A site for medical students - Practical,Theory,Osce Notes

>

Posterior cerebral artery syndromes


  • In 75% of cases, both PCAs arise from the bifurcation of the basilar artery
  • In 20%, one has its origin from the ipsilateral internal carotid artery via the posterior communicating artery
  • 5%  both originate from the respective ipsilateral internal carotid arteries 
The precommunal or P1, segment of the true posterior cerebral artery is atretic in such cases.
PCA syndromes usually result from atheroma formation or emboli that lodge at the top of the basilar artery; 
posterior circulation disease may also be caused by dissection of either vertebral artery and fibromuscular dysplasia.

Two clinical syndromes are observed with occlusion of the PCA
P1 syndrome : midbrain, subthalamic, and thalamic signs, this is due to P1 segment of PCA or of its penetrating branches such as thalamogeniculate, Percheron, and posterior choroidal arteries
P2 syndrome : cortical temporal and occipital lobe signs, due to occlusion of the P2 segment distal to the junction of the PCA with the posterior communicating artery.
P1 syndromes 
Infarction usually seen in the following areas
  • Ipsilateral subthalamus
  • Medial thalamus 
  • Ipsilateral cerebral peduncle
  • Midbrain 
A third nerve palsy with contralateral ataxia (Claude’s syndrome)
A third nerve palsy with contralateral hemiplegia (Weber’s syndrome) 
Structure affected
  • The ataxia is due to involvement of the red nucleus or dentatorubrothalamic tract
  • The hemiplegia is localized to the cerebral peduncle 
  • If the subthalamic nucleus is involved, contralateral hemiballismus
  • Occlusion of the artery of Percheron produces the following deficit
  • Paresis of upward gaze and drowsiness
Extensive infarction in the midbrain and subthalamus occurring with bilateral proximal PCA occlusion presents as
  • Coma
  • Unreactive pupils
  • Bilateral pyramidal signs,
  • Decerebrate rigidity.
Occlusion of the penetrating branches of thalamic and thalamogeniculate arteries result in less extensive thalamic and thalamocapsular lacunar syndromes. 
The thalamic Dejerine-Roussy syndrome consists of contralateral hemisensory loss followed later by an agonizing, searing or burning pain in the involved  areas. It is persistent and will responds poorly to analgesics. Anticonvulsants (carbamazepine or gabapentin) or tricyclic antidepressants may be beneficial in treating it.
P2 syndrome
P2 syndromes occlusion of the distal PCA produce infarction of the medial temporal and occipital lobes. 
  • Contralateral homonymous hemianopia with macula sparing is the common manifestation. Sometimes , only the upper quadrant of visual field is involved. 
  • If the visual association areas are spared and only the calcarine cortex is, the patient may be aware of visual defects. 
  • Medial temporal lobe and hippocampal involvement may cause an acute disturbance in memory, especially if it occurs in the dominant hemisphere. As the memory has bilateral representation the defect usually clears.
  • If the dominant hemisphere is affected and the infarct extends to affect the splenium of the corpus callosum, the patient sometimes demonstrate alexia without agraphia. 
Visual agnosia for faces, objects, mathematical symbols, and colors and anomia with paraphasic errors (amnestic aphasia) are seen in this setting, this is seen even without callosal involvement. 
Occlusion of the posterior cerebral artery can produce peduncular hallucinosis it is manifested as visual hallucinations of brightly colored scenes and objects.
Bilateral infarction in the distal PCAs produces
Cortical blindness (blindness with preserved pupillary light reaction). 
Antons syndrome -The patient is often unaware of the blindness or he or she may  even deny it .it is called as Anton’s syndrome
Tiny islands of vision may persist, and the patient may sometime report that vision fluctuates as images are captured in the preserved portions. 
Rarely, only peripheral vision is lost and central vision is spared,which will result in “gun-barrel” vision. 
Balints syndrome-Bilateral visual association area lesions may result in Balint’s syndrome , a disorder of the orderly visual scanning of the environment .It is due infarctions secondary to low flow in the “watershed” between the distal PCA and MCA territories, as occurs after cardiac arrest. 
Patients may experience persistence of a visual image for several minutes despite gazing at another scene called as palinopsia 
An inability to synthesize the whole of an image termed as asimultanagnosia. 
Top of basilar artery
Embolic occlusion of the top of the basilar artery can produce any or all of the central or peripheral territory symptoms. 
The hallmark is the sudden onset of bilateral signs, including 
  • Ptosis
  • Pupillary asymmetry or lack of reaction to light
  • Somnolence