AVC

AVC
Prof. M. Gavriliuc
Department of
Neurology,

Medical and
Pharmaceutical
Nicolae Testemitsanu
State University,
Republic of Moldova

FACULTATEA STOMATOLOGIE, CICLUL NEUROSTOMATOLOGIE
EPILEPSIA
BAZELE ANATOMICE ALE CONSTIENTEI
COMA: koma (gr.) somn adnc

Pacientul aparent doarme, dar nu
poate fi trezit de stimuli externi sau
de necesiti interne (areactivitate).

Trei procente din bolnavii admii n
serviciile de urgen sunt afectai
de o leziune responsabil de
tulburrile de contien.

Este o problem psihologic i
filozofic.
FIZIOPATOLOGIA COMEI
PRINCIPALELE CAUZE CARE PRODUC COMA:
1. O leziune a trunchiului
cerebral sau tulburri
metabolice ce lezeaz sau
deprim Sistemul Reticular
Activator (SRA).
2. O leziune emisferic
bilateral sau o inhibiie a
activitii emisferelor.
1 + 2
OBSERVAIA PRACTIC A BOLNAVULUI COMATOS
COMA nu este o entitate
nozologic per se , dar face parte
dintr-o problem medical
(hipoxie, AVC, traumatism,
insuficient renal sau hepatic
etc.). Toat atentia, n cauz
evident, este focalizat asupra
bolii primitive.

n foarte multe cazuri, ns, cauza
comei la admitere nu se
cunoate.

DIAGNOSTICUL DIFERENTIAL AL COMEI
I. Maladii ce nu provoac semne neurologice de focar sau de
lateralizare, cu pstrarea funciilor trunchiului cerebral. Examenul
CT i RM cerebral, numrul de celule n LCR este normal.
A. Intoxicaii: alcool, barbiturate i alte droguri sedative, opiate,
etc.

B. Afeciuni metabolice: anoxia, acidoza diabetic, uremia, coma
hepatic, hipoglicemia, boala Addison, deficiena nutriional
profund.

C. Infecii de sistem severe : pneumonia, febra tifoid, malaria,
septicemia, sindromul Waterhouse-Friderichsen.

D. Colapsul (ocul) circulator de orice cauz.

E. Starea postcritic (dup acces epileptic).

F. Encefalopatia hipertensiv i eclampsia.

G. Hipertermia sau hipotermia.

H. Comoia cerebral.

I. Stupoarea i coma idiopatic.

J. Hidrocefalia acut.
I. Maladii ce nu provoac semne neurologice de focar sau de
lateralizare, cu pstrarea funciilor trunchiului cerebral. Examenul
CT i RM cerebral, numrul de celule n LCR este normal.
II. Maladii care cauzeaz iritaie meningeal cu sau fr febr, cu
un exces de eritrocite sau leucocite n LCR, de obicei fr semne de
focar, de lateralizare sau de implicare a trunchiului cerebral. CT sau
RMN care preced puncia lombar este normal sau anormal.
A. Hemoragie subarahnoidian din erupie de anevrism,
malformaie arterio-venoas, ocazional post-traumatic.

B. Meningit acut bacterian.

C. Unle forme de encefalite virale.
III. Maladii care provoac semne de lezare de focar a
trunchiului cerebral sau semne de lateralizare cerebral,
cu sau fr modificri ale LCR. CT i RMN de obicei sunt
anormale.
A. Hemoragie sau infarct cerebral emisferial.
B. Infarct de trunchi cerebral prin tromboz sau embolism.
C. Abces cerebral, empiem subdural.
D. Hemoragie cerebral epidural i subdural, contuzie
cerebral.
E. Tumori cerebrale.
F. Cauze mixte: tromboz de vene corticale, unele forme de encefalite
virale, encefalomalacie de focar embolic pe motiv de endocardit
bacterian, leucoencefalit hemoragic acut, encefalomielit acut (post-
infecioas), i altele.

