פרק 33 Chapter 33: Stroke and Cerebrovascular Diseases Flashcards
בן 38 הגיע למיון עם אוטם מוחי חריף תת קורטיקלי מימין. בעברו שני אירועים תת קורטיקליים ישנים. במשפחתו סיפור של מיגרנה עם המיפלגיה, אוטמים מוחיים ודמנציה
MRI:
מראה לזיות מרובות, בעיקר בחומר לבן תת קורטיקלי
האבחנה הסבירה במקרה הזה היא:
א. CADASIL
ב. familial hemiplegic migraine
ג. Binswanger disease
ד. Cerebral amyloidosis
ה. familial atrial fibrillation with extensive brain infarcts
א. CADASIL
- CADASIL – Cerebral AD Arteriopathy with Subcortical infarcts and leukoencephalopathy
AD – assoc’ with missense mutation on chrom 19 – NOTCH3. Migraines precede recurrent small strokes which lead to dementia.
Imaging– white matter lesions bilateral of various sizes - around basal gnglia and periventricular. Lesions anterior to temporal horns of lat vetricles are characteristic
NOTCH 3 – same locus as the gene from Familiar Hemiplegic Migraine.
Diagnosis on genetic testing as well as eosinophilic inclusions in arterioles of skin biopsy - CARASIL – AR variant with precending alopecia and lumbar spondylosis. HTAR1 gene
- Famillial Hemiplegic migraine: episodes of unilateral weakness that overlasts migraine. Most cases mutation of ion channel – P/Q type calcium channel alpha subunit CACNA1A. Other sites are ATPASA of Na/ K and SCNA1
- Binswanger – widespread degeneration of cerebral whiate matter having a vadcular causation and observed in the context of hypertension, atherosclerosis and multiple strokes. Leukoaraiosis – hypotinenseperiventricularwhiate matter by chronic ischaemia.
Clinically – Dementia, pseudobulbar state and gait disorder constitute the clinical presentation. - CAA – deposition of amyloid in media and adventita of small vessels predominantly in meninges, cortex and cortical pentrating vessels. Amyloid Ab40 (in contrast to AD AB42). Amyloid deposition leads to several small haemorrhages at various ages , mainly depostied in cerebral hemispheres with propensty to posterior parts.
Strong assoication with homozygous apoe4/e4 genotype
MRI – gradient ECHO – location pfheamorrhages on posterior subcortical, subpialcharateristic.
PCA infarcts are associated with
PCA infarcts
homonymus hemianopsia
Occipital infarcts of the dominant
hemisphere may cause alexia without agraphia, anomia
(amnesic aphasia), a variety of visual agnosias, and rarely
some degree of impaired memory.
דברים שלא נראה בהיפופרפוזיה של רקמת מח :
א. אשלגן חוץ תאי עולה
ב. הגדלת המרווח הבין תאי
ג. סידן תוך תאי יורד
ד. ATP is depleted
בהיפופרפוזיה של רקמת מוח סידן תוך תאי עולה…
Table 33-1
CAUSES OF ISCHEMIC AND HEMORRHAGIC STROKE
Table 33-2
CEREBROVASCULAR DISEASES CHARACTERISTIC OF EACH AGE PERIOD
Table 33-3
SCORING SYSTEMS TO PREDICT THE RISK OF STROKE IN PATIENTS WITH ATRIAL FIBRILLATION (CHADS2 AND CHA2DS2-VASC)
Table 33-4
MRI SEQUENCES IN THE DIAGNOSIS OF STROKE
Table 33-5
INTRAMEDULLARY BRAINSTEM SYNDROMES
Table 33-6
INCLUSION AND EXCLUSION CHARACTERISTICS OF PATIENTS WITH ISCHEMIC STROKE WHO COULD BE TREATED WITH IV rtPA WITHIN 3 HOURS FROM SYMPTOM ONSET
Table 33-7
STROKE ASSOCIATED WITH GENETIC DISORDERS
Table 33-8
CAUSES OF CEREBRAL HEMORRHAGE (INCLUDING INTRACEREBRAL, SUBARACHNOID, AND VENTRICULAR)
Table 33-9
SCORING SYSTEMS FOR PREDICTION OF OUTCOME IN INTRACEREBRAL HEMORRHAGE (ICH AND FUNC SCORES)
Table 33-10
CONDITIONS THAT HAVE BEEN ASSOCIATED WITH DIFFUSE OR WIDESPREAD CEREBRAL VASOSPASM
הפרעה תחושתית של צד שמאל , לאחר שעה הפרעה במבט ורטיקלי ולטרלי .איפה הפגיעה?
א.תלמוס
ב.פוטמן
ג.פונס
ד.קורטקספריאטלי
תלמוס (כנראה מדובר בדימום תלמי שמתרחב)
תאור של שבץ עם פגיעה תחושית מבודדת - כאב, טמפרטורה ותחושה עמוקה, היכן הפגיעה ?
1. פריאטלית
2. תלמית
3. פרונטלית
4. מדולה
תלמית
A lacune of the lateral thalamus or (less often of the deep parietal white matter) is the cause of hemisensory defect involving the limbs, face, and trunk extending to the midline with no motor or language difficulty, a pure sensory stroke.
Parietal –dejerine mouisson- Pseudothalamic –pain and touch no deep sense
מטופלת התקבלה בתמונה של אוטמים במספראיזורים, בבדיקתה לאנימושדופק רדיאלי . איזה טיפולתתןבשלב המיידי?
א. סטרואידים
ב.פלזמהפרזיס
ג.IVIG
ד.אזהתיופירין
סטרואידים
Takayasu Disease (“Pulseless Disease”)
ארטריטיס כרונית לא ספציפית המערבת את האאורטה וענפיה, דומה מאוד ל-
Giant cell arteritis
פרט לנטייתה לערב ענפים פרוקסימלים במקום דיסטלים. המחלה אופיינה באוכלוסיה של נשים אסיאתיות צעירות, אך קיימים דיווחים על מקרים בכל העולם. המנגנון אינו ידוע, אך חושדים כי מדובר במחלה אוטואימונית.
שקיעת דם תהיה מוגברת בשלבים הפעילים הראשונים של המחלה, בהמשך מתחילות להיות מודגמות חסימות של העורקים הברכיו-צפלים, סאב-קלביאן, קרוטיסים וורטברלים שלעיתים הינן אסימפטומטית. קיימת גם מעורבות של עורקי הכליה והריאות.
החולים ידגימו קרירות של הידיים עם היעדר דופק רדיאלי (משם הכינוי) וכאב ראש, לצד תלונות נוירולוגיות שהינן חולפות בעיקרן ונוטות להופיע בזמן מאמץ, חום או בתנוחות מסויימות, דוגמת טשטוש ראיה בזמן מאמץ או חום, סחרחורת והימפרזיס או תסמונת המיסנסורית.
רבים מהחולים מתים תוך 3-5 שנים, מתן סטרואידים בשלב הפעיל משפר את הפרוגנוזה, לעיתים מבצעים פעולות שחזור כירורגיות בשלב מתקדם.
.
מוצאשלanterior choroidal artery
א.ICA
ב.MCA
ג.PCA
ד.בזילר
anterior choroidal artery is a branch of the ICA
ANTERIOR CHOROIDAL ARTERY
This is a long, narrow artery that springs from the internal Carotid, just above the origin of the posterior communicating artery. it supplies the internal segment of the globus pallidus and posterior limb of the internal capsule and several contiguous structures including (in most patients) the optic tract. It then penetrates the temporal horn of the lateral ventricle, where it supplies the choroid plexus and anastomoses with the posterior choroidal artery.
contralateral hemiplegia, hemihypesthesia, and homonymous sectorial hemianopia (not reaching the vertical meridian of the visual fields) as a result of involvement of the posterior limb of the internal capsule and white matter posterolateral to it, through which the geniculocalcarine tract passes, and the lateral geniculate nucleus.
This combination of extensive unilateral motor, sensory, and visual impairment in an individual with well-preserved language and cognition distinguishes this stroke syndrome from the more common ones involving the major cerebral arteries.
With right-sided lesions, there may be a left spatial neglect and constructional apraxia; slight disorders of speech and language may accompany left-sided lesions.
————
Posterior choroidal artery occlusion uncommonly presents as an isolated stroke syndrome. It usually coexists with posterior cerebral artery and often superior cerebellar artery involvement.
When seen in isolation damage is characteristically limited to the:
* lateral geniculate body
* pulvinar
* posterior thalamus
* hippocampus
* parahippocampal gyrus
When infarction is limited to to the lateral posterior choroidal artery territory, the most common clinical manifestations include:
homonymous quadrantanopsia +/- hemisensory loss
neuropsychological dysfunction (trans-cortical aphasia, memory disturbances).
homonymous horizontal sector anopsia (uncommon but highly suggestive of the involvement of the lateral geniculate body).
anterior choroidal artery
ANTERIOR CHOROIDAL ARTERY
This is a long, narrow artery that springs from the internal Carotid, just above the origin of the posterior communicating artery. it supplies the internal segment of the globus pallidus and posterior limb of the internal capsule and several contiguous structures including (in most patients) the optic tract. It then penetrates the temporal horn of the lateral ventricle, where it supplies the choroid plexus and anastomoses with the posterior choroidal artery.
contralateral hemiplegia, hemihypesthesia, and homonymous sectorial hemianopia (not reaching the vertical meridian of the visual fields) as a result of involvement of the posterior limb of the internal capsule and white matter posterolateral to it, through which the geniculocalcarine tract passes, and the lateral geniculate nucleus.
