Neuroscience: Dermatomes and Pain Pathways

Area of skin supplied by a single spinal nerve.

Single afferent neuron and its receptor endings.

Precise sensory pathway for location and intensity.

Pain and temperature pathway (slower, less precise).

Nociceptors (pain receptors) signaling to brain via spinal cord then thalamus.

Opiate receptors in the spinal cord block pain signals from reaching the brain. This is achieved by substances like morphine or natural compounds like endorphins.

These nerve fibers transmit sharp, fast pain signals. They have a myelin sheath, allowing faster conduction.

These fibers carry dull, aching pain signals slowly due to a lack of myelin sheath.

An exaggerated pain response to a normally painful stimulus.

Pain caused by a normally non-painful touch.

Pain caused by activation of pain receptors in response to tissue damage or injury.

Pain arising from nerve damage, affecting the pathways from the periphery to the brain.

Pain perceived in a different location than its actual source.

Pain lasting less than 6 months, often accompanied by increased heart rate, anxiety, and muscle tension.

Pain lasting 6 months or more, often leading to depression, fatigue, and sleep disturbances.

A specific area of skin that is innervated by a single spinal nerve. It's like a dedicated 'territory' for each nerve.

The discriminative pathway, a superhighway for precise sensory information, transmits sharp pain signals quickly. Think of it as a direct line to the brain.

The anterolateral pathway carries pain and temperature information more slowly and less precisely compared to the discriminative pathway. It's like a slower, less clear radio signal.

Nociceptors are pain receptors that detect tissue damage and send alarm signals to the spinal cord and then to the brain, triggering the pain experience.

Opioids interfere with pain signals by blocking their transmission from the spinal cord to the brain, effectively turning down the volume of pain signals.

An increased response to a normally painful stimulus.

A painful response to a normally non-painful stimulus.

Pain caused by activation of pain receptors in response to tissue damage or injury.

Pain arising from nerve damage, affecting the pathways from the periphery to the brain.

Pain perceived in a different location than its actual source.

Acute pain lasts less than 6 months and often has strong physical reactions (increased heart rate, anxiety). Chronic pain lasts 6 months or more and is often accompanied by emotional and psychological changes like depression and fatigue.

Cognitive behavioral therapy, physical therapy, and massage.

Activating the periaqueductal gray area in the midbrain using electrodes to decrease pain transmission.

Sensory disturbances like numbness and tingling caused by nerve damage.

Severe, brief attacks of pain.

The discriminative pathway transmits sharp, localized pain quickly. The anterolateral pathway transmits dull, less localized pain and temperature information more slowly. Think of one as a highway, the other a back road.

They interfere with pain signals, blocking them from reaching the brain. Think of it like a gatekeeper that stops bad news from going through.

The thalamus is a relay station, taking pain signals from the spinal cord and sending them to the brain for interpretation. Think of it like a switchboard, connecting incoming calls to the right extension.

Opiate receptors in the spinal cord block pain signals from reaching the brain.

Pain triggered by normally non-painful stimuli, like a light touch.

Electrical stimulation in the midbrain (periaqueductal gray) to decrease pain transmission.

Nerve damage causing sensory disturbances like numbness, tingling, and pain.

Opioid receptors are specialized sites in the nervous system that bind to opioid molecules, like morphine or endorphins, to reduce the transmission of pain signals.

Acute pain is generally short-lived, lasting less than 6 months, and often accompanied by physiological changes like increased heart rate and anxiety.

Chronic pain persists for longer than 6 months and can be associated with psychological changes like depression, anxiety, and fatigue.

Deep brain stimulation (DBS) involves implanting electrodes in the brain, specifically in the periaqueductal gray area, to modulate pain signals.

By stimulating the periaqueductal gray area in the midbrain, deep brain stimulation releases endogenous opioids, which act as natural pain relievers.

Pain receptors that detect tissue damage and send alarm signals to the brain. Think of them like smoke alarms when something is wrong with your body.

Opioids interfere with pain signals in the spinal cord, preventing them from reaching the brain. It's like turning down the volume of the pain signal.

Acute pain is short-term (less than 6 months) and often comes with strong physical reactions. Chronic pain lasts longer (6 months or more) and can have emotional and psychological effects.

Nociceptive pain is caused by tissue damage. Neuropathic pain comes from nerve damage. Referred pain is felt in a different location than the source.

Pain signals travel from nociceptors in the body to the spinal cord, then to the thalamus, and finally to the somatosensory cortex in the brain.