GCS variaz de la 3 pn 15 puncte, 3 fiind valoarea cea mai proast, iar 15
cea mai bun. Este compus din trei compartimente : Rspunsul Ocular,
Rspunsul Verbal, Rspunsul Motor, n modul dup cum urmeaz :

Rspunsul ocular. (4) Rspunsul verbal. (5)
O1.Deschiderea ochilor lipsete. V1. Rspunsul verbal lipsete.
O2. Ochii se deschid la stimul dureroi. V2. Sunete nenelese.
O3. Ochii se deschid la cerere verbal. V3. Cuvinte/expresii neadecvate.
O4. Ochi deschii spontan, cu clipit. V4. Vorbire confuz.
V5. Adecvat.
Rspunsul motor. (6)
M1. Lipsete.
M2. Extensie la stimul dureros.
M3. Flexie la stimul dureros.
M4. Retrage membrul la stimul dureros.
M5. Localizeaz durerea (ncearc s nlture stimulul dureros).
M6. ndeplinete instruciunile.

Este important a specifica GCS dup compartimentele din care este compus,
adic O3V3M5 = GCS 11. GCS 13 puncte i mai mult denot o alterare
cerebral uoar, 9 12 puncte - moderat, iar 8 i mai puin sever.

Teasdale G., Jennett B., LANCET (ii) 81-83, 1974.
Glasgow Coma Score
Scala Glasgow

Scor total O+V+M

Stare de contien 15
Somnolen 14 - 13
Obnubilare, stupoare 12 - 9
Com 8 - 4
Moarte cerebral 3
Care of the Comatose Patient
1. The management of shock, if it is present, takes precedence
over all other diagnostic and therapeutic measures.

2. Shallow and irregular respirations, stertorous breathing
(indicating obstruction to inspiration), and cyanosis require the
establishment of a clear airway and delivery of oxygen. The
patient should initially be placed in a lateral position so that
secretions and vomitus do not enter the tracheobronchial tree.
Secretions should be removed by suctioning as soon as they
accumulate; otherwise they will lead to atelectasis and
bronchopneumonia. Arterial blood gases should be measured
and further observed by monitoring of oxygen saturation. A
patient's inability to protect against aspiration and the presence
of either hypoxia or hypoventilation dictates the use of
endotracheal intubation and a positive-pressure respirator.
ACCIDENT VASCULAR CEREBRAL
Ictusul cerebral este un
sindrom clinic, caracterizat
prin acuze aprute n mod
rapid i/sau simptome de
deficit cerebral de focar i
uneori de ordin general, cu
o durat mai mare de 24 ore
sau care conduc la deces,
fr oricare alt motiv n
afara celui de proces
patologic vascular (Hatano,
1976).
Informaia epidemiologic
Accidentul vascular cerebral reprezint a treia cauz de
mortalitate dup afeciunile cardiace i boala neoplazic
i prima cauz n rndul bolilor neurologice.

Incidena anual i mortalitatea prin AVC au sczut
considerabil (pe plan mondial) n ultimii ani, acest lucru
datorndu-se unui bun control al factorilor de risc.

Republica Moldova se afl printre primele tari ale
Europei la capitolul mortalitii prin boli cerebro-
vasculare.

Rata mortalitii pacienilor cu AVC n lume constituind
8% pentru pacienii ce au benifeciat de tratament n
unitile de STROKE i 27% - 33% pentru cei care nu a
fost posibil internarea n unitile specializate.

