Cranial Nerve Deficits Affecting the Pupil: A Review and Clinical Cases

Dukes, Joanna (1991) Cranial Nerve Deficits Affecting the Pupil: A Review and Clinical Cases. MVM(R) thesis, University of Glasgow.

Abstract

The pupil is an important indicator of the neurological health of the central and peripheral nervous systems (Scagliotti, 1990). Pupil size is determined by the afferent input, i. e. the amount of light illuminating the retina, and the autonomic balance of the parasympathetic and sympathetic nervous systems, as they innervate the reciprocal pupillary constrictor and pupillary dilator muscles respectively, of the iris. The parasympathetic system is dominant and through this efferent arm, light will drive pupillary size; the pupillary light reflex pathway (PLR). The afferent arm of this shares optic fibres with the proximal part of the central visual pathway and evaluation of conscious visual perception, resting pupil size and the response of each pupil to light illuminating the ipsilateral or contralateral eye (direct and consensual PLRs) will aid localisation of any lesion affecting these projections. A series of 36 cases presenting with an abnormality affecting at least one pupil is recorded here, together with the spectrum of associated clinical or neurological signs, the investigations of the cases and, where possible, confirmation of diagnoses. They illustrate the wide spectrum of abnormalities which may affect the pupil in a referral veterinary hospital population. Although retinal disease, affecting the photoreceptors or the first order neurons of the central visual pathway, will result in abnormalities in visual acuity and pupil size, such cases are not included in this series - it was limited to cases with neuro-ophthalmological disease. However, a number of cases did have retinal abnormalities obvious on fundoscopy and careful ophthalmoscopy is essential in investigating these cases. Some cases showed fundic evidence of their underlying lesions? cases 3, 4, 6, 7 & 12 with papillitis subseguent to their optic neuritis, case 1 had an obviously hypoplastic optic disc and case 10 had a retinopathy occurring concurrently with the neurological signs reflecting the diffuse granulomatous feline corona virus infection. Cases 3 and 5 developed retinal degeneration subsequent to optic nerve involvement. Some cases, however, had a retinopathy which was presumed not to be associated with the neurological signs, although this could only be an assumption - cases 8, 9 & 11. A number of cases showed bizarre and aggressive central nervous system involvement which did not appear to respond to any symptomatic therapy; 3, 6, 7, 8, 10, 11, 12, 20 and 23. These ranged from confirmed or assumed inflammatory disease (3, 8, 10, 11, 12 & 20) to unexplained severe widespread cord haemorrhage (23) and confirmed or assumed neoplasia (6 & 7). Other cases had multifocal signs which could not be explained by a single lesion which remained fairly stable; 5, 13, 15, 16, 18 and case 36 where a space occupying lesion was considered but no progression was documented. Underlying systemic disease was evident in a number of cases, and, indeed, was the primary reason for presentation; cases 28 and 29 both had coexistent diabetes mellitus and hyperadrenocorticism and Horner's syndrome. Case 14 had diabetes mellitus and an internal ophthalmoplegia. Case 15 had been receiving treatment for lymphoma and developed a facial palsy contralateral to a partial internal and external ophthalmoplegia. Although many of the cases were readily predictable and logical in the way neurological signs resulted from a distinct lesion, such as otitis media / interna with Horner's syndrome and a facial palsy (cases 31, 32 & 33) or as in cases 21 (cervical disc extrusion), 24 (spinal cord tumour with meningitis) & 25 (thyroid adenocarcinoma), other cases required pharmacological localisation to determine the site of the lesion. To be accurate and informative, pharmacological diagnosis requires a well defined protocol, and this is distinctly lacking in the literature with a huge variation of agents used, concentrations of these agents and time intervals described in determining the level of involvement in the parasympathetic or sympathetic innervation of the eye. Although in the cases where pharmacological localisation was attempted in this series a standard protocol was followed, and events were carefully timed, a number of problems in interpretation were noted and there was insufficient post mortem follow up to confirm the accuracy of the pharmacological diagnosis. Of note are two cases with parasympathoparesis which completely failed to respond to pilocarpine (cases 17 & 18). Also worthy of mention are some cases of Horner's syndrome which responded rapidly (within 30 seconds) to phenylephidrine 10% administration with presumed post-ganglionic (third order neuron) lesions (cases 33, 34, 35 & 36). This reaction, due to denervation supersensitivity to the sympathomimetic agent, was much more rapid and complete than any references in the literature would suggest. However, in another case, case 5, the presumed post-ganglionic sympathoparesis was shown inexplicably on pharmacological testing to be due to a second order lesion.

• Item Type: Thesis (MVM(R))
• Qualification Level: Masters
• Keywords: Veterinary science, Neurosciences
• Date of Award: 1991
• Depositing User: Enlighten Team
• Unique ID: glathesis:1991-78362
• Copyright: Copyright of this thesis is held by the author.
• Date Deposited: 30 Jan 2020 15:31
• Last Modified: 30 Jan 2020 15:31
• URI: https://theses.gla.ac.uk/id/eprint/78362