Page 1 of 2 Case report Licensee OA Publishing London 2013. Creative Commons Attribution License (CC-BY) For citation purposes: Hantson P, Wittebole X, Van Den Bergh P. Critical illness polyneuropathy or axonal Guillain-Barre syndrome triggered by subarachnoid haemorrhage? OA Case Reports 2013 Sep 10;2(9):86. Competng interests: none declared. Confict of interests: none declared. All authors contributed to concepton and design, manuscript preparaton, read and approved the fnal manuscript. All authors abide by the Associaton for Medical Ethics (AME) ethical rules of disclosure. Anaesthetics & Critical Care Critical illness polyneuropathy or axonal Guillain–Barré syndrome triggered by subarachnoid haemorrhage? P Hantson¹*, X Wittebole¹, P Van Den Bergh² Abstract Introduction This article reports a case of the diffi- culty to differentiate between critical illness polyneuropathy and axonal Guillain–Barré syndrome when trig- gered by subarachnoid haemorrhage. Case report An 81-year-old man was admitted comatose (Glasgow coma scale score 4/15) after a subarachnoid haemor- rhage. His neurological condition gradually improved with as best mo- tor response (M4) withdrawal from pain at the four limbs. The patient developed early complications such as septicaemia and acute renal inju- ry. After 3 weeks, a marked decrease of motor response (M1) was noted in the lower, and, to lesser extent, upper limbs. Deep tendon reflexes were abolished. The cerebrospinal fluid examination showed elevated protein level. After electrophysi- ological examination, the diagnosis of acute motor axonal neuropathy, a variant of Guillain–Barré syndrome, was discussed versus critical illness polyneuropathy. Specific therapy for Guillain–Barré syndrome could not be administered. No significant mo- tor recovery was observed after 7 months. Conclusion The distinction between critical ill- ness polyneuropathy and Guillain– Barré syndrome remains difficult in critically ill patients. It is not known if subarachnoid haemorrhage could be considered as a possible triggering factor for Guillain–Barré syndrome. Introduction After subarachnoid haemorrhage (SAH), the patient’s neurological condition may fluctuate over the first hospital days or weeks according to the magnitude of the bleeding and related complications. In patients with deeply altered consciousness, the testing of the best motor re- sponse may be challenging and defi- cits appear to be mainly due to cen- tral injury. The discrepancy between a progressive recovery of conscious- ness manifested as spontaneous eye opening or response to verbal com- mand in the oro-facial territories and a persisting quadriplegia or quadri- paresia should prompt further inves- tigations to rule out peripheral in- jury. Numerous conditions have been associated with critical illness poly- neuropathy (CIP) and myopathy and Guillain–Barré syndrome (GBS), in- cluding head trauma or intracerebral haemorrhage 1–4 . The potential role of subarachnoid bleeding is specu- lative, but the following observation illustrates the difficulties of the dif- ferential diagnosis between CIP and GBS when consciousness is impaired. Case report An 81-year-old man was admitted comatose in the emergency depart- ment. He had a medical history of arterial hypertension and type 2 dia- betes mellitus; there was no evidence for a recent infection or vaccination. The initial Glasgow coma score (GCS) was 4/15 (E1V1M2) and intubation was required for mechanical ventila- tion in the intensive care unit (ICU). The diagnosis of SAH was made on the admission brain computed to- mography (CT) (grade IV according to Fisher classification). No intrac- ranial aneurysm could be demon- strated after contrast enhancement at CT and conventional angiography. The patient developed as an immedi- ate complication a mild hydrocepha- lus, but the GCS gradually improved up to 10/15 (E4V1M6). However, the progression of hydrocephalus resulted in a neurological worsening (GCS ranging from 5 to 8). Despite ventricular drainage, the neurologi- cal condition remained unchanged. The best motor response was M4 in the four limbs. The patient developed a septicaemia due to Staphylococcus aureus, and a worsening of renal function was also noted. Haemody- namic instability was observed with alternating hypo- and hypertension. The repeated brain CT showed a re- gression of subarachnoid bleeding and hydrocephalus. After 3 weeks in the ICU, a marked decrease of motor response (M1) was noted in the low- er, and, to lesser extent, upper limbs. The patient was able to open the eyes and the mouth on verbal command. Cranial nerve examination was nor- mal. The deep tendon reflexes were abolished. The analysis of the cer- ebrospinal fluid (CSF) revealed ele- vated CSF protein level (122 mg/dl), with normal CSF cell counts. In the blood investigations, there was a pol- yclonal increase of immunoglobulins A and G; antibodies against myelin- associated glycoproteins were nega- tive. Serum creatinine phosphoki- nase levels were elevated at the time of admission, but rapidly decreased. Routine serological investigations for common viral or bacterial infections were also negative. The differential * Corresponding Author E-mail: philippe.hantson@uclouvain.be 1 Department of Intensive Care, Université catholique de Louvain, Brussels, Belgium 2 Neuromuscular Reference Centre, Université catholique de Louvain, Brussels, Belgium