Hyper-reflexia in Acute Motor Axonal Neuropathy Child Case Secondary to Mycoplasma Pneumonia

GBS is a group of syndromes with several distinctive subtypes classified on a pathologic basis into demyelinating and axonal forms. Axonal GBS has been classified into 2 groups: AMAN and acute motor and sensory axonal neuropathy [3]. Although hyporeflexia or areflexia is the hallmark of GBS, normal reflexes or hyperreflexia does not exclude GBS diagnosis. AMAN commonly reported to be associated with retained or brisk reflexes [4]. The incidence of hyper-reflexia in AMAN is reported to be between 33% and 48% [2]. In a review of AMAN cases with hyperreflexia, diarrhea or gastroenteritis was reported in 77.8% of patients before the disease, and Campylobacter jejuni infection was demonstrated iby isolation from stool or serological evidence in all these patients [5]. However, unlike the literature, in our case AMAN presented secondary to M. pneumonia. At the same review, limb weakness was present in 80% of patients and was usually mild to moderate. Weakness generally involved all four limbs being limited to upper or lower limbs in only three patients (8.3%) [5]. Our patient, like many other patients noted, had mild weakness and his deep tendon reflexes were globally brisk.

Hyper-reflexia and reflex spread are considered signs of upper motor neuron or corticospinal tract lesion [6]. Only a few studies attempted to elucidate the pathophysiology of hyper-reflexia in GBS. Early in the disease, electrophysiologic abnormalities are often mild or nonspecific. A high soleus H:M ratio that correlates with hyper-reflexia and the recording of H reflex in muscles where it is not normally elicitable (ie, considered a pathological sign) and prolongation of central conduction time have been reported [7,8]. These findings indicate a lower motoneuron hyperexcitability and have been interpreted as a possible consequence of the dysfunction of spinal inhibitory interneurons and the involvement of distal motor nerves, the proximal segments, and the sites prone to compression [2,9].

Despite these findings, the absence of upper motor neuron damage findings such as spasticity and Babinski sign suggests a functional involvement of the corticospinal tract, although no structural damage was demonstrated by MRI. Involvement of corticospinal pathways may also increase the excitability of motoneurons by reducing presynaptic inhibition at the Ia fiber-α motoneuron synapse and increasing axonal sprouting of terminal Ia fibers [10]. Diagnostic approach to GBS is based on clinical, laboratory, and electrophysiological criteria. The history is of paramount importance and is characterized by symmetric flaccid paresis associated with varying combinations of pain, paresthesia and weakness.