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Showing posts with label cerebral circulation. Show all posts
Showing posts with label cerebral circulation. Show all posts

The vertebral artery

The vertebral artery arises from the following vessels
  Innominate artery on the right
 Subclavian artery on the left

     Segments of vertebral artery
Vertebral artery has four segments
The first (V1) -extends from its origin to its entrance into the sixth or fifth transverse vertebral foramen.
The second segment (V2) -traverses the vertebral foramina from C6 to C2.
·    The third segment (V3) -passes through the transverse foramen and circles around the arch of the  atlas to pierce the dura at the foramen magnum.
·   The fourth segment (V4) -segment courses upward to join the other vertebral artery to form the  basilar artery; Only the fourth segment gives rise to branches that perfuse the brainstem and cerebellum
      Course of verebral artery
Each vertebral artery passes upwards through the vertebral foramina to enter the cranial cavity through the foramen magnum and runs upwards on each side of the medulla. Both arteries meet at the lower border of the pons to form one midline single artery, the basilar artery, which runs upwards on the ventral surface of the pons were it gives small branches known as the paramedian arteries to the brain stem and divides into its two terminal branches the posterior cerebral arteries. Each posterior cerebral artery supplies the whole occipital lobe and the posterior part of the temporal lobe (posterior 2/5 of the cerebral hemisphere).
Branches of vertebral artery
In its course the vcrtebro-basilar system gives:
Two spinal arteries which unit to form the anterior spinal artery.
Three cerebellar arteries on each side. The superior middle and inferior cerebellar arteries.

Etiology of VBI
·       Atherothrombotic lesions have a predilection for V1 and V4 segments of the vertebral artery.
·  Atheromatous disease rarely narrows the second and third segments of the vertebral artery, thisregion is prone  to dissection, fibromuscular dysplasia, and, rarely, encroachment by osteophytic spurs situated within the vertebral foramina.
Clinical features of VBI
The first segment may become diseased at the origin of the vessel and it produce posterior circulation emboli; If there is sufficient  collateral flow from the contralateral vertebral artery or the ascending cervical, thyrocervical, or occipital arteries it is usually sufficient to prevent low-flow TIAs or stroke.
When one vertebral artery is atretic and an atherothrombotic lesion threatens the origin of the other, the collateral circulation, which may also include retrograde flow down the basilar artery, is often insufficient. This will promote, low-flow TIAs
This state also sets the stage for thrombosis.
Disease of the distal fourth segment of the vertebral artery can promote thrombus formation it will manifest as embolism or with propagation as basilar artery thrombosis.
Stenosis occurring proximal to the origin of the PICA can threaten the lateral medulla and posterior inferior surface of the cerebellum.
Embolic occlusion or thrombosis of a V4 segment causes ischemia of the lateral medulla.
What is “subclavian steal.”?
If the subclavian artery is occluded proximal to the origin of the vertebral artery this will result in reversal in the direction of blood flow in the ipsilateral vertebral artery. Exercise of the ipsilateral arm may result in  increase demand on vertebral flow, producing posterior circulation TIAs, or “subclavian steal.”
Clinical manifestations of Vertebrobasilar insufficiency
Clinicalfeatures of VBI consist of syncope, vertigo, and alternating hemiplegia
Hemiparesis is not a feature of vertebral artery occlusion, however, quadriparesis may result from occlusion of the anterior spinal artery.

