Isolated focal dystonia is a neurological disorder that manifests as repetitive involuntary spasms and/or aberrant postures of the affected body part. Craniocervical dystonia involves muscles of the eye, jaw, larynx, or neck. The pathophysiology is unclear, and effective therapies are limited. One mechanism for increased muscle activity in craniocervical dystonia is loss of inhibition involving the trigeminal sensory nuclear complex (TSNC). The TSNC is tightly integrated into functionally connected regions subserving sensorimotor control of the neck and face. It mediates both excitatory and inhibitory reflexes of the jaw, face, and neck. These reflexes are often aberrant in craniocervical dystonia, leading to our hypothesis that the TSNC may play a central role in these particular focal dystonias. In this review, we present a hypothetical extended brain network model that includes the TSNC in describing the pathophysiology of craniocervical dystonia. Our model suggests the TSNC may become hyperexcitable due to loss of tonic inhibition by functionally connected motor nuclei such as the motor cortex, basal ganglia, and cerebellum. Disordered sensory input from trigeminal nerve afferents, such as aberrant feedback from dystonic muscles, may continue to potentiate brainstem circuits subserving craniocervical muscle control. We suggest that potentiation of the TSNC may also contribute to disordered sensorimotor control of face and neck muscles via ascending and cortical descending projections. Better understanding of the role of the TSNC within the extended neural network contributing to the pathophysiology of craniocervical dystonia may facilitate the development of new therapies such as noninvasive brain stimulation.

Background: Endometriosis is a debilitating chronic condition that is commonly associated with chronic pelvic pain, affecting approximately 10% of women of reproductive age worldwide. The general principle of pain management in this population involves both pharmacological and surgical interventions. There is also increasing interest in the use of exercise as an alternative non-pharmacological analgesic, but adherence and accessibility to face-to-face exercise-delivery modalities are poor. This study aims to determine the immediate impact of a single session of ‘supervised’ telehealth-delivered exercise compared to ‘self-managed’ virtual reality (VR)-delivered exercise on pelvic pain associated with endometriosis. Methods: Twenty-two women experiencing pelvic pain due to endometriosis were included and randomized into three groups: (i) VR-delivered exercise group (n = 8); (ii) telehealth-delivered exercise group (n = 8); and (iii) control group (n = 6). The visual analogue scale (VAS) was used to assess the severity of pelvic pain. Results: There was no statistically significant between-group difference (p = 0.45) in the participants’ pain score following a single session of the study interventions (VR or telehealth) or the control. However, a ‘medium-to-large’ group x time interaction effect (η² = 0.10) was detected, indicating a more favorable pain score change following a single session of telehealth- (pre-post ∆: +10 ± 12 mm) and VR-delivered exercise (pre-post ∆: +9 ± 24 mm) compared to the control group (pre-post ∆: +16 ± 12 mm). Conclusions: Our study suggests that a single bout of a ‘self-managed’ VR-delivered exercise may be as efficacious as a single session of ‘supervised’ telehealth-delivered exercise in providing immediate relief from pelvic pain associated with endometriosis.

Vulvodynia is an idiopathic chronic pain disorder and a leading cause of dyspareunia, or pain associated with sexual intercourse, for women. The key pathophysiological features of vulvodynia are vaginal hyperinnervation and nociceptor sensitization. These features have been described consistently by research groups over the past 30 years, but currently there is no first-line recommended treatment that targets this pathophysiology. Instead, psychological interventions, pelvic floor physiotherapy and surgery to remove painful tissue are recommended, as these are the few interventions that have shown some benefit in clinical trials. Recurrence of vulvodynia is frequent, even after vestibulectomy and questions regarding etiology remain. Vestibular biopsies from women with vulvodynia contain increased abundance of immune cells including macrophages as well as increased numbers of nerve fibers. Macrophages have multiple roles in the induction and resolution of inflammation and their function can be broadly described as pro-inflammatory or anti-inflammatory depending on their polarization state. This state is not fixed and can alter rapidly in response to the microenvironment. Essentially, M1, or classically activated macrophages, produce pro-inflammatory cytokines and promote nociceptor sensitization and mechanical allodynia, whereas M2, or alternatively activated macrophages produce anti-inflammatory cytokines and promote functions such as wound healing. Signaling between macrophages and neurons has been shown to promote axonal sprouting and nociceptor sensitization. This mini review considers emerging evidence that macrophages may play a role in nociceptor sensitization and hyperinnervation relevant to vulvodynia and considers the implications for development of new therapeutic strategies.

Introduction: Subarachnoid hemorrhage (SAH) is associated with significant morbidity and mortality, even for patients who receive early neurointerventionist management. Areas covered: Early mechanisms of secondary brain injury precede the delayed vasospasm phase and contribute to the poor outcome. These mechanisms and their intervention are discussed, including high intracranial pressure (ICP), low cerebral perfusion pressure (CPP), acute vasospasm, disturbed cerebral autoregulation, cerebral edema, oxidative stress, seizures, microvascular damage and hyperglycemia. Erythropoietin, statins and magnesium have been particularly promising in experimental studies. Expert opinion: Multiple mechanisms, including delayed vasospasm, may contribute to cerebral ischemia and poor outcome following SAH. Treatments that simultaneously target multiple secondary injury pathways show significant potential as therapeutic agents, particularly those that attenuate vasospasm in addition to having other neuroprotective properties.