused by an arteriovenous fistula in the overlying dura of the lumbar region. Closure of the vascular shunt may lead to rapid reversal of paraplegia-a treatable form of paraplegia.
With infarction of the spinal cord in the territory of supply
of the anterior spinal artery or with other lesions that
affect the ventral portion of the cord predominantly, as in some cases of myelitis, one finds a loss of pain and temperature sensation below the level of the lesion but with relative or absolute sparing of proprioceptive sensation. Because the corticospinal tracts and the ventral gray matter also lie within the area of distribution of the anterior spinal artery, spastic paralysis is a prominent feature.
Thus, the branches of the anterior median spinal artery supply roughly the ventral two-thirds of the spinal cord. Infarction of the region supplied by this artery give rise to an anterior spinal cord syndrome that consists of loss of pain and temperature and paralysis below the level of the lesion, but with sparing of proprioception and vibration sense that correspond to transaction of the spinothalamic and corticospinal tracts but not of the posterior columns.
בן 28, ברקע מחלת הודג’קין, לפני שנה וחצי טופל בכימותרפיה והקרנות באיזור המדיאסטינום והגב. בחודש האחרון סובל מזרם בעת כיפוף הראש, נימול בגפיים, קושי בהליכה. בבדיקה חולשה קלה ברגליים עם סימנים פירמידליים, הפרעה בתחושת מנח ברגליים, מה הפתולוגיה בחוט השדרה המסבירה את הסימפטומים?
1. Perivascular inflammation of white matter
2. infarction of anterior spinal artery
3. arterioles necrosis and thrombotic occlusion in the cord
4. intra-myelinic vacuoles in the dorsal ascending tracts
5. necrosis without vascular changes in the cord.
- arterioles necrosis and thrombotic occlusion in the cord
The late-delayed process is the most serious of radiation complications. Here one finds-in structures adjacent to a cerebral neoplasm, the pituitary gland, or other structures of the head and neck-necrosis of the white matter of the brain and, occasionally, of the brainstem. In some areas, the tissue undergoes softening and liquefaction, with cavitation. With lesser degrees of injury,
the process is predominantly a demyelinating one, with partial preservation of axons. Later reactions are thought to be caused by diffuse vascular changes as a result of radiation energy. Endothelial cells frequently multiply and, because ionization injures dividing cells, the vessels are most vulnerable. The result is hyaline thickening of vessels with fibrinoid necrosis and widespread microthrombosis. There is a lesser degree of damage to glial
cells
בן 61 עבר תאונת דרכים וספג פגיעה בחוט שדרה צווארי. בבדיקתו, שיתוק רפה, ארפלקסיה.
איזה ממצא נוסף יימצא?
א. אטוניה של הקיבה.
ב. טכיקרדיה.
ג. פריאפיזם.
ד. שלפוחית ספסטית.
אטוניה של הקיבה כחלק משוק ספינאלי
בן 24, עבר תאונת דרכים לפני שבועיים ונחבל בצווארו. נשאר משותק עם חולשה פלסידית ב4 גפיים, החזרים אינם מופקים והחזרים פלנטרים אדישים. גובה החבלה הינו
C5
. אילו מההחזרים הבאים יחזור קודם?
א. פלנטרי פלקסורי
ב. פלנטרי אקסטנסורי
ג. החזר פיקה
ד. החזר אכילס
ה. החזר בולבוקוונרוזוס
החזר בולבוקוורנוזוס
Usually the bulbocavernosus reflex is the first to return. Contraction of the anal sphincter can be elicited by plantar or perianal stimulation, and other genital reflexes reappear at about the same time. The F-waves, electrophysiologic responses that reflect the functioning of the motor neurons of the isolated segment of the cord, are suppressed until spasticity supervenes, at which time they become overly easy to elicit. Noxious stimulation of the plantar surfaces evokes a tremulous twitching and brief flexion or extension movements of the great toes.
בן 45, לאחר תאונת דרכים, סבל משבר בעמוד השדרה עם פגיעה בחוט השדרה בגובה
T3
נותר עם שיתוק ספסטי בגפיים תחתונות, אי שליטה על סוגרים, לאחרונה הופיעו אירועים של הזעת יתר עם הסמקה של פלג גוף עליון, מה יהיו הסימנים החיוניים של החולה בזמן אירוע מסוג זה?