Symptoms of Posterior cerebral artery infarct

Origin of Posterior cerebral artery
  • The two PCAs are the terminal branches of the basilar artery in majority of people
  • In 20%—25% one of the posterior cerebral artery (PCAs) may originate from the internal carotid artery (ICA) via a posterior communicating artery
The clinical presentation of PCA territory infarction is determined by the  
  • Site of occlusion 
  • Availability of collaterals. 
1.Occlusion of the precommunal PI segment results in midbrain, thalamic, and hemispheric infarction.
2.Occlusion of the PCA in the proximal ambient segment before branching in the thalamogenictulate pedicle results in lateral thalamic and hemispheral symptoms 
3.Sometimes the occlusions may affect a single PCA branch, primarily the calcarine artery cause a large hemispheric infarction of the PCA territory.
Causes of PCA infarct
PCA infarct may be due to
  • Embolic
  • Thrombotic
  • Migrainous
  • Intrinsic atherosclerotic disease
  • PCA infarcts can also occur  due to compression of the artery against the tentorium during uncal herniation
Whether embolic, thrombotic, migrainous, or due to intrinsic atherosclerotic disease, partial syndromes of the PCA are the rule
1.Visualfield defect in PCA infarct
1.Infarction in the distribution of the hemispheric branches of the PCA may cause a contralateral homonymous hemianopia
This is due to infarction of
  • Striate cortex
  • Optic radiations
  • Lateral geniculate body
There is partial or complete macular sparing if the infarction does not reach the occipital pole.
2.The visualfield defect may be sometimes limited to a quadrantanopia. 
A superior quadrantanopia is due to infarction of the striate cortex inferior to the calcarine fissure or due to involvement of the inferior optic radiations present  in the temporo-occipital lobes.
An inferior quadrantanopia is the caused by an infarction of the striate cortex superior to the calcarine fissure or due to the superior optic radiations in the parietooccipital lobes
3.Complex visual changes observed in  PCA infarct are 
  • Formed or unformed visual hallucinations
  • visual and color agnosias 
  • Prosopagnosia.
Right hemispheric PCA infarctions may result in cause contralateral visual field neglect
2.Sensory findings in PCA infarct
Some alteration of sensation are also observed in PCA infarct
They  are paresthesiae, or altered position, pain, and temperature sensations
Sensors findings are due to thalamic ischemia  as a result of occlusion  of the precommunal or proximal postcommnual segments of the PCA
Thalamoparietal ischemia due to occlusion of the more distal PCA or its parieto-occipital branches
Brainstem ischemia is caused by vasoocclusive disease in the proximal vertebrobasilar arterial system
3.Alexia without agraphia (pure word blindness)
Infarction in the area of distribution of the callosal branches of the Posterior cerebral artery (PCA) tha affect  the left occipital region and the splenium of the corpus callosum results in alexia without agraphia (pure word blindness), occasionally this is associated with color anomia and object and photographic anomia .
In this syndrome, patients is able to write, speak, and spell normally but are they are unable to read words and sentences. The ability to name letters and numbers is intact, but there may be inability to name colors, objects, and photographs.
 .4.Behavioural disturbance in PCA infarct
Agitated delirium is seen with unilateral or bilateral penetrating mesiotemporal infarctions .
Large infarctions in the left posterior temporal artery territory may produce an anomic or transcortical sensory aphasia
Infarctions in the area of distribution of the penetrating branches of the PCA to the thalamus can result in aphasia
If the left pulvinar is involved, akinetic mutism, global amnesia, and the Dejerine-Roussy syndrome can be seen
5.Occlusion of calcarine artery
Occlusion of calcarine artery may be associated with pain in the ipsilateral eye .
Bilateral infarctions in the area of distribution of the PCA may result in bilateral homonymous hemianopia.
Anton’s syndrome
Bilateral occipital or occipitoparietal infarctions may cause  cortical blindness with preserved pupillary reflexes. Patients often deny or unaware of their blindness this is called as Anton’s syndrome.
Bilateral altitudinal visual held defects rarely result from bilateral occipital lobe infarcts
Infarction in the territory of the hemispheric branches of the PCA may also be accompanied by formed or unformed visual hallucinations called as release hallucinations ,
Visual and color agnosias
Prosopagnosia (agnosia for familiar faces). 
Apraxia of ocular movements is often present with bilateral lesions.
Balints syndrome
Some patients with bilateral occipital or parietooccipital infarctions present with  Balints syndrome.
Some patient with Proximal PCA occlusion may simulate MCA occlusion when it result in
  • Hemiparesis
  • Hemianopsia
  • Hemispatial neglect
  • Aphasia
  • Sensory  inattention .
Cortical signs are probably explained by thalamic involvement

The Circle of Willis

The Circle of Willis is a grouping of arteries at the base of the brain
It is named after an English physician named Thomas Willis, he discovered it and then published the findings in 1664
It is the joining area of several arteries at the inferior (bottom) side of the brain.The internal carotid arteries branch into smaller arteries at the Circle of Willis and supply oxygenated blood over 80% of the cerebrum

Formation of  Circle of Willis
The brain receives its blood supply from four main arteries:
2 internal carotid arteries 
2 vertebral arteries 
The vertebral arteries on each side  unite to form Basilar artery 
The basilar artery and the carotids together  form the circle of Willis below the hypothalamus
The circle of Willis is the origin of six large vessels that supply the cerebral cortex
The clinical presentation of vascular disease in the cerebral circulation is depended upon the  vessels or combinations of vessels that are involved.

Peculiarities of cerebral blood flow
The arteries and arterioles that supply blood to the brain are highly specialized,they include both vascular smooth muscle and endothelial cells and unlike vascular cells from the peripheral circulation or other vascular beds. 
The vascular smooth muscle is highly responsive to changes in pressure, a process called myogenic activity,which contributes to autoregulation of cerebral blood flow. 
The endothelial cells in the cerebral circulation are also highly specialized and they provide a barrier to fluid movement called the blood-brain barrier.