Neuroscience Hilary Notes

Neuroscience- Hilary term 2014

Vestibular system/posture:

• Though NYSTAGMUS can be demonstrated physiologically as part of the VOR in an experiment whereby a subject is rotated in a chair and their eyes movements are tracked, it can also happen PATHOLOGICALLY In unilateral vestibular hypofunction, there is a pattern of afferent vestibular signalling analogous to that stemming from rotation away from that side: there is a strong feeling of SPINNING (vertigo) and the VOR responds by generating the pathological nystagmus. If lesion is PERIPHERAL, nystagmus can be suppressed by vision and will recover over time (relies on calibration by cerebellum). If lesion is central in VESTIBULAR NUCLEI, there is little suppression and less recovery.

• Bilateral vestibular hypofunction (e.g. from OTOTOXICITY caused by antibiotics) can be devastating. Patients appear normal but cannot read street signs or recognise friends’ faces whilst walking in the street (lack of VOR; they have to stop to see). They can ever ‘see’ their own HEARTBEAT no VOR compensating for the tiny head movements caused by one’s own pulse. Lack of orientation whilst SWIMMIMG; marked LOSS of STABILITY when subject asked to stand and CLOSE one’s EYES.

• The CEREBELLAR FLOCCULUS is essential for the ADAPTIVE CHANGES in the VOR. It normally learns to correlate visual input with the vestibular input through experience. This is important as the VOR has to be constantly CALIBRATED to maintain its accuracy in the face of changes such as INJURY or AGEING to vestibular and visual organs or pathways (or indeed in patients who wear glasses). Patients with LESIONS in the lateral part of the vestibulocerebellum DO NOT undergo these adaptive changes.

• SINGLE-CELL RECORDINGS in the “vestibular cortex” (S-1, parietal association cortex, area near S-2) show that these areas receive visual AND somatosensory inputs, in addition to the vestibular ones. Site of integration of these modalities so that a UNIFYING PERCEPTION of position and movement in space can be experienced? A few patients with LESIONS in the PARIETAL CORTEX perceive their visual environments to be rotated by 90-180 degrees. (Primarily probably an interference with otolithic processing).

• ZEBRAFISH KNOCKOUTS for the gene “starmaker” causes malformation of the OTOCONIA (calcium carbonate crystals in the otolithic organs) and loss of otolithic function.

• BENIGN PAROXYSMAL POSITIONAL VERTIGO is where pieces of the otolithic membrane BREAK OFF and fall into the semicircular canal, displacing fluid. Common in elderly. The EPLEY MANOEUVRE is used to treat this, and works by allowing the free floating particles from the affectedsemicircular canalto be relocated back to the utricle using gravity, where they can no longer stimulate the cupula.

• MENIERE’S DISEASE is where there is mild to severe vertigo due to IMPROPER DRAINAGE of the endolymphatic duct and thus DILATION of the endolymph system. Sometimes this is treated SURGICALLY to reduce this build-up; however as a last-resort STREPTOMYCIN can be injected to KILL the vestibular hair cells.

• Generally DAMAGE to the vestibulospinal system results in ATAXIAand POSTURAL INSTABILITY. For example, if unilateral damage occurs to the lateral vestibulospinal tract, the person will likely sway to that side and fall when walking. This occurs because the healthy side "over powers" the weak side in a way that will cause the person to veer and fall towards the injured side.Potential early onset of damage can be witnessed through a positiveROMBERG’S TEST. Patients will likely regain postural stability over weeks and months through a process called VESTIBULAR COMPENSATION, related to a greater reliance on OTHER sensory information (nevertheless there may still be residual deficits during COMPLEX movements).

• Nevertheless, SHERRINGTON showed that interrupting the pathway from brain/midbrain to spinal cord through using the DECEREBRATE CAT model (whilst keeping the MEDULLA connections intact) still resulted in a RIGID ANTIGRAVITY STANCE; presumably this represents the residual importance of the CUTAENOUS MECHANORECEPTORS on the soles of the feet.

• When visual info DOESN’T MATCH vestibular info, MOTION SICKNESS occurs. (E.g. travelling in a car and reading; microgravity). As above though, over time this RECTIFIES due to vestibular compensation. Most common hypothesis for the cause is that it functions as a DEFENSE mechanism againstNEUROTOXINS. As a result of the discordance, the brain will come to the conclusion that one of the inputs ishallucinatingand further conclude that the hallucination is due to poison ingestion. Thebrainresponds by inducing vomiting, to clear the supposed toxin.

• VISION strongly influences posture: place a subject on a tilted chair in a dummy room tilted the other way and they report the height to be between the apparent height and actual height Static visual and vestibular contributions. The STATIC visual contributions are from the LEARNT horizontal and vertical elements of the environment around us in modern society (though were they important in more natural environments from which we evolved?) Moreover OPTOKINETIC REFLEXES can compensate for VORs once the semicircular canals ADAPT. Movements of the eyes, or visual info moving across the retina, informs about movement of head because of EFFERENCE COPY of oculomotor output (eyes not subject to same external influence as limbs so proprioceptive input not necessary). Visual and vestibular info are weighted about equally: RECORDINGS from vestibular nuclei show they receive info from both as mentioned the CEREBELLUM is needed to calibrate both inputs.

• The POSITIVE SUPPORTING REACTION: is a decerebrate animal is suspended in the air with its legs hanging down, PUSHING UP on the sole of one of its feet will elicit an EXTENSOR RESPONSE in that limb. Variations include STEPPING and HOPPING reactions.

• NECK REFLEXES: before info can be used about the position of the head in space to inform about body...

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