1. לחץ דם גבוה ודופק נמוך
2. לחץ דם נמוך ודופק נמוך
3. לחד דם גבוה ודופק גבוה
4. לחץ דם תקין ודופק גבוה
5. לחץ דם נמוך ודופק גבוה
לחץ דם גבוה ודופק נמוך
With cervical cord lesions, there is a loss of the sympathetically mediated cardiovascular changes in response to stimuli reaching the medulla. However, cutaneous stimuli (pinprick or cold) in segments of the body below the transection will raise the blood pressure. However, a fall in blood pressure is not compensated by sympathetic vasoconstriction. Hence tetraplegics are almost obligatorily prone to orthostatic hypotension. Pinching the skin below the lesion causes gooseflesh in adjacent segments. Heating the body results in flushing and sweating over the face and neck, but not in the trunk and legs, because of the loss of connections from the hypothalamus. Bladder and bowel, including their sphincters, which are at first flaccid, become automatic as spinal reflex control returns. There may be reflex penile erection or priapism and even rarely ejaculation.
With lesions in the upper thoracic cord, similar but lesser degrees of labile blood pressure are seen; in several of our patients with destructive myelitis, a viral infection of fever brought out episodes of a drop in blood pressure to approximately 80 I 60 mm Hg and a subsequent rapid rise to 190/110 mm Hg.
After a time, the tetraplegic patient may develop a mass reflex in which flexor spasms of the legs and involuntary emptying of the bladder are associated with a marked rise in blood pressure, bradycardia, and sweating and pilomotor reactions in parts below the cervical segments (autonomic dysreflexia). These reactions may also be evoked by pinprick, passive movement, contractual stimuli of the limbs and abdomen, and pressure on the bladder.
מטופלת צעירה לאחר חבלת בתאונת דרכים לפני כמה חודשים. כעת הפרעה תחושתית שטחית וחולשת כפות ידיים ללא הפרעה ברגליים. מה הסינדרום?
1. צנטרל קורד
2. פוסטריור קורד
3. אנטריור קורד
Central cord
central cord (“schneider) syndrome
- פגיעה צווארית המערבת את מרכז החוט ומתבטאת יותר בחולשת גפיים עליונות מאשר רגליים ובעיקר מתבטאת בכפות הידיים.
- תתכן דיספונקציה של שלפוחית
- יתכן אובדן סנסורי מינורי (היפרפתיה בכתפיים וזרועות)
- רטרופלקסציה של הצוואר הוא לרוב המנגנון האחראי, אך ייתכן סיבות אחרות כמו המטומיאליה, אמבוליזם פיברוקארטילאז’ או שבץ משני לדיסקציה ורטברלית באזור צומת המדולוספינאלית.
-
crucicate paralysis–
פגיעה צווארית גבוהה באזור חוליות צוואריות 1-2, מיוחס להצטלבות במסילות הפיראמידאליות של הידיים (כאשר אלו של הרגליים נמצאות נמוך יותר). חולשת הידיים יכולה להיות אסימטרית, סלקטיבית מאוד, תתכן אפילו פגיעה יונלטרלית. עדיין לא הובן האם הפגיעה היא בסיבים המצטלבים או שמערבים גם חומר אפור.
Central Cord (“Schneider”) Syndrome and Cruciate Paralysis A special from of acute cervical cord injury implicates mainly central cord damage, resulting in the loss of motor function solely or more severely in the upper limbs than in the lower ones, and it particularly affects the hands. Bladder dysfunction with urinary retention occurs in some cases and sensory loss is often slight (hyperpathia over the shoulders and arms may be the only sensory abnormality). Many of these instances are reversible but damage to the centrally situated gray matter may leave an atrophic, areflexic paralysis of the arms and hands and a segmental loss of pain and thermal sensation from interruption of crossing pain and thermal fibers. Retroflexion injuries of the head and neck are the ones most often associated with the central cord syndrome, but other causes include hematomyelia, fibrocartilaginous embolism, and infarction from dissection of the vertebral artery in the medullary-cervical region.
* 4 percent of patients who survive injuries of the very rostral cervical cord demonstrate *a very limited form of the central cord syndrome- cruciate paralysis.” The weakness is very selective, being practically limited to the arms, a feature that is attributable to the segregation within the pyramidal decussation of
corticospinal fibers to the arms (being rostral) and to the legs (more caudally situated).
The arm weakness may be asymmetrical or even
unilateral and sensory loss is inconsistent. The patients
described have had contusions of the Cl-C2 region.
