UNASSIGNED: Muscle cramps are typically regarded as benign muscle overactivity in healthy individuals, whereas spasms are linked to spasticity resulting from central motor lesions. However, their striking similarities made us hypothesize that cramping is an under-recognized and potentially misidentified aspect of spasticity.
UNASSIGNED: A systematic search on spasms and cramps in patients with Upper Motor Neuron Disorder (spinal cord injury, cerebral palsy, traumatic brain injury, and stroke) was carried out in Embase/Medline, aiming to describe the definitions, characteristics, and measures of spasms and cramps that are used in the scientific literature.
UNASSIGNED: The search identified 4,202 studies, of which 253 were reviewed: 217 studies documented only muscle spasms, 7 studies reported only cramps, and 29 encompassed both. Most studies (n = 216) lacked explicit definitions for either term. One-half omitted any description and when present, the clinical resemblance was significant. Various methods quantified cramp/spasm frequency, with self-reports being the most common approach.
UNASSIGNED: Muscle cramps and spasms probably represent related symptoms with a shared pathophysiological component. When considering future treatment strategies, it is important to recognize that part of the patient\'s spasms may be attributed to cramps.

Stiff-person syndrome (SPS) is an uncommon autoimmune neurological disorder marked by painful muscle stiffness, muscle spasms, and limb weakness. Neurological symptoms in SPS can mimic a psychogenic movement disorder in which symptoms are triggered by sudden movement and emotional distress, which might delay proper treatment. However, psychiatric symptoms are far less common, and there is limited understanding regarding the co-occurrence of psychiatric conditions. Psychiatric symptoms include nonspecific anxiety, agoraphobia, and depression, which can be triggered by sudden movement, noise, or emotional stress. This case report dives into the psychiatric manifestations seen in a patient with SPS. The case report focuses on a 42-year-old female with SPS, migraines, systemic lupus erythematosus, Sjogren\'s syndrome, and a psychiatric history of anorexia, depression, and anxiety. Her unique presentation underscored the necessity for a multidisciplinary approach to psychiatric care. The patient was evaluated and managed during her admission to the psychiatric unit for unspecified psychosis. Her course included a complicated medical evaluation for cardiovascular and neurologic symptoms and comprehensive psychiatric management. She manifested resistance to specific psychiatric medications and care strategies. She had atypical presentations, like sensory symptoms and left-sided chest pain. She exhibited paranoia and psychosis, which were managed with a combination of pharmacologic treatments, including aripiprazole. Psychotic symptoms were resolved upon discharge, with an emphasis on strict outpatient follow-up. This case report enhances our understanding of the clinical nuances associated with SPS and its intersection with psychiatric symptoms. The objective of this case report is to detail the diagnostic and therapeutic complexities of managing psychosis in a patient with SPS, along with a pre-existing complex medical and psychiatric profile, and to contribute to a deeper understanding of SPS and associated psychiatric conditions and more effective management strategies.

Muscle spasms are common in chronic spinal cord injury (SCI), posing challenges to rehabilitation and daily activities. Pharmacological management of spasms mostly targets suppression of excitatory inputs, an approach known to hinder motor recovery. To identify better targets, we investigated changes in inhibitory and excitatory synaptic inputs to motoneurons as well as motoneuron excitability in chronic SCI. We induced either a complete or incomplete SCI in adult mice of either sex and divided those with incomplete injury into low or high functional recovery groups. Their sacrocaudal spinal cords were then extracted and used to study plasticity below injury, with tissue from naive animals as a control. Electrical stimulation of the dorsal roots elicited spasm-like activity in preparations of chronic severe SCI but not in the control. To evaluate overall synaptic inhibition activated by sensory stimulation, we measured the rate-dependent depression of spinal root reflexes. We found inhibitory inputs to be impaired in chronic injury models. When synaptic inhibition was blocked pharmacologically, all preparations became clearly spastic, even the control. However, preparations with chronic injuries generated longer spasms than control. We then measured excitatory postsynaptic currents (EPSCs) in motoneurons during sensory-evoked spasms. The data showed no difference in the amplitude of EPSCs or their conductance among animal groups. Nonetheless, we found that motoneuron persistent inward currents activated by the EPSCs were increased in chronic SCI. These findings suggest that changes in motoneuron excitability and synaptic inhibition, rather than excitation, contribute to spasms and are better suited for more effective therapeutic interventions.Significance Statement Neural plasticity following spinal cord injury is crucial for recovery of motor function. Unfortunately, this process is blemished by maladaptive changes that can cause muscle spasms. Pharmacological alleviation of spasms without compromising the recovery of motor function has proven to be challenging. Here, we investigated changes in fundamental spinal mechanisms that can cause spasms post-injury. Our data suggest that the current management strategy for spasms is misdirected toward suppressing excitatory inputs, a mechanism that we found unaltered after injury, which can lead to further motor weakness. Instead, this study shows that more promising approaches might involve restoring synaptic inhibition or modulating motoneuron excitability.

