Cerebrovascular diseases in human .ppt

Cerebrovascular diseases

1. CEREBROVASCULAR
DISEASES
Professor Taras A.Skoromets
Department of Neurology and
Neurosurgery
SPbSMU

2. SUBARACHNOID HEMORRHAGE
(SAH)
•The frequency of spontaneous (nontraumatic) SAH
is 10 – 19 new cases per 100 000 annualy
•Arterial hypertension, cerebral atherosclerosis,
infections, alcohol ingestion are the causes of SAH
•But rupture of cerebral arterial aneurysm or
intracranial Vascular Malformation causes SAH in
50 – 60 % of cases
•Nontraumatic SAH has more severe course than
traumatic one

3. SUBARACHNOID HEMORRHAGE
(SAH)
•Usually rupture of an aneurysm or intracranial Vascular
Malformation becomes the source of SAH
•Half of patients die during the next 2 weeks
•60% of them die before reaching the hospital, 20% die during
first hours after admitting to the hospital and 20% die later on
•The patients of 2 final groups die from cardiac insufficiency

4. The cerebral aneurysm
•Aneurysm is formed as a local arterial
wall protrusion
•The aneurysm consists of 3 parts:
- cupola (bottom)
- corpus (body)
- neck
Aneurysm’s cupola has no intima, no
muscle layer or elastic membrane inside
(normal artery wall consists of: 1- intima,
2 –internal elastic membrane, 3 - muscle
layer, 4 –adventitia)
Aneurysm consists of adventitia only
Because of that aneurysm’s rupture starts
from this very place

5. The cerebral aneurysm classification
•Cerebral aneurysms dispose at places of
artery’s bifurcations
•1 – a. cerebri anterior – a. communicantis
anterior (49%)
•2 - a. cerebri media (25%)
•3 - a. carotis int.(17%)
•4 - a. communicantis posterior (3%)
•5 - a. cerebri posterior (1%)
•6 – a. basilaris (3%)
•7 – a. cerebellaris posterior and inferior
(1%), 8 – a. vertebralis (1%)

6. Classification of aneurisms
•Aneurisms can be sole and multiple as well
•According to their size aneurisms can be
divided into small (2 –3 mm), of average size
(4 – 20 mm), big (2 – 2,5 cm), gigantic (more
2,5 cm)
•Their form can be saccular and fusiform

7. Etiology of aneurisms
•Congenital
•Inflammatary
•Degenerative
•Posttraumatic

8. Clinical picture of aneurisms
•There are two periods of aneurism’s clinical
course: prehemorrhagic and hemorrhagic
•The prehemorrhagic period can be one
of two variants: asymptomatic and paralytic
•The paralytic course occurs in gigantic
aneurisms and has a tumor like character
•In rare cases carotid aneurisms remind clinical
course of middle fossa or cella turcica tumors
or meningiomas of other localization

9. Hemorrhagic period
Hemorrhagic period is divided into 4 stages:
acutissimus stage
stage of complications
recovery stage
residual stage

10. Acutissimus stage (1 – 3 days)
•HEMORRHAGIC forms :
•SUBARACHNOID HEMORRHAGE
•Intracerebral and SUBARACHNOID
HEMORRHAGE
•Subdural and SUBARACHNOID
HEMORRHAGE
•Intracerebral, intraventricular and
SUBARACHNOID HEMORRHAGE

11. Clinical presentation of
acutissimus stage
•The signs of intracranial hypertension
syndrome:
•Severe (or mild) headache
•Vomiting
•Vertigo
•Impairment of consciousness

