The role of surgery in AIN syndrome remains controversial. Indications for considering surgery include a known space-occupying lesion that is compressing the nerve (a mass) or fascial compression, and persistent symptoms beyond 1 year of conservative treatment. Symptoms and signs
Patients may experience poorly localised, transient pain in the wrist, i.e. where the sensory branch of the AIN is mapped in the brain. The pain is sometimes referred into the cubital fossa and elbow pain has been reported as being a primary complaint.⁠
The characteristic severe impairment of the pincer movement of the thumb and index finger is most striking. Clinical signs
In a pure lesion of the anterior interosseous nerve there is weakness of the long flexor muscle of the thumb (Flexor pollicis longus), the deep flexor muscles of the index  and middle fingers (Flexor digitorum profundus I & II), and the pronator quadratus muscle.There is no sensory deficit since the anterior interosseous nerve has no cutaneous branch to skin, but there is a large sensory branch to the volar carpus, and transient wrist pain may be experienced.
Another difference that has been cited between organic and psychogenic amnesia is the temporal gradient of retrograde loss of autobiographical memory. The temporal gradient of loss in most cases of organic amnesia is said to be steepest at its most recent premorbid period, whereas for psychogenic amnesia the temporal gradient of retrograde autobiographical memory loss is said to be quite consistently flat. Although there is much literature on psychogenic amnesia as dissimilar to organic amnesia, the distinction between neurological and psychological features is often difficult to discern and remains controversial. Diagnosis
Functional assessment of brain activity can be assessed for psychogenic amnesia using imaging techniques such as fMRI, PET and EEG, in accordance with clinical data. Some research has suggested that organic and psychogenic amnesia to some extent share the involvement of the same structures of the temporo-frontal region in the brain. It has been suggested that deficits in episodic memory may be attributable to dysfunction in the limbic system, while self-identity deficits have been suggested as attributable to functional changes related to the posterior parietal cortex. To reiterate however, care must be taken when attempting to define causation as only ad hoc reasoning about the aetiology of psychogenic amnesia is possible, which means cause and consequence can be infeasible to untangle. Treatments
Because psychogenic amnesia is defined by its lack of physical damage to the brain, treatment by physical methods is difficult. Nonetheless, distinguishing between organic and dissociative memory loss has been described as an essential first-step in effective treatments.