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Fulminant Guillain–Barré Syndrome Post Hemorrhagic Stroke: Two Case Reports

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Fulminant Guillain–Barré Syndrome Post Hemorrhagic Stroke: Two Case Reports Case Report Fulminant Guillain–Barré Syndrome Post Hemorrhagic Stroke: Two Case Reports Sameeh Abdulmana 1, Naif Al-Zahrani 1, Yahya Sharahely 2, Shahid Bashir 1 and Talal M. Al-Harbi 1,* 1 Neuroscience Centre, Neurology Department, King Fahad Specialist Hospital-Dammam, Dammam 31444, Saudi Arabia; [email protected] (S.A.); [email protected] (N.A.-Z.); [email protected] (S.B.) 2 Neurology Division, Medical Department, Dammam Medical Complex, Dammam 31444, Saudi Arabia; [email protected] * Correspondence: [email protected]; Tel.: +96-6138442222 (ext. 2270/2278); Fax: +96-6138150315 Abstract: Guillain–Barré syndrome (GBS) is an acute, immune-mediated inflammatory peripheral polyneuropathy characterized by ascending paralysis. Most GBS cases follow gastrointestinal or chest infections. Some patients have been reported either following or concomitant with head trauma, neurosurgical procedures, and rarely hemorrhagic stroke. The exact pathogenesis is not entirely understood. However, blood–brain barrier damage may play an essential role in triggering the autoimmune activation that leads to post-stroke GBS. Here, we present two cases of fulminant GBS following hemorrhagic stroke to remind clinicians to be aware of this rare treatable complication if a stroke patient develops unexplainable flaccid paralysis with or without respiratory distress. Keywords: Guillain–Barré syndrome; Guillain–Barré following stroke; intracranial hemorrhage; Citation: Abdulmana, S.; Al-Zahrani, hemorrhagic stroke complicated by radiculopathy N.; Sharahely, Y.; Bashir, S.; M. Al-Harbi, T. Fulminant Guillain–Barré Syndrome Post Hemorrhagic Stroke: Two Case Reports. Neurol. Int. 2021, 13, 190–194. 1. Introduction https://doi.org/10.3390/ Guillain, Barré, and Strohl first reported Guillain–Barré syndrome (GBS), or acute neurolint13020019 inflammatory demyelinating polyradiculoneuropathy, in 1916 [1]. It is characterized by acute ascending progressive weakness, areflexia, and dysautonomia [2]. Clinically, the Academic Editor: incidence of GBS is rare, at 0.8–1.9/100,000 people/year [1]. Several subtypes of GBS are Takehiko Yanagihara well recognized, including acute inflammatory demyelinating polyradiculoneuropathy (AIDP), acute motor axonal neuropathy (AMAN), acute motor-sensory axonal neuropathy Received: 8 January 2021 (AMSAN), and Miller Fisher syndrome (MFS). Accepted: 31 March 2021 GBS is thought to result from an immune response that leads to acute polyneuropathy. Published: 6 May 2021 It is often triggered by an antecedent infection. Two-thirds of patients report symptoms suggesting an initial respiratory or gastrointestinal disease [3]. A minority of patients Publisher’s Note: MDPI stays neutral develop GBS following a vaccine, bone marrow transplant, neurosurgery, or head trauma. with regard to jurisdictional claims in However, in the last few years, growing reports about the concurrence of GBS with unusual published maps and institutional affil- events like intracerebral hemorrhage (ICH) have increased with unfavorable prognosis due iations. to cardiovascular autonomic instability [4]. Here, we report two cases of patients who were diagnosed with GBS following hem- orrhagic stroke. The first patient developed GBS after endovascular mechanical thrombec- tomy for acute ischemic stroke complicated by a hemorrhagic transformation. In compari- Copyright: © 2021 by the authors. son, the second patient developed GBS after hematoma evacuation. Licensee MDPI, Basel, Switzerland. This article is an open access article 2. Case Presentation distributed under the terms and 2.1. Case 1 conditions of the Creative Commons Attribution (CC BY) license (https:// The patient was a 74-year-old right-handed woman. She was known to have type 2 creativecommons.org/licenses/by/ diabetes (DM), hypertension (HTN), and dyslipidemia. She presented to the emergency 4.0/). department (ED) after six hours of left-sided weakness and dysarthria in February 2019. Neurol. Int. 2021, 13, 190–194. https://doi.org/10.3390/neurolint13020019 https://www.mdpi.com/journal/neurolint Neurol. Int. 2021, 13, FOR PEER REVIEW 2 2. Case Presentation Neurol. Int. 2021, 13 2.1. Case 1 191 The patient was a 74-year-old right-handed woman. She was known to have type 2 diabetes (DM), hypertension (HTN), and dyslipidemia. She presented to the emergency department (ED) after six hours of left-sided weakness and dysarthria in February 2019. Her neurological examination was remarkable for dysarthria, as she was able to obey Her neurological examination was remarkable for dysarthria, as she was able to obey sim- simple commands, and showed right gaze preference, left facial (sparing the