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Trigeminal Isolated Sensory Neuropathy (TISN) and FOSMN

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Trigeminal Isolated Sensory Neuropathy (TISN) and FOSMN Cruccu et al. BMC Neurology (2014) 14:248 DOI 10.1186/s12883-014-0248-2 RESEARCH ARTICLE Open Access Trigeminal isolated sensory neuropathy (TISN) and FOSMN syndrome: despite a dissimilar disease course do they share common pathophysiological mechanisms? Giorgio Cruccu1*, Elena M Pennisi2, Giovanni Antonini3, Antonella Biasiotta1, Giulia di Stefano1, Silvia La Cesa1, Caterina Leone1, Salvatore Raffa4, Claudia Sommer5 and Andrea Truini1 Abstract Background: Patients presenting with bilateral trigeminal hypoesthesia may go on to have trigeminal isolated sensory neuropathy, a benign, purely trigeminal neuropathy, or facial-onset sensory motor neuronopathy (FOSMN), a malignant life-threatening condition. No diagnostic criteria can yet differentiate the two conditions at their onset. Nor is it clear whether the two diseases are distinct entities or share common pathophysiological mechanisms. Methods: Seeking pathophysiological and diagnostic information to distinguish these two conditions at their onset, in this neurophysiological and morphometric study we neurophysiologically assessed function in myelinated and unmyelinated fibres and histologically examined supraorbital nerve biopsy specimens with optic and electron microscopy in 13 consecutive patients with recent onset trigeminal hypoesthesia and pain. Results: The disease course distinctly differed in the 13 patients. During a mean 10 year follow-up whereas in eight patients the disease remained relatively stable, in the other five it progressed to possibly life-threatening motor disturbances and extra-trigeminal spread. From two to six years elapsed between the first sensory symptoms and the onset of motor disorders. In patients with trigeminal isolated sensory neuropathy (TISN) and in those with FOSMN neurophysiological and histological examination documented a neuronopathy manifesting with trigeminal nerve damage selectively affecting myelinated fibres, but sparing the Ia-fibre-mediated proprioceptive reflex. Conclusions: Although no clinical diagnostic criteria can distinguish the two conditions at onset, neurophysiological and nerve-biopsy findings specify that in both disorders trigeminal nerve damage manifests as a dissociated neuronopathy affecting myelinated and sparing unmyelinated fibres, thus suggesting similar pathophysiological mechanisms. Keywords: Trigeminal nerve, Neuronopathy, Trigeminal neuropathy, FOSMN, Facial pain Background related to connective tissue disease or seldom labelled as Trigeminal neuropathy is a relatively frequent clinical con- idiopathic [3,4]. dition that poses major diagnostic problems to centres This condition has received attention in sparse case re- treating orofacial pain and headache [1,2]. Although most ports, and in three main studies. In the first case series, patients have unilateral trigeminal neuropathy secondary Spillane and Wells in 1959, described 16 patients with a to focal lesions, a few present with a bilateral, symmet- purely sensory, unilateral or bilateral, trigeminal neur- ric, initially purely sensory trigeminal neuropathy, often opathy [5]. Several years later, Lecky and colleagues re- ported 13 patients with idiopathic sensory disturbances restricted to the trigeminal territory, and referred to this * Correspondence: [email protected] condition as “idiopathic trigeminal sensory neuropathy” 1 Department of Neurology and Psychiatry, Sapienza University, Rome, Italy [3]. More recently, Vucic and colleagues demonstrated Full list of author information is available at the end of the article © 2014 Cruccu et al.; licensee BioMed Central. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. Cruccu et al. BMC Neurology (2014) 14:248 Page 2 of 9 that in patients with bilateral trigeminal neuropathy a se- with the Medical Research Council score. Patients were vere motor involvement might ultimately develop [6,7]. also asked to report dysautonomic symptoms. They studied nine patients with bilateral facial-onset All patients underwent laboratory testing, including tests sensory deficits in whom, after a mean of 4 years, motor to exclude identifiable causes of trigeminal neuropathy: deficits developed and progressed in a rostral-caudal dir- autoantibody essays to detect connective tissue disease (an- ection. In two autopsy studies, Vucic et al. specified that tinuclear antibodies, anti-double-stranded DNA, antinu- the disease primarily involved cell bodies in the sensory clear extractable antigens, including anti Sm, anti