The phenomenon of ""phantom limb"" is difficult to explain using the direct pathway model of pain.
The phantom pain may be at least partially explained as a response to mixed signals from the brain. After an amputation, areas of the spinal cord and brain lose input from the missing limb and adjust to this detachment in unpredictable ways.
The direct pathway starts from the cortex and projects to the striatum (caudate nucleus and putamen) with excitatory glutamatergic (glu) neurons. The neurons from the striatum, which are inhibitory GABAergic, send their axons to the medial (internal) globus pallidus and substantia nigra, pars reticulata (SNr).
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