12. The appraisal of severity of patient’s
state during acutissimus period
(HUNT AND HESE, 1965)

13. Grad
e
HUNT-HESE Cooperative aneurism
study
World federation
Neurosurgests
I Mild headache Asymptomatic Asymptomatic(GCS
15)
II Severe headache, cranial
nerve deficit
meningismus,
Headache awake/alert
mildly ill
Headache/
meningism, no focal
signs (GCS 15)
IIIAltered level of
consciousness ± focal
sings
Moderately ill, or alert
with focal sings
Headache/
meningismus, no
focal signs GCS 13
IV Sopor ± hemiparesis Severely ill (Sopor) or
drowsy with local
signs
Headache/
meningismus and
GCS 9 - 12, or focal
signs and GCS 13
V Coma ± posturing Not available Headache/
meningismus ±
focal sings (GCS<
9)
 
 

14. NEUROSURGERY DURING
ACUTISSIMUS PERIOD
•If patient’s state is similar to
IV – Vth grade of HUNT-HESE
scale, then intracranial
hematoma is present as a rule
•In these cases operations bear
life-saving character
•Very rarely a neurosurgeon
doesn’t find an aneurysm
during operation, then
hematoma is removed only

15. •If patient’s state is similar to
Ist – I I Id grade of HUNT-
HESE scale, then there arises
the necessity in more deep
investigation for the further
pathogenetic operative
treatment
•This investigation is named
cerebral angiography
•This investigation makes it
possible to localize an
aneurism
NEUROSURGERY DURING
ACUTISSIMUS PERIOD

16. •After this procedure the patient undergoes
a neurosurgical operation
•Two types of operations are used in this
pathology:
•1) the open method (clip application)
•2) Intravascular method, when the foreign
agent (balloon, coils, glue) is introduced
into the aneurism’s cavity
NEUROSURGERY DURING
ACUTISSIMUS PERIOD

17. Clipping of an aneurism
•Arterial bifurcation
•Clip application at
aneurism’s neck
•Aneurism
•Clip-holder

18. Clipping of an aneurism
•Osteoplastic trepanation of
the skull
•Discharge of an aneurism
•Clipping of an aneurism

19. Academician Serbinenko A.F. – the founder of
endovascular neurosurgery
•
• Balloon-
• catheter
Those are
introduced
inside the
cavity
of aneurism

20. The endovascular method
After introduction of
balloon-catheter inside an
aneurism’s cavity
Aneurism

21. The results of neurosurgical
treatment
•The results of neurosurgical
treatment in IV – Vth grade of
HUNT-HESE scale don’t differ from
such at severe brain injury

22. The results of neurosurgical
treatment
•The patients with Ist – IIId grade of HUNT-
HESE scale recover as a rule
•At contemporary point of view early surgery
is more apologized in this group of patients
•An operation is fulfilled during 1 – 2 days
after SAH (before vasospasm develops)

23. Conservative treatment of SAH
•Triple H therapy:
•Arterial Hypertension
•Hemodelution
•Hypervolimia

24. Stage of complications (4 - 21
days)
Intracranial
•Vasospasm
•Obstructive hydrocephalus
•Rebleeding


Extracerebral

25. Vasospasm
•In SAH the blood cells
dissolve
•Very many decay products fill
CSF (serotonin,
prostaglandin, angiotensin,
etc.)
•These substances obtain
vasoconstriction nature
•Vasospasm helps these
substances to appear
consequently inside CSF

26. Cerebral vasospasm is a delayed narrowing
capacity of arteries and arterioles that occurs
after SAH
•Usually it develops in 3-5
days after hemorrhage and it
is maximal after 7-10 days. It
abates during next 2-3 weeks
•It develops in 70% of patients
•Patients with a thick blood
clot inside basal cisterns are
considerably more likely to
develop vasospasm than those
who have thin scant amount
of subarachnoid blood

27. Clinical manifestation of vasospasm
•The onset of vasospasm symptoms is usually
heralded by worsening of headache or
diminished level of consciousness. Less
frequently, patients may develop focal
neurological deficit
•These symptoms occur because the ischemic
brain edema develops
•Less frequently, local ischemic exchange takes
place

28. DIAGNOSIS
•The clinical picture
•Cerebral Angiography
•Duplex scannng

29. The treatment of vasospasm
•Lumbal puncture every day or once in
two days
•Intra-venous introduction of nimotop
(nimodipin) with constant blood pressure
monitoring

