Medications that should not be used
Carbamazepine, vigabatrin, and tiagabine are contraindicated in the treatment of absence seizures, irrespective of cause and severity. This is based on clinical and experimental evidence. In particular, the GABA agonists vigabatrin and tiagabine are used to induce, not to treat, absence seizures and absence status epilepticus. Similarly, oxcarbazepine, phenytoin, phenobarbital, gabapentin, and pregabalin should not be used in the treatment of absence seizures because these medications may worsen absence seizures. Data limitations
In the treatment of absence seizures there is often insufficient evidence for which of the available medications has the best combination of safety and efficacy for a particular patient. Nor is it easily known how long a medication must be continued before an off-medication trial should be conducted to determine whether the patient has outgrown the absence seizures, as is often the case in children. To date there have been no published results of any large, double-blind, placebo-controlled studies comparing the efficacy and safety of these or any other medications for absence seizures. A 2019 Cochrane review found that ethosuximide was the best mono-therapy for children and adolescents but noted that if absence seizures co-exist with tonic-clonic seizures then valproate should be preferred. References
External links

Mechanisms of absence seizures (Scholarpedia)
Thalamocortical oscillations (Scholarpedia)
Absence (a comic about an affected persons experiences)
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 ==