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Hyperacute Guillain-Barré syndrome mimicking stroke: Report of 3 cases Guillain-Barré and stroke

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Abstract

Stroke is the leading cause of acute neurological deficit. However, several potentially life threatening diseases can mimic stroke symptoms. Herein we report 3 cases of sudden onset neurological deficits with a final diagnosis of hyperacute Guillain-Barré syndrome (GBS). Two cases mimicked brain stem stroke while the last suggested a spinal cord infarct. No specific characteristics in terms of electrophysiological parameter, underlying etiology, response to treatment or prognosis was found between these hyperacute forms of hyperacute GBS and more common subacute forms. These cases remind us that acute inflammatory demyelinating neuropathy should always be evoked in front of stroke-like symptoms with negative brain imaging study.

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... An atypical presentation constitutes a diagnostic challenge for medical specialists given the symptomatic heterogeneity and diverse diagnostic possibilities. There have been very few reports on GBS patients presenting with unilateral limb weakness or facial palsy as onset symptoms (4)(5)(6)(7)(8)(9)(10)(11). Among them, the symptoms of some patients were suspected of indicating the onset of stroke (8)(9)(10)(11). ...
... There have been very few reports on GBS patients presenting with unilateral limb weakness or facial palsy as onset symptoms (4)(5)(6)(7)(8)(9)(10)(11). Among them, the symptoms of some patients were suspected of indicating the onset of stroke (8)(9)(10)(11). Brainstem stroke sometimes presents with symptoms similar to GBS. The clinical manifestations of brainstem stroke are varied and depend on the site of occlusion. ...
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Introduction: Guillain–Barre syndrome (GBS) is an acute immune-mediated inflammatory demyelinating polyneuropathy characterized by symmetrical limb weakness and areflexia. GBS can have different clinical manifestations; hence, the initial symptoms are also varied. Here, we describe a rare case of GBS presenting as hemiparesis and cranial nerve palsy, which mimic brainstem stroke. Case Presentation: A 53-year-old man was admitted to the hospital with a 3-h history of left-arm weakness, glossolalia, and right eyelid droop. After admission, his condition suddenly worsened, with quadriplegia, bilateral peripheral facial palsy, bilateral ophthalmoplegia, and other neurological symptoms. Based on the findings from a neurological examination, MRI, cerebrospinal fluid analysis, and nerve conduction study, a diagnosis of GBS was made. He received intravenous immunoglobulin (0.4 kg/day) for 5 days. After 20 days of systematic therapy, his dysphagia, dyspnea, facial paralysis, ocular movement disorder, and leg weakness recovered almost completely, but his arms were still moderately impaired, with a power of 4/5. Fortunately, the patient recovered well without any sequelae after 2 years of follow-up. Conclusions: In patients with an atypical presentation, the diagnosis of GBS is often delayed. With this case report, we intend to highlight the fact that some symptoms mimicking stroke may be a feature of GBS at onset; close observation and timely diagnosis are crucial for clinicians. Neuroimaging is a valuable diagnostic tool in differentiating stroke from GBS.
... Hyper-acute GBS refers to the cases in which the nadir is reached in one to two days [11]. Hyper-acute GBS is rare [11] and only recorded in a few case reports and case series [12][13][14][15], where the time to reach the nadir ranged from 12 to 48 hours. In our case, the nadir was reached within one hour, which is unique. ...
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A 46-year-old man with a prior history of cervical spondylosis and myelopathy needing cervical spinal surgery three years back presented to the emergency department with acute onset areflexic flaccid weakness of both lower extremities, with a sensory level at T10. Magnetic resonance imaging studies (MRI) of the cervical, thoracic, and lumbar spine ruled out significant cord compression, spinal cord ischemia, spinal shock, or findings to suggest transverse myelitis. CSF analysis showed normal albumin and protein; however, with the features of paraplegia with flaccidity, areflexia, absence of bowel and bladder symptoms, and MRI ruling out other possibilities, a diagnosis of Guillain-Barre syndrome (GBS) was made. The patient was treated with intravenous immunoglobulin (IVIG) and showed a clinical response, with improvement in strength in both lower extremities. This case is rare and unique, as it exhibits atypical features for a GBS case, including a sensory level and hyper-acute presentation, with the onset of weakness to a nadir within an hour. This case highlights the importance of awareness of such atypical GBS presentations so that the diagnosis is not missed and is appropriately managed for favorable patient outcomes.
