Neuroanatomy, Medial Lemniscus (Reils Band, Reils Ribbon)

Structure and Function

The primary function of the medial lemniscus as a second-order neuron of the DCML is to transmit sensory information related to conscious proprioception, vibration, fine touch, and 2-point discrimination from the skin and joints of the body and head. This information travels from the caudal medulla to the ventral posterolateral nucleus of the thalamus and subsequently to the primary somatosensory cortex.

Embryology

The medial lemniscus, like the entire nervous system, originates from the neural ectoderm during embryonic development. This neural ectoderm divides into 3 primary subdivisions that contribute to the DCML pathway. The neural plate, which forms the central nervous system, gives rise to several cerebral vesicles, which include the myelencephalon, which develops into the medulla oblongata; the metencephalon, which forms the pons; the mesencephalon, which becomes the midbrain; the diencephalon, which develops into the thalamus; and the telencephalon, which matures into the cerebral cortex. (Source: Betts et al, 2022)

As previously described, all these structures are essential components of the DCML tract and its development. Additionally, the protein Netrin-1, secreted by the floor plate of the medulla oblongata, plays a critical role in the development and migration of axons forming the medial lemniscus.[1]

Neural crest cells originating from the dorsal neural tube are pivotal in forming the peripheral nervous system. These cells differentiate into various types, including the somatic sensory neurons that act as 1st-order neurons in the DCML pathway. These neurons transmit fine touch, vibration, and proprioceptive information from peripheral receptors to the central nervous system.[2]

Furthermore, neural crest cells contribute to the development of specialized tactile mechanoreceptors that are critical for somatosensation. Meissner corpuscles detect light touch and low-frequency vibrations. Ruffini endings respond to skin stretch and sustained pressure.[3] Merkel cell-neurite complexes are sensitive to steady pressure and texture, facilitating fine tactile discrimination. (Source: Andrusca, 2023) Pacinian corpuscles detect deep pressure and high-frequency vibrations (Source: Molnar and Gair, 2015). These mechanoreceptors are integral to the somatosensory system, enabling the perception of various tactile stimuli.

The ectodermal placodes give rise to cranial sensory ganglia, which develop into the chief sensory nucleus of the trigeminal nerve. The axons from this nucleus join the medial lemniscus pathway, conveying conscious proprioception, vibration, fine touch, and two-point discrimination from the head.

Blood Supply and Lymphatics

The blood supply of the medial lemniscus varies according to the level of the brainstem. The nuclei gracilis and cuneatus, located in the medial posterior aspect of the medulla, receive vascular supply from the posterior spinal artery. The arcuate fibers decussate in the medial-anterior aspect of the medulla and are irrigated predominantly by the anterior spinal artery. The medial lemniscus begins ascending contralaterally in the medial aspect of the medulla and is also supplied by the anterior spinal artery. As the fibers ascend, the medial lemniscus shifts posteriorly and laterally. At the level of the pons, the medial lemniscus receives blood supply from the basilar artery. By the time it reaches the midbrain, the medial lemniscus is located predominantly in the posterior lateral aspect, where it is perfused by the posterior cerebral artery.[4]

Infarction in specific regions of the brainstem or thalamus can cause loss of conscious proprioception, vibration, fine touch, and 2-point discrimination. This presentation may be explained by the medial lemniscus occupying different positions along its pathway.

Surgical Considerations

The medial lemniscus, a 2nd-order neuron of the DCML pathway, lies mostly within the brainstem. The brainstem’s high density of neurological tracts and nuclei makes surgery targeting specific pathways particularly complex. Surgical intervention in this area risks damage to additional neurological tracts. Consequently, surgery has traditionally been reserved for clear-cut cases where potential benefits outweigh the risks.

A prospective randomized clinical trial evaluated motor deficit and neurological outcomes in patients undergoing surgery for cavernous brainstem malformations. Preoperative diffusion tensor imaging (DTI) and diffusion tensor tractography (DTT) were used to assess these outcomes. While definitive conclusions cannot yet be drawn, the results appear promising. The ability to visualize specific tracts and pathologies may improve surgical planning, decision-making, and potentially reduce morbidity.

While these findings are encouraging, further research is needed to confirm the efficacy of DTI and DTT in routine clinical practice for brainstem surgeries. Continued advancements in imaging technology could enhance surgical precision and improve patient outcomes in this challenging anatomical region.[5]

Clinical Significance

The DCML pathway may be impaired at multiple points along its 1st-, 2nd-, and 3rd-order neurons. Clinical presentations may be complex due to the fibers' proximity to other neurological tracts. However, the loss of conscious proprioception, vibration, fine touch, and 2-point discrimination of the skin and joints is pathognomonic for DCML pathway damage. The specific symptoms depend on the level at which the pathway is affected. Common pathologies impacting the DCML pathway are described below.

