The infrared absorption of charge density waves coupled to a magnetic background is first observed in two manganites La1−xCaxMnO3 with x = 0.5 and x = 0.67. In both cases a BCS-like gap 2∆(T ), which for x = 0.5 follows the hysteretic ferro-antiferromagnetic transition, fully opens at a finite T0 < T Neel , with 2∆(T0)/kBTc ≃ 5. These results may also explain the unusual coexistence of charge ordering and ferromagnetism in La0.5Ca0.5MnO3.The close interplay between transport properties and magnetic ordering in the colossal magnetoresistance (CMR) manganites La(Nd) 1−x Ca(Sr) x MnO 3 is presently explained in terms of magnetic double exchange promoted by polaronic carriers along the path Mn +3 -O −2 -Mn +4 .[1] Charge hopping promotes the alignment of Mn +3 and Mn +4 magnetic moments, and vice versa. The polaronic effects are due to the dynamic Jahn-Teller distortion of the oxygen octahedra around the Mn +3 ions. The above mechanism explains how, in manganites with 0.2 < x < 0.48, any increase in the magnetization enhances the dc conductivity, and vice versa. However, La 0.5 Ca 0.5 MnO 3 shows an unpredicted coexistence of ferromagnetism and incommensurate charge ordering (CO). This compound is paramagnetic at room temperature, becomes ferromagnetic (FM) at T c ≃ 225 K and, by further cooling (C), antiferromagnetic (AFM) at a Néel temperature T C N ≃ 155 K.[2] Upon heating the sample (H) the FM-AFM transition is instead observed at T H N ≃ 190 K .[3] The dc conductivity σ(0) of La 0.5 Ca 0.5 MnO 3 is quite insensitive to the PM-FM transition at T c . [3] Xray, neutron [4] and electron diffraction [5] show quasicommensurate charge and orbital ordering in the AFM phase with wavevector q = (2π/a)( 1 2 − ǫ, 0, 0). The incommensurability ǫ increases with temperature and follows the hysteretic behavior of the AFM-FM transition, until charge ordering disappears above the Curie point T c .[5] At higher Ca doping, for 0.5 < ∼ x < ∼ 0.75, a transition to a charge ordered phase [6] is observed in the paramagnetic phase at T CO . T CO is a maximum (265 K) for x = 0.67 ≃ 2 3 , where the charge ordering is commensurate with the lattice. Below T CO , the system enters at T N an antiferromagnetic phase. For x = 0.67, T N ≃ 140 K.
A specific diagnostic protocol including the caloric test, C-VEMPS, O-VEMPS, could be useful when employed for identifying vestibular damage in CIDP patients.
The aim of this paper was to evaluate prospectively, in a group of patients affected by VN, a diagnostic protocol employing C-VEMPs, O-VEMPs and vHIT together. The diagnosis of vestibular neurolabyrinthitis was based on the clinical history, absence of associated auditory or neurological symptoms, and a neuro-otological examination with an evaluation of lateral semicircular canal function using the Fitzgerald-Hallpike caloric vestibular test and ice test. Our series revealed an incidence of 55% of superior and inferior vestibular neurolabyrinthitis, 40% of superior vestibular neurolabyrinthitis and 5% of inferior vestibular neurolabyrinthitis. These data, however, comprised different degrees of vestibular involvement considering the evaluation of each single vestibular end-organ with potential different prognosis. Four patients had only deficits of the horizontal and superior semicircular canals or their ampullary nerves. The implementation of C-VEMPs, O-VEMPs and vHIT in a vestibular diagnostic protocol has made possible to observe patients with ampullary VN, unidentifiable with other types of vestibular exams. The effect of age seems to have some impact on the recovery. When recovery firstly involves the utricular and saccular nerves and subsequently the ampullary nerves, it may be reasonable to expect a more favorable and successful outcome.
To our knowledge, these are the first reported cases in which selective damage to the lateral and superior semicircular canals and their nerves caused by neurolabyrinthitis was demonstrated clinically. Our clinical results indicate that the damage can be selective for specific vestibular end organs.
The implementation of C-VEMPs, O-VEMPs, and the vHIT in a vestibular diagnostic protocol has made it possible to observe patients with ampullary VN in a way that has not been feasible with other types of vestibular examinations. The age of the patient seems to have some impact on recovery from VN. When recovery occurs in the utricular and saccular nerves first and in the ampullary nerves subsequently, it may be reasonable to expect a more favorable outcome.
Objective Usher's syndrome type II (USH2) is characterized by moderate to profound congenital hearing loss, later onset of retinitis pigmentosa, and normal vestibular function. Recently, a study investigating the vestibular function of USH2 patients demonstrated a pathologic response to vestibular tests. In this cross-sectional study we performed vestibular tests of a group patients with genetic diagnosis of USH2 syndrome to demonstrate if vestibular damage is present in USH2 patients. Study Design Cross-sectional study. Setting Tertiary referral center. Subjects and Methods Mutated genes of 7 patients with a clinical diagnosis of USH2 were evaluated. Vestibular function was investigated by audiometry, Fitzgerald-Hallpike caloric vestibular testing, cervical vestibular evoked myogenic potentials (C-VEMPs), ocular vestibular evoked myogenic potentials (O-VEMPs), and video head impulse test (v-HIT). Results Genetic tests confirmed the USH2 diagnosis in 5 of 7 patients examined, with 1 patient reporting a unique mutation on genetic tests. Four (80%) of the 5 patients with a genetic diagnosis of USH2 showed pathological O-VEMPs. Two patients (40%) reported bilateral absent or abnormal values of C-VEMPs. The superior semicircular canal presented a significant deficit in 2 (40%) patients. The same 2 cases showed a pathologic response of the v-HIT of the horizontal semicircular canal. Finally, the posterior semicircular canal presented a significant deficit in 4 (40.0%) patients. Conclusion A vestibular evaluation with vestibular evoked myogenic potentials and v-HIT seems to identify latent damage to the vestibular receptors of USH2 patients.
Hypoglycaemia, common in diabetic patients treated with insulin, can induce various neurological disturbances. Of these, seizures are the most common acute symptom, mainly of the generalised tonic-clonic type, with focal events only exceptionally being reported and documented. Hypoglycaemia can modify cortical excitability by determining an imbalance between excitation and inhibition; some brain structures, such as the temporal lobe and hippocampus, appear to be particularly susceptible to this insult. We describe a case of a 61-year-old diabetic patient in whom insulin-induced transient hypoglycaemia triggered a focal seizure of temporal origin that was well documented by EEG during 24-hour ambulatory monitoring. This is, to our knowledge, one of the few, well-documented cases of this type of seizure.
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