Page 137 - Edited - Webster HEAD AND NECK - part 2-Merge PDF
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HN 325






               upon descending axons from the cerebral cortex. (It is “half” the movement required to shift lateral gaze
               from one side to the other.)
               Caloric testing:  In simple terms, increased tonic vestibular activity in one ear "attracts the eyes' attention",
               and "the gaze slowly wanders over to that side in order to see what is happening". Similarly, the eyes are
               attracted to look at cold ears: pouring cold (~30°C) water into one external auditory meatus (HN 326)
               causes endolymph convection currents in such a direction as to attract the eyes "slowly to investigate the
                       3
               intrusion" . (Using warm - ~44°C - water reverses the direction: the eyes slowly and stupidly wander over
               to look at the relatively colder but unmolested ear.) In each case, the cortex eventually snatches back the
               gaze, but then the process starts again - the vestibular system is a real nag. Clinicians perversely describe
               horizontal nystagmus according to the direction of the quick component - which is the normal, cortically
               controlled  correcting movement  - rather  than the  slow,  which  is the  abnormal  (the  sluggard labyrinth,
               asking the  eyes  to  have  a  look  at  it  ….).  For  example,  a  nystagmus  with  a  fast  right  and  slow  left
               component is  called  a  right  nystagmus.  Usually  the  slow  component  is  towards  the  pathological  side
               (come over and see my lesion …. and the eyes sneak over until the cerebral cortex, like a good parent,
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               realises what is going on and snatches them back - see HN 326) .
               "Doll's Eyes": Disruption of the connection between the medial longitudinal bundle and the cervical cord
               or destruction/death of the midbrain (controlling convergent and vertical gaze movements) prevents co-
               ordination of head and eye movements and results in the "doll's eyes phenomenon" - the direction of gaze
               remains fixed irrespective of the appropriate direction of gaze in relation to the position of the head.

               (See also Neuro notes Vol. I, pp. 112-113 for Ménière's disease).




                                 6.   THE GLOSSOPHARYNGEAL AND VAGUS NERVES

                       Pathology of these nerves is fortunately rare. Glossopharyngeal palsy: it becomes impossible to
               elicit the gag reflex from the affected side, since the mucous membrane of that half of the posterior third of
               the tongue and of the oro-pharynx is anaesthetic. The quality of "bitter" in tastes is also impaired. Death of
               the medulla oblongata abolishes the gag reflex - the entire om-pharynx is anaesthetized and the nucleus
               ambiguus, innervating the pharyngeal and laryngeal muscles, is destroyed.
                       "Vaso-vagal" (Stokes-Adams) attacks are syncope (fainting) associated with profound depression
               of the heart rate, and thought to be due to some peculiarity of the  vagus. Unilateral destruction of the
               nucleus ambiguus  (or,  most  commonly,  of  one  superior,  or  especially  the  recurrent,  laryngeal  nerve)
               produces paralysis of one vocal fold and causes dysphonia - in this case, a hoarse voice - and, in the case
                                                                 5
               of the central lesion, difficulties with swallowing - dysphagia . The paralyzed vocal fold makes it difficult
                                                                                   6
               to cough properly, since the glottis cannot be closed (see Coughing, Volume I, p. 170) . In addition, the soft
               palate  is  substantially  paralyzed  on  the  homolateral  side  (only  tensor  veli  palatini  is  supplied  by  the
               trigeminal nerve), so that when the patient is asked to say "AH" while the observer is examining the back of
               his or her mouth, the soft palate fails to rise on the side of the lesion (HN 216, Fig. 3). Bilateral laryngeal
               paralysis is life-threatening because both vocal folds adduct, shutting off the lower larynx and trachea from
               the outside world.

                                             7.   THE ACCESSORY NERVE

                       The cranial accessory nerve derives from the nucleus ambiguus and is motor to the larynx (HN
               60). The spinal accessory nerve arises from the upper three or four cervical segments and is motor to the
               trapezius and sternocleidomastoid muscles (HN 60; 61). Complete paralysis of one trapezius leads to


               3 Note:   For caloric testing, the subject lies down with the head inclined at about 30° to the horizontal: this ensures that
                       the plane  of the two lateral semicircular canals is  vertical  and therefore ideal for  allowing  endolymph flow
                       induced by convection. Notice that 'warm' and 'cold' are 37 ± 7°C.
               4 Note:   This is the easy way to understand and remember the two components of jerk nystagmus. It is, however, an
                       oversimplification, since vestibulo-ocular nystagmus can be elicited in the absence of cerebral cortex.
               5 Note:   Neurological dysphagia is relatively rare. Think of pharyngitis!
               6 Note:   This distinguishes a true neurological dysphonia from an hysterical or assumed one: such patients talk with a
                       low, hoarse voice, but quite happily cough normally on request.


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