Factorii de risc
Nemodificabili
Vrsta
Rasa
Sexul
Greutatea ponderal mic la natere
Anamnestic familial de AVC sau AIT
Factorii de risc modificabili, bine documentai
Hipertensiune arterial
Tabagism
Diabet zaharat
Patologia carotidian
Fibrilaie atrial
Anemia falciform
Dislipidemia
Stilul alimentar
Obezitatea
Inactivitatea fizic
Terapia hormonal postmenopauzal
BOLILE CEREBRO-VASCULARE
Etiologia alteraiilor arterelor i venelor rezultnd n anormaliti
cerebrale
1. Tromboza aterosclerotic.
2. Spasme de arter cerebral (atac ischemic cerebral tranzitoriu).
3. Embolia.
4. Hemoragia hipertensiv.
5. Anevrismul sacular sau malformaia arterio-venoas cu sau fr
ruptur.
6. Arterita
a. Sifilisul meningovascular, arterita secundar ca consecin a
meningitei piogenice sau tuberculoase, infecii rare (tifos, schistosomiasis,
malarie, micoze, etc.)
b. Bolile esutului conjunctiv (poliarterita nodoas, lupus
erythematosus), arterita necrotizant, arterita Wegener, arterita
temporal, boala Takayasu, granulomatoza sau arterita cu celule gigante
a aortei, angiita arterelor cerebrale.
Etiologia alteraiilor arterelor i venelor
rezultnd n anormaliti cerebrale
1. Tromboza
aterosclerotic.
cerebrale
2. Spasme de arter cerebral (atac ischemic cerebral
tranzitoriu).
3. Embolia.
5. Anevrismul sacular sau malformaia arterio-venoas cu sau fr ruptur.
6. Arterita
erythematosus), arterita necrotizant, arterita Wegener, arterita temporal,
boala Takayasu, granulomatoza sau arterita cu celule gigante a aortei,
angiita arterelor cerebrale.
cerebrale
3. Embolia.
ruptur.
6. Arterita
3. Embolia.
cerebrale
3. Embolia.
ruptur.
6. Arterita
cerebrale
3. Embolia.
5. Anevrismul sacular sau malformaia arterio-venoas cu sau
fr ruptur.
6. Arterita
5. Anevrismul sacular sau malformaia arterio-
venoas cu sau fr ruptur.
cerebrale
3. Embolia.
ruptur.
6. Arterita
6. Arterita
a. Sifilisul
meningovascular,
arterita secundar
ca consecin a
meningitei
piogenice sau
tuberculoase,
infecii rare (tifos,
shistosomiasis,
malarie, micoze,
etc.).
BOLILE CEREBROVASCULARE
cerebrale
7. Tromboflebita cerebral: secundar otogen, infeciei sinusurilor
paranazale, a feei, etc.; n cadrul meiningitei i empiemului subdural; stri
de slbire general a organismului, postpartum, postoperativ, insuficien
cardiac, sau de cauz nedeterminat.
8. Boli hematologice: utilizare de anticoagulante i trombolitice, policitemia,
talassemia, purpura trombocitopenic trombotic, trombocitopeniile,
angioendotelioza neoplastic, etc.
9. Traumatismul i disecia arterei carotide i bazilare.
10. Angiopatia amiloid.
11. Anevrismul disecant al aortei.
12. Complicaiile arteriografiei.
Tromboflebita sinusului
longitudinal superior cu
infarct hemorrhagic
bilateral. Femeie n vrst
de 21 ani cu cefalee,
tetraparez, i stupoare.
7. Tromboflebita
cerebral secundar
otogen, infeciei
sinusurilor paranazale,
a feei, etc.; n cadrul
meningitei i
empiemului subdural;
stri de slbire
general a
organismului,
postpartum,
postoperativ,
insuficien cardiac,
sau de cauz
nedeterminat.
cerebrale
8. Boli hematologice: utilizare de anticoagulante i trombolitice,
policitemia, talassemia, purpura trombocitopenic trombotic,
trombocitopeniile, angioendotelioza neoplastic, etc.
8. Boli hematologice: utilizare
de anticoagulante i
trombolitice, policitemia,
talassemia, purpura
trombocitopenic trombotic,
trombocitopeniile,
angioendotelioza neoplastic,
etc.
cerebrale
9. Traumatismul i
disecia arterei
carotide i bazilare.

