What is the physiology behind numbness and tingling in the context of spinal ascending and descending tracts?

Physiology of Numbness and Tingling in Spinal Tract Pathology

Numbness and tingling (paresthesias) result from dysfunction in the ascending sensory pathways of the spinal cord, specifically affecting the dorsal column-medial lemniscal pathway (for fine touch, vibration, proprioception) and the spinothalamic tract (for pain and temperature), with the clinical presentation depending on which specific tract is damaged and at what level. 1

Anatomical Organization of Ascending Sensory Pathways

Dorsal Column-Medial Lemniscal System

• Carries fine touch, vibration, and proprioception information through the gracilis fasciculus (lower body, medial) and cuneatus fasciculus (upper body, lateral) 1
• These tracts ascend ipsilaterally in the posterior white matter of the spinal cord before decussating in the medulla 1
• Damage to these pathways produces ipsilateral sensory deficits below the level of the lesion, manifesting as numbness to light touch and loss of vibration sense 1

Spinothalamic Tract (Anterolateral System)

• Conveys pain, temperature, and crude touch from the periphery to the brain 2, 3
• Primary sensory neurons synapse in the dorsal horn (laminae I-V), then second-order neurons decussate within 1-2 spinal segments and ascend contralaterally in the anterolateral white matter 1, 2
• Damage produces contralateral loss of pain and temperature sensation beginning 1-2 dermatomes below the lesion level 1
• Spinothalamic tract cells project to both the ventroposterolateral thalamus (sensory-discriminative processing) and intralaminar thalamic nuclei (motivational-affective components) 2

Spinoparabrachial Pathways

• TACR1-expressing and GPR83-expressing projection neurons form parallel circuits conveying thermal, tactile, and noxious signals to the lateral parabrachial nucleus 3
• GPR83-expressing neurons are particularly sensitive to mechanical stimuli and can mediate both positive and negative valence depending on stimulus intensity 3

Mechanisms of Paresthesias

Compression and Ischemia

• Spinal cord compression from metastases, disc herniation, or stenosis produces numbness and tingling as alarm symptoms indicating potential myelopathy or cauda equina compression 4
• Numbness or tingling radiating down from chest, stomach, groin, and/or legs indicates spinal instability and/or myelum compression requiring urgent evaluation 4
• Metabolic failure occurs at the mitochondrial respiratory chain level when spinal cord tethering causes physical stretching, leading to impaired blood flow and diminished oxidative metabolism 4

Incomplete Injury Patterns

• Sensory deficits may begin distally in the leg and progress proximally, or present as "suspended" sensory loss with preserved sensation both above and below the abnormal area 4
• In spinal cord injury without fracture-dislocation (SCIwoFD), patients commonly present with numbness and weakness in hands with burning dysesthesias in forearms, reflecting central cord syndrome patterns 4

Cauda Equina Syndrome

• Perianal or saddle numbness combined with sensory changes or numbness in lower limbs indicates cauda equina nerve root compression 4
• Back pain with radicular symptoms, weakness, and absent lower limb reflexes are associated findings 4

Descending Modulatory Pathways

Pain Modulation Systems

• Descending pathways from cerebral structures to the dorsal horn either suppress (descending inhibition) or potentiate (descending facilitation) nociceptive transmission 5
• Serotonin and norepinephrine play critical roles in descending pain inhibitory pathways, which is why SNRIs are effective for neuropathic pain 6, 5
• Opioid peptides (endorphins, enkephalins, dynorphins) bind to receptors in the dorsal horn to modulate pain transmission 6

Neurotransmitter Systems

• Glutamate is the primary excitatory neurotransmitter involved in excitatory postsynaptic potentials in sensory pathways 6
• Substance P is a key neuropeptide in pain transmission and inflammatory responses in the dorsal horn 6
• Noradrenergic reuptake inhibition is the main mechanism for controlling visceral pain through descending modulation 6

Clinical Correlation for STEP 1

Lesion Localization Rules

• Ipsilateral motor weakness (corticospinal tract) + ipsilateral loss of vibration/proprioception (dorsal columns) + contralateral loss of pain/temperature (spinothalamic tract) = Brown-Séquard syndrome (hemisection) 1
• Bilateral "girdle" sensory level with suspended sensory loss = damage to commissural fibers crossing in the anterior white commissure (syringomyelia pattern) 1
• Autonomic dysfunction occurs with bilateral cord involvement, affecting bladder, bowel, and sexual function 1

Gray Matter Organization

• Laminae 1-5 in the posterior horn carry sensory neuron information and are the site of second-order neuron cell bodies for the spinothalamic tract 1, 2
• Lamina 9 in the anterior horn contains most lower motor neuron cell bodies 1
• Nociceptive-specific cells in lamina I project to ventroposterolateral thalamus with restricted, contralateral receptive fields 2
• Multireceptive cells in lamina V projecting to intralaminar thalamus often have large, bilateral receptive fields 2

Prognosis and Recovery

• The majority of recovery following spinal cord injury occurs during the initial 9-12 months, with relative plateau by 12-18 months post-injury 7
• Approximately 10-20% of complete injuries convert to incomplete during the first year, but robust functional motor recovery distal to the zone of injury is rare in complete injuries 7
• MRI findings of intramedullary hemorrhage and extended segments of edema are associated with clinically complete spinal cord injury and poor prognosis 7

Critical Pitfalls

• Do not rely on conventional x-rays, CT scans, or bone scintigraphy to exclude spinal metastases—full spinal column MRI is required 4
• Urgent MRI within 12 hours is mandatory when cauda equina syndrome is suspected based on new-onset urinary symptoms with back pain or saddle numbness 4
• In cervical spine injury with numbness and tingling, early surgical decompression may worsen neurological deficits in some SCIwoFD cases, as metabolic disturbances can be exacerbated by manipulation 4