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Paratrigeminal” Paralysis of the Oculopupillary Sympathetic System P J Goadsby

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Paratrigeminal” Paralysis of the Oculopupillary Sympathetic System P J Goadsby J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.72.3.297 on 1 March 2002. Downloaded from 297 NOSOLOGICAL ENTITIES? ”Paratrigeminal” paralysis of the oculopupillary sympathetic system P J Goadsby ............................................................................................................................. J Neurol Neurosurg Psychiatry 2002;72:297–299 Raeder described five patients with mixed features of attribution of cases that did not respect the anat- trigeminal nerve pathology and oculosympathetic omy. Conditions such as carotid disease, particu- larly dissection, may give rise to pain and a impairment, with or without other cranial nerve lesions. Horner’s syndrome,3 and cluster headache may This constellation of clinical features drew the original lead to oculosympathetic loss and impaired sym- author’s attention to the paratrigeminal region as a pathetic facial sweating56In both situations fore- head sweating may be impaired. I will set out the likely site for the causative lesion in this syndrome. An relevant anatomy of the paratrigeminal region, analysis of the anatomy of the oculosympathetic then review Raeder’s patients, and finally make innervation supports the view that a restricted lesion in some suggestions for the postimaging era based on an anatomical/pathophysiological designation the middle cranial fossa might cause the syndrome of for such patients. trigeminal nerve involvement, neuralgic pain or sensory change, with ptosis or miosis, or both, but no ANATOMY anhidrosis. Such a paratrigeminal oculosympathetic The key anatomical feature to be understood for Raeder’s syndrome is the relation between the syndrome (POSS) usefully reminds clinicians to pursue trigeminal nerve and the oculopupillary sympa- vigorously possible lesions of the middle cranial fossa thetic fibres. The trigeminal nerve lies in the mid- with careful, and possibly repeated, imaging studies. dle cranial fossa and in close proximity, par- atrigeminally as Monrad-Krohn suggested, there Attaching the eponym Raeder’s syndrome or Raeder’s are other cranial nerves. Most particularly for a paratrigeminal neuralgia to this syndrome adds nothing short course the fibres that will innervate the valuable to the anatomical description (POSS), which levator palpebrae superioris, specifically Müller’s muscle, and the pupilodilator fibres without the might be preferred for clarity. sudomotor fibres for the forehead. Therein is the .......................................................................... anatomical lesson of Raeder. 1 Cranial sympathetic innervation n 1924 Raeder wrote a classic clinical- http://jnnp.bmj.com/ The sympathetic outflow ultimately arises in the anatomical colocalisation paper that described hypothalamus and can be modulated by brain five patients, one of whom had been reported in I stem neurons. Preganglionic fibres arise from 1918. The patients had two key features: involve- ment of the trigeminal nerve and the oculosym- neurons in the lateral column of grey matter of pathetic nerves. He sought to differentiate the the thoracic and upper two to three lumbar restricted oculosympathetic findings from the segments. The fibres emerge through the ventral classic Horner’s syndrome: cervical sympathetic roots of the corresponding spinal roots, passing dysfunction characterised by ptosis, miosis, an- into the spinal nerve trunks and their ventral on September 30, 2021 by guest. Protected copyright. hidrosis and enophthalmos. Since that time vari- rami. The fibres leave the ventral rami in the ous terms have been employed, meanings de- white rami communicantes to synapse in the cor- fined, and classifications developed.23It is against responding ganglion or, in the circumstance of this background that one ventures into the interest for the cervical sympathetic ganglia, to 7 Coliseum that is the history of medicine to play ascend before synapsing The sympathetic ganglia out the academic battle. An eponym is useful if it give rise to non-myelinated postganglionic fibres, conveys a very clear meaning, or perhaps ac- which, for the head, arise as the internal carotid knowledges some contribution that was so pivotal nerve from the superior cervical ganglion, which as to provide insight well beyond the describer’s is, in effect, the rostralmost section of the sympa- ....................... demise. Raeder made an interesting clinical thetic trunk. The cervical sympathetic ganglia Correspondence to: ProfessorPJGoadsby, observation that pointed out the likely localisa- destined to innervate the eye derive their input Institute of Neurology, tion of a lesion adjacent to the trigeminal nerve in from the upper