cerebrale
cerebrale
cerebrale
cerebrale
12.
Complicaiile
arteriografiei.
Etiologia alteraiilor arterelor i venelor rezultnd n
anormaliti cerebrale
13. Migrena cu deficit neurologic persistent.
14. Hernii cerebrale supratentoriale i subtentoriale, n gaura rupt
posterioar.
15. Cauze mixte: displazia fibromuscular cu disecare local de carotid,
arter cerebral medie, or arter vertebral, bazilar; iradiere cu raye X,
infarct cerebral n teritoriu a. Cerebrale medii n cadrul traumatismului
cranio-cerebral nchis, compresie prin anevrism sacular fr ruptur,
complicaii de utilizare a contraceptivelor orale.
16. Cauze nedeterminate ale vrstei copilreti i adultului tnr: boala
moyamoya; ocluzia arterial multipl progresiv (Taveras).
13. Migrena
cu deficit
neurologic
persistent.

14. Angajri (hernii) cerebrale supratentoriale i subtentoriale,
n gaura rupt posterioar.
arter cerebral medie, or arter vertebral, bazilar; iradiere cu raye X,
14. Angajri
(hernii) cerebrale
supratentoriale
i subtentoriale,
n gaura rupt
posterioar.
14. Angajri (hernii) cerebrale supratentoriale i subtentoriale, n gaura
rupt posterioar.
15. Cauze mixte: displazia fibromuscular cu disecare local de
carotid, arter cerebral medie, or arter vertebral, bazilar;
iradiere cu raye X, infarct cerebral n teritoriu a. Cerebrale
medii n cadrul traumatismului cranio-cerebral nchis,
compresie prin anevrism sacular fr ruptur, complicaii de
utilizare a contraceptivelor orale.
14. Angajri (hernii) cerebrale supratentoriale i subtentoriale, n gaura
rupt posterioar.
arter cerebral medie, or arter vertebral, bazilar; iradiere cu raze X,
16. Cauze nedeterminate ale vrstei copilreti i adultului
tnr: boala moyamoya; ocluzia arterial multipl progresiv
(Taveras).
CEREBROVASCULAR DISEASES
Circle of Willis
At the base of the brain, the
carotid and vertebrobasilar
arteries form a circle of
communicating arteries
known as the circle of Willis.
From this circle other arteries --
the anterior cerebral artery
(ACA), the middle cerebral
artery (MCA), the posterior
cerebral artery (PCA) - arise
and travel to all parts of the
brain.
Because the carotid and
vertebrobasilar arteries form
a circle, if one of the main
arteries is occluded, the
distal smaller arteries that it
supplies can receive blood
from the other arteries
(collateral circulation).
More than any other organ, the brain
depends from minute to minute on an
adequate supply of oxygenated blood.
Constancy of the cerebral circulation is
assured by a series of baroreceptors
and vasomotor reflexes under the
control of centers in the lower
brainstem.
Brain tissue deprived of blood undergoes
ischemic necrosis or infarction (also
referred to as a zone of softening or
encephalomalacia). Obstruction of an
artery by thrombus or embolus is the
usual cause of focal ischemic damage,
but failure of the circulation and
hypotension from cardiac
decompensation or shock, if severe and
prolonged, can produce focal as well as
diffuse ischemic changes.
Ischemic cascade
Free radicals, arachidonic acid, and nitric oxide are generated
by this process, leading to further neuronal damage. Within
hours to days after a stroke, specific genes are activated,
leading to the formation of cytokines and other factors that
in turn cause further inflammation and microcirculatory
compromise. Ultimately, the ischemic penumbra is
consumed by these progressive insults, coalescing with the
infarcted core, often within hours of the onset of the stroke.
The central goal of therapy in acute ischemic stroke is to
preserve the ischemic penumbra. This can be
accomplished by limiting the severity of ischemic injury (ie,
neuronal protection) or reducing the duration of ischemia
(ie, restoring blood flow to the compromised area).
day 1 2 6 20 50
Ischemic lesion, development
on non-enhanced CT
SCOPUL TRATAMENTULUI
PACIENTULUI CU ICTUS
CEREBRAL:
1. PACIENTULUI I SE OFER O
ANS OPTIMAL DE
SUPRAVIEUIRE.
2. REDUCEREA LA MINIMUM A
CONSECINELOR ICTUSULUI
PENTRU BOLNAV I PENTRU
PERSOANELE CARE NGRIJESC
DE EL.

