Stereognosis is the ability to identify the shape and form of a three-dimensional object, and therefore its identity, with tactile manipulation of that object in the absence of visual and auditory stimuli. The etymology of the word stereognosis is from the Greek for “stereo,” meaning solid and “gnosis” meaning knowledge. A distinction is necessary between manual stereognosis and oral stereognosis, which take place in the hands and mouth, respectively.[1]
Manual stereognosis requires intact peripheral sensory pathways, namely the dorsal column-medial lemniscus tract (DCMLT), to receive discriminative touch and proprioceptive information. Receival of this information is necessary but not sufficient for stereognosis because the information also requires functioning processing centers, which are in the cortex of the parietal lobe.
To properly understand the clinical relevance of stereognosis, one must first appreciate the primary pathway that allows perception of the size and shape of the object, the DCMLT, and how this information is processed in the parietal cortex.
The first-order neurons of the DCMLT have cell bodies in dorsal root ganglia with peripheral processes extending out to sensory receptors (Pacinian corpuscles, Merkel cells, Golgi tendon organs, and muscle spindles) and central processes that enter the spinal cord in the large sensory fiber entry zone of the dorsal horn ascending ipsilaterally in the dorsal columns.[2]
Nerve fibers introduced to the dorsal columns from the lower extremities localize to the medial aspect as they ascend ipsilaterally, forming bundles of axons called the fasciculi gracilis. Similar proprioceptive and discriminative touch information from the upper extremities (spinal level T5 and above) localizes to adjacent lateral axon bundles called the fasciculi cuneatus. The fact that nerve fibers enter the spinal cord and add to the dorsal column fascicles in a medial to lateral manner is an important concept. This somatotopic organization of the ascending tracts allows for precise localization of these stimuli when they eventually reach the primary somatosensory cortex of the parietal lobe.[3]
Before this can occur, however, the fasciculi cuneatus and gracilis must ascend ipsilaterally until they reach the caudal medulla. As these axon bundles enter the caudal medulla, the neurons synapse in their respective nuclei; the nuclei cuneatus and nuclei gracilis. Second-order neurons of the DCMLT decussate, or cross over, in the caudal medulla forming crossing tracts termed the internal arcuate fibers. This is an important anatomic process that explains why the interpretation of right-sided discriminative touch information is via the left somatosensory cortex and vice versa. After decussation, the internal arcuate fibers are now referred to as the medial lemnisci and travel through the pons and midbrain until reaching the thalami of the diencephalon. Here, second-order neurons synapse with third-order neurons in the ventral posterolateral nuclei of the thalami. Third-order neurons from each tract pass through their respective internal capsule en route to the primary somatosensory cortices of the anterior parietal lobes, located in the postcentral gyri.[2][4][5]
The organization of the primary somatosensory cortices of the parietal lobes is in a somatotopic manner such that the inferior anatomic structure information (from the lower extremities) is interpreted in the superomedial aspect of the postcentral gyrus, and the more superior anatomic structure information (from the face and arms) is interpreted in the lateral aspect of said gyrus. The representation of this organization is as a diagrammatic homunculus overlying the precentral gyrus with areas of the body being displayed in their appropriate location along the gyrus and the anatomic structure size being proportional to their relative tactile sensitivity. During manual stereognosis, information from the hand portion of the primary somatosensory cortex is sent to the tertiary somatosensory association cortex located in the superior parietal lobule. Localization of stimuli and integration of information within this cortical processing area represents the physiologic basis for stereognosis.[6]
Terminology Confusion
It is crucial to understand stereognosis relative to a set of related terms: astereognosis, agnosia, and tactile object agnosia. Recall that stereognosis is the ability to perceive the physical form and identity of an object based on tactile stimuli alone. Astereognosis refers to the inability to perceive the form and identity of an object when physically manipulating it through active touch. By definition, astereognosis necessitates functioning peripheral sensory modalities (pain, temperature, fine touch, and vibration sense) and is a result of pathology within the central cortical integration of this sensory information. Astereognosis falls under a family of conditions called agnosias, which are classified based on the sensory modality involved (auditory, visual, or tactile). In the context of this terminology, one should also be aware that the term tactile object agnosia is used interchangeably and is practically synonymous with astereognosis.[7][8]