בן 54 היה מעורב בתאונת דרכים לפני חודשיים. הגיע עם חולשה ספסטית של הידיים עם ערות החזרים והפרעה במתן שתן. כמו כן הפרעה בתחושת כאב וטמפרטורה בידיים. מה סביר שיש לו?
1. central cord
2. spinal cord concussion
3. Brown Sequard
3. anterior spinal artery syndrome
Central cord
central cord (“schneider) syndrome
- פגיעה צווארית המערבת את מרכז החוט ומתבטאת יותר בחולשת גפיים עליונות מאשר רגליים ובעיקר מתבטאת בכפות הידיים.
- תתכן דיספונקציה של שלפוחית
- יתכן אובדן סנסורי מינורי (היפרפתיה בכתפיים וזרועות)
- רטרופלקסציה של הצוואר הוא לרוב המנגנון האחראי, אך ייתכן סיבות אחרות כמו המטומיאליה, אמבוליזם פיברוקארטילאז’ או שבץ משני לדיסקציה ורטברלית באזור צומת המדולוספינאלית.
-
crucicate paralysis–
פגיעה צווארית גבוהה באזור חוליות צוואריות 1-2, מיוחס להצטלבות במסילות הפיראמידאליות של הידיים (כאשר אלו של הרגליים נמצאות נמוך יותר). חולשת הידיים יכולה להיות אסימטרית, סלקטיבית מאוד, תתכן אפילו פגיעה יונלטרלית. עדיין לא הובן האם הפגיעה היא בסיבים המצטלבים או שמערבים גם חומר אפור.
Central Cord (“Schneider”) Syndrome and Cruciate Paralysis A special from of acute cervical cord injury implicates mainly central cord damage, resulting in the loss of motor function solely or more severely in the upper limbs than in the lower ones, and it particularly affects the hands. Bladder dysfunction with urinary retention occurs in some cases and sensory loss is often slight (hyperpathia over the shoulders and arms may be the only sensory abnormality). Many of these instances are reversible but damage to the centrally situated gray matter may leave an atrophic, areflexic paralysis of the arms and hands and a segmental loss of pain and thermal sensation from interruption of crossing pain and thermal fibers. Retroflexion injuries of the head and neck are the ones most often associated with the central cord syndrome, but other causes include hematomyelia, fibrocartilaginous embolism, and infarction from dissection of the vertebral artery in the medullary-cervical region.
* 4 percent of patients who survive injuries of the very rostral cervical cord demonstrate *a very limited form of the central cord syndrome- cruciate paralysis.” The weakness is very selective, being practically limited to the arms, a feature that is attributable to the segregation within the pyramidal decussation of
corticospinal fibers to the arms (being rostral) and to the legs (more caudally situated).
The arm weakness may be asymmetrical or even
unilateral and sensory loss is inconsistent. The patients
described have had contusions of the Cl-C2 region.
בת 74 עם היצרות ספינלית צווארית ידועה בגובה
C6-C7
מעדה ונפלה עם חבלות בפנים. בבדיקה לאחר הנפילה, ללא חולשה בגפיים, הולכת ועומדת יציב גם עם עיניים עצומות. מהי הפרעת התחושה האופיינית בעקבות טראומה לחוט השדרה במקרה זה?
א. הפרעה בתחושת מנח בידיים
ב. הפרעה בתחושת ויברציה ברגליים
ג. הפרעה בתחושת מגע עם פלס בגובה
C7
ד. הפרעה בתחושת כאב בכפות הידיים.
הפרעה בתחושת כאב בכפות הידיים
central cord (“schneider) syndrome
- פגיעה צווארית המערבת את מרכז החוט ומתבטאת יותר בחולשת גפיים עליונות מאשר רגליים ובעיקר מתבטאת בכפות הידיים.
- תתכן דיספונקציה של שלפוחית
- יתכן אובדן סנסורי מינורי (היפרפתיה בכתפיים וזרועות)
- רטרופלקסציה של הצוואר הוא לרוב המנגנון האחראי, אך ייתכן סיבות אחרות כמו המטומיאליה, אמבוליזם פיברוקארטילאז’ או שבץ משני לדיסקציה ורטברלית באזור צומת המדולוספינאלית.
