Alessia Nicotra

Slow Breathing and Hypoxic Challenge: Cardiorespiratory Consequences and Their Central Neural Substrates

Controlled slow breathing (at 6/min, a rate frequently adopted during yoga practice) can benefit cardiovascular function, including responses to hypoxia. We tested the neural substrates of cardiorespiratory control in humans during volitional controlled breathing and hypoxic challenge using functional magnetic resonance imaging (fMRI). Twenty healthy volunteers were scanned during paced (slow and normal rate) breathing and during spontaneous breathing of normoxic and hypoxic (13% inspired O2) air. Cardiovascular and respiratory measures were acquired concurrently, including beat-to-beat blood pressure from a subset of participants (N = 7). Slow breathing was associated with increased tidal ventilatory volume. Induced hypoxia raised heart rate and suppressed heart rate variability. Within the brain, slow breathing activated dorsal pons, periaqueductal grey matter, cerebellum, hypothalamus, thalamus and lateral and anterior insular cortices. Blocks of hypoxia activated mid pons, bilateral amygdalae, anterior insular and occipitotemporal cortices. Interaction between slow breathing and hypoxia was expressed in ventral striatal and frontal polar activity. Across conditions, within brainstem, dorsal medullary and pontine activity correlated with tidal volume and inversely with heart rate. Activity in rostroventral medulla correlated with beat-to-beat blood pressure and heart rate variability. Widespread insula and striatal activity tracked decreases in heart rate, while subregions of insular cortex correlated with momentary increases in tidal volume. Our findings define slow breathing effects on central and cardiovascular responses to hypoxic challenge. They highlight the recruitment of discrete brainstem nuclei to cardiorespiratory control, and the engagement of corticostriatal circuitry in support of physiological responses that accompany breathing regulation during hypoxic challenge.

Asymmetry of visual function in migraine with aura: Correlation with lateralisation of headache and aura

Background: Asymmetry of visual phenomena and headache is an important feature of migraine with aura. Methods: This asymmetry was explored by assessment of visual illusions, hemifield spatial contrast detection (HCD) and hemifield pattern reversal visual evoked potentials (HVEPs) in 47 migraineurs with aura (MA), who were not taking prophylactic medications, and 62 controls with the same age range (16–59). Results: Illusions were greater and HCD was poorer in MA than in controls. There were no group differences with respect to P100 amplitude. The longer the duration of migraine the poorer the HCD. When the aura was consistently unilateral it was associated with greater illusions, reduced HCD and reduced hemifield P100 amplitude. These findings were not related to the side of headache. Conclusion: The lateralised changes suggest that the visual dysfunction occurs at a cortical level, and the correlation with the side of the aura suggests that dysfunction is most likely to occur in an area of preexisting anomaly of neural function.

Peripheral Nerve Dysfunction in Middle-Aged Subjects Born with Thalidomide Embryopathy.

Background Phocomelia is an extremely rare congenital malformation that emerged as one extreme of a range of defects resulting from in utero exposure to thalidomide. Individuals with thalidomide embryopathy (TE) have reported developing symptoms suggestive of peripheral nervous system dysfunction in the mal-developed limbs in later life. Methods Case control study comparing TE subjects with upper limb anomalies and neuropathic symptoms with healthy controls using standard neurophysiological testing. Other causes of a peripheral neuropathy were excluded prior to assessment. Results Clinical examination of 17 subjects with TE (aged 50.4±1.3 [mean±standard deviation] years, 10 females) and 17 controls (37.9±9.0 years; 8 females) demonstrated features of upper limb compressive neuropathy in three-quarters of subjects. Additionally there were examination findings suggestive of mild sensory neuropathy in the lower limbs (n = 1), L5 radiculopathic sensory impairment (n = 1) and cervical myelopathy (n = 1). In TE there were electrophysiological changes consistent with a median large fibre neuropathic abnormality (mean compound muscle action potential difference -6.3 mV ([-9.3, -3.3], p = 0.0002) ([95% CI], p-value)) and reduced sympathetic skin response amplitudes (-0.8 mV ([-1.5, -0.2], p = 0.0089)) in the affected upper limbs. In the lower limbs there was evidence of sural nerve dysfunction (sensory nerve action potential -5.8 μV ([-10.7, -0.8], p = 0.0232)) and impaired warm perception thresholds (+3.0°C ([0.6, 5.4], p = 0.0169)). Conclusions We found a range of clinical features relevant to individuals with TE beyond upper limb compressive neuropathies supporting the need for a detailed neurological examination to exclude other treatable pathologies. The electrophysiological evidence of large and small fibre axonal nerve dysfunction in symptomatic and asymptomatic limbs may be a result of the original insult and merits further investigation.

Pathological yawning as an ictal seizure manifestation in the elderly

Excessive yawning has been reported in the peri-ictal period preceding or following seizures. We describe an exceptional case of an elderly man with impairment of consciousness and paroxysmal excessive yawning. We hypothesise that this can be regarded as an autonomic seizure originating from diencephalic/brainstem structures, manifesting with yawning as an ictal phenomenon.

Entrapment of the lateral cutaneous nerve of the calf.

Isolated lesion of lateral cutaneous nerve of the calf (LCNC), particularly due to entrapment, is rarely reported in the literature. Patients usually present with sensory symptoms in the lateral aspect of the calf. Treatment is usually by local applications or local steroid/anaesthetic injection. We report the first case of LCNC entrapment in a 35-year-old man which is documented by nerve conduction studies. The patient had a temporary improvement following a local anaesthetic/steroid injection. Owing to the recurrence of symptoms, the patient opted for surgery. About 1 year after surgery, the symptoms disappeared completely.

PTMS 1 Pre-and post-surgical assessment of cervical myelopathy: a transcranial magnetic stimulation study

cortical stimulation, absence of response on the right side and abnormal response for latency and amplitude on the left side; after lumbar stimulation normal response was elicitated bilaterally. Over time the patient partially recovered her neurological deficit spontaneously and on the ten days a MEP for cortical stimulation was recorded bilaterally, although reduced for amplitude. After four months her recover was complete and the MEP investigations documented a normal cortical response for amplitude and latency on both sides. Discussion: Brain mechanisms underlying conversion symptoms haven’t been elucidated so far. Dysfunction at thalamus level (Sackeim et al 1979) or at prefrontal cortex (Oakley et al, 1999) have been postulated; moreover, a distorsion of sensory or motor representation has been suggested (Brown et al 2004). Our results could reveal an inhibition of motor cortex, maybe through changing in its connectivity with midline brain regions, as documented in functional MRI studies (Cojan Y et al 2009). Conclusions: Unlike commonly reported MEP abnormalities seem to be compatible with conversion disorders and could explain the pathophysiology of these conditions.