This combination of extensive unilateral motor, sensory, and visual impairment in an individual with well-preserved language and cognition distinguishes this stroke syndrome from the more common ones involving the major cerebral arteries.
With right-sided lesions, there may be a left spatial neglect and constructional apraxia; slight disorders of speech and language may accompany left-sided lesions.
———–
Posterior choroidal artery occlusion uncommonly presents as an isolated stroke syndrome. It usually coexists with posterior cerebral artery and often superior cerebellar artery involvement.
When seen in isolation damage is characteristically limited to the:
* lateral geniculate body
* pulvinar
* posterior thalamus
* hippocampus
* parahippocampal gyrus
When infarction is limited to to the lateral posterior choroidal artery territory, the most common clinical manifestations include:
homonymous quadrantanopsia +/- hemisensory loss
neuropsychological dysfunction (trans-cortical aphasia, memory disturbances).
homonymous horizontal sector anopsia (uncommon but highly suggestive of the involvement of the lateral geniculate body).
what are the MCA Branch syndromes?
MCA Branch Syndromes
* Superior Division supplying the rolandic and prerolandic areas (Compared to the inferior division supplying the lateral temporal and inferior parietal lobes).
Major infarction in the territory of the superior division causes a dense sensorimotor deficit in the contralateral face, arm, but, to a lesser extent the leg, as well as ipsilateral deviation of the head and eyes; i.e., it differs from the MCA stem occlusion syndrome in that the leg and foot are partly spared and less involved with weakness than the arm and face (“brachiofacial,” or chierobrachial “paralysis”);
there is no impairment of alertness. If the occlusion is long-lasting (not merely transient ischemia with disintegration of the embolus) there will be slow improvement; after a few months, the patient is able to walk with a spastic leg, while the motor deficits of the arm and face Remain. The sensory deficit may be profound, resembling that of a thalamic infarct. but more often it is less severe than the motor deficit, taking the form of stereoanesthesia, agraphesthesia, impaired position sense, tactile localization, and two point discrimination, as well as variable changes in touch, pain, and temperature sense.
With left-sided lesions there is initially a global aphasia, which changes to a
predominantly nonfluent (Broca’s) aphasia, with the emergence of an effortful, hesitant, grammatically simplified, and dysmelodic speech; or quite often there is Broca’s aphasia from the outset.
Embolic occlusion limited to one of the distal branches of the superior division, perhaps the most common stroke seen in clinical practice, produces a more circumscribed infarct that further fractionates the above-described syndrome. With occlusion of the ascending frontal branch, the motor deficit is limited to the face and arm with little or no weakness of the leg, and the latter, if weakened at all, soon improves; with left-sided lesions, there is dysfluent and agrammatic speech and normal comprehension
(Broca’s aphasia). Embolic occlusion of the left Rolandic branch alone results in sensorimotor paresis with severe dysarthria but little evidence of aphasia. A cortical subcortical branch occlusion may give rise solely to a brachial monoplegia or hand weakness that simulates a problem in the peripheral nervous system. Embolic occlusion of ascending parietal and other posterior branches of the superior division may cause no sensorimotor deficit but only a conduction aphasia and ideomotor apraxia. There are many other limited stroke syndromes or combinations of the aforementioned deficits relating to small regions of damage in the frontal, parietal, or temporal lobes. Among these are the Gerstmann syndrome and various forms of agnosia (in some patients, these may be in the territory of the inferior division of the MCA discussed below).
As indicated earlier, the distal territory of the middle cerebral artery may also be rendered ischemic by failure of the systemic circulation, especially if the carotid artery is stenotic; this situation may simulate embolic branch occlusions.
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Occlusion of the inferior division of the MCA is slightly less frequent than occlusion of the superior one, but again is nearly always the result of embolism. The usual result in left-sided lesions is a Wernicke’s aphasia, which generally remains static for days or weeks after which some improvement can be expected. In less-extensive infarcts that are the result of selective distal branch occlusions (superior parietal, angular, or posterior temporal), the deficit in comprehension of spoken and written language may be especially severe. Again, after a few months, the deficits usually improve, often to the point where they are evident only in self-generated efforts to read and copy visually presented words or phrases. With either right- or left-hemispheric lesions, there is usually a superior quadrantanopia or homonymous hemianopia and, with right-sided ones, a left visual neglect and other signs of amorphosynthesis. Rarely, an agitated confusional state, presumably from nondominant temporal lobe damage, may be a prominent feature of dominant hemispheral lesions and sometimes of nondominant
ones. Some of the syndromes applicable to the angular gyrus and the supramarginal gyrus may occur in strokes within this division, depending on the distributions of the vessels in an individual.
מה הסיבה הכי שכיחה לאוטם בפיזור שלheubner?
1. אמבוליה
2. וסקוליטיס
3. אתרוסקלרוזיס
4. ואזוספאזם
אמבוליה
The largest of these deep branches is the artery of Heubner (“recurrent artery of Heubner”; Fig. 33-8). This artery, which may, in fact, be up to four small vessels, shares its territory of supply with anteriorly placed lenticulostriate arteries that emanate from the middle cerebral artery. Strokes in this territory cause infarction of the head of the caudate and adjacent white matter. In the past, this was a common stroke syndrome from meningovascular syphilis. Now usually the stroke is usually due to emboli.
PCA
PCA
The thalamoperforate branches (also called paramedian thalamic arteries) arise slightly more distally from the stem, nearer the junction of the posterior cerebral and posterior communicating arteries (P2 segment of the artery) and supply the inferior, medial, and anterior parts of the thalamus. The thalamogeniculate branches arise still more distally, opposite the lateral geniculate body, and supply the geniculate body and the central and posterior parts of the thalamus.
פרשרון
אם מדובר על אוטם איסכמי התשובה היא מידבריין שמאלי
אם מדובר על דימום בשלב ההתחלתי שלו מדובר בפוטמן שמאלי.
Midbrain- A unilateral lesion in the rostral midbrain tegmentum, by interrupting the cerebral pathways for horizontal conjugate gaze before their decussation, will also cause a paresis of gaze to the opposite side.
Putamen- The most common syndrome is the one caused by putaminal hemorrhage with extension to the adjacent internal Capsule. Neurologic symptoms and signs vary slightly with the precise site and size of the extravasation, but hemiplegia from interruption of the capsule is a consistent feature of medium-sized and large clots. Vomiting occurs in about half the patients. …Within a few minutes or less the face sags on one side, speech becomes slurred or aphasic, the arm and leg weaken and are flaccid, and the eyes tend to deviate away from the side of the paretic Limbs. These events, occurring gradually over a period of several minutes or more, are strongly suggestive of intracerebral bleeding.
בפונס המבט סוטה לכיוון ההמיפרזיס
putamen
Putamen- The most common syndrome is the one caused by putaminal hemorrhage with extension to the adjacent internal Capsule. Neurologic symptoms and signs vary slightly with the precise site and size of the extravasation, but hemiplegia from interruption of the capsule is a consistent feature of medium-sized and large clots. Vomiting occurs in about half the patients. …Within a few minutes or less the face sags on one side, speech becomes slurred or aphasic, the arm and leg weaken and are flaccid, and the eyes tend to deviate away from the side of the paretic Limbs. These events, occurring gradually over a period of several minutes or more, are strongly suggestive of intracerebral bleeding. (look at the lesion)
in the ventral pons, the lacunar syndrome
may be one of pure motor hemiplegia, mimicking
that of internal capsular infarction except at times
for relative sparing of the face and the presence of an ipsilateral paresis of conjugate gaze in some cases (Look at the weakness)
מטופל מפתח וורטיגו כאשר משתמש ביד ימין. מה הסיבה?
1. חסימה פרוקסימלית בעורק ורטברלי ימני
2. חסימה דיסטלית בעורק ורטברלי ימני
3. חסימה בעורק תת בריחי מימין
4. חסימה בעורק תת בריחי משמאל
חסימה בעורק תת בריחי מימין
Subclavian steal syndrome-
אם העורק התת בריחי חסום פרוקסימלית למוצא העורק הורטברלי הימני- פעילות של הזרוע בצד ימין עשויה “למשוך” דם רטרוגרדית מהבזילר והורטברלי השמאלי, אל הורטבלי הימני ולתת הבריחי הימני הדיסטאלי. לעיתים הדבר גורם סימני אי ספיקה בזילרת. הסימן העיקרי הוא ורטיגו וסימני גזע מוח אחרים יחד עם חולשה בעת פעילות של זרוע ימין. ייתכנו גם כאב ראש וקלאודיקציה של כאב בזרוע.
Paramedian branch of basilar artery
“Medial mid-pontine syndrome”
As mentioned, in the ventral pons, the lacunar syndrome may be one of pure motor hemiplegia, mimicking that of internal capsular infarction except at times for relative sparing of the face and the presence of an ipsilateral paresis of conjugate gaze in some cases; or
there is another highly characteristic lacunar syndrome of a combination of dysarthria and clumsiness of one hand. This “clumsy hand-dysarthria” stroke is usually located in the paramedian midpons on the side opposite the clumsy limb but a lacune in the posterior portion of the internal capsule on the side opposite the affected limb.
