Q 1.3. General sensation: anatomy and physiology. Somatosensory disorders.

Somatic sensation encompasses the perception of touch or pressure, vibrations, awareness of joint position, pain, and temperature, as well as more intricate functions derived from these foundational sensory experiences. These complex functions include abilities like two-point discrimination, stereognosis, and graphesthesia. Notably, somatic sensation does not involve the special senses of smell, vision, taste, and hearing.

 

1) Sensory Pathway Overview:

The pathway from peripheral tissues to the cerebral cortex involves three neurons and two central synapses.

 

First-Order Sensory Neurons:

  – Originate from limbs and trunk with cell bodies in dorsal root ganglia.

  – Send peripheral processes to sensory receptors and central processes to spinal cord.

  – Sensory receptors include free nerve endings, MeissnerMerkel corpuscles, hair cells, Krause end-bulbs, and Ruffini corpuscles.

  – Synapse centrally depending on sensation type: fine touch/pressure/vibration ascend in posterior columns to the medulla through nucleus gracilis and cuneatus, while pain/temperature/itch synapse in posterior horns – substantia gelatinosa.

  – Face sensations processed via trigeminal ganglion and nerve to the pons.

 

Second-Order Sensory Neurons:

  – Cell bodies in gracile/cuneate nuclei (in the medulla) cross midline and ascend through the medial lemniscus.

  – Cell bodies in posterior horns cross the midline (1-3 levels above their entry i the spinal cord) and ascend through: a) anterior spinothalamic tract (touch), b) lateral spinothalamic tract (pain, itch, temperature).

  – Face sensations join limb/trunk fibers in brainstem, project via trigeminal lemniscus (facial touch, pressure) or trigeminothalamic tract (facial pain, itch, temperature) to the ipsilateral side of the thalamus.

 

Thalamic Processing:

  – Fibers synapse in ventral posterolateral (VPL), ventral posteroinferior (VPI), and intralaminar (ILa) nuclei for spinothalamic and ventral posteromedial (VPM) nucleus for trigeminal.

 

Third-Order Sensory Neurons:

  – Project from thalamus to ipsilateral cerebral cortex.

  – Fibers from VPL, VPI, and VPM mainly go to primary somatosensory cortex, while ILa fibers also target striatum, cingulate gyrus, and prefrontal cortex.

The postcentral gyrus, nestled just behind the central sulcus in the cerebral cortex, plays a pivotal role in processing sensory information from various parts of our body. But what makes it truly captivating is its somatotopic organization. Imagine the postcentral gyrus as a topographical map etched onto the brain’s surface. Different body parts—like the hands, face, lips, and toes—each have their designated regions within this map. The larger the representation, the more sensitive or significant that body part is in terms of sensory perception. Now, let’s introduce our whimsical friend—the homunculus. Picture a tiny, cartoon-like figure residing within the postcentral gyrus. But here’s the twist: The homunculus stands upside-down! Its head points downward, and its legs stretch upward. Why? Because this arrangement mirrors the distorted proportions of sensory input. So, the hands and face get prime real estate, while the legs and trunk squeeze into smaller spaces.

2) Sensory Examination

Primary Sensory Modalities:

  A) Light Touch:

    – Evaluated with cotton wool on skin bilaterally, patient indicates sensation.

    – Depends on fibers in posterior columns of spinal cord and anterior spinothalamic tract.

  B) Pinprick & Temperature:

    – Pinprick: Patient differentiates sharpness from pressure.

    – Temperature: Hot/cold water or metal tuning fork applied.

    – Integrity of lateral spinothalamic tracts is crucial.

  C) Deep Pressure:

    – Sensibility tested on tendons like Achilles tendon.

  D) Vibration:

    – Tuning fork (128 Hz) applied over bony prominence.

    – Indicates whether vibration is felt.

  E) Joint Position:

    – Patient indicates direction of passive movements of finger/toe joints.

    – Impaired sense may cause pseudoathetoid movement.

 

Complex Sensory Functions:

A)   Romberg Test:

    – Assesses balance with eyes closed; unsteadiness indicates impaired joint position sense.