-
crucicate paralysis–
פגיעה צווארית גבוהה באזור חוליות צוואריות 1-2, מיוחס להצטלבות במסילות הפיראמידאליות של הידיים (כאשר אלו של הרגליים נמצאות נמוך יותר). חולשת הידיים יכולה להיות אסימטרית, סלקטיבית מאוד, תתכן אפילו פגיעה יונלטרלית. עדיין לא הובן האם הפגיעה היא בסיבים המצטלבים או שמערבים גם חומר אפור.
Central Cord (“Schneider”) Syndrome and Cruciate Paralysis A special from of acute cervical cord injury implicates mainly central cord damage, resulting in the loss of motor function solely or more severely in the upper limbs than in the lower ones, and it particularly affects the hands. Bladder dysfunction with urinary retention occurs in some cases and sensory loss is often slight (hyperpathia over the shoulders and arms may be the only sensory abnormality). Many of these instances are reversible but damage to the centrally situated gray matter may leave an atrophic, areflexic paralysis of the arms and hands and a segmental loss of pain and thermal sensation from interruption of crossing pain and thermal fibers. Retroflexion injuries of the head and neck are the ones most often associated with the central cord syndrome, but other causes include hematomyelia, fibrocartilaginous embolism, and infarction from dissection of the vertebral artery in the medullary-cervical region.
* 4 percent of patients who survive injuries of the very rostral cervical cord demonstrate *a very limited form of the central cord syndrome- cruciate paralysis.” The weakness is very selective, being practically limited to the arms, a feature that is attributable to the segregation within the pyramidal decussation of corticospinal fibers to the arms (being rostral) and to the legs (more caudally situated). The arm weakness may be asymmetrical or even unilateral and sensory loss is inconsistent. The patients
described have had contusions of the Cl-C2 region.
בת 87, חולת פרקינסון נפלה ונחבלה בסנטר, מתלוננת על כאבים בצוואר, בבדיקתה: ללא חולשת גפיים או הפרעה תחושתית. טונוס ריגידי. מה הממצא הסביר ביותר בהדמיית עמוד שדרה צווארית?
1. Dislocation of facet C1-C2
2. central disc protrusion C5-C6 with cord compression
3. fractures of pedicles C7 and T1
4. compression fracture with spondylolisthesis
5. occipital condyle dislocation
dislocation of facet C1-C2
מה לא מתאים לשוק ספינאלי?
1. Detrusor contraction
2. flaccid paralysis
3. abolished vasomotor tone
Detrusor contraction is not a part of the spinal shock syndrome.
The loss of motor function at the time of injury, tetraplegia with lesions of the fourth to fifth cervical segments or above, and paraplegia with lesions of the thoracic cord, are accompanied by immediate atonic paralysis of bladder and bowel, gastric atony, loss of sensation below a level corresponding to the spinal cord lesion, muscular flaccidity, and almost complete suppression of spinal segmental reflex activity below the lesion. Also impaired in the segments below the lesion is the control of autonomic function. Vasomotor tone, sweating, and piloerection in the lower parts of the body are temporarily abolished. As a result, there may be severe systemic hypotension that itself contributes to spinal cord damage. The lower extremities lose heat if left uncovered, and they swell if dependent. The skin over time becomes dry and pale, and ulcerations may develop over bony prominences. The sphincters of the bladder and the rectum remain contracted to some degree because of the loss of the normal inhibitory influence of higher centers, but the detrusor of the bladder and smooth muscle of the rectum become atonic. Urine accumulates until the intra vesicular pressure is sufficient to overcome the sphincters, causing overflow incontinence. There is also passive distention of the bowel, retention of feces, and absence of peristalsis (paralytic ileus). Genital reflexes (penile erection, bulbocavernosus reflex, contraction of dartos muscle) are abolished or profoundly depressed.
בת 52, ברקע ראומטאויד ארטריטיס, לאחר שטיפת שיער עם מתיחת ראש לאחור הרגישה חולשה פתאומית ב-4 גפיים ונפלה. לאחר מספר דקות החולשה חלפה. מה הפתולוגיה האופיינית במקרה זה?