* Occasionally a lacunar infarction of the pons, midbrain, internal capsule, or parietal white matter gives rise to a hemiparesis with ataxia on the same side as the weakness . Some of the brainstem syndromes may blend with basilar branch syndromes.
מטופל צעיר עם שינוי התנהגות והפרעות בראיה. בהדמיה:
ממה עוד יסבול?
1. הפרעה תחושתית
2. ירידה בשמיעה
3. מונונויריטיס מולטיפלקס
ירידה בשמיעה- מתאים לסוסאק ווסקוליטיס
Susac Syndrome
This is yet another poorly understood form of vasculitis, consisting of a microangiopathy affecting mainly the brain and retina. Psychiatric symptoms, headache, dementia, sensorineural deafness, vertigo, and impairments of vision are the clinical manifestations. These are generally young patients, more often women and present with an incomplete syndrome, without one or more of the core features of deafness or branch retinal artery occlusion or encephalopathy. Funduscopy shows multiple retinal artery branch occlusions and retinal angiography shows multiple additional infarctions and evidence of diffuse vascular leakage from endothelial injury. The MRI may show characteristic white matter lesions, particularly in the central portion of the corpus callosum. Antibodies to endothelial cells have been
Identified by Magro and colleagues in many of their cases. The patients seem to respond to steroid therapy and most cases are singular and do not relapse but there are exceptions.
.
מטופל עם שבץ מוחי בעבר, סובל מכאבי ראש, מנינגיזמוס, אפטות בפה ובאיבר המין, איך נטפל?
1. קומאדין
2. IVIG
3. סטרואידים
4. השגחה בלבד
סטרואידים
בכצ’ט
Behcet Disease
chronic, recurrent vasculitis, involving small vessels, with prominent neurologic manifestations. men more often than women. originally distinguished by the triad of relapsing iridocyclitis and recurrent oral and genital ulcers, but it is now recognized to be a systemic disease with a much wider range of symptoms, including erythema nodosum, thrombophlebitis, polyarthritis, ulcerative colitis, and a number of neurologic manifestations, some of them encephalitic or meningitic in nature.
The most reliable diagnostic criteria were recurrent aphthous or herpetiform oral ulceration, recurrent genital ulceration, anterior or posterior uveitis, cells in the vitreous or retinal vasculitis, and erythema nodosum or papulopustular lesions.
The nervous system is affected in approximately 30 percent of patients with Behcet disease; the manifestations are:
- recurrent meningoencephalitis,
- cranial nerve (particularly abducens) palsies,
- cerebellar ataxia,
- corticospinal tract signs,
- and venous occlusion disease.
- There may be episodes of diencephalic and brainstem dysfunction resembling minor strokes
The neurologic symptoms usually have an abrupt onset and are accompanied by a brisk spinal fluid pleocytosis (lymphocytes or neutrophils may predominate), along with elevated protein but normal glucose values (in one of our patients, 3,000 neutrophils per cubic millimeter were found at the onset of an acute meningitis).
* As a rule, neurologic symptoms clear completely in several weeks, but they have a tendency to recur, and some patients are left with persistent neurologic deficits.
Rarely, the clinical picture is that of a progressive confusional state or dementia.
The cause of Behcet disease is unknown. Administration of corticosteroids has been the usual treatment, on the assumption of an autoimmune etiology. Because the episodes of disease naturally subside and recur, evaluation of treatment is difficult.
נוירופתיה אינה חלק מבכצ’ט!
Behcet Disease
chronic, recurrent vasculitis, involving small vessels, with prominent neurologic manifestations. men more often than women. originally distinguished by the triad of relapsing iridocyclitis and recurrent oral and genital ulcers, but it is now recognized to be a systemic disease with a much wider range of symptoms, including erythema nodosum, thrombophlebitis, polyarthritis, ulcerative colitis, and a number of neurologic manifestations, some of them encephalitic or meningitic in nature.
The most reliable diagnostic criteria were recurrent aphthous or herpetiform oral ulceration, recurrent genital ulceration, anterior or posterior uveitis, cells in the vitreous or retinal vasculitis, and erythema nodosum or papulopustular lesions.
The nervous system is affected in approximately 30 percent of patients with Behcet disease; the manifestations are:
- recurrent meningoencephalitis,
- cranial nerve (particularly abducens) palsies,
- cerebellar ataxia,
- corticospinal tract signs,
- and venous occlusion disease.
- There may be episodes of diencephalic and brainstem dysfunction resembling minor strokes
The neurologic symptoms usually have an abrupt onset and are accompanied by a brisk spinal fluid pleocytosis (lymphocytes or neutrophils may predominate), along with elevated protein but normal glucose values (in one of our patients, 3,000 neutrophils per cubic millimeter were found at the onset of an acute meningitis).
* As a rule, neurologic symptoms clear completely in several weeks, but they have a tendency to recur, and some patients are left with persistent neurologic deficits.
Rarely, the clinical picture is that of a progressive confusional state or dementia.
The cause of Behcet disease is unknown. Administration of corticosteroids has been the usual treatment, on the assumption of an autoimmune etiology. Because the episodes of disease naturally subside and recur, evaluation of treatment is difficult.
גיל מעל 75
יתר לחץ דם!
In approximate order of frequency, the most common sites of a cerebral hemorrhage are:
(1) the putamen and adjacent internal capsule (SO percent);
(2) the central white matter of the temporal, parietal, or frontal lobes (lobar hemorrhages, not strictly associated with hypertension);
(3) the thalamus;
(4) one or the other cerebellar hemisphere;
and (5) the pons.
Bleeding in areas other than those listed above, specifically in the subcortical white matter of one of the lobes of the cerebral hemisphere, is not associated strictly with hypertension. Any number of other causes are usually responsible, the main ones being anticoagulation or thrombolytic
therapy; acquired coagulopathies, cranial trauma, arteriovenous Malformation (discussed further on), trauma, and, in the elderly, amyloidosis of the cerebral vessels. however- Cerebral Amyloid angiopathy – commonly multiple lesion and posterior Location – e.g. occipital.
the usuall cause is still hypertension
אספירין.
The separate issue of the endovascular treatment of intracranial atherosclerosis is considered here for convenience.
The risks of manipulating intracranial vessels are obvious, particularly those of the circle of Willis with no surrounding tissue because they are located within the subarachnoid space.
In an attempt to determine if a stent and angioplasty would improve outcome in patients who had TIAs or minor strokes as a result of an intracranial stenosis, Chimowitz and colleagues (2011) reported that
their trial was stopped early because of poor outcomes of the group who were treated by stent in comparison to medical management. The treatment of symptomatic intracranial atherosclerosis therefore remains problematic and is delegated to the antiplatelet drugs and lipidlowering agents
טיפול ללחץ דם- מוריד סיכון המשמעותי ביותר- גם לשבץ המורגי וגם איסכמי
This is an area of major public health importance in that several modifiable factors are known to increase the liability to stroke. The most important of these are hypertension, atrial fibrillation, diabetes mellitus, cigarette smoking, and hyperlipidemia. Others, such as systemic diseases associated with a hypercoagulable state and the use of contraceptives, also contribute, but only in special circumstances. Hypertension is also the most readily recognized factor in the genesis of primary intracerebral Hemorrhage. It appears that the stroke-producing potential of hypertension is as much the product of heightened systolic pressure, as of diastolic pressure (Rabkin et al).
The cooperative studies of the Veterans Administration (see Freis et al) and the report by Collins and associates (collating 14 randomized trials of antihypertensive drugs) convincingly demonstrated that the long-term control of hypertension decreased the incidence of both ischemic infarction and intracerebral hemorrhage.
—–
Numerous clinical trials have also shown a marked reduction in stroke incidence with the use of cholesterol-lowering drugs. As in the case of coronary artery disease, the level of low-density lipoprotein (LDL) cholesterol has the most impact on the incidence of stroke but elevated triglycerides may also confer risk.
מטופל עם אירועים מוחיים רבים, סובל מ
binswagner
מה לא נכון?
1. הפרעת הליכה
2. דמנציה
3. נגלקט
4. לויקואראוזיס
נגלקט אינו חלק מהותי ממחלת בינסווגנר
widespread degeneration of cerebral
white matter having a vascular causation and observed in the context of hypertension, atherosclerosis of the small blood vessels, and multiple strokes. Hemiparesis, dysarthria, TIAs, and typical lacunar or cortical strokes are admixed in many cases. The process has been associated with a particular radiologic appearance that reflects confluent areas of white matter signal change. The term leukoaraiosis describes the imaging appearance of hypointense periventricular tissues, presumably damaged by chronic ischemia.
Dementia, a pseudobulbar state, and a gait disorder, alone or in combination, are the main features of Binswanger cases
החולה בהכרה אך לא יכול להזיז עיניים לצדדים.
Yet another configuration, the result of occlusion of the midbasilar artery; gives rise to the locked-in syndrome, in which the patient is mute and quadriplegic but conscious, reflecting interruption of descending motor pathways in the base of the pons but sparing of the reticular activating system (“locked-in” syndrome; see Chap. 17). Horizontal eye movements are obliterated but vertical ones and some ability to elevate the eyelids are
Spared. The pupils become extremely small but retain some reaction to light. Midbasilar disease may also cause coma if the posterior communicating arteries are inadequate to perfuse the distal basilar artery territory.