30. REBLEEDING
•Rebleeding is a very severe complication
•More frequently it occurs in 10 and 20 days
after SAH
•It develops in 45 % of patients during first 30
days after SAH
•Mortality rate associated with rebleeding is
higher than that associated with the initial
bleeding, with fatality rate of approximately
70%

31. REBLEEDING
•To prevent rebleeding, the clinician must
focus one’s attention at pertinent risk
factors:
•blood pressure control,
•mild sedation,
•stool regulation,
•treatment by anticonvulsants,
•strict bed regime, etc.

32. Obstructive hydrocephalus
•Acute obstructive hydrocephalus occurs in
approximately 25% of patients with
aneurismal SAH, most often with
intraventricular blood location and/or inside
the envelopment (ambient) cisterns
•The patients develop the signs of increasing
intracranial hypertension within 1 – 2 days

33. Obstructive hydrocephalus
•Patients with obstructive
hydrocephalus need for
special external
ventriculostomy
•By means of external
ventriculostomy brain
ventricles are washed with the
help of some thrombolytic (for
example – streptokinase)
•If the patient survives,
venrticuloperitoneal shunt is
posed

34. The extracranial
complications
•Pulmonary Cardiac Gastrointestinal
Bedsores Sepsis

35. Pulmonary complications
Hypostatic pneumonia Aspiration pneumonia
Pulmonary edema
(complication of 3-H therapy)
Traditional treatment + tracheostomy +
bronchoscopic removing of sputum

36. Cardiac complications
•ECG changes are evident in 50% -90% of patients who
had had aneurismal SAH
•Cardiac complications appear to be more common in
elderly patients and in those who developed more severe
neurological deficit
•These complications are believed to result from
excessive activation of the sympathetic nervous system,
with catecholamine mediated myocardial injury
•Presence of these disorders is a contraindication for
surgical treatment

37. Gastrointestinal complications
Development of acute stress-ulcers (“Cushing ulcers”)
Bleeding Perforation Penetration
Traditional therapy

38. The recovery stage (1 – 6 months)
•This stage is characterized by gradual
regress of consciousness disturbances,
neurological deficit, psychic disorders, etc.

39. The residual stage (more 6 months)
•This stage is characterized by stable
neurological deficit

40. Cerebral arteriovenous malformations
•Cerebral arteriovenous
malformations (AVMs) are
congenital lesions with primitive
arteries inside that shunt directly
into veins with no intervening
capillary or venule network
•They are high-pressure and high-
flow vascular malformations that
cause significant damage to the
surrounding brain when they
rupture
•AVMs are usually posed at brain
surface and are often cone shaped
and extend towards ventricular
system

41. Cerebral arteriovenous malformation
•The arteries vary in width and often have
duplication or absence of the internal elastic
membrane and tunica media layer
•In response to the high arterial pressure veins
become dilated, tortuous, and elongated
•Rapid arterial shunting leads to a poor perfusion and
ischemia in the surrounding brain tissue
•Capillaries can be dilated and irregular in size and
may represent a transitional zone from capillary
telangiectasias to AVM itself

42. Clinical manifestations
•Similar to a rupture of an aneurism AVM’s clinical course
undergoes two periods: prehemorrhagic and hemorrhagic
•Hemorrhage in AVM’s occurs more rarely than in
aneurisms
•The prehemorrhagic period has a tumor like course (similar
to extracerebral tumors)
•Epileptic seizures often become common at manifestation of
AVMs
•This sign can help in the early AVM’s diagnostics
•The hemorrhagic period doesn’t differ from such of
aneurisms

43. Cerebral arteriovenous malformations
Diagnosis
•MRI
•Cerebral angiography
•Operation (surgery)

44. Treatment
•Two types of surgical operations are used in this
pathology: the open method (clip application and
removal of an AVM)
•Intravascular method: AVM’s embolization,
balloonization (ballooning)
•Stereotaxic operation
•Radiosurgery