Limitations of Testing
Because stereognosis is a function of cortical sensory areas, it is worth noting that cortical sensory function is not testable if the patient has peripheral lesions that cause dysfunction in the afferent pathways that supply the cerebrum. For example, if a patient has peripheral neuropathy that limits the ability for tactile signals to reach the brain, it can be challenging to ascertain whether or not the patient's stereognosis limitations are secondary to their peripheral neuropathy or a cortical processing deficit.[9]
Clinical Testing
It is important to understand stereognosis assessments in the context of general sensory function due to the dependent relationship between cortical sensory processing and afferent sensation. Tests of peripheral sensation often include sensation to light touch (using fingertip palpation or cotton swab), pain (alternating between relatively sharp and dull stimuli), temperature (often using a cool metallic object), vibration (using a tuning fork), and two-point discrimination (using calipers). If all of these functions are intact, the patient's cortical sensory function can then undergo assessment. To test stereognosis specifically, clinicians often perform a tactile object recognition (TOR) test. The TOR test involves asking the patient to close their eyes and placing a series of common objects in the patient's hand and asking him or her to identify the object. The objects frequently used in the TOR test include a pen, key, comb, and paperclip. If the patient can recognize the object placed in his or her hand, their stereognosis is said to be intact. If they are unable to identify the object despite having an intact peripheral sensory function, they are said to have astereognosis.[9][10]
Astereognosis
Astereognosis indicates that a patient is suffering from a lesion of the primary somatosensory cortex or somatosensory association area of the parietal lobe; this is commonly described as a cortical sensory loss. As previously discussed, afferent sensory fibers located in the periphery decussate before reaching the cerebral cortex, which means that defects in these cortical processing regions will produce contralateral deficits. Fine motor functions involved with activities of daily living, such as feeding one's self, require coordination between sensory and motor processing areas of the cortex. Therefore, defects in the processing of haptic information can result in difficulty performing activities of daily living and impede the recovery of patients with cortical injuries. Many conditions precipitate astereognosis, including but not limited to, cortical dementias, cerebral palsy, cerebrovascular stroke, and meningioma.[11]
Cerebrovascular Strokes
Between 2013 and 2016, approximately 7 million Americans reported having a stroke, with a significant proportion of these individuals (17%) being above the age of 85. It is widely recognized that the motor and sensory deficits following strokes, including cortical sensory modalities like stereognosis, represent a large portion of the burden of disease and recovery. With the high prevalence of cerebrovascular strokes, there is a great opportunity for improving outcomes and recovery. This is of particular interest in the elderly populations who tend to have poorer outcomes. In cases of cortical sensorimotor stroke, tracking recovery and rehabilitation status often include an assessment of tactile object recognition. Also, many of the therapeutic modalities that allow stroke patients to regain their functional status focus on sensory discrimination and recognition skills. Thus, stereognosis provides great clinical utility in prognostication and maximizing sensorimotor recovery following cerebrovascular strokes.[12][13][14][15][16]
Post-Stroke Sensory Retraining
Studies have suggested that there is a degree of sensorimotor neuronal recovery following strokes, particularly for proprioception and stereognosis. It has also been recognized that sensorimotor deficits contribute to interference with activities of daily living and return to functional status in patients recovering from a stroke. That said, there is significant variability in the standardized outcomes that physicians, physical therapists, and occupational therapists use to monitor stroke patient recovery status. Also, the rehabilitation community lacks consensus about the physical therapy protocol, which optimizes sensorimotor recovery. The American Stroke Association guidelines indicate that the use of somatosensory retraining to improve sensory discrimination can be an option for stroke survivors who demonstrate sensory deficits [Level IIb Evidence]. For these reasons, it may benefit patients if physicians and physical/occupational therapy staff coordinate to construct a regimen that includes sensory retraining to improve the performance of activities of daily living in stroke survivors.[12][17][18][19]
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