Year : 2021  |  Volume : 63  |  Issue : 1  |  Page : 109--110

Miller Fischer syndrome? A harbinger of obsessive compulsive disorder - A case report


P Liji, Keya Das 
 Department of Psychiatry, PESIMSR, Kuppam, Andhra Pradesh, India

Correspondence Address:
Keya Das
Department of Psychiatry, PESIMSR, Kuppam, Andhra Pradesh
India




How to cite this article:
Liji P, Das K. Miller Fischer syndrome? A harbinger of obsessive compulsive disorder - A case report.Indian J Psychiatry 2021;63:109-110


How to cite this URL:
Liji P, Das K. Miller Fischer syndrome? A harbinger of obsessive compulsive disorder - A case report. Indian J Psychiatry [serial online] 2021 [cited 2021 Apr 13 ];63:109-110
Available from: https://www.indianjpsychiatry.org/text.asp?2021/63/1/109/309487


Full Text



Sir,

Miller-Fisher syndrome (MFS) is a variant of Guillain-Barre syndrome, first described by Dr. Miller Fisher. It is an autoimmune nerve disorder consisting of the triad of ophthalmoplegia, ataxia, and are flexia. The less frequent symptoms consist of blepharoptosis; limb dysesthesia; face, bulbar, and pupillary palsies; micturition disturbance; and motor weakness.[1] Psychiatric symptoms could accompany MFS due to the immunological interaction, which is a rare phenomenon.[2] Here, we present a male patient who was diagnosed with MFS and thereafter developed obsessive–compulsive disorder (OCD).

Mr. X, a 38-year-old, married, Muslim male presented to the Psychiatry Department of a tertiary care teaching hospital, with 2 years' history of repeated thoughts of contamination and associated hand washing. Obsessions of symmetry and arrangement with fear of travelling alone, to crowded places were present. Occasional panic attacks were discovered in interview. Three months prior to onset of these symptoms, Mr. X developed diplopia, ophthalmoplegia, ataxia, and facial palsy with distal motor weakness and was diagnosed with MFS by a Neurologist. Documents revealed treatment with intravenous immunoglobulin and steroids with significant clinical improvement. No other medical comorbidities was discovered. The family history was noncontributory. Alcohol abuse was present with no substance dependence. Results of standard blood tests, urinalysis, thyroid stimulating hormone, and electrocardiogram were normal. A diagnosis of OCD with agoraphobia as per ICD 10 was made. He was managed by Escitalopram 25 mg, Olanzapine 5 mg, and Clomipramine 50 mg with follow-up every 2 weeks until decreased symptom severity was noted in 2 months. He continued to be apprehensive for trivial reasons but remission was sustained during the follow-up.

OCD is a relatively common psychiatric disorder with a lifetime prevalence of 2.3%. It is characterized by recurrent intrusive thoughts or images (obsessions) that create significant distress and drive individuals to perform repetitive behaviors or mental rituals (compulsions) in an attempt to reduce the distress.[3] Existence of antineuronal antibodies blocking the brain serotonin receptors in conjunction with the antibodies to somatostatin and prodynorphin that act as neuromodulators in the basal ganglia indicates the autoimmune mechanisms in the etiology of the disease.[4] Findings of antineural ganglioside antibodies, the IgG anti-GQ1b antibody have disclosed immune mediated mechanisms in MFS via molecular mimicry.[5] This explains a common etiological link between MFS and OCDs. While the association between rheumatic fever – particularly its neurological manifestation, Sydenham's chorea, Pediatric Autoimmune Neuropsychiatric Disorder Associated with Streptococcus B and OCD has been well established, the link with other classic autoimmune disorders is far less clear.[6]

To date, we are not aware of any studies investigating the relationship between OCD and MFS, which may make a significant contribution in terms of both providing insight to the etiopathogenesis of the disorder and paving the way for new therapeutic approaches to the cases refractory to conventional treatments. To conclude, the current report points to the association of MFS and OCD, hence we propose that clinicians should be vigilant about neuropsychiatric sequelae when dealing with an autoimmune disorder patient in the clinic.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understand that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

References

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4Swedo SE, Leonard HL, Kiessling LS. Speculations on antineuronal antibody-mediated neuropsychiatric disorders of childhood. Pediatrics 1994;93:323-6.
5Yuki N, Taki T, Takahashi M, Saito K, Yoshino H, Tai T, et al. Molecular mimicry between GQ1b ganglioside and lipopolysaccharides of Campylobacter jejuni isolated from patients with Fisher's syndrome. Ann Neurol 1994;36:791-3.
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