  B) Two-Point Discrimination:

    – Tests ability to distinguish simultaneous touch at neighboring points.

    – Impaired discrimination suggests sensory cortex disorder.

  C) Graphesthesia, Stereognosis, & Barognosis:

    – Agraphesthesia: Inability to identify number traced on palm or gaiter area implies contralateral parietal lobe lesion.

    – Astereognosis: Inability to distinguish shapes/textures by touch.

    – Abarognosis: Impaired ability to distinguish weights.

  D) Bilateral Sensory Discrimination:

    – Reveals neglect or inattention to sensation from one side due to contralateral cerebral lesion in some patients with apparently normal sensation.

 

3) Sensory Syndromes

Peripheral Nerve Lesions:

  A) Mononeuropathy:

    – Usually less sensory loss than expected due to overlap from adjacent nerves.

    – Compressive lesions often affect large touch fibers.

  B) Polyneuropathy:

    – Symmetric sensory loss, more distal than proximal (stocking-and-glove pattern).

    – Commonly affects hands and feet.

    – Diabetes, amyloidosis, and certain metabolic disorders affect small fibers, preserving tendon reflexes and causing no motor deficit.

 

Root Lesions:

  – Segmental sensory loss; overlap prevents sensory loss unless multiple roots are affected.

  – Pain common with compressive root lesions; reflex changes occur.

 

Spinal Cord Lesions:

  – Central cord lesions cause loss of pain and temperature appreciation.

  – Anterolateral lesions cause contralateral impairment of pain and temperature appreciation below lesion level.

  – Anterior cord lesions impair pain and temperature appreciation below lesion level; motor deficits may occur.

  – Posterior column lesions result in reduction in fine-touch perception, loss of vibration and joint position sense below lesion – Multiple sclerosis, B12 deficiency, Tabes dorsalis.

 – Spinal cord hemisection leads to Brown–Séquard syndrome – contralateral pain and temperature anesthesia, ipsilateral loss of fine tactility and proprioception.

 

Brainstem Lesions:

  – Sensory disturbances accompanied by motor deficit, cerebellar signs, and cranial nerve palsies.

  – Dorsolateral lesions cause contralateral loss of pain and temperature appreciation in limbs and trunk.

 

Thalamic Lesions:

  – Loss or impairment of sensation on contralateral side; may present with spontaneous pain.

 

Lesions of Sensory Cortex:

  – Impair discriminative sensory function on opposite side of body.

  – Difficulty localizing stimuli or recognizing body parts.

 

Distinguishing Organic vs. Psychogenic Sensory Disturbances:

  – Organic: Follows neuroanatomic pattern, transitions between normal and affected areas gradual.

  – Nonorganic: No specific neuroanatomic pattern, abrupt transitions between normal and affected areas, dissociated sensory loss may occur.

 

Peripheral Nerve Lesions:

  – Sensory symptoms prominent; may follow specific patterns (stocking-and-glove or individual nerve).

Classification:

  – Mononeuropathy simplex: Single nerve involvement.

  – Mononeuropathy multiplex: Multiple non-contiguous nerve involvement.

  – Polyneuropathy: Multiple peripheral nerve involvement; may be axonal, demyelinating, or neuronopathic.

 

Clinical Findings:

  Sensory Disturbances:

    – Numbness, abnormal sensations, hyperpathia.

  Pain:

    – Prominent in certain neuropathies; mechanisms unclear.

  Dissociated Sensory Loss:

    – Impaired pain and temperature with preserved touch, vibration, and proprioception.

  Motor Deficits:

    – Weakness, wasting, fasciculation; reflect lower motor neuron deficit.

  Tendon Reflexes:

    – Impaired or lost due to interruption in reflex arcs.

  Autonomic Disturbances:

    – Present in some neuropathies; include postural hypotension, impaired sweating, bladder dysfunction.

  

 

 

 

 

References: 

1)    Clinical Neurology LANGE Roger P. Simon etc. 10th edition

2)        Neurology handbook for medical students. Prof. Penko Shotekov, MD, Ph.D., Sc.D.

Verifiziert von Dr. Petya Stefanova

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