thoracic (T1) sympathetic white Queen Square, London the middle cranial fossa. In the era before cranial rami communicantes. WC1N 3BG, UK; imaging this was a wonderful piece of neurology; [email protected] in the modern era the eponym is much less Oculosympathetic innervation Received 11 September useful. Solomon and Lustig4 recently set out the The internal carotid nerve ascends with the inter- 2001 clinical cases that in many respects have illus- nal carotid artery dividing into medial and lateral In revised form trated the trigeminosympathetic anatomy of the branches in the bony carotid canal, and forming a 1 November 2001 plexus known as the carotid plexus. The medial Accepted carotid artery, concluding that the use of the term 8 November 2001 Raeder’s paratrigeminal neuralgia had become plexus communicates with the trigeminal gan- ....................... corrupted to the point of being useless by careless glion and abducens nerve, and the lateral plexus www.jnnp.com J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.72.3.297 on 1 March 2002. Downloaded from 298 Goadsby Table 1 Raeder’s cases Trigeminal sensory Oculosympathetic Patient (age, sex: pathology) Pain† Sensory change Ptosis Miosis Anhidrosis Other cranial nerves 18, male: parasellar endothelioma + − ++−Trigeminal motor loss Intermittent diplopia Cranial parasympathetic activation 65, male: not described +(*) + (V1 loss) + + − Diplopia 48, male: run over by a car ? + (hypaesthesia) + + ? Paracentral scotoma 28, male: not described +(*) − ++−None 48, male: injured by runaway horse ? + (V1–V3 loss) − + − Trigeminal motor loss Hearing impaired Reduced visual acuity †Although often described as a neuralgia only the patients marked * had clear neuralgia. ? Indicates data not described in case. communicates with the oculomotor, trochlear, ophthalmic, oculosympathetic involvement, as well as other relevant clini- and abducens nerves, as well as the ciliary ganglion. The dila- cal features. Several features emerge from such an analysis. tor pupillae fibres travel with either of the ophthalmic artery, nasociliary or long ciliary nerves, and those for levator palpe- Trigeminal involvement brae superioris travel with the oculomotor nerve. Considering three possible types of trigeminal involvement— pain, sensory change and motor signs—what is constant in Sympathetic control of facial flushing Raeder’s patients? Only three patients had pain and only two The cervical sympathetic pathway is responsible for facial had neuralgia. Thus the term Raeder’s paratrigeminal neural- sweating and flushing, among other roles. The oculosympa- gia is fanciful. Three patients had sensory change; one patient thetic and facial flushing roles seem well differentiated func- had pantrigeminal loss indicating that the lesion had moved tionally given that central lesions have been reported in which lateral to the unique paratrigeminal region, and similarly the facial sweating is spared in the presence of an oculosym- patient 1 had motor loss indicating a more extensive lesion. pathetic lesion.8 Indeed whereas oculosympathetic fibres arise from T1 those for sudomotor function arise at lower levels; Oculosympathetic loss certainly at T2/3.9 Sudomotor fibres destined for the forehead All five of Raeder’s patients had miosis, and four of five had traverse the internal carotid plexus, whereas those for the ptosis. Four of five also had normal sudomotor function. Thus remainder of the face traverse the external carotid plexus, oculosympathetic loss which must be peripheral was demon- excepting those for the cheek, which may take either route10 strated but without anihydrosis. Sudomotor fibres destined for the forehead join the ophthal- mic nerve in the region of the cavernous sinus reaching the Other signs skin through the supraorbital nerve11 Sweating of the forehead Four out of five of the original patients had other cranial http://jnnp.bmj.com/ is, therefore, normally mediated by fibres that exit the internal nerves involved. It is interesting that one had cranial parasympathetic activation, most likely simply as a result of carotid plexus relatively laterally when compared with the 12 oculosympathetic fibres. It must be borne in mind that pain and activation of the trigeminal-autonomic reflex parasympathetic neurons may reinnervate the sweat glands,8 Status of Raeder’s patients so that intact sweating may not necessarily imply sympathetic An analysis of Raeder’s patients demonstrates several issues. It sudomotor integrity. is notable that only two of the patients had neuralgia and two had lesions not restricted to the paratrigeminal region. Thus Trigeminal nerve and oculosympathetic outflow perhaps one patient at most, patient 4, really illustrated in a on September 30, 2021 by guest. Protected copyright. As the internal carotid artery passes from being inferior to the pure fashion the anatomical
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