Parsonage-Turner Syndrome Following SARS-CoV-2 Infection: A Systematic Review

Abstract

Parsonage-Turner syndrome (PTS) is an inflammatory disorder of the brachial plexus. Hypothesized underlying causes focus on immune-mediated processes, as more than half of patients present some antecedent event or possible predisposing condition, such as infection, vaccination, exercise, or surgery. Recently, PTS was reported following the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. We aimed to investigate data on PTS triggered by SARS-CoV-2 infection to provide an extensive perspective on this pathology and to reveal what other, more specific, research questions can be further addressed. In addition, we aimed to highlight research gaps requiring further attention. We systematically reviewed two databases (LitCOVID and the World Health Organization database on COVID-19) to January 2023. We found 26 cases of PTS in patients with previous SARS-CoV-2 infection. The clinical and paraclinical spectrum was heterogeneous, ranging from classical PTS to pure sensory neuropathy, extended neuropathy, spinal accessory nerve involvement, and diaphragmatic palsy. Also, two familial cases were reported. Among them, 93.8% of patients had severe pain, 80.8% were reported to present a motor deficit, and 53.8% of patients presented muscle wasting. Paresthesia was noted in 46.2% of PTS individuals and a sensory loss was reported in 34.6% of patients. The present systematic review highlights the necessity of having a high index of suspicion of PTS in patients with previous SARS-CoV-2 infection, as the clinical manifestations can be variable. Also, there is a need for a standardized approach to investigation and reporting on PTS. Future studies should aim for a comprehensive assessment of patients. Factors including the baseline characteristics of the patients, evolution, and treatments should be consistently assessed across studies. In addition, a thorough differential diagnosis should be employed.

Parsonage–Turner Syndrome following COVID-19 Vaccination: A Systematic Review

“…In most cases, further PTS symptoms appeared within two weeks after the onset of pain; only two patients with a history of viral vector vaccination presented motor and sensory signs after three weeks [ 42 ] and one month, respectively [ 44 ]. These findings contrast the data from the literature, including patients with or without COVID-19, where authors found that in 27.2% [ 1 ] and 25% [ 62 ] of cases, paresis did not manifest itself until over two weeks later [ 1 ].…”

“…In the mRNA group, 64% of cases were males, similar to other cohorts from the literature, including PTS of all causes [ 1 ]. The proportion of males in the viral vector group was higher (83.3%), comparable to the gender distribution reported by a previous systematic review on PTS following SARS-CoV-2 infection [ 62 ]. A family history was absent in all patients, but most authors did not report on it.…”

“…After the COVID-19 vaccination, sensory symptoms were less frequent, but muscle wasting occurred at similar rates only in the viral vector vaccines group. Sensory loss presented similar rates compared to PTS after SARS-CoV-2 infection [ 62 ].…”

“…Although in the literature, 15.4% of PTS patients presented autonomic nervous system involvement (e.g., vegetative and trophic skin changes, edema, temperature dysregulation) [ 1 ], autonomic dysfunction was not reported after COVID-19 vaccination or infection [ 62 ]. The development of nerve involvement outside the brachial plexus was documented solely following viral vector immunization, including the lumbosacral plexus [ 33 ] and phrenic nerve [ 28 , 32 ].…”

“…The development of nerve involvement outside the brachial plexus was documented solely following viral vector immunization, including the lumbosacral plexus [ 33 ] and phrenic nerve [ 28 , 32 ]. Lumbosacral PTS was also diagnosed in patients with COVID-19 [ 62 ] and hereditary PTS [ 6 ]. However, lower limb involvement was not found in patients in large cohorts of sporadic neuralgic amyotrophy [ 63 ].…”