a Gioi

Involvement of GABA in mirror focus: A case report

Mirror focus (MF) is a cortical epileptogenic lesion that is posited to develop in the contralateral site to a cortical primary focus (PF) by secondary epileptogenic mechanisms. Previous animal evidence supports the implication of gamma-aminobutyric acid (GABA) in this phenomenon, but this contention has not yet been substantiated by clinical findings. Here we report for the first time clinical evidence suggesting the involvement of GABAergic cortical transmission in MF pathogenesis, in a 37-year-old man affected by a lesional PF in the right frontal lobe and a homotopic MF in the contralateral hemisphere, triggered by hyperventilation. One year after surgical excision of the PF, the electric activity of the MF remained unchanged, but was accompanied by a significant increase in the density of GABA(A)/benzodiazepine receptor binding in the left frontal lobe, as measured by (123)I-Iomazenil SPECT. These results extend previous evidence on the involvement of GABAergic signaling in MF pathophysiology.

Diffusion tensor imaging tractography and MRI perfusion in post traumatic brain injury hypersomnia

Three years ago, a 48-year-old female patient had head trauma with commotion followed by a four-month coma. After hospital discharge, she complained of bilateral frontal headache, amnesia related to the episode and excessive daytime sleepiness with prolonged non-restorative naps at any time of day. Previous patient history did not report neurological or psychiatric illness. At our first outpatient sleep service (besides a normal neurological exam), she did report severe sleep disturbances, particularly an incoercible daytime sleepiness followed by non-refreshing and prolonged naps (Epworth Scale 18), prolonged night-time sleep with snoring and a noteworthy morning sleep inertia. Multiple repeated night videopolysomnography (PSG) excluded limb movements and respiratory disturbances and no REM behavior disorder was evident (preserved regular REMmuscle atonia). Nocturnal PSG showed four complete cycles [sleep latency 4.5 min, TST 6 h and 40 min, sleep efficiency 91% with normal NREM\REM alternationwhile increased N3 rate (N14%, N2 33%, N3% 41, REM 22%)]. Next-daymultiple sleep latency test (MSLT) showed a pathological mean sleep latency of 5.1 min without evidence of SOREMPs (mean REM-latency

F-Wave Duration as a Specific and Sensitive Tool for the Diagnosis of Restless Legs Syndrome/Willis-Ekbom Disease

STUDY OBJECTIVES Restless legs syndrome, also known as Willis-Ekbom disease (RLS/WED), is a frequent condition, though its pathophysiology is not completely understood. The diagnosis of RLS/WED relies on clinical criteria, and the only instrumental tool, the suggested immobilization test, may lead to equivocal results. Recently, neurophysiological parameters related to F-wave duration have been proposed as a diagnostic aid. The aim of this study is to assess and compare the diagnostic values of these parameters in diagnosis of RLS/WED. METHODS Fifteen women affected by primary RLS/WED and 17 age- and sex- matched healthy subjects. A complete electroneurographic evaluation, including nerve conduction studies (NCS), cutaneous silent period (CSP), and F-wave parameters, namely amplitude, F-wave duration (FWD), and the ratio between FWD and duration of the corresponding compound muscle action potential (FWD/CMAPD). RESULTS No subject showed alterations of the NCS. However, FWD and FWD/CMAPD of both upper and lower limbs were significantly longer in patients than controls. Tibial FWD/CMAPD best discriminated RLS/WED patients from controls. A cutoff of 2.06 yielded a sensitivity of 69.2%, a specificity of 94.1%, a positive predictive power of 90%, and a negative predictive power of 80% (area under the curve = 0.817; 95% confidence interval = 0.674-0.959). The combination of ulnar or tibial FWD/CMAPD increases the sensitivity (85.7%) while slightly decreasing the specificity (87.5%, positive predictive value: 85.7%, negative predictive value: 87.5%). CONCLUSIONS Lower limb FWD/CMAPD ratio may represent a supportive diagnostic tool, especially in cases of evening lower leg discomfort of unclear interpretation.

Sleep in Parkinson’s Disease with Impulse Control Disorder

Purpose of ReviewThis paper aims to explore the relationship between impulse-control disorders (ICDs) and sleep problems in patients with Parkinson’s disease (PD) among scientific literature.Recent FindingsPreviously published results are controversial and sometimes inconclusive. ICDs and sleep disruption represent important non-motor features of Parkinson’s disease, responsible for reducing quality of life and increasing burden of disease. The relationship between sleep problems and ICDs is complex and bidirectional. Indeed, sleep disturbances and fragmentation may play a crucial role in increasing susceptibility to impulsive behavior and may represent a risk factor for developing ICDs in PD patients. Moreover, REM sleep behavior disorder (RBD) and restless legs syndrome (RLS) have been indicated as independent risk factors for ICDs in PD patients. On the other hand, also ICDs may lead to sleep restriction and fragmentation, suggesting a bidirectional relationship.SummaryThe association between sleep problems and ICDs in PD is far from being completely understood. Further studies are needed to confirm the nature of this relationship and its pathophysiology.

Dissociation Between Neurovegetative Signs and Subjective Symptoms in a Case of Idiopathic Pilomotor Seizures

ObjectivePilomotor seizure (PS) is a rare subtype of simple and complex partial seizures, often related to temporal lobe epilepsy and occasionally linked to alterations of amygdala. The physiologic role played by this latter region in the coordination of autonomic responses to fear-induced emotional changes raises the question as to whether the involvement of amygdala in PS might elicit a disconnection between subjective symptoms and neurovegetative signs. MethodsWe report a case of idiopathic bilateral PS studied with video electroencephalogram, polygraphic 24-hour Holter electroencephalogram, and magnetic resonance imaging, plus spectral functional magnetic resonance imaging, in which the seizures were associated with abrupt tachycardia occurring in a state of emotional neutrality, without either clouding or loss of consciousness. ResultsElectroencephalogram documented PS episodes occurring during waking, rapid eyes movements, and nonrapid eye movement sleep stages. Although no morphologic alteration was detected, spectral magnetic resonance imaging visualized alterations of the metabolic ratios of N-acetylaspartate and creatine-phosphocreatine in hippocampus and amygdala, whereas no apparent involvement of the temporal lobe was found. ConclusionsThese findings suggest that the limited involvement of amygdala and hippocampus in PS triggers the repertoire of fear-related sympathetic responses uncoupled from alterations in emotional status. This phenomenon supports the possibility that autonomic responses involved in fear or extreme alertness follow a kind of “ethological” modularity.