1. Atlanto-axial dislocation
2. C4/C5 central disc protrusion
3.C5/C6 facet joint dislocation
4. Tearing of posterior longitudinal ligament
5. Carotid artery dissection
Atlanto- axial dislocation
Spinal rheumatoid arthritis may be restricted to or include the cervical zygapophysial (facet) joints and the atlantoaxial articulation. The usual manifestations are pain, stiffness, and limitation of motion in the neck and pain in the back of the head. In contrast to ankylosing spondylitis, rheumatoid arthritis is rarely confined to the spine. Because of evident disease of other joints, the diagnosis is relatively easy to make, but significant involvement of the cervical spine may be overlooked. In the advanced stages, one or several of the vertebrae may become displaced anteriorly, or a synovitis of the atlantoaxial joint may damage the transverse ligament of the atlas, resulting in forward displacement of the atlas on the axis, i.e., atlantoaxial subluxation. In either instance, serious and even life-threatening compression of the spinal cord may occur gradually or suddenly.
The spinal changes of rheumatoid arthritis differ somewhat from those of ankylosing spondylitis although the latter too may be a cause of atlantoaxial dislocation (see further on under “Anomalies at the Craniocervical Junction”). The ligaments that attach the odontoid to the atlas and to the skull and the joint tissue are weakened by the destructive inflammatory process. The subsequent dislocation of the atlas on the axis may remain mobile or become fixed and give rise to an intermittent or persistent paraparesis or quadriparesis.
paraparesis.
Lathyrism
Consumption of Lathyrus sativus ( chickling vetch, vetch pea, or grass pea). The disease is still common in some parts of India and Africa. In these districts, during periods of famine when wheat and other grains are in short supply, the diet may for months consist of flour made of the grass pea. In individuals so exposed, a gradual weakening of the legs accompanied by spasticity and cramps occurs. Paresthesias, numbness, formication in the legs, and frequency and urgency of micturition, erectile dysfunction, and sphincteric spasms are added. The upper extremities may exhibit coarse tremors and involuntary movements.
These symptoms, once established, are more or less permanent but not progressive, and most of the patients live out their natural life span
The African acute spastic paraplegia called konzo has a similar toxic pathogenesis; it is caused by cyanide-like compounds in flour made from cassava.
תשובה 2
4000 RBC, 4 WBC, protein 50, glucose 40
Spinal Subdural Hemorrhage
This is an unusual process, but we have reported cases that presented with excruciating thoracic back pain of such severity as to cause a bizarre, almost psychotic, reaction The neck becomes slightly stiff and there may be a headache, suggesting subarachnoid hemorrhage. However, signs of a myelopathy do not appear, indicating that the bleeding is confined to the pliable subdural spaces surrounding the cord, thereby allowing the blood to spread over several segments.
Lumbar puncture yields a distinctive dark yellow brown spinal fluid that resembles, to us, used motor oil. The color is imparted by methemoglobin and reflects the presence of an adjacent, decomposing walled-off clot. Usually there are also red blood cells in the CSF, suggesting seepage into the subarachnoid space from the adjacent collection.
MRI or CT myelography shows a subdural collection, with characteristically smooth borders. When drained operatively, this is found to be clotted blood. Usually, no vascular malformation is demonstrable and the cause remains obscure. Trauma or anticoagulation underlies a few cases but many are spontaneous.
The symptoms resolve in 1 or 2 weeks after removal of the subdural hematoma. Small collections may be managed without surgery, in which case corticosteroids may be helpful in reducing the pain.
תיאור של חולה עם פוליומייליטיס בהדמיה האדרה של קרן קדמית דו”צ. מה המחולל?
1. קוקסאקי
סטפילוקוקוס אארוס. 2
3. לגיונלה
קוקסאקי
ACUTE ANTERIOR POLIOMYELITIS
In the past, this syndrome was almost invariably the result of infection by one of the three types of poliovirus. However, illnesses that clinically resemble poliovirus infections can be caused by other enteroviruses such as the Coxsackie groups A and B and Japanese encephalitis, as well as by West Nile virus. The poliomyelitis agent is a small RNA virus that is a member of the enterovirus group. Poliomyelitis is a highly communicable disease. The main reservoir of infection is the human intestinal tract (humans are the only known natural hosts), and the main route of infection is fecal-oral – (incubation period 1-3 weeks).
The prodromal symptoms consist of listlessness, generalized, nonthrobbing headache, fever of 38 to 40°C (100.4 to 104°F), stiffness and aching in the muscles, sore throat in the absence of upper respiratory infection, anorexia, nausea, and vomiting. These symptoms may subside to a varying extent, to be followed after 3 to 4 days by recrudescence of headache and fever and by symptoms of nervous system involvement; more often the second phase of the illness blends with the first. Tenderness and pain in the muscles, tightness of the hamstrings (spasm), and pain in the neck and back become increasingly prominent. Other early manifestations of nervous system involvement include irritability, restlessness, and emotional instability; these are frequently a prelude to paralysis. Weakness becomes manifest while the fever is at its height, or, just as frequently, as the temperature falls and the general clinical picture seems to be improving. Muscle weakness may develop rapidly, attaining its maximum severity in 48 h or even less; or it may develop more slowly or in stuttering fashion over a week, rarely even longer.