———
* Top of the basilar – coma, somnolence, memory deficit, akinetic mutism, visual hallucinations, ptosis, disorders of occular movements Convergence spasm, vertical gaze paralysis, retraction nystagmus, skew deviation, collier’s lid).
- Superior cerebellar - ipsilateral cerebellar ataxia (mid and sup cerebellar peduncle), N&V, slurred speech, loss of pain and thermal sensation contralaterally.
- AICA – vertigo, N&V, tinnitus, facial weakness, ipsilateral cerebellar ataxia, ipsilateral horner, contralat loss of pain and temp sensation Tinnitus – SCREAMING, there may be an associated hemiplegia
In the absence of one of the localizing crossed cranial nerve signs it is often not possible to distinguish a hemiplegia of pontine origin from one of deep cerebral origin on the basis of motor signs alone. In both, the face, arm, hand, leg, and foot are affected because of the compression of the descending motor fibers into a small segmental region. With brainstem lesions as with cerebral ones, a flaccid paralysis gives way to spasticity after a few days or weeks, and there is no satisfactory explanation for the occurrence in some cases of spasticity from the onset of the stroke. There is also often a combined hemiparesis and ataxia of the limbs on the same side. With a hemiplegia of pontine origin, however, the eyes may deviate to the side of the paralysis, i.e., the opposite of what occurs with supratentorial lesions.
The pattern of sensory disturbance may also be helpful.
- A dissociated sensory deficit over the ipsilateral face and contralateral half of the body usually indicates a lesion in the lower brainstem,
- while a hemisensory loss including the face and involving all modalities indicates a lesion in the upper brainstem, in the thalamus, or deep in the white matter of the parietal lobe.
- **When position sense, two-point discrimination, and tactile localization are affected relatively more than pain or thermal and tactile sense, a cerebral lesion is suggested; the converse indicates a brainstem localization.
- *Bilateral motor and sensory signs are almost certain evidence that the lesion lies in the brainstem. When hemiplegia or hemiparesis and sensory loss are coextensive, the lesion usually lays supratentorially. Additional manifestations that strongly favor a brainstem site are rotational dizziness, diplopia, cerebellar ataxia, a Horner syndrome, and deafness.
מהם הסינדרומים של
midbrain
- Weber- CN III palsy (ipsilesional); hemiplegia and vertical gaze palsy (contralesional).
- Claude- CN III palsy (ipsilesional); ataxia, tremor and vertical gaze palsy (contralesional)
- Benedict- CN III palsy (ipsilesional); ataxia, tremor and hemiplegia (contralesional)
- Nothnagel- CN III palsy (ipsilesional); ataxia and vertical gaze palsy (contralesional)
- Parinaud- Paralysis of upgaze, convergence-retraction nystagmus, lid retraction and light near dissociation
מהם הסינדרומים של
Pons
- Raymond-Cestan- Internuclear ophthalmoplegia (ipsilesional); ataxia and weakness (contralesional)
- Raymond- CN VI palsy (ipsilesional); weakness (contralesional)
- Ataxic hemiparesis- Weakness and ataxia (contralesional)
- Millard-Gubler- CN VI and VII palsy (ipsilesional); weakness (contralesional)
- Foville- CN VI and sometimes VII palsy (ipsilesional); weakness and sensory loss (contralesional)
מהם הסינדרומים של
Medulla
- Wallenberg- Ataxia, loss of pain and temperature for face, weakness of soft palate, larynx and pharynx, Horner’s (ipsilesional); loss of pain and temperature for body (contralesional).
- Babinski-Nageotte-Ataxia, loss of pain and temperature for face, weakness of soft palate, larynx and pharynx, Horner’s (ipsilesional); hemiparesis and loss of pain and temperature for body (contralesional)
- Cestan-Chenias- Loss of pain and temperature for face, weakness of soft palate, larynx and pharynx, Horner’s (ipsilesional); weakness and loss of pain and temperature for body (contralesional)
- Reinhold- Ataxia, loss of pain and temperature for face, weakness of soft palate, larynx, pharynx and tongue, Horner’s (ipsilesional); hemiparesis and loss of touch, pain and temperature for body (contralesional)
- Avellis- Weakness of soft palate, larynx, and pharynx (ipsilesional); weakness and loss of touch for body (contralesional).
- Vernet- Weakness of palate, CN XI palsy, decreased taste posterior tongue (ipsilesional); weakness (contralesional)
- Jackson- CN XII palsy, weakness of soft palate, larynx, and pharynx (ipsilesional); weakness (contralesional)
- Dejerine- CN XII palsy (ipsilesional); hemiplegia and sometimes loss of position and vibration (contralateral)
בן50עםיתרלחץדםודיספליפידמיה.
פנהבשלהופעהחדהשלורטיגו,ניסטגמוס,ירידהבתחושהמימין,הורנרמשמאל,אטקסיהבגפייםשמאליות,
הפעהבבליעהוצרידות.איזהעורקפגוע?
1. VA
2. AICA
3. עורקבאזילרי.
4. PCA
vertebral artery
wallenberng syndrome
- Wallenberg- Ataxia, loss of pain and temperature for face, weakness of soft palate, larynx and pharynx, Horner’s (ipsilesional); loss of pain and temperature for body (contralesional).
Lateral Medullary Syndrome- Known also as the Wallenberg syndrome (who described a case in 1895), this common stroke is produced by infarction of a wedge of lateral medulla lying posterior to the inferior olivary nucleus (see Fig. 34-12). The complete syndrome, as outlined by Fisher and colleagues (1961),
Comprises:
* (a) symptoms derived from the vestibular nuclei (vertigo, nystagmus, oscillopsia, vomiting);
* (b) spinothalamic tract (contralateral or, less often, ipsilateral impairment of pain and thermal sense over half the body);
* (c) descending sympathetic tract (ipsilateral Horner syndrome-miosis, ptosis, decreased sweating);
* (d) issuing fibers of the ninth and tenth nerves (hoarseness, dysphagia, hiccough, ipsilateral paralysis of the palate and vocal cord, diminished gag reflex);
* (e) utricular nucleus (vertical diplopia and illusion of tilting of vision and rotation of the vertical meridian, rarely so severe as to produce upside down vision);
* (f) olivocerebellar, spinocerebellar fibers, restiform body and inferior cerebellum (ipsilateral ataxia of limbs, fallingor toppling to the ipsilateral side, and the sensation of lateropulsion);
* (g) descending tract and nucleus of the fifth nerve (pain, burning, and impaired sensation over ipsilateral half of the face);
* (h) nucleus and tractus solitarius (loss of taste);
* and rarely, (i) cuneate and gracile nuclei (numbness of ipsilateral limbs).
fragmentary syndromes are more frequent, especially at the onset of the stroke.
Vertebral artery
medial medullary syndrome * Jackson- CN XII palsy, weakness of soft palate, larynx, and pharynx (ipsilesional); weakness (contralesional).
- With occlusion of the anterior inferior cerebellar artery (AICA), the extent of the infarct is extremely variable, as the size of this artery and the territory it supplies vary inversely with the size and territory of supply of the PICA. The principal findings are vertigo, vomiting, nystagmus, tinnitus, and sometimes unilateral deafness; facial weakness; ipsilateral cerebellar ataxia (inferior or middle cerebellar peduncle); an ipsilateral Horner syndrome and paresis of conjugate lateral gaze; and contralateral loss of pain and temperature sense of the arm, trunk, and leg (lateral spinothalamic tract)
- The main signs of occlusion of the superior cerebellar artery, the most rostral circumferential branch of the basilar, are ipsilateral cerebellar ataxia of the limbs (referable to middle and superior cerebellar peduncles); nausea and vomiting; slurred speech; and loss of pain and thermal sensation over the opposite side of the body (spinothalamic tract). Partial deafness, static tremor of the ipsilateral upper extremity, an ipsilateral Horner syndrome, and palatal myoclonus have also been reported.
- The results of vertebral artery occlusion are quite variable. If the occlusion of the vertebral artery is so situated as to block the posterior inferior cerebellar artery supplying the lateral medulla and inferior cerebellum (PICA), a characteristic syndrome results with vertigo being a prominent symptom (see “Lateral Medullary Syndrome” ).
- If the subclavian artery is blocked proximal to the origin of the left vertebral artery, exercise of the arm on that side may draw blood from the right vertebral and basilar arteries, retrograde down the left vertebral and into the distal left subclavian artery sometimes resulting in the symptoms of basilar insufficiency. This phenomenon, described in 1961 by Reivich and colleagues, was referred to by Fisher (1961) as the subclavian steal. Its most notable features are vertigo and other brainstem signs coupled with transient weakness on exercise of the left arm. There may also be headache and claudication or pain of the arm. In an unusual configuration in which one vertebral artery is occluded just proximal to the origin of its PICA branch, and the opposite vertebral artery is open and sufficient in size, there may be no symptoms because the PICA is still filled by retrograde flow through its vertebral artery.
בן 65 ברקע גורמי סיכון וסקולרים, מתקבל בשל הפרעה פתאומית של סחרחורת וקשיי דיבור. בדקתו מודגם פטוזיס ומיוזיס מימין, ירידה בתחושת כאב בפנים מימין, דיספגיה ודיסארטריה וירידה בתחושה של כאב וטמפרטורה בגפיים משמאל. חסימה באיזו מעורקים הבאים:
- Post. Inf. Cerebellar
- Basilar artery
- Sup cerebellar artery
- Post cerebral artery
- Ant cerebral artery
PICA= lateral medullary syndrome
- Wallenberg- Ataxia, loss of pain and temperature for face, weakness of soft palate, larynx and pharynx, Horner’s (ipsilesional); loss of pain and temperature for body (contralesional).
