Discussion:
GBS manifests itself in a variety of ways, ranging from typical peripheral 4 limb weakness with areflexia to numerous variants that complicate diagnosis and management. Typical GBS usually presents with ascending limb weakness with hyporeflexia/areflexia with minor sensory symptoms and usually involves the 4 upper limbs [4]. Besides the typical presentation of GBS, clinical variants are based on the types of nerve fibers involved (motor, sensory, sensory, and motor, cranial, or autonomic) and the mode of fiber injury (demyelinating vs axonal) [5, 6]. The most common mode of nerve fiber injury is demyelinating, while axonal motor and axonal sensory variants have been described [6] and are associated with rapid progression and poor prognosis [7]. Axonal variants are usually preceded by campylobacter jejune infection [8].
GBS typically has ascending weakness, but descending variants have been described, including the Miller-Fischer variant, which consists of ophthalmoplegia, ataxia, and areflexia [9]. Another cranial variant is the Bickerstaff brainstem encephalitis, which is characterized by alteration in consciousness, hyperreflexia, ataxia, and ophthalmoplegia [10].
A less common paraparetic motor variant affects the legs selectively with areflexia, mimicking an acute spinal cord lesion, and is associated with back pain [11]. In most cases, the paraparetic variant is usually milder compared to the classical GBS, and in 50% of the cases, there are abnormalities in upper limb nerves observed in NCS [12].
While the sensory symptoms in GBS are typically mild, pure sensory variants have been described and are usually characterized clinically by exclusive sensory symptoms and signs that reach their nadir in a maximum of 6 weeks without related systemic disorders and other diseases or conditions [13].
Our case is a 62-year-old lady who presented with progressive ascending lower limb weakness with areflexia in addition to the sensory level of T6. MRI excluded spinal cord compression and demyelination. CSF studies showed albumin-cytological dissociation. NCS showed absent F-waves of both the perineal and tibial nerves. She was given intravenous immunoglobulin followed by five days of IV methylprednisolone, and her symptoms improved over four weeks. Our most likely diagnosis was GBS based on the presentation of acute flaccid paralysis, areflexia, preceding diarrheal illness, CSF studies, and lack of evidence of demyelination and cord compression on MRI, in addition to the duration and course of her illness. We think that our case is like the case reported by Khoo et al. and may represent a new variant of GBS [14]. It is important to note that typical NCS findings are not always present in GBS as it is affected by timing and multiple studies at different times are needed [15].
Another argument is the possibility of transverse myelitis provided that our patient has sensory level and with the onset of symptoms typical of transverse myelitis, but the diagnostic criteria [16] don’t apply in our case as there is an absence of demyelination in repeated MRI and no CSF leukocytosis.