As a general rule, there is no progression of weakness after the temperature has been normal for 48 h. The distribution of spinal paralysis is quite variable; rarely there may be an acute symmetrical paralysis of the muscles of the trunk and limbs as occurs in the Guillain-Barre syndrome. Excessive physical activity and local injections during the period of asymptomatic infection were thought to favor the development of paralysis of the exercised or injected limbs. Coarse fasciculations are seen as the muscles weaken; they are transient as a rule, but occasionally they persist. Tendon reflexes are diminished and lost as the weakness evolves and paralyzed muscles become flaccid. Atrophy of muscle can be detected within 3 weeks of onset of paralysis, is maximal at 12 to 15 weeks, and is permanent.
Bulbar paralysis is more common in young adults, but usually such patients have spinal involvement as well. The most frequently involved cranial muscles are those of deglutition, reflecting involvement of the nucleus ambiguous. The other great hazards of medullary disease are disturbances of respiration and vasomotor Control-hiccough, shallowness and progressive slowing of respiration, cyanosis, restlessness and anxiety from air hunger, hypertension, and, ultimately, hypotension and shock.
* The enteroviruses, of which Coxsackie and poliomyelitis are examples, herpes zoster, arboviruses such as West Nile and the equine encephalitic viruses, and HIV are the important members of this category. *The enteroviruses in particular have an affinity for neurons of the anterior horns of the spinal cord and the motor nuclei of the brainstem (i.e., they are neuronotropic and cause a disease that can be generically termed poliomyelitis), and herpes zoster virus has a clear affinity for the dorsal root ganglia; hence the disturbances of function are in terms of motor and sensory neurons, respectively, not of spinal tracts. We have cared for several patients who have had destruction of anterior horn cells as a consequence of an enterovirus other than poliomyelitis virus. West Nile virus shows the same proclivity to damage anterior horn cells.
צעיר חזר מדרום אפריקה. במהלך ביקורו שם מתאר כי שחה באגם, לאחר מכן הבחין בפריחה אדומה חולפת ברגליים. כעת כעבור מספר חודשים התפתחות של פאראפרזיס ופלס תחושתי גבי. בניקור מותני 500 תאים מונונוקלארים, חלבון מוגבר, אוליגוקלונל בנדס חיוביים. מה הטיפול?
1. IVIG
2. IV methylprednisolone
3. ampicillin + chloramphenicol
4. praziquantel
5. Zidovudine
praziquantel
Some types of Schistosoma infections (also called Bilharzia), mainly mansoni, tend to localize in the spinal cord, causing an acute or subacute myelitis that is concentrated in the conus medullaris. The clinical picture is of a subacutely developing transverse cord lesion. There is often preceding leg or radicular pain and bladder control is affected prominently. We have observed a few cases in students returning from Africa; their lesions were in the conus. Unless treated immediately, there may be permanent paralysis of the legs and bladder from inflammatory and microvascular destruction of the lower cord.
Eosinophilia is common in symptomatic individuals and there is a serologic test but it often becomes negative soon after the initial infection. Examination of the CSF in the myelitic form discloses a pleocytosis, sometimes with an increase in eosinophils (more than half of patients), increased protein content, and increased pressure. Diagnosis is made by the finding of eggs in stool or urine. Treatment consists of praziquantel orally in a dosage of 20 mg/kg tid. Surgical excision of spinal granulomatous tumors is sometimes indicated, but the results are unpredictable. Corticosteroids are often given concurrently.
Myelitis Caused by Fungus and Parasitic Diseases
* Actinomyces, Blastomyces, Coccidioides, and Aspergillus may invade the spinal epidural space via intervertebral foramina or by extension from a vertebral osteomyelitic focus.
* Cryptococcus, which causes meningoencephalitis and, rarely, a cerebral granuloma, in our experience, seldom causes spinal lesions.
* Hematogenous metastases to the spinal cord or meninges may occur in both blastomycosis and coccidioidomycosis.