45. Open method
Before operation After operation

46. Radical embolization of an AVMRadical embolization of an AVM

47. Radiosurgery (γ-knife)

48. Carotid-cavernous fistula (CCF)
•Anatomy of
carotidcavernous zone:
Superior wall of cavernous
sinus is removed
Carotid artery is found in
sinus cavity
•N. opticus, n.
oculomotorius (short
needles)

49. Carotid-cavernous fistula
•Anatomy of
carotidcavernous zone:
•Ophthalmic vein (short
needle)

50. Carotid-cavernous fistula
•Rarely CCF develops as a complication of skull and
brain trauma
•The rupture of intracavernous part of carotid
artery’s wall can occur in consequence to a severe
and significant change of hydraulic pressure inside
cavernous sinus cavity (hydrodynamic stroke)
•Fistula formation is a result of this process
•Such situation is similar to that in AVM (shunting of
blood flow develops)
•Blood flow shunting increases constantly in time

51. Carotid-cavernous fistula
2
3
4
1
5
1

1

A.Carotis interna
V. Ophtalmica
Sinus cavernosis
Fistula
Plexus ptherigoideus

52. Carotid-cavernous fistula
•The pressure inside cavernous sinus increases, that
leads to a breach of venous drainage
•What is more, the arterial blood with a high pressure
rushes into veins
•Inside cranium cavity the venous blood enters
collateral anastomosis which fall into other sinuses
•The ophthalmic vein is a unique one that falls into
cavernous sinus only and has no large
anastomosing vein

53. Carotid-cavernous fistula
•That’s why venous blood flow is more
difficult in this region (eye orbit)
•Blood plasma comes out trough the vein’s
wall and remains inside fat tissue behind of
an eye
• It results in exophthalmos (bulging eye)
•Such exophthalmos has pulsating character

54. Clinical manifestation of carotid-
cavernous fistula
•The pulsating exophthalmos
•During auscultation the blowing murmur is heard
upon an eye and at the same temporal region
•The rate of blowing murmur coincides with pulse
rate
•The blowing murmur disappears after clamping of
unilateral common carotid artery (Matthias test)

55. The development of exophthalmos

56. Complications
•1. Ophthalmologic
•2. Lesion of cranial nerves
•3. Cerebral blood circulation trouble:
Compensation
Decompensation

57. Ophthalmologic complications
• Severe conjunctival edema with strangulation of
conjunctiva between eyelid margins (chemosis)
• Conjunctivitis
• Keratitis
• Corneal ulcer
• Panophthalmitis

58. Lesion of cranial nerves
•Lesion of optic nerve (ophthalmoscopy: simple optic disc
atrophy, perimetry: narrowing of visual fields; drop of
vision, amaurosis)
•Lesion of oculomotor nerve (mydriasis, divergent
strabismus)
•Lesion of trochlear and abducens nerves (diplopia,
strabismus, limitation of horizontal eye movements)
•Lesion of trigeminal nerve (ramus ophthalmicus)

59. Lesion of cerebral blood circulation
Compensatory stage: CCF like AVM is a
”parasite”of brain. All cerebral blood passes through
this side. Situation with cerebral blood circulation is
controlled by collateral blood circulation (circle of
Willis)
The shunting of cerebral blood constantly increases.
It results in possible decrease of collateral blood
circulation and development of the stage of
decompensation

60. Lesion of cerebral blood circulation
•Decompensatory stage starts when resources of collateral blood
circulation are severely diminished
•Decompensatory stage leads to development of cerebroastenia (loss of
memory, attention, intellect; development of debility or total disability)

61. Treatment of CCF
•Different balloon
occlusion
operations:
optimal variant
а б
в г

62. Result of balloon occlusion
•Disappearance of
arterial blood
shunting
•Reestablishment
of blood flow
through middle
and anterior
cerebral arteries

63. Thank you for attention!