Question

draw and explain the pain pathway of trigomenialthalamic tract

Answer 1

The trigeminal lemniscus, also called the trigeminothalamic tract, is composed of the ventral trigeminal tract, and the dorsal trigeminal tract – nerve tracts that convey tactile, pain, and temperature impulses from the skin of the face, the mucous membranes of the nasal and oral cavities, and the eye, as well as proprioceptive information from the facial and masticatory muscles.

The main sensory trigeminal pathway carries and processes discriminative touch and proprioceptive information from the face (Figure 4.7). Consequently, it is the cranial homologue of the medial lemniscal pathway.

The cranial 1° main sensory trigeminal afferent neurons

• peripheral processes are located in the trigeminal (predominantly), facial, glossopharyngeal and vagus nerves.
• form mechanoreceptors in the skin, mucous membranes, muscles and joints of the face. The relationship between receptor type formed and the axon Type/Group are similar to those of the medial lemniscal 1° afferents.
• have pseudounipolar cell bodies in the cranial ganglia of the trigeminal, facial, glossopharyngeal and vagus nerves (Table II).
• send their central axons to the brain stem.
• synapse in the main sensory trigeminal nucleus (2° afferents).

The main sensory trigeminal 2° afferent axons

• decussate immediately on leaving the main sensory trigeminal nucleus.
• join the contralateral ventral trigeminal lemniscus.
• above the level of the main sensory trigeminal nucleus (i.e., the mid pons), carries information about the contralateral face (i.e., the right ventral trigeminal lemniscus carries information about the left side of the face).

The 2° main sensory trigeminal afferents in the ventral trigeminal lemniscus

• ascend to the diencephalon.
• terminate in the ventral posteromedial (VPM) nucleus of the thalamus.

The axons of the 3° main sensory trigeminal afferents (VPM neurons)

• travel in the posterior limb of the internal capsule.
• end in the postcentral gyrus of the parietal lobe.

These descending pathways originate in the somatosensory cortex (which relays to the thalamus) and the hypothalamus. Thalamic neurons descend to the midbrain. There, they synapse on ascending pathways in the medulla and spinal cord and inhibit ascending nerve signals. This produces pain relief (analgesia). Some of this relief comes from the stimulation of natural pain-relieving opiate neurotransmitters called endorphins, dynorphins and enkephalins.

Pain signals can set off autonomic nervous system pathways as they pass through the medulla, causing increased heart rate and blood pressure, rapid breathing and sweating. The extent of these reactions depends upon the intensity of pain, and they can be depressed by brain centers in the cortex through various descending pathways.

As the ascending pain pathways travel through the spinal cord and medulla, they can also be set off by neuropathic pain -- damage to peripheral nerves, spinal cord or the brain itself. However, the extent of the damage may limit the reaction of the brain's descending pathways.

The influences of the descending pathways might also be responsible for psychogenic pain (pain perception with no obvious physical cause).

P.S if this helped you please like the answer.Thankyou.