* Occasionally an echinococcal infection of the posterior mediastinum may extend to the spinal canal (epidural space) via intervertebral foramina and compress the spinal cord.
* Schistosomiasis (bilharziasis) is a recognized cause of myelitis in the Asia, Africa, and South America. The spinal cord is a target for all three common forms of Schistosoma: S. haematobium, S. japonicum, and S. mansoni, but most particularly the last of these (see “Schistosomiasis” in Chap. 31). The schistosomal ova evoke an intense granulomatous myelomeningoradiculitis. The lesions are destructive of gray and white matter, with ova in arteries and veins leading to vascular obstruction and ischemia.
Less often, a localized granuloma gives rise to a cord syndrome and, rarely, the disease takes the form of an acute transverse myelitis with massive necrosis of cord tissue A pruritic “swimmer’s itch**” at the site of entry of the parasite is reported by many patients in the days prior to the myelopathy.
the latency between exposure and symptoms was **38 days to several years. We have cared for several patients over the years in whom the spinal cord in the low thoracic and lumbar region was infected approximately 3 weeks after they swam in contaminated water during an east African vacation and then returned home to the United States The CSF showed only a slight elevation of protein, but in almost all cases there is a pronounced pleocytosis ranging from 5 to 500 lymphocytes/mm3 and the glucose is normal or minimally reduced. Systemic and CSF eosinophilia are variable so are not dependable for diagnosis. The diagnosis is confirmed by the finding of elevated titers of antibody directed against the schistosome in the CSF or blood. There are usually oligoclonal bands of IgG in the CSF as well. The parasite can sometimes be found in biopsies of the rectosigmoid mucosa. The administration of praziquantel arrested the course of the illness, but all but one of our patients was left disabled.
בחורה בת 30 עם הופעה סוב אקוטית של הליכה אטקטית ורומברג חיובי. מה הסיבה הסבירה?
1. חסר תיאמין
2. חסר בפירידוקסין
3. מייאליטיס
4. מנינגיטיס
מייאליטיס
HTLV
* HTLV: chronic infective inflamamtory disease of Spinal Cord – tropical spastic paraparesis.
Slowly progressive paraparesis with increased reflexes, disorder of **sphincteric control, reduced vibratory and position sense*.
May be associated with polyneuropathy. Upper extremities and cerebrum spared.
Dx: detection of antibodies in serum.
MRI – thin SC – inflammatory myelitis with focal spongiform, demyelinative, necrotic lesions, perivascular and meningeal infiltrates,
Focal destruction of grey matter. Posterior column and corticospinal tract most affected – commonly in thoracic cord.
קצת על המסיחים האחרים (וגם בתמונה המצורפת)
* Diphtheria: inflammatory exudates of throat – exotoxin formed – affects heart and NS- biphasic pattern - : PALATAL PARALYSIS (nasal
Voice, regurgitation, dysphagia) followed by OTHER CN INVOLVEMENT. CILIARY BODY PARALYSIS – loss of accommodation and blurring
Of vision – PRESERVED LIGHT REACTION – followed in some cases by sensorimotor polyneuropathy of limbs to rapidly evolving Ascending paralysis – GBS like.
* Campylobacter – the most frequent identifiable antecedent infection of GBS
* Tick-Borne paralysis – acute onset, GBS like
Figure 42-1.
The relationship of spinal segments and roots to the vertebral bodies and spinous processes. The cervical roots (except C8) exit through foramina
above their respective vertebral bodies, and the other roots issue below these bodies. (From Haymaker W, Woodhall B: Peripheral Nerve Injuries, 2nd ed. Philadelphia, Saunders, 1953, by permission.)
Figure 42-2.
MRI of spinal epidural abscess compressing the dorsolateral cervical spinal cord. Sagittal (left) and axial (right) T1 gadolinium-enhanced
images show the peripherally enhancing pyogenic collection (arrows) which extends over several vertebral segments.
Figure 42-2.
MRI of spinal epidural abscess compressing the dorsolateral cervical spinal cord. Sagittal (left) and axial (right) T1 gadolinium-enhanced
images show the peripherally enhancing pyogenic collection (arrows) which extends over several vertebral segments.
Figure 42-3.
Sagittal T2-weighted
MRI in Pott tuberculous spine disease. The angulated deformity of the thoracic spine is highly characteristic. (Courtesy of Dr. Randall Edgell, New York University Medical Center.)
Figure 42-4.
