Continuing Education Activity

Astereognosis is the inability to identify objects by feel only, in the absence of input from the visual system. It may also be defined as the impairment of recognition of the objects by somatosensory discrimination of the size, texture, weight, and shape of the objects, in the absence of any major somatosensory deficit. This activity reviews the etiopathology, evaluation, and treatment of astereognosis and emphasizes the role of the interprofessional team in improving the disability due to astereognosis.

Objectives:

• Describe the etiology of astereognosis.

• Explain the evaluation of patients with astereognosis.

• Review the management options available for patients with astereognosis.

• Summarize the importance of communication and coordination amongst the interprofessional team members to enhance the care of patients with astereognosis.

Introduction

Astereognosis is the inability to identify objects by feel only, in the absence of input from the visual system. Stereognosis is the ability to know ('gnosis'- knowledge) the three-dimensional form of an object ('stereo'- solid) with tactile manipulation.[1] The shape, texture, size, and weight of the object are assessed. Usually, this is done with hands. Manual stereognosis requires the dorsal column-medial lemniscus tract (DCMLT) to receive discriminative touch and proprioceptive information, and the parietal cortex to process the information. Oral stereognosis is the ability to identify objects by mouth.[2] This is done using the perception of various receptors in the oral structures, including teeth.

Astereognosis may also be defined as the impairment of recognition of the objects by somatosensory discrimination of the size, texture, weight, and shape of the objects, in the absence of any major somatosensory deficit.[3] Somatosensory agnosia is a synonym. Postcentral, parietal lesions produce astereognosis clinically.[3][4] This is a marker of cognitive impairment in dementia.[5] Astereognosis can be divided into primary and secondary recognition defects.

The primary recognition deficit, called morphognosia, is the impairment in recognition of the physical features of the object. The secondary recognition deficit is a specific impairment in object recognition with spared primary recognition. The patient can feel the object and sense the dimensions and texture but is unable to correlate with the stored information and identify.

Etiology

Astereognosis indicates a lesion of the contralateral parietal lobe (see Image. Parietal Meningioma Causing Contralateral Sensory Syndrome). Small postcentral lesions can produce astereognosis, whereas complete parietal lesions produce hemianesthesia on the contralateral side.[4] Bilateral astereognosis can occur with a left postcentral lesion if there is dominance for stereognosis in the left hemisphere. Stroke and neoplasms are common causes. Astereognosis is also seen in diseases with cognitive impairment, such as Alzheimer's disease.[5] Trauma to the parietal regions such as depressed fracture also has been reported to cause this.

Other etiologies include ischemic infarction of the parietal lobe.[6] Arteriovenous malformation in the same site also can cause tactile agnosia. Rarely, lesions of the anterior corpus callosum and thalamic radiations also have been reported to cause astereognosis. Brainstem tumor also has caused unilateral astereognosis.[7] Brainstem ischemic lesions involving the medial lemniscus also are causative.[8] It has also been reported in extramedullary tumors of the foramen magnum. High posterior cord lesions due to multiple sclerosis also produce impaired stereognosis.[9]

Astereognosis is associated with the severity of stroke.[10] Somatosensory impairment is associated with motor impairment.[11] A defect in stereognosis is also found in children with cerebral palsy.[12]

Epidemiology

On analysis of the lateralized vascular, neoplastic, or traumatic cerebral lesions for their effect on sensory functions, it was found that cerebrovascular accidents caused severe impairment.[13] The global incidence of stroke is increasing and is around 258/100000/year.[14] Although primary prevention reduced the incidence of stroke in high-income countries, the incidence is increasing in middle-to-low-income countries. The survivors exhibit many impairments. The incidence of brain tumors has increased over the past 40 years.[15] However, this is probably secondary to the increased availability of imaging modalities. The established risk factors for brain tumors are ionizing radiation, mutations of penetrant genes, hereditary syndromes, and immunosuppression.[16] Around 14% of gliomas occur in the parietal lobes.[17] Head injuries can cause astereognosis. The parietal lobe is a common site of depressed skull fracture.[18]

Pathophysiology

Octave Landry formulated the fundamental concepts in the physiology of sensation as proprioception and stereognosis.[19] Manual stereognosis requires the dorsal column-medial lemniscus tract (DCMLT) to receive discriminative touch and proprioceptive information, and the parietal lobe for processing the information.[1] The movement of mechanoreceptors relative to one another helps to perceive the three-dimensional structure of objects.[20]

There are four types of mechanoreceptors:

1. Merkel cell receptors respond to slowly moving stimuli
2. Ruffini corpuscles responding to skin stretch
3. Meissner corpuscles for low-frequency vibrations
4. Pacinian corpuscles for high-frequency vibrations

They perceive information about the size, shape, texture, and motion of the objects. The spatial pattern of the activation of the mechanoreceptor in response to the forces applied to the skin and the relative receptive field of each receptor determine the perception. The information from the forelimb is carried in the dorsal column-medial lemniscal pathway to the cuneate nucleus in the medulla and from there to the ventroposterior lateral nucleus of the thalamus. From the thalamus, the inputs go to the primary somatosensory cortex, Brodmann areas 3,1, and 2. The information is then carried to the association areas in the posterior parietal cortex and the second somatosensory cortex.

Astereognosis occurs in cortical sensory syndrome secondary to superior-posterior parietal stroke.[21] The parietal cortex is also involved in Alzheimer's disease in addition to the medial temporal lobe, resulting in cognitive impairment.[22] The cortical sensory syndrome is seen in parietal gliomas regardless of hemispheric dominance.[23]

History and Physical

If the tests of peripheral sensations such as light touch, pain, temperature, and vibration are normal, the cortical sensory function can be assessed.[1] The tactile object recognition (TOR) test is to be done for stereognosis. A series of common objects such as pen, key, comb, and paperclip is placed in the hands of the patient after the eyes are closed. If the patient can recognize the object, stereognosis is intact. In the Nottingham sensory assessment, the test of light touch is with cotton wool, pressure by deforming the skin by the index finger, pinprick with a neurotip, and temperature with test tubes filled with hot and cold water.

In the assessment for stereognosis, an object such as a coin, pencil, scissor, cup, glass, comb, or sponge is placed in the hands of the patient for 30 seconds. The patient is asked to identify by naming or description. The score is given as 2 for normalcy, 1 for impairment (identification of some features of the object), and 0 for absence. The Nottingham method of stereognosis assessment is found to be a reliable tool between raters, in patients that have had a stroke.[24]

The sensory deficits in cortical sensory syndrome are loss of position sense, inability to localize noxious stimulus, astereognosis, agraphesthesia, and loss of two-point discrimination. This is seen contralaterally in either parietal lobe disease along with hemiparesis, hemianopia, hemineglect, and loss of optokinetic nystagmus. Additional features in the involvement of the dominant parietal lobe will be aphasia, ideomotor apraxia, and Gerstmann syndrome consisting of agraphia without alexia, left-right confusion, digit agnosia, and acalculia.[25] Bilateral astereognosis can occur in dominant parietal lobe dysfunction. The clinical features peculiar to non-dominant parietal lobe disease are loss of topographic memory, anosognosia, and dressing apraxia.

Evaluation

Computerized tomography (CT) and magnetic resonance imaging (MRI) are the imaging modalities to assess intracerebral pathology. CT is often the initial imaging in emergencies as it is quick, with no contraindications, and can identify hemorrhage. The use of MRI in acute stroke is increasing.[26] MRI has more sensitivity in acute stroke. In the case of brain tumors, CT may be the initial investigation done for the detection.[27] CT may show calcification, hemorrhage, herniation, mass effect, and hydrocephalus associated with tumors. But MRI is more useful in characterizing the tumors. Contrast-enhanced T1 weighted images can show the vascularity and necrosis of the tumor. MR spectroscopy will show the metabolic profile. Functional MRI (fMRI) assesses the activities of parts of the brain by detecting the changes in the blood oxygen level-dependent (BOLD) signals. It is widely used to determine the relationship of the tumor to the eloquent areas of the brain.[28]

A study of the somatosensory network after stroke, using resting-state fMRI, has shown the strong associations between the interhemispheric network connectivity indices and stereognosis.[29] The higher functional network connectivity is related to better somatosensory function. fMRI has been used to study the primary and secondary somatosensory areas of patients with congenital hemiplegia.[30] Diffusion tensor imaging (DTI) can be used to assess the sensory tract connectivity of the dorsal column medial lemniscus pathway in children with hemiparesis.[31]

Somatosensory evoked potentials (SEP) help in the correlation of sensory impairments such as astereognosis and hemianesthesia with parietal lesions seen in imaging.[4] SEP can be used as a diagnostic test as well.

Treatment / Management

The treatment of astereognosis is directed towards the underlying etiology. Treatment of acute ischemic stroke includes intravenous and intraarterial thrombolysis, mechanical thrombectomy, control of blood pressure, antiplatelet drugs, statins, etc.[32] Treatment of neoplasm of the brain may include a combination of surgery, radiotherapy, and/or chemotherapy, depending on the location, tumor type, and the age of the patient.[33]

Cognitive rehabilitation therapy (CRT) may improve cognitive deficits due to brain trauma, stroke, brain tumor, and dementia.[34][35] Sensory training can improve sensory discrimination after stroke.[36] Active sensory training consists of manual exploration and discrimination of different surfaces, textures, figures, shapes, weights, and objects with the hands, and tactile object recognition.[37] SENSe (Study of the Effectiveness of Neurorehabilitation on Sensation), a randomized controlled trial, showed that sensory discrimination training could give a functional improvement in those with impaired tactile object recognition after stroke.[38]

Differential Diagnosis

There are mainly three syndromes in the differential diagnosis of hemisensory disturbances in a parietal lesion.[21]

• The cortical sensory syndrome, including astereognosis, agraphesthesia, and loss of position sense, is due to a superior-posterior parietal lesion.
• The pseudothalamic sensory syndrome consists of a faciobrachiocrural impairment of touch, pain, temperature, and vibration, due to an inferior-anterior parietal lesion.
• The atypical sensory syndrome with a sensory loss involving all modalities of sensation in a partial distribution is produced by parietal lesions of different topography.

Astereognosis is used to describe both the inability to discriminate shape and size by touch and the inability to recognize objects by touch. These are apperceptive and associative types of agnosia. The term tactile agnosia is used for the associative type. The deficits in discrimination are most commonly seen with lesions in the primary somatosensory area and its connections. Lesions in the parietal somatosensory association areas result in tactile agnosia. 

Tumors at the craniovertebral junction also can produce astereognosis with the involvement of the dorsal column medial lemniscus tract.[39] In addition, amyotrophy of hand muscles may also be seen. Impairment of stereognosis due to lesions in the spinal cord and brainstem is termed stereoanesthesia.[40] Impairment of ipsilateral vibration and joint position senses are noted.

Prognosis

Astereognosis is a frequent somatosensory impairment after stroke.[10] Recovery occurs over time. Patients with stroke improve over days to months, depending on the location and severity of the stroke.[41] Larger parietal gliomas are associated with neurological deficits.[23] Either improvement or deterioration of deficit can occur after resection. Patients with traumatic brain injury show functional improvement with rehabilitation therapy such as sensory re-education even in the chronic phase.[42]

Complications

Somatosensory loss has a negative influence on functional outcomes. Discriminative sensory impairment of the upper limb is seen in about half of the patients with stroke in the phase of rehabilitation. The sensory impairment of the upper limb results in a hindrance to its usage in daily life.[37] It has been found that impairment of discriminative sensation is common in patients with stroke and causes clumsiness, which is not explained by the main deficits.[43] Astereognosis is associated with a neurocognitive decline in Alzheimer's disease.[5] Astereognosis or stereoanesthesia is associated with useless hand syndrome or numb clumsy hands in high cervical lesions due to multiple sclerosis or cervical spondylosis.[9][44][45] Impaired stereognosis in parietal lobe disease can lead to tactile apraxia, as a disturbance of hand movements for interaction with an object.[46]

Deterrence and Patient Education

Patients are given sensory re-education to improve the deficits. This is by giving graded tactile stimuli to restore sensory areas.[37] Sensory re-learning comprises the tactile exploration of surfaces, tactile discrimination of shapes, textures, weights, and temperatures, and tactile object recognition of objects. The patients are asked to do repeated exercises with grades of increasing difficulty. The feedback is taken with vision or by the unaffected hand. Individualized home exercises are also advised.

Enhancing Healthcare Team Outcomes

Health professionals should be trained to elicit discriminatory and cortical sensations. The Nottingham sensory assessment is a good method to assess the tactile and kinesthetic sensations and stereognosis. Patients with astereognosis are best managed with an interprofessional team approach. There is a significant role in rehabilitation after the acute treatment of neurological diseases. This may include neurologists, physiatrists, occupational therapy, physical therapy, and speech therapy. Sensory training should be given as much importance as motor training. The involvement of therapists early in the course of the disease is important for optimal outcomes. The competence and training of physical and occupational therapists in astereognosis are vital.