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13 Decreased and Increased facial sensation

Many animals, mentally obtunded because of marked systemic illness and particularly severe brain disease, are slow to respond to noxious stimuli anywhere on the body, including the face. The problem of decreased facial sensation is identified when the degree of hypalgesia detected is greater than that to be expected by any accompanying somnolent or moribund state or is demonstrably asymmetric.

In defining this problem, care must be taken to distinguish facial hyporeflexia from facial hypalgesia—and these signs can occur together. The facial reflex (CN V sensory → CN VII motor) can be poorly functional with lesions involving the sensory trigeminal nerve, ganglion or nucleus, or the facial motor nucleus or nerve. With lesions involving the sensory branches of the trigeminal nerve, these facial reflexes will not function. Degrees of facial hypalgesia or analgesia also occur and the animal does not pull its head away from the noxious facial stimulus, for example in a cow that had an ocular squamous cell carcinoma invading the trigeminal nerve resulting in facial analgesia.¹

Sensation from at least the rostral third of the tongue of horses is mediated via fibers in the mandibular nerve and that has been inadvertently sectioned during surgical debulking of intermandibular tumors, resulting in analgesia and areflexia from the ipsilateral rostral circa 10 cm of the tongue. Expansile retrobulbar tumors including lymphosarcoma, melanoma, squamous cell carcinoma, and parotid adenocarcinoma have caused facial hypalgesia, usually with other overt evidence of face and eye lesions.^2,3 Partial facial analgesia resulting from trauma to single branches of CN Vs is not common and is usually associated with trauma to the face, nasal region, and sinuses. Because distal portions of sensory trigeminal nerves are distributed with branches from autonomic nerves, processes such as perineuritis that affect distal nerves may result in signs of autonomic denervation. For example, trigeminal innervation of the nasal membranes includes parasympathetic branches of CN VII, thus resulting in rhinitis sicca when these nerves are damaged (Figure 13.1). A similar involvement of oculomotor branches to the eyeball that are confluent with the ophthalmic branch of CN V may also result in poor pupillary constrictor function (Figure 13.2).

Figure 13.1 Facial analgesia is evident in the bright and alert horse shown here, by the needle holders clamped on the distal face (arrow). There was a cranial—believed immune‐associated—polyneuritis particularly involving the trigeminal nerves, with bilateral facial and rostral nasal analgesia. The presence of severe rhinitis sicca as also shown was unusual. In the right clinical setting, this sign is regarded as almost pathognomonic for equine dysautonomia, but this horse had no other signs of enteric or autonomic nervous dysfunction. As is the case often with polyneuritis equi, the trigeminal neuritis was accompanied by a prominent perineuritis. Also, the neuritis involved not just proximal cranial nerves but spread along the distal branches. It was believed that the more distal perineuritis involving the maxillary nerve also involved the autonomic fibers innervating the nasal membranes, mimicking the rhinitis sicca seen with grass sickness.

Figure 13.2 This case of polyneuritis involved the trigeminal nerves, and quite distinctly the ophthalmic branch on the left side was clinically affected. The latter resulted in conjunctival and corneal hypalgesia demonstrated here in the left eye (OS). Likely because of perineuritis, and the fact that branches of the ophthalmic nerve are confluent with the oculomotor fibers and the ciliary ganglion, a degree of pupillary dilation was also present in the left eye (OS) compared with the right (OD) (yellow bars).

Medullary (and cranial cervical spinal cord) diseases such as equine protozoal myeloencephalitis and listeriosis in ruminants are the more common central causes of decreased facial sensation due to involvement of the sensory tract and/or nucleus of the trigeminal nerve in the caudal medulla oblongata and cranial cervical spinal cord (Figure 13.3).

Central pathways for sensory perception from the face pass from the trigeminal sensory nucleus to the contralateral thalamus, contralateral internal capsule, and somesthetic, sensory cerebral cortex, mostly in the frontoparietal lobe. Lesions in these structures rostral to CNs V and VII can result in degrees of contralesional facial hypalgesia or analgesia but no interruption to the facial (CN V sensory → CN VII motor) reflex (Figure 13.4). This facial hypalgesia or analgesia is most evident when the noxious stimulus is applied to the sensitive nasal septal membranes on the side opposite to such rostral lesions. Several severe, particularly focal or selective, diseases of the thalamus, internal capsule, and forebrain including cerebral abscess, cholesterinic granuloma, Fusarium verticillioides (ex. moniliforme) leukoencephalomalacia, intracarotid injection, and Sarcocystis neurona encephalitis have resulted in this contralesional facial hypalgesic and analgesic syndrome.

Figure 13.3 Oblivious to the presence of a straw stuck in its left nasal cavity, this lamb suffering from listeriosis is demonstrating facial analgesia. There were accompanying facial and vestibulocochlear nerve deficits with ataxia and weakness. Indeed, involvement of the sensory branch of the trigeminal nerve is a very common sign with listeriosis and possibly reflects one of the routes of bacterial infection reaching the medulla oblongata in that disease.