Here, we present a case of a 55-year-old male, who was admitted with a spider bite, which caused swelling of the hand and painful muscle spasms along with palpitations. The patient made a complete recovery after the administration of intravenous calcium gluconate, followed by oral calcium supplements. Although no specific treatment exists in Sri Lanka for spider bites, calcium supplements can be beneficial for Sri Lankan ornamental tarantula (Poecilotheria fasciata) bites.

OBJECTIVE: To report a case of sudden onset vertical diplopia, blurred vision, and muscle spasms.
METHODS: This is a case report of a 57-year-old female who presented to the accident and emergency department with a one day history of vertical diplopia and a two week history of lower limb spasticity secondary to muscle spasms.
RESULTS: The patient had no significant medical or ocular history. Orthoptic investigation initially revealed a left inferior rectus (IR) underaction. Possible diagnoses at this point were thought to be isolated IR weakness, myasthenia gravis or skew deviation. An urgent MRI scan was arranged and blood tests were taken. MRI showed no abnormalities. Blood tests were normal, however, the acetylcholine receptor antibody serum test (ACH-R) was 0.43 nmol/L, which is at the high end of normal. At the follow-up visit, the IR weakness had deteriorated and the patient had also developed gaze-evoked nystagmus. An appointment with the neurologist and neuro-ophthalmologist was expedited. When the patient returned, she reported that her neurologist had diagnosed her with stiff-person syndrome (SPS). The patient had also developed a laterally alternating skew deviation and reported that she had undergone a course of intravenous immunoglobulin (IVIG). The patient was prescribed diazepam and gabapentin. Due to the lack of recovery, persistent diplopia and oscillopsia, monthly IVIG have been prescribed.
CONCLUSIONS: There is currently a paucity of literature relating to ophthalmic problems with SPS and how they are best treated. Previous reports have established that there is a link with myasthenia gravis, with many patients going on to develop myasthenia. Treatment of SPS is lacking large evidence-based studies. However, treatment with muscle relaxants and anticonvulsants has provided a good outcome for some. Further research is required to develop an evidence-based approach to treating the ophthalmological problems patients with SPS experience. This case report highlights the importance and value of orthoptists in investigating and monitoring patients with stiff-person syndrome.