... Steiner et al reported in a study of five adult cases a time to nadir between 20 and 36 hours with favourable outcome on follow up (6) . Montaudouin M,et al reported three adult cases of sudden onset neurologic deficits with a final diagnosis of hyperacute GBS of which two cases mimicked brain stem stroke and another one as spinal cord infarct clinically (7). However, we have to keep in mind that GBS is often taught as a differential diagnosis of hyperacute onset of paraparesis in children. ...
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Guillain-Barre Syndrome (GBS) is an acute auto immune mediated inflammatory polyradiculoneuropathy. It is characterized by acute onset, gradually progressive ascending muscular weakness with absent or depressed tendon reflexes. Typically more than 90% of patients reach the nadir of their function within two to four weeks. Very rarely it can happen less than one week. In our case report child developed hyperacute onset paraparesis which was very rare. This presentation will mimic acute spinal cord lesion like trauma or spinal artery infract. MRI brain with spinal cord was normal. Nerve conduction study revealed low compound motor action potential (CMAP) in lower limb motor nerves which was suggestive of acute motor axonal neuropathy, variant of GBS. Child was treated with immunoglobulin therapy, which was useful to arrest the clinical progression of disease. Child was recovered slowly with physiotherapy. Hence, in our case report, we conclude that hyperacute paraparesis which mimic acute spinal cord lesion, clinicians must suspect GBS as one of the differential diagnosis.
... Our second case presented with nonspecific generalized weakness and hyperreflexia following a gastrointestinal infection. Although ascending motor symptoms constitute the typical pattern of GBS (like our third case), presenting symptoms from upper limbs or cranial nerves as well as generalized weakness are often seen [1,2,13]. ...
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Guillain-Barré syndrome (GBS) is mainly classified into acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN). Although diagnosis of GBS requires progressive weakness and universal areflexia or hyporeflexia, cases of GBS with preserved or increased deep tendon reflexes (DTRs) have been increasingly recognized. We report three cases of GBS, presenting at a single unit in six months. Our first case presented with pure sensory symptoms. The second case had nonspecific generalized weakness, while the third presented with typical ascending weakness. One of our patients had preserved DTRs, while the other two had increased DTRs. Our two cases with hyperreflexia were found to have a preceding Campylobacter jejuni infection and anti-ganglioside antibodies, and their electrophysiological studies revealed AMAN. The other case had an AIDP. Only one case was offered a diagnosis and treatment from the first emergency department (ED) visit and had a better clinical outcome. Clinical diagnosis of GBS in the ED can be challenging. Delay in diagnosis of GBS in the ED is common due to cases with intact or increased DTRs, atypical pattern of weakness, or pure sensory symptoms. Emergency physicians should be aware of GBS clinical heterogeneity, because early diagnosis and treatment improve clinical outcome.
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Guillain–Barré syndrome (GBS) is a heterogeneous disease, and it usually develops after an antecedent infection, while rare cases develop following a central nervous system disease. Given the indeterminacy of prodromal infection symptoms and the overlap of symptoms with other neurological disorders, a rigorous clinical and neurological examination in conjunction with history is necessary for early diagnosis and treatment of GBS. Here we present a rare case of GBS following acute ischemic stroke which was different from previous reports such as GBS following hemorrhagic stroke or head trauma. Moreover, intravenous immunoglobulin was effective in this patient after 6 months of follow-up despite the potential risk of thrombotic events.
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We herein report an unusual case of a 58-year-old man with polycythemia presented with sudden right leg and right arm weakness. He was treated for a stroke but continued to worsen, leading to quadriparesis. He was referred to the emergency department after experiencing progressive weakness in all four limbs for five days. No prior history of fever, cough, chest pain, diarrhea, backache, or trauma was found. The patient had normal neurological examination, MRC scores, and bilateral weak hand grips. Sensory examination was normal. The patient had normal blood tests, electrolytes and brain MRI. CSF examination revealed protein an albumin-cytological dissociation pattern. An electrodiagnostic study showed evidence of acute motor axonal polyneuropathy. The patient received IVIg for five days, and symptoms improved significantly.
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