Tabes Dorsalis

Tabes dorsalis is a late manifestation of tertiary syphilis caused by the spirochete Treponema pallidum. Although rare today due to the pathogen's penicillin sensitivity, the condition leads to demyelination of the dorsal columns and dorsal roots, predominantly affecting the lumbosacral region and, thus, the lower limbs. The resulting loss of conscious proprioception, vibration, fine touch, and 2-point discrimination contributes to neuropathic osteoarthropathy (Charcot joint). This condition manifests as progressive degeneration of weight-bearing joints, with the midfoot being the most commonly affected site. Complications include bone fractures and ulcerations at the injury site. Management focuses on treating the underlying infection with intravenous penicillin.[6] 

Vitamin B12 Deficiency

Subacute combined degeneration is characterized by demyelination of the dorsal columns, lateral corticospinal tracts, and spinocerebellar tracts due to vitamin B12 deficiency.[7] Although rare in the U.S., vitamin B12 deficiency should be considered in high-risk groups such as strict vegans, patients with inflammatory bowel disease, chronic malabsorption, pernicious anemia, history of gastrectomy, Diphyllobothrium latum infection, and cystic fibrosis.[8] Diagnosis relies on measuring methylmalonic acid levels. Treatment consists of vitamin B12 supplementation.[9] However, recovery depends on the duration and severity of neuronal damage.[10]

Brown-Sequard Syndrome

Brown-Séquard syndrome is a theoretical spinal cord hemisection injury rarely seen in its textbook form. This condition typically results from trauma, ischemia, large unilateral tumors, or infections. The hemisection causes ipsilateral loss of the DCML pathway and corticospinal tract, contralateral spinothalamic tract damage, and flaccid paralysis with sensory loss at the level of injury. Clinically, patients present with loss of conscious proprioception, vibration, fine touch, and 2-point discrimination on the ipsilateral side, accompanied by spasticity and hyperreflexia. Loss of pain and temperature sensation is observed on the contralateral side. Flaccid paralysis and complete sensory loss occur at the injury level. Diagnosis involves magnetic resonance imaging and neurological examination. Treatment targets the underlying pathology.[11]

Medial Medullary Syndrome

Medial medullary syndrome results from infarction of the medial medulla oblongata due to occlusion of the paramedian branches of the anterior spinal artery. Damage to the medial lemniscus causes loss of conscious proprioception, vibration, fine touch, and 2-point discrimination on the contralateral side of the body. Contralateral hemiparesis occurs due to corticospinal tract damage before decussation at the medullary pyramids. Ipsilateral tongue deviation results from injury to hypoglossal nerve fibers. Diagnostic evaluation includes coagulation studies, echocardiography, and computed tomography angiography (CTA). Management depends on stroke type, whether ischemic or hemorrhagic, and time since onset.

Paramedian Artery Occlusion

The paramedian arteries, branches of the basilar artery, supply the medial basal pons, pontine nuclei, corticospinal fibers, and the medial lemniscus as it ascends through the pons. Although rare, occlusion of these arteries can cause significant neurological deficits. Evaluation involves coagulation studies, echocardiogram, and CTA. Treatment depends on the stroke type and timing.

Upper Dorsal Pontine Syndrome

Also known as Raymond-Cestan syndrome, this condition arises from occlusion of the long circumferential branches of the basilar artery. Damage to the medial lemniscus pathway causes contralateral loss of conscious proprioception, vibration, fine touch, and 2-point discrimination. Additional symptoms include ipsilateral ataxia, paralysis of muscles of mastication, sensory loss of the face, horizontal gaze palsy, contralateral loss of pain and temperature sensation, and contralateral hemiparesis affecting both face and body. Diagnostic workup includes coagulation studies, echocardiography, and CTA. Management is guided by stroke type and time of onset.[12]

Medial Lemniscus Pathway Conditions Beyond Brainstem Syndromes

In addition to the syndromes described above, other conditions may also involve damage to the medial lemniscus pathway. Dorsal midbrain syndrome, caused by occlusion of the paramedian branches of the basilar artery, can lead to medial lemniscus injury if the occlusion extends laterally. Thalamic strokes affecting the ventral posterolateral nucleus, due to occlusion of thalamic branches of the posterior cerebral artery, can damage the 3rd-order neuron of the DCML pathway, resulting in characteristic sensory deficits.