tcomes were not uniform. Within the transport and leisure domains, physical activity was inversely associated with pain-related outcomes, whereas household physical activity was positively associated with pain scores within the working sample. Fatigue-related group III/IV muscle afferent firing from agonist, antagonist or distal muscles impairs the ability to drive the elbow flexors maximally, that is, reduces voluntary activation. In the lower limb, the effect of feedback from distal muscles on the proximal knee extensors is unknown. Here, we test whether maintained group III/IV afferent feedback from the plantarflexor muscles reduces voluntary activation of the knee extensors. On 2 d, voluntary activation of the knee extensors during maximal voluntary contractions (MVCs) was assessed in 12 participants before and after a 3-min fatiguing task of the plantarflexors. On 1 d, an inflatable cuff around the calf occluded blood flow for 2 min immediately postexercise (cuff day). The other day had no occlusion (no-cuff day). Supramaximal stimulation of the femoral nerve elicited superimposed twitches during MVC of the knee extensors and resting twitches 2 to 3 s after relaxation. Pain (0-10 point scale) was reported throughout. In the 2 min after the 3-min fatiguing plantarflexor task, voluntary activation was 5.3% (SD, 7%) lower on the cuff day than on the no-cuff day (P = 0.045), and MVC force was reduced by 13% (SD, 16%) (P = 0.021). The resting twitch was similar on both days (P = 0.98). Pain rated 4.9 points higher with the cuff inflated (P = 0.001). Maintained group III/IV afferent feedback from the fatigued plantarflexor muscles reduced maximal force and voluntary activation of the unfatigued knee extensors, suggesting that afferents from the calf act centrally to inhibit the ability to drive the motoneurones of the knee extensors. Maintained group III/IV afferent feedback from the fatigued plantarflexor muscles reduced maximal force and voluntary activation of the unfatigued knee extensors, suggesting that afferents from the calf act centrally to inhibit the ability to drive the motoneurones of the knee extensors.Transcranial magnetic stimulation (TMS) is a safe and effective therapeutic modality for a rapidly expanding range of neuropsychiatric indications. Among psychiatric conditions, it is presently approved by the US Food and Drug Administration for treatment-resistant unipolar major depressive disorder and obsessive-compulsive disorder, 2 highly prevalent conditions with a considerable public health impact. There is also mounting evidence for its clinical utility in numerous other neuropsychiatric conditions. Nonetheless, many mental health providers, as well as primary care and other providers, remain unfamiliar with its clinical use. In this primer, we seek to describe in nontechnical terms how the magnetic field is applied to the brain, the unmet needs that may be remediated with TMS, the present state of evidence for clinical effectiveness, particularly in major depressive disorder, the safety profile of TMS, what patients experience during TMS, and some recent developments that serve to advance the use of this still novel intervention. TMS is poised to assume an important place in the armamentarium of interventions to better serve our patients, especially those with serious, chronic conditions with high rates of resistance to more conventional treatments. Consequently, it is essential that mental health providers gain as adequate a working knowledge of device-based interventions such as TMS as they currently have of psychopharmacological and psychosocial interventions. https://www.selleckchem.com/products/sbfi-26.html Among other potential benefits, this information should aid the process of obtaining informed consent from patients who are candidates for these treatments.Hypothyroidism is associated with a wide array of medical, neurological, and psychiatric symptoms. Severe hypothyroidism may present as myxedema coma, a medical emergency. In addition, patients may present with myxedema psychosis, a psychiatric emergency manifested as hyperactive encephalopathy, hallucinations, delusions, and suicidal ideation. In rare instances, patients may present with symptoms of mania with psychosis. We present the case of a 26-year-old woman with no known psychiatric history who presented with gradual onset of altered mental status, distractibility, decreased need for sleep, pressured speech, and religious and paranoid delusions. Her medical history was significant for a surgically absent thyroid gland and nonadherence to thyroid hormone. The patient was found to have a severely elevated level of thyroid-stimulating hormone, low level of triiodothyronine, and undetectable thyroxine. Thyroid ultrasound demonstrated a surgically absent thyroid gland. The patient's metabolic panel and random serum cortisol level were normal. Rapid plasma reagin was nonreactive, and toxin screening was negative. It was concluded that severe hypothyroidism was the cause of the patient's mania with psychotic features, given her thyroid hormone levels and lack of history of a psychiatric or substance use disorder. Thyroid hormone monitoring and treatment of hypothyroidism is necessary in all patients who have undergone surgical excision of the thyroid gland. All patients presenting with a first episode mania should be screened for thyroid dysfunction. The preferred treatment includes an atypical antipsychotic and thyroid replacement therapy. Rapid resolution of symptoms can occur with combined levothyroxine and liothyronine. Correction of hypothyroidism improves response to antipsychotics.Steroid-responsive encephalopathy associated with autoimmune thyroiditis (SREAT) is a rare phenomenon that manifests with nonspecific psychiatric and neurological signs and symptoms, an elevated serum thyroid peroxidase antibody level, and a positive treatment response to corticosteroids. Current literature describes highly varied presentations of the disease, which makes its diagnosis a challenging endeavor. The psychiatric symptoms of SREAT, in particular, are very difficult to ascribe to the correct diagnosis, as there are few laboratory or imaging modalities available to workup these manifestations. As a result, authors have attempted to compose rough guidelines that would help clinicians more easily recognize SREAT, which is important given the wide accessibility and efficacy of the main treatment for this condition. We present the case of a young woman diagnosed with SREAT who presented after a suicide attempt. Although signs and symptoms of depression, psychosis, and mania have been well described as potential manifestations of the disorder, attempted suicide as a primary presentation of SREAT has not been well captured in the current literature.