T2-weighted MRI of acute postinfectious myelitis in the sagittal (A) and axial (B) planes. There is abnormal T2 hyperintensity within the dorsal spinal cord and the cord is mildly enlarged. Mild enhancement following gadolinium infusion was noted (not shown).
Figure 42-5.
MRI of necrotic myelopathy in a patient with neuromyelitis optica. Note the long extent of the lesion and thinning of the cord as the acute illness subsides.
Figure 42-5.
MRI of necrotic myelopathy in a patient with neuromyelitis optica. Note the long extent of the lesion and thinning of the cord as the acute illness subsides.
Figure 42-6.
Anterior view of the spinal cord with its segmental blood supply from the aorta. (Reproduced with permission from Prasad S, Price RS, Kranick SM, et
al: Clinical reasoning: A 59yearold
woman with acute paraplegia. Neurology 69:E41, 2007.)
Figure 42-6.
Anterior view of the spinal cord with its segmental blood supply from the aorta. (Reproduced with permission from Prasad S, Price RS, Kranick SM, et
al: Clinical reasoning: A 59yearold
woman with acute paraplegia. Neurology 69:E41, 2007.)
Figure 42-7.
Spinal cord infarct: Sagittal (left) and axial (right) T2 MRI of a man who experienced sudden onset of bilateral flaccid arm weakness. Note the abnormal T2 hyperintensity restricted to the ventral spinal cord, including both ventral horns.
igure 42-8.
Dural arteriovenous fistula of the cord. A. Sagittal T2 weighted MRI of the lower spinal cord of a 50 year old
man with progressive myelopathy. Cord edema (T2 hyperintensity at the conus medullaris) and multiple vascular flow voids surrounding the spinal cord and extending up to the midthoracic vertebral levels are seen, both the result of the arteriovenous fistula.
B. Angiographic injection of the left T12 radicular artery from the patient whose MRI is shown in A, demonstrating abnormal early filling of veins surrounding the spinal cord, confirming the presence of an arteriovenous fistula. The
fistula was repaired and the patient’s symptoms partially improved.
Figure 42-9.
Sagittal T2 MRI in a patient with symptomatic cervical spondylosis. The spinal cord is severely compressed at the C5-C6 intervertebral disc space. Faint abnormal T2 hyperintensity of the spinal cord can be seen at the point of compression. Following surgical decompression, the patients myelopathic symptoms partially improved.
Figure 42-10.
Sagittal (left) and axial (right) gadolinium enhanced T1 weighted
MRI of an intraspinal meningioma that displaced and compressed the spinal cord, causing incontinence and leg weakness. As in intracranial meningiomas, homogenous contrast enhancement and a dural attachment are seen.
Figure 42-10.
Sagittal (left) and axial (right) gadolinium enhanced T1 weighted
MRI of an intraspinal meningioma that displaced and compressed the spinal cord, causing incontinence and leg weakness. As in intracranial meningiomas, homogenous contrast enhancement and a dural attachment are seen.
Figure 42-11.
Sagittal T2-weighted
MRI of a primary glioma of the thoracic spinal cord in a middle aged man. Note the expansion of the spinal cord.
Figure 42-11.
Sagittal T2-weighted
MRI of a primary glioma of the thoracic spinal cord in a middle aged man. Note the expansion of the spinal cord.
Figure 42-12
Sagittal T1weighted
MRI showing multiple spinal metastases from carcinoma of the lung. The metastases exhibit low signal intensity due to tumor
replacement of bone marrow, which is normally T1 hyperintense.
Figure 42-13.
Sagittal T2 MRI of an intramedullary metastasis from breast cancer. The expansile lesion is at the T2 vertebral level (arrow) and the adjacent edema
extends superiorly and inferiorly over a great length of the spinal cord.
Figure 42-13.
Sagittal T2 MRI of an intramedullary metastasis from breast cancer. The expansile lesion is at the T2 vertebral level (arrow) and the adjacent edema
extends superiorly and inferiorly over a great length of the spinal cord.
Figure 42-14.
Sagittal T2-weighted
MRI showing a developmental syringomyelia without Chiari malformation. The cervical spinal cord is greatly expanded but there
were only signs of spinothalamic sensory loss over the arms.
Figure 42-14.
Sagittal T2-weighted
MRI showing a developmental syringomyelia without Chiari malformation. The cervical spinal cord is greatly expanded but there
were only signs of spinothalamic sensory loss over the arms.
