A person with ALO may complain of occasionally being unable to open the eye at will, typically after prolonged closure. Oftentimes, ALO only persists momentarily and the ptosis resolves upon manually lifting the eyelid. During attempted<unk><unk> , there may be forceful frontalis muscle contraction, backward thrusting of the head, or<unk>  of the mouth noted. Causes== The exact cause of ALO is not yet fully understood. Despite its name, it is not a true<unk> , but thought to be due to a supranuclear origin of abnormal neuronal activity. Voluntary eyelid<unk>  involves the simultaneous activation of the levator palpebrae superioris muscle and the inhibition of the orbicularis oculi muscle. Electromyographic studies have shown that ALO may involve either involuntary levator palpebrae superioris muscle inhibition, persistent pretarsal orbicularis oculi muscle contraction, or both. Hypometabolism of glucose may play a part, and has been documented in the basal ganglia, frontal lobe, and the primary visual cortex in some cases of ALO. While often an isolated condition, ALO sometimes occurs in conjunction with blepharospasm, which may complicate the diagnosis and treatment. Additionally, several diseases as well as medications have been reported in association with ALO. It has been reported in cases of extrapyramidal disorders, including Parkinson’s disease, parkinsonism, progressive supranuclear palsy, hydrocephalus, motor neuron disease, Shy–Drager syndrome, and various lesions in the brain. Medications that have been associated include Lithium, sulpiride, and a meperidine analog, 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine.
Apraxia of lid opening
Ocular dysmetria
Horizontal gaze palsy
Facial toning
Binocular dysphoria
Ocular tremor
Emmasofia
Hemifacial spasm