Virus Lesions of the Cranial Nerves with Special Reference to the VIII Nerve

fibres of taste and not for those of skin sensation. In fact the herpetic lesion may be on the anterior two-thirds of the tongue without taste being affected; therefore the lesion is more likely to be in the trigeminal than the geniculate ganglion. The facial paralysis of herpes oticus is associated with herpetic lesions in the unquestionable distribution of the cervical posterior root ganglia and the trigeminal ganglion. Denny-Brown et al. (1944) examined a geniculate ganglion in a case of herpes oticus with facial paralysis and found it unaffected. The 2nd cervical ganglion was infected and the brain stem showed minor encephalitic changes, with neuronal damage to the facial nucleus. With zoster of the face, multiple cranial nerve palsies may occur without gross clinical evidence of encephalitis. Further, herpes of the pinna and postural herpes occur without facial paralysis and it would be thought likely, if such lesions resulted from infection of the geniculate ganglion, that the inflammatory reaction in the ganglion would produce a facial paralysis. There is no evidence to suggest that the facial paralysis of herpes oticus is due to a lesion of the geniculate ganglion and, in all probability, herpes oticus is a zoster lesion ofmore than one cranial nerve. Consequently the evidence for a wide sensory distribution of the VII nerve on the pinna and palate does not exist. There are no sensory neurones in the facial nucleus and the only sensory fibres known to be carried by the nerve are proprioceptive and taste fibres. The proprioceptive fibres probably end in the trigeminal nucleus; the sensory fibres found in the peripheral distribution of the VII nerve are likely to be of V nerve origin, being merely an example of a trigeminal sensory branch using the peripheral branches of the facial nerve as a final route.