Lateral Medullary Syndrome- Known also as the Wallenberg syndrome (who described a case in 1895), this common stroke is produced by infarction of a wedge of lateral medulla lying posterior to the inferior olivary nucleus (see Fig. 34-12). The complete syndrome, as outlined by Fisher and colleagues (1961),
Comprises:
* (a) symptoms derived from the vestibular nuclei (vertigo, nystagmus, oscillopsia, vomiting);
* (b) spinothalamic tract (contralateral or, less often, ipsilateral impairment of pain and thermal sense over half the body);
* (c) descending sympathetic tract (ipsilateral Horner syndrome-miosis, ptosis, decreased sweating);
* (d) issuing fibers of the ninth and tenth nerves (hoarseness, dysphagia, hiccough, ipsilateral paralysis of the palate and vocal cord, diminished gag reflex);
* (e) utricular nucleus (vertical diplopia and illusion of tilting of vision and rotation of the vertical meridian, rarely so severe as to produce upside down vision);
* (f) olivocerebellar, spinocerebellar fibers, restiform body and inferior cerebellum (ipsilateral ataxia of limbs, fallingor toppling to the ipsilateral side, and the sensation of lateropulsion);
* (g) descending tract and nucleus of the fifth nerve (pain, burning, and impaired sensation over ipsilateral half of the face);
* (h) nucleus and tractus solitarius (loss of taste);
* and rarely, (i) cuneate and gracile nuclei (numbness of ipsilateral limbs).
fragmentary syndromes are more frequent, especially at the onset of the stroke.
בחורה צעירה שמעשנת, גלולות , הופיעה כוראה למשך שבוע וחלפה. בהמשך הופעה שלאמרוזיספוגסשחלף. מה נצפה למצוא ?
א.APLA
ב. אנטיאנדותל
ג.binswanger
ד.ANA
APLA
The most frequent neurologic abnormality is a TIA, often taking the form of amaurosis fugax (transient monocular blindness), with or without retinal arteriolar or venous occlusion (Digre et al). Stroke-like phenomena are more frequent in patients who also have migraine, hyperlipidemia, or antinuclear antibodies, and in those who smoke or take birth control pills. Almost one-third of the 48 patients reported by Levine and associates (1990) had thrombocytopenia and 23 percent had a false-positive Venereal Disease Research Laboratory (VDRL) test. The vascular lesions are mainly in the cerebral white matter and are infarcts, seen well with MRI. Angiography reveals occlusions of arteries at unusual sites (Brey et al). The mechanism of stroke is not entirely clear and may derive from emboli originating on mitral valve leaflets similar to nonbacterial thrombotic endocarditis; alternatively, and more likely in our view, there is a noninflammatory in situ thrombosis of medium-sized cerebral vessels, as suggested by the limited pathologic material studied by Briley and colleagues. These circulating antibodies may be associated with a syndrome of transient bilateral chorea or hemichorea; some patients have an additional slight hemiparesis or other subtle focal signs
Almost all of the affected patients we have seen have been women with thrombocytopenia, some of whom probably had systemic lupus, at least on the grounds of laboratory studies.
Autoantibodies directed at the binding protein of phospholipids thereby induce blood clotting. The first of the antibodies to be described were lupus anticoagulant and Anticardiolipin. Most classifications of the anti phospholipid syndrome also include antibodies to beta2 -glycoprotein 1, a protein that may be necessary for the binding and procoagulant effect of anticardiolipin antibody.
The formal criteria for the diagnosis of the syndrome require that an ischemic event be accompanied by the detection of autoantibodies on two occasions at least 6 weeks apart.
Testing for this disease consists of detection of IgM, IgG, and mixed antibodies to each of these three main phospholipids; there is a partial overlap in many patients, in which more than one antibody subclass is present against more than one lipoprotein—80 percent of patients with lupus anticoagulant have anticardiolipin antibody but fewer than 50 percent of those with anticardiolipin antibody have lupus anticoagulant. Antibodies to beta2 -glycoprotein 1 are most specific for the disease.
APLA – false VDRL
The most frequent neurologic abnormality is a TIA, often taking the form of amaurosis fugax (transient monocular blindness), with or without retinal arteriolar or venous occlusion (Digre et al). Stroke-like phenomena are more frequent in patients who also have migraine, hyperlipidemia, or antinuclear antibodies, and in those who smoke or take birth control pills. Almost one-third of the 48 patients reported by Levine and associates (1990) had thrombocytopenia and 23 percent had a false-positive Venereal Disease Research Laboratory (VDRL) test. The vascular lesions are mainly in the cerebral white matter and are infarcts, seen well with MRI. Angiography reveals occlusions of arteries at unusual sites (Brey et al). The mechanism of stroke is not entirely clear and may derive from emboli originating on mitral valve leaflets similar to nonbacterial thrombotic endocarditis; alternatively, and more likely in our view, there is a noninflammatory in situ thrombosis of medium-sized cerebral vessels, as suggested by the limited pathologic material studied by Briley and colleagues. These circulating antibodies may be associated with a syndrome of transient bilateral chorea or hemichorea; some patients have an additional slight hemiparesis or other subtle focal signs
Almost all of the affected patients we have seen have been women with thrombocytopenia, some of whom probably had systemic lupus, at least on the grounds of laboratory studies.
Autoantibodies directed at the binding protein of phospholipids thereby induce blood clotting. The first of the antibodies to be described were lupus anticoagulant and Anticardiolipin. Most classifications of the anti phospholipid syndrome also include antibodies to beta2 -glycoprotein 1, a protein that may be necessary for the binding and procoagulant effect of anticardiolipin antibody.
The formal criteria for the diagnosis of the syndrome require that an ischemic event be accompanied by the detection of autoantibodies on two occasions at least 6 weeks apart.
Testing for this disease consists of detection of IgM, IgG, and mixed antibodies to each of these three main phospholipids; there is a partial overlap in many patients, in which more than one antibody subclass is present against more than one lipoprotein—80 percent of patients with lupus anticoagulant have anticardiolipin antibody but fewer than 50 percent of those with anticardiolipin antibody have lupus anticoagulant. Antibodies to beta2 -glycoprotein 1 are most specific for the disease.
מה הכי רגיש לאבחנה
APLA
1. LAC
2. אנטי קרדיוליפין IgG
3. anti beta 2 glycoprotein
anti beta 2 glycoprotein
The most frequent neurologic abnormality is a TIA, often taking the form of amaurosis fugax (transient monocular blindness), with or without retinal arteriolar or venous occlusion (Digre et al). Stroke-like phenomena are more frequent in patients who also have migraine, hyperlipidemia, or antinuclear antibodies, and in those who smoke or take birth control pills. Almost one-third of the 48 patients reported by Levine and associates (1990) had thrombocytopenia and 23 percent had a false-positive Venereal Disease Research Laboratory (VDRL) test. The vascular lesions are mainly in the cerebral white matter and are infarcts, seen well with MRI. Angiography reveals occlusions of arteries at unusual sites (Brey et al). The mechanism of stroke is not entirely clear and may derive from emboli originating on mitral valve leaflets similar to nonbacterial thrombotic endocarditis; alternatively, and more likely in our view, there is a noninflammatory in situ thrombosis of medium-sized cerebral vessels, as suggested by the limited pathologic material studied by Briley and colleagues. These circulating antibodies may be associated with a syndrome of transient bilateral chorea or hemichorea; some patients have an additional slight hemiparesis or other subtle focal signs
Almost all of the affected patients we have seen have been women with thrombocytopenia, some of whom probably had systemic lupus, at least on the grounds of laboratory studies.
Autoantibodies directed at the binding protein of phospholipids thereby induce blood clotting. The first of the antibodies to be described were lupus anticoagulant and Anticardiolipin. Most classifications of the anti phospholipid syndrome also include antibodies to beta2 -glycoprotein 1, a protein that may be necessary for the binding and procoagulant effect of anticardiolipin antibody.
The formal criteria for the diagnosis of the syndrome require that an ischemic event be accompanied by the detection of autoantibodies on two occasions at least 6 weeks apart.
Testing for this disease consists of detection of IgM, IgG, and mixed antibodies to each of these three main phospholipids; there is a partial overlap in many patients, in which more than one antibody subclass is present against more than one lipoprotein—80 percent of patients with lupus anticoagulant have anticardiolipin antibody but fewer than 50 percent of those with anticardiolipin antibody have lupus anticoagulant. Antibodies to beta2 -glycoprotein 1 are most specific for the disease.
בן 50 התקבל למיון עקב כאב ראש פתאומי ועז.
CT- דמם באיזור הסילביאן פישר
מה מקום המפרצת שגרמה לדמם?
1. ACA
2. ACOM
3. MCA
4. PCA
5. Basilar
MCA
saccular anurisms
Thrombotic Thrombocytopenic Purpura (TTP, Moschcowitz Syndrome) and Hemolytic Uremic Syndrome.
the main features of this disease are fever, anemia, symptoms of renal and hepatic disease, and thrombocytopenia-the latter giving rise to the common hemorrhagic manifestations (petechiae and ecchymoses of the skin, retinal hemorrhages, hematuria, gastrointestinal bleeding, etc.).