COMPARTIMENTELE TRATAMENTULUI
ACCIDENTULUI VASCULAR
CEREBRAL:
1. Tratamentul nedifereniat n perioada
acut.
2. Tratamentul conservator difereniat i
tratamentul neurochirurgical n perioada
acut.
3. Reabilitarea.
4. ngrijirea de lung durat.

Most Common Sites and Sources of Intracerebral
Hemorrhage.

Intracerebral
hemorrhages
most commonly
involve cerebral
lobes, originating
from:

penetrating
cortical branches
of the anterior,
middle, or
posterior cerebral
arteries (A);
basal ganglia,
originating from
ascending
lenticulostriate
branches of the
middle cerebral
artery (B);
the thalamus,
originating from
ascending
thalmogeniculate
branches of the
posterior cerebral
artery (C);
the pons, originating
from paramedian branches of the basilar artery (D);

and the
cerebellum,
originating from
penetrating
branches of the
posterior
inferior, anterior
inferior, or
superior cerebellar
arteries (E).
The bleeding occurs
within brain tissue,
and rupture of
arteries lying in the
subarachnoid space
is practically
unknown apart from
aneurysm. The
extravasation forms a
roughly circular or
oval mass that
disrupts the tissue
and grows in volume
as the bleeding
continues.
INTRACRANIAL HEMORRHAGE
An unenhanced CT scan showing the typical picture of a massive primary
(hypertensive) hemorrhage in the basal ganglia. The third ventricle and opposite
lateral ventricle are compressed and displaced by the expanding mass (12 h after
onset of stroke).
Pathogenesis The nature of the
hypertensive vascular lesion that
leads to arterial rupture is not fully
known, but in the few cases studied
by serial sections, the hemorrhage
appeared to arise from an arterial
wall altered by the effects of
hypertension, i.e., the change
referred to in a preceding section
as segmental lipohyalinosis and the
false aneurysm (microaneurysm) of
Charcot-Bouchard. Ross Russell
has affirmed the relationship of
these aneurysms to hypertension
and hypertensive hemorrhage, and
their frequent localization on
penetrating small arteries and
arterioles of the basal ganglia,
thalamus, pons, and subcortical
white matter.
Clinical Picture Of all the cerebrovascular diseases,
brain hemorrhage is the most dramatic and from
ancient times has been surrounded by "an aura of
mystery and inevitability." It has been given its own
name, "apoplexy." The prototype is an obese,
plethoric, hypertensive male who, while sane and
sound, falls senseless to the ground - impervious to
shouts, shaking, and pinching - breathes stertorously,
and dies in a few hours. A massive blood clot escapes
from the brain as it is removed postmortem. With
smaller hemorrhages, the clinical picture conforms
more closely to the usual temporal profile of a stroke,
i.e., an abrupt onset of symptoms that evolve
gradually and steadily over minutes, hours, or a day
or two, depending on the size of the ruptured artery
and the speed of bleeding.
Laboratory Findings. Among laboratory methods for the
diagnosis of intracerebral hemorrhage, the CT scan
occupies the foremost position. This procedure has proved
totally reliable in the detection of hemorrhages that are 1.0
cm or more in diameter. Smaller pontine hemorrhages are
visualized with less certainty. The CT scan is particularly
useful in the diagnosis of brain hemorrhages that do not
spill blood into the CSF and were heretofore clinically
unrecognizable. At the same time, coexisting
hydrocephalus, tumor, cerebral swelling, and displacement
of the intracranial contents are readily appreciated. MRI is
particularly useful for demonstrating brainstem
hemorrhages and residual hemorrhages, which remain
visible long after they can no longer be seen by the CT
scan (after 4 to 5 weeks). Hemosiderin and iron pigment
have their own characteristic appearances, as described
earlier.
Treatment. The general medical management of the
comatose patient with intracerebral hemorrhage is the
same as that of patients with ischemic or embolic
infarction. The management of patients with large
intracerebral hemorrhages and coma includes the
maintenance of adequate ventilation, use of controlled
hyperventilation to a PCO2 of 25 to 30 mmHg, monitoring
of intracranial pressure and its control by the use of
tissue-dehydrating agents such as mannitol (osmolality
kept at 295 to 305 mosmol/L and Na at 145 to 150 meq),
and limiting fluid intake to 1200 mL/day, given as
intravenous infusions of normal saline.
Treatment Rapid reduction in blood pressure, in the hope of
reducing further bleeding, is not recommended, since it
risks compromising cerebral perfusion in cases of raised
intracranial pressure. On the other hand, sustained mean
blood pressures of greater than 110 mmHg may
exaggerate cerebral edema and risk further bleeding. It is
at approximately this level of acute hypertension that the
use of beta-blocking (esmolol, labetalol), or angiotensin-
converting enzyme inhibitory drugs is recommended.
Diuretics are helpful in combination with any of the
antihypertensive medications. More rapidly acting and
titratable agents such as nitroprusside may be used in
extreme situations, recognizing that they may further raise
intracranial pressure.