暂无摘要。

Cutaneous reflexes were tested to examine the neuronal mechanisms contributing to muscle spasms in humans with chronic spinal cord injury (SCI). Specifically, we tested the effect of Achilles and tibialis anterior tendon vibration on the early and late components of the cutaneous reflex and reciprocal Ia inhibition in the soleus and tibialis anterior muscles in humans with chronic SCI. We found that tendon vibration reduced the amplitude of later but not earlier cutaneous reflex in the antagonist but not in the agonist muscle relative to the location of the vibration. In addition, reciprocal Ia inhibition between antagonist ankle muscles increased with tendon vibration and participants with a larger suppression of the later component of the cutaneous reflex had stronger reciprocal Ia inhibition from the antagonistic muscle. Our study is the first to provide evidence that tendon vibration attenuates late cutaneous spasm-like reflex activity, likely via reciprocal inhibitory mechanisms, and may represent a method, when properly targeted, for controlling spasms in humans with SCI.
The neuronal mechanisms contributing to the generation of involuntary muscle contractions (spasms) in humans with spinal cord injury (SCI) remain poorly understood. To address this question, we examined the effect of Achilles and tibialis anterior tendon vibration at 20, 40, 80 and 120 Hz on the amplitude of the long-polysynaptic (LPR, from reflex onset to 500 ms) and long-lasting (LLR, from 500 ms to reflex offset) cutaneous reflex evoked by medial plantar nerve stimulation in the soleus and tibialis anterior, and reciprocal Ia inhibition between these muscles, in 25 individuals with chronic SCI. We found that Achilles tendon vibration at 40 and 80 Hz, but not other frequencies, reduced the amplitude of the LLR in the tibialis anterior, but not the soleus muscle, without affecting the amplitude of the LPR. Vibratory effects were stronger at 80 than 40 Hz. Similar results were found in the soleus muscle when the tibialis anterior tendon was vibrated. Notably, tendon vibration at 80 Hz increased reciprocal Ia inhibition between antagonistic ankle muscles and vibratory-induced increases in reciprocal Ia inhibition were correlated with decreases in the LLR, suggesting that participants with a larger suppression of later cutaneous reflex activity had stronger reciprocal Ia inhibition from the antagonistic muscle. Our study is the first to provide evidence that tendon vibration suppresses late spasm-like activity in antagonist but not agonist muscles, likely via reciprocal inhibitory mechanisms, in humans with chronic SCI. We argue that targeted vibration of antagonistic tendons might help to control spasms after SCI.

BACKGROUND: Vismodegib demonstrated 60% response rates in the ERIVANCE trial. Basal cell carcinoma has various histopathologies. Their effect on response is unclear.
OBJECTIVE: The purpose of this study was to determine whether basal cell carcinoma histopathology affected vismodegib response.
METHODS: This phase 2b, single-center, prospective case series study compared the efficacy of vismodegib in infiltrative, nodular, and superficial basal cell carcinomas treated for 12 or 24 weeks in 27 patients. Patients had 1 target lesion and up to 3 nontarget lesions.
RESULTS: Twenty-seven patients were enrolled, with 65 tumors (27 target lesions/38 nontarget lesions). At 24 weeks, most basal cell carcinomas achieved histologic clearance, with positive biopsy results in 10.5% of target lesions, 30.4% of nontarget lesions, and 21.4% overall. No statistical differences were observed between histopathologic subtypes. One hundred percent of patients experienced an adverse event, 94% grade 1 or 2. The most common adverse events were dysgeusia/loss of taste (86%), muscle spasms (82%), and alopecia (71%). Clinically progressive disease during treatment was low (1.5%). Two patients had recurrence within 1 year of treatment.
CONCLUSIONS: Limitations included sample size of basal cell carcinoma histopathologic subtypes, sampling punch biopsies, and short follow-up.
CONCLUSIONS: Basal cell histopathologic subtype did not significantly affect response to vismodegib. Each subtype was observed to completely respond at 12 weeks of therapy, 24 weeks, or both.

暂无摘要。

Satoyoshi syndrome is a multisystemic rare disease of unknown etiology, although an autoimmune basis is presumed. Its main symptoms are: painful muscle spasms, diarrhea, alopecia and skeletal abnormalities. Clinical course without treatment may result in serious disability or death. A review of treatment and its response is still pending.
Sixty-four cases of Satoyoshi syndrome were published between 1967 and 2018. 47 cases described the treatment administered. Drugs used can be divided into two main groups of treatment: muscle relaxants/anticonvulsants, and corticosteroids/immunosuppressants. Dantrolene improved muscle symptoms in 13 out of 15 cases, but not any other symptoms of the disease. Other muscle relaxants or anticonvulsant drugs showed little or no effect. 28 out of 30 cases responded to a regimen that included costicosteroids. Other immunosuppressive drugs including cyclosporine, mycophenolate mofetil, azathioprine, methotrexate, tacrolimus and cyclophosphamide were used to decrease corticosteroid dose or improve efficacy. Immunoglobulin therapy was used in nine patients and four of them obtained a favorable response.
Corticosteroids was the most widely treatment employed with the best results in Satoyoshi syndrome. Further studies are needed to determine optimal dose and duration of corticosteroids as well as the role of other immunosuppressants and immunoglobulin therapy. Genetic or autoimmune markers will be useful to guide future therapies.