Special Senses
Olfaction, Gustation, Vision, Audition, Equilibrium
Olfaction: Olfactory Nerve (CN1)
Olfactory receptors
Cilia (hair cells) of nostrils and nasal membranes
Olfactory pathway
Nasal membrane
Olfactory bulb and tract
Olfactory cortex of temporal lobe (part of the limbic system)
Takes information from hippocampus and projects it to hypothalamus
Goes from hypothalamus to thalamus to orbitofrontal cortex for conscious association of odor with previous memories
Therapeutic significance of olfactory stimulation
Olfaction can be used with comatose patients to increase CNS arousal
Aromatherapy can have moos enhancement properties
Bilateral lesion will lead to Anosmia (loss of sense of smell)
Lesion to olfactory cortex may lead to seizure activity of pre-seizure aura scent hallucinations
Gustation:
Facial Nerve (CN7), Glossopharyngeal (CN9), Vagus Nerve (CN10)
Receptors = taste buds on the surface of the tongue
Papillae: bumps on the tongue (contains taste receptors)
Physiology
Saliva dissolves food in mouth
Dissolved food enters pores of papillae and taste buds
A membrane potential is activated
If membrane potential is strong enough, causes action potential
Gustatory Pathway
Taste receptors → CN 7,9,10 → Medulla → Thalamus → Gustatory cortex (in insula)
Sense of smell is critical to taste (loss of smell will lead to loss of taste)
Therapeutic Significance
Gustatory stimulation used for comatose patients
Can facilitate oral motor function in children and adults with oral musculature dysfunction
Vision: Optic Nerve (CN 2)
Visual Receptor Pathway
Light Waves
Fovea or periphery → Action Potential
Visual Signals
Optic Nerve → Optic Chiasm → Optic Tracts → Superior colliculi of midbrain or thalamus
Occipital lobe
Detection: Primary visual cortex
Interpretation: Visual association cortex
Visual fields pathways
Nasal field - lateral optic nerve
Temporal field - medial optic nerve (cross at optic chiasm)
Visual Pathway Pathology
Contralateral homonymous hemianopia: Loss of either right
or left visual field
Bitemporal Hemianopia: lose both temporal fields of vision
Optic Nerve Lesion: lose whole visual field on that side
Complete severance at optic chiasm: Fully blind
Visual field blind spot: damage to the retina
Nystagmus: Involuntary, rapid, repetitive eye movement
Normal: Response to rotation, tracking a moving target, caloric testing
Pathological: Damage to labyrinths, CN8 damage, cerebellar damage
Audition: Vestibulocochlear nerve (CN8)
Sensory receptors = Hair cells
Stimulus = sound (vibrations) mechanical input
Vibrates tympanic membrane (ear drum)
Hammer, Anvil, Stirrup (inner ear bones)
Hearing Impairment
Sensorineural: Damage to inner ear, CN8, or brain
Conductive: Damage to outer/inner ear structure
Lesion to auditory portion of CN8: Deafness or tinnitus
Lesion to primary auditory cortex: Cortical deafness
Lesion to auditory association cortex: Auditory agnosia or inability to interpret sounds
The Vestibular System
Function: Equilibrium and Balance
Input= Vestibulocochlear nerve
Relates to cerebellum (balance)
Vestibular apparatus in the middle ear
Vestibular pathway
Sensory input → Vestibulospinal tract → motor neurons synapse with spinal nerves → Antigravity muscles → feedback loop to cerebellum
Reticular Formation–Brainstem
Autonomic nervous system- Vagus nerve
Signs and Symptoms of Vestibular Dysfunction
Nystagmus (involuntary, rapid, eye movement)
Vertigo
Tinnitus
Hearing loss
Loss of balance and possible falls
Broad-based stance
Sweating, nausea and vomiting