Abstract:Miller Fisher syndrome (MFS) is characterized by a clinical triad of ophthalmoplegia, ataxia, and areflexia, and is closely associated with serum anti-GQ1b antibody. Although the clinical triad is the cardinal diagnostic clue, a variety of other symptoms and signs beyond the triad have been reported. To elucidate the frequency and characteristics of atypical clinical manifestations of MFS, we recruited 38 patients with MFS and evaluated the symptoms or signs beyond the classic triad. Eleven (29%) of 38 patient… Show more
“…Cranial mononeuropathy with brachial diparesis, albumincytologic dissociation, and areflexia in the second case can suggest an atypical MFS overlap [17].…”
Objective To report two cases of cranial multineuritis after severe acute respiratory syndrome caused by coronavirus-2. Methods Patients' data were obtained from medical records of the clinical chart of dell'Angelo Hospital, Venice, Italy. Results The first patient is a 42-year-old male patient who developed, 10 days after the resolution of coronavirus-2 pneumonia and intensive care unit hospitalization with hyperactive delirium, a cranial multineuritis with asymmetric distribution (bilateral hypoglossus involvement and right Claude Bernard Horner syndrome). No albumin-cytologic dissociation was found in cerebrospinal fluid; severe bilateral denervation was detected in hypoglossus nerve, with normal EMG of other cranial muscles, blink reflex, and cerebral magnetic resonance with gadolinium. He presented a striking improvement after intravenous human immunoglobulin therapy.The second case is a 67-year-old male patient who developed a cranial neuritis (left hypoglossus paresis), with dyslalia and deglutition difficulties. He had cerebrospinal fluid abnormalities (albumin-cytologic dissociation), no involvement of ninth and 10 th cranial nerves, diffuse hyporeflexia, and brachial diparesis. Discussion Cranial neuritis is a possible neurological manifestation of coronavirus-2 pneumonia. Etiology is not clear: it is possible a direct injury of the nervous structures by the virus through olfactory nasopharyngeal terminations. However, the presence of albumin-cytological dissociation in one patient, the sparing of the sense of smell, and the response to human immunoglobulin therapy suggests an immune-mediated genesis of the disorder.
“…Cranial mononeuropathy with brachial diparesis, albumincytologic dissociation, and areflexia in the second case can suggest an atypical MFS overlap [17].…”
Objective To report two cases of cranial multineuritis after severe acute respiratory syndrome caused by coronavirus-2. Methods Patients' data were obtained from medical records of the clinical chart of dell'Angelo Hospital, Venice, Italy. Results The first patient is a 42-year-old male patient who developed, 10 days after the resolution of coronavirus-2 pneumonia and intensive care unit hospitalization with hyperactive delirium, a cranial multineuritis with asymmetric distribution (bilateral hypoglossus involvement and right Claude Bernard Horner syndrome). No albumin-cytologic dissociation was found in cerebrospinal fluid; severe bilateral denervation was detected in hypoglossus nerve, with normal EMG of other cranial muscles, blink reflex, and cerebral magnetic resonance with gadolinium. He presented a striking improvement after intravenous human immunoglobulin therapy.The second case is a 67-year-old male patient who developed a cranial neuritis (left hypoglossus paresis), with dyslalia and deglutition difficulties. He had cerebrospinal fluid abnormalities (albumin-cytologic dissociation), no involvement of ninth and 10 th cranial nerves, diffuse hyporeflexia, and brachial diparesis. Discussion Cranial neuritis is a possible neurological manifestation of coronavirus-2 pneumonia. Etiology is not clear: it is possible a direct injury of the nervous structures by the virus through olfactory nasopharyngeal terminations. However, the presence of albumin-cytological dissociation in one patient, the sparing of the sense of smell, and the response to human immunoglobulin therapy suggests an immune-mediated genesis of the disorder.
“…In this case, enhancement along the neural sheath of the oculomotor nerve was observed on the orbital MRI, as well as the fast recovery of the patient’s symptoms, supporting the theory of demyelination. Moreover, the atypical presentation of Fisher syndrome could be considered as one of possible diagnoses of this case, considering various clinical manifestations and the ganglioside antibody profile of Fisher syndrome [15, 16]. Although CSF profile and negative anti-GQ1b antibody were not compatible with Fisher syndrome, the self-limiting disease course of our case and previous reports of GBS and Fisher syndrome after vaccination were suggestive of a diagnosis of Fisher syndrome in this case.…”
Influenza vaccines are known to have a few neurological complications, such as Guillain-Barre syndrome, chronic inflammatory demyelinating polyneuropathy, and acute disseminated encephalomyelitis. However, oculomotor palsy caused by influenza vaccination is extremely rare. We present a case report of a 25-year-old woman without any medical history who developed complete oculomotor palsy 2 weeks after influenza vaccination. Other possible causes of oculomotor nerve palsy, such as stroke, compressive lesions, infections, and autoimmune disorders, were eliminated by blood tests, cerebrospinal fluid examination, and imaging studies. Hence, influenza vaccine was considered as the likely cause.
“…In other recent study, six of the 38 patients (16%) with MFS experienced headache during the acute phase. Three of them complained of pain with over moderate (over 5 score by Wong-Baker FACES Pain Rating Scale), and NSAIDs was not effective in all patients [5].…”
Anti-GQ1b antibody syndrome, including Miller Fisher syndrome, Guillain-Barré syndrome with ophthalmoplegia, Bickerstaff's brainstem encephalitis, and acute ophthalmoplegia without ataxia, has overlapped clinical symptoms and mostly associated with anti-GQ1b immunoglobulin (Ig) G antibody. We report two cases of anti-GQ1b antibody syndrome mainly presenting with a severe headache. The 60-year-old man was admitted for severe headache and gait disturbance. Neurological examination revealed limb and truncal ataxia, areflexia, nystagmus, and ophthalmoplegia. Serum IgG anti-GQ1b antibody was positive. He recovered after intravenous (IV) immunoglobulin and steroid. The 23-year-old man suffered from severe headache (visual analogue scale=10) within the periorbital area. Ophthalmoplegia with gaze-evoked nystagmus were revealed. Serum IgG anti-GQ1b and anti-GT1a antibodies were positive. Headache was improved by IV immunoglobulin and steroid. The pathophysiology of headache in anti-GQ1b antibody syndrome is largely unknown. The affected nerve or structures in the brainstem including the trigeminovascular system may induce intractable severe headache.
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