RNP, ganglia and motor nuclei and named this condition “facial anti Scl70, and anti-phospholipids, antineutrophil cyto- onset sensory and motor neuronopathy” (FOSMN) [6-8]. plasmic antibodies and anti Ro/SSA and anti-La/SSB for Some reports suggest that FOSMN is a primary neu- Sjögren’s disease). Some patients also underwent the gen- rodegenerative disorder resembling amyotrophic lateral etic serum test for Kennedy’s disease, cholesteryl esters sclerosis, others that it is an immune-mediated neur- and low serum cholesterol for Tangier disease, glycosphin- opathy [8-13]. golipid accumulation for Fabry’s disease, and serum- These studies indicate that a recent onset bilateral tri- angiotensin converting enzyme for neurosarcoidosis. geminal sensory hypoesthesia may subsequently follow one All patients underwent brain and spinal cord gadolinium- of two clinical courses: in some patients the disease will re- enhanced magnetic resonance imaging (MRI). main a trigeminal isolated sensory neuropathy (TISN) in others it will progress to FOSMN, a life-threatening condi- Trigeminal neurophysiology tion manifesting with severe motor involvement. We tested trigeminal motor evoked potentials after No diagnostic criteria can differentiate these two con- transcranial magnetic stimulation [14], the temporalis H ditions. Nor do we know whether they are distinct dis- reflex, assessing Aα fibre (Ia fibre) in the monosynaptic ease entities or share similar pathophysiological features. trigeminal reflex [15]. We also tested the early blink Having this information would make it easier to predict reflex components (R1) after electrical supraorbital nerve a favourable or unfavourable outcome, and help in plan- stimulation and the masseter inhibitory reflex (SP1) after ning the most appropriate treatment. mental nerve stimulation, assessing Aβ fibres [16]. We re- Seeking pathophysiological and diagnostic information corded laser evoked potentials (LEPs) to investigate Aδ to distinguish these two conditions, we enrolled 13 con- nociceptors (Aδ-LEPs) and unmyelinated warmth recep- secutive patients presenting with bilateral facial sensory tors (C-LEPs) [17]. hypoesthesia, did complete neurophysiological trigemi- All patients underwent nerve conduction studies (NCS) nal function testing (assessing all myelinated and unmy- using surface recording electrodes placed in the standard elinated fibre groups), and in 10 patients analysed by light manner. We recorded sensory nerve action potentials and electron microscopy the morphometric features in (SNAPs) and conduction velocities from sural, ulnar and supraorbital nerve biopsy samples. superficial radial nerves. Other nerve function variables ex- amined were compound motor action potential (CMAP) amplitude and peroneal, tibial and ulnar nerve conduction Methods velocities. Electromyographic (EMG) investigation in- In the period 1997-2013, in the Policlinico Umberto I and cluded pontobulbar muscles (orbicularis oris muscle, gen- the Ospedale Sant’Andrea (both being University Hospitals ioglossus muscle, sternocleidomastoid muscle, masseter of the Sapienza University of Rome), we enrolled 13 con- muscle), limb muscles (biceps brachii, extensor digitorum secutive patients with recent onset bilateral trigeminal communis, first dorsal interosseus, lateral vastus, tibialis hypoesthesia and pain (Table 1). Exclusion criteria were anterior), and cervical paraspinal muscles. connective tissue disease, cognitive disturbances, and other Neurophysiological testing adhered to the technical re- neurological diseases. All patients gave their informed con- quirements issued by the International Federation of sent to the procedures and the publication of clinical Clinical Neurophysiology [18,19]. details. The Institutional Review Board of the Policlinico Umberto I – Sapienza University approved the protocol. Nerve biopsy and nerve morphometry Supraorbital nerve biopsies were performed by a trained Clinical, neuroimaging and laboratory investigations plastic surgeon, in a period ranging between 3 and 6 All patients underwent a detailed neurological examin- years from beginning of disease. Specimens fixed with ation using bedside tools. Trigeminal and extra-trigeminal 2% glutaraldehyde in phosphate-buffered saline (PBS) at sensory function were assessed: touch was investigated 4°C. Samples were post-fixed in 1% osmium tetroxide in with a piece of cotton wool, vibration with a tuning fork veronal acetate buffer (pH 7.4) for 1 h at 25°C, stained (128 Hz), and pinprick sensation with a wooden cocktail with uranyl acetate (5 mg/ml) for 1 h at 25°C, dehy- stick. Gait impairment, and muscle strength were
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