forehead) ple commands, and showed right gaze preference, left facial (sparing the forehead) flaccid flaccid weakness (power 0/5), and an extensor plantar reflex. weakness (power 0/5), and an extensor plantar reflex. A computerized brain tomography (CT) and CT arteriogram (CTA) showed acute right A computerized brain tomography (CT) and CT arteriogram (CTA) showed acute middle cerebral artery (MCA) ischemic infarction with complete occlusion of the suitable right middle cerebral artery (MCA) ischemic infarction with complete occlusion of the M1 and a partial filling defect in the distal M2 segment. She underwent endovascular suitable M1 and a partial filling defect in the distal M2 segment. She underwent endovas- thrombectomy with partial recanalization and was kept in an intensive care unit (ICU) for cular thrombectomy with partial recanalization and was kept in an intensive care unit close monitoring. A follow-up CT brain showed interval development of hemorrhagic (ICU) for close monitoring. A follow-up CT brain showed interval development of hem- transformation (Figure1). orrhagic transformation (Figure 1). FigureFigure 1. 1.Brain Brain CTCT scan.scan. ThreeThree daysdays later,later, she she had had movedmoved toto thethe wardward inin aa stablestable condition,condition,with with minimalminimal im-im- provementprovement in in her her left left side side weakness. weakness. On On the the fifth fifth day day of of admission, admission, she she developed developed breathing breath- difficultying difficulty and consciousnessand consciousness level level deterioration. deterioration. Her arterial Her arterial blood blood gas (ABG) gas (ABG) revealed revealed high PaCo2high PaCo2 65 mm 65 Hg mm (45–45 Hg mm(45– Hg),45 mm normal Hg), bicarbonatenormal bicarbonate HCO3 23 HCO3 mEq/L 23 (22–26 mEq/L mEq/L), (22–26 lowmEq/L), oxygen low PO2 oxygen 70 mm PO2 Hg 70 (80–100mm Hg mm(80– Hg),100 mm and Hg), low and Ph 7.24low (Ph7.35–7.45 7.24 (7.3); subsequently,5–7.45); subse- shequently, required she ICUrequired admission, ICU admission, was intubated, was andintubated, was connected and was to connectedmechanical to ventilation.mechanical ventilation.Her neurological examination at that time revealed absent brain stem reflexes with bilateralHer facial neurological weakness. examination She had at flaccid that time quadriplegia revealed withabsent areflexia. brain stem Her reflexes metabolic with workup,bilateral includingfacial weakness. electrolytes She level, had renal,flaccid liver, quadriplegia and thyroid with function, areflexia. was normal.Her metabolic There wasworku nop, clinical including nor metabolicelectrolytes evidence level, renal, of infection. liver, and Chest thyroid X-ray, function, blood culture,was normal. and urineThere culturewas no wereclinical negative nor metabolic for any evidence abnormalities. of infection. The brain Chest MRI X-ray, (Supplementary blood culture, Figure and urine S1) demonstratedculture were negative an interval for evolution any abnormalities. of the known The rightbrain MCA MRI territories(Supplementary infarctions Figure with S1) ademonstrated hemorrhagic an transformation interval evolution and of no the brain known stem right involvement. MCA territories Because infarctions she was with un- a conscious, electroencephalography (EEG) was done, which showed generalized diffuse hemorrhagic transformation and no brain stem involvement. Because she was uncon- slowing with no epileptiform activity. Based on her clinical progression, a diagnosis of GBS scious, electroencephalography (EEG) was done, which showed generalized diffuse slow- was considered. ing with no epileptiform activity. Based on her clinical progression, a diagnosis of GBS Two weeks later, the nerve conduction study demonstrated absent motor responses was considered. of the common peroneal, tibial, median, and ulnar nerves and absent sensory responses Two weeks later, the nerve conduction study demonstrated absent motor responses from the sural, superficial peroneal, median, and ulnar nerves with stimulation of the four of the common peroneal, tibial, median, and ulnar nerves and absent sensory responses limbs (Supplementary Table S1). Moreover, the needle examination for the non-paralyzed from the sural, superficial peroneal, median, and ulnar nerves with stimulation of the four side from the stroke, including right tibialis anterior, gastrocnemius, vastus medialis, first dorsal interosseous, biceps, triceps, and deltoid, showed diffuse abnormal spontaneous discharges in forms of positive sharp waves (PSWs) and fibrillation potentials, which were more abundant in the distal muscles with no voluntary motor units, which is highly compatible with AMSAN variant. The cerebral spinal fluid (CSF) analysis showed albu- Neurol. Int. 2021, 13 192 minocytological dissociation with a normal white blood cells (WBCs) of 1 and
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