Research directions
Studies have been done with electromyography to trace skeletal muscle activity in some hyperkinetic disorders. The electromyogram (EMG) of dystonia sometimes shows rapid rhythmic bursts, but these patterns can almost always be produced intentionally. In the myoclonus EMG, there are typically brief, and sometimes rhythmic, bursts or pauses in the recording pattern. When the bursts last for 50 milliseconds or less they are indicative of cortical myoclonus, but when they last up to 200 milliseconds, they are indicative of spinal or brainstem myoclonus. Such bursts can occur in multiple muscles simultaneously quite quickly, but high time resolution must be used in the EMG trace to clearly record them. The bursts recorded for tremor tend to be longer in duration than those of myoclonus, although some types can last for durations within the range for those of myoclonus. Future studies would have to examine the EMGs for tics, athetosis, stereotypies and chorea as there are minimal recordings done for those movements. However, it may be predicted that the EMG for chorea would include bursts varying in duration, timing, and amplitude, while that for tics and stereotypies would take on patterns of voluntary movements.In general, research for treatment of hyperkinesia has most recently been focusing on ameliorating symptoms rather than attempting to correct the pathogenesis of the disease. Therefore, now and in the future it may be beneficial to inform the learning of the diseases pathology through carefully controlled, long-term, observation-based studies.
Symptoms
The most common symptoms of acquired and transient cortical blindness include:

A complete loss of visual sensation and of vision
Preservation/sparing of the abilities to perceive light and/or moving, but not static objects (Riddoch syndrome)
A lack of visual fixation and tracking 
Denial of visual loss (Anton–Babinski syndrome)
Visual hallucinations 
Macular sparing, in which vision in the fovea is spared from the blindness. Causes
The most common cause of cortical blindness is ischemia (oxygen deprivation) to the occipital lobes caused by blockage to one or both of the posterior cerebral arteries. However, other conditions have also been known to cause acquired and transient cortical blindness, including:

Congenital abnormalities of the occipital lobe
Head trauma to the occipital lobe of the brain
Bilateral lesions of the primary visual cortex
Infection
Creutzfeldt–Jakob disease (CJD), in association with a rapid onset of dementia
rarely Dissociative identity disorder (DID)
Side effect of some anti-epilepsy drugs (AEDs)
Hyperammonemia
Eclampsia and, rarely, pre-eclampsiaThe most common causes of congenital cortical blindness are:

Traumatic brain injury (TBI) to the occipital lobe of the brain
Congenital abnormalities of the occipital lobe
Perinatal ischemia
Encephalitis
Meningitis

Diagnosis
A patient with cortical blindness has no vision but the response of his/her pupil to light is intact (as the reflex does not involve the cortex). Therefore, one diagnostic test for cortical blindness is to first objectively verify the optic nerves and the non-cortical functions of the eyes are functioning normally. This involves confirming that patient can distinguish light/dark, and that his/her pupils dilate and contract with light exposure. Then, the patient is asked to describe something he/she would be able to recognize with normal vision.