Treatment Surgical removal of the clot in the acute
stage, either by evacuation or aspiration, may
occasionally be lifesaving, and we have referred
numerous patients, in whom hemispheral hemorrhages
were more than 3 cm in diameter and whose clinical
state was deteriorating, for surgical treatment. The most
successful surgical results have been in patients with
lobar or putaminal hemorrhages. Although selected
patients may be saved from progression to brain death,
the underlying focal neurologic deficit is not altered.
Moreover, even this degree of success requires that
operation be carried out before or very soon after coma
supervenes. Once the patient becomes deeply
comatose, with dilated fixed pupils, the chances of
recovery are negligible.
Clinical Picture Prior to rupture, saccular aneurysms are usually
asymptomatic. Exceptionally, if sufficiently large to compress pain-
sensitive structures, they may cause localized cranial pain. With a
cavernous or anterolaterally situated aneurysm on the first part of the
middle cerebral artery, the pain may be localized to the orbit. An
aneurysm on the posterior-inferior or anterior-inferior cerebellar artery
may cause unilateral occipital or cervical pain. The presence of a partial
oculomotor palsy with dilated pupil may be indicative of an aneurysm of
the posterior communicating-internal carotid junction (rarely posterior
communicating-posterior cerebral junction). Occasionally, large
aneurysms just anterior to the cavernous sinus may compress the optic
nerves or chiasm, third nerve, hypothalamus, or pituitary gland. In the
cavernous sinus they may compress the third, fourth, or sixth nerves, or
the ophthalmic division of the fifth nerve. A monocular visual field defect
may also develop with a supraclinoid aneurysm near the anterior and
middle cerebral bifurcation or the ophthalmic-carotid bifurcation.
Spontaneous Subarachnoid Hemorrhage (Ruptured Saccular Aneurysm)
In summary, the clinical sequence of sudden severe headache, collapse, relative
preservation of consciousness with a paucity of lateralizing signs, and neck
stiffness is diagnostic of subarachnoid hemorrhage due to a ruptured saccular
aneurysm.
Almost all patients are hypertensive for one or several days following the bleed,
but preceding hypertension is not more common than in the general population.
Levels of 200 mmHg systolic are seen occasionally just after rupture but usually
the pressure is elevated only moderately and fluctuates with the degree of head
pain. Spontaneous intracranial bleeding with normal blood pressure should
always suggest ruptured aneurysm or arteriovenous malformation, a bleeding
diathesis, and, rarely, hemorrhage into a cerebral tumor. Nuchal rigidity is usually
present but occasionally absent, and the main complaint of pain may be referable
to the interscapular region or even the low back rather than to the head.
