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INTRODUCTION Lyme disease, caused by spirochete Borrelia burgdorferi, is a multisystemic infectious disorder with prominent neurologic involvement, affecting both the peripheral and the central nervous system. Meningitis, cranial neuritis and radiculoneuritis are the usual manifestations in the acute phase, and peripheral neuropathy in the chronic phase. Other less common manifestations have been also described. Here we report one case of Lyme disease confirmed by PCR, with a previously undescribed neurological manifestation, and the neurophysiological studies performed before and after treatment. CLINICAL CASE Our patient showed a chronic and progressive clinical picture consisting of instability on walking and distal paresthesia of lower limbs, suggestive of posterior column disfunction. The neurophysiological exam performed prior to treatment with ceftriaxone revealed bilateral absence of lower limbs somatosensory evoked potentials (SEPs), without alterations in the distal nervous conduction or in upper limbs SEPs. The exam performed after treatment revealed a partial recovery of lower limb SEP with presence of an evoked response in SEP of left lower limb, coincident with a transitory clinical improvement of paresthesia in the same extremity. CONCLUSIONS Our findings reveal that posterior column disfunction can be a neurological manifestation of Lyme disease. Furthermore the neurophysiological study shows that this manifestation is partially reversible following treatment. Our study emphasize the importance of the neurophysiological tests for the diagnosis and follow up of neurological manifestations of Lyme disease.

The exact location of the pontine gustatory pathway has not yet been clarified, probably because there are so few studies of taste in patients with well localised brainstem lesions.1-3 Here we report on a patient with isolated hemiageusia and trigeminal sensory neuropathy from a single small pontine lesion. A 46 year old woman experienced a burning sensation on the left side of the tongue. The next day she discovered a loss of taste on the entire left half of her tongue and numbness on the left side of her face. Neurological examination was normal except for hypaesthesia to pain, touch, and temperature sensation in all three divisions of the left trigeminal nerve, with decreased left corneal reflex and no weakness of masseters. Taste sensation was tested using separate solutions of 1.2 …

INTRODUCTION In typical Guillain-Barre syndrome the clinical symptomatology is more pronounced in lower extremities. So, this is the territory of election to demonstrate electrophysiological abnormalities early in the disease. PATIENTS AND METHODS We presented the results of the electrophysiological study of 37 patients, who showed abnormalities in peroneal nerve territory as soon as 15 days from the onset of the disorder, and were maintained at least up to 30 days later. Since Guillain-Barre syndrome is an heterogeneous syndrome, which can differ in extension and severity in the different patients, is necessary a more extensive electrophysiological study. Furthermore, subtypes of the disorder are recognized in relation to different electrophysiological patterns. Therefore, it is important to analyze data of each patient individually and to make control evolutive studies. For these reasons we also describe in detail the electrophysiological study of a selected patient affected by Guillain-Barre syndrome. In this case motor and sensory abnormalities were localized in distal nerve segments, and there was not denervation potentials in EMG. RESULTS We considered these findings indicative of a mainly distal sub-pattern with a good prognosis. The occurrence of A-waves was an early finding in this case of Guillain-Barre syndrome. During the course of the disease the behavior of these A-waves was variable in the different nerves of the lower extremities, and they disappeared in parallel with the clinical improvement of the patient.

OBJECTIVE The object of the present study is to show the spectrum of neurophysiological findings during clinical course of Miller Fisher syndrome (MFS), avoiding the controversy over a combined central and peripheral pathology. PATIENTS AND METHODS We report five patients with a syndrome of ophthalmoplegia, ataxia and areflexia. A similar episode had been suffered previously by 2 of these patients, 14 and 13 years before. In one of them the second episode evolved to a typical Guillain-Barre syndrome (GBS). Motor and sensory conduction velocity of upper and lower limbs, F waves, blink-reflex and somatosensory evoked potentials were recorded in all cases. Needle electromyography in four and brainstem evoked potentials in three of them and the jaw-reflex in another one. RESULTS In all patients there was a markedly reduced amplitude of the distal sensory evoked response, and no signs of denervation in the EMG. The other results were variable both interindividually and intraindividually. The severity of abnormalities was also different between different patients. The clinical recovery was always accompanied by a improvement of neurophysiological parameters. CONCLUSIONS The electrophysiological findings in MFS can be variable but they appear always related with the clinical symptomatology. We report for the first time a case in whom the jaw-reflex was abnormal whereas the blink-reflex was normal.