* Neurologic symptoms are practically always present and are the initial manifestation of the disease in about half the cases. Confusion, delirium, seizures, and hemiparesis -sometimes remittent or fluctuating in nature–are the usual manifestations of the nervous system disorder and are readily explained by the widespread microscopic ischemic lesions in the brain.
אספירין
בין אירוע וסקולרי למיגרנה עם אאורה, בכל מקרה למיגרנה הטיפול הוא אספירין ואם אירוע וסקולרי אין הנחייה ברורה לטיפול תחת הנושא בע”מ 855, במאמר ההמלצה היא לקלקסן או קומדין בטרימסטר ראשון ואספירין לטרימסטר שני ושלישי.
טרימסר ראשון 0-12 שני 13-26 שלישי 27 עד לידה- אז בשאלה הזו אספירין
RA does not have vascullitis
meningovascular syphilis, tuberculous meningitis, fungal meningitis, and the subacute (untreated or partially treated) forms of bacterial meningitis may be accompanied
by inflammatory changes in the walls of vessels.
The nature of the cerebral vasculitis that
may rarely accompany AIDS is unclear.
Typhus, schistosomiasis, mucormycosis, aspergillosis, malaria, and trichinosis are infrequent causes of inflammatory arterial disease, which, unlike the above-mentioned infections, are not secondary to meningeal infections.
a diverse group of arteritides that have little in common except their tendency to involve the cerebral vasculature. One group involves
the larger caliber vessels and includes the giant cell arteritides-extracranial (temporal) arteritis; granulomatous arteritis of the brain; and aortic branch arteritis, one form of which is known as Takayasu disease.
A second group that affects the medium- and
smaller-sized vessels includes polyarteritis nodosa, the Churg-Strauss type of arteritis, Wegener granulomatosis, systemic lupus erythematosus, Behcet disease, hypersensitivity angiitis, Kohlmeier-Degos disease, and the small vessel disorder of Susac syndrome.
מהי בדיקת הבחירה לאבחון קברנומה מוחית
1. CT
2. CTA
3. MRI
4. angiography
5. biopsy
MRI
CAVERNOUS MALFORMATIONS:
Vascular malformations composed mainly of clusters of thin-walled veins without important arterial feeders and with little or no intervening nervous tissue .
Their tendency to bleed is probably no
less than that of the more common AVMs, and far more often, the hemorrhages are small and clinically silent.The incidence of bleeding is uncertain but is estimated to
be less than 1 percent per year per lesion but quite often they are multiple lesions so that the cumulative risk in any one patient is higher.
approximately 10 percent of these lesions are multiple and 5 percent are familial.
The diagnosis is based on clinical manifestations and MRl, which discloses a cluster of vessels surrounded by a zone of hypodense ferritin in the T1-weighted images, the product of previous small episodes of bleeding.
About one-half of all cavernous angiomas lie in the
brainstem.
Lesions that cause recurrent bleeding and are surgically accessible with little risk are often removed but incidentally discovered angiomas, even if they have caused a small hemorrhage, and those that are inaccessible may be left alone
קברנומה
MRI
CAVERNOUS MALFORMATIONS:
Vascular malformations composed mainly of clusters of thin-walled veins without important arterial feeders and with little or no intervening nervous tissue .
Their tendency to bleed is probably no
less than that of the more common AVMs, and far more often, the hemorrhages are small and clinically silent.The incidence of bleeding is uncertain but is estimated to
be less than 1 percent per year per lesion but quite often they are multiple lesions so that the cumulative risk in any one patient is higher.
approximately 10 percent of these lesions are multiple and 5 percent are familial.
The diagnosis is based on clinical manifestations and MRl, which discloses a cluster of vessels surrounded by a zone of hypodense ferritin in the T1-weighted images, the product of previous small episodes of bleeding.
About one-half of all cavernous angiomas lie in the
brainstem.
Lesions that cause recurrent bleeding and are surgically accessible with little risk are often removed but incidentally discovered angiomas, even if they have caused a small hemorrhage, and those that are inaccessible may be left alone.
——
* cortical dysplasia- The increasingly
refined techniques of MRI now also reveal small zones of developmental cortical dysplasia and hippocampal sclerosis, both of which tend to be epileptogenic.
* The lower-grade astrocytomas (grade II in the WHO classification), which constitute between 25 and 30 percent of cerebral gliomas, may occur anywhere in the brain or spinal cord. The median survival in cases of anaplastic astrocytoma is considerably longer than for glioblastoma. Favored sites of occurrence are
the cerebrum, cerebellum, hypothalamus, optic nerve and chiasm, and pons. In general, the location of the tumor appears to be influenced by the age of the patient. Astrocytomas of the cerebral hemispheres arise mainly in adults in their third and fourth decades or earlier; astrocytomas in other parts of the nervous system, particularly the posterior fossa and optic nerves, are more frequent in children and adolescents.
קברנומה
CAVERNOUS MALFORMATIONS:
Vascular malformations composed mainly of clusters of thin-walled veins without important arterial feeders and with little or no intervening nervous tissue .
Their tendency to bleed is probably no
less than that of the more common AVMs, and far more often, the hemorrhages are small and clinically silent.The incidence of bleeding is uncertain but is estimated to
be less than 1 percent per year per lesion but quite often they are multiple lesions so that the cumulative risk in any one patient is higher.
approximately 10 percent of these lesions are multiple and 5 percent are familial.
The diagnosis is based on clinical manifestations and MRl, which discloses a cluster of vessels surrounded by a zone of hypodense ferritin in the T1-weighted images, the product of previous small episodes of bleeding.
About one-half of all cavernous angiomas lie in the
brainstem.
Lesions that cause recurrent bleeding and are surgically accessible with little risk are often removed but incidentally discovered angiomas, even if they have caused a small hemorrhage, and those that are inaccessible may be left alone.
אישה בת 60 עם כאבי ראש ופרכוס לראשונה בחייה.
CT מוח תקין
וגם ניקור מותני.
MRI מוקדים היפואינטנסיים ב
GRE
ונגעים קשים היפראינטנסיים בפלייר.
מה האבחנה הסבירה?
1. PRES
2. CAA
3. RCVS
CAA
Cerebral Amyloid Angiopathy
This angiopathy consists of the deposition of amyloid in the media and adventitia of small vessels, predominantly in the meninges, cortex, and cortical penetrating vessels. The incidence at autopsy of vascular amyloid deposition in the brain is related to the age of the population studied; rates of 12 percent are cited in patients older than 85 years of age (the same changes are present in more than 25 percent of individuals with Alzheimer disease, but the nature of the amyloid [Aβ40 in the pure cerebrovascular form] is different in the two conditions). The result of this deposition is several large or numerous small cerebral hemorrhages of various ages. There is a propensity for hemorrhages in the posterior parts of the brain. An association has been found with the homozygous APOE ε4/ε4 genotype by Greenberg and colleagues (1995) but others have found an association with the E2 allele. As alluded to in earlier sections on cerebral hemorrhage, cerebral amyloid angiopathy is a cause of otherwise unexplained single of multiple cerebral hemorrhage in older people.
- inflammatory type of cerebrovascular amyloidosis which is referred to as cerebral amyloid angiopathy-related inflammation. Included in the clinical picture are encephalopathy, seizures, headache, and focal cerebral symptoms such as aphasia. The MRI appearance is of large subcortical and cortical patches of abnormal T2 hyperintensity suggestive of cerebral edema. The findings are similar to the mainly white matter encephalitis that was found in some patients with Alzheimer disease who were treated with a monoclonal antibody directed against a-beta amyloid. This disease subtype has a significantly younger age at presentation compared to cerebral amyloid angiopathy and is strongly associated with the APOE ε4/ε4 genotype. It is treated with a course of high-dose corticosteroids or other forms of immunosuppression and some improvement is to be expected though outcomes may be unfavorable
-
PRES:
Rapidly evolving syndrome of severe hypertension in association with headache, N&V, visual disturbances and confusion, might lead to stupor and coma. Seizures may occur.
The syndrome may be dominated by symptoms referable to the occipital and parietal regions with field deficits, hallucinations, balint syndrome, cortical blindness, Encephalopathy. Hence PRES. Eclampsia – special form of PRES.
A clustering of multiple microinfarcts and petechial haemorrhages in any region may result in focal neurological signs – hemiparesis, aphasia, distortion of vision.
MRI – large areas of white matter signal change which tend to normalize over weeks.
Hypertensive encephalopathy and eclampsia may cause SAH – though small and may be asymptomatic only appreciated on MRI
Rx- lower BP, Magnesium Sulfate, CCB – nifedipine, Labetalol -
RCVS:
Widespread multifocal or diffuse reduction in caliber of cerebral vessels and their branches.
Rx by stopping offending agent and give CCB orally.
נשאות ל
APOE2
מעלה סיכון לאיזו מהמחלות הבאות?