Examination of the fundi frequently reveals smooth-surfaced, sharply outlined
collections of blood that cover the retinal vesselsthe so-called preretinal or
subhyaloid hemorrhages; Roth spots are seen occasionally. Bilateral Babinski
signs are found in the first few days following rupture. Fever to 39C may be
seen in the first week. Rarely, escaping blood enters the subdural space and
produces a hematoma, evacuation of which may be lifesaving.
Laboratory Findings A CT scan will detect
blood locally or diffusely in the subarachnoid
spaces or within the brain or ventricular
system. This should be the initial investigative
procedure, since it confirms a subarachnoid
hemorrhage in more than 95 percent of cases.
The blood may appear as a subtle shadow
along the tentorium, difficult to distinguish from
the veins in this area, or in the sylvian or
adjacent fissures. A large localized collection of
subarachnoid blood may indicate the location
of the aneurysm and the region of subsequent
vasospasm as already noted. When two or
more aneurysms are visualized by
arteriography, the CT scan may identify the
one that had ruptured by the clot that
surrounds it. Also, a coexistent hydrocephalus
will be demonstrable. If the CT scan
documents subarachnoid blood with certainty,
a spinal tap is not necessary.
Blood fills the subarachnoid
space over the cerebral
hemispheres as well as
entering the sulci and
interhemispheric fissure.
Laboratory Findings In all other cases a lumbar puncture should be
undertaken when the clinical features suggest a subarachnoid hemorrhage.
Usually the CSF is grossly bloody, with RBC counts up to 1 million per cubic
millimeter or even higher. With a relatively mild hemorrhage, there may be
only a few thousand cells. It is unlikely that an aneurysm can rupture entirely
into brain tissue without some leakage of blood into the subarachnoid fluid,
so that the diagnosis of ruptured saccular aneurysm (by lumbar puncture)
cannot be confirmed unless blood is present in the CSF. Usually deep
xanthochromia is found after centrifugation if several hours have elapsed.
Carotid and vertebral angiography is the only certain means of
demonstrating an aneurysm and does so in some 85 percent of patients in
whom the correct diagnosis of spontaneous subarachnoid hemorrhage is
made on clinical grounds. MRI and MRA detect most aneurysms of the
basal vessels but are as yet of insufficient sensitivity to replace conventional
angiography.
Treatment This is influenced by the neurologic and general medical state of
the patient as well as by the location and morphology of the aneurysm.
Ideally, all patients should have the aneurysmal sac surgically obliterated,
but the mortality is high if the patient is stuporous or comatose (grade IV or
V, see below). Before deciding on a course of action, it has been useful to
assess the patient with reference to the widely employed scale introduced
by Botterell and by Hunt and Hess, as follows:

