Occlusions of the branches of the PCA that supply the thalamus can result in central post-stroke pain and lesions to the subthalamic branches can produce “a wide variety of deficits”.Left posterior cerebral artery syndrome presents alexia without agraphia; the lesion is in the splenium of the corpus callosum. Signs and symptoms
Peripheral Territory Lesions

Contralateral homonymous hemianopsia
cortical blindness with bilateral involvement of the occipital lobe branches
visual agnosia
prosopagnosia
dyslexia, Anomic aphasia, color naming and discrimination problems
memory defect
topographic disorientationCentral Territory Lesions

central post-stroke (thalamic) pain: spontaneous pain, dysesthesias and sensory impairments
involuntary movements: chorea, intention tremor, hemiballismus
contralateral hemiplegia
Weber’s syndrome: occulomotor nerve palsy
Bálints syndrome: loss of voluntary eye movements optic ataxia, asimultagnosia (inability to understand visual objects)

Diagnosis
1.CT
2.MRI

Treatment
References


== External links ==
In 2006, approximately 1540 kilotonnes of ethylene glycol were manufactured in Canada by three companies in Alberta, with most of the production destined for export. Pathophysiology
The three main systems affected by ethylene glycol poisoning are the central nervous system, metabolic processes, and the kidneys. The central nervous system is affected early in the course of poisoning as the result of a direct action of ethylene glycol. Similar to ethanol, it causes intoxication, followed by drowsiness or coma. Seizures may occur due to a direct effect. The toxic mechanism of ethylene glycol poisoning is mainly due to the metabolites of ethylene glycol. Initially it is metabolized by alcohol dehydrogenase to glycolaldehyde, which is then oxidized to glycolic acid by aldehyde dehydrogenase. The increase in metabolites may cause encephalopathy or cerebral edema. The metabolic effects occur 12 to 36 hours post ingestion, causing primarily metabolic acidosis which is due mainly to accumulated glycolic acid. Additionally, as a side effect of the first two steps of metabolism, an increase in the blood concentration of lactic acid occurs contributing to lactic acidosis. The formation of acid metabolites also causes inhibition of other metabolic pathways, such as oxidative phosphorylation.The kidney toxicity of ethylene glycol occurs 24 to 72 hours post ingestion and is caused by a direct cytotoxic effect of glycolic acid. The glycolic acid is then metabolized to glyoxylic acid and finally to oxalic acid.