The paper reports on someone developing MS like symptoms 2-3 weeks after symptom onset for COVID-19 They say…..
“SARS-CoV-2 infection can produce neurological features. The most common are headache, anosmia and dysgeusia but patients may also develop other central nervous system (CNS) injuries.
We present a patient affected by Covid-19 who initially consulted for decreased visual acuity. The MRI showed inflammation in the right optic nerve and demyelinating lesions in the CNS.
We speculate that an immune mechanism induced by SARS-CoV-2, which can activate lymphocytes and an inflammatory response, plays a role in the clinical onset of the disease. This pathogen may be associated with either the triggering or the exacerbation of inflammatory/demyelinating disease”.
I think I will start to write my next paper…can a Mars bar cause MS? It’s as plausible as this. Statistically it is bound to happen that someone will develop MS, after they have eaten a Marsbar. This may be the first case of MS after COVID, but if it is not the last, it will be a question of who believes this? By the time they were tested there was no virus to be seen but they were positive for anti-COVID antibodies and also had oligoclonal bands.
However if true it rather throws away all the stuff about the MS prodrome (grumbling MS years before it shows itself), the function of the migration studies, the American service studies after BV infection and begs the question of why JC virus is not a cause of MS as it seems far more plausible. We can go on an on and we can have a good old book shredding exercise. We have to wait until a pattern emerges to determine whethet this is exploitism of not.
There have been a number of case reports linking COVID-19
The Emerging Spectrum of COVID-19 Neurology: Clinical, Radiological and Laboratory Findings. Brain. 2020 Jul 8;awaa240. doi: 10.1093/brain/awaa240. Online ahead of print
There were quite a few cases at the National Hospital Queen Square
Five major categories emerged:
(i) encephalopathies (n = 10) with delirium/psychosis and no distinct MRI or CSF abnormalities, and with 9/10 making a full or partial recovery with supportive care only;
(ii) inflammatory CNS syndromes (n = 12) including encephalitis (n = 2, para- or post-infectious), acute disseminated encephalomyelitis (n = 9), with haemorrhage in five, necrosis in one, and myelitis in two, and isolated myelitis (n = 1). Of these, 10 were treated with corticosteroids, and three of these patients also received intravenous immunoglobulin; one made a full recovery, 10 of 12 made a partial recovery, and one patient died;
(iii) ischaemic strokes (n = 8) associated with a pro-thrombotic state (four with pulmonary thromboembolism), one of whom died;
(iv) peripheral neurological disorders (n = 8), seven with Guillain-Barré syndrome, one with brachial plexopathy, six of eight making a partial and ongoing recovery;
Guillain-Barré syndrome is known to develop following viral infection
(v) miscellaneous central disorders who did not fit these categories. SARS-CoV-2 infection is associated with a wide spectrum of neurological syndromes affecting the whole neuraxis, including the cerebral vasculature and, in some cases, responding to immunotherapies. The high incidence of acute disseminated encephalomyelitis, particularly with haemorrhagic change, is striking. This complication was not related to the severity of the respiratory COVID-19 disease.