During ancient Greek times, touch was considered to be an unrefined perceptual system because it differed from the other senses on the basis of the distance and timing of
sensation.[1]Weber distinctly identified these two types of sensation as the sense of touch and common bodily sensibility.[1] This distinction further helped 19th century psychiatrists to distinguish between tactile hallucinations and cenesthopathy
.
During the 19th century, tactile hallucinations were classified as symptoms associated with
tactile
sensory input creating a sensation of touch with an imaginary object.
In schizophrenia
snakes crawling over their body.[1] Such vivid tactile sensation of an object that is not present results from the unsuccessful attempt of the brain trying to perceive objects that are novel and that represent unreal situations usually triggered by guilt and fear.[4] Patients with schizophrenia also have a hard time portraying emotions as they divert most of their energy to control the pain from their tactile hallucinations.[4]
hallucinations associated with different modalities such as taste and sight.[5] However, the study failed to recognize the pathophysiology
of tactile hallucinations in individuals with schizophrenia.
In Parkinson's disease
About 7% of individuals with
narcoleptic rapid eye movement sleep disorders due to its concordance with visual hallucinations.[6] Moreover, it emphasizes that individuals who have had PD for a longer period of time have a more severe form of tactile hallucinations than with individuals who have succumbed to this disease for just a short period of time.[6]
Restless legs syndrome (RLS) causes unpleasant or uncomfortable sensations in the legs and an irresistible urge to move them.[9][10] Tactile hallucinations in RLS include feelings of itching, pulling, crawling or creeping mainly in the legs, with the accompanying overwhelming urge to move them.[9][10] These symptoms are more prominent in the late afternoon and at night, often causing insomnia.[9] The causes of RLS are generally unknown, though there are three major hypotheses: iron deficiency, dopamine insufficiency and genetic inheritance.[9][10] RLS can also occur due to nerve damage, or neuropathy.[9] Treatments for RLS typically focus on symptom relief through supplementing iron, blocking nerve receptors through the use of alpha-2 delta drugs such as gabapentin, or through the use of opioids or benzodiazepines.[10]
Phantom limbs
Main articles:
Mirror box
brain plasticity
. The vivid tactile sensation of the arm that is no longer present suggest the highly complex nature of the brain to reorganize different functions which were once thought to be hardwired to specific regions (localization).
Inducement through drugs
insects. Cocaine and alcohol can induce rapid firing of neuronal cells of the somatosensory region of the brain leading to vivid perception of illusionary bugs on the skin.[12] Additionally, as mentioned above, Trihexyphenidyl
is an antiparkinsonian drug that creates tactile hallucination. The mechanism through which these drugs induce tactile hallucinations is still unknown.
Cenesthopathy
ill and this feeling is not localized to one region of the body.[1] Cenesthopathic hallucinatory experiences are caused by the hyperactive neuronal stimulation of the primary somatosensory cortex due to a disorder or a damage to this area. There are two theories that are established to portray sensation of unified bodily feeling. One of these theories is called associationism, which states that cenesthesia is an amalgamation of propioceptive and interoceptive sensations.[1] Faculty psychology is the other theory which states that there is a particular brain region where all of the sensory information converged and the integration of this information gives one cenesthetic sensation. The latter theory became more predominant and it established two types of cenestopathic hallucinations namely "painful" and "paraesthetic". Patients that experience "painful" type of cenesthopathic hallucination felt that their organs were stretched apart and twisted.[1] On the other hand, patients with "paraesthetic" cenesthopathic hallucination experience severe hallucinatory itching.[1]
Pathophysiology
Tactile hallucinations are the result of a dysfunctional somatosensory and a dysfunctional
premotor areas.[2] The intensity of the tactile stimulus is directly proportional to the area of the primary somatosensory region activated.[13] A feedback mechanism from different cortical areas results in the awareness of touch. Even with complete sensory deprivation, discrete tactile memories can trigger spontaneous firing of impaired neurons.[2]
Therefore, individuals with various psychiatric disorders are more prone to tactile hallucinations than normal individuals.
Tactile hallucinations are especially possible due to faulty sensory integration of neuronal signals in the primary and secondary somatosensory system with neuronal signals in the
parietal cortex
, insular cortex and premotor cortex. Moreover, the posterior insula is responsible for mental body schema representation and can produce tactile hallucination if defected. Additionally, the regions of the brain involved in tactile hallucinations are similar to the regions of the brain involved in pain.