1. פרקינסון
2. אלצהיימר בגיל מוקדם
3. דמם תוך- מוחי
4. דמנציה פרונטוטמפורלית
5. MSA
דמם תוך מוחי
Cerebral Amyloid Angiopathy
This angiopathy consists of the deposition of amyloid in the media and adventitia of small vessels, predominantly in the meninges, cortex, and cortical penetrating vessels. The incidence at autopsy of vascular amyloid deposition in the brain is related to the age of the population studied; rates of 12 percent are cited in patients older than 85 years of age (the same changes are present in more than 25 percent of individuals with Alzheimer disease, but the nature of the amyloid [Aβ40 in the pure cerebrovascular form] is different in the two conditions). The result of this deposition is several large or numerous small cerebral hemorrhages of various ages. There is a propensity for hemorrhages in the posterior parts of the brain. An association has been found with the homozygous APOE ε4/ε4 genotype by Greenberg and colleagues (1995) but others have found an association with the E2 allele. As alluded to in earlier sections on cerebral hemorrhage, cerebral amyloid angiopathy is a cause of otherwise unexplained single of multiple cerebral hemorrhage in older people.
- inflammatory type of cerebrovascular amyloidosis which is referred to as cerebral amyloid angiopathy-related inflammation. Included in the clinical picture are encephalopathy, seizures, headache, and focal cerebral symptoms such as aphasia. The MRI appearance is of large subcortical and cortical patches of abnormal T2 hyperintensity suggestive of cerebral edema. The findings are similar to the mainly white matter encephalitis that was found in some patients with Alzheimer disease who were treated with a monoclonal antibody directed against a-beta amyloid. This disease subtype has a significantly younger age at presentation compared to cerebral amyloid angiopathy and is strongly associated with the APOE ε4/ε4 genotype. It is treated with a course of high-dose corticosteroids or other forms of immunosuppression and some improvement is to be expected though outcomes may be unfavorable
מה מהבאים לא יכול לחקות
TIA
1. אאורה של מיגרנה
2. דימום תוך מוחי
3. מטסטזה
4. המטומה סובדורלית
5. מנינגיומה
דימום תוך מוחי.
Differential Diagnosis of TIA
Transient focal neurologic symptoms are ubiquitous in neurologic practice. They may be a result of seizures, migraine, syncope, or other conditions such as transient global amnesia, and they occur occasionally in patients with multiple sclerosis. The clinical setting in which they occur assists in making clear the nature of the attack. Furthermore, transient and reversible episodes
of focal cerebral symptoms, indistinguishable from TIAs, are known to occur in patients with meningioma, glioblastoma, metastatic brain tumors situated in or near the cortex, and even with subdural hematoma
שקיעה של קומפלקסים אימונים
Some of the neurologic manifestations can be accounted for by widespread microinfarcts in the cerebral cortex and brainstem; these, in turn, are related to destructive and proliferative changes in arterioles and capillaries. The acute lesion is subtle; it is not a typical fibrinoid necrosis of the vessel wall, like that in hypertensive encephalopathy, and there is no cellular infiltration. Attachment of immune complexes to the endothelium is the postulated mechanism of vascular injury. Thus, the changes do not represent a vasculitis in the strict sense of the word.
NOTCH 3
The acronym CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy) is now applied. In these patients recurrent small strokes beginning in early adulthood culminate in a subcortical dementia. Migraine headaches, often with neurologic accompaniments, may precede the strokes by several years, as may numerous and varied TIAs that are attributed, probably incorrectly, to the migraine.
The responsible mutation is a missense change on chromosome 19 of the NOTCH 3 gene, in the same locus as the gene for familial hemiplegic migraine, and has been characterized by Joutel and colleagues; this provides a diagnostic test that can be performed on the blood or skin. The gene may now be sequenced in commercial laboratories. The diagnosis can also be confirmed by
finding eosinophilic inclusions in the arterioles of a skin biopsy
Post partum cerebral vasculopathy
AKA
RCVS
ווגנר
Wegener Granulomatosis
This is a rare disease of unknown cause, affecting adults as a rule and favoring males slightly. A subacutely evolving vasculitis with necrotizing granulomas of the upper and lower respiratory tracts followed by necrotizing glomerulonephritis are its main features. Neurologic complications come later in one-third to one-half of cases and take two forms:
1. a peripheral neuropathy either in a pattern of polyneuropathy or, far more frequently, in a pattern of mononeuropathy multiplex.
2. multiple cranial neuropathies as a result of direct extension of the nasal and sinus granulomas into adjacent upper cranial nerves and from adjacent to pharyngeal lesions to the lower cranial nerves.
בת 37 מובאת למלר”ד במצב בלבולי, עם כאבי ראש והפרעה בראייה. במהלך שהותה במלר”ד מופיע
התקף פרכוסי כללי. ב- CT נראים שינויים היפודנסיים עם גבול לא ברור באונות האוקסיפיטליות. איזו תרופה
עלולה לגרום לתמונה קלינית זו:?
א. Amantadine .
ב. Isoniazid .
ג. Natalizumab .
ד. Tacrolimus
נטליזומב= אינטרפרון
igure 33-1. Arrangement of the major arteries on the right side carrying blood from the heart to the brain. Also shown are collateral vessels that may modify the effects of cerebral ischemia. For example, the posterior communicating artery connects the internal carotid and the posterior cerebral arteries and may provide anastomosis between the carotid and basilar systems. Over the convexity, the subarachnoid inter-arterial anastomoses linking the middle, anterior, and posterior cerebral arteries are shown, with inset A illustrating that these anastomoses are a continuous network of tiny arteries forming a border zone between the major cerebral arterial territories. Occasionally a persistent trigeminal artery connects the internal carotid and basilar arteries proximal to the circle of Willis, as shown in inset B. Anastomoses between the internal and external carotid arteries via the orbit are illustrated in inset C. Wholly extracranial anastomoses from muscular branches of the cervical arteries to vertebral and external carotid arteries are indicated in inset D.
Figure 33-2. Diagram of the base of the brain showing the principal vessels of the vertebrobasilar system (the circle of Willis and its main
branches). The term M1 is used to refer to the initial (stem) segment of the middle cerebral artery; A1 to the initial segment of the anterior cerebral
artery proximal to the anterior communicating artery; A2 to the postcommunal segment of the anterior cerebral artery; and P1 and P2 to the corresponding
pre- and post-communicating segments of the posterior cerebral artery. The letters and arrows on the right indicate the levels of the
four cross-sections following: A = Fig. 33-16; B = Fig. 33-15; C = Fig. 33-14; D = Fig. 33-13. Although vascular syndromes of the pons and medulla
have been designated by sharply outlined shaded areas, one must appreciate that because satisfactory clinicopathologic studies are scarce, the
diagrams do not always represent established fact. The frequency with which infarcts fail to produce a well-recognized syndrome and the special
tendency for syndromes to merge with one another must be emphasized.
Figure 33-3. MRI showing acute infarctions. The upper images show a right middle cerebral artery infarction that appears bright on diffusionweighted
imaging (DWI) (upper left). There is subtle hyperintensity representing early vasogenic edema on T2-FLAIR sequence (upper right). The
lower images show an acute cerebellar infarction in the territory of the posterior inferior cerebellar artery (PICA) that is bright on DWI (lower left)
and faintly bright on T2-FLAIR (arrow, lower right). There is also a previous infarction just anterior to the acute cerebellar stroke, that is dark on
DWI and bright on T2 due to gliosis.
Figure 33-4. In perfusion imaging, a time-intensity curve (A) is generated by measurement of the passage of contrast material through brain
tissue. The slope of the curve represents blood flow and the area under the curve represents blood volume. Voxel measurements of these parameters
are converted to color maps showing blood flow, volume, and contrast transit time throughout the brain. Arterial occlusions alter the time- intensity curve by either flattening the slope of the curve or reducing the area under the curve. As an example, an acute occlusion of the proximal
segment of the right middle cerebral artery produces a region of signal abnormality on diffusion-weighted imaging (B) that is matched in size
by an area of reduced blood volume (C). This area represents infarcted tissue. The area of prolonged transit time (D) affects a larger territory,
particularly posteriorly. The difference between this territory and the infarcted zone represents the ischemic penumbra, and is often referred to
as the diffusion-perfusion mismatch.
Figure 33-5. Diagram of the left cerebral hemisphere, lateral aspect, showing the courses of the middle cerebral artery and its branches and
the principal regions of cerebral localization. Below is a list of the clinical manifestations of infarction in the territory of this artery and the corresponding
regions of cerebral damage.
Figure 33-6. Diagram of one cerebral hemisphere, coronal section, showing the regions of blood supply of the major cerebral vessels.
Figure 33-7. A. Diagram of the right cerebral hemisphere, medial aspect, showing the branches and distribution of the anterior cerebral artery
and the principal regions of cerebral localization. Below is a list of the clinical manifestations of infarction in the territory of this artery and the
corresponding regions of cerebral damage. Also shown is the course of the main branch of the posterior cerebral artery on the medial side of
the hemisphere. Note: Hemianopia does not occur; transcortical aphasia occurs rarely (isolation of the language areas) (see Chap. 22). B. Axial
diffusion-weighted MRI showing an acute ischemic infarction in the anterior cerebral artery territory.
Figure 33-8. Corrosion preparations with plastics demonstrating penetrating branches of the anterior and middle cerebral arteries. The medial and lateral lenticulostriate arterioles are labeled, along with the recurrent artery of Heubner. (Reproduced by permission from Krayenbühl and Yasargil.)
Figure 33-9. Diagram of the regions of blood supply of the diencephalon.
Distribution of the (1) anterior cerebral artery, (2) posterior
cerebral artery, (3) anterior and posterior choroidal arteries, (4)
posterior communicating artery, and (5) internal carotid artery.
(Reproduced by permission from Krayenbühl and Yasargil.)