Figure 13.4 Definitive facial hypalgesia and analgesia are best detected over the distal face as shown and particularly on the nasal membranes. When this is found, the main question to arise is whether it is due to a central forebrain (thalamus or cerebral hemisphere) lesion or it relates to an afferent sensory lesion of the trigeminal distribution. In this horse with a lesion in the forebrain causing facial analgesia, the facial reflexes remained intact and voluntary movement of the face was good. With peripheral sensory CN Vs lesions, the loss of facial sensation can be very well demarcated particularly with more distal lesions. Also, facial reflexes will be reduced or absent to the same degree as the hypalgesia or analgesia. The central distribution of the afferent fibers from the trigeminal nerve is quite spread out in the medulla oblongata and cranial cervical spinal cord within the sensory trigeminal nucleus and its tract. Thus, a central medullary lesion causing dense analgesia over the face would entail a very extensive lesion such that there would be many other signs of brain disease such as recumbency and (semi)coma. Thus, dense facial sensory loss alone, due to an afferent lesion, is most likely in the peripheral trigeminal nerve or ganglion.

Equine protozoal myeloencephalitis caused by S. neurona and filariid nematode encephalitis have caused ipsilesional facial hypalgesia and no interference to the facial (CN V sensory → CN VII motor) reflexes with brainstem lesions involving pontine and midbrain sites, but with no lesion(s) in thalamus or cerebrum. It is likely that the ascending impulses for conscious sensory perception from the face cross in the region of the rostral brainstem to join the contralateral medial lemniscus on its path to the ventral caudal lateral thalamic nucleus. Also, it is probable that facial sensory input is perceived not only at the somatosensory cerebral cortex, but also at the level of the thalamus as a few newborn ruminants with no cerebral cortices (agenesis) appeared to react with avoidance movements when the nasal septal region was stimulated strongly.

Facial analgesia can be seen in cattle with extensive basilar empyema adjacent to and invading the sensory branches of the trigeminal nerves along with accompanying signs of dropped mandible, head and neck extension, bradycardia, peripheral blindness, dilated pupils, and facial, tongue and pharyngeal paralysis. The full syndrome results from extension to involve CNs II, III, V, IX, X, XI and XII, the ventral brainstem, and the hypothalamus.

Facial and body regional hypersensitivity to firm stimuli (hyperesthesia) but not to light touch stimuli (allodynia) is seen with trigeminal and diffuse neuritis in early stages of diffuse bacterial meningitis. Trigeminal neuritis is the presumed diagnosis in the syndrome of pernicious head rubbing in horses, wherein there is an acquired, profound irritation such that the patient severely self‐traumatizes the side of the face. Such a syndrome has been replicated during (presumed) regrowth of infraorbital nerve axons following compression or cauterization of that nerve to attempt to ameliorate signs of headshaking in horses.⁴ Facial hyperesthesia with allodynia to light touch (Figure 13.5) has been seen in association with fluctuating signs of facial hyporeflexia and hypalgesia to firm stimuli. This has occurred in cases of paranasal sinusitis and following sinus surgery when the trigeminal nerve within or adjacent to the sphenopalatine sinus and within the infraorbital canal have been involved.^5,6 The syndrome has resolved in a few cases as the sinusitis was controlled. The absence of true, stable allodynia alone does seem to differentiate these cases from cases of regional pain syndrome with prominant allodynia as well as from the enigmatic syndrome of headshaking with no facial hypalgesia. (see Chapter 28).

Figure 13.5 Accompanying the obvious nasal and distal facial hypalgesia to firm pressure in this case, there was evidence of nasal and facial allodynia to light touch in the form of self‐inflicted injury to the affected area of the face as indicated here. This horse was suffering from a squamous cell carcinoma affecting the left side of the sphenopalatine sinus region and the trigeminal nerve. It rubbed its distal face on objects spontaneously and with stimulation to the face, despite the demonstrable hypalgesia, but did not demonstrate headshaking.

References

1 1 Samuel JL, Kelly WR and Vanselow BA. Intracranial invasion by bovine ocular squamous cell carcinoma via cranial nerves. Vet Rec 1987; 121(18): 424–425.

2 2 Rebhun WC. Diseases of the bovine orbit and globe. J Am Vet Med Assoc 1979; 175(2): 171–175.

3 3 Guard CL, Rebhun WC and Perdrizet JA. Cranial tumors in aged cattle causing Horner's syndrome and exophthalmos. Cornell Vet 1984; 74(4): 361–365.

4 4 Roberts V. Trigeminal‐mediated headshaking in horses: prevalence, impact, and management strategies. Vet Med Auckl 2019; 10: 1–8.

5 5 Tucker R, Windley ZE, Abernethy AD, et al. Radiographic, computed tomographic and surgical anatomy of the equine sphenopalatine sinus in normal and diseased horses. Equine Vet J 2016; 48(5): 578–584.

6 6 McCann JL, Dixon PM and Mayhew IG. Clinical anatomy of the equine sphenopalatine sinus. Equine Vet J 2004; 36(6): 466–472.