SPD has been added to the diagnostic criteria of ASD in DSM-5 in 2013, but the relation between SPD and the other diagnostic criteria of ASD was not in focus in Egyptian literature.
SPD may be considered central in autistic symptomatology as it precedes and predicts the occurrence of social interaction impairment and repetitive behaviors in the developmental cascade [14].
Although the presence of SPD may pass unnoticed, if it is not treated it reduces the response to treatment of other symptoms in ASD [15].
In our study, the most affected sensory processing was in under-responsive/seeks sensation (57.5%), followed by tactile sensitivity (52.5%), auditory filtering (50.0%), taste/ smell sensitivity (47.5%), and visual/ auditory sensitivity (42.5%), while the least affected sensory processing was hypo-activity (low energy/ weak subscale) (35.0%).
Our results were consistent with a study by Kojovic et al. [14] who found sensory processing abnormalities in items of under-responsiveness/sensation seeking, auditory filtering, and tactile sensitivity sections in autistic children.
In agreement with the present study, came a study by Posar and Visconti [15] who found three main sensory patterns in children with ASD namely hypo-responsiveness, hyper-responsiveness, and sensory seeking.
Under-responsiveness/seeks sensation may reflect response to multiple sensory stimuli. Our participants seemed to seek sensory input from multiple sensory systems (e.g., auditory, vestibular, tactile, proprioception). Tasks involving multisensory input include difficulty paying attention, getting lost easily, fidgeting in an active environment, or leaving clothing twisted on the body.
Proper working of the multisensory system is mandatory for the integration of stimuli obtained from different sensory systems to perceive the environment accurately [16]. Several studies revealed multisensory abnormalities in autistic children [17,18,19].
As regards tactile sensitivity subscale, our participants seemed to be hyper-responsive to tactile stimuli in some items such as reacting emotionally or aggressively to touch, irritated when wearing shoes or socks, or avoiding being barefoot. While they were hypo-responsive in other items such as decreased awareness to pain and temperature, and not noticing when face or hands are messy.
Both hyper- and hypo-responsiveness to tactile stimuli are reported in autistic children [20,21,22]. and were steered together as the strongest predictors of social interaction deficits [23].
In contrast to under-responsiveness/seeks sensation and tactile sensitivity subscales which were among the highest definite difference from normal among our study participants, came the hypo-activity (low energy/ weak) subscale as the lowest in difference from normal. Most of the participants’ parents reported that their children were strong, were active, had good tolerance, and were exploring their environment without a purpose.
This came in disagreement with various studies which found that this subscale is often seen in autistic children manifested by difficulty with sustained engagement in daily routines. The low energy/ weak domain includes items such as the following: seems to have weak muscles, poor tolerance/ tires easily, especially when standing or holding particular positions and props to support self [24].
In the present study, there was a negative correlation between the ADI-R reciprocal social interaction domain (A) and SSP (the SSP total and all subscales scores except for low energy/weak domain). This means that participants with more sensory symptoms showed more impairment in social interaction.
Thye and colleagues [18] revealed that primary sensory processing deficits in visual, auditory, tactile, and olfaction/gustatory responses could lead to social difficulties in ASD.
Also, our results came in agreement with a study done by Kojovic et al. [14] who confirmed the association between sensory processing and social impairments and its presence at a younger age before 6 years old.
We found a negative correlation relation between the ADI-R communication abnormalities (B) and the SSP total and all subscales scores except for movement sensitivity, low energy/weak, and visual/ auditory sensitivity domains. This means that participants with more sensory symptoms showed more impairment in communication.
Caminha and Lampreia [25] agreed with us as they related that sensory deficits were reflected in language and communication developmental deficits.
Studies revealed that SPD may have an effect on the essential sensorimotor skills concerned in non-verbal language and communication like gesture and imitation, therefore resulting in what is perceived as idiosyncratic behaviors, i.e., eye gaze aversion, limited non-verbal communication, and restricted facial expression. These atypical behaviors may later affect social learning opportunities, with a huge impact on development of effective social communication skills [26].
The present study revealed a negative correlation between the ADI-R restricted, repetitive, and stereotyped patterns of behavior (C) and the SSP total and all subscale scores except for low energy/weak and visual/auditory sensitivity in our study. This means that participants with more sensory symptoms showed more restricted, repetitive, and stereotyped patterns of behavior.
Restricted and repetitive behaviors (RRBs) are core symptoms of ASD. Analytical studies applying ADI-R showed a pair of subclasses: repetitive motor and sensory behaviors like repetitive hand or finger movements, and insistence on sameness, together with limited interests, rigid routines, and rituals [27]. These classes of behaviors are usually correlative and frequently occur along within the same individual [28].
Previous studies discovered that SPD is often related to RRBs, where SPD were more obvious in people experiencing more RRBs [27, 29].
Indeed, sensory hypersensitivity could clarify the co-occurrence of anxiety and RRBs in ASD. RRBs may act as a coping mechanism to reduce anxiety resulting from sensory hypersensitivity [30].
In a study by Gal et al. [31], they found that stereotyped movements are initiated or terminated in response to sensory stimulation.
RRBs appear to reflect trials to control a chaotic perceived environment caused by sensory deficits in children with autism [25].
Better understanding of the effect of sensory profiles on adaptive behavior and therefore the development of behavioral issues in children with ASD should urge creating higher tailored clinical support [32].
Collectively, our study found a negative correlation between SPD and the symptom triad in autistic children.
Tavassoli et al. [33] agreed with our results as they suggested a negative correlation between SPD and other autistic symptoms.
Caminha and Lampreia [25] said sensory problems would promote the triad of impairment in autistic children from a developmental perspective.
In our study, children with more severe autism had more sensory deficits. CARS was negatively correlated with the SSP total and all subscales scores. These findings are consistent with several previous studies in which the severity of ASD had been associated with the severity of sensory deficits [34,35,36,37].
However, other studies found no significant difference between low and high functioning autism subgroups in the frequency of sensory symptoms [38].
In the present study, there was a high percentage of parental consanguinity (80% of the participants), 37.5% of them were mildly autistic, 15% were moderately autistic, and 47.5% were severely autistic, suggesting that parental consanguinity is a risk factor for ASD and predicts its severity. This highlights the importance of early screening of ASD in families with parental consanguinity.
The nearest percentage of paternal consanguinity in families with autistic children to our study was in a study conducted in Qatar who found paternal consanguinity in 45% of their studied sample and linked it to the ASD severity [39].
In another Egyptian study, there was parental consanguinity in 20% of the forty studied autistic cases [40].
Meanwhile in Israel, there was a significant difference regarding parental consanguinity in families of autistic children between Arabs (21.1%) and Jews (2.3%) [41].
And in the first epidemiological Iranian study of autistic children, the paternal consanguinity was 32.4% [42].
The high percentage of parental consanguinity in our results may be due to small sample size or such a coincidence as the participants were selected randomly from the autistic children attending the ASD clinic. This issue needs further studies.