Figure 33-10. A. Inferior aspect of the left hemisphere showing the branches and distribution of the posterior cerebral artery and the principal
anatomic structures supplied. The vessel is considered from the perspective of its proximal and distal territories. Listed below are the clinical
manifestations produced by infarction in these territories and the corresponding regions of damage. Tremor in repose has been omitted because
of the uncertainty of its occurrence in the posterior cerebral artery syndrome. Peduncular hallucinosis may occur in thalamic-subthalamic
ischemic lesions, but the exact location of the lesion is unknown. B. Axial diffusion-weighted MRI showing an acute ischemic infarction in the
posterior cerebral artery territory.
Figure 33-11. The posterior cerebral and basilar arteries. A. The terminus of the basilar artery and branches originating from the P1 through P3 segments. (Reproduced by permission from Stroke 34:2264, 2003.) B. Lateral view of the brain showing the branches of the posterior cerebral artery. (Reproduced by permission from Krayenbühl and Yasargil.) C. Axial diffusion-weighted MRI showing an acute ischemic infarction due to occlusion of an artery of Percheron, an anatomic variant, in which an azygos paramedian artery supplies both sides of the posterior-medial thalamus.
Figure 33-12. Regions supplied by the posterior segment of the circle
of Willis, lateral view (A) and basal view (B). A. (1) Posterior cerebral
artery; (2) superior cerebellar artery; (3) basilar artery and superior
cerebellar artery; (4) posterior inferior cerebellar artery; (5) vertebral
artery (posterior inferior cerebellar artery, anterior spinal artery,
posterior spinal artery). B. (1) Posterior cerebral artery; (2) superior
cerebellar artery; (3) paramedian branches of the basilar artery and
spinal artery; (4) posterior inferior cerebellar artery; (5) vertebral
artery; (6) anterior inferior cerebellar artery; (7) dorsal spinal artery.
(Reproduced by permission from Krayenbühl and Yasargil.)
Figure 33-13. Transverse section through the upper medulla, reflecting regions supplied by the vertebral arteries and their branches.
Figure 33-14. Transverse section through the lower pons, reflecting the regions supplied by the lower basilar artery including its anterior inferior
cerebellar artery branch.
Figure 33-15. Transverse section through the midpons in the regions supplied by the mid-basilar artery and its short circumferential and paramedian branches.
Figure 33-16. Transverse section through the upper pons and the regions supplied by the upper basilar artery and its superior cerebellar artery branch.
Figure 33-17. Axial diffusion-weighted MRI of acute lacunar infarctions. A. Left capsular infarction causing a right pure motor hemiplegia. B.
Left pontine infarction causing a clumsy hand–dysarthria syndrome.
Figure 33-18. Large ischemic infarction of the left cerebral hemisphere mainly in the distribution of the superior division of the middle cerebral
artery. CT at 24 h (left) and 72 h (right) following the onset of stroke symptoms. The second scan (right) demonstrates marked swelling of the
infarcted tissue and rightward displacement of central structures.
Figure 33-19. A. Axial diffusion-weighted MRI showing multifocal acute infarctions in the left ACA-MCA arterial border zone (watershed).
B. Magnetic resonance angiography displays severe stenosis of the left internal carotid artery (arrow), just above the common carotid artery
bifurcation.
Figure 33-20. Cervical artery dissections. T1 MRI with fat saturation (left) and magnetic resonance angiography (right). The upper images show bilateral internal carotid artery dissections (arrows). The lower images show a left vertebral artery dissection (arrows). The T1 hyperintensity that is shown in the left upper and lower images is due to thrombus within the false lumen of the vessel.
Figure 33-21. Moyamoya disease. Digital subtraction angiography in the coronal plane of the left common carotid artery. On the left image, there
is occlusion of the left internal carotid artery near its terminus, and evidence of abnormal vascular proliferation involving the lenticulostriate
vessels (arrow). The external carotid artery branches fill normally. The right image shows the same contrast injection during the early capillary
phase; the characteristic “puff of smoke” is encircled.
Figure 33-22. Axial T2-FLAIR MRI of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL).
There is confluent symmetric abnormal hyperintensity within the periventricular white matter and internal and external capsules (left) and characteristically,
also in the anterior temporal lobes (right).
Figure 33-23. Two axial T2-FLAIR images of mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS). Multifocal
asymmetric areas of cortical and subcortical T2 hyperintensity are seen.
Figure 33-24. Unenhanced CT showing hypertensive hemorrhages in the putamen (A), thalamus (B), pons (C), and cerebellum (D). The thalamic
hemorrhage (B) has extended into the posterior horn of the right lateral ventricle and the cerebellar hemorrhage (D) has extended into
the fourth ventricle.
Figure 33-25. Diagram of the circle of Willis
showing the principal sites of intracranial aneurysms.
Approximately 90 percent of aneurysms
arise from branches of the anterior half of the
circle. The sizes of the aneurysms depicted correspond
roughly to the frequency of occurrence
at those sites.
Figure 33-26. Subarachnoid hemorrhage as a result of rupture of a basilar artery aneurysm. Left: Axial CT at the level of the lateral ventricles
showing widespread hyperdense blood in the subarachnoid spaces and layering within the ventricles with resultant hydrocephalus. There is a
blood–CSF level in the posterior horns of the lateral ventricles, typical of recent bleeding. Right: At the level of the basal cisterns, blood can be
seen surrounding the brainstem, in the anterior sylvian fissures, and the anterior interhemispheric fissure. The temporal horns of the lateral
ventricles are enlarged, reflecting acute hydrocephalus.
Figure 33-27. Aneurysm of the anterior communicating artery. Left: CT angiogram showing the aneurysm (arrow) arising from the branch point
of the anterior communicating artery and the A1 segment; Right: Reconstructed image from CT angiogram data showing the aneurysm (arrow)
in relation to the adjacent bony and vascular structures.
Figure 33-28. Vasospasm following subarachnoid hemorrhage due to rupture of an anterior communicating artery aneurysm. Sagittal CT angiography reveals multifocal narrowing of segments of the anterior cerebral artery (arrows).
Figure 33-29. Giant aneurysm of the anterior cerebral artery. Left: T1-weighted MRI without gadolinium infusion. The white signal is thrombus
within the anterior aspect of the aneurysm; there is some blood flow within the lesion evidenced by the darker signal. Right: Cerebral angiogram,
left common carotid injection, lateral view, showing the residual flow in the posterior aspect of the aneurysm.
Figure 33-30. Left parietal arteriovenous malformation. Upper left: T2-weighted MRI shows a tangle of vessels interspersed throughout the parietal lobe. The largest of these vessels are dilated draining veins. Upper right: CT angiography demonstrates enhancement of the abnormal vessels throughout the left hemisphere. The AVM is fed primarily via branches of the left MCA. Cerebral angiography. Contrast injected into the left internal carotid artery reveals the feeding arteries (lower left) and abnormal early filling of dilated draining veins (lower right) due to blood bypassing the capillary bed.
Figure 33-31. Cerebral angiogram of a cerebral dural arteriovenous malformation. The nidus is located at the cerebral convexity (arrow). There is rapid filing of the cerebral venous system after injection of contrast into one internal carotid artery.
Figure 33-32. Cavernous malformation in the right parietal lobe. Axial T2 MRI (left) shows a round lesion which is heterogeneously hyperintense
and hypointense. This appearance is due to vascular channels which are immediately adjacent to each other without interspersed normal brain
tissue, containing blood products in different stages of degradation. An axial gradient echo MRI (right) shows that the lesion is hypointense, again
due to blood products.
Figure 33-33. A developmental venous anomaly (DVA) and its collecting vein in the left cerebellum on a T1-weighted MRI with contrast.
Figure 33-34. Axial susceptibility-weighted MR images from a 65-year-old man with cerebral amyloid angiopathy. The left image shows innumerable cortical and subcortical microhemorrhages. The right panel shows cortical gyriform hemosiderosis, with additional cortical and subcortical microhemorrhages.
Figure 33-35. Hypertensive encephalopathy. Axial T2-FLAIR images showing fairly symmetric abnormal hyperintensity predominately in the parietooccipital lobes. The lesion affects the cortex and subcortical white matter and there is little mass effect. In severe cases, there may be hemorrhage and heterogeneous infarction in the cerebral cortex. The same imaging findings may occur in eclampsia (see also Chap. 41).
Figure 33-36. Reversible cerebral vasoconstriction syndrome. Axial (left) and sagittal (right) CT angiogram showing segmental narrowing of the
middle and anterior cerebral artery branches (arrows).
Figure 33-37. Granulomatous angiitis of the brain. Cerebral arteriogram from a common carotid artery injection, lateral projection, demonstrating numerous areas of irregular narrowing (arrows) and, in some areas, contiguous slight dilatation (“beading”), particularly in the anterior cerebral artery.
Figure 33-38. Typical lesions of Susac syndrome in the central portion of the corpus callosum shown in a sagittal T-2 FLAIR MRI. These abnormal areas may show restriction of diffusion.
Figure 33-39. Venous sinus thrombosis. Coronal (left) and sagittal (center) magnetic resonance venogram demonstrating absence of flow in the superior sagittal and left transverse sinuses (arrows). Note that the straight sinus and right transverse sinuses remain patent. Axial T2-FLAIR MRI shows left otomastoiditis, which was the cause of the extensive thrombosis. The clot can be seen in the MRI (right) (arrow).