Grade I. Asymptomatic or with slight headache and stiff neck

Grade II. Moderate to severe headache and nuchal rigidity but no focal or
lateralizing neurologic signs

Grade III. Drowsiness, confusion, and mild focal deficit

Grade IV. Persistent stupor or semicoma, early decerebrate rigidity and
vegetative disturbances

Grade V. Deep coma and decerebrate rigidity.
Treatment The general medical management in the acute
stage includes the following, in all or part: bed rest, fluid
administration to maintain above-normal circulating volume
and venous pressure, use of elastic stockings and stool
softeners; administration of propranolol, intravenous
nitroprusside, or other medication - to reduce greatly elevated
blood pressure and then maintain systolic blood pressure at
150 mmHg or less; and pain-relieving medication for
headache (this alone will often reduce the hypertension). The
prevention of systemic venous thrombosis is critical, usually
through the use of cyclically inflated whole leg compression
boots. The use of anticonvulsants is controversial; many
neurosurgeons administer them early, with a view of
preventing a seizure-induced risk of rebleeding. We have
generally avoided them unless a seizure has occurred.
Treatment Calcium channel blockers are being used extensively to reduce
the incidence of stroke from vasospasm. Nimodipine, 60 mg administered
orally every 4 h, is currently favored. Although calcium channel blockers do
not alter the incidence of angiographically demonstrated vasospasm, they
have reduced the number of strokes in each of five randomized studies.
Patients with stupor or coma who have massive hydrocephalus often benefit
from decompression of the ventricular system. This is accomplished initially
by external drainage and may require permanent shunting if the
hydrocephalus returns. The risk of infection of the external shunt tubing is
high if it is left in place for much more than 3 days.
The timing of surgery for grade III patients is still controversial, but if their
general medical condition allows, they probably also benefit from the same
aggressive approach. In grade IV patients, the outcome is generally dismal,
no matter what course is taken, but we have usually avoided early
operation. The insertion of ventricular drains into both frontal horns has
occasionally raised a patient with severe hydrocephalus to a better grade
and prompted early operation. In the hands of experienced
anesthesiologists and cerebrovascular surgeons using microdissection, the
operative mortality, even in grades III and IV patients, has now been
reduced to 2 to 3 percent.
Treatment
The timing of surgery for grade III patients is still
controversial, but if their general medical condition allows,
they probably also benefit from the same aggressive
approach. In grade IV patients, the outcome is generally
dismal, no matter what course is taken, but we have usually
avoided early operation. The insertion of ventricular drains
into both frontal horns has occasionally raised a patient with
severe hydrocephalus to a better grade and prompted early
operation. In the hands of experienced anesthesiologists
and cerebrovascular surgeons using microdissection, the
operative mortality, even in grades III and IV patients, has
now been reduced to 2 to 3 percent.
Treatment
The timing of surgery for grade III patients is still
controversial, but if their general medical condition allows,
they probably also benefit from the same aggressive
approach. In grade IV patients, the outcome is generally
dismal, no matter what course is taken, but we have usually
avoided early operation. The insertion of ventricular drains
into both frontal horns has occasionally raised a patient with
severe hydrocephalus to a better grade and prompted early
operation. In the hands of experienced anesthesiologists
and cerebrovascular surgeons using microdissection, the
operative mortality, even in grades III and IV patients, has
now been reduced to 2 to 3 percent.
EPILEPSIA
Epilepsia -

este o maladie cronic a encefalului de divers
origine, care se caracterizeaz prin apariia
repetat a strilor paroxistice, cauzate de
descrcarea excesiv a neuronilor cerebrali, i care
are o multitudine de manifestri clinice i
manifestri speciale nregistrate prin investigaii
complementare (EEG).
Clasificarea acceselor epileptice
I. Pariale (debut local):
1.Pariale simple.
2.Pariale complexe (cu dereglri de contien).
3.Pariale secundar generalizate.
II. Generalizate:
1.Absene.
2. Mioclonice.
3.Clonice.
4. Tonico-clonice.
5. tonice.
Accesul tonico-clonic (accesul major generalizat)
I. Aura.
II. Faza convulsiilor tonice.
III. Faza convulsiilor clonice.
IV. Compa postcritic care treptat se transform n
somn.

I. .

II. .

III. - .
Encefalita herpetic
Investigaii complementare.
EEG: Descrcri periodice i paroxistice de vrfuri uni- sau bitemporal
THE END

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