**3. Neurologic correlation**

The complexity of sensorimotor systems requires deep knowledge of anatomy and physiology to analyze and localize the symptoms and the signs of the patients. Joint sense and vibration sense examination is an important component of neurological examination.

The classic diseases causing sensory ataxia are tabes dorsalis, polyneuropathies (especially involving large fibers), dorsal root ganglionopathies and subacute combined degeneration. With parietal lobe lesion, position sense is often impaired and vibration preserved [5]. Vibratory sensation may also be impaired in lesions of the peripheral nerves, plexopathies, radiculopathies, dorsal root ganglion, posterior columns and medial lemniscus. In patients with peripheral neuropathies, vibration sensation is lost in the lower extremities first. Impaired vibration from posterior column disease is more likely to be uniform at all sites in the involved extremities. In spinal cord diseases, detecting a "level" of vibration sensory (segmental demarcation) loss over the spinous processes is crucial for diagnosis [5]. In patients with diabetic neuropathy, the decline in proprioceptive function may be caused by impairment in muscle spindle function and or the spindle receptors itself [47].

In patients with hereditary sensory and autonomic neuropathy type III patients (Riley-Day Syndrome, familial dysautonomia) ataxic gait is explained by poor proprioceptive acuity at the knee joint [48]. In mitochondrial ataxias sensory ataxia (which classically include gait ataxia worsened by loss of visual fixation) is due to the involvement of proprioception, secondary to peripheral neuropathy or neuronopathy [49]. In patients following whiplash type injuries involving soft tissues of cervical spine leads to proprioceptive deficits affecting head and position sense. Also in patients with chronic whiplash associated disorders are reported to have balance and dizziness problems, head and eye movement impairments reflecting mismatch od afferent input from the proprioceptive, visual and vestibular systems [8, 50]. Lesions of the dorsal columns impairs sensation of touch, vibration and proprioception in the ipsilateral side of the body below the injury level [51]. In patients with non-specific low back pain, postural control is impaired during standing and slow performance movements. This is due to an altered use of ankle compared to back proprioception related activity in right primary motor cortex and frontoparietal cortex [52]. Brainstem lesions resemble those in spinal cord disease as it selectively involves spinothalamic tract or medial lemniscus causing contralateral loss of position sense and vibration sense [5].

Neglect is a condition in which patients loose self-spatial awareness opposite to the damaged site of the brain. It is proposed that it is associated with the lesions of the dorsal stream causing dysfunction of proprioceptive space which is encoded in the bilateral parietal cortex [53]. Loss in the position sense may cause pseudochoreoathetosis as well. This abnormal involuntary, spontaneous movements are restricted to the parts with proprioceptive sensory loss. It is proposed that failure to integrate cortical proprioceptive sensory inputs in striatum may explain this situation [5, 54].

There are experimental evidence of proprioception impairments in Parkinson's disease. Parkinsonian gait is affected by the involvement of lower limb proprioceptive deficits as well as the involvement contralateral somatosensory and premotor lateral cortices and posterior cingulate cortex and basal ganglia and bilateral prefrontal cortex [10, 55, 56]. It was also shown that conscious perception of kinaesthetic stimuli is impaired in Parkinson's disease as cerebro-basal loops are not intact [9].

Weeks and colleagues showed that patients with cerebellar damage had reduced dynamic proprioceptive acuity which was also parallel to their motor deficits [3]. Diseases of the primary somatosensory cortex do not generally produce sensory symptoms but deteriorate fine and delicate manipulations in the contralateral part depending on position sense [2, 5]. Many patients with stroke

**25**

erative rehabilitation [77].

*Proprioception and Clinical Correlation DOI: http://dx.doi.org/10.5772/intechopen.95866*

neuroplasticity [58, 60].

our five major joints.

joint to the brain [65].

ception is disrupted [66, 67].

**4.1 Knee joint**

**4. Proprioception after orthopedic surgeries**

experience proprioceptive deficits. Recovery of proprioception increases in the chronic phase [57, 58]. In study by Pope it was shown that proprioceptive input from the neck also may change cerebellar output affecting M1 plasticity [59]. In the study of Vidoni and colleagues preserved motor learning after stroke was related to the degree of proprioceptive deficit suggesting the relation between proprioceptive perception from muscle spindles and motor learning and central

Studies on changes in joint proprioception after orthopedic surgeries are available in the literature. This section consists of the information in the literature about

Knee proprioception is necessary to achieve normal joint coordination during movement as well as providing joint stabilization [61, 62]. The anterior cruciate ligament (ACL), posterior cruciate ligament, collateral ligaments and menisci contribute to proprioception with the help of proprioceptors they have [63, 64]. The mechanoreceptors of the cruciate ligaments, together with the mechanoreceptors of the joint capsule, transmit information about the extension and flexion of the knee

The ACL is the most important ligament involved in knee mechanical and neuromuscular stability. It contributes to proprioception in joint movement. However, the ACL is the most frequently injured ligament. After ACL rupture, knee proprio-

Various autografts and allografts are used for ACL reconstruction. Patellar tendon or hamstring tendons may be preferred in patients using autografts. In addition, different techniques and materials are used. However, there is no gold standard in graft and technique selection [68]. In order for ACL reconstruction to be successful, not only mechanical but also neuromuscular stability is required. Neuromuscular stability depends on obtaining proprioception [69]. ACL injury leads to degradation of mechanoreceptors and a histologic study revealed that free nerve endings disappear after 1 year [70]. The effectiveness of ACL reconstruction in regaining proprioception has been tried to be revealed by some studies [71–74]. While some studies argue that ACL reconstruction is not sufficient to restore joint position [71–73], some studies advocate the adverse opinion [74]. The lack of a test to distinguish about whether the proprioception is derived from the soft tissues around the knee and capsule or from mechanoreceptors on ACL prevents to reach a

Even after total knee arthroplasty, the contribution of the soft tissues around the knee to proprioception continues. In order to take advantage of this effect and ensure satisfactory outcomes in these patients, the soft tissue and gap must be well adjusted. Unicompartmental replacement protecting the ACL may be more advantageous in not reducing proprioception due to the proprioceptive effect of ACL. Also Ishii et al. [76] conclude that balance is improved after the postoperative period in bilateral total knee arthroplasty. It is stated that the first 6-week period is the critical period for adaptation time and proprioceptive loss after total knee replacement, and a new pattern in the knee load distribution occurs with postop-

certain decision about the mechanoreceptors of ACL [75].

experience proprioceptive deficits. Recovery of proprioception increases in the chronic phase [57, 58]. In study by Pope it was shown that proprioceptive input from the neck also may change cerebellar output affecting M1 plasticity [59]. In the study of Vidoni and colleagues preserved motor learning after stroke was related to the degree of proprioceptive deficit suggesting the relation between proprioceptive perception from muscle spindles and